Postpartum toxemia: Hypertension, edema, proteinuria and unresponsiveness in an unknown female

The Journal of Emergency Medicine, Vol13, No 5, pp 643448, 1995 Copyright 0 1995Elsevier ScienceLtd Printed in the USA. All rights reserved 0736-4679/95 $9.50 + .oo

Pergamon

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Clinical Communications: OBIGYN

POSTPARTUM TOXEMIA: HYPERTENSION, EDEMA, PROTEINURIA AND UNRESPONSIVENESS IN AN UNKNOWN FEMALE William J. Brady,

MD,*

Daniel J. DeBehnke, MD,?and C. Tom Carter,

MD*

*Department of Emergency Medicine, University of Virginia Health Sciences Center, Charlottesville, Virginia tDepartment of Emergency Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin Reprint Address: William J. Brady, MD, Department of Emergency Medicine, Box 523, University of Virginia Health Sciences Center, Charlottesville, VA 22908

0 Abstract - Kclampsia, or toxemia of pregnancy, is a disorder of pregnancy characterized by seizures associated with hypertension, edema, and proteinuria. Toxemia of pregnancy carries significant maternal and fetal morbidity and mortality. Eclampsia most commonly occurs in the antepartum period. A minority of cases, however, may initially manifest in the postpartum period. We present the case of a 2&year-old female with postpartum eciampsia presenting to the Emergency Department with altered mental status. A review of the literature concerning postpartum toxemia and a discussion of appropriate management strategies follows.

20th week of pregnancy, usually approaching term. Preeclampsia progresses to eclampsia with the onset of generalized convulsive activity. Eclampsia, or toxemia of pregnancy, complicates 0.05 to 0.2% of deliveries ( 1,2) and constitutes a significant life threat to both mother and fetus. Maternal mortality is reported to approach 13% (3-S), and perinatal mortality ranges from 10 to 28% (2,3,5,6). Toxemia occurs most often antepartum. A significant minority of cases, however, develops in the postpartum period with an incidence ranging from 13% (7) to 37% (8). In general, postpartum eclampsia represents onefifth of all cases of toxemia. 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. An altered sensorium in the postseizure state resulting from toxemia must be added to the differential diagnosis for female patients of child-bearing age presenting with changes in mentation.

•i Keywords - pregnancy; postpartum; seizure; eclampsia; toxemia INTRODUCTION

Preeclampsia, a hypertensive disorder of pregnancy associated with edema and proteinuria, develops in a minority of obstetric patients. Preeclampsia frequently occurs in nulliparas, most often after the Presented at the Clinicopathologic Conference Competition at the Society of AcademicEmergencyMedicineMeeting, Washington, DC, 1994.

Clinical Communications: Obstetrics and Gynecology is coordinated by Elizabeth Honingford, MD, of the University of California, San Diego Medical Center, San Diego, California RECEIVED: 17 October 1994; FINALSUBMISSIONRECEIVED: 6March 1995; ACCEPTED: 21 March 1995 643

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CASE PRESENTATION A 28-year-old female was “found down” on the floor of a restroom of the hospital. She was transported to the Emergency Department (ED) on a stretcher by the nursing supervisor. The patient was found unconscious on the floor of the restroom located adjacent to the main lobby by a visitor to the hospital. According to witnesses, the patient had entered the restroom approximately 5 to 7 min prior to being found. No companions could be found in the restroom or the lobby area. According to the nursing supervisor, the patient was unresponsive when found. The patient was breathing spontaneously at a rate of 24 breaths/min; she had a blood pressure of 180/105 mm Hg and a pulse rate of 120 beats/min. She was transported to the ED for further evaluation. No further details regarding the patient’s medical history were available. Physical examination on arrival in the ED showed a lethargic, minimally obese, young black female; she was arousable only to painful stimuli. The patient was not diaphoretic; no significant odors were appreciated on the examination. The vital signs were a blood pressure of 160/100 mm Hg, a pulse of 110 beats/min, a respiratory rate of 20 breaths/min, a temperature of 37.5OC (99.5OF), and a Glasgow Coma Score of 9 (eyes 2, verbal 2, motor 5). No evidence of trauma was found on the head, neck, trunk, or extremities. The pupils were equal (3 mm), round, and reactive to light; no papilledema was noted. The tympanic membranes were normal. The mucous membranes were moist. A gag reflex was found. The neck was supple, the trachea was midline, and no JVD was present. The cardiac examination demonstrated a tachycardia but regular rhythm without murmur, rub, or gallop. The lung examination was normal with equal aeration bilaterally. The abdomen was soft and nontender with normal bowel sounds. The rectal examination demonstrated normal sphincter tone and no evidence of occult or gross blood loss. The patient had been incontinent of urine prior to her arrival. The skin was warm and dry without rash. The extremities were warm with both normal capillary refill time and palpable pulses. No puncture marks were noted; trace ankle edema was discovered. The neurologic examination demonstrated brisk localization to painful stimuli bilaterally, normal Babinski responses, and symmetric hyper-reflexia. The pulse oximetry on high-flow oxygen was 100%; the cardiac monitor revealed a sinus tachycardia with normal intervals and no ectopy. A fingerstick determination of the serum glucose was 150. A search for a medical alert warning or other

