Anesthesia challenges in robotic surgery

Dr. Azam’s....
Notes in Anesthesiology
Postgraduates appearing
Updated up to December 2013, 3rd Edition for MD, DNB & DA Exams
General Anesthesia
Edited by:
Dr. Azam
Consultant Anesthesiologist
& Critical Care Specialist
!
www.drazam.com
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2
Dr Azam’s Notes in Anesthesiology 2013
Dedication
To Mohammed Shafiulla, my father, my oxygen, companion, and best friend; for

being my major pillar of support and making this vision a reality. Thank you for your
continual sacrifices with boundless love and limitless gratitude, for the sake of your
children. I owe you a debt I can never repay.
I also would like to thank my mom (Naaz Shafi), my wife (Roohi Azam), my two lovely
kids (Falaq Zohaa & Mohammed Izaan), for their support, ideas, patience, and
encouragement during the many hours of writing this book.
Finally, I would like to thank my teachers (Dr.Manjunath Jajoor & team) & Dr T. A. Patil . The
dream begins with a teacher who believes in you, who tugs and pushes and leads you to the next
plateau, sometimes poking you with a sharp stick called "truth."

A NOTE TO THE READER
Anesthesiology is an ever-changing field. Standard safety precautions must be followed, but as new research and clinical experience
broaden our knowledge, changes in treatment and drug therapy may become necessary or appropriate. Readers are advised to check the
most current product information provided by the manufacturer of each drug to be administered to verify the recommended dose, the
method and duration of administration, and contraindications.
However, in view of the possibility of human error or changes in medical sciences, neither the author nor the publisher nor any other party
who has been involved in the preparation or publication of this work warrants that the information contained herein is in every respect
accurate or complete, and they disclaim all responsibility for any errors or omissions or for the results obtained from use of the information
contained in this work. Readers are encouraged to confirm the information contained herein with other sources. It is the responsibility of the
licensed prescriber, relying on experience and knowledge of the patient, to determine dosages and the best treatment for each individual
patient. Neither the publisher nor the editor assumes any liability for any injury and/or damage to persons or property arising from this
publication.
Dr. Azam

Contents Dr Azam’s Notes in Anesthesiology 2013
1. Anesthesia For Robotic surgery or Anesthesia problems during 27. Describe clinical presentation, pathophysiology & management of
Robotic surgery - 5 Malignant Hyperthermia. - 84
2. Intraoperative hypercarbia - 8 28. What is the criteria for discharge from post anesthesia care unit -
3. Awareness in Anesthesia - 10 & 31 86
4. Causes of Perioperative Seizures and Management - 12 & 6 29. What is post operative jaundice? Describe its causes - 88
5. Difficult Airway - 15 30. What is Minimum Alveolar Concentration(MAC)? Discuss the
6. Substance abuse - 19 & 180 factors which effects the alveolar concentration of an inhalation
7. Neuroleptic Malignant Syndrome - 22 agent. - 89
8. Positional hazards under anaesthesia - 24 31. What is Monitored anesthesia care? Discuss the discharge criteria
9. Transport of the Critically ill patient - 26 for a patient after day care surgery - 90
10. Balanced Anesthesia - 28 32. Discuss measures to attenuate pressor response to laryngoscope -
11. Stages of Anesthesia - 29 91
12. Theories of Anesthesia - 30 33. What is oculo-cardiac reflex? Discuss measures to attenuate
13. Depth of Anesthesia - 33 pressor response to laryngoscope - 92
14. Pressor Response Pathway - 37 34. Write briefly on Research Ethics - 93
15. Stress Response & Anesthesia - 39 35. Meth-hemoglobinemia & anesthesiologist - 94
16. Positioning in Anesthesia - 47 36. Microcirculation in Shock - 95
17. Physiological Changes during different positions - 59 37. Clinical manifestations & Management of patient with acute
18. Cricoid Pressure ( Sellickʼs Maneuver) - 66 anaphylaxis - 97
19. Nausea & Vomiting - 67 38. Describe the techniques for anesthetizing airway for awake
20. Perioperative seizures - 70 fiberoptic laryngoscopy and intubation through nasal route in an
21. Enumerate classical Biological Warfare Agents. Describe adult with restricted mouth opening - 98
physical findings, pathogenesis and treatment of Anthrax - 71 39. American Society of anaesthesiologist(ASA) physical status
22. What is Low Flow Anesthesia? Discuss the advantages and classification - 101
disadvantage - 73 40. Activated Protein - C (APC) - 102
23. Anesthetic problem in prone position - 75 41. Phantom limb pain - 103
24. Discuss the physiological changes due to pneumoperitoneum during 42. Capillary Circulation - 104
Laparoscopic abdominal surgery. list the intraoperative 43. Uses of CO2 in Anesthesia - 107
complications. - 77 44. Nitric Oxide - 108
25. Post operative Visual loss - 79 45. Total Intravenous Anesthesia - 110
26. What are the major causes of Hypoxemia? What is Hypoxic 46. French Gauge 114
Pulmonary Vasoconstriction? How can general anesthesia 47. Temperature Monitoring - 115
worsens V/Q mismatch - 81

Contents Dr Azam’s Notes in Anesthesiology 2013
48. Malignant Hyperthermia - 120

49. Thermoregulation, Monitoring effect of anesthesia on
Thermoregulation & Vice versa - 123
50. Airway assessment & Management of Difficult Airway - 136
51. N2O, Anesthetic agents, Properties, impurities & Methods to
purify - 163
52. Organ retrieval from beating heart Donor or Anesthetic
management of a brain dead patient for multiple organ
harvesting - 169
53. Sterilization & Disinfection of anesthetic equipments in the OR
and ICU - 171
54. First Aid - 176
55. Neuroleptic Malignant Syndrome - 178
56. Rapid Airway assessment - 183

1. Anesthesia For Robotic surgery or Anesthesia problems during Robotic surgery Dr Azam’s Notes in Anesthesiology 2013
Itʼs the surgery performed by the Robot which have a specialized Anesthetic consideration:
program which governs the articulation and motion of the • Patient intubated with ET Tube in a rapid sequence manner using
specialized instrument. thiopentone and scholine/NDMR and opioids in supine position
So, there is presence of three things. • Maintenance with volatile agent and NDMR and Opioids (titrated)
• Telesurgery • Patient should not move during surgery when instruments are in the
• Telemanipulation abdomen.
• Telepresence • Abdominal cavity is insufflated with CO2 to a pressure not to exceed
• i.e., ability to perform surgery, manipulate instrument movements 20 mmHg.
and visualize robotic movements from a remote distance. • The side cast of the robot will be placed very close to the head of the
• Some of the robotic machines have three dimensional image in patient, so it provides very limited access to the airway, so airway
form of CT Scan from which it can recognize surface anatomy should be properly fixed and secured
and perform specific task. • After the robot is engaged, the patient body position cannot be
changed, if there is decrease in BP, trendlenberg position can be
done ony after disengaging the robot.
Advantages of Robotic Surgery
• The surgical team should be able to rapidly disengage the robotic
• Less pain and trauma system if an airway or anesthesia emergency arises.
• Shorter hospital stays
• It is important to have large peripheral intravenous access with 16g
• Quicker recovery cannula to overcome the decrease blood pressure situation.
• Better cosmetic result
• Precise control over surgery and instruments with minimally Cardiac Surgery:
invasive procedure
• First endoscope CAB and surgery done in 1998
• Repetitive robot motions and tasks are not prone to fatigue
• Other surgeries done by robotic system:
• Robot can filter the surgeons hand tremor and scale the
• ASD closure, mitral valve repairs, PDA ligation
movements of instruments to the level of high precision and
• Sternatomy is not required and hence surgical stress is decreased.
stability required for microsurgery.
Surgeries done by Robot and Associated Anesthetic

Problems
1. Gastrointestinal Surgeries:
• First laparoscopic cholecystectomy in 1997 by Robot
• Other surgery - splenectomy, Heller myotomy, bowel resection
pylorophy adrenalectomy and exploratory laparotomy with
antireflux surgery (Nissen fundoplication)
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Anesthesia For Robotic surgery or Anesthesia problems during Robotic surgery. Dr Azam’s Notes in Anesthesiology 2013
Mitral valve surgery (anesthetic implications) Internal mammary artery harvest and CABG
• Patients are initially evaluated by cardiac catheterization to • Single lung ventilation with DLT is required.
estimate degree of coronary artery stenosis and to assess valve • CO2 insufflation is needed (5-10 mmHg) in to left hemithorax which
function. pushes mediastinal fat pad medially and enlarge space between
• Patients may be taking antihypertensive (ACEI), anticoagulant, heart and sternum. Caution should be taken when installing thorax in
rate controlling drugs for AF and drugs for pulmonary patient who have poor left ventricular function or are hypovolemic
hypertension (CVP < 5mmHg). Patient should have their volume status augmented
• All the monitors to be attached to the patient and CVP, IA BT to before proceeding to full insufflation
be taken. • Femur femoral CPB is achieved
• Patients well preoxygentated and anasthetized with combination • Right lung is allowed to collapse and left lung ventilation is begun
of midazolam and fentanyl and isoflurane and NDME. • Ventilator adjusted to provide ETCO2 35-40 mmHg.
• Patient is intubated with DLT and proper tube position is • CO2 insufflated into right hemithorax and continued a pressure of
confirmed by bronchoscopy. 5-10 mmHg. This allows affected lung to collapse further and
• Right femoral vessels are exposed and left sided single lung provides larger visual field.
ventilation is established with FiO2I, PEEP to ventilated lung and
CPAP to non ventilated lung to decrease shunted blood (HPV) Contraindication for CABG:
• Heart is exposed with right sided mini thoracotomy and • Age > 80 years,
pericardial opening • clinical features for one lung ventilation,
• Patient is heparinized based on an ACT. • EF > 40%,
• Femoral femoral cardiopulmonary bypass is established • severe non cardiac health issues,
canulating femoral vessels. • PVD MI > 7 days,
• Anterograde and retrograde Cardioplegia cannulas are placed • calcified LAD or diffuse disuse
some surgeons prefer to cannulate the ascending are using a • Morbid obesity BMI > 32.
heart port straight shot.
• A transthoracic aortic cross clamping is passed percentage using Thoracic Surgery:
through right axilla and applied to ascending aorta. • Lung tumor (< 5cm, Stage I status) resection and esophagectomy
• Robotic arms are engaged through lateral to mini thoracotomy thoracic epidural used as postoperative pain relief.
incision and camera passes directly through thoracotomy
incision. Left atrium is entered for MVR or MCR
Contraindications for MVR:

• Severe calcified mitral annulus
• Severe pulmonary hypertension
• IHD, surgery for multiple value repairs
• Severe aortic and peripheral atherosclerosis
8

Anesthesia For Robotic surgery or Anesthesia problems during Robotic surgery. Dr Azam’s Notes in Anesthesiology 2013
Neurosurgery:
Especially spinal surgery involving cervical lumbar regions.
Urologic surgery: TURP, radical prostatectomy also done
Gynecologic SA: Tubal anastomosis after sterilization procedures
• In this pneumoperitoneum is created
• Patient will be in a modified dorsal lithitomy with
trendelenberg position.
Orthopedic SA: THR, TKR and Ophthalmic Surgery
Summary:
• Due to use of a large size robot there is a limited access
because iv access should be secured with large base cannulas
preoperatively.
• ET Tube should be properly secured and fixed.
• ECG electrodes and other monitoring equipment should properly
placed and checked.
• Be careful about DLT presence exerted by the arms of robot may
result in its kinking.
• Patient is positioned well to avoid injury to pressure points.
• Prolonged surgical hours, so drugs given should be titrated for
recovery BIS can be used.
• In case of hypotension it is difficult for the anesthetist to put a
patient into trendelenberg position.
• So to anticipate blood loss 1 CVP line and two 16g peripheral iv
lines should be put and it is important during laparoscopic
surgeries where CO2 insufflations pressure may decrease
venous return and compromise blood pressure.
• During airway emergencies which may include disconnection
bronchospasm anesthetist should make sure that surgeon
disengage the robot from the surgical site as quickly as possible.
• Adequate muscle relaxation should be given. Any coughing,
bucking or movement during surgery can prone to be disastrous.
• Anesthesiologists should also play an important role in selection
of patients for robotic surgery.
• All complications and management of OT and laparoscopic
surgery to be known by the anesthetist.
9

2.Intraoperative hypercarbia. Dr Azam’s Notes in Anesthesiology 2013
• Hypercarbia exists when PaCO2 > 45mHg which can be Effects of hypercarbia on various organ systems
detected by ABG analysis. CNS:
Causes: • For each increase of 1mmHg CO2, cerebral blood flow (CBF)
1. Increased production of CO2: Fever, dextrose containing increases 1.8ml/100gm/min.
solutions. Thyrotoxicosis sepsis, total parenteral nutrition • Increased CO2 crosses across the BBB and results in decrease in
malignant hypothermia pheochromocytoma. pH of CSF and causes vasodilation of arterials and thus decreases
2. Impairment of transportation of CO2: ICP.
• Decreased cardiac output due to hypotension/ • PaCO2 (CO2 narcosis) > 90mmHg causes reduction in seizures
hypovolemia threshold - convulsions.
• Pulmonary embolism, occlusion of vessels (V/Q
mismatch) CVS:
3. Impairment of ventilation/hypoventilation • As CO2 rises heart rate, blood pressure and cardiac output
• Anesthesia related: increases
• Faulty inspiratory and expiratory valves • At very high levels hypercarbia causes reduction in CO, blood
• Disconnection or kinked ET Tube pressure and heart rate with resultant cardiac collapse.
• Leaks in the breathing circuit • Arrhythmias associated with hypercarbia especially during
• Exhausted soda line administration of halothane.
• Low TV with low RR
• Spontaneous ventilation with low flow of gases RS:
• Respiratory muscle weakness due to • Hypercarbia causes increase in pulmonary vascular resistance and
• Muscle spinal epidural acidosis augments hypoxic pulmonary vasoconstriction.
• Peripheral nerve blocks causing phrenic nerve palsy • Maximal stimulation occurs at PaCO2 of about 100mmHg any further
• Depression of respiratory centre due to volatile anesthetics and increase in PaCO2 results in ventilator depression.
sedatives, narcotics
• Atelectasis Gastrointestinal System and Renal System:
• Pulmonary embolism • Increases hepatic and portal venous blood flow
• Pneumothorax • Retention of HCO3 in renal tubules and causes metabolic alkalosis
• Aspiration pneumonitis
• Bronchospasm Metabolic Effects:
• Surgical related • Plasma levels of epinephrine and norepinephrine increase
• Laparoscopic surgeries with CO2 insufflations • Increased leakage of K+ from cell into plasma and reuptake of K+ by
• Hipper abdominal surgeries causing pain cells is slow - Hyperkalemia
• One lung ventilation associated surgeries
• Respirator tract infections
• Bronchopneumonia, COPD, pleural effusion
10

Intraoperative hypercarbia.Continuation: Dr Azam’s Notes in Anesthesiology 2013
Management: 17. Malignant hyperthermia - dantrolene 2-10mg

1. Any pathological states or infections treated with antibiotics 18. Pulmonary edema - PPV with PEEP, inj lasix 1mg/kg
preoperatively. 19. Pneumothorax - IGG needle insertion 2nd ICS in the mid clavicular
2. Avoid dextrose containing solutions if there is increased line followed by IC drainage in 4th ICS mid axillary line.
chances of hypercarbia. 20. Pulmonary embolism - 100% O2, inotropic support avoid N2O,
3. Hypotension or hypovolemia head down position, covering of surgical site with wet gauge piece
4. Any disconnection ET Tube kink leak in breathing circuit to be if not improving hypobaric O2 therapy.
corrected. 21. Bronchospasm - 100% O2, deeper level of anesthesia,
5. Increase fresh flow gas during spontaneous ventilation • Inhaled B2 agonists (salbutamol)
according to minute volume needed. • Inj. Aminophylline 5mg/kg bolus,
6. Adjust the tidal volume and RR according to PaCO2/EICO2 • Inj. Hydrocortisone / Dexamethasone
7. Titrated doses of sedatives or narcotics or volatile agents to be
given to avoid respiratory centre depression
8. Avoid high spinal epidural anesthesia. Caution to be taken
during peripheral nerve blocks, ultrasound guided nerve blocks
can be done
9. Use neuromuscular monitoring devices to avoid excess muscle
relaxation. Give adequate dose of reversal
10. During laparoscopic surgeries CO2 insufflations pressures
should not go beyond 20mmHg.
11. Adequate intraoperative analgesia should be given.
12. Avoid increase in HPV in one lung ventilation by giving FIO2 of
1, PEEP to dependent lung and CPAP to non dependent lung
and maintain PaCO2 just less than 40mmHg.
13. If sodalime got exhausted, increase E and F and change from
close to open circuit. To decrease rebreathing.
14. If hypoventilation due to high spinal epidural diaphragm
paralysis due to nerve blocks, then should be treated with
airway support.
15. Pheochromocytoma - maintain blood pressure by NT and SNP
16. Thyroid storm - maintain Heart Rate < 100/minute esmolol
100-200μg/kg/min
11

3. Awareness in Anesthesia. Dr Azam’s Notes in Anesthesiology 2013
• Awareness is defined as the spontaneous recall of events Predisposing factors:

occurring under general anesthesia. The term spontaneous is • Faulty techniques
important since some auditory inputs occur even in sufficiently • Drug requirement varies according to age, obesity, addictions,
deep anesthesia and some meaningful images are retained. previous exposure, systemic disease etc.
• This awareness is may be due to the practice of balanced • Psychiatric illness and certain personality make ups.
anesthesia or increase in reporting. George Crile was one of the • Inadequate premedication
earliest person to report about awareness (1908) under N2O • Switching on N2O late and putting off early
anesthesia. • Keeping O2 flush on
• Early reversal
There are three types of true awareness: • Ventilators contribute by leaks and entraining air when gas flows are
• Conscious awareness without amnesia response to verbal inadequate.
command present but no memory afterwards. • A sudden powerful surgical stimulus may provoke awareness at
• Conscious awareness with amnesia sufficient depth.
• Subconscious awareness with amnesia: No response to verbal
command but retention of verbal information can still occur. Detection of Awareness:
• Requires utmost vigilance
Incidence: • Symptoms of ANS stimulation like tachycardia, hypertension,
• In general around 2% papillary dilation, increased secretions, tear and sweating.
• In obstetrics 2-17% • Movements of limbs, eyelids and swallowing
• EEG and Evoked potential monitoring (as a cerebral/function
• Many patients do not report spontaneously and clinical monitor)
assessment depends on the experience of anesthetist. • Power spectrum analysis offers bet hope for future
• Awareness leads to considerable psychiatric morbidity, • EMG of frontalis muscle is possible even at clinical neuromuscular
wakefulness in a paralysed patient can lead to the syndrome of blockade
traumatic neurosis. • Bispectral index scale (BIS) monitoring
• Repetitive nightmares, irritability, anxiety, preoccupations with
death and suicidal tendencies make their life miserable. There
are also intraoperative problems, since there are hemodynamic,
pseudomotor and hormonal responses to noxious stimuli which
are harmful.
12

Awareness in Anesthesia.Continuation: Dr Azam’s Notes in Anesthesiology 2013
Prevention of Awareness: Total iv anesthesia: Tailored doses should be given and maintained
• Adequate preparation of patient carefully monitoring anesthetic depth is not often possible with TIVA.
• Check apparatus before anesthesia During one long ventilation because of high FIO2 awareness is
• Faultless technique and usage of certain adjuvants common
• Preoperative discussion with patient and explaining the “Awareness with analgesia is regrettable and with pain is
possibility of dreams and warning about awareness in special unforgivable”
situations (wakeup tests obstetrics)
• Premedication with larazepom, hyoscine and adequate narcotics
• Proper induction dose rather than sleep dose. Ketamine is
reportd as good induction agent in this respect.
• Use N2O, volatile agents and iv agents in adequate proportions
and duration in increments etc., all contribute to avoid awareness
• Do not entirely on E-O-R technique. Relaxants are better given
as infusion
• If intubation is found difficult, add incremental anesthetic
• At the end of surgery maintain N2O till relaxants are reversed.
Special Situations:
Obstetrics:
The practice of keeping the patient under light anesthesia till
delivery to avoid neonatal depression leads to decreased
uteroplacental blood flow due to the sympathetic stimulation
caused by awareness. From induction till delivery a low dose
volatile agent (e.g., halothane 0.5%) can help to prevent
awareness; this does not cause uterine relaxations hemorrhage.
Bronchoscopy:
Apneic oxygenation and jet ventilation are associated with high
incidence of awareness.
Pediatrics:
It is faulty concept that small bodies do not require much
anesthetics.
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4. Causes of Perioperative Seizures and Management Dr Azam’s Notes in Anesthesiology 2013
Causes: Halothane, isoflurane and N2O:

• Idiopathic • Report of seizures like activity during exposure is present but no
• Hypoxia related postoperative seizures.
• Metabolic disorders • Desflurane:
• Hypoglycemia • No seizures activity
• Hypocalcemia, hypoglycemia • Seveflurane
• Uremia • There are few case reports upon emergence from anesthesia with
• Hepatic failure sevoflurane
• Fever (febrile convulsions)
• Concomitant CNS diseases INTRAVENOUS AGENTS
• Cerebrovascular diseases Methohexital:
• Brain tumors • Produces excitatory phenomena such as tremor and muscle
• Degenerative diseases movements. Does not precipitate clinical / EEG demonstrated
• Anesthetic agents seizures in generalized convulsive disorder, but epilectogenic in
•
patient with psychomotor epilepsy.
Inhalation agents
• Intravenous agents Etomidate:
• Produces involuntary myoclonic movements during induction of
INHALATION AGENTS anesthesia but occasionally persist in post operative.
Influence:
• In non epileptic these myoclonic movements occasionally associated
• It produces epileptiform EEG activity in both normal and with EEG spikes but donʼt progress to seizures.
epileptic, that is influenced by the depth of anesthesia and
• In epileptic patients seizures occurs in 30% of non epileptic patients,
PaCO2. seizures occur (patient undergoing open heart surgery)
• At a given influence concentration hyperventilation increases
seizures activity, but hypoventilation decreases seizures activity. Ketamine:
• Minimal epileptogenic concentration is approximately 1% less at • Activates epileptogenic foci and increases seizures frequency in
a PaCO2 of 20mmHg and 1% greater at PaCO2 of 60mmHg patients with a seizures disorders.
than it is at 40mmHg.
• No EEG changes/seizures in non epileptic patients.
• EEG documentation of post operative seizures activity is rare.
14

Causes of Perioperative Seizures and Management. Continuation: Dr Azam’s Notes in Anesthesiology 2013
Propofol: Mental alterations:

• Associated with excitatory activity such as movement, • Irritability, depression, psychosis, demention also associated with
myoclonus, muscle tremors during induction. heart failure, hypotension, arrhythmias, insensitivity to digitalis,
• But does not precipitate epileptic form activity in patients without impaired adrenergic action.
pre existing CNS pathology; but activate preexisting seizures foci
in patients with CNS pathology. Diagnosis:
• In epileptic patients effects of propofol are dose dependant • History and physical examination
depresses EEG activity at high doses increases spike activity at • History of duration of hypocalcemia
sedative doses. • Laboratory evaluation of renal function.
• Serum Po4 -3, Ca2+, mg2+ level noted
Opioid analgesics: • Serum PO4-3 if high à renal failure hypoparathyroidism
• Meperidine (metabolite nor pethidine) produces tremulousness, • Low or normal à Vitamin D /Mg2+ deficiency
myoclenus and seizures. • Children and ill adults cause of hypocalcemia - malabsorption,
• 1 ½ 14-21 hours, 50 effort persists into post operative in patients Osteomyelitis osteoblastic metastasis.
with reduced clearance because of renal failure or in those
receiving very large doses of meperidine for chronic pain. Treatment:
• Fentanyl and Alfentanil • Hypo Ca2+ due to low Mg2+ à repletion of Ca2+
• Produces electro corticographic seizures in patients with • High PO43- à removal of phosphate
preexisting epilepsy • Hypokalemia protects against hypo Ca2+ tetany
• Hyper K+ and hypo Mg2+ à potentiation hypo Ca2+ induced cardiac
Hypocalcemia: and neuromuscular irritability.
• Hallmark feature is ionized Ca2+ < 4mg/dl which increases
membrane irritability and tetany. Symptomatic:
• Ionized hypocalcemia (< 0.07 mmol)
Symptoms: • Treatment is (Rule of 10) - 10ml of 10% calcium gluconate over 10
• Numbness and tingling sensation involving fingers toes minutes followed by continuous infusion of calcium
circumoral region. • 0.3 – 2mg/kg/hr (3-16ml/hr of 10% calcium gluconate)
Latent hypocalcemia:
• Diagnosed by tapping on facial nerve or inflating a
sphygmomanometer to 20mmHg above SBP causes carpal
spasm (Troassessous sign)
• Frank tetany characterized by laryngospasm bronchospasm
respiratory arrest.
15

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5. Difficult Airway Dr Azam’s Notes in Anesthesiology 2013
ASA definitions: Acquired:

Difficult airway: • Infectious- croup, Ludwigʼs angina, abscess
• It is existence of clinical factors that complicate either ventilation • Arthritis
administered by face mask or intubation performed by • Rheumatoid
experienced and skilled clinicians • Enclosing spondylitis
• Airway malignancy
Difficult ventilation: • Trauma
• As the inability of a trained anesthetist to maintain the oxygen • Obesity
saturation > 90% using a face mask for ventilation and 100% • Acute burns and acromegaly
inspired oxygen, provided that the pre ventilation oxygen
saturation level was within the normal range.
Local examination:
Difficult intubation: 1. Teeth:
• Defined by the need for >3 intubation attempts or attempts at • Look for teeth, missing teeth and dentures long incisors and buck
intubation that last >10min. teeth(difficulty in insertion of soppy blade)
• Ability protrude mandibular teeth anterior maxillary is test of TMJ
AIRWAY ASSESSMENT: functioning
General examination: • Interincisor distance should be> 3cm to enable easy insertion of 2cm
flange
• Short and stumpy individuals, pregnant women and women with
large breasts have difficult intubation 2. Inside of the mouth
• Certain congenital and acquired conditions predispose to difficult • Relative tongue and pharyngeal size:
• Assessed by mullampatti test: performed with patient
airway.
Congenital: upright, head in neutral position, mouth opened widely and
tongue protrusion as far as possible patient should not
• Pierre robin syndrome- micrognathia, macroglossia, cleft palate
phonate during test
• Treaties Collin syndrome- malas and mandibular hypoplksia • Class 1- uvula, faucal pillars, soft palate seen
• Goldenharʼs syndrome- malas and mandibular hypoplksia • Class 2- faucal pillars, soft palate
• Downʼs syndrome- absent bridge of nose and macroglossia • Class 3- soft palate
• Klippel flail syndrome- congenital fusion of nose of cervical • Class 4- hard palate(Sassoon and young modification)
vertebra restricted neck movements
• Goiter- compression of trachea, deviation of larynx/trachea
17

Difficult Airway.Continuation: Dr Azam’s Notes in Anesthesiology 2013
ASSESSMENT DURING DIRECT LARYNGOSCOPY WILSONʼS SCORE:

(CORMACK AND LEHANE) • This score takes into account five risk factors, which are likely to
• Grade 1- visualization of entire laryngeal aperture constitute a difficulty in laryngoscope and intubation
• Grade 2- visualization of posterior portion of laryngeal aperture Risk factor level
• Grade 3- visualization of epiglottis only
• Grade 4- visualization of only soft palate Weight 0. <90kg
1. 90-110kg
Narrowness of palate: 2. >110kg
• A narrow palate decreases or pharyngeal volume and room for
both blade and end tracheal tube Head and neck Movement 0. Above 90 degree
1. Mandibular space length: 1. Above 90 degree
• This is space anterior to larynx and expressed as “thyromental 2. below 90 degree
distance”.
• This space will determines how easily the laryngeal axis will fall Jaw movement 0. 1G>5cm and flux>0
in line with pharyngeal axis when Atlanta- occipital joint is 1. 1G>5cm and flux=0
extended. 2. 1G>5cm and flux<0
• This distance should be at least 6cm. This would ensure that
larynx is relatively posterior to other upper airway structures. If it D. Receding mandible 0. Normal
is short , the laryngeal axis will make an acute angle with 1. Moderate
pharyngeal axis and it will more difficult for Atlanta occipital 2. Severe
extension to bring these two axes into line.
2. Neck: E. Buck teeth 0. Normal
a. Atlanta occipital joint extension: When the neck is flexed on the 1. Moderate
chest(25-35 degree) and Atlanta occipital joint is well extended 2. Severe
the oral, laryngeal and pharyngeal axis are brought into a
straight line(sniff position).
• Normal Atlanta occipital extension is 35 degree when this joint
cannot be extended attempts to do so will increase convexity of
cervical spine, thus pushing larynx anterior making laryngoscopy
view difficult.
b. Length and thickness of neck:
• A short decreases the ability to align the upper airway axis, thus
making glottis visualization difficult.
18

Difficult Airway.Continuation: Dr Azam’s Notes in Anesthesiology 2013
LEMON SCORE Four Dʼs also suggests difficult airway:-

• L= Look externally (facial trauma, large incisors, beard or 1. Dentition:- prominent upper incisors, receding chin
moustache and large tongue) 2. Distortion:- edema, blood, vomit, tumor, infection
• E= Evaluate 3-3-2 rule 3. Disproportion:- short chin to larynx distance, bull neck, large
• Incisor distance<3 finger breadths tongue, small mouth
• Hyoid/mental distance<3 finger breadths 4. Dysmobility:- TMJ and cervical spine
• Thyroid to mouth distance< 2 finger breadths
• M=Mullampatti score ≥ 3 Radiological assessment:
• O=Obstruction • Posterior mandibular depth:- distance between the alveolus
• N=Neck mobility (limited neck mobility) immediately behind 3rd molar to the lower boreler of the mandible.
This distance is related to the effective mandibular length
The five predictors of difficult bag and mask ventilation and • Effective mandibular length:-
oxygenation:- • distance from the tip of lower incisor to TM joint
• O- Obese (BMI>26(kg/m2)) • direct laryngoscopy is difficult if the effective mandibular
• B- Bearded length is 3-6 times the posterior mandibular depth
• E- Elderly (>55 years) • decrease in gap between the occiput and c1vertebrae.
• S- Snorers
• E- Edentulous
• The presence of to indicates high likelihood of difficulty in bag
and mask ventilation and oxygenation.
LM-MAP criteria:
• L=Look for external face deformities
• M=Mallampatti grading
• M=Measurements 3-3-2-1 or 1-2-3-3 fingers
• 3- fingers mouth opening
• 3- fingers hypo mental distance( 3 fingers between tip of the jaw
and beginning of the neck (under the chin))
• 2- fingers between thyroid notch and the floor of mandible(top of
neck)
• One Finger lower jaw anterior subluxation
• A=A-O extension (Atlanta- occipital)
• Normal angle between A-O extensions is 35 degree. Limited A-O
joint extension is present in spondylosis, Rh.Arthritis, halo-jacket
fixation etc
• P=Pathological obstructive conditions, edema/glottis trauma. 19

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7.Substance abuse. Dr Azam’s Notes in Anesthesiology 2013
Definition: Anesthesia:
• Self administration of a substance that is not for normal • Maintain opioid administration with a suitable opioid in a dose
medicinal purposes and that may lead to physical and/ or equivalent to addicts routine daily requirement
psychological dependence • Methadone is useful. Avoid opioid antagonists/ agonist- antagonists
• The analgesic effect of entonox is reduced
Physical dependence: • Hypotension is common, treated with fluids in first instance
• It occurs when the presence of substance is necessary for • Cross tolerance to other CNS depressants may be seen with an
normal physiological wall being and when specific symptoms increase in the requirements of anesthesia
occur if the substance is not taken • If hypotension does not respond to fluids/ vasopressors, a dose of
morphine has been reported to restore the BP
Psychological dependence: • For rehabilitated addicts avoid drugs of opioid family use inhalational
• Occurs when the substance produces a desire to repeat the agent + regional block
experience again and again • Opioid addicts are usually difficult and manipulative it may be difficult
to determine post operative pain requests for additional doses of
Tolerance: opioid are genuine or not
• It develops such that increasing doses are required to produce
the same effect Alcohol: affects all age group
• Many of the alcohol effects appear to result from an action on GABA
Associated complications with drug abuse: • Alcohol increases GABA medicated increase in chlorine conductance
• Diseases- hepatitis, AIDS • Alcohol withdrawal shows- tremor, hallucinations, agitation,
• Personality disorders confusion, tachycardia, HTN, arrhythmias, nausea, vomiting,
• Unwanted pregnancy insomnia
• Antisocial behavior • Chronic alcohol ingestion shows- cerebellar neuron loss with vitB12
• Drug over dose deficiency (wryneckʼs encephalopathy or korsakoffʼs psychosis)
Opioids:
• Produce physical dependence and also tolerance develops
• Effects seen when overdose taken- slow RR, very small
constricted pupils, impaired conscious level, dysarthria, slurred
speech later coma and death pulm.edema may complicate
overdose
• Opioid addicts have high incidence of- anemia, nutritional
deficiencies sepsis, phlebities and cellulitis, bacterial
endocarditis.
21

Substance abuse.Continuation: Dr Azam’s Notes in Anesthesiology 2013
Anesthesia: Anesthesia:-
• When there is acute intoxication delay anesthesia if possible but • Acutely intoxicated high chances of arrhythmias and MI
if it is necessary use reduced aruovnts of anesthetics and • An anesthetic requirement increases. Premedication with BZD or
sedatives barbiturates
1. Rapid sequence induction to be done because of increased • Nitrate infusion for hypertension
chance of aspiration • Avoid volatile agents which can sensitive myocardium to
2. Hypoglycemia is common repeated blood glucose levels catecholamine
monitored • Platelet count to be checked before doing regional block
• Opioid effects of sedation and respiratory depression potentiated • Ketamine, pancuronium, gallamine to be avoided
• When there is moronic alcoholism tolerance to anesthesia is
often present Barbiturates and BZD:
• Later stage hepatic dysfunction leads to slow drug metabolism • Chronic abuse causes tolerance to sedative drugs
and reduced plasma protein measurements , produces an • They are CNS depressants and hyperpolarization of postsynaptic
exaggerated responses to some agents neural membranes, so that farther excitation wont occurs
• Hepatic cirrhosis and nutritional deficiencies present • Acute ingestion of barbiturate- hypotension, hypothermia, and ataxia
• Regional techniques beneficial but alcohol induced polyneuritis slurred speech In high doses- myocardial depression coma, ARF
may present • Acute withdrawal shows-tachycardia, anxiety, tremor, hyper reflexia,
• Disaffirm treatment potentiates B2D and other sedative agents. hypotension, convulsions and cardiovascular collapse
A reduced dose may be needed Anesthesia:
• Metaraminol used vasopressors • Cross tolerance to anesthetic agent(s), needs high dose
• Avoid alcohol containing skin preparations and medications • Acute intoxication increases MAC and chronic use increases MAC
• Chronic induction of hepatic enzymes will alter pharmacy kinetics of
Cocaine: Produces profound high central stimulation mediated number of drugs like warfarin, digoxin and Phenytoin
through enhancement of adrenergic and dopaminergic pathways • Overdose needs- NG lavage, urine alkalization flumazenil for BZD
It is metabolized by plasma cholinesterase levels
Withdrawal causes:- fatigue, depression and increased appetite
Acute administration shows- increased HR, HTN, arrhythmia (VF),
coronary spasm, MI, lung damage, nasal septum atrophy,
pulm.edema, agitation, paranoid thoughts, hyperglycemia, hyper
reflexia, convulsions, asphyxia
22

Substance abuse.Continuation: Dr Azam’s Notes in Anesthesiology 2013
Amphetamine:
• Stimulates catecholamine release causing heightened
awareness and reduced need for sleep
• Appetite is suppressed, tolerance develops rapidly leading to an
escalation of dose
• Chronic amphetamine abuse leads to- daytime somnolence,
weight loss, malnutrition
• In overdose – anxiety, hyperreflexia, hyperthermia, convulsions
• Withdrawal- increased appetite, lethargy, depression
Anesthesia:
• If acutely intoxicated anesthetic requirements
• Chronic abuse reduced requirements for anesthesia
• Profound hypotension on induction, may not respond to
ephedrine Metaraminol preferred
Marijuana:
• Increasingly used for medicinal purposes ( antiemetic and in
certain chronic neurological disorders )
• Produces euphoria, drowsiness, tachycardia, postural
hypotension
• Long term use causes deposits in lungs
Anesthesia:
• Reduced dose of anesthetic agent may be required delayed
recovery and respiration depression are possible.
23

8. Neuroleptic Malignant Syndrome. Dr Azam’s Notes in Anesthesiology 2013
• NMS caused either by treatment with dopamine receptor Death from NMS due to:-
antagonists or by withdrawal of dopamine receptor agonist. • Respiratory failure (comment)
• Renal failure secondary to myoglobinuria
Pathogenesis • Cardiac arrest.
1. Central mechanism
2. Excitatory aminoacids Criteria for diagnosis:-
3. Peripheral mechanism Major:
1. Fever
2. Rigidity
1. Central mechanism: 3. Raised serum creatinine kinase
There is acute dopaminergic.
• Transmission block in Minor:
• Nigrostriatum à produces rigidity. 1. Tachycardia
• Hypothalamus à produces hyperthermia. 2. Tachypnea
• Corticolimbic system à produces altered mental state. 3. Increased blood pressure
4. Altered consciousness
2. Excitatory aminoacids: 5. Sweating
• Relative glutaminergi excess transmission is as consequence of
dopamine block. Complications:
1. Respiratory: Secondary infection aspiration pneumonia
3. Peripheral mechanism: 2. Central Venous System: Arrhythmia pulmonary embolism.
• Not clear, may be some intracellular association between MH 3. Muskuloskeletal:-
and NMS leads to disease process. • Peripheral neuropathy
• Rhabdomyolysis (myoglobinuria)
Clinical Features and diagnosis:-
• It develops over a period of 24-72hours/ following exposure to Differential diagnosis:
neuroleptic agents or sometimes several days to months and 1. NMS versus fatal catatonia: Rigidity is intermittent in catatonia and
may even follow a low dose of neuroleptic agent. it demonstrates severe psychotic excitement in early stages.
• It will continue upto 10 days even after stopping triggering agent. 2. MH versus NMS:
• NMS demonstrates:-
1. Slow in onset
2. Rigidity of central origin
3. Latency of effect of dantrolene
4. Lack of familial tendency(MH is autosomal dominant)
5. Uneventful anesthesia with triggering agents
• Drugs 24
of abuse: ethanol and sedative, hypnotic withdrawal cocaine
and amphetamine intoxication MAO overdoses.
Dr Azam’s Notes in Anesthesiology 2013 • Neuroleptic heat stroke: here flaccid muscle tone will be present.
Neuroleptic Malignant Syndrome.Continuation: Dr Azam’s Notes in Anesthesiology 2013
MANAGEMENT Treatment:
I. Nonspecific therapy 1. Access rapidly airway, breathing and circulation if not maintaining
II. Specific therapy hemodynamic stability incubate and put the pt on ventilator
2. Stop further beta adrenergic drugs.
I. Nonspecific therapy: 3. Monitor and correct blood glucose level, electrolytes and acid base
• Basic resuscitation measures balance.
• Withdrawal of triggering agents 4. If arrhythmias present pharmacological cardio version done by
• Cooling using ant arrhythmic drugs or by electric cardio version if
hemodynamic unstable.
5. If hypotension present treat with adequate fluids.
II. Specific therapy: 6. If hypertension present use vasodilators(NTG/SNP) or ion dilators
• Bromocriptine- helpful in pts with hepatic dysfunction (phosphodiesterase inhibitors)
• Dantrolene- reduces death rate below 9% 7. Control HR and BP with beta blockers(propranolol)
• Avoid anticholinergic agents(when rigidity ass with pyrexia)

• Glutamate antagonists
• Amantadine acts on NMDA type
• Glutamate receptors: These drugs act on NMDA type
glutamate receptors.
• Amantadine
• Mimantine
• Restore balance between dopaminergic and glutaminergic
system
• Exhibit hypothermic and central muscle relaxant properties
Anesthesia:
• Anesthetic management is important during pts posted for ECT.
• The technique should not increase muscle disorder or produce
complications of NMS.
• Avoid scoline in presence of active muscle disease. It may
release k+ of course rhabdomyolysis.
• Propofol is best avoided in ECT because it shortens duration of
seizures and increase frequency of treatment.
25

9. Positional hazards under anaesthesia. Dr Azam’s Notes in Anesthesiology 2013
commonest causes of complications: Lithotomy position:-

• Accidental trauma a. Straight leg sling systems will damage sciatic and femoral nerve.
• External pressure • Common personal nerve trapped against head of the fibula
• Extreme passive movement • Saphenous nerve trapped against supporting posts
• Physiological tress pass • Extreme flexion of thighs will kink femoral nerve around inguinal
• Failure support the head adequately during shifting of pt from ligament
trolley to operation theatre tableàwhiplash injury to neck b. Prolonged elevation of lower limbs with or without superadded
• Failure to apply brakes on transfer trolley or to raise side guard- pressure on calf muscles from leg supports will result in reduction iv
rails on narrow transfer trolley àallows the pt to fall. perfusion pressure and lends to lower limbs compartment syndrome.
• Intra operative movement may cause eyes to be c. Ligamentous damage of hip and knee joints occur if parinive
damagedàblindness. movement exceeds the normal active range.
• Fingers can get amputated by hinged sections of operation • Sacroiliac joint strains is a risk if the legs are not raised
theatre table. symmetrically.
• Skin abrasions because of careless sliding of patients d. Extent of surgically induced hypovolemia may be marked by entrap
àpressure sores auto transfusion from the legs, which is lost when the pt is returned
• Accidental traction on iv lines, urine catheters and drainage to supine.
tubeà internal damage • Increased intra abdominal pressure enhances the possibility of
• Orthopaedic traction table cause à genital and pudendal nerve gastric regurgitation- GA should never be induced in this position.
tracema. Lateral position:
Positional hazards during supine position • Stability of the position is essential. Which is best achieved through
use of an evacuatable mattress
• Pressure necrosis of skin and mucosa
• Alopecia in occipital region • Skin covering the iliac crest undergo pressure necrosis
• Sacral thermal damage therefore use of circulating water • Underlying sciatic nerve get damaged in emaciated pts.
warmers • Underlying common peroneal nerve damaged around neck of fibula.
• Heels get damaged in diabetic patients • Head and neck damaged during positioning.
• LMA may cause mucosal compression and resultant ischaemia • Accidental ETT extubation can occur.
• Supra orbital nerve compressed because of airway tubing • Deltoid muscle crush syndrome can occur if support is not kept
between lateral thorax and OT table
• Brachial plexus neuroproxia because of faulty arm board
positioning • Chest wall movements are restricted – V/G mismatch
• Radial nerve trapped against a head-screen support
• Ulnas nerve get compressed against edge of the matters
26

Positional hazards under anaesthesia.Continuation: Dr Azam’s Notes in Anesthesiology 2013
Sitting position:
• Venous air embolism
• Postural hypotension
• Quadriplegia following head and neck flexion and cervical
• Spine rotation – decreased blood flow to spinal card
• Brachial plexus damage because if arms are not properly
supported
Prone position:
• Restricted chest wall movement and diaphragmatic excursions
because of free abdominal movement and increased intra-
abdominal pressure
• Mohammedan prayer position leads to lower limb congestion
and cause myoglobinuria- acute renal failure
• Increased intraabdominal pressure and occlusion of one femoral
neurovascular bundle because of improper positioning, back
pressure will be transmitted to epidural veins may cause
troublesome surgical hemorrhage
• Pressure necrosis of weight bearing skin areas
• Pts with previous CABG surgery are at risk of graft occlusion
• Neurapraxia both brachial and auxiliary nerve if arms are
positioned above the head
• Blindness from external orbital pressure
• Sudden hidden intra peritoneal hemorrhage due to damage to
major vessels – leads to acute hypovolemic shock.
• Bowel may get perforated in prone position
• ET tube may get kinked/dislodged/ endobronchial intubation may
occurs
• Obesity and respiratory disease will hamper adequacy of
ventilation
• Suction effect of pendulous abdomen can potentiate negative
venous pressure within the epidural veins during prone position-
venous gas embolism.
27

10. Transport of the Critically ill patient. Dr Azam’s Notes in Anesthesiology 2013
Reason for transport of patient is Aeromedical transfer:

1. Lack of functioning ICU bed • Helicopter fly at relatively low attitude and because avoid some
2. Referral for specialist services problems of aero-plane.
• High attitude decrease PaO2 (i.e., 75mmHg at 1500m), so high FiO2
Principles of safe transfer: • Decreased barometric pressure loads expansion of air filled cavities
• Staff experienced in ICU and transfer (specialist transport teams) so, NGT chest drain needed.
• Use of appropriate equipment, vehicle, extensive monitoring, • Pressurizing cabin pressure to sea level can decrease those
careful stabilization, continuing reassessment, direct handover problems but fuel cost increases
documentation, audit • Air ETT cuff to be replaced with saline.
• Risk of transfer should be weighed against the potential benefits
of treatment at the receiving unit before any transfer. Specific Consideration:
• Vibration leads to failure and in accuracy of NIBP so invasive blood
Danger of transfer: pressure monitoring used.
• Deranged physiology worsened by movement – cardiovascular • Access to the patient may be limited
instability hypoxia, hypotension • Acceleration deceleration lead to CV instability
• Cramped conditions, isolation, temperature and pressure • Hypothermia is a risk factor in children because core temperature
changes monitored. Warming mats, hats, warm fluids to be used.
• Vehicular crashes • To line to be secured before transferring
• Patient should be fully stabilized with invasive monitoring
The transfer vehicle: • Blood tests, radiographs and CT taken prior to transfer
• There should be adequate space, light, gases, electricity and • Adequate full gas cylinders and infusion pumps with good battery life
communications to be taken.
• Mode: Consider urgency, mobilization time, geography, weather,
traffic and costs Minimum monitoring standards for transfers:
• Consider air if over, 150 miles (remember PaO2 may decrease • Continues ECG
at attitude, so FiO2 to be high expanding air space requiring • NIBP / IABP is must
naso orogastric tube, temperature, noise and vibration. • SaO2
• EtCO2
• Core and peripheral temperature
• Presence appropriately trained staff (at least one ICU consultant)
28

Transport of the Critically ill patient.Continuation: Dr Azam’s Notes in Anesthesiology 2013
Check List of Preparation:

• All emergency airway equipments (ETT, LMA, laryngoscopes,
airways, face masks, tracheostomy tubes, bougie) and
emergency drugs to be kept (adrenaline, atropine,
hydrocortisone, NA, amiodarone, lasix, nebulizers, lignocaine,
CA++, Naloxane, Metoprolol etc.,)
• Sedation / muscle relaxants (propofol,
midazolam,scoline,vecuronium, rocuronium, atracurium)
• Paediatric equipments: Masks, iv cannulae, ETT, intrasseous
needle laryngoscopes, stylets, 10% Dextrose solution.
• Iv fluids and iv set, syringes, needles, cannula, iv dressing and
tape
• Suction apparatus
• All the monitors, infusion pumps, gas cylinders, inotropes
Preparation of patient:
• Stabilize if necessary intubate and ventilate
• Chest drains not to be clamped
• Long bones fracture are splinted
• Transfer document to be handed over to the receiving medical
personnel.
29

