Puerperal eclampsia in the immediate postoperative period of cesarean section: a critical obstetric emergency

INTRODUCTION

Eclampsia is a serious and potentially fatal complication of hypertensive disorders of pregnancy, characterized by the onset of new-onset seizures (tonic-clonic, focal, or multifocal) in the absence of other identifiable neurological causes.(1) It affects approximately 2-8 % of pregnancies worldwide(2,3) and occurs in 2-3 % of patients with preeclampsia.(4) As one of the leading causes of maternal and perinatal mortality, its timely diagnosis and immediate management, including seizure control with magnesium sulfate and appropriate termination of pregnancy, are crucial to mitigate maternal and fetal complications. Most cases of eclampsia occur in the postpartum period, with the first 48 hours being the highest risk period. 1Classically, preeclampsia and, by extension, eclampsia have been defined by the concomitant presence of significant hypertension and proteinuria. In fact, most women who develop these conditions exhibit these signs between 20 weeks of gestation and 48 hours postpartum. However, recent literature has documented the emergence of atypical forms of eclampsia, in which seizures can occur in the absence of hypertension or proteinuria.(1) These atypical presentations account for approximately 8 % of eclampsia cases, and studies have found that up to 38 % of eclampsia convulsions occur before these signs are documented.(2,5) The unpredictable nature of these cases makes timely diagnosis and management difficult.(5) This case report of a primigravida patient who developed generalized tonic-clonic seizures four hours after a cesarean section, with no history of hypertension or proteinuria at baseline, although mild hypertension and slight proteinuria were subsequently identified.

The objective is to highlight the unusual presentation of puerperal eclampsia in the immediate postoperative period in the initial absence of the classic diagnostic criteria of hypertension and proteinuria, which is of significant academic and clinical value. This case underscores the need to maintain a high index of clinical suspicion and consider the diagnosis of eclampsia even in the absence of typical features, given that early recognition is critical for the prevention of maternal and neonatal morbidity and mortality.(6)

CLINICAL CASE

A 29-year-old female patient, primigravida, from and residing in La Paz, Bolivia, with a relevant personal medical history of moderate anemia in childhood, treated intermittently with ferrous sulfate. In December 2024, she was diagnosed with fungal colpitis, for which she was prescribed treatment with vaginal clotrimazole, which she did not complete. She reports no allergies, tobacco, alcohol, or drug use. Her gynecological and obstetric history includes menarche at age 15 with regular menstrual cycles (28/4 days), onset of sexual activity at age 17, nulliparous (G0), nulliparous (P0), null abortions (A0), and no cesarean sections (C0). Her last menstrual period (LMP) was on April 29, 2024. The estimated gestational age at admission was 40,6 weeks. The patient denied using contraception and had no history of sexually transmitted infections. Her last cervical smear was in 2013, with normal results. She had 10 adequate prenatal checkups.

The patient presented to the emergency department with prodromal labor, with a clinical picture of progressively intense contractile abdominal pain radiating to the lumbar region, accompanied by the expulsion of a mucous plug. On physical examination upon admission, the following vital signs were recorded: blood pressure 100/70 mmHg, heart rate 102 beats per minute (bpm), respiratory rate 20 breaths per minute (rpm), temperature 37 °C, and oxygen saturation 93 %.

An obstetric ultrasound was performed, which reported a pregnancy of 37,2 weeks according to fetal biometry, with a single live fetus in cephalic presentation, estimated fetal weight of 3 556 g, and pathological findings of severe oligohydramnios (amniotic fluid index: 2 cm) and an altered fetal Doppler profile. Given the diagnosis of risk of fetal distress, an emergency segmental cesarean section was decided. During the surgical procedure, a live female newborn was delivered, weighing 3 030 g and measuring 50 cm, with no immediate neonatal complications. The estimated intraoperative blood loss was 350 ml. Approximately four hours after the cesarean section, while in the recovery room, the patient had two generalized tonic-clonic seizures without sphincter relaxation. Intravenous midazolam was administered as immediate treatment. Based on the clinical picture, a diagnosis of puerperal eclampsia was established, and her transfer to the intensive care unit (ICU) was coordinated. Upon admission to the ICU, the patient was in a stable neurological state (Glasgow Coma Scale 15/15), with no signs of neurological focalization. Blood pressure readings of 135/90 mmHg were documented, with a subsequent peak of 145/90 mmHg. Initial laboratory studies showed mildly impaired renal function (creatinine: 1,1 mg/dL), mild hyponatremia (133 mmol/L), mild anemia (hemoglobin: 9,7 g/dL), and proteinuria on urine examination. No criteria for HELLP syndrome were found.

