By Dr Lee June Lyng

OUTLINE
y Physiolo ical cha

es y Classificatio a d defi itio of hyperte sive disorders of pre a cy y Pathophysiolo y y Ma a eme t i pre-eclampsia a d eclampsia y RA or GA

MATERNAL CHANGES DURING PREGNANCY

1.

CVS changes:
1.

Aortocaval a d IVC compressio (s pi e)

d/t compressio by pre a t ter s Thus, decreased VR a d CO ecreased place ta blood flow a d causes fetal hypoxia Mater al dizzi ess, ausea, vomiti , A kle edema, varices

y I creased i CO y d/t i creased SV a d HR y

y I travascular fluid

volume i creases
y Relative a emia i pre

CSF pressure i creases duri uteri e co tractio thus, re io al a aesthetic mus t ive duri uetri e co tractio

2. Respiratory changes: y Capillary engorgement

y The upper respiratory

of respiratory tract.
y The mucosa of the

nasopharynx, larynx, trachea and bronchi are congested.

y Increased risk of obs fr

tract must be treated very gently especially during intubation and suction.

tissue edema and bleeding with instrumentation

y Minute volume

increased by 50%
y d/t increased tidal

y FRC(functional

volume and respiratory rate

residual capacity) decreased

y d/t exp reserve

volume(ERV) and RV Affects the changes in alveolar decreased decreased

concentration

So,both induction and recovery from an inhalation agents are faster

y Anesthetic implication y During induction of GA, PaO2 decreases rapidly d/t decreased FRC and increased O2 intake(increased metabolic rate) y Thus, it is important to administer O2/preO2 prior to GA

3. GI Changes y A raised intragastric pressure at term y A delayed gastric emptying time and reduced esophageal sphincter
y

Increased risk of GERD and aspiration Used of aspiration prophylaxis

4. Renal changes y increased GFR with an increase in urine output and a decrease in the UN. y Decreased tubular resorption of both protein and glucose
y Increased protein and

glucose excretion

y Fluids and elecrolytes y Sodium and water retention occur during pregnancy y The IV fluid of choice is Hartmann s solution, or 0.9% saline. y Avoid dextrose 5% esp in pre-eclampsia

Classification of hypertensive disorders in pregnancy

Disorder PIH definition Hypertension after 20 wks of POG and settles within 6 wks of delivery, characterized by a rise in P > 140/90 Chronic HPT diagnosed b4 pregnancy or earlier than 20wks of POG and persisting after delivery, characterized by a rise of P> 140/90 s above Subtype Gestational HPT preeclampsi a

Preexisting HPT

Preexisting HPT superimposed with preeclampsia Eclampsia

Generalized convulsions during hypertensive pregnancy, labour or within 7days of delivery( presence of fits may not correlate with degree of HPT

Pre eclampsia
y Pre eclampsia are y It is a SYNDROME y The clinical spectrum

common in :
y Primigravida y Chronic hypertension y GDM/preexisting DM y Obesity y Pre-eclamptic family

ranges from mild to severe

history y Multiple gestation

Mild Pre-eclampsia
y Definition y BP > 140/90 after 20 weeks of POG with previous normal BP y Proteinuria defined as urinary excretion of 0.3g protein or higher in a 24 hour urine specimen(>1+ on urine dipstick)

Severe pre-eclampsia
y Definition: y BP>160/110 or higher on 2 occasions at least 6 hours apart while pt is on bed rest y Proteinuria
y y

y oilguria <500 ml in 24 y y y y y y

>5g in 24 hr urine >3+ on dipstick

hr Cerebral or visual disturbances Pul edema Epigastric pr rt upper quadrant pain Impaired liver fx Thrombocytopenia Fetal growth restriction

Factors differentiating mild from severe pre-eclampsia

mild SBP DBP Urine protein Urine output Epigastric pain or rt upper quadrant pain Pulmonary edema Headache Visual disturbances Platlet count HE P >140 >90 >0.3g/24hr dipstick + or 2+ >500ml/24hr no no no no >100,000/mm3 no Severe pre eclampsia >160 >110 5g/24hr dipstick 3+ or 4+ 500ml/24hr Yes Yes Yes Yes <100,000/mm3 Yes

Pathophysiology
y Placenta y Failure of secondary invasion of trophoblastic tissue to myometrial segments of spiral artery
y

 Normal, y Replacement of smooth muscle and endothelium of spiral artery with trophoblastic tissue
y Become refractory to all

eading to vasospasm of spiral artery

vasocontrictor factors
y Decreased uteroplacental

flow y Widespread endothelial damage

y d/t vasospasm of spiral artery, it causes endothelial dysfx y Thus, released of

y thromboxane(powerful

y Platelet aggregation and

thrombin activation
y y

vasospasm and platlet aggregration y Increased sensitivity to angiotensin y Decreased prostagladins, antioxidants, EDRF(endothelial derived relaxing factor) wic normally causes vasodil.

