Late subacute peripancreatic hematoma secondary to walled-off necrotizing pancreatitis: a case report

Delayed intra-abdominal hemorrhage is a rare clinical entity, most commonly associated with abdominal trauma, anticoagulation therapy, or underlying coagulation disorders. In exceptional cases, it has been reported as a complication of inflammatory abdominal conditions, including acute pancreatitis, particularly in necrotizing pancreatitis or in pancreatic pseudocysts complicated by vascular erosion. Nevertheless, the occurrence of a delayed hemorrhagic collection secondary to focal necrotizing inflammatory pancreatitis, without a history of trauma or hemorrhagic risk factors, represents an exceedingly rare clinical presentation. (1) Hemorrhagic complications associated with acute pancreatitis are uncommon but potentially life-threatening and are generally related to vascular erosion secondary to the proteolytic activity of pancreatic enzymes. Atypical hemorrhagic manifestations have been described in the literature, including subcapsular splenic or hepatic hematomas, as well as intrahepatic hemorrhage, which may develop in the setting of acute or necrotizing pancreatitis. (2,3) However, these presentations are exceedingly rare, and their diagnosis often represents a clinical challenge due to their low incidence and the nonspecific nature of the initial findings. In particular, the formation of intra-abdominal hemorrhagic collections distant from the pancreatic parenchyma has been scarcely reported. In this context, the aim of the present report is to describe a case of a hemorrhagic collection secondary to walled-off necrotizing pancreatitis with the development of an internal pancreatic fistula, contributing to the recognition of this uncommon complication and highlighting the importance of early diagnostic suspicion.

A clinical case report was conducted to document a rare late hemorrhagic complication associated with walled-off necrotizing pancreatitis, characterized by the development of a peripancreatic hematoma and a concomitant internal pancreatic fistula. This case was considered clinically relevant because of the uncommon nature of this presentation, its nonspecific clinical manifestations, and the diagnostic challenge it may represent, particularly in the absence of a history of trauma, anticoagulant use, or other recognized hemorrhagic risk factors. A retrospective review of the patient’s medical record was performed, including relevant medical history, clinical course, laboratory findings, imaging studies, intraoperative findings, biochemical analysis of the drainage fluid, treatment, and subsequent clinical follow-up. Abdominal magnetic resonance imaging and contrast-enhanced computed tomography findings were reviewed, together with the findings obtained during exploratory laparotomy, to characterize the hemorrhagic collection and its relationship with the underlying pancreatic inflammatory process. The biochemical characteristics of the postoperative drainage fluid were also evaluated to support the diagnosis of an internal pancreatic fistula. The case was documented for academic and scientific purposes, with the aim of increasing awareness of this uncommon complication and emphasizing the importance of maintaining a high index of clinical suspicion and timely use of appropriate imaging modalities in patients with atypical or delayed complications of necrotizing pancreatitis.

