Intensive Care Management of Severe Pre-eclampsia and Eclampsia

IN

NTENSIVE

CARE MA

ANAGEMENEC

NT OF SEVCLAMPSIA

VERE PRE--ECLAMPSSIA AND

end organ ischaemia. There may be a variety ofpresentations and classic features are not always present.Changes have occurred in the recommended treatment foreclamptic seizures and are considerably different fromother seizure disorders (including management ofhypertension and careful fluid balance).

INCIDENCE, MORTALITY AND MORBIDITY

A significant contributor to maternal and perinatalmorbidity and mortality[6,7], hypertension is estimated tocomplicate approximately 7-10% of all pregnancies[8]. Inthe developing and underdeveloped world, the incidencesare thought to be 20 times more than in the developedworld.

Eclampsia is responsible for approximately 50,000maternal deaths worldwide each year. A prospectivedescriptive survey of every case of eclampsia in the UKwas carried out in 1992[9]. Two hundred and seventy nineconsultant led obstetric units were surveyed. Five hundredand eighty two possible cases were reported and 383 weresubsequently confirmed as cases of eclampsia. This gave arate of 4.9 per 10 000 maternities. This incidence is similarto that reported in the USA in 1983-1986 of 4.3 per 10 000[10]. Sixty eight per cent of seizures occurred in hospital;44% were postpartum; 18% were intrapartum. Theremainder were antepartum.

A recent study at the All India Institute of MedicalSciences (AIIMS) shows the incidence of toxaemiaincluding eclampsia to be 16.4% (1995-1997) in 46,443admissions (116 maternal death)[11]. A study at

Apollo Medicine, Vol. 3, No. 1, March 2006 102

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INTENSIVE CARE MANAGEMENT OF SEVERE PRE-ECLAMPSIA AND ECLAMPSIA

V. Murlidhar* and Sameer Bolia**Senior Consultant*, Senior Resident**, Department of Anaesthesia, Indraprastha Apollo Hospitals,

Sarita Vihar, New Delhi 110 076, India.Correspondence to: Dr. V. Murlidhar, Senior Consultant, Department of Anaesthesia, Indraprastha Apollo Hospitals,

Sarita Vihar, New Delhi 110 076, India.

Pregnancy induced hypertension is a common medical complication of pregnancy and is a significantcontribution to maternal and perinatal morbidity and mortality. Early diagnosis, increased patient awarenessand appropriate medical intervention, especially intensive care management of severe preeclampsia andeclampsia have led to marked fall in mortality in this group of patients. In this review article, thepathophysiology, effect on different organ systems, choice of drugs (anticonvulsants and antihpertensives),support of a critically ill patient in the intensive care, monitoring, anaesthetic considerations and managementof the neonate are discussed.

Key words: Intensive care, Pre-eclampsia, Eclampsia, Pregnancy induced hypertension, anticonvulsants,HELLP syndrome, Convulsions.

INTRODUCTION

HYPERTENSIVE disorders are the most common medicalcomplication of pregnancy[1,2]. Two basic types ofhypertension occur during pregnancy: chronic hypertensionand pregnancy-induced hypertension (PIH). Chronic hyper-tension is that which predates pregnancy or continuesbeyond 42 weeks postpartum. Pregnancy-induced hyper-tension generally occurs after 20 weeks of pregnancy.Clinically chronic hypertension and pregnancy-inducedhypertension (PIH) may coexist. Further, PIH is classifiedaccording to the maternal organ systems affected. Pre-eclampsia is the progression of PIH and is classified assevere or mild based on maternal and fetal clinical findings(Table 1).

Eclampsia is defined as the development of convulsionsand/or unexplained coma during pregnancy or postpartumin patients with signs and symptoms of pre-eclampsia. In thewestern world, the reported incidence of eclampsia rangesfrom 1 in 2,000 to 1 in 3,448 pregnancies. The reportedincidence is usually higher in tertiary referral centres,in multifetal gestation, and in populations with no prenatalcare[3,4]. Current definitions place less reliance on thepresence of pre-eclampsia as eclampsia can develop withoutpreceding symptoms or signs in up to 38% of cases.extra.Late postpartum eclampsia is defined as eclampsia thatoccurs more than 48 hours, but less than 4 weeks, afterdelivery[5].