11. Balanced Anesthesia. Dr Azam’s Notes in Anesthesiology 2013
The concept of using several agents each with a specific purpose was proposed and
applied by CRILE between 1900 and 1911.
• The term balanced anesthesia was first coined by LUNDY in 1926.
• Balanced anesthesia is a descriptive terms, and may be defined as anesthesia
produced by a combination of drugs and technique, each with a primary purpose and
specific effect but with overlapping secondary effects. The following is implied.
• Surgical anesthetic conditions are produced by several agents often administered by
different routes, the amount of any one agent used is diminished if the administrate
does not need to rely for all effects on any one drug (deep levels of general
anesthesia); the drugs may be detoxified and excreted in several different ways and
thus not burden any one later. Thus components of general anesthesia, as noted by
Wood Bridge, one each achieved by a specific drug, and these drugs may interact
and be interdependent in part;
• Mental block by sedatives, hypnotics, and small conc. of anesthetic agents.
• Sensory blocks: Including pain relief, by large doses of sedative hypnotics,
large doses of opiates and low concentrations of potent volatile inhalation
anesthetics, Nitrous oxide analgesia
• Relaxation by peripheral relaxants and secondarily by the anesthetic agents.
• Autonomic block by some anesthetic and sympathetic blocking agents.
• An ideal agents would be one which achieves all these objectives but with
limited toxicity.
The techniques of administration of widely accepted anesthetic agents in combination
fall into four main categories.
1. General anesthesia administered by combinations of inhalation, parenteral and
rectal anesthesia.
2. General anesthesia combined with regional anesthesia, including spinal anesthesia.
3. General anesthesia combined with relaxants
4. General anesthesia combined with neuroleptics and relaxants.
30

12.Stages of Anesthesia. Dr Azam’s Notes in Anesthesiology 2013
• General anesthesia cause an irregularly descending depression STAGES OF ANALGESIA:

of CNS i.e., The higher functions are lost first and progressively • Starts from beginning of anesthetic inhalation and lasts upto the loss
lower areas of the brain are involved, but in the spinal cord of consciousness. Pain is progressively abolished during this stage
lower segments are affected some what earlier than the higher patient remains conscious, can hear and see, and feels a dream like
segments. state. Reflexes and respiration remains normal.
GUEDEL described four stages with ether anesthesia.
They are: STAGE OF DELIRIUM:
I. Stage of analgesia • From loss of consciousness to beginning of regular respiration.
II. Stage of delirium Apparent excitement is seen, patient may shout, struggle and hold
III. Surgical anesthesia his breath, muscle tone increases, jaws are tightly closed, breathing
IV. Medullary paralysis. is jerky vomiting, involuntary maturation or defecation may occur. HR
and BP may rise and pupils dilate due to sympathetic stimulation.
STAGES OF ANALGESIA: • No stimulus should be applied or operative procedure carried out
• Starts from beginning of anesthetic inhalation and lasts upto the during this stage. This stage can be cut short by rapid induction.
loss of consciousness. Pain is progressively abolished during STAGE OF ANESTHESIA:
this stage patient remains conscious, can hear and see, and From onset of regular respiration to cessation of spontaneous
feels a dream like state. Reflexes and respiration remains breathing.
normal. Plane 1: Rolling eyeballs. This plane ends when eyes become fixed.
Plane 2: Loss of corneal and laryngeal reflexes.
Plane 3: Pupil starts dilating and light reflex is lost.
Plane 4: Intercostal paralysis. Shallow abdominal Respiration, dilated
pupil
Medullary paralysis
Cessation of breathing to failure of circulation and DEATH.
31

13. Theories of Anesthesia. Dr Azam’s Notes in Anesthesiology 2013
Substances capable of producing GA are remarkable • Altered membrane structure could produce anesthesia in number of
• Inert elements – xenon ways.
• Simple inorganic compounds – N2O • Electrolyte permeability could be changed by disrupting ion
• Halogenated hydrocarbons – Halothane channels
• Complex organic compounds – barbiturates
C. GA can be due to change in any of these.
A. Various Agents produce anesthesia by different methods.
1) Agents specific theory.
2) Various sites of action are:
• Reticular activating system
• Cerebral cortex
• Cuneate nucleus
• Olfactory cortex
• Hippocampus
3) Unitary hypothesis:
• All inhalational agents share a common mechanism of action at
molecular level. Potentiation of inhalational agents depend on
lipid solubility (Meyer-overton rule). This states that anesthesia
results from molecules dissolving at specific hydrophobic sites.
Meyer overton theory: Alteration in the structure of nerve

covering results in anesthesia.
4) Critical volume hypothesis:
• Neuronal membranes contain a multitude of hydrophobic sites in
their phospholipids bi-layer. Anesthetic binding to these sites
could expand the bi-layer beyond a critical amount, altering
membrane function. As per this reversal of anesthesia is by
increased pressure. As hydrostatic pressure is elevated
resistance to anesthetic agent is increased by displacing the
number of molecules from membrane
B. Disturbances in membrane form suggest 2 theories:
1. Fluidization theory of anesthesia
2. Lateral phase separation theory.
32

14. Awareness Under Anesthesia. Dr Azam’s Notes in Anesthesiology 2013
Definition: 10. Oxygen by-pass being accidentally left in the switched on position.
The ability to recall events occurring during GA. 11. Entrainment of gas through faulty connections.
4 levels of awareness have been described. 12. Failure on the part of the anesthesiologists to understand
I. Conscious awareness without amnesia. functioning of anesthetic breathing systems.
II. Conscious awareness with amnesia
III. Subconscious awareness with amnesia Fundamental clinical dilemma is whether awareness occurs during
IV. No awareness otherwise adequate G.A. or whether it is merely the consequence of
• Stage I is normal wakefulness inadequate or “too light” anesthesia. This basic problem is due to the
• Stage III is associated with implicit expression of memory when lack of definitive parameters for monitoring the depth when muscle
the patient has no voluntary recall of events. relaxants preclude movement as a clinical sign.
• Awareness does not occur during adequately controlled depth.
Incidence: • Subconscious awareness with amnesia can be demonstrated by
testing for a behavioral response to an intra-operative suggestion.
• 0.2-1.6%
8% for cesarean section • Positive verbal suggestions presented intra operatively and subject
•
to implicit recall may reduce the duration of postoperative recovery.
• Upto 45% during accident and emergency surgery.
Stage I can be converted to stage II by use of benzodiazepines. • Postoperative visits by the anesthetist are recommended as part of a
•
good clinical practice.
But, removing the memory of awareness is not the same as
preventing awareness. • Relatively few incidences of awareness have been reported using
TIVA without N2O.
• Implicit recall of events may still be present even after the
Prevention of awareness:
retrograde disruption of explicit memory with an amnesic agent.
The target of anesthetists should be prevention of awareness, to avoid
Causes:
medico-legal claims.
1. Administration of low doses of anesthetic agents.
2. E.g. In caesarean section. In moribund patients. • Stage I may be converted to stage II with benzodiazepines.
3. Delay in reaching adequate blood levels of inhalation agents. • Morphine and diazepam combination cause both anterograde and
retrograde amnesia.
4. E.g.: Nitrogen washout in low flow breathing system.
5. Reliance on IV agents given by bolus without inhalation agents, • Maintenance of an adequate depth of anesthesia.
leading to awareness between doses. • Adequate checking of equipment.
6. E.g.: During bronchoscope • Absolute ban on leaving the patients unattended during surgery.
Detection:
7. Repeated attempts at difficult intubation
8. Equipment failure or malfunction • Using clinical signs of depth of anesthesia is next to impossible.
9. Dilution of inhaled anesthetic gas mixture caused by • Vital signs are both insensitive and non-specific of detection of
awareness
undetected emptying of N2O cylinder.
33

Awareness Under Anesthesia.Continuation: Dr Azam’s Notes in Anesthesiology 2013
What should be done when awareness is reported?

• Most patients who have experienced awareness under GA report
their suffering during the first few postoperative days.
• Many patients do not wish to discuss experience for fear of being
labeled insane.
• Personally visit and talk to his / her patient in the postoperative
period and give a sympathetic hearing / a convincing explanation
and appropriate counseling can help patient from awareness
under anesthesia.
• One need to maintain good anesthesia records to defend in the
event of litigation.
34

15. Depth of Anesthesia. Dr Azam’s Notes in Anesthesiology 2013
History: 1. Autonomic changes:

• Progressive loss of consciousness was first staged by SNOW, • Sudden changes in BP and / or heart rate may incline to lightening
into 5 stages of narcotics. levels that result in awareness.
• GUEDEL, subsequently refined it. PSRT score system for systemic evaluation of the autonomic signs of
• Staging the depth is not the same as staging potential levels of light anesthesia:
accursedness. INDEX CONDITION SCORE
Guedelʼs classification: Systolic pressure (mm Hg) Less than control—15 0
I. Stage I à Stage of Analgesia Less than control—30 1
II. Stage II à Stage of Excitement More than control—30 2
III. Stage III à Stage of Surgical anesthesia Heart rate ( beats/min ) Less than control—15 0
1) Plane I à From automatic respiration or regular breathing
Less than control—15 1
to cessation of eye movement.
More than control—30 2
2) Plane II à Commencement of inter-costal muscle paralysis.
3) Plane III à Complete intercostal paralysis Sweating Nil 0
4) Plane IV à Diaphragmatic paralysis Skin moist to touch 1
IV. Stage IV à Stage of over dosage, ranging from onset of Visible beads of sweat 2
diaphragmatic paralysis to apnea and death. Tears No excess of tears in open eye 0
• Excess of tears in open eye 1
• Muscle relaxants removed the need for deep anesthesia to Tears overflow in open eye 2
reduce muscle tone.
1. Pupil Diameter:
Measurement of Anesthetic Depth: is by 2 main means.
• Pupil dilates after initial contraction with progressively deeper
• Subjective measurement. anesthesia.
• Objective measurement. • The dilatation is due to
SUBJECTIVE MEASUREMENT: 1) Changing level of catecholamine
Rely on the opinion and experience of the anesthetist, is by 2) Direct effect on the CNS.
observing 3 parameters
• Some anesthetics do not give the same change in catecholamine
• Autonomic changes and so pupil diameter does not change reliably with depth.
• Papillary diameter • E.g. Opioids induced meiosis.
• Isolated forearm technique. • Atropine / Hyoscine induced mydriasis.
• Presence of an unresponsive pupil (not reacting to light) does not
Type to enter text necessarily mean that the patient is deeply anaesthetized.
35

Depth of Anesthesia.Continuation: Dr Azam’s Notes in Anesthesiology 2013
2. Isolated forearm technique (IFT):

METHODS:
• Is a simple method of preventing the suppression of movement Frontalis Electromyogram (FEMG):
by competitive neuromuscular blockade. A tourniquet is placed
Frontalis muscle is the one muscle that is less affected by
on an arm. The arm is free to move during surgery. Purposeful
neuromuscular blockade.
movements in response to instruction indicate excessively light
A stick on electrode positioned over the frontalis can record the FEMG.
anesthesia.
The level of FEMG activity declines during anesthesia and rises to pre-
• Ischemia is prevented by periodically releasing the tourniquet, induction levels at recovery.
usually before topping up the level of neuromuscular blockade.
Lower Oesophageal Contractility (LOC):
Disadvantages:
• Oesophagus has striated muscles in the upper portion and smooth
1. Movements during surgery may make the surgeon
muscle in the lower.
uncomfortable.
• During wakefulness esophagus exhibits regular spontaneous
2. Levels of anesthesia needed to prevent movements in all
contractions (SLOC) of several types, under the control of autonomic
patients during IFT higher than those routinely used since the
nervous system. During anesthesia, these contractions reduce in
advent of relaxants.
both frequency and amplitude.
3. IFT does not act as an indicator of subsequent recall.
• A probe inserted into esophagus measures SLOC and also has an
inflatable cuff with provoke contractions of the lower esophagus.
3. OBJECTIVE MEASUREMENT:
• The provoked contractions (PLOC) may continue as anesthesia is
An IDEAL objective monitor of depth should meet the following
deepened, even when the SLOC have ceased.
requirement.
1. It should indicate the stage during light anesthesia preceding
EEG and DERIVED INDICES:
conscious awareness.
EEG:
2. It should closely reflect changing concentrations of anesthetic
• Excitatory past synaptic potentials cause an upward deflection in the
agents.
scalp-recorded EEG if the synapse is in the superficial layers of
3. It should be sensitive to stimuli of different modalities
cortex but cause a downward deflection if originating in deeper
especially surgical simulation.
layers.
4. It should have a high temporal resolution.
• (Vice versa with inhibitory potentials)
5. It should be able to stage the depth of anesthesia.
• EEG varies from periods of intense, high-frequency fluctuations to an
6. It should be easy to use and easy to set up in a short time.
almost flat line.
7. It should work for all modern anesthetic agents
Waves are:
8. Economical
• α à 8-13 Hz
• β à 13.30 Hz % %
• δ à 0.5 – 4.5 Hz
• θ → 4.7 Hz%
36

• Wakefulness with eyes closed is associated with higher levels of

α in contrast to lower levels of δ. BIS SCORE CLINICAL ENDPOINT
• Sleep is associated with more low frequency activity, including δ 100 Awake sedated
and θ waves. 70 Light hypnotic effect—very low possibility of recall
Spectral Analyses:
60 Moderate hypnotic effect—unconscious. General
• Electronic filtering of the EEG, with the integrated amplitude of
the EEG waveform indicates the level of brain activity. Anesthesia
• E.g.: CFM à Cerebral function monitor. 40 Deep hypnotic effect.
• CFAM à Cerebral frequency analyzing monitor. 0 EEG suppression.
• CFM, gives a single tracing of integrated EEG amplitude,
increased levels of cerebral activity appearing as broadening of Evoked Potentials:
the trace, ranging from 5-18 μV peak to peak amplitude. • Show the response of more localized areas of the brainstem,
• CFAM filters the EEG into five frequency bands and adds one midbrain and cerebral cortex to specific stimuli.
extra trace demonstrating period of burst suppression, as Auditory Evoked Potentates (AEP):
encountered in deep anesthesia. • Halothane, isoflurane and enflurane increase the latencies of the
• Microcomputers using algorithms filter the EEG waveform into brainstem AEP waves III and IV as the anesthesia is deepened
its spectral components. (same response with IV barbiturate)
• Most common algorithm is FFT à Fast Fourier Transform. • Increasing the depth increases the latency and decreases the
• By squaring the results of the FFT, the power spectrum of the amplitude of the early cortical AEP components Pa and Nb.
EEG may be obtained, which when plotted as power against • Surgical stimulation affects the amplitude of the early cortical wave
frequency gives a frequency distribution of the EEG. Nb during light halothane anesthesia.
• The individual distributions can be considered as ʻtime- slicesʼ
and joined together into a 3-dimensional plot, most frequently 2 main problems with AEP are:
termed is compressed Spectral Array (CSA). 1. Significant changes in evoked potentials during mild hypoglycemia.
• Characteristic changes in CSA during anesthesia have been 2. Its applicability in patient with hearing defects.
documented. Deeper anesthesia results in low frequency 3. Used in acoustic neuroma excision to monitor 8th C.N in posterior
activity, shifting the peaks of CSA from higher frequencies. cranial fossa
• At recovery, there is a progressive increase in the amount of
high frequency activity with a corresponding decrease in low Visual Evoked Potentials (VEP):
frequency activity. • Commonly generated by the presentation of bright flashes through
• Though CSA is a considerably more compact than raw EEG, it the closed eyelid using light emitting diodes mounted with goggles.
is still a complex display that takes time to comprehend and • 3 components of VEP have been studied P60, N70 and P100.
changes within it are difficult to quantify. • Origin of P100 is primary visual cortex. Earlier components from
lateral geniculate nucleus.
37

Somatosensory Evoked Potentials (SEP):

• Takes 80 seconds to calculate.
• Typical recording sites are
• 5th cervical vertebra.
• Scalp above the contra-lateral somatosensory cortex.
Recent Trends:
1. Position emission tomography (PET) has been used in a
limited number of studies to monitor brain function during
anesthesia.
2. Ultrasensitive superconducting quantum interference devices
(SQUIDS) have been used to provide a new insight into
cerebral function by non-invasively measuring not only
structures as resolved with more conventional MRI but also
functional activity in the brain
3. Second messenger function
4. Neurotransmitter receptor
5. GABA inhibition.
38

16. Pressor Response Pathway. Dr Azam’s Notes in Anesthesiology 2013
I. Reflex pathways of pressor response: Efferent pathway:"

Parts of the airway Sensory innervations 1) Hypothalamo spinal tracts.
• Anterior 2/3rd of tongue • (Trigeminal N) Lingual Nerve 2) Efferent sympathetic nerves
Posterior 1/3 rd of tongue 3) Efferent sympathetic nerves to adrenal medulla.
• • Glossopharyngeal N (IX)
• Oropharynx • Glossopharyngeal N (IX)
• Posterior pharynx and • Plexus formed by IX, X and XI Effector sites:
hypopharynx Nerves • Peripheral vessels
• Epiglottis • IX, N (Glossopharyngeal) • Myocardium, conduction pathways.
• Anterior surface • Internal laryngeal N. (SLN of
• Posterior surface vagus) Pressor Pathway:
! !"#$%#&'$(")('$*+&(%' ,-./01#&#2*3''
• Periepiglottic tissue, valleculla, •
pyriform fossa upto vocal •
• Inferior surface of true vocal • Internal laryngeal N 789',-./01#&#2/'
3.%$#&'0"#+03''
cords and trachea • Recurrent laryngeal nerve X
:*."#5&/ 4%0*%0#"-'5&#$6''
00%+'B<'CD<'
!"#$%&'( :.%$#&'+/"6'' 789'(@@("($0'
D<'DC'
&")"*+%&(( 3-2.#01(0%+'$(")(3''
II. Types of reflexes:
!;,<'!=:,<'!>:,'!' 88' 88' 88'
1. Supraglottic reflex: by stimulation of supraglottic structures. It C$@"#5&/00%+'
D' ."/&#+0%$'
occurs during laryngoscopy without intubation. ?"0("%/&(3''' ,(#"0'''' ?6"($#&3'''''
2. Infraglottic reflex: due to stimulation of infraglottic sensory area. 88' 88'
It occurs during intubation along with supraglottic reflex. !?!=,'
III. Components of reflex pathway:
Receptors: Sensory receptors of supra and infraglottic mucosa. !'A/"'?6"($#&%$(''
!'?6"($#&%$(''
?6"($#&3' !,E' '
Afferents: V, IX, X and XI cranial nerves. !F4'
!'4("%.1("#&')#3+*&#"'
"(3%30#$+('#""1-012%#3''
Centers:% !'!/"0%3/&''
1) Cranial nerve nuclei
2) Hypothalamus – sympathetic centers.
Efferent pathway:"
1) Hypothalamo spinal tracts.
2) Efferent sympathetic nerves
3) Efferent sympathetic nerves to adrenal medulla.
39

Pressor Response Pathway.Continuation: Dr Azam’s Notes in Anesthesiology 2013
Essentially there are 3 large groups to attenuate these reflexes:

1. Block of the sensory peripheral receptors and the afferent input.
2. Achieved by topical application infiltration of nerves e.g. 4% and 10% lidocaine, spray.
3. Block of the central mechanism of sensory input
4. Achieved by narcotics such as fentanyl, morphine and Droperidol.
5. Block of the efferent pathway and effector receptor
6. IV lignocaine, ß.blockers etc.
Attenuation of Pressor response pathway.

Prevention:
• A large number of drugs and techniques have been tried to obtund the hyperactive
sympatho-adrenal pressor response to laryngoscopy and intubation but none has been
accepted as universal technique due to the complexity and lack of total efficacy of each
method.
Some methods are:
1. Duration of laryngoscopy should be as short as possible ideally < 15 seconds.
2. Deepening the level of anesthesia with volatile agent for 5-10 min.
3. Use of IV propofol prior to laryngoscopy
4. Use of local anesthetic spray (or) (gargles) 3 minutes prior to intubation with 4% to 10%
lidocaine.
5. I.V. lidocaine 1.5 mg / kg IV / intratratheacly.
6. Low dose opioids fentanyl 2.5 to 5 μg / kg.
6.1. Sufentanil 0.25 – 0.5 μg/kg
6.2. Refimentanil 0.5 – 1 μg/kg
6.3. Alfentanil 15-25 μg/kg
7. β adrenergic blockade %Esmolol 0.5 – 1.5 mg/kg
7.1. Propronolol 1-3 mg IV
7.2. Labetalol 5-20 mg IV
7.3. Droperidol
8. S/L Nifidepine prior to induction
9. ACE inhibitors 45 min prior to intubation
10. Clonidine 4 μg/kg premedicate 1 ½ hr before induction.
11. SNP infusion 1-2 μg/kg issues prior to intubation
12. IV hydralazine / topical / transdermal NTG
40

17. Stress Response & Anesthesia. Dr Azam’s Notes in Anesthesiology 2013
Stress response The net effect of stress response “The Neuro endocrinal outflow”
• Thy body reacts to external stimuli, ranging from minor to • Cardiovascular changes: Rise in-cardiac output, heart rate, blood
massive insult both locally and generally. The general response pressure, increased myocardial contractility, increase oxygen
is in form of wide spread endocrinal, metabolic and biochemical demand.
reaction throughout the body. The magnitude of response is • Blood volume distribution: Peripheral and splanchnic
highly dependent on the severity, intensity and duration of vasoconstriction coronary and cerebral vasodilatation.
stimulus. • Respiratory Changes: Increased respiratory rate.
• For triggering such reflex response and presenting a complex • Fluid and electrolyte changes: Sodium and water retention.
interplay of substances between the hypothalamic pituitary axis, • Coagulation: Hypercoagubility and fibrinolysis
the classical neuro – endocrinal hormone system and autonomic • Immunosupression: Wound infections
nervous system is brought to action and is called “stress • Metabolic Changes: Substrate mobilization- hyperglycemia.
response “ or “alarm reaction . • Urinary changes: Reduced urinary output.
• The local response is of great importance for healing and • The stress changes are well tolerated by normal healthy patients
defense against infection. This involves mediators, vascular (ASA grade I). The changes return to normal in due course of time.
endothelial cell products and even the intracellular products of In patients with hypertension, coronary artery disease, myocardial
single cells. infarction, valvular heart disease, aortic aneurysm, cerebral
• The stress response leads to secretion of many anabolic and aneurysm or intracranial hypertension, diabetes mellitus, liver
catabolic hormones resulting in hypermetabolism, with the diseases, renal insufficiency, geriatric age group, (ASA grade III, IV,
acceleration of most of the biochemical reactions. and V), these changes are life threatening.
• The response play as compensatory mechanism and provides • The review will highlight the causes, development in the
maximum chances of survival because of the increased cardio- understanding of the release mechanism involved in the stress
vascular functions, fluid preservation and supply of the increased response to injury, effects on various systems and the methods that
demands for energy generating substrates. If the stress can modulate these responses for better outcome.
response is prolonged, the continuous hypermetabolic state may
result in exhaustion of essential components of the body e.g.
glucose, fat, protein, minerals, leading to delayed ambulation
and increased morbidity and mortality.
41

Stress Response & Anesthesia.Continuation: Dr Azam’s Notes in Anesthesiology 2013
The primary stimuli of neuro-endocrine reflexes

Hypotension: Anxiety and Emotions:
• The reduction in the effective circulating volume due to any • Fear, anxiety, emotions, tension significantly reduces pain tolerance.
reason (trauma, hemorrhage, burns, MI, CCF, tamponade, The stimuli pass to the limbic system especially in the region of
sepsis, neurogenic collapse etc.) is sensed by the pressure amygdale, hippocampus and lower brainstem nuclei then
sensitive baro-receptors in aorta, carotid and renal arteries, transmitting the signals to the posterior hypothalamus. Stimulation of
proportional to the magnitude of the volume loss, directly through which controls the release of various hormones from pituitary.
central autonomic pathway to activate release of pituitary Pituitary secretes AVP, ACTH, cortisol, aldosterone and
hormones such as ACTH, vasopressin, growth hormone, beta catecholamine through the stimulation of the ANS causing rise in
endorphin and indirectly through the sympathetic nervous heart rate, blood pressure.
system to activate the release of pituitary hormones such as Temperature:
ACTH, vasopressin, growth hormone, beta endorphin and • The change in the core temperature is sensed by the pre-optic area
indirectly through sympathetic nervous system to activate the of hypothalamus induces the secretion of the stress hormones. The
release of catecholamine, glucagon, inhibiting insulin release stress hormones increases the heat production but temperature
and resulting in retention of sodium and water and rise in heart alterations in certain clinical situations can be seen. The conditions
rate, blood pressure and blood sugar. like hypovolemia with inadequate hepatic blood flow, starvation,
• Decrease in renal blood flow due to splanchnic vasoconstriction sepsis with peripheral vasomotor control, burn with loss of thermal
is sense by the high pressure stretch receptors at juxta- insulation and induced hypothermia during cardiopulmonary bypass
glomerular complexes of kidney resulting in renin and or neurosurgery, profound hypothermia for total circulatory arrest are
angiotensin secretion which results in rise of blood pressure and known to induce neuro-endocrinal responses.
reduction in urinary output. Uneven blood flow for longer time
may lead to renal dysfunction. Anesthesia:
Oxygen, carbondioxide and hydrogen ion: • Certain drugs or procedures, light planes of anesthesia and during
• The changes in the concentration of oxygen, carbon-dioxide and the period of maximum stimulation (skin incision, tissue handling,
hydrogen ions in the blood initiate cardiovascular, pulmonary and stretching of mesentery or gut) show exaggerated responses.
neuroendocrine responses through the activation of the Anesthetic drugs:
peripheral chemoreceptors, aortic and carotid bodies. Decrease • The use of cyclopropane, ether causes release of catecholamine.
in arterial blood flow or oxygen tension, decreases the Laryngoscopy and intubation
chemoreceptor oxygen extraction, decreasing venous PO2. The • The mechanical stimulation of upper respiratory tract viz nose,
9th and 10th cranial nerves carry these sensation to the epipharynx, laryngopharynx, the afferents are carried by glosso-
hypothalamus resulting in to cardiac sympathetic outflow causing pharyngeal nerve and from tracheobronchial tree via the vagus
rise in heart rate, cardiac contractility and hyperventilation. nerve, which enhances the activities of the cervical sympathetic
Further hypovolemia may potentiate the hormonal reflex afferent fibres resulting in transient rise in heart rate and blood
response to hypoxia. pressure.
42

Light anesthesia Surgery:

• The use of poly-pharmacy such as sedatives, anxiolytics, • The surgery is a created injury for the treatment. The stress response
narcotics, muscle relaxants of different onset, peak action and depends on the extent of injury. The procedures of short duration,
duration may result in fluctuation of the depth of anesthesia is diagnostic procedures, body surface, eye, ear surgeries, the
assessed by PSRT scores (pressure, sweating, rate, tear). abdominal endoscopic surgeries requiring small incisions, minimum
Inadequate drug titration may result in light or deep anesthesia. tissue handling evoke only a slight response. The major procedures
During light planes of anesthesia feeling of pain, inadequate elicit more pronounced response in which the flow phase may last up
sleep, amnesia or muscle relaxation results in stress response. to several days or weeks. This result in excessive weight loss, also
Pain delays the recovery and ambulation resulting in increased morbidity
• The superficial layer of the skin is densely supplied with the pain and mortality.
nerve endings. It is stated that the surgical procedures are not Wound:
possible without producing damage to the nerve tissue which • The tissue injury during surgical incision and tissue handling
then become sensitized by the release of the inflammatory activates inflammation and host defense system. The magnitude of
mediators ,resulting in severe pain (cry of the injure nerves) the wound has direct relationship with the manifestations of the host
Such pain is characterized by both “peripheral and central response. The quantity of the mediators and spill over of these
sensitization”. mediators affects the neuroendocrine reflexes. Various substances
• Peripheral sensitization – The damaged tissues evoke the typical like exotoxin, heat labile proteins produced by gram positive bacteria,
local inflammatory response. The release of the traditional the endotoxins the lipopolysacharide moiety of gram negative
inflammatory mediators like cytokine, leukotrienes, nerve growth bacteria cell walls, cause the release of the mediator substances,
factor, histamine, serotonin, kallikrenin, prostaglandins etc, such as interleukin I (IL-I and tumor necrosis factor (TNF) from
increase the sensitivity of nociceptors. various cells stimulate the neuro-immune axis release of the
• Central sensitization – The high intensity pain sensation is hormones such as ACTH.
carried through the finely myelinated nociceptive fibres. A-delta
and smaller C fibres, cutaneous nerve fibres pass through the The stress response is divided into two phases:
lamina, where the change in the excitability of neurons in the • Acute ebb or shock phase – This is very transient and characterized
spinal cord is triggered by the afferent impulses. by a hypodynamic state, a reduction in metabolic rate and
• The exaggerated pain sensation affects the ascending reticular, depression of most of the physiologic processes.
limbic system, thalamus and hypothalamus which regulate the
autonomic, neuroendocrine response by stimulating the
hypothalamic-pituitary-adrenal-sympathetic axis resulting in
release of all catabolic and anabolic hormones, before reaching
the cortex. The pain sensation causing sympathetic stimulation
even in deeper planes of anesthesia during skin incision (e.g.
rise in heart rate and blood pressure during sternotomy).
43

Flow phase: This hyperdynamic phase may last for few days to Cortisol: The central key is the excitation of the hypothalamus during
weeks depending on the magnitude of the surgical insult or stress resulting in the secretion of ACTH which in turn initiates sudden
occurrence of the complication. The flow phase corresponds to the increase in cortisol level. The metabolic effects of cortisol are directed
period of compensation, with increase in metabolic rate, enzyme to overcome the stressful state. There is a direct feedback mechanism
modulation directed to glucose production and consequent for cortisol to both hypothalamus and pituitary gland to decrease the
restitution of blood volume and stimulation of the immune system. concentration of cortisol in plasma but the potent stress stimuli always
If the compensatory system prevails, energy expenditure initiates either periodic exacerbations of cortisol secretion at multiple
diminishes and metabolism shifts to anabolic pathways. times during the day or prolonged cortisol secretion during chronic
The stress hormones: The reflex neuroendocrine response to the stress.
injury is considered as autocrine, endocrine and paracrine. Cortisol has widespread effects on the metabolism and utilization of
glucose, amino acid and fatty acids in hepatic and extra-hepatic
1. Autocrine (Autonomic response): Catecholamines, insulin tissues. The cortisol causes rapid mobilization of amino acids and fat
and glucagon. from their cellular stores, making them immediately available both for
Catecholamines: The plasma catecholamines increase energy and synthesis of other compounds including glucose needed
immediately after injury and achieve peak concentration in 24 to by different tissues.
48 hours depending on the severity. This exerts metabolic, Effect of cortisol on glucose metabolism
hemodynamic and hormone modulating actions. Epinephrine • The cortisol and other glucocorticoids have the ability to stimulate
causes hepatic glycogenolysis, gluconeogenesis, lypolysis in the gluconeogenesis by liver as much as 6 to 10 folds during stress. One
adipose tissues, ketogenesis, increased insulin resistance, of its effect is increase in glycogen storage in the liver cells which is
preventing glucose uptake by cells. The direct cardio-respiratory the primary source of glucose production. The glucose production
effect increases heart rate, myocardial contractility, blood pressure during flow phase is mediated through glucagon and insulin using
and respiratory rate. amino acids, lactates, pyruvates and glycerol etc. Cortisol mobilizes
Glucagon: The glucogan release is modulated by plasma amino acids from the extra-hepatic tissues and converts it into
glucose, amino acid concentration, ANS and CNS activities. glucose. It also decreases and delays the rate of glucose utilization
Glucagon along with catecholamine and cortisol promotes and in-spite of increased insulin secretion, blood glucose concentration
prolongs the liver glycogenesis. It does not exert its effect during increases, up to 50% of the normal, 7 to 30mg% rise in BSL in non
acute hyperglycemia. diabetic patients. In diabetic patients excess of glucose provides a
Insulin: The plasma concentration of insulin during stress has ready source of energy to obligate tissues such as CNS, wound and
been noted to be biphasic, characterized by the suppression of red cells. Since these cells do not require insulin for glucose
insulin secretion followed by a normal secretion, which has been transport and utilization.
termed as the phase of physiologic insulin resistance.
2. Endocrines: Hormones under hypothalamic -pituitary control
like cortisol, thyroxine, AVP, growth Hormone.
44

Aldosterone
Protein metabolism
• ACTH and angiotensin increases and stimulates aldosterone
• Cortisol mobilizes amino acids from the extra-hepatic cells concentration following injury. The primary aldosterone secretion is
thereby diminishing the tissue stores, increase in catabolism and
related to sodium and water resorption from the distal convoluted
decreased protein synthesis results in thinning and weakness of
tubules.
muscles. In contrast, liver increases the formation of essential
Renin-Angiotensin
plasma proteins and glucose.
• Renin release is under the control of juxta-glomerular neurogenic
Fat metabolism
receptors and the macula densa. Decreased circulating volume,
• Cortisol helps in mobilization of fatty acids from the adipose ACTH, AVP, glucagon, prostaglandins, potassium, magnesium and
tissues and also increases oxidation of fatty acids in the cells,
calcium influence the renin secretion. Angiotensin II acts directly on
changing the metabolic system of the cells in times of starvation
cardiovascular system, fluid electrolyte balance, hormonal modulation
or stress from utilization of glucose for energy. Ketogenesis
and metabolism. It is a potent vasoconstrictor, also stimulates heart
depends on the severity of injury but is suppressed by the high
rate, myocardial contractility and increases vascular permeability.
insulin level.
Paracrine:
TRH-TSH-T3/T4
The activated local tissue, vascular endothelial cell system and single
• During injury the peripheral conversion of T4 to T3 is impaired. cell initiates response during hemorrhage, sepsis, inflammation and
The plasma concentrations of free and total T3 are decreased
other form of injury. It releases the cell derived mediator likes cytokine,
after injury.
leukotrines, prostaglandins, histamine, serotonin, TNF, interleukin I, II,
Growth hormone
VI, plasminogen activator, ecosanoids, kallikreins-kinins and other
• The secretion of growth hormone is governed by hypothalamic mediators. These mediators are also released as a consequence of cell
factors, autonomic stimulation and non hormonal signals. The
injury or death, which have direct effect on the ANS and CNS on the
primary metabolic action of GH during stress is to promote
classical hormone system releasing cortisol, EP and NE and other stress
protein synthesis and enhance lipid break down, and glucose
hormones in small quantity. Some mediators affect the vascular,
stores.
metabolic, coagulation, angiotensin and immunological system. The
Arginine vasopressin
preventive measures for the release of such mediators may play an
• Secretion of AVH is increased after major trauma, hemorrhage, important role in reducing the stress hormones.
sepsis, pain. Immediate AVH release, following acute reduction
of circulating volume, is a complex event acting through afferents
Cytokines and other mediators
including baro, chemoreceptors and left atrial receptors. The
The mediators may be the result of cellular injury or death due to
preservation of water and sodium reduction in the urine volume
hypoxia, sepsis, inflammation. They exert paracrine, autocrine and
occurs as a compensatory phenomenon.
endocrine effects even in very low concentration.
45

a. Interleukins: IL-l, IL-2, IL-6- The release of interleukins is e. Histamine: Elevated concentration of histamine has been observed
during inflammatory, infectious and immunologic process. They act during hypotension, trauma, thermal injury, endotoxemia. It causes
on CNS inducing fever by stimulating local release of severe vasodilatation resulting in hypotension, peripheral pooling,
prostaglandins in the anterior hypothalamus, inducing anorexia but increased capillary permeability and ultimately cardiac failure.
increasing the basal metabolic rate and oxygen consumption. f. Kallikreins-Kinins: The kinins are potent vasodilators, causes
They promote the synthesis of hepatic acute proteins and tissue oedema, evoke pain, increases hepatic prostaglandins, inhibit
breakdown of muscle protein to amino acids, necessary for the gluconeogenesis, reduction in renal blood flow, increase in renin
immune stimulation, defence and energy production. They also formation during injury.
have central hormonal modulating effects causing release of g. Heat shock proteins: A group of intracellular proteins named after
ACTH, CRF and marginal increase in catecholamines. the heat stimulation induced by hypoxia, ether anesthesia, trauma and
b. Tumour necrosis factor: During injury the TNF stimulates the haemorrhage. This protects the cells from the deleterious effects of
release of prostaglandin E2, neutrophils aggregation, thromboxane stress. The experimental work has shown that the HSP action is in
synthesis (potent vasoconsistrictor and promotes platelet parallel with the hypothalamic - pituitary- axis activation, adrenal cortex
aggregation), cytotoxicity, ecosanoids, platelet activating factor. and specific vascular cells providing evidences for stress induced
They also cause decrease in lipoprotein lipase activity in adipose interaction of the neuro-endocrinal system and the molecular response
cells and reduces the transmembrane potential in skeletal muscle. to stress.
c. Eicosanoids: The eicosanoids are derived from the arachidonic Immune response
acid of the cell membrane phospholipids of all nucleated cells. The • Infectious complications continue to be one of the causes of post-
stimuli for the increased synthesis of eisosanoids are hypoxia, operative morbidity. The body protects itself against foreign
ischemia, tissue injury, NE, AVP, angiotensin II, serotonins. organisms or substances. The mechanism of immune-suppression in
They are the prostaglandins, from kidney, platelets, blood vessels, the post-operative period is not fully understood. The known
thromboxane from platelets and macrophages, leukotrines from mediators of immune depression are neuro-endocrine response as
WBC, synovial tissues, lung parenchyma. They have wide spread well as intravenous opioids and inhalational agents which have
effects on systemic, pulmonary, regional vasoregulation, effect on shown an increase in the susceptibility to infection through a
central and peripheral neurotransmission. They are powerful significant decrease in the cytotoxic activity of the natural killer cells.
vasodilators and vasoconsistrictors and proaggregatory It is found that a significant reduction in post-operative infections in
substances. patients receiving epidural anesthesia and analgesia due the
d. Serotonin: It is found in the enterochromoffin cells of intestines cytoprotective and anti-inflammatory effects of local anesthetics.
and platelets during tissue injury. It stimulates vasoconsistriction, Modifying factors of the stress response:
bronchospasm, platelet aggregation, increases heart rate and • The stress response to surgery, anesthesia and other injuries has
myocardial contractility. been considered as the homeostatic defence mechanism, important
for the body for adaptation and developing resistance to the noxious
insults. But such exaggerated physiological changes in patients with
co-existing diseases is always life threatening.
46

• This can be prevented by appropriate fluids, electrolytes and • The efferent pathway is also involved in the release of cortisol, rennin
glucose to reduce nitrogen loss. Timely therapeutic intervention angiotensin and epinephrine. Extensive neural blockade T4 to S5
can reduce the myocardial strain. Absolute post operative pain during lower abdominal surgery, prevents cortisol response & the
relief reduces the catecholamine release and pulmonary hyperglycemic response to surgery apparently due to the release of
complications. The feeling of well being, less weight loss, early stress hormones through the afferent and efferent neural pathway.
recovery and ambulation reduces the morbidity. The insulin response to hyperglycemia and plasma glucagon
• The pre-anesthetic screening plays an important role in response to peripheral glucose are inhibited only by higher thoracic
identifying, quantifying and optimization of the disease T2 to T6 dermatome block. The T9 to T10 block for lower abdominal
processes. The recognition of the factors which initiate the stress surgeries has no influences on insulin secretion.
response can be considered for modification in the pre-operative 3. Alleviation of anxiety
period. • Anxiety initiates catecholamine release harming the cardio-
1. General anesthesia respiratory impulses due the exaggeration of the oxygen
• General anesthesia may limit the perception of sensation due to consumption and hemodynamic responses. The pre-operative use of
injury, but does not abolish the response completely as various anxiolytic drugs, cardiac drugs eg-beta-blockers, anti-
hypothalamus reacts to the noxious stimuli even in the deeper hypertensive and anti-anginal can prevent the morbidity.
planes of anesthesia (e.g. rise in HR and blood pressure, during 4. Pre-operative fluid balance
sternotomy). All the intravenous agents and volatile anesthetics • The appropriate pre-operative fluid therapy with sufficient amount of
in normal doses have minor influence on the endocrine and glucose, is essential to maintain fluid balance and caloric
metabolic functions. requirement to avoid undue catabolism.
5. Peri-operative management
2. Regional blockade: • It is essential to prevent the hemodynamic changes during induction
• The neural blockade by regional anesthesia with local endotracheal intubation, skin incision and maintenance of the depth
anesthetics have direct influence on endocrinal and metabolic of anesthesia are adequate to attenuate the stress response. The
response. The basic mechanisms of neural blockade on stress careful titration of inhalational anesthetic drugs, short acting opioids,
response to surgery is the total prevention of the nociceptive use of cardio-stable muscle relaxants are helpful. The continuous
signals from the surgical area from reaching the central nervous infusion of anesthetic drugs, relaxants and opioids technique has
system. The inhibitory effect of neural blockade on endocrine proved to be excellent in preventing the fluctuation of the depth of
and metabolic response to surgery is involved through both anesthesia.
afferent and the efferent pathway but differ among the individual • The continuous monitoring of vital parameters HR, BP, ECG, CVP,
endocrine glands. The afferent pathway is involved in the release SpO2, PCO2, temperature, blood sugar, the timely interpretation of
of pituitary hormones whereas adrenocortical hormones release any changes and instant therapeutic intervention throughout the
is complex. The cortisol release is through the efferent neural to procedure plays an important role in stabilizing the patientʼs
pituitary and neural efferent pathway to adrenal cortex by ACTH. condition.
47

General anesthesia combined with neural blockade – The G.A. f) Peripheral blocks: Retrobulbar block reduces the effect of stress
plus epidural analgesia in hip replacement, thoracic surgery, response as compared to general anesthesia.
abdominal surgeries certainly reduces circulatory, hyperglycemic g) Prevention of deep vein thrombosis: Vasodilatation due to
responses due to inhibition of the cortisol and catecholamines. sympathetic block during spinal or epidural blockade, use of aspirin
The postoperative care including multi-component regimen: and early ambulation reduces the hypercoagulation response in the
Absolute pain relief during the peri and postoperative period is a postoperative period.
“gold standard” for preventing protein breakdown. h) Anabolic and catabolic hormone modulation: Beta blockers,
a) The local wound infiltration: Use of local anesthetic during growth hormone and insulin reduces protein breakdown and improves
wound infiltration completely block the pain transmission, local nitrogen balance.
inflammation and pituitary response. i) Substrate administration: The demand of certain substrates
b) Pre-emptive analgesia: The pre operative NSAIDs or increases during starvation and injury. The administration of glucose
continuous infusion of local anesthetic bupivacaine at low and amino acids, though the fundamental characteristic of catabolism
concentration, through epidural catheter provides excellent is not abolished but it reduces to great extent during stress.
perioperative analgesia which can be continued postoperatively.
c) NSAIDs: The NSAIDs has no direct effect on the classical
stress response but the arachidonic cascade metabolites are
involved in various steps of the response to injury. The use of
NSAIDs and aspirin may help as an anti-prostaglandins, anti-
serotonins, antihistamines, anti-inflammatory, anticoagulant and
immune-suppressive effects may result in slight modification.
d) Systemic opioids: Epidural morphine does not abolish the
stress response. High doses of fentanyl (50µg/kg) and etomidate
selectively inhibit the hypothalamus thus preventing endocrinal
and metabolic response.
e) Stimulation of inhibitory descending pathway and alpha-2-
agonist: The stimulation of the descending inhibitory pathway
from brain stem using electrical stimulation or administration of the
final serotonin, clonidine and enkephalins reduces pain sensation.
48

18. Positioning in Anesthesia. Dr Azam’s Notes in Anesthesiology 2013
DORSAL DECUBITUS POSITIONS:

Physiological changes
• Circulation:
• In the horizontal supine position, the influence of gravity on the
vascular system is minimal. The pressure gradient between the
heart and the arteries is almost non-existent. The venous
gradient depends on the intrathoracic pressure changes that
occur with respiration. But if the patient is tilted, the effects of
gravity on blood flow in the head or feet can become quite
significant. Pressures may change by 2mm Hg for each 2.5 cm
that a given point varies in vertical height above or below the
reference point at the heart.
• With the head-up tilt, blood pools in distensible dependent
vessels, reduces effective circulating volume, cardiac output and
systemic perfusion. If the head is tilted down, pressure in the
cerebral veins increases, alert patients complain of pounding
vascular headache. Acute volume loading of the heart may occur
and may lead to myocardial ischemia. The enlarged central
blood mass activates baroreceptors on the great vessels of the
chest and neck, results in rapid peripheral vasodilatation,
unchanged or reduced cardiac output, and decreased organ
perfusion.
• Spontaneous fluctuations of blood flow in microcirculation fail
after about 1 hour of immobility. The patient then becomes
uncomfortable and restless, the normal pattern returns. The
same is true with anaesthetized patients and when the patient
reacts after reversal.
• The pulmonary circulation is the most congested along the
dorsal body wall and least congested substernally. With head-up
tilt, Zone 3 moves toward the lung bases. If the tilt is head-down,
Zone 3 shifts cephalad, abnormal ventilation –perfusion ratio
intensify.
49

Positioning in Anesthesia.Continuation: Dr Azam’s Notes in Anesthesiology 2013
Variations of the Dorsal Decubitus Position:

Supine
Horizontal supine
• In the traditional horizontal supine position, patient lies on his back,
with a small pillow under the head. Arms are well padded, restrained
by the side or abducted.
Contoured supine
• Also called “Lawn Chair Position”. The trunk-thigh hinge is angulated
about 150, the thigh-knee hinge is angulated the same degree in the
opposite direction.
Frog-Leg
• The patient is placed supine with the knees bent and the soles
touching each other. This is useful when the surgeon wants access is
useful when the surgeon wants access to the patientʼs perineum and
vagina.
Respiration: Lithotomy
• In supine position, the diaphragm is pushed cephalad, it Standard:
lengthens the muscle fibres in that part of the diaphragm, hence • The patient lies supine, each lower extremity is flexed at the hip and
increased the strength and effectiveness of its contractions. With the knee. Both lower limbs are simultaneously lifted and separated,
head-up tilt, the visceral weight shifts away and ventilation is so that the perineum is exposed.
enhanced. In the head-down position, the visceral mass causes Low:
significant respiratory embarrassment by impeding causes • The degree of thigh elevation is only about 30-45 degrees. Used
excursions of the diaphragm prevents adequate expansion of the mostly in urological surgeries.
lung bases. To avoid significant V/Q mismatch, one may have to High:
use larger tidal volumes under anesthesia. • The patientʼs legs are fully extended on the thighs; the thighs flexed
more than 90 degrees over the trunk.
Exaggerated:
• The thighs are forcibly flexed on the trunk, lower legs aimed skyward.
50

51

Head-down tilt 1.Nerve Injuries.

