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Acute & Chronic Pancreatitis 11/01/2005 11/01/2005 Chp. 87 Tintinalli Chp. 87 Tintinalli Bogdan Irimies D.O. Bogdan Irimies D.O.

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Presentation on theme: "Acute & Chronic Pancreatitis 11/01/2005 11/01/2005 Chp. 87 Tintinalli Chp. 87 Tintinalli Bogdan Irimies D.O. Bogdan Irimies D.O."— Presentation transcript:

1 Acute & Chronic Pancreatitis 11/01/ /01/2005 Chp. 87 Tintinalli Chp. 87 Tintinalli Bogdan Irimies D.O. Bogdan Irimies D.O.

2 Acute Pancreatitis: Epidemiology Clinical presentation can vary from mild abdominal pain to refractory shock Clinical presentation can vary from mild abdominal pain to refractory shock 90% of acute pancreatitis is secondary to acute cholelithiasis or ETOH abuse 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 List if causes is extensive: Cholelithiasis, ETOH, drugs, infection, inflammation, trauma, metabolic disturbances

3 Drug Induced Pancreatitis Drugs assoc. w/pancreatitis: Drugs assoc. w/pancreatitis: Amiodarone, amlodipine Amiodarone, amlodipine Antibiotics(macrolides,sulfa, FQ’s, rifampin) Antibiotics(macrolides,sulfa, FQ’s, rifampin) Antiepileptics (carbamazepine, valproic acid, topiramate) Antiepileptics (carbamazepine, valproic acid, topiramate) Hyperlipidemic drugs Hyperlipidemic drugs Antineoplastic agents Antineoplastic agents Antipsychotics (risperdal) Antipsychotics (risperdal)

4 Drug Induced Pancreatitis Drugs cont’d: Drugs cont’d: Antiretrovirals: all types Antiretrovirals: all types Diuretics Diuretics GI agents: H2 blockers, PPI’s GI agents: H2 blockers, PPI’s Glucocorticoids Glucocorticoids NSAIDS NSAIDS ASA ASA

5 Pathophysiology Central cause appears to be activation of the digestive zymogens in the pancreatic acinar cells and subsequent autodigestion of the pancreas. 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 Number of factors(endotoxins, toxins, ischemia, infections, anoxia) trigger activation of proenzymes

6 Pathophysiology Activated proteolytic enzymes such as trypsin digest cellular membranes within pancreas and cause edema, interstitial hemorrhage, vascular damage, coagulation and cellular necrosis. 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 This can lead to extension of localized process into generalized systemic inflammatory response Can lead to shock, ARDS, Multi-organ system failure Can lead to shock, ARDS, Multi-organ system failure

7 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. 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 Nausea/vomiting or abdominal bloating PE: low grade fevers, tachycardia, +/- hypotension PE: low grade fevers, tachycardia, +/- hypotension

8 Clinical Features Respiratory symptoms: atelectasis, pleural effusion, ARDS Respiratory symptoms: atelectasis, pleural effusion, ARDS Abdominal exam: epigastric tenderness, peritonitis, Cullen sign(bluish discoloration around umbilicus), Grey Turner sign (bluish discoloration of flanks) 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 Pts. May present in hypovolemic shock and MOSF Hypotension secondary to 3 rd spacing, hemorrhage, increased vascular permeability, vasodilation, cardiac depression, vomiting Hypotension secondary to 3 rd spacing, hemorrhage, increased vascular permeability, vasodilation, cardiac depression, vomiting

9 Diagnosis Amylase: found in pancreas & salivary glands Amylase: found in pancreas & salivary glands Low levels found in many tissues so this test is nonspecific Low levels found in many tissues so this test is nonspecific Amylase may be even normal in acute pancreatitis Amylase may be even normal in acute pancreatitis Poor specificity Poor specificity

10 Diagnosis Lipase: found predominantly in pancreas but also in gastric, intestinal mucosa and liver Lipase: found predominantly in pancreas but also in gastric, intestinal mucosa and liver Cleared by the kidney so renal failure will elevate levels Cleared by the kidney so renal failure will elevate levels Most appropriate cut-off is 2-3 x normal level Most appropriate cut-off is 2-3 x normal level More accurate test than amylase, better specificity (90% vs. 75%) More accurate test than amylase, better specificity (90% vs. 75%)

11 Diagnosis Xrays of chest/abdomen: useful for r/o other diagnosis. Xrays of chest/abdomen: useful for r/o other diagnosis. Calcification of pancreas seen in chronic pancreatitis Calcification of pancreas seen in chronic pancreatitis May see sentinel loop, elevated hemi- diaphragm, pleural effusion May see sentinel loop, elevated hemi- diaphragm, pleural effusion U/S may detect gallstones U/S may detect gallstones CT best study for grading severity if disease, prognosis. CT best study for grading severity if disease, prognosis.

