Download Free Medical Acute Pancreatitis PowerPoint Presentation

Acute Pancreatitis PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical presentation on Hereditary Pancreatitis, which is titled "Acute Pancreatitis", to know about Acute pancreatitis, Acute Inflammatory process of pancreatic parenchyma.

Tags : Hereditary Pancreatitis, Acute Pancreatitis, Acute Inflammatory, pancreatic parenchyma

Published on : May 18, 2021 | Views : 8195 | Downloads : 125

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Acute Pancreatitis Rachel Dunagin, MD
Slide 2-

Background Acute Inflammatory process of pancreatic parenchyma A stimulus leads to release of activated digestive enzymes from acinar cells into interstitium Results in autodigestion of pancreas and adjacent tissue Activated inflammatory mediators convert a localized inflammatory response into a systemic inflammatory process, resulting in increased tissue and vascular permeability End result: hypovolemia, shock, ARDS, multisystem organ failure Majority: mild self-limited course; 15-25% severe, complicated course; 5% mortality
Slide 3-

Pathophysiology
Slide 4-

ppt slide no 4 content not found
Slide 5-

Etiology Gallstone (35%) Microlithiasis Alcoholism (30%) Medication Trauma/Sphincter of Oddi Dysfunction Infection Duodenal Diverticula Hypercalcemia Vascular Abnormalities Post-operative Neoplasm Pancreas Divisum Autoimmune Hereditary Idiopathic (30%) Hypertriglyceridemia Cystic Fibrosis
Slide 6-

Etiology: Gallstones ½ of all cases of acute pancreatitis 3-8% patients with symptomatic cholelithiasis develop pancreatitis Older women 80% patients previously thought to have idiopathic etiology are due to microlithiasis, tiny gallstones, and biliary sludge Mechanism unclear – pancreatic ductal obstruction does not full explain pathogenesis
Slide 7-

Etiology: Alcohol Interferes with normal process of pancreatic secretion Excessive deposition of GP-2 (protein involved in maintaining normal pancreatic secretion) leads to ductal obstruction Daily consumption 80g alcohol over 5-15 years before first attack of alcoholic pancreatitis occurs Acute attacks 1-3 days after drinking
Slide 8-

Etiology: Hypertriglyceridemia >1000mg/dL 50% with hyperTG have falsely normal amylase level due to interference of lipemic specimen with assay Therefore, must dilute serum to get accurate serum amylase level
Slide 9-

Etiology: Medications Uncommon cause Azathioprine, 6-mercaptopurine and ddI have 5-10% risk of acute pancreatitis >100 meds implicated
Slide 10-

Definitely Cause Pancreatitis Azathioprine Asacol Cytosine arabinoside Estrogens Norethindrone/mestr-anol Isoniazid 6-mercaptopurine Metronidazole Pentamidine Tetracycline Trimethoprim/sulfamethoxazole (TMP/SMX) Valproic Acid
Slide 11-

Implicated Agents Industrial chemicals (Parathion) Scorpion venom
Slide 12-

Viral Infections Mumps – most common in adults Coxsackie-B Epstein-Barr Rubella Influenza A Varicella Hepatitis A, B, C, E
Slide 13-

AIDS and Pancreatitis 10% with AIDS develop acute pancreatitis Asymptomatic pancreatic lesions in 30-50% of autopsy cases Common infectious etiologies: CMV, MAC, Crypto, M. TB, Toxoplasma Common medication etiologies: pentamidine, ddI, ddC and TMP/SMX
Slide 14-

Rare Etiologies SLE Polyarteritis Nodosum Autoimmune pancreatitis Fungal infections Bacterial infections: Legionella, Brucellosis Ampullary tumors Metastatic tumors (breast, lung) Pancreas Divisum
Slide 15-

Pancreatic Divisum Debatable cause Represents 5-7% of population per autopsy and ERCP studies Normal Pancreatic Development: Dorsal and ventral pancreatic buds fuse during 8th week gestation to form main pancreatic duct; drains through major papilla. Small duct often persists between the main pancreatic duct and the minor papilla
Slide 16-

Pancreatic Divisum Embryonic dorsal and ventral ducts fail to migrate and fuse abnormally. Two noncommunicating duct systems: Inferior portion of head of pancreas drained by rudimentary ventral duct through the major papilla. Remainder of pancreas drained by dorsal duct through the minor papilla.
Slide 17-

