Gastrointestinal Bleeding in Acute Pancreatitis: Etiology, Clinical Features, Risk Factors and Outcome
Gastrointestinal Bleeding in Acute Pancreatitis: Etiology, Clinical Features, Risk Factors and Outcome
Gastrointestinal Bleeding in Acute Pancreatitis: Etiology, Clinical Features, Risk Factors and Outcome
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Article in Tropical gastroenterology: official journal of the Digestive Diseases Foundation · January 2015
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ABSTRACT
Department of Gastroenterology1, Background: There is paucity of data on the effect of interventions on risk of gastrointestinal
Surgery2 and Radiodiagnosis3, bleeding (GIB) in acute pancreatitis (AP). Methods: Retrospective study of records of patients
Post Graduate Institute of Medical
with AP and GIB. Results: 16 (3.7%) patients (14 males; mean age 39.3±12.8 years) had
Education and Research (PGIMER),
Sector 12, Chandigarh – 160012, gastrointestinal bleeding. Two patients had peptic ulcer disease related GIB. The cause of GIB
India in remaining patients was: pseudoaneurysms in 5, gastrointestinal fistulization in 4, and no
identifiable lesion in 5. Two patients with pseudoaneurysms were treated with angio-
Correspondence:
embolisation whereas 3 needed surgery. The patients with gastrointestinal fistula had
Dr. Surinder Singh Rana
Email: drsurinderrana@yahoo.co.in complicated course and 3 of these 4 patients died due to sepsis and multi organ failure. Rest
5 patients with no identifiable lesion were managed conservatively and there was no recurrence
of GIB. Of the 14 patients with AP related GIB, a previous intervention had been done in
11(79%) patients. Fifty-three patients (12.7%) without GIB died whereas 5 (31.2%) patients
with GIB succumbed to the illness (p=0.04). Conclusions: The majority of our patients of AP
with GIB had antecedent history of interventions. The mortality was higher in patients with
GIB, which was not due to hemorrhage but to sepsis and related complications.
Introduction
Acute pancreatitis (AP) is a perplexing gastrointestinal disease demonstrated that although organ failure had more adverse
with variable degree of severity, course and outcome. effects on the outcome of AP than did GIB, the bleed still
Necrotizing pancreatitis is a more severe form of AP associated modestly increased the risk of mortality as well as the length of
with pancreatic parenchymal necrosis and/or peri-pancreatic the hospital stay in patients with AP.3
necrosis.1 Gastrointestinal bleeding (GIB) is an infrequent but The cause of GIB in acute pancreatitis can be varied and
potentially fatal complication of AP. It was considered a marker includes non-pancreatic causes like peptic ulcer disease,
of severity in the original Atlanta classification but was removed aggravated or induced by stress and nonsteroidal anti-
in the revised version as it is a late manifestation and does not inflammatory drug use for pain relief or due to local vascular
represent organ failure.1,2 A recent large population-based study complications of acute pancreatitis like thrombosis of the portal
venous system leading to formation of varices, erosions of the severe acute pancreatitis.1 Presence of local complications and/
upper abdominal arteries by the inflammatory process or by or transient organ failure (<48 hours) defined moderately severe
the collections, formation of pseudoaneurysms or fistulization AP and absence of local/systemic complications and organ
into the gastrointestinal tract.3-5 The combination of severe failure signified mild AP.
necrotizing pancreatitis and massive gastrointestinal bleed can
be a therapeutic challenge and is associated with high Assessment of gastrointestinal bleeding
mortality.6,7
Because of the rarity of GIB in AP, its risk factors have been We recorded the presentation of bleed (hematemesis, melena),
infrequently studied. The presence of pancreatic necrosis, presence or absence of hemodynamic compromise, need for
sepsis, collection and organ failure might be more common in transfusion, and results of evaluation for the cause of bleeding
bleeders compared with non-bleeders.5 The impact of surgical including endoscopy and computed tomography guided
and radiological interventions of local complications of AP on angiography. All patients received standard therapy including
the risk of GIB has also rarely been studied. One study reported intravenous proton pump inhibitors, intravenous fluids and
increased frequency of bleeding in patients who underwent correction of coagulopathy and thrombocytopenia, if present,
early surgical intervention as compared to patients with delayed by transfusion of appropriate blood component. Death,
intervention. 8 However, the impact of percutaneous discharge and readmission were recorded. The management of
interventions in increasing the risk of GIB in AP is not clear. pancreatitis was as per standard guidelines including
We retrospectively studied the etiology, clinical and analgesia, management of organ dysfunction, antibiotics on
endoscopic features, impact of prior interventions and outcome suspicion of infection and drainage of infected collections
of our patients with AP having GIB. using radiology guided pigtails.