A 38-year-old female patient was referred to a secondary level hospital for evaluation of acute abdominal syndrome. Her relevant medical history included a previous hospitalization for mild acute pancreatitis, classified according to the revised Atlanta criteria, of biliary etiology secondary to biliary tract obstruction. During that episode, early cholecystectomy was performed in accordance with the recommendations of the American Gastroenterological Association guidelines. Intraoperatively, the gallbladder was classified as Parkland grade II, with no surgical complications. The patient had an uneventful postoperative course and was discharged without evidence of complications. Approximately 60 days after the initial hospitalization, the patient presented with a new episode characterized by epigastric pain, accompanied by nausea and subsequent vomiting on five occasions. Her condition progressively deteriorated over the following hours, with increasing abdominal pain. Upon admission, physical examination revealed tenderness to superficial palpation and a palpable mass in the epigastric region and right hypochondrium, without muscular rigidity or evidence of periumbilical or flank ecchymosis. Initial laboratory studies showed a hemoglobin concentration of 9.2 g/dL, serum glucose of 230 mg/dL, hyperbilirubinemia with total bilirubin of 1.44 mg/dL, direct bilirubin of 0.65 mg/dL, and indirect bilirubin of 0.80 mg/dL, as well as elevated alkaline phosphatase levels of 1,657 IU/L. C-reactive protein (CRP) was elevated at 12.35 mg/L. Serum amylase and lipase levels were requested, revealing elevated concentrations of lipase (1,345 IU/L) and amylase (845 IU/L). Forty-eight hours after admission, the patient showed clinical deterioration, with a marked increase in CRP levels to 161 mg/dL and a decrease in hemoglobin concentration to 7.2 g/dL, requiring transfusion of three units of packed red blood cells. Given the laboratory findings and clinical progression, a non-contrast magnetic resonance cholangiopancreatography (MRCP) was performed, revealing the following findings: a septated collection with hemosiderin remnants in the gastrohepatic space measuring 15 × 15 × 6 cm (approximately 700 mL) (Figure 1), and a retroperitoneal collection adjacent to the pancreatic tail measuring 9 × 6 × 7 cm (approximately 240 mL) (Figure 2), both findings compatible with organized hematomas. Additional findings included perihepatic free fluid, right basal atelectasis, left pleural effusion, and an interloop collection in the left flank measuring 6 × 5 cm (Figure 3). To assess pancreatic viability and further characterize the collections, a contrast-enhanced abdominal computed tomography (CT) scan was obtained. The study demonstrated findings consistent with focal pancreatitis, including absence of contrast enhancement of the pancreatic parenchyma during both arterial and venous phases (Figure 4). An encapsulated heterogeneous collection adjacent to the pancreas with hemorrhagic and inflammatory content was identified (Figure 5), suggestive of a hematoma with an estimated chronicity of 2–7 days, with possible communication toward the perihepatic Morrison’s pouch and the lesser sac. During hospitalization, the patient developed intermittent fever episodes with peaks of up to 38.5 °C. Due to their temporal association with blood product administration, these episodes were attributed to a probable non-hemolytic febrile transfusion reaction. The case was evaluated by the Hematology Department, which recommended symptomatic management and prophylactic measures in case additional transfusions were required. The patient showed adequate clinical response, with resolution of fever within the following 48 hours. On the eighth day of hospitalization, after hemodynamic stabilization and optimization of hemoglobin levels, the patient was taken to the operating room for exploratory laparotomy. During the procedure, approximately 2,000 mL of chronic-appearing hemorrhagic fluid undergoing coagulation was identified, predominantly located in the suprahepatic region (left hepatic lobe), anterior to the stomach, within interloop spaces, and in the lesser sac. Additionally, approximately 100 mL of inflammatory fluid was observed. No active bleeding source was identified during intraoperative exploration. Extensive surgical lavage of the abdominal cavity was performed, and Penrose drains were placed for postoperative monitoring and control. Subsequently, the patient remained under close postoperative surveillance. Biochemical analysis of the fluid obtained through the Penrose drain revealed elevated amylase (8,788 U/L) and lipase (>25,000 U/L) concentrations, findings consistent with a pancreatic leak. The patient's clinical course was favorable, with progressive improvement, adequate oral intake tolerance, hemodynamic stability, and no evidence of infection. These findings allowed hospital discharge with outpatient follow-up for monitoring of drain output and clinical surveillance. At the three-week follow-up evaluation, the patient was asymptomatic and showed no evidence of complications; therefore, she was discharged from medical care with a diagnosis of a type A pancreatic fistula.

