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Acute pancreatitis.dr behmanesh
 

Acute pancreatitis.dr behmanesh

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sideeffects and treatment Acute pancreatitis on based Schwartz's Principles of Surgery 9th Edition (2010)

sideeffects and treatment Acute pancreatitis on based Schwartz's Principles of Surgery 9th Edition (2010)
by DR MOHSEN BEHMANESH

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    Acute pancreatitis.dr behmanesh Acute pancreatitis.dr behmanesh Presentation Transcript

    • Anatomy
    • Definition and Incidence Acute pancreatitis is an inflammatory disease of the pancreas that is associated with little or no fibrosis of the gland
    • Etiology
    • Biliary Tract Disease • Although acute pancreatitis is documented in association with acalculous biliary tract disease, bile duct stones (choledocholithiasis) represent the most common form of associated biliary abnormality
    • Alcohol • spasm of the sphincter of Oddi • ethanol is a metabolic toxin to pancreatic acinar cells interfere with enzyme synthesis and secretion • increases ductal permeability improperly activated enzymes to leak out of the pancreatic duct into the surrounding tissue • The inappropriate activation of trypsin • decreases pancreatic blood flow, possibly causing focal ischemic injury to the gland
    • Iatrogenic Pancreatitis • pancreatic biopsy, biliary duct exploration, distal gastrectomy, and splenectomy • cardiopulmonary bypass • cardiac transplantation
    • Drugs • thiazide diuretics, furosemide, estrogens, azathioprin e, L-asparaginase, 6mercaptopurine, methyldopa, the sulfonamides, tetracycline, pentamidine, proc ainamide, nitrofurantoin, dideoxyinosine, val proic acid, and acetylcholinesterase inhibitors.
    • • A tumor should be considered in a nonalcoholic patient with acute pancreatitis who has no demonstrable biliary tract disease. Approximately 1 to 2% of patients with acute pancreatitis have pancreatic carcinoma, and an episode of acute pancreatitis can be the first clinical manifestation of a periampullary tumor. In both conditions, the pancreatitis possibly results from blockage of secreted juice and its upstream consequences
    • Infections • coxsackievirus, and Mycoplasma pneumoniae • infecting the acinar cells
    • Hyperlipidemia • lipase can liberate large amounts of toxic fatty acids into the pancreatic microcirculation • endothelial injury, sludging of blood cells, and consequent ischemic states • types I and V hyperlipoproteinemia often experience attacks of abdominal pain that are thought to indicate episodes of acute pancreatitis hypertriglyceridemia and lactescent serum and can be prevented
    • • Hyperparathyroidism Hypercalcemic states • hypersecretion and the formation of calcified stones
    • • azotemia, vasculitis, and the sting of the Trinidadian scorpion Tityus trinitatis neurotransmitter discharge from cholinergic nerve terminals, leading to massive production of pancreatic juice
    • • perforated peptic ulcer, a gangrenous small bowel obstruction, and acute cholecystitis
    • Abdominal pain Amylase or lypase>3* Physical exam IV contrast CT scan Abdominal pain: severe following a substantial meal max=30 min Amylase+3-5 d tachycardia, Conteneuse>24h tachypnea, Lypase+7-14 Supine hypotension dleukocytosis(15000-20000) epygastric Bend to front tenderness • Sonography:stone of bile Hyperglycemia guarding involuntary nasia duct Hypocalcemia subcotaneous necrosis vomiting after abd pain Hyperbillirobinemia(10%0 •fever contrast Ct:sign IV Cullen's gold HTC Grey standardTurner's sig knifing" or "boring through" to icter •the back Contraindication:MRI BUN,CR
    • Symptom • acute pancreatitis begin with severe pain, generally following a substantial meal • The pain is usually epigastric, but can occur anywhere in the abdomen or lower chest • "knifing" or "boring through" to the back • relieved by the patient leaning forward • onset of nausea and vomiting • often continuing after the stomach has emptied
    • examination • tachycardia, tachypnea, hypotension, and hyperthermia • involuntary guarding • The bowel sounds are decreased or absent • There are usually no palpable masses • The abdomen may be distended with intraperitoneal fluid • pleural effusion, particularly on the left side
    • • sequestration of edematous fluid in the retroperitoneum intravascular fluid loss elevated hematocrit Hemoconcentration • Cullen's sign (periumbilical discoloration Grey Turner's sig (periumbilical discoloration severe fluid loss prerenal azotemia elevated blood urea nitrogen and creatinine levels
    • Serum Markers • amylase, lipase, trypsinogen, and elastase • Serum amylase concentration increases almost immediately with the onset of disease and peaks within several hours. It remains elevated for 3 to 5 days before returning to normal • magnitude of serum amylase elevation and severity of pancreatitis no significant correlation
    • • hyperamylasemia can occur in a patient with small bowel obstruction, perforated duodenal ulcer, or other intra-abdominal inflammatory conditions • (p-amylase specific (88 to 93%). • Specificity lipase 77 to 96%