Pancreatic Divisum: Hypothesis of pancreatitis etiology First proposed in 1977 Increased resistance to flow through a small minor papilla. If so, would reason that recurrent pancreatitis would stop after endoscopic minor papilla sphincterotomy, or insertion of endoscopic stent across the minor papilla. Some disagree on basis that incidence of pancreas divisum is the same in patient with or without pancreatitis and 95% with pancreatic divisum do not develop pancreatitis Other arguments against: pancreatitis develops in adulthood, not childhood in those with pancreatic divisum Still remains controversial.
Slide 18-

Diagnosis Clinical signs and symptoms, confirmed with lab/radiologic studies Symptoms: Acute abdominal pain Location: entire abdomen or localized in midepigastric, RUQ or left flank Intensity: maximized within 10 – 20 min of acute attack Quality: steady, moderate to severe, little relief with change of position, unbearable, refractory to narcotics Radiation: band-like to the back Anorexia, nausea, emesis CNS manifestations: disorientation, hallucinations, agitation, or coma
Slide 19-

Diagnosis Signs: Mild Pancreatitis – mild abdominal tenderness, no guarding Severe Pancreatitis - epigastric tenderness and guarding, rebound tenderness, abdominal distention (due to gastric ileus or dilatation of transverse colon) Decreased or absent bowel sounds May be mistaken for acute abdomen If severe, extensive peripancreatic fat necrosis with hemorrhagic fluid within the peritoneum and/or retroperitoneum → Cullen’s sign, Grey-Turner’s sign Palpable epigastric mass = pseudocyst or large inflammatory mass Subcutaneous nodular fat necrosis, thrombophlebitis in legs, polyarthritis
Slide 20-

Cullen’s Sign
Slide 21-

Grey-Turner’s Sign
Slide 22-

Diagnosis Due to third-space fluid loss and systemic toxicity Pulse 100-150 BP hypertensive in beginning, then hypotensive due to 3rd spacing and hypovolemia Temp: initially normal, then increase to 101-103 within 1-3d Tachypnea and shallow respirations
Slide 23-

Nonspecific Lab Findings Leukocytosis Hyperglycemia Hypocalcemia LFTs: ⁭ AST, ⁭⁭⁭⁭ ALT, ⁭ AlkPhos, ⁭ Bilirubin Hypertriglyceridemia Hypoxemia
Slide 24-

Laboratory Testing Serum Amylase Most widely accepted 2-3x upper limit of normal Does not correlate with severity of disease 30% of Alcoholics with acute pancreatitis have normal amylase levels ? of using elevated lipase to amylase level to predict alcoholic acute pancreatitis ALT 3x upper limit of normal + elevated amylase is highly sensitive for gallstone pancreatitis (95% PPV)
Slide 25-

Laboratory Tests Caution!! -- Other causes of elevated amylase level Can be of pancreatic or salivary origin Any inflammatory process of abdomen: Perforated peptic ulcer Intestinal obstruction Cholecystitis Generalized peritonitis Mesenteric ischemia Ruptured AAA/ectopic pregnancy Renal failure Macroamylasemia: due to benign change in peptide processing in Golgi (amylase is bound to immunoglobulin or abnormal serum protein), forms a large complex which is difficult to clear through the kidneys
Slide 26-

Laboratory Testing Serum Lipase More sensitive and specific than amylase Greater than 2-3x upper limit of normal Does not correlate with severity of disease
Slide 27-

Other Lab Tests Pancreatitis associated protein (PAP), heat shock protein Trypsinogen activation peptide (TAP), 5-amino acid peptide cleaved from trypsinogen to produce active trypsin Non-specific Markers: CRP, neutrophil elastase, complement, TNF, IL6 Methemalbumin level
Slide 28-

Radiology Sonography Computer Tomography (CT) Magnetic resonance imaging (MRI)
Slide 29-

Ultrasound Fails to completely to completely image the pancreas 2/2 overlying bowel gas Superior to CT in visualizing gallbladder and biliary tree for gallstones Negative US does not rule out gallstone as etiology because: 1. Not sensitive for common bile duct stones. 2. Only 50% of those with microlithiasis have + US. 3. View may be obstructed by ileus and underlying structures obscured by bowel gas.
Slide 30-

A Acute Pancreatitis. A. Transverse scan. B. Longitudinal scan. The head of the pancreas (H) is enlarged as revealed by the red arrowheads and decreased in echogenicity because of edema. The surrounding structures are superior mesenteric vein (v), superior mesenteric artery (a), abdominal aorta (A), and inferior vena cava (IVC). B
Slide 31-