Acute pancreatitis is one of the most common causes of hospitalization due to gastrointestinal disease and may progress to multiple local and systemic complications. Among these, vascular complications represent an uncommon but potentially fatal group, primarily resulting from enzymatic autodigestion of pancreatic tissue and adjacent vascular structures. This inflammatory process may lead to weakening of the vascular wall, pseudoaneurysm formation, or vessel rupture, resulting in intra-abdominal hemorrhage. Vascular complications have been estimated to occur in approximately 1–23% of patients with pancreatitis, whereas hemorrhagic arterial complications occur in approximately 1.3–10% of cases. (4-9) Furthermore, when significant bleeding occurs, mortality rates may reach 34–52%, emphasizing the importance of early recognition and timely management. (10) In most reported cases, intra-abdominal hemorrhage is associated with abdominal trauma or postoperative complications. (11) Consequently, during the initial evaluation of the present case, a complication related to the previous surgical procedure was considered the primary diagnostic hypothesis. However, this possibility was definitively excluded based on the intraoperative findings. The differential diagnosis included mesenteric vascular disorders, anticoagulant therapy, and neoplastic processes. Nevertheless, the absence of relevant medical history, together with the lack of compatible clinical, biochemical, and radiological findings, allowed these etiologies to be ruled out. The nonspecific clinical presentation, combined with the limited diagnostic sensitivity of medical history and physical examination in this setting, highlights the need for advanced imaging modalities, including computed tomography and magnetic resonance imaging, for the timely detection of hemorrhagic complications associated with pancreatitis. (7-8, 12-13) During the postoperative period, biochemical analysis of the fluid obtained through the Penrose drain revealed markedly elevated amylase and lipase concentrations, directing the pathophysiological assessment toward the presence of a pancreatic fistula. According to the International Study Group on Pancreatic Fistula (ISGPF) classification, the condition was initially considered a type C pancreatic fistula due to its significant clinical impact, characterized by the development of an extensive intra-abdominal collection, the requirement for surgical intervention, and its influence on the patient's clinical course. These findings suggest focal erosive damage of the peripancreatic vascular structures secondary to walled-off necrotizing pancreatitis localized in the pancreatic head, with extravasation of pancreatic secretions into the peritoneal cavity. Anatomically, the vessels most frequently involved include the celiac trunk, superior mesenteric artery, and, predominantly, the splenic artery and its distal branches. Subsequently, following favorable clinical evolution and progressive resolution of the condition, the fistula was reclassified as a less severe type A pancreatic fistula during follow-up. (14-15) Additionally, intracavitary hemorrhage may occur when vascular rupture extends into a pancreatic pseudocyst or an encapsulated necrotic collection, appearing on imaging studies as hyperattenuating or hyperintense areas depending on the modality used. (4, 6, 9, 12-15) In the present case, non-contrast magnetic resonance cholangiopancreatography demonstrated a peripancreatic collection with a thin, well-defined wall, heterogeneous peripancreatic tissue, and alterations in the morphology of the pancreatic tail. These radiological findings, together with the clinical evolution, supported the diagnosis of a focal and localized vascular erosive injury.(12, 13, 16) Furthermore, Thomas R. Gadacz et al. performed a meta-analysis on vascular lacerations associated with pancreatitis, reporting an incidence of hemorrhagic complications ranging from 1.7% to 2.5%. (17, 18) In a review of 44 cases, the splenic artery and gastroduodenal artery were identified as the most frequently affected vessels, with incidences of 34% and 9%, respectively. In 28% of cases, the injured vessel could not be identified, which is consistent with the present case, in which no vascular injury was identified during surgical exploration. Notably, these complications were more frequently observed in patients with chronic pancreatitis of alcoholic etiology, accounting for up to 75% of reported cases. (19) In 2020, Vikas Gupta et al. published a meta-analysis focused on hemorrhagic complications associated with acute pancreatitis. Among 183 cases of severe acute pancreatitis analyzed, only 13% (24 patients) developed hemorrhagic complications. Of these, 50% presented with intra-abdominal or intraluminal hemorrhage, 52% experienced massive bleeding, and the remaining patients developed mild hemorrhage. Sixteen cases were classified as de novo hemorrhage, whereas eight were categorized as postoperative hemorrhage. Based on these findings, the authors proposed a clinical classification according to bleeding location and severity: intraluminal hemorrhage (presenting as hematemesis or melena), intra-abdominal hemorrhage (identified as a hemorrhagic collection on imaging studies), massive hemorrhage (defined as a hemoglobin decrease >2 g/dL or hemodynamic instability), and mild hemorrhage. According to this classification, the present case was categorized as a de novo massive hemorrhage, as the patient had not undergone a previous surgical procedure directed toward the management of peripancreatic hemorrhage. Notably, within that study, only four cases presented with these characteristics; two were associated with pseudoaneurysm formation, whereas the underlying etiology could not be determined in the remaining two cases. (20)

The management of this case represented a considerable diagnostic and therapeutic challenge, mainly due to the atypical location of the hematoma, limitations in access to advanced imaging modalities such as angiography, and the prolonged clinical course. Ultimately, it was concluded that the late subacute hemorrhagic event was secondary to walled-off necrotizing pancreatitis localized in the pancreatic head, documented by magnetic resonance imaging, which resulted in peripancreatic vascular injury and the concomitant development of a type C internal pancreatic fistula as a complication of a localized inflammatory process in this region. (6, 14-15) Spontaneous peripancreatic hemorrhagic collections associated with acute pancreatitis represent an uncommon complication with a frequently nonspecific clinical presentation, which may delay the timely recognition of hemorrhagic events. Therefore, maintaining a high index of suspicion is essential in patients presenting with clinical deterioration or atypical findings during the course of the disease, even in the absence of classical criteria for severe or necrotizing acute pancreatitis. Early recognition of these complications allows optimization of diagnostic and therapeutic strategies, potentially improving patient outcomes.