The cause is a pregnancy specific, underlyingmultiorgan disorder involving vascular endothelial damage,intravascular coagulation, and vasoconstriction leading to

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OBJECTIVES OF INTENSIVE CAREMANAGEMENT1. Organ support and management of multiorgan failure2. Prevention and management of the critical incidents

such as airway obstruction, aspiration etc.3. Medical and obstetric management of a potentially

reversible and manageable state4. Neonatal management

The understanding of the disease has changedconsiderably in the last two decades. It was realized thatearly shifting of these patients to an intensive care unit led toa drastic fall in the mortality and morbidity. The questionarises at what point of time these patients should be shiftedto an intensive care unit. Sengupta, et al[12] were using thecriteria of (a) severe hypertension, (b) prolongedunconsciousness, (c) multiple convulsions, (d) respiratorydistress and respiratory failure. But these criteria haveexpanded with the understanding of the disease and havegrown to include hepatic and renal problems. Even signs ofcerebral irritation should be considered a warning sign andnecessitate close monitoring. The individual predictivevalue of these risk factors for risk identification has beenquestioned. In a recent study Nisell, et al have identifiedfactors predicting maternal and fetal complications[14].The only factor, which they found to be of predictive value,was diastolic blood pressure.

Severe pre-eclampsia and eclampsia need to be referredand managed in a well-equipped center. The center shouldhave facilities to diagnose and define the disease and itscomplications. It should have facilities to intensivelymanage various problems, e.g., ICU with facilities for

Safdarjung Hospital (1975-84) studied the various causesof maternal mortality and morbidity between 1975 to 1984and came up with the following facts:

(a) Mortality rate of eclampsia was 7.05/1000 births (1975-84);

(b) Rising eclampsia mortality from 10.2% (1975) to15.02% (1984). Managing them in an intensive care unit(1984-86) led to a marked fall in mortality [12]. This issupported by a number of studies and it is mandatoryto manage severe pre-eclampsia and eclampsia in theICU.

Eclampsia and pre-eclampsia continue to be responsiblefor very high morbidity and mortality in the developingworld due to inadequate antenatal care, absence of a referralnetwork and management in ill-equipped centres.

Pregnancies complicated by eclampsia are alsoassociated with increased rates of maternal morbidities[13], such as abruptio placentae (7-10%), disseminatedintravascular coagulopathy (7-11%), pulmonary edema(3-5%), acute renal failure (5-9%), aspiration pneumonia(2-3%), and cardiopulmonary arrest (2-5%). Adultrespiratory distress syndrome and intracerebral haemorr-hage are rare complications among eclamptic seriesreported from the developed world. The risks of diffuseintravascular coagulation (8%); haemolysis, elevated liverenzymes, low platelets (HELLP) syndrome (10-15%); andliver haematoma (1%) are similar in eclamptic and severelypreeclamptic patients. It is important to note that maternalcomplications are significantly higher among women whodevelop antepartum eclampsia, particularly among thosewho develop eclampsia remote from term.

Table 1: Features under mild and severe pre-eclampsia.

Abnormality Mild Severe

Diastolic blood pressure <100 >110 or higherProteinuria Trace to 1+ Persistent 2+ or moreHeadache Absent PresentVisual disturbances Absent PresentUpper abdominal pain Absent PresentOliguria Absent PresentConvulsions Absent Present (eclampsia)Sr. creatinine Normal ElevatedThrombocytopenia Absent PresentLiver enzymes elevation Minimal MarkedFetal growth restriction Absent ObviousPulmonary edema Absent Present


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The first priority in the management of eclampsia is toprevent maternal injury and to support respiratory andcardiovascular functions. During or immediately after theacute convulsive episode, supportive care should be givento prevent serious maternal injury and aspiration, assess andestablish airway potency, and insure maternal oxygenation.During this time, the bed’s side rails should be elevated andpadded, a padded tongue blade is inserted between the teeth(avoid inducing gag reflex), and physical restraints may beneeded[15]. To minimize the risk of aspiration, the patientshould lie in lateral decubitus position, and vomitus and oralsecretion are suctioned as needed.

Left lateral position is used while transporting andnursing an unconscious patient to avoid airway obstructionand aspiration. If the airway reflexes are diminished, thenthe patient may need endotracheal intubation for airwayprotection.

