acute chronic pancreatitis l.
Skip this Video
Loading SlideShow in 5 Seconds..
Acute & Chronic Pancreatitis PowerPoint Presentation
Download Presentation
Acute & Chronic Pancreatitis

Loading in 2 Seconds...

play fullscreen
1 / 38

Acute & Chronic Pancreatitis - PowerPoint PPT Presentation

  • Uploaded on

Acute & Chronic Pancreatitis. 11/01/2005 Chp. 87 Tintinalli Bogdan Irimies D.O. Acute Pancreatitis: Epidemiology. Clinical presentation can vary from mild abdominal pain to refractory shock 90% of acute pancreatitis is secondary to acute cholelithiasis or ETOH abuse

I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
Download Presentation

PowerPoint Slideshow about 'Acute & Chronic Pancreatitis' - liam

An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.

- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
acute chronic pancreatitis
Acute & Chronic Pancreatitis
  • 11/01/2005
  • Chp. 87 Tintinalli
  • Bogdan Irimies D.O.
acute pancreatitis epidemiology
Acute Pancreatitis: Epidemiology
  • Clinical presentation can vary from mild abdominal pain to refractory shock
  • 90% of acute pancreatitis is secondary to acute cholelithiasis or ETOH abuse
  • List if causes is extensive: Cholelithiasis, ETOH, drugs, infection, inflammation, trauma, metabolic disturbances
drug induced pancreatitis
Drug Induced Pancreatitis
  • Drugs assoc. w/pancreatitis:
    • Amiodarone, amlodipine
    • Antibiotics(macrolides,sulfa, FQ’s, rifampin)
    • Antiepileptics (carbamazepine, valproic acid, topiramate)
    • Hyperlipidemic drugs
    • Antineoplastic agents
    • Antipsychotics (risperdal)
drug induced pancreatitis4
Drug Induced Pancreatitis
  • Drugs cont’d:
    • Antiretrovirals: all types
    • Diuretics
    • GI agents: H2 blockers, PPI’s
    • Glucocorticoids
    • NSAIDS
    • ASA
  • Central cause appears to be activation of the digestive zymogens in the pancreatic acinar cells and subsequent autodigestion of the pancreas.
  • Number of factors(endotoxins, toxins, ischemia, infections, anoxia) trigger activation of proenzymes
  • Activated proteolytic enzymes such as trypsin digest cellular membranes within pancreas and cause edema, interstitial hemorrhage, vascular damage, coagulation and cellular necrosis.
  • This can lead to extension of localized process into generalized systemic inflammatory response
    • Can lead to shock, ARDS, Multi-organ system failure
clinical features
Clinical Features
  • Major symptom is midepigastric or left upper quadrant pain: described as constant, boring pain that radiates to back, flanks, chest or lower abdomen.
  • Nausea/vomiting or abdominal bloating
  • PE: low grade fevers, tachycardia, +/- hypotension
clinical features8
Clinical Features
  • Respiratory symptoms: atelectasis, pleural effusion, ARDS
  • Abdominal exam: epigastric tenderness, peritonitis, Cullen sign(bluish discoloration around umbilicus), Grey Turner sign (bluish discoloration of flanks)
  • Pts. May present in hypovolemic shock and MOSF
    • Hypotension secondary to 3rd spacing, hemorrhage, increased vascular permeability, vasodilation, cardiac depression, vomiting
  • Amylase: found in pancreas & salivary glands
    • Low levels found in many tissues so this test is nonspecific
    • Amylase may be even normal in acute pancreatitis
    • Poor specificity
  • Lipase: found predominantly in pancreas but also in gastric, intestinal mucosa and liver
    • Cleared by the kidney so renal failure will elevate levels
    • Most appropriate cut-off is 2-3 x normal level
    • More accurate test than amylase, better specificity (90% vs. 75%)
  • Xrays of chest/abdomen: useful for r/o other diagnosis.
    • Calcification of pancreas seen in chronic pancreatitis
    • May see sentinel loop, elevated hemi-diaphragm, pleural effusion
    • U/S may detect gallstones
    • CT best study for grading severity if disease, prognosis.
  • Prognostic markers: Ranson criteria predicts pt. outcome
    • Age >55
    • BS >200
    • WBC >16,000
    • AST >250
    • LDH >700
    • Features portend a worse prognosis, but they have poor predictive value in acute setting and does not improve clinical judgment
  • CT of abdomen:
    • Estimates severity and prognosis
    • Complications include phlegmons, abscesses or pseudocysts.
      • Usually seen 2-3 weeks after acute pancreatitis
complications of acute pancreatitis
Complications of Acute Pancreatitis
  • Pulmonary: pleural effusions, atelectasis, hypoxemia, ARDS
  • CV: myocardial depression, hemorrhage, hypovolemia
  • Metabolic: Hypocalcemia, hyperglycemia, Hyperlipidemia, coagulopathy/DIC
  • Others: Colonic perforation, ARF. Arthritis, pseudocyst, abscess
  • General principle: rest the pancreas
  • Fluid resuscitation
  • NG tube only if needed
  • Pain control, anti-emetics
  • ATBX only in severe disease
    • Cover polymicrobial, GNB
    • IV imipenem or quinolone in combination w/Flagyl
  • Pts. w/mild pancreatitis w/no evidence of systemic disease and low likelihood of biliary disease may be managed as outpts. if tolerating oral fluids and pain control is adequate
  • All others need to be admitted
chronic pancreatitis
Chronic Pancreatitis
  • Defined as chronic inflammatory condition that causes irreversible damage to pancreatic structure and function
  • Causes: ETOH abuse, malnutrition, hyperPTH, pancreas divisum, ampullary stenosis, cystic fibrosis, hereditary, trauma, idiopathic
chronic pancreatitis18
Chronic Pancreatitis
  • Chronic pancreatitis results in interstitial inflammation w/duct obstruction and dilation leading to parenchymal loss and fibrosis.
  • Loss of both exocrine and endocrine
  • Clinicically significant malabsorption occurs when 90% of pancreas is lost.
chronic pancreatitis19
Chronic Pancreatitis
  • Presents as midepigastric abdominal pain, nausea, vomiting
  • Pts. May appear chronically ill, w/sign of pancreatic insufficiency such as weight loss, steatorrhea, clubbing, polyuria
  • Differentiating acute vs chronic pancreatitis is difficult b/c primary distinction is based on disease reversibility
chronic pancreatitis20
Chronic Pancreatitis
  • Amylase and lipase may be normal if pancreas is fibrotic
  • CT scan may help ID pseudocyst or abscess
  • Tx: IVF’s anti-emetics, narcotics
  • Pancreatic extracts to improve absorption and pain
  • If pain is increasing or intractable, image pancreas to look for complications
  • Pts. Maybe discharged home if all the complications have been ruled out
  • Hospitalize if intractable pain.
  • 1. Which of the following are common causes of pancreatitis
    • A. infection
    • B. Gallstones
    • C. ETOH
    • D. Drugs
    • E. all of above
  • 2. Which of the following are complications of pancreatitis:
    • A. ARDS
    • B. Shock
    • C. pancreatic insufficiency
    • D. pleural effusions
    • E. all of above
  • 3. True or false: many meds can cause pancreatitis?
  • 4. True or false: Grey Turner and Cullens sign are signs of hemorrhagic pancreatitis?
  • 5. True or false: There is no single lab test that can reliably diagnose pancreatitis?
  • 1. E
  • 2. E
  • 3. T
  • 4.T
  • 5. T
case of the day
Case of the Day:
  • HPI: 54 y/o WF presented to ER after being found on the ground s/p fall by her son. Pt. was found to be lethargic, weak, dizzy. Pt. had been vomiting the preceding 2-3 days. C/O diffuse abdominal pain.
  • ROS: + weight loss 50 lbs. over past year, rest of ROS neg.
case of the day27
Case of the Day
  • PMHx: 1. Anemia 2. GERD 3. HLD 4. Hypokalemia 5. Herniated disc
  • PSHX: 1. TAH 2. Chole
  • NKDA
  • Meds: Urocrit, Zyprexa, Prevacid, Vicodin
  • Soc Hx: Denies ETOH, + 1pk. Day smoker, no drugs
  • Fam Hx: N/C
physical exam
Physical Exam
  • VS: 36.3, 96/60, 109, 14, 97% RA
  • Gen: A&o x1 , cachetic, difficult to arouse
  • ENT: mm dry, otherwise normal
  • CV: Tachy, S1,S2 no m/c/r
  • Pulm: LCTAx2
  • GI: + BS, soft, diffuse TTP, No R/R/G
  • Rectal: heme + stools (done by Dr. Holencik)
  • Neuro: intact, no focal deficits
  • Ext: good pulses, no edema
  • EKG: ST 109 bpm
  • CBC: WBC 8.5 10.7/32.4 Plt 440 MCV 102.2, Fe+ def. anemia
  • CMP: Na 143, K 3.6, Cl 109 CO2 12, GLU 63 BUN 17 Cr. 1.0 Alb. 3.3 AST/ALT nml, Amylase,lipase normal Mg 1.8
  • CPP neg. x 1, CXR: NAD CT head: neg.
  • UA: 1+ protein, 2+ blood
  • ABG: 7.24/26/95/10/96% RA
  • APAP/ASA neg.
  • UDS: + BZD TSH 0.23 (L) L.A. 1.6
  • ETOH 0.002
  • Serum acetones: large amount
  • Serum Osm: 294
d dx mental status change metabolic acidosis




