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 Table of Contents  
CASE REPORT
Year : 2013  |  Volume : 3  |  Issue : 2  |  Page : 111-113

Acute pancreatitis in early postpartum period: A case report


Department of Critical Care Medicine, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India

Date of Web Publication19-Dec-2013

Correspondence Address:
Mohan Gurjar
Department of Critical Care Medicine, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh - 226 014
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2249-4472.123312

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  Abstract 

Acute pancreatitis (AP) during peripartum is a rare life-threatening condition which poses as a real challenge for clinician to diagnose it early. Here, we present a case of severe AP occurring in early postpartum period.

Keywords: Pancreatitis, postpartum, intensive care


How to cite this article:
Sharma A, Gurjar M, Azim A, Baronia AK. Acute pancreatitis in early postpartum period: A case report. J Obstet Anaesth Crit Care 2013;3:111-3

How to cite this URL:
Sharma A, Gurjar M, Azim A, Baronia AK. Acute pancreatitis in early postpartum period: A case report. J Obstet Anaesth Crit Care [serial online] 2013 [cited 2019 Dec 6];3:111-3. Available from: http://www.joacc.com/text.asp?2013/3/2/111/123312


  Introduction Top


Acute pancreatitis (AP) during pregnancy is a rare life threatening clinical problem with variable incidence of approximately less than 1-14 cases per 10,000 births. [1],[2],[3] Most of the case series showed highest incidence during third trimester, and least during postpartum period. [1],[3],[4] Due to rarity of incidence, it is a real challenge for clinician to diagnose AP especially in early postpartum period. Here, we present a case of severe AP occurring in early postpartum period.


  Case Report Top


A 24-year-old nulliparous woman had full-term normal vaginal delivery with uneventful antenatal course. On the second day of delivery, she was having severe pain abdomen with distension and multiple episodes of vomiting. Laboratory investigations were: Hemoglobin (Hb) 11.9 g/dl, total leukocyte counts (TLC) 10,800/mm 3 , S. creatinine 1.1 mg/dl. Over next 1 day, she started to have respiratory distress along with worsening of her abdominal symptoms. So, she was referred to our hospital for further management. On admission in intensive care unit (ICU), she was conscious and oriented. Her vitals were: Heart rate 106/min, BP 147/76 mmHg, respiratory rate 32/min [Chest X-ray, [Figure 1]]. Abdomen was distended and slightly tender, having intra-abdominal pressure 14-16 mmHg. Arterial blood gas on venturi mask (FiO 2 0.4) was pH 7.43, PaO 2 80.7 mmHg, PaCO 2 36.3 mmHg, HCO 3 23.7, BE -0.2, Na 133 meq/L, K 3.6 meq/L. On admission day, her Acute Physiology and Chronic Health Evaluation II (APACHE II) and Sequential Organ Failure Assessment (SOFA) score were 10 and 4, respectively. Repeat laboratory investigations revealed Hb 11.3 g/dl, TLC 31.4/mm 3 , platelet 268,000/mm 3 , prothrombin time 14.7 s (control 12.2 s), blood urea nitrogen 12 mg/dl, creatinine 0.7 mg/dl, amylase of 320 U/L, and lipase of 62 U/L and triglyceride 128 mg/dl. In further workup, both ultrasonography (USG) and contrast-enhanced computed tomography (CECT) of abdomen confirmed pancreatitis which revealed a bulky pancreas with free fluid in abdomen and pelvis [Figure 2]. There was no evidence of gall stone or biliary sludge in the imaging. Later on, she had worsening of respiratory distress (respiratory rate 40/min), and presence of shock (noradrenaline infusion 0.05 μg/kg/min, lactate 22.2 mg/dl) for that, invasive mechanical ventilation initiated. Noninvasive ventilation was not tried due to raised intra-abdominal pressure. She was managed conservatively with broad-spectrum antibiotics and other supportive care. Over the next few days, multiple percutaneous drainage tubes were placed under CT guidance for the drainage of multiple intrabdominal collections and to reduce intra-abdominal pressure. During initial days, parenteral nutrition initiated because of intra-abdominal hypertension. Blood sugar levels were in the range of 64-175 mg/dl during ICU stay. Her clinical condition improved gradually and weaned off from the ventilator over 5 days, and later on shifted to the ward for further management. At the time of shifting to the ward she was afebrile, hemodynamically stable, breathing at room air, mild abdominal distension with percutaneous drains (PCDs) in situ, receiving enteral feed by nasojejunal tube and adequate urine output. In follow-up USG of abdomen, there was resolution of intra-abdominal collection and later on drains were removed. She was discharged from the hospital after 16 days of stay in the ward and having good clinical recovery during her follow-up visit after 1 month.
Figure 1: Chest X-ray at admission

