DOCTOR-PATIENT RELATIONSHIP

Interaction that is established between a doctor and patient with the goal of
restoring health, alleviate suffering, and preventing disease
The doctor needs to establish a dialogue with the patient that plays a
significant role in the success of therapy, as well as to apply theoretical and
technical knowledge for DX & TX
There is a dialogue of the relevant medical procedures
Also need to remember the family members, because the suffering can either
bring a family together or tear them apart
Respect for the patient consists of reciprocity, communication, and concern
It is not shown in the informed consent but in the sensitive and attentive
response to the nuances of patient behavior, both verbal and non-verbal
The doctor-patient relationship
It is not only professional, but humane
It displays the dignity of each party
Dignity is an emotional need of having public recognition by authority,
personal, friends, family, social circles of having done things well
It is an intrinsic quality of being human
It is based on the recognition that the person is worthy of respect
It is developed in the hope of curing and being cured
It needs empathy, trust, compassion, and sensitivity
It is unequal in professional terms, but not in human terms
The characteristics of the doctor needed to maintain a doctor-patient
relationship:
Knowledge
Wisdom
Humanity
Empathy
Willingness to help when facing difficulties
Types of relationships
Active-passive
Is provided for patients w/ a coma or if the patient is in a state where
active participation is not possible
Guided cooperation
Is established w/ patients that are in a condition where they can
cooperate with the doctor in their DX & TX, such as in some acute &
chronic diseases such as pneumonia or arterial HTN
Mutual participation
Not only compliance w/ TX, but the patient is actively participating in
the discussion of situations and attitudes related with the cause &
evolution of the disease
In reality, seeing the patient as a client and the use of modern technology in
medical practice has increased errors in the practice of medicine, violating
the principles of medical ethics & facilitating the participation of lawyers in

malpractice claims
The dilemma of the specialist: they know more about the disease, but
understand less of being humane
Rights of the patient
To receive adequate medical attention for their state of health and the
specific circumstances of their case, and to be informed when there is a
need for references of any other doctor
To be treated w/ trust and that their health information is not divulged to
those not expressively authorized
To be treated in a dignified & respectful manner. The doctor, nurses, and
all personnel must identify themselves and respect at all times the patients
personal and moral convictions
Have the option to obtain a second opinion on DX, TX, or PX
To receive information that is sufficient, clear, timely, and accurate of DX,
PX, and TX
To receive medical care in case of emergency at any health establishment,
whether public or private
To be able to decide on the type of care without any form of pressure, as
well as to accept or reject each diagnostic procedure offered and the person
performing the procedure
To have a clinical record w/ information that is truthful, clear, accurate,
legible, and complete
Stress and surgery
The response to all stressful stimuli, real or symbolic, is a complete
response of the individual, integrated at all levels, from the molecular level
and the psychologic level, to the biochemical modifications and changes in
behavior
The surgical procedure has many symbolic meanings, different for each
operation and for each patient
The surgical procedure is a brutal assault, adding to the aggression of the
disease itself, as it consists of pain, danger of death, violation of the body
itself by a stranger, mutilation, and of transitory state of death with no
guarantee of the brevity
Why is a good doctor-patient relationship important?
b/c with it, you can arrive at a more precise DX for the disease
b/c we will be able to motivate the patient to the extent possible
b/c the patient and the family will be better able to appreciate our work
b/c it is important to develop a good clinical history, a document that is
essential in the scientific and legal aspect
How to have empathy for a patient? SMILING IS FREE
By first greeting the patient and encouraging them to introduce us to their
problem
By being quiet during the interrogation
By smiling and exhibiting the ability to listen with sincerity
By talking when you need, and giving explanations about their condition

 By maintaining orderly records

SMILING DOESNT CURE, BUT ALLEVIATES. PRESENCE IS NOT
ENOUGH, BUT IS GRATIFYING
PREOPERATIVE EVALUATION
Integral determination of state of health of a patient that will be submitted for
surgery, with the goal of identifying diseases that can affect the prognosis, the
surgery itself, or the recuperation from surgery
Objective
To evaluate surgical patients to determine if it is necessary to
implement therapeutic measures (prophylaxis) so that the patient can
tolerate the surgery without any major problems
To reduce Perioperative morbidity and mortality
Requirements
Definition of actual physiological state of the patient
To determine all pathological processes and their grade of activity
Evaluation of nutritional status
To delineate physical, cognitive, and emotional state
To identify the surgical risk factors (pre/trans/post-operative)
Plan of action to minimize risks
Advantages
Evaluation of anesthetic risk
ASA
1 = healthy patient, w/o physical/metabolic abnormalities
2 = patient w/ mild-moderate deterioration of physical state
that does not interfere w/ their daily activities
3 = patient w/ severe metabolic/physical disorders that
interfere w/ daily activities
4 = patient w/ severe life-threatening disorders
5 = moribund patient w/ limited life-expectancy w/in the next
24 hours
Preparation of surgery includes recommendation for fasting & any
indication for pre-medication
Prevention of possible complications
Treatment of existing pathologies
Formulation of anesthetic plan
Obtainment of informed consent
Document which establishes communication from the doctor to the
patient informing them of the surgical process that is to come, the
alternative options, potential complications, risks and benefits, that
the patient accepts with their signature
Separate authorization for:
Blood transfusions
Anesthesia & its risks
Risks

 Respiratory
Pulmonary dysfunction
It is important to evaluate respiratory function in patients w/
pulmonary problems in case they deteriorate, which represents
a major risk of presenting w/ complications such as atelectasis,
hypoxia, and pneumonia postoperatively
Risk factors
Intense smoker
Cough
Obesity
Advanced age
Intra-thoracic operations
Pre-existing lung disease
Risk I = normal
Risk II = chronic smoker, controlled chronic pulmonary
disease, acceptable VC & respiratory volume
Risk III = chronic smoker, controlled chronic pulmonary
disease, acceptable VC & respiratory volume, limited
pulmonary function tests
Risk IV = Acute or active chronic pulmonary disease, w/ poor
pulmonary function, hypoxia, hypercapnia
Pulmonary thromboembolism
Low risk = TX w/ compressive measures
Moderate risk = TX w/ compressive measures, low-dose
heparin (5000 U tid or bid)
High risk = TX w/ compressive measures, heparin, or LMWH,
or warfarin
Cardiovascular
Based on:
Risk I = normal patient
Risk II = patient older than 40 or less than 40 & arrhythmic, or w/
previous heart surgery, or hypertensive, or MI more than 6 months
ago
Risk III = patient older than 40 or less than 40 & arrhythmic, or w/
previous heart surgery, or hypertensive, MI more than 6 months
ago, or with history of infarct less than 6 months ago
Risk IV = decompensated cardiac function, need to evaluate for
risk in arterial & venous system studies
Goldman Cardiac Risk Index
S3 = 11
Elevated JVP = 11
MI in past 6 months = 10
ECG: premature arterial contractions or arrhythmia = 7
ECG shows > 5 premature ventricular contractions/min = 7
Age > 70 = 5

Emergency procedure = 4
Intra-thoracic, intra-abdominal, or aortic surgery = 3
Poor general or metabolic status, bedridden = 3
Severe aortic stenosis = 3
Patients w/ scores > 25 had a 56% incidence of death, w/ a
22% incidence of severe CV complications
Patients w/ scores < 26 had a 4% incidence of death w/ a 17%
incidence of severe CV complications
Patients w/ scores < 6 had a 0.2% incidence of death w/ a
0.7% incidence of severe CV complications

