122 Acute and Chronic

Pancreatitis is defined as acute or chronic. Acute pancre- Clinical signs associated with acute and chronic pan- atitis is associated with the abrupt onset of symptoms that creatitis are similar. It is often difficult to distinguish dissipate once the attack resolves. Chronic pancreatitis the two entities without knowledge of previous attacks. occurs as multiple acute attacks.The most common causes Common symptoms include epigastric abdominal pain, of pancreatitis are gallstone disease and alcohol abuse. nausea, and vomiting.The pain is often described as sharp Other causes include pancreatitis induced by drugs, pan- and radiates to the mid-back. Patients may report partial creatic duct obstruction, hereditary factors, trauma, and relief of pain with sitting up and leaning forward. Fever, idiopathic causes. The development of tachycardia, shortness of breath, and hypotension can is often associated with the passage of gallstones through also be associated with an acute episode. Fluid losses the biliopancreatic tract. The mechanism by which this from capillary leak syndrome and repeated emesis result takes place has been debated. A common theory is that in hypovolemia and hypotension. Abdominal distension obstruction of the biliopancreatic tract results in a brief with tympani and absent bowel sounds suggest an asso- outflow obstruction, which causes bile reflux through ciated ileus. Patients with severe pancreatitis may also the tract. The bile reflux in turn causes inflammation in show signs of retroperitoneal hemorrhage in the form of the . Newer studies, however, have shown stone flank ecchymoses (Grey Turner’s sign) and periumbilical passage to result in pancreatitis without direct evidence ecchymoses (Cullen’s sign). Chest radiographs may show of bile reflux through the pancreatic duct. The latest line a pleural effusion and occasionally evidence of adult of thought implicates pancreatic ductal obstruction and respiratory distress syndrome in severe cases. ductal hypertension with stone passage as the cause of Amylase and lipase levels are often elevated. The acute pancreatitis. Injury to pancreatic acinar cells leads rise in the two pancreatic enzymes occurs in parallel; to intracellular activation of digestive enzymes such as however, the amylase level may return to baseline before trypsinogen. An inflammatory response within the pan- the lipase level. Prolonged amylase elevation (>1 week) creas then ensues. Circulating proinflammatory cytokines may be a clue to the presence of pancreatic abscess, cause major systemic changes in the body. With severe pseudocyst, or ascites. Leukocytosis with a left shift is attacks, capillary leak syndrome may develop, leading to common. Hypovolemia may manifest itself as elevations fluid sequestration in areas such as the lungs. of hematocrit and hemoglobin levels.This is confirmed by The cause of chronic pancreatitis is most often alcohol a simultaneous elevation of blood urea nitrogen level and abuse. This occurs more often in men, and patients gen- a creatinine ratio of 20:1. Endocrine dysfunction is indi- erally report an extensive history of alcohol abuse. The cated by elevated serum glucose level. Hypoalbuminemia popular theory behind chronic pancreatitis is that it is the and hypocalcemia can also be present; however, a result of multiple and repeated subclinical episodes of decrease in ionized calcium in the setting of severe pan- acute inflammation. The repeated episodes of inflamma- creatitis has a poor prognosis. tion eventually lead to pancreatic necrosis and fibrosis. Imaging studies are helpful for determining the extent Over time, the accumulated tissue loss leads to loss of of the disease and for evaluating possible complications. endocrine and exocrine function. The nature of alcohol Chest radiographs may reveal pleural effusions (com- injury has been attributed to a number of mechanisms monly on the left side) and basilar atelectasis. Abdomi- that include free radical production in the pancreas, nal plain films may show paralytic ileus. In the case induced hypertriglyceridemia, and direct pancreatic of chronic pancreatitis, calcified intraductal protein acinar injury. plugs may appear as pancreatic calcifications. Computed