The Trendelenberg Position
• This maneuver of tilting the patient 30-45 degrees head down
was adopted and popularized by FRIEDRICH
TRENDELENBERG OF BONN and LEIPZIG before 1870.
Wristlets and shoulder braces are needed to prevent the patient
from sliding cephalad.
The Scultetus position

• The angulation is only 10-15 degrees head-down. This position
threatens to dislodge the patient cephalad.
Complications of Dorsal Decubitus Positions:

Pressure Alopecia.
• Prolonged compression of hair follicles can produce hair loss. Brachial Plexus Injuries:
Alopecia occurs between 3rd and 28th day and re-growth is • The principal means of brachial plexus injury under general
complete in 3 months. Other causes are use of tight head straps anesthesia is stretching. Unfortunately this type of injury does not
to hold facemask, prolonged hypotension and hypothermia. allow regeneration and restoration of function.
• It can be avoided by frequently turning the patientʼs head during • When the patientʼs arm is abducted and/or rotated, flexion and
long surgeries, and by using padded, soft head supports. rotation of the neck to the opposite side stretches the plexus. The
awake patient will not tolerate this because of the pain and
Pressure-point Reactions restlessness caused by nerve ischemia. Under general anesthesia,
• Weight-bearing bony prominences produce ischemic necrosis of there is no feedback, hence the increased risk of ischemic injury.
overlying tissues. Hypothermia and hypotension enhance the • Median sternotomies have been known to cause rib fractures and
process. brachial plexus injuries.
• The heels, the elbows and the sacrum are vulnerable. • Diagnosis of brachial plexus injury is suspected if the patient has
Prophylactic padding is a must. unusual pain in the neck and upper arm on the first postoperative
day. There may be numbness and motor function loss. Prognosis is
better, if the patient presents with incomplete nerve defects and
regeneration should occur over 3 to 6 months
52

Radial Nerve Injury:

• May be caused by pressure from the vertical bar of an
anesthesia screen over the lateral aspect of the arm and Saphenous Nerve Injury:
excessive cycling of an automatic blood pressure cuff. • Because of the superficial location at the medial thigh, the
• Diagnostic features are wrist drop, weakness of abduction of saphenous nerve can be directly compressed by pneumatic
thumb, inability to extend the metacarpophalangeal joints and tourniquets when used for prolonged duration and by the stirrups.
loss of sensation in the web space between the thumb and the
index finger.
Ulnar Nerve Injury:
• Injury occurs by direct compression on the olecranon notch.
Blankets, table edges are the causes of direct compression.
Neuroapraxia follows prolonged ischemia. Special foam or gel
padding at the elbow is wise. Supination of the hand shifts the
weight of the elbow onto the olecranon process and offers a high
degree of protection.
%
• Ulnar nerve injury can be detected if the grip strength is weak Sciatic Nerve Injury:
and there is weakness of the ulnar functions of the hand. If a • Positioning the buttock of a thin or malnourished patient over an
complete lesion, there can be wasting and contracture, resulting edge of the table or positioning device can cause compression injury
in clawing of the hand to the sciatic nerve. Severe abduction or flexion of the leg stretches
the sciatic nerve and can cause injury.
• With sciatic nerve injury, all muscles below the knee are weak or
paralysed, and numbness of the anterolateral calf and the foot
occurs. Injury to the common peroneal nerve can lead to ʻfoot dropʼ.
53

Backache: LATERAL DECUBITUS POSITIONS:

• Lumbar backache is due to ligamentous relaxation and further, PHYSIOLOGY
loss of normal lumbar curvature. Place several folded towels or Circulation:
an inflatable bladder of a blood pressure cuff under the lumbar • If the legs are maintained in the long axis of the body, almost no
spine to retain the lordosis and to reduce the discomfort. pressure gradients exist along the great vessels. If the lower
Perineal Crush Injury: extremities are flexed at the hips and remain below the heart, blood
• On the fracture table, the countertraction post is placed in the pools in the distensible vessels of the legs.Wrapping the legs and
perineum and the external genitalia are at risk if compressed. things in compressive bandages can combat venous pooling. Marked
The correct position for the pole is against the pelvis between the flexion at hips and knees can partially or completely obstruct venous
genitalia and the uninjured limb. Pubic hair must also not be return.
under stretch, lest, painful folliculitis may occur later in the • Vascular congestion of the down-side lung resembles a zone 3 while
postoperative period. the relatively hypoperfused up-side lung resembles a zone 2.
Respiratory:
Compartment Syndrome: • In lateral ducubitus position, the volume of the down-side hemithorax
• If perfusion to a lower extremity is hampered, compartment is reduced by the pressure of the up-side hemithorax mediastinum.
syndrome may develop. It is characterized by ischemia, hypoxic Abdominal viscera force the down side diaphragm cephalad.
edema, elevated tissue pressures within the fascial Spontaneous ventilation can partially compensate by the increased
compartments of the leg and extensive rhabdomyolysis, further contractile efficiency of the elongated diaphragmatic muscle fibres.
direct toxicity on renal tubular epithelium, and likely renal failure. • Positive pressure ventilation, preferentially, reaches the more
• Causes of a compartment syndrome can be (1) Systemic compliant upside lung, hence there is excessive ventilation of the
hypotension, elevation of the extremity, (2) Vascular obstruction underperfused up-side lung and hypoventilation of the congested
by excessive flexion of knees or hips and (3) External down-side lung. This leads to clinically significant ventilation –
compression of the elevated extremity by tight straps or leg perfusion mismatch
wrappings.
• Surgical fasciotomies are the only means of managing and
alkalizing the urine and diuresis may reduce the degree of renal
damage.
54

VIBRATIONS OF THE LATERAL DECUBITUS POSITIONS: The Simsʼ position:

Standard (Horizontal) Lateral Position: • J. MARION SIMSʼ modification of the lateral position is used for
• The patient is rolled onto one side on a flat table surface and operations on the perineum, rectum, vagina and bladder. It
stabilized in that posture by flexing the down-side thigh to 90 resembles semi prone position with down-side leg extended, up-side
degrees on the trunk. The peroneal nerve is padded on the is flexed at the hip and knee to expose the perineum, the patient rolls
down-side is padded on the down side to minimize compression slightly ventral.
damage. The heat is supported by pillows so that the cervical
and thoracic spines are properly aligned. A small pad placed just
caused to and out the down-side axilla prevents excessive
compression of the shoulder, prevents stretching of
supraclavicular nerve.
• Arms may be extended ventrally, retained on a single arm board
with suitable padding or may flex each elbow and place the
hands on the table in front of the patientʼs face.
• The patients is stabilized in the lateral position by retaining tapes
across the hips and thorax
Flexed Lateral positions
Lateral Jackknife:
• Usually intended to stretch the up-side flank and widen the
intercostals spaces to facilitate a thoracotomy incision. The patientʼs
iliac crest is placed over the hinge between the back and the thigh
sections of the table. The table is then angulated at that hinge. The
legs are usually strapped to mid-thigh to reduce the pooling of the
blood.
• It is of no value once the rib-spreading retractor is placed in the
Semi supine and Semi prone: incision
• In the semi supine position, the up-side arm must be carefully
supported, it should not be hyper extended so that no traction or
compression is applied to the brachial or axillary neurovascular
bundles. The supporting bar should be well wrapped to prevent
electrical grounding.
• In semi-prone position, the down-side arm should be placed
behind the patients to avoid stress on the shoulder.
55

Neck:
• Lateral flexion of the arthritic neck, if not supported, leads to
troublesome post-operative pain. The neck should be placed in
neutral position at all times under anesthesia.
Suprascapular Nerve Injury:

• Can occur due to ventral circumduction of the down-side shoulder.
Causes dull and diffuse shoulder pain. A supporting pad under the
thorax, just caudal of the axilla should prevent the circumduction
stretch injury.
Long Thoracic Nerve:
• Lateral flexion of the neck may stretch the long thoracic nerve,
causing postoperative winging of the scapula. A firm head pillow
pressed against the down-side thoracic outlet can traumatize the
long thoracic nerve or root of the brachial plexus.
Compartment syndrome of the Down-side Upper Extremity:

• The misnamed “axillary roll” must not compromise the circulation to
Kidney position: the down-side upper extremity by pressing against the contents of
• Resembles the lateral jackknife position, but it adds an elevated the axilla, thus preventing the compartment syndrome.
kidney rest (or kidney bridge) under the down-side iliac crest to
increase lateral flexion. Unstable Thorax:
• If the ribcage is unstable and the patients turned onto the injured
COMPLICATIONS OF THE LATERAL DECUBITUS POSITIONS side, sharp ends of fractured ribs can puncture the down-side lung.
Eyes and Ears: Atelectasis:
• If the patientʼs face turns toward the mattress and the eye lids • Of an imprisoned and poorly expanding dependent lung can occur in
are not closed, abrasions on the ocular surface can occur. Direct the lateral decubitus positions, particularly in the flexed lateral
pressure on the globe can displace the crystalline ions or cause positions. Careful positioning and adequate passive positive
retinal ischemia, if systemic hypotension exists. pressure ventilation, application of PEEP should reduce the risk.
• The pressure of the head over the pinna, if not padded properly, Peroneal Nerve Injury:
can cause severe pain post-operatively. • Padding the area of the head of the fibula on the down-side leg can
prevent common peroneal nerve compression.
56

VENTRAL DECUBITUS (PRONE) POSITIONS PHYSIOLOGY

Circulatory:
• If the legs remain horizontally, pressure gradients in the blood
vessels are minimal. If the patient is kneeling or has head high,
significant pooling of venous blood can occur.
• The pressure of compressed viscera is transmitted on to the
dorsal surface of abdominal cavity, mesenteric and paravertebral
vessels are compressed, causing engorgement of veins within
the spinal canal.
• If the head is below the atria level, venous congestion of the face
and neck is evident. Conjunctival edema is usual. Turning the
head can alter the arterial perfusion and venous drainage in both
intracranial and extra-cranial vessels.
• The perfusion of the entire lung fits into zone 3. There can be a
significant fall in stroke volume and cardiac index. No significant
changes occur in mean arterial pressure, right atrial pressure or
pulmonary artery occlusion pressure. Prone Jackknife
Respiratory:
• Used to provide access to sacral, perineal regions and lower
• The compliance of the compacted prone lung decreases, may alimentary canal. The thighs are flexed more than usual on the trunk.
need higher inflation pressures during positive pressure
ventilation. If the abdomen hands free, the loss of FRC is
minimal.
Variations of the ventral decubitus position:
Full (Horizontal) prone
• In this full prone position, the head and the lower extremities
remain below the spinal level, if the abdomen is made to hand
freely. To minimize the venous pooling, one may use
compressive bandages on the legs or full-length elastic hosiery.
If the neck is pain-free, head can be turned laterally and
supported on a sponge device.
• Arms can be snugly retained alongside the torso or are placed
alongside the head i.e. extended at the shoulder, flexed at the
elbow. Ulnar nerves at the elbow should be padded
57

Kneeling Breast Injuries

• Used to improve operative conditions in the lumbar and cervico- • Average sized breasts of a pronated woman, if forced laterally by
occipital areas. chest supports, can be stretched and injured along the sterna
borders. Medial and cephalad displacement seems better tolerated,
Complications of the ventral decubitus positions: Massive breasts, if forced laterally, may not cause distress to the
Eyes and Ears patient. Direct pressure can rupture enhancement prostheses.
• Eyes should be lubricated, the lids closed, and light weight Abdominal Compression
protective goggles may prevent accidental opening. Monitoring • May cause viscera to force diaphragm cephalad enough to impair
wires and intravenous tubing should not migrate underneath the ventilation. The increased intra-abdominal pressure may be
head after pronation. transmitted onto perivertebral and intraspinal surgical field, the
homeostasis becomes difficult.
Neck problems HEAD-ELEVATED POSITION PHYSIOLOGY
• Pain and impaired cerebral perfusion are the consequences of Circulatory:
bad positioning. • As the head is raised above the level of the heart, pressure gradients
develop, blood shifts from the upper body to the feet. Atrial filling
Brachial plexus injuries pressures decrease, sympathetic tone increases, parasympathetic
• Stretch injuries to the roots on the side opposite to the turned tone decreases, the renin-angiotensin-aldosterone system is
face are possible. If the arm is placed alongside the head, care activated, fluid and electrolytes are retained by the kidneys.
should be taken not to stretch the humeral head and compress Intrathoracic blood volume decreases by as much as 500 ml. cardiac
the axillary neurovascular bundle. output decreases 20-40%, stroke volume by 50%, heart rate
• Ulnar nerve, in the cubital tunnel, is vulnerable to being increases by 30%. Systemic vascular resistance increases 30-60%
compressed by the weight of the elbow. Hence, medial aspect of to maintain a steady or increased mean arterial pressure. Oxygen
the elbow must be well padded. consumption is unchanged.
• Radial nerve injury due to repeated inflation of blood pressure • Cerebral blood flow decreases by 20% renal blood flow by 30%,
cuff may occur. glomerular filtration decreases.
• Significant changes are not encountered with less than 60 degrees of
Thoracic Outlet Syndrome head up tilt. These alterations increase progressively for more than 1
• It the patient presents with a history suggestive of thoracic outlet hour after the final posture is achieved.
syndrome such as dysesthesias caused by having the arms
overhead, it may be prudent to keep the arms alongside the Respiratory:
trunk in the prone position. • Less pressure is needed to inflate the lungs in an upright position.
FRC increases.
58

Variations of the Head-elevated positions

Sitting
• The full sitting position is uncommon in current practice. The
classic sitting position places the patient in a semi-reclining
posture, with the legs elevated to the heart level, head flexed
ventrally on the neck. Elastic stockings or compressive wraps
around the legs reduce the venous pooling.
Supine, Tilted Head Up
COMPLICATIONS OF THE HEAD-ELEVATED POSITIONS

Postural hypotension
• In an anesthetized patient, head-elevated position is frequently
accompanied by some reduction in systemic blood pressure.
• Measurement of mean arterial pressures at the circle of Willis is
• A dorsal recumbent position with the head elevated is used for recommended to assess cerebral perfusion pressures. Treatment of
many surgeries on the head and neck. It improves access to be hypotension consists of temporarily delaying the elevation of head,
surgical target, helps to drain blood and irrigation solutions way reducing the concentration of anesthetic drugs, infusing fluids and
from the field. Though the tilt is not great, the venous pooling in using a small dose of vasopressors.
the legs can still occur and venous air embolism is a possibility. Air Embolus
Lateral, Tilted Head UP • Venous air embolization is potentially lethal. Though the occurrence
• Is also referred to as “park bench position”. The threat of air of air emboli is frequent in head-elevated positions, most of the
embolism persists. emboli are small in volume, clinically silent.
Prone, Tilted Head up

• Is the widely used replacement for the sitting position to access
dorsal structures of head and neck. The perceived advantage is
the avoidance of air embolism, but the hazard is not eliminated
59

The diagnosis is by: a change in heart sounds noted by a General Principles of safe patient positioning:
parasternal Doppler probe; ʻmill wheelʼ murmur; cardiac • Safe positioning of a patient is a team work involving the
dysrhythmias; hypotension; a decrease in expired carbon dioxide anesthesiologist, the surgeon and others. All the aspects of
and sudden appearance of vigorous spontaneous respiration; positioning are ---planned in advance and co-operating and
transesophageal echocardiography. coordinating with the head of the group form part of the teamwork.
• Positions associated with major physiological changes should be
Pneumocephalus achieved in a stepwise fashion, checking the hemodynamic status
• If the incision is made through the dura in the posterior fossa or repeatedly. Endotracheal tube position should be checked at the end
cervical spine of a seated patient, air gets trapped in the upper of positioning.
region of the cranium. If the brain mass is reduced by steroids • Padded cushions should be kept under areas vulnerable for nerve
and diuresis, the space available for pneumocephalus is compression. Bony areas may be left in contact with the mattress;
enlarged. Diffusion of nitrous oxide can produce tension but if the surgical time is prolonged or in the presence of hypotension
penumocephalus with signs of increased intracranial pressures or hypothermia, even these areas need to be well padded. It is
and delayed awakening from anesthesia. preferable to have all the joints in the body, with the exception of the
ankle joint, in minimal flexion.
Ocular Compression • Eyes need to be kept closed and padded, with eye ointment
• Pressure from a padded head-rest on the eyes can dislocate a containing water-soluble base. Finally, barring the surgical area, the
crystalline lens or cause global ischemia. patient should be covered so that heat loss in minimized. Patient
Edema of the Face, Tongue and Neck positioning should be done methodically and unhurriedly.
• Due to venous and lymphatic obstruction caused by prolonged
and marked neck flexion.
Mid-cervical Tetraplegia
• This occurs due to marked flexion of the neck, with or without
rotation of the head, is attributed to stretching of the spinal cord
with resulting compromise of its vasculature in the mid cervical
area. The result is paralysis below C5. May occur even following
prolonged, non forced head flexion for intracranial surgery in the
supine position.
Sciatic Nerve Injury
• Can occur if the hips are markedly flexed without bending the
knees. Foot drop is the result and can be bilateral.
60

19. Physiological Changes during different positions. Dr Azam’s Notes in Anesthesiology 2013
• Change of position from supine to any other position. In a patient Supine position:
is associated with both anatomical as well as physiological • Cardio-respiratory changes in the supine position are different in
changes (hazards) unless, specific precautions are taken to awake and anesthetized persons. Contrary to the upright position,
prevent or minimize them. The anatomical changes are related to the pulmonary perfusion at the apex and base of the lung becomes
abnormal movements as well as the pressure effects. Acute homogenous in this position. However, the perfusion in the anterior
postural homeostasis is largely governed by the autonomic parts of lung is lesser than posterior part due to gravity. Even the
reflexes (sympathetic nervous system) while long standing ventilation in supine position is even from apex to base.
postural homeostasis is maintained by renin-angiotensin system. • Hence in a spontaneously breathing patient, the posterior parts of the
Constant monitoring during the intra-operative and preoperative lungs are better ventilated as well as perfused because of better
periods can identify these physiological changes. diaphragmatic movement over those areas. With IPPV, the reverse is
• Physiological changes of positioning the patients are primarily seen and the anterior aspects of the lung are better ventilated.
manifested in cardiovascular system, pulmonary system and
central nervous system. State of consciousness, type of Upright to supine position:
anesthetic technique and the preexisting pulmonary pathology • (Conscious patient) when a patient is turned from upright to supine
influence these changes. position, the following changes are noted.
• Before going into the details of various posture related changes, 1. Pulmonary changes: A fall in functional residual capacity (FRC) by
it is imperative to briefly mention the distribution of pulmonary 24% is seen along with the alveolar collapse.
perfusion in the upright position. 2. Cardiovascular changes: These changes are due to gravity and the
Conscious upright position: physiological adaptations there to. There may not be any changes
•% Gravity plays a dominant role in determining the distribution at all. Venous return to the right heart increases resulting in
of blood flow within the lungs. The mechanism of gravity increased cardiac output. Peripheral resistance either decreases or
mediated distribution of blood flow in the upright lung is shown in remains unchanged.
fig.1. On the basis of the relationship between the alveolar For every 2.5cm height above or below the heart level, systemic BP
pressure (PA), the pulmonary artery pressure (Pa) and the changes by 2mmHg.
pulmonary venous pressure (Pv), the lung has been divided into
three zones. At the top of the lung is zone 1 where the blood flow
is little or none. In zone 2, the blood flow is partial and in zone 3
the blood flow continues to increase. Hence it can be seen from
fig.2 that in passing from the apex to the base of the lung, the
blood flow alters from 0.07 Lmin-1 to 1.29 Lmin-1. In the normal
upright lung the ventilation per unit lung volume like perfusion is
also greater at the base than it is at the apex. The change in
ventilation decrease linearly with the distance up the lung. The
normal lung ventilation. VA=4L/min while the lung perfusion
Q=5L/min. hence VA/Q=4/5=0.8.
61

Physiological Changes during different positions.Continuation: Dr Azam’s Notes in Anesthesiology 2013
Supine, anaesthetized position

Pulmonary changes:
• State of consciousness has a particular bearing on the
pulmonary system. Anesthesia is associated with some degree
of arterial hypoxemia unless FiO2 is kept greater than 33%.
Factors contributing to arterial hypoxemia under general
anesthesia are as follows: Fall in FRC (15-30%) fall in lung
compliance, increased intrapulmonary shunts (10-15% of cardiac
output), increase in PAO2 – PaO2. All these changes lead to
airway closure, V/Q mismatch and atelectasis of the lungs. Also 1. Anaesthetized patient breathing spontaneously:
these changes occur both on spontaneous as well as controlled • In this position perfusion of the lower most lung is encouraged at the
ventilation. There is an associated decrease in the constrictor cost of the upper lung. Ventilation of the lower lung also increases
response of pulmonary arterioles to hypoxemia. Anesthesia also because the diaphragm can contract more efficiently.
impairs the efficiency of CO2 excretion. 2. Anaesthetized patient on controlled ventilation turned lateral:
Cardiovascular changes: • In this patient, FRC of the upper lung increases while the dependent
• Mean arterial blood pressure falls by 20%. Heart rate also falls. lung has a moderate fall in FRC and hence is predisposed to
Cerebral dural sinus pressure: atelectasis. In addition, zone 1 of lung increases. It has been seen
• The dural sinus pressure is approximately 6 cm H2O if patientʼs that V/Q mismatch is the highest in lateral, position in patients with
head and legs are not elevated. normal lungs. On the contrary, if patient has one lung disease and is
turned laterally with the diseased lung uppermost, both PaO2 and V/
Lateral Decubitus position: Q mismatch improve. Lateral position does not help patients with
• This position is a good compromise between the sitting and fully bilateral pulmonary infiltrates especially in the dependent lung
prone positions specially in the elderly patients or seriously ill regions.
patients as the abdominal compression is lesser and the In addition to this, faulty position may lead to vascular obstruction in
respiratory movement are least interfered with. Physiological the neck and abdomen, injury to the brachial plexus, eyes, knees etc.
changes in lateral decubitus position vary depending upon patients can get rolled over also. Some of these problems can be
whether the patient is anaesthetized and then turned laterally taken care of by putting the patient in the modified lateral position.
with spontaneous breathing or is paralyzed first and then turned
laterally
62

a. Standard prone position:

• The patient lies on his ʻFace Downʼ or is rotated to one side. Arms
are either alongside the trunk or abducted at 900. The physiological
changes mainly are in the pulmonary system. Central nervous
system and cardiovascular system. Increased abdominal pressure
leads to a fall in pulmonary compliance. Raised venous pressure in
inferior vena cava leads to increased cerebrospinal fluid pressure via
lumbar and vertebral venous channels, increased cerebrospinal fluid
pressure via lumbar and vertebral venous channels, increased
Park bench position: bleeding and even hypotension. If abdominal pressure is prevented,
• This position was specially designed for acoustic neuroma FRC does not change significantly.
surgery but is not satisfactory for midline craniotomies. Special
advantage of this position over the lateral decubitus position is
only a better surgical field. Physiological changes and problems b. Modified prone position:
of this position are similar to those of lateral position. • In this position the abdomen is kept free by special rolls/support
across the chest as well as across the anterior superior iliac spine.
The arms are also along the trunk on board. Too much of head
rotation is avoided and lateral cutaneous nerve is also protected.
Head is flexed into a head rest or held by pins and the table is tilted
100 head up.
The following physiological changes take place:
I. FRC is the highest in normal awake prone patients.
II. FRC in anaesthetized prone patients does not alter if abdominal
pressure is prevented.
Prone position:
• This position is ideal for surgery on patients with hypoxemic
respiratory failure and patients with bilateral pulmonary infiltrates
on chest X-ray. Prone position could either be (a) standard prone
position or (b) modified prone position.
63

III. Pulmonary functions do not alter much in healthy patients under

general anesthesia. However, pulmonary functions of patients with
respiratory failure improve in this position whether they are
conscious and breathing spontaneously or are being mechanically
ventilated. Patients with bilateral basal infiltrates and those with
pathology of the base as well as the dorsal aspects of lungs are
said to be benefited from this position. The possible explanation is a
decrease in the hydrostatic forces opposing the passive movement
of the dorsal aspect of the diaphragm thereby expanding and
ventilating the dorsal aspects of the lungs. Cardiac output and
mixed venous PO2 increase in patients with acute respiratory failure
resulting in an improved PaO2.
IV. Cerebral effect: The cerebral dural sinus pressure in this position is
higher as compared to supine position. The following table shows
the dural sinus pressure in cm H2O, in supine and prone positions.
Head elevation Leg elevation Dural sinus pressure
(in degrees) (in degrees) (cm H2O)
Supine 0 0 6
Prone 20 20 +6
• Metabolic changes: Pressure on the lower limbs in this position may
lead to ischemia of the muscles which in turn may release muscle
myoglobin leading on to renal Sitting position is the ʻNearestʼ to the
normal erect posture and producers the fewest changes in the
pulmonary functions. The standard sitting position is not used
nowadays. Instead, modified recumbent position is preferred for
better failure
Sitting position:
• cardiovascular stability, better resuscitation and lower incidence of
venous air embolism. The popularity of sitting position has declined
over the years.
64

a. Pulmonary system:
• The blood gravitates to the dependent parts and since the lung
volumes do not change significantly, the alveoli remain open. The
extent of blood gravitation will depend on the precise nature of the
position. It is worse in the full sitting position and is the least if the
feet are at the level of the heart. The end result is an increase in FRC
as well as PAO2-PaO2. O2 transport and PaO2 decrease.
b. Cerebral effects:
• Cerebral blood flow falls by 15%. Intracranial pressure (ICP)
decreases as there is gravitational drainage of blood and CSF. The
dural sinus pressure varies, depending upon the degree of head and
leg elevation. The following table illustrates this.
Head elevation Leg elevation Dural sinus pressure
(in degrees) (in degrees) (cm H2O)
Supine 0 0 6
Sitting 25 0 0
Sitting 60 0 -6
Sitting 90 0 -13
Sitting 20 20 +3
Physiological changes with this position could be seen in any
of the following systems. • Since central venous pressure is also low, the incidence of venous
1. Pulmonary system air embolism rises. It could vary between (8-15%) and (25-50%)
2. Cerebral system depending upon the monitoring device used.
3. Cardiovascular system c. Cardiovascular effects:
4. Miscellaneous Cardiovascular responses in sitting position are variable. It may vary
from mild hypotension of 20-30 mm Hg (in 1/3 cases) to marked
hypotension of 50% in 2-5% cases. These changes occur immediately
and are maximal at 1hour. Old age, hypovolemia; vital centre
disturbances and electrolytic imbalance, alter these responses. In
addition to these factors, the cardiovascular (CV) responses are
influenced by the state of consciousness and type of anesthetic
technique. The fall in CV parameters seem to be related to induction of
anesthesia rather than the position itself. Various CV changes seen
while patient is sitting up and conscious as well as patient is sitting up
65
and conscious as well as under anesthesia as shown below.
Sitting the patient up while Sitting the patient up when he is Induction of

conscious (% changes) anaesthetized anesthesia then
Heart rate +12 Unchanged or increased Sitting position
patient is scated and +N2O
Mean systemic BP BP falls by 0.40% with patient Innovar Morphine +N2O
surgical stimulus +O2
RAP No change Falls awake
applied (enflurane/
PAP No change Cardiac output decreases by
halothane)
Stroke vol. index -11 12-80%
22.25 20.50
PAP No change H.R ↑ 12% SAP ↓ 22.27% SAP ↓ SVI ↓
PCW -22 SVR increases by 50-80% % %
25.29
Cardiac index No change SAP ↑ 11% Cl ↓ 20% SVI ↓ Cl ↓ 25%
%
• Right atrial pressure (RAP): Pulmonary artery pressure (PAP): CPP is
Pulmonary capillary wedge pressure (PCWP): Systemic vascular
SVRI ↑ 12% SVI ↓ 30-33% Cl ↓ 14-20 best
resistance (SVR)
maintained
• Anesthetic technique also greatly influences the cardiovascular RAP &
changes in sitting position. They used 4 anesthetic techniques PVR ↑ 37% SVRI ↑
PCWP↑
after positioning the anesthetic techniques after positioning the
RAP, PCWP-No
patient in sitting position and anaesthetizing them. After PaO2 ↑ 10% MAP do
traditional induction, anesthesia was maintained with either of change
the following agents: PCW
1. Enflurane 0.7% ↓ 22%
P
2. Halothane 0.4%
3. Innovar (Fentanyl: Droperidol)0.1 ml/kg-1 SVI ↓ 11%
4. Morphine 0.5 mg/kg-1 SVI
• It was found that PaO2 was better in seated awake patients and PAP No
during induction of anesthesia, no changes was seen. Later on
CV changes were seen to occur gradually. Left ventricular RAP change
functions are depressed by all techniques but CPP an MAP are Cl
best maintained with morphine. Various CV changes as seen in
the 4 different anesthetic groups are as follows:
66

SAP% :% Systolic arterial pressure

PVR% :% Pulmonary vascular resistance
SVI % :% Systemic vascular index
PAP% :% Pulmonary artery pressure
RAP% :% Right atrial pressure
CI% :% Cardiac index%
CPP% :% Cerebral perfusion pressure
• It was also found that although there is high sympathetic tone,
anesthesia avoids fall in systemic BP, yet, and increase in SVR
occurs resulting in a fall in myocardial performance. It is
concluded that morphine with N2O and O2 technique is the most
cardio-stable. Innovar is the worst, while halothane/enflurane
technique are intermediate.
• The cardiovascular instability during the sitting position can be
minimized by taking certain precautions which are summarized
under ʻconclusionsʼ.
Miscellaneous effects:
The following changes are also observed in sitting position.
I. Fall in body temperature
II. Increase in blood pH and base excess
III. Unchanged plasma renin levels and tissue perfusion
IV. Hypertension and tachycardia subsequent to pin insertion in
the scalp
V. Accidental intubation of right bronchus
VI. Edema tongue due to flexion of neck
VII. Pneumocephalus
VIII. Injury to brachial plexus, cervical plexus, common peroneal
nerve and sciatic nerve.
67

20. Cricoid Pressure ( Sellickʼs Maneuver) Dr Azam’s Notes in Anesthesiology 2013
• Cricoid pressure is applied during Rapid sequence induction. • The cricoid pressure is applied once the patient is induced just
This technique is employed to guard against regurgitation of before consciousness is lost and should be maintained until tracheal
aspiration of gastric contents. placement of the ETT is confirmed and the cuff has been inflated.
• The cricoid cartilage is the only cartilage in the upper airway to This is an important concept to stress when training supporting staff.
form a complete ring. So the correct technical standard has to be taught and practiced both
• Cricoid pressure is a backward pressure on this cartilage, with by the anesthetists and by their assistants.
the head extended on the neck. The pressure occludes the • The correct amount of force to be applied for effective cricoid
esophagus by pinching it between the cricoid cartilage in front pressure is said to be 30N or 3kg or 66 lb. The digital sensation of
and the vertebral bodies behind and thus prevents regurgitation. applying this force can be mimicked by pressing on weighting scales
Indications for cricoid pressure: to produce a reading of 3 kg.
1. Pregnant patients undergoing General Anesthesia with full Complications:
stomach and as a prophylaxis against aspiration of gastric General:
contents (Mendelsonʼs syndrome) especially in pregnant 1. Difficult to monitor
status. 2. May be applied inaccurately.
2. In any patient with full stomach undergoing General 3. Can contribute to difficult intubation.
Anesthesia. 4. Can contribute to esophageal rapture.
3. Patients with Raised intra abdominal pressure.
Identification of cricoid cartilage: Two handed:
The easiest and best way to identify the cricoid cartilage is Requires two assistants, one dedicated to cricoid pressure
1. Position the patient with neck flexed and head extended.
2. Palpate the sternal notch
3. Keeping the palpating finger in the midline, move it cephalad
until the first hard tracheal bump is felt. This is the cricoid
cartilage.
4. Confirmation of the cartilage can be achieved by moving the
finger a few mm cephaloid, where the cricothyroid membrane
can be felt as a small depression between the lower cricoid and
upper thyroid cartilage.
Technique:
One hand technique:
• 3 digits of the hand usually the thumb and first and second
fingers Two to maintain the trachea in the midline and one finger
to exert the force.
Two hand technique: One hand is positioned comfortably behind
the neck to maintain neck flexion and head extension. The other
hand is used as described. 68

#
#
21. Nausea & Vomiting. Dr Azam’s Notes in Anesthesiology 2013
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Nausea & Vomiting.Continuation: Dr Azam’s Notes in Anesthesiology 2013
Mechanism of nausea and vomiting: • N2O when used alone: Entonox – emetogenic but during balanced
• In the prodromal or preejection phase, relaxation of gastric anesthesia effect is uncertain.
muscles followed by small intestinal retrograde peristalsis, • Modern volatile agents are less emetogenic compared to older
forcing intestinal contents into the relaxed stomach. agents (ether, trilene)
• During ejection phase, a series of forceful contractions of • Hypotension – during spinal or epidural anesthesia
muscles of abdomen, diaphragm and appropriate portions of • Inflation of stomach with air during manual ventilation.
intestines and stomach occurs and contents forced out of d. Other factors:
relaxed upper esophageal sphincter. • Hypotension
Factors Associated with PONV: • Hypoxemia
a. Patient factors: • Intra abdominal pathology, psychological factors, fluid intake, naso
• A previous history PONV gastric tube, pain, antibiotics.
• Age: children are more susceptible Management:
• Gender: females. 1. Prevention rather than treatment of PONV should be the
• Influence of menstrual cycle and obesity. anesthetistʼs aim.
• Anxiety: sympathetic activity and air swallowing 2. Prophylactic antiemetic therapy should be given to all patients.
b. Surgical factors:
• ENT surgeries: Stimulation of pharynx and blood in GIT stimulate Treatment:
vomiting Treating the cause of PONV is very important.
• Abdominal surgeries: All the efferent limbs of vomiting reflex are • Post operative hypotension should be treated seeing its cause rather
stimulated. than treating with antiemetic.
• Major and minor gynecological surgery consistently associated • Hypoxemia should be treated with O2 and investigated if necessary
with PONV. • Early fluid intake and mobilization after day-case surgery should be
• Ophthalmic surgery: Squint correction. prevented.
• Inadequate pain relief in post op period • Anxiety should be treated with anxiolytics and reassurance.
c. Anesthetic factors: • Opioids should be administered judiciously or changing to a local
• The perioperative use of opioids [oral, IM, IV, epidural, spinal] is anesthetic technique or adopting a more balanced approach to
associated with increased incidence of PONV. Paradoxically post analgesia may solve the problem.
operative pain may cause PONV, which may be alleviated by
judicious use of opioids.
• The choice of induction – agent
• Etomidate and Methohexital à emetogenic
• Propofol – less emetogenic rather have antiemetic effect.
70

Nausea & Vomiting.Continuation: Dr Azam’s Notes in Anesthesiology 2013
Pharmacological treatment:
I. Antiemetics:
• Antagonists of Dopamine
• E.g. Metoclopramide, droperidol
II. Antagonists of 5HT3
• Ondansetron, Granisetron.
• Anticholinergics
• Atropine, Hyoscine, Cyclizine.
• Dexamethasone , Cannabinoids
71

22. Perioperative seizures. Dr Azam’s Notes in Anesthesiology 2013
I. Causes: Management:
• Uncontrolled / inadequately treated epilepsy Preventions:
• Severe hypoxia 1. Continue anticonvulsants in perioperative period.
• Severe hypercarbia 2. Avoid drugs lowering convulsive threshold.
• Perioperative strokes 3. Avoid hypertensive responses.
• Increased ICP [Trauma, Tumors, Infection] By avoiding pressor responses of laryngoscope intubation
• HTN crisis • Smooth and rapid intubation
• Cerebral Ischemia • Adequate analgesia
• Electrolyte imbalance [hyponatremia, hypocalcaemia] • Avoid lighter planes of anesthesia.
• Local anesthetic toxicity. • Suppress pressure response before extubation or extubate at deeper
• High spinal anesthesia. plane.
• Drugs which decrease threshold for convulsions. 1) Avoid hypoxia / hypercarbia.
• Ketamine, Methohexital, propofol, atracurium [Laudanosine] 2) Supplementation of O2 after opioid premedication
• Alcohol withdrawal. 3) Preoxygenation with 100% O2 – 5 min.
• Metabolic disorders hypoglycemia, uremia, hepatic 4) Use of closed circuit.
encephalopathy 5) Adequate ventilation - Tidal volume, rate, flow rates
• Severe pre-eclampsia, eclampsia 6) Check malfunctioning of circuits.
• Arterial air embolism 7) Anesthetic agents.
II. Types: • Thiopentone is preferred.
• In pre/post operative periods and in intraoperative period with no • Avoid ketamine, Methohexital, pancuronium, volatile agents used
relaxants, grandmal epilepsy seen. Patients relaxed with cautiously with increased ICP
relaxants do not show convulsive movements. [only EEG 1. Perioperative correction of electrolyte imbalance.
monitoring can detect seizure activity] 2. Limit LA agents to below toxic level.
III. Hazards of perioperative convulsions: Monitoring:
• Injuries [Tongue bite etc] Pulse oximeter, ECG, ETCO2, EEG, arterial line, NIBP ABG
• Displacement of monitors Electrolytes.
• Dislodgement of airway devices Treatment:
• Loss of airway control and aspiration • Cut off N2O, inhalational agents
• Increased CMRO2 and CBF increase ICP • 100% O2; secure airway with ETT.
• Bleeding / dislodgement of clots /grafts • Inj thiopentone 3-5mg/kg IV.
• Displacements / dislocations of joints / fractures • Continue with muscle relaxants – vecuronium
• Hypoxia /hypercarbia. • Continue anticonvulsants in perioperative period
72

23 Enumerate classical Biological Warfare Agents. Describe physical findings, pathogenesis and treatment of Anthrax
Biological warfare (BW) — also known as germ warfare — is the deliberate use of disease-causing biological agents
such as bacteria, viruses, fungi, or biological toxins, to kill or incapacitate humans, animals or plants as an act of war.
Physical Findings:
B.anthracis is a large aerobic, spore-forming, gram-positive bacillus that grows well on common culture media, such as blood
agar. Stained B. anthracis from culture media appears as long parallel chains of organisms with square ends, referred to as
“boxcars.” B. anthracis spores can remain viable and infective in the soil for many years, even decades.
Pathogenesis:
The replicating bacteria produce at least three proteins—lethal factor (LF), protective antigen (PA), and
edema factor (EF). These proteins combine to form two toxins known as lethal toxin and edema toxin.
Anthrax Toxins
Lethal Factor Protective Antigen Edema Factor
Biological Warfare Agents
Neurotoxins
Lethal Toxin Edema Toxin Anthrax
Staphylococcal
Bioregulators
Enterotoxin B (SEB)
Botulinal toxins
Plague
Brucellosis
Q-fever
Cholera
Ricin
Clostridium perfringens
Shigella
Encephalomyelitis viruses
Tissue damage Shock Edema Smallpox
Glanders
Tularemia
Hemorrhagic Fever viruses
Typhus
Mycotoxins
73
Dr Azamʼs Notes in Anesthesiology - 2013
Clinical Feature:
Medical Management:
Antibiotics are the most important therapeutic intervention in any form
There are three clinical forms of anthrax: cutaneous, gastrointestinal, of anthrax and should be started as soon as the disease is
and inhalation. The symptoms and incubation period of human anthrax suspected.B. anthracis are typically sensitive to several antibiotics,
are determined by the route of transmission of the organism. including penicillin, tetracycline, and oral fluoroquinolones
Cutaneous Anthrax
(ciprofloxacin and ofloxacin). B. anthracis produces a
Most (more than 95%) naturally occurring B. anthracis infections are cephalosporinase that inhibits the antibacterial activity of
cutaneous and occur when the bacterium enters a cut or abrasion on the cephalosporins such as ceftriaxone.
skin (e.g., when handling B. anthracis–contaminated animals, animal
products, or other objects). The reported incubation period for cutaneous Anthrax Medical Management
anthrax ranges from 1 to 12 days.symptoms may include swelling of • Antibiotics o Ciprofloxacin or doxycycline and >1 additional drug
adjacent lymph nodes, fever, malaise, and headache. active against B. anthracis*
•IV, then PO •30–60 days duration
Gastrointestinal Anthrax *Rifampin, vancomycin, penicillin, ampicillin, chloramphenicol,
The intestinal form of anthrax usually occurs after eating contaminated meat. imipenem, clindamycin, clarithromycin
The incubation period for intestinal anthrax is believed to be 1–7 days.
Involvement of the pharynx is characterized by lesions at the base of the • For cutaneous anthrax, ciprofloxacin or doxycycline is
tongue or tonsils, with sore throat, dysphagia, fever, and regional recommended as first-line therapy. Intravenous therapy with a
lymphadenopathy. Involvement of the lower intestine is characterized by acute multidrug regimen is recommended for cutaneous anthrax with
inflammation of the bowel. Initial signs of nausea, loss of appetite, vomiting, signs of systemic involvement, for extensive edema, or for lesions
and fever are followed by abdominal pain, vomiting of blood, and bloody on the head and neck. Cutaneous anthrax is typically treated for 7–
diarrhea. 10 days.
• Amoxicillin is recommended for patients who cannot take
Inhalation Anthrax fluoroquinolones or tetracycline- class drugs
Originally known as Woolsorter's disease, inhalation anthrax results from
inhalation of 8,000– 50,000 spores of B. anthracis.Rapid deterioration then
occurs, with high fever, dyspnea, cyanosis, and shock. Chest x-ray often shows
pleural effusion and mediastinal widening due to lymphadenopathy.Meningitis,
often hemorrhagic, occurs in up to half of patients with inhalation anthrax.
Laboratory Diagnosis
• The diagnosis of cutaneous anthrax should be suspected by the characteristic painless, shallow ulcer with a
black crust. Gram stain of vesicular fluid will reveal typical gram-positive bacteria. Diagnosis can be confirmed by
culture.Gastrointestinal anthrax is difficult to diagnose because of its similarity to other severe gastrointestinal
diseases.clinical specimens, such as pleural fluid, skin biopsy lesion material, oropharyngeal ulcers, or
cerebrospinal fluid. Diagnosis is usually confirmed with a positive culture for B. anthracis. Standard blood
cultures should show growth in 6–24 hours.Other laboratory tests that may assist in the diagnosis are
polymerase chain reaction (PCR), which detects B. anthracis DNA in pleural fluid or blood, serology (PA-based
74
ELISA), and tissue immunohistochemistry, in which tissue is stained with specific cell wall and capsular
antibodies. Dr Azamʼs Notes in Anesthesiology
2013
24.What is Low Flow Anesthesia? Discuss the advantages and disadvantage? THE PRACTICE OF LOW FLOW ANAESTHESIA:
Primary aim at the start of The
low practice of low flow anaesthesia
flow anaesthesia is to achievecan
anbealveolar
dealt with
concentra
Definition: under the following three categories:
the anaesthetic
• Technique that utilizes a fresh gas flow (FGF) that is less than the agent that is adequate I. Initiation of Low flow surgical
for producing anaesthesia anaesthesia (approximat
alveolar ventilation can be classified as Low flow anaesthesia II. Maintenance of Low flow anaesthesia
• Technique wherein at least 50% of the expired gases hadMAC). been The factors that can influence III. Termination of Low flow anaesthesia.
the build up of alveolar concentration should
returned to the lungs after carbon dioxide absorption.
• For most practical considerations, utilization of a fresh gasconsidered
flow Initiation of Low flow anaesthesia:
while trying to reach the desired alveolar concentration. These factors can bro
less than 2 liters/min may be considered as low flow anaesthesia. Primary aim at the start of low flow anaesthesia is to achieve an alveolar
concentration of the anaesthetic agent that is adequate for producing surgical
Flows: classified into three groups
anaesthesia (fig. 1); 1)1.3
(approximately Factors
MAC) governing the inhaled tension of the anaesth
classified the FGF used in anaesthetic The factors that can inBluence the build up of alveolar concentration:
practice into the following categories: Factors responsible
1) Factors gfor rise inthe
overning alveolar
inhaled ttension,
ension of 3)
the Factors responsible for uptake from the
anaesthetic,
• Metabolic flow: about 250 ml /min 2) Factors responsible for rise in alveolar tension,
• Minimal flow : 250-500 ml/min thus reducing the alveolar
3) Factors tension.
responsible for uptake from the lungs thus reducing the alveolar tension.
• Low flow: 500- 1000 ml/min
• Medium flow: 1 - 2 l/min
• High flow: 2- 4 l/min
• Super high flow: > 4 l/min Fig 1. Factors affecting the build up of alveolar tension
Equipment:
The minimum requirement for conduct of low flow
FACTORS AFFECTI NG THE 1. BREATHI NG CI RCUI T VOLUM E
anaesthesia is effective absorption of CO2 from the I NHALED TENSI ON 2. RUBBER GAS SOLUBI LI TY
expired gas, so that the CO2 free gas can be reutilized for 3. SET I NSPI RED CONCENTRATI ON
alveolar ventilation.
The circle system should have the basic configuration: FACTORS AFFECTI NG THE 1. CONCENTRATI ON EFFECT
• Soda lime canisters RI SE I N ALVEOLAR TENSI ON 2. ALVEOLAR VENTI LATI ON
• Two unidirectional valves on either side of the soda lime
canister, Fresh gas entry
• reservoir bag UPTAKE BY THE 1. CARDI AC OUTPUT
• pop off valve BLOOD 2. BLOOD GAS
• corrugated tubes and SOLUBI LI TY
3. ALV ± VENOUS
• Y piece to connect to the patient
GRADI ENT
Monitoring:
Regular monitoring plus
1. Inspired O2 concentration
2. EtCO2
3. Monitoring of end tidal anesthetic 75
concentration if available
Disadvantages of LFA:
THE MAINTENANCE OF LOW FLOW ANAESTHESIA: 1. The need to accurately adjust the flows of gases. The system is
This is the most important phase, This phase is characterized by inherently stable once a steady state is reached and small errors
• Need for a steady state anaesthesia often meaning a steady alveolar in the dosage of the agents or the gases would be of no concern.
concentration of respiratory gases. 2. Accumulation of trace gases20. It has, however, been often
• Minimal uptake of the anaesthetic agents by the body. overestimated.
• Need to prevent hypoxic gas mixtures. 3. Need for monitoring equipment. Oxygen monitor is necessary but
not mandatory if the recommended flow rates are used. EtCO2
TERMINATION OF LOW FLOW ANAESTHESIA: monitor is indicated to ensure satisfactory CO2 absorption and
There are only two recognized methods of termination of the maintenance of normocarbia. With a proper understanding of the
closed circuit. concepts of practice, the low flow anaesthesia technique can
First Method: Towards the end of the anaesthesia, the circuit is safely be used in all surgical procedures lasting more than an
opened and a high flow of gas is used to flush out the hour.
anaesthetic agents which accelerates the washout of the 4. The formation of compound A had been a matter of concern for
anaesthetic agents. several years.
5. The use of sevoflurane with a fresh gas flow rate of at least 1.0 L/
Second Method: Use of activated charcoal Activated charcoal min is assumed to be safe even in longer anaesthetic procedures.
when heated to 220oC adsorbs the potent vapors almost Sevoflurane, like all currently used volatile anaesthetics, is
completely. Hence, a charcoal-containing canister with a bypass degraded by carbon dioxide absorbents. The most significant
is placed in the circuit. degradant is a haloalkene known as "compound A" being
nephrotoxic in rats at an exposure of 150 – 340 ppm-h.
Advantages of LFA:
The low flow closed circuit anaesthesia has many advantages Absolute contraindications:
to offer. Smoke or gas intoxication,
1. Enormous financial savings due to use of low fresh gas Malignant hyperthermia
flows as well as the agent.
2. High humidity in the system leads to fewer post anaesthetic
complications.
3. Maintenance of body temperature during prolonged
procedures due to conservation of heat.
4. Reduction in the theatre pollution.
5. Low flow anaesthesia performed with markedly reduced
fresh gas flow rates improves climatisation of the
anaesthetic gases.
76
25. Anesthetic problem in prone position Dr Azam’s Notes in Anesthesiology 2013
Recommend invasive hemodynamic monitors in

patients with precarious cardiovascular status
Physiological Effect:
Respiratory
Cardiovascular System: System:
Respiratory
Circulatory
• Cephalad shift of diaphragm, compression abdominal viscera
• ↑ intra-abdominal & intrathoracic pressure→ ↓cardiac output, ↓BP
→ ↓ FRC, ↑work of breathing, ↑airway pressures
• IVC obstruction → vertebral venous plexus engorgement → ↑ • Ventral supports: improved lung volumes, oxygenation, and
bleeding, ↑ risk of thrombosis compliance, especially in obese patients
• Head low position: venous congestion of face and neck → facial, • Ventilation and perfusion are more uniform in prone position
conjunctival and airway edema → ↓ V/Q mismatch → Improved oxygenation
• Head high position: risk of venous air embolism
To assess hemodynamic response to prone position
• ↓Stroke volume, ↓ Cardiac index
• ↑SVR, ↑PVR
• HR, PAOP, Right atrial pressure: no change
Risk Factors for Prone Position:
• Peripheral neuropathies
• Advanced age
• Nerve entrapment syndromes e.g. carpal tunnel
• Alcohol abuse
• Diabetes mellitus
• Malnutrition
• Osteoarthritis, Rheumatoid arthritis
• Vitamin deficiencies
• Pre-existing decubiti
• Corticosteroid use
• Venous stasis
• Contractures
• Previous traumatic injury, fractures
• Morbid obesity
• Hypothyroidism 77
• Renal disease
Anesthetic problem in prone position Continuation:
Complications & Problems:
Airway & Facial injuries: Nerve Injuries: Eye Injury: Skin & Soft Tissue injuries: Others:
Mechanisms • Corneal abrasions • Key factors: amount and duration of