Hepatic
The patient w/ hepatic disease constitutes a challenge for the medical
team in perioperative management, and the determination of potential
surgical risk is proportional to the severity of hepatic compromise
Must evaluate immunologic, metabolic, and circulatory function of
the liver
Hepatic surgery risk
I = normal
II = Group A of Child classification
Albumin > 3.5 g/L
Bilirubin < 2 mg/dL (w/ cholestasis, < 4)
PT% > 50% or INR < 1.7
Ascites absent
No encephalopathy
III = Group B of Child classification
Albumin 2.8-3.5 g/L
Bilirubin 2-3 mg/dL (4-10)
PT% 30-50% or INR 1.8-2.3
Mild ascites
Grade 1 or 2 encephalopathy
IV = Group C of Child classification, in case of acute disease
evaluation of LFT
Albumin < 2.8 g/L
Bilirubin > 3 mg/dL (>10)
PT% < 30% or INR > 2.3
Moderate ascites
Grade 3 or 4 encephalopathy
Renal
Renal surgery risk
I = normal evaluation
II = slightly elevated BUN & creatinine, creatinine clearance of 4060 ml/min
III = creatinine clearance of 20-40 ml/min
IV = creatinine clearance < 20 ml/min or patient on dialysis

 Hematologic
Hematologic surgery risk
I = normal
II = Hb & Hct up to 20% less than normal value, slightly elevated
coagulation factors
III = Hb & Hct b/w 20-40% less than normal, altered coagulation
factors, thrombocytopenia, active hematologic disease
IV = Hb & Hct more than 40% less than normal, w/ severely
affected coagulation factors
Endocrine-metabolic
Endocrine-metabolic surgery risk
I = normal
II = slightly decompensated (diabetic w/ hypoglycemia)
III = decompensated (insulin-dependent)
IV = severely decompensated (decompensated diabetic)
Neuro-psychiatric
Neuropsychiatric surgery risk
I = normal
II = GCS 11-13, controlled neurologic disease, anxiety, depression
III = GCS 9-11, psychiatric problems in TX
IV = GCS < 9, schizophrenia, psychosis
Glasgow Coma Scale
Open eyes
None = 1
To painful stimuli = 2
To vocal command = 3
Spontaneously = 4
Best verbal response
None = 1
Incomprehensible sounds = 2
Utters inappropriate words = 3
Confused, disoriented = 4
Oriented, converses normally = 5
Best motor response
None = 1
Extension to painful stimuli = 2
Abnormal flexion to painful stimuli = 3
Flexion/withdrawal to painful stimuli = 4
Localizes painful stimuli = 5
Obeys commands = 6
Nutritional
Nutritional surgery risk
I = normal
II = loss of 10% of body weight w/ hypoproteinemia w/o

associated diseases
III = loss of 20% of body weight w/ hypoproteinemia, associated to
chronic disease, albumin 2-2.5 mg/dL
IV = loss of > 20% of body weight w/ hypoproteinemia, associated
to chronic disease, albumin < 2 mg/dL
Infection & sepsis
Surgical risk
I = normal
II = patient w/ chronic controlled process
III = acute infectious process, septic syndrome
IV = septic shock
Age
Surgical risk
18-40, 41-60, 61-80, >81
Condition of surgical intervention
Risk
I = elective
II = urgent
III = very urgent
IV = immediate or life/death
Initial evaluation form
ID & profile of patient
Type of condition
Acute, acquired, localized, complicated w/
Manifested by: synopsis of clinical case
Acknowledgement of following syndromes (list in order of severity)
Acknowledgement of primary cause & any complications
Proposal of DX studies
Lab
Imaging
Proposal of following management
Immediate TX
Mediate TX
Post-mediate TX
Late TX
Preoperative evaluation
General measures
Informed consent
Fasting
Bed position
Vital signs (SVPT)
Nursing general care (CGE)
Obtain IV access
Elastic measures (anti-thrombotic prophylaxis)

 Parenteral solutions
Begin or continue w/ previously indicated plan
Reset solutions
Maintenance solutions
Medications
Continue w/ medications already initiated
Abx
Anaglesics, KCL
Add
Omeprazole 40 mg c/24 hours
Enoxaparin 20 mg c/ 12 hours SC
Special measures
Supplemental O2 (nasal points 4-5 L)
Vigilance of tubes (NG, urinary, catheters)
Note entry and exit of balance of liquids every 12 hours
Solicit CXR, interconsult w/ cardio, w/ anesthesiologist
Justification of indications
Pass to operating room at 7 AM
Transoperative evaluation
Anesthesia
Anti-sepsis of operating region
Technique of preparation of operating field
Technique of laparotomy
Description of surgical technique
Technique of closure of laparotomy
Postoperative evaluation
Recuperation: ICU, hospital bed
General measures
Position
Mobilization of bed
O2
Vital signs every 15 min
General nursing care
Parenteral solutions
Mixed solution 1 L for 4 hours
NaCl 1 L for 4 hours
Dextrose 5% 1 L for 8 hours + 2 ampules of KCL
Medications
Ketorolac or Meperidine every 4-6 hours
Continue Abx, enoxaparin, omeprazole
Special measures
O2 nasal
Monitor functioning of tubes & catheters

Change of position & exercise every 4-6 hours

Form of balance of liquids
Removal of NG tube when hear intestinal sounds
Initiate PO
De-ambulation in 12-36 hours
Discharge the following day w/ appointment to remove sutures in 8
days

PERIOPERATIVE ANALGESIA
Pain
Characteristics of postoperative pain
Nociceptive
Involve inflammatory mediators such as:
Prostaglandins
Histamine
Serotonin
Bradykinin
Involves A delta fibers
Is acute, w/ variable intensity
30% of recently operated patients suffer from intense pain
40% of recently operated patients suffer from moderate pain
20% of recently operated patients suffer from mild pain
Objective of perioperative analgesia
Decrease the stress response, which fundamentally consists of a
neurovegetative response manifested by:
Elevation of BP, HR, CO
Greater oxygen consumption (organic respiration to surgical stress)
Avoid hyper-excitability of neurons of dorsal horn, by a single dose of
preoperative analgesia
Permit normal activity of patient, with supplemental analgesics
Decrease hospital stay and costs
Decrease postoperative complications
Thrombosis d/t delayed de-ambulation
Pulmonary alterations d/t retention of secretions or hypoventilation
Atelectasis
Eschar
Thromboembolism
Muscular contraction d/t pain
International Association for the Study of Pain (IASP) Recommendations
NSAIDs for parenteral use in acute pain
Antipyretic analgesics
Propacetamol ampoule of 1-2g IV qid
Metamizol ampoule of 2g IV/IM tid/qid
Ketorolaco ampoule of 30mg IV/SC/IM qid

 Potent analgesic, but w/ moderate anti-inflammatory activity

w/ similar analgesic & anti-inflammatory actions to other
NSAIDs, but 350 times more potent than aspirin
Inhibits platelet aggregation & can damage gastric mucosa
Administration (PO, IV, IM, SC, rectal): the max plasma
concentration can be achieved in 30-60 min, w/ max effects in
2 hours, and lasts 6 hours
It is partially metabolized in the liver & excreted in the urine
Renal elimination is prolonged in renal insufficiency & elderly
Efficacy
30mg of ketorolac IM = 100mg of meperidine IM (12 mg
of morphine IM)
Dosage
Ketorolac 30mg qid (no more than 120mg/d for 5 days IV)
In elderly above 65, 15mg qid (no more than 60mg/d
for 5 days IV)
Anti-inflammatory analgesics
Ketoprofeno ampoule of 100mg IV tid
Diclofenaco ampoule of 75mg IM bid
Dipirona 1g IV slow infusion (max 4g/d) repeated tid/qid
Opioid analgesics
Tramadol 100mg diluted in 100ml physiologic fluid passed in 10
minutes, repeated qid (max 400mg/d)
Dextropropoxifeno 38mg/dipirona 1g in 100ml physiologic fluid,
repeated tid (max 152mg/4g/day)
Morfina
Full agonist of receptors mu, delta, and kappa
Fundamental activity on mu receptors
Absorbed via all routes except transdermal
Excreted via urine (half-life of 2-4 hours)
Epidural analgesia
Most used epidural analgesics are local anesthetics (bupivacaine,
ropivacaine, and lidocaine) and opioids
Opioid (fentanyl)
Duration of action is relatively short w/ lipophilic character
(prevents the incidence of late respiratory depression
associated with epidural morphine)
Most probable side effect of fentanyl is pruritis, which
responds normally to a decrease in dose or antihistamines
Can resemble sedation, especially in the elderly, that only
respond to a decrease in velocity of perfusion or to removal of
medication
Other possible secondary effects are nausea, delay of intestinal
motility, and occurrence of distended bladder
Protocol of epidural analgesia w/ PCA pump

