Anaesthetic Implications and Management in Preeclampsia & Eclampsia

Anaesthetic Implications and Management in Preeclampsia & Eclampsia
Dr. Shilpa Agarwal Moderator: Dr. JP Sharma University College of Medical Sciences & GTB Hospital, Delhi

Contents Classification of hypertensive disorders of pregnancy
Diagnosis of preeclampsia Risk factors Obstetric and Anaesthetic management Complications of preeclampsia Diagnosis and risk factors of Eclampsia Obstetric and Anaesthetic management in Eclampsia Complications of Eclampsia

Introduction Hypertensive disorders complicate nearly 5-10% of all pregnancies Deadly triad with infection and haemorrhage In developed countries, 16% of maternal deaths due to hypertensive disorders Preeclampsia – a multifactorial, multi-system hypertensive disorder of pregnancy ,is most dangerous etiology remains unknown evidence-based management

History 1903 Chesley -Preeclampsia word included in books 1961 Chesley
Year Milestones 1903 Chesley -Preeclampsia word included in books 1961 Chesley -Preeclampsia-eclampsia restricted to obstetric definition. 1966 Eastman and Hellmann -Toxemia of pregnancy -Diagnostic criteria of preeclampsia: hypertension, proteinuria, edema after 24 weeks 1976 Pritchard and Mc Donald -Hypertensive disorders of pregnancy -Diagnostic criteria of preeclampsia: hypertension, proteinuria, edema after 20 weeks 1988 Hibbard -Under classification Hypertensive disorders of pregnancy, preeclampsia grouped into Pregnancy induced Hypertension -Classified into mild-moderate and severe preeclampsia

Classification In 2000, National High Blood Pressure Education Program classified hypertensive disorders complicating pregnancy as: Gestational hypertension Preclampsia- eclampsia chronic hypertension chronic hypertension with superimposed preeclampsia

Gestational Hypertension
Blood Pressure ≥ 140/90 on two or more occasions - in a previously normotensive patient - after 20 weeks gestation - without proteinuria - returning to normal 12 weeks after delivery Almost half of these develop preeclampsia syndrome

Chronic Hypertension Blood Pressure ≥ 140/90 before 20 weeks of gestation Or Persistence of hypertension beyond 12 weeks after delivery.

Preeclampsia superimposed on Chronic Hypertension
New-onset proteinuria ≥ 300 mg/24 hours in hypertensive women but no proteinuria before 20 weeks’ gestation A sudden increase in proteinuria or blood pressure or platelet count <1 lakh/mm3 in women with hypertension and proteinuria before 20 weeks’ gestation More adverse outcome than preeclampsia alone

Preeclampsia New onset of hypertension & proteinuria in a previously normotensive woman after 20 weeks of gestation Returning to normal after 12 weeks of pregnancy. Edema not a part of diagnosis now. A retrospective diagnosis Eclampsia : new onset of seizures or unexplained coma during pregnancy or postpartum period in patients with pre-existing preeclampsia and without pre-existing neurological disorder.

PREECLAMPSIA

Epidemiology Preeclampsia complicates nearly 6% - 10% of all pregnancies. maternal ICU admission Leading cause of preterm delivery-NICU Birth of LBW babies- economic, social and medical burden Leading cause of maternal and fetal morbidity and mortality.

Classification of Preeclampsia
Mild PE Severe PE Blood pressure >140/90 >160/110 Proteinuria On 2 occasions, >4hrs apart >0.3gm/ 24 hrs Dip stic > 1+ >5gm/24 hrs Dipstic > 3+ S. creatinine normal elevated Pulmonary edema _ + oliguria IUGR headache Visual disturbance Epigastric pain HELLP syndrome

Risk Factors Preconception - Partner related -Non partner related
Nulliparity limited exposure to paternal sperms Partner who fathered a preeclamptic pregnancy in another women -Non partner related History of Preeclampsia in previous pregnancy Advanced maternal age Family history of Preeclampsia History of placental abruptio, IUGR, fetal death Non hispanic black race

Risk factors contd.. -Maternal disease related -Behaviour-
Obesity, BMI>35 doubles the risk Hypertension Diabetes Thrombotic vascular diseases -Behaviour- Smoking : preventive -Pregnancy associated- Multiple gestation Molar pregnancy

