Jaundice: Key Teaching Points

CHAPTER 8
Jaundice
KEY TEACHING POINTS

• B edside examination is accurate in four settings: diagnosing the etiology of
jaundice (i.e., hepatocellular disease versus obstructed biliary ducts), recog-
nizing cirrhosis, diagnosing hepatopulmonary syndrome, and diagnosing por-
topulmonary hypertension.
• In patients with jaundice, dilated abdominal veins, palmar erythema, spider
angiomas, and ascites all increase the probability of hepatocellular disease. A
palpable gallbladder increases the probability of extrahepatic obstruction.
• In patients with chronic liver disease, dilated abdominal veins, asterixis,
reduced body hair, gynecomastia, ascites, spider angiomas, jaundice, palmar
erythema, and a firm liver edge all increase the probability of cirrhosis.
• In patients with cirrhosis, clubbing and cyanosis increase the probability of
hepatopulmonary syndrome.
• In patients with cirrhosis, a loud P2, right ventricular heave, and blood
pressure of 140/90 or more increase the probability of portopulmonary
hypertension.
I. INTRODUCTION
Jaundice is an abnormal yellowish discoloration of the skin and mucous membranes
caused by accumulation of bile pigment. There are three forms: (1) hemolytic jaun-
dice (due to increased bilirubin production from excessive breakdown of red cells),
(2) hepatocellular jaundice (due to disease of the liver parenchyma, e.g., alcoholic
liver disease, drug-induced liver disease, viral hepatitis, or metastatic carcinoma),
and (3) obstructive jaundice (due to mechanical obstruction of the biliary ducts
outside the liver, e.g., choledocholithiasis or pancreatic carcinoma). In most pub-
lished series of jaundiced patients, hemolysis is uncommon, and the usual task of
the clinician at the bedside is to distinguish hepatocellular disease from obstructed
biliary ducts.1,2
II. THE FINDINGS

A. JAUNDICE
Jaundice is usually first noted in the eyes, but the traditional term for this finding
(scleral icterus) is actually a misnomer because pathologic studies reveal most of
the pigment to be deposited in the conjunctiva, not the avascular sclera.3 As jaun-
dice progresses and the serum bilirubin increases, the face, mucous membranes, and
eventually the entire skin acquire a yellow or orange hue.
59
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60 PART 3 GENERAL APPEARANCE OF THE PATIENT
Prominent yellowish subconjunctival fat may be mistaken for conjunctival jaun-

dice, but fat is usually limited to the conjunctival folds and, unlike jaundice, spares
the area near the cornea. Patients with carotenemia (from excess carrot or multivita-
min ingestion) also develop a yellowish discoloration of the skin, especially the palms,
soles, and nasolabial fold, but in contrast to jaundice, the conjunctiva are spared.4
B. ASSOCIATED FINDINGS
According to classic teachings, several findings distinguish hepatocellular disease
from obstructed biliary ducts.
1. HEPATOCELLULAR JAUNDICE
Characteristic findings are spider telangiectasia, palmar erythema, gynecomastia,
dilated abdominal wall veins, splenomegaly, asterixis, and fetor hepaticus.
A. SPIDER TELANGIECTASIA (SPIDER ANGIOMAS)

Spider telangiectasia are dilated cutaneous blood vessels with three components:
(1) a central arteriole (the “body” of the spider) that can be seen to pulsate when
compressed slightly with a glass slide; (2) multiple radiating “legs”; and (3) sur-
rounding erythema, which may encompass the entire lesion or only its central por-
tion.5 After blanching, the returning blood fills the central arteriole first before
traveling to the peripheral tips of each leg. Spiders are most numerous on the face
and neck, followed by the shoulders, thorax, arms, and hands. They are rare on
the palms, scalp, and below the umbilicus. This peculiar distribution may reflect
the neurohormonal properties of the microcirculation, because it is similar to the
distribution of where blushing is most intense.5
Acquired vascular spiders are associated with three clinical conditions: liver
disease, pregnancy, and malnutrition.6 In patients with liver disease, the spiders
advance and regress with disease severity,7 and their appearance correlates some-
what with an abnormally increased ratio of serum estradiol to testosterone levels.8
In pregnant women, spiders typically appear between the second and fifth months
and usually disappear within days after delivery.6 Vascular spiders also have been
described in normal persons, but these lesions, in contrast to those of liver disease,
are always small in number (with an average of three) and size.5
Vascular spiders were first described by the English physician Erasmus Wilson
in 1867.5
B. PALMAR ERYTHEMA
Palmar erythema is a symmetric reddening of the surfaces of the palms, most pro-
nounced over the hypothenar and thenar eminences.6 Palmar erythema occurs in
the same clinical conditions as vascular spiders, and the two lesions tend to come
and go together.6
C. GYNECOMASTIA AND DIMINISHED BODY HAIR

