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TABLE 9.7.1 Common Causes of Gastrointestinal Bleeding and Diagnostic
Clues
Cause Diagnostic clue
Peptic ulcer (55%) Nonsteroidal anti-inflammatory drug use, Helicobacter pylori
infection, stress
Esophagogastric varices (14%) Ethanol use, umbilical or rectal varices, palmar erythema,
ascites, spider hemangiomas
Arteriovenous malformations (6%) History of previous episodes
Mallory-Weiss tears (5%) Vomiting prior to hematemesis, ethanol use, occurs in
young men
Tumors (4%) Ethanol use, smoking, smoked foods, gastroesophageal
reflux disease, Barrett’s esophagus, weight loss
From Jutabha RJ, Jensen DM. Approach to the patient with upper gastrointestinal bleeding.
UpToDate June 2005.
II. PATHOPHYSIOLOGY. Bleeding from the upper GI tract usually results when disruption
occurs between the protective barriers to the vasculature and the harsh environment of the
digestive tract. The most common causes (as percentages) are listed in Table 9.7.1.
III. EVALUATION. The key to successful evaluation and diagnosis is a systematic approach with
emphasis on the overall hemodynamic status of the patient (see Figure 9.7.1).
A. History. Clinical history accurately points to the source of bleeding in only 40% of cases
(3). Hematemesis and melena are the most common presentations of acute upper GI bleed-
ing. Other historical features include abdominal pain, coffee-ground emesis, dysphagia,
black tarry stools, bright red blood per rectum, hematemesis, or chest pain. It is important
to ask about a prior history of bleeding as 60% rebleed from the same site (3). History of
other comorbid diseases (peptic ulcer disease, pancreatitis, cirrhosis, and cancer) may point
to an etiology as well as a review of medication use (i.e., clopidogrel, coumadin, nonsteroidal
anti-inflammatory drugs, aspirin, SSRIs, or corticosteroids) (1). A history of alcohol or drug
use is also improtant to elucidate. Particular attention must be given to the patient’s cardio-
pulmonary status because this affects urgency and degree of resuscitative efforts. Table 9.7.1
lists other diagnostic clues to common causes, and Table 9.7.2 lists the less common causes.
B. Physical Examination
1. Vital Signs. The single most important aspect of the initial physical examination is
determining the patient’s hemodynamic stability. Unstable patients should be managed
as trauma patients. A nasogastric (NG) tube is often placed at presentation to help con-
firm the diagnosis. After ensuring hemodynamic stability, the initial physical examina-
tion should eliminate a nasal or oropharyngeal source of bleeding.
2. Skin Examination. Ecchymoses, petechiae, and varices should be noted. Conjunctival
pallor is a sign of chronic anemia. Numerous mucosal telangiectasias can point to an
underlying vascular abnormality.
3. Abdominal Examination. Look for stigmata of chronic liver disease (hepatospleno-
megaly, spider angiomata, ascites, palmar erythema, caput medusae, gynecomastia, and
testicular atrophy).
4. Rectal Examination. Rectal varices, hemorrhoids, and fissures should be noted and
hemeoccult testing done.
C. Testing. Basic laboratory studies should include a complete blood count (CBC), with
particular attention to the hematocrit, coagulation studies (prothrombin time [PT]) and
partial thromboplastin time [PTT]), liver function tests (LFTs), serum chemistries (blood
urea nitrogen is elevated disproportionate to creatinine in patients with GI blood loss),
198
Taylor’s DifferenTial Diagnosis Manual
Initial Clinical
Assessment
(Vital Signs and
Orthostatics)
Resuscitation and
Stabilization
Risk Assessment
(Amount of Bleed and
Patient‘s Comorbid
Conditions)
High Low
Suspected Upper
Gastrointestinal Bleeding
(Hematemesis, Melena)
Admit to Intensive Care
Unit, Urgent Endoscopy
Admit to Ward or Hold
in Emergency
Department
Endoscopic Evaluation for
Source of Bleeding and
Treatment
Figure 9.7.1. Approach to upper gastrointestinal bleeding. (Modified from Eisen GM, Dominitz JA,
Faigel DO. An annotated algorithmic approach to upper gastrointestinal bleeding. Gastrointest Endosc
2001;53:853–858.) (2)
TABLE 9.7.2 Uncommon Causes of Upper Gastrointestinal Bleeding
Cause Diagnostic clue
Dieulafoy’s lesion Congenital lesion usually diagnosed during endoscopy
Gastric antral vascular
ectasia
Associated with cirrhosis and elderly women
Hemobilia Usually associated with recent biliary tree injury
Aortoenteric fistulas Primary cases associated with AAA, secondary cases with fistulas
from AAA repairs; may present with back pain and fever
AAA, abdominal aortic aneurysm.