ETIOPATHOGENESIS Exact mechanism unknown, disease of theories.
ABNORMAL PLACENTATION Stage1: failure of trophoblastic invasion into myometrium Penetrates only decidua superficial placentation  ↓placental perfusion stage2 : endothelial damage systemic manifestations of Preeclampsia

1.Abnormal placentation

2. Inflammatory mediators
↓PGI2 ↑TXA2 Vasoconstriction Platelet aggregation ↑Vasopressor response ↑uterine activity

3. GENETIC Family history of pre eclampsia: genetic origin
Mutations in Complement Regulatory Protein gene Genes assoc.: MTHFR, F5 leiden, AGT, HLA, NOS3, F2(prothrombin), ACE Early onset Late onset onset < 34 wks POG > 34 wks POG frequency 20% 80% Association with IUGR High negligible Familial component yes no Placental morphology abnormal normal etiology placental maternal Risk factos Family history DM, HTN, Maternal age, ↑BMI, CVS disorder Risk of adverse outcome high

4. IMMUNOLOGIC Exposure to sperms of different partner
long term exposure to paternal antigen in sperms of same partner- protective activated auto antibodies to angiotensin receptor-1 AA-AT1activate AT1 receptorsincreased sensitivity to angiotensins  hypertension

5.ANTIANGIOGENIC PROTIENS

Markers of Preeclampsia
↑ plasma Homocystiene ↑ serum sFlt1(soluble fms-like tyosine kinase) ↓serum and urinary Platelet Growth Factor ↓ Vascular Endothelial Growth Factor

Pathophysiology

Respiratory Airway is edematous; ↓ internal diameter of trachea
Pharyngolaryngeal edema  risk of pulmonary edema; 3% women with preeclampsia.

CNS CNS manifestations include: headache,
visual disturbances, hyperexcitability, hyperreflexia, coma,seizures Cause: cerebral edema and hypoperfusion

CVS Vasospasm and exaggerated responses to catecholamines
Increased vascular permeability ↓ Colloid Oncotic Pressure hypertension endorgan ischemia Intravascular volume deficit

Haemat ology Hemoconcentration (pts with anemia may appear to have normal hematocrit) Thombocytopaenia  most common Platelet count correlates with disease severity and incidence of abruptio placentae DIC due to activation of coagulation cascadeoverconsumption of coagulants and platelets spontaneous haemorrhage.

Hepatic HELLP syndrome Periportal haemorrhage subcapsular bleeding
hepatic rupture: 32% maternal mortality

Renal Decreased GFR - oliguria Glomerulopathy - proteinuria
- renal failure - uric acid, creatinine is elevated Glomerulopathy - proteinuria

Uteroplacental circulation
Uteroplacental insufficiency Fetal complications: - hypoxia -IUGR -Prematurity -IUD -Placental abruptio

Prediction of Preeclampsia
No screening test is really helpful Various screening methods are: Diastolic notch at 24weeks by doppler ultrasonography Absence or reversal of end diastolic flow Average mean arterial pressure ≥ 90 mmHg in second trimester Angiotensin infusion test: angiotensin infusion required to raise the blood pressure >20 mm Hg from baseline Roll over test: rise in blood pressure >20 mmHg from baseline on turning supine at weeks gestation is positive.

Prevention Regular Antenatal checkup: rapid gain in weight
rising blood pressure edema proteinuria/deranged liver or renal profile Low dose Aspirin in High risk group: ↑PGs and↓TXA2 Calcium supplementation: no effects unless women are calcium deficient Antioxidants- Vitamin C and E Nutritional supplementation: zinc, magnesium, fish oil, low salt diet

Obstetric Management

Obstetrics management
1. Maternal evaluation : Hemoglobin and hematocrit platelet count : decreased, if < 1 lakh coagulation profile LFTs : indicated in all patients KFTs : raised (S.urea creatinine is decresaed in Normal pregnancy) Urine Routine : proteinuria

Obstetrics management contd..
2. Fetal evaluation: Daily fetal movement count Ultrasound Doppler ultrasound for fetal blood flow Velocimetry

Obs. Manag contd.. 3. Treatment of Acute Hypertension:
Goal: to prevent adverse maternal sequalae Aim: to keep DBP below 100 mm Hg and to lower MAP not >15-25%