12 Diagnosis Prognostic markers: Ranson criteria predicts pt. outcome Prognostic markers: Ranson criteria predicts pt. outcome Age >55 Age >55 BS >200 BS >200 WBC >16,000 WBC >16,000 AST >250 AST >250 LDH >700 LDH >700 Features portend a worse prognosis, but they have poor predictive value in acute setting and does not improve clinical judgment Features portend a worse prognosis, but they have poor predictive value in acute setting and does not improve clinical judgment

13 Diagnosis CT of abdomen: CT of abdomen: Estimates severity and prognosis Estimates severity and prognosis Complications include phlegmons, abscesses or pseudocysts. Complications include phlegmons, abscesses or pseudocysts. Usually seen 2-3 weeks after acute pancreatitis Usually seen 2-3 weeks after acute pancreatitis

14 Complications of Acute Pancreatitis Pulmonary: pleural effusions, atelectasis, hypoxemia, ARDS Pulmonary: pleural effusions, atelectasis, hypoxemia, ARDS CV: myocardial depression, hemorrhage, hypovolemia CV: myocardial depression, hemorrhage, hypovolemia Metabolic: Hypocalcemia, hyperglycemia, Hyperlipidemia, coagulopathy/DIC Metabolic: Hypocalcemia, hyperglycemia, Hyperlipidemia, coagulopathy/DIC Others: Colonic perforation, ARF. Arthritis, pseudocyst, abscess Others: Colonic perforation, ARF. Arthritis, pseudocyst, abscess

15 Treatment: General principle: rest the pancreas General principle: rest the pancreas Fluid resuscitation Fluid resuscitation NG tube only if needed NG tube only if needed Pain control, anti-emetics Pain control, anti-emetics ATBX only in severe disease ATBX only in severe disease Cover polymicrobial, GNB Cover polymicrobial, GNB IV imipenem or quinolone in combination w/Flagyl IV imipenem or quinolone in combination w/Flagyl

16 Disposition: 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 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 All others need to be admitted

17 Chronic Pancreatitis Defined as chronic inflammatory condition that causes irreversible damage to pancreatic structure and function 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 Causes: ETOH abuse, malnutrition, hyperPTH, pancreas divisum, ampullary stenosis, cystic fibrosis, hereditary, trauma, idiopathic

18 Chronic Pancreatitis Chronic pancreatitis results in interstitial inflammation w/duct obstruction and dilation leading to parenchymal loss and fibrosis. Chronic pancreatitis results in interstitial inflammation w/duct obstruction and dilation leading to parenchymal loss and fibrosis. Loss of both exocrine and endocrine Loss of both exocrine and endocrine Clinicically significant malabsorption occurs when 90% of pancreas is lost. Clinicically significant malabsorption occurs when 90% of pancreas is lost.

19 Chronic Pancreatitis Presents as midepigastric abdominal pain, nausea, vomiting Presents as midepigastric abdominal pain, nausea, vomiting Pts. May appear chronically ill, w/sign of pancreatic insufficiency such as weight loss, steatorrhea, clubbing, polyuria 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 Differentiating acute vs chronic pancreatitis is difficult b/c primary distinction is based on disease reversibility

20 Chronic Pancreatitis Amylase and lipase may be normal if pancreas is fibrotic Amylase and lipase may be normal if pancreas is fibrotic CT scan may help ID pseudocyst or abscess CT scan may help ID pseudocyst or abscess Tx: IVF’s anti-emetics, narcotics Tx: IVF’s anti-emetics, narcotics Pancreatic extracts to improve absorption and pain Pancreatic extracts to improve absorption and pain If pain is increasing or intractable, image pancreas to look for complications If pain is increasing or intractable, image pancreas to look for complications

21 Disposition Pts. Maybe discharged home if all the complications have been ruled out Pts. Maybe discharged home if all the complications have been ruled out Hospitalize if intractable pain. Hospitalize if intractable pain.

22 Questions 1. Which of the following are common causes of pancreatitis 1. Which of the following are common causes of pancreatitis A. infection A. infection B. Gallstones B. Gallstones C. ETOH C. ETOH D. Drugs D. Drugs E. all of above E. all of above

23 Questions 2. Which of the following are complications of pancreatitis: 2. Which of the following are complications of pancreatitis: A. ARDS A. ARDS B. Shock B. Shock C. pancreatic insufficiency C. pancreatic insufficiency D. pleural effusions D. pleural effusions E. all of above E. all of above

24 Questions 3. True or false: many meds can cause pancreatitis? 3. True or false: many meds can cause pancreatitis? 4. True or false: Grey Turner and Cullens sign are signs of hemorrhagic 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? 5. True or false: There is no single lab test that can reliably diagnose pancreatitis?

25 Answers 1. E 1. E 2. E 2. E 3. T 3. T 4.T 4.T 5. T 5. T

26 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. 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. ROS: + weight loss 50 lbs. over past year, rest of ROS neg.

