EM guidemap - Eclampsia

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Introduction

History of the present illness

Examination

Diagnostic testing

Medical decision-making and treatment Appendix
Introduction

- pre-eclampsia occurs in ~ 5% of pregnancies and eclampsia complicates < 1% of pre-eclamptic pregnancies

Definition of eclampsia = generalised convulsions occurring after the 20th week of pregnancy in a patient with underlying pre-eclampsia

(* altered mental status and coma can occur, but an altered LOC is not part of the definition of eclampsia)

- most eclamptic convulsions are typical tonic-clonic grand mal seizures and the convulsions usually cease spontaneously within two minutes

- the underlying pre-eclampsia is usually severe, although eclampsia can occur in pre-eclamptic patients with only mild hypertension and minimal edema

- eclampsia occurs between the 20th week of pregnancy and term (50% of cases), during labour (25% of cases), and up to ~ 48 hours post-partum (25% of cases)

- it is not known what precipitates an eclamptic convulsion and there are no clinical or laboratory markers that can accurately predict an eclamptic convulsion

- the cause of pre-eclampsia has not been elucidated and a number of clinical and laboratory features are variably present in pre-eclamptic patients

- pre-eclamptic patients usually have an elevated cardiac output, a high SVR and a relatively low plasma volume

- pre-eclamptic patients usually have hypertension (> 140/90), edema and proteinuria

- other clinical features of pre-eclampsia include:-

- HELLP syndrome (Hemolysis with schistocytosis, Elevated Liver function tests, Low Platelets) is a specific syndrome that occurs in ~ 10% of severe pre-eclampsia patients and ~ 30 - 50% of eclampsia patients

- many HELLP syndrome patients present without significant hypertension or marked proteinuria, and initial symptoms include vague nausea, malaise and mild abdominal (epigastric or RUQ) pain

- although ICH is a rare complication, it is the leading cause of materal death in eclampsia

History of the presenting illness

- the patient can present with vague symptoms of pre-eclampsia and then suddenly have a seizure during the ED evaluation period, or a sudden generalised convulsion without any preceding symptoms may be the presenting complaint

- symptoms suggestive of severe pre-eclampsia include:-

- a severe headache often precedes an eclamptic convulsion

- other common premonitory symptoms include visual disturbances, abdominal pain and nausea

- sudden weakness or syncope due to hypovolemic shock (+/- preceding abdominal pain) suggests rupture of a subcapsular liver hematoma

Examination

- first check the vital signs and LOC

- an altered mental status (persisting beyond any post-ictal period) is unusual and suggests severe pre-eclampsia or an intracranial complication eg. CVA

- a variable degree of hypertension is common

- generalised edema is common, while petechiae/mucosal bleeding suggest the rare complication of DIC

- respiratory distress + bilateral basal rales suggest the complication of pulmonary edema

- RUQ tenderness may be present and suggests hepatic involvement or HELLP syndrome

(* cautious palpation of the liver is advisable to avoid an iatrogenic rupture of a "contained" subcapsular liver hematoma)

- uterine tenderness suggests the complication of abruptio placentae

- hyperreflexia and clonus are commonly present in severe pre-eclampsia

- check for any focal neurological signs and specifically check the confrontational visual fields for evidence of a posterior visual pathway homonymous hemianopia

- check the eyes for vitreous/retinal hemorrhages and retinal detachment

Diagnostic testing

Routine blood work

- includes a CBC, peripheral smear for fragmented red cells, type-and-screen, coagulation profile (PT, aPTT, serum fibrinogen +/- fibrin degradation products), BUN and creatinine, serum glucose and electrolytes, liver function tests, serum uric acid

Chest X-ray

- to look for evidence of pulmonary edema and/or aspiration pneumonia

CT scan of the head

- if the patient has an altered LOC, an excessively prolonged post-ictal period,  any focal neurological signs, cortical blindness or a severe headache

Medical decision-making and treatment

The definitive treatment of severe pre-eclampsia/eclampsia is delivery of the fetus and placenta

- immediately initiate cardiac monitoring, blood pressure monitoring, continuous pulse oximetry, and cardiotocographic montoring of fetal heart activity and uterine contractions

- stabilise the vital signs by optimizing oxygenation and hemodynamic recuscitation of the hypotensive patient

- if the patient is normotensive or hypertensive, IV fluids should be limited to 50 - 100 ml/hour to avoid fluid overload and secondary pulmonary edema