The therapeutic plan in the ICU included the infusion of phenytoin as an anticonvulsant, antihypertensive management with alphamethyldopa, hemodynamic support, correction of electrolyte imbalance, and empirical antibiotic therapy for suspected urinary tract infection. In addition, two units of packed red blood cells and three units of fresh frozen plasma were transfused due to anemia and an initial alteration in coagulation parameters. After 48 hours of management and stabilization in the ICU, the patient was transferred to the postpartum ward. Her subsequent evolution was favorable, remaining afebrile, hemodynamically stable, and without recurrence of seizures. Oral antihypertensive treatment was continued, and progressive improvement in laboratory results was observed. Neurologically, she remained alert, oriented, and without deficits. Finally, she was discharged with instructions for outpatient follow-up by the Gynecology and Obstetrics service.

DISCUSSION

Eclampsia is classically defined as the onset of seizures in a woman with preeclampsia, without other attributable causes. Traditionally, preeclampsia is associated with hypertension and significant proteinuria. Overall, the modeled incidence of preeclampsia and eclampsia is approximately 4,6 % and 1,4 % of all deliveries, respectively, with wide regional variation. Eclampsia can occur before, during, or after delivery.About one-third of women with eclampsia have their first seizure after the birth of their baby.(4,7) The highest risk of eclampsia occurs in the first week postpartum, with early postpartum eclampsia occurring within the first 48 hours after delivery, as in the case presented. The peculiarity of our case lies in the absence of classic signs of preeclampsia (hypertension or overt proteinuria) before the onset of seizures. The literature has documented that eclampsia can occur without warning.(1) In fact, a significant percentage of women, between 20 % and 38 %, do not show the classic signs of preeclampsia before the convulsive episode. (2) In addition, it has been observed that 21 % of female patients with eclampsia had normal blood pressure (≤140/90 mmHg).(7) This challenges the notion of a linear progression from preeclampsia to eclampsia.(1,2) Our case, where the patient was normotensive and norm us in the prenatal period and only showed a slight elevation in blood pressure and proteinuria after the seizures, is a clear example of this atypical presentation.(1,6) Regarding pathophysiology, it has been debated whether the neurological symptoms of eclampsia are due to vasospasm or cerebral hyperperfusion causing cerebral edema formation. Current evidence suggests that eclampsia is a form of posterior reversible encephalopathy syndrome (PRES), characterized by reversible abnormalities on neuroimaging that are suggestive of cerebral edema.(7) Endothelial cell dysfunction is central to the pathogenesis of preeclampsia, leading to vasospasm, plasma transudation, and ischemia, and in atypical cases, organ involvement may begin with the brain.(2) PRES lesions mainly affect the posterior brain, occipital and parietal cortices, although other areas may also be involved. Interendothelial cell leakage, associated with preeclampsia, develops at much lower blood pressure levels than would normally cause vasogenic edema, and is accompanied by a loss of autoregulation of the upper limit of cerebral blood flow.(11,12) The clinical implications are significant. It is crucial to maintain a high index of clinical suspicion for eclampsia, even in patients who do not present with classic signs of preeclampsia during pregnancy or before delivery. The need for neurological surveillance in the postpartum period, especially in patients without a history of hypertension, is essential for early detection.(13,14) In a post-cesarean context, it is imperative to consider eclampsia in the differential diagnosis when seizures occur, as timely diagnosis and treatment, such as the administration of magnesium sulfate, are critical to prevent serious maternal and fetal complications.(1) It is important to highlight the flowchart-based approach used in our hospital. (figure 1)

CONCLUSIONS

The clinical case describes the onset of generalized tonic-clonic seizures, with no history of hypertension or proteinuria. This presentation challenges the classic profile of eclampsia and aligns with curry evidence indicating that up to 38 % of cases may present without prior diagnosis of hypertension or proteinuria and even with normal blood pressure readings. This case highlights the importance of maintaining a high index of clinical suspicion for eclampsia in the immediate postpartum period, even in the absence of previous criteria for preeclampsia. Assessment of clinical symptoms and blood pressure monitoring remain the most effective methods for diagnosing eclampsia, allowing for early intervention. Close neurological monitoring and the inclusion of eclampsia in the differential diagnosis of any neurological symptoms are also highlighted. Post-seizure treatment includes monitoring and management of potential complications. Early recognition and timely use of magnesium sulfate are essential to reduce maternal morbidity and mortality.