27 Case of the Day PMHx: 1. Anemia 2. GERD 3. HLD 4. Hypokalemia 5. Herniated disc PMHx: 1. Anemia 2. GERD 3. HLD 4. Hypokalemia 5. Herniated disc PSHX: 1. TAH 2. Chole PSHX: 1. TAH 2. Chole NKDA NKDA Meds: Urocrit, Zyprexa, Prevacid, Vicodin Meds: Urocrit, Zyprexa, Prevacid, Vicodin Soc Hx: Denies ETOH, + 1pk. Day smoker, no drugs Soc Hx: Denies ETOH, + 1pk. Day smoker, no drugs Fam Hx: N/C Fam Hx: N/C

28 Physical Exam VS: 36.3, 96/60, 109, 14, 97% RA VS: 36.3, 96/60, 109, 14, 97% RA Gen: A&o x1, cachetic, difficult to arouse Gen: A&o x1, cachetic, difficult to arouse ENT: mm dry, otherwise normal ENT: mm dry, otherwise normal CV: Tachy, S1,S2 no m/c/r CV: Tachy, S1,S2 no m/c/r Pulm: LCTAx2 Pulm: LCTAx2 GI: + BS, soft, diffuse TTP, No R/R/G GI: + BS, soft, diffuse TTP, No R/R/G Rectal: heme + stools (done by Dr. Holencik) Rectal: heme + stools (done by Dr. Holencik) Neuro: intact, no focal deficits Neuro: intact, no focal deficits Ext: good pulses, no edema Ext: good pulses, no edema

29 Labs EKG: ST 109 bpm EKG: ST 109 bpm CBC: WBC /32.4 Plt 440 MCV 102.2, Fe+ def. anemia CBC: WBC /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 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. CPP neg. x 1, CXR: NAD CT head: neg.

30 Labs UA: 1+ protein, 2+ blood UA: 1+ protein, 2+ blood ABG: 7.24/26/95/10/96% RA ABG: 7.24/26/95/10/96% RA APAP/ASA neg. APAP/ASA neg. UDS: + BZD TSH 0.23 (L) L.A. 1.6 UDS: + BZD TSH 0.23 (L) L.A. 1.6 ETOH ETOH Serum acetones: large amount Serum acetones: large amount Serum Osm: 294 Serum Osm: 294

31 D/Dx: mental status change/metabolic acidosis Methanol Methanol Uremia Uremia Dka Dka Inh/iron Inh/iron Lactic acidosis Lactic acidosis Ethylene glycol Ethylene glycol ASA ASA CO CO Cyanide Cyanide AKA/starvation AKA/starvation Tolulene Tolulene

32 Alcoholic ketoacidosis(AKA): AKA is a wide anion gap metabolic acidosis often assoc. w/acute cessation of ETOH consumption after chronic ETOH abuse. 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 Key features are ingestion of large amounts of ETOH, relative starvation, volume depletion

33 AKA Relative starvation, lack of glucose/glycogen stores, insulin deficiency, production of counter- regulatory hormones Relative starvation, lack of glucose/glycogen stores, insulin deficiency, production of counter- regulatory hormones Lipolysis promoted w/conversion of acetyl Co A to ketones Lipolysis promoted w/conversion of acetyl Co A to ketones

34 Clinical Features: N/V abd. Pain N/V abd. Pain Tachycardia & Tachypnea Tachycardia & Tachypnea SOB SOB Tremulousness Tremulousness Dizziness Dizziness Hematemesis, melena Hematemesis, melena Hepatomegaly Hepatomegaly Mental status change Mental status change Seizure/syncope Seizure/syncope Muscle pain Muscle pain Fever Fever

35 Lab: ETOH: low or none ETOH: low or none Elevated anion gap caused by ketones Elevated anion gap caused by ketones Serum ketones: maybe neg. or high (assay detects AcAc/acetone, BHB predominant ketone in AKA) Serum ketones: maybe neg. or high (assay detects AcAc/acetone, BHB predominant ketone in AKA) Electrolytes: hypophosphatemia, hypokalemia, hyponatremia, hypoglycemia Electrolytes: hypophosphatemia, hypokalemia, hyponatremia, hypoglycemia Acid Base: maybe mixed met. Acidosis & met. Alkalosis(vomiting, volume depletion) Acid Base: maybe mixed met. Acidosis & met. Alkalosis(vomiting, volume depletion)

36 Treatment: Glucose administration to promote insulin secretion Glucose administration to promote insulin secretion IVF: D5NS, HCO3 if pH<7.1 IVF: D5NS, HCO3 if pH<7.1 Thiamine Thiamine Admit for acidosis Admit for acidosis

37 Hyperkalemia: EKG see III-19 Tall, tenting of T-waves Tall, tenting of T-waves Prolongation of QRS & P-R interval Prolongation of QRS & P-R interval Low amplitude p-waves Low amplitude p-waves AV blocks AV blocks Sine wave, V. Fib, asystole Sine wave, V. Fib, asystole

38 Hypokalemia: see III-20 Flattening of T-waves, U waves present Flattening of T-waves, U waves present ST-depression ST-depression T-wave inversion T-wave inversion Advanced: PAT w/block Advanced: PAT w/block


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