 200ml saline + 200mg bupivacaine + 600microg fentanyl at 510 ml/hour w/ bolus of 1 ml

200ml of 0.2% ropivacaine + 600microg fentanyl at 5-10
ml/hour w/ bolus of 1 ml
Examples of perioperative analgesia
Infiltration of wound: at the end of surgery, a local anesthetic of long
duration (0.25% bupivacaine)
Peribulbar or retrobulbar block for ocular surgery or topical analgesics
In children, regional anesthesia before surgery reduces the
requirements of general anesthesia w/ subsequent lower incidence of
N/V and early & high tolerance
Patterns of treatment
Once the surgery is completed, the patient is moved to recuperation
Pain is controlled = initiate IV analgesic protocol
Pain is not controlled
Mild pain = NSAID
Metamizol 2g
Ketorolaco 30mg
Propacetamol 2g
Moderate pain = NSAID + Tramadol 50mg +
Metoclopramida 10mg in 100cc saline
Severe pain = potent opiate
Meperidine 25mg every 4-6 hours until pain is controlled
Morphine 2-5mg & later 1mg until pain is controlled
COMPLICATIONS IN SURGERY
Any divergence from the predicted course in the systemic recuperation of
operated patient
Are the result of the primary disease, the surgical intervention, and other
non-related factors
For early detection, it is necessary to repeatedly evaluate the patient
Prevention of complications begins before surgery
Important factors in postoperative stage
Early mobilization
Adequate respiratory care
Liquid and electrolyte balance
Classification
Anatomical area
Neurologic
Respiratory
Cardiovascular
Digestive
Renal
Extension of anatomical area

 Local
Systemic
Time of presentation
Immediate (first phase): w/in OR & up to recuperation area
Anesthetic induction-beginning of surgery
Dysrhythmias
HR alterations
Cardiac arrest
Bleeding
Defective hemostasis
During the time of surgery
Prolongation of estimated operative time
Change in route of access
Shock state
Transfusions
w/ conclusion of surgery-anesthetic reversion
Sutures
Installation of drainage systems
Equipment for immobilization
Late recuperation of alert state
Odontologic (loss of dental pieces)
Ocular (conjunctivitis, corneal lesions)
Musculoskeletal (lumbalgia, pharyngitis, laryngitis, phlebitis)
Dehiscence of wounds, rupture of sutures, N/V, headache
Recent (second phase): in bed or intensive therapy
Respiratory
Dyspnea
Respiratory insufficiency
Pulmonary infection
Pulmonary thromboembolism
Pneumonia
Pneumothorax
Atelectasis
Cardiovascular
Tachycardia
Arrhythmias
Shock
HF
Phlebitis
DVT
Neurologic
Disorientation
Loss of consciousness

 Headache
Renal
Renal insufficiency
Oliguria
Hydroelectrolytic disequilibrium
Late (third phase): w/ discharge and until full recovery
Headache
Pulmonary infections
Respiratory insufficiency
Phlebitis
DVT
Depression
GI dysfunction
Hepatic insufficiency
Renal insufficiency
Eschar
Anemia
Muscular weakness
Myalgia
Anorexia
Probability of presentation
Avoidable vs inevitable
Predictable vs unpredictable
Complications of surgical wounds
Evaluate health status of patient
Anti-sepsis of operative area, as well as adequate hemostasis
Prophylactic antibiotic therapy
Seroma
Accumulation of ECF
Separates layers of skin
Cuts numerous lymphatic vessels
TX
Drain by puncture
Tetracycline 1g in 150ml saline
Re-intervention to ligate lymphatics
Hematoma
Accumulation of blood & clots
Frequent, imperfect hemostasis
Pain
Increase in local temperature
Swelling
Ecchymoses
If small, drain w/ open puncture & give prophylactic Abx

 Keloids
Excessive accumulation of collagen tissue in response to trauma
TX
Extirpation w/ or w/o graft
Partial resection
Radiotherapy
Local steroids (triamcinolone)
Dehiscence of wounds
Partial or total rupture of any of the layers of a wound
5% in older than 60
M>F
On postoperative day 5-8
Etiology
Infection
Poor surgical technique
Poor selection of suture material
Anemia, DM, uremia, malnutrition, cirrhosis
Deficient tissue perfusion
3 important risk factors
Inadequate closure: use of insufficient amount of sutures or placement
too close to the border
Increase in intra-abdominal pressure: obesity, cirrhosis, cough
Deficient curing of wound d/t seroma, hematoma
Evisceration
Exposure of abdominal contents outside the limits of the parietal
peritoneum
Increase in intra-abdominal pressure
Dehiscence of surgical wound
Syndrome of abdominal compartmentalization
Cellulitis
Inflammatory process d/t bacterial infection which extends via skin or
subcutaneous tissue
Edema
Redness
Heat/hyperthermia
Headache
Local measures
Cold compression
Local cleaning
Topical Abx
Systemic measures
Abx therapy
Synthetic & selective
Necrotizing fascitis

 Local
Erythema
Distant tumefaction
Distant cellulitis
Absence of crepitus
Systemic
Toxemia
Mental apathy
Dehydration
Negative cultures
Associated w/ DM, Immunosuppression
TX
Ample debridement
Systemic Abx therapy
Gaseous gangrene
Rare, is produced by anaerobic bacteria
Is related to the type of surgery
Clinical presentation
Intense pain at wound 12-72 hours postoperatively
Hyperthemia (39.5-41)
Tachycardia (120-140)
Grayish pallor
Severe shock
Subcutaneous crepitus
Alterations in consciousness
Diaphoresis
TX
Debridement of wound
Abx
Hyperbaric oxygen therapy
Amputation
MC systemic complications in surgery
S/S
Fever = atelectasis/infections/post-transfusion/drugs/thrombophlebitis
Tachycardia & anxiety = hypovolemia
Dyspnea = hypoxemia, arrhythmias, sepsis, pain
Hypotension = hypovolemia, sepsis, HF, anaphylaxis, bleeding
Oliguria = hypovolemia, ARF
MANAGEMENT OF BURN PATIENTS
Burns
Lesions in skin d/t physical (temperature), chemical, electrical, and
radiational over-exposure
Differ in severity, extension, and depth of affected tissue

 Superficial (epidermal)
Dress w/ tulle gras and gauze if extensive until healed (usually
w/in 1 week)
Superficial partial thickness
Dress w/ tulle gras and gauze & re-assess at 48 hours
Heal w/in 2-3 weeks
Low exudate
May be suitable for Hypafix, wash dressing daily
and take off with oil in 1 week
High exudate
If contaminated or signs of infection, apply
antimicrobials & need to refer
If not contaminated, continue w/ tulle gras or
Bactigras and review every 2 days until healed
If not healed w/in 2-3 weeks
Requires surgery (refer to burn unit)
Deep partial thickness
Obvious deep dermal injury
Requires surgery, preferably w/in 5 days, unless < 1cm2 in
area
If no obvious deep dermal injury
Dress w/ tulle gras and gauze, reassess at 48 hours
Signs of improvement in healing
Re-dress and review every 2 days
If unhealed at 2 weeks, requires surgery &
refer to burn unit
If no signs of improvement in healing
If unhealed at 2 weeks, requires surgery & refer to
burn unit
Management
Airway: compromised or at risk of compromise?
Yes = intubate
No = BREATHING
Breathing: compromised?
Yes = cause
Mechanical: escharotomies
CarboxyHb: intubate & ventilate
Smoke inhalation: nebulizers, ventilation
Blunt injury: invasive ventilation, chest drain
CIRCULATION
Circulation: compromised perfusion to an extremity?
Yes = escharotomies
No = NEUROLOGICAL DISABILITY
Neurologic disability: impaired GCS score?