items in the patient’s personal property did not yield any useful information. No patient identification was found. She was dressed in ordinary street clothing (i.e., not inpatient attire:). While the examination was being performed, the patient was placed on oxygen supplementation, cardiac monitoring was initiated, and a peripheral IV was started. Naloxone (2 mg) and thiamine (100 mg) were both administered intravenously without response. The cervical spine was not immobilized. During the initial 15 min of patient examination and stabilization, she demonstrated an increase in her level of alertness. The patient would open her eyes and move all extremities to command. She was able to furnish only her first name. A computed tomography (CT) scan of the head was performed and was normal. Approximately 35 min after arrival in the ED, the patient experienced a generalized tonicclonic seizure lasting 2 min without obvious eye deviation. The seizure activity terminated spontaneously. The cardiac monitor, oxygen saturation, and vital signs showed no significant change. The patient received lorazepam (2 mg ) IV. The laboratory studies demonstrated normal chemistries with the exception of the HCO, which was 18 mEq/dl. The hematocrit was 33, the white cell count was 17.0 with a left shift, and the platelet count was 105,000/mm3. Toxicologic studies were negative for ethanol, benzodiazepine, and barbiturate. Urine toxicologic studies were negative (notably for cocaine metabolite and amphetamine). Urinalysis with microscopic examination revealed 2 + protein and was otherwise negative. The patient again became more responsive and followed commands appropriately. The vital signs were unchanged with the exception of the blood pressure, which was 150/105 mm Hg. She was able to furnish her name at this point. She then asked about “her baby.” She was unable to comment on the possibility of pregnancy. The abdomen was reexamined for the presenceof a palpable uterus; none was found transabdominally. A bimanual vaginal examination revealed a soft, 12-week uterus without blood or purulent discharge. No fetal heart tones were heard. A urine pregnancy test was added to the laboratory studies. The possibility of pregnancy-related seizure activity, toxemia, was then considered. The medical records were ordered. The urine pregnancy test returned “positive” as the medical records arrived in the ED. The patient was five days postpartum from a normal spontaneous vaginal delivery. Her pregnancy was complicated by preeclampsia; she had been admitted to the hospital for bed rest for the last 15 days of the pregnancy. She

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did not receive magnesium sulfate antepartum. The infant had developed a fever of 38.3OC (101 OF) approximately 20 h after birth and remained in the hospital. The mother had been discharged 24 h ago and had apparently returned to visit her new baby. The diagnosis of postpartum toxemia was made. Magnesium was given intravenously while nifedipine was administered orally. The mental status improved; a repeat neurologic examination showed only symmetric hyper-reflexia. The blood pressure was lowered to 130/90 mm Hg while in the ED. The patient was admitted to the obstetrical ward of the hospital and was discharged four days later with normal vital signs, using no medications other than prenatal vitamins, and without neurologic deficit.

