Table of Contents  
CASE REPORT
Year : 2015  |  Volume : 8  |  Issue : 4  |  Page : 537-539  

Ascites in a case of severe preeclampsia with twin gestation


Department of Obstetrics and Gynaecology, Dr. D. Y. Patil Medical College, Hospital and Research Centre, Dr. D. Y. Patil Vidyapeeth, Pune, India

Date of Web Publication14-Jul-2015

Correspondence Address:
Priyanka Gupta
Department Obstetrics and Gynaecology, Dr. D. Y. Patil Medical College Pimri, Pune - 411 018, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0975-2870.160832

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  Abstract 

We report a rare case of massive maternal ascites complicating severe preeclampsia in a case of twin gestation. This complication developed in association with severe hypertension and marked proteinuria. Ascites has been reported at cesarean section delivery in pregnancies complicated by preeclampsia. Hypoproteinemia caused by the excretion of large amounts of protein in the urine seems to be a partial etiological factor aggravated by the renal retention of sodium and water. The onset of massive ascites causes respiratory compromise in all the patients. Careful antenatal assessment and informed anticipation may help in detecting more cases with this complication, which is often missed and thereby help in reducing both maternal and perinatal morbidity and mortality. The purpose of this report is to increase the awareness of such nonclassical and atypical features of preeclampsia.

Keywords: Ascites, hypoproteinemia, preeclampsia


How to cite this article:
Gupta P, Bal H, Chaudhari S, Gosavi A. Ascites in a case of severe preeclampsia with twin gestation. Med J DY Patil Univ 2015;8:537-9

How to cite this URL:
Gupta P, Bal H, Chaudhari S, Gosavi A. Ascites in a case of severe preeclampsia with twin gestation. Med J DY Patil Univ [serial online] 2015 [cited 2022 Oct 5];8:537-9. Available from: https://www.mjdrdypu.org/text.asp?2015/8/4/537/160832


  Introduction Top


Preeclampsia, a pregnancy-specific syndrome characterized by new onset hypertension and proteinuria, is a major obstetric problem and a significant cause of maternal and neonatal morbidity and mortality. [1] Although preeclampsia and related hypertensive disorders of pregnancy continue to affect ~8% of all pregnancies, the incidence of preeclampsia has seen a 40% increase in recent years. [2] Preeclampsia can present to a clinician with a variety of features. However, the presence of fluid in various body cavities is rarely seen in preeclampsia, and the presence of the same is associated with increased morbidity to the mother. [3] Surveillance, appropriate therapeutic strategies to minimize the complications of preeclampsia and delivery of the fetus remain the mainstay of management of the disease. [4]


  Case Report Top


A 25 year old G 2 P 1 L 1 unbooked patient at 36.5 weeks with twin gestation reported to our casualty with abdominal pain and leaking per vaginum. She had one full term normal vaginal delivery without any antenatal and postnatal complication. She had no family history of preeclampsia. On examination she was severely pale, pulse 102/min, blood pressure (BP) 162/110 mm of Hg, respiratory rate 24/min, pedal edema ++, hemic murmur heard on auscultation, knee jerks were normal. Obstetric examination revealed abdomen over-distended foetus1 cephalic, fetus 2 transverse, fetal heart sound regular for both the twins. Internal examination showed absent membranes with crowning of the head of the first fetus. Bedside urine albumin test found to be 3+, hemoglobin was 7 gm%, platelet count −1.98 lakh/mm 3 , serum proteins −5.8 gm% with serum albumin −2.7 gm%, blood urea −22 mg/dL, creatinine −0.8 mg/dL, rest all other investigations were within normal limits. She was given the nifedipine −10 mg orally with a sip of water. Twin 1 was delivered normally, and 1.6 kg male child shifted to neonatal Intensive Care Unit for respiratory distress syndrome. Twin 2 remained in transverse lie, external cephalic version tried but failed, and thereafter patient was shifted to operation table for emergency caesarean section. Lower segment caesarean section was done under general anesthesia. On opening the abdomen there was free fluid in the abdomen and around 1.5-2 liters of ascitic fluid were drained. A male baby of 3 kg was delivered, baby cried immediately after birth, and rest of the surgery was uneventful. Postoperative BP was 150/100 mm Hg. She was continued on cap nifedipine 10 mg blood donor (BD) and 2 units of blood were transfused. On the third postoperative day, patient had marked abdominal distension. Her abdominal girth measured 98 cm, shifting dullness and fluid thrill were positive, pulse rate was 132/min, and BP140/90 mm Hg. Urgent ultrasonography was done, and it showed the presence of moderate ascites. Her postoperative Hb was 6.8 gm%. Biochemical investigations were repeated. The reports were serum bilirubin - 1.6 mg%, serum glutamic pyruvic transaminase −238 IU/L, alkaline phosphatase −135 IU/L, serum proteins −5.8 gm%, serum albumin −2.7 gm%, serum globulin −3.1 gm% and renal function test within normal limits. On postoperative day 4, injection. Furosemide was started, 2 units packed red blood cell were transfused, and patient was advised high protein diet. In view of persistent tachycardia, nifedipine was omitted and tablet labetalol 100 mg BD along with injection. Furosemide −40 mg oral dose (OD) were started. On postoperative day, 5 patient was switched over to tablet furosemide 40 mg OD. Ascites gradually resolved over a period of 8-10 days. Patient was discharged on postoperative day 24 on tablet labetalol 100 mg OD and tablet furosemide −40 mg OD on alternate day for 10 days and asked to come for review after 2 weeks in out-patient department. On follow-up visit, she was asymptomatic and had become normotensive. All medications except hematinics were stopped. Thereafter, patient was lost to follow-up.