From Jutabha RJ, Jensen DM. Approach to the patient with upper gastrointestinal bleeding.
UpToDate June 2005 (4).
Chapter 9 • Gastrointestinal Problems
199
electrocardiogram (ECG), and NG aspirate analysis. Initially, the hematocrit is a poor indica-
tor of blood loss; however, serial hematocrits can be useful in assessing ongoing blood loss. The
CBC indices, particularly an elevated red cell distribution width and low mean corpuscular
volume, point toward a chronic bleed. A prolonged PT or PTT suggests an underlying coagu-
lopathy. Elevated LFTs suggest underlying liver disease. An ECG is important, especially in
elderly patients, to search for evidence of cardiac ischemia. If the aspirate is bright red, or “cof-
fee ground” in appearance, an upper GI source of bleeding is likely. Additionally, NG lavage
removes blood and helps with the performance of endoscopy. In cases in which no source can
be identified, lower endoscopy should be considered in the search for a lower GI bleed.
IV. DIAGNOSIS. The differential diagnosis of an upper GI bleed should include bleeding from the
upper airways or pharynx that is swallowed and regurgitated and lower GI bleeding that may
be manifested as melanic stools due to delay in transit through the colon. Endoscopy is typi-
cally preformed within 24 hours (1). In most cases, diagnosis can be confirmed and the source
localized and treated. In rare cases in which upper endoscopy is unable to adequately identify
the source of GI bleeding, specialized nuclear medicine and angiographic studies can be used.
Colonoscopy would also be considered.
REFERENCES
1. Wilkins T, Khan N, Nabh A, Schade R. Diagnosis and management of upper gastrointestinal bleeding.
Am Fam Phys 2012;469–476.
2. Eisen GM, Dominitz JA, Faigel DO. An annotated algorithmic approach to upper gastrointestinal
bleeding. Gastrointest Endosc 2001;53:853–858.
3. McGuirk TD, Coyle WJ. Upper gastrointestinal tract bleeding. Emerg Med Clin North Am 1996;14:523–545.
4. Laine L. Acute and chronic gastrointestinal bleeding. In: Feldman M, Sleisinger MH, Scharschmidt
BF, eds. Gastrointestinal and liver disease: pathophysiology, diagnosis, and management. Philadelphia, PA:
WB Saunders, 1998:198–218.
9.8
I. BACKGROUND. Hepatitis involves inflammation of the liver resulting from infectious or non-
infectious causes. Among infections, viral hepatitis accounts for 50% of acute hepatitis in the
United States but bacterial, fungal, and parasitic etiology can also be responsible.
II. PATHOPHYSIOLOGY. Hepatitis involves hepatocellular injury and subsequent necrosis.
Injury can be acute or chronic. Progressive damage of liver parenchyma causes fibrosis, which
eventually causes cirrhosis and portal hypertension with loss of hepatic function. Once 80–90%
of hepatic function is affected, liver failure ensues with a mortality of 70–95%.
A. Etiology. Multiple viruses can cause hepatitis. Hepatitis A is most common for acute hepa-
titis and hepatitis B (HBV) and hepatitis C mostly result in chronic infection. Hepatitis D
virus can occur as coinfection or superinfection in persons with established HBV infection
especially in intravenous drug users. Hepatitis E is mostly seen in endemic areas in under-
developed nations. Clinically, it presents similar to hepatitis A. During pregnancy, hepatitis
E infection can lead to fulminant hepatic failure.
1. Drug-induced liver injury (DILI) is the most common cause for liver transplantation.
The exposure could be acute or chronic. Most common drug culprit is acetaminophen.
Other offenders are antibiotics (augmentin is most common), medications for central
nervous system, musculoskeletal, and gastrointestinal system. Antiretroviral agents (espe-
cially protease inhibitors) and lipid lowering agents are other offenders. Alcohol causes
hepatitis either due to its direct long-term effect or due to its effect on the metabolism
of other drugs. Few herbal and dietary supplements can also be responsible for DILI.