DISCUSSION

Preeclampsia 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 including: “H” for hemolysis, “EL” for elevated liver enzymes, and “LP” for low platelet or thrombocytopenia (9). Preeclampsia is noted less commonly in patients during the first half of pregnancy, 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. Criteria for the diagnosis of eclampsia include seizure activity occurring in the pregnant or recently pregnant patient who has at least two of the following three clinical signs: hypertension, peripheral edema, and proteinuria. Eclampsia occurs in 0.05 to 0.2% of pregnancies ( 1,2), representing a significant life threat to the mother and fetus. Impending seizures - the development of eclampsia- may be signalled by headache, visual changes, epigastric pain, and hyper-reflexia. Alternatively, toxemia may appear suddenly without prior warning symptoms or signs in a patient with unrecognized preeclampsia. The pathophysiology of preeclampsia and eclampsia remains largely unknown, yet it is clear that the pathogenesis involves the uteroplacental bed. The pathophysioiogic end-point is severe vasospasm with resultant hypertension. It is speculated that this vaso-

spasm may be secondary to increased vasoactive prostaglandins (10). The concentration of the vasodilating prostaglandin, prostacyclin, is lower in women with preeclampsia and eclampsia, causing vasospasm due to unopposed action of the vasoconstricting agent angiotensin II (10). 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 ( 11). Such a pathophysioiogic failure supports the clinically proven theory that the best anticonvulsant therapy is proper management of of hypertension. An analysis of the incidence of toxemia relative to the period of pregnancy reveals that the majority of patients experience the onset of seizure activity antepartum (Table 1). In general, 80% of toxemic patients (range 63 to 87%) will have the first seizure in the ante- or intrapartum periods. (l-3,7,8,12-16) A significant minority of patients, however, will develop eclampsia after delivery of the infant. A review of past eclampsia studies (Table 1) demonstrates that approximately 20% of patients will convulse initially in the postpartum period (range 13 to 37% ) ( l3,7,8,12-16). 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 (13,17). 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 (13,16-20). One perspective (13,18,19) maintains that the vast majority of such caseswill occur in the first 24 h postpartum with the remainder taking place in the second day after delivery. Further, seizures first appearing beyond 48 h postpartum, theorized to result from eclampsia, “should be regarded with skepticism” (18). Bhose reported that approximately 50% of postpartum toxemic patients initially seized within the first 3 h after delivery and that 98.4% initially convulsed during the first postpartum day (13). One additional study (19) noted that 100% of patients with postpartum toxemia manifested the disorder within 14 h of delivery. Other authors (16,17,20,21) 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 h after delivery of the infant. Watson et al. (16)

W. J. Brady et al.

646 Table 1. Time of Onset of Toxemia Relative to Stage of Pregnancy: A Compilation of Studies’ Principal Author of Study

Year

Country

Total Patients per Study

Percent Antepartum b

Whitcare( 10) Bhose( 11) Harbert( 12) Mojadidi( 7) Pritchard( 3) Wightman( 1) Porapakkham( 2) Sibai( 8) Lopez-Llera( 13) Watson( 14) Lubarsky( 27) TOTAL/MEAN”

1947 1964 1968 1973 1975 1978 1979 1981 1982 1983 1994 -

China India USA (VA) USA (FL) USA (TX) UK Thailand USA (TN) Mexico USA (TN) USA (TN) -

200 367 168 30 154 43 298 67 704 132 334 2497

84 83 78 83 82 68 81 63 83 73 71 79.5

Percent Postpartum 16 17 22 17 18 32 19 37 17 27 29 20.5

%tudies were selected as representative from the literature spanning 1947 to 1994. These studies used criteria as noted in the Discussion Section for the diagnosis of eclampsia. bDefined as the total of ante- and intrapanum. 7he mean percentage for the incidence of ante- and postpartum toxemia was calculated from the total number of patients in the above studies (n = 2497).