  Discussion Top


As early as 1949 Golden stated that the cause of ascites in pregnancy was either low concentration of proteins with an altered albumin/globulin ratio, portal obstruction or hemoconcentration in the portal circulation. After Golden, there have been only sporadic case reports of massive ascites complicating preeclampsia. [5] Preeclampsia is a condition involving multiple organ systems. The basic pathophysiology involves the release of vasoconstrictive agents, endothelial damage, hyperpermeability of the capillaries and microangiopathic hemolysis. This results in the entity presenting in various forms like hypertension, HELLP syndrome, seizures, pulmonary edema, proteinuria. [5,6] Excess sodium retention occurs in preeclampsia. Total body sodium is increased, but plasma volume is usually decreased with shift of fluid to the interstitium. [7] The reduced plasma volume is the result of intense vasoconstriction that also results in hypertension. In preeclampsia renin activity and aldosterone concentration in plasma in the third trimester are less than those observed in normal pregnancy or indeed those found in pregnancy associated with essential hypertension. Further atrial natriuretic peptide (ANP) concentrations are significantly increased above those found in normal pregnancy. [7] ANP appears to be released in maternal circulation in response to vasoconstriction and increased volume load to cardiac atria. Thus in preeclampsia as compared to normal pregnancy renin, aldosterone and ANP all act as if to promote the natriuresis but for reasons not clearly understood natriuresis is impaired. [7] The most recent concept of pathophysiology of preeclampsia involves widespread endothelial cell dysfunction. [8] Impairment of endothelial barrier function is suggested by generalized capillary leak, which is responsible for edema, proteinuria and decreased colloid osmotic pressure. [8] The low colloid osmotic pressure results in effusion such as ascites. [9],[10] It was concluded that ascites in severe preeclampsia is an indication of termination of pregnancy as it cannot be cured by medical treatment. Our case had hypoproteinemia and continued to manifest with tachycardia that was most likely due to generalized leaking of capillaries and microangiopathy. The trigger for sudden and massive ascites may have been hypoproteinemia. This patient had massive or large volume ascites as defined by amount equal to or more than 2 liters of peritoneal fluid. Neither the textbooks nor the case reports available give a clear definition of massive ascites although they described massive ascites in subjective terms of two or more liters. [6]

Therefore, this definition of massive ascites is arbitrary but at the same time it is based on the clinical criteria of ascites causing significant respiratory distress to the mother and the arterial blood gas analysis showing respiratory acidosis and maternal hypoxia. We did not keep any intraperitoneal drain in our patient and ascites resolved with supportive therapy. She received four units of blood transfusion postoperatively. This patient did not have any evidence of thrombocytopenia and elevated liver enzymes. Wood et al. have reported 10% incidence of large volume ascites with hemolysis, elevated liver enzymes and low platelet count. [6] We conclude that massive ascites developing in preeclampsia is an unusual complication and massive ascites leading to maternal respiratory compromise calls for active termination of pregnancy within 24-48 h. The paucity of reports in the literature may be due to under reporting and also difficulty in recognizing this condition clinically as seen in our case.