• Accidental extubation • ↑ stretch, compression → • Orbital edema pressure
• Obstruction of ETT ischemia • Postoperative visual loss
bloody • High risk areas: face, breasts,
• Occur despite adequate ( POVL) genitalia & bony prominences e.g.
• secretions/ sputum protection → other factors? • Rare; unclear etiology malar regions, chin, iliac crests,
plugs Prone patient knees, toes
• Facial, Airway edema Mechanism:
• Supraorbital, facial, mandibular • Uncontrollable factors e.g. duration
• Prolonged head low nerves • First is direct pressure to the of surgery may override protective
position, eye - incorrect positioning
• Brachial plexus and its peripheral measures → pressure injury
• ↑ crystalloid infusion components leading to the weight of the
Problems with •
head being supported by the
extubation globe will intuitively result in
damage secondary to Other
ischaemia. • Compartment
Ischemic Optic Neuropathy (ION) syndrome,
• The second is a result of poor
Etiology: perfusion. Rhabdomyolysis
• Intraoperative decrease in BP • Venous air embolism
• Prolonged surgery • Visceral ischemia:
• Increased Blood loss Central Retinal Artery Occlusion (CRAO): pancreatitis
• Increased Crystalloid infusion Etiology: • Undiagnosed space
Mechanism: occupying lesions
• Direct external pressure
• Ischemia • Emboli •
• Orbital edema leading to stretch and Mechanism:
compression of ON • Decreased “Ocular perfusion pressure
C/F: C/F:
• Painless • Painless
• Bilateral • Unilateral
• Decreased Light perception • Periorbital swelling or ecchymosis
• DecreasedVisual Bields 78

26. Discuss the physiological changes due to pneumoperitoneum during Laparoscopic abdominal surgery. Dr Azam’s Notes in Anesthesiology 2013
list the intraoperative complications.
Physiological Changes:
CVS Effects: Respiratory Effects: CNS: Liver:
Effect of Position: • Increase in Decrease

• Trendelenberg < 15 degree Renal: CBF and in portal
• Due to position Increase in ICP venous
• minimal shift in blood volume
• Alteration in gas exchange Increase in IAP - flow
• Trendelenberg >15 degree
• Head up position - V/Q better • decrease RBF &
• Increase in venous return
• Head down - minimal change decrease GFR
• Increase in CVP & Stroke • Mechanics of respiration Because of
volume
• Head up position - minimal decrease in Venous
• Head Up change
• Blood pooling return to the heart. Temperature:
• Head down - decrease FRC &
• Decrease venous return Decrease compliance
• Decrease cardia output All changes are significantly affected in • Hypothermia
These are related to steepness obese & respiratory disabled patients
Patients with comprised cardia • Due to insufflation
function have increase in O2 • Increase PaCO2
consumption • Increase V/Q mismatch - more in
• Effect of Increased IAP: ASA II & III patients
• decreased preload - RA Regional blood flow:
pressure does not reflect • decrease splenic, mesenteric & intestinal blood flow
• Due to anesthesia • decrease RBF, decrease GFR, Increase renal
preload
• Local - No changes vascular resistance
• Increased after-load
• GA spontaneous - increase in PaCo2 • Normal or increased coronary blood flow
• changes will depend on the IAP:
• GA controlled constant minute
• Up to 20 cm of H2O -
volume increase in PaCO2
Normal CO
In cardiac & respiratory disabled increase
• Above 20 cm of H2O -
in PaCO2 is exaggerated
Increase CVP & SVP PVR &
decrease CI
• Above 40 cm of H2O
• increase HR, BP, CVP & CO
79

Intraoperative Complications: Laparoscopic Surgery Dr Azam’s Notes in Anesthesiology 2013
Cardiovascular Complications: Nerve Injury:

Traumatic Complications: Respiratory Complications:
Arrhythmia: • Care must be

• Surgical emphysema taken
• Pneumothorax • Hypercarbia + Halothane
Vascular Trauma: Hypotension & CO • Avoid nerve
• Pneumomediastinum compression &
• pneumopericardium
• Major complication Gas embolism: hyperextension
• Veress needle into • Most fatal & dangerous complication
one of the vessels • Due to intravascular injection of gas
of the abdominal • occurs during induction of
wall - aorta, Vena pneumoperitoneum
cava, and
retroperitoneal Treatment of Gas embolism:
vessels • Immediate cessation of insufflation Endotracheal
and release of pneumoperitoneum Aspiration of gastric
Trauma to the abdominal viscera: Intubation:
• Patient in head down & left lateral content & Nausea vomiting:
• Hepatic tear • Head down &
position • Because of increase in
insufflation of gas
• Splenic tear • Discontinue N2O abdominal pressure
causing the shift of
• perforation of the stomach or intestinal tract • Aspirate gas from the CVP • Preoperative
the diaphragm
• Maintain oxygenation administration of antacids
causing downward & anti-emetics
shift of the
endotracheal tube
80

27. Post operative Visual loss: Dr Azam’s Notes in Anesthesiology 2013
Mechanism:
• First is direct pressure to the eye -
Visual loss after anesthesia and incorrect positioning leading to the
surgery is rare. weight of the head being supported
by the globe will intuitively result in
Anatomy of Visual Pathway: damage secondary to ischaemia.
• The second is a result of poor
• Cornea & lens focus light on the perfusion.
retina
• Iris controls the amount of light
reaching the retina
• The cillary body produces aqueous
humor Ischemic Optic Neuropathy (ION) Central Retinal Artery Occlusion
Etiology: (CRAO):
Blood supply & Nerve supply: Etiology:
• Intraoperative decrease in BP
• Opthalmic artery - 1st intracrainal • Direct external pressure
• Prolonged surgery
branch of internal carotid artery • Emboli
• Increased Blood loss Mechanism:
• optic nerve • Increased Crystalloid infusion
Mechanism: • Decreased “Ocular perfusion
Factors: pressure
• Ischemia
• Decrease in MAP diminishes ocular C/F:
• Orbital edema leading to stretch
perfusion pressure • Painless
and compression of ON
• Increase in IOP decreases retinal & C/F: • Unilateral
choridal blood flow Painless • Periorbital swelling or ecchymosis
•
• Anesthetics alter blood flow. Both • Bilateral
halothane & enflurane produces does • Decreased Light perception
related increase in retinal & decrease in • DecreasedVisual Bields
choridal blood flow further it decreases
perfusion pressure
Investigations: Special Investigations:

• ophthalmologist Consultation • Visual field testing
• Examination of pupil reactivity • Fluorescein angiography
• Opthalmoscopy • Electronretinography (ERG)
• IOP • Visual evoked potentials (VEPʼs)
• Eye movement and Visual field • CT
• MRI
81

Causes:
I. Cortical Blindness:
complete cortical blindness is defined as bilateral
visual loss, absence of optokinetic nystagmus implies
damage to both the left & right occipital cortex IV. Pregnancy Induced Hypertension:
Mechanism: • Blurring of vision
• Oxygen delivery to the visual pathway between the • Diminision of vision
optic nerve & occipital cortex decreased • Complete blindness
II. Acute Glaucoma: Causes:

more in women & elderly • Spasm of retinal vessels
Clinical features: • Edema
• Painful red eye • retinal detachment ( rare)
• cloudy or blurred vision • Cortical Blindness
• headache nausea vomiting
Treatment:
• Beta adrenergic antagonists
• Alpha adrenergic agonist
• carbonic anhydrase
• Steroids
• Iridectomy
III. Glycine Toxicity:

• Glycine crosses BBB and depresses the
spontaneous & evoked activity of retinal neuroma &
hyperpolarize cells through blocked of chloride
channels
• Serine plays an important role in causing visual loss
• Cerebral edema, decreased Na, & increased IOP
may cause blindness
IV. Prone positioning:

• refer mechanism of visual loss and refer problems of
prone position.
82

28. What are the major causes of Hypoxemia? What is Hypoxic Pulmonary Vasoconstriction? How
can general anesthesia worsens V/Q mismatch?
Five Causes of Hypoxemia (↓ PaO2):

1. Hypoventilation
2. Low inspired Oxygen
3. Right to Left shunt
4. Ventilation-Perfusion mismatch
5. Diffusion impairment
Five Causes of Hypoxemia (↓ PaO2):
Hypoventilation: Low inspired Oxygen:

• P(A-a)O2 is normal Right to Left shunt: Ventilation-Perfusion
• A decrease in Barometric
• PaCO2 is elevated ( Hypercapnia) pressure (High Altitude) • Healthy Individuals: mismatch:
• A portion of the • V/Q mismatch is the
• A decrease in FIO2 - bronchial circulation most common cause of
Causes of Hypoventilation: accidental disconnection
• Depression of CNS by drugs (blood supply to the hypoxemia in disease
of the ETT, leak or conducting zone of the state.
• Upper airway obstruction exhausted central supply airways) venous blood
• Disease of Neuromuscular of O2 drains into the
junction pulmonary vein
• Disease of respiratory muscles • A portion of coronary Diffusion impairment:
• Abnormality of the chest wall circulation venous blood
• Disease of motor neurons of the • PaCO2 is normal
drains through the
brain stem/Spinal cord thebesian veins into the
• P(A-a)O2 is normal at rest
• Inflammation, trauma or left ventricles
but may be elevated during
hemorrhage in the brain stem • Congenital abnormalities:
exercise
• TOF, VSD + PAS
• Intrapulmonary
Hypoxic pulmonary vasoconstriction is a paradoxical, physiological fistulas
phenomenon in which pulmonary arteries constrict in the presence of
hypoxia without hypercapnia, redirecting blood flow to alveoli with a higher
oxygen content.
83

Book Text Dr Azam’s Notes in Anesthesiology 2013
Pagina 2 di 8
How can general anesthesia worsens V/Q mismatch? Continuation:
V/Q Ventilation Perfusion:

Definition: It is relationship between
alveolar ventilation & total perfusion
In zone 1, alveolar pressure (PA) exceeds pulmonary

artery pressure (Ppa), and no flow occurs because the
intra-alveolar vessels are collapsed by the compressing
alveolar pressure.
In zone 2, Ppa exceeds PA, but PA exceeds

pulmonary venous pressure (Ppv). Flow in zone 2 is
determined by the Ppa-PA difference (Ppa - PA) and
has been likened to an upstream river waterfall over a
dam. Because Ppa increases down zone 2 whereas
PA remains constant, perfusion pressure increases,
and flow steadily increases down the zone.
In zone 3, Ppv exceeds PA, and flow is determined by
the Ppa-Ppv difference (Ppa - Ppv), which is constant
down this portion of the lung. However, transmural
pressure across the wall of the vessel increases down
this zone, so the caliber of the vessels increases
(resistance decreases), and therefore flow increases.
In zone 4, pulmonary interstitial pressure becomes
positive and exceeds both Ppv and PA. Consequently,
flow in zone 4 is determined by the Ppa-interstitial Figure 17-1 Schematic diagram showing the distribution of blood flow in the upright lung. In zone 1, alveolar pressure
pressure difference (Ppa - PISF) (PA) exceeds pulmonary artery pressure (Ppa), and no flow occurs because the intra-alveolar vessels are collapsed by the
compressing alveolar pressure. In zone 2, Ppa exceeds PA, but PA exceeds pulmonary venous pressure (Ppv). Flow in
zone 2 is determined by the Ppa-PA difference (Ppa - PA) and has been likened to an upstream river waterfall over a dam.
Because Ppa increases down zone 2 whereas PA remains constant, perfusion pressure increases, and flow steadily
• Ventilation (V) is approximately - 4 liters, & total perfusion (Q) - 5 liters
increases down the zone. In zone 3, Ppv exceeds PA, and flow is determined by the Ppa-Ppv difference (Ppa - Ppv),
• V/Q = 4/5 = 0.8 liters/min which is constant down this portion of the lung. However, transmural pressure across the wall of the vessel increases
down this zone, so the caliber of the vessels increases (resistance decreases), and therefore flow increases. Finally, in
zone 4, pulmonary interstitial pressure becomes positive and exceeds both Ppv and PA. Consequently, flow in zone 4 is
determined by the Ppa-interstitial pressure difference (Ppa - PISF). (Redrawn with modification from West JB:
Ventilation/Blood Flow and Gas Exchange, 4th ed. Oxford, Blackwell Scientific, 1970.)
84
In this region, alveolar pressure (PA) then exceeds Ppa and pulmonary venous pressure (Ppv), which
is very negative at this vertical height. Because the pressure outside the vessels is greater than the
Dr Azam’s Notes in Anesthesiology 2013 pressure inside the vessels, the vessels in this region of the lung are collapsed, and no blood flow
How can general anesthesia worsens V/Q mismatch? Continuation:
General anesthesia worsens V/Q mismatch
V/Q mismatch occurs very commonly during anaesthesia because the FRC falls leading to a change in the position
of the lung on the compliance curve. The apices, therefore, move to the most favourable part of the curve whilst the
bases are located on a less favourable part at the bottom of the curve.
At the extremes of V/Q mismatch, an area of lung receiving no perfusion will have a V/Q ratio of (infinity) and is
referred to as alveolar dead-space, which together with the anatomical dead-space makes up the physiological
dead-space. Ventilating the dead space is, in effect, wasted ventilation, but unavoidable.
In contrast an area of lung receiving no ventilation, owing to airway closure or blockage, its V/Q ratio will be zero
and the area is designated as shunt. Blood will emerge from an area of shunt with a PO2 unchanged from the
venous level (5.3kPa or 40mmHg) and produce marked arterial hypoxaemia. This hypoxaemia cannot be corrected
by increasing the FiO2, even to 1.0, as the area of shunt receives no ventilation at all. The well-ventilated parts of
the lung cannot compensate for the area of shunt because Hb is fully saturated at a normal PO2 . Increasing the
PO2 of this blood will not increase the oxygen content substantially.
In the case of shunt, therefore, adequate oxygenation can only be re-established by restoring ventilation to these
areas using measures such as physiotherapy, PEEP or CPAP, which clear blocked airways and re-inflate areas of
collapsed lung. Because closing capacity (CC) increases progressively with age, and is also higher in neonates,
these patients are at particular risk during anaesthesia as the FRC may fall below CC and airway closure result.
85

29. Describe clinical presentation, pathophysiology & management of Malignant Hyperthermia. Dr Azam’s Notes in Anesthesiology 2013
Definition: MH is a rare myopathy characterized by on acute hypermetabolic state Clinical Presentation:
with in the muscle tissue following induction of general anesthesia.
Early signs:
• Masseter spasm, Tachypnea (increased minute
• Genetic predisposition:
• Pharmacogenetic disorder: Susceptible patient have a genetic ventilation)
predisposition which does not manifest until they are exposed to • Rapid exhaustion of soda lime/(increasing ETCO2–
triggering agents or stressful environment. doubling /tripling earliest and most sensitive indicator)
• Heterogeneous genetic disorder: Genes on chromosomes 1, 3, 7, 17 and • Warm soda lime canister
19 have been linked with MH. • Tachycardia
• Ch -19 à skeletal muscle, ryanodine (Ryr1) receptor Ca+2 channel • Irregular HR
receptor
Intermediate signs:
• Midwest in US – has highest incidence of MH. Patient warm to touch (increased core temperature)
Pathophysiology: cyanosis ( decrease HbO2 saturation)
• Uncontrolled increase in intracellular calcium in skeletal muscle from Dark blood – Irregular HR.
sarcoplasmic reticulum, removes inhibition of troponin à Intense muscle
contractions Late signs:
• Enhanced and sustained ATPase activity à uncontrolled increase in Aerobic Generalized skeletal muscle rigidity
and Anaerobic metabolism prolonged bleeding
Dark urine - Myoglobinuria
•↓ Oliguria
• Increased O2 consumption Irregular HR.
• Increased CO2 production
• Severe Lactic acidosis
• Hyperthermia
• Hyperkalemia - K+ efflux from muscle Trigger agents:
Acidosis • Halogenated anesthetics: Ether,
Cyclopropane, Halothane, Methoxyflurane,
a) Increased Sympathetic tone
Enflurane, Isoflurane, Desflurane,
Sevoflurane
• Succinylcholine
86

Management of Malignant Hyperthermia: Continuation Dr Azam’s Notes in Anesthesiology 2013
Anesthetic Management:
Dantrolene prophylaxis for MH susceptible patients.
Treatment of MH: 5mg/kg PO in 3 or 4 divided doses every 6 hrs with last dose 4 hrs
• Etiologic treatment: preoperatively (OR) 2-4 mg/kg IV over 10-30min as prophylaxis prior to
Dantrolene – Hydantoin derivative – directly interferes with muscle induction – ½ dose is repeated 6 hrs.
contraction by binding the Ryr1 ca+2 channel receptor inhibiting Ca+2 Drug selection – % Barbiturates %% % N2O
release from sarcoplasmic reticulum. % % % Propofol % % % NDMR
Intracellular dissociation of E-C coupling. 20mg of Lyophilized powder to be % % % Etomidate % % % Anticholinesterase
dissolved in 60 ml of sterile H2O. (t ½ -6 hr). Safe% % % Benzodiazepines % % Anticholinergics%
Decreased temperature in thyroid strom and Neuroleptic Malignant – Drugs%% % Ketamine % % % Sympathomimetics
% % % Opioids % % % Local Anesthetics
Syndrome .
(esters amides)
2.5mg/kg IV every 5 min until episode is terminated Premedication: Well sedated – to avoid from stress triggering MH.
↓ % % Anticholinergics – Avoided (confusion regarding HR
Max 10mg/kg or interference with normal body heat loss)
↓ Anesthesia Machine: “Dedicated” anesthesia machines never used to
1 mg/kg IV every 6 hrs for 24-48 hrs to prevent relapse. deliver volatile anesthetics for use for MH patients.
• Symptomatic treatment Conventional Anesthesia Machine with disposable breathing circuit
- Immediately discontinue inhaled anesthetics and conclude surgery and fresh gas outlet hoses, fresh CO2 absorbent, no vaporizer
at soon as possible (removed) and continuous flow of O2 at 10L/min for 5 to 10 min before
- Hyperventilate lungs with 100% oxygen. using the machine.
- Initiate active cooling (increased saline 15ml/kg IV every 10 min) Regional Anesthesia:
Gastric and bladder lavage with iced saline, surface cooling. - Avoid stress – patients well sedated
- Correct Metabolic acidosis – NaHCO3 1-2 mEq/kg based on ABG - Acceptable choice.
- Maintain urine output (Hydration, Mannitol 0.25 G/kg IV, furosemide - Local anesthetic agents both esters & amide are acceptable.
1mg/kg IV)
- Treat cardiac dysrrhythmias (procainamide 15 mg/kg IV)
- Monitor in intensive care unit (urine output, ABG, pH, electrolytes)
- Hyperkalemia treated with insulin glucose and diuresis.
87

30. What is the criteria for discharge from post anesthesia care unit? Dr Azam’s Notes in Anesthesiology 2013
Post-anesthesia Recovery Score (Modified Aldrete Score) Post-anesthesia Discharge Scoring System
Activity Vital signs (BP and Pulse)
2 = Moves all extremities voluntarily/on command 1 2 = Within 20% of preoperative baseline
= Moves two extremities 1 = 20%–40% of preoperative baseline
0 = Unable to move extremities 0 = >40% of preoperative baseline
Respiration Activity
2 = Breathes deeply and coughs freely 2 = Steady gait, no dizziness
1 = Dyspneic, shallow or limited breathing 1 = Requires assistance
0 = Apneic 0 = Unable to ambulate
Consciousness Pain
2 = Fully awake Acceptable to patient; control with PO medications
1 = Arousable on calling 2=Yes
0 = Not responding 1 = No
88

What is the criteria for discharge from post anesthesia care unit: Continuation
Oxygen Saturation Surgical Bleeding
2 = SpO2 >92% on room air 2 = Minimal: no dressing change required
1 = Supplemental O2 req. to maintain SpO2 >90% 1 = Moderate: up to 2 dressing changes
0 = SpO2 <92% with O2 supplementation 0 = Severe: more than 3 dressing changes
10 = Total score 10 = Maximum score
Score >9 required for discharge Score >9 required for discharge
89

31. What is post operative jaundice? Describe its causes.
Postoperative jaundice occurs as a result of overproduction and underexcretion

of bilirubin, direct hepatocellular injury, or extrahepatic obstruction. [130] Most
etiologies of postoperative jaundice become manifested within 3 weeks of
surgery and can be classified as either mild (<4 mg/dL) or severe (>4 mg/dL).
The primary mechanisms by which certain drugs cause hemolysis and subsequent jaundice are:
(1) the drug adsorption type, whereby an antibody (IgG) reacts with a drug bound to the red blood cell membrane;
(2) (2) the neoantigen type (so-called innocent bystander), whereby the drug combines with the erythrocyte membrane and an antibody reacts
with the newly formed antigenic site to activate the complement cascade;
(3) The autoimmune type caused by an autoantibody (IgG) to erythrocytes.
Classifications: Etiology of postoperative jaundice by time course:
Immediate postoperative jaundice (<3 wk)

• Hemolysis
• Anesthesia
• Hypotension/hypovolemia Delayed postoperative jaundice (>3 wk)
• Drugs • Drugs
• Infection/sepsis • Blood transfusion
• Bleeding/resorption of hematoma • Post-intestinal bypass status
• Bile duct ligation/stricture/surgical injury • Total parenteral nutrition
• Hepatic artery ligation
• Retained common duct stone
• Postoperative pancreatitis/cholecystitis
• Acute viral hepatitis
• Gilbert's syndrome/Dubin-Johnson syndrome
• Inflammatory bowel syndrome
• Heart failure
• Pulmonary postoperative jaundice
• Blood transfusion
90

32. What is Minimum Alveolar Concentration(MAC)? Discuss the factors
which effects the alveolar concentration of an inhalation agent.
Definition: The minimum alveolar concentration (MAC) of an inhaled anesthetic is the alveolar concentration
that prevents movement in 50% of patients in response to a standardized stimulus (e.g., surgical incision).
Points:
• Developed to compare the potency of an agent
• MAC values are roughly additive ( i,e, 0.5 MAC of N2O + 0.5 MAV of sevoflurane = 1.0 MAC)
• MAC-BAR (1.5-2.0 MAC): concentration required to block autonomic reflex to nociceptive stimuli
• MAC-Aware: concentration at which 50% of patients will not be forming long-term memory MAC of different agents:
• MAC-Awake (0.3 - 0.5 MAC): concentration required to block voluntary reflex & control
perceptive awareness (i,e, opening eyes on command)
• MAC greatest at 1 year of age & reduced by 6% per decade of life Agent MAC
Nitrous Oxide 105

Factors Affecting MAC
Halothone 0.75
Isoflurane 1.2
Factors that increases MAC
Factors that decreases MAC Desflurane 6.0
( IDecreasing Potency):
( Increasing Potency):
• Very Young age( closer to 1 year of age)
• Anemia Sevoflurane 2.0
• Increased temperature (>42 degree)
• Elderly patients
• decreased altitude
• BNZ Enflurane 1.7
• Drugs: MAOʼs TCAʼs, cocaine, acute
• Intravenous anesthetics
amphetamine use
• Opiates
• Pregnancy
• Acute alcohol Use
• Hypothermia ! ! ! ! ! ! ! ! ! ! ! ! ! !
• Acidosis - Hypoxia
• Severe Hypotension
• High Altitude
• Hyponatremia
91

30. What is Monitored anesthesia care? Discuss the discharge criteria for a patient Dr Azam’s Notes in Anesthesiology 2013
after day care surgery.
ASA definition of MAC is: "Monitored anesthesia care refers to instances in which an anesthesiologist has been
called upon to provide specific anesthesia services to a particular patient undergoing a planned procedure, in
connection with which a patient receives local anesthesia, or in some cases, no anesthesia at all.
Additional requirements are:

1. Performance of a preanesthetic examination and evaluation.
2. Prescription of anesthetic care.
3. Personal participation in, or medical direction of, the entire plan of care.
4. Continuous physical presence of the anesthesiologist or, in the case of medical direction, of the resident or
nurse anesthetist being medically directed.
5. Proximate presence, or in the case of medical direction, availability of the anesthesiologist for diagnosis and
treatment of emergencies.
MAC does not necessarily imply the administration of sedatives. Facilities to secure the airway should always
be immediately available.
For Discharge criteria refer question # 27
92

31. Discuss measures to attenuate pressor response to laryngoscope. Continuation Dr Azam’s Notes in Anesthesiology 2013
A large number of drugs and techniques have been tried to obtund the hyperactive sympatho-adrenal pressor response to
laryngoscopy and intubation but none has been accepted as universal technique due to the complexity and lack of total efficacy of
each method.
Some methods are:
1. Duration of laryngoscopy should be as short as possible ideally < 15 seconds.
2. Deepening the level of anesthesia with volatile agent for 5-10 min.
3. Use of IV propofol prior to laryngoscopy
4. Use of local anesthetic spray (or) (gargles) 3 minutes prior to intubation with 4% to 10% lidocaine.
5. I.V. lidocaine 1.5 mg / kg IV / intratratheacly.
6. Low dose opioids fentanyl 2.5 to 5 μg / kg.
• Sufentanil 0.25 – 0.5 μg/kg
• Refimentanil 0.5 – 1 μg/kg
• Alfentanil 15-25 μg/kg
7. β adrenergic blockade % Esmolol 0.5 – 1.5 mg/kg
Propronolol 1-3 mg IV
Labetalol 5-20 mg IV
Droperidol
8. ACE inhibitors 45 min prior to intubation
9. Clonidine 4 μg/kg pre-medicate 1 ½ hr before induction.
10. SNP infusion 1-2 μg/kg issues prior to intubation
11. IV hydralazine / topical / transdermal NTG
93

32. 40. What is oculo-cardiac reflex? Discuss measures to attenuate pressor response to Dr Azam’s Notes in Anesthesiology 2013
laryngoscope
Oculo-cardiac Reflex: (Also called as Aschenrʼs reflex or Trigemino-

vagal reflex)
Pressure on the globe or traction on extra-ocular muscles
i+
Stretch receptors on extra-ocular muscles
i+
Short & long ciliary nerves + Ophthalmic division of V CN
i +
Gasserian ganglion
i + PNS
i
Bradycardia
Incidence: 30% - 90% of ocular surgeries. Can be attenuated by
administration of an antimusarmic drug (atropine / glycopyrrolate).
Cardiovascular responses to Anesthetic maneuvers and to surgery
Pathway :
• The afferent pathway follows the long and short ciliary nerves to
the cilliary ganglion and then to the gasserian ganglion along the
ophthalmic division of the trigeminal nerve.
• This afferent pathways terminate it the main trigeminal sensory
nucleus in the floor of the fourth ventricle.
• The efferent impulses starts in muscles of the vagal cardiac
depressor nerve and cause negative ionotropic and conduction
effects.
94

33. Write briefly on Research Ethics Dr Azam’s Notes in Anesthesiology 2013
Research ethics involves the application of fundamental ethical principles to a variety of topics
involving scientific research.
Ethical conduct of human subjects research follows 3 principles:
• Respect, with autonomy & obligation to protect the subject with limited autonomy
• Beneficence, with obligations to minimize risk, maximize benefits and ensure that the
research design is scientifically sound
• Justice, the obligation to treat each person with regard to what is normally right & to ensure
fair distribution of benefits & burdens.
• The disclosure of research must include the possibility of commercialization of the

results, financial interests.
• Subjects must be free to refuse or end participation at any time without penalty.
• Situational coercion - in which subjects believe that they are not true they are free to
refuse
• Monetary or other inducements to participate in research are permissible, if they refuse
do undermine the freedom of the subject to refuse under reasonable circumstances
• Researchers are obligated to maximize benefits and minimize potential harm, including
physical,psychological, social, legal and financial harm.
• The research must address a question of sufficient value to justify the level of risk & must
follow the approved protocol
• The research must be terminated immediately if it is suspected to be harmful to the
participants.
In terms of research publications, a number of key issues include

and are not restricted to:
• Honesty. Honesty and integrity is a duty of each author and
person, expert-reviewer and member of journal editorial boards.
• Review process. The peer-review process contributes to the
quality control and it is an essential step to ascertain the standing
and originality of the research.
• Ethical standards. Recent journal editorials presented some
experience of unscrupulous activities.
95

34. Meth-hemoglobinemia & anesthesiologist. Dr Azam’s Notes in Anesthesiology 2013
• Methemoglobinemia results from the oxidation of the ferrous iron in hemoglobin to the ferric iron state.
• It is incapable of carrying O2 high levels of methemoglobin may impact O2 delivery to the tissues, resulting in tissue hypoxia
• Known oxidant substance used most commonly in anesthetic practice include the local anesthetic agents (prilocaine, lidocaine, benzocaine),
metoclopramide, nitric oxide,Phenytoin, nitroglycerin, and sodium nitroprusside.
• Neonates may be at greater risk because of more readily available oxidized fetal Hb
• Normal Meth-hemoglobin constitutes < 1% of total Hb.
• Central cyanosis when methHb > 15% • Perioperative care includes arrival at the correct diagnosis
when there is a discrepancy between pulse oximetry and
clinical findings, determination of the cause with removal of
Meth-Hemoglobin Concentration % Clinical sign & symptoms the offending agent, treatment with intravenous methylene
blue, and maintenance of O2 delivery to tissue.
• Perioperative monitoring may be problematic because of
10 to 20 % central cyanosis of trunk & limbs usually the interference of methemoglobin with pulse oximetry
asymptomatic function.
20 to 45% CNS depression ( headache,
dizziness,fatigue,lethargy, syncope) Treatment:
• Methylene blue is the primary emergency treatment
45 - 55% Coma, arrhythmia, shock & convulsions for documented, symptomatic methemoglobinemia.
• The methylene blue dose is 1-2 mg/kg administered as a
> 70% High risk of Death 1% solution in intravenous saline over 3-5 minutes. This
dose may be repeated at 1 mg/kg every 30 minutes as
necessary to control symptoms. Doses of methylene blue
should not exceed 7 mg/kg, because this agent in itself
Diagnosis: can be toxic and cause dyspnea, chest pain, and
• Difference between calculated & measured arterial O2 saturation. hemolysis.
• Qualitative measurement of meth-hemoglobin by Co-oximetry. • Riboflavin (vitamin B-2) for Chronic cases
• The co-oximeter is an accurate device for measuring methemoglobin • Ascorbic acid (vitamin C) tendency to form Stones
and is the key to diagnosing methemoglobinemia. • Avoid drugs causing Meth-hemoglobin.
96

35. Microcirculation in Shock Microcirculation during Shock:
The disruption of microvasculature appears to be a final common path in all shock
Definition: states.
• The microcirculation is a term used to describe the small The resistance can occur at:
vessels in the vasculature which are embedded within organs 1. The arterioles
and are responsible for the distribution of blood within tissues. 2. Pre capillary sphincter
3. Post capillary sphincter
The microcirculation refers to the smallest blood The sphincters perform two functions:
vessels in the body: • They maintain hydrostatic pressure with in the capillary.
• the smallest arterioles • They maintain the direction of net flow across the capillary wall between the wall
• the metarterioles and extracellular fluid.
• the pre & Post capillary sphincters
• the capillaries
• the small venules
Structure:
There are two Stages:

I. Reversible Stage ( Compensated Mechanism)
II. Irreversible Stage
Reversible Stage ( Compensated Mechanism):
• The transport of nutrient to the tissue and Decrease in BP – Sympathoadrenal stimulation

removal of cellular excreta occurs in the ↓
microcirculation. PRE CAPILLARY SPHINCTER CONSTRICTION
• In general, each nutrient artery entering an
↓
organ, branches six to eight times before the
Decreases CAPILLARY HYDROSTATIC PRESSURE.
arteries become small enough (20 μm diameter)
to be called arterioles. ↓
FLUID MOVES INTO INTRAVASCULAR SPACE
• Arterioles themselves branch two to five times
(5-9 μm diameter) at their ends where they • HR increases because of stimulation of baroreceptors.
supply blood to the capillaries. • Renal conservation of fluid through renin-angiotensin mechanism
• Maintains adequate perfusion pressure to vital organs. 97

Irreversible Stage:
If hypoperfusion continues
↓
Hypoxia – Anaerobic metabolism
↓
↑ LACTIC ACID + ↑ [H+]
↓
↑ CAP. HYDR. PRES ←↑ Post cap. Sphincter tone
↓+
Weakening of pre cap sphincter tone
↓
Fluid loss into extra vascular space.
• Adhesion of activated leukocytes to endothelial cells - Increases capillary Permeability +
obstruction to micro vessels
• Accumulation of micro thrombi because of activation of coagulation system with fibrin
deposition.
Factors that influence the Sphincters:

• sympathetic activity
• local metabolites
• pH
• hypoxia.
• Metabolic acidosis
• Metabolic acidosis, and hypoxia relax the precapillary more

than the post capillary sphincter.
• In the late stages of hemorrhagic shock, the resistance of
the post capillary sphincter exceeds that of the precapillary
sphincter the direction of fluid flow is reversed and
interstitial edema occurs.
98

36. Clinical manifestations & Management of patient with acute anaphylaxis. Dr Azam’s Notes in Anesthesiology 2013
Definition:
Anaphylaxis is acute, severe, potentially life Management of Acute Anaphylaxis:
threatening allergic reaction characterized by
respiratory distress, cardiovascular collapse
and angioneurotic oedema in a sensitized
person on exposure to an offending antigen. Secondary or Subsequent Treatment:
Immediate Treatment:
Antihistamines:
Clinical Manifestations: • Stop injection or infusion in process
• Chlorpheniramine 10-20mg iv slow
CVS manifestations: • Switch to 100% O2 with low
injection
1. Tachycardia concentration of volatile agent
Steroids:
2. Hypotension • Mainstay of initial pharmacological
treatment is Adrenaline (epinephrine). • Glucocorticoids may be useful in
3. Dysrrhythmias. preventing potential late phase
If the patients are being monitored, it is • 0.01ml /kg increments of 1:1000 solution
reactions, but they have no immediate
characterized by decrease in MAP, DBP and IV. (0.01 to 0.5mg/ml).
effects. Hydro Cortisone 5 mg/kg up to
SBP. • If risk of laryngeal edema present, as
200mg initial dose and then 2.5 mg/kg
Respiratory System manifestations: evidenced by stridor and dyspnoea, the
every 6 hours OR Methylprednisolone
1. Wheeze – Bronchospasm patient should be intubated immediately
1 mg/kg IV every 6 hrs.
2. Cyanosis and ventilated with 100% O2.
• For persistent bronchospasm, it is
3. Laryngeal edema. • Rapid intravascular volume expansion.
prudent to use Aminophylline 5 mg/kg
Sudden decrease in pulmonary compliance is 25-50ml/kg (total2-4lit) of colloid or
IV in loading dose followed by 0.5 mg/
manifested by an increase in airway pressure crystalloid may be needed for correcting
kg/ by in infusion.
during positive pressure ventilation. Cyanosis hypotension.
• For persistent hypotension
or ↓PaO2 may be noted. • Discontinue all anaesthetic agents,
catecholamine infusion may be needed.
Cutaneous manifestations because they have negative inotropic
effects and may interfere with reflex • Epinephrine may be helpful for both
1. Flushing hypotension and bronchospasm.It is
2. Erythema response to hypotension.
given as 0.05 µg/kg/min infusion.
3. Urticaria and angioedema
• Dopamine in the dose of 5-10 µg//kg/
min helps to maintain Cardiac output,
thereby maintaining cerebral, coronary
and mesenteric blood flow.
• If acidosis is suspected, NaHCO3 (1
mEq/kg) should be administered.
99

37. Describe the techniques for anesthetizing airway for awake fiberoptic laryngoscopy and Dr Azam’s Notes in Anesthesiology 2013
intubation through nasal route in an adult with restricted mouth opening.
Awake intubation: Innervation:

• Modalities for awake intubation is fibreoptic bronchoscope • The nasal cavity is innervated by the greater and lesser palatine nerves and the
is the 1st choice anterior ethmoidal nerve.
• The oropharynx is innervated by branches of the vagus, facial and
Preoperative Preparation: glossopharyngeal nerves
• Preanesthetic evaluation • The internal branch of the superior laryngeal nerve is a branch of CN X (vagus
• Routine hemogram, urine exam,ABO group/cross match nerve). The superior laryngeal nerve provides sensory innervation to the base of
• Discuss the plan with the patient, explained consent for the tongue, posterior epiglottis, aryepiglottic folds, and arytenoids.
awake intubation. psychological preparation should be • This branch originates from the superior laryngeal nerve lateral to the greater cornu
performed with the mentating patient: the patient should be told of the hyoid bone. The recurrent laryngeal nerve provides sensory innervation of
the rationale for the procedure and what to expect, with the vocal folds and trachea and motor function of all intrinsic laryngeal muscles
reassurance except the cricothyroid supplied by the external branch of the superior laryngeal
• Consent for cricothyrotomy /mini tracheostomy / nerve.
tracheostomy (for emergency airway access, if required)
• Premedication with oral Ranatidine 150 mg night before & Techniques for Anesthetizing the Airway:
morning of the surgery. Topical Anesthesia of the Nose, Mouth, Tongue, & Pharynx:
• Nil orally after midnight • Vasoconstriction of the nasal mucosa can be achieved with phenylephrine 0.5% or
• Nasal decongestant, glycopyrrolate 0.4 mg I.M 1 hour oxymetazoline drops.
before the procedure (effective penetration of local • The nares can be anesthetized by applying 2% lidocaine jelly to, and inserting a
anesthetic into the mucosa) nasopharyngeal airway, or using a cotton pledget soaked with 2% lidocaine with
epinephrine.
In the operative room: Superior Laryngeal Nerve Block:
• Check the anesthesia machine & suction • The internal branch originates from the superior laryngeal nerve lateral to the
• Check the difficult airway tool chart greater cornu of the hyoid bone. In most patients, the nerve should pass
• Check the emergency & anesthetic drug chart approximately 2–4 mm inferior to the greater cornu of the hyoid bone.
• Check experienced help • A 5/8 -in., 25-gauge needle is inserted in an anteroinferomedial direction until the
• patient in supine position with extended neck arms well lateral aspect of the greater cornu is contacted.
supported • the needle is retracted slightly after contacting the hyoid, both the internal and
• Talk to the patient again, explain and allay the anxiety external branches of the superior laryngeal nerve are blocked. The syringe is then
• Two IV line access (18, 20G) aspirated, and if aspiration is negative for air and blood, 2 mL of local anesthetic
• Monitor ECG lead II, NIBP, Spo2,(Etco2 with mask, circuit) (2% lidocaine) with or without epinephrine (1:300,000) are then injected.
• If H/O of snoring airway obstruction avoid sedation
• Topical anesthesia of oral cavity, superior laryngeal nerve
block, and intratracheal lignocaine instillation.
100

Describe the techniques for anesthetizing airway for awake fiberoptic laryngoscopy and
intubation through nasal route in an adult with restricted mouth opening.Continuation:
Superior Laryngeal Nerve Block: continuation: Recurrent Laryngeal Nerve Block:

• Some patients may be unwilling or unable to undergo such injections. • The needle is advanced until air is freely aspirated,
Common reasons include patient refusal, anticoagulation, and signifying that the needle is now in the larynx. Instillation of
distorted anatomy due to tumors, arteriovenous malformations, local anesthetic at this point invariably results in coughing.
surgical deformities, or reconstruction Through coughing, the local anesthetic is dispersed,
• In patients in whom injection is contraindicated or overly challenging, diffusely blocking the sensory nerve endings of the recurrent
a less invasive technique for blocking the superior laryngeal nerve laryngeal nerve. Motor function remains completely
can be accomplished by using soaked pledgets. After topicalization, unaffected.
the patient is asked to stick the tongue out. The tongue is then
grasped using a gauze pad.With a right-angled forceps (Jackson-
Krause forceps) the anesthetic-soaked pledgets are placed in the
pyriform fossae located on either side of the root of the tongue. After
5–10 minutes, a sufficient degree of anesthesia should be present for
intubation.
Recurrent Laryngeal Nerve Block:

• The recurrent laryngeal nerve provides sensory innervation to the
vocal folds and the trachea. Blockade of this nerve is necessary to
provide comfort and prevent coughing while the endotracheal tube is
being paused between the vocal cords.
• Technique for blocking the sensory input of the recurrent laryngeal
nerve is the transtracheal block. In this technique, the cricothyroid
membrane is located in the midline of the neck. It can be located by
palpating the thyroid prominence and proceeding in a caudad
direction. The cricothyroid membrane is identified as the spongy
fibromuscular band between the thyroid and cricoid cartilages . After
sterile skin preparation, the overlying skin is anesthetized by raising a
small skin wheal of local anesthetic. Then a 22- or 20-gauge needle
on a 10-mL syringe with 4mL of 4%lidocaine is passed perpendicular
to the axis of the trachea and pierces the membrane.While the
needle is being advanced, the syringe is continuously aspirated.
101

Describe the techniques for anesthetizing airway for awake fiberoptic laryngoscopy and intubation Dr Azam’s Notes in Anesthesiology 2013
through nasal route in an adult with restricted mouth opening.Continuation:
Step-by-Step Method for Orotracheal Fiberoptic Intubation Using Topical Anesthesia Only
1. Administer antisialogogue (glycopyrrolate 0.2–0.4 mg + dyphenhydramine (Benadryl) 20 mg IM) at least
20–30 minutes before fiberoptic instrumentation.
2. Provide judicious sedation using appropriate doses of midazolam and fentanyl/alfentanil and/or
dexmedetomidine.
3. Use benzocaine spray to anesthetize the oral cavity and pharynx.
4. Apply a generous amount of2%lidocaine ointment on the Ovassapian airway, and insert the tip of the
airway in the patientʼs mouth. As the lidocaine ointment is dissolved, it is carried deeper into the pharynx
and swallowed by the patient. The airway is then advanced deeper as tolerated by the patient every 2–3
minutes. Eventually, the patient should be able to swallow the entire airway without discomfort.
5. Attach a 5-mL syringe containing a solution of 4% lidocaine to the insufflating port of the flexible
bronchoscope.
6. Advance the bronchoscope until the epiglottis and vocal chords are seen and proceed as follows:
7. Inject 2 mL of local anesthetic over the epiglottis, wait 15 seconds, and advance the scope (anesthetizes
the epiglottis and superior aspect of the cords).
8. Inject 1mL of local anesthetic when the tip of the scope is just above the vocal cords; wait 15 seconds and
advance the scope (anesthetizes cords).
9. Inject 2 mL of local anesthetic when the tip of the scope passes underneath the vocal cords (anesthetizes
the trachea).
10. Advance the scope until the carina is seen.
11. Advance the endotracheal tube over the fiberoptic scope.
12. If unable to intubate using the above method, attempt appropriate blockade of individual nerves until the
patient is able to tolerate intubation.
102

38. American Society of anaesthesiologist(ASA) physical status classification. Dr Azam’s Notes in Anesthesiology 2013
ASA Physical Status (PS) Classification System*:

American Society of Anesthesiologists Physical Status Classification
ASA 1 ASA:
Healthy patient without organic, biochemical, or psychiatric disease
ASA 2 • If the surgery is an emergency, the physical
A patient with mild systemic disease, e.g., mild asthma or well- controlled hypertension. No status classification is followed by “E”
significant impact on daily activity. Unlikely to have an impact on anesthesia and surgery • The purpose of the grading system is simply to
ASA 3 assess the degree of a patient’s "sickness" or
Significant or severe systemic disease that limits normal activity, e.g., renal failure on "physical state" prior to selecting the anesthetic
dialysis or class 2 congestive heart failure. Significant impact on daily activity. Probable or prior to performing surgery.
impact on anesthesia and surgery
ASA 4 • Describing patients’ preoperative physical status
Severe disease that is a constant threat to life or requires intensive therapy, e.g., acute is used for record-keeping, for communicating
myocardial infarction, respiratory failure requiring mechanical ventilation. Serious limitation between colleagues, and to create a uniform
of daily activity. Major impact on anesthesia and surgery system for statistical analysis.
ASA 5
• The grading system is not intended for use as a
Moribund patient who is equally likely to die in the next 24 hours with or without surgery
measure to predict operative risk.
ASA 6
Brain-dead organ donor
“E” added to the classification indicates emergency surgery. Available from
103

39. Activated Protein - C (APC) Dr Azam’s Notes in Anesthesiology 2013
• Activated protein C (APC) is an important mediator of the bodyʼs Adult drotrecogin alfa guidelines:
response to sepsis as it possesses antithrombotic, anti-fibrinolytic • Do not prescribe if more than 48 hours has passed
and anti-inflammatory properties. since patients first met criteria
• APC inactivates clotting factors Va and VIIIa, thereby preventing the • At least three of the following four criteria of systemic
generation of thrombin. inflammatory response syndrome:
• Inhibition of thrombin formation decreases inflammation by inhibiting • Core temperature > 380 C or < 360 C
platelet activation, neutrophil recruitment and mast-cell • Heart rate more than 80 beats/min
degranulation. • Respiratory rate > 20 breaths/min or PaCO2 < 32
• APC has direct anti-inflammatory properties by blocking the mm Hg
production of the pro-inflammatory cytokines tumour necrosis • White cell count > 12,000/mm or < 4,000/mm
factor, interleukin-1 and interleukin-6 and limiting the adhesion of • At least one organ or system dysfunction presumed
immune cells to endothelium. due to sepsis.
Mechanism of Action:
• APC inhibits iNOS(inducible Nitric Oxide synthetase) expression Dosage, Form & strengths :
• Decreases level of TNF - ɑ • Infuse intravenously at 24 mcg/kg/hr (based on actual
• Reduces leucocyte activation, decreases adherence plasma body weight) for a total duration of 96 hours.
extravasation • Single-use vials of 5 mg and 20 mg Xigris as a sterile,
• Reduces release of reactive O2 species preservative-free, lyophilized powder for reconstitution.
• The 5 and 20 mg vials of Xigris contain 5.3 mg and 20.8
• Improves capillary density
mg of drotrecogin alfa (activated), respectively.
• Acts on coagulation pathway by inhibiting factors Va & VIIIa • The 5 and 20 mg vials of Xigris (drotrecogin alfa) also
& promotes fibrinolysis. contain 40.3 and 158.1 mg of sodium chloride, 10.9 and
• Decreases systemic cytokine IL - 1β 42.9 mg of sodium citrate, and 31.8 and 124.9 mg of
• Decreases Apoptosis sucrose, respectively.
• Inhibits synthesis of plasminogen activators inhibitor 1.
Indications:
• Patients with severe sepsis
• APACHE II score ≥ 25
• Dysfunction of 2 or more organs
Contraindications:
• Thrombocytopenia ( platelets < 30,000)
• Recent stroke
104

40. Phantom limb pain Dr Azam’s Notes in Anesthesiology 2013
• This is the sensation of the continued presence of an amputated New treatments:

limb. • An electrical prosthetic limb moved by signals from the
• It is most common after arm amputation and if the amputation is patient's muscle reduced the pain if used for several hours
delayed after the initial injury. per day.
• It is associated with tingling or pain, which is severe in 15% of cases.
• The perceived limb may be felt to be in an abnormal position. Visual trickery:
• It is believed to be a state of central pain. • Stimulation of the motor cortex can reduce phantom limb
pain.
Mechanisms • These new approaches are all based on a shift in emphasis
in phantom limb pain away from the site of damage – the
There may be many mechanisms underlying phantom limb pain: stump – to the centre of pain processing: the brain. It
• Damage to nerve endings is often important; subsequent erroneous appears that disordered inputs from the limb's sensory
regrowth can lead to abnormal and painful discharge of neurones in systems, combined with disrupted motor signal back to the
the stump, and may change the way that nerves from the amputated limb, generate a mismatch between the brain's built-in map
limb connect to neurones within the spinal cord. of the physical body and what is actually perceived. It would
• There is also evidence for altered nervous activity within the brain as appear that this mismatch results in pain.
a result of the loss of sensory input from the amputated limb.
• Phantom limb pain is generable intractable and chronic; once it
develops, it persists and is rarely improved by present medical
treatments.
Traditional treatment of phantom limb pain:

Traditional treatments include:
• Phenytoin, carbamazepine, sympathetic nerve blocks,
transcutaneous electrical nerve stimulation (TENS), dorsal
column stimulation and cordotomy. Pre-emptive analgesia with
epidurals has been claimed to prevent the development of
phantom limb pain when instituted before surgical amputation.
105

41. Capillary Circulation. Dr Azam’s Notes in Anesthesiology 2013
Capillaries: • True capillaries are devoid of smooth muscle and are therefore
• Capillaries serve as the site for the transfer of O2 and nutrients to incapable of active constriction.
tissues and receipt of metabolic byproducts. • Endothelial cells contain actin and myosin and can alter their shape
• Capillaries are numerous is metabolically active tissues (cardiac in response to certain chemical Stimuli.
and skeletal muscles) • The thin cells of capillaries are able to withstand high intraluminal
• Anatomy: Arterioles give rise to metarterioles which give rise to pressures, because their small diameter prevents excessive cell
capillaries. tension.
• Capillaries drain via short collecting venules to the veins. Blood flow:
• Blood flow through capillaries is regulated by muscular • BF in capillaries is intermittent rather than continuous.
precapillary sphincters present at the capillary opening. • Intern BF reflects contraction and relaxation of metarterioles and
• Arterioles metarterioles and venules contain smooth muscle. As precapillary sphincters. This phenomenon is known as vasomotion.
a result the arterioles serve as the major resistance vessels and • O2 is the most important determinant of the degree of opening and
regulate regional blood flow to the capillary beds. closing of metarterioles precapillary sphincters.
• Venules and veins serve primarily as collecting channels and • Low PO2 allows more blood to flow through capillaries to supply
storage or capacitance vessels. tissues.
• Capillary walls are about 1 mm thick consisting of a single layer • So nutritive blood flow is regulated by O2 and there is also
of endothelial cells surrounded by a thin basement membrane on nonnutritive BF regulated by A.N.S.
the outside. • The nonnutritive BF is characterized by direct vascular connections
• The structure of capillary wall varies from tissue to tissue between arterioles and venules.
• The interdigitated junction between endothelial cells allows • In some parts of the skin these arteriovenous anastomosis provide a
passage of molecules upto 10nm in diameter. much to permit rapid inflow of arterial blood to warm the skin i.e.
• The cytoplasm of endothelial cells is attenuated to form, gaps or important in regulating temperature of the body.
pores that are 20 to 100nm in diameter.
• These pores permit the passage of relatively large molecules. Fluid movement:
• Plasma and its dissolved proteins are taken up by endocytosis • Solvent and solute movement across capillary endothelial cells
transported across the endothelial cells and discharged by occurs by filtration, diffusion and pinocytosis via endothelial vesicles.
exocytosis into the interstitial fluid. • Filtration is the net outward movement of fluid at the arterial end of
• In the brain – the interdigitated junctions between endothelial capillaries.
cells are tighter. • Diffusion of fluid occurs in both directions across capillary
• The diameter of H2O molecule is 0.3 nm that can normally pass membranes.
through endothelial cells.
• O2 and CO2 are both lipid soluble and readily pass through
endothelial cells.
106

Capillary Circulation.Continuation: Dr Azam’s Notes in Anesthesiology 2013
Filtration: • Interstitial fluid is held in a gel that fills the spaces between cells. This
• 4 pressures that determine whether fluid will move outward gel contains large quantities of mucopolysaccharides (hyaluronic
across capillary membranes (Filtration) or inward across capillary acid)
membrane (reabsorption) are • Loss of negative interstitial fluid pressure allows fluid to accumulate
1. Capillary pressure (Mean capillary pressure: 17 mmHg) in tissue space as edema.
2. Interstitial fluid pressure (6.3 mm Hg)
3. Plasma colloid osmotic pressure (28 mm Hg) Plasma Colloid Osmotic Pressure (PCOP):
4. Interstitial fluid colloid osmotic pressure (5 mm Hg) • Plasma proteins are responsible for the PCOP that tends to cause
• The net effect of these 4 pressures is a positive filtration movement of fluid Inward through capillary membranes.
pressure of the arterial end of capillaries – causing fluid to move • 70% of total PCOP results from albumin and only 30% from globulin
outward across cell membranes into interstitial fluid spaces. and fibrinogen.
• At the venous end of capillaries the net effect of these and • A special phenomenon known as Donnan Equilibrium causes the
pressures is positive reabsorption pressures causing fluid to PCOP to be about 50% greater than that caused by proteins alone.
move inward across capillary membranes into capillaries. • This reflects the negative charge characteristic of proteins that
• Over all the mean values of the 4 pressures acting across necessitates the presence of an equal number of positively charged
capillary membrane are nearly identical such that the amount of ions mainly negative.
fluid filtered= the amount of fluid reabsorption • About 1/3 of the normal PCOP of 28 mmHg is caused by positively
• Any fluid that is not reabsorbed enters the lymph vessels. charged ions held in the plasma by proteins.
Capillary pressure: • So replace of dextran cannot maintain normal PCOP.
• Capillary pressure tends to move fluid outward across the arterial
ends of capillary membranes. Interstitial Fluid colloid Osmotic Pressure (ICOP):
• Capillary pressure at the arterial end of capillaries is 25 mm Hg. • Proteins present in the interest fluid are responsible for ICOP
Pressure at the venous end of capillaries is 10 mm Hg. So the • It tends to cause movement of fluid outward across capillary
mean capillary pressure is about 17 mmHg. membranes. Normal ICOP is about 5 mmHg.
• Changes in arterial pressure have little effect on capillaries • The total protein content of interest fluid is similar to the total protein
pressure content of plasma, but the volume of the interstitial fluid is 4 times the
Interstitial Fluid Pressure: % volume of plasma, the average interstitial fluid protein content is only
• It tends to move fluid outward across capillary membrane ¼ that in plasma or about 1.8 g/dl
• Average interstitial fluid pressure is 6.3 mmHg. Diffusion: (Depends on concentration gradient)
• The negative pressure act as a vacuum to hold the tissues • Is the important much to transfer of nutrients between the plasma
together and maintain a minimal distance for diffusion of and the interstitial fluid.
nutrients. • O2, CO2, anesthetic gases are lipid soluble, which can diffuse
directly through capillary membranes.
107

Capillary Circulation.Continuation: Dr Azam’s Notes in Anesthesiology 2013
• Na, K, Cl and glucose are insoluble in lipid capillary membranes,

so they pass through pores à((20-200 nm)
• Diffusion depends on concentration difference.
• So O2 moves from capillaries to tissues and CO2 in opposite
direction.
Pinocytosis:
• Is the process by which capillary endothelial cells ingest small
amounts of plasma or interstitial fluid followed by migration to the
opposite surface where the fluid is released.
• Transport of high mol wt substances such as plasma proteins,
glycoprotein, dextran – occurs by pinocytosis.
108

42. Uses of CO2 in Anesthesia. Dr Azam’s Notes in Anesthesiology 2013
Discovered by JEAN BAPTISTE VON HELMONT and isolated by Other therapeutic uses:
(JOSEPH BLACK in 1757.) • Management of CO-poisoning
• Colorless gas, pungent odour in high concentration mol. wt. 44. • Treatment of hiccups
Boiling point – 78.50C. Critical temperature 310C. Sp. Gr. 1520. • Use in petit mal seizures.
In atmosphere at and concentration 0.03 vol%.(Air is 1000) • Counteraction of deleterious effects of low O2 levels on intellectual
• Prepared –from fermentation in brewing of beer function and improvement of the abnormal EEG pattern associated
• By product of manufacture of hydrogen in petrol refining with hypoxemia.
• From combustions of other fuels.
• By heating magnesium and CaCo3 in presence of their
oxides.
• Stored in grey cylinders at 50 bar.
• Breathing 5% CO2 in air or oxygen is tolerable, but high amounts
cause dyspnea, headache etc.
• Above 10% - Narcotic effect more marked, CO2 narcosis
• 30% - Isoelectric EEG and coma
• 40% - Breathing depressed.
Clinical uses in anesthesia:

1. To raise PaCO2 when discontinuing IPPV so that spontaneous
respiration is established more quickly. Patients ventilated
during operations are frequently hypocapnic, so that use of
CO2 under these circumstances is reasonable.
2. To hasten inhalation induction especially with agents of high
solubility. Adding 5% CO2 for to longer than 5 min, stimulates
respiration and helps to overcome laryngeal spasm and break
holding. It also speeds elimination of such agents at end of
surgery.
3. To widen glottis and facilitate blind intubation.
4. To insufflate abdomen for laparoscopy
5. As a cerebral vasodilator in studies of cerebral blood flow.
6. For cryoprobe
7. To confirm breath death.
8. 5% CO2 will raise PaCO2 by about 35 mmHg for a given
alveolar ventilation.
109

43. Nitric Oxide. Dr Azam’s Notes in Anesthesiology 2013
• An endogenous, endothelium derived relaxing factor. CLINICAL USES:

• NO is synthesized from the amino acid L- arginine by NO • Inhaled NO can diffuse from alveoli to pulmonary vascular muscle
synthetase and produces pulmonary vasodilation but will not produce systemic
• NO activates guanylate cyclase effects because NO that diffuses into blood is immediately
• ↓ inactivated by Hb thus inhaled NO functions as a selective
• Increase GMP à vasodilatation pulmonary vasodilator for the management of a disease associated
• No has half time of <5 seconds with pulmonary hypertension.
• Inhaled NO 10 to 20 ppm has been used for therapy persistent
Physiological effects: pulmonary hypertension of the newborn.
1. CVS – NO regulates SVR and PVR under baseline conditions. • ARDS à Inhaled NO in concentration ranging from 5 to 40 ppm
Its a major factor in autoregulation. NO release is important for decrease PVR and improves arterial oxygenation. Inhaled NO gets
opposing the pulmonary hypertensive response to multiple distributed according to ventilation so that the associated
stimuli, including arterial hypoxemia. vasodilatation increases blood flow to the well ventilated alveoli.
2. NO has negative inotropic and chronotropic effects. Toxicity:
3. Pulmonary system Pulmonary toxicity due to its reactive metabolite NO2
• Bronchodilator ← NO à selective vasodilatation of • 6 days – 6 months at 10-40 ppm safe.
ventilated segments • NO2; cause acid pneumonitis and oedema
% % % % ↓ • Upper limit of NO2 is 5
Increase ventilation – perfusion matching Technique of administration:
• NO ventilation delivery system: Add NO to ventilator in a Inhaled NO is dispersed in cylinders (high concentration) along with N2
constant proportion to minute ventilation. (200-2000 ppm) this needs to be diluted with inspiratory gases to attain
• Rapidly inactivated by Hemoglobin, hence lacks systemic effects. therapeutic concentration.
1. CNS – Endogenous NO is a neurotransmitters in the brain, 2 major system of administration:
spinal cord and peripheral nervous system. 1. Upstream delivery system
2. NO may be important for the formation of memory involved in 2. Downstream delivery system.
antinociception and in modulating anesthetic effects. Upstream delivery system: This system premix required flow of NO in
3. Platelets à NO inhibits platelet aggregation and activation, N2, air and O2 to obtain the concentration of NO necessary for
useful in maintaining antithrombotic properties of endothelium. therapeutic effect and deliver the gas mixture into gas inlet of
4. Immune function: Kills bacteria, virus and fungi. Increase ventilator. This system enables stable administration of NO
phgocytosis by macrophages. Modulates inflammation. concentration.
Disadvantage: 1) Long contact time between NO and O2 leads to
formation of high concentration of NO2 à which can cause acid
pneumonitis and pulmonary edema. 2) It can damage components of
ventilators.
110

Nitric Oxide. Dr Azam’s Notes in Anesthesiology 2013
Downstream delivery system:

This stem delivers constant flow of NO into proximal end of
inspiratory limb of ventilator circuit.
1. Continuous administration: Constant flow of NO both during
inspiration and expiration phase of ventilation.
2. Sequential administration: Constant flow of NO only during
inspiratory phase of ventilation.
3. Monitoring NO concentration by electrochemical cell monitor
4. Metabolism and toxicity: NO has higher affinity towards Hb.
NO+Hb=Methhemoglobin and carboxy hemoglobin.

• These undergo complex metabolic process which finally results
in formation of nitrates which are excreted in urine.
Toxicity:
1. NO itself
2. NO2 ; Acid pneumonitis and edema
3. Methemoglobinemia
4. Nitrates.
111

44. Total Intravenous Anesthesia. Dr Azam’s Notes in Anesthesiology 2013
Definition: DRUGS USED FOR TIVA:

THIOPENTONE
• The complete provision of anesthesia by the intravenous route.
History: • Infusion rates of 150-300μg/kg/min with N2O (67%). This produces
• 1934 – Introduction of barbiturates. plasma concentration of 15-25 μg/ml.
• 1969 – Use of morphine as sole anesthetic agent for cardiac • Continuous infusion causes saturation of the peripheral tissue
surgeries. storage sites resulting in slow recovery. This is due to low hepatic
• 1975 – Use of Althesin + pethidine. clearance rate.
IDEAL PROPERTIES OF DRUGS REQUIREMENT FOR TIVA: • At infusions rates > 300μg/kg/min, the concentration will increase
1. Should be soluble in water exponentially as the peripheral stores become saturated. So, use is
2. Should be stable in solution. associated with prolonged recovery.
3. Should not be adsorbed onto plastic infusion sets • After a 2 hr infusion, 20% of the total drug dose will be present as
4. Should not cause venous damage or tissue damage phenobarbitone à an active metabolite.
5. Sleep should be produced in one arm brain circulation • Other disadvantages of this infusion are,
6. Should have a short duration of action • Low therapeutic index
7. Should form inactive, non-toxic and water soluble metabolites • Porphyrinogenicity
8. Should have minimal cardiovascular and respiratory side • Hepatoxicity with large doses.
effects. Advantages are
INDICATIONS FOR TIVA: 1. Minimal cardiovascular depression.
1. By infusion as an alternative to volatile agents used to 2. Brain protection during cerebral ischemia.
supplement N2O and O2 anesthesia
2. To provide sedation during local or regional anesthetic METHOHEXITONE
techniques. • Used as a sole agent or as supplement to N2O or opioids in
3. For ambulatory surgery when the speed and completeness of • Body surface operations
recovery are important. • Intra-abdominal operations
4. For situations in which conventional anesthetics may be difficult • Neurosurgical operations
to administer. • Dose: 50-120μg/kg/min
5. In circumstances where N2O is undesirable or contraindicated. • Recovery prompt unless the total dose is >500-600 μg/kg
DISADVANTAGES OF TIVA: Disadvantages:
1. Possibility of awareness. 1. Excitatory movements.
2. Likelihood of post-op respiration depression. 2. Pain on injection.
3. Requirement for a separate and dedicated IV access site and 3. Predisposition for convulsions.
appropriate infusion pumps
4. Inability to control the depth of anesthesia as well as with
volatile agents.
5. Once given cannot be removed.
112

Total Intravenous Anesthesia.Continuation: Dr Azam’s Notes in Anesthesiology 2013
Advantages: Disadvantages:
1. Faster recovery 1. Cardiovascular stimulation
2. No hepatotoxicity 2. Intra & post-op dreaming and hallucinations
3. No adverse effects on adrenal cortex 3. Excessive salivation, emergence delirium.
ETOMIDATE Contraindications:
• Plasma concentration for anesthesia -- 300-500 ngm/ml
Disadvantages: 1. Cerebrovascular disease
• High incidence of nausea and vomiting 2. Hypertension
• Excitatory movements ( especially in unpremedicated patients) 3. Ischemic or valvular heart disease.
• Dose dependent depression of adrenal steroidogenesis which 4. Increase IOP and / or increased ICP.
may lead is increase mortality. By inhibiting 11β - 17 - α PROPOFOL "
hydroxylases and 20,22-lyase • Induction -2-2.5mg/kg (1-1.5 mg/kg)
• Pain on injection • Infusion – 100-200 μg/kg/min.
• Venous thrombosis and phlebitis. • Only real advantage over Thiopentone is in day-care surgery.
Advantages: Advantages:
1. Sleep in one arm-brain circulation 1. Rapid clearance and faster recovery
2. No detectable histamine release 2. Short duration of action
3. Low incidence of allergic reactions 3. No effect on steroidogenesis or haeme synthesis
4. Minimal cardiovascular and respiratory depressive effects 4. Act on CTZ chemoreceptor trigger zone.
5. No inhibition of HPV Plasma therapeutic level: 4-6 µg/ml (with N2O ).
6. Reduction in cerebral metabolism, CBF and ICP • IDEAL agent for TIVA due to its high clearance rapid initial decline in
7. Rapid recovery drug concentration in the blood.
8. Advantageous in patients with poor cardiac reserve • Different anesthetists hold differing news on whether the hypnotic
hypovolemia or acute intermittent porphyria. component of TIVA regimens or the analgesic components should be
KETAMINE altered according to patient response.
• Only hypnotic agent that has also analgesic properties. TIVA IN CHILDREN: %
• Analgesic threshold: 200 ngm/ml • ED 95 dose of propofol required is twice that compared to adults
• For hypnosis (with N2O): 1.5 – 2.5 μg./ml (10.5 mg/kg/hr. V/S 5 mg/kg/hr). But achieved blood concentration
• Loading dose: 2mg/kg were similar.
• Infusion: 40 μg/kg/min. • Alfentanil – propofol regimen results in only minor decreases in BP
• When used as the sole agent, infusion rates of 60-80μg/kg/min and heart rate (less than that seen in adults).
provides clinical anesthesia.
• Metabolite I: Nor-ketamine à Active with 30% potency (Appears
in 5 minutes)
• Metabolite II: Dehydro-ketamine à 1% active (Appears in 20
min) 113

ANALGESIA FOR TIVA TECHNIQUES Effects on respiration and ventilatory performance:

• Drugs with either limited respiratory depressant effects E.g.: • Apnea 4-30 % more in those premedicate with an opioid or
partial opioid agonists or the careful titration of drug dose to benzodiazepine (Dose related with propofol)
effect. • Bronchospasm / laryngospasm common with barbiturates
• Morphine and pethidine are now replaced by newer drugs -- • Increased salivation with ketamine.
Anilino – piperidine derivatives. • Depression of HPV reflex with resultant V/Q mismatch with all
• Fentanyl, Alfentanil or Sufentanil à All can be used either by volatile agents.
multiple increments or by continuous infuse. • Bronchodilator with volatile agents and ketamine
Disadvantages of Alfentanil: • All agents cause a dose dependent respiratory center depression
1. Less potent than the parent drug Fentanyl. and depression of chemoreceptor responses.
2. Emetic effect. Effects on cerebral hemodynamic function and cerebral pressures
3. Laryngeal and chest wall rigidity. • Decrease CSF with Thiopentone / methohexitone / etomidate (when
4. Post-op respect depression. used in high doses)
Plasma concentration of Fentanyl: 3-5 ng/ml for superficial body • Increased cerebrovascular resistance and decrease in ICP due to
surface surgery. 4-8 ng/ml for intra abdominal surgery. decreased CBF and decrease in cerebral blood volume.
Dose: • Decrease CMRO2
5-10 μg/kg – loading • N2O increases CBF.
3 μg/kg/hr and 2 μg/min maintenance rate. Awareness during TIVA is a major concern. Titration of drug doses is
Effects of hypnotic and analgesic drugs on systemic responses to important in blocking awareness.
anesthesia and surgery Effect on liver, renal & other tissues :
1. On central hemodynamics: • Decreases hepatic blood flow with volatile anesthetics.
• Decrease in BP (Both SBP and DBP) max within 1 min and • Decreases RBF/GFR/urine with volatile anesthetic (Greatest
sustained for 5 min with barbiturates with Isoflurane)
• Compensatory tachycardia • IV hypnotic agents (Except ketamine) also decrease HBF
• Increase in IOP. and RBF
• With ketamine à Increase BP /HR/ cardiac output/ increase left Anaphylactic and Anaphylactoid reactions to IV agent:
ventricular force of contraction. • All IV agents are liable.
2. CVS effects of infusions of hypnotic agents in TIVA: • Incidence 1/5000 – 1/20,000 (less with Barbiturates)
• Propofol: ↓ MAP by 15.20% to due to decreased cardiac output • Cross-sensitivity with Methohexitone and thio-barbiturates
SVR unaltered.
• ↓ in preload accompanies ↓ in cardiac output
• Does not impair baro-receptor sensitivity but rather resets the
control gain.
114

NEW HYPNOTIC AND ANALGESIC AGENTS POTENTIALLY

USEFUL IN TIVA
1. Emulsion formulations of propanidid, methohexitone and
etomidate.
2. Steroid agents + althesin
3. 5β- pregnanolone à eltanolone
4. Opioids
5. Remifentanyl à Rapid onset; shorter elimination ½ life
6. A-3665 à potency similar to alfentanil
7. α2 Adrenergic agonists.
115

45. French Gauge Dr Azam’s Notes in Anesthesiology 2013
Definition:
• It is one of systems used to designate the size of tubular
equipments (Instruments)
• It signifies the circumference of the tube.
• History à Developed by Joseph Frederisk charrire (1803-1876)
who is a French Instrument maker.
• Originally French gauge was meant for urologic instruments like
rubber catheters, semi rigid catheters. Later it was adopted for
tubular instruments like bronchoscope and ET tube.
Points to be noted are:

• To convert ED (external diameter) into Fr. Gz.
• 1 Fr. Gauge = 3 x ED in mm
• To convert ID (internal diameter) into Fr. Gz
• 1 Fr. Gauge = 4 x ID mm +2
In case of semi rigid /rubber tubes:

• Length (size) of tube has 40 perforations
• Each perforation varies from adjacent one by 0.33 mm in
diameter.
• Size of the hole ranges between 0.3 mm to 1.6 cm so each
perforation represents a French gauge catheter size.
116

46. Temperature Monitoring. Dr Azam’s Notes in Anesthesiology 2013
Introduction:
Variations in temperature of patients in the operating room during
anesthesia and surgery may be considerable.
Indications:
Most patients should be monitored during anesthesia and many
during regional anesthesia.
• There are specific situations however, where it is necessary,
particularly where heat loss may be great or the ability of the
patient to produce heat or maintain a normal thermic state is
deficient.
• The neonate and the infant as well as children, are not capable
of good thermal balance.
• Elderly are more likely to loose heat readily, but are subject to a
definite inability for heat production.
• Situations that are mandatory for temperature monitoring include
those patients who have an infectious process, who already
have an elevated temperature or who are at risk for malignant
Measurement of body temperature:
hyperthermia. Surgical procedures requiring hypothermia like
Probe positions: The sites for body temperature measurement relate
CPB, craniotomies organ transplantations.
to core, peripheral and intermediate temperatures. The later are used
Sites: to reflect changes in core temperature and are 0.5 – 10C lower.
• Tympanic membrane, the nasopharynx, the distal esophagus The site chosen must be accessible, comfortable, convenient to the
and the pulmonary artery when a catheter is in place. user, hygienic, efficient, safe and reliable.
• Nasopharynx and tympanic membrane à commonly used. It is The tympanic membrane temperature has been used during surgery,
noted that these do not differ from core temperature by more closely follows rapid fluctuations in hypothalamic temperatures and
than 0.20C. has been instrumental in determining the mechanisms of human
thermoregulation.
• Skin
Difficulties: Cerumen may act as an insulator and bleeding can occur
• Mouth % % %
from around the tympanic membrane when anticoagulants are used.
• Tympanic membrane
Perforation can occur. The external auditory meatus was chosen to
• Axilla % % %
overcome these difficulties.
• Nasopharynx
• Rectum% % %
• Distal oesophagus
• Bladder % % %
• Pulmonary artery catheter
117

Temperature Monitoring.Continuation: Dr Azam’s Notes in Anesthesiology 2013
• A nasopharyngeal temperature probe can also be situated close Techniques:

to the brainstem and hypothalamus. • Intra operatively temperature is monitored by using a Thermistor or
• Pulmonary artery temperature requires invasive catheterization. Thermocouple
Reperfusion or a sudden influx alterations during of cold blood. 1. Thermistor – Semiconductors whose resistance decreases
• Oesophageal temperature probe kept in the lower quarter of the predictably with warming.
oesophagus. Because upper quarter temperature affected by 2. Thermocouple: Is a circuit of 2 dissimilar metals joined so that a
ventilation, an open pleural cavity and malpositioning. potential is generated when the metals are at different
• The rectum is not close to metabolically active tissues and rectal temperatures.
temperature shows a large drift after rewarming from mild INTRA OPERATIVE AND POST OPERATIVE HYPERTHERMIA
hypothermia. It is commonly used to monitor childrenʼs • Body temperature depends on an intricate interplay between
temperature. environmental temperature and the mechanisms of heat gain and
• Urinary catheters can have a temperature probe incorporated heat loss controlled by the temperature thermoregulatory centers.
into the tip and if urine flow is high, the temperature may relate to • Hyperthermia may therefore be a result of an inadequate or
core, since the kidney is well perfused. inappropriate response to increased environmental temperature, an
• Peripheral or skin temperature depends upon the ambient alteration of the internal set point of the thermostat located in the
temperature, blood flow to the area, local heat production and hypothalamus or overwhelming peripheral heat production.
insulation. Intra operative causes of hyperthermia.
Probe design: A) Iatrogenic causes: During anesthesia, hyperthermia results from
1. Skin probe: Require good thermal contact with an area of skin a) active warming of patients (particularly pediatric patients) b) During
so they are made flat. long procedures when the patient covered with non permeable drapes
2. Orifice probes: Depth markings are useful. and the operative area is small (e.g., eye surgery) c) Application of
3. Tympanic: Probes should be prevented from penetrating the tourniquets to extremities for prolonged periods of time, especially in
auditory canal. Resistance devices have been attached to limit children induces hyperthermia. Secondary to constraint of body heat to
probe insertion to 25 mm. the core, and the reduction of body surface area. d) Injection of A-V
4. Oesophageal, oral, Nasopharyngeal and rectal: malformation with sclerosing solution may increase body temperature
5. A rounded tip is designed at the end of a flexible probe for e) Induced hyperthermia for patients undergoing treatment for
atraumatic use. malignancy
5.1. The probe diameter should permit insertion without
resistance. For the rectal probe, a variable size ball is
positioned a few millimeters from the end to aid retention.
6. Incorporated probes: Incorporated into pulmonary artery (swan-
ganz) catheters, urinary catheters, oesophageal stethoscopes
etc.
7. Needle probes: Are used to measure the temperature of
tissues, such as the myocardium and a steam of air of liquid.
118

B) Hyperthermia secondary to diseases D) Transfusion related

1. Pheochromocytoma Causes of post operative hyperthermia
2. Increase in circulating CatecholamineàVasoconstrictionà • Malignant hyperthermia
Inhibition of dissipation of heat àIncrease body temperature. • Thyroid storm
3. Thyrotoxicosis and thyroid storm • Pheochromocytoma
4. Present with hypertension, hyperthermia and tachycardia. • Sepsis
5. Riley- Day syndrome • Drug reactions
6. Deficiency of dopamine ß hydroxylase. • Reaction to blood and blood products.
7. Patients exhibits profound instability of ANS with wide • CNS catastrophe
variations in BP, heart rate and temperature, apparently • Vomiting and aspiration
unrelated to external stimuli. • Exogenous hypothermia
8. Osteogenesis imperfecta Physiologic Alterations induced by Hyperthermia
9. CNS dysfunctions 1. Metabolic à Increased BMR by 10-12% with increase O2
9.1. In status epilepticus, hyperthermia secondary to intense consumption and increase CO2 production and increase fluid and
muscle activity nutritional requirements.
9.2. Hypoxic encephalopathy 2. CVS à Myocardial hemorrhage, myofibril degeneration,
9.3. After resuscitation from cardiac arrest occasional necrosis of left ventricular myocardium, elevated
10. Infectious agents. catecholamines à tachycardia, dysryhtmias, conduction changes
Bacteremia, Viremia and a host of infectious agents produce and demand induced myocardial ischemia.
sepsis and fever. 3. Endocrine à Increase ADH, increase Aldosterone, increased GH,
C) Drug induced hyperthermia. increase corticosteroids, increase Thyroid hormone.
1. Malignant hyperthermia (MH) following volatile anesthesia or 4. CNS à Alterations in sensorium and cognitive skills and seizure
succinylcholine in susceptible patients activity.
2. Neuroleptics malignant syndrome (NMS) 5. Hematologic à Decrease platelet, decrease fibrinogen, decrease
3. Precipitated by haloperidol coagulation factors V, VI, VII and DIC
% Phenothiazines Monitoring: Includes temperature probe selection and temperature
% Antidepressants monitoring site selection
4. Other drug induced hyperthermia Temperature probes:
• Cocaine toxicity in association with PCP, LSD ecstasy, alcohol • Mercury thermometer
abuse • Thermocouples and thermistor
• Anticholinergics serotonin Syndrome: MAOI + Mepirdine • Liquid crystals
% % % % % MAOI + SSRI • Needle probes.
• Infra red detectors
119

Temperature monitoring sites: 2) Neuroleptics Malignant syndromes.(NMS)

• Oral, Tympanic membrane, Nasopharynx, Esophagus, Bladder, • Discontinue offending agent
Rectum, Skin, Forehead, Axilla, Toe. • Administer Dantrolene and Bromocriptine
Prevention of hyperthermia: • Supportive treatment.
• A thorough history of MH and NMS, drug history.
• Familiarity with patients preoperative condition. 3) Other syndromes .
• Careful attention to application of heating devices • Specific treatment for Pheochromocytoma, hyperthyroidism and
• Screening for the disorders mentioned previously are essential in status epilepticus should be instituted when these are the
the prevention of hyperthermia precipitating causes of hyperthermia.
• Treatment of Endocrine disorders – PCC, Thyrotoxicosis. Malignant Hyperthermia:
Treatment of hyperthermia: • MH is a rare myopathy characterized by an acute hyper metabolic
Non-specific: state with in muscle tissue following induction of G.A.
• Cooled I.V. solutions • Signs:
• Removal of warming devices Hypermetabolism ↑ Sympathetic activity Muscle damage
• Blowing cool air and cooling the room
Placement of ice packs over neck, scalp, axilla and groin 1. ↑ CO2 production Tachycardia Masseter spasm
•
• Iced solution lavage of stomach and rectum provides internal 2. ↑ O2 consumption Initial Hypertension Generalized rigidity
cooling 3. Low MVSO2. Arrhythmia (VF) ↑ serum CK.
• Peritoneal lavage where abdomen is not opened. 4. Met Acidosis Hyperthermia ↑ k+ ↑ Na + ↑ Po4
• In extreme cases cardio pulmonary bypass rapidly cools the
patient 5. Cyanosis Fever 10C ↑ every 5 min Myoglobinemia ,
• Use of antipyretics Myoglobinuria(dark
Specific: urine)
1) MH à
Withdraw offending agent and the hyperventilate with O2.Measure • Incidence:-
temperature, blood gases and electrolytes. Acidosis is corrected • 1:15, 000 – pediatric
with bicarbonates. • 1: 40,000 – adults
• Give Dantrolene 1-2 mg /kg and repeated up to 10mg/kg Earliest signs -‐ Masseter muscle rigidity (MMR), tachycardia, hypercarbia.
• Promote a diuresis Complications: VF – Death; ARF; DIC; cerebral edema; seizures;
• Give Dexona 20mg, methylprednisolone 10 mg/kg or other Hepatic failure.
steroids. Pathophysiology: Uncontrolled increase in intracellular Ca+2 in
skeletal muscles à removes inhibition of troponin à intense muscle
contraction enhanced an sustained ATPase activity à uncontrolled
increase in aerobic and anaerobic metabolism.
120

• Abnormal Ryr1(Rp) receptor. Neuroleptics Malignant Syndrome NMS:

• Abnormalities in second messengers and modulators of Ca2 • Characterized by hyperthermia, autonomic liability, muscle rigidity,
+ release. dyskinesia, altered consciousness in patients receiving
• Drugs known to trigger MH - Halogenated volatile anesthetics, antidopaminergic drugs.
ether, cyclopropane, halothane, methoxyflurane, enflurane, • Imbalance of neurotransmitters in CNS. Functional dopamine
isoflurane, desflurane, sevoflurane and scoline. deficiency results in hyperactivity of excitatory amino acids in basal
• Conditions considered at increased risk- Musculoskeletal ganglia and hypothalamus.
disease, • Drug therapy with antidopaminergic agents – phenothiazines,
• Orthopedic, ophthalmic, head and neck, family H/O anesthetic butyrophenones thioxanthines, dibenzoxapines, Metoclopramide.
complications, intolerance to caffeine containing food. • Withdrawal of dopaminergic agents in parkinsonian patient –
Treatment: Levodopa and amantadine.
1. Triggering agents stopped- succinylcholine and volatile • Develops in hrs to weeks –Within 2 wks of dose adjustments.
anesthetic • Not inherited.
2. 100 of O2 Mild NMS: resolves after withdrawal of causative agent or restarting
3. Cooling measures. anti-parkinsonian treatment.
4. Dantrolene: A hydantoin derivative directly interferes with Severe NMS: O2 treatment, endotracheal intubation, muscle paralysis
muscle contraction by binding the Ryr1 receptor Ca+2channel with NDMR (Muscle rigidity), Dantrolene, Dopaminergic agonists –
and inhibiting Ca+2 ion release from sarcoplasmic reticulum. Amantadine, Levodopa, Bromocriptine or others.
Dose -2 to 5mg/kg IV every 5 min until MH episode is terminated,
upper limit 10 mg/kg. t ½ - 6hrs after control – 1mg /kg IV every 6
hrs for 24-48 hrs to prevent relapse.
• Also used in NMS and Thyroid storm, Phlebitis – given in central
venous line, acute – generalized muscle weakness, chronic –
hepatic dysfunction.
1. Acidosis -NaHCO-3
2. Inotropes and anti arrhythmic drugs – as necessary
3. Treatment for hyperkalemia
121

47. Malignant Hyperthermia. Dr Azam’s Notes in Anesthesiology 2013
1 Definition: • Sweating
• MH is a rare myopathy characterized by on acute • Muscle damage –
hypermetabolic state with in the muscle tissue following induction Masseter spasm
of general anesthesia. • Generalized rigidity
• Incidence 1 in 15,000 in pediatric anesthesia. • Increased creatinine kinase
• 1 in 40,000 in Adult anesthesia. • Hyperkalemia
2 Genetic predisposition: • Hypernatremia
• Pharmacogenetic disorder: Susceptible patient have a genetic • Hyperphospnatemia
predisposition which does not manifest until they are exposed to • Myoglobinuria (Dark urine)
triggering agents or stressful environment. • Myoglobinemia.
• Heterogeneous genetic disorder: Genes on chromosomes 1, 3, 1. Early signs:
7, 17 and 19 have been linked with MH. • Masseter spasm, Tachypnea (increased minute ventilation)
• Ch -19 à skeletal muscle, ryanodine (Ryr1) receptor Ca+2 • Rapid exhaustion of sodalime/(increasing ETCO2–doubling /
channel receptor tripling earliest and most sensitive indicator)
• Midwest in US – has highest incidence of MH. • Warm sodalime canister
3. Pathophysiology: • Tachycardia
1. Uncontrolled increase in intracellular calcium in skeletal muscle • Irregular HR
from sarcoplasmic reticulum, removes inhibition of troponin à 2. Intermediate signs:
Intense muscle contractions • Patient warm to touch (increased core temperature)
2. Enhanced and sustained ATPase activity à uncontrolled • cyanosis ( decrease HbO2 saturation)
increase in Aerobic and Anaerobic metabolism • Dark blood – Irregular HR.
% % ↓ 3. Late signs:
3. Increased O2 consumption • Generalized skeletal muscle rigidity
Increased CO2 production • prolonged bleeding
Severe Lactic acidosis • Dark urine
Hyperthermia • Oliguria
4. Hyperkalemia - K+ efflux from muscle • Irregular HR.
Acidosis 4. Trigger agents:
5. Increased Sympathetic tone • Halogenated anesthetics: Ether, Cyclopropane, Halothane,
4. Signs of MH: Methoxyflurane, Enflurane, Isoflurane, Desflurane, Sevoflurane
• Hypermetabolism– Increased CO2 production, increased O2 • Succinylcholine
consumption, low mixed venous O2 tension, Metabolic acidosis,
cyanosis, mottling.
• Increased Sympathetic activity– Tachycardia, Initial HTN (à
Hypotension) Arrhythmias (vent fibrillation à death)
• Hyperthermia – Fever @ 0.5 every 15 min & as high as 460C 122

Malignant Hyperthermia.Continuation: Dr Azam’s Notes in Anesthesiology 2013
5. Increase Risk: • Correct Metabolic acidosis – NaHCO3 1-2 mEq/kg based on ABG
1. Musculoskeletal diseases • Maintain urine output (Hydration, Mannitol 0.25 G/kg IV, furosemide
a. Ducheneʼs muscular dystrophy. 1mg/kg IV)
b. Central core disease. • Treat cardiac dysrrhythmias (procainamide 15 mg/kg IV)
c. Osteogenesis imperfecta. • Monitor in intensive care unit (urine output, ABG, pH, electrolytes)
2. King- Denborongh syndrome • Hyperkalemia treated with insulin glucose and diuresis.
3. Orthopedic cases, ophthalmic surgery (strabismus)
4. Head and Neck procedures 7. Identification of Susceptible Patients:
5. F/H of Anesthetic complications • Biopsy of a fresh section of living skeletal muscle (vastus muscle –
6. H/O unexplained fever or muscular cramps. thigh)
• Halothane – caffeine contracture test: False negative rate is close to
6. Treatment of MH: zero. False positive rate 10-20.
Etiologic treatment: • Genetic counseling
• Dantrolene – Hydantoin derivative – directly interferes with
muscle contraction by binding the Ryr1 ca+2 channel receptor 8. Anesthetic Management:
inhibiting Ca+2 release from sarcoplasmic reticulum. • Dantrolene prophylaxis for MH susceptible patients.
• Intracellular dissociation of E-C coupling. 20mg of Lyophilized • 5mg/kg PO in 3 or 4 divided doses every 6 hrs with last dose 4 hrs
powder to be dissolved in 60 ml of sterile H2O. (t ½ -6 hr). preoperatively (OR) 2-4 mg/kg IV over 10-30min as prophylaxis prior
• Decreased temperature in thyroid strom and Neuroleptic to induction – ½ dose is repeated 6 hrs.
Malignant – Syndrome . Drug selection – % Barbiturates %N2O.
2.5mg/kg IV every 5 min until episode is terminated Non-triggering drugs:
↓ • Propofol % % %
Max 10mg/kg • NDMR
↓ • Etomidate % % %
1 mg/kg IV every 6 hrs for 24-48 hrs to prevent relapse. • Anticholinesterase
Symptomatic treatment • Benzodiazepine
• Immediately discontinue inhaled anesthetics and conclude • Anticholinergics% % %
surgery at soon as possible • Ketamine % % %
• Hyperventilate lungs with 100% oxygen. • Sympathomimetics
• Initiate active cooling (increased saline 15ml/kg IV every 10 min) • Opioids
Gastric and bladder lavage with iced saline, surface cooling. • Local Anesthetics
• (esters amides)
123

Malignant Hyperthermia.Continuation: Dr Azam’s Notes in Anesthesiology 2013
Premedication:
• Well sedated – to avoid from stress triggering MH.
• Anticholinergics – Avoided (confusion regarding HR
• or interference with normal body heat loss)
Anesthesia Machine:
• “Dedicated” anesthesia machines never used to deliver volatile
anesthetics for use for MH patients.
• Conventional Anesthesia Machine with disposable breathing
circuit and fresh gas outlet hoses, fresh CO2 absorbent, no
vaporizer (removed) and continuous flow of O2 at 10L/min for 5
to 10 min before using the machine.
Regional Anesthesia:
• Avoid stress – patients well sedated
• Acceptable choice.
• Local anesthetic agents both esters & amide are acceptable.
Post op period:
• Overnight observation even for day care surgeries.
• Discharge after minor surgery is not associated with increase
risk.
124

48. Thermoregulation, Monitoring effect of anesthesia on Thermoregulation & Vice versa. Dr Azam’s Notes in Anesthesiology 2013
INTRODUCTION Body heat is lost by

• Mammals are homoeothermic species where thermoregulatory • Radiation < 60%
system co-ordinates defenses against environmental Convection 12%
•
temperature to maintain internal body temperature within a Conduction 3%
•
narrow range of 36.3 – 37.1o C or 97.3 – 98.8o F there by Vaporization of sweat 25%
•
optimizing the body function. Respiration 2%
•
• Hypothermia is a common peri-operatively due to anesthetic • Urination and defecation 1%.
induced inhibition of thermoregulation and exposure to cold OT
environment. Factors associated with heat loss:
• Hypothermia is defined as body temperature below 36o C. • Environmental temperature and humidity.
Hyperthermia is defined as body temperature more than 38.3o C • Artificial control imposed on clothing.
• An understanding of normal anesthetic induced thermoregulation • Metabolic rate and activity of person.
will facilitate prevention and management of complication.
RADIATION
NORMAL THERMOREGULATION • This is a major type of heat loss in most of surgical patient. All
• Body temperature represents a balance between heat produced surfaces above absolute 0 will radiate heat and similarly all surfaces
in body, to heat lost to environment. This is regulated by will absorb radioactive heat from surrounding surfaces.
hypothalamus by a feedback mechanism. • Skin over neoplasm or abscess is a 2 – 3 o C greater than normal
temperature hence heat loss is proportionately greater.
BODY HEAT PRODUCTION AND HEAT LOSS
• Body heat is produced by CONDUCTION
• Basic metabolic process • Heat loss is proportional to temperature difference between 2
• Food intake (specific dynamic action) adjacent surfaces and strength of thermal insulation separating them.
• Muscular activity. • Heat conduction to OT table, blankets and other objects with which
the patient is in contact represents < 3% of heat loss because these
Factors objects warm up rapidly.
• Age
• Sex CONVECTION
• Basal metabolic rate • When still air layer around the body adjacent to skin is disturbed by
• Muscular activity air current the insulating property diminishes and heat loss occurs.
• Hormones like thyroxin, growth hormone and catecholamines This is 2nd most common type of heat loss but can be reduced by
like epinephrine and nor epinephrine. surgical drapes.
• In infants ; brown fat it is the major source of heat production
since this fat has a high rate of metabolism.
125

Thermoregulation, Monitoring effect of anesthesia on Thermoregulation & Vice Dr Azam’s Notes in Anesthesiology 2013
versa.Continuation:
Evaporation AFFERENT THERMAL SENSING

!"##$
!"#$%&'()#*+,-)#./#$/-),0-)1+2+34###### • Temperature information is obtained from thermally sensitive cells
• This is the process whereby a liquid is changed into gaseous
state by absorbing heat. 56-7+/8#981,1+/# throughout body. Thermo sensitive neurons that respond to small
changes in temperature are located in different areas of CNS, which
• # Heat loss is about 10% of metabolic heat production in adults.
Evaporation occurs without any change in temperature of liquid include nuclei of hypothalamus, spinal cord and lower brain stem
• %&'(%)*+,'-$$
and heat absorbed by liquid is called heat of evaporation. medulla.
>01)#1)#,0-#?"+7-))#<0-"-@4#&#21AB18#1)#70&/3-8#1/,+#3&)-+B)#),&,-#@4#&@)+"@1/3#0-&,=##
• For every gram of water evaporated 0.58 K.cal of heat is lost at • Cold sign travel via A α fibers, warm signals via unmyelinated C
C-&,#2+))#1)#&@+B,#:DE#+F#'-,&@+217#0-&,#?"+8B7,1+/#1/#&8B2,)=## fibers although there is some overlap.
normal temperature, but this amounts to 25% of heat loss. The
9G&?+"&,1+/#+77B")#<1,0+B,#&/4#70&/3-#1/#,-'?-"&,B"-#+F#21AB18#&/8#0-&,#&@)+"@-8#@4#
heat loss is more when humidity is low. • The C fiber also conveys pain, and hence intense heat canʼt be
21AB18#1)#7&22-8#0-&,#+F#-G&?+"&,1+/=##
Sweating: Itself causes little heat loss, is effective only when it distinguished from sharp pain.
• H+"#-G-"4#3"&'#+F#<&,-"#-G&?+"&,-8#D=IJ#K=7&2#+F#0-&,#1)#2+),#&,#/+"'&2#,-'?-"&,B"-L#@B,#
,01)#&'+B/,)#,+#MIE#+F#0-&,#2+))=##>0-#0-&,#2+))#1)#'+"-#<0-/#0B'181,4#1)#2+<=##
vaporizes. Hence humid environment is unfavorable because of • Most of the ascending thermal information travel via anterior
./0123456$.,)-2F#7&B)-)#21,,2-#0-&,#2+))L#1)#-FF-7,1G-#+/24#<0-/#1,#G&?+"1%-)=##C-/7-#0B'18#
interference with vaporization. spinothalamic tract and eventually arrive at hypothalamus.
-/G1"+/'-/,#1)#B/F&G+"&@2-#@-7&B)-#+F#1/,-"F-"-/7-#<1,0#G&?+"1%&,1+/=##
)%789*+,'-$':$;'<=$+%>(%)*+8)%$$
REGULATION OF BODY TEMPERATURE CENTRAL CONTROL
The processing of thermoregulation has 3 components • Preoptic region of anterior hypothalamus is dominant autonomic
>0-#?"+7-))1/3#+F#,0-"'+"-3B2&,1+/#0&)#;#7+'?+/-/,)## thermoregulatory controller in mammals.
I.%.=# Afferent thermal sensing
$FF-"-/,#,0-"'&2#)-/)1/3##
II.% Central regulation • Much of excitatory input to warm sensitive neurons comes from
..=# N-/,"&2#"-3B2&,1+/##
III.%
...=# Efferent responses
9FF-"-/,#"-)?+/)-)##
hippocampus which links limbic system (emotion, memory, behavior)
##########################################################################################################################O&"'#"-)?+/)-)## to thermoregulatory responses.
"#$%&'()(*+,!! ! "#$%&'()(*+,!! • Although inputs are integrated by hypothalamus most of thermal
-&'./!$(/&,!%0!1/(23!! ! 43&./&'/.,'%)5!! D8&2C.!C(,%52)(&(&2%3!
information is preprocessed in spinal cord and other parts of CNS.
6723!,+/0(8.!! 9:;< =!!! % ! !!!!!9>;< =!!% 6H.(&23@!!
I.'(C2%/!! • The anterior hypothalamus contains mechanism to cool body, while
6$23()!=%/5!! ! ! ?(3@.!!
A..$!8.3&/()!&2,,+.,!!
posterior hypothalamus initiates heat producing and heat preserving
mechanisms.
! J(,%8%3,&/28&2%3!! • The mechanism by which the body determines absolute body
K%3L,'2C./23@!!
# temperature thresholds appears to be influenced by circadian
B'./*%!@.3.,2,!!
N+28#"-)?+/)-)##
6'2C./23@!! rhythm, exercise, food intake, thyroid function, anesthetics and other
I.'(C2%/!! drugs and cold and warm adaptation.
B'./*())#!,.3,2&2C.!! D!!!021./!8%)5!! "#$%&'()(*+,!! • Central regulation is intact from infancy but may be impaired in
=.)),!23!&'.!1%5#!! E(/*!+3*#.)23.5!=!021./!! ,$23()!8%/5!! elderly and extremely ill patient.
! F(23!! G%H./!1/(23!,&.*!(35!*.5+))(!!
EFFERENT RESPONSES
Multiple inputs are integrated in to a common efferent signal to effector
system.
The body responds to thermal perturbation via effector mechanism that
increases heat production and later environmental heat loss. 126
::;#
#
Dr<<<=!"$%&'=7+'
Azam’s Notes in###############################################################!"#"$%&'(#")*+"),%
Anesthesiology 2013 !
#
versa.Continuation:
Non shivering thermo genesis: (in infants)
• The energy efficient effectors such as vasoconstriction are
maximized before metabolically costly responses like shivering • Metabolic heat production without producing mechanical work
are initiated. (shivering)
• Effectors determine the ambient temperature range that the body • it doubles heat production in infants but increases slightly in adults.
will tolerate while maintaining core temperature as normal. • Main source is from brown fat which is a specialized lipid located
between scapula, nape of neck, along great vessels in thorax and
Mechanisms activated by cold abdomen, peri renal region etc.
↑ Heat production % -% Shivering • The brown fat cells and blood vessels have extensive sympathetic
% % % -% Hunger innervations.
• It also contains many mitochondria where inward proton
% % % -% ↑ Voluntary activity
conductance, generate ATP so that more heat is produced.
% % % -% ↑ Secretion of nor epinephrine and
• Stimulation of sympathetic innervations to brown fat release nor
% % % % epinephrine epinephrine, which acts via β 3 adrenergic receptors to lipolysis and
↓ Heat Loss %-% Cutaneous vasoconstriction increased fatty acids production.
% % -% Curling up Sweating:
Mechanism activated by heat
• Is mediated by post ganglionic cholinergic fibers, which is an active
↑ Heat Loss %-% Cutaneous vasodilatation process. Where body can dissipate heat in an environment
% % -% Sweating exceeding core temperature.
% % -% ↑ Respiration • It is inhibited by anticholinergic drugs like atropine, Hyoscine,
↓ Heat Production% - anorexia scopolamine etc.
% % % - apathy Active vasodilation:
Cutaneous vasoconstriction: • Is mediated by unknown factors released from sweat glands. During
• Is most consistently used autonomic nervous system. It extreme heat stress blood flow to the top mm of skin is equal to 7.5
prevents metabolic heat lost by radiation and convection from lit / min.
skin surface through AV shunting of blood which is mediated by • All most all anesthetic drugs causes vasodilatation.
local α adrenergic sympathetic nerves. Behavioral regulation:
Sustained shivering: • Like dressing appropriately, modifying environmental temperature,
It is an involuntary, oscillatory unsynchronized muscular activity. assuming positions that oppose skin surface and voluntary
• It increases metabolic heat production by 100% in adults. movement is most effective effector mechanism.
• Efferent shivering pathway arises and descends from posterior
hypothalamus.
• Shivering does not occur in infants and is not fully effective in
children until they are several years old.
• Shivering is inhibited by muscle relaxants. But still the
temperature remains normal unless other effectors canʼt
compensate for imposed stress. 127

versa.Continuation:
THERMOREGULATION IN PEDIATRICS: THERMOREGULATION INGERIATRIC PATIENTS

