Hx: A male in his 30s presents with abdominal pain and vomiting. He relates that he was recently hospitalized for 4 days for alcoholic pancreatitis, at an outside institution. He was feeling better when he was discharged but the pain recurred 2 days ago and has been increasing steadily. He states it is now more severe than when he was hospitalized. It is sharp, stabbing, in the upper abdomen and left upper quadrant, and associated with repetitive vomiting each time he attempts to eat or drink anything. He adamantly denies any alcohol or drug use.
SocHx: regular smoker, regular alcohol consumption until 1 week ago, no drugs.
- Vitals: BP 150/85, HR 110, RR 20, sat 100% on room air, temp 98.6 F (37 C)
- HEENT: normal
- Neck: supple
- Resp:clear bilaterally, increased abdominal pain with deep inspiration
- Cardiovascular: tachycardia, regular, pulses symmetrical bilaterally.
- Abdomen: soft, non-distended, no skin abnormalities. There is focal tenderness to palpation of the epigastrium and left upper quadrant without guarding or rebound. Lower abdomen non-tender.
- Extremities: normal pulses, warm
- Neuro: normal
- Recurrent pancreatitis
- Peptic ulcer disease
- Bowel Obstruction
- Lower Lobe pneumonia
- Biliary Obstruction
- Aortic Aneurysm
- Descending Aortic Dissection
Interval History: Review of records from outside institution shows patient had a normal CT scan of the abdomen and pelvis during his most recent admission for pancreatitis. No evidence for aortic, hepatic , or gallbladder pathology. Lipase was elevated at prior admission.
- IV hydration is initiated with normal saline.
- Laboratory analysis includes: CBC, CMP, lipase, urinalysis, and urine drug screen
- Chest xray is obtained
- Laboratory analysis reveals an elevated WBC at 15,000, normal hemoglobin and hematocrit, and platelets. Liver enzymes and renal function are normal. Lipase is elevated. Urinalysis and drug screen are negative.
- Given normal CT at last admission, the patient is admitted with a diagnosis of recurrent pancreatitis.
- The patient’s abdominal pain continues to be severe requiring escalating doses of pain medication.
- Due to an inability to obtain adequate pain relief and the patient’s continued complaint of pain worse than previous admission, repeat imaging of the abdomen is obtained and reveals a splenic hematoma indicative of splenic rupture, in addition to fluid around the pancreas and fluid around the stomach and duodenum. No bowel obstruction. There is evidence for splenic vein thrombosis.
Splenic rupture due to pancreatitis is rare and reported in both acute and chronic pancreatitis. What we know about it comes from case reports and a handful of systematic reviews. It is present in up to 36% of pancreatitis cases with splenic pathology1, second only to splenic vein thrombosis. In addition, spontaneous splenic rupture due to any inflammatory process (pancreatitis included) carries a 10% mortality2 making timely diagnosis important. The pathophysiology is believed to result from peri-pancreatic inflammation leading to splenic vein thrombosis, vascular congestion, splenomegaly, and eventually rupture. Direct injury to the splenic capsule from pancreatic enzymes and inflammatory change is also thought to play a role. There are often peri-pancreatic fluid collections complicating the disease by the time splenic injury occurs. Given the presence of splenic pathology in both acute and chronic pancreatitis, the timeline for presentation is variable. This case highlights the occurrence of splenic injury after a case of acute pancreatitis.
Treatment is dependent on the severity of rupture. Since the symptoms occur due to inflammatory changes, case reports demonstrate that presentation may occur multiple days after the initial diagnosis of pancreatitis. Reported treatments included:
- observation of asymptomatic small peri-splenic hematoma
- ultrasound guided drainage of symptomatic sub-capsular splenic hematoma
- splenic artery embolization of enlarging symptomatic hematoma
- emergent laparotomy and splenectomy due to intra-abdominal hemorrhage with or without partial pancreatectomy.
Regardless of the selected treatment, hospitalization is required. In addition to pain management, blood transfusion and significant resuscitation may be necessary. Delayed intra-abdominal hemorrhage may occur as the hematoma expands resulting in shock and emergent laparotomy. Additionally, splenic vein thrombosis is known to result in gastric varices, visible on CT or endoscopy. Although previously believed to require splenectomy in order to reduce the risk of variceal bleeding, a 2004 review suggests this only occurs in 4% of patients and that observation is a safe approach. In our case, the patient remained hemodynamically stable and underwent splenic artery embolization. Patients with hemodynamic instability require emergent splenectomy and may also require partial pancreatectomy 4.
Another interesting factor in this case is the potential for premature closure. This phenomenon is described as a cognitive error that leads to early termination of the diagnostic investigation when a presumptive diagnosis is made early. The patient had been previously treated for acute alcoholic pancreatitis with demonstrated improvement. However, several days after discharge, his return to the ED was triggered by worsening pain. Pain location was similar, epigastric and left upper quadrant of the abdomen, but more severe and included radiation to the left shoulder. Initial examination and testing showed an elevation of the patient’s lipase, at a level higher than previously seen on admission. Record review included a CT completed during the prior admission. Given the alcoholic pancreatitis diagnosis, assumptions regarding his alcohol use and non-compliance could easily be made. The patient’s symptoms and examination could easily have been dismissed as simple recurrent pancreatitis. Premature closure of the diagnostic pathway and lack of further evaluation is a common cognitive error and one that is prone to occur in a similar scenarios. Fortunately, the patient’s pain severity and lack of response to pain management prompted further investigation. In this case, a repeat CT scan was performed demonstrating the new pathology.
References and further reading:
- S S, Olakkengil S, Rozario AP. Occult splenic rupture in a case of chronic calcific pancreatitis with a brief review of literature. Int J Surg Case Rep. 2015;14:95-7. PubMed
- Renzulli P, Hostettler A, Schoepfer AM, Gloor B, Candinas D. Systematic review of atraumatic splenic rupture. Br J Surg. 2009;96:1114–1121. PubMed
- Heider TR, Azeem S, Galanko JA, Behrns KE. The natural history of pancreatitis-induced splenic vein thrombosis. Ann Surg. 2004;239(6):876-80. PubMed
- Malka D, Hammel P, Lévy P, et al. Splenic complications in chronic pancreatitis: prevalence and risk factors in a medical-surgical series of 500 patients. Br J Surg. 1998;85(12):1645-9. PubMed
- Hernani BL, Silva PC, Nishio RT, Mateus HC, Assef JC, De campos T. Acute pancreatitis complicated with splenic rupture: A case report. World J Gastrointest Surg. 2015;7(9):219-22. PubMed
- Aubrey-bassler FK, Sowers N. 613 cases of splenic rupture without risk factors or previously diagnosed disease: a systematic review. BMC Emerg Med. 2012;12:11. PubMed
- Cengiz F, Yakan S, Enver İ. A rare cause of acute abdomen: Splenic hematoma and rupture resulting from pancreatitis. Ulus Cerrahi Derg. 2013;29(2):81-3. PubMed
- Habib E, Elhadad A, Slama JL. [Diagnosis and treatment of spleen rupture during pancreatitis]. Gastroenterol Clin Biol. 2000;24(12):1229-32. PubMed
- Sriaroon C, Dalal P, Sompalli S, Thethi I, Huq S. Splenic rupture: a rare delayed complication of acute necrotizing pancreatitis. Am J Gastroenterol. 2007;102(5):1136-7. PubMed
- Toro H, González P, Moyano D, Villanueva C, Enríquez J. [Splenic rupture in the course of pancreatitis]. Rev Esp Enferm Dig. 1993;83(1):51-2. PubMed