1. Causes
1.1. Chronic alcoholism
1.1.1. most common cause
1.2. hereditary pancreatitis
1.3. tropical pancreatitis
1.3.1. commonly found in children and young adults.
1.4. idiopathic
1.5. Hypercalcaemia
2. Acute Pancreatitis
2.1. Definition
2.1.1. Sudden inflammation of the pancreas.
2.1.2. a process that occurs on the background of a previously normal pancreas and can return to normal after resolution of the episode.
2.2. pathophysiology
2.2.1. consequence of premature intracellular trypsinogen activation, releasing proteases which digest the pancreas and surrounding tissue.
2.2.1.1. elevation of intracellular calcium <leads to activation of intracellular proteases<cellular necrosis.
2.3. Causes
2.3.1. Alcohol abuse
2.3.2. Gallstones
2.3.3. Post-ERCP
2.3.4. Viral infections
2.3.4.1. mumps, Coxsackievirus B
2.3.5. Drugs
2.3.5.1. sulfonamides,thiazide diuretics,furosemide, estrogens, HIV medication
2.3.6. Scorpion bites
2.3.7. Hypertriglyceridemia, hypercalcemia
2.3.8. Blunt abdominal trauma
2.3.8.1. most common cause of pancreatitis in children
2.4. investigation
2.4.1. Laboratory studies
2.4.1.1. Serum amylase
2.4.1.1.1. (nonspecific) and (nonsensitive)
2.4.1.2. Serum lipase
2.4.1.2.1. more specific for pancreatitis than amylase
2.4.1.3. LFTs
2.4.1.3.1. to identify cause (gallstone pancreatitis)
2.4.2. Abdominal radiograph
2.4.2.1. Has a limited role in the diagnosis of acute pancreatitis. More helpful in chronic pancreatitis
2.4.3. Abdominal ultrasound
2.4.3.1. help in identifying cause of pancreatitis
2.4.4. CT scan
2.4.4.1. Most accurate test for diagnosis of acute pancreatitis
2.4.4.2. identifying complications of the disease
2.4.5. ERCP
2.4.5.1. Severe gallstone pancreatitis with biliary obstruction
2.5. Complications
2.5.1. Pancreatic necrosis
2.5.1.1. Sterile pancreatic necrosis
2.5.1.2. Infected pancreatic necrosis
2.5.1.2.1. high mortality rate
2.5.2. Pancreatic pseudocyst
2.5.2.1. Complications of untreated pseudocysts include rupture, infection, gastric outlet obstruction, fistula, hemorrhage into cyst, and pancreatic ascites.
2.5.3. Hemorrhagic pancreatitis
2.5.3.1. Characterized by Cullen sign, Grey Turner sign, and Fox sign
2.5.4. Adult respiratory distress syndrome
2.5.4.1. life-threatening complication
2.5.5. ascites/pleural effusion
2.5.6. Ascending cholangitis
2.5.7. Pancreatic abscess
2.5.7.1. (rare)
2.6. Treatment
2.6.1. Bowel rest (Nothing by mouth)— to rest the pancreas
2.6.2. IV fluids
2.6.3. Pain control
2.6.4. Prophylactic antibiotics
2.6.4.1. should be considered to prevent infection (which has high morbidity and mortality).
2.6.5. Feeding
2.6.5.1. severe acute pancreatitis
3. Chronic Pancreatitis
3.1. Definition
3.1.1. continuing inflammation with irreversible structural changes.
3.1.2. endocrine and exocrine functions of the pancreas are impaired(Diabetes mellitus occurs in advanced cases)
3.1.3. presents as chronic unrelenting pain with episodic flare-ups.
3.2. pathophysiology
3.2.1. Alcohol and other risk factors may trigger acute pancreatitis through multiple mechanisms. The first episode of acute pancreatitis initiates an inflammatory response involving T-helper cells. Ongoing exposure to alcohol drives further inflammation but this is modified by regulatory T cells with subsequent fibrosis, via activation of pancreatic stellate cells. A cycle of inflammation and fibrosis ensues, with development of chronic pancreatitis.
4. Prognosis
4.1. Ranson criteria are used to determine prognosis and mortality rates.
4.2. Patients with more than 3 or 4 Ranson criteria should be monitored in an ICU .
4.3. Ranson criteria
4.3.1. Age >55 years
4.3.2. WBC >15 ×109/L
4.3.3. Blood glucose >10 mmol/L
4.3.4. Serumurea >16 mmol/L Serum
4.3.5. albumin <30 g/L Serum
4.3.6. aminotransferase >200 U/L Serum
4.3.7. calcium < 2 mmol/L Serum
4.3.8. LDH > 600 U/L
4.3.9. Pao2 <8.0 kPa(60 mmHg)