Possible causes of impaired thermoregulation
• The neonateʼs thermoregulatory range is significantly limited and
easily overwhelmed by environment influences. Aging lowers skin temperature thresholds required for initiation of
cutaneous vasoconstriction, exposure to cold stress and broadens the
• The neutral thermal environmental in infants is between 32 – 35o
C instead of 28 – 32oC as in adults. inter threshold range. Thermoregulatory responses occur but are less
vigorous.
• New born infants < 30 week of gestation have immature sweat
glands resulting in defective sweat mechanism. • Exposure to cold environment – hypothermia can result from illness,
falls or cold other mishaps which can render victim immobile and
• Cooling of face alone produces 23% increase in oxygen
consumption in full term, but in premature babies it is 36%. exposed to cold environment.
• They have less subcutaneous fat. • Elderly if inactive will have slow metabolic rates and low heat
production. Depressed lipolysis could contribute to limited
• They have 2 – 2.5 times more the surface area than body
weight. generation of body heat.
• The main source of heat production is by non shivering thermo • Concomitant medications can blunt shivering and vasoconstriction –
genesis i.e. by brown fat. drugs which can cause hypothermia include phenothiazines, tricyclic
antidepressants, benzodiazepines, narcotics, barbiturates, ethanol,
• Newborn and infants and small children are more sensitive to
hypothermia because of less effective effector mechanism, heat gluthetimide and reserpine demonstrate anticipated vasomotor
production is limited and potential for heat loss is more. responses to temperature changes, they have diminished peripheral
vasoconstriction during cold exposure and diminished vasodilatation
• They have increased thermal conduction and they lose
proportionately more metabolic heat though skin. during warming.
Prevention • Autonomic aging defects lead to low peripheral perfusion and
• Heat loss by radiation is decreased by use of double shelled reduced ability to regulate peripheral flow through vasoconstriction
isolettes during transport. and vasodilatation.
• Heat lost by conduction is reduced by placing baby on a warming • Shivering is less effective means with increasing age.
mattress and warming the OT room. The afferent limb of thermoregulation is impaired so they lack a full
• Heat lost through convection is minimized by keeping the infant capacity to perceive cold especially in those who have low resting
in an incubator, covered by blankets and by covering heat. body temperature.
• Heat lost through evaporation is lessened by humidification of
inspired gases, use of plastic wrap to decrease water loss
through skin and by warming the preparation solutions.
128

versa.Continuation:
THERMOREGULATORY RESPONSES IN ANESTHETIZED PATIENT Phase II: Thermal imbalance

During anesthesia initial cooling is not accompanied by any • Core temperature decreases in a slow linear fashion for 2 – 3 hours.
thermoregulatory response. However when temperature reaches This is because heat loss >metabolic heat production. The mean
34.5o C significant peripheral vasoconstriction occurs and loss is 0.5 – 1o C/ hr.
temperature decline decreases. • Anesthesia contributes to decrease in production by limiting
We can divide human body into 3 compartments. muscular activity, decrease in metabolic rate and diminishing work of
I. Central: Related to core temperature which corresponds to breathing.
vessel rich group of organs. • Convection and radiation > 85% heat loss.
II. Peripheral: Largest which consists of musculoskeletal conduction and evaporation > 15%, but 25% in infants
system. It acts as dynamic buffer which function to • Respiratory losses 5 – 10% of total heat loss. But it represents 1/3 of
accommodate any changes in core temperature by total heat loss in infants because minute ventilation on per kg basis is
vasodilatation or vasoconstriction. higher than in adults.
III. Shell / Skin: Composed of skin, subcutaneous fat, represents Phase III: Plateau phase or re-warming phase
barrier between previous 2 compartments and environments • It occurs after 3-4 hours of anesthesia and virtually remains constant
and acts as an insulator to the body. for the duration of surgery. It is a steady state where heat
Temperature changes under general anesthesia follows 3 phases: production = heat loss.
Phase I% :% Internal redistribution • It is associated with peripheral thermoregulatory vasoconstriction
Phase II% :% Thermal imbalance when the core temperature is between 33 – 35o C.
Phase III % :% Plateau phase or Rewarming phase • Another factor which contributes to plateau is the restriction of
Phase I: Internal redistribution metabolic heat produced to core compartment in contrast to
• It results from vasodilatory effects of anesthetics mainly caused peripheral tissue which continues to decrease the temperature since
by reducing the threshold for vasoconstriction to a level below heat is no longer supplied by central compartment.
the current body temperature leading to opening of AV shunts. • In comparison to adults, infants and children replaced this steady
This increases size of central compartment. There is decrease state with rewarming phase. GA decreases heat production by
in metabolic heat production caused by anesthesia which inhibiting muscular activity and decreases metabolic rate, but there is
reduces the amount of energy available to compensate for simultaneous increase in oxygen consumption, CO2 production and
increase in central compartment. nor adrenaline level in infants because of occurrence of non
• Rapid core temperature decreases by 0.5 – 1.5o C during first shivering thermogenesis. Infants differ from adults in that
hour due to redistribution of core heat to periphery. This intraoperative thermoregulatory responses are sufficiently effective to
decreases core temperature but mean body temperature and increase central temperature significantly despite constant ambient
body heat content is unchanged. temperature.
129

versa.Continuation:
TEMPERATURE REGULATION DURING REGIONAL ANESTHESIA • Enflurane – In adults with 1.3% or (0.77 MAC). Thermoregulatory
• Spinal and epidural anesthesia can have several effects on threshold (TRT) for vasoconstriction was 35.1o without and 35.5o C
thermoregulation. with painful stimulation. 1 – 12 years, 1.67% or 1 adult MAC in
• The vasoconstriction and shivering thresholds are decrease in oxygen with caudal bupivacaine caused profound depression of TRT
regional anesthesia, which suggests an alteration in central for vasoconstriction, failing to vasoconstriction even when
control because of altered thermal input i.e. an apparent temperature is 33.9o C.
elevation of leg temperature and administration of opioids and • Isoflurane – TRT is inversely proportional to inhaled concentration
sedatives. The perception of temperature is largely determined and decreases by about 0.3o C for every 1% increase in end tidal
by skin rather than core temperature. In regional anesthesia inhaled concentration.
there is core hypothermia which increase temperature in the 2). IV agents:
periphery, below the level of block. The result is continued • Midazolam minimally impairs TRT.
perception of warmth accompanied by autonomic • Ketamine minimally alters in dose dependent manner.
thermoregulatory response including shivering which is more Muscle relaxants reduce capacity of body to respond to hypothermia
pronounced in the area which is unblocked. even though slight decrease in oxygen consumption (2%) occurs in
• This mechanism of heat loss persist in the regional anesthesia normothermic and hypothermic patient with pancuronium.
until the block wears off, whereas in general anesthesia patients 3). Opioids:
begin to rewarm immediately on emergence. • Decreases the vasoconstriction and shivering thresholds.
• Shivering with epidural is less vigorous than compared to after • Alfentanil – slight increase in sweating threshold and linear decrease
GA and therefore has fewer hemodynamic metabolic in vasoconstriction and shivering thresholds.
consequence. • Meperidine – has antishivering action which is due to
EFFECTS OF ANESTHETIC DRUGS ON THERMOREGULATION disproportionate drop in shivering threshold.
1).Inhalation agents: • Tramadol – has slight effect on thermoregulatory control.
4). Adjuvants:
• All inhalational agents augment inter-threshold range in dose
dependent manner. • Clonidine – decreases shivering by lowering vasoconstriction and
shivering thresholds.
• N2O →↓ in shivering thermogenesis.
• Intraoperative tourniquets induces hyperthermia, due to reduction in
• Halothane ↓ thermoregulatory threshold to 34.4o C at 1.3 MAC. peripheral compartment and containment of heat in core
In children – anaesthetized with 1 MAC with 7-% N2O with compartment, which explains drop in core temperature when
oxygen ↓ thermoregulatory threshold to 35.8o C. vascular clamp is withdrawn.
130

versa.Continuation:
HYPOTHERMIA • AF
• Usually defined as body temperature less than 36o C. • Ectopics
Causes of hypothermia: • Heart block
1. OT temperature – most of OT temperature is between 18 – 21o • Conduction disorders
C, increased temperature produces perspiration and increase • Suppression of higher pacemakers
chances of microbial transfer and seeding of wounds. Patients • Hypotension and decreased cardiac output
looses heat when temperature is < 21o C. • Terminal events – VF or asystole.
2. Administration of cold blood or IV fluids.
3. Prolonged surgery. • Hematologic: Left shift of ODC which impede oxygen delivery and
4. Intra abdominal surgery or intrathoracic surgery due to leading to cellular hypoxia and metabolic acidosis. Increases blood
exposure of large viscera, body cavities. viscosity.
5. Use of repeated large volumes of irrigating fluids. • Can hinder homeostasis with sequestration of platelets which can
6. Direct effects of anesthetic drugs which depress bodyʼs lead to DIC.
feedback for maintenance of thermoregulation. Muscle • Metabolic: Decreases metabolic rate by 5 – 8% per degree C to
relaxants impede thermogenesis by eliminating shivering. approximately ½ of normal rate at 28o C. Decrease tissue perfusion
Effects of hypothermia: → can lead to metabolic acidosis → lipolysis → increased FFA →
• Inadvertent hypothermia can have a variety of manifestations. glucose use → hypoglycemia. Increases tissue oxygen consumption
• CNS – altered mental status, disturbances in gait and speech, by 400 – 500%.
sluggish deep tendon reflexes, slow and shallow respiratory
• Pulmonary: Respiratory strength is decreased at 33o C. Increased
pattern. Increase in cerebral vascular resistance (CVR). PVR, MVV which is required for additional oxygen demand.
• CBF is proportional to decrease in metabolic rate because of • Decreases hepatic blood flow – decreases the liver function,
autoregulatory CVR. decreases metabolism and excretion of drugs.
• AV PO2 remains constant and venous lactate doesnʼt increase. • Decreases renal blood flow – renal perfusion decreases, GFR
• Cerebral function is well maintained until core temperature is decrease, tubular insufficiency.
equivalent to 33o C but consciousness is lost when temperature
• ʻCold diuresisʼ
is < 28o C. Treatment:
• Primitive reflexes like gag, cough, papillary constriction and • Warmed IV fluids, heated humidified gases
monosynaptic spinal reflexes remain intact until 25o C. supporting treatment of cardiac renal, metabolic consequences
• Nerve conduction decreases but tone of peripheral muscle Inadvertent hypothermia can best be corrected with gradual
increase at 26o C. spontaneous rewarming with blankets in a warm room.
• CVS – Cardiac rhythm disturbances
-% SVT
131

versa.Continuation:
POST ANESTHETIC SHIVERING 2. Cutaneous heat loss can be decreased by covering the skin with
• Shivering is common complications occurring in 40% of patient surgical drapes which decreases heat loss by 30%.
during post anesthetic recovery. It is considered as a normal 3. Radiant heat lamps can be used during preparation and catheter
thermoregulatory shivering only when placement.
• Mean body temperature is below threshold for shivering 4. OT room temperature can be increased to 25o C until the patient is
• Tremor is preceded by peripheral cutaneous vasoconstriction. fully draped.
• Tremor patterns match those produced by centrally mediated 5. Forced air system can transfer more than 50 W across skin surface
shivering. there by rapidly increasing the body temperature (Bair Hugger).
• The cause for tremors has been attributed to uninhibited spinal 6. Heated humidifiers and airway heating is effective in rewarming
reflexes, pain, decreased sympathetic activity, pyrogen release, children and infants rather than adults who help in retaining the heat
adrenal suppression, respiratory alkalosis and most commonly and moisture within respiratory system.
due to intraoperative hypothermia. 7. Fluid warmers- 1 L of crystalloid solution at room temperature or 1
EMG show 2 patterns for tremors. point of refrigerated blood will decrease the mean body temperature
1). Tonic pattern typically having 4- 8 cycles / min. Waxing and by 0.25o C. So fluids or blood should be warm.
waning component. 8. Water circulating warming blankets may be of value when placed on
2). Phasic pattern having 4 – 7 Hz of bursting pattern which top of patient. The temperature of water should not exceed 40o C.
resembles clonus.
Effect: 25% of post. Op patient reach a core temperature of 38o C Treatment of hypothermia and shivering in PACU:
and 50% reach 38.4o C and this will eventually lead to increase in • Supplemental oxygen until patient are fully warm.
thermoregulatory set point. • Stop shivering by giving pharmacological agents
Prevention: Inj. Meperidine 25 mg IV
• PAS is defense mechanism against reduction of core Inj. Clonidine 75 µg IV
temperature, so it should not be prevented, rather warming of Inj. Ketonserin 10 mg IV
patient should be undertaken than administering medication to • Cutaneous heat source – forced air system, warming blankets,
inhibit it. radiant heat lamps. Paralysis and ventilation in severely hypothermic
1. PAS can be treated with skin surface warming because the sick patients.
regulatory system will tolerate more core hypothermia when HYPERTHERMIA:
cutaneous warm input is augmented. • Hyperthermia is defined as increase in body core temperature higher
2 factors contribute to rapid intra op. transfer of heat from than 38.3o C whereas fever is an endogenously triggered process
periphery to core. with metabolic and functional changes that alter hypothalamic set
• Vasodilatation induced by central inhibition of thermoregulatory point.
control.
• GA itself induces peripherally mediated vasodilatation which
facilitates intra-compartmental transfer of heat.
132

versa.Continuation:
Pathophysiology of hyperthermia: Endocrine:

• The primary injury in hyperthermia is direct cell toxicity above 42o • Temperature regulation has physiologic priority over maintenance of
C (critical thermal maximum) cell function deteriorates with salt and water balance. Sweating continues in phase of severe
cessation of mitochondrial activity, alteration in cellular enzyme dehydration and salt loss leading to circulatory failure.
function and loss of cell membrane integrity. Irreversible • There is increase in ADH, aldosterone, growth hormone,
changes of coma, cerebral hypoxia, acidosis, rhabdomyolysis, corticosteroids and thyroid hormone.
dehydratation and organ damage can occur leading to death. CNS:
The manifestation of hyperthermia on organ function are – • Seizures
1).% CVS % -Vasodilatation • Delirium
% % -Increased heart rate 10 beats / o C rise in temp. • Coma
% % -Increased stroke volume • Death
% % -Decreased venous return • Survivors show ataxia and dysarthria.
% % -Hypotension
GIT
• Oxygen demand is increased initially leading to increase in
cardiac output. Later increase in oxygen extraction by tissue • Bleeding from gut
outstrips the supply. • Acute liver failure
• Myocardial damage occur in the form of myocardial
Hematologic system %
haemorrhage, dysrrhythmias, heart failure and demand induced
ischemia. • Coagulopathy
• DIC
Metabolic: Muscle – Degeneration and necrosis occurs leading to rhabdomyolysis
• 1o C rise in body temperature increases BMR by 7% with a and myoglobin release.
parallel increase in oxygen consumption, CO2 production and Causes of hyperthermia "
fluid and nutrition requirements. This increased systemic • Exogenous
demands can impose a great burden on marginal CVS. Endogenous
Respiratory: Exogenous
• Decreases tidal volume • Draping the patient
• Increases respiratory rate • High humidity
• Increased ventilatory response to hypoxemia & hypercapnea • Elevated room temp.
• Increased hypoxic pulmonary vasoconstriction • Use of warm blankets, heated mattress or blood warmers.
• Shift of ODC to right • Circle system with soda lime
• Heated humidifiers
• Large operating room lights
Exogenous causes rarely lead to marked increase in body temperature
and the resulting mild hyperthermia usually responds to withdrawal of
offending cause. 133

versa.Continuation:
Endogenous: I). MALIGNANT HYPERTHERMIA:

• Malignant hyperthermia Is a rare disorder that appears to involve excessive release of Ca from
• Neuroleptic malignant syndrome sarcoplasmic reticulum in response to anesthetic agents. The increase in
• Drug Induced Ca initiates a severe muscle hypermetabolism. It is a autosomal dominant
Cocaine, amphetamines disorder, hence a positive family history is always present.
MAOIs Incidence % :% Adults 1: 50,000
Diethyl either % % % Children 1: 15,000
• Infection • Onset: Is acute during induction with inhalation anesthesia or with
Bacteremia administration of scoline but recurrence of the syndrome can occur within
Meningitis, encephalitis first 24 to 36 hours.
Peritonitis • MH can be diagnosed by muscle biopsy or by caffeine halothane
Surgical wound infection contracture test.
Phlebitis • Triggering agents – halogenated general anesthetic like ether, halothane,
• Transfusion cyclopropane, methoxyflurane, enflurane, isoflurane, desflurane
Febrile reaction (pyrogens, cell debris endotoxins) sevoflurane.
Incompatibility • Non depolarizing muscle relaxants like scoline
Reactions against leukocytes, platelets Signs and symptoms are:
• Endocrinopathy
Pheochromocytoma Hypermetabolism
Thyroid Storm % Increased CO2 production
• CNS % Increased O2 consumption
Hypothalamic bleed % Metabolic acidosis
Acute hydrocephalus % Cyanosis
Increased sympathetic activity
Diabetes insipidus
Impairment of sweating (atropine, scopolamine) • Tachycardia
• Inflammatory response Initial hypertension
Arrhythmias
Systemic inflammatory disease
Muscle damage
Tissue trauma and inflammation
% Masseter spasm
Gastric content aspiration
• Miscellaneous % Generalized rigidity
% Elevated serum creatinine Kinase
Methyl methacrylate
% Hyperkalemia
Sclerosing solution
% Hypophosphatemia
% Myoglobinuria
134

versa.Continuation:
Management:
• Hyperthermia
Body temperature often exceeds 41o C and may be as high as • Involves promoting heat loss and reducing heat production.
45o C. • Temperature < 39oC
Look for cause
• MH of anesthesia has high mortality rate upto 70%. But with
advent of Dtc it has dropped to 10% which is a muscle relaxant Remove covers and warming devices
that inhibits the release of calcium from sarcoplasmic reticulum. Discontinued triggering agents
Other important measures include prompt interruption of Discontinued blood transfusion if any.
anesthesia, correction of hypoxia and metabolic disturbances • Temperature > 39o C or 0.5o C / 15 min.
and CVS support. 1) Give 100% oxygen.
2) Initiate active cooling measures by blowing cool air, wet
• Physical cooling with ice packs, core cooling with parenteral
fluids have been advocated. drapers, reduce OT temp. Ice packs, ice solution lavage into
DIAGNOSIS: stomach, rectum and operative sites, peritoneal dialysis.
• Monitoring of body temperature should be mandatory in all 3) Consider terminating surgery.
patients undergoing general anesthesia. The 4 most common 4) Send for blood analysis.
temperature transducers are • Temperature equivalent 40o C.
Thermocouple • Patient should be paralysed and mechanically ventilated using high
Thermistor minute volume to eliminate CO2.
Infrared tympanic thermometer • Dantrolene should be administered.
Liquid crystal thermometer Temperature > 40o C
Once hyperthermia is established. • Hemofiltration should be considered.
• Evaluate patient history, physical examination and rule out • Other symptomatic measures
Other symptomatic measures:
predisposing condition.
• Antiseizures medication like phenytoin can be given prophylactically
• Evaluate drugs which might trigger.
once temp. pouches 39o C. if convulsion are present diazepam can
• Assess signs and symptoms
be given.
Lab Tests
-% Electrolytes and lactate • Renal function should be monitored with urine output maintained with
fluid replacement or administration of mannitol, Frusemide.
-% Plasma free Hb or heptoglobin
-% Urine myoglobin • Cardiac dysrrhythmias can be caused by hyperkalemia and acidosis,
so administration of glucose and insulin to correct hyperkalemia.
-% Creatinine kinase
Bicarbonate can be given in severe acidosis Cacl2 can be given once
-% Antiglobulin test
hypocalcemia is confirmed.
-% Blood Cultures
-% Compliment levels
-% Complete blood count and clotting time
-% LP for CSF analysis
135

versa.Continuation:
TEMPERATURE MONITORING: • Both have equilibration period of 20 – 30 sec.

The objective of temperature monitoring and perioperative. • Liquid crystal thermometer – These are recently used thermometers
Thermal management is to detect thermal disturbances and to for constant monitoring of skin temperature during anesthesia and
maintain appropriate body temperature during anesthesia. into recovery phase. These devices use the thermal optic
1. Core body temperature should be measured in most patient transmission qualities of crystals. The temp. is read from adhesive
given GA for > 30 minutes, both to detect MH and to quantify strip as the colour of liquid crystal changes with temp.
hyper and hypothermia. • The liquid crystal material which is commonly a cholesteric base
2. Temperature should be measured during regional anesthesia alters its molecular arrangement in response to temperature
when changes in body temperature are intended. variation. This configuration change permit some crystals to reflect
3. Unless hypothermia is specially indicated efforts should be or scatter light at given temp. While rest transmit light without
made to maintain intraoperative. Core temperature > 36o C. aberration. This is used to monitor skin temp.
Temperature monitoring involves – Advantages:

• Temperature probe selection. • Commercial kits are available
• Temperature monitoring site selection • Ease of application
Temperature probes: • Continuous information output
• Contact probes: The prototype is mercury thermometer. It has • Simplicity in screening for MH.
equalization time of 3-5 min.
• Use of mercury in glass is now economically unsound and Disadvantages
represents a hazardous waste disposable problem. • Skin surface temp may not reflect core temp. accurately.
Thermocouples and thermistors:
• Electrical thermometers are now commonly used for Infrared sensors
intraoperative monitoring of temperature. • Infrared temperature detectors look like otoscopes and are used to
• Electrical resistance of thermistor varies as a function of measure tympanic membrane temp.
temperature. Thermistors are fundamentally devices which are
thermal sensitive resistances whose resistance changes with Advantages:
temperature. • Response time is < 5 sec
• The principle of thermocouple is that if a circuit is made up of 2 • Very good index of core temp.
dissimilar mental elements the current in the circuit will be • Disposable thin plastic film cover reduces risk of infection.
directly proportional to temp. difference between 2 junctions of Disadvantages
dissimilar metals. Here one of junction is always kept at • Only intermittent spot checks can be made.
standard reference temp. (OO c) while other junction is located • Probe must be accurately placed aimed at tympanic membrane
in temp. probe. otherwise false low reading are a problem.
136

versa.Continuation:
ANATOMIC SITES FOR MONITORING Disadvantages

Oral: The classic location for oral location of temperature probe is • Perforation of tympanic membrane
sublingual on either side of frenulum. • Bleeding in external auditory canal in patients on anticoagulants.
The site is subjected to a number of external factors such as • Cerumen in ear canal act as insulator and can dampen the changes
mouth breathing, crying, and recent ingestion of hot or cold food. in temp.
Skin: It is not a reliable index of core temp. because the degree of • Oesophagus: Measurements of upper oesophagela temperature
vasoconstriction or vasodilatation can significantly affect the reflects temperature of inflow gases because of close approximation
measurements obtained. with trachea. So the probe is placed in lower ¼ of oesophagus i.e.
Forehead: It has received a lot of attention as an anatomic site for 20 cm below from pharyngoesophageal junction, which shows
temperature monitoring because of introduction of liquid crystal accurate core temp. because of close proximity with great vessels
temp. sensitive adhesive strips. and heart.
At normal OT room temperature heat lost from forehead is equal to
heat lost from any other part of body with same surface area
exposed.
Rectal temp: It is an adequate indicator of core temp. during
steady state. But drawback is that it seldom reflects actual core
temperature in anaesthetized patient when temp changes are
relatively rapid.
Can be used easily in infants than in adults. Major problem is of
execution, patient discomfort.
Bladder: It is reliable index of core temp. But lower abdominal
surgeries and irrigation with large amounts of fluids lowers the
measured temp.
Nasopharynx: The temperature is close approximation with brain
temp.
Measurements can be adversely affected by gas flow from
ventilation resulting in lower temp. with high flows.
The danger of causing Epistaxis is a consideration especially in
patient who are on anticoagulants.
Tympanic membrane: It approximates brain temp. better than any
other tissue. The blood supply to tympanic membrane is by
internal carotid artery which also supplies hypothalamus where the
central thermostat is located.
137

49. Airway assessment & Management of Difficult Airway. Dr Azam’s Notes in Anesthesiology 2013
INTRODUCTION DIFFICULT AIRWAY:

• The major responsibility of the anesthesiologist is to provide • The American society of anesthesiologists (ASA) defined a difficult
adequate ventilation for the patient. Expertise in airway airway as “The clinical situation in which a conventionally trained
management is important for every medical specialist and is a anesthesiologist experiences difficulty with mask ventilation, difficulty
lifeline for the anesthesiologist. Maintaining a patent airway is with tracheal intubation or both”.
vital aspect of providing adequate oxygenation and ventilation. • Any situation where operator requires more than 3 attempts or
• Failure to do so for even a brief period can be life threatening. A greater than 10 minutes is considered a difficult intubation according
quarter of preventable deaths related to anesthesia are due to to ASA guidelines.
airway management. Hence assessment of airway DIFFICULT MASK VENTILATION
preoperatively is most important to prevent such mishaps. • The ASA task force defined difficult mask ventilation as occurring
• The 3 main causes of respiratory related injuries are inadequate when “It is not possible for the unassisted anesthesiologist to
ventilation oesophageal intubation and difficult tracheal maintain oxygen saturation more than 90% using 100% oxygen and
intubation, Airway assessment helps in recognizing before positive pressure mask ventilation in a patient whose oxygen
anesthesia ; the potential for a difficult airway (DA) and allows saturation was more than 90% before anesthetic intervention; and /
time for optimal patient preparation, proper selection of or, it is not possible for the unassisted anesthesiologist to prevent or
equipment and technique and participation of personal reverse signs of inadequate ventilation during positive pressure mask
experienced in difficult airway management. ventilation.
DEFINITION OF TERMS: DIFFICULTY LARYNGOSCOPY
• AIRWAY: Airway is the passage through which the air/gas • The ASA task force has defined difficult laryngoscopy as occurring
passes during respiration. It may be divided into an upper and a when “It is not possible to visualize any portion of the vocal cords
lower airway. Upper airway structures comprise mouth, with conventional laryngoscope”. This usually corresponds to
nasopharynx, oropharynx, pharynx and the larynx. The Cormark and lehaneʼs Grade IV laryngoscopic view.
nasopharynx consists of nasal cavity, septum, turbinates and DIFFICULT AIRWAY CLINICS
adenoids. The oropharynx comprises the oral cavity, including • Recognizing before anesthesia the potential for a difficult airway (DA)
the teeth and tongue. The pharynx, includes the tonsils, uvula, is designated difficult airway clinics. It allows time for optimal patient
and the epiglottis. The lower airway includes the trachea, preparation, proper selection of equipment and technique and
bronchi and the bronchioles, which terminate in the alveoli. participation of personnel experienced in DA management.
• It is the epiglottis, which separates the larynx (which leads to
trachea) from the hypopharynx (which leads to oesophagus).
• In the practice of airway management it has also been used to
describe any artificial device with a lumen to serve as a conduit
to endotracheal intubation or a passage to aid ventilation. These
include intubation LMA, oropharyngeal airway, nasopharyngeal
airway or the severe varieties of LMA.
138

Airway assessment & Management of Difficult Airway.Continuation: Dr Azam’s Notes in Anesthesiology 2013
Anesthetic implication
Pediatric Adult
(in pediatric cases)
Nose Cartilages are very thin, not Thick and developed Increased risk of
fully developed, mucosa highly bleeding
vascular
Tongue Relatively large Smaller Oral cavity is small
difficult for insertion of
laryngoscope blade.
Straight blade is better
choice
Larynx More cephalad, funnel shaped, More caudal cylindrical Larynx is higher position.
C3C4 levels. Narrowest part – shape. C4, C5, C6 level. Choice of ETT is 1 size
just below the vocal cords at Narrowest part – is glottis lesser than visual
cricoid ring (subglottic region) appearance
Epiglottis V or Omega shaped stubby, Leaf shaped, flat thin To visualize larynx,
more horizontal close to the floppy more flexible. epiglottis should be lifted
base of the tongue along with laryngoscopic
blade
Hyoid and Cartilages intimately close Cartilages separated Thyromental distance is
thyroid less
Glottis One half is cartilaginous One fourth is cartilaginous Resistance to
endotracheal tube is
more
Arytenoids Inclined inferiorly, vocal cords Horizontal cards Passing of endotracheal
concave tube is difficult
Cricoid Inclined posteriorly Vertical
Narrowest Below the vocal cords cricoid The area between vocal
part ring cords
139

PAEDIATRIC AIRWAY: CAUSES OF DIFFICULT AIRWAY

• Difficulty with airway maintenance in children may be 1). Common Anatomical Factors
encountered due to the presence of large tongue, narrow and % -% Short muscular neck
short epiglottis, non calcified hyoid and thyroid cartilage. High % -% Protruding upper incisors
position of larynx (C3 4) trachea is downward and posterior. % -% A high arched, palate associated with long narrow mouth
OBSTETRIC AIRWAY: % -% Receding lower jaw and small mouth opening
• Incidence of difficult intubation is 1 in 280 patients and it is due to % -% Large tongue
the result of oedema of airway due to water retention in
pregnancy. Also due to increased vascularity of the larynx and a 2). Infection
friable mucosa and in pre-eclampsia there will be laryngeal % -% Epiglottitis
edema. The presence of large breast may also cause difficult % -% Abscess – Submandibular, retropharyngeal
intubation. These patients have decreased FRC and compliance % -% Croup
and increased oxygen consumption. % -% Bronchitis
AIRWAY ASSESSMENT / EVALUATION OF THE AIRWAY % -% Tetanus
1). HISTORY
• A history of difficult airway management in the past may be the 3). Neoplastic (Tumours and cysts)
best predictor of a challenging airway. If old medical records are % -Oropharyngeal, laryngeal, head and neck, anterior mediastinal,
available, prior anesthetic records should be reviewed for the % papillomatosis etc.
ease of intubation and ventilation (number of intubation attempts,
ability mask ventilate, type of laryngoscope blade – used, use of 4). Scarring of Tissues
stylet, or any other modifications of technique). Particular % -Post surgical, post burn, radiation, temporomandibular joint
importance should also be placed on diseases that may affect % ankylosis.
the airway. Specific symptoms related to airway compromise
should be sought, including hoarseness, stridor, wheezing, 5). Inflammatory
dyspnoea, dysphagia etc. % -% Rheumatoid arthritis
• Some diseases such as rheumatoid arthritis, and morbid obesity % -% Ankylosing spondylitis
might have progressed in the interim and created a more difficult % -% Subluxation of cervical vertebra.
airway than suggested by the previous record.
• History of previous surgery, burns, trauma or tumour in and
around the oral cavity, neck or cervical spine should be asked.
Many congenital syndrome that involve the airway may make
mask ventilation or endotracheal intubation difficult. Other
diseases of infections, traumatic, neoplastic or inflammatory
origins may also profoundly affect airway management.
140

6). Congenital II). GENERAL, PHYSICAL AND REGIONAL EXAMINATION

• Pierre Robin Syndrome – Micrognathia (small mouth), A global assessment should include the following:
macroglossia, mandibular hypoplasia, cleft soft palate. I. Patency of nares: Look for masses inside nasal cavity (eg. Polyps)
• Treacher Collins Syndrome (Mandibulofacial Dysostosis) – DNS etc.
Auricular and ocular defects malar and mandibular II. Mouth Opening of at least 2 large finger breadths between upper
hypoplasia. and lower incisors in adults is desirable.
• Goldenhars Syndrome (Oculoauricular vertebral anomalies) – III. Teeth: Prominent upper incisors, or canines can impose a
auricular and ocular defects, malar and mandibular limitation on alignment of oral or pharyngeal axes during
hypoplasia, cervical spine anomaly. laryngoscopy and especially in association with a large base of
• Downʼs Syndrome – Poorly developed or absent bridge of the tongue, they can compound the difficulty during the direct
nose, macroglossia, small mouth makes laryngoscopy laryngoscopy or bag mask ventilation.
difficult. Atlantoaxial instability. IV. Palate: A high arched palate or a long, narrow mouth may present
• Klippel – Feil Syndrome – Congenital fusion of a variable difficulty.
number of cervical vertebrae, restriction of neck movement V. Assess patientʼs ability to protrude the lower jaw beyond the upper
and neck rigidity. incisors (Prognathism).
VI. Temporomandibular joint movement: it can be restricted
7). Endocrine disorders ankylosis / fibrosis, tumours etc.
% - Acromegaly, Goitre / Thyromegaly, Obesity VII. Measurement of submental space (hyomental/thyromental length
should ideally be > 6 cm).
8)." Traumatic VIII. Observation of patientʼs neck: A short, thick neck is often
• Multiple trauma to face / mandible; cervical spine fractures, associated with difficult intubation. Any masses in neck, extension
basilar skull fractures, neck trauma, laryngeal fractures. of neck, neck mobility and ability to assume ʻSniffingʼ position
should be observed.
9)." Miscellaneous IX. Presence of hoarse voice / stridor or previous tracheostomy may
• Angioedema, scleroderma, Sarcoidosis, head traction, body suggest stenosis.
casts, Masseter spasm, poor technique and poor equipment. X. Any systemic or congenital disease requiring special attention
during airway management.
XI. Infections of airway (e.g. Epiglottis, abscess, croup, bronchitis,
pneumonia).
XII. Physiologic conditions; pregnancy and obesity.
141

DIFFICULT MASK VENTILATION I.E. BONES / OBESE Reduction of a-o extension

• B: Bearded individual – presence of beard – difficulty in creating i).% No reduction
proper seal with a mask leading to loss of ventilated volume. ii).% 1/3rd reduction
• O: Obesity – Body mass index > 26 kg / m2 iii).% 2/3rd reduction
• N: No teeth – lack of teeth – difficult to establish effective seal. iv).% Complete reduction
• E: Elderly age > 55 YEARS • 2/3rd or complete reduction of extension of a-o joint is a clear pointer
• S: Snorer – Varying degrees of obstructive sleep apnoea and are to difficult laryngoscopy.
difficult to mask ventilate. • Indirect assessment: Approximately 1/3rd of long term diabetic
• In addition Hair bun: Placing such a patient in the sniffing patients presents with laryngoscopic difficulties due to “Stiff Joint
position is difficult as the bun prevents extension of the atlanto- Syndrome”.
occipital joint. It is advisable to undo the bun prior to positioning i).Palm print: The patient is made to sit ; palm and fingers of right hand
the head and neck. are painted with blue ink. Patient then presses the hand firmly against
• Jewellery: worn by piercing of lips, tongue, cheek, chin, a white paper placed on a hard surface. It is categorized as –
eyebrows and ear may also create difficulty in mask ventilation. • Grade 0: All the pharyngeal areas are available
• Grade 1: DeBiciency in the inter-‐pharyngeal areas of the 4th & 5th digits
III. SPECIFIC TESTS FOR ASSESSMENT (Clinical Tests)
• Grade 2: DeBiciency in the inter-‐pharyngeal areas of 2nd to 5th digits
• These are used in an attempt to predict difficult laryngoscopy
and tracheal intubation. No single test can be used to predict • Grade 3: Only the tips of digits are seen.
difficult – laryngoscopy with certainty. Combining 2 or more tests ii). Prayer sign: Patient is asked to bring both the palms together as
improves the positive predictive value. “Namaste” and sign is categorized as –
• Positive: When there is gap between palms
TESTS: Negative: When there is no gap between palms
A). ASSESSMENT OF CERVICAL AND ATLANTO – OCCIPITAL • If prayer sign is positive, it should alert the laryngoscopy to the
JOINT (A-O) FUNCTION: possibility of cervical spine involvement and limited a-o movement
• These function may be assessed directly and also indirectly leading to difficult laryngoscopy and intubation.
especially in patients of stiff joint syndrome (as in diabetics) B)." ASSESSMENT OF TEMPORO – MANDIBULAR JOINT (TMJ)
• Direct assessment: Laryngoscopic view becomes easier when FUNCTION:
the neck is flexed on the chest by 25 – 35o and the a-o joint is • 1).Inter-incisor gap (distance): It is the distance between the upper
well extended (85o). It assesses the feasibility to make “Sniffing” and lower incisors. Ask the patient to open his mouth as wide as
or the “Magillʼs position” for intubation i.e. Alignment of oral, possible and place his 3 fingers (index, middle and ring) in the
pharyngeal and laryngeal axes into arbitrary straight line. opening. If done this is > 5 cm and is adequate for direct
Assess the first movement by asking the patient to touch his laryngoscopy and intubation < 3 cms (2 finger breadth) is associated
manubrium sterni with his chin. If done, this assures neck flexion with difficult laryngoscopy.
of 25 – 30o. Following this ask the patient to look at the ceiling
without raising eyebrows to test a – o joint function.
142

2). Place index finger in front of the tragus and the thumb in front • In Sampson and Youngʼs modification (1987) of Mallampati
of the lower part of the mastoid process behind the ear. Ask the classification a IV class was added.
patient to open his mouth wide. As the condyle of the mandible • Class IV: Hard palate visible.
slides forward, the index finger in front of the tragus can be • Class III & IV: Views are associated with difficulty intubation when
indented in its space and the thumb can feel the sliding of the used in isolation the Mallampati test predicts approximately about
condyle. This suggests good sliding function of mandible 50% difficult intubations.
(Subluxation of the lower jaw). ASSESSMENT OF MANDIBULAR SPACE:
3). Protrusion of the mandible: Ask the patient to protrude their 1)." Thyromental distance (Patilʼs test)
mandible. Look at the position of the lower teeth in relation to the • It is defined as the distance from the mentum to the thyroid notch.
upper teeth. While the patientʼs neck is fully extended. This measurement helps
Class A : % The lower incisors can be protruded anterior to the in determining how readily the laryngeal axes will fall in line with the
upper incisors. pharyngeal axes when the atlanto occipital joint is extended. It
Class B : % The lower incisors can be brought edge to edge with estimates the potential space into which the tongue can be displaced
the upper incisors. on laryngoscopy. This should be greater than 6.5 cm.
Class C:% The lower incisors cannot be brought edge to edge. • > 6.5 cm: No problem with laryngoscopy and intubation.
Class B & C: %are associated with difficulty laryngoscopy. • 6 to 6.5 cm: Without other concomitant anatomical problems
MALLAMPATI TEST (With Samson and Youngʼs modification laryngoscopy and intubation are difBicult but possible.
1987): • < 6 cm: Associated with difficult laryngoscopy and predicts 75%
• This is probably the most commonly employed test for predicting difficult laryngoscopy.
difficult airway. It indicates the amount of space within the oral 2). Sternomental distance:
cavity to accommodate the laryngoscope and ETT. The Savva (1948) estimated the distance from the suprasternal notch
Mallampati classification correlates tongue size to pharyngeal (upper border of manubrium) to the mentum with neck fully extended
size. Sit in front of the patient who should be sitting up with their and mouth closed. A value of less than 12.5 cm is associated with
head in the neutral position. Ask the patient to open their mouth difficult laryngoscopy and intubation.
maximally and protrude their tongue without phonating, as it can 3). Mandibulohyoid distance or hyomental distance
result in contraction and elevation of the soft palate leading to This is the distance between the mentum to hyoid bone. It is graded
spurious picture. as
• Note which of the following structures visible – Grade I % :% > 6.0 cm
• Class 0: Epiglottis is seen Grade II % :% 4.0 – 6.0 cm
• Class I : Faucial pillars, uvula, soft and hard palate visible. Grade III % :% < 4.0 cm
Class II : Uvula, soft and hard palate visible Grade III hyomental distance is usually associated with difficulty
Class III :Soft palate and base of Uvula visible. laryngoscopy and intubation.
143

WILSONʼS RISK SCORE

• M.E. Wilson and colleagues in 1988 identified 5 risk factors in predicting difficult airway. These include
(1) Body weight (2) Extent of head and neck movement (3) presence of receding mandible (4) Jaw
movement (5) Buck teeth.
• These factors were given scores varies between 0 to 10. The greater than score, greater the risk for
difficult intubations.
Risk factor 0 1 2
Weight (Kg) < 90 90 – 110 > 110
Head and neck movement > 90o 90o < 90o
Jaw movement " - (IG) > 5 cm 5 cm < 5 Cm
" " " - (SL) > 0 =0 <0
Receding mandible None Moderate Severe
Buck teeth Normal Moderate Severe
Total score 10
BENUMOFʼS 11 PARAMETER ANALYSIS ;

• Benumof has suggested 11 step airway examination that can be completed in less than a minuteʼs time.
It is easy to follow this scheme if one remembers that it follows the line of sight from the upper incisors to
the glottis. Another way is by remembering 4-2-2-3 rule, i.e there are 4 steps focusing on the teeth, 2
steps inside the mouth, 2 steps for the mandibular space and 3 steps in neck examination.
144

Parameter evaluated Minimal acceptable value Significance

1. Inter incisor gap in cm > 3 cm Gap > 3 cm permits easy insertion of laryngoscope blade
2. Look for buck teeth, i.e. No overriding Buck teeth if present cause the laryngoscope blade to
involuntary anterior overriding of enter in cephalic direction
maxillary teeth on the mandibular
teeth
3. Length of upper incisors Short incisors (< 1.5 cm) Long incisors prevent easy aligning of oropharyngeal axes
4. Voluntary protrusion of the Mandibular teeth can be protruded suggests optimal TMJ function, both rotatory and sliding,
mandibular teeth anterior to beyond the maxillary teeth thereby permitting easy laryngoscopy
maxillary teeth
5. Mallampati class Class II or less Suggests optimal tongue size in relation to oropharyngeal
cavity permitting easy laryngoscopy
6. Palate configuration No arching or narrowness of the A narrow, arched palate reduces room for laryngoscope
palate blade and ETT
7. Length of mandibular space < 5 cm or > 3 ordinary sized finger Suggests optimally placed larynx, permitting easy aligning
(thyromental distance) breadth of axes
8. Compliance of mandibular space Mandibular space is soft to palpation A complaint mandibular space allows easy tongue
compressibility during laryngoscopy
9. Neck thickness Qualitative exact values need A thick, short neck decreases the ability to align the upper
determination airway axes.
10. Neck thickness - do - Not well defined significantly
11. Head and neck Sniffing position = Neck flexion 35o The 3 axes of the upper airway (oro pharyngeal laryngeal)
head extension 80o the best aligned in sniffing position
145

ROCKE et al (1992) combined Mallampati grading with factors SIX STANDARDS IN THE EVALUATION OF AIRWAY:
such as obesity, short neck, abnormality in teeth (missing, 1. Temporomandibular mobility.
protruding or single maxillary incisors), receding mandible, facial 2. Inspection of mouth, oropharynx
edema and swollen tongue in obstetric population and showed a 3. Measurement of mentohyoid distance (4 cm) in adults. Grade I – 6
significant correlation between classification of airway and cms, Grade – II – 4-6 cms, Grade – III - < 4 cms.
laryngoscopic grade. 4. Measurement of distance form chin to thyroid notch (5 to 6 cm).
LEMON AIRWAY ASSESSMENT METHOD / MELON: 5. Ability flex head towards chest, extend head to atlanto – occipital
The score with a maximum of 10 point sis calculated by assigning joint and rotate head to right and left.
1 point for each of the following. LEMON CRITERIA. 6. Symmetry of nose and patency of nasal passage.
• L: Look externally (short neck, facial trauma, facial hair – beard
or moustache, edentulous patient, obesity, large tongue etc. CORMACK AND LEHANE CLASSIFICATION
• E :Evaluate the 3-3-2 rule (Incisor distance 3 finger breadths Direct laryngoscopy
hyoid – mental distance 3 finger breadths, thyroid to mouth On basis of clinical examination if a difficult intubation is expected,
distance – 2 finger breadths) direct laryngoscopy should be done under topical anesthesia to assess
• M :Mallampati (Mallampati Score > 3) the grade of difficulty. Graded into 4 grades according to degree of
• O: Obstruction (Presence of any condition like epiglottis, glottic exposure.
peritonsillar abscess, trauma, tumour etc). • Grade I: Glottis fully exposed visualization of entire laryngeal
• N :Neck mobility (limited neck mobility) aperture. No difficulty expected, No extrinsic pressure required.
Patients in the difficult intubation group have higher LEMON • Grade II : Visualization of only posterior commissure of laryngeal
scores. aperture. Optimal external laryngeal manipulation cricoid pressure
CLINICAL CHECK TEST FOR INTUBATION i.e. 12” Tʼs required to intubate)
1). Teeth – Loose / Missing / Prosthesis / Bucked • Grade III : Visualization of only epiglottis
2). Tongue May have difficulty in intubation and can be overcome by the use of
3). Tonsils stylet / Bougie.
4). Temporomandibular joint • Grade IV: No glottic structures seen
5). Torticollis (flexion, extension, rotation of the neck) Difficult and may even be impossible to intubate
6). Thyroid notch Planned intubation required.
7). Trachea
8). Tumours
9). Turbinates
10). Tuberculum pharyngeum
11). Talk (Voice)
12). Tales (history)
146