The present study was a retrospective analysis of AP patients The descriptive data was presented as percentages for
with GIB seen at our unit at a large tertiary care referral teaching categorical variables and mean ± SD for quantitative variables.
hospital in North India over the last four years. The diagnosis The continuous variables were compared using student t-test
of acute pancreatitis was based on the presence of two of the whereas the categorical variables were compared using the
three features including presence of typical abdominal pain, Chi-square test. A p value of <0.05 was considered significant.
elevation of serum amylase or lipase to more than thrice the
upper limit of normal or presence of radiological evidence of Results
acute pancreatitis.1 We noted the clinical details including
duration of pain, onset to bleeding, age, gender, and etiology Of 432 patients with AP seen at our unit over the last four
of acute pancreatitis as well the hematological and biochemical years, 16 (3.7%) patients (14 males; mean age 39.3±12.8 years)
investigations and endoscopic findings. Details of the invasive had gastrointestinal bleeding. All our patients presented with
procedure prior to bleed including insertion of percutaneous overt gastrointestinal bleeding and hemodynamic instability
drains (PCD) and surgery were recorded. The outcome i.e. was seen in 13 (81%) patients. Blood transfusion was required
sepsis, organ failure, recurrence of bleeding and mortality was in all patients. The etiology of acute pancreatitis was alcohol
noted. The details of the therapeutic interventions done for in 11 (68.75%), gall-stones in 1 (6.25%), blunt abdominal trauma
hemostasis were also retrieved and noted. The various in 1 (6.25%), and idiopathic in 3 (18.75%) patients. These patients
definitions used in the study include: had GIB 3-12 weeks after the onset of AP. Twelve (75%) patients
Pancreatic necrosis: The presence of non-enhancing areas had severe AP whereas 4 patients had moderately severe AP.
in the pancreas as noted on contrast enhanced computed None of the patients had mild AP. All patients had pancreatic
tomography scan. necrosis on computed tomography (Table 1).
Severity of acute pancreatitis: Severity of AP was defined Upper gastrointestinal endoscopy revealed duodenal ulcer
using revised Atlanta definitions where the presence of in 1, and severe esophagitis in 1 patient and these two patients
persistent organ failure (>48 hours) was the central feature of were successfully treated with proton pump inhibitors and
GI bleeding in acute pancreatitis 33
Table 1:Details of 16 patients with acute necrotizing pancreatitis and gastrointestinal bleed
Age Sex Etiology Preceding Intervention Cause Pseudoaneurysm Location Death
18 M Idiopathic N Pseudoaneurysm Splenic No
60 F GSD P Pseudoaneurysm Left hepatic No
50 M Alcohol N Pseudoaneurysm Splenic No
38 M Alcohol P, S Fistula Duodenum No
52 M Alcohol P, S, Fistula Duodenum Yes
32 F Idiopathic N Pseudoaneurysm Splenic No
46 M Alcohol P Fistula Stomach Yes
34 M Trauma P Not Identified No Yes
42 M Alcohol P, S Not Identified No No
21 M Alcohol P Pseudoaneurysm Transverse mesocolic Yes
61 M Alcohol P Fistula Duodenum Yes
28 M Alcohol T Not Identified No No
28 M Idiopathic T Not Identified No No
46 M Alcohol N Duodenal Ulcer No No
32 M Alcohol N Esophagitis No No
42 M Alcohol P, S Not Identified No No
M: Male, F: Female; P: Percutaneous drainage, S: Surgery, T: Transmural drainage; D: Digital Subtraction angiography; N: None; GSD:
Gall stone disease
endoscopic intervention (Figure 1). Although 4 (25%) patients angiography and pseudoaneurysms were identified in 4 patients
had splenic vein thrombosis, none of them had esophageal or (splenic artery in 3 and left hepatic artery in 1). Two of the 4
gastric varices. The remaining 14 patients had AP related GIB patients with pseudoaneurysms were successfully treated with
and endoscopy revealed fistulous opening in the duodenum angioembolisation whereas 2 needed immediate surgery
and stomach in 3 and 1 patient, respectively (Figure 2). Necrotic because of hemodynamic compromise. One patient initially
material with granulation tissue was seen from the fistulous treated by angioembolisation needed surgery for worsening
opening in the gastrointestinal lumen. Although the sepsis and succumbed to the illness.
bleed was self-limiting in all 4 patients but these patients had a Of the remaining 6 patients, 1 patient was operated on
complicated course, and all required surgery for infected because of hemodynamic compromise and intra operatively
necrosis and 3 of these 4 patients died due to sepsis and multi- pseudoaneurysm of transverse mesocolic artery could be
organ failure. identified and successfully ligated. However, this patient died
Upper gastrointestinal endoscopy did not identify any due to sepsis and organ failure. The remaining 5 patients with
bleeding lesion in the remaining 10 patients. All these 14 no identifiable lesions were managed conservatively and there
patients also underwent computed tomographic (CT) was no recurrence of GIB in these patients.
Discussion