Lactic acidosis

Ethylene glycol






D/Dx: mental status change/metabolic acidosis
alcoholic ketoacidosis aka
Alcoholic ketoacidosis(AKA):
  • AKA is a wide anion gap metabolic acidosis often assoc. w/acute cessation of ETOH consumption after chronic ETOH abuse.
  • Key features are ingestion of large amounts of ETOH, relative starvation, volume depletion
  • Relative starvation, lack of glucose/glycogen stores, insulin deficiency, production of counter-regulatory hormones
  • Lipolysis promoted w/conversion of acetyl Co A to ketones
clinical features34
N/V abd. Pain

Tachycardia & Tachypnea




Hematemesis, melena


Mental status change


Muscle pain


Clinical Features:
  • ETOH: low or none
  • Elevated anion gap caused by ketones
  • Serum ketones: maybe neg. or high (assay detects AcAc/acetone, BHB predominant ketone in AKA)
  • Electrolytes: hypophosphatemia, hypokalemia, hyponatremia, hypoglycemia
  • Acid Base: maybe mixed met. Acidosis & met. Alkalosis(vomiting, volume depletion)
  • Glucose administration to promote insulin secretion
  • IVF: D5NS , HCO3 if pH<7.1
  • Thiamine
  • Admit for acidosis
hyperkalemia ekg see iii 19
Hyperkalemia: EKG see III-19
  • Tall, tenting of T-waves
  • Prolongation of QRS & P-R interval
  • Low amplitude p-waves
  • AV blocks
  • Sine wave, V. Fib, asystole
hypokalemia see iii 20
Hypokalemia: see III-20
  • Flattening of T-waves, U waves present
  • ST-depression
  • T-wave inversion
  • Advanced: PAT w/block