Anti Hypertensive Drugs
MOA SIDE EFFECTS C/I & PREVENTION Methyldopa 250mg-1g tds or mg iv Central and pripheral anti adrenergic action Maternal-postural hypotension, hemolytic anemia, sodium retention, excessive sedation Fetal-intestinal ileus Hepatic disorders, psychic pts., CCF Labetalol Oral-100mg tds till 800mg/d Iv- 20 mg till desired effect (max. 220mg) Alpha + beta blocker Maternal-tachycardia, hypotension Fetal-bradycardia, hypotension Hepatic disorders Hydralazine Oral-100mg/d in 4 divided doses Peripheral vasodilation Maternal-hypotension, tachycardia, arrythmia, palpitations, lupus like syndrome Fetal- safe Neonate- thrombocytopenia Causes sodium retention so use diuretic Ace $ avoid

Anti Hypertensives contd..
DRUGS MOA SIDE EFFECTS C/I & PREVENTION Nifedipine Oral: 5-10mg tds Arteriolar vasodilation Flushing, hypotension, tachycardia, inhibition of labor With MgSO4 and NMBs Nitroprusside mcg/kg/min Direct vasodilator Maternal- nausea, vomitting, severe hypotension Fetal- cyanide toxicity Bed rest Avoid Diuretics, ACE inhibitors, ARBs Avoid uterotonics

Obs Manag contd.. 4. Seizure Prophylaxis Routinely used in severe PE
Magnesium sulphate: most commonly used Initiated with onset of labor till 24h postpsrtum For caesarean, started 2hrs before the section till 12hrs postpartum

Recommended regime for MgSO4
Zuspan or sibai regime: 4-6 gm i.v over 15 min f/b infusion of 1-2 gm/hr Pritchard regime: 4 gm i.v over 3-5min f/b 5 gm in each buttock with maintenance of 5 gm i.m in alternate buttock 4 hrly

Side effects of MgSO4 Maternal : flushing, perspiration, headache,
muscle weakness, pulmonary edema Neonatal: lethargy, hypotonia, respiratory depression

Magnesium levels Monitoring
Normal Serum levels mg/dl Therapeutic range- 5- 9mg/dl Patellar reflex lost- >12mg/dl Respiratory depression mg/dl Cardiac arrest- >25mg/dl

Management of MgSO4 Toxicity
Stop infusion Intravenous Calcium 10 ml 10% over 10 minutes Endotracheal intubation in respiratory depression

Anaesthetic implications during MgSO4 therapy
MgSO4 potentiate and prolong the action of both depolarizing non-depolarizing muscle relaxants At higher doses Mg2+ rapidly crosses the placental barrier, has been found to significantly ↓ FHR variability Should be given cautiously with Ca2+ as may antagonize the anticonvulsant effect of MgSO4 Also be cautious in patients with renal impairment May ↑ the possibility of hypotension during regional block

Obs. Manag. Contd.. 5. Delivery The only definitive treatment
Preeclamptic patients divided into 3 categories A- Preeclampsia features fully subside B- partial control, but BP maintains a steady high level C- persistently increasing BP to severe level or addition of other features

Gp A: can wait till spontaneous onset of labor
Management: Gp A: can wait till spontaneous onset of labor don’t exceed Expected Date of Delivery Gp B: >37wk terminate w/o delay <37wk, expectant management at least till 34wks Gp C: terminate irrespective of POG, start seizure prophylaxis and steroids if<34wks

Anaesthetic management

Pre anaesthetic Evaluation
1.Airway 2. Haemodynamic monitoring : blood pressure, ECG, Pulse oxymetry 3. Fluid status: volume depleted patients higher risk of hypotension with induction of anaesthesia 4. BP control 5. Coagulation status

Invasive Haemodynamic monitoring
Invasive central blood pressure monitoring not routinely indicated Does not improve patient outcome Indications: -oliguria patients -pulmonary edema -poorly controlled maternal blood pressure - massive hemorrhage -frequent arterial blood gas measurements Poor correlation between central venous and pulmonary capillary wedge pressure

Anesthetic Goals of Labor Analgesia in Preeclampsia
To establish & maintain hemodynamic stability (control hypertension & avoid hypotension) To provide excellent labor analgesia To prevent complications of preeclampsia Pulmonary edema Eclampsia Intracerebral haemorrhage Renal failure To be able to rapidly provide anesthesia for Caesarean Section

