Case Report


A series of unfortunate events: Eclampsia with massive post-partum ascites

,  ,  ,  

1 Internal Medicine Resident, Mountain Vista Medical Centre, 1301 S Crismon Rd., Mesa, AZ 85209, USA

Address correspondence to:

Spogmai Saeed Khan

MD, Mountain Vista Medical Centre, PGY2, 1301 S Crismon Rd., Mesa, AZ 85209,

USA

Message to Corresponding Author


Article ID: 101375Z01SK2023

doi:10.5348/101375Z01SK2023CR

Access full text article on other devices

Access PDF of article on other devices

How to cite this article

Khan SS, Roalkvam SN, Harmse ADR, Saddouk Y. A series of unfortunate events: Eclampsia with massive post-partum ascites. Int J Case Rep Images 2023;14(1):18–22.

ABSTRACT


Postpartum ascites in preeclampsia and eclampsia is a rare complication associated with increased maternal morbidity and mortality. Here, we present a case of postpartum ascites, primarily localized in the gastrointestinal interstitium. Medical management with intravenous albumin to increase oncotic pressure, with piggybacked intravenous diuretics to facilitate fluid removal, showed significant clinical improvement.

Keywords: Eclampsia, Interstitial edema, Postpartum ascites, Pre-eclampsia, Pregnancy

Introduction


Preeclampsia is defined as new-onset hypertension with clinical signs of organ dysfunction presenting at >20 weeks of gestation [1]. The development of one or more tonic-clonic seizure in a patient with preeclampsia is called eclampsia [2]. Eclampsia is on the severe end of the disease spectrum that is associated with increased fetomaternal morbidity and mortality [2],[3],[4]. In our case, we aim to elucidate a rare complication of massive postpartum ascites in the setting of eclampsia presenting as extravasated fluid primarily within the interstitium of the gastric and intestinal walls along with its medical management.

Case Report


A 32-year-old, gravida 3, para 2, aborta 0, Caucasian female with history of intrauterine growth restriction during second pregnancy and no past medical history presented at 37.1 weeks of gestation presented to ER after a seizure episode. She received prenatal care from a midwife with the last visit at 23.5 weeks gestation was brought to the ER. She had complaints of headache overnight and subsequently had an episode of seizure. In the ER, the patient was postictal but followed one step command. Vitals revealed a blood pressure of 160/116 mmHg, heart rate of 71 bpm, respiratory rate of 22 bpm with an oxygen saturation of 98% on room air. On examination, the patient is a well-nourished young female, somnolent, alert, and oriented x1, her extremities showed deep tendon reflex of 3+. Her uterine fundus measured 35 cm in height. The rest of the physical exam was unremarkable. Lab values are mentioned in Table 1. She was given a 10 mg hydralazine, and 2 mg magnesium initiated. Ultrasound (US) abdomen revealed single live intrauterine pregnancy with ultrasound estimated fetal age of 34 weeks 3 days in vertex presentation with fetal heart rate (HR) of 150 bpm. Placenta was fundal. No previa noted. Amniotic fluid index equals 7.5 cm. No free fluid was noted on this US. An emergent C-section was performed and healthy male fetus was delivered.

On post-operative day (POD) 1, the patient remained altered. On exam, she was somnolent and had a soft abdominal with mild tenderness at the scar site. No guarding or distension noted, with palpable uterine fundus.

  • CT brain: Abnormal low attenuation in the brainstem, cerebral peduncle, and white matter of the right posterior occipital lobe.
  • MRI and MRA brain: findings consistent with extensive posterior reversible encephalopathy syndrome (PRES).

POD-2, the patient complained of dull diffuse abdominal pain. She was noted to have significant abdominal distension and tenderness.

  • US pelvis: Involuting uterus with moderate intra-abdominal fluid.
  • CT abdomen and pelvis: A large amount of ascites and severe interstitial edema of the gastric and intestinal walls. Small bilateral pleural effusions were also noted (Figure 1).
  • Transthoracic echocardiogram: small pericardial effusion.
  • Chest X-ray: Bilateral edema/infiltrates and pleural effusions. Left lower lobe consolidation, and cardiomegaly.

Urine output decreased to less than 30 cc/h. Although, computed tomography (CT) abdomen showed worsening abdominal ascites but the ultrasound failed to identify a safe pocket for drainage via paracentesis. The majority of ascitic fluid was confined to the walls of the visceral mucosa. No demonstrable organic cause, other than pre-eclampsia could be found to explain the ascites.

