pancreatitis.pdf

Pancreas ¨ The pancreas is an organ located in the abdomen. It plays an essential role...

Pancreas ¨ The pancreas is an organ located in the abdomen. It plays an essential role in converting the food we eat into fuel for the body's cells. ¤ Trypsin n Digests proteins ¤ Chymotrypsin n Digests proteins ¤ Amylase n Digests Carbohydrates ¨ The pancreas has two main functions: an exocrine function that helps in digestion and an endocrine function that regulates blood sugar such as PANCREATITIS insulin and glucagon 1) Exocrine -->conversion of food into energy -->realese enzyme to digest food 2) Endocrine --> regulates blood sugar -->Insulin= Alpha cells -->glucagon= Beta cells Pancreatitis Acute Pancreatitis Source ¨ Acute pancreatitis (AP) is an inflammatory disorder ¨ Gallstones and alcohol abuse account for most cases of the pancreas characterized by upper abdominal in the United States. Diabetes mellitus and pain and pancreatic enzyme elevations. autoimmune disorders such as inflammatory bowel ¨ Chronic pancreatitis (CP) is a progressive disease disease are also associated with an increase in characterized by long-standing pancreatic acute pancreatitis. A cause cannot be identified in inflammation leading to loss of pancreatic exocrine some patients (idiopathic pancreatitis). and endocrine function. =necrosis Atorvastatin==> Hmg-coa reductase inhibitors Cimetidine==> (-) H2 Receptor Ifosfamide==> Anti cancer/chemotherapy Enalapril==> (-) ACE Methyldopa==> DOC for HTN in preganant women Erythromycin==> Macrolide antibiotic Simvastatin==> Hmg-coa reductase inhibitors Furosemide==> High ceiling diuretics Oxaliplatin==> platin compound Use for chemotherapy Hydrochlorothiazide==> thiazide diuretics that acts on distal convoluted tubule Cisplatin==> Cancer chemotherapy Tamoxifen==> commonly used as tx for breast cancer Suindac==> NSAID Drug induced Pancreatitis ¨ Well supported Association ¨ Probable Association ¨ AP is initiated by premature activation of trypsinogen ¤ Cimetidine ¤ Acetaminophen to trypsin within the pancreas, leading to activation of ¤ Enalapril other digestive enzymes and autodigestion of the gland ¤ Atorvastatin ¤ Erythromycin ¤ Ifosfamide ¨ Activated pancreatic enzymes within the pancreas and ¤ Furosemide surrounding tissues produce damage and necrosis to ¤ Methyldopa pancreatic tissue, surrounding fat, vascular endothelium, ¤ Hydrochlorothiazide ¤ Simvastatin and adjacent structures. Lipase damages fat cells, ¤ Cisplatin ¤ Oxaliplatin producing noxious substances that cause further ¤ Tamoxifen pancreatic and peripancreatic injury. ¤ Sulindac Releases cytokinin==> activates inflammatory responses ==>systemic inflammatory response syndrome ==> releases kinin= permeable  ¨ Release of cytokines by acinar cells injures those ¨ Pancreatic infection may result from increased cells and enhances the inflammatory response. intestinal permeability and translocation of colonic Injured acinar cells liberate chemoattractants that bacteria. attract neutrophils, macrophages, and other cells to ¨ Local complications in severe AP include acute fluid the area of inflammation, causing systemic collection, pancreatic necrosis, infection, abscess, inflammatory response syndrome (SIRS). Vascular pseudocyst formation, and pancreatic ascites. damage and ischemia cause release of kinins, which ¨ Systemic complications include respiratory failure make capillary walls permeable and promote tissue and cardiovascular, renal, metabolic, hemorrhagic, edema. and CNS abnormalities Permeability=Increase pancreatic infection Pancreatic ascites= from buildup fluid in the abdomen Clinical Presentation ¨ The initial presentation ranges from moderate abdominal discomfort to excruciating pain, shock, and respiratory distress ¤ Abdominal pain occurs in 95% of patients and is usually epigastric, often radiating to the upper quadrants or back. ¨ Onset is usually sudden, and intensity is often described as Òknife-likeÓ or Òboring.Ó (stab like pain) ¤ Pain usually reaches maximum intensity within 30 minutes and may persist for hours or days. ¤ Nausea and vomiting occur in 85% of patients and usually follow onset of pain. Alcoholism==> common cause Treatment SRS ¨ Signs include ¤ epigastric tenderness on palpation with rebound tenderness and guarding in severe cases. ¤ The abdominal distention with tympanic sound and decreased or absent bowel sounds in severe disease. ¤ Vital signs may be normal, but hypotension, tachycardia, and low-grade fever are often observed, especially with widespread pancreatic inflammation and necrosis, Dyspnea and tachypnea are signs of acute respiratory complications. ¤ Jaundice and altered mental status may be present; other signs of alcoholic liver disease may be present in patients with alcoholic pancreatitis No Borborygmus==>Absence of gargling of the stomach  Pharmacologic Therapy ¨ IV anti emetics for nausea ¨ Patients should