Complications
Seen in patients with severe acute pancreatitis. May be caused by circulating toxins or rhabdomyolysis. Hypovolaemia and inflammatory mediators. Acute renal failure is a complication with poor outcome.[192]
Can occur in severe acute pancreatitis and has a reported mortality rate of 49%.[201] Associated with over-aggressive fluid resuscitation. Defined by a sustained intra-abdominal pressure >20 mmHg that is associated with new-onset organ failure. Cannot be diagnosed by physical examination; measurement of intra-abdominal pressure should be considered in mechanically ventilated patients with severe acute pancreatitis, especially in the event of deterioration.[54] Treatment options include percutaneous drainage of intra-abdominal fluid or decompressive laparotomy.[201]
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).[197][198] Approximately 20% of patients with acute pancreatitis develop diabetes mellitus within 5 years.[199] The pathophysiology of acute pancreatitis-related diabetes mellitus is poorly understood.[197]
Recurrent attacks of acute pancreatitis may lead to chronic scarring, and, if the aetiological factor is not treated, may present with the classic characteristics of chronic pancreatitis: glucose intolerance, pancreatic insufficiency, and calcifications.[15] Around 8% to 16% of patients will go on to develop chronic pancreatitis.[50]
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) in patients with recurrent pancreatitis, splenomegaly, and bleeding from gastric varices.[5][15] It is more common in patients with severe disease, pancreatic necrosis, and/or acute pancreatitis caused by long-term alcohol misuse.[200]
Resulting from inflammation surrounding the pancreas and adjacent duodenum or transverse colon.
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.[193][194][195] Gram-negative bacteria are the main 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 anatomical barrier by providing enteral nutrition.[196]
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 hypoxaemia, 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][15]
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 raised levels of split fibrin products and D-dimer with low fibrinogen.[5]
Pancreatic ascites consists of accumulated pancreatic fluid in the peritoneal cavity and is defined by high amylase concentration in ascitic fluid (usually >1000 IU/L). The term encompasses people with ascites and pleural effusion and is a rare complication of acute pancreatitis (<5%). Leakage from a pancreatic pseudocyst or disruption of the pancreatic duct is the most common underlying cause. Patients may present with pain and symptoms caused by irritant abdominal ascites or with shortness of breath due to amylase-rich pleural effusion. It remains unclear whether conservative, medical, endoscopic, or surgical management is most effective. Advice on management should be sought from a specialist pancreatic centre.[8]
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