Hepatitis
Manoj Kumar and Milton (Pete) Johnson
200
Taylor’s DifferenTial Diagnosis Manual
2. Fatty liver disease aka hepatic steatosis involves lipid droplets accumulation within
hepatocytes. In alcoholics, it leads to alcoholic hepatitis and finally to alcoholic cirrhosis.
Nonalcoholic fatty liver disease results from insulin resistance. It follows a spectrum of
disease from hepatic steatosis to nonalcoholic steatohepatitis and eventually leads to cir-
rhosis and even liver failure.
3. Autoimmune hepatitis is four times more common in females. α1-antitrypsin (A1AT)
deficiency disease affects the lung as well as liver. Unlike lungs, in liver, A1AT accumu-
lates within the hepatocytes due to a failure in its export into the circulation and causes
hepatitis. Hereditary hemochromatosis (HFE gene on chromosome 6) is characterized
by excess iron deposition in the liver and several other organs. Hepatic iron overload
can also occur due to excess iron supplement, multiple frequent transfusions, or hema-
topoietic disorders. Wilson’s disease (ATP7B gene, on chromosome 13) involves defect
of intrahepatic copper metabolism resulting in excess copper deposition in the liver and
other organs. These patients have normal copper absorption from proximal bowel, but
their capability of biliary copper excretion is severely decreased leading to its accumula-
tion in the hepatocytes which causes hepatitis due to free radical injury. Deficiency of
ceruloplasmin is not a cause of Wilson’s disease. Ischemia in the presence of hypovolemic
shock or hypoxemia can also cause hepatitis.
B. Epidemiology. In 2009, a total of 1,987 acute symptomatic cases of hepatitis A, 3,371 of
hepatitis B, and 781 cases of hepatitis C were reported in the United States (1). An incidence
rate of 0.6 (lowest ever) cases per 100,000 population of hepatitis A, 0.1–4.6 for hepatitis
B, and 0.3 for hepatitis C was recorded (2, 3). There are approximately 800,00–1.4 million
people living with chronic hepatitis B and 2.7–3.9 million with chronic hepatitis C. About
5% of all acute cases of hepatitis B and 60–85% of hepatitis C develop into chronic infec-
tion. Many cases present just with asymptomatic elevations in their liver-associated enzymes.
Fatty liver disease is considered the most common cause of mild liver-associated enzyme
elevation mostly seen in obese patients.
III. EVALUATION
A. History.
Risk factors should be identified while obtaining the history from hepatitis
patients. If acute hepatitis is suspected, the history of recent drug intake as well as risk fac-
tors for viral hepatitis should be obtained. History of alcohol is very important in any form
of liver injury including hepatitis. History of travel to endemic areas, ingestion of shell fish,
children in day care centers, and institutionalization are other important components espe-
cially if hepatitis A is suspected. History of sexual promiscuity, intravenous drug use, blood
transfusions should be elicited if hepatitis B or C is suspected. History containing exposures
to hepatotoxins and family history of A1AT deficiency, hereditary hemochromatosis, or
Wilson’s disease are other useful components while obtaining history (4, 5).
B. Physical Examination. Physical examination helps in identifying the severity and some-
times the cause of hepatitis. Low-grade fevers, jaundice, and signs of dehydration are some
of the common features of acute hepatitis. Liver can be diffusely enlarged, firm, and tender
with a smooth edge. Nodules or mass-like appearance can also be encountered. In early
chronic hepatitis, the liver may or may not be tender and other constitutional signs may be
masked. During advanced chronic disease, new signs may appear. Liver can be hard, nodular
along with the signs of liver failure (e.g., alopecia, palmar erythema, gynecomastia, testicular
atrophy, and spider angioma). Ascites can be seen in patients who have portal hypertension
secondary to cirrhosis. Signs of iron overload like hyperpigmentation in hereditary hemochro-
matosis and Kayser-Fleischer ring encircling the iris in Wilson’s disease are important findings.
C. Testing
1. While ordering the lab test, the clinician should be mindful of various causes of hepatitis.
Most of the time the basic labs ( serum alanine and aspartate aminotransferases, alkaline
phosphatase, γ-glutamyl transpeptidase, serum albumin, bilirubin levels) provide great
information about the severity and possible mechanism of the liver injury. Tables 9.8.1
and 9.8.2 show commonly used tests and their clinical significance. Specific tests (e.g.,
serum antigen, antibody test, iron studies, quantitative tissue copper analysis) are used
to identify the type of viral hepatitis as well as other causes of hepatitis.