(* most patients with pre-eclampsia have a decreased plasma volume and are vasoconstricted => the patients cannot tolerate aggressive fluid therapy)

Treatment of seizures

- ensure a quiet and darkened enviroment because bright lights and loud noises can precipitate eclamptic convulsions

Magnesium sulfate

- magnesium sulfate is the anticonvulsant drug-of-choice in patients with severe pre-eclampsia or eclampsia

- loading dose of magnesium sulfate for an active/recent seizure = 4 - 6g IV over 20 minutes IV (dilute the 50% solution with normal saline and administer the 20% solution using an infusion pump)

- maintenance dose of magnesium sulfate = 2g/hour IV

- a repeat IV bolus of magnesium sulfate is indicated if seizures recur => 2g IV over 3 - 5 minutes

(* recurrent seizures occur in 10 - 15% of eclamptic patients and usually respond to the repeat dose of magnesium sulfate)

- measure the serum magnesium  ~ 4 hours after commencing magnesium therapy and attempt to keep the serum magnesium in the therapeutic range (4 - 8 mg/dl)

(* the serum magnesium should be measured hourly if there is evidence of renal failure or decreased urine output)

- monitor the patellar reflexes and the respiratory rate q hourly and ensure that the urine output > 60 ml/hour => use 5 - 10 cc of 10% calcium gluconate IV if significant respiratory depression occurs due to magnesium toxicity

(* see the appendix for a table of "clinical signs suggesting magnesium toxicity")

- decrease the maintenance dose of magnesium sulfate to 1g/hour if the serum magnesium is > 10 mg/dl, or if the patellar reflexes become depressed

- increase the maintenance dose of magnesium sulfate to 3g/hour if the urine output is brisk and the serum magnesium level is falling, or if the serum magnesium is <  4 mg/dl

- if the patient has to be transferred to a higher level facility and an IV infusion cannot be maintained during transport => give a loading dose of 4g of magnesium sulfate IV followed by10g of magnesium sulfate IM using a three-inch 20g needle and inject half of the dose deep into each buttock

- magnesium sulfate should be given prophylactically to patients with severe eclampsia and ? "impending eclampsia" - heralded by symptoms/signs such as a severe unrelenting headache, scotomata or hyperreflexia - although it is not proven that prophylactic magnesium therapy actually decreases the subsequent incidence of eclamptic convulsions

- the prophylactic loading dose of magnesium sulfate = 4g IV over 20 mins followed by a maintenance infusion of 1 - 2g/hour

(* serial serum magnesium levels do not need to be routinely performed if low doses of magnesium are used => monitor the patellar reflexes q hourly)

Phenytoin

- used if the patient has a recurrent seizure despite optimum magnesium sulfate therapy

- dose of phenytoin = 20 mg/kg at a maximum rate of 50 mg/min IV

Diazepam

- used if the patient does not respond to magnesium and phenytoin, or if the patient has status epilepticus and continuous (ongoing) seizures

- dose of diazepam = 10 mg at a rate of 1mg/min

- causes maternal sedation and fetal respiratory depression, hypotonia and decreased beat-to-beat heart rate variability

(* see the "status epilepticus" guidemap for further details about the managment of status epilepticus)

Treatment of hypertension

- the blood pressure should be treated emergently if the systolic blood pressure is > 160 mmHg, or if the diastolic blood pressure is > 110 mmHg

Hydralazine

- hydralazine is the drug-of-choice for the treatment of hypertension in pre-eclampsia/eclampsia

- give 10 mg IV over 2 mins and repeat the dose q 20 minutes prn to decrease the systolic blood pressure to ~ 120 - 140 mmHg and the diastolic blood pressure to ~ 90 mmHg

(* do not decrease the diastolic blood pressure to < 90 mmHg because of the risk of iatrogenic utero-placental hypoperfusion and secondary fetal distress)

Labetalol

- an alternative first-line drug

- give 10mg IV (over 2 mins) and double the dose q 10 - 20 mins to a maximum dose of 300 mg

Nitroprusside

- a second-line drug that can cause fetal cyanide toxicity, and nitroprusside should only be used if satisfactory control of the blood pressure cannot be obtained with a first-line drug

(* see the "hypertensive emergencies" guidemap for further details on anti-hypertensive drug therapy)

Delivery of the fetus and placenta

- consult an obstetrician stat => leave it to the obstetrician to decide on the optimum time and method of delivery of the fetus and placenta

