Transcript Jaundice - Cleveland Clinic Regional Hospitals

Jaundice
Presented by Dr. Pollock
Prepared by Christopher Edwards
Tintanalli Chapter 84, pgs. 560-561
October 2005
Jaundice
Clinical marker of defect in metabolism
&/or excretion of bilirubin.
ER task to initiate lab eval or imaging
studies to identify cause and determine
admission or outpt therapy.
Pathophysiology
Yellow discoloration of sclera, skin,
mucous membranes due to deposition
of bile pigment
Clinically detected with serum bilirubin
2-2.5mcg/dL or  (2 times nl)
What is bilirubin?
The breakdown product of Hgb from
injured RBCs and other heme
containing proteins.
Produced by reticuloendothelial system
Released to plasma bound to albumin
Hepatocytes conjugate it and extrete
through bile channels into small intest.
What causes  bilirubin?
Overproduction by reticuloendothelial
system
Failure of hepatocyte uptake
Failure to conjugate or excrete
Obstruction of biliary excretion into
intestine
Unconjugated vs. Conjugated
Unconjugated
 production
exceeds ability of
liver to conjugate
Ex. Hemolytic
anemias,
hemoglobinopathies,
in-born errors of
metab., transfusion
rxn.
Conjugated
Can produce but not
excrete
Metabolic defect
Intra- or
extrahepatic
obstruction
Clinical Features
Careful history and PE
Family history (Gilbert, Rotor, CriglerNajjar, Dubin-Johnson, Sickle Cell)
Healthy young person with fever,
malaise, myalgias = viral hepatitis (try
to locate source)
Clinical Features
Gradually develops symptoms =
hepatic/bile duct obstruction (consider
ETOH liver dz/cirrhosis)
Develops acutely with abd pain = acute
cholangitis 2° to choledocholithiasis
Clinical Features
Painless jaundice in older person with
epigastric mass & weight loss = biliary
obstruction from malignancy
Hepatomegaly with pedal edema, JVD,
and gallop = CHF
Laboratory Tests
Serum bilirubin level
(total and direct)
Liver
aminotransferase
levels
Alk. Phos
U/A for bilirubin and
urobilogen
CBC
PT
Other labs pertinent
to history
Coombs test
Hgb electrophoresis
Viral hepatitis panel
U/S Gallbladder
Disposition
Hemodynamically stable, new-onset
jaundice, no evidence of liver failure or
acute biliary obstruction  discharge
with follow up
If one of above violated  admission
with surgery consult
Cholecystitis and Biliary Colic
Tintanalli Chapter 85
Pages 561-566
Biliary Tract Emergencies
Related to Gallstones
1)
2)
3)
4)
Biliary Colic
Cholecystitis
Gallstone pancreatitis
Ascending cholangitis
Gallstones
Most gallstones are asymptomatic
Usually seen in obese females 20-40
yoa and pregnancy (Remember fat,
fertile, flatulent, female, forty)
Associated with upper abdominal pain
Gallstones
Uncommon in children (seen with hemolytic
d/o, idiopathic, cystic fibrosis, obesity, ileal
resection, long term use of TPN)
Elderly


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14-27% symptomatic gallstone dz.
More likely biliary sepsis/gangrenous GB
 perioperative morbidity
Mortality rate 19%
Gallstone Risk Factors
Familial
Asian descent
Chronic biliary tract infections
Parasitic infections (ascaris lumbricoides)
Chronic liver dz (ETOH)
Chronic intravasular dz (Sickle Cell, Hereditary
Scherocytosis)
Hepatitis A, B, C, E
HIV
Herpesvirus
Pathophysiology
Bile

Manufactured & secreted from hepatocytes
GB storage in canaliculi, ductiles, & bile
ducts bile ducts enlarge form R and L
hepatic ducts form common hepatic duct
joins cystic duct from GB to form CBD
Ampulla of Vater duodenum
Pathophysiology
Release of bile stimulated by
cholecystokinin secreted from small int.
mucosal cells when fats & AA enter
duodenum
Pathophysiology
Symptomatic cholelithiasis = stone
migration from GB into biliary tract with
eventual obstruction obstruction of
hollow viscus pain, nausea & vomiting
acute cholecystitis
Pathogens Involved in Acute
Cholecystitis
E. coli/Klebsiella-70%
Enterococci-15%
Bacteroides-10%
Clostridium-10%
Group D Strep
Staphylococcal species
Clinical Features
Overlap of s/s of PUD, gastritis, GERD,
nonspecific dyspepsia
RUQ pain
Upper abd/epigastric pain
Radiation to L upper back
Pain persisant lasting 2-6h
Clinical Features
Clinical studies show no coorelation
with fatty food
Peak symptoms 9PM-4AM –follows
circadium rhythm
Infrequent pain-intervals more than
1wk
Not related to meals in 1/3 of pts.
Clinical Features of Acute
Cholecystitis
Pain lasts beyond 6h
N,V
Anorexia
Fever, chills
+Murphy’s sign ( pain or inspiratory
arrest with deep, subcostal palpation on
inspiration)
See Table 85-2
Acalculous Cholecystitis
5-10% incidence
Elderly
DM
Multiple trauma
Extensive burns
Prolonged Labor
Major surgery
GB torsion
Systemic vasculitis
states
Bacterial or parasitic
infection of biliary
tract
Differential Diagnosis
Gastritis
GERD
Pancreatis
Hepatitis
PUD
AMI in elderly
Acute renal colic
Acute pyelo
Appendicitis
(pregnancy,
retrocecal)
PID
Fitzhugh-Curtis Syn.
Ectopic
Pneumonia
Pleural Effusion
Diagnostic Studies
Most important is high clinical suspicion
and U/S.
Usually labs nl. (CBC, bilirubin, Alk. Phos,
LFTs, U/A, UHCG, Lipase)
CXR- r/o pneumonia, pleural effusion
12 Lead EKG- r/o ACS
U/S shows stones small as 2mm
CT when ? other intraabdominal path
HIDA Scan
Complications
Fluid & Electrolyte deficiencies- due to
vomiting & anorexia
Upper GI hemorrhage- Mallory-Weiss tears
Gallstone pancreatitis
Ascending cholangitis
Cholecystitis
GB Empyema
Emphysematous (gangrenous) GB
Treatment
Uncomplicated Symptomatic Cholelithiasis–
No immediate surgery, Elective
cholecystectomy, Control symptoms





