By Dr Lee June Lyng

OUTLINEPhysiological changesClassification and definition of hypertensive

disorders of pregnancyPathophysiology Management in pre-eclampsia and eclampsiaRA or GA

MATERNAL CHANGES DURING PREGNANCY1. CVS changes:

1. Aortocaval and IVC compression(supine)• d/t compression by

pregnant uterus

• Thus, decreased VR and CO

• Decreased placenta blood flow and causes fetal hypoxia

• Maternal dizziness, nausea, vomiting,

• Ankle edema, varices

Increased in COd/t increased SV and

HR

CSF pressure increases during uterine contraction thus, regional anaesthetic musnt given during uetrine contraction

Intravascular fluid volume increases

Relative anemia in preg

2. Respiratory changes:

Capillary engorgement of respiratory tract.

The mucosa of the nasopharynx, larynx, trachea and bronchi are congested.

Increased risk of obs fr tissue edema and bleeding with instrumentation

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

Minute volume increased by 50% d/t increased tidal

volume and respiratory rate

FRC(functional residual capacity) decreasedd/t exp reserve

volume(ERV) and RV decreased decreased

Affects the changes in alveolar concentration

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

Anesthetic implicationDuring induction of

GA, PaO2 decreases rapidly d/t decreased FRC and increased O2 intake(increased metabolic rate)

Thus, it is important to administer O2/preO2 prior to GA

3. GI Changes A raised

intragastric pressure at term

A delayed gastric emptying time and reduced esophageal sphincter

Increased risk of GERD and aspiration

Used of aspiration prophylaxis

4. Renal changesincreased GFR with

an increase in urine output and a decrease in the BUN.

Decreased tubular resorption of both protein and glucose

Increased protein and glucose excretion

Fluids and elecrolytesSodium and water

retention occur during pregnancy

The IV fluid of choice is Hartmann’s solution, or 0.9% saline.

Avoid dextrose 5% esp in pre-eclampsia

Classification of hypertensive disorders in pregnancy

Disorder definition Subtype

PIH Hypertension after 20 wks of POG and settles within 6 wks of delivery, characterized by a rise in BP > 140/90

•Gestational HPT•preeclampsia

Preexisting HPT

Chronic HPT diagnosed b4 pregnancy or earlier than 20wks of POG and persisting after delivery, characterized by a rise of BP> 140/90

Preexisting HPT superimposed with preeclampsia

As above

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

Pre eclampsiaPre eclampsia are

common in :PrimigravidaChronic

hypertensionGDM/preexisting

DMObesityPre-eclamptic family

historyMultiple gestation

It is a SYNDROMEThe clinical

spectrum ranges from mild to severe

Mild Pre-eclampsiaDefinition

BP > 140/90 after 20 weeks of POG with previous normal BP

Proteinuria defined as urinary excretion of 0.3g protein or higher in a 24 hour urine specimen(>1+ on urine dipstick)

Severe pre-eclampsiaDefinition:

BP>160/110 or higher on 2 occasions at least 6 hours apart while pt is on bed rest

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

oilguria <500 ml in 24 hr

Cerebral or visual disturbances

Pul edemaEpigastric pr rt

upper quadrant painImpaired liver fxThrombocytopeniaFetal growth

restriction

Factors differentiating mild from severe pre-eclampsia

mild Severe pre eclampsia

SBP >140 >160

DBP >90 >110

Urine protein >0.3g/24hrdipstick + or 2+

≥5g/24hrdipstick 3+ or 4+

Urine output >500ml/24hr ≤500ml/24hr

Epigastric pain or rt upper quadrant pain

no Yes

Pulmonary edema no Yes

Headache no Yes

Visual disturbances no Yes

Platlet count >100,000/mm3 <100,000/mm3

HELLP no Yes

Pathophysiology Placenta

Failure of secondary invasion of trophoblastic tissue to myometrial segments of spiral artery

Leading to vasospasm of spiral artery

Decreased uteroplacental flow

Widespread endothelial damage

Normal,Replacement of

smooth muscle and endothelium of spiral artery with trophoblastic tissue

Become refractory to all vasocontrictor factors

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

Thus, released of thromboxane(powerful

vasospasm and platlet aggregration

Increased sensitivity to angiotensin

Decreased prostagladins, antioxidants, EDRF(endothelial derived relaxing factor) wic normally causes vasodil.

