Acute Pancreatitis

Acute pancreatitis: Acute inflammation of the pancreas Spillage of pancreatic enzymes into surrounding pancreatic tissue can cause auto digestion and severe pain Varies from mild edema to severe hemorrhagic necrosis Most common in middle age men and women and effects both equally Rates higher in Afro Americans than whites Etiology: - Gallbladder disease/Gallstones (most common cause) Chronic alcohol intake (2nd most common cause) Smoking Genetic factors Biliary sludge(Microlithiasis): - mixture of cholesterol crystals and calcium salts found I 20-40% of acute p. pts formation seen in pts with bile statsis Acute attack causes: - associated with hypertriglyceridemia(over 1000mg/dL) trauma to pancreas viral infections penetrating duodenal ulcers cysts abscesses cystic fibrosis kaposi sarcoma certain drugs (corticosteroids, thiazide diuretics, oral contraceptives, sulfonamides, NSAIDS) Metabolic disorders (hyperparathyroidism, renal failure) Vascular disease Can be idiopathic(unknown) Pathogenic mechanism: Auto digestion of pancreas - - Etiologic factors injure pancreatic cells or activate the pancreatic enzymes in the pancreas rather than the intestine; this may be due to bile acids in pancreatic duct tough an open or distended sphincter of Oddi. Reflex may be caused by blockage by gallstones Obstruction can lead to pancreatic ischemia Classification of pancreatitis: 43-12 Mild: edemantous or interstitial pancreatitis Severe: necrotizing pancreatitis; ½ of pts have permanent decrease in exocrine and endocrine function; pts also at high risk of developing pancreatic necrosis, organ failure, and septic compilations S/S: - Abd pain(predominate symptom) in LUQ or mid-Epigastric and can radiate to lower back Distention of pancreas Peritoneal irritation Obstruction of biliary tract N/V Low grade fever Leukocytosis Hypotension Tachycardia Jaundice Abd tenderness Muscle guarding Decreased bowel sounds or absent Paralytic ileus due to abd distention Crackles in lungs Intravascular damage from circulating trypsin; may cause areas of cyanosis or greenish or yellow brown discoloration of abd wall Ecchymosis are flanks and the peri-umbilical area(pg1000) Shock may occur Toxemia from activated pancreatic enzymes Hypovolemia as a result of fluid shift into the retroperitoneal pace Pain: - Sudden onset Sever, deep, piercing, and continuous or steady Aggravated by eating Has it sudden onset when the pt is recumbent - Not relieved by vomiting Accompanied by flushing, cyanosis, and dyspnea Pt may flex spine in attempt to relieve severe pain Complications: Depends on pancreatic destruction Psuedocyst: Pancreatic pseudocyst: accumulation of fluid, pancreatic enzymes, tissue deris, and inflammatory exudates surrounded by a wall adjacent to the pancreas. Can resolve spontaneously or may perforate Can rupture and cause peritonitis or rupture into the stomach or duodenum s/s of pancreatic pseudocyst: - Abd pain Palpable epigastric mass N/V Anorexia Elevated serum amylase Diagnostics: - CT MRI Endoscopic Ultrasound Treatment: - Surgical drainage Percutaneous catheter placement and drainage Endoscopic drainage Pancreatic Abscess: Can result from an infected pseudocyst causing extensive necrosis May rupture or perforate into adjacent organs S/S: - Upper and pain High fever Leukocytosis Sepsis: prompt surgical drainage to prevent it Systemic complications: Pulmonary: likely due to exudate containing pancreatic enzymes enzyme induced inflammation of the diaphragm occurs resulting in atelectasis caused by reduced diaphragm movement - Pleural effusions Atelectasis Pneumonia Acute respiratory distress syndrome (ARDS) Cardiovascular: hypotension Trypsin can activate prothrombin and plasminogen increasing risk of thrombi formation, pulmonary emboli, and disseminated intravascular coagulationDIC) Tetany caused by hypocalcemia is a sign of severe disease; combining of calcium and fatty acids during fat necrosis Acute severe pancreatitis complications: Abd compartment syndrome secondary to intra-abdominal hypertension and