During the convulsive episode, hypoventilation andrespiratory acidosis often occur. Although the initial seizurelasts only a few minutes, it is important to maintainoxygenation by supplemental oxygen administration via aface-mask with or without oxygen reservoir at 8-10 L/min[15]. After the convulsion has ceased, the patient begins tobreathe again and oxygenation is rarely a problem.However, maternal hypoxemia and acidosis may develop inwomen who have had repetitive convulsions and in thosewith aspiration pneumonia, pulmonary edema, or acombination of these factors. Transcutaneous pulseoximetry to monitor oxygenation should be used in alleclamptic patients. Arterial blood gas analysis is required ifthe pulse oximetry results are abnormal (oxygen saturationat or below 92%).

The next step in the management of eclampsia is toprevent recurrent convulsions. Magnesium sulphate(MgSO4) IV is preferred for controlling convulsions. It isused as an anticonvulsant in eclampsia due to a generalizeddepression of the nervous system. Magnesium sulphatedoes not seem to be an anticonvulsant but is known to be apotent cerebral vasodilator. It is thought to reverse cerebralvasoconstriction by blocking calcium influx through theNMDA (N-methyl-D-aspartate) subtype of the glutamatechannel. Magnesium sulphate increases the uteroplacentalblood flow and behaves as a mild tocolytic agent. It has anumber of side effects which includes flushing, reddeningof the face and respiratory depression. The loading dose is4 g (IM) plus 5 g in each buttock. For an IV loading dose it isadministered 4-6 g IV. The maintenance dose is 5 g IMevery four hourly and 1-2 g/hr infusion respectively.Approximately 10% of eclamptic women will have asecond convulsion after receiving MgSO4. In these women,another bolus of 2 g magnesium sulfate can be givenintravenously over 3-5 minutes A magnesium level of

management of the critically ill patients, operation theatre, awell-equipped blood bank and neonatal intensive care.

PATHOPHYSIOLOGICAL BASIS OF CRITICALCARE IN SEVERE PRE-ECLAMPSIA ANDECLAMPSIA (Table 2)

1. Central nervous system (CNS)

(a) Cerebral irritation and convulsions

In severe pre-eclampsia and eclampsia, there is anincreased CNS irritability (headache, visual disturbances,hyperreflexia, convulsions). The occurrence of convulsionsis not related to an elevation in blood pressure as comparedto hypertensive encephalopathy (40% seizures are postnatal, 38% seizures are antepartum, 18% seizures areintrapartum). Also, retinal changes are less common in pre-eclampsia and eclampsia as compared to hypertensiveencephalopathy. Some of the etiologic mechanisms that areimplicated in the pathogenesis of eclamptic convulsionshave included cerebral vasoconstriction or vasospasmhypertensive encephalopathy, cerebral edema or infarction,cerebral haemorrhage, and metabolic encephalopathy.However, it is not clear whether these findings are causes oran effect of the convulsions.

Prophylaxis for convulsions should be started with signsof cerebral irritability such as headache, visual distur-bances, epigastric pain or hyperreflexia. Following asingle eclamptic convulsion, prophylaxis with magnesiumsulphate should always be instituted, unless there are majorcontraindications. Conclusions may occur at moderatelyelevated blood pressures and blood pressure alone is a poorpredictor of the likelihood of occurrence of a convulsion.Although phenytoin was widely used in past for theprevention and control of eclamptic convulsions, recentevidence no longer supports its use.

Table 2: Pathophysiology of PIH.

CNS Ischemic foci; CVA; ICP maybe raised

CVS Vasospasm; hypertension; poorperfusion;diastolic dysfunction

Respiratory V/Q imbalance; airway oedema(pulmonary and laryngeal)

Renal Protenuria; renal failureGIT Periportal necrosis; oedema;

reduced metabolismCoagulation Low platelets; DICHaemodynamics Raised PCV; low blood volumeFeto-placental Unit Reduced IUBF; IUGR; abruptio

placenta


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4-6 mmol/L causes nausea, vomiting, somnolence, doublevision, slurred speech, and loss of patellar reflex. A rise to6.5-7.5 mmol/L can cause muscle paralysis and respiratoryarrest. If it rises above 10 mmol/L then there is a high chanceof a cardiac arrest. A serum magnesium level of more than5 mmol/L is a warning (physiological level: 0.75-1.1mmol/L, therpeutic 2-4 mmol/L). Some points to be kept inmind are

(a) Hourly measurement of patellar reflex, respiratory rateand volume are carried out to avoid toxicity. If deeptendon reflexes are absent, withhold MgSO4 untilreflexes return.