 Yes = consider hypoxia or hypovolemia

No = EXPOSURE
Exposure: fully assess burn areas & depth, full examination of
concomitant injuries, keep warm
Fluids: calculate resuscitation formula based on surface area & time
since burn
Heat burns
Cutaneous cellular damage caused by increase in temperature at the cellular
level
T < 45 = w/o evident damage
T = 45-50 = diverse grades of lesion
T > 50 = evident cellular damage w/ presence of denaturation of
cellular proteins
Skin
0.25 sq m in children (up to 1.8 sq m in adults)
Epidermis
Stratum corneum
Stratum lucidum
Stratum granulosum
Stratum spinosum
Stratum basale
Dermis
Formed by fibroconnective tissue
Amorphous in the region of blood vessels
Nervous plexus
2 layers
Papillary dermis
Reticular dermis
Hypodermis
Subcutaneous tissue
Etiology
Multiple causes
MCC
Direct flame
Hot liquids
Direct contact w/ hot metals
Electric current
Other causes
Chemical (acidic/alkali)
Spark
Atomic radiation
Extension of burn
Should be quantified while taking into account the extent of the burn
Rule of 9 (in children)

 Head = 9 (18)
Anterior thorax = 9
Anterior abdomen = 9
Right superior extremity = 9
Left superior extremity = 9
Right inferior extremity = 18 (14)
Left inferior extremity = 18 (14)
Genitals = 1
Rule of palm
Adults = palm of the hand including fingers = 1% of total surface
area
Children = palm of hand including fingers = 2% of total surface
area
Classification
Depth
First degree = epidermis
Painful erythema
Intact basal membrane
Management
Healthy in 5-7 days spontaneously apart from basal layer
Only require application of moisturizer
In case of important discomfort (burning), prescribe an
analgesic
Second degree
Superficial
Erythema
Presence of ampoules
Underlying tissue is white w/ pressure
Is painful
Management
Debridement of ampoules
Cleaning w/ water & soap everyday is there is no NaCl
Apply sterile dressing
Healthy in 3-4 weeks
Generally do not require reconstructive procedures
Deep
More pallor
Can be gray or opaque
Hypoesthetic
Third degree
Extensive destruction of skin
Painless lesions
Coffee-colored or black lesions
Dry, hard, w/ no elasticity

 No vesicles
No sensitivity
Management
In burn unit
Always require reconstruction
First, only apply sterile dressing
Immediate IV fluid therapy
Burn of airways
Symptoms: can cause swelling that blocks airflow
Charred mouth
Burned lips
Burns on head, face, or neck
Wheezing
Change in voice
Difficulty breathing, coughing
Singed nose hairs or eyebrows
Dark, carbon-stained mucus
Incidence of burns
Mortality & frequency of burns
Scalding = 22% (mortality of 10%)
Inflammatory liquids = 16% (6%)
Explosions = 11% (13%)
Burning homes = 5% (44%)
Causes of burns in children
Scalding = 42%
Inflammatory liquids = 10%
Oils = 7%
Sites of burns
Forearm
Hand/wrist
Arm
Face
Special burns
Chemical burns
Acids = cause denaturation of cellular proteins
Alkali = cause caseation of cellular proteins
Management
Immediate removal of whatever is causing damage
Apply continuous irrigation (running water) for 1-2 hours (2-4
hours for alkali burns)
Do not apply neutralizing agents
If burns for phosphorus, lithium, or sodium, no water
Electric burns
Low-voltage < 1000 V

High-voltage > 1000 V

Non-evident lesions
Can cause arrhythmias
At least, maintain medical observation for 24 hours, w/ ECG every 8
hours & continual monitoring
Management
Definitive management of burns
Apply graft
Partial thickness
Complete thickness
Fluid therapy
Restoration of liquids when possible
Begin application of formulas when the burnt surface is at least 20% or
if lesions are of second/third degree
Remember that fist degree burns do not require restoration of liquids
Formulas
Evans
Brooke
Parkland
First 24 hours: Hartman (Ringers lactate) 4ml/kg/%SA burnt
of second/third degree
Half in the first 8 hours
Quarter in the next 8 hours
Quarter in the next 8 hours
Diuresis of 30-70 ml/h
Second 24 hours
Dextrose 5% in water to conserve Na at 140 mEq/L
Colloid solution (plasma) to conserve blood volume in
patients w/ burns of second/third degree affecting more
than 40% of total body surface area
Diuresis of 30-100 ml/h
Hypertonic (Monafo)
Half
Carbajal
First 24 hours
Ringers lactate: 5000ml/sq m burnt in adults
2000ml/sq m burnt in children
Colloid: 12.5g/L of Ringers lactate
Second & third 24 hours
Ringers lactate: 2500ml/sq m burnt in adults
2000ml/sq m burnt in children
Colloid: 12.5g/L of Ringers lactate
Escharectomy
Cut skin to free the tension of eschar

 When there is vascular compromise distally or w/ respiration

Performed in ER
Factors for hospitalization
Burns of > 10% of total body surface area in patients under 10 & over 50
Burns of > 20% of total body surface area in patients b/w 10-50
Burns of third degree greater than 5% in any age
Pre-existing medical disorders
Extremes of life
Chemical burns
Inhalation lesions
Presence of other major trauma
Burns of special areas
Control of pain
Meperidine 25-50mg infusion every 2-4 hours
Morphine sulfate 2.5-5.0mg IV
Hydromorphine chlorhydrate 0.5-1.0mg IV repeated every 2-4 hours
Antihistamine
TX
A,B,C
Initiate fluid therapy w/ strict control of liquids
Realization of ambulatory surgical process in case it is needed
Complete evaluation & transfer to burn unit
Debridement & excision of necrotic tissue
Autografts
Grafts: mallados
Flaps
Cultivated skin
Heterografts & allografts
Synthetic substitute for skin (Integra)
Split skin graft donor site management
Split-thickness skin grafting is recommended for third & fourth degree
burns
Involves harvesting skin from an unaffected part of the patient
(epidermis & superficial dermis)
Donor sites heal in 10-14 days but can be very uncomfortable
Potential for complications
Extreme discomfort
Intense pain
Leakage of blood
Serous fluid & infection
Traditional dressing w/ open-weave tulle impregnated w/
petroleum jelly, covered by an absorbent layer of gauze & cotton
wool
Goals

 Promote rapid wound healing

Reduce pain
Provide a barrier to infection
Absorb copious amounts of exudate
Be easy to handle & apply
Be removable w/o traumatizing the new epidermis
Not impede the morality of the patient
No antigenic or allergenic
Reduce the risk of hypertrophic scarring
Inexpensive & accessible
Dressings
Tulle gras: tulle adheres firmly to raw surface until healing is
complete
Silver sulfadiazine: Abx cream that is effective in reducing risk of
infection
Calcium alginates: promote blood clotting & wound healing by
creating a moist environment
Film dressings
Biological dressings
Topical antibiotics
Silver sulfadiazine
Sodium mafenide
Platinum nitrate of 0.5%
Iodopolivinilpirrolidona (isodyne)
Complications of burn patients
Cardiovascular
Hypovolemic shock
Acute MI
HTN
Myocarditis
Respiratory
Inhalation wound
Pneumonia
Acute respiratory insufficiency
Pulmonary edema
Renal
Renal insufficiency
Myoglobinuria
GI
Curling ulcers
Hepatic dysfunction
Alithiasic cholecystitis
Metabolic & nutritional
Lack of nutrition