    • Ultrasound • in suspected biliary pancreatitis confirm the presence of gallstones • detect extrapancreatic ductal dilations and reveal pancreatic edema, swelling, and peripancreatic fluid collections • 20% of patients presence of bowel gas CT
    • Acute pancreatitis. Focal pancreatitis involving pancreatic head. Pancreatic head is enlarged with adjacent ill-defined peripancreatic inflammation and fluid collections
    • Axial CT in a patient with acute exudative pancreatitis showing extensive fluid collections surrounding the pancreas
    • Iv contrast CT scan Enhancemet Microcirculation is intacted ICU NPO NGT H2 blocker Atropin Calcitonin Flurouracil metabolic support, and maintenance of fluid balance: Vomiting,sudorosis:hypovolom ia:visceral ischemia: Assesedevery buprenorphine, pentazocine, procaine hydrochloride, and meperidine : controlling abdominal pain Morphine: spasm odi Canservative treatment ABDOMinal pain and tenderness+ nl amylase+hungry:PO interstitial pancreatitis(mild) With Interstitial edema CT scan rules out necrotizing pancreatitis low APACHE-II scores and Ranson's signs sustained clinical improvement
    • Iv contrast scan TPN Syst:ARDS:PEEP ASCIT:peritoneal lavage CHF/cardiogenic shock/cardic arrhythemia/CHF Enhancement microcirculation is disrupted ICU necrotizing pancreatitis(sever) crateria:ICU encephalopathy, hematocrit >50%, urine output <50 mL/h, hypotension, fever peritonitis Eldery =>3ranson s
    • Nonnecrotizing acute pancreatitis
    • Infections • Infection is a serious complication of acute pancreatitis and is the most common cause of death. It is caused most often by translocated enteric bacteria and is seen commonly in necrotizing rather than interstitial pancreatitis. If there is an indication of infection (e.g., retroperitoneal air on CT scan), then a CT- or USguided fine-needle aspiration (FNA) should be performed for Gram's stain and culture of the fluid or tissue, and the indicated antibiotic therapy initiated. • necrotizing pancreatitis= Abt (metronidazole, imipenem, and third-generation cephalosporins) +Debridment
    • Necrotizing (infected) acute pancreatitis
    • Sterile Necrosis • have a far better prognosis than those with infected necrosis • may evolve into a chronic pseudocyst • A CT-guided, FNA then confirms or disproves infection, and in the latter instance, the patient can be managed medically. • The last and most serious condition is that of the patient who appears to be very ill, has high APACHE-II and Ranson's scores, and shows evidence of systemic toxicity, including shock. Patients in this category have a poor chance of survival without aggressive débridement, and a decision may be made to proceed with exploration simply due to a relentless course of deterioration despite maximal medical therapy.
    • Nutritional Support • Which is better: TPN > enteral nutrition through a jejunal tube • NGT: no dangerous
    • Pancreatic necrosis
    • Pancreatic Abscess • occurs 2 to 6 weeks after the initial attack • in contrast to infected necrosis, which occurs in the first few hours or days. • The mechanism of delayed infection is not clear, but the treatment consists of external drainage, whether established by surgical or by percutaneous catheter-based methods.
    • Pancreatic abscess
    • Treatment of Biliary Pancreatitis • Gallstones are the most common cause of acute pancreatitis worldwide • General consensus favors either urgent intervention (cholecystectomy) within the first 48 to 72 hours of admission, or briefly delayed intervention (after 72 hours, but during the initial hospitalization) to give an inflamed pancreas time to recover. • Cholecystectomy and operative common duct clearance is probably the best treatment for otherwise healthy patients with obstructive pancreatitis. • However, patients who are at high risk for surgical intervention are best treated by endoscopic sphincterotomy, with clearance of stones by ERCP. • Stone in CBD or AMPULAWATTER :CTscan,MRCP,EUS
    • A. Pancreatic phlegmon B. Pancreatic abscess C. Pancreatic pseudocyst D. Pancreatic ascites E. Involvement of adjacent organs, with hemorrhage, thrombosis, bowel infarction, obstructive jaundice, fistula formation, or mechanical obstruction
    • D. A. Pulmonary nervous systemB. Cardiovascular GI hemorrhage G. Central E. Renal 1. Pneumonia,ulcer Psychosis 1. Peptic atelectasis 1. H. FatF. Metabolic C. Hematologic necrosis 1. 1. Hyperglycemia Hemoconcentration 1. Intra-abdominal 2. Acute respiratory distress 2. Hypocalcemia 2. Hypovolemia 2. Erosive gastritis 2. Disseminated 2. Azotemia 2. saponification syndrome Fat emboli intravascular 3. Hypertriglyceridemia 3. Sudden death 3. Portal vein or splenic vein 3. Renal artery/vein Subcutaneous tissue necrosis 2. coagulopathy 3. Pleural effusion 3. Alcoholvarices withdrawal syndrome thrombosis with 4. Encephalopathy thrombosis wave 4. Nonspecific ST-T changes 5. Sudden blindness (Purtscher's retinopathy 5. Pericardial effusion 1.1. Oliguria Hypotension