(b) Significant respiratory depression is treated withcalcium gluconate 1 g IV over 10 minutes.

(c) Monitoring of Mg level to be considered in patients witholiguria (urine output <100 mL/4 hr). Therapeutic Mgrange is 2-4 mmol/L. If serum levels are not availablethe maintenance dose should be reduced to 0.5 g/hr.

(d)If seizure continue despite MgSO4, use diazepam orthiopentone infusion. Thiopental is preferred in theprepartum period since large doses of diazepam may beassociated with neonatal hypotonia and impairedthermoregulation Intravenous solutions of diazepamalso contain sodium benzoate, which may compete withbilirubin for binding sites on albumin. This isparticularly hazardous for the preterm neonate in whomdiazepam administration may precipitate kernicterus.

(e) Intubation may become necessary in order to protectairway and ensure adequate oxygenation. Furtherseizures should be managed by IPPV and musclerelaxation.

(f ) The next step in the management of eclampsia is toreduce the blood pressure to a safe range but at the sametime avoid significant hypotension. The objective oftreating severe hypertension is to avoid loss of cerebralautoregulation and to prevent congestive heart failurewithout compromising cerebral perfusion or jeo-pardizing uteroplacental blood flow that is alreadyreduced in many women with eclampsia.

(g) Parenteral MgSO4 should be continued for at least 24hours after delivery and/or for at least 24 hours after thelast convulsion[16].

Choice of anticonvulsant[17,18]

The Collaborative Eclampsia Trial [16] was aninternational multicentre randomised trial involving 1680women with eclampsia. The trial was divided into two arms.The first compared magnesium sulphate with diazepam andthe second compared magnesium sulphate with phenytoinin the prevention of recurrent seizures. Maternal and

neonatal morbidity and mortality were the outcomemeasures. This study concluded that magnesium sulphateshould be the drug of choice for eclampsia. Phenytoinappeared to cause more maternal and neonatal morbidityand diazepam and phenytoin were associated withincreased recurrence of seizures compared with magnesiumsulphate.

(b) Cerebrovascular accidents

Patients having convulsion and unconsciousness mayhave a spectrum of intracranial changes e.g., petichialhaemorrhages, white matter oedema, intraventricularhaemorrhage. Studies in these patients with MRI has shownlesions most common in the distribution of posteriorcerebral artery and are associated with visual disturbances.Lesions in the basal ganglia and deep white matter are lesscommon and are associated with mental changes.Intaventricular haemorrhages are the most severe formleading to prolonged unconsciousness. Cerebral imaging(MRI & CT) is not indicated in eclampsia. However,imaging is necessary to exclude haemorrhage and otherserious abnormalities in women with focal neurologicaldeficits or prolonged coma[19].

(c) Raised intracranial pressure

Some patients may have a raised intracranial pressureand this may be managed on standard guidelines: (a)elevated head 30º, (b) mannitol, (c) IPPV with normocarbiaor mild hypocarbia (hyperventilation) with PCO2 not lessthan 25 mmHg.

(d) Prolonged unconsciousness

An unconscious patient needs nursing care to protecteyes, pressure points, feeding etc. Monitoring of the level ofunconsciousness may be done with Glasgow coma scale.

2. Cardiovascular system

The haemodynamic changes of pre-eclampsia can bedescribed as hypertension, increased systemic vascularresistance, decreased intravascular volume and decreasedcardiac output. Pulmonary edema may occur because ofiatrogenic fluid overload, decreased left ventricularfunction, increased capillary permeability and narrowingof the colloid osmotic-pulmonary capillary wedge pressuregradient. This is more likely to occur after delivery,particularly in patients who are older or multiparous or havepreexisting hypertension.

Haemodynamic monitoring and assessment

Blood pressure measurement: The cuff size used for themeasurement of blood pressure has to be appropriate as thiscould lead to fallacies in the diagnosis. The cuff has to beappropriate to the arm circumference. A regular cuff size


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(12 × 23 cm) is used if the arm circumference is less than33cms. A larger cuff (15 × 33 cm) is used if the armcircumference is 33-41 cm and a thigh cuff (18 × 36 cm)must be used if the arm circumference is greater than41 cm. The sphyngomanometer and the heart must be at thesame level while measuring the blood pressure. Korotokoff4 sounds may be better in defining the level of diastolicpressure[20].

