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,
hemoglobinopathi
es, 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, newonset 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 2040 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

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
+Murphys 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, lowgrade 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:

A.
B.
C.
D.
E.

RUQ abdominal pain

Radiation to R upper back
Nausea, Vomiting
+ Murphys 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!!