FURTHER EVALUATION: Advanced indices for predicting difficult airway

Radiographic assessment: a. Flow volume loops: Recording of flow volume loops is an advanced
Following measurements are found to be of use in predicting test in which forced expiratory volume and forced inspiratory
difficulty in direct laryngoscopy. volumes are recorded in spirogram. Flow volume loops help in
1. Posterior depth of the mandible (PDM): It is the distance distinguishing between large and small airway obstruction.
between the bony alveolus immediately behind the 3rd molar b. Acoustic response measurement: Here the airway is assessed by
tooth and the lower border of the mandible. Increase in this reflection of sound waves from the upper airway.
distance is thought to hinder displacement of soft tissues by the c. MRI: Sagittal MRI of upper airway may be valuable in specialized
laryngoscopic blade. cases.
2. Effective mandibular length (EML): It is the distance between Recently, Ezri et al (2003), have demonstrated that quantifying the
the tip of lower incisors to TMJ. If EML is less than 3.6 times anterior neck soft tissue by ultrasound is a good method to predict
the PDM, direct laryngoscopy will be difficult. difficult laryngoscopy in obese patients. In this method, the distance
3. Atlanto – occipital (distance) A- O gap is the major factor which from the skin to the anterior aspect of the trachea is measured at 3
limits the extension of head on neck. Longer the A-O gap, level.
more space is available for mobility of head at that joint with • i).% Vocal cords (Zone I)
good axis for laryngoscopy and intubation. ii).% Thyroid Ishthmus (Zone – II)
4. Interspinous gap C1-C2 gap: Look for loss of atlanto – iii).% Suprasternal notch (Zone – III)
occipital / atlanto axial gap. (C1-C2) when head is extended, The amount of soft tissue at each zone is calculated by averaging the
movement takes place at both joints. Loss of these gaps may amount of soft tissues in mm obtained in the central axis of the neck
indicate limitation of neck movements. and 15 mm to the left and right of the central axis. A soft tissue
5. Relation of mandibular angle and hyoid bone with cervical thickness of more than 25mm in Zone – I is a clear pointer to difficult
vertebra and laryngoscopic grading: A definite increase in laryngoscopy.
difficult laryngoscopy was observed when the mandibular angle A rapid assessment of the airway by the rule of 1-2-3:
tended to be more rostral and hyoid bone to be more caudal, Three factors determine the ease of visualization of glottis in an
position of mandibular angle being more important. emergency situation, with severe time constraint, done in < 15
Other assessment aids: seconds.
1. Fluoroscopy for dynamic imaging (cord mobility, airway i).% Movement of the Temporomandibular joint
malacia, and emphysema). ii).% Extent of mouth opening
2. Oesophagogram (Inflammation, foreign body, extensive mass iii).% Size of mandibular space
or vascular ring).
3. Ultrasonography (assessment of anterior mediastinal mass,
lymphadenopathy)
4. Computed tomography MRI (congenital anomalies, vascular
airway compression).
5. Video optical intubation stylets (combines viewing capability
with the familiar handling of intubation devices). 147

This consists of 3 basic steps: INDICATORS OF DIFFICULT INTUBATION

• Step I : Ability to insinuate 1 finger in front of the tragus while
patient opens his mouth (establishes movement at TM joint).
a. Poor flexion – extension mobility of the head on neck
• Step II: Determining the adequacy of mouth opening by b. A receding mandible and presence of prominent teeth.
quantifying the interincisor gap which should be at least 2 finger
c. A reduced a-o distance, a reduced space between C1 and the
breadths.
occiput.
• Step III: Measurement of thyromental distance which should be d. Large tongue size – Related more to the ratio of the anterior length
at least 3 finger breadths.
of the tongue to the length of the chin or mandible.
Tests to predict prolonged laryngoscopy time:
A COMPREHENSIVE SCORING SYSTEM:
Saghei and Safavi (2001) have reported the use of 6 parameters Type variable score:
to predict prolonged laryngoscopy time. 1).% Receding chin or TMD < 7 cm % % -% 3 Points
1).% Weight of the patient % -% > 80 Kg 2).% Mallampati sign (Uvular not visible)% -% 2 Points
2).% Tongue Protrusion% % -% < 3.2 cm 3).% Restricted head extension% % % -% 2 Points
3).% Mouth Opening % % -% < 5 cm 4).% Protruding teeth % % % % -% 2 Points
4).% Upper incisor length% % -% < 1.5 cm 5).% Mouth opening < 4 cm % % % -% 2 Points
5).% Mallampati class % % -% >1 6).% Vertical neck length < 7.5 cm % % -% 1 Point
6).% Head extension% % -% < 70o 7).% Neck circumference > 33 cm % % -% 1 Point
A score of 6 more correctly identified 22 out of 23 difficult intubation.
The presence of 3 of these factors predicts prolonged The standard intubating position: “Sniffing position” or “Magillʼs
laryngoscopy. Position”
Upper lip bite test:
• This test have been proposed b Khan et al (2002) as a simple
new assessment method in predicting difficulty in endotracheal
intubation. It basically tests the range and freedom of
mandibular movement and the architecture of the teeth. The
upper lip bite test is performed as follows.
• Class I :Lower incisors can bite the upper lip above the vermilion
line
Class II : Lower incisors can bite the upper lip below the
vermilion line
Class III : Lower incisors cannot bite the upper lip.
• Patients having class III of upper lip bite test may be expected to
have Cormack and Lehaneʼs grade III and IV laryngoscopic view
of the larynx. With this test 88% of easy and difficult intubations
were correctly predicted. 148

PREMEDICATION AND PREPARATION OF THE PATIENT TEN COMMANDMENTS OF AIRWAY MANAGEMENT

• Patients with underlying medical conditions should be optimized 1). Have an organized plan
because the stress elicited during difficult intubation will be 2). Remain Calm
greater than usual. 3). First use bag – mask ventilation
• Repeated airway manipulation may cause 4). Call for help early
Transient hypoxemia and hypercarbia 5). If you canʼt ventilate, intubate
Will cause tachycardia / hypertension thereby increasing the risk 6). Keep track of time
of ischaemia in a known CVS disturbed patients. 7). If at first you donʼt succeed try again
• Secure a good IV line 8). If you canʼt intubate, ventilate
• Oxygen administration 9).If you canʼt ventilate with a bag mask and canʼt intubate, open the
• Sedation and anxiolytics neck
• Anticholinergics: These patients are known to produce increased 10). Practice whenever you can, These re perishable skills.
secretions in airway which may provoke laryngospasm /
bronchospasm during the procedure. ANTICIPATED DIFFICULT INTUBATION FOR ELECTIVE SURGERY
• H2 receptor blockers – For those with risk of gastric aspiration. • Only about one quarter of anticipated difficult intubation may actually
• Inhaled B1 blockers – patients with bronchospatic airway be difficult. Of these approximately 85 – 90% can be managed by
condition require inhaled B1 blockers. experienced anesthesiologist with simple maneuvers.
• If intubation is expected to be difficult, a senior Anesthesiologist
MANAGEMENT OF DIFFICULT AIRWAY properly equipped to deal with the situation should be present and it
Difficult Airway is logical to secure the airway with Awake tracheal intubation.
• The ASA has defined difficult airway as a situation where a
conventionally trained. Anesthesiologist experiences difficulty AWAKE INTUBATION:
with mask ventilation, intubation or both. 1). Indications: Awake oral or nasal intubation should be considered
• Any situation where operator require more than 3 attempts or when there is
greater than 10 min. is considered a difficult intubation a). A difficult intubation anticipated in a patient at risk of aspiration.
according to ASA guidelines. Incidence is 0.5 to 13.6%. b). Uncertainty about the ability to ventilate or intubate after induction
• The approach to difficult intubation will depend on whether it is of GA (e.g.: Morbidly obese patients)
expected or unexpected. Other factors include – c). A need to assess neurologic function after intubation or positioning
1) Status of the patient for surgery.
2) Type of surgery
3) Urgency of surgery TOPICAL ANESTHESIA
4) Type and grade of difficulty Topical Anesthesia is the primary anesthesia for awake intubation.
5) Skin and experience of individual. Allow sufficient time to anaesthetize all the relevant portions of airway.
149

Nose, Mouth, Nasopharynx / Oropharynx: Translaryngeal Injection: Here the local anesthetic solution is
• Nasal mucosa can be anaesthetized by sprays, pledgets and injected through the Cricothyroid membrane to anesthetize supraglottic
nasal drops, 4% lignocaine spray may be used to anaesthetize structures and upper trachea. This blunts cough reflex.
oral mucosa. Gargling 2-4 ml of lignocaine viscus will also help. Procedure: The procedure is easy to perform and very effective and
It is more convenient and reasonable effective to use a causes minimal discomfort provided patients are adequately sedated
lidocaine / phenylephrine combination i.e. 4% lidocaine and 1% beforehand. Patients should be warmed about the possibility of an
phenylephrine in 3:1 combination. episode of uncontrollable coughing during and immediately after the
• Nasopharynx: Local anesthetic aerosol is a good option. This procedure. With the neck extended, the cricothyroid space is palpated
may be done through a nasopharyngeal airway. Topical and a 23 G needle attached to a syringe is inserted into the trachea in
anesthetic solution may be injected through the airway using a the midline. Following aspiration of air, 4 ml of 2% lignocaine injected.
syringe and IV catheter. Coughing dissipates the solution within the trachea. The use of 50 to
• Tongue and Oropharynx: Can be anesthetized with 10% 100 µg of fentanyl prior to injection helps to reduce the severity of
lidocaine spray, which is placed progressively further into the coughing. Some recommend the use of a “Catheter over the needle”
pharynx using the laryngoscope blade or a tongue depressor. technique to reduce the possibility of laryngeal trauma.
• Supraglottic and glottic structures: Once the tongue and
oropharynx are sufficiently anaesthetized the long applicator Contraindications:
adaptor for 10% lidocaine spray can be blindly placed through • Unstable cervical fracture
the airway to spray anesthetic directly onto the supraglottic and • Localized infection
glottic structures. Nebulization of 5 ml of 4% lidocaine can also • Malignant tumor
be employed. • Enlarged thyroid
• Larynx: It can be sprayed with additional lidocaine directly on the • Bleeding diathesis
visualized structures. There are a number of prefilled devices
available to achieve topical anesthesia of the larynx and trachea. Complications
One such device is the laryngotrachela topical anesthetic spray • Hematoma formation
(LTA). This consists of a prefilled disposable syringe with a long • Oesophageal perforation
plastic cannula that has multiple perforations. Using a • Subcutaneous emphysema
laryngoscope, the cannula is advance to topically anesthetize the
supraglottic region, larynx and trachea.
• In the presence of full stomach, the topical anesthesia of the
airway should be used with caution.
150

Aerosol inhalation: This can be done with the help of nebulizer. 5 DIFFICULT AIRWAY (DA) CART:
ml of 4% lignocaine with an oxygen flow of 10 lit / min is used. • Face masks – appropriate sizes
Patient is advised to breath deeply and slowly. About 15 – 20 min • At least 2 working laryngoscopes with all sizes of blades both curved
should be allowed for the inhaled anesthesia to be effective. and straight.
However even careful topical anesthesia may not be adequate for • Endotracheal tubes – all sizes with patent lumens and intact cuffs.
laryngoscopy, as the pressure receptors at the root of the tongue • Magillʼs forceps both small and large
that cause gag reflex are submucosal and are not blocked • Gum elastic Bougie
topically. In such situations, block of 2 nerves done. • Tongue depressor
There are 2 nerve blocks which are easy to perform with low risk. • Malleable stylets
1).% Bilateral internal branch of superior laryngeal nerve block. • Airways of suitable sizes both oropharyngeal and nasopharyngeal
2).% Bilateral lingual branch of glossopharyngela nerve block • Suction apparatus with suction catheters
• Oxygen source
• A ventilating apparatus with suitable adaptors to the mask and tube
1). Superior laryngeal nerve block (internal branch) • A head rest or pillow with a minimum height of 10 cm.
• It can be blocked either externally, where the nerve pierces the • LMAs of assorted sizes, this may include ILMA and Proseal LMA.
thyrohyoid membrane or internally as it passes through the • Combitube
pyriform fossa and lies submucosally. Pledgets soaked in local • Flexible fibro optic laryngoscope / bronchoscope
anesthetic solution are placed in the fossa with a curved forceps. • Cricothyrotomy and tracheostomy kit
(eg. Krause forceps) and left in place for 3 to 5 min for effective • Light wand, Huffman prism
anesthesia. • Equipment for retrograde intubation.
• The external block is performed as follows: • Emergency kit for transtracheal ventilation
• Patient is placed supine with the neck extended. Grip the hyoid • Monitors – Pulse oximetry, BP, Capnography and temperature
bone transversely with thumb and index finger, then palpate a
depression felt bilaterally between the superior horn of thyroid
cartilage and hyoid bone. Following a negative aspiration test,
inject 3 ml of 2% lidocaine bilaterally using a 23 G needle.
2). Glossopharyngeal nerve block (lingual branch)
• Performed bilaterally it abolishes gag reflex.
• Technique: Ask the patient to open the mouth wide. After
identifying the posterior tonsillar pillar (palatopharyngeal fold) an
angled tonsillar needle is inserted at the midpoint of the pillar and
2-3 ml of 1% lignocaine is injected. The same is repeated on
other side.
151

PROBLEM ORIENTED APPROACH: D). EXPOSURE OF GLOTTIS EXPECTED TO BE INADEQUATE

A). PATIENT CANNOT BE POSITIONED FOR DIRECT i). Grade III exposure expected
LARYNGOSCOPY • Optimize position, give pressure on thyroid cartilage i.e. BURP
Restricted flexion of cervical spine. maneuver, %use stylet use straight blade, Mc Coy Blade, Bullard
Use of miller blade, McCoy blade, Huffman Prism laryngoscope, upsherscope, WuScope, Huffman prism or Howland
Restricted movement at atlantoccipital joint: adapter and try nasal intubation.
a. Mild to moderate restriction ii). Grade IV exposure expected.
• Raise occiput above level of shoulder • Under local anesthesia, attempt nasal intubation, retrograde
• Use malleable stylet to increase the curvature of the tube. intubation, intubation with light wand, LMA, fibroscope aided
• b. No extension possible intubation.
under local anesthesia, use retrograde intubation / fiberoptic E). INTRODUCTION OF TUBE IN THE TRACHEA EXPECTED TO BE
aided intubation. DIFFICULT
• c. Fixed flexion of the neck Use a malleable stylet, use Magill forceps
Under local anesthesia, use retrograde intubation or fiberoptic If the ability to ventilate by mask has also been lost then a true CVCI
scope aided intubation situation exists. Four acceptable responses to this situation are:
• Insertion of LMA
B)." MOUTH OPENING RESTRICTED
• Insertion of combitube
a. Restriction due to pain / spasm • Institution of TTJV
• Intubate under vision after induction • Surgical airway
b. Restriction due to fibrosis / ankylosis There are 4 important steps from the ASA difficult airway algorithm:
i). Minimal restriction A).% If suspicious – secure airway awake
Use miller bade, McCoy blade or intubate nasally. B).% If can ventilate but cannot intubate – awaken the patient
• ii). Severe restriction C).% If CVCI – immediately employ CVCI options.
Under local anesthesia, attempt blind nasal intubation, D).% Always have a plan for B & C Immediately available and think
retrograde intubation, fiberoptic scope aided intubation or ahead
% transtracheal jet ventilation. A few clarifications are appropriate while reviewing the ASA difficult
C)." DIFFICULTY IN INTRODUCTION OF LARYNGOSCOPE
algorithm.
• Use polio blade, shorthanded blade or blade detached from handle.
152

A). What is optimal best attempt at conventional laryngoscopy: ANTICIPATED DIFFICULT INTUBATION FOR EMERGENCY SURGERY
i).% Reasonably experienced laryngoscopist • Awake intubation should be considered whenever there is a risk of
ii).% No restrictive muscle tone present aspiration during induction of anesthesia, with the patient breathing
iii).% Use of optimal sniffing position spontaneously, there need be little urgency to complete tracheal
iv).% Use of optimal external laryngeal manipulation intubation and the risk of hypoxia is minimized. Even when local
v).% Change of length of blade anesthetics are used to blunt airway reflexes, an awake patient can
vi).% Change of type of blade usually respond to regurgitation by clearing the pharynx. For
preventing a possible aspiration, intubation under local anesthesia
MANAGEMENT OF DIFFICULT AIRWAY: without sedation is safer than intubation under sedation without local
DOʼs anesthesia.
• Use an antisialagogue in the premedication. UNEXPECTED DIFFICULT INTUBATION (Failed intubation)
• If nasal intubation is chosen, use a topical vasoconstrictor for the Nearly 50% difficult airway are unexpected.
nasal mucosa. These are risk to the patient and a challenge to the skill of the
• Check and keep ready in advance all special equipment likely to anesthesiologist. When first 2 – 3 attempts of intubation fails,
be needed, all sizes of airway, LMA, ETT, kept ready. a). Ensure adequate ventilation and oxygenation
• Tracheostomy and emergency cricothyrotomy kits b). Continue cricoid pressure in a patient at risk of aspiration.
• Pre-oxygenate the patient If conventional laryngoscopy fails, after a best attempt, other choices
• Take all precautions to prevent regurgitation and aspiration of include
gastric contents 1. Laryngoscopy with different sizes of blades
• Monitor ventilation and oxygenation continuously by pulse 2. Blind orotracheal / Nasotracheal technique
oximetry, ECG, capnography and temperature monitor. 3. Flexible fiberoptic aided intubation
• Confirm successful intubation by all available means before 4. Illuminating stylet ; light wand aided ETI
proceeding. 5. Intubating laryngeal mask airway aided ETI
• Keep help – a senior anesthesiologist or one more colleague. 6. Indirect rigid fiberoptic laryngoscope assisted ETI
DONʼTʼs 7. Retrograde technique
• Do not induce unconsciousness unless you are certain that 8. Pharyngeal airway express aided ETI
spontaneous respiration be maintained. 9. Percutaneous transtracheal jet ventilation
• Do not produce deep anesthesia unless you are sure that you 10. Percutaneous tracheostomy / cricothyroidotomy
can maintain patient airway.
• Do not render the patient apnoeic unless artificial ventilation can
be rapidly instituted.
• Do not use a technique you are not familiar with
153

BLIND NASAL INTUBATION

Causes of failure of fiberoptic intubation
• Used when mouth opening is very limited or absent but at the
• Lack of experience
same time there is no difficult in adopting the standard intubation
• Presence of secretions
position. Can be used in spontaneously breathing patients.
Technique • Fogging of objective / focusing lens
• Poor topical anesthesia
• A well lubricated endotracheal tube is introduced along the floor
of the nose with the bevel facing nasal septum. • Epiglottis touching the pharyngeal wall
• Distorted airway anatomy
• The ET tube is advanced through the nostril into the
Contraindications
hypopharynx to a point just above the glottic opening.
• An absolute contraindication is lack of time
• Then the ET tube is advanced while the operator is listening to
breath sounds. It is advanced as long as breathing is tubular in • Relative contraindications – 1(1) Edema of pharynx or tongue,
tracking infection with inflammation and hematoma. In all these
quality until it is in the trachea.
situations the field of vision of fiberscope is greatly reduced. (2)
• This should not be used in patients with bleeding diathesis and
Blood and secretions in the oral cavity (3) Presence of pharyngeal
laryngeal pathology.
abscess, which can be disrupted as the ETT is railroaded over the
FIBEROPTIC INTUBATION fiberscope.
The main components of the flexible fiberscope system are –
• The flexible fiberoptic bronchoscope was introduced into clinical
a). % Eyepiece
practice in 1964. It was used for first time in managing difficult
b). % Control Section
intubation in 1967 by Peter Murphy. Since then the use of
c).% Insertion cord
fiberoptic intubation has gained its popularity and has become an
d).% Universal cord for light transmission
established procedure to manage difficult airway.
Indications e).% Light source
Routine intubations • The flexible fiberoptic laryngoscope consists of glass fibres (10,000
•
Difficult intubation (anticipated and unanticipated) glass fibres, 25 µ each in diameter) that re bound together to provide
•
Congenital abnormalities a flexible unit for the transmission of light and images. The fiberoptic
•
High risk of dental damage bundle is fragile and excessive bending can damage the fibres.
•
High risk of aspiration Working channels are usually present that can be used to administer
•
Acquired abnormalities – cervical spine spondylitis, TMJ topical anesthetics / saline and provide suction and insufflation of
•
ankylosis. oxygen. The visual field often becomes limited as the fiberoptic
Movement of neck not desirable as in cervical spine instability. bronchoscope nears the glottic opening. Secretions, blood or
•
Previous tracheostomy or prolonged intubation. fogging of the lens may obscure the view. Immersion of the tip of the
•
Anticipated problems: obesity, micrognathia, protruding teeth etc. fiberoptic scope in warm water helps to prevent fogging.
•
• Confirm correct placement of ET tube
• Confirm correct placement of DLT.
• To evaluate possible obstruction of ETT
154

• Standard equipment for oral or nasal fiberoptic intubation • Maintaining midline head and fiberscope position, negotiate upper
includes an oral bite block or Ovassapian airway, topical airway, and emerge into the pharynx above the epiglottis and the
anesthetics and vasoconstrictors suction and a sterile fiberoptic vocal cords. Once the adequacy of topical or inhalational anesthesia
scope with light source. is verified, the scope is advanced under the epiglottis and through
• Technique: FOI can be performed by either oral or nasal route. the vocal cords. The trachea is entered and scope advanced until
the carina is in view. The fiberscope is carefully maintained in this
NASAL FOI position until ETT is advanced into the trachea over the scope. The
• Nasal FOI is often preferred to oral FOI because, it is easier to tip of the ETT and the carina should both be watched closely as the
maintain midline position of the fiberscope, the patient cannot scope is carefully withdrawn.
bite or chew on the scope and the anatomy of the nasopharynx Oral:
naturally directs the scope into the trachea. • Technique: An ETT is placed over a lubricated fiberoptic scope,
There are several technique for achieving nasal FOI suction tubing is attached to the suction port, and the control lever is
1. Pass a soft nasal airway to ascertain good patency. Replace grasped with one hand while the scope is advanced or maneuvered
this airway, with the nasotracheal tube (ETT) to the same with the other hand. An oral ovassapian airway is helpful and well
length. Perform fiberscopy through the ETT. tolerated for oral laryngoscopy. It is important to heep the fiberoptic
2. Load the ETT over the insertion cord upto the level of the scope in the midline to prevent entering the piriform fossa. The tip of
control section. Remove the nasal airway and introduce the the scope is positioned anteriorly when in the hypopharynx and
fiberscope directly through the nose. advanced toward the epiglottis.
3. Introduce fiberscope through a slit nasal airway and • If mucosa or secretions impair the view, the scope should be
subsequent removal of the nasal airway by disengaging at via retracted or removed to clean the tip and then reinserted in the
the split. midline. As the scope slides beneath the epiglottis, the vocal cords
4. Access the airway through anesthetic mask designed to will be seen. The scope is advanced with the tip in a neutral position
accommodate the fiberscope. until tracheal rings are noted. The scope is stabilized within the
• Before embarking of FOI, the fiberscope and the light source are trachea and the ETT is advanced over it and into the trachea.
checked a three way stopcock may be attached to the suction • If there is resistance to passage, the ETT may need to be turned 90o
channel for suction and O2 insufflation. The lens is focused for a in the counter clockwise direction to avoid the anterior commissural
clear view prior to use. A lubricant is applied over the cable and permit passage through the vocal cords.
(avoiding the lens) and a cut to size ETT is mounted over it. The
scope is now held in one hand, thumb on the control knob and Key to successful intubation include –
index finger on the suction port. The scope is now introduced a).Control of secretions b) Bronchoscopic intervention before extensive
via the more and index finger on the suction port. The scope is bleeding and oedema have occurred c) Adequate topical anesthesia
now introduced via the more patent nares using any of the four and sedation, d) Proper defogging of the lens, e) Aligning the scope in
techniques described earlier. midline.
155

LARYNGEAL MASK AIRWAY (LMA): • The inner aspect of the mask is called the bowl, which is comprise of
It was designed and developed between 1981 and 1988 by Dr. the distal aperture, MAB, back plate and the inner aspect of the
Archie Brain, a British Anesthesiologist. LMA is a supraglottic inflatable cuff.
device that is intermediate in design and function between a face • The mask inflation line consists of 4 parts, the long narrow inflation
mask and an endotracheal tube. Although originally developed for line itself, the pilot balloon, a metallic valve and the syringe port. The
airway management of routine cases with spontaneous ventilation, valve which has a white coloured core is made from polypropylene
it is now listed in the ASA difficult airway algorithm in 5 different and has a stainless steel spring valve. The LMA is available in eight
places as an airway (ventilatory device) or a conduit for sizes from neonates to large adults.
endotracheal intubation. It can be used in both pediatric and adult Classic LMA specification:
patients in whom ventilation with a face mask or intubation is Mask size Patient weight (Kg) Maximum inflation volume (ml)
difficult or impossible.
1 <5 4
DESIGN:
• The LMA is manufactured from medical grade silicon rubber and 1.5 5 – 10 7
is reusable. There are 3 main components of the LMA classic: 2 10 – 20 10
An airway tube, mask and mask inflation line. The airway tube is 2.5 20 – 30 14
a large bore tube with a 15mm standard male adopter. Its other
end is fitted to the small elliptical (oval) mask, which has an 3 30 – 50 20
inflatable rim (cuff). The cuff can be inflated or deflated via a 4 50 – 70 30
valve located on the inflation line. Two aperture bars i.e. Mask 5 70 – 100 40
aperture bars guard the distal opening of the tube. They prevent
56 > 100 50
the epiglottis from entering and obstructing airway.
• The airway tube is slightly curved to match the oropharyngeal
anatomy, semi grid to facilitate atraumatic insertion and • LMA sits in hypopharynx where it forms a circumferential pressure
semitransparent, so that condensation and regurgitated material seal around the glottis. When inflated it lies with the tip resting
is visible. A black line runs longitudinally along its posterior against upper oesophageal sphincter, the sides facing pyriform fossa
curvature to aid in orientation. The distal aperture of the airway with the upper surface behind the base of the tongue and the
tube opens into the lumen of an inflatable mask and is protected epiglottis pointing upwards.
by 2 flexible vertical rubber bars called mask aperture bass • Insertion of LMA is relatively unstimulating. To obtain optimal
(MAB). placement, appropriate size LMA should be inserted. Reflexes
• The inflatable mask is oval shaped with a broad round proximal should be obtunded by general or topical anesthesia.
end and a narrow, more pointed distal end. It has a inflatable
cuff and semi-rigid, concave shield like back plate. The cuff is
attached to the outer rim of the back plate.
156

Technique: Indications
• After the patient is sufficiently anaesthetized, the head is put into • Elective short surgical procedures under GA.
sniff position. Before insertion mask is well lubricated and cuff is • Rescue airway in cannot intubate – can ventilate and cannot
deflated. The standard technique involves a completely deflated intubate, cannot ventilate scenario.
LMA, held like a pen, guided into the pharynx with the index • In ASA difficult airway algorithm in 5 different places, both as a
finger of the operator at the junction of the tube and the bowl. ventilatory device (Airway) and a conduit for endotracheal intubation.
With the operator at the head of the patient and the LMA • Cardiopulmonary resuscitation.
aperture facing caudally. With the head extended and neck Contraindications
flexed by using the hand under the occiput, under direct vision, • Mouth opening less than 1.5 cm
the lip of the cuff is pressed upwards against the hard plate. The • Poor lung compliance
LMA is advanced into the hypopharynx till a resistance is felt. • Airway pressure more than 20 cm of H2O.
The cuff is then inflated with just enough air to seal. • Non fasting states
• A common alternative technique popular in children described by • Oropharyngeal, pharyngeal or hypopharyngeal mass.
Mc Niol, consists of inserting a partially inflated LMA into the LMA Variants
pharynx above the epiglottis with the aperture facing cranially, • Reinforced / flexible LMA (LMA flexible), LMA specifically designed
the LMA is then turned 180 degrees before advancing it into its for tracheal intubation (LMA fastrack), single use LMA / LMA Unique
final position. and LMA with as integral gastric access / venting port (LMA Proseal)
• The LMA should then be secured after insertion, so as to prevent
rotation and movement cranially. Before taping the LMA in place, LMA as an airway intubator:
a bite block inserted to stabilize the LMA and prevent tube Practical considerations -
occlusion. • The LMA will accommodate only a relative small ET tube.
• LMA can be modified by splitting it vertically to accommodate larger
Signs of correct LMA placement: ET tube.
a). Slight outward movement of the tube upon LMA inflation. • LMA tube is long and the mean distance from mask aperture bar
b). Presence of small oval swelling in the neck around the thyroid (MAB) to the vocal cords is 3.6 cm in adults. The tracheal tube must
and cricoid area. protrude 9.5 cm beyond the MAB to ensure complete passage into
c). No cuff visible in the oral cavity. trachea.
d).Expansion of chest wall on bag compression.
Emergency Technique:
• Removal of the LMA can be accomplished during deep
anesthesia or after protective reflexes returned.
157

Technique INTUBATING LMA (Fastrach)

a)." Blind intubation via the LMA: • Since the classic LMA was not ideally suited to aid blind tracheal
• Done GA / topical anesthesia – LMA is inserted in the standard intubation, the primary design goal for a new intubating LMA was to
way. produce an intubating system that eliminated the need fro anatomical
• Holding the LMA, a well lubricated tracheal tube is inserted and distortion and that did not require manipulation of head and neck and
rotated 90o to the left. This enables the bevel to pass through thus increased its utility in patients with cervical spine pathology. The
the central aperture in MAB. ILMA has a rigid, stainless steel anatomically curved airway tube with
• Oxygen is administered during the procedure. a 15mm connector, capable of accommodating specially designed
• Once through MAB, tracheal tube is rotated anteriorly. The neck 8mm ET tube. Here the MAB of standard LMA is replaced by a
is extended to enable the tube tip to pass anterior to the single Epiglottis Elevator Bar that lifts the epiglottis out of the way of
arytenoids. Put the tracheal tube until resistance is felt at the ET tube. It also has rigid handle that facilitates one handed
approximately 3 cm down. insertion of LMA. It is available in 3 sizes i.e. 3, 4, 5.
• Flex the head to free the tube from impaction to permit further LMA PROSEAL
passage of tracheal tube into the trachea. • It is the most recent and most complex and potentially the most
• Tracheal tube cuff is inflated and correct position of tube is influential of the specialized LMA device. The principle new features
confirmed. are the modified cuff and drainage tube.
b)." Fiberoptic guided intubation via the LMA: Advantage:
• Here well lubricated full deflated tracheal tube is threaded over • Prevents lungs from aspirations and the stomach from gastric
the bronchoscope with the rotated bevel 90o to the left. insufflations. It also facilitates passage of gastric tubes and
• The tip of the fiberoptic bronchoscope is then introduced through monitoring devices into the oesophagus. It can be inserted like the
a revealing connector and passed into LMA tube. classic or intubating LMA and has its own built in bite block.
• Oxygen is administered throughout the procedure. Malposition is detected more readily. Limitations are that it is more
• Once the vocal cords are visualized the tip of the fiberscope is difficult to insert.
passed through them and into the trachea. COMBITUBE (Esophagotracheal combitube – ETC)
• The tracheal tube is gently threaded downwards into the trachea • Oesophagela tracheal combitube (ETC) are the successor of the
over the fiberscope. oesophagela obturator airway (EOA). It was invented and brought
• The tip of the tracheal tube is rotated anteriorly as it passes the into clinical use in 1987 by Frass. The combitube is a double lumen
MAB. supraglottic device with 2 inflatable balloons. Designed for use in
• The fiberscope then removed, the tracheal tube cuff is inflated emergency situations and difficult airways. It can be inserted blindly
and placement checked. into oropharynx and usually enters the oesophagus. It has a large
• The LMA is left in place with cuff deflated. proximal oropharyngeal balloon and a distal oesophageal low
pressure cuff with 8 ventilatory holes in between, ventilation is
possible with either tracheal or oesophageal intubations. Two adult
sizes are available. The 2 sizes are 37 and 41 French for adult
patients upto 5 feet and over 5 ½ feet height respectively.
158

Indications Disadvantages
• Securing the airway in emergency situations such as – 1. Not recommended for use in patients with laryngeal inflammatory
Cardiopulmonary resuscitation, trauma, facial burns, upper disorders such as epiglottis or tracheal stenosis.
airway bleeding and vomiting where there was an inability to 2. Should not be used in patients with foreign body in the airway.
visualize the vocal cords. 3. Not recommended in patient with laryngeal or tracheal
• In patients in whom neck movements is contraindicated and abnormalities such as polyps tumors or retropharyngeal abscess.
predicted or unpredicted difficult airways. 4. In morbidly obese patients, the ability to see the glow may be
Contraindications diminished. On the contrary, in thin or frail patients, some
• Intact gag reflex. transillumination may occur even when the tube tip is in the
• Patients < 4 feet in height oesophagus.
• Known oesophageal disease INDIRECT RIGID FIBEROPTIC LARYNGOSCOPY AND INTUBATION
• Caustic – substance (acid or dye) ingestion 1.% Bullard Elite Laryngoscope
• Allergy or sensitivity to latex 2.% Upsher – Scope
3.% Wu – Scope
LIGHTWAND AIDED TRACHEAL INTUBATION Indications
• One of the alternative techniques of ETI is the trans illumination • Predicted difficult intubation
of the soft tissue of the neck using a light wand. • In failed intubation
• Unstable cervical spine mandating minimal cervical movement.
Advantages of trach-light aided ETI Contraindications
1. Easy technique, relatively easy to learn and requires less • Blood and secretions in the upper airway.
experience. • Distorted upper airway anatomy.
2. Relatively un-expensive. • Upper airway obstruction due to foreign body.
3. Used as an aid in the placement of the ETT or in the Advantages
positioning of an already placed ETI. • Compared to flexible fiberscope, they are sturdier.
4. Useful adjunct in difficult airway. • Can control soft tissues much better.
5. Does not require extensive neck manipulation and can be used • Allow for improved management of the secretions
in patients with potential cervical spine instability. • Are more portable and cost lesser than the flexible fiberscope
6. Useful in patients with poor or irregular definition.
7. TL is useful in patients with limited mouth opening. Disadvantages
8. Less traumatic than blind nasal intubation may be applied after • Cannot be used in the presence of blood or secretions.
failed intubation using rigid laryngoscopy. • Being made of non-malleable metal, it can damage teeth or soft
9. Presence of secretion is of no consequence while using the tissue.
instrument.
159

RETROGRADE INTUBATION CLASSIC METHOD:

• The first reported case of retrograde intubation was by Butler • It is done using a 17 G Touhy needle and epidural catheter. The
and Cirillo in 1960. the first person to perform RI as presently anesthetist stands on the right side of the supine patient. The left
practiced was WATERʼS a British Anesthesiologist in Nigeria in hand is used to stabilize trachea by holding thumb and third digit on
1963. either side of thyroid cartilage. The index finger is used to identify
Indications midline of cricothyroid membrane. A small skin incision is made on
• Failed attempts at laryngoscopy / fiberoptic intubation. the midline on the cricothyroid membrane. The Tuohy needle is held
• Emergent establishment of an airway, where visualization of the in right hand with syringe filled with normal saline like a pencil and a
vocal cords is prevented by blood, secretions or anatomic cricothyroid membrane puncture is done in the 90o plane. Air is
derangement. aspirated to confirm placement. Following this the angle of the
• Electively, as an unstable cervical spine, mandibular fracture or needle is changed to 45o with the bevel pointing cephalad. The
anatomic anomaly. syringe is removed and epidural catheter passed into the trachea.
Contraindications While doing this, tongue should be pulled anteriorly to prevent the
1). Unfavorable anatomy catheter coiling up. The catheter will exit either by oral / nasal cavity.
• Lack of access to CTM (eg. Severe flexion deformity of neck) If this does not happen it may be fished out with nerve hook or Magill
• Poor anatomic landmarks (eg. Obesity) forceps. The epidural catheter is pulled out of the mouth for
• Pretracheal mass (eg. Thyroid goiter) appropriate length. A well lubricated endotracheal tube is threaded
2). Laryngotracheal pathology over the epidural catheter and advanced forwards, while at the same
• Malignancy time maintaining a moderate amount of tension on the epidural
• Stenosis catheter. As endotracheal tube passes the vocal cords, small click is
3). Bleeding diathesis felt. When the ET tube reaches the cricothyroid membrane maintain
4). Infection (e.g. Pretracheal abscess) pressure with the tip of the endotracheal tube on the cricothyroid
Technique: membrane, remove the hemostat and then remove the epidural
• Positioning, Supine Sniffing position with the neck hyper catheter.
extended is ideal. In patients with cervical spine injury, head Complications
should be kept in neutral position. It can also be performed in • Bleeding
sitting position. • Subcutaneous traveling caudally
• Entry site: It may be above or below cricoid cartilage. • Guide wire fracture
• Pneumothorax
160

TRANSTRACHEAL JET VENTILATION • Use only when well defined anatomic landmarks are visible.
• In the CVCI situation, when oxygenation cannot be maintained, a • Use non kinkable catheters
formal tracheostomy is impractical as time does not permit it, in • Hold catheter / needle device in place
this situation percutaneous transtracheal jet ventilation (PTJV)
using a large bore intravenous catheter inserted through a SUPRAGLOTTIC AIRWAY DEVICES
cricothyroid membrane is a simple, safe and effective treatment. • They cause minimal resistance in the patient supper airway.
But it must be emphasized that TTJV is only a interim solution till • They produce lower hemodynamic instability during placement.
a definitive airways is established. It also must be emphasized • They do not cause translocation of oral / nasal bacterial colony and
that the TTJV should be used only in desperate situations. secretions into the lower respiratory tract.
• Inadvertent bronchial intubation is totally avoided.
Principle: • Ease of insertion and smooth awakening.
During TTJV the lungs are inflated in 2 ways. Some of the supraglottic devices are:
a). Delivery of oxygen through the needle / cannula. 1).% Cuffed oropharyngeal airway (COPA)
b). Entertainment of air translaryngeally (venture principle) 2).% Glottic aperture seal airway
Technique: 3).% Streamlined pharynx airway liner (SLIPA)
• A 14-16G standard IV catheter or needle may be used. After 4).% Soft seal laryngeal mask
identification of cricothyroid membrane the needle is advanced 5).% Laryngeal tube airway
through the cricothyroid membrane. A change of resistance will 6).% Laryngeal tube suction (LTS)
be felt and air should be aspirated freely. Remove needle and 7).% Pharynx airway express
advance catheter and then attach jet ventilation system. 8).% Cobra pharyngeal lumen airway.
Complications INVASIVE TECHNIQUES:
• Subcutaneous emphysema • Cricothyrotomy
• Pneumo mediastinum, pneumothorax, pneumopericardium • Tracheostomy
• Oesophageal perforation • A patient who has upper airway obstruction that cannot be removed
• Bleeding into trachea by positive pressure mask ventilation or by passed by tracheal
• Tracheal mucosal damage intubation must have an immediate surgical airway.
Failure of TTJV: This is mostly due to • For obstruction above the level of the cricoid cartilage a
• Catheter dislodgement cricothyrotomy is indicated. For obstruction at the level of cricoid or
• Catheter kinking below, a tracheostomy will be necessary.
Contra indications:
Complete airway obstruction leading to inability to exhale. To
summarize TTJV has a place in the CVCI situations but only as a
last resort. The following recommendations should be considered
when TTJV used.
161

CRICOTHYROTOMY
• Is a life saving procedure in critical airway conditions like a).
Failed Intubation, b). Foreign body, c). Tumor, d). Trauma, e).
Hematoma
• Is a rapid effective method for relieving severe upper airway
obstruction. With the neck extended a small incision is made in
the cricothyroid membrane in the midline. The handle of a
scalpel or a Kelley forceps is used to separate the tissues and
dilate the space, while a tracheostomy tube or ETT is inserted
percutaneously.
TRACHEOSTOMY:
• May be performed under local anesthesia before the induction of
GA for a patient with a particularly difficult airway.
• a). Technique: After careful dissection of vessels, nerves and the
thyroid isthmus, a tracheal incision is made, usually between the
third or fourth cartilaginous rings. Percutaneous dilatational
tracheostomy using commercially available techniques and a
modified. Seldinger technique may also be performed.
• b). Complication – Haemorrhage, false passage and
pneumothorax.
CONCLUSION:
• Each anesthesiologist must develop a plan, consistent with his or
her expertise, to deal with the unexpected DA and must always
be prepared both mentally and physically for the unrecognized
DA and periodically review the DA algorithm.
162

Airway assessment & Management of Difficult Airway.Continuation:
Airway Management in the Adult 1607 50
Plan A: Succeed
Initial tracheal Direct laryngoscopy Tracheal intubation
intubation
Failed intubation
Succeed Confirm–then
Plan B:
Secondary tracheal ILMA or LMA fiberoptic tracheal
intubation plan intubation through
Failed oxygenation ILMA or LMA
Section IV Anesthesia Management

Plan C: Figure 50-19 Basic algorithm of the Difficult Airway
Maintenance of Succeed Society (DAS) guidelines for the management of
oxygenation, ventilation, Revert to face mask Postpone surgery unanticipated difficult tracheal intubation. (From
postponement of Oxygenate and ventilate Awaken patient Henderson JJ, Popat MT, Latto IP, et al: Difficult
surgery and awakening Airway Society guidelines for management of the
Failed oxygenation unanticipated difficult intubation. Anaesthesia 59:675-
694, 2004.)
Improved
Plan D: oxygenation
Rescue techniques for Awaken patient
LMA
“can’t intubate, can’t
ventilate” situation Increasing hypoxaemia
or
Cannula Surgical
cricothyroidotomy cricothyroidotomy
Fail
the two-person technique and the use of an oral or nasal airway.