Analgesia For Labor & delivery
Neuraxial analgesia: Lumbar Epidural- gradual onset of sympathetic blockade cardiovascular stability ↓ stress response maintains uteroplacental circulation avoids neonatal depression extended analgesia if cesarean required excellent post op analgesia

Neuraxial analgesia contd..
Combined Spinal Epidural Analgesia- advantages of both Spinal - rapidity requires only small dose of LA ↑vasopressor response-better control of hypotension disadvantage: immediate verification of catheter function not possible

Anaesthesia for Caesarean
Epidural anaesthesia Spinal anaesthesia: advantage: rapidity requires only small dose of LA ↑vasopressor response-better control of hypotension Combined Spinal Epidural Anaesthesia Indications: Patient preference Contraindications to general anaesthesia Hemodynamically stable patient

Anaesthesia for caesarean contd..
General anaesthesia: Indications - coagulopathy -sustained fetal bradycardia with reassuring maternal airway - severe ongoing maternal hemorrhage - contraindications to neuraxial technique

Concerns with neuraxial anaesthesia
Adequate hydration: - risk of pulmonary edema -Lower concentration of local anesthetics: hypotension less common Treatment of hypotension if any: - small doses of vasopressors Epinephrine containing test dose should be avoided Coagulation status -mild preeclampsia-: hypercoagulable -severe preeclampsia-: hypocoagulable -bleeding time poor indicator of platelet function

Platelets and neuraxial anaesthesia
platelets >1lakh/mm3, coagulation profile not indicated Platelets <1 lakh/mm3 -clinical evidence of bleeding -platelet trend-Every 6hourly if stable, every 1-3hrly if declining -coagulation profile: PT/PTTK/INR -quality of platelets -risk vs benefit Platelets <50,000: contraindication

Platelets contd.. - remove epidural catheter only when platelet count returns normal (at least /mm3) emergency imaging studies and neurologic evaluation if epidural hematoma suspected In various studies, it has been found that low dose aspirin doesn’t significantly affect bleeding time, neuraxial analgesia can be given safely without any complication

Coagulopathy and Neuraxial Anaesthesia
ASRA guidelines Frank coagulopathy is an absolute contraindication Subcutaneous (minidose) heparin thromboprophylaxis: not a contraindication, however Assess platelet count before needle placement and removal of catheter, if > 4days heparin therapy Stop heparin 4-5 days prior to needle placement With Low Molecular Weight Heparin: - needle placement and catheter removal hours after last dose, at higher doses after 24h - first post operative dose after 6-8 hours -repeat dose after at least 2hours of catheter removal

Hazards of General Anaesthesia
1.Difficult intubation- -smaller size tube -difficult airway cart ready 2. Exaggerated and prolonged hypertensive response to laryngoscopy and intubation: -risk of intracranial hemorrhage. -labetalol(5-10 mg), local anesthetics, esmolol( 2mg/kg ), nitroglycerine(200mcg/ml), nitroprusside 0.5mcg/kg/min, remifentanyl (1mcg/kg) used before intubation and extubation

Hazards contd.. 3.MgSO4 with neuromuscular blockers, calcium channel blockers, uterotonics and uterine relaxants 4. Uterotonics avoided: risk of acute hypertension and eclampsia

General Anaesthesia administration in severe Preeclampsia
Place a radial canula for continuous BP monitoring i.v line secured Arrange smaller size endotracheal tubes Antacids and perinorm given 30 minutes before 100% oxygen for 3 min. Labetalol 10 mg iv bolus and titrate to effect before induction, while monitoring fetal heart rate Rapid Sequence Induction Labetalol 5-10 mg before extubation Give opioids or BZDS after delivery .

Post op concerns Post op analgesia: Post partum management:
intravenous opioids, neuraxial opioids concern : monitor for respiratory depression Post partum management: risk of pulmonary edema, sustained hypertension, stroke, Venous thromboembolism, seizures, HELLP, postpartum hemorrhage.

