In the name of God

Acute Pancreatitis

INTRODUCTION — Acute pancreatitis is an acute inflammatory process of the pancreas. It is usually associated with severe acute upper abdominal pain and elevated blood levels of pancreatic enzymes

Acute Pancreatitis – Epidemiology 180,000 - >200,000 Hospital Admissions / Year 20% have a severe course –> 30% mortality for this group, which has not significantly changed during the past few decades despite improvement in critical care and other interventions

Etiology Gallstones (35%-60%) –Gallstone pancreatitis risk is highest among patients with small GS < 5mm and with microlithiasis –GS pancreatitis risk is also increased in women > 60 yrs

Alcohol (30-40%) –Not all alcoholics get pancreatitis (only about 15%)

Etiology – Drugs and Toxins (5%) Azathioprine Cimetidine Estrogens Enalapril Erythromycin Furosemide Scorpion Bites

Blunt Trauma Iatrogenic – ERCP (1-7%) Infection Cystic Fibrosis –2-15% of patients Idiopathic (20-25%).

Infection Ascaris CMV EBV Enterovirus HIV/AIDS Mycoplasma Varicella

Clinical Presentation Clinical –Continuous mid-epigastric / peri-umbilical abdominal pain  Radiating to back, lower abdomen or chest

One characteristic of the pain that is present in about one-half of patients, and that suggests a pancreatic origin, is band-like radiation to the back.

Clinical Presentation More severe cases –Jaundice –Ascites –Pleural effusions – generally left-sided –Cullen’s sign – bluish peri-umbilical discoloration –Grey Turner’s sign – bluish discoloration of the flanks

Grey Turner sign Cullen’s sign

Physical examination fever, tachycardia, and, in severe cases, shock and coma. tenderness and guarding Respirations may be shallow due to diaphragmatic irritation from inflammatory exudate, and dyspnea may occur if there is an associated pleural effusion.

Diagnosis – Amylase Elevates within HOURS and can remain elevated for 4-5 days High specificity when using levels >3x normal Many false positives (see next slide)

Diagnosis – Amylase Elevation –Biliary obstruction –Bowel obstruction –Perforated ulcer –Appendicitis –Mesenteric ischemia –Peritonitis –Parotitis –DKA –Fallopian tube –Malignancies Unknown Source –Renal failure –Head trauma –Burns

Diagnosis – Lipase Begins to increase 4-8H after onset of symptoms and peaks at 24H Remains elevated for days Sensitivity % and Specificity 60-99% >3X normal S&S ~100%

phospholipase A, trypsin, carboxypeptidase A, and co-lipase

RADIOLOGIC FEATURES Important radiologic features may be seen on a plain film of the abdomen, chest radiograph, and spiral (helical) CT scan, Abdominal ultrasound

Diagnosis – Imaging CT –CT scan — CT scan is the most important imaging test for the diagnosis of acute pancreatitis and its intraabdominal complications and also for assessment of severity. –Search for necrosis – will be present at least 4 days after onset of symptoms

CT shows significant swelling and inflammation of the pancreas

Diagnosis - Imaging ERCP (endoscopic retrograde cholangiopancreatography) –Diagnostic and Therapeutic –Can see and treat: Ductal dilatation Strictures Masses / Biopsy

Diagnosis – Imaging ERCP indications (should be done in the first 72hr) –GS etiology with severe pancreatitis – needs sphincterotomy –Cholangitis –Dilated CBD –If no GS found sphincterotomy is indicated anyway –Pregnant patient

Abdominal ultrasound — A diffusely enlargement, hypoechoic pancreas is the classic ultrasonographic image of acute pancreatitis; it can also detect gallstones in the gallbladder

Prognosis – Ranson’s (Severe > 3) Ranson’s Score –5 on Admission Age > 55 y Glucose >200 WBC > LDH > 350 AsT > 250 –6 after 48 hours from presentation Hct > 10% decrease Calcium < 8 Base Deficit > 4 BUN > 5 Fluid Sequestration >4L PaO2 < 60

5% mortality risk with <2 signs 15-20% mortality risk with 3-4 signs 40% mortality risk with 5-6 signs > 50% mortality risk with >7 signs

Management The first step in managing patients with acute pancreatitis is determining the severity.

Management SUPPORTIVE CARE — Mild acute pancreatitis is treated with supportive care including pain control, intravenous fluids, and correction of electrolyte and metabolic abnormalities. The majority of patients require no further therapy, and recover and eat within three to seven days. In severe acute pancreatitis, intensive care unit monitoring and support of pulmonary, renal, circulatory, and hepatobiliary function

Management – Necrosis All severe pancreatitis should be managed in the ICU Necrosis associated Infection generally requires debridement (surgical)

Management – Pain Meperidine has been favored over morphine for analgesia in pancreatitis because studies showed that morphine caused an increase in sphincter of Oddi pressure.Meperidinemorphine Hydromorphone

Complications – Local Necrosis –Sterile –Infected - abscess Pseudocyst Ascites Intraperitoneal hemorrhage Thrombosis Bowel infarction Obstructive jaundice

Complications – Systemic Pulmonary –Pleural effusions –Atelectasis –Mediastinal abscess Cardiovascular –Hypotension –Sudden death –Pericardial effusion –DIC Gastrointestinal –PUD –Erosive gastritis –Portal vein thrombosis Renal –Oliguria –Azotemia –Renal artery/vein throbosis –ATN

Complications – Long Term Chronic Pancreatitis –Abdominal Pain –Steatorrhea –Exocrine insufficiency (pancreas has a 90% reserve for the secretion of digestive enzymes) –DM, i.e.Endocrine Insufficiency

ارائه دهنده : حسام الرفاعی