POD-3, the lab testing continued to show significant persistent proteinuria 3+, urine random total protein of 2000 mg/dL, and protein/creatinine ratio of 16.2. Serum albumin was low at 1.8 g/dL.

We hypothesized that increasing her intravascular oncotic pressure with intravenous (IV) albumin with piggybacked IV diuretics with bumetanide would facilitate fluid removal. Following this intervention, her urine output increased to 250 cc/h and her abdominal distention resolved over the next 48 hours. She was weaned off IV blood pressure medications and transitioned to oral labetalol. She was discharged home on day 7 of her hospitalization. Flowchart in Figure 2 summarizes the patient management while inpatient.

Follow-up at three months showed a complete resolution of all her neurological symptoms and an uneventful postpartum course.

Table 1: Serum chemistries including CBC, CMP, magnesium, phosphates, uric acid, coagulation profile, and urine studies

Share Image:

Figure 1: Severe interstitial edema of the gastric and intestinal walls; arrowheads marking the area of interstitial edema.

Share Image:

Figure 2: Flowchart denoting the management of patient.

Share Image:

Discussion


Eclampsia is defined as the occurrence of one or more generalized, tonic-clonic convulsions unrelated to other medical conditions in women with hypertensive disorder of pregnancy [2]. The estimated prevalence of pre-eclampsia and eclampsia globally is 4.6% and 0.3%, respectively [5]. The exact pathophysiology of the disease spectrum is unknown; however, endothelial damage and decreased oncotic pressure resulting in generalized capillary, and alteration of autoregulation in the cerebral circulation are the proposed mechanisms [2],[3],[6],[7].

Antenatal ascites in preeclamptic women have been reported in numerous case reports [3]. 8 in 1000 cases during pregnancy develop ascites which develop between 27 and 31weeks of gestation [8]. Preeclamptic/eclamptic patients are at risk of limited literature that describes the incidence of massive ascites in preeclamptic patients during the postpartum period [9]. As per our literature review, only one case of post-partum ascites associated with etiopathology of preeclampsia has so far been reported [10]. The development of post-partum ascites is hypothesized to be due to the sudden change in intra-abdominal pressure (IAP) from the involuting uterus resulting in negative IAP [10]. This, in addition to reduced intravascular oncotic pressure and endothelial damage results in trans-endothelial movement of fluid into the intra-abdominal space resulting in abdominal distention.

Our case is unique in its presentation because the majority of the extravascular volume was located within the mucosa and interstitial walls of the stomach and small intestine. Paracentesis was not a consideration because of the absence of a safe window of approach, medical management by increasing the intravascular oncotic pressure with IV albumin, followed by IV diuresis with bumetanide that facilitated volume removal. Within 24 hours, urine output increased and abdominal distention improved significantly.

There is no evidence-based guideline that describes the management of postpartum ascites associated with preeclampsia or eclampsia [3]. Various case studies have reported a wide range of approach for management from watchful waiting to aggressive intervention via paracentesis and even exploratory laparotomy. [3],[6],[7],[8],[9],[10],[11],[12]. Additionally, underlying etiology should be the focus of management to prevent recurrence of this complication. Continued postpartum hypertension should be administered a long-acting oral antihypertensive agents, i.e., labetalol and nifedipine that are compatible with breastfeeding [13]. Women with a history of eclampsia are at increased risk of preeclampsia in a subsequent pregnancy [2]. Additionally, low-dose aspirin (dosage ranging 60–150 mg daily) has been proven to reduce the risk of preeclampsia by 10%to 15% [14].

The paucity of reports in the literature regarding massive postpartum ascites may be due to under reporting. This can be a daunting situation for new mothers and their families. To facilitate healthcare professionals in clinical decision making, reduce patient distress, length of stay, and better clinical outcomes, further data collection and controlled trials are required to prevent recurrence in future pregnancies.

Conclusion


Antepartum eclampsia can manifest wide range of postpartum complications. Massive ascites is a rare complication but can present as gastrointestinal interstitial edema. We recommend intravascular albumin infusion followed by diuretic therapy that facilitates raising intravascular oncotic pressure and offloading interstitial fluid, respectively.

REFERENCES


1.

Mignini LE, Villar J, Khan KS. Mapping the theories of preeclampsia: The need for systematic reviews of mechanisms of the disease. Am J Obstet Gynecol 2006;194(2):317–21. [CrossRef] [Pubmed]   Back to citation no. 1  

2.