Platelet aggregation and thrombin activation Fibrin deposit in

capillary bed thrombosis

CVSIncreased

myocardial contractility

Vasoconstriction causing hypertension and hypoperfusion

Oedema secondary to leaky capillaries and salt retention d/t endothelial dysfx

and increased in HP

Respiratorylaryngeal edema with

potential difficult airway

pulmonary edema non cardiogenic

Decreased COP(protein loss to renal and tissue)

Cap endothelial damage(increased cap permeability)

Cardiogenic Dilated cardiomyopathy

Renal Arterioalar

vasospasm Decreased GFR Oliguria and

proteinuria Increased risk of ATN

if hemorrhage, hypoxia or HELLP

Hematology Thr will be

increased of fibrin, fibrinogen and platelet turnover Platelet reduced d/t

thrombosis Increased risk of DIC Better avoid spinal

anaesthesia esp if platelet <75k d/t spinal hematoma

HepaticIntravascular

deposits of fibrin in liver sinusoids causes periportal necrosis Increased transaminase

and LDHLiver distension from

blood flow obstruction in HELLP Hepatomegaly Epigastric/RUQ pain

NeurologicalCerebral vasospasm

and thrombosisUncontrolled HPT

leading to hypertensive encephalopathy Seizures Headache Blurred vision microinfarction

HELLP syndromeHemolysisElevated Liver enzymesLow Platelets

RUQ painNausea and

vomitingEdemaDICRisk of liver rupture

– 75% mortality

Management Aim of treatment:

Control of BPPrevention of eclampsiaFluid resuscitationAssessment of urgency and delivery of baby

Multidisiplinary approachInvolved obstetric, anaesthetic and paediatric

teams CURRENTLY, DEFINITIVE treatment is

DELIVERY OF BABY!!!!

Immediate managementABCAirway Maintain the airway, using airway

adjuncts as necessary, position patient on the left side, give oxygen via face

BreathingIncreased RR – early sign of pul edemaAuscultate – to exclude pul edema

CirculationMeasure BP, PR, O2

saturationIV accessBl Ix- FBC, RP,

PT/INR, GXM, uric acid, LFT

Insert CBD monitor urine output If oliguric,( < 30ml/hr),

consider a modest fluid challenge(250 ml 0.9%NS)

DisabilityAny IE sxAssess reflex,

looking for clonus, perform fundoscopy

Principle of treatment1. Control of BP

Considered invasive BP mnitoring Aim MAP 100-140 mmHg

Sudden drop may compromise placental perfusion

Non severe HPT—oral agents Severe HPT- IV route

BP controlNon severe HPT:

defined as BP 140-159/90-109 mmHg most guidelines recommend lowering of non-

severe blood pressure to levels of SBP 140-150/DBP 90-100

Eg:methyldopa, labetalol, nifedipine

BP controlSevere HPT:

defined as systolic ≥160 mmHg or diastolic ≥ 110mmHg

BP should be lowered to levels of SBP 140-150/DBP 90-100 at a rate of 10-20 mmHg every 10-20 minutes

The choice should be made on clinician familiarity and experience with a particular agent

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.

EG:hydrallazine, labetolol, nifedipine

BP controlHydrallazine

1st linedirect peripheral

arteriolar vasodilator slow onset of action

(10-20 min) and peaks approximately 20 minutes after administration

IV bolus at a dose of 5-10 mg and admin every 20 min

Max dose is 20 mg 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:headache, nausea, and

vomitingReflex tachycardia

BP controlLabetolol:

selective alpha blocker and a nonselective beta blocker that produces vasodilatation and results in a decrease in systemic vascular resistance

IV lab 10 mg over 1 min at least 5 min interval with max dose of 50mg

And then infusion of 25mg/hr and titrate every 30 min until desired.

Max dose: 160mg/hrMaybe given orally(100-

200mg PO hourly until BP controlled and maintainence dose is given 12 hrly

Faster onsetDecreased BP and HRNo efect on uteroplacental

flowno neonate hypoglycemia or hypotension

BP controlNifedipine

CA channel blockeract on arteriolar

smooth muscle and induce vasodilatation

The dosage of nifedipine is 10 mg PO every 15-30 minutes, with a maximum of 3 doses

Maintainence – tds with max of each dose is 20mg

s/e:tachycardia,

palpitations, and headaches

Augments effect of Mg Severe hypotension Myocardial

depression

SNPUsed in severe HPT

whn other medications failed

VasodilatorOnset is rapid May cause rebound

HPTMay cause fetal

cyanide toxicity

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

Preventions of eclampsia2. Preventions /treatment of eclampsia

1st line :MgSO4 causes cerebral arterial dilatation

Indication: 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

Further 2g over 15 min and maintain with infusion of 1g/hr for 24 hrs after last seizure

Recurrent seizure 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 monitoringMg levels(mmol/l) effects

0.7-1.0 Normal level

2.0-3.5 Therapeutic level

>3.0 Widened QRS, prolonged PR

>4.0(symptomatic) Sedation, headache, blurred vision

>5.0 Loss of patellar reflex

7.5-14 Heart block, resp paralysis, cardiac arrest

MgSO4 monitoringMeasure hourly:

Urine output: aim for urine output >120ml over 4 hours (average 30ml/hour). If low, assess for symptoms or signs of MgSO4 toxicity.