Fibrin deposit in capillary bed thrombosis

y CVS y Increased myocardial contractility y Vasoconstriction causing hypertension and hypoperfusion y Oedema secondary to leaky capillaries and salt retention
y

y Respiratory y laryngeal edema with potential difficult airway y pulmonary edema

y

non cardiogenic
y

d/t endothelial dysfx and increased in HP

Decreased COP(protein loss to renal and tissue) Cap endothelial damage(increased cap permeability) Dilated cardiomyopathy

Cardiogenic
y

y Renal y Arterioalar vasospasm

y y y

Decreased GFR Oliguria and proteinuria Increased risk of ATN if hemorrhage, hypoxia or HE P

y Hematology y Thr will be increased of fibrin, fibrinogen and platelet turnover

y

y y

Platelet reduced d/t thrombosis Increased risk of DIC Better avoid spinal anaesthesia esp if platelet <75k d/t spinal hematoma

y Hepatic y Intravascular deposits of fibrin in liver sinusoids causes periportal necrosis

y

Increased transaminase and DH

y Neurological y Cerebral vasospasm and thrombosis y Uncontrolled HPT leading to hypertensive encephalopathy
y y y y

iver distension from blood flow obstruction in HE P

y y

Hepatomegaly Epigastric/RUQ pain

Seizures Headache Blurred vision microinfarction

y HE P syndrome y Hemolysis y Elevated y Liver enzymes y Low y Platelets

y RUQ pain y Nausea and vomiting y Edema y DIC y Risk of liver rupture

75% mortality

Management
y Aim of treatment: y Control of BP y Prevention of eclampsia y Fluid resuscitation y Assessment of urgency and delivery of baby y Multidisiplinary approach y Involved obstetric, anaesthetic and paediatric teams y CURRENT Y, DEFINITIVE treatment is DE IVERY

OF BABY!!!!

Immediate management
y ABC y Airway

y Maintain the airway, using airway adjuncts as

necessary, position patient on the left side, give oxygen via face
y Breathing y Increased RR early sign of pul edema y Auscultate to exclude pul edema

y Circulation y Measure BP, PR, O2 saturation y IV access y Bl Ix- FBC, RP, PT/INR, GXM, uric acid, FT y Insert CBD monitor urine output
y

y Disability y Any IE sx y Assess reflex, looking for clonus, perform fundoscopy

If oliguric,( < 30ml/hr), consider a modest fluid challenge(250 ml 0.9%NS)

Principle of treatment
1. Control of BP y Considered invasive BP mnitoring y Aim MAP 100-140 mmHg
y

Sudden drop may compromise placental perfusion

y y

Non severe HPT oral agents Severe HPT- IV route

BP control
y Non severe HPT: y defined as BP 140-159/90-109 mmHg y most guidelines recommend lowering of non-severe blood pressure to levels of SBP 140-150/DBP 90-100 y Eg:methyldopa, labetalol, nifedipine

BP control
y Severe HPT: y defined as systolic 160 mmHg or diastolic 110mmHg y BP should be lowered to levels of SBP 140-150/DBP 90100 at a rate of 10-20 mmHg every 10-20 minutes y The choice should be made on clinician familiarity and experience with a particular agent y Particular care should be taken to avoid precipitous falls in BP which may induce maternal or fetal complications as a result of falling below critical perfusion thresholds. y EG:hydrallazine, labetolol, nifedipine

BP control
y Hydrallazine y 1st line y direct peripheral arteriolar vasodilator y slow onset of action (10-20 min) and peaks approximately 20 minutes after administration y IV bolus at a dose of 5-10 mg and admin every 20 min

y Max dose is 20 mg y

y y

OR Infusion of 40mg in 40ml of NS run at 2mg/hr and if DBP>100, increased rate by 1mg/hr(max 5mg/hr) If DBP maintain 90-100, remain at same rate & cont BP monitoring every 30min If DBP <90, reduced infusion by 1 mg/hr S/e: y headache, nausea, and vomiting y Reflex tachycardia