- most obstetricians will induce labour if the pregnancy is > 30 weeks and the cervix is favorable, and perform a C-section if the pregnancy is < 30 weeks

Appendix

Definition of severe eclampsia

- two-or-more of the following:-

Classification of HELLP syndrome

Thrombocytopenia

Class1: < 50,000/dl
Class 2: > 50,000/dl but < 100,000/dl
Class 3: > 100, 000/dl but < 150,000/dl

Hepatic dysfunction

LDH > 600 IU/L
AST or ALT > 40 IU/L

Hemolysis with fragmented red cells

- evidence of thrombocytopenia + liver dysfunction + hemolysis must be present to diagnose HELLP syndrome

- early HELLP syndrome is suggested by mild elevation of the liver enzymes and mild thrombocytopenia (class 3), while renal impairment and coagulation abnormalities (prolonged PT/PTT and decreased serum fibrinogen) are not usually found in early HELLP syndrome and suggest an impending DIC

- the amount of red cell fragmentation does not correlate with the degree of multi-organ involvement

- a small percentage of HELLP syndrome patients eventually develop significant renal compromise

- severe RUQ pain, or RUQ pain that increases markedly in intensity, or RUQ pain that radiates to the back suggests impending subcapsular liver hematoma rupture => diagnostic studies (CT scan or MRI of the abdomen) should be performed before free rupture into the peritoneal cavity occurs

(* subcapsular liver hematomas are more common in older multiparous HELLP patients)

- emergency surgery is necessary if a subcapsular liver hematoma ruptures into the peritoneal cavity, while angiographic embolisation of the hepatic artery can be successfully used to treat a "contained" rupture of a subcapsular liver hematoma

- prophylactic magnesium therapy to prevent eclamptic convulsions is recommended, and anti-hypertensive therapy is indicated if the systolic blood pressure > 160 mmHg (or if the diastolic blood pressure > 110 mmHg)

- a platelet transfusion is required if the platelet count is < 20,000/dl in a patient undergoing a vaginal delivery, or if the platelet count is < 50,000/dl in a patient undergoing a C-section or abdominal surgery

- dexamethasone (10mg IV q 12 hourly) can possibly decrease the need for platelet transfusions, and steroids also enhance fetal lung maturity - even if delivery cannot be postponed the ideal 24 - 48 hours

- acute fatty liver of pregnancy, thrombotic thrombocytopenic purpura, and hemolytic-uremic syndrome can mimic HELLP syndrome and they can all appear indistinguishable late in their disease-courses when severe complications (DIC, ICH, renal failure, pulmonary edema, abruptio placenta) develop

Clinical and laboratory characteristics of HELLP, TTP-HUS and AFL
  HELLP TTP-HUS AFL
Hypertension ++ +/- +/-
Proteinuria ++ +/- +/-
Thrombocytopenia +++ +++ +/-
Serum LDH ++ +++ ++
Anemia + ++ +/-
Bilirubin + ++ ++
Serum AST ++ +/- ++
Serum fibrinogen Normal Normal Decreased
Serum antithombin III Decreased  Normal  Decreased
Serum ammonia Normal Normal +
Serum glucose Normal Normal Decreased
Serum creatinine + ++ ++

- acute fatty liver of pregnancy is suggested by jaundice, significantly increased liver enzymes, hypoglycemia, increased serum ammonia + normal platelets + abnormal PT/PTT; while HELLP patients have minimal jaundice, no/minimally increased "cholestatic" liver enzymes + thrombocytopenia + normal PT/PTT + schistocytes in the peripheral blood smear

Clinical signs of magnesium toxicity
Serum magnesium level (mg/dl) Clinical findings
1.5 - 2.5 Normal range
4 - 8 Therapeutic range
9 - 12  Loss of patellar reflexes, slurred speech, somnolence, flushing
15 - 17 Muscle paralysis and respiratory arrest
30 - 35 Cardiac arrest

Disclaimer: My EM guidemaps reflect my personal approach to problem-solving/managing clinical cases in an ED setting and they should not be regarded as the standard of care. They merely represent the personal opinions of the author and they should only be used in clinical practice if the reader-user has substantial reason to believe that the clinical advice contained in the guidemaps is valid and accurate. The guidemaps are not meant to be "authoritative" and the reader-user should consult standard medical textbooks and expert opinion articles/guidelines for more authoritative advice. The reader-user should particularly confirm all drug doses, their indications and contra-indications, prior to their use.