acute & chronic pancreatitis 11/01/2005 11/01/2005 chp. 87 tintinalli chp. 87 tintinalli bogdan...

Acute & Chronic PancreatitisAcute & Chronic Pancreatitis

11/01/200511/01/2005Chp. 87 TintinalliChp. 87 TintinalliBogdan Irimies D.O.Bogdan Irimies D.O.

Acute Pancreatitis: Acute Pancreatitis: EpidemiologyEpidemiology

Clinical presentation can vary from mild Clinical presentation can vary from mild abdominal pain to refractory shockabdominal pain to refractory shock

90% of acute pancreatitis is secondary 90% of acute pancreatitis is secondary to acute cholelithiasis or ETOH abuseto acute cholelithiasis or ETOH abuse

List if causes is extensive: Cholelithiasis, List if causes is extensive: Cholelithiasis, ETOH, drugs, infection, inflammation, ETOH, drugs, infection, inflammation, trauma, metabolic disturbancestrauma, metabolic disturbances

Drug Induced PancreatitisDrug Induced Pancreatitis

Drugs assoc. w/pancreatitis:Drugs assoc. w/pancreatitis:Amiodarone, amlodipineAmiodarone, amlodipineAntibiotics(macrolides,sulfa, FQ’s, Antibiotics(macrolides,sulfa, FQ’s,

rifampin)rifampin)Antiepileptics (carbamazepine, valproic Antiepileptics (carbamazepine, valproic

acid, topiramate)acid, topiramate)Hyperlipidemic drugsHyperlipidemic drugsAntineoplastic agentsAntineoplastic agentsAntipsychotics (risperdal)Antipsychotics (risperdal)

Drug Induced PancreatitisDrug Induced Pancreatitis

Drugs cont’d:Drugs cont’d:Antiretrovirals: all typesAntiretrovirals: all typesDiureticsDiureticsGI agents: H2 blockers, PPI’sGI agents: H2 blockers, PPI’sGlucocorticoidsGlucocorticoidsNSAIDSNSAIDSASAASA

PathophysiologyPathophysiology

Central cause appears to be Central cause appears to be activation of the digestive zymogens activation of the digestive zymogens in the pancreatic acinar cells and in the pancreatic acinar cells and subsequent autodigestion of the subsequent autodigestion of the pancreas.pancreas.

Number of factors(endotoxins, Number of factors(endotoxins, toxins, ischemia, infections, anoxia) toxins, ischemia, infections, anoxia) trigger activation of proenzymestrigger activation of proenzymes

PathophysiologyPathophysiology

Activated proteolytic enzymes such as Activated proteolytic enzymes such as trypsin digest cellular membranes within trypsin digest cellular membranes within pancreas and cause edema, interstitial pancreas and cause edema, interstitial hemorrhage, vascular damage, hemorrhage, vascular damage, coagulation and cellular necrosis.coagulation and cellular necrosis.

This can lead to extension of localized This can lead to extension of localized process into generalized systemic process into generalized systemic inflammatory responseinflammatory response Can lead to shock, ARDS, Multi-organ system Can lead to shock, ARDS, Multi-organ system

failurefailure

Clinical FeaturesClinical Features

Major symptom is midepigastric or Major symptom is midepigastric or left upper quadrant pain: described left upper quadrant pain: described as constant, boring pain that radiates as constant, boring pain that radiates to back, flanks, chest or lower to back, flanks, chest or lower abdomen.abdomen.

Nausea/vomiting or abdominal Nausea/vomiting or abdominal bloatingbloating

PE: low grade fevers, tachycardia, +/- PE: low grade fevers, tachycardia, +/- hypotensionhypotension

Clinical FeaturesClinical Features

Respiratory symptoms: atelectasis, pleural Respiratory symptoms: atelectasis, pleural effusion, ARDSeffusion, ARDS

Abdominal exam: epigastric tenderness, Abdominal exam: epigastric tenderness, peritonitis, Cullen sign(bluish discoloration peritonitis, Cullen sign(bluish discoloration around umbilicus), Grey Turner sign around umbilicus), Grey Turner sign (bluish discoloration of flanks)(bluish discoloration of flanks)

Pts. May present in hypovolemic shock and Pts. May present in hypovolemic shock and MOSFMOSF Hypotension secondary to 3Hypotension secondary to 3rdrd spacing, spacing,

hemorrhage, increased vascular permeability, hemorrhage, increased vascular permeability, vasodilation, cardiac depression, vomitingvasodilation, cardiac depression, vomiting