 Prolonged catabolism
Endocrine
Suprarenal bleeding
Insulin/glucagon disequilibrium
Neurologic
Burn encephalopathy w/ carbon monoxide intoxication
ACID-BASE DYSEQUILIBRIUM
The respiratory apparatus have sensitive chemoreceptors in the concentration of
H+ in the CNS, in the aorta, and in the bifurcation of the carotids
The principal function of the cardio-respiratory function is supplying the
cells of the body with the blood flow to enable to be viable in ideal
conditions
The kidney participates in the maintenance of acid-base equilibrium via:
Regulates urinary excretion of circulating bicarbonate
Excretes hydrogen ions
The most important buffer is sodium bicarbonate which reacts w/ carbonic acid
Other substances that act as significant buffers are Hb, other proteins,
phosphates, and carbonates
Arterial blood gases (ABG)
Evaluate the state of acid-base equilibrium (used preferentially in
peripheral venous blood)
Evaluate hemodynamic state, using venous saturation of oxygen in central
venous blood
Essential applications
The evaluation of diffusion of gases at the pulmonary & systemic level
The evaluation of the relation b/w acids & bases of ECF
pH
Measures the global results of acid-base equilibrium
It is not a parameter of evaluation of respiratory function
Time of respiratory alteration
If a respiratory process is acute or chronic, or when a chronic process
becomes acute
PaCO2
Measures partial pressure of CO2 in arterial blood
Is a parameter that is related to respiration
PaO2
Measures the partial pressure of oxygen in arterial blood
Is a parameter which uses oxygenation in respiration
HCO3
Measures basic component of acid-base equilibrium
Acute or chronic process
Anion gap
To maintain electroneutrality

 Positive load (cations) must equal negative load (anions)

If not, normal anion gap is 8-16 mEq/L calculated by:
Na Cl HCO3
Metabolic acidosis
When HCO3 decreases, pH decreases = acidosis
The body tends to increase the level of ventilation (hyperventilation) and
the CO2 decreases
pH < 7.35
HCO3 < 22 mEq/L
PaCO2 < 35 mmHg (if there is compensation)
Uncompensated metabolic acidosis (compensated)
pH < 7.23 (7.32)
PaCO2 = 35 mmHg (< 27 mmHg)
HCO3 < 19.2 mEq/L (< 13 mEq/L)
Etiology
Loss of bicarbonate d/t diarrhea
Excessive production of organic acids d/t hepatic diseases a/o
endocrine alterations
Shock
Intoxications d/t drugs (salicylates)
Inadequate excretion of acids d/t renal insufficiency
Parenteral nutrition
S/S
Rapid & deep breathing
Fruity breath
Hypotension
Ventricular arrhythmias
N/V
Deterioration of level of consciousness, headache, confusion, & coma
TX
Correct the cause of acidosis
Correct the input of deficit of bases (input of bicarbonate if pH < 7.2)
Complications
Hypovolemic shock, septic shock
Hyperchloremia
Deficiency of insulin
High-output diarrhea
Terminal phase of renal failure
Fistula (pancreatic, duodenal, ileal)
Non-adaptive ileostomy
Metabolic alkalosis
If bicarbonate increases & produces an increases of pH, and is produced by
an increases in bases or HCO3
The body produces hypoventilation by increasing the level of CO2

 pH > 7.45
HCO3 > 26 mEq/L
PaCO2 > 45 mmHg (if there is compensation)
Etiology
Loss of acids d/t prolonged vomiting or gastric aspiration
Loss of K+ by increase in renal excretion (w/ diuretics)
Alkaline antacids
S/S
Slow & shallow breathing
Muscular hypertonia
Restlessness
Fasciculations
Confusion
Irritability
Coma
TX
Administration of NaCl or KCl depends on the severity of
hypokalemia, before cases of severe or persistent alkalosis can require
NH4Cl
Complications
Hyperchloremic
Loss of chloride
Gastric aspiration
Vomiting
Cerebral edema
Respiratory acidosis
When bicarbonate increases, pH decreases
The organism increases bases, eliminates acidic urine by the kidney,
pH < 7.35
HCO3 > 26 mEq/L (if there is compensation)
PaCO2 > 45 mmHg
Uncompensated respiratory acidosis (compensated)
pH < 7.22 (7.36)
PaCO2 > 70 mmHg
HCO3 > 27.4 mEq/L
Etiology
CNS depression d/t drugs, lesions, or illness
Asphyxia
Hypoventilation d/t pulmonary disease, cardiac disease,
musculoskeletal disease, or neuromuscular disease
S/S
Diaphoresis
Headache
Tachycardia

TX

Confusion
Nervousness

Treat the disease

Mechanical ventilation in severe forms a/o accompanied by hypoxemia
Assisted ventilation before a chronic hypercapnia is indicated only if
there is an acute increase in PCO2
Respiratory alkalosis
If the bicarbonate decreases & CO2 also decreases d/t hyperventilation,
there is an increase in pH
pH > 7.45
HCO3 < 22 mEq/L (if there is compensation)
PaCO2 < 35 mmHg
Etiology
Hyperventilation for pain, anxiety, or inadequate use of ventilator
Respiratory stimulation for drugs, asthma, hypoxia, fever
Hepatic insufficiency
Exercise
Uncompensated respiratory alkalosis (compensated)
pH > 7.53 (7.38)
PaCO2 < 23 mmHg
HCO3 < 18.7 mEq/L (< 14.2 mEq/L)
S/S
Rapid and deep breathing
Paresthesia
Anxiety
Fasciculations
TX
First treat the cause
Then treat the hyperventilation w/ sedatives or have the patient breathe
into a brown paper bag
Complications
Sepsis
Pneumonia
Thoracic trauma
Pain
Hyperthermia
Anxiety
Tachycardia
Hepatic failure
Mechanical ventilation
ABG
Renal compensatory conditions or primary respiratory situations, are slow
to be evident w/in 48 hours, however respiratory compensation to

metabolic abnormalities subsequent to primary metabolic alterations are

done in a matter of minutes, given the large volume of CO2 that is managed
by the lungs in the short term
Acidosis
Alteration of electrical status of multiple proteins
Enzymatic systems fail
Hyperkalemia
Hyperchloremia
Alterations in state of consciousness
Muscular weakness
Failure of cardiac rhythm
Coronary & cerebral vasodilation
Pulmonary vasoconstriction
Decrease in RV pressure
Myocardial depression
Alkalosis
Tetany (reduction of Ca++ ions)
Hypokalemia (entry of K+ into ICF)
Coronary & cerebral vasoconstriction
Pulmonary vasodilation
Diaphragmatic depression
Hypokalemia & Hypochloremia
Surgery
Acid-base disorders most frequent in surgical patients is metabolic acidosis
Non-lethal acid-base disorders in surgical patients are metabolic alkalosis
& respiratory alkalosis
ORGANIC RESPONSE TO SEVERE LESION
Response to lesion
Set of organizational changes that occur during the process of
convalescence following an organic lesion.
In what is lost in the acute form, the local & systemic homeostasis, and
the favorable circumstances, permitting anatomical, functional, and
psychic re-establishment:
Physiologic field
Series of events aimed at restoring homeostasis & repairing the
tissue damage as quickly as possible
Courses w/ a self-immune response, but do not develop SIRS
Express clinically the presence of generalized systemic
endothelial inflammation, independent of the productive
cause
3 or more of the following conditions
Temperature > 38 or < 36
HR > 90/min
Respiratory rate > 20/min or PaCO2 < 32

 WBC > 12000 or < 4000 or 10% bands

w/ a duration of 5-10 days from surgery, ADH & aldosterone
levels returned to normal & to recover and a tenth of cortisol
recuperates its circadian rhythm of secretion
Pathophysiologic field
Set of events, beyond the horizon of their physiological
development & lead to the extremes of the body:
Immunologic dissonance
Hypercatabolic state
Cardio-circulatory instability
Consisting of all previous events that decimate the functional
reserve, to the extent that the response itself becomes a threat
to life
Etiology of acute & deep loss of homeostasis
Severe accidental lesion
Multiple trauma
Severe burns
Extensive elective lesions
Transplants
Surgical TX of cancer
Surgical control of abdominal sepsis
Orthopedic surgery of extremities under ischemia
Hip surgery
Colon surgery
Cardiac surgery w/ extra-corporeal pump
Severe disease
Shock
Sepsis
Organic failure: renal, hepatic, intestinal
Acute respiratory failure
Pneumonia
Severe asthma
Acute pulmonary edema
Decompensated COPD
Severe disease
Extensive tissue infarct
Severe intoxications
Systemic vasculitis
Cancer in advanced stages
DKA
Severe pancreatitis
AIDS
Triggers therapeutics
Blood-derived transfusions