Complications CVA: main leading cause of death in pts with PE
absolute risk is low reversible cerebral edema is m/c Pulmonary edema, pleural effusion, ARDS: head end elevation oxygen therapy restrict fluids diuretics mechanical ventilation laryngeal edema Placental abruptio

Complications contd.. Renal failure: oliguria most common
haemodynamic monitoring diuretics Liver: Subcapsular liver hematoma: avoid trauma to liver, HELLP Syndrome, hepatic rupture with shock : surgical emergency DIC: treat the cause platelets/Fresh Frozen Plasma/cryoprecipitate Eclampsia Maternal death

HELLP syndrome Diagnosis: Hemolysis: Peripheral smear
↑bilirubin >1.2mg/dL, LDH>600 IU/L Elevated liver enzymes: SGOT> 70 IU/L Low platelets: <1 lakh /mm3

Management of HELLP syndrome
Immediate hospitalisation Stabilise mother antihypertensives anti seizure prophylaxis correct coagulation abnormalities Assess fetal condition- FHR, doppler ultrasound, biophysical profile

HELLP contd.. Ultimate goal: >34 wks gestation deliver
<34wks expectant management if stable maternal and fetal conditions Platelet transfusion if: <40,000/mm3 before cesarean <20,000/mm3 before delivery

Eclampsia

ECLAMPSIA Is the new onset of seizures or unexplained coma during pregnancy or postpartum period in patients with pre-existing PE and without pre-existing neurological disorder.

Epidemiology 0.1- 5.5 per 10,000 pregnancies
Decreasing incidence with time Antepartum(50%): mostly in third trimester Intrapartum(30%): Postpartum(20%): usually within 48hours, fits beyond 7days generally rules out eclampsia

Risk factors Maternal age less than 20 years Multigravida
Molar pregnancy Triploidy Pre-existing hypertension or renal disease Previous severe Preeclampsia or Eclampsia Nonimmune hydrops fetalis Systemic Lupus Erythematosus

Clinical features Eclamptic convulsions are epileptiform and consist of four stages Premonitory stage: twitching of muscles of face, tongue, limbs and eye. Eyeballs rolled or turned to one side, 30s Tonic stage: opisthotonus, limbs flexed, hands clenched, 30s Clonic stage: 1-4 min, frothing, tongue bite, stertorous breathing Stage of coma: variable period.

Physical Examination Sustained rise in blood pressure
Tachycardia, Tachyponea Rales Mental status changes Hypereflexia Clonus Papilloedema Oliguria or anuria Right upper quadrant or epigastric abdominal tenderness Generalized edema Small fundal height for the estimated gestational age

Pathogenesis Loss of normal cerebral auto regulatory mechanisms
cerebral hyperperfusion Edema & ↓cerebral blood flow

Differential Diagnosis
meningitis encephalitis space occupying lesion electrolyte disturbance vasculitis amniotic fluid embolism medications organ failure stroke

Prediction and Prevention
Early detection and judicious treatment with termination of pregnancy in Preeclamptic patients Adequate sedation, Anti hypertensives and prophylactic Anticonvulsant in peripartum period Observe for hrs postpartum

Management of Eclampsia
Prevention of seizures Control of seizures

Prevention of convulsions
MgSO4 therapy: DOC for prophylaxis of eclamptic convulsions M.O.A: blocks Ca2+ ion influx into neurons leading to cerebral vasodilatation Other actions: -lowers endothelin-1 levels - ↑ production of PG I2 - tocolytic action - attenuates the release of Ach and sensitivity to Ach at myoneuronal junction

Control of seizures -turn patient head to one side,
-apply jaw thrust if airway compromised nasopharyngeal airway Adequate oxygenation - ensure adequate breathing , bag and mask ventilation can be done - secure an i.v line - Drugs- Antiepileptics Antihypertensives - Delivery

Anticonvulsants Drugs Mechanism of action Contraindications
Side effects MgSO4 Zuspan or sibai regime: 4-6g iv over 15 min f/b infusion of 1-2g/h Pitchard regime: 4g i.v over 3-5min f/b 5g in each buttock with maintenance of 5g i,.m in alternate buttock 4hrly Competitive inhibition of calcium ions at motor end plate or cell membrane, ↓ Ach release & sensitivity Patients with MG and impaired renal function, heart block, digitalis Maternal : flushing Perspiration, headache, muscle weakness, pulmonary edema Neonatal: lethargy, hypotonia, respiratory depression Diazepam 10-20 mg I.V f/b 40 mg diazepam in 500ml normal saline at 30 drops per minute Cerebral muscle relaxant and anticonvulsants Maternal : hypotension Fetal : respiratory depression, may last even 3 weeks after delivery Phenytoin 10 mg/kg IV at not more than 50 mg/min f/b 2 hrs later by 5 mg/kg for 12 hrs, thereafter 200mg orally till 48hours Centrally acting anticonvulsants Maternal: hypotension, cardiac arrythmias, phlebitis, hyperglycemia, respiratory arrest, cardiac arrest, bradycardia Fetal: Fetal hydantoin syndrome