DiagnosisDiagnosis

Amylase: found in pancreas & Amylase: found in pancreas & salivary glandssalivary glandsLow levels found in many tissues so this Low levels found in many tissues so this

test is nonspecifictest is nonspecificAmylase may be even normal in acute Amylase may be even normal in acute

pancreatitispancreatitisPoor specificityPoor specificity

DiagnosisDiagnosis

Lipase: found predominantly in Lipase: found predominantly in pancreas but also in gastric, pancreas but also in gastric, intestinal mucosa and liverintestinal mucosa and liverCleared by the kidney so renal failure Cleared by the kidney so renal failure

will elevate levelswill elevate levelsMost appropriate cut-off is 2-3 x normal Most appropriate cut-off is 2-3 x normal

levellevelMore accurate test than amylase, better More accurate test than amylase, better

specificity (90% vs. 75%)specificity (90% vs. 75%)

DiagnosisDiagnosis

Xrays of chest/abdomen: useful for Xrays of chest/abdomen: useful for r/o other diagnosis.r/o other diagnosis.Calcification of pancreas seen in chronic Calcification of pancreas seen in chronic

pancreatitispancreatitisMay see sentinel loop, elevated hemi-May see sentinel loop, elevated hemi-

diaphragm, pleural effusiondiaphragm, pleural effusionU/S may detect gallstonesU/S may detect gallstonesCT best study for grading severity if CT best study for grading severity if

disease, prognosis.disease, prognosis.

DiagnosisDiagnosis

Prognostic markers: Ranson criteria Prognostic markers: Ranson criteria predicts pt. outcomepredicts pt. outcome Age >55Age >55 BS >200BS >200 WBC >16,000WBC >16,000 AST >250AST >250 LDH >700LDH >700 Features portend a worse prognosis, but they Features portend a worse prognosis, but they

have poor predictive value in acute setting have poor predictive value in acute setting and does not improve clinical judgmentand does not improve clinical judgment

DiagnosisDiagnosis

CT of abdomen:CT of abdomen:Estimates severity and prognosisEstimates severity and prognosisComplications include phlegmons, Complications include phlegmons,

abscesses or pseudocysts.abscesses or pseudocysts.Usually seen 2-3 weeks after acute Usually seen 2-3 weeks after acute

pancreatitispancreatitis

Complications of Acute Complications of Acute PancreatitisPancreatitis

Pulmonary: pleural effusions, Pulmonary: pleural effusions, atelectasis, hypoxemia, ARDSatelectasis, hypoxemia, ARDS

CV: myocardial depression, CV: myocardial depression, hemorrhage, hypovolemiahemorrhage, hypovolemia

Metabolic: Hypocalcemia, Metabolic: Hypocalcemia, hyperglycemia, Hyperlipidemia, hyperglycemia, Hyperlipidemia, coagulopathy/DICcoagulopathy/DIC

Others: Colonic perforation, ARF. Others: Colonic perforation, ARF. Arthritis, pseudocyst, abscessArthritis, pseudocyst, abscess

Treatment:Treatment:

General principle: rest the pancreasGeneral principle: rest the pancreasFluid resuscitationFluid resuscitationNG tube only if neededNG tube only if neededPain control, anti-emeticsPain control, anti-emeticsATBX only in severe diseaseATBX only in severe disease

Cover polymicrobial, GNBCover polymicrobial, GNBIV imipenem or quinolone in IV imipenem or quinolone in

combination w/Flagylcombination w/Flagyl

Disposition:Disposition:

Pts. w/mild pancreatitis w/no Pts. w/mild pancreatitis w/no evidence of systemic disease and low evidence of systemic disease and low likelihood of biliary disease may be likelihood of biliary disease may be managed as outpts. if tolerating oral managed as outpts. if tolerating oral fluids and pain control is adequatefluids and pain control is adequate

All others need to be admittedAll others need to be admitted

Chronic PancreatitisChronic Pancreatitis

Defined as chronic inflammatory Defined as chronic inflammatory condition that causes irreversible condition that causes irreversible damage to pancreatic structure and damage to pancreatic structure and functionfunction

Causes: ETOH abuse, malnutrition, Causes: ETOH abuse, malnutrition, hyperPTH, pancreas divisum, hyperPTH, pancreas divisum, ampullary stenosis, cystic fibrosis, ampullary stenosis, cystic fibrosis, hereditary, trauma, idiopathichereditary, trauma, idiopathic

Chronic PancreatitisChronic Pancreatitis

Chronic pancreatitis results in Chronic pancreatitis results in interstitial inflammation w/duct interstitial inflammation w/duct obstruction and dilation leading to obstruction and dilation leading to parenchymal loss and fibrosis.parenchymal loss and fibrosis.

Loss of both exocrine and endocrineLoss of both exocrine and endocrineClinicically significant malabsorption Clinicically significant malabsorption

occurs when 90% of pancreas is lost.occurs when 90% of pancreas is lost.

