Article

Spontaneous rupture of spleen masquerading as acute pancreatitis

Unlabelled imageSpontaneous rupture of spleen masqueradi”>American Journal of Emergency Medicine 32 (2014) 394.e1-394.e3

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Case Report

Spontaneous rupture of spleen masquerading as acute pancreatitis

Abstract

Splenic rupture most commonly follows blunt abdominal trauma. Nontraumatic rupture of the spleen is rare. Nontraumatic rupture of the spleen has been described in a variety of Pathologic conditions, which include neoplastic, infectious, and Hematologic diseases affecting the spleen. Spontaneous rupture of nondiseased spleen is extremely rare. We report a case of spontaneous rupture of spleen in a chronic alcoholic clinically simulating acute pancreatitis.

Splenic rupture is a potentially life-threatening abdominal emer- gency and usually follows blunt abdominal trauma. Nontraumatic rupture of the spleen is rare. Nontraumatic or spontaneous rupture of the spleen (SRS) has been described in a variety of pathologic conditions, which include neoplastic, infectious, and hematologic diseases affecting the spleen. Spontaneous rupture of nondiseased spleen is extremely rare. We report a case of spontaneous rupture of spleen in a chronic alcoholic clinically simulating acute pancreatitis.

A 45-year-old man was brought to the emergency department (ED) of a tertiary care service hospital late night (0330 hours) with the complaints of sudden onset pain abdomen with progressive distension of the abdomen for 4-hour duration. The pain was of abrupt onset, started after an alcoholic binge, and was initially located in the left hypocondrium and epigastrium. Gradually, the pain spread over to involve the entire abdomen. The pain increased in severity with movement and coughing. Along with the increase in the severity of pain, there has been progressive distension of the abdomen, and he did not pass flatus since then. His personal history revealed that he used to consume 50 to 60 g of alcohol everyday for the last 5 years. He did not have any other known comorbid illness. There was no definite history of trauma in the preceding 6 months.

At the ED evaluation, he was found to be in hypovolumic shock (blood pressure, 88/56 mm of Hg; pulse, 126 per minute). He had severe pain in the abdomen and was lying still on the bed. There was marked pallor, and the extremities were cold and clammy. Abdomen was grossly distended with diffuse tenderness and board-like rigidity. Shifting dullness was present and bowel sounds were absent. Per rectal and hernial sites examination was unremarkable. Chest was clear and there were no added sounds. He was vigorously fluid re- suscitated, placed on broad spectrum Intravenous antibiotics, and simultaneously all urgent investigations were ordered. Initial inves- tigations revealed hemoglobin level of 8.4 g/dL and polymorphonu- clear leucocytosis (total leucocytes count, 18 600/mm3). His Biochemical parameters were follows: Blood sugar (random): 310 mg/dL; Serum glutamic-oxaloacetate transaminase/Serum glutamic- pyruvic transaminase, 242/94 u/L; Serum bilirubin,1 mg/dL; serum amylase, 124 u/L; lipase, 120 u/L. Chest and abdominal portable radiographs did not reveal any evidence of pneumoperitoneum.