Chapter 9 • Gastrointestinal Problems
201
TABLE 9.8.2 Diagnostic Tests for Suspected Hepatitis
Hepatitis A Anti-HAV IgM
Hepatitis B Hepatitis B surface antigen, antihepatitis B core IgM
Hepatitis C
Non alcoholic fatty liver
disease (NAFLD)
Anti-HCV antibody (ELISA or RIBA), HCV RNA
Ultrasound of liver, liver biopsy
Alcoholic liver disease Liver biopsy, improvement with alcohol abstinence
A1AT deficiency Serum A1AT activity, A1AT phenotyping or genotyping, liver biopsy
Autoimmune hepatitis First exclude other causes of hepatitis, antinuclear, antismooth muscle,
liver–kidney microsomal antibodies, soluble liver antigen antibody, IgG,
liver biopsy
Iron overload Serum ferritin and transferrin saturation, HFE gene test, liver biopsy
Wilson’s disease Serum ceruloplasmin, 24-h urine copper, slit lamp examination for Kayser
Fleisher rings, liver biopsy, and quantitative tissue copper analysis
A1AT, α
1
-antitrypsin; ELISA, enzyme-linked immunosorbent assay; HAV, hepatitis A virus; HCV,
hepatitis C virus; Ig, immunoglobulin; RIBA, recombinant immunoblot assay.
From Goldman L, Ausiello D, eds. Cecil textbook of medicine, 22nd ed. Philadelphia, PA: Saunders,
2003; Green RM, Flamm S. AGA technical review on the evaluation of liver chemistry tests.
Gastroenterology 2002;123:1367–1384. http://www2.us.elsevierhealth.com/inst/serve?action=
searchDB&searchDBfor=art&artType=abs&id=agast 1231367&nav=abs&special=hilite&query=
[all_fields](liver+chemistry+tests,).
TABLE 9.8.1 Common Laboratory Tests for Evaluating Liver Disease
Test Implication Notes
ALT and AST Hepatocellular injury
or necrosis
ALT is more specific than AST for liver injury;
AST/ALT ≥ 2 in alcoholic liver disease.
Improvement in ALT level (longer half-life)
lags behind AST
Bilirubin (conjugated/
unconjugated)
Hepatobiliary disease Conjugated hyperbilirubinemia patients have
dark urine (hyperbilirubinuria) and light
colored stool
GGT Hepatobiliary disease Increased by alcohol ingestion or medications;
used to confirm hepatic origin of alkaline
phosphatase
Alkaline phosphatase Cholestatic disease Not liver specific (also in placenta and bone);
used to rule out cholestasis
Prothrombin time
and albumin
Marker of hepatic
synthesis function
Short-term and long-term indicators; not
specific
ALT, alanine aminotransferase; AST, aspartate aminotransferase; GGT, γ-glutamyl transpeptidase.
From Goldman L, Ausiello D, eds. Cecil textbook of medicine, 22nd ed. Philadelphia, PA: Saunders,
2003; Green RM, Flamm S. AGA technical review on the evaluation of liver chemistry tests.
Gastroenterology 2002;123:1367–1384. http://www2.us.elsevierhealth.com/inst/serve?action=
searchDB&searchDBfor=art&artType=abs&id=agast 1231367&nav=abs&special=hilite&query=
[all_fields](liver+chemistry+tests,).
202
Taylor’s DifferenTial Diagnosis Manual
TABLE 9.8.3 Differential Diagnosis of Hepatitis
Biliary tract obstruction Conditions such as choledocholithiasis, neoplasm, pancreatitis, primary
sclerosis cholangitis
SURGICAL CAUSES MUST BE EXCLUDED EARLY
Liver infiltration Granulomatous liver disease: immunologic and hypersensitivity disorders;
fungal, mycobacterial, parasitic, other infections; inflammatory bowel
disease; lymphoma; primary biliary cirrhosis; drug, foreign body, toxic
reactions; rheumatic diseases; sarcoidosis; infiltrating malignancy
Other infections Bacterial: ehrlichiosis, gonococcal perihepatitis, Legionnaires’ disease, lep-
tospirosis, listeriosis, Lyme disease, pyogenic abscess, Q-fever, Rocky
Mountain spotted fever, salmonellosis, secondary syphilis, tularemia
Fungal: candidiasis
Parasitic: amebic abscess, babesiasis, malaria, toxoplasmosis
Viral: adenovirus, cytomegalovirus, Epstein-Barr virus, herpes simplex
virus
Pregnancy Acute fatty liver of pregnancy, HELLP syndrome, hyperemesis
gravidarum
HELLP, hemolysis, elevated liver enzymes, and low platelet count.