Computer Tomography (CT) Imaging modality of choice for diagnosis, determining severity, and identifying complications Sensitivity: 90% for diagnosis of acute pancreatitis Specificity: 98-100% Not necessary for mild acute pancreatitis; however is useful to rule out other abdominal processes presenting with abdominal pain. Mild disease: no abnormalities, diffuse enlargement of pancreas, loss of normally sharp border, homogenous attenuation, inflammatory stranding in peripancreatic fat and adjacent soft tissue, fluid collections, pseudocysts, pancreatic necrosis
Slide 32-

Computer Tomography (CT) Necrotizing pancreatitis: Non-enhancement of ≥ 1/3 of pancreas or >3cm of non-enhancement of the pancreas on dynamic, IV contrast-enhanced CT. If > 30% gland involved, sensitivity approaches 100%
Slide 33-

Indications for CT Severe acute pancreatitis (Ranson score ≥3 or APACHE II score ≥8) Mild pancreatitis with no response to conservative management after 48-72 hours (confirm dx, re-assess severity, identify complications) May repeat q7-10 day if no improvement or if deterioration.
Slide 34-

ppt slide no 34 content not found
Slide 35-

ppt slide no 35 content not found
Slide 36-

Severity: Open Drainage due to Pancreatic Necrosis
Slide 37-

Severity Not predicted by degree of pain, etiology or serum amylase level. CRP: > 120mg/L in pts with acute pancreatitis typically have necrotizing pancreatitis. Phospholipase A2: elevated in severe disease, esp those who develop necrosis, ARDS, and shock Urinary trypsinogen activation peptide: ≥ 10ng/mL has 100% PPV of severe pancreatitis Peritoneal Lavage: any volume of peritoneal fluid with a dark color or recovery of at least 20mL of free intraperitoneal fluid = 33% mortality
Slide 38-

Trypsinogen Activation Pathway
Slide 39-

Severity Hematocrit ≥ 47% at admission or failure of admission hematocrit to decrease at 24hrs is strong predictor of development of pancreatic necrosis. Compromised microcirculation of pancreatic parenchyma precipitated by fluid sequestration with intravascular volume depletion and hemoconcentration leads to development of necrotizing pancreatitis. Therefore, intense hydration is important.
Slide 40-

Severity Ranson Criteria ≥ 3 APACHE II score ≥ 8 Hematocrit ≥ 44 CT severity index ≥ 6 1992 Atlanta Symposium: evidence of organ failure or local complications
Slide 41-

Ranson Criteria **Can not be applied fully for 48 hours **Poor predictor later in the disease **Single snapshot in time
Slide 42-

APACHE II Criteria Multivariate scoring system 12 measurable variables: temperature, heart rate, respiratory rate, mean arterial BP, oxygenation, arterial pH, serum potassium, sodium and creatinine, hematocrit, WBC, and Glasgow Coma Scale Account for premorbid state and age Can be used throughout course of illness, but is complex and cumbersome
Slide 43-

CT Severity Index A: Normal pancreas B: Enlargement of pancreas, heterogeneous enhancement without peripancreatic disease C: Pancreatic abnormalities with peripancreatic disease D: Small or single fluid collection E: 2 or > fluid collection or pancreatic abscess
Slide 44-

Atlanta Symposium Criteria 40 Internationally renowned experts on pancreatic disease met to define severity of pancreatitis Defined based on outcome: organ failure and/or anatomic complications Mild acute pancreatitis: minimal or no organ system dysfunction with complete and uneventful recovery; interstitial edema of parenchyma Severe acute pancreatitis: evidence of life-threatening systemic complications or pancreatic collection.
Slide 45-

Severe Acute Pancreatitis Systemic Complications: Shock: SBP <90mm Hg Pulmonary Insufficiency: PaO2 ≤ 60mm Hg Renal failure: Cr > 2mg/dL after rehydration GI bleeding: > 500ml/24hr DIC: platelets < 100,000/mm3, fibrinogen < 1g/L, fibrin degradation products > 80mug/mL Hypocalcemia: < 7.5mg/dL
Slide 46-

Severe Acute Pancreatitis Pancreatic Collections Pancreatic Necrosis: diffuse or focal areas of nonviable pancreatic parenchyma Pancreatic Abscess: well-circumscribed collection of pus containing little or no necrotic tissue Acute Pseudocyst: collection of enzyme-rich, pancreatic fluid enclosed by a wall of fibrous tissue
Slide 47-

Treatment Goals: halt progression of local disease and prevent remote organ failure Nutritional Support: Pancreatitis is catabolic state Benefit of pancreatic “rest” by limiting oral intake is unproven, however is widely used Evidence that early enteral nutrition is safe Nasojejunal feeding limits pancreatic secretion Preferable to oral or nasogastric feeding
Slide 48-