reported 132 cases of eclampsia, 36 of which were postpartum. Of those patients with postpartum toxemia, 47% occurred after the initial 48 h period. Patients were noted to initially seize as late as the ninth and eleventh days postpartum. Sibai and colleagues (17) described a series of six patients experiencing late postpartum toxemia an average of six and onehalf days postpartum (range of 3 to 11 days). Brown et al. (20) reported a series of eight patients with late postpartum convulsions occurring 3 to 10 days postdelivery. Two of the eight casesin this serieswere found to have seized from etiologies other than toxemia (newly diagnosed epilepsy on postpartum day 3 and hemolytic uremic syndrome on day 14). The remaining six patients, after thorough metabolic and neurologic evaluations, were felt to have experienced late postpartum eclampsia. Samuels (21) treated four patients presenting with postpartum toxemia that occurred on postpartum days 7, 8, 11, and 23. The authors of these studies stress several important issues: ( 1) a significant number of toxemic patients will first manifest the syndrome more than 48 h after delivery; (2) a thorough medical evaluation is warranted in all such patients to rule out other causesof convulsion; and (3) that, while excluding other causes of seizure, such patients should be aggressively treated for presumed postpartum eclampsia. The use of magnesium sulfate, a frequently administered medication in the management of preeclampsia, may have delayed the progression to toxemia in several cases. In the series published by Watson et al. (16), approximately 70% of the patients with late postpartum toxemia had received such therapy peripartum; two patients were being treated with magnesium at the time of seizure onset.

Sibai et al. (17) reported that 100% of patients with late postpartum toxemia were treated with magnesium sulfate peripartum; none were undergoing such therapy at the time of convulsion. Bhose (13) and Jeffcoate et al. (19), in their reports of patients with postpartum eclampsia occurring no later than 48 h after delivery, rarely used magnesium in the management of preeclampsia. The findings of these studies may suggest that the peripartum administration of magnesium prevents the occurrence of toxemia in certain patients and delays the development of eclampsia in others to the late postpartum period. 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, not unlike patients presenting with antepartum eclampsia (2,7,8). Headache and visual changes were common in one study ( 16) with abdominal pain occurring less often (16,21). Patient age and parity also are similar in both antepartum and postpartum toxemias; young, nulliparous patients are most frequently affected (2,7,8,13,18). Physical examination and laboratory findings such as edema, hyperreflexia, 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 (7,8,16,17). A previous diagnosis of preeclampsia at the time of convulsion is available in 50 to 75% of patients with postpartum eclampsia. The remaining patients represent cases in which the diagnosis was

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missed or the process appeared suddenly with rapid progression in the postpartum period (13,16,17). The severity of eclampsia appears to differ between the ante- and postpartum varieties. Postpartum toxemia is described as mild in 65% 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 62% 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( 13). 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 looking for agents capable of producing seizures 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 transaminase;, are frequently elevated, especially in the HELLP syndrome variant. A CT scan of the head should also be performed at the time of presentation in 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 (Table 2) for such convulsions includes metabolic, toxic, infectious, neurologic, and traumatic etiologies as well as preexisting or new-onset epilepsy. Additionally, epidural anesthesia has been reported as a potential cause of seizure in postpartum patients (22). Patients presenting with a seizure due to a variety of causes such as epilepsy, hemolytic uremic syndrome, pheochromocytoma, water intoxication, hypoglycemia, central nerv-ous system hemorrhage, and central venous thrombosis have been incorrectly diagnosed with eclampsia in the past due to an incomplete evaluation and a lack of physician understanding of the entity. The initial management of postpartum eclampsia is similar to the approach used in the treatment of antepartum toxemia. Attention to the ABCs with

Table 2. The Diffwentkl Diafposis in the of conv Postpartum Period I_ .- ..Infectious Meningitis Encephalitis Brain abscess Central nervous system Tumor Cerebrovascular Embolic stroke intracranial hemorrhage Central venous thrombosis Hypertensive encephalopathy Metabolic/endocrine Hypo-/hyperglycemia Hyponatremia Hypocalcemia Water intoxication Pheochromocytoma Toxic Traumatic head injuries Idiopathic (epilepsy) Psychogenic (pseudoseizure)

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 diphenylhydantoin 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 (23) though not universally accepted among the obstetrical and neurologic communities (24). It is administered in a 4 to 6 g intravenous bolus over 30 min, followed by a constant infusion of 1 to 2 g per hour. Manifestations of excessivemagnesium 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 eight 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 to antepartum toxemia due to the absence of the fetus. Patients presenting with toxemia or a constellation of clinical findings (i.e., headache, visual changes, epigastric pain, or hyper-reflexia) suggestive of toxe-