From Goldman L, Ausiello D, eds. Cecil textbook of medicine, 22nd ed. Philadelphia, PA: Saunders,
2003; Green RM, Flamm S. AGA technical review on the evaluation of liver chemistry tests.
Gastroenterology 2002;123:1367–1384. http://www2.us.elsevierhealth.com/inst/serve?action=
searchDB&searchDBfor=art&artType=abs&id=agast 1231367&nav=abs&special=hilite&query=
[all_fields](liver+chemistry+tests,).
2. Ultrasound and computed tomography scan of biliary tract and liver is helpful in biliary
tract obstruction or fatty liver disease. Genetic testing is done in hereditary hemochro-
matosis, Wilson’s disease, or A1AT deficiency. Liver biopsy plays an important role in
diagnostic confirmation as well as to evaluate the severity of the disease.
IV. DIAGNOSIS
A. Differential Diagnosis.
Table 9.8.3 represents the differential diagnosis of hepatitis.
B. Clinical Manifestations
1. Acute Hepatitis. It may manifest as completely asymptomatic (like in hepatitis C)
or with symptoms such as flu-like illness, lethargy, jaundice, fever, nausea, vomiting,
anorexia, etc., as in acute hepatitis A or B. Approximately 1% cases of acute hepatitis
A or B may develop into fulminant hepatic failure. Acute hepatitis C as the cause of
fulminant failure remains controversial. The acute viral hepatitis follows a classic pattern
of four phases, which is described in Table 9.8.4.
2. Chronic Hepatitis. Hepatitis with a sustained elevation in aminotransferases (>3
months) is described as chronic hepatitis. The symptoms of chronic hepatitis are either
mild or may be absent. They can present with nonspecific signs of fatigue, weight loss,
insomnia, and malaise. In advanced stages, patients may present with upper or lower GI
bleeding due to variceal bleed. Endocrinologic abnormalities like hypogonadism, hypo-
thyroidism (in hereditary hemochromatosis), and arthropathies can also be encountered.
In very advanced cases, patients can show signs of encephalopathy, ascites, and anasarca
(due to liver function abnormality). Generalized bleeding can also occur due to throm-
bocytopenia secondary to hypersplenism from portal hypertension or coagulopathic liver
disease. Since prognosis is poor in advanced liver disease secondary to chronic hepatitis,
serial clinical and laboratory checkups and follow-ups play a crucial role in the manage-
ment of patients once they get diagnosed with hepatitis (4).
Chapter 9 • Gastrointestinal Problems
203
9.9
Hepatomegaly
Zoilo O. Lansang and John C. Huscher
I. BACKGROUND. Hepatomegaly is a physical finding associated with hepatobiliary disease. It is
not specific or sensitive to one cause and defining it can be enigmatic because of the highly vari-
able liver size that makes establishment of what constitutes normal somewhat difficult. The nor-
mal adult liver has a midclavicular range of 8–12 cm for men and 6–10 cm for women, with most
studies defining hepatomegaly as a liver span greater than 15 cm in the midclavicular line (1).
II. PATHOPHYSIOLOGY
A. Etiology.
Liver enlargement can have multiple pathophysiologic pathways. Enlargement
occurs in the early hepatic inflammatory response to viral pathogens, toxic substances, and
other stimulants and is then followed by scarring and shrinking in chronic conditions.
Fatty infiltration causes enlargement in obesity and metabolic syndrome. Vascular conges-
tion results in liver swelling in acute and chronic heart diseases as well as in conditions of
decreased vascular outflow. Focally enlarging lesions such as vascular cysts, infectious cysts,
and cancerous growths also occur. Abnormal deposition of amyloid, lipids, or iron can also
result in liver enlargement. Common causes are listed in Table 9.9.1.