receive aggressive fluid replacement ¨ Patients requiring ICU admission should be treated to reduce the risks of persistent SIRS and organ with antisecretory agents if they are at risk of failure. stress-related mucosal bleeding. ¨ Different guidelines recommend goal-directed IV ¨ Vasodilation from the inflammatory response, fluid with either lactated RingerÕs at an initial rate vomiting, and nasogastric suction contribute to of 5 to 10 mL/kg/hour or crystalloids at a rate of hypovolemia and fluid and electrolyte 250 to 500 mL/hour. abnormalities, necessitating replacement. IV Fluid 1) Ringer's= 5-10 ml/kg/hr 2) Crystalloids= 250-500 ml/hr ¨ Parenteral opioid analgesics are used to control ¨ Patients with known or suspected infected AP should abdominal pain. Parenteral morphine is often used, receive broad-spectrum antibiotics that cover the and patient-controlled analgesia should be range of enteric aerobic gram-negative bacilli and considered in patients who require frequent opioid anaerobic organisms ¤ Imipenem-Cilastatin: now replaced by Meropenem dosing (eg, every 2Ð3 hours). ¤ Fluoroquinolones ( Ciprofloxacin, Levofloxacin) plus ¨ empiric antimicrobial therapy may be considered in Metronidazole ( if patient is allergic to penicillin) patients with necrosis who deteriorate or fail to ¨ Parenteral histamine2-receptor antagonists and improve within 7 to 10 days, but not for those proton pump inhibitors do not improve the overall without signs or symptoms outcome of patients with AP. prescence of fats and oil in feces Azotorrhea--> nitrogenous compound in feces or urine ¨ Steatorrhea and azotorrhea occur in most patients. ¨ Diagnosis is based primarily on clinical presentation Steatorrhea is often associated with diarrhea and and either imaging or pancreatic function studies. bloating. Noninvasive imaging includes ¨ Weight loss may occur. ¨ abdominal ultrasound, ¨ Computed tomography (CT), ¨ Pancreatic diabetes is a late manifestation commonly associated with pancreatic calcification. ¨ magnetic resonance cholangiopancreatography (MRCP). ¨ Invasive imaging includes ¨ endoscopic ultrasonography (EUS) and ERCP. (Invasive) Enzyme ¨ Serum amylase and lipase are usually normal or ¨ Pancreatic function tests include only slightly elevated but may be increased in acute ¤ Serum trypsinogen ( produce oxidants in the body depression and malnutrition. Palliative care/treatment==>slows down the progress of the disease ¨ Reduction in dietary fat may be needed if ¨ Enteral nutrition via a feeding tube is recommended symptoms are uncontrolled with enzyme for patients who cannot consume adequate calories, supplementation. have continued weight loss, experience ¨ Consumption of a low-fat purified amino acid complications, or require surgery. elemental diet may reduce pain. ¨ Invasive procedures and surgery are used primarily ¨ Supplementation with medium-chain triglycerides to treat uncontrolled pain and the complications of should be considered for patients with steatorrhea chronic pancreatitis who are unable to gain weight Pharmacologic Therapy ¨ Pain management should begin with weak opioid ¨ Severe pain requires more potent opioids. Unless analgesics (eg, tramadol, codeine) scheduled contraindicated, oral opioids should be used before around the clock (rather than as needed) to parenteral, transdermal, or other dosage forms maximize efficacy (ATC) ¨ Administration of short-acting analgesics prior to meals may decrease postprandial pain Take note Pregablain==> 75mg b.i.d (max 300mg) ¨ Adjuvant agents should be added if patients have ¨ Adding pancreatic enzyme supplements for pain inadequate relief from opioids alone. Pregabalin control (eg, 4Ð8 tablets/capsules of a preferred (75 mg twice daily initially; maximum 300 mg twice product with each meal plus a histamine2-receptor daily) has the best evidence. antagonist or proton pump inhibitor) may be ¨ Selective serotonin reuptake inhibitors (eg, considered in select patients, but no clinical trial paroxetine), serotonin/norepinephrine reuptake data support this approach for pain management. inhibitors (eg, duloxetine), and tricyclic ¨ Pancreatic enzyme supplementation and reduction in antidepressants can be considered in difficult-to- dietary fat intake are the primary treatments for manage patients. malabsorption due to CP Algorithm in treating Malabsorption/steartorrhea ¨ This combination enhances nutritional status and reduces steatorrhea. The enzyme dose required to minimize malabsorption is 30,000 to 50,000 units of lipase administered with each meal. ¨ The dose may be increased to a maximum of 90,000 units per meal. ¨ Products containing enteric-coated microspheres or mini-microspheres may be more effective than other dosage forms Improvement==>Continue treatment No improvement ==> decrease dietary fat (0.5g/kg/day) ==> increase enzyme dose (90,000 max) ==>if still no improvement add (H2 blocker, PPI and RA)