 Idiosyncratic & drug response

Anaphylaxis
Malignant hyperthermia
Epidermal necrolysis
Immunotherapy, chemotherapy, a/o radiotherapy
Prolonged transoperative hypotension
Alveolar recruitment
Thrombolysis (follows w/ ischemia-reperfusion)
Metabolic response to trauma
Ebb phase
Defend homeostasis (perfusion volumes, pH)
3-24 hours
Decreased balance of N2
Diminished tissue perfusion
Cold, clammy skin
Slow capillary filling
Diminished central temperature
Flux phase
Lesion has priority: mobilization of protein stores
1-14 days
Catabolic phase
Increased metabolic load
Decreased balance of N2
Lesion & body have priority: reconstitution of protein stores
Weeks
Anabolic phase
Increased balance of N2
High cardiac output
Hypermetabolism
Increased energy output
Accentuated protein catabolism
Pathophysiology of the problem (sepsis)
The monocyte-macrophage system is being stimulated by bacteria or its
products, and secretes inflammatory mediators or pro-inflammatory
cytokines including TNF, IL1, IL2, IL6, IL8
Simultaneous secretion of anti-inflammatory cytokines such as IL4,
IL10, w/ the goal of modulating of action of pro-inflammatory
cytokines
Monocytes release an inflammatory response
Pro-inflammatory = SIRS = death
Balanced response = resolution
Anti-inflammatory = CARS = death
Apoptosis & necrobiosis
The type of cellular death determines immunologic function of

surviving cells (CD4 T cells)

Apoptotic cells: induce anergy or presence of anti-inflammatory
cytokines & block the immune response: auxillary Th2 cells & IL4 &
IL10
Necrotic cells: Induce an inflammatory state creating an immune
response & incrementing antimicrobial defenses: Th1
Neuroendocrine response
Physiologic
Retain Na & water for guaranteeing circulating volume
Maintain catabolism of macromolecules that provide substrates for
synthesis of energy, conservation of acid-base state
Modulate the immunologic response, maintenance of epithelial barriers
& reparation of sites of lesion
Nutrition
Set of interconnected factors to achieve:
Homeostasis
Energy
Growth
Restoration of organism
The nutrition of human organism, depends on cellular metabolism which
consists of 2 fundamental phases
Anabolism
Biosynthesis of macromolecules
To grow & maintain structure (proteins)
For caloric-energy reserve (glycogen, lipids)
Catabolism
Oxidation of nutrients for the production of energy (AcCoA + O2 =
ATP) and the elimination of waste products (CO2, NH2)
Nutrition in fasting & stress (trauma, surgery, sepsis)
The stimulus of the neural & endocrine systems block the adaptation &
establish a hypercatabolism, which in these situations is proportional to
the magnitude of stress
Greater requirement for glucose, fat, and protein for muscle repair
of injured tissues
The effects of catabolic hormones will be reflected in the
proteolysis
Increments of Basal Energy Needs following type of stress:
Elective surgery: 10-25%
Trauma: 10-30%
Sepsis: 50-80%
Burns: 100-200%
Complications of malnutrition
Delay of scarring
Depression of immunocompetence
Decrease in resistance to infection

 Sepsis
Death
CV response
Physiologic
Adequate flow & perfusion pressure to organic demand
Its ability to generate pressure produces interstitial fluid continually w/
continual flow, carrying oxygen & energetic substrates of cells
Transporters & mediators leads to the elimination of substances
Intravascular volume depletion and hypotension
Generalized or localized reduction in renal blood flow = ischemic ARF
GI, renal, and dermal losses: hemorrhage, shock
Large vessel renal vascular disease
Renal artery thrombosis/embolism, operative arterial crossclamping, renal artery stenosis
Small vessel renal vascular disease
Vasculitis
Atheroembolism
HUS
Malignant hypertension
Scleroderma
Preeclampsia
Sickle cell anemia
Hypercalcemia
Transplant rejection
Sepsis
Hepatorenal syndrome
Medications
Cyclosporine
Tacrolimus
ACE inhibitors
NSAIDs
Radioconstrast agents
Amphotericin B
Decreased effective intravascular volume
CHF
HF
Cirrhosis
Nephrosis
Peritonitis
Immunoendothelial response
At the local level, limits the damage, destroys infecting agents, removes
dead tissue, and limits necrosis & apoptosis
Promotes local hemostasis & tissue repair
At the systemic level protects the body against invasive pathogens

 Pathophysiology (in sepsis)

Bacterial aggression, triggers a series of immunologic responses to
combat the aggression that also causes damage to the body
Vascular endothelium
Rolling mediated by selectins
PMN: L-selectin
Endothelium: P/E-selectin
Firm adhesion mediated by integrins
PMN: LFA-1, Mac-1
Endothelium: ICAM-1, VCAM-1
Transmigration
PECAM, VLA-4
Identification of organic dysfunction like markers of severe sepsis
Altered consciousness, confusion, psychosis
Tachypnea
PaO2 < 70 mmHg
SaO2 < 90%
PaO2/FiO2 < 300
Icterus
Positive enzymes
Decreased albumin
Increased PT
Tachycardia
Hypotension
Decreased central venous pressure
Oliguria/anuria
Increased creatinine
Decreased platelets
Increased PT
Decreased protein C
Increased D-dimers
LIQUIDS & ELECTROLYTES
Homeostasis is maintained by coordinated action of hormonal adaptations
TBW (50-75%) of body mass, and changes w/ sex, age, & fat content
In newborns, 75-77%
In children 1-12 months, 65.5%
In children 1-10 years, 61.7%
In adults, b/w 50-60% of body mass
In relation to sex, in adolescence, there is a greater water content in
males d/t the higher fat content in women
ICF represents 40% of mass
ECF represents 20% of mass
Plasma constitutes 5% of mass

 Interstitium constitutes 15% of mass

Transcellular fluid (lymph, peritoneal, pericardial, pleural, CSF) 1-2%
Regulation of body water
Regulation of entry & excretion
Thirst, which is regulated by the medial hypothalamic center, is a major
defense against depletion of liquid & hypertonicity
Kidneys: RAS & ADH
Excretion of body water is regulated by a variation in the rhythm of
urinary flow
ADH or vasopressin
Controls reabsorption of water in renal tubules
Regulates hydroelectrolytic balance of body fluids
Increases cellular permeability in distal tubules & in collecting
ducts
Decrease formation of urine
Sufficient kidney is a major ally to a patient undergoing inadequate
management of liquids & electrolytes
The kidney is the effector organ in the response to loss of
hydroelectrolytic homeostasis
The kidney makes fine adjustments on the volume of body water &
electrolyte concentration
Effective circulating volume
The proportion of circulating volume that inhibits compensatory response
of homeostatic receptors
Entry
Liquids: 1200 ml
Food: 1000 ml
Metabolic: 350 ml
Loss
Urine: 1500 ml
Passive loss: 900 ml
Sweat 50 ml
Feces 100 ml
Electrolytes
Cations in body water include Na, K, Ca, Mg
Na+
Excreted via the kidneys & via skin by sweating
Excreted in great quantities when body temperature is high, during
exercise, fever, or emotional tension
Hyponatremia < 135 mEq/L
Causes
Pseudo-hyponatremia induced by active osmotic molecules
(glucose, mannose, glycine)
Provoke a displacement of water, w/o altering the

quantity of sodium, which decreases the concentration

(dilutional hyponatremia)
An increase of 100 g/dL glucose provokes a decrease
in 1.7 mEq/L of Na
Pseudo-hyponatremia induced by active non-osmotic
molecules (TG, proteins)
These molecules reduce the relative % of water in a
determined volume of plasma
Elevation of 1 g/dL of TG decreases natremia by 1.7
mEq/L
Elevation of 1 g/dL of plasma proteins cuases a
decrease in natremia of 1 mEq/L
Loss of Na
Renal
Diuretics
Osmotic diuretics
Hypoaldosteronism
Nephropathy w/ salt loss
Diuresis
Postobstructive
Digestive
Vomiting
Drainage tube
Fistulas
Obstruction
Diarrheas
Cutaneous
Sweating
Burns
Drugs
Physical exercise
CNS alterations: hemorrhage, astrocytomas,
hypopituitarism
S/S
GI: N/V
Peripheral nervous system: muscle tremors, visual
alterations
CNS: lethargy, convulsions, coma
TX
Hyponatremia w/ diminished ECF
Administration of isotonic saline solutions
Na = (140 mEq/L Na actual) x (0.6 x weight)
Hyponatremia w/ minimally increased ECF
Initial TX is based on restriction of fluids

