Special Feature
Postpartum Toxemia
By William Brady, MDPreeclampsia is characterized by hypertension, edema, and proteinuria and frequently occurs in nulliparous women. The syndrome, noted in a minority of pregnancies, usually becomes apparent after the 20th week of pregnancy, most often near the end of the third trimester. A variant of the syndrome (the HELLP syndrome) includes the above clinical findings as well as hemolytic anemia, thrombocytopenia, coagulopathy, and elevations in liver enzymes. The acronym "HELLP" describes the characteristics of the syndrome: "H" for hemolysis, "EL" for elevated liver enzymes, and "LP" for low platelets. Preeclampsia is noted less commonly in patients during the first half of pregnancy, and is usually associated with molar or hydropic degeneration of the placenta. With the appearance of generalized seizure activity, preeclampsia has progressed to eclampsia, or toxemia of pregnancy. Eclampsia complicates less than 1% of deliveries and constitutes a significant life threat to both mother and fetus. Maternal mortality is reported to approach 15% and perinatal mortality ranges from 10% to 30%. 1-4 Toxemia occurs most often antepartum; however, a significant minority of cases develop in the postpartum period. Postpartum toxemia may have its onset only moments after delivery is complete or, alternatively, the disorder may manifest as late as three weeks after delivery. Emergency physicians must be familiar with the presentation and management of toxemia. Further, they must recognize that a significant minority of toxemic patients will experience the onset of eclampsia following uncomplicated delivery and discharge from the hospital.
Epidemiology
An analysis of the incidence of toxemia relative to the timing of pregnancy reveals that the majority of patients experience the onset of seizure activity antepartum. In general, 80% of toxemic patients will have the first seizure in the ante- or intrapartum periods. A review of past eclampsia studies demonstrates that approximately 20% of patients will convulse initially in the postpartum period.5 The past several decades have demonstrated a decline in the occurrence of eclampsia, most likely reflecting not only increased recognition of preeclampsia, but also improved means of treating such patients, perhaps preventing the progression to toxemia. During the same time period, a relative increase in the proportion of postpartum cases has been noted.
Significant controversy exists in the obstetrical community, however, concerning the definition of postpartum toxemia in terms of the time of onset of the convulsions relative to delivery. One perspective maintains that the vast majority of such cases will occur in the first 24 hours postpartum, with the remainder taking place during the second day after delivery. Further, seizures first appearing beyond 48 hours postpartum, theorized to result from eclampsia, are regarded with skepticism by this group. Others have placed less emphasis on the time of onset of the first seizure and have adopted the term "late postpartum eclampsia" to describe patients who develop toxemia more than 48 hours after delivery of the infant. Regardless of one’s perspective, the emergency physician should consider the following issues in the approach to such a patient: 1) a significant number of toxemic patients will first manifest the syndrome more than 48 hours after delivery; 2) a thorough medical evaluation is warranted in all such patients to rule out other causes of convulsion; and 3) that, while excluding other causes of seizures, such patients should be aggressively treated for presumed postpartum eclampsia.
Pathophysiology and presentation
The pathophysiology of preeclampsia and eclampsia remains largely unknown, yet it is clear that the pathogenesis involves the uteroplacental bed. The pathophysiologic end point is severe vasospasm with resultant hypertension. It is speculated that this vasospasm may be secondary to increased vasoactive substances. The concentration of the vasodilating prostaglandin, prostacyclin, is lower in women with preeclampsia and eclampsia, likely causing vasospasm due to unopposed action of the vasoconstricting agent angiotensin II. The seizure activity in eclampsia is a direct manifestation of a failure of the cerebral autoregulatory mechanisms in the control of intracranial perfusion at elevated blood pressures. Such a pathophysiologic failure supports the clinically proven theory that the best anticonvulsant therapy is proper management of hypertension.