Invasive blood pressure monitoring should be usedwhile administering intravenous antihypertensive agents.

Central venous pressure monitoring

Controversy exists as to whether central venouspressure monitoring is helpful, as it may not accuratelyreflect pulmonary capillary wedge pressure. Most cases aremanaged without such monitoring. One study, usinginvasive monitoring in 49 patients with severe pre-eclampsia, demonstrated normal or high cardiac output inthe presence of normal wedge and central venous pressure,and inappropriately high systemic vascular resistance [20].It concluded, that because filling pressures were normal,fluid should be given cautiously to avoid precipitatingpulmonary oedema.

In patients with severe pre-eclampsia or eclampsia,induction of anaesthesia or starting a labour epidural can bedone after the CVP is brought to a level of 6-7 cm of water.This would avoid precipitous falls in blood pressure. Whenan internal jugular or a subclavian cannulation is planned,one has to keep the coagulation disorders these patientscould have in mind and it has to be performed by anexperienced person. It may be preferable to insert centralvenous catheter via a peripheral site such as the antecubitalfossa.

Pulmonary artery catheterization

The central haemodynamic changes occurring inpatients with severe pre-eclampsia or eclampsia have beenstudied by Mabie, et al and in these patients there is ageneralized arterial vasospasm with a 30-40% decrease inblood volume[21]. Systemic vascular resistance (SVR) isincreased with increased left ventricular stroke work index(LVSWI) leading to left ventricular strain due to chronichypertension. There is also a low pulmonary capillarywedge pressure (PCWP). Consequently there may be a leftventricular diastolic dysfunction with poor correlationbetween CVP and PCWP. Measurement/monitoring ofthese parameters needs a pulmonary artery catheter (Swan-Ganz) in pulmonary oedema, intractable HTN, refractoryoliguria, haemorrhagic hypovolaemia requiring massivefluid resusctitation. Catheter as only a central venouspressure monitoring may be unreliable guide for fluidreplacement in a small percentage of cases. There is an

increased sensitivity to circulating adrenaline, nor-adrenaline and angiotensin II. In addition to the low plasmavolume, the plasma albumin is also reduced as a result ofloss in urine and loss across leaky capillaries leading to areduced colloid osmotic pressure. A normal colloid osmoticpressure is 22 mmHg in normotensive patients at term. Thecolloid osmotic pressure in moderate to severe pre-eclampsia drops to 15-20 mmHg.

Control of hypertension

Aim is to keep mean arterial pressure between 100-140mmHg (130/90-170/110 mmHg) to maintain adequateplacental blood flow. Management includes:

(a) Bed rest with avoidance of aortocaval compression maybe all that is required.

(b) Vasodilation should be preceded by intravascularexpansion to avoid fall in blood pressure.

(c) Pain management using epidural catheter may be used ifthere is no coagulopathy.

(d) Antihypertensive drug therapy: It is preferable to useinvasive blood pressure monitoring when intravenousantihypertensive drugs are used.

Hydralazine: This is the first line drug if available.Administered as increments of 5 mg titrated against bloodpressure. Onset is seen in 15 minutes. Therefore 15-20minutes intervals should be allowed between increments orsevere hypotension may occur. Hypotension and tachy-cardia generally respond to fluids. Hydralazine crosses theplacenta and can cause neonatal hypotension. Hydralazinehas been seen to produce fetal tachycardia with latedecelerations. Neonatal thrombocytopenia has also beenreported in association with the use of hydralazine. Needsfetal monitoring. Its duration of action is six to eight hours.Side effects include hypotension, tachycardia, tremor,headache, nausea, and vomiting. Unfortunately, this maymimic impending eclampsia.

Nifedipine: Principal use has been in acute management ofvery high blood pressures with 5-10 mg (orally) being theusual dose and can be repeated after 30 minutes. This drugmay be administered orally or sublingually. This can beused in graded doses sublingually to achieve the necessaryclinical effect. Rebound hypotension could be a problem ifthe dose is excessive. It has also been seen to exacerbate theeffect of MgSO4.

