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
List if causes is extensive: Cholelithiasis,
ETOH, drugs, infection, inflammation,
trauma, metabolic disturbances
 Drug Induced Pancreatitis
Drugs assoc. w/pancreatitis:
Amiodarone, amlodipine
Antibiotics(macrolides,sulfa, FQs,
rifampin)
Antiepileptics (carbamazepine, valproic
acid, topiramate)
Hyperlipidemic drugs
Antineoplastic agents
Antipsychotics (risperdal)
 Drug Induced Pancreatitis
Drugs contd:
Antiretrovirals: all types
Diuretics
GI agents: H2 blockers, PPIs
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
 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
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
 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
 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
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.
 Diagnosis
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
 Diagnosis
CT of abdomen:
Estimates severity and prognosis
Complications include phlegmons,
abscesses or pseudocysts.
Usuallyseen 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
 Treatment:
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
 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
 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: IVFs anti-emetics, narcotics
Pancreatic extracts to improve
absorption and pain
If pain is increasing or intractable, image
pancreas to look for complications
 Disposition
Pts.
Maybe discharged home if all the
complications have been ruled out
Hospitalize if intractable pain.
 Questions
1.
Which of the following are
common causes of pancreatitis
A. infection
B. Gallstones
C. ETOH
D. Drugs
E. all of above
 Questions
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
 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 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
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.
 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
 D/Dx: mental status
change/metabolic acidosis
Methanol CO
Uremia Cyanide
Dka AKA/starvation
Inh/iron Tolulene
Lacticacidosis
Ethylene glycol
ASA
 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
 Clinical Features:
N/V abd. Pain Hepatomegaly
Tachycardia & Mental status
Tachypnea change
SOB Seizure/syncope
Tremulousness Muscle pain
Dizziness Fever
Hematemesis,
melena
 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)
 Treatment:
Glucose administration to promote
insulin secretion
IVF: D5NS , HCO3 if pH<7.1
Thiamine
Admit for acidosis
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
Flattening of T-waves, U waves
present
ST-depression
T-wave inversion
Advanced: PAT w/block