Many patients with liver disease have gynecomastia (defined as a palpable, discrete
button of firm subareolar breast tissue 2 or more cm in diameter) and diminished
pubic and body hair, both findings attributed to increased circulating estrogen-to-
testosterone levels.
D. DILATED ABDOMINAL VEINS

In some patients with cirrhosis, elevated portal venous pressures lead to the
development of collateral vessels from the portal venous to systemic venous
CHAPTER 8 Jaundice 61
systems. One group of such vessels surrounds the umbilicus, decompressing the
left portal vein via paraumbilical vessels into abdominal wall veins.9 Sometimes
these abdominal wall veins become so conspicuous they resemble a cluster of
serpents, thus explaining their common label caput medusae.10 Collateral vessels
may generate a continuous humming murmur heard during auscultation between
the xiphoid and umbilicus.11
Collateral abdominal vessels also may appear in patients with the superior vena
cava syndrome (if the obstruction also involves the azygous system)12 or inferior
vena cava syndrome.13 In these disorders, however, the vessels tend to appear on
the lateral abdominal wall. A traditional test to distinguish inferior vena cava
obstruction from portal hypertension is to strip abdominal wall veins below the
umbilicus and see which way blood is flowing. (In portal-systemic collaterals, blood
should flow away from the umbilicus toward the patient’s feet, whereas in inferior
vena cava collaterals, flow is reversed toward the head.) Even so, this test is unreli-
able because most dilated abdominal vessels lack competent valves, and the clini-
cian can “demonstrate” blood to flow in either direction in most patients with both
conditions.
E. PALPABLE SPLEEN
One of the principal causes of splenomegaly is portal hypertension from severe
hepatocellular disease.14 Therefore, a traditional teaching is that the finding of
splenomegaly in a jaundiced patient increases the probability of hepatocellular
disease.
F. ASTERIXIS
Originally described by Adams and Foley in 1949,15,16 asterixis is one of the earli-
est findings of hepatic encephalopathy and is thus a finding typical of hepatocel-
lular jaundice. To elicit the sign, the patient holds both arms outstretched with
fingers spread apart. After a short latent period, both fingers and hands commence
to “flap,” with abrupt movements occurring at irregular intervals of a fraction of a
second to seconds (thus earning the name liver flap). The fundamental problem in
asterixis is the inability to maintain a fixed posture (the word asterixis comes from
the Greek sterigma, meaning “to support”), and consequently asterixis can also be
demonstrated by having the patient elevate the leg and dorsiflex the foot, close
the eyelids forcibly, or protrude the tongue.15 Because some voluntary contraction
of the muscles is necessary to elicit asterixis, the sign disappears once coma ensues
(although some comatose patients exhibit the finding during the grasp reflex; see
Chapter 63).15
Electromyography reveals that asterixis represents the abrupt disappearance of
electrical activity in the muscle (i.e., negative myoclonus).17 Asterixis is not spe-
cific to liver disease but also appears in encephalopathy from other causes, such
as hypercapnia or uremia.18 Unilateral asterixis indicates structural disease in the
contralateral brain.19,20
G. FETOR HEPATICUS
Fetor hepaticus is the characteristic breath of patients with severe hepatic paren-
chymal disease, an odor likened to a mixture of rotten eggs and garlic. Gas chroma-
tography reveals that the principal compound causing the odor is dimethylsulfide.21
Fetor hepaticus correlates best with severe portal-systemic shunting, not encepha-
lopathy per se, because even alert patients with severe portal-systemic shunting
have the characteristic breath.22
2. OBSTRUCTIVE JAUNDICE: PALPABLE GALLBLADDER

(COURVOISIER SIGN)
The presence of a smooth, nontender, distended gallbladder in a patient with jaun-
dice is a traditional sign of obstructive jaundice. Courvoisier sign refers to the asso-
ciation of the palpable gallbladder and extrahepatic obstruction, a sign discussed
fully in Chapter 51.
III. CLINICAL SIGNIFICANCE

