Diagnostic Tests for Chronic Hepatitis B
Chronic Hepatitis B Tests: Book Excerpts
Home Diagnostic Testing
These home medical tests may be relevant to Chronic Hepatitis B:
- Liver Health & Hepatitis: Home Testing
Chronic Hepatitis B Diagnosis: Book Excerpts
Diagnostic Tests for Chronic Hepatitis B: Online Medical Books
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HEPATOMEGALY:
DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)
Routine diagnostic studies include a CBC, sedimentation rate, ANA test, Monospot test, chemistry panel, chest x-ray, EKG, and flat plate of the abdomen.
If viral hepatitis is suspected, a hepatitis profile should be ordered. If congestive heart failure is suspected, a venous pressure and circulation time and pulmonary function tests should be done. A CT scan of the abdomen will assist in the diagnosis of metastatic carcinoma and often find a primary source for the metastasis. Metastatic neoplasms and the various forms of cirrhosis may be diagnosed by liver biopsy, but one should keep in mind that it is dangerous to do a liver biopsy if biliary cirrhosis is suspected. Gallbladder ultrasound or cholecystography should be done if cholecystitis and cholelithiasis are suspected. Transhepatic cholangiography or ERCP may need to be done. Exploratory surgery may be the only way to get a diagnosis, especially in obstructive jaundice.
The various infectious diseases will need antibody titers and skin tests to pin down the diagnosis. For example, a brucellin antibody titer or a Monospot test can be done. Skin tests for the various fungi and tuberculosis can be done.
The various hemolytic anemias may be diagnosed by blood smears, a sickle cell preparation, serum haptoