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XIII. Ulusal Perinatoloji Kongresi 13-16 Nisan 2011, ‹stanbul

Perinatoloji Dergisi 2011;19(Suppl 1): S63-S70 e-Adres: http://www.perinataldergi.com/20110191122

Eclampsia Management: Our Experience

Dr Girija Wagh, MD

FICOG Dip in Endoscopy Professor and Head, OBGYN, Bharati Vidyapeeth University Medical College, Pune, India

Introduction are complicated by PIH and therefore we need to have a high index of suspicion. As a country the biggest challenge faced today by us obstetricians is the maternal mortality and mor- • By definition Eclampsia is defined as the occur- bidity. Also what we encounter as the most challeng- rence of one or more superim- ing disorder is preeclampsia and eclampsia. As said posed on pre-eclampsia. when we do not know the makers of PIH what can • Preeclampsia is -induced hyperten- we know about the markers? Truly we donot know sion in association with (> 0.3 g in why PIH occurs and lifetimes have gone by in burst- 24 hours) ± and virtually any organ sys- ing this mystery. tem may be affected Preeclampsia and eclampsia are obstetric dis- We also know that there are four major types of eases, and obstetricians are the group best equipped hypertensive disorders during pregnancy. And we to diagnose, evaluate and manage them. Today as a need to classify them.It is important that we do so as clinician however we need to tackle what we have that helps in better prognostication and treatment from the experiences gathered and try to deliver the planning. best to our patients.We should not falter there and 1. Chronic should try to deliver the best.From making the diag- 2. Preeclampsia eclampsia syndrome nosis to treating atypical eclampsia, management of preeclampsia involves serious, often unpredictable 3. Superimposed preeclampsia challenges. In this article, we highlight several chal- 4. lenges that obstetricians face when managing Attempts should be made to establish these diag- preeclampsia and eclampsia, and offer useful strate- noses antenatally, intranatally, postnatally and in sub- gies to help minimize morbidity and mortality in sequent pregnancy both mother and infant. Although severe preeclampsia represents only a Optimum Antenatal Care is a Must fraction of those amounts, and eclampsia an even Early and adequate cannot me more lower percentage, they are potentially catastrophic emphasized ! Although the diagnostic criteria for complications of pregnancy and one of the leading preeclampsia have been widely established – persis- causes of . They also are responsible tent BP elevation above 140/90mmHg and protein- for a large percentage of infants born prematurely as uria exceeding 300mg over a 24hr collection period- a result of a worsening maternal or fetal condition. the condition does not always play by the rules. With The National Eclampsia Registry interim statistics close monitoring of weight, urine protein, and BP, reveals that the incidence of hypertensive diseases the clinician can identify and follow the patient and during pregnancy to be quite high with quite a sub- detect a condition much early stantial incidence of eclampsia. These are actually Risk Factors for Preeclampsia: cases reported by the FOGSI members. There can be • Chronic hypertension quite some more which are being treated by periph- eral health workers and the incidence can actually be • Chronic renal disease higher.What we know for sure is 1in 10 • Connective tissue disease 64 Wagh G, Eclampsia Management: Our Experience

• Current foetal growth restriction fulfilled, along with one or more of the findings list- • Gestational hypertension in the current preg- ed below: nancy • Persistent pressure above 160/110 • History of prior preeclampsia mmHg • Insulin dependent • Proteinuria • Refractory (<500cc over 24 hours) • Multiple gestation • Renal failure (minimal criterion would be a rise • Nulliparity in serum creatinine of 1mg/dl above baseline) • Obesity • Persistent right upper quadrant or epigastric • Thrombophilia. pain or both It is important to diagnose it early: • Persistent headache Early identification of preeclampsia may allow • Scotomata/blurred vision for interventions, including delivery, that will lessen • Shortness of breath with reduced oxygen satu- the risk of progression to severe preeclampsia and ration or eclampsia and reduce foetal and maternal morbidity • (platelets <100,000 / and mortality. It is, therefore, essential for the clini- cu.mm) cian to ask specifically about of • (based on peripheral smear analysis preeclampsia and to listen carefully to the answers. or increased Bilirubin) Signs and symptoms may sometimes be typical: • Impaired liver function of unclear etiology • Eclampsia • Weight gain • Estimated foetal weight below 5th percentile • Increasing edema for • Persistent headache • Blurred vision Prediction • Malaise Attempts to predict preeclampsia have met with poor results. Measurement of the ratio of uterine • Nausea artery systolic to diastolic flow has not been informa- • Epigastric discomfort tive in the general healthy population of pregnant • Right upper quadrant discomfort. women. Nor has uric acid determination been useful; Although a number of tests have been proposed it generally has very poor predictive value and to predict who may be at greatest risk for preeclamp- should be interpreted with caution. sia, none have risen to the level that they can be rec- ommended for general population screening. When to Hospitalize? Mild preeclampsia can be managed expectantly Diagnostic Criteria until foetal maturity or 37weeks of gestation.But hos- The diagnosis of preeclampsia is based on persis- pitalization can be offered in the Indian context. This tent BP elevation above 140/90 mmHg and protein- offers an opportunity to investigate the patient prop- uria exceeding 300 mg over a 24-hour collection peri- erly,monitor the urine output, BP and the fetal con- od. Other criteria have been applied, such as rise in dition through USG and Doppler if necessary.Also systolic or diastolic BP above baseline and urine dip- the patient can be offered dietary advice and the cor- stick criteria for proteinuria, but BP above rect categorization after her BP has been monitored 140/90mmHg and proteinuria above 300mg are round the clock.But any serious presentations such most frequently used in medical centres Gestational as severe edema, ascites, high BP, severe proteinuria, hypertension and chronic hypertension do some- headache, pain, sever IUGR,convulsions etc demand times coexist with superimposed preeclampsia, but a hospital care. should not be confused with preeclampsia or lead to Assessment: management decisions that should apply only to patients with preeclampsia. Initial evaluation consists of: Before severe preeclampsia can be diagnosed, • Foetal non stress testing the initial criteria for preeclampsia should have been • index Perinatoloji Dergisi 2011;19(Suppl 1): S63-S70 65

• Serial BP determination cated and should be administered in a timely fashion. • 24-hour urine collection( if dipstick proteinuria , nifedipine have been used effectively is negative ) in such acute settings, when administered parenter- • Initial laboratory evaluation comprising of a ally (except nifedipine, which can be given orally with platelets and aspar- and should never be given sublingually) and when tate amino transferase (AST), alanine amino given in proper dosage. transferase (ALT), and creatinine levels and Pharmacotherapy of acute hypertension: LDH levels The tests should be directed to assess the mater- Table 1. Pharmacotherapy of acute hypertension. nal conditions as Preeclampsia is a multisystemic dis- order. Constant vigilance should be undertaken to Drug Dosage Directions prevent eclampsia as far as is possible and to diag- nose HELLP early. There is a tendency to prolong the Labetalol 10-20 mgIV push Repeat every 10-20mins, doubling pregnancy as much as possible to be able to achieve the dosage each time until a salvagibility in the .But one needs to weigh the maximum total cumulative dosage risk to the mothers system such a prolongation could of 300mg has been given. cause. Also LDH levels above 600 have proved to be Nifedipine 10 mg Repeat in 20mins for four doses a better parameter to guide a clinician regarding the (maximum 40mg); then give presence of hemolysis. This can help one guide 10-20 mg orally (never sublingually) regarding the intervention and rising LDH levels every 4-6h to achieve a stable BP of would help this decision.While interpreting renal 140-150/90-100 mmHg. parameters in Pregnancy one should muster care as these parameters are already reduced in a normal pregnancy due to increased GFR and hemodilution Preventing Additional tests may be ordered as indicated but sulfate is the drug of choice to pre- are of limited value in making management deci- vent both initial and recurrent eclamptic seizures. sions. If foetal and maternal evaluations are reassur- Two large clinical trials ended any doubts about its ing, and if the patient has remained stable, then out- efficacy, demonstrating its superiority over both patient management may be considered. In general, and in the settings of if proteinuria exceeds one gram in 24 hours, in-hos- preeclampsia and eclampsia. pital management is recommended, regardless of other parameters. Magnesium sulfate is best administered intra- venously(iv) via continuous infusion pump. An ini- Controlling : tial bolus of 4-6gm is given over 15-30mins; this Why? and How? amount does not need be adjusted to the patient’s level of renal function. A continuous infusion of mag- Cerebrovascular accident(stroke) is the leading cause of maternal mortality from preeclampsia. Not nesium sulfate is usually initiated at a rate of all cases can be prevented, but one suggested pre- 2gm/hour. It is this infusion dosage that may need to ventive strategies is adequate BP control. Some cases be altered, based on the patients urine output and of stroke in the setting of preeclampsia will occur renal function. despite systemic BP reading that are not considered Evidence of magnesium toxicity includes: to be in a dangerous range. One reason may be an • Loss of deep tendon reflexes over ride of normal cerebral blood flow auto regula- • Respiratory depression tion mechanisms, resulting in increased cerebral • Blurred vision blood flow, rising cerebral pressures, and vessel rupture. Such occurrences may sometimes, • Cardiotoxicity but not always, be related to . Each of these toxicities can occur at ostensible When a patient has elevated BP, generally therapeutic levels of serum magnesium, so there can defined as persistent systolic pressures above 160 to be no substitute for the regular (atleast every 2hours) 170mmHg and persistent diastolic pressures above clinical assessment of the patient who is receiving a 105 to 110 mmHg, antihypertensive therapy is indi- continuous infusion of magnesium sulfate. 66 Wagh G, Eclampsia Management: Our Experience

There is no debate about the utility of magnesium Risks of Regional Anesthesia: sulfate in severe preeclampsia, but when it comes to Women who have preeclampsia are volume intrapartum management of mild preeclampsia or depleted. As such, they are prone to hypertension cases in which preeclampsia first manifests in the after administration of regional anesthesia if the post partum period, data are not so clear. This debate block sets up too rapidly. For this reason, epidural will not be resolved to anyone’s satisfaction in the anesthesia or some of the newer combined tech- course of this article. Historically, the practice has niques offer optimal analgesia by allowing for slow- been to use magnesium in these circumstances, but er implementation of the regional block. the pendulum has begun to shift based on the few Women who have preeclampsia, especially arguments: severe preeclampsia, are usually candidates for • Eclampsia is a rare event (about 1 case for regional analgesia and anesthesia. Some requisites every 300 to 1000 deliveries) for regional anesthesia under these conditions • Most cases occur outside of the hospital include the following: • Some women experience seizures before • The patient can tolerate preblock hydration preeclampsia has been diagnosed • She has adequate IV access • Some patients experience seizures while tak- • There is reproducible means of determining ing magnesium sulfate. BP One might argue that number of potentially pre- • The patient has a normal profile. (a ventable cases of eclampsia is lower-perhaps in the normal platelet count with normal transami- range of one in every 3000 to 10,000 deliveries-and nase should be sufficient to confirm this; that this low rate does not justify routine use of the women who have preeclampsia are not at drug. increased risk of having altered prothrombin Regardless of one’s position on this debate, there time, partial thromboplastin time, or fibrino- is broad consensus that regular careful clinical assess- gen levels, provided there are no other mitigat- ment of the patient who has preeclampsia is essential ing clinician circumstances). to minimize the morbidity and mortality. This disease • The anesthesiology team is skilled in the can progress from mild to severe rapidly. Only thor- administration of regional anesthesia. ough regular careful assessment can a physician If Eclampsia Occurs: observe this change soon enough to alter manage- ment as necessary. Do not proceed to emergent cesaerean section. Rather, stabilize the mother, protect her from injury Treatment of Magnesium Toxicity: during the , protect her airway, and allow the 10% calcium gluconate (1g) is administered IV seizure to take its course. to reverse the effects of suspected magnesium toxici- Begin magnesium at once. If it was being infused ty. before the seizure, consider giving an additional 2g In addition, because magnesium freely crosses bolus over several minutes. As the mother stabilizes, the , it is recommended that a new born the foetal heart rate will recover and she can be resuscitation team be present at all deliveries during reassessed to determine optimal timing and route of the mother was receiving magnesium sulfate delivery. because neonatal respiratory and cardiac depression In case of fetal compromise cesarean section may have been reported in this setting. be a better choice than a vaginal delivery

Delivering The Patient: Practice AMTSL Preeclampsia, severe preeclampsia, and eclamp- Whether a vaginal delivery or a CS active man- sia present a dilemma for the managing clinician: agement with oxytocis should be practiced to pre- subject her to the rigors of labor, or to the height- vent PPH. It is safe to use Oxytocin 5 U bolus equally ened risk of cesarean delivery? Overall, a properly diluted over 2-3 minutes or Prostaglandin injections. vaginal delivery is less hemodynamically stressful PG can be used also as misoprostol sublingually or than cesarean delivery for the mother. To accomplish transvaginally. due to hemoconcentration even aver- vaginal delivery, it is necessary to provide optimal age loss maynot be well tolersated by these patients. anesthesia and analgesia. Also hyopertension, use of magnesium sulpahte and Perinatoloji Dergisi 2011;19(Suppl 1): S63-S70 67

endpthelis dysfunction can contribute to more blood • Central loss which maynot be well compensated and tolerat- - Cerebral over perfusion due to loss of ed by these patients. All attempts to reduce blood autoregulation loss should be undertaken. The fluids used should - be liberal but judicious recommendation is 80 ml - Cerebral hemorrhage /kg/hr as over infusion can cause pulmonary edema very fast in these women. Eclampsia and preeclampsia account for approx- imately 63,000 maternal deaths worldwide annual- Post Delivery Management ly.1 In developed countries, the maternal death rate has been reported as 0-1.8%. A CDC study found an It involves close vigilance for eclampsia, PPH, overall preeclampsia-eclampsia case-fatality rate of HELLP, Pulmonary edema and thromboembolic 6.4 per 10,000 cases at delivery with a rate twice as complications. Delivery of the baby is the treatment high for black women compared with white women. but the 72 hours post delivery are an important peri- This same study found an increased risk of death od when hemodynamic transition is occurring in the among women older than 30 years and those with no mother which need close observation and early prenatal care. The highest risk for maternal death detection of eclampsia. The NER data has shown a was found in pregnancies at 28 weeks’ gestation or high index of postpartum eclampsia and it has to be remembered that such a occurrence leading to mor- less. The maternal mortality rate is as high as 14% in bidity has to be avoided by all means developing countries.2 The perinatal mortality rate from eclampsia in recent reviews in the United States Preventing Complications and Great Briton ranges from 5.6-11.8%.3 4 Preeclampsia/eclampsia produces multiple sys- Maternal complications of eclampsia may include temic derangements that can involve a diversity of permanent CNS damage from recurrent seizures or organ systems including hematologic, hepatic, renal, intracranial bleeds, disseminated intravascular coag- and cardiovascular systems as well as the central ner- ulopathy, renal insufficiency, pulmonary edema, and vous system. The severity of these derangements cardiopulmonary arrest. A majority of maternal often correlates with maternal medical (eg, pre-exist- deaths associated with eclampsia have concurrent ing renal or vascular pathology) or obstetric factors HELLP syndrome.4 Causes of neonatal death include (eg, multifetal gestations or ). prematurity, placental infarcts, intrauterine growth Systemic derangements associated with eclampsia retardation, abruptio placentae, and fetal . can include the following: Complications As many as 56% of patients with • Cardiovascular eclampsia may have transient deficits, including cor- tical blindness.Studies have failed to demonstrate - Generalized vasospasm evidence of persisting neurologic deficits after - Increased peripheral vascular resistance uncomplicated eclamptic seizures during the follow- - Increased left ventricular stroke work index up period.3 Maternal, as well as fetal, death can be a - Decreased central venous pressure consequence of eclampsia and its complications. - Decreased pulmonary wedge pressure Etiopathogensis of Complications: The failure of • Hematologic cytotrophoblastic epithelial-to-endothelial transfor- - Decreased plasma volume mation and a subsequent lack of adhesion mole- - Increased blood viscosity cules, integrins, and cadherins results in a damaged - Hemoconcentration placenta which in turn secretes the antiangiogenic - Coagulopathy factors, sFlt1 and endoglins into the maternal circula- • Renal tion. These factors lead to impaired VEGF/PlGF and β - Decreased glomerular filtration rate TGF- signaling, resulting in systemic endothelial cell dysfunction mediated by a variety of factors. - Decreased renal plasma flow Endothelial dysfunction, in turn, results in the sys- - Decreased uric acid clearance temic manifestations of preeclampsia. Endothelial • Hepatic dysfunction, vasoconstriction and platelet aggrega- - Periportal necrosis tion and edema result all over the body with various - Hepatocellular damage manifestations which can conglomerate into compli- - Sub capsular hematoma cations 68 Wagh G, Eclampsia Management: Our Experience

Maternal Complications: Maternal complica- quickest means of diagnosis although computerized tions are those related to the effect of severe tomography is more sensitive. The management of preeclampsia on multiple organ systems, together contained hematoma is to support the patient, with with those associated with medical complications surgery reserved for those who are hemodynamical- during pregnancy and the course of labor. ly unstable or documented expansion of hematoma. 1. Eclampsia: The term comes from the Greek Surgical management includes stitching of the word for lightning. While the risk of death from com- lesions, packing, argon laser ablation, use of gelatin plications of eclampsia is relatively high in the devel- sponge, hepatic artery ligation, embolization of oping world-ranging from about 14 to 22% -- the risk hepatic artery, use of recombinant factor VII A and is much lower in developed nations. Compared to liver transplantation. women without seizures, eclamptic women had sig- 5. Renal complications: Typically in preeclamp- nificantly higher rates of headache, visual changes, sia, renal blood flow and GFR fall with a decreased epigastric pain, and nausea and vomiting. HELLP syn- urate clearance and increased calcium reabsorption drome, disseminated intravascular coagulation, leading to hyperuricemia and hypocalciuria. acute renal failure, neurological complications, and Histopathologically, there is swelling of the glomeru- acute respiratory distress syndrome. More than half lar endothelial cells, referred to as glomeruloen- of patients need cesarean delivery. Early neonatal dotheliosis. Pre-renal oliguria may develop to acute mortality rate is also high. tubular necrosis, most often with a good prognosis 2. HELLP Syndrome: One of the most severe Acute cortical necrosis is rare and has poor progno- forms of preeclampsia it occurs in 4 percent to 12 sis Renal failure is relatively unusual even with severe percent of the women who have preeclampsia. cases, unless there is significant or hemo- HELLP stands for: hemolysis, elevated liver enzymes, dynamic instability or marked DIC. The renal and and lowered platelets. The criteria of the syndrome extrarenal abnormalities typically resolve sponta- are debated but include hemolysis as evidenced by neously within the first two weeks postpartum. an abnormal peripheral blood smear; platelet count 6. Hematological Complications: Thrombocyto- of less than 100 x 109/L; and serum AST value of penia, Disseminated intravascular coagulation and greater than 70 U/L, serum lactate dehydrogenase associated bleeding disorders including massive value of greater than 600 U/L, or total bilirubin value PPH. of greater than 1.2 mg/dL. Clinically the diagnosis of 7. Cardiovascular dysfunction: Untreated HELLP syndrome may be challenging because preeclamptic women almost always have low filling patients may present with vague symptoms includ- pressures and a hyperdynamic circulation, Hence car- ing nausea, vomiting, headache, malaise, or viral-like diac failure can occur. Some cases of peripartum car- symptoms and is often mistaken for the flu acidity or diomyoipathy may be associated with preeclampsia. gallbladder problems. 8. Respiratory dysfunction 3. Antepartum hemorrhage: Abruption placenta plus preeclamspsia is a serious condition with a high A. Pulmonary edema: The main cause of mater- risk for maternal death. It is important to remember nal mortality in severe preeclampsia is now pul- that many patients with abruption placentae have monary edema. Incidence is 3-6% in severe underlying preeclampsia because signs of shock preeclampsia. Patients with preeclampsia are usually may be present even with a normal blood pressure. volume depleted, and pulmonary edema most com- These patients are hemodynamically very unstable. monly occurs in the early and is Although initially they also require active resuscita- often associated with aggressive fluid replacement. tion, they quickly become fluid overloaded, resulting Other predisposing factors include: a. Reduced albu- in pulmonary edema. Renal complications, such as min concentration and myocardial dysfunction con- acute tubular necrosis, commonly occur. tribute to edema formation. b. Reduced Colloid Osomotic Pressure (COP ) c. Increased capillary per- 4. Hepatic complications: Subcapsular hematoma meability probably due to endothelial damage and hepatic rupture are very unusual catastrophic of preeclampsia/eclampsia The report- B. Adult respiratory distress syndrome: appears ed incidence of this condition varies from 1 in 40,000 to have become more common, it is not known to 1 in 2, 50,000 deliveries. Infarction with vascular whether this is a consequence of modern methods of disruption leads to intrahepatic hemorrhage and respiratory support rather than of the disease itself. parenchymal destruction. Ultrasound scan is the 9. Neurological complications Perinatoloji Dergisi 2011;19(Suppl 1): S63-S70 69