Refractory seizures Thiopentone sodium 0.5 g in 20 ml of 5% Dextrose intravenously slowly Propofol infusion Midazolam infusion if fails then General Anaesthesia Seizures still not controlled then termination of pregnancy

Delivery in Eclampsia Unless contraindicated: Eclamptic women should undergo normal vaginal delivery Indications for cesarean section - Fetal distress Placental abruption Extreme prematurity Unfavorable cervix Failed induction of labor Recurrent seizures

Anaesthetic Management
Assess seizure control and neurologic function Fluids : ml/hr avoid cerebral edema, CVP guided fluid therapy BP control : appropriate anti hypertensives Monitoring :Pulse oxymeter , ECG, Fetal Heart Rate, Urine output, NM monitoring, Mg monitoring, Lab inv: CBC, Bld sugar, Bld urea, S.creatinine, S.uric acid level with S.E, LFTs, Coagulation profile, 24 hrs specimen for protein Choice of anaesthesia: GA preferred with thiopentone or propofol (both decreases ICP) Avoid hypo or hyperglycaemia, hypoxia, hyperthermia Peripartum : manage for shock, sepsis, psychosis thrombocytopenia, DIC, coagulopathy

Choice of Anaesthesia in Eclampsia
Neuraxial: - indications seizures controlled - no coagulopathy - patient cooperative GA: - Indications seizures not controlled -coagulopathy -reassuring airway -uncooperative patients

General anesthesia in eclamptic pt.
Careful preanesthetic evaluation to be done Aspiration prophylaxis to be given Secure an i.v line Small endotracheal tubes ( 6 and 6.5mm) should be ready Difficult airway cart should be ready All monitors to be attached Start preoxygenation with100% oxygen via well fitting mask for 3-5 minutes Exaggerated CVS response should be pretreated with either lignocaine or beta blockers Induces anesthesia with : inj. Thiopentone 4-5mg/kg inj Sch 1-1.5mg/kg RSI #If pt. is on MgSo4 therapy, the usual fasciculation following Sch may not occur and it may take 60 sec.

General anesthesia in eclamptic pt.
Maintain anesthesia with 50% N2o+50% O2 +0.5% isoflurane until delivery of neonate, with inj. Vecuronium #Neuromuscular monitoring to be done and dosage of NDMR to be titrated accordingly Extubation: Should be done after hrs later in view of- Postpartum seizure, Cerebral edema, Aspiration pneumonia, Hypertensive crisis, Pulmonary edema, ARDS DIC, HELLP syndrome Persistent oliguria

Summary Preeclampsia is a multisystem disorder.
Management is supportive, delivery is the only definitive. Preeclampsia patients: High risk for difficult intubation. Hypertensive response to laryngoscopy intracranial hemorrhage. Spinal Anaesthesia not contraindicated in severe Preeclampsia Eclampsia can be prevented by prophylactic MgSO4 therapy Eclamptic patients should be monitored for at least 24 hrs post partum.

References Chestnut’s Obstetric Anaesthesia: Principles and Practice, “Hypertensive disorders” 4th Ed, Ch 45, Miller’s Anaesthesia, “Anaesthesia for Obstetrics” 7th Ed,Ch 69, Wylie and Churchill Davidson’s A Practice of Anaesthesia, “Obstetric Anaesthesia” 7th Ed, Ch57, 934 Morgan’s Clinical Anaesthesiology, “Obstetric Anaesthesia” 4th Ed, Ch 43, Textbook of Obstetrics, D.C. Dutta, “Hypertensive Disorders in Pregnancy” 6th Ed, Ch 17, William obstetrics, “Pregnancy Hypertension” Ch34, Bell M.J, BSN, RN, A Historical Overview of Preeclampsia-Eclampsia J Obstet Gynecol Neonatal Nurs September ; 39(5): 510–518

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Anaesthetic Implications and Management in Preeclampsia & Eclampsia

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