A. DETECTION OF JAUNDICE
Although many textbooks claim jaundice becomes evident once the serum biliru-
bin exceeds 2.5 to 3 mg/dL, clinical studies reveal that only 70% to 80% of observ-
ers detect jaundice at this threshold.23,24 The sensitivity of examination increases to
83% when bilirubin exceeds 10 mg/dL and 96% when it exceeds 15 mg/dL.
B. HEPATOCELLULAR VERSUS OBSTRUCTIVE JAUNDICE

Studies show that clinicians accurately distinguish hepatocellular from obstruc-
tive jaundice more than 80% of the time by just using bedside and basic laboratory
findings (i.e., before clinical imaging).25,26 In EBM Box 8.1, disease is arbitrarily
defined as hepatocellular disease: therefore, likelihood ratios (LRs) with large
positive values increase the probability of hepatocellular disease, whereas those
with values close to zero decrease it and thus increase probability for obstructive
disease.
These studies show that in patients presenting with jaundice, the physical signs
of portal hypertension (dilated abdominal veins, LR = 17.5; ascites, LR = 4.4; and
palpable spleen, LR = 2.9), palmar erythema (LR = 9.8), and spider angiomas (LR
= 4.7) all increase the probability of hepatocellular jaundice. The only finding argu-
ing strongly against hepatocellular jaundice is the palpable gallbladder (LR = 0.04;
in other words, the finding of a palpable gallbladder argues for obstructed bile ducts
with an LR of 26, the inverse of 0.04).
Weight loss does not help discriminate between hepatocellular and obstructive
etiologies. Other unhelpful signs are liver tenderness and a palpable liver. The pal-
pable liver remains unhelpful even when defined as a liver edge extending more
than four to five fingerbreadths below the right costal margin.25
C. DIAGNOSIS OF CIRRHOSIS
The diagnosis of cirrhosis in patients with liver disease has important prognos-
tic and therapeutic implications. EBM Box 8.2 displays the diagnostic accuracy
of physical findings in detecting cirrhosis, determined from hundreds of patients
presenting with diverse chronic liver diseases. According to this EBM Box, the
findings increasing the probability of cirrhosis the most are dilated abdominal wall
veins (LR = 9.5), encephalopathy (irrational behavior, disordered consciousness,
or asterixis; LR = 8.8), reduced body or pubic hair (LR = 8.8), gynecomastia (LR
= 7), ascites (LR = 6.6), spider angiomas (LR = 4.2), jaundice (LR = 3.8), palmar
erythema (LR = 3.7), a liver edge that is firm to palpation (LR = 3.3), and periph-
eral edema (LR = 3). Other helpful findings (though less compelling ones) are a
palpable liver in the epigastrium (LR = 2.7) and splenomegaly (LR = 2.5). The only
findings decreasing the probability of cirrhosis in these patients are the absence of
a palpable liver in the epigastrium (LR = 0.3) and the absence of a firm liver edge
(LR = 0.4).
EBM BOX 8.1

Diagnosing Hepatocellular Disease in Patients With
Jaundice*
Likelihood Ratio‡ if
Finding Is
Finding Sensitivity Specificity
(Reference)† (%) (%) Present Absent
General Appearance
Weight loss25,27 10-49 21-97 NS NS
Skin
Spider angiomas25,27 35-47 88-97 4.7 0.6
Palmar erythema25 49 95 9.8 0.5
Dilated abdominal 42 98 17.5 0.6
veins25
Abdomen
Ascites25 44 90 4.4 0.6
Palpable spleen25,27 29-47 83-90 2.9 0.7
Palpable gallblad- 0† 69 0.04 1.4
der25
Palpable liver25,27 71-83 15-17 NS NS
Liver tenderness25,27 37-38 70-78 NS NS
*Diagnostic standard: for nonobstructive (vs. obstructive) jaundice, needle biopsy of liver, surgical
exploration, or autopsy.
†None of the 41 patients with medical jaundice in this study had a palpable gallbladder; for
calculation of the LRs, 0.5 was added to all cells of the 2 × 2 table.
‡Likelihood ratio (LR) if finding present = positive LR; LR if finding absent = negative LR.
NS, Not significant.

