INTRODUCTION: Pancreatitis (inflammation of the pancreas) is a serious disorder that can range in severity from a relatively mild, selflimiting disorder to a rapidly fatal disease that does not respond to any treatment. Acute pancreatitis is commonly described as an autodigestion of the pancreas by the exocrine enzymes it produces, principally trypsin. [Readabout biochemistry of enzymes]
Eighty percent of patients with acute pancreatitis have biliary tract disease or a history of long-term alcohol abuse. Other less common causes of pancreatitis include bacterial or viral infection, with pancreatitis occasionally developing as a complication of mumps virus. Many disease processes and conditions have been associated with an increased incidence of pancreatitis, including surgery on or near the pancreas, medications, hypercalcemia, and hyperlipidemia. Up to 10% of cases are idiopathic, and there is a small incidence of hereditary pancreatitis. Mortality is high because of shock, anoxia, hypotension, or fluid and electrolyte imbalances. [Readabout shock]
Attacks of acute pancreatitis may result in complete recovery, may recur without permanent damage, or may progress to chronic pancreatitis.
CLINICAL MANIFESTATIONS: Severe abdominal pain is the major symptom. Pain in the midepigastrium may be accompanied by abdominal distention; a poorly defined, palpable abdominal mass; decreased peristalsis; and vomiting that fails to relieve the pain or nausea. Pain is frequently acute in onset (24 to 48 hours after a heavy meal or alcohol ingestion); may be more severe after meals and unrelieved by antacids. Patient appears acutely ill, Abdominal guarding; rigid or boardlike abdomen (generally an ominous sign, usually indicating peritonitis). Ecchymosis in the flank or around the umbilicus, which may indicate severe hemorrhagic pancreatitis. Nausea and vomiting, fever, jaundice, mental confusion, agitation. Hypotension related to hypovolemia and shock. May develop tachycardia, cyanosis, and cold, clammy skin. Acute renal failure common. Respiratory distress and hypoxia. May develop diffuse pulmonary infiltrates, dyspnea, tachypnea, and abnormal blood gas values. Myocardial depression, hypocalcemia, hyperglycemia, and disseminated intravascular coagulation (DIC).
ASSESSMENT AND DIAGNOSTIC FINDINGS: Diagnosis is based on history of abdominal pain, the presence of known risk factors, physical examination findings, and diagnostic findings (increased urine amylase level and white blood cell [WBC] count; hypocalcemia; transient hyperglycemia; glucosuria and increased serum bilirubin levels in some patients). X-rays of abdomen and chest, ultrasound, and contrast-enhanced computed tomography (CT) scan may be performed. Hematocrit and hemoglobin levels are used to monitor the patient for bleeding. Serum amylase and lipase levels are most indicative (elevated within 24 hours; amylase returns to normal within 48 to 72 hours; lipase remains elevated for longer period). Peritoneal fluid is evaluated for increase in pancreatic enzymes.
MEDICAL MANAGEMENT:
Acute Phase: During the acute phase, management is symptomatic and directed toward preventing or treating complications. Oral intake is withheld to inhibit pancreatic stimulation and secretion of pancreatic enzymes. Parenteral nutrition (PN) is administered to the debilitated patient. Nasogastric suction is used to relieve nausea and vomiting and to decrease painful abdominal distention and paralytic ileus. Histamine-2 (H2) receptor antagonists (cimetidine, ranitidine) or, sometimes, proton pump inhibitors are given to decrease hydrochloric acid secretion. Adequate pain medication, such as morphine, is administered. Antiemetic agents may be prescribed to prevent vomiting. Correction of fluid, blood loss, and low albumin levels is necessary. Antibiotics are administered if infection is present. Insulin is necessary if significant hyperglycemia occurs. Aggressive respiratory care is provided for pulmonary infiltrates, effusion, and atelectasis. Biliary drainage (drains and stents) results in decreased pain and increased weight gain. Surgical intervention may be performed for diagnosis, drainage, resection, or debridement.
MEDICAL MANAGEMENT:
Postacute Phase. Antacids are given when the acute episode begins to resolve. Oral feedings low in fat and protein are initiated gradually. Caffeine and alcohol are eliminated. Medications (eg, thiazide diuretics, glucocorticoids, or oral contraceptives) are discontinued.
RELATED;
1. INSULIN
2. GLUCAGON
No comments:
Post a Comment