Chronic PancreatitisChronic Pancreatitis

Presents as midepigastric abdominal Presents as midepigastric abdominal pain, nausea, vomitingpain, nausea, vomiting

Pts. May appear chronically ill, w/sign of Pts. May appear chronically ill, w/sign of pancreatic insufficiency such as weight pancreatic insufficiency such as weight loss, steatorrhea, clubbing, polyurialoss, steatorrhea, clubbing, polyuria

Differentiating acute vs chronic Differentiating acute vs chronic pancreatitis is difficult b/c primary pancreatitis is difficult b/c primary distinction is based on disease distinction is based on disease reversibilityreversibility

Chronic PancreatitisChronic Pancreatitis

Amylase and lipase may be normal if Amylase and lipase may be normal if pancreas is fibroticpancreas is fibrotic

CT scan may help ID pseudocyst or CT scan may help ID pseudocyst or abscessabscess

Tx: IVF’s anti-emetics, narcoticsTx: IVF’s anti-emetics, narcoticsPancreatic extracts to improve Pancreatic extracts to improve

absorption and painabsorption and pain If pain is increasing or intractable, If pain is increasing or intractable,

image pancreas to look for image pancreas to look for complicationscomplications

DispositionDisposition

Pts. Maybe discharged home if all the Pts. Maybe discharged home if all the complications have been ruled outcomplications have been ruled out

Hospitalize if intractable pain.Hospitalize if intractable pain.

QuestionsQuestions

1. Which of the following are 1. Which of the following are common causes of pancreatitiscommon causes of pancreatitisA. infectionA. infectionB. GallstonesB. GallstonesC. ETOHC. ETOHD. DrugsD. DrugsE. all of aboveE. all of above

QuestionsQuestions

2. Which of the following are 2. Which of the following are complications of pancreatitis:complications of pancreatitis:A. ARDSA. ARDSB. ShockB. ShockC. pancreatic insufficiencyC. pancreatic insufficiencyD. pleural effusionsD. pleural effusionsE. all of aboveE. all of above

QuestionsQuestions

3. True or false: many meds can 3. True or false: many meds can cause pancreatitis?cause pancreatitis?

4. True or false: Grey Turner and 4. True or false: Grey Turner and Cullens sign are signs of hemorrhagic Cullens sign are signs of hemorrhagic pancreatitis?pancreatitis?

5. True or false: There is no single lab 5. True or false: There is no single lab test that can reliably diagnose test that can reliably diagnose pancreatitis?pancreatitis?

AnswersAnswers

1. E1. E2. E2. E3. T3. T4.T4.T5. T5. T

Case of the Day:Case of the Day:

HPI: 54 y/o WF presented to ER after HPI: 54 y/o WF presented to ER after being found on the ground s/p fall by being found on the ground s/p fall by her son. Pt. was found to be her son. Pt. was found to be lethargic, weak, dizzy. Pt. had been lethargic, weak, dizzy. Pt. had been vomiting the preceding 2-3 days. C/O vomiting the preceding 2-3 days. C/O diffuse abdominal pain. diffuse abdominal pain.

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

Case of the DayCase of the Day

PMHx: 1. Anemia 2. GERD 3. HLD PMHx: 1. Anemia 2. GERD 3. HLD 4. Hypokalemia 5. Herniated disc4. Hypokalemia 5. Herniated disc

PSHX: 1. TAH 2. CholePSHX: 1. TAH 2. CholeNKDANKDAMeds: Urocrit, Zyprexa, Prevacid, Meds: Urocrit, Zyprexa, Prevacid,

VicodinVicodinSoc Hx: Denies ETOH, + 1pk. Day Soc Hx: Denies ETOH, + 1pk. Day

smoker, no drugssmoker, no drugsFam Hx: N/CFam Hx: N/C

Physical ExamPhysical Exam

VS: 36.3, 96/60, 109, 14, 97% RAVS: 36.3, 96/60, 109, 14, 97% RA Gen: A&o x1 , cachetic, difficult to arouseGen: A&o x1 , cachetic, difficult to arouse ENT: mm dry, otherwise normalENT: mm dry, otherwise normal CV: Tachy, S1,S2 no m/c/rCV: Tachy, S1,S2 no m/c/r Pulm: LCTAx2Pulm: LCTAx2 GI: + BS, soft, diffuse TTP, No R/R/GGI: + BS, soft, diffuse TTP, No R/R/G Rectal: heme + stools (done by Dr. Rectal: heme + stools (done by Dr.