Bedside ultrasonography (USG) done by the attending surgeon revealed free fluid in the peritoneal cavity, which, on aspiration, appeared hemorrhagic. Pancreas was not visualized. A provisional diagnosis of hemorrhagic pancreatitis was made. At this stage, computed tomographic (CT) scan of abdomen was requested. Ultrasound abdomen before the CT scan revealed gross hemoper- itoneum. The pancreas was not visualized due to gas-filled floating bowel loops in the epigastric region. The liver was enlarged (craniocaudal, 18 cm) and showed grade III fatty changes within. The gall bladder was contracted. The splenic outline was ill defined with diffuse heterogeneous echotexture. Heteroechoic collections were noted within and around the spleen with complete disruption of the splenic architecture (Fig. 1). Based on Sonographic findings, a diagnosis of splenic rupture with hemoperitoneum was made. He immediately underwent Non contrast computed tomography fol- lowed by Contrast enhanced computed tomography abdomen (Somatom sensation 40; Siemens, Erlangen, Germany). Computed tomographic scan abdomen confirmed splenic rupture with massive hemoperitoneum (Fig. 2). The liver was enlarged with diffuse fatty changes within. The portal vein and spleno-portal axis appeared normal. There were no collaterals present. The pancreas was also normal in attenuation and enhancement pattern. There was no bony injury, recent or past, noted in the visualized rib cage. With vigorous ongoing resuscitation, he was taken up for urgent laparotomy which revealed completely shattered spleen (Fig. 3) with more than 2 L of frank blood within the peritoneal cavity. Emergency splenectomy was carried out along with peritoneal lavage and drainage. Per- operatively, it was difficult to secure control of the splenic hilum due to ongoing brisk bleeding. Intraoperative injury to the pancreatic tail was also suspected. Postoperatively, for 3 days, his general condition, Vital parameters, and laboratory parameters appeared to improve. However, his drain output continued to be high: 1500 to 2000 mL/d with drain amylase more than 200 on the fourth postoperative day. He was managed for postoperative pancreatitis. However, his condition took a downhill course from the fifth day and became mentally obtunded. His drain and serum amylase progressively increased with deranged hepatic and renal function. He finally succumbed to multiorgan failure on the 25th postoperative day. Autopsy study confirmed splenic rupture, gross hepatomegaly with diffuse fatty changes along with features of early portal hyper- tension. The spleen was histologically normal.

Spontaneous rupture of the spleen is an extremely rare yet im-

portant and potentially life-threatening condition. The exact inci- dence and epidemiology of SRS have not been clearly defined in the literature. Most of the information about Spontaneous splenic rupture is limited to case reports. In one of the largest case series, Gorg et al [1] described sonographic patterns, diagnosis, and follow-up in 41 cases of SRS. In this study, infectious and various Malignant diseases

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394.e2 J. Debnath et al. / American Journal of Emergency Medicine 32 (2014) 394.e1394.e3

Fig. 1. Ultrasonography (5 MHz Convex probe, P5- Wipro GE) of left hypochondrium reveals near complete loss of splenic architecture with heterogeneous internal echogenicity consistent with multiple splenic lacerations.

Fig. 2. Computed tomographic scan of abdomen (Somatom Sensation 40; Siemens). A and B, Noncontrast scan image at the level of liver and spleen (A) and flank (B). Note multiple irregular linear hypodense tracks seen throughout visualized splenic parenchyma (white arrows). Also note diffusely hypodense liver parenchyma (curved arrow) consistent with diffuse fatty liver. Image B demonstrates presence of free fluid (hemoperitoneum) in bilateral flanks (block arrows). Contrast-enhanced axial (C) and coronal reconstruction images confirm presence of multiple splenic lacerations. Note the pancreas and peripancreatic region appears normal. Sp, Spleen.

J. Debnath et al. / American Journal of Emergency Medicine 32 (2014) 394.e1394.e3 394.e3

Fig. 3. Photograph of splenectomy specimen demonstrates splenic rupture through the hilum in an otherwise normal-appearing spleen.

affecting the spleen were associated with more than 82% of cases of SRS. Cirrhosis of liver was associated with SRS in 2 cases (4.8%). However, it is not mentioned, whether portal hypertension was associated with these 2 cases. Gedik et al [2] reported 7 cases of Nontraumatic splenic rupture in which 4 patients had malaria and only 1 case had spontaneous splenic rupture.