Antispasmodics
Opiates (Meperidine preferred)
Antiemetics
Ketorolac (relieves GB distention)
Replace fluids & electrolytes
Treatment
Acute Acalculous/Calculous Cholecystitis
If septic – wide spectrum abx and
immediate surgery
If not septic – single agent abx (3rd gen
cephalosporin), surgery within 24-72
hours
Hepatic Disorders & Hepatic
Failure
Tintanalli Chapter 86
Pages 566-573
Acute & Chronic Liver Disease
CLD- 12th leading cause of death in US
However, decreased inf with hepatitis
viruses A, B, & C in last decade.
Other causes: ETOH, CMV, HSV,
Coxsackie, EBV, Drugs, autoimmune,
metabolic
Pathophysiology
Hepatocellular
Cholestatic
Immunologic
Infiltrative Disorder
Clinical Features
Acute Viral –anorexia, N, V, low-grade
fever
Cholestatic –jaundice, pruritis, claycolored stools, dark urine
Chronic –complications of advanced
cirrhosis, portal HTN (abd pain, ascites,
GI bleed, fever, AMS)
History, History, History
Sexual behaviors
Travel
ETOH
Illicit drug use
Natural supplements (Vitamin A)
Herbal remedies
Mushroom ingestion
Raw oysters
Family history
Physical Findings
Acute

Moderate liver enlargement, tenderness,
+/- jaundice
Chronic

Sallow complexion, extremity muscle
atrophy, palmar erythema, cutan spider
nevi, parotid enlargement, testicular
atrophy, gynecomastia, splenomegaly,
ascites
LFTs
1) Markers of acute hepatocyte injury &
death: AST (SGPT), ALT (SGOT), Alk Phos.
2) Measures of hepatocyte synthetic fxn :
PT, Albumin
3) Indicators of hepatocyte catabolic activity:
direct & indirect bilirubin, ammonia
4) Others: Lactate dehydrogenase, viral
hepatitis serology
Cirrhosis & Complications of
End Stage Liver Dz
Gastroesophageal Varices & Hemorrhage
Medical literature shows no evidence of
 risk of iatrogenic hemorrhage from
placement of naso- or orogastric
catheters!!!
Tx: Hemodynamic & airway stabiliz.
Endoscopy-banding/sclerotherapy
Vasoactive drugs: Somatostatin, Octreotide
Abx. to cover enteric organisms
Ascites & Spontaneous
Bacterial Peritonitis
Paracentesis (U/S guided or not)
Lab Testing of Ascitic Fluid (WBC, diff,
glucose, protein, gram stain, C&S)



SBP = WBC>1000/L, low glucose, high
protein
Abx coverage of enterobacteriaceae
(63%), S. Pneumoniae (15%), Enterococci
(6-10%), Anaerobes (<1%)
See table 86-4
Hepatorenal Syndrome
Acute renal failure with acute or chronic
hepatic failure
Etiology unknown
Median survival 21 days
Tx: Liver transplant & kidneys will
spontaneously recover
Hepatic Encephalopathy
Accumulation of nitrogenous waste
products
Diagnosis of exclusion
Tx: Decreased protein intake, lactulose
(traps ammonia & allows stool
excretion), neomycin
THE END!!!
Questions???????
Questions
1) Unconjugated hyperbilirubinemia usually
results from a intra- or extrahepatic biliary
obstruction.


A. True
B. False
2) All patients with jaundice should be
admitted to the hospital for further workup.


A. True
B. False
3) All of the following are risk factors
for development of gallstones except:





A.
B.
C.
D.
E.
Pregnancy
>50 yoa
Female
Obesity
Asian descent
4) Clinical features of cholecystitis
include all of the following except:



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
A.
B.
C.
D.
E.
RUQ abdominal pain
Radiation to R upper back
Nausea, Vomiting
+ Murphy’s sign
Fever
5) A marker of acute hepatocyte injury
&/or hepatocyte death is:





A.
B.
C.
D.
E.
PT
ALT
Albumin
Direct bilirubin
Ammonia
Answers
All answers are B!!