Holencik)Holencik) Neuro: intact, no focal deficitsNeuro: intact, no focal deficits Ext: good pulses, no edemaExt: good pulses, no edema

LabsLabs

EKG: ST 109 bpmEKG: ST 109 bpmCBC: WBC 8.5 10.7/32.4 Plt 440 MCV CBC: WBC 8.5 10.7/32.4 Plt 440 MCV

102.2, Fe+ def. anemia102.2, Fe+ def. anemiaCMP: Na 143, K 3.6, Cl 109 CO2 12, CMP: Na 143, K 3.6, Cl 109 CO2 12,

GLU 63 BUN 17 Cr. 1.0 Alb. 3.3 GLU 63 BUN 17 Cr. 1.0 Alb. 3.3 AST/ALT nml, Amylase,lipase normal AST/ALT nml, Amylase,lipase normal Mg 1.8Mg 1.8

CPP neg. x 1, CXR: NAD CT head: neg.CPP neg. x 1, CXR: NAD CT head: neg.

LabsLabs

UA: 1+ protein, 2+ bloodUA: 1+ protein, 2+ bloodABG: 7.24/26/95/10/96% RAABG: 7.24/26/95/10/96% RAAPAP/ASA neg.APAP/ASA neg.UDS: + BZD TSH 0.23 (L) L.A. 1.6UDS: + BZD TSH 0.23 (L) L.A. 1.6ETOH 0.002ETOH 0.002Serum acetones: large amountSerum acetones: large amountSerum Osm: 294Serum Osm: 294

D/Dx: mental status D/Dx: mental status change/metabolic acidosischange/metabolic acidosis

MethanolMethanol UremiaUremia DkaDka Inh/ironInh/iron Lactic acidosisLactic acidosis Ethylene glycolEthylene glycol ASAASA

COCO CyanideCyanide AKA/starvationAKA/starvation ToluleneTolulene

Alcoholic ketoacidosis(AKA):Alcoholic ketoacidosis(AKA):

AKA is a wide anion gap metabolic AKA is a wide anion gap metabolic acidosis often assoc. w/acute acidosis often assoc. w/acute cessation of ETOH consumption after cessation of ETOH consumption after chronic ETOH abuse.chronic ETOH abuse.

Key features are ingestion of large Key features are ingestion of large amounts of ETOH, relative starvation, amounts of ETOH, relative starvation, volume depletionvolume depletion

AKAAKA

Relative starvation, lack of Relative starvation, lack of glucose/glycogen stores, insulin glucose/glycogen stores, insulin deficiency, production of counter-deficiency, production of counter-regulatory hormonesregulatory hormones

Lipolysis promoted w/conversion of Lipolysis promoted w/conversion of acetyl Co A to ketonesacetyl Co A to ketones

Clinical Features:Clinical Features:

N/V abd. PainN/V abd. Pain Tachycardia & Tachycardia &

TachypneaTachypnea SOBSOB TremulousnessTremulousness DizzinessDizziness Hematemesis, Hematemesis,

melenamelena

HepatomegalyHepatomegaly Mental status Mental status

changechange Seizure/syncopeSeizure/syncope Muscle painMuscle pain FeverFever

Lab:Lab:

ETOH: low or noneETOH: low or noneElevated anion gap caused by ketones Elevated anion gap caused by ketones Serum ketones: maybe neg. or high Serum ketones: maybe neg. or high

(assay detects AcAc/acetone, BHB (assay detects AcAc/acetone, BHB predominant ketone in AKA)predominant ketone in AKA)

Electrolytes: hypophosphatemia, Electrolytes: hypophosphatemia, hypokalemia, hyponatremia, hypokalemia, hyponatremia, hypoglycemiahypoglycemia

Acid Base: maybe mixed met. Acidosis & Acid Base: maybe mixed met. Acidosis & met. Alkalosis(vomiting, volume depletion)met. Alkalosis(vomiting, volume depletion)

Treatment:Treatment:

Glucose administration to promote Glucose administration to promote insulin secretioninsulin secretion

IVF: D5NS , HCO3 if pH<7.1IVF: D5NS , HCO3 if pH<7.1ThiamineThiamineAdmit for acidosisAdmit for acidosis

Hyperkalemia: EKG see III-19Hyperkalemia: EKG see III-19

Tall, tenting of T-wavesTall, tenting of T-wavesProlongation of QRS & P-R intervalProlongation of QRS & P-R intervalLow amplitude p-wavesLow amplitude p-wavesAV blocksAV blocksSine wave, V. Fib, asystoleSine wave, V. Fib, asystole

Hypokalemia: see III-20Hypokalemia: see III-20

Flattening of T-waves, U waves Flattening of T-waves, U waves presentpresent

ST-depressionST-depressionT-wave inversionT-wave inversionAdvanced: PAT w/blockAdvanced: PAT w/block