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.[174]
Occurs when the peri-pancreatic fluid collections become colonised and infected. Invariably fatal if not treated surgically. Follows secondary bacterial contamination of necrotic pancreatic tissue and haemorrhagic exudates. It is unknown whether prophylactic antibiotics given early in the course of the disease decrease the incidence of abscess. Generally patients present 2 to 4 weeks after the onset of pancreatitis, with fever, and clinically worsen.
Computed tomography is diagnostic, showing a ring-enhancing fluid collection with gas. Its treatment is drainage (surgical versus percutaneous) and antibiotics to cover Esterichia coli, Bacteroides, Staphylococcus, Klebsiella, Proteus, and Candida albicans.[5]
For information on management of infected pseudocysts, see Management Recommendations.
Can occur in severe acute pancreatitis and has a reported mortality rate of 49%.[179] 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.[48] Treatment options include percutaneous drainage of intra-abdominal fluid or decompressive laparotomy.[179]
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.[17] Around 8% to 16% of patients will go on to develop chronic pancreatitis.[96]
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.[175][176][177] 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.[178]
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][17]
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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