 In the presence of neurologic symptoms, administer

hypertonic saline solution (20%) along w/ small doses
of loop diuretics (furosemide)
For more severe cases, administer urea at 10-30%
which provokes osmotic diuresis
Hyponatremia w/ increased ECF
Characterized by the presence of edema, and is related
with HF, nephrotic syndrome, and cirrhosis
TX is based on restriction of liquids & salt along w/
administration of loop diuretics
Hypernatremia > 150 mEq/L
Pathophysiology
Insufficient action of ADH
Deficit of central production
Loss of renal response
Excessive loss of water
Renal
Extra-renal
Positive salt balance
Iatrogenic
Primary hyperaldosteronism
S/S
Thirst
Can be accompanied by polyuria
Diarrhea
Sweating
Neurologic disorders
TX
Objectives
Correct triggering cause
Correct osmolarity
Normalization of ECF
Hypernatremia w/ hypovolemia
Isotonic solutions until no signs of dehydration
Continue to use hypotonic solutions until correction of
hypernatremia
0.45% saline solution
5% dextrose solution
Hypernatremia w/o hypovolemia
Water PO
If not possible, parenteral 5% dextrose
K+
Renal excretion is accelerated w/ ACTH & cortisone
Increased serum concentration of K+ produces a clinical effect on

cardiac muscle
Decreased ECF concentration of K+ produces weakness w/ loss of
smooth & striated muscle tone, along w/ circulatory failure
Hypokalemia < 3.5 mEq/L
Severity
Mild: 3-3.5 mEq/L or a deficit of 150-300 mEq
Moderate: 2.5-3 mEq/L or a deficit of 300-500 mEq
Severe: < 2.5 mEq/L or a deficit of > 500 mEq
Causes
GI loss: diarrhea, laxatives
Renal loss: hyperaldosteronism, K+-wasting diuretics,
penicillin, Amphotericin B
Intracellular changes (alkalosis)
Malnutrition
S/S
Weakness, fatigue
Paralysis, respiratory difficulty
Muscle disorder (rhabdomyolysis)
Constipation
Paralytic ileus
Leg tremors
TX
Minimize extensive loss of K+ & replace K+
Administration of IV K+ is recommended when
arrhythmias are present or hypokalemia is severe
When indicated, max replacement of K+ IV is 1020 mEq/h w/ continuous ECG monitoring
Hyperkalemia > 5.0 mEq/L
Repeat test
Confirm test w/ ECG
Peaked T wave
Short QT interval
Fat QRS complex
Slow conduction velocity
TX
Average elevation (5-6 mEq/L): remove K+ from body
Diuretic: Furosemide 1mg/kg IV slow infusion
Kayexalate: 15-30 in 50-100 mL of 20% sorbitol
solution
Dialysis: peritoneal or hemodialysis
Moderate elevation (6-7 mEq/L): change ICF K+
NaHCO3 50 mEq IV
Glucose-insulin IV
Albuterol nebulizers 10-20 mg

 Severe elevation (> 7 mEq/L)

10% CaCl2 at 5-10 mL IV over 2-5 minutes
50 mEq IV NaHCO3 for over 5 minutes
Glucose-insulin IV
Albuterol 20 mg
Diuresis (40-80 mg IV furosemide)
Kayexalate enema
Dialysis
Anions in body water include Cl-, HCO3-, HPO4 Organ monitor of hydro-electrolytic disorders
Of volume
Substance: water
Organ: kidney
Manifestation: oliguria, anuria
Of concentration
Substance: sodium
Organ: brain
Manifestation: coma
Of composition
Substance: potassium
Organ: muscle
Manifestation: ileus, arrhythmias, weakness
Increase in requirements
Increase HR
Postural changes in pulse
Hypotension
Decrease in diuresis
Decrease in capillary filling
Lab data: Na, urea, osmolarity
Hydro-electrolytic management
Delay recuperation of patients
Is a frequent cause of morbidity
Is a cause of death
MC in surgical patients
Combined depletion w/ dehydration
Depletion vs dehydration
Depletion (dehydration)
Affects intravascular & interstitial space (ICF &
interstitial)
Loss of isotonic fluid (hypotonic)
Fast velocity of development of disorder (slow)
Shock hemodynamic state (normal)
Fluid therapy w/ isotonic solution (w/ hypotonic solution)
Velocity of TX in minutes (infusion in hours)

 Hyponatremia
Hypokalemia
Loss in surgical patients
Internal loss
Sequestration of liquids
Severe pancreatitis
Sepsis
Metabolic ileus
Intestinal obstruction
Blood loss
Transoperative hemorrhage
GI hemorrhage
Hemorrhagic phase of DIC
Fractures of the pelvis & long bones
External loss
Evaporation via integral barriers
Hyperthermia
Hyperventilation
Evaporation via loss of barriers
Extensive burns
Transoperative exposure of serous cavities
Open abdomen for management of abdominal sepsis
GI loss
V/D
Drainage or GI aspiration
Spontaneous fistulas
Crohns disease
Posttraumatic fistulas
Surgical fistulas: external derivation of biliary tree
Ileostomy, colostomy, jejunostomy, duodenostomy
Loss d/t drains
Peritoneal drains
Pleural drains
Drains in spaces created by surgical dissection
UTI loss
Osmotic polyuria (mannitol, hyperglycemia)
Use of diuretics
Fluid therapy: restoration of liquids
Fluid therapy in shock is based on the rescue & maintenance of renal
function, considering diuresis as a monitor of perfusion
Depending on the type & rate of loss, establish the type & speed of
replacement
The correction of intravascular volume depletion must be made
in minutes, while a hydro-electrolytic correction (which is not

life-threatening) must be made w/in 24-48 hours

In patients w/ hypovolemia, 50% of the volume is given in the
first administration, and then given in thirds or quarters
Crystalloids
Establish circulating volume (Na concentration)
Short half-life (30-40 sec)
Spread to interstitium (edema)
Dilution of plasma proteins
Contains water, electrolytes, a/o sugars
Prepared
NaCl 0.9%
Dextrose 5%
Ringers lactate
Colloids
Increase plasma osmotic pressure & retain water in intravascular
space
Prolonged half-life
Establish circulating volume
Natural colloids
Plasma
Albumin
Hyper-oncotic
Half-life of 24 hours
High cost
Risk of anaphylaxis
Synthetic colloids
Gelatin: half-life of 4-5 hours
Haemaccel: 330-390 mmHg
Gelofusin: 465 mmHg
Dextran
Dextran 40
Dextran 70
Heta-almidon
Penta-almidon
Combination of crystalloids & colloids
Parameters of suspending liquids
Decrease in HR below 120
BP
Normal urinary flow
High pressure of filling
Acute loss
Pathologic: replenish volume-by-volume w/ Hartmann solution
Insensitive: 0.5 ml/kg/hr + 10% for each C of temperature above 38C
Care in management w/ liquids