Methyldopa: Reserved for patients with an element ofchronicity to their hypertension.

Labetelol: One mg/kg of labetelol blocks response toendotracheal intubation without neonatal effects. The drugmay be administered in progressively increasing doses(20, 40, 80 mg) every 10-15 minutes to a maximum dose of


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300 mg. This may cause fetal bradycardia, hypotension, andhypoglycemia. Fear of the effects of betablockade on thefetus makes the use of other betablocking drugs in the highrisk pregnancies unadvisable. Needs fetal monitoring. Thisis contraindicated in patients with history of asthma and firstdegree heart block. This drug improves uteroplacentalperfusion, decreases uterine vascular resistance.

Sodium Nitroprusside: This drug has limited use due tofear of cyanide toxicity in the fetus. There are also doubts asto its safety in the presence of raised intracranial pressuresuch as may occur in a patient who has had severalconvulsions.

Nitroglycerine: Acts on venous capacitance vessels. Doesnot prevent response to intubation. Patients receivingvolume expansion are markedly resistant. Initial intra-venous infusion rate is 5 mg/min and titrated to desiredresponse by doubling the dose every 5 minutes. Side effectsinclude tachycardia, nausea, vomiting, pallor, sweating,headache and methaemoglobinaemia.

Once delivery has occurred, other oral antihypertensiveagents such as labetalol or nifedipine can be used to keepsystolic blood pressure below 155 mm Hg and diastolicblood pressure below 105 mm Hg. The recommended doseof oral labetalol is 200 mg every 8 hours (maximum dose of2,400 mg/d), and the recommended dose of nifedipine is10 mg orally every 6 hours (maximum dose of 120 mg/d).We would prefer oral nifedipine because it offers the benefitof improved diuresis in the postpartum period[16].

Fluid management

Fluid management is a challenge in severe pre-eclamptics and eclamptics complicated by decreased urineoutput, poor CVP-PCWP correlation, and wide variabilityof haemodynamic profile. In severe pre-eclamptics andeclamptics, low plasma oncotic pressure and left ventriculardysfunction can combine to produce high incidence ofpulmonary oedema and cerebral oedema. Diuretics and theadministration of high concentrations of colloid solutions(albumin, hetastarch) should not be used to decreaseperipheral edema caused by further depletion ofintravascular volume and an increased risk of pulmonaryedema and uteroplacental insufficiency. Severe pre-eclamptics poorly tolerate overhydration (preloading)before regional anaesthesia if ventricular dysfunction ispresent. They are also sensitive to sympathetic blockade as aresult of regional anaesthesia due to decreased bloodvolume. However, 400-500 colloid preloading prior toregional anaesthesia may reduce the risk of hypotension andfetal distress.

3. Hepatic

In hepatic disorders raised enzymes may occur due to

periportal or focal necrosis with large hyaline deposits offibrin-like material in sinusoids. Decreased synthesis ofpseudo cholinesterase may prolong suxamethonium,chloroprocaine or tetracaine. Hyperbilirubinemia, how-ever, is not a common feature. Hepatic dysfunction mayform part of the HELLP syndrome, which complicates0.3% of all pregnancies and up to 20% of women withsevere pre-eclampsia. The syndrome comprises haemo-lysis, increased liver enzymes, and low platelets withepigastric or right upper quadrant pain. Thrombocytopenia(platelets <100,000/mL) and also qualitative plateletdysfunction can occur[20,22,23]. Subcapsular hematomaof the liver can cause intense epigastric pain and, rarely, theliver may rupture. Disseminated intravascular coagulationoccurs in 7% of patients with eclampsia but the cause isunclear[23]. More than 50% patients may need blood orblood products if they develop HELLP syndrome. Massivetransfusion may be required in some case of HELLPsyndrome. These patients may manifest a number ofproblems associated with massive transfusion. In caseswhere patients have a coagulopathy, regional anaesthesia iscontraindicated. Deferential diagnosis is preeclampsiaversus acute fatty liver of pregnancy, viral hepatitis andother hepatic disorders. Assessments and management ofthe woman diagnosed with HELLP syndrome are the sameas for the woman with severe preeclampsia.