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Figure 2: Computed tomography (CT) scan of abdomen showing acute pancreatitis

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  Discussion Top


During pregnancy and postpartum period, differential diagnosis for abdominal pain commonly includes acute fatty liver of pregnancy, HELLP syndrome, acute appendicitis, biliary colic, acute cholecystitis, acute cholangitis, AP, obstructive intestinal pathology, and postpartum intra-abdominal sepsis. Classically, AP is characterized by nausea, vomiting, epigastric pain radiating to back, and elevated serum amylase level.

The leading cause of AP in pregnancy is biliary disease followed by hypertriglyceridemia. [2],[3],[4] During pregnancy changes occurs in hepatobiliary functions lead to more lithogenic environment (stones or sludge up to 10%), and also mild hypertriglyceridemia. [2],[5] In a recent study, biliary disease was found to be etiology of mild AP, while severe hypertriglyceridemia was the main cause of severe AP. [4] Other rare etiologies described are alcohol, preeclampsia-eclampsia, diuretics, hyperparathyroidism, systemic lupus erythematosus. [2] However, in literature, there are no strong evidence exits that pregnancy itself is a specific etiologic factor for pancreatitis.

Women with AP were younger than those with non-pregnancy-related pancreatitis. [6] There are no consistent relationships of incidence AP with parity of women has been found. [2],[3] Advanced gestational age was found to be associated factor for increased incidence of AP in many studies. [3],[4]

The general management of AP in pregnancy is mainly supportive (intravenous fluid, analgesia, bowel rest), while management of underlying cause should also be considered like cholecystectomy for gall stones, preferably during second trimester; and for hypertriglyceridemia induced AP consider low fat diet, antihyperlipidemic therapy, insulin, heparin and/or plasmapheresis. [7] Other key issues in management of severe AP are nutritional support, drainage of peripancreatic collection in case of raised intra-abdominal pressure that may lead to abdominal compartment syndrome, timely support of other organ dysfunction like respiratory, cardiovascular, and renal as well as prevention of hospital acquired infection. The overall outcome substantially improved in last decade due to better and advanced imaging that leads to early diagnosis and intensive care management.

So, in presence of abdominal pain during pregnancy or postpartum period, imaging of abdomen with ultrasonography and/or CT scan should be considered as one of the diagnostic tests of choice along with routine hematology and clinical chemistry including serum amylase that could be helpful in early diagnosis and timely supportive management of AP by clinician/intensivist to improve the outcome, as onset of AP in postpartum period is reported as early as 2 h-1 year after delivery. [6],[8]

 
  References Top

1.Ramin KD, Ramin SM, Richey SD, Cunningham FG. Acute pancreatitis in pregnancy. Am J Obstet Gynecol 1995;173:187-91.  Back to cited text no. 1
    
2.Khan AS, Latif SU, Eloubeidi MA. Controversies in the etiologies of acute pancreatitis. JOP 2010;11:545-52.  Back to cited text no. 2
    
3.Li HP, Huang YJ, Chen X. Acute pancreatitis in pregnancy: A 6-year single center clinical experience. Chin Med J (Engl) 2011;124:2771-5.  Back to cited text no. 3
    
4.Sun L, Li W, Geng Y, Shen B, Li J. Acute pancreatitis in pregnancy. Acta Obstet Gynecol Scand 2011;90:671-6.  Back to cited text no. 4
    
5.Ko CW, Beresford SA, Schulte SJ, Matsumoto AM, Lee SP. Incidence, natural history, and risk factors for biliary sludge and stones during pregnancy. Hepatology 2005;41:359-65.  Back to cited text no. 5
    
6.Maringhini A, Lankisch MR, Zinsmeister AR, Melton LJ 3 rd , DiMagno EP. Acute pancreatitis in the postpartum period: A population-based case-control study. Mayo Clin Proc 2000;75:361-4.  Back to cited text no. 6
    
7.Pitchumoni CS, Yegneswaran B. Acute pancreatitis in pregnancy. World J Gastroenterol 2009;15:5641-6.  Back to cited text no. 7
    
8.Fukami T, Chaen H, Imura H, Sudou K, Eguchi F. Acute pancreatitis occurring in the early postpartum period: Acase report. J Perinat Med 2003;31:345-9.  Back to cited text no. 8
    


    Figures

  [Figure 1], [Figure 2]



 

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