It may be necessary to reduce cricoid pressure to achieve satisfac- Summary
tory ventilation. If satisfactory oxygenation cannot be achieved 163
with a facemask, an SAD should be used instead. Insertion of an Airway management is at the core of care of anesthetized and
LMA inNotes
Dr Azam’s the “cannot intubate, cannot
in Anesthesiology 2013 ventilate” situation has a unconscious patients. Though straightforward much of the time,
43
significant failure rate. it can be very difficult. Many new devices and techniques have
IV 1576 Anesthesia Management
Difficult Airway Algorithm

1. Assess the likelihood and clinical impact of basic management problems:
A. Difficult ventilation
B. Difficult intubation
C. Difficulty with patient cooperation or consent
D. Difficult tracheostomy
2. Actively pursue opportunities to deliver supplemental oxygen throughout the process of difficult airway management:
3. Consider the relative merits and feasibility of basic management choices:
Awake intubation vs. Intubation attempts after induction

of general anesthesia
A
Noninvasive technique for initial Invasive technique for initial
vs.
B approach to intubation approach to intubation
Preservation of spontaneous Ablation of spontaneous

vs.
ventilation ventilation
C
4. Develop primary and alternative strategies:
A Awake intubation
B Intubation attempts after
induction of general anesthesia
Airway approached by Invasive

non-invasive intubation airway access(b)* Initial intubation Initial intubation
attempts successful* attempts UNsuccessful
Succeed* FAIL From this point

onwards, consider:
1. Calling for help 3. Awakening
2. Returning to the patient
Cancel Consider feasibility Invasive spontaneous ventilation
case of other options(a) airway access(b)*
Face mask ventilation Face mask ventilation

adequate not adequate
Nonemergency pathway LMA adequate* Consider/attempt LMA LMA not adequate

ventilation adequate, or not feasible
intubation successful
Emergency pathway
ventilation not adequate,
intubation unsuccessful
Alternative approaches If both face mask

to intubation(c) and LMA ventilation Call for help
become inadequate
Emergency non-invasive
airway ventilation(e)
Successful intubation* FAIL after multiple attempts
Successful ventilation* FAIL

Invasive airway Consider feasibility Awaken
access(b)* of other options(a) patient(d)
Emergency invasive
airway access(b)*
*Confirm ventilation, tracheal intubation, or LMA placement with exhaled CO2
a. Other options include (but are not limited to) surgery utilizing face b. Invasive airway access includes surgical or percutaneous d. Consider re-preparation of the patient for
mask or LMA anesthesia, local anesthesia infiltration, and regional tracheostomy or cricothyrotomy. awake intubation or canceling surgery.
nerve blockade. Pursuit of these options usually implies that mask c. Alternative noninvasive approaches to difficult intubation include e. Options for emergency noninvasive airway
ventilation will not be problematic. Therefore, these options may be (but are not limited to) use of different larynoscope blades, LMA ventilation include (but are not limited to): rigid
of limited value if this step in the algorithm has beed reached via as an intubation conduit (with or without fiberoptic guidance), bronchoscope, esophageal-tracheal Combitube
the Emergency Pathway. fiberoptic intubation, intubating stylet or tube changer, light wand, ventilation, or transtracheal jet vantilation.
retrograde intubation, and blind oral or nasal intubation.
A Figure 50-2 American Society of Anesthesiologists Difficult Airway Algorithm. (From American Society of Anesthesiologists Task Force on Management of the
Difficult Airway. Practice guidelines for management of the difficult airway. An updated report by the American Society of Anesthesiologists Task Force on
Management of the Difficult Airway. Anesthesiology 98:1269-1277, 2003.)
164

50. N2O, Anesthetic agents, Properties, impurities & Methods to purify. Dr Azam’s Notes in Anesthesiology 2013
NITROUS OXIDE: Preparation: In the laboratory – small amounts may be prepared by

• The use of Nitrous Oxide dates back to the earliest days of allowing iron to react with nitric acid. Nitric Oxide (NO) is first
anesthesia and itʼs reflection of its safety and versatility that its produced, but this is reduced to nitrous oxide by an excess of iron:
still being used today.
History:
• 2 NO + Fe → FeO + N2O
Commercially, by heating Ammonium nitrate (NH4NO3), as a solid or as
1772 % - Prepared by priestly.
an aqueous solution of 83% NH4NO3 to 250o C (245 – 270o C)
1799% - Anesthetic properties suggested by Sri. Humphry Davy
1844% - Horace Wells used it in dentistry for tooth extraction • NH4NO3 → 250O C → N2O + 2H2O + 85.6 KJ
1868 % - Edmund Andrews combined it with O2 to give longer • At high temperature, NH4NO3 dissociates to N2 and other oxides like
% anesthesia. nitric oxide and nitrogen dioxide.
1956 % - Lassen reported prolonged use of N2O could cause bone
% marrow aplasia. Impurities: Include
Physical Properties a). Ammonia
• Sweet smelling, non-irritating, colorless gas. b). Nitric acid
• Potent analgesic, weak anesthetic c). Nitrogen
• MAC → 104 (i.e.ʼs why itʼs a weak anesthetic) d). Nitric oxide
• Blood gas coefficient → 0.47 (least soluble in blood and e). Nitrogen dioxide
therefore rapid induction & recovery) f). Water vapour
Mol. Wt → 44 g). Carbon monoxide (produce by burning particles of sacks in which
•
NH4NO3 is stored)
• Boiling point → - 88.5o C.
• Critical temp → 36.4o C Adverse effects of impurities
• Specific gravity → 1.5, i.e. 1 ½ times heavier than air.
• Higher oxides of N2 dissolves in water to form nitrous and nitric acids.
• Density (at 15o C and 1 atm) → 1.875 g/l These substances are toxic and can produce Methemoglobinemia
• Saturated vapour pressure at 15o C → 44.1 bar. and pulmonary edema (occurs when NO2 > 50 vpm)
• Physical state in cylinder → liquid • CF: In acute stage,
• Combustion characteristics → non inflammable, but strongly 1. Cyanosis (due to Methemoglobinemia)
supports combustion. 2. Respiratory difficulty (due to pulmonary edema / laryngospasm)
• Elimination – unchanged from the body, mostly via lungs 3. Circulatory failure (hypotension due to effect of nitrate ions on
• Stable and unaffected by soda lime. % vascular smooth muscles)
• Patients can have either respiratory acidosis from associated
ventilatory failure or metabolic acidosis – from productions of nitric /
nitrous acids.
165

N2O, Anesthetic agents, Properties, impurities & Methods to purify. Dr Azam’s Notes in Anesthesiology 2013
Treatment: Test for contamination

1). Oxygen either by spontaneous / assisted ventilation. • The best method involves the use of a starch iodide paper.
2). IV methylene blue (2 mg / kg) is required initially to overcome • Put a piece of moistened starch iodide paper into a 20 ml syringe
cyanosis from methemoglobinimia. and 15 ml of O2 is dawn up followed by 5 ml of sample gas. Any
3). IV Fluids and vasopressors may be needed to correct nitric oxide in sample gas will be oxidized by O2 to nitrogen dioxide.
hypotension. The nitrogen dioxide in turn oxidizes iodide to iodine, turning starch
4). ABG should be done to check for acid base status. paper from purple to blue. The sensitivity of the test is 300 VPM.
• 5). Cardiovascular monitoring is done by ECG and occasionally
central venous pressure monitoring is needed. Mechanism of Action:
• In chronic cases, chemical pneumonitis with pulmonary fibrosis • Mainly in the brain and spinal cord.
may follow. • In the brain it causes amnesia by in inhibiting the synaptic
• Bronchial lavage and suction, together with endobronchial and transmission mainly in the reticular activating system, hippocampus
parental steroids have been suggested for chemical and cerebral cortex.
pneumonitis. • Anesthetic induced immobility to noxious stimuli is caused by action
• Nitric oxide – combines with Hb and form anemic type of hypoxia in the spinal cord.
• N2 – Dilutes the anesthetic • Analgesic action of nitrous oxide is due to the marked increase in
• Water vapour – Great care is taken during manufacture to proenkephalin derived endogenous peptides. The endorphins binds
prevent moisture being included in the cylinder contents, since to the opioid receptors and causes analgesia.
water vapour tends to freeze as it passes through the reducing
valve and may lead to obstruction of gas flow. Pharmacological actions:
Purification • Nitrous oxide is rapidly absorbed from the alveoli and 100 ml of blood
• After cooling, ammonia and nitric acid are reconstituted to will carry 45 ml of nitrous oxide in its plasma. It does not combine
NH4NO3 and returned to the beginning of the process. with hemoglobin nor does it undergo any chemical combination
• The gases are then passed through water scrubbers which within the body.
remove any residual ammonia and nitric acid. CNS:
• Purification of the remaining gases are done by removing higher • N2O increases cerebral blood flow, CMR and ICP as a result of
oxides of N2 by passing them through potassium permanganate sympatho adrenal stimulatory effect. The magnitude of the effects
scrubbers. vary considerably in the presence or absence of other anesthetic
• The purified gases are then compressed and dried (removing agents.
water vapour) by passing it through columns of activated • N2O alone → substantial increase in CBF and ICP.
alumina. N2O + other volatile agents → moderate increase in CBF.
• The compressed gas is expanded in a liquefier with N2 escaping N2O + IV drugs → decrease in CBF & ICP.
as gas. Itʼs then evaporated, compressed and passed through (Barbiturates, BZD, narcotics)
another aluminum dryer before being stored in the cylinder.
166

EEG: • Also causes a minimal reduction in Hypoxic pulmonary

When used alone, it causes decrease in amplitude and frequency of vasoconstriction (HPV), which may increase the right to left shunt.
dominant alpha rhythm. With the onset of analgesia and depressed
consciousness, frontally dominant fast oscillatory activity is seen. Hematopoietic and Neurologic systems:
CVS:
• N2O is the only anesthetic reported to produce hematologic toxicity
Myocardial contractility:
and neurotoxicity with long term administration. Both these toxicities
• Direct myocardial depressant and causes decreases in cardiac are the result of interaction of N2O and vitamin B12 and disruption of
output. This is caused by dose-related reduction in intracellular several pathways in one-carbon chemistry. The biochemical basis of
Ca2+ content. However increased sympathetic nervous system this effect is the oxidation of cobalt in vit. B12 by N2O).
activity resulting in peripheral vasoconstriction offsets the
• N2Oconverts cobalt in vitamin in B12 from monovalent to bivalent
myocardial depression and maintains the blood pressure. from. In the bivalent form, vitamin B12 can no longer carry out its
• N2O in clinical concentration (40-70%) cause modest increase in function as a methyl carrier. This oxidation reaction is irreversible
HR. and depends on the replacement of vitamin B12.
Cardiac electrophysiology:
• In humans, there is an irreversible inactivation of the enzyme
• Addition of N2O to halothane lowers the threshold for methionine synthase, which requires vitamin B12 as a cofactor.
arrhythmias. This is due to the combined effect of sympathetic
Methionine synthase catalyse the conversion of methyl – THF to THF
NS stimulation N2O and myocardial sensitization by halothane.
and Homocysteins to methionine. Failure to produce these products
Coronary Circulation:
leads to reduce synthesis of thymidine which is required for DNA
• It redistributes transmural coronary blood flow preferentially to
synthesis. The oxidation of vitamin B12 leads to megaloblastic
the subepicardium. In the presence of volatile anesthetics, N2O
hematopoesis and sub acute combined degeneration of the spinal
decreases MVO2 and myocardial O2 extraction.
RS: cord, since methionine synthetase is required for myelin formation.
• Pleasant to inhale and non-irritant to the airways. • The time required to produce megaloblastic hematopoesis varies
with patients. Itʼs not usually seen in healthy patients undergoing
• It increases the uptake of the accompanying agent. (2nd gas
effect). It also helps in reducing MAC of the accompanying routine surgery (< 6 hours).
volatile anesthetic. a. mild megaloblastic bone marrow a. > 12 hours to 50% N2O
• N2O decreases the tidal volume. However the resultant changes
depression of minute ventilation may be partially offset by b. Marked changes b. > 24 hours
concomitant increase in respiratory rate. c. Complete bone marrow failure c. continuous exposure for several
• In clinically used concentration (50-75%), N2O depresses the (agranulocytosis) days.
ventilatory response to CO2 / hypoxia.
• It has no effect on bronchial smooth muscles.
• All inhaled anesthetics, including N2O, decreases ciliary
movement in a dose dependent manner. They decrease ciliary
beat frequency or disrupt metachronism or by altering the
characteristics or quantity of mucous produced.
167

• The bone marrow changes are preventable by pre treating the Hepatic system:
patients with large doses of folic acid. This further is converted • Hepatic blood flow probably falls during N2O anesthesia, but to a
to 5, 10-methylene THF needed for thymidine synthesis. lesser extent than with other volatile agents.
• The neurologic disease, subacute combined degeneration of
spinal cord, develops only after several months of daily exposure Renal system:
to N2O. • Decreased renal blood flow by increased renal vascular resistance
• The failure to synthesis S-adenosyl methionine from methionine thereby leading to decreased GFR and urine output.
and ATP leads to failure of methylation of basic proteins in the
myelin sheath. Neuromuscular system:
Symptoms and signs: • Potentiates neuromuscular blockade but to a lesser extent than other
a.% Numbness and paresthesia in extremities. volatile agents.
b.% Loss of balance and unsteady gait PROPERTIES OF NITROUS OXIDE
c.% Impairment of touch 1. The concentration effect
d.% Muscle weakness 2. The second gas effect
It occurs in individuals whose abuse N2O on a long term basis and 3. Diffusion hypoxia.
in individuals who work in environment grossly contaminated with 4. Effect of N2O on closed gas spaces.
this gas.
Reproduction and Development: 1. The concentration effect:
N2O presents potential for adverse reproductive and development • The inspired anesthetic concentration influences both the alveolar
effects for patients administered anesthesia during pregnancy and concentration that may be attained and the rate at which itʼs attained.
for health care personnel exposed to it. During early part of induction, using higher concentration of N2O,
• Increased incidence of premature labor/LBW babies/abortions. more rapidly the alveolar concentration reaches the inspired
• Increase incidence of teratogenicity (mainly in 1st trimester). concentration. This is referred to as concentration effect.
This is due to the interference of DNA synthesis by N2O The concentration effect results from two factors:
• Adverse effects have been seen in the rates of fertilization and a. Concentrating effect
cleavage of oocytes, pregnancy and carriage to term. b. Augmentation of inspired ventilation.
• High exposure to N2O can cause situs inversus Itʼs due to the • The concentrating effect reflects concentration of the inhaled
stimulation of alpha 1 receptors by N2O. anesthetic in a smaller lung volume due to uptake of all gases in the
• However, most anesthetics that are given during pregnancy are lung. At the same time, augmentation of inspired ventilation is
of short duration, which may not cause these adverse effects. increased to fill the space produced by uptake of gases.
168

2) Second Gas effect: 4. Effect of N2O on closed gas spaces:

• The second gas effect reflects the ability of high volume uptake • During N2O administration, appreciable volumes of N2O can move
of one gas (first-gas) to accelerate the rate of increase of a into the closed spaces within the body.
concurrently administered “companion” gas (second gas). Two types of closed cavities in the body:
• E.g. Initial large volume uptake of N2O accelerates the uptake of a. Those enclosed by compliant walls.
second gases such as O2 ad volatile anesthetics. b. Those enclosed by non-compliant walls.
• N2O has low-blood gas coefficient (0.47), has low blood
solubility and therefore it ensues a rapid equilibration of FA/FI Compliant gas spaces include (increase in volume):
ratio. But N2 is still less soluble in blood than N2O (0.013) is, 35 a. Bowel
times less soluble than N2O. b. Pneumothorax
• When a patient starts breathing higher concentrations of N2O, its c. Pneumoperitoneum
concentration in alveoli rises rapidly. Since N2O is more soluble d. Surgical emphysema.
in blood than nitrogen, the volume of N2O taken up by blood is e. Air embolus
more than that of N2 leaving the blood. The alveoli therefore Non-compliant gas spaces include 9increase in pressure):
gets smaller and the fractional concentration of remaining gases a. Middle ear
in the alveoli rises. Although the volume of N2O has decreased, b. Nasal sinuses
the concentration is not decreased because the volume of the c. Vitreous cavity
lung has also decreased. Therefore if another volatile agent is d. Intracranial cavity.
given with N2O, itʼs concentration will also increase. This • These spaces contain N2 (from air) whose low solubility limits its
phenomenon is called second gas effect. removal by blood. The entrance of N2O into these closed spaces is
not encountered by an equal loss of nitrogen and there is a net
3. Diffusion hypoxia (Fink effect): increase in volume of these spaces leading to adverse effects like.
• At the end of anesthesia, the N2Oin the blood diffuses faster into a. Expansion of air embolus and pneumothorax.
the alveoli than the blood can take up N2 (because N2 is less b. Aggravating bowel obstruction.
soluble). The volume of N2O in the lung increases and the c. Displacement of the middle ear graft.
concentration of other gases in the alveoli falls. This is called d. Vacuum headache → due to increase in nasal sinuses pressure.
ʻdiffusion hypoxiaʼ or fink effect. e. Pneumoretinopexy. Gases can be instilled into vitreous to create a
tamponade effect to stick retina back to sclera. The 3 gases used
Hypoxia is caused by two mechanisms: are air, SF6 and perfluropropane (C3 F8). The gases get absorbed
a. They may directly affect oxygenation by displacing O2. over a variable period. Air in one week, SF6 in 2 week and C3 F8 in
b. By building CO2, they decrease the respiratory drive. 2 months. N2O readily gets diffused into the bubble and enlarges it
To avoid this, 100% O2 is administered for the first 3-5 minutes of 3 times and can cause retinal artery occlusion and blindness. Hence
recovery. N2O should be discontinued 15 min prior to injection of bubble.
Postoperatively, these patients should carry a wrist band to caution
anesthetists about the use of nitrous oxide if they happen to
undergo GA. Instead if silicone gel is used, this problem is avoided.
169
f. It also diffuses into the tracheal tube cuff, increasing the pressure
Dr Azam’s Notes in Anesthesiology 2013 against tracheal mucosa.
Supply and storage: The pointing effect;

N2O is available as: • The pointing effect is an effect where the critical temperature and
1. Pure N2O pressure of one gas is altered by the presence of the other here O2
2. Mixture in equal parts of N2O & O2 (50:50) (ENTONOX). alters the behavior of N2O so that it does not liquefy at this pressure
unless the temperature drops to below – 70C. Below 70C, N2O will
1. Pure N2O: liquefy and O2 still remain in gaseous form and two gases separate
• Supplied and stored in cylinder as liquid under pressure of 745 out.
psig at 200 C. • This will result in high con. Of O2 over N2O liquid. If the cylinder is
• The cylinder are filled only upto a filling ratio of 0.67, filling ratio used at this time, high concentration of O2 will be released first
is the weight of the gas in a cylinder to the weight of the water leaving N2O behind which can cause hypoxia in the patient.
the cylinder would hold at 600 F. this is to prevent a cylinder Therefore thorough mixing of the gases in the cylinder is necessary
containing liquefied gas from being overfilled. when temperature falls below - 70C.
• The pressure gauge in cylinder only measures the pressure of • Pin index of entonox cylinder is 7.
the gas (vapour) above the liquid level. It remain constant till all Color – French – blue body with white shoulders.
the liquid is converted to gas and therefore is not an accurate
measurement of the contents. The contents can be accurately Uses of entonox:
measured by weighing the cylinder. 1. Labour analgesia
• As the gas is used, the cylinder becomes cool because energy is 2. Dental analgesia
required to convert the liquid N2O to gas. Latent heat is required 3. Relief of pain from dressing surgical wounds.
for the vaporization of liquid nitrous oxide and this is obtained 4. Chest physiotherapy.
from the casing of the metal cylinder, which, as a result, rapidly
cools. This in turn leads to freezing of the water vapour in the air Uses:
immediately surrounding the cylinder, and to the formation of the • 99% of manufactured N2O is used for medical purpose – in
layer of ice on the cylinder. anesthesia and cryosurgery.
• Pin index of N2O cylinder is 3,5. Non-medical uses:
• Colour – French – blue. a. A propellant in aerosols.
b. A source of O2 in superchargers of high performance engines.
2) ENTONOX (50 N2O: 50 O2) c. A drug of abuse.
• Supplied in cylinder pressurized at 15000 kpa at 200 C.
Here both O2 & N2O are in gaseous form.
170

51. Organ retrieval from beating heart Donor or Anesthetic management of a brain dead Dr Azam’s Notes in Anesthesiology 2013
patient for multiple organ harvesting.
Pathophysiology of brain death: Preoperative Preparation:

• Acute ischemia due to sudden rise in ICP or alteration in blood • Confirm and certify brain stem death and take consent form relatives
flow commonly initiates a series of pathophysiological • Emphasis in management changes from cerebral resuscitation to
responses. optimal organ perfusion and oxygenation.
• In earlyl phase, short lived massive sympathetic outflow occurs • Ensure intravascular volume resuscitation with blood and gelatin
during brain stem herniation, causing hypertension, tachycardia, based colloids using CVP monitoring. Avoid overhydration in patients
myocardial dysfunction, impaired organ perfusion and acute with lung donors, which may precipitate pulmonary edema, increase
tissue ischemia. A-a O2 gradient, causes cardiac over distension and liver
• Then paralytic autonomic collapse follows with a fall in cardiac congestion.
output, hypotension and atropine resistant bradycardia. • If optimal adjustment of preload fails to achieve target values
Circulatory collapse can ensure within 24-72 hours without inotropes should be started (use dopamine up to 10µg/kg/min as first
intervention. choice, then adrenaline 0.01-0.05 µg/kg/in if necessary).
• Lung function will be deteriorated because of neurogenic • PAEG and TEE should be considered for heart donors with high
pulmonary edema ALI or preexisting lung disease. inotrope requirements. They allow assessment of cardiac structure
• Reduced circulating T3 and T4 with increased peripheral and function, and prevent intravascular overload.
conversion of T4 to (reverse T3) causes depletion of myocardial • Lung toilet should continue with regular chest physiotherapy and
energy stores, myocardial dysfunction and a global shift to suctioning.
anaerobic metabolism. • If desmopresin (DDAVP) has been used to control diabetes insipidus
• Hyperglycemia due to reduced circulating insulin and insulin it should be changed to vasopressin (ADH) à restores vascular tone
resistance. and arterial pressure without a direct myocardial effect.
• Reduced ADH output leads to neurogenic diabetes insipidus with • Hormone resuscitation is often commenced empirically seen after
hypovolemia and electrolyte disorders (hyper Na, hyper Mg2+, diagnosis of brain stem death and continued throughout organ
hypo K+, hypo P, hypo Ca2+) procurements to stabilize hemodynamics.
• Systemic inflammatory response with increased serum and
organ cytokine and up regulation of endothelial adhesion
molecules.
• Release of tissue fibrinolytic agents and plasminogen activators
from necrotic brain causes a coagulopathy.
• Temperature regulation is lost due to hypothalamic dysfunction
resulting in poikilothermia.
171

Organ retrieval from beating heart Donor or Anesthetic management of a brain dead Dr Azam’s Notes in Anesthesiology 2013
patient for multiple organ harvesting.
Perioperative Management:
Bolus Infusion
• Standard monitoring plus CVP, arterial line, core temperature, urine
Tri iodothyronine T3 4µg 3µg/hr Reverses myocardial output. Maintain core temperature > 350C. frequent analysis of
dysfunction and decreases
ABGʼs, electro Hct, glucose and clotting. Large bore iv access (right
iotrope requirements
Vasopressin (ADR) 1U 0.5-2u/hr Treats DI and restore vascular
upper limb) is mandatory for replacement of fluid losses (upto 8
tene titrated to MAP > litres) with crystal colloid or blood (keep Hcl > 30%)
60mmHg or SVR 800-1200 • Need for GA is controversial we can use upto 1 MAC isoflurane
dur fentanyl (5-7µg/kg) to control reflex pressure responses during
Insulin -- Sliding To maintain blood sugar surgery
scale 4-6mmol/ltr • Labetalol NTG can also be used to control hypertensive episodes
Methylpertnisolone 15mg/kg - Improves oxygenation and intraoperatively.
increases donar lung • NDMR are administered to obtunded reflex muscular contractions to
procurement by reducing the preserved spinal arc and improve surgical access. Pancuronium
cytokine mediated cellular and vecuronium are cardio stable and preferred.
injury. • Large and frequent haemodynamic fluctuations occurs due to
compression of IVC, manipulation of adrenals and blood fluid loss.
• Correct hypernatremia with 5% dextrose (Na+ < 155mmol/ltr) Hypotension is treated with colloid titrated to CVP, vasopressin
dextrose 4% saline 0.18% with potassium chloride should be infusion or metaraminol (0.5g/increments)
used to replace normal urinary water and electrolyte losses. • Brad spectrum antibiotics are given as per local transplant protocol
• Clotting abnormalities should be corrected with clotting factors • Full heparinization (3001 u/kg) should be administered centrally prior
and platelet to surgical cannulation of the major vessels.
• Central venous access via right IJV and left radial artery access • Prostacyclin (5-20mg/kg/min) may be needed for 10 min via
are preferred due to early ligation of the left innominate vein right pulmonary artery if lugs are to be harvested
subclavian artery respectively. • PAFC / CVC withdrawn before ligation of SVC
• Chest X-ray, ECG, Echocardiography and 4 hourly ABG for • Note time of aortic cross clamp as beginning of organ ischemic time
heart / lung donor • At the end discontinue mechanical ventilation monitoring and remove
Target parameters ETT after lung inflation and trachea cross clamp.
• CVP! ! ! 4-10mmHg • The abdominal surgical team continues to operate in circulatory
• MAP!! ! 60-80mmHg arrest.
• PCWP! ! ! 10-15mmHg • In the event of cardiac arrest CPR should be commenced. Procuring
• O Index! ! ! > 2.1/min/m2 of liver and kidney should be proceed rapidly with cross clamping of
• Hb! ! ! ! 10gm/dl (HC+ 30%) aorta at the diaphragm and infusion cold preservation solution into
• SaO2! ! ! > 95% (with lowest FIO2 and PEEP) the distal aorta and portal vein.
• Tidal Volume! ! < 10ml/kg
• PaCO2! ! ! 4.5-5.5 kPa
• Urine Output! ! 1-3ml/kg/hr
172
• Peak inspiratory pressure < 30cm H2O

52. Sterilization & Disinfection of anesthetic equipments in the OR and ICU. Dr Azam’s Notes in Anesthesiology 2013
Methods of Sterilization of Equipments:

Theatre Sterilization Schedule
• Equipments must be clean, free from organic contaminants and
A. Carbolising:
should not cause cross infection. Methods used re
Daily:
1. Cleaning and decontamination:
• Wipe with a disinfect or germicide for floor and wall upto a height
Physical removal of infected matter micro organisms and organic
of 5 ½ feet e.g., Chlrocresol, Lysol, Dettol
matter like tissue debris, blood etc., by following steps
• Wipe all the articles like trolleyʼs Mayoʼs table, operation table,
Thorough soaking
top with disinfectant
• Scrubbing
• Washing with detergents
Weekly: Decontamination can be done as follows
1. Washing the theatre through including roof after making 1) Manual: Thorough cleaning by scribbling with brush and soap
suitable protective arrangements for switch boards, lights etc., water detergent antiseptic will be better option. Then rinse with
first with plain water and then with 1% Lysol in water clean water.
2. Fumigation with formalin with one of following method 2) Automatic washing machine:
• Micronebulisers: For 1000 cubic feet 350ml of 40% formalins in a. It combines cleaning and disinfection it uses treated
water nebulized, leave fumes for 6 hours and then exhaust water with detergent and cleans articles by pumping
• Boiling: For one cubic feet 0.5 to 1ml of 40% formalin keep water as jets
formalin over kerosene / electric stove to boil b. Then disinfection is done by circulating water at 800C
• KMnO4 and formalin: 50gms of KMnO4 + 1 litre of 40% formalin and holding it for 10 minutes (pasteurization)
kept in centre of OT, formalin furiously fumes to fill the 3) Ultrasonic Washer:
atmosphere, one has to rush out and close the door. Open after a. Instruments are kept immersed in water bath and are
6 hours and exhaust. subjected to ultrasonic vibrations which cleans the
debris, contaminants that cannot be reached by brush,
Ultraviolet light: e.g., instruments used for microsurgeries.
• This can be used to s terlie the whole area overnight
• Control switch can be kept out side the OT Disinfection:
• Exposure to ultra Violet light may cause skin burn and retinal • Killing of all infected organisms ʻexcept the bacterialʼ. Those that are
damage not killed are reduced to the level that is not harmful to health, e.g.,
Assess the adequacy of asepsis in theatre done by intermediate risk items (face mask, airways)
• Check every fortnightly • Methods:
• Microbiological test using petridish to assess growth and number • Cold chemical methods
of colonies the number must be within the permissible limits. • Pasteurization
• Boiling
173

Sterilization & Disinfection of anesthetic equipments in the OR and ICU. Dr Azam’s Notes in Anesthesiology 2013
Cold chemical methods: • Ideal packing: Articles are packed in bin with sufficient space in
• Many organic agents are capable of killing bacteria and viruses between for passage of steam, it should not be tightly packed,
• Factors modifying their effects are concentration duration of instruments need not be packed, it needs 15 minutes for sterilization
contact and individual potency and for linen it is 30 minutes.
• Most of them are liquids • For rubber and plastic 15 psi for 15 minutes at 1210C
• Vapors à formaldehyde • Sharp instruments will be dulled by this process at the end of
• Gases à ethylene oxide or prophylone oxide procedure things must be dry
• Liquidsà glutaraldehyde, formaldehyde
Advantages of autoclaving:
1. Sterilization • Efficient, rapid, simple, cost effective
Classification: • Suitable for smallest hospital
• Physical methods (heat) • Spores destroyed
• Chemical • Linen and rubber not destroyed
• Gamma rays
• Ultra violet rays Testing:
• Filtration • Signaloc tape changes colour indicates adequacy of sterilization
• Culture by test bin once in a month
Physical methods: • Introduce bacillus subtilis in the bin and autoclave. Then this bin sent
• Bacteria, viruses and spores destroyed for bacterial examination (ideal method)
• Time required depends upon temperature and size of particle
• Heat can be moist dry Low pressure autoclaving:
a. Moist heat • 730C storm at 290 mmHg pressure for 2 hours good method for
• Moisture increases cellular permeability heating coagulates the delicate objects, if formaldehyde is added, spores are also killed.
protein, kills bacteria This process automatically carried not in the machine.
• Boiling: 1000C for 15 minutes, kills bacteria not pores
• Pasteurization: 700C for 20 minutes or 800C for 10 minutes b. Dry Heat:
materials which can be damaged by boiling can use this method 1. Hot air oven: temperature 1600C needs 1 hour to sterilize powder
• Autoclave: Steam at 1340C with 32 psi pressure applied for 3 ½ grease glass syringes
minutes steam is evacuated and sterile air is filled to remove 2. Flames: Ophthalmic instruments are directly heated on flames
moisture. This cycle takes 10 minutes. (10000C)
• This method kills the all organisms provided steam is allowed to
penetrate all the parts. Common method is using bins
174

Chemical Methods: b. GAS (Ethylene oxide)

• Used for objects which cannot stand heat • Colourless gas with high bactericidal powder
• Chemicals kills by coagulations or alkylation of proteins • Very toxic to inhale, inflammable, explosive at 3% concentration
Criteria to be satisfied are; • Has high penetrating power, does not harm any objects
• Must be capable of killing spores • Kills organisms by alkylation of proteins, but action is slow 12-18 hours
• Non corrosive, non toxic • 10% gas in CO2 or from gas with humidity of 30-50% used.
• Non irritant to skin stable • Indicated à pump oxygenator, rubber valve, plastic pump tubing, Teflon
• Should penetrate grease and fibres prosthesis grafts, catheters
• Puling of CO post sterilization vaccum and shelf store of 6 days is advised to
Disadvantages: remove absorbed ET oxide
• Act only on exposed surface • For sterilizing ventilators used in infected cares 4 hours of flushing of air after
• Some react with metal sterilization. This needs autoclave and cylinders
• Some impregnate with materials (rubber plastic) • Cylinders contain ET O + CO2 mixture are identified by aluminium colour
• Residual chemicals forms source of irritation body with red shoulders (red + explosive) below that circular band of yellow
• Some agents destroy rubber and plastics colour (Yellow à poisonous). At room temperature this gas can be a liquid
with boiling point of 10.60C.
Advantages:
• Technically easier c. Liquids:
• Suitable for equipments damaged by heat sterilization • Phenol: 1-5% used to clean the surface of equipment does not kill spores
• Ethylene oxide achieve perfect sterilization • Iodine: 0.5 – 2% in alcohol tincture iodize is irritant povidone iodine
(betadine) less irritant and is in aqueous solution
a. Vapour (formaldehyde)
• Ethyl alcohol: 70-80% - isopropyl alcohol (50-70%) used in cat gut
• Useful for endoscopic equipments
sterilization in pack itself
• Formaldehyde vapour requires moisture for action
• Chlorhexidine gluconate: 0-1% aqueous solutions for 20 minutes for ET
• Their action depends upon sublimation
tube decontamination. 0.5% in 50% ethyl-alcohol for skin sterilization in 30
• Takes 2 hours for sterilization
seconds.
• 40% formalin can be nebulized in a chamber
Glutaraldehyde cidex:
• 2% solution made alkaline by adding 0.3% sodium carbonate
• Potency is 15 days, kills bacteria in 15 minutes and spores in 3 hours.
• Used for endoscopes, ETT, breathing equipments
• Rinse before use with clean water to skin irritant.
175

Nucidex: • Spore bearing organisms not transmitted from corrugated tubes, so

• Similar to cidex autoclaving is not essential
• Stabilized buffered peracetic acid solution • Common organisms transmitted are.
• Acts as oxidizing agent on cell wall and nuclei • Streptococci
• Chlorine compounds: For floor sterilization • Staphylococci, TB bacilli, pseudomonas pyogenes
• Detergents (cetavalon cetrimide): Quaternary ammonium • Boiling or pasteurization can be ideally used
compounds, lower surface tenion of solution good against gram
positive and negative organisms. Tracheal tubes
Suction catheters airways:
Gamma rays: • Washed with soap and water and rinsed with the help of frush
• Derived from cobalt 60 source • Dipped in 0.1% chlorhexidine solution for 30-60 minutes
• Lethal dose for bacteria 2.5 megarads • Autoclaving effective but replaced after 6 uses
• Tuber, catheters, ETT, plastic equipments, all can be sterilized in • γ radiation satisfactory
a transparent plastic envelop with an indicator
• Needs protected environment, highly expensive, commonly used Face masks
for disposable equipments after manufacturing Wash with soap and water donʼt boil it
UV Rays: Keep in water 60-700C for 20 minutes
• Special lights emitting ultra violet fixed on roof in appropriate
angles so that OT and equipments are exposed for 6 hours or
more. Skin and eyes protected. Laryngoscope blade
Filtration: • Boiled or autoclaved
• Used for prevention of entry of organisms into breating system of • Stand in carbolic acid 1-20% for 30 minutes – may spoil electric
ventilators. The efficiency lasts for 200 hours connections
• It filters any particle down diameter of 0.5µ • Keep in formalin oven, wipe with 70% alcohol
• They can be autoclaved • Wipe in 0.1% chlorhexidine in 70% alcohol
• 99.99% efficient • Non rebreathing values à ETO
• Modern filters available with 0.22µ size • Mcintosh spray à BTO
• Liters with least resistance can be placed in between ETT and
breathing system Breathing tubes and reservoir bags
Equipments are classified: • Wash, rinse, dry it in air
1. Direct contact with respiratory: ETT, airways suction catheters • Pasteurized at 750C for 10 minutes
2. Nearer to respiratory tract: Corrugated tubes, reservoir bags • ETO effective
3. Remote ones: Circle absorber, ventilators • Waterʼs canister à washed, boiled, autoclaved
Circle absorber: γ radiation, ETO, Formalin chamber, filters can be
used
176

Ventilators:
• Fillers used, ETO, nebulization with alcohol, irrigation with
antiseptics
• Ultrasonic nebulization with H2O2
• Breathing circuits placed immersed in cidex for 1 hour and then
washed thoroughly.
Humidifiers:
• 600C running temperature when in use keeps it in pasteurized,
frequent and thorough working
•
Syringes and needles:
• Ideally γ irradiated (disposable)
• Glass syringes ideally autoclaved in case emergency boiled in
distilled water for 5 minutes
Instruments for local blocks:

• Disposable sets of γ irradiated
Tests of adequacy of sterilization:

• Colour changes in Brownʼs tube in autoclaves or signaloc tapes in
autoclaves
• They are temperature sensitive tapes
177

53. First Aid. Dr Azam’s Notes in Anesthesiology 2013
Definition: • If victim is unresponsive, difficulty in breathing due to secretions/

• The National First Aid Science Advisory Board defined first aid as vomiting and we are alone and have to leave the patient to got help,
assessments and interventives that can be performed by a place the victim in a modified HAINES recovery position by extending
bystander or by the victims with minimal or no medical one of the victims arm above the head and rolling the body to the
equipment. side so that victims head resist on the extended arm. Bend both legs
• First aid provider is defined as someone with formal training in to stabilize the victim.
first aid, emergency care or medicine who provides first aid.
• First aid should be medically sound and based on scientific Organ:
evidence or on export consensus Insufficient evidence to recommend or against use of O2 by
• Administration of first aid must not delay activation of EMS administration may delay other interventions.
system or other medical assistance when required.
• The National first aid science advisory board believes that
education in first aid should be universal everyone can learn first Medical Emergencies:
aid and everyone should • First aid providers may assist the victim in using prescribed
bronchodilator medication if victim states that he / she is a asthma
Call for help: patient and unable to administer the drug without assistance.
• First aid provider is to know how to get help • First aid providers should be familiar with the epinephrine auto-
• Learn how and when to access the EMS system, how to active infector so that they can help someone having an (anaphylactic
or site emergency response plan (ERP) and reaction) self administer.
• Non to contact that poison control center.
Seizures:
Position the Victim: • Protect the head with a pillow or other soft material
• As a general rule victim should not be moved, but there are • Do not restrain the victim during and seizures or place any object in
times when we should do so. mouth victims – (tongue bite is common at the onset) (causes
• If area is unsafe, move the victim to safe location muscle skeletal injury or soft tissue injury)
• If victim is facedown and needs CPR turn him face up. • To prevent aspiration of secretions and maintain an open airways
• If victim is unresponsive has an open airway and breathing place the victim in a recovery position after the seizure stops.
spontaneously turn the victim onto his/her side (recovery Injury Emergencies:
position) with victims hand in front. Because of nerve vessel Bleeding:
injury if he lies on one arm • Manual pressure on guaze or other cloth placed ever the bleeding
• If we suspect victim might have spinal injury it is best not to more source.
the patients. • Elastic bandage firmly wrapped over the guaze to hold it in place with
pressure.
178

First Aid. Dr Azam’s Notes in Anesthesiology 2013
Wounds and abrasions Type to enter text

• Irrigate with clean running tap water for ≥ 5 minutes or until
there appears to be no foreign matter in wound.
• Antibiotic ointment or cream applied only if the victim wound
is an abrasion or is superficial.
Burns:
Thermal burns
• Cool the burns with cold water as soon as possible and
continue at least until pain is relieved
• Avoid cooling with ice or ice water for > 10 minutes
especially if burn is large (> 20% body surface area)
Burn blisters:
• Loosely cover burn blisters with a sterile dressing but leave
them intact
Electrocution and electrical burns:
• Do not place our self in danger by touching electrical victim
while power is on. Turn off power at release
• Try to remove wires or other materials which conducts
electricity with other materials like wooden ones.
• Assess the victim, who may need CPR defibrillation
treatment for shock or thermal burns.
179

54. Neuroleptic Malignant Syndrome. Dr Azam’s Notes in Anesthesiology 2013
NMS caused either by treatment with dopamine receptor Criteria for diagnosis:-
antagonists or by withdrawal of dopamine receptor agonist. Major:
Pathogenesis 1. Fever
1. Central mechanism 2. Rigidity
2. Excitatory aminoacids 3. Raised serum creatinine kinase
3. Peripheral mechanism
Minor:
1. Central mechanism: 1. Tachycardia
There is acute dopaminergic transmission block in. 2. Tachypnea
• Nigrostriatum à produces rigidity. 3. Increased blood pressure
4. Altered consciousness
• Hypothalamus à produces hyperthermia.
5. Sweating
• Corticolimbic system à produces attered
• mental state. Complications:
2. Excitatory amino acids: Relative glutaminergi excess 1. Respiratory: Secondary infection aspiration pneumonia
transmission is as consequence of dopamine block. 2. Central Venous System: Arrhythmia pulmoembolism.
3. Peripheral mechanism: Not clear, may be some intracellular 3. Musculoskeletal:-
association between MH and NMS leads to disease • Peripheral neuropathy
process. • Rhabdomyolysis (myoglobinuria)
Clinical Features and diagnosis:-
• It develops over a period of 24-72hours/ following exposure Differential diagnosis:
to neuroleptic agents or sometimes several days to months 1. NMS versus fatal catatonia: Rigidity is intermittent in catatonia and it
and may even follow a low dose of neuroleptic agent. demonstrates severe psychotic excitement in early stages.
• It will continue upto 10 days even after stopping triggering 2. MH versus NMS:
agent. NMS demonstrates:-
• Slow in onset
Death from NMS due to:- • Rigidity of central origin
• Respiratory failure (comment) • Latency of effect of dantrolene
• Renal failure secondary to myoglobinuria • Lack of familial tendency(MH is autosomal dominant)
• Cardiac arrest. • Uneventful anesthesia with triggering agents
1. Drugs of abuse: ethanol and sedative, hypnotic withdrawal cocaine
and amphetamine intoxication MAO overdoses.
2. Neuroleptic heat stroke: here flaccid muscle tone will be present.
180

Neuroleptic Malignant Syndrome.Continuation: Dr Azam’s Notes in Anesthesiology 2013
MANAGEMENT Treatment:
I. Nonspecific therapy • Access rapidly airway, breathing and circulation if not maintaining
II. Specific therapy hemodynamic stability incubate and put the pt on ventilator
• Stop further beta adrenergic drugs.
I. Nonspecific therapy: • Monitor and correct blood glucose level, electrolytes and acid base
• Basic resuscitation measures balance.
• Withdrawal of triggering agents • If arrhythmias present pharmacological cardio version done by using
• Cooling ant arrhythmic drugs or by electric cardio version if hemodynamic
unstable.
II. Specific therapy: • If hypotension present treat with adequate fluids.
• Bromocriptine- helpful in pts with hepatic dysfunction • If hypertension present use vasodilators(NTG/SNP) or ion dilators
• Dantrolene- reduces death rate below 9% (phosphodiesterase inhibitors)
• Avoid anticholinergic agents(when rigidity ass with pyrexia) • Control HR and BP with beta blockers(propranolol)

Glutamate antagonists
• Amantadine acts on NMDA type
• Glutamate receptors: These drugs act on NMDA type
glutamate receptors.
• Amantadine
• Mimantine
• Restore balance between dopaminergic and glutaminergic
system
• Exhibit hypothermic and central muscle relaxant properties
Anesthesia:
• Anesthetic management is important during pts posted for
ECT.
• The technique should not increase muscle disorder or
produce complications of NMS.
• Avoid scoline in presence of active muscle disease. It may
release k+ of course Rhabdomyolysis.
• Propofol is best avoided in ECT because it shortens duration
of seizures and increase frequency of treatment.
181

55. Substance Abuse. Dr Azam’s Notes in Anesthesiology 2013
Definition: Anesthesia:
• Self administration of a substance that is not for normal • Maintain opioid administration with a suitable opioid in a dose
medicinal purposes and that may lead to physical and/ or equivalent to addicts routine daily requirement
psychological dependence • Methadone is useful. Avoid opioid antagonists/ agonist- antagonists
• The analgesic effect of entonox is reduced
Physical dependence: • Hypotension is common, treated with fluids in first instance
• It occurs when the presence of substance is necessary for • Cross tolerance to other CNS depressants may be seen with an
normal physiological wall being and when specific symptoms increase in the requirements of anesthesia
occur if the substance is not taken • If hypotension does not respond to fluids/ vasopressors, a dose of
morphine has been reported to restore the BP
Psychological dependence: • For rehabilitated addicts avoid drugs of opioid family use inhalational
• Occurs when the substance produces a desire to repeat the agent + regional block
experience again and again • Opioid addicts are usually difficult and manipulative it may be difficult to
determine post operative pain requests for additional doses of opioid
Tolerance: are genuine or not
• It develops such that increasing doses are required to
produce the same effect Alcohol: affects all age group
• Many of the alcohol effects appear to result from an action on GABA
Associated complications with drug abuse: • Alcohol increases GABA medicated increase in chlorine conductance
• Diseases- hepatitis, AIDS • Alcohol withdrawal shows- tremor, hallucinations, agitation, confusion,
• Personality disorders tachycardia, HTN, arrhythmias, nausea, vomiting, insomnia
• Unwanted pregnancy • Chronic alcohol ingestion shows- cerebellar neuron loss with vitB12
• Antisocial behavior deficiency (wryneckʼs encephalopathy or korsakoffʼs psychosis).
• Drug over dose
Opioids: Anesthesia:
• Produce physical dependence and also tolerance develops • When there is acute intoxication delay anesthesia if possible but if it is
• Effects seen when overdose taken- slow RR, very small necessary use reduced aruovnts of anesthetics and sedatives
constricted pupils, impaired conscious level, dysarthria, • Rapid sequence induction to be done because of increased chance of
slurred speech later coma and death pulm.edema may aspiration
complicate overdose • Hypoglycemia is common repeated blood glucose levels monitored
• Opioid addicts have high incidence of- anemia, nutritional • Opioid effects of sedation and respiratory depression potentiated
deficiencies sepsis, phlebities and cellulitis, bacterial • When there is moronic alcoholism tolerance to anesthesia is often
endocarditis present
• Later stage hepatic dysfunction leads to slow drug metabolism and
reduced plasma protein measurements , produces an exaggerated
responses to some agents.
182

Substance Abuse.Continuation: Dr Azam’s Notes in Anesthesiology 2013
• Hepatic cirrhosis and nutritional deficiencies present • Acute ingestion of barbiturate- hypotension, hypothermia, and ataxia
• Regional techniques beneficial but alcohol induced slurred speech In high doses- myocardial depression coma, ARF
polyneuritis may present • Acute withdrawal shows-tachycardia, anxiety, tremor, hyper reflexia,
• Disaffirm treatment potentiates B2D and other sedative hypotension, convulsions and cardiovascular collapse
agents. A reduced dose may be needed Anesthesia:
• Metaraminol used vasopressors • Cross tolerance to anesthetic agent(s), needs high dose
• Avoid alcohol containing skin preparations and medications • Acute intoxication increases MAC and chronic use increases MAC
• Chronic induction of hepatic enzymes will alter pharmacy kinetics of
Cocaine: number of drugs like warfarin, digoxin and Phenytoin
• Produces profound high central stimulation mediated through • Overdose needs- NG lavage, urine alkalization flumazenil for BZD
enhancement of adrenergic and dopaminergic pathways
• It is metabolized by plasma cholinesterase levels Amphetamine:
• Withdrawal causes:- fatigue, depression and increased • Stimulates catecholamine release causing heightened awareness and
apetite reduced need for sleep
• Acute administration shows- increased HR, HTN, arrhythmia • Appetite is suppressed, tolerance develops rapidly leading to an
(VF), coronary spasm, MI, lung damage, nasal septum escalation of dose
atrophy, pulm.edema, agitation, paranoid thoughts, • Chronic amphetamine abuse leads to- daytime somnolence, weight
hyperglycemia, hyper reflexia, convulsions, asphyxia loss, malnutrition
• Anesthesia:-acutely intoxicated high chances of arrhythmias • In overdose – anxiety, hyper-reflexia, hyperthermia, convulsions
and MI • Withdrawal- increased appetite, lethargy, depression
• An anesthetic requirement increases. Premedication with
BZD or barbiturates Anesthesia:
• Nitrate infusion for hypertension • If acutely intoxicated anesthetic requirements
• Avoid volatile agents which can sensitive myocardium to • Chronic abuse reduced requirements for anesthesia
catecholamine • Profound hypotension on induction, may not respond to ephedrine
• Platelet count to be checked before doing regional block Metaraminol preferred.
• Ketamine, pancuronium, gallamine to be avoided.
Barbiturates and BZD: Marijuana:
• Chronic abuse causes tolerance to sedative drugs • Increasingly used for medicinal purposes ( antiemetic and in certain
• They are CNS depressants and hyperpolarisation of chronic neurological disorders )
postsynaptic neural membranes, so that farther excitation • Produces euphoria, drowsiness, tachycardia, postural hypotension
wont occurs. • Long term use causes deposits in lungs
183

Substance Abuse.Continuation: Dr Azam’s Notes in Anesthesiology 2013
Anesthesia:
• Reduced dose of anesthetic agent may be required delayed
recovery and respiration depression are possible.
184

Flow Charts & Diagrams Dr Azam’s Notes in Anesthesiology 2013
Rapid Assessment of Airway: FUN - M - MAPing with MOANS, RODS, BANGS, Assessment of risk factors for aspiration
& difficulties for removal of airway maintenance device. It Can be classified as 1. Global (Head to Toe Examination), 2.
Regional (Head & neck) & 3. Radiological (effective Mandibular length, A-O & A-A joint)
Assessment Test
Face Unusual or deformed facies, any obvious abnormality in face, beard, Syndrome - Pierre-robin Syndrome,
klippel-Feil, Goldenhar and Fetal Alcohol.
Upper Incisors Absent, Loose Protruding
Nose Nasal Patency
MMAP”ing Mallampati Class III & IV.
Measurements: 3-3-1;
•Thyromental span = < 3 fingers breath, Mouth Opening = < 3, Jaw Protrusion = < 1 cm or upper lip bite
test.
A-O extension ( in absence of C-Spine precautions), Inability to adequately to flex & extend the atlanto-
occipital joint.
Pathology in the mouth & Upper airway. Swellings in and around the airway H/O snoring & stridor.
MOANS (Specific for BMV) Mask Seal, Obesity/Obstruction, Age > 55, No teeth, Stiff lungs
RODS (Specific for Restricted mouth opening, Obstruction in upper airway, Disrupted upper airway e.g trauma, intra-oral burns,
supraglottic devices) Stiff lungs (Poor compliance)
BANG (specific for surgical Bleeding tendency, Agitated patient, Neck scarring and flexion deformity, Growth or vascular abnormalities
airway) in the region of the surgical airway
Factors for higher risk of NPO status & Full stomach, GE Reflex, Pregnancy, Obesity Hiatus Hernia, presence of Ryleʼs tube.
aspiration.
Difficulties during and after Any cause encountered as above

removal of airway
maintenance device.
185

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Anesthesia challenges in robotic surgery

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Anesthesia challenges in robotic surgery

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Dr. Azam’s....

To Mohammed Shafiulla, my father, my oxygen, companion, and best friend; for

Dr Azam’s Notes in Anesthesiology 2013

A NOTE TO THE READER

Dr Azam’s Notes in Anesthesiology 2013

Dr Azam’s Notes in Anesthesiology 2013

48. Malignant Hyperthermia - 120

Dr Azam’s Notes in Anesthesiology 2013

Surgeries done by Robot and Associated Anesthetic

Dr Azam’s Notes in Anesthesiology 2013

Contraindications for MVR:

Dr Azam’s Notes in Anesthesiology 2013

Dr Azam’s Notes in Anesthesiology 2013

Dr Azam’s Notes in Anesthesiology 2013

Management: 17. Malignant hyperthermia - dantrolene 2-10mg

Dr Azam’s Notes in Anesthesiology 2013

• Awareness is defined as the spontaneous recall of events Predisposing factors:

Dr Azam’s Notes in Anesthesiology 2013

Dr Azam’s Notes in Anesthesiology 2013

Causes: Halothane, isoflurane and N2O:

Dr Azam’s Notes in Anesthesiology 2013

Propofol: Mental alterations:

Dr Azam’s Notes in Anesthesiology 2013

ASA definitions: Acquired:

Dr Azam’s Notes in Anesthesiology 2013

ASSESSMENT DURING DIRECT LARYNGOSCOPY WILSONʼS SCORE:

Dr Azam’s Notes in Anesthesiology 2013

LEMON SCORE Four Dʼs also suggests difficult airway:-

Dr Azam’s Notes in Anesthesiology 2013

• treat infection if suspected = 1; &JGCJ!)Y!EF2KHE3F!!QF3CIG4!HG4EF6R;

Dr Azam’s Notes in Anesthesiology 2013

Dr Azam’s Notes in Anesthesiology 2013

Dr Azam’s Notes in Anesthesiology 2013

Dr Azam’s Notes in Anesthesiology 2013

commonest causes of complications: Lithotomy position:-

Dr Azam’s Notes in Anesthesiology 2013

Dr Azam’s Notes in Anesthesiology 2013

Reason for transport of patient is Aeromedical transfer:

Dr Azam’s Notes in Anesthesiology 2013

Check List of Preparation:

Dr Azam’s Notes in Anesthesiology 2013

Dr Azam’s Notes in Anesthesiology 2013

• General anesthesia cause an irregularly descending depression STAGES OF ANALGESIA:

Dr Azam’s Notes in Anesthesiology 2013

Meyer overton theory: Alteration in the structure of nerve

Dr Azam’s Notes in Anesthesiology 2013

Dr Azam’s Notes in Anesthesiology 2013

What should be done when awareness is reported?

Dr Azam’s Notes in Anesthesiology 2013

History: 1. Autonomic changes:

Dr Azam’s Notes in Anesthesiology 2013

2. Isolated forearm technique (IFT):

Dr Azam’s Notes in Anesthesiology 2013

• Wakefulness with eyes closed is associated with higher levels of

Dr Azam’s Notes in Anesthesiology 2013

Somatosensory Evoked Potentials (SEP):

Dr Azam’s Notes in Anesthesiology 2013

I. Reflex pathways of pressor response: Efferent pathway:"

Dr Azam’s Notes in Anesthesiology 2013

Essentially there are 3 large groups to attenuate these reflexes:

Attenuation of Pressor response pathway.

Dr Azam’s Notes in Anesthesiology 2013