Pancreatitis Aguda (Inglés)

Acute pancreatitis
Varies from interstitial pancreatitis that is usually mild and self-limited to necrotizing pancreatitis in which degree necrosis correlates with severity.
Etiology:
• Gallstones: 30-60%
• Alcohol: 15-30%
• Hypertriglyceridemia
• After ERCP
• Trauma
• Drugs (sulfonamides, tetracycline’s)
• Sphincter of Oddi dysfunction

PathophysiologyInitial event is injury to acinar cells, and activation of proteolytic enzymes. Inflammatory cells like neutrophils and macrophages are recruited. Pancreatic hemorrhage, edema and eventually pancreatic necrosis.
Proteolytic enzymes and cytokines act on distant organs. SIRS and ARDS mar occur.

Clinical
Cardinal symptom is dull and steady abdominal pain in epigastrium that may radiate to the back.Nausea and vomiting are often present along with anorexia.
Fever and tachycardia are common. A minority has jaundice.

Lab data:
• Amylase and lipase are elevated usually more than 3 times. Serum amylase elevation only last for 48-72h and is not specific (intestinal obstruction, mesenteric ischemia, renal insufficiency). Lipase remains elevated for 7-14 days and is more specific forpancreas. Level of amylase or lipase does not indicate severity.
• Alkaline phosphatase, total Bilirubin and ALAT/ASAT may be elevated in gallstone panecreatitis
• CBC count of 15-20 000 and elevated CRP, Hematocrit > 44% due to plasma loss into peritoneal cavity.
• Hyperglycemia due to decreased release of insulin. Hypocalcemia

Imaging studies:
• Abdominal radiography: mainly todetect free air (perforated)
• US: initial test to detect gallstones.
• CT scans are used in more severe cases, and used for assessing complications.
• MRCP for diagnosis of biliary and pancreatic duct obstruction

Complications
In the first 2-3 weeks after pancreatitis patients frequently develops an inflammatory mass, which may be due to organized pancreatic necrosis or apseudocyst. Pancreatic abscess develops later, usually after 6 weeks. Systemic complications include pulmonary (effusions, atelectasis), cardiovascular (hypotension), hematologic (DIC), renal (azotemia), metabolic (hyperglycemia) and CNS abnormalities.

Treatment
In 85-90% self-limited. General measures includes analgesis, and IV fluids and colloids.
Antibiotics as prophylaxis is controversial.Infected pancreatic necrosis, abscess and pseudocysts
Infected pancreatic necrosis occurs often in first 2-4 weeks after onset. An abscess often develops after 4-6 weeks.
Both should be treated with surgical debridement or with drainage (abscess). Characteristic signs of abscess are fever, leukocytosis, ileus and rapid deterioration.
Pseudocysts are collection of fluid that differs from realcysts in that they don’t have any epithelial lining.

Pancreatic ascites is usually due to disruption of the main pancreatic dut, often by a internal fistula between the duct and peritoneal cavity or a leaking psudocysts.

Chronic pancreatitis
Continuing chronic inflammation process characterized by irreversible morphological changes. Pancreas is usually seen as atrophic fibrotic gland withdilated ducts and calcifications. Progressive destruction of both endocrine and eventually exocrine tissue. Cardinal symptoms are abdominal pain, steatorrhea and diabetes mellitus.

Etiology
1. Toxic-metabolic: Alcohol, tobacco, hypercalcemia, hyperlipidemia, Chronic renal failure, medications (phenacetin), toxins
1. Autoimmune
2. Genetic
3. Obstructive: duct obstruction, sphincterof oddi
4. Idiopathic
5. Recurrent and severe acute pancreatitis
Alcoholism is the most common, while CF in children. In 25% the cause is unknown. Genetic is often due to defects in trypsinogen

Autoimmune pancreatitis has characteristic clinical features. Symptoms are often mild abdominal pain without frequent attacks and presents with obstructive jaundice. Head of pancreas is...