 H2O: During input of load, can auscultate frequently wheezing in the

pulmonary fields that can indicate volume overload
Na: The correction of sodium is not done rapidly, but the max changes per
day in serum sodium concentration is 8 mEq/L/d for women (10 for men)
K: Via peripheral vein, the max concentration of K per L of solution is 40
mEq/L, and the max velocity of input is 10 mEq/hour. No input of K+ in
the immediate postop period
Dextrose: in patients w/ metabolic response in the lesion, 100 g/d of
dextrose limits 50% of catabolism of proteins (Gamble principle), which
is approximately 1.5 g/kg/day. In cases of hyperglycemia, dextrose
solutions can initiate when the glucose level reaches 250 mg/dL, and an
insulin scheme is established
NUTRITION IN THE SURGICAL PATIENT
40-70% of hospitalized patients in any moment, have malnutrition
MC is marasmus-type malnutrition (protein-caloric malnutrition)
Input of preop nutrition during 7-10 days diminishes morbidity & mortality
associated w/ surgery
Surgical patients present 3 problems in basic nutrition
Secondary malnutrition to prolonged postop fast related to postop
complications
Chronic malnutrition in surgical candidates that have lost weight as a
consequence of their disease
High energy demands in polytraumatic & burn patients, due to the severity
of their disease
Transcendence of salvation of proteins
Intestinal mucosa, immune system, and renal metabolism requires high
quantities of glutamine
Proteins meet a un-substitutable biologic function
Its consumption to obtain energy corresponds to loss of specific
functions
Malnutrition
Any state in which nutritional deficit affects health
Disorder of body composition characterizes by excess of ECF & deficit of
muscle mass
Causes of malnutrition in surgery
Previous & prolonged situation of fast & semi-fasting
Uncompensated increase in nutritional requirements taxing the disease
Malattention on the part of professionals in attending to the patient
Complication of medical/surgical TX of disease
Nutrients administered via an inadequate route
Consequences of malnutrition
Affect musculature
Affect function of respiratory muscles
Facilitate the presence of cardiac abnormalities (loss of muscle mass &

decrease in CO)
Harmful effects over mass & function of enterocytes & colonocytes
Delay of scarring of wounds
Alter immune response
Evaluation of nutritional status
Capacity of protein synthesis
Visceral: pre-albumin, transferring
Muscular: nitrogen balance
Immunity
Lymphocyte count
Response to Ag
Markers of inflammation
Organic reserve
Fat: impedance
Muscle: force
Visceral proteins
The mass of visceral proteins can be evaluated from serum concentrations
of transport proteins synthesized in the liver
Albumin is easy to determine
2.8-3.5 g/dL = mild malnutrition
2.1-2.7 g/dL = moderate malnutrition
< 2.1 g/dL = severe malnutrition
Preoperative nutritional support
Conserve or improve nutritional status before surgery
Diminish perioperative morbidity & mortality
Prevent postoperative malnutrition
Prevent depletion in hypercatabolic states
Contraindications
Hemodynamic instability
Not recuperable patient
Parenteral nutrition
Administration of nutrients via venous route w/ specific catheters to cover
the energy needs & maintain an adequate nutritional status in those patients
where enteral route is inadequate, insufficient or contraindicated
TPN = when it is the only input of nutrients
PPN (partial parenteral nutrition) = when other inputs of nutrients as well
The complications in perfusion of parenteral nutrition are related to the
catheter, the manipulation of system, and the solution of parenteral nutrition
Peripheral parenteral nutrition
In smaller veins
In relatively low requirements
For short time (max 2 weeks)
Indications
Intestinal inflammatory diseases

Malabsorption syndrome
Pancreatic insufficiency
Gastrectomy
Radiotherapy & chemotherapy
Central parenteral nutrition
Used in patients w/ greater requirements
Resectable gastric cancer, in which you can recuperate nutritional
status as fast as possible
In ICU
Digestive indications
Neonatal, congenital, or acquired pathologies
Surgical interventions
Intestinal malabsorption
Severe acute pancreatitis
Post-chemotherapy, post-radiation
Intestinal pseudo-obstruction
Irreversible vomiting
Cheilous ascites
Chylothorax
Extra-digestive indications
Hypercatabolic state: sepsis, polytruauma, burns, neoplasias,
transplants, cachexia
Pre-term newborns of low weight
Visceral failure: hepatic insufficiency or acute renal insufficiency
Oncology: severe mucositis
Proteins
In fasting, catabolized 75g of muscle protein
Need to ingest 1-1.5g of protein per kg to maintain reserve
6.25 g of protein contains 1 g of nitrogen
CHO
Constitutes 50% of caloric input in diet
Each g of monohydrate dextrose inputs 3.4 calories
W/ administration of 100-150 g of glucose in fasting, which is 50% of
protein
Lipids
Require 25g to favor absorption of lipid soluble vitamins
In fast, break down 160g of fat in 24 hours
Oxidation of 1g of lipids yields 9 Kcal
Oligoelements: Zn, Cu, Cr, Se
Deficit of zinc doesnt help wound scarring
Cr potentiates action of insulin
Se is an antioxidant
Mn is a procoagulant
Iron

 Men: 1000mg (women: 300-500mg)

Parenteral dosage is 0.5-1.0 mg/day
Vitamin C
Cofactor in collagen synthesis
Participates in tissue reparation
Standard formulas
Dextrose = 10-25% of central parenteral nutrition (5% of peripheral)
AA = 4.25% of central parenteral nutrition (same)
Na+ = 36.5 mEq/L or a K+ = 36.5 mEq/L
Advantages of parenteral nutrition
100% absorption
Continuous infusion
Very complete
Does not use digestive use, which is still useful in a specific group of
patients
Disadvantages of parenteral nutrition
Alter the quality of mucosa & intestinal transit, producing bacterial
translocation & problems of eating later
More expensive: require major manipulation, monitorization & special
physical place
Complications are grave, w/ infection of the central venous catheter, w/
sepsis for nosocomial microorganisms
Require change in all of central venous system
Increment of caloric dose
Elective surgey = 10% of stress factor
Trauma = 10-30% of stress factor
Sepsis = 50-80% of stress factor
Enteral nutrition
Technique to support nutrition which consists of administration of nutrients
Directly into GI tract, find tube in liquid environment
Indications
GI tract is functional but
Not able to use optimally nutrients PO
d/t severe D, short intestinal syndrome
If the needs are extremely increased and the patient cannot cover
them w/ ingestion
burn patients, malnutrition
When the patient cannot swallow
Advantages
Most physiologically normal means of input
More trophic stimulation of GI tract
Cheaper
Easier to care for
Require less invasive procedures for the patient

 Contraindications
Intestinal obstruction
Intolerance to formula
Diarrhea
Gluten enteropathy
Hypoperfusion
Routes of choice
NG tube
Trans-pyloric tube: nasoduodenal or nasojejunal
Gastrostomy
Percutaneous endoscopy
Radiology
Surgery
Jejunostomy
Types of solution
Polymeric
Ensure/ Ensure fiber
Osmolite 1 cal/cc (low osmolarity)
Pulmocare (low in CHO high in proteins)
Glucal Bott (low in CHO)
Nephro, Suplena (nephropathy)
Advera (1 cal/cc)
Alitreg (metabolic distress)
Sevite 1 cal/cc (low osmolarity, to correct D or constipation)
Peptidic: when proteins are hydrolyzed
Elemental: when proteins are in the form of AA
Complications
Bronchoaspiration
Infectious
Metabolic (inadequate nutrients)
Mechanic (obstruction of NG tube)
For specific pathologies
Hepatic: decrease dosage of lipids or suppress input
Pneumo: decrease CHO & increase lipids
Renal: decrease input of proteins, Na, K, P, Mg
Sepsis: increase immuno-nutrients, input AA for catabolism
Immuno-nutrition
Arginine
High demand in catabolic states and in growth
Improves the response of T cells to mitogens
Improves the response to late sensitivity
Glutamine
Energetic substrate of enterocyte

 Its precursor, glutamate, represents 61% of AA in plasma

Favors support of enteral mass & mucosal integrity
Nucleotides
Forms part of nucleic acids
Are necessary for production of T cells, epithelial cells, &
interleukins
Omega-3 FA
Does not produce Immunosuppression of
Burns: increase proteins and non-protein calories