BP control
y Labetolol: y selective alpha blocker and a nonselective beta blocker that produces vasodilatation and results in a decrease in systemic vascular resistance y IV lab 10 mg over 1 min at least 5 min interval with max dose of 50mg

y And then infusion of 25mg/hr

y y

y y y

and titrate every 30 min until desired. Max dose: 160mg/hr Maybe given orally(100200mg PO hourly until BP controlled and maintainence dose is given 12 hrly Faster onset Decreased BP and HR No efect on uteroplacental flowno neonate hypoglycemia or hypotension

BP control
y Nifedipine y CA channel blocker y act on arteriolar smooth muscle and induce vasodilatation y The dosage of nifedipine is 10 mg PO every 15-30 minutes, with a maximum of 3 doses y Maintainence tds with max of each dose is 20mg y s/e: y tachycardia, palpitations, and headaches y Augments effect of Mg
y y

Severe hypotension Myocardial depression

y SNP y Used in severe HPT whn other medications failed y Vasodilator y Onset is rapid y May cause rebound HPT y May cause fetal cyanide toxicity

y should be reserved for

use in postpartum care or for administration just before the delivery of the fetus.

Preventions of eclampsia
2. Preventions /treatment of eclampsia y 1st line :MgSO4 causes cerebral arterial dilatation
y

y y

Indication: y Severe PE with increased irribility of CNS (headache, visual disturbances, hyperreflexia) first-line treatment for the prevention of primary and recurrent eclamptic seizures. Loading dose of 4g over 15-20 min Persistent convulsion y Further 2g over 15 min and maintain with infusion of 1g/hr for 24 hrs after last seizure Recurrent seizure y be treated with an additional bolus of 2 g or an increase in the infusion rate to 1.5 g or 2 g per hour.

MgSO4 monitoring
Mg levels(mmol/l) 0.7-1.0 2.0-3.5 >3.0 >4.0(symptomatic) >5.0 7.5-14 effects Normal level Therapeutic level Widened QRS, prolonged PR Sedation, headache, blurred vision Loss of patellar reflex Heart block, resp paralysis, cardiac arrest

MgSO4 monitoring
y Measure hourly: y Urine output: aim for urine output >120ml over 4 hours (average 30ml/hour). If low, assess for symptoms or signs of MgSO4 toxicity. y Respiratory system: stop infusion if RR <10/min and/or general condition deteriorates (drowsiness, difficulty speaking y Check patellar reflex (knee-jerk) every 2-4 hours.If knee-jerk depressed, stop infusion. y monitor serum Mg2+ levels 4-6 hrly y After delivery: check uterus is contracted and whether there is any vaginal bleeding

MgSO4 monitoring
y If any sign of overdose: y Stop MgSO4 infusion. y Call for help. y Assess and resuscitate guided by ABC. y Calcium gluconate should be available to treat
y

administer 10ml 10% calcium gluconate (1g) IV over 2-3 minutes

y For eclamptic seizures that are refractory to

magnesium sulfate, IV Diazepam and phenytoin may be used as second-line agents.

Fluid management
y Careful fluid balance y Risk of fluid overload and pulmonary edema y Guided by urine output >0.5ml/kg/hr y Preferred IV Hartmann and 0.9% NS

Timing of delivery
y Definitive treatment y Start steroids if gestation is < 36 weeks y d/w obstetrician regarding urgency of delivery y Close collaboration btw obstetric, anaesthetic and

paeds y Avoid ketamine and ergometrine

Anaesthetic problems
1. 2. 3. 4.

5.

Uncontrolled hypertension. Imminent convulsions Hypovolaemia (shift of fluid). Electrolyte imbalance: sodium may be low because of diet and diuretics. The potassium level may be low because of the use of diuretics. The foetus is premature, placental function is impaired and foetal hypoxia is likely.

6. The magnesium level in the blood may be high if oliguria is present.Magnesium is excreted through the kidneys, so if an oliguric patient has been treated with magnesium sulphate, look for signs of magnesium toxicity. Prolonged neuromuscular block is common,potentiating nondepolarising drugs. Note however that magnesium improves renal blood flow and hence urine output 7. The foetus is often depressed because of decreased placental blood flow or as a result of the drugs used in treating of the eclampsia.

