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Pancreatitis

Ramesh.k PB 2nd yr

ROLL NO:03 SVCP

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Sudden onset of unrelenting upper abdominal pain resulting from inflammation of the pancreas

Patients commonly present to ER due to severe abdominal pain

Requires admission to the hospital for medical management

Acute Pancreatitis

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Ethanol abuse Biliary diseases

◦ Gallstones◦ Choledocholithiasis◦ Biliary sludge◦ Microlithiasis

Mechanical/structural injury◦ Sphincter of Oddi dysfunction◦ Pancreas divisum◦ Trauma◦ Postendoscopic retrograde

cholangiopancreatography◦ Pancreatic malignancy◦ PUD◦ IBD

Causes of Acute PancreatitisMedications

Azathioprine/6-mercaptopurinePentamidineSulfonamidesThiazide diureticsACEI

MetabolicHypertriglyceridemiaHypercalcemia

InfectiousViralBacterialParasitic

VascularVasculitis

Genetic predispositionidiopathic

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Initial insult•Zymogen activation•Ischemia•Duct obstruction

Acute injuryIntial insult• Zymogen activation• Ischemia

• Duct obstructionRelease of

active enzymes

Release of vasoactive substances

Generation of cytokines

Inflammation Vascular damage ischemia

Tissue damage and cell death

Pathophysiology

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Common Complications of Acute Pancreatitis Pulmonary

◦ Atelactasis◦ Pleural effusions

Cardiovascular◦ Cardiogenic shock

Neurologic◦ Pancreatic encephalopathy

Metabolic◦ Metabolic acidosis◦ Hypocalcemia◦ Altered glucose metabolism

Hematologic◦ GI bleeding

Renal◦ Prerenal failure

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Clinical Presentation Upper abdominal pain rapidly increasing in

severity, often within 60 minutes Epigastric pain Right-sided pain Diffuse abdominal pain with radiation to back Pain rarely only in left upper quadrant Restless Prefer to sit and lean N/V Fever Tachycardia

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Abdominal Examination

Decreased or absent bowel sounds Abdominal tenderness Guarding Palpable mass in epigastric area Biliary colic Jaundice if there’s obstruction of the bile

duct Cullen’s sign Grey Turner’s Sign

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Clinical Manifestations

Abdominal distention Abdominal guarding Abdominal tympany Hypoactive bowel sounds Severe disease: peritoneal

signs, ascites, jaundice, palpable abdominal mass, Grey Turner’s sign, Cullen’s sign, and signs of hypovolemic shock

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Diagnostic Evaluation Patient’s history Physical examination Diagnostic findings

◦Serum amylase levels greater than three times the upper limit

◦Serum amylase levels may be normal in patients with pancreatitis related to alcohol abuse or hypertriglyceridemia

◦Levels greater than five times the top normal value should be expected in patients with renal failure because amylase is cleared by the kidneys

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Imaging Modalities Plain abdominal x-rays for visualizing

gallstones or a gas-filled transverse colon ending at the area of pancreatic inflammation◦colon cut-off sign

Abdominal ultrasound◦Cholelithiasis, biliary sludge, bile duct

dilation, and pseudocysts CT of abdomen MRCP (magnetic resonance

cholangiopancreatography)

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Ranson’s Criteria The severity of acute pancreatitis is determined by the

existence of certain criteria, called Ranson’s criteria On admission

◦ Patient older than 55◦ WBC > 16,000◦ Serum glucose >200◦ Serum lactate dehydrogenase >350◦ Aspartate aminotransferase > 250

During initial 48 hours after admission◦ 10% decrease in Hct◦ BUN increase > 5◦ Serum calcium < 8◦ Base deficit > 4◦ PaO2 < 60◦ Estimated fluid sequestration > 6 liters

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Management

Fluid Management Nutritional support

◦ Rest gut◦ TPN

Pain management Supporting other organ systems

IV replacement of fluids, proteins, and electrolytes

Fluid volume replacement and blood transfusions

Withholding food and fluids to rest the pancreas

NG tube suctioning Peritoneal lavage Surgical drainage Laparotomy to remove

obstruction

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Acute pancreatitis General approach: Initial treatment usually involves

withholding foods or liquids . Nasogastric aspiration Aggressive fluid resucitation Intravenous colloids Drotrecogin alfa Insulin

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Nonpharmacologic therapy: Nutritional therapy.

Pharmacologic therapy:

Relief of abdominal pain Analgesics:-pethidine,morphine Prevention of infection Antibiotics:-Imipenem+cilastatin, Quinolones+metronidazole

Anti emetics:-Ondansetron

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Chronic Pancreatitis

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Chronic Pancreatitis It is characterised by permanent damage to

pancreatic structure and function because of progressive inflammation and long standing pancreatic injury

Permanent destruction of pancreatic tissue usually leads to exocrine and endocrine insufficiency.

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AUTOIMMUNE PANCREATITIS

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Pathophysiology Pathogenesis of chronic pancreatitis is not well

defined. Few hypothesis have been proposed to account for development of chronic pancreatitis

These include: Ductal obstruction : chronic alcohol ingestion

causes changes in pancreatic fluid that creates intraductal protein plugs that blocks small ductules.

This results in progressive structural damage in ducts and acinar tissue.

Calcium complexes with protein plugs ,eventually resulting in injury and pancreatic tissue destruction

Toxic metabolic: toxins ,alcohol and its metabolites has direct effect on acinar necrosis .

Leads to accumulation of lipids in acinar cells .

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Oxidative stress Abdominal pain is related in part to increased

intraductal pressure secondary to continued pancreatic secretion,pancreatic inflammation, abnormalities of pancreatic nerves

Malabsorption of protein and fat occurs when the capacity for enzyme secretion is reduced by 90%.

Lipase secretion decreases more rapidly than proteolytic enzymes.

Decreased bicarbonate leads to duodenal pH of less than 4.

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Clinical Manifestations Abdominal pain

◦ Located in the same areas as in acute pancreatitis Abdominal tenderness Malabsorption with weight loss Constipation Mild jaundice with dark urine Steatorrhea Frothy urine/stool Diabetes mellitus

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Diagnostic tests

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Management Nonpharmacologic therapy:- Abstinence from alcohol is the most

important factor in preventing abdominal pain in the early stages of alcoholic CP.

Small and frequent meals (six meals per day) and a diet restricted in fat (50 to 75 g/day) are recommended to minimize postprandial pancreatic secretion and pain

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PAIN MANAGEMENT Treatment of chronic pain: Analgesics Acetaminophen NSAIDS Tramadol Codeine TREATMENT OF MALABSORPTION AND STEATORRHEA Pancreatic enzyme supplements –Amylase, lipase Antisecretory drugs –Somatostatin, octreotide GIT- proton pump inhibitor H2 receptor antagonist SURGERY

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References Pharmacotherapy, A Pathophysiologic

approach by J.T.Dipiro 7 th edition, page.no:659-673

Ross and wilson anatomy and physiology http://gastro.ucsd.edu/Chronic

%20Pancreatitis http://www.webmd.com/digestive-disorders/

digestive-diseases-pancreatitis

THANK YOU

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