4. Renal

Glomerular involvement, probably due to a vascularbasis of the disease leads to proteinuria. Examination showssubendothelial deposits, electron dense droplets in theglomerular epithelial cells that contain albumin, immuno-globolin, fibrinogen and complement. Oligouria is commondue to hypoproteinaemia and decreased renal blood flowrather than a primary renal pathology[24]. This may be dueto prerenal cause and may be distinguished from othercauses by giving a fluid challenge. But one has to avoidgiving repetitive, unmonitored fluid challenges. Dopaminemay be started in a low dose 2-3 mcg/kg/min to improverenal perfusion. Progression to acute renal failure iscommon especially with hypertension and HELLPsyndrome. Renal outcomes are usually good.

5. Pulmonary

Respiratory assessments are performed to identifysigns of pulmonary oedema, respiratory compromise, ormagnesium toxicity. Respiratory rate is evaluated for ratequality and pattern, especially if receiving MgSO4, toidentify early signs of toxicity. Laboured respiration or useof the accessory muscles is assessed; pulmonary oedemacan develop very quickly. Tachypnoea and tachycardia areearly signs of evolving pulmonary oedema. Skin color andmucous membranes are assessed for the presence of


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cyanosis, which may indicate problems with oxygenation.Oxygenation status is assessed with pulse oximetry.However, pulse oximetry should not replace clinicalassessments.

During active convulsion, maternal injury should beavoided. Since the woman may have vomiting, the airwaymust be protected. Maintain adequate oxygenation. Oncethe convulsion has stopped and the patient has begunspontaneous respirations, oxygenation status is monitored.If spontaneous respirations are not present, ventilatorysupport will be required.

Minimize the risk of aspiration. The woman should bepositioned to facilitate drainage from the mouth. Suctionequipment should be readily available and in workingorder. Also, if supplemental oxygen is being administeredby facemask, be aware of the possibility of vomiting andaspiration. Correct maternal acidaemia. Blood gas analysiswill allow monitoring oxygenation and pH status.Respiratory acidaemia is possible after convulsion, butsodium bicarbonate is not administered unless the pH is lessthan 7.10[12]. Ensuring adequate respiratory status isessential. Since all anticonvulsant drugs are respiratorydepressants and may interact with each other, poly-pharmacy should be avoided.

Respiratory failure is diagnosed clinically and by bloodgas analysis. A fall in PaO2 to less than 60 mmHg or/and arise in PCO2 to more than 45 mmHg would needmechanical support. Airway is protected with a cuffedendotracheal tube.

Ventilation is also required temporarily after emergencylower segment caesarean section or in uncontrollableconvulsive states. Once the delivery has occurred the bloodgas analysis is satisfactory and convulsions are controlled,and other systems are in an acceptable condition, a decisionto wean off is taken. Patient is weaned from the ventilatorand is put on T-piece trial. Once the reflexes have returned

and the patient is conscious and oriented (after withdrawalof sedation) and able to breathe around the tube, the tracheais extubated.

MANAGING THE NEONATE

Ultimate goal of any protocol for management ofpreeclampsia must be maternal safety first followed bydelivery of a live, mature (if possible) newborn in optimalcondition (Table 3)[25-28]. Essentially two managementoptions are available:

• Immediate delivery for maternal benefit and subsequentneonatal intensive care.

• Pregnancy prolongation (expectant management or 4hour delay with corticosteroid therapy for maturation oflungs).

The study by Witlin, et al has the following results[29].

1. No correlation between severity of maternal disease andfetal outcome.

2. No correlation between fetal variables (5 min APGAR,cord pH, PDA, O2 requirements, necrotizing entero-colitis) and fetal outcome.

3. Incidence of RDS (respiratory distress syndrome) isinversely proportional to gestational age.

4. Expectant management and steroid use did not decreaseRDS.

5. Incidence of RDS is directly proportional to cesareandelivery (incidence of cesarean decreased withincreased gestation).

6. Birth weight was the most important determinant ofsurvival (IUGR decreased survival).

7. Any delivery after 34 weeks is safe as the lung is matureafter this period.

LABOUR ANALGESIA

Mild to moderate preeclampsia may be allowed toproceed with normal labour. Epidural block may beinstituted early if the coagulation parameters are normal.This may be useful in controlling stress and pain. It is alsothought that an epidural block may improve the placentalintervillous blood flow.