TABLE 9.8.4 Phases of “Classic” Acute Hepatitis
Phase Symptoms Findings Duration
Preicteric/
prodromal
Anorexia, nausea,
fatigue, malaise,
vague right upper
quadrant pain
Greater than tenfold
elevation of ALT
and AST
2 weeks after exposure till
appearance of jaundice
Icteric Worsening of preicteric
symptoms, dark
urine, jaundice
Jaundice, liver tender-
ness, hyperbilirubi-
nemia
Begins 1–2 weeks after
prodromal phase and
lasts 2–6 weeks
Convalescent/
recovery
Gradual resolution Gradual resolution 6–8 weeks after exposure
until full recovery of
liver function and injury
ALT, alanine aminotransferase; AST, aspartate aminotransferase.
From Goldman L, Ausiello D, eds. Cecil textbook of medicine, 22nd ed. Philadelphia, PA: Saunders,
2003.
REFERENCES
1. Surveillance Data for Acute Viral Hepatitis—United States, 2009, CDC. Accessed at http://www.cdc
.gov/hepatitis/Statistics/2009Surveillance/index.htm#
2. Recommendations for identification and public health management of persons with chronic hepatitis
B virus infection. MMWR 2008;57(No. RR-8).
3. Armstrong GL et al. The prevalence of hepatitis C virus infection in the United States, 1999 through
2002. Ann Int Med 2006;144:705–714.
4. Goldman L, Ausiello D, eds. Cecil textbook of medicine, 22nd ed. Philadelphia, PA: Saunders, 2003.
5. Mersy DJ. Recognition of alcohol and substance abuse. Am Fam Physician 2003;67:1529–1532.
Accessed at http://www.aafp.org/afp/20030401/1529.html
204
Taylor’s DifferenTial Diagnosis Manual
TABLE 9.9.1 Common Causes of Hepatomegaly
Infective
• Glandular fever (infectious mononucleosis) caused by the Epstein-Barr virus (EBV).
• Hepatitis (not all hepatitis viruses cause hepatomegaly)
• Liver abscess (pyogenic and amoebic abscess)
• Malaria
• Amoeba infections
• Hydatid cyst
• Leptospirosis
• Actinomycosis
Neoplastic
• Metastatic tumors (most common)
• Hemangiomas
• Hepatocellular carcinoma
• Myeloma
• Leukemia
• Lymphoma
• Carcinoma
Cirrhotic
• Portal
• Biliary
• Cardio
• Hemochromatosis
Metabolic
• Fatty infiltration
• Amyloidosis
• Gaucher’s disease
• Niemann Pick disease
• Von Gierke disease (glycogen storage disease type 1)
• Glycogen storage disease types III, VI and IX
Drugs and toxins
• Alcoholism
• Poisoning
Congenital
• Hemolytic anemia
• Riedel’s lobe is an extended, tongue-like, right lobe of the liver
• Polycystic disease
• Cori’s disease
Others
• Hunter syndrome
• Zellweger’s syndrome
(Continued)
Chapter 9 • Gastrointestinal Problems
205
TABLE 9.9.1 Common Causes of Hepatomegaly
• Carnitine palmitoyltransferase I deficiency
• Right ventricular failure
• Granulomatous: Sarcoidosis
• Glycogen storage disease type II
B. Epidemiology. The incidence of hepatomegaly has not been studied in any large popula-
tion group. However, a recent summary article of multiple studies found that a palpable liver
margin had a likelihood ratio of 2.5 (confidence interval [CI], 2.2–2.8) for hepatomegaly
and a nonpalpable liver margin had a negative likelihood ratio of 0.45 (CI, 0.38–0.52) (2).
III. EVALUATION
A. History
1. Risk Factors. See Table 9.9.2
2. Symptoms associated with liver disease. See Table 9.9.3
B. Physical Examination. Examination of the liver is difficult given its irregular shape and
its location within the abdomen.
1. It is typical to use one of the two directions for palpation of the right upper quadrant: pal-
pate from below using the fingertips to palpate superiorly or from above with the finger-
tips hooked over the lower rib. Either method is facilitated by the patient’s deep inspira-
tion. Palpation must include the midline to identify an enlarged left lobe of the liver. On
palpation, note the liver position, the extent of its palpation below the costal margin, and
its texture and consistency. Palpate for the lower edge and percuss for the upper margin.
