Transcript Acute & Chronic Pancreatitis

Acute & Chronic Pancreatitis
11/01/2005
 Chp. 87 Tintinalli
 Bogdan Irimies D.O.
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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
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Drug Induced Pancreatitis
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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 Pancreatitis
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Drugs cont’d:
 Antiretrovirals:
all types
 Diuretics
 GI
agents: H2 blockers, PPI’s
 Glucocorticoids
 NSAIDS
 ASA
Pathophysiology
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
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Pathophysiology
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
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Can lead to shock, ARDS, Multi-organ system failure
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
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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
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Hypotension secondary to 3rd spacing, hemorrhage,
increased vascular permeability, vasodilation, cardiac
depression, vomiting
Diagnosis

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
Diagnosis

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%)
Diagnosis
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Xrays of chest/abdomen: useful for r/o
other diagnosis.
 Calcification
of pancreas seen in chronic
pancreatitis
 May see sentinel loop, elevated hemidiaphragm, pleural effusion
 U/S may detect gallstones
 CT best study for grading severity if disease,
prognosis.
Diagnosis
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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
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Diagnosis
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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
Pulmonary: pleural effusions, atelectasis,
hypoxemia, ARDS
 CV: myocardial depression, hemorrhage,
hypovolemia
 Metabolic: Hypocalcemia, hyperglycemia,
Hyperlipidemia, coagulopathy/DIC
 Others: Colonic perforation, ARF. Arthritis,
pseudocyst, abscess
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Treatment:
General principle: rest the pancreas
 Fluid resuscitation
 NG tube only if needed
 Pain control, anti-emetics
 ATBX only in severe disease
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 Cover
polymicrobial, GNB
 IV imipenem or quinolone in combination
w/Flagyl
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
 All others need to be admitted
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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 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 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 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
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Disposition
Pts. Maybe discharged home if all the
complications have been ruled out
 Hospitalize if intractable pain.
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Questions

1. Which of the following are common
causes of pancreatitis
 A.
infection
 B. Gallstones
 C. ETOH
 D. Drugs
 E. all of above
Questions
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2. Which of the following are
complications of pancreatitis:
 A.
ARDS
 B. Shock
 C. pancreatic insufficiency
 D. pleural effusions
 E. all of above
Questions
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?

Answers
1. E
 2. E
 3. T
 4.T
 5. T
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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.
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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
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Physical Exam
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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
Labs
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.
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Labs
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
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D/Dx: mental status
change/metabolic acidosis
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Methanol
Uremia
Dka
Inh/iron
Lactic acidosis
Ethylene glycol
ASA
CO
 Cyanide
 AKA/starvation
 Tolulene
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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

AKA
Relative starvation, lack of
glucose/glycogen stores, insulin deficiency,
production of counter-regulatory
hormones
 Lipolysis promoted w/conversion of acetyl
Co A to ketones
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Clinical Features:
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N/V abd. Pain
Tachycardia &
Tachypnea
SOB
Tremulousness
Dizziness
Hematemesis, melena
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Hepatomegaly
Mental status change
Seizure/syncope
Muscle pain
Fever
Lab:
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)
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Treatment:
Glucose administration to promote insulin
secretion
 IVF: D5NS , HCO3 if pH<7.1
 Thiamine
 Admit for acidosis
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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
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Hypokalemia: see III-20
Flattening of T-waves, U waves present
 ST-depression
 T-wave inversion
 Advanced: PAT w/block
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