Treatment Fluids IV hydration, aggressive (300-500ml.hr) especially in the early phase of illness with goal hemodilution to Hct 30% May need NG tube (if persistent nausea and vomiting or ileus), Foley catheter and central line or Swan-Ganz catheter to monitor hydration status Analgesics Adequate pain control is essential 50-100mg Meperidine (Demerol) IV q3-4hr Hydromorphone (Dilaudid) PCA Avoid Morphine b/c it increases sphincter of Oddi tone and increases serum amylase ERCP If severe acute gallstone pancreatitits or ascending cholangitis is indicated, then early ERCP with sphincterotomy and stone extraction is indicated. Is not to be used in mild acute pancreatitis
Slide 49-

Pancreatic Infection: A Word on Antibiotics Antibiotics – there is no role for routine use Indicated if severe attack with necrosis of pancreas Typical organisms: from gut = E coli, Pseudomonas, Klebsiella, Enterococcus Treatment: selective decontamination of gut with oral nonabsorbable antibiotics, systemic antibiotics, and enteral feedings to avoid catheter-related infections. Imipenem/cilastin penetrate pancreatic parenchyma and reduces incidence of intra-abdominal infection. Unfortunately, there is a tendency for fungal superinfection to develop later in clinical course. Other options: 3rd gen cephalosporin, piperacillin, mezlocillin, fluoroquinolones and metronidazole
Slide 50-

Treatment
Slide 51-

Complications of Acute Pancreatitis EARLY COMPLICATIONS Cardiovascular Collapse Respiratory Failure Renal Failure GI bleeding DIC Visual Disturbance Change in mental status Metabolic disturbance Acute fluid collections Pancreatic Necrosis LATE COMPLICATIONS Pseudocysts Pseudoaneurysms Perforation Obstruction Fistulization Infection (abscess, infected necrosis)
Slide 52-

ppt slide no 52 content not found
Slide 53-

Pancreatic Necrosis
Slide 54-

Pancreatic Necrosis: Sterile Clinically mild, low mortality rate Systemic antibiotics to prevent secondary pancreatic infection Enteral nutrition with advancement to oral feedings once organ failure subsides. If no improvement in 1st 7-10d, ? of severe sterile or infected necrosis, proceed to CT-guided percutaneous aspiration to r/o infection
Slide 55-

Pancreatic Necrosis
Slide 56-

Pancreatic Necrosis
Slide 57-

Pancreatic Necrosis: Infective Infected Necrosis: Guided percutaneous aspiration to demonstrate pancreatic infection Common bugs – Klebsiella, E coli, Staph aureus Occasional bugs – Candida Prompt debridement preceded by appropriate antibiotic based on Gram stain or culture Surgical debridement – gentle blunt finger dissection followed by closure of abdomen with external Penrose or JP drain, closure of abdomen with large soft drain within retroperitoneum for intermittent or continuous saline lavage or open packing of abdomen for pancreatic debridement q2-3d
Slide 58-

ppt slide no 58 content not found
Slide 59-

Complications: Pseudocysts Fibrous walled peri-pancreatic fluid collection Present for > 1 month No epithelial lining Fluid has high amylase content 35% of patients develop peri-pancreatic fluid collections > 50% resolve spontaneously over 3 month period Complication rate increases over 6 weeks Diagnosis may be suggested by persistent elevation of serum amylase Planned intervention at 6 weeks.
Slide 60-

Classification of Pseudocysts Type 1 – normal duct anatomy; no fistula between duct and cyst. Type 2 – abnormal duct anatomy; no fistula Type 3 – abnormal duct anatomy and fistula
Slide 61-

Investigation of Pseudocysts Ultrasound – assess change in size of cyst Endoscopic Ultrasound – used increasingly CT – define relationship to adjacent organs ERCP – define duct anatomy
Slide 62-

Treatment of Pseudocyst Percutaneous Drainage - US or CT guided - 80% successful in Type 1 cyst - Less successful if fistula to duct is present - Occasionally associated with pancreatic abscess or fistula
Slide 63-

Treatment of Pseudocysts 2. Endoscopic drainage and insertion of pigtail catheter - transpapillary - transmural
Slide 64-

Treatment of Pseudocysts 3. Surgical Drainage - cystogastrotomy or Roux Loop Cystojejunostomy - allows adequate internal drainage - perform biopsy of cyst wall to exclude cystadenocarcinoma - mortality (~5%) = percutanous drainage - lower recurrence rate (5% vs 20%)