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mia in the postpartum period should be admitted to a monitored setting with both urgent obstetrical and neurologic consultations. Such patients presenting with complaints and 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 the progression to convulsive activity. The subject in our case is a member of a small yet challenging group of unidentified patients with altered mental status presenting with a potentially serious disorder, accounting for 0.44% of all visits in one urban emergency department (25). This specific population is a category of patients with a wide range of life-threatening disorders including traumatic, metabolic, toxicologic, and neuropsychiatric syndromes requiring rapid diagnostic evaluation and therapy. According to two studies (25,26) addressing such patients, the etiology of the altered sensorium was traumatic (most often to the head) in 41 to 47% of cases, followed by overdose in 7.8 to 22%. Other causesof altered mental status included neuropsychiatric disorders, acute ethanol intoxication, seizures, hypothermia, and miscellaneous medical conditions.

Seizures accounted for 3.8 to 10% of such patients, The mortality rate for these unknown patients is relatively high, ranging from 23 to 47% (25,26). Additionally, the inability to initially identify these patients was felt to have compromised their care and may have contributed to the high mortality rate (25). The initial inability to identify our patient undoubtedly impacted on her early management.

CONCLUSION

We report the case of an unknown female who presented to the ED in an unresponsive state after an apparent seizure related to postpartum toxemia. Emergency physicians must be familiar with the presentation and management of toxemia, both the ante- and postpartum varieties. Further, they must recognize that a significant minority of casesof toxemia will occur after both delivery of the infant and discharge from the hospital. An altered sensor-mmfollowing a seizure resulting from postpartum toxemia must be added to the differential diagnosis for female patients presenting with changesin mentation.

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rience in a referral medical center. Am J Obstet Gynecol. 1982; 142:28-35. 16. Watson DL, Sibai BM, Shaver DC, Dacus JV, Anderson GD. Late postpartum eclampsia:an update. S Med J. 1983;76:1487-9. 17. Sibai BM, Schneider JM, Morrison JC, et al. The late postpartum eclampsia controversy. Obstet Gynecol. 1980;55:74-81 18. Cunningham FG, MacDonald PC. et al.. eds. Hvnertensive disorders in pregnancy. In: Williams obstetrics. New York: Appleton-Century-Crofts; 19th ed; 1993:763-817. 19. Jeffcoate TNA, Scott JS. Some observations on the placental factor in pregnancy toxemia. Am J Obstet Gynecol. 1959;77: 475-89. 20. Brown CEL, Cunningham FG, Pritchard JA. Convulsions in hypertensive, proteinuric primiparas more than 24 hours after delivery: eclampsia or some other cause?J Reprod Med. 1987; 32:499-503. 21. Samuels B. Postpartum eclampsia. Obstet Gynecol. 1960;15: 748-52. 22. Vercauteren MP, Vundelinckx GJ, Hanegreefs, GH. Postpartum headache, seizures and bloodstained C.S.F. Intensive Care Med. 1988;14:176-7. 23. Pritchard JA, Cunningham FG, Pritchard SA. The Parkland Memorial Hospital protocol for treatment of eclampsia: evaluation of 245 cases.Am J Obstet Gynecol. 1984;148:951-60. 24. Kaplan PW, Lesser RP, Fisher RS, Repke JT, Hanley DF. No, magnesium sulfate should not be used in treating eclamptic seizures. Arch Neurol. 1988;45:1361-3. 25. Claps PJ, Berk WA. The John Doe syndrome: diagnosis and outcome of patients unidentified at the time of emergency department admission. Am J Emerg Med. 1992;10:217-8. 26. kothari m, bazil c, syed j, et al. patients of unknown identity: a neurodiagnostic challenge. Am J Emerg Med. 1994;12:510-1. 27. Lubarsky SL, Barton JR, Friedman SA, Nasreddine S, Ramaddan MK, Sibai BM. Late postpartum eclampsia revisited. Obstet Gynecol. 1994;83:502-5.