References

1. 1 Magley M, Hinson MR. Eclampsia. [Updated 2024 Oct 6]. En: StatPearls [Internet] [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 [citado el 24 de junio de 2025]. Available at: https://www-ncbi-nlm-nih-gov.translate.goog/books/NBK554392/?_x_tr_sl=en&_x_tr_tl=es&_x_tr_hl=es&_x_tr_pto=tc
2. 2 American College of Obstetricians and Gynecologists’ Committee on Practice Bulletins-Obstetrics. Gestational hypertension and preeclampsia: ACOG Practice Bulletin, number 222. Obstet Gynecol [Internet]. 2020;135(6):e237–60. Available at: http://dx.doi.org/10.1097/AOG.0000000000003891
3. 3 Duley L. The global impact of pre-eclampsia and eclampsia. Semin Perinatol [Internet]. 2009;33(3):130–7. Available at: http://dx.doi.org/10.1053/j.semperi.2009.02.010
4. 4 Pérez Nisperuza MJ, Sarmiento Lombana MV, Gómez Rodríguez RA, Ortega López NP, Ordosgoitia Betín ME, Soto Lara KM, et al. Actualización del Manejo de la Eclampsia ¿Que ha Cambiado? Ciencia Latina [Internet]. 2024;8(3):220–32. Disponible en: http://dx.doi.org/10.37811/cl_rcm.v8i3.11205
5. 5 Albayrak M, Ozdemir I, Demiraran Y, Dikici S. Atypical preeclampsia and eclampsia: report of four cases and review of the literature. J Turk Ger Gynecol Assoc [Internet]. 2010;11(2):115–7. Available at: http://dx.doi.org/10.5152/jtgga.2010.014
6. 6 Ghadiali T, Nguyen MT, Lee RH, Sasso EB. Atypical eclampsia in a normotensive patient with altered mental status and severely elevated transaminases: Case report and review. Int J Gynaecol Obstet [Internet]. 2024;164(2):476–81.Available at: http://dx.doi.org/10.1002/ijgo.14975
7. 7 Cipolla MJ. Cerebrovascular function in pregnancy and eclampsia. Hypertension [Internet]. 2007;50(1):14–24. Available at: http://dx.doi.org/10.1161/hypertensionaha.106.079442
8. 8 Acosta Aguirre Y, Bosch Costafreda C, López Barroso R, Rodríguez Reyes O, Rodríguez Yero D. Preeclampsia y eclampsia en el período gravídico y puerperal en pacientes ingresadas en cuidados intensivos. Rev Cuba Obstet Ginecol [Internet]. 2019 [citado el 24 de junio de 2025];45(1):14–24. Disponible en: http://scielo.sld.cu/scielo.php?script=sci_arttext&pid=S0138-600X2019000100014&lang=es
9. 9 Abalos E, Cuesta C, Grosso AL, Chou D, Say L. Global and regional estimates of preeclampsia and eclampsia: a systematic review. Eur J Obstet Gynecol Reprod Biol [Internet]. 2013;170(1):1–7. Available at: http://dx.doi.org/10.1016/j.ejogrb.2013.05.005
10. 10 Diaz V, Long Q, Oladapo OT. Alternative magnesium sulphate regimens for women with pre-eclampsia and eclampsia. Cochrane Database Syst Rev [Internet]. 2023;10(10):CD007388. Disponible en: http://dx.doi.org/10.1002/14651858.CD007388.pub3
11. 11 Cunningham FG, Leveno KJ, Bloom SL, Dashe JS, Hoffman BL, Casey BM, et al. Williams Obstetrics. 26th ed. New York: McGraw-Hill; 2022.
12. 12 Hassan H, Zaarour M. Case of postpartum eclampsia in a patient with isolated proteinuria. ijcriog [Internet]. 2019;5:1. Disponible en: http://dx.doi.org/10.5348/100053z08hh2019cr
13. 13 Anandan S, Rajendran SS, Kumar JP, Shajee DS. Late postpartum eclampsia with “normal” blood pressure. J Assoc Physicians India [Internet]. 2024;72(10):e37–8. Disponible en: https://japi.org/article/japi-72-10-e37
14. 14 Norwitz E. Eclampsia [Internet]. UpToDate. 2025 [citado el 24 de junio de 2025]. Disponible en: https://www.uptodate.com/contents/eclampsia.