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 86-100% 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 showssignificantswellingand inflammationof 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 > 16000• 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.

• 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

الرفاعی : حسام دهنده ارائه