ANAESTHETIC CONSIDERATIONS

1. Airway assessment to predict a difficult maskventilation or intubation is a must. Mallampatti scoringmust be done prior to anaesthesia. Post convulsionlaceration of the tongue or mucosa may be predictive ofa difficult ventilation or intubation. Presence of a stridoror excessive facial oedema may be predictive of airwayoedema. In these patients it is important to take care thatthe endotracheal tube used is smaller than usual and

Table 3: Indications of immediate delivery.

1. Non-reassuring fetal status2. Vaginal bleeding3. Uncontrolled severe hypertension4. Pulmonary oedema5. Persistent severe headache or visual changes6. Compromised renal function7. Platelet count of <100,000/mm3 or raised liver

enzymes (AST/ALT)8. Uncontrolled seizures9. Attainment of 34 weeks of gestation


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extreme care is taken to avoid trauma during intubation.However, in many of these patients it is not possible topredict all the problems and there may be anunanticipated difficult airway so the anaesthesiologistmust be ready with the equipment needed in thissituation (introducers, bougie, laryngeal masks, surgicalairway, fiberoptic bronchoscopes etc.). Awakeintubation may be necessary in predicted difficultairway but nasotracheal intubation requires a normalcoagulation status.

2. A rapid sequence induction is carried out and generalanaesthesia is preceded with a 3-minute pre-oxygenation. Theopentone 4-5 mg/kg or etomidate 0.2mg/kg with suxamethonium (1-1.5 mg/kg) withSellick’s maneuver should be used for achieving rapidairway access.

3. Haemodynamic response to intubation can cause adangerous rise in blood pressure and drugs to controlthis may have to be used in some cases. Lignocaine,betablockers, opioids, nitroglycerine and sodiumnitroprusside have been seen to affect the fetus. Newernarcotics such as alfentanil when administered prior tosuxamethonium can decrease the haemodynamicresponse to intubation and has a short duration of actionin the fetus.

4. When MgSO4 or nifedepine has been administered tothe patient there may be an interaction with thenondepolarising muscle relaxant in causing a prolongedblock. Neuromuscular monitoring is preferable in thesecases.

5. Regional anaesthesia is contraindicted in patients withabnormal coagulation parameters, patients with ahistory of convulsions or unconsciousness. The othercontraindications to regional anaesthesia also apply inthese situations. The patients must be well hydratedprior to anaesthesia as there could be precipitous fall inblood pressure. Newer techniques like the combinedspinal epidural are preferable to a single dose spinal asthere is a better control over the haemodynamics.

6. Depending on the preoperative problems and theconditions of the patient, postoperative ventilation andsupportive intensive care are continued in the post-operative period. All patients with severe preeclampsianeed intensive care for 24-48 hours in the postoperativeperiod. The same standard of care must be continued.One must remember that convulsions can occur upto 7days in the postoperative period.

In a randomized study by Wallace, et al three groups of27 patients received GA, epidural or Combined spinalepidural[22].1. All methods are equally acceptable and no serious

maternal or fetal complications were attributable to anymethod if steps are taken to ensure careful approach tothe method used.

2. Vasopressor and fluid requirements are more withregional anaesthesia. Delivery is the ultimate care forthe maternal disease. However, maternal benefits mustbe weighed against the neonatal risks of pretermdelivery. Delivery of infants less than 24 weeksgestation with immature fetal pulmonary profiles resultin intensive and prolonged neonatal care associatedwith significant neonatal mortality and morbidity.

CONCLUSION

Eclampsia is the commonest obstetritic conditionrequiring ICU admission in the developing countries.Women diagnosed with the HELLP syndrome or eclampsiapresent a variety of management issues and problems forthe health care provider. Regardless of the diagnosis, severepre-eclampsia, the HELLP syndrome, or eclampsia canprofoundly affect the woman and her fetus. The underlyingpathophysiology must be evaluated and treated with bothpatients in mind at all times. Nurses caring for the womandiagnosed with severe preeclampsia, the HELLPsyndrome, and eclampsia must be fully aware of the riskfactors, diagnostic criteria, appropriate managementregimes, and the potential complications for both thewoman and her fetus. The Collaborative Eclampsia Trialhas shown that magnesium sulphate is the drug of choice forroutine anticonvulsant management of women witheclampsia; a similar study is warranted to establish theantihypertensive drug of choice.

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Health & Medicine

Intensive Care Management of Severe Pre-eclampsia and Eclampsia