These two points give the highest accuracy in estimating liver size (3). If the margin is not
palpated but hepatomegaly is suspected, attempt direct percussion of both margins. The
“scratch method” (gently stoking or scratching the skin surface in a parallel plane while
listening with the stethoscope for change in sound and intensity of frequency) has been
used to identify margins; however, a recent study comparing ultrasound to the results of
the scratch test found that this test was unreliable and inaccurate (4).
2. Auscultation of the right upper quadrant has poor clinical utility. Other physical exami-
nation findings consistent with liver disease include jaundice, vascular spiders, palmar
erythema, gynecomastia, ascites, splenomegaly, testicular atrophy, peripheral edema,
Dupuytren’s contracture, parotid enlargement, and encephalopathy. Although none of
these physical examination signs are pathognomonic for hepatobiliary disease, their pres-
ence prompts further diagnostic tests for hepatic disease.
C. Testing. Diagnostic tests should include computed tomography (CT) scan of the right
upper quadrant and initial laboratory tests (complete blood count, serum blood tests
[CHEM-7]), liver enzyme tests (aspartate aminotransferase, alanine aminotransferase,
γ-glutamyl transpeptidase, and alkaline phosphatase), and true liver function tests (albumin,
prothrombin time, partial thromboplastin time, and bilirubin). If liver enzymes are elevated,
TABLE 9.9.2 Risk Factors for Liver Disease
Acupuncture Alcoholism Bisexuality
Blood product transfusion Dietary supplements Family history of liver disease
Gallstones Gastrointestinal bleeding Irritable bowel disease
Sexually transmitted disease Male homosexuality International travel
Tattoos
(Continued)
206
Taylor’s DifferenTial Diagnosis Manual
TABLE 9.9.3 Symptoms of Liver Disease
Abdominal pain Pruritus Nausea Loss of appetite
Confusion Arthralgias Rashes Night sweats
Fatigue Diarrhea Chills Sleep disturbance
Gastric bleeding Fever Easy bruisability Vomiting
Myalgia Heavy menses Frequent epistaxis
proceed with hepatitis serology. Ultrasound can be used when CT scan is contraindicated
or not available. Further testing used to elucidate the differential diagnosis is listed in
Table 9.9.4.
IV. DIAGNOSIS
A. Differential Diagnosis.
This can be approached on the basis of the findings of the physi-
cal examination.
1. Smooth nontender liver. Suspect fatty infiltration, congestive heart failure (CHF), portal
cirrhosis, lymphoma, portal obstruction, hepatic vein thrombosis, lymphocystic leuke-
mia, amyloidosis, schistosomiasis, or kala-azar.
2. Smooth tender liver. Suspect early CHF, acute hepatitis, amoebic abscess, or hepatic
abscess.
3. Nodular liver. Suspect late portal cirrhosis, tertiary syphilis, hydatid cyst, or metastatic
carcinoma.
4. Very hard nodular liver. This nearly always indicates metastatic carcinoma.
B. Clinical Manifestations. The clinical manifestations of hepatomegaly, although some-
what ill defined, should prompt a thorough evaluation and workup. Appropriate diagnostic
tests generally provide a quick and accurate diagnosis. New therapies for chronic liver
diseases make early diagnosis critical for obtaining good results.
REFERENCES
1. Unal B, Bilgili Y, Kocacikli E, et al. Simple evaluation of liver size on erect abdominal plain
radiography. Clin Radiol 2004;59:1132–1135.
2. Seupaul RA, Collins R. Physical examination of the liver. Ann Emerg Med 2005;45:553–555.
3. Naylor CD. Physical examination of the liver. JAMA 1994;27:1859–1865.
4. Tucker WN, Saab S, Leland SR, et al. The scratch test is unreliable for determining the liver edge.
J Clin Gastroenterol 1997;25:410–414.
TABLE 9.9.4 Specific Tests to Evaluate hepatomegaly
Suggested diagnosis Test
Autoimmune hepatitis Smooth muscle antibody, anti–liver–kidney microsomal antibody
Biliary cirrhosis Antimitochondrial antibody
Hemochromatosis Ferritin
Wilson’s disease Ceruloplasmin
Hepatocellular cancer
α-Fetoprotein
α
1
-Antitrypsin deficiency
Enzyme assay of the same
Chapter 9 • Gastrointestinal Problems
207