Complications
Seen in patients with severe acute pancreatitis. May be caused by circulating toxins or rhabdomyolysis. Hypovolemia and inflammatory mediators. Acute renal failure is a complication with poor outcome.[120]
Occurs when the peripancreatic fluid collections (pseudocysts) become colonized and infected. Generally patients present 2-4 weeks after the onset of pancreatitis, with fever, and clinically worsen. See Management recommendations for further information on detection and management of infected pseudocysts.
Recurrent attacks may lead to exocrine pancreatic insufficiency more commonly than endocrine failure, although exocrine disorders of the pancreas can cause or precede the onset of diabetes (pancreatogenic or type 3c diabetes).[125][126] Approximately 20% of patients with acute pancreatitis develop diabetes mellitus within 5 years.[127] The pathophysiology of acute pancreatitis-related diabetes mellitus is poorly understood.[125]
Recurrent attacks of acute pancreatitis may lead to chronic scarring, and, if the etiologic factor is not treated, may present with the classic characteristics of chronic pancreatitis: glucose intolerance, pancreatic insufficiency, and calcifications.[19]
Ongoing pancreatic inflammation may cause irritation and inflammation of the portal vein and/or splenic vein, leading to portal hypertension. Suspect splenic vein or portal vein thrombosis (splanchnic vein thrombosis) patients with recurrent pancreatitis, splenomegaly, and bleeding from gastric varices.[5][19] It is more common in patients with severe disease, pancreatic necrosis, and/or acute pancreatitis caused by long-term alcohol misuse.[128]
Resulting from inflammation surrounding the pancreas and adjacent duodenum or transverse colon.
Ileus may be frequently seen in pancreatitis: a result of dehydration, electrolyte abnormalities, or adjacent bowel inflammation. Intestinal obstruction can be seen later in the course of the disease, when a pseudocyst or abscess causes a mechanical compression of the bowel (generally duodenum or transverse colon).[19]
The gut mucosa plays a central role in the development of sepsis. Several descriptions about how the gut modulates the inflammatory response by priming neutrophils and secreting cytokines can be found in the literature.[121][122][123] Gram-negative bacteria are the number one cause of sepsis in patients with acute pancreatitis, and the gut mucosa is considered as the source of such organisms. Therefore, it is important to maintain integrity of the anatomic barrier by providing enteral nutrition.[124]
From arterial pseudoaneurysm.
The production and excretion of inflammatory mediators (such as cytokines, prostaglandins, and thromboxanes) during pancreatitis may damage the alveolocapillary membrane, leading to destruction of pneumocytes and decrease in the amount of surfactant. This leads to airway destruction, increase in superficial tension, and inadequate oxygenation. Patients usually present with hypoxemia, requiring higher levels of supplemental oxygen, with bilateral interstitial infiltrates, PaO₂:FiO₂ ratio <300, and a normal pulmonary capillary wedge pressure. Patients may require mechanical ventilation during the course of their disease.[1][4][19]
Severe acute pancreatitis, especially if associated with necrosis, has been linked to liberation of cytokines and systemic inflammatory response, with activation of the complement, coagulation, and fibrinolytic cascades, leading to a state of coagulopathy and disseminated intravascular coagulation with elevated levels of split fibrin products and D-dimer with low fibrinogen.[5]
From adjacent inflamed stomach or duodenum, ruptured pseudocyst, arterial pseudoaneurysm, or peptic ulcer.
From celiac or splenic artery rupture or acute splenic vein thrombosis.
Consists of accumulated pancreatic fluid in the peritoneal cavity. It is due to chronic leakage of a pseudocyst, but some cases may be due to duct disruption. Clinically manifested by weight loss and unresponsiveness of the ascites to diuretics. Initial treatment involves hyperalimentation and somatostatin analogs. If no improvement is obtained in 2 to 3 weeks, endoscopic retrograde cholangiopancreatography and surgery should be considered.[5]
Secondary to pancreatic fistula draining into the chest. The diagnosis is based on thoracentesis with fluid rich in amylase and a computed tomography scan/retrograde pancreatogram that shows the fistula. Its treatment consists of drainage with a chest tube, somatostatin analogs, and total parenteral nutrition. If fistula persists, operative intervention with fistula resection or distal pancreatectomy should be performed.[5]
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