Respiratory system: stop infusion if RR <10/min and/or general condition deteriorates (drowsiness, difficulty speaking

Check patellar reflex (knee-jerk) every 2-4 hours.If knee-jerk depressed, stop infusion.

monitor serum Mg2+ levels 4-6 hrlyAfter delivery: check uterus is contracted and

whether there is any vaginal bleeding

MgSO4 monitoringIf any sign of overdose:

• Stop MgSO4 infusion.• Call for help.• Assess and resuscitate guided by ‘ABC’.• Calcium gluconate should be available to

treat administer 10ml 10% calcium gluconate (1g) IV

over 2-3 minutes

For eclamptic seizures that are refractory to magnesium sulfate, IV Diazepam and phenytoin may be used as second-line agents.

Fluid managementCareful fluid balanceRisk of fluid overload and pulmonary edemaGuided by urine output >0.5ml/kg/hrPreferred IV Hartmann and 0.9% NS

Timing of deliveryDefinitive treatmentStart steroids if gestation is < 36 weeksd/w obstetrician regarding urgency of

deliveryClose collaboration btw obstetric, anaesthetic

and paedsAvoid ketamine and ergometrine

Anaesthetic problems1. Uncontrolled hypertension.2. Imminent convulsions3. Hypovolaemia (shift of fluid).4. Electrolyte imbalance: sodium may be low

because of diet and diuretics. The potassium level may be low because of the use of diuretics.

5. 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 non-depolarising 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 hypoxia10.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 PRE-ECLAMPSIARegional techniques are superior to general

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

pre-eclampsia have increased oedema of the airway

provide maximum analgesia, eliminating the risk of pain, which can raise the blood pressure

no direct effect on the patient's heart, lungs, kidneys or liver(if the spinal is given carefully). However, coagulation tests needed.

Pre-operative careAt least 2 large bore cannulas Monitor vital signs until the patient is brought to

the operating room.Intra-arterial monitoring is very useful in severe pre-eclampsia

Check the following:The drugs given pre-operatively, especially the

central depressants like pethidineThe time and dose of drugs givenThe availabilty of naloxone

-

Premedicate with ranitidine, metoclopramide and sodium citrate

Make sure all the equipment necessary for a general anaesthetic is available, especially suction, oxygen, airways, endotracheal tubes,laryngoscopes.

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 pre-eclamptic GA is the anaesthetic of choice in all patients

withdiminished level of consciousness e.g.

those who have had eclamptic convulsions or are showing signs of increased cerebral irritability.

coagulation problems, maternal haemorrhage, severe fetal distress

GA technique in pre-eclamptic and eclamptic ptAssess airway as there may be damage or

swelling as a result of seizureBP should be controlled until SBP<160Prepare all equipment for difficult intubationPreoxygenate as for any emergency caseInduce anaesthesia with thiopentone (4-5mg/kg)

followed by suxamethonium (1-1.5mg/kg) as per rapid sequence induction with cricoid pressure.

Ketamine is contra-indicated because it causes hypertension

To prevent the hypertensive response during laryngoscopy and intubation in severe pre-eclampsialignocaine (1-1.5mg/kg)fentanyl (1-1.5 micrograms/kg) or alfentanil (5

micrograms/kg). The neonate may need naloxone if opioids are

used.BP and intraop blood loss shld be closely

monitored.If DIC suspected, shld be corrected with

cryoprecipitate, platelet, FFP and blood

Maintain anaesthesia with small doses of a non-depolarising relaxant and a low concentration of volatile agent.

An opioid can be given as soon as the baby is delivered.

Administered oxytocin 5u diluted to 5ml by slow IV bolus

Infusion of oxytocin 40-80 u in 500ml NS in presence of uterine atonyAVOID ERGOMETRINE causes acute increases

in BP

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/HDWPt has fittedPt is drowsy and the ability to protect her

airway is in doubtThere is inadequate reversal of neuromuscular

blockadePresence of C/F of aspiration pneumoniaPresence of DIC with hemodynamic instabilityUnstable CVS: severe hyper 0r hypotension,

cardiac failure, APOMarked acidosis or low PaO2 on ABG

Postpartum MxControl fluid balanceEncourage diuresis using low dose frusemide

if necessary esp if CVP cont to riseGradual reduction of hydralazine and/or

MgSO4Conversion to oral hypertensive drugsProvision of good analgesic

Take home messageDefinitive treatment

DELIVERY OF THE BABY

Drugs to control BP and seizures

RA or GAMultidisplinary

approach

Reference Manual of anaesthesia by CY Leehttp://www.anzca.edu.au/fellows/sig/obstetric

-anaesthesia-sig/obstetric-anaesthesia-scientific-evidence/management-of-pre-eclampsia-and-eclampsia.html

http://update.anaesthesiologists.org/wp-content/uploads/2009/09/Eclampsia-and-Preeclampsia-Pharmacological-Management.pdf

http://www.frca.co.uk/article.aspx?articleid=100463