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HEPATOCELLULAR JAUNDICE
Probability
Decrease Increase
–45% –30% –15% +15% +30% +45%
LRs 0.1 0.2 0.5 1 2 5 10 LRs
Palpable gallbladder Dilated abdominal veins

Palmar erythema
Spider angiomata
Ascites
Palpable spleen
EBM BOX 8.2
Diagnosing Cirrhosis in Patients With Chronic Liver
Disease*
Likelihood Ratio‡
if Finding Is
(Reference)† (%) (%) Present Absent
Skin
Spider angiomas28-39 33-84 48-98 4.2 0.5
Palmar erythe- 12-70 49-98 3.7 0.6
ma29,31,32,34,37,39
Gynecomastia29,37 18-58 92-97 7.0 NS
Reduction of body or 24-51 94-97 8.8 NS
pubic hair29,37
Jaundice29,33,35,37,40 16-44 83-99 3.8 0.8
Dilated abdominal wall 9-51 79-100 9.5 NS
veins29,34,37
Abdomen
Hepatomegaly29,32-36,38,41 31-96 20-96 2.3 0.6
Palpable liver in 50-86 68-88 2.7 0.3
epigastrium35,38
Liver edge firm to 71-78 71-90 3.3 0.4
palpation32,39,41
Splenomegaly28,30-36,38,40,41 5-85 35-100 2.5 0.8
Ascites28,29,31,33-35,40 14-52 82-99 6.6 0.8
Other
Peripheral edema29,33,34 24-56 87-92 3.0 0.7
Encephalopathy28,29,31 9-29 98-99 8.8 NS
*Diagnostic standard: For cirrhosis, needle biopsy of liver.
†Definition of findings: For hepatomegaly and splenomegaly, examining clinician’s impression using
palpation, percussion, or both; for encephalopathy, disordered consciousness and asterixis.15

‡Likelihood ratio (LR) if finding present = positive LR; LR if finding absent = negative LR.
CIRRHOSIS
Probability
Decrease Increase
–45% –30% –15% +15% +30% +45%
LRs 0.1 0.2 0.5 1 2 5 10 LRs
Liver not palpable in Dilated abdominal wall

epigastrium veins
Liver edge not firm to palpation Encephalopathy
Diminished body or pubic hair
Gynecomastia
Ascites
Spider angiomata, jaundice, or
palmar erythema
D. DETECTING LARGE GASTROESOPHAGEAL VARICES IN

PATIENTS WITH CIRRHOSIS
In studies of more than 750 patients with cirrhosis who have not had prior gas-
trointestinal bleeding, no physical finding reliably predicts which patients have
significant gastroesophageal varices (as detected by endoscopy). For all findings—
caput medusae, spider angiomas, jaundice, hepatomegaly, splenomegaly, or hepatic
encephalopathy—the LRs are 1.5 or less or not significant.42-46
E. DETECTING HEPATOPULMONARY SYNDROME

Hepatopulmonary syndrome is a serious complication of cirrhosis, causing intrapul-
monary vascular shunting and significant hypoxemia. In eight studies of over 550
patients with cirrhosis, most of them awaiting liver transplantation, the findings of
finger clubbing (LR = 4) and cyanosis (LR = 3.6) increased the probability of hepa-
topulmonary syndrome (EBM Box 8.3). The Child prognostic score (for chronic
liver disease)* is also useful: Child class C increases the probability of hepatopulmo-
nary syndrome (LR = 3.1), whereas Child class A or B decreases it (LR = 0.4).51,52
F. DETECTING PORTOPULMONARY HYPERTENSION

Some patients with end-stage liver disease develop pulmonary hypertension, a sig-
nificant complication because it greatly increases the surgical risk of liver transplan-
tation. In one study of 80 consecutive liver transplant candidates, three physical
findings accurately detected pulmonary hypertension (mean pulmonary artery pres-
sure of 25 mm Hg or higher): a loud P2 (pulmonary component of the second heart
sound, EBM Box 8.3; LR = 17.6), right ventricular heave (LR = 8.8), and systemic
hypertension (blood pressure 140/90 or higher, LR = 7.3).54 At first glance, the
association between systemic and pulmonary hypertension may be unexpected, but
most patients with end-stage liver disease actually have a normal or low blood pres-
sure from systemic vasodilation, suggesting that the association between pulmonary
and systemic hypertension represents a generalized abnormality of vascular tone.
The presence of oxygen desaturation, elevated neck veins, ascites, and edema
does not affect the probability of pulmonary hypertension in these patients (EBM
Box 8.4).
The references for this chapter can be found on www.expertconsult.com.
* The Child score (or Child-Pugh score) predicts the prognosis of patients with chronic liver
disease by addressing five clinical variables (bilirubin, albumin, prothrombin time, ascites,
and hepatic encephalopathy) and scoring each 1 to 3 based on levels of abnormality. The
combined score distinguishes Child classes A (best prognosis), B, and C (worst prognosis).
EBM BOX 8.3