Fishel Bartal M, Sibai BM. Eclampsia in the 21st century. Am J Obstet Gynecol 2022;226(2S):S1237–53. [CrossRef] [Pubmed]   Back to citation no. 1  

3.

Suriya JY, Keepanasseril A, Manikandan K, Maurya DK, Veena P, Soundara Raghavan S. Maternal ascites an independent prognostic factor in severe preeclampsia: A matched cohort study. Arch Gynecol Obstet 2017;296(1):63–8. [CrossRef] [Pubmed]   Back to citation no. 1  

4.

Gustavo Vázquez-Rodríguez JG, Guadalupe Veloz-Martínez M. Pleural effusion and ascites in severe preeclampsia: Frequency and correlation with plasma colloid osmotic pressure and renal filtration function. Cir Cir 2011;79(4):299–305. [Pubmed]   Back to citation no. 1  

5.

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 2013;170(1):1–7. [CrossRef] [Pubmed]   Back to citation no. 1  

6.

Koseoglu SB, Deveer R, Camuzcuoglu A, Kasap B, Camuzcuoglu H. Massive ascites and pleural effusion in preeclampsia. J Clin Diagn Res 2017;11(2):QD08–9. [CrossRef] [Pubmed]   Back to citation no. 1  

7.

El-Agwany AS, Abdelsadek AA. A rare case of normotensive HELLP syndrome complicated with massive ascites: Spontaneous resolution. Egypt J Anaesth 2016;32(1):155–8. [CrossRef]   Back to citation no. 1  

8.

Bharathi BK, Vijayalakshmi S, Mahendra G. Massive ascites complicating severe preeclampsia: A case report. Global Journal of Medical Research: E Gynecology and Obstetrics 2017;17(2).   Back to citation no. 1  

9.

Kumar R, Dey M. Massive ascites and bilateral pleural effusion causing respiratory embarrassment in a postnatal case of severe preeclampsia. Med J Armed Forces India 2014;70(3):290–2. [CrossRef] [Pubmed]   Back to citation no. 1  

10.

Higami S, Kondo E, Shibata E, et al. A case of preeclampsia developing massive ascites after delivery. Clin Case Rep 2022;10(5):e05830.   Back to citation no. 1  

11.

Le Y, Ye J, Lin J. Expectant management of early-onset severe preeclampsia: A principal component analysis. Ann Transl Med 2019;7(20):519. [CrossRef] [Pubmed]   Back to citation no. 1  

12.

Ko ML, Huang LW, Chang JZ, et al. Massive ascites complicating pre-eclampsia. Taiwan J Obstet Gynecol 2005;44(3):267–9. [CrossRef]   Back to citation no. 1  

13.

Magee L, von Dadelszen P. Prevention and treatment of postpartum hypertension. Cochrane Database Syst Rev 2013;(4):CD004351. [CrossRef] [Pubmed]   Back to citation no. 1  

14.

Roberge S, Nicolaides K, Demers S, Hyett J, Chaillet N, Bujold E. The role of aspirin dose on the prevention of preeclampsia and fetal growth restriction: Systematic review and meta-analysis. Am J Obstet Gynecol 2017;216(2):110–20.e6. [CrossRef] [Pubmed]   Back to citation no. 1  

SUPPORTING INFORMATION


Author Contributions

Spogmai Saeed Khan - Conception of the work, Design of the work, Acquisition of data, Analysis of data, Drafting the work, Revising the work critically for important intellectual content, Final approval of the version to be published, Agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Sher Naidoo Roalkvam - Conception of the work, Design of the work, Acquisition of data, Analysis of data, Drafting the work, Revising the work critically for important intellectual content, Final approval of the version to be published, Agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Albert De Ridder Harmse - Revising the work critically for important intellectual content, Final approval of the version to be published, Agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Yamine Saddouk - Revising the work critically for important intellectual content, Final approval of the version to be published, Agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Guarantor of Submission

The corresponding author is the guarantor of submission.

Source of Support

None

Consent Statement

Written informed consent was obtained from the patient for publication of this article.

Data Availability

All relevant data are within the paper and its Supporting Information files.

Conflict of Interest

Authors declare no conflict of interest.

Copyright

© 2023 Spogmai Saeed Khan et al. This article is distributed under the terms of Creative Commons Attribution License which permits unrestricted use, distribution and reproduction in any medium provided the original author(s) and original publisher are properly credited. Please see the copyright policy on the journal website for more information.