278 122. Acute and Chronic Pancreatitis 279

Table 122.1. Ranson’s criteria for nongallstone pancreatitis. endoscopic duct clearance in the early stages of gallstone Admission Initial 48 hours pancreatitis has been debated. In mild pancreatitis, duct Age >55 years Hematocrit decrease >10 clearance can be delayed, because most cases resolve WBC >16k BUN increase >5mg/100mL spontaneously. In the case of severe pancreatitis, there is Serum glucose >200mg/100mL Calcium <8mg/100mL no clear evidence of its merit. > > AST 250U/100mL Base deficit 4mEq/L Complications of pancreatitis include fluid collections, LDH >350IU/L pO2 < 60mmHg Fluid loss >6L abscesses, ascites, fistulas, false aneurysms, splenic vein thrombosis, necrosis, and pseudocysts. The consensus is that sterile pancreatic and peri-pancreatic fluid collec- tomography is useful in evaluating the degree of pancre- tions should be treated conservatively. The conditions atic edema, necrosis, and fluid collection. The magnitude eventually resolve, and, therefore, surgical intervention of an episode of pancreatitis is determined during the first may simply complicate matters. In the case of infected 48 hours.A clinical scoring system known as Ranson’s cri- fluid collections, intravenous antibiotic therapy in combi- teria (Tables 122.1 and 122.2) was devised to determine nation with percutaneous drainage is necessary. Infected the severity and prognosis of an attack. pancreatic necrosis is less likely to respond to antibiotic Patients with fewer than three criteria are categorized therapy alone or in conjunction with percutaneous as having a mild attack.The mortality rate associated with drainage. Surgical debridement of all necrotic tissue with less than three criteria is less than 1%. However, the mor- antibiotics provides the optimal therapy in this case. bidity and mortality rates rise as more criteria are asso- Pancreatic pseudocysts result from communication of ciated with the attack. If a patient meets three to four the pancreatic duct system into a cystic cavity created by criteria, the mortality rate approaches 15%. When seven localized inflammation. Pseudocysts lack an epithelial or more criteria are met, the mortality rate is as high as lining and therefore are not true cysts. They generally 90%. contain high levels of pancreatic enzymes, and persistent The treatment of acute pancreatitis is aimed at limit- elevation of amylase or lipase can be a clue to their exis- ing progression and alleviating symptoms. In the acute tence. Intervention is only necessary in pseudocysts that setting, hypovolemia should be addressed by aggressive are symptomatic or continue to enlarge. Large pseudo- volume resuscitation. Complications such as adult respi- cysts (greater than 6cm) are more likely to be sympto- ratory distress syndrome may hamper the resuscitation matic due to mass effect and encroachment onto adjacent efforts. In such cases, a Swan Ganz catheter proves useful. organs or vessels. Some common complications include Electrolyte abnormalities are common because of poor early satiety, gastric outlet obstruction, obstructive jaun- nutritional status and frequent emesis. Electrolyte dice, pseudoaneurysm, and hemorrhage. There are many replacement is mandatory, especially for decreased treatment options for Pseudocysts, including internal and ionized calcium level. Nausea and vomiting can be alle- external drainage, endoscopic drainage, laparoscopic viated with nasogastric decompression. Studies have drainage, and open . External drainage shown a benefit to administering prophylactic antibiotics increases the risk of infection and external pancreatic to patients with severe pancreatitis. Patients are given fistula; therefore, it is generally reserved for patients who parenteral nutrition via a central venous catheter. Proton are poor surgical candidates. The treatment of a pseudo- cyst is directed by its anatomic make up. Pseudocysts that pump inhibitors or H2-blockers are used for prophylaxis against the formation of stress ulcers. Good pulmonary are directly adjacent to the or duodenum may toilet and pain control have a role in preventing pul- be effectively treated by endoscopic cystogastrostomy or monary complications. cystoduodenostomy. Patients with pseudocysts at the With pancreatitis caused by gallstones, surgery should head of the pancreas may be amenable to transpapillary be delayed until resolution of the attack. The benefit of stent placement via endoscopic retrograde cholan- giopancreatography. Surgical drainage consists of cystogastrostomy, Roux-en-Y cyst , or cyst Table 122.2. Ranson’s criteria for gallstone pancreatitis. duodenostomy. Pancreatic ascites and pleural fistulas Admission Initial 48 hours can be treated conservatively in up to 60% of patients. Age >70 years Hematocrit decrease >10 Endoscopic therapy includes sphincterotomy and stent- WBC >18k BUN increase >2mg/100mL ing. Surgical options include partial or Serum glucose >220mg/100mL Calcium <8mg/100mL Roux-en-Y drainage. Splenic vein thrombosis responds > > AST 250U/100mL Base deficit 5mEq/L to splenectomy when left-side , gas- LDH >40IU/L Fluid sequestration >4L troesophageal varices, and bleeding develop.