Diagnosing Hepatopulmonary Syndrome in Patients
With Chronic Liver Disease*
Likelihood Ratio†
if Finding Is
(Reference) (%) (%) Present Absent
Clubbing47-52 22-80 64-95 4.0 0.5
Cyanosis47,48,52 8-86 78-99 3.6 NS
Palmar ery 57-80 54-70 NS NS
thema47,53
Spider angioma47-53 39-97 26-87 1.6 0.5
Ascites49-51 55-94 20-57 NS NS
*Diagnostic standard: For hepatopulmonary syndrome, all three of the following criteria were
present: (1) cirrhosis, (2) contrast echocardiography revealing intrapulmonary right → shunting,
and (3) hypoxemia, variably defined as arterial pO2 <70 mm Hg,53 or <80 mm Hg,47,51 alveolar-
arterial pO2 gradient ≥15 mm Hg50,52 or >20 mm Hg,48 or either pO2 <70 mm Hg or AapO2
>20 mm Hg.49
†Likelihood ratio (LR) if finding present = positive LR; LR if finding absent = negative LR.

HEPATOPULMONARY SYNDROME
Probability
Decrease Increase
–45% –30% –15% +15% +30% +45%
LRs 0.1 0.2 0.5 1 2 5 10 LRs
Clubbing
Cyanosis
EBM BOX 8.4

Diagnosing Pulmonary Hypertension in Patients With
Cirrhosis*
Likelihood Ratio† if
Finding Is
Sensitivity Specificity
Finding54 (%) (%) Present Absent
Vital Signs
Blood pressure 63 91 7.3 NS
≥140/90
Oxygen saturation 25 89 NS NS
<92%
Heart Examination
Elevated neck 13 94 NS NS
veins
Right ventricular 38 96 8.8 NS
heave
Loud P2 38 98 17.6 NS
Other
Ascites, edema, or 75 36 NS NS
both
*Diagnostic standard: For pulmonary hypertension, measured mean pulmonary artery pressure ≥25
mm Hg.
†Likelihood ratio (LR) if finding present = positive LR; LR if finding absent = negative LR.

PORTOPULMONARY HYPERTENSION
Probability
Decrease Increase
–45% –30% –15% +15% +30% +45%
LRs 0.1 0.2 0.5 1 2 5 10 LRs
Loud P2
Right ventricular heave
Blood pressure 140/90 or higher
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Jaundice: Key Teaching Points

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Jaundice: Key Teaching Points

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CHAPTER 8

KEY TEACHING POINTS

II. THE FINDINGS

Prominent yellowish subconjunctival fat may be mistaken for conjunctival jaun-

A. SPIDER TELANGIECTASIA (SPIDER ANGIOMAS)

C. GYNECOMASTIA AND DIMINISHED BODY HAIR

D. DILATED ABDOMINAL VEINS

2. OBSTRUCTIVE JAUNDICE: PALPABLE GALLBLADDER

III. CLINICAL SIGNIFICANCE

B. HEPATOCELLULAR VERSUS OBSTRUCTIVE JAUNDICE

EBM BOX 8.1

NS, Not significant.

Palpable gallbladder Dilated abdominal veins

palpation, percussion, or both; for encephalopathy, disordered consciousness and asterixis.15

Liver not palpable in Dilated abdominal wall

D. DETECTING LARGE GASTROESOPHAGEAL VARICES IN

E. DETECTING HEPATOPULMONARY SYNDROME

F. DETECTING PORTOPULMONARY HYPERTENSION

The references for this chapter can be found on www.expertconsult.com.

EBM BOX 8.3

NS, Not significant.

EBM BOX 8.4

NS, Not significant.

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