High-dose corticosteroids (dexamethasone 10 mg every 12 h) have shown transient benefit in HELLP syndrome. Some studies [11] have shown that high-dose corticosteroids may help in improving platelet count and liver enzyme abnormalities. A case report by Chawla et al. showed that a patient with ascites and preeclampsia who was treated with steroid in tapering dose regimen recovered faster, had less morbidity, and less need for other interventions. [12]


  Conclusion Top


A high index of suspicion, careful clinical and ultrasonographic examination to detect ascites will help in elucidating the true incidence of this complication. The incorporation into clinical practice of monitoring for ascites in preeclampsia might alert the obstetrician toward more intensive and more frequent maternal and fetal surveillance to avoid maternal and fetal hypoxia and also to find the true incidence of this entity.

 
  References Top

1.
Sibai B, Dekker G, Kupferminc M. Pre-eclampsia. Lancet 2005;365:785-99.  Back to cited text no. 1
    
2.
Roberts JM, Pearson GD, Cutler JA, Lindheimer MD, National Heart Lung and Blood Institute. Summary of the NHLBI Working Group on Research on Hypertension During Pregnancy. Hypertens Pregnancy 2003;22:109-27.  Back to cited text no. 2
    
3.
Daponte A, Skentou H, Dimopoulos KD, Kallitsaris A, Messinis IE. Massive vulvar edema in a woman with preeclampsia: A case report. J Reprod Med 2007;52:1067-9.  Back to cited text no. 3
    
4.
Lewis G. The Confidential Enquiry into Maternal and Child Health (CEMACH). Saving Mothers' Lives: Reviewing maternal deaths to make motherhood safer 2003-2005, The Seventh Report on Confidential Enquiries into Maternal Deaths in the United Kingdom. London: CEMACH; 2007. p. 72-6.  Back to cited text no. 4
    
5.
Vaijyanath AM, Nayar B, Malhotra N, Deka D. Massive ascites in severe pre-eclampsia: A rare complication. J Obstet Gynaecol Res 2002;28:199-202.  Back to cited text no. 5
    
6.
Woods JB, Blake PG, Perry KG Jr, Magann EF, Martin RW, Martin JN Jr. Ascites: A portent of cardiopulmonary complications in the preeclamptic patient with the syndrome of hemolysis, elevated liver enzymes, and low platelets. Obstet Gynecol 1992;80:87-91.  Back to cited text no. 6
    
7.
Marshall W, Lapsley M, Day A, Ayling R. Clinical Biochemistry: Metabolic and Clinical Aspects. 3 rd ed. London: Churchill Livingstone Elsevier; 2014. p. 55-7.  Back to cited text no. 7
    
8.
Brown MA, Zammit VC, Lowe SA. Capillary permeability and extracellular fluid volumes in pregnancy-induced hypertension. Clin Sci (Lond) 1989;77:599-604.  Back to cited text no. 8
    
9.
Robson S. Hypertension and renal disease in pregnancy. In: Edmond's DC, editors. Dewhurst's Textbook of Obstetrics and Gynaecology for Post Graduates. 6 th ed. Oxford: Blackwell Science Publisher; 1999. p. 166-85.  Back to cited text no. 9
    
10.
Sullivan JM. Hypertension and Pregnancy. Chicago: Year Book Medical Publishers; 1986. p. 73-81.  Back to cited text no. 10
    
11.
O'Brien JM, Shumate SA, Satchwell SL, Milligan DA, Barton JR. Maternal benefit of corticosteroid therapy in patients with HELLP (hemolysis, elevated liver enzymes, and low platelet count) syndrome: Impact on the rate of regional anesthesia. Am J Obstet Gynecol 2002;186:475-9.  Back to cited text no. 11
    
12.
Chawla S, Kumar P, Bhalla M. Case of ascites in pre-eclampsia. Med J Armed Forces India 2012;68:257-9.  Back to cited text no. 12
    




 

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