The term SRS has often been applied to cases of splenic rupture with no clinical history of trauma. These cases often included splenic rupture in otherwise diseased spleen. Hence, the appropriateness of the term SRS in such cases has been a subject of debate from time to time. In the year 1958, Orloff and Peskin [3] had laid out 4 criteria needed to diagnose true SRS, which included (a) no history of trauma or unusual effort, (b) no evidence of disease that could involve the spleen, (c) no evidence adhesion or scarring of the spleen, and (d) the spleen should be otherwise normal on gross and histologic examina- tion. In a true sense, the term SRS should include only those cases of splenic rupture where the spleen has been found to be histologically normal, which itself is a rarity. In a systematic review of 632 publications involving 845 patients, Renzulli et al [4] classified atraumatic splenic rupture (ASR) into 2 broad categories: atraumatic idiopathic (7%) where the spleen is normal and atraumatic pathologic (93%) where the spleen is diseased. Besides the idiopathic group, 5 major causes of ASR were identified, which included neoplastic, infectious, inflammatory noninfectious, drug/treatment related, and mechanical disorders in 30%, 27%, 20%, 9%, and 7% cases, respectively. Overall mortality rate related to ASR was found to be 12%, with splenomegaly, older than 40 years, and neoplastic conditions being increasingly associated with mortality.

Splenic rupture is a potentially life-threatening condition, which

necessitates earliest possible diagnosis and appropriate management for a favorable outcome. Traumatic rupture of spleen can be diagnosed in time given the positive history and clinical and imaging findings. Diagnosis of ASR requires a high index of clinical suspicion because of its rarity, lack of supporting history, and atypical clinical presenta- tions. Particularly difficult is the diagnosis of SRS in the absence of any underlying disease conditions. Nevertheless, it is important to

understand here that inordinate delay in the diagnosis of splenic rupture can be fatal. Atypical clinical presentation in cases of SRS is another facet that needs to be kept in mind for an early diagnosis. Our case, a known alcoholic, presented with acute onset abdominal pain in the left hypochondrium and epigastrium with progressive Abdominal distention after an alcoholic binge. The initial working diagnosis was acute pancreatitis with hypovolumic shock. Surgeon performed bedside USG revealed free intraperitoneal fluid, which was diagnosed as hemoperitoneum on aspiration. Subsequent imaging (USG fol- lowed by NCCT and CECT) by the radiologist revealed SRS as the actual cause for the massive hemoperitoneum and hemodynamic instability. Our case is unique in the sense that the initial presentation mimicked acute pancreatitis in the background of patient being a known alcoholic and pain starting after an alcoholic binge in the character- istic location. Although, at autopsy, there were signs of early portal hypertension, the spleen was found to be normal histologically. To the best of our knowledge, such a presentation of SRS has not been reported in the literature.

Spontaneous rupture of the spleen is a rare, yet clinically significant entity that merits consideration and urgent attention in hemodynam- ically unstable patients, although history and clinical features are nonspecific. A low threshold for carrying out Cross-sectional imaging (eg, USG/CT scan) can help early and Timely diagnosis of SRS, which is crucial for successful management and outcome.

Jyotindu Debnath MD

Department of Radiodiagnosis, Armed Forces Medical College

Pune, India E-mail address: [email protected]

Samrat Sonkar MBBS, DNB

167 Military hospital, Pathankot, Punjab, India

Vivek Sharma MD, DNB Samar Chatterjee MD

Department of Radiodiagnosis, Armed Forces Medical College

Pune, India

Vikash Srivastava MD

Anesthesia and Critical Care Medicine, Command Hospital (CC)

Lucknow, India

Shiv Pankaj Khanna MD

Pathology 167 Military Hospital, Pathankot, Punjab, India

http://dx.doi.org/10.1016/j.ajem.2013.10.036

References

  1. Gorg C, Colle J, Gorg K, Prinz H, Zugmaier G. Spontaneous rupture of the spleen: ultrasound patterns, diagnosis and follow-up. Br J Radiol 2003;76:704-11.
  2. Gedik E, Girgin S, Aldemir M, Keles C, Tuncer MC, Aktas A. Non-traumatic splenic rupture: report of seven cases and review of the literature. World J Gastroenterol 2008;14:6711-6.
  3. Orloff MJ, Peskin GW. Spontaneous rupture of the normal spleen; a surgical enigma. Int Abstr Surg 1958;106:1-11.
  4. Renzulli P, Hostettler A, Schoepfer AM, Gloor B, Candinas D. Systematic review of atraumatic splenic rupture. Br J Surg 2009;96:1114-21.

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