Headache: The most common neurologic symp- include: a. Intrauterine growth retardation b. tom in preeclampsia/eclampsia is headache. Premature delivery: c. /fetal demise Headache occurs in about in 75% women with Managing complications: Managing complica- seizures (eclampsia) and always precedes the tions of eclampsia needs a multidisciplinary approach seizure. Headache can be bitemporal, frontal, occipi- and an institutional care. Eclampsia is unfortunately tal, or diffuse. known to afflict the population which is many a times Seizures: Convulsions are the other most com- far away from such settings and therefore are mon feature of this syndrome. Convulsions are usu- deprived from such care. It therefore is important to ally generalized tonic-clonic in nature. train the first contact medical personnel catering to Visual disturbances: The most common symp- deliveries to be able to identify the possibilities of these complications well ahead of their occurrence. tom is blurring of vision. The visual disturbances are Abnormal blood pressure reading should be the first ominous and may indicate impending seizure. important alarm bell which mandates the patient to be Blindness in women with eclampsia is rare and can fully investigated. The first approach to a pregnant be due to involvement of the occipital cortex or reti- patient with PIH is to classify the hypertension and the na. may cause altered vision second step is to assess the possibility of a complica- although it is usually one sided and seldom causes tion. Deterioration of these patients is very swift and total visual loss. Most women with varying degree of therefore proper evaluation is important. There amaurosis are found to have radiographic evidence always has to be a proper evaluation of the systemic of extensive occipital lobe hypodensities. Blindness parameters through the various laboratory evalua- persists from 24 hrs to 72 hrs, it subsequently tions. In country like India where anemia and infec- resolves completely. tions which cause thrombocytopenia are so rampant : Coma is a dreaded complication in that Platelet count itself cannot suffice. We have eclampsia. Coma may be a result of intracerebral hem- observed that lactose dehydrogenase can help as a orrhage that, at times, may dissect into the ventricular good marker for identifying the deterioration in the system or over the surface of the brain, creating a mas- hemolysis and help guide a clinician as a decision sive subarachnoid hemorrhage. Investigations include making tool in situations of dilemma. head CT, which involve exposure to ionizing radiation and MRI which is safer in pregnancy. Table 2. Eden’s criteria for risk assessment: can help guide Cerebrovascular accident: The association the clinician to assess risks inpatients of eclampsia. between eclampsia and cerebral hemorrhage has been recognized since 1881, and this is reported to be • Long interval bet the onset of fit and commencement of treatment the most common cause of death in patients with • Antepartum eclampsia with long delivery interval eclampsia • Fits >10 10. Gastrointentinal Complications: Ischemia • Coma in between the fits associated with pre-eclampsia cannot only damage • Temp> 102 ° F : the liver but also the pancreas and gallbladder. • PR 120/min 11. Musculoskeletal complications: • BP > 200 mmHg : SBP • Oliguria < 400 ml/24 hrs Dislocation of shoulder is a very rare complica- • Proteinuria > 5g/24 hrs tion of eclampsia. Other reported musculo-skeletal • Non response to treatment complication of eclampsia include simultaneous • bilateral central dislocation of hip 12. Maternal death: Events associated with Prognosis: About 25% of women with eclampsia maternal deaths include cerebral hemorrhage (45%), have hypertension in subsequent pregnancies. 5% of cardiopulmonary arrest (40%), disseminated patients with hypertension develop severe intravascular coagulopathy (39%), adult respiratory distress syndrome (28%), renal failure (28%), sepsis preeclampsia. About 2% of women with eclampsia (23%), hepatic hemorrhage (20%), and hypoxic develop eclampsia with future pregnancies. ischemic encephalopathy (16%). Multiparous women with eclampsia have a higher risk for development of essential hypertension and a Fetal Complications: Severe preeclampsia is asso- higher mortality rate in subsequent pregnancies as ciated with different degrees of fetal injury and compared with primiparous women 70 Wagh G, Eclampsia Management: Our Experience