edema Dx studies: Labs - Serum amylase and lipase; usually elevated Test for other disorders that might increase amylase levels Elevated liver enzymes Elevated triglycerides Elevated glucose Elevated bilirubin Decrease in calcium Imaging: - Ultrasound - X-ray: may show pulmonary changes such as atelectasis and pleural effusions CT scan; best test ERCP(can cause acute pancreatitis along with EUS) EUS Magnetic resonance Cholangiopancreatography(MRCP) Angiography Interprofessional Care/ conservative therapy : 43-17 &18 - - Hydration Pain management: IV morphine, other pain meds, may be combined with antispasmodic, atropine and other anticholinergic drugs should be avoided when paralytic ileus is present as it could reduce motility even more Management of metabolic complications Minimize pancreatic stimulation; NPO, NG suction to reduce vomiting, gastric distention Antispasmodics (relax smooth muscles): nitroglycerin or paparative Supplemental O2 Monitor for hyperglycemia Blood volume replacements: Plasma volume expanders may be given: dextran or albumin IV fluids for electrolyte imbalance Vasoactive drugs such as dopamine (Intropin) may be used to increase systemic vascular resistance in pts with ongoing hypotension Enteral nutrition for pt who can not resume orla intake Prevent infections Monitor pt closely for infection so antibiotics can be given early if necrosis and infection occur Gram stains to help determine bacteria; endoscopic to CT guided percutaneous aspiration may be used Surgical therapy: - When acute p. urgent ERCP plus endoscopic sphincterectomy may be done May be indicated when dx is uncertain and pts don’t respond to conservative therpay Drainage of necrotic fluid Drug therapy:43-19 Nutritional therapy: - NPO status reduce pancreatic secretion Enteral feedings via nasojejenual tube Parenteral reserved for pts who cannot tolerate enteral nutrition - If IV lipids are ordered, triglycerides must be closely monitored Jejunal feeding tube for moderate to severe cases When food is given, it is given in small frequent feedings Diet is high in carbs because it is the least stimulating to the exocrine portion of the pancreas Suspect intolerance when pt complains of pain, increased abd girth, and increased amylase and lipase levels Supplemental fat-soluble vitamins may be given Nurse assessment: 43-20 Nursing implementation: Health promotion - assessment of predisposing factors Encourage early treatment of these factors Acute care: - Monitor vitals Monitor hemodyanmic stability for complication such as hypotension, fever, tachypnea Monitor response to IV fluids Monitor electrolyte balance and factors that might upset it Assess respiratory function and monitor for complications such as respiratory failure If ARDS develops pt may need to intubated and on mechanical ventilation Monitor for signs of tetany r/t hypocalcemia such as jerking, irritability, muscular twitching, numbness or tingling around lips and fingers Give calcium gluconate as ordered to relieve symptomatic hypocalcemia Assess for positive chvosteks or trousseaus sign Monitor magnesium levels as hypomagnesaemia can develop Assess, document and institute pain relief measures Repositioning pt may help with pain, N/V, and reduce restlessness Assume positions that draw knees up to abd to decrease pain and side lying position with head elevated 45 degrees to decrease tension and pain Frequent oral (prevent parotitis) and nasal care for NG tube and NPO pts Monitor for fever and other manifestations of infection Prevent respiratory infections Observe for signs of paralytic ileus, renal failure and mental changes Determine blood glucose levels to asses damage to beta cells in pancreas Wound care and prevent skin breakdown Ambultory care: - Diet restricted from fats as this could stimulate pancrease Diet high in carbs because less stimulating Avoid crash diets and bingeing because they can precipitate attacks Report symptoms of infection, diabetes, and steatorrhea; changes indicate ongoing destruction of pancreatic tissue and pancreatic insufÏciency