8. Inadequate pain relief may cause the blood pressure

to increase further result in seizures 9. Pulmonary oedema causing hypoxia 10. Detoxification and excretion of drugs are interfered with because of impaired liver and renal function in severe cases. 11. Increased of bleeding, DIC, HELLP syn

ANAESTHETIC TECHNIQUE IN PREECLAMPSIA

y Regional techniques are superior to general

anaesthesia in pre-eclamptic patients without cerebral symptoms for the following reasons:
y Avoids difficult/failed intubation. Patients with pre-

eclampsia have increased oedema of the airway y provide maximum analgesia, eliminating the risk of pain, which can raise the blood pressure y no direct effect on the patient's heart, lungs, kidneys or liver(if the spinal is given carefully). However, coagulation tests needed.

Pre-operative care
y At least 2 large bore cannulas y Monitor vital signs until the patient is brought to the operating room.Intra-arterial monitoring is very useful in severe pre-eclampsia y Check the following: y The drugs given pre-operatively, especially the central depressants like pethidine y The time and dose of drugs given y The availabilty of naloxone y-

y Premedicate with ranitidine, metoclopramide and sodium citrate y Make sure all the equipment necessary for a general anaesthetic is available, especially suction, oxygen, airways, endotracheal tubes,laryngoscopes. y Follow the routine for a spinal anaesthetic for an obstetric patient,taking the usual precautions. Following spinal anaesthesia there maybe a large drop in the patient's BP which treated with small doses of ephedrine (3-6mg) and 250-500 ml boluses of HM

Contraindication of RA in preeclamptic
y GA is the anaesthetic of choice in all patients with y diminished level of consciousness e.g. those who have had eclamptic convulsions or are showing signs of increased cerebral irritability. y coagulation problems, y maternal haemorrhage, y severe fetal distress

GA technique in pre-eclamptic and eclamptic pt

y Assess airway as there may be damage or swelling

as a result of seizure y BP should be controlled until SBP<160 y Prepare all equipment for difficult intubation y Preoxygenate as for any emergency case y Induce anaesthesia with thiopentone (4-5mg/kg) followed by suxamethonium (1-1.5mg/kg) as per rapid sequence induction with cricoid pressure. y Ketamine is contra-indicated because it causes hypertension

y To prevent the hypertensive response during

laryngoscopy and intubation in severe pre-eclampsia

y lignocaine (1-1.5mg/kg) y fentanyl (1-1.5 micrograms/kg) or alfentanil (5

micrograms/kg).

y The neonate may need naloxone if opioids are used. y BP and intraop blood loss shld be closely monitored. y If DIC suspected, shld be corrected with cryoprecipitate, platelet, FFP and blood

y Maintain anaesthesia with small doses of a non-

depolarising relaxant and a low concentration of volatile agent. y An opioid can be given as soon as the baby is delivered. y Administered oxytocin 5u diluted to 5ml by slow IV bolus y Infusion of oxytocin 40-80 u in 500ml NS in presence of uterine atony
y AVOID ERGOMETRINE causes acute increases in BP

y At the end of surgery, reverse the neuromuscular

blockade and remove ETT whn pt fully awake and able to protect her airway

Criteria admission to ICU/HDW

y Pt has fitted y Pt is drowsy and the ability to protect her airway is in

doubt y There is inadequate reversal of neuromuscular blockade y Presence of C/F of aspiration pneumonia y Presence of DIC with hemodynamic instability y Unstable CVS: severe hyper 0r hypotension, cardiac failure, APO y Marked acidosis or low PaO2 on ABG

Postpartum Mx
y Control fluid balance y Encourage diuresis using low dose frusemide if

necessary esp if CVP cont to rise y Gradual reduction of hydralazine and/or MgSO4 y Conversion to oral hypertensive drugs y Provision of good analgesic

Take home message

y Definitive treatment y DELIVERY OF THE BABY y Drugs to control BP and

seizures y RA or GA y Multidisplinary approach

Reference
y Manual of anaesthesia by CY Lee y http://www.anzca.edu.au/fellows/sig/obstetric-

anaesthesia-sig/obstetric-anaesthesia-scientificevidence/management-of-pre-eclampsia-andeclampsia.html y http://update.anaesthesiologists.org/wpcontent/uploads/2009/09/Eclampsia-andPreeclampsia-Pharmacological-Management.pdf y http://www.frca.co.uk/article.aspx?articleid=100463