Patient Education: The patient should be advised gestation), the diagnosis of hydatiform mole or and educated on the course of the disease and any choriocarcinoma should be considered.Eclampsia residual problems.The patient should be educated always should be considered in a pregnant patient on the importance of adequate prenatal care in sub- with a seizure episode.A pregnant patient who has sequent pregnancies.If the patient has preexisting been involved in an unexplained trauma (such as a hypertension, she should have good control prior to single-vehicle auto accident) and has exhibited conception and throughout pregnancy. Her case seizure activity should be evaluated for eclampsia. should be followed for recognition and treatment of preeclampsia. Post Partum Care Miscellaneous Medicolegal Pitfalls: The mode of Every patient of preeclampsia should be moni- delivery should be based on obstetric indications, tored closely for 6 weeks with proper advice regard- with the understanding that vaginal delivery is ing the use of antihypertensives and should report at preferable from a maternal standpoint.When emer- regular intervals. they should be guided and encour- gent cesarean delivery is indicated, substantiating the aged to use contraception atleast for a period of 2-3 absence of coagulopathy prior to the procedure is years. The preferred method would be an IUCD. They important.Fetal is common following an should be counseled regarding the importance of pre- eclamptic seizure and usually resolves within 10 min- natal checkup counseling and the necessary care peri- utes. Consider if uterine hyper- conceptionally in the subsequent pregnancy. activity remains and fetal bradycardia persists. References Cervical examination should not be overlooked. The 1. Vigil-De Gracia P. Maternal deaths due to eclampsia and delivery mode may be largely dependent on the cer- HELLP syndrome. Int J Gynaecol Obstet. Feb vical status.Fluid management is critical in patients 2009;104(2):90-4. [Medline] with eclampsia.Avoid the use of multiple agents, 2. Sibai BM. Diagnosis, prevention, and management of unless necessary, to abate eclamptic seizures.Ruling eclampsia. Obstet Gynecol. Feb 2005;105(2):402-10. out eclampsia in an obstetrical patient who has been [Medline]. involved in an unexplained trauma is important. 3. Sibai BM, Sarinoglu C, Mercer BM. Eclampsia. VII. Pregnancy outcome after eclampsia and long-term progno- Special ConcernsDo not overlook other neuro- sis. Am J Obstet Gynecol. Jun 1992;166(6 Pt 1):1757-61; dis- logic causes, particularly if the seizure occurs more cussion 1761-3. [Medline]. than 24 hours after delivery. When preeclampsia 4. Douglas KA, Redman CW. Eclampsia in the United occurs in the early second trimester (ie, 14-20 weeks' Kingdom. BMJ. Nov 26 1994;309(6966):1395-400. [Medline]