The clinical presentation of eclampsia in the postpartum period is not markedly different from the antepartum version of toxemia, with the obvious exception of the lack of a fetus. Patients may present in the postpartum period with complaints suggestive of impending convulsion including headache, visual changes, and epigastric pain of several days duration. Patient age and parity also are similar in both antepartum and postpartum toxemia; young, nulliparous patients are most frequently affected. Physical examination and laboratory findings such as edema, hyper-reflexia, hypertension, and proteinuria are noted at similar rates. Hypertension and hyper-reflexia are found in the majority of cases, while edema and proteinuria are present in approximately 50% of patients. A previous diagnosis of preeclampsia at the time of convulsion is available in 50-75% of patients with postpartum eclampsia. The remaining patients represent cases in which the diagnosis was missed or the process appeared suddenly with rapid progression in the postpartum period. The severity of eclampsia appears to differ between the ante- and postpartum varieties. Postpartum toxemia is described as mild in two-thirds of cases with both fewer than five seizure episodes and less pronounced elevations in blood pressure in the majority of patients. Conversely, antepartum eclampsia is characterized as severe in approximately 60% of cases, with the majority of patients experiencing greater than 10 convulsive episodes. Further, postpartum patients receiving adequate therapy are more likely to respond favorably in terms of suppression of seizure activity and control of blood pressure when compared with antepartum toxemic cases.6
Evaluation and management
The evaluation of postpartum patients presenting with findings potentially consistent with eclampsia must include a thorough physical examination with special emphasis on the nervous system. A metabolic panel including electrolytes and glucose is essential. A rapid, bedside determination of the serum glucose is mandatory to rule out hypoglycemia as a cause of the seizure. Toxicologic studies for epileptigenic agents such as cocaine or amphetamine must be considered in appropriate cases. The urine must be examined for the presence of protein. The complete blood count may reveal hemoconcentration as well as thrombocytopenia; coagulation studies may demonstrate prolongation of the prothrombin and partial thromboplastin times. The liver function tests, specifically the transaminases, are frequently elevated, especially in the HELLP syndrome variant. A CT scan of the head should also be performed at the time of presentation to the ED. Analysis of the cerebrospinal fluid may be warranted depending on the clinical presentation. The above evaluation is performed to rule out other causes of seizure in the postpartum patient. The differential diagnosis for such convulsions includes metabolic, toxic, infectious, neurologic, and traumatic etiologies, as well as pre-existing or new-onset epilepsy.
The initial management of postpartum eclampsia is similar to that of antepartum toxemia. Attention to the ABC’s with maintenance of an airway, satisfactory ventilation and oxygenation, and adequate perfusion is essential. For patients presenting with active seizure, a parenteral benzodiazepine such as lorazepam or diazepam followed by intravenous phenytoin or fosphenytoin at conventional doses is a reasonable approach. If the diagnosis of postpartum eclampsia is suspected, treatment with intravenous magnesium sulfate with its anticonvulsant and antihypertensive properties is suggested, though not universally accepted among the obstetrical and neurologic communities. It is administered in a 4-6 g intravenous bolus over 30 minutes followed by a constant infusion of 1-2 g/h. Manifestations of excessive magnesium therapy include lethargy, loss of reflexes, hypotension, and, ultimately, respiratory depression. The continuous infusion should be stopped if reflexes disappear or the serum magnesium level exceeds 8 mEq/L. Parenteral calcium may be used to treat magnesium toxicity if profound. Hypertension may be further managed with hydralazine (the traditional agent) or other medications (such as nifedipine, labetolol, or nitroprusside) titrated to the clinical picture. Diuretic agents are not helpful and may actually worsen the situation by impairing already compromised perfusion. In general, the emergency physician has more flexibility in the choice of medications in the management of postpartum eclampsia as compared with antepartum toxemia, due to the absence of the fetus. Patients presenting with toxemia or a constellation of clinical findings suggestive of toxemia in the postpartum period should be admitted to a monitored setting with both urgent obstetrical and neurologic consultations. Such patients presenting with complaints and/or physical findings consistent with impending seizure or in the postictal state should be aggressively treated with magnesium sulfate as well as antihypertensive agents, with the aim of halting disease progression.
References
1. Porapakkham S. An epidemiologic study of eclampsia. Obstet Gynecol 1979;54:26-30.
2. Pritchard JA, Pritchard SA. Standarized treatment of 154 consecutive cases of eclampsia. Am J Obstet Gynecol 1975;123:543-554.
3. Lopez-Llera M. Eclampsia 1963-1966. Evaluation of the treatment of 107 cases. J Obstet Gynecol Brit Commonw 1967;20:379-384.
4. Zuspan FP, Ward MC. Improved fetal salvage in eclampsia. Obstet Gynecol 1965;26:893-897.
5. Brady WJ. et al. Postpartum toxemia: Hypertension, edema, proteinuria, and unresponsiveness in an unknown female. J Emerg Med 1995;13:643-648.
6. Bhose L. Postpartum exlampsia: A clinical study. Am J Gynecol 1964;89:898-902.
Reasonable pharmacologic adjuncts in the treatment of postpartum toxemia include all of the following except:
a. phenytoin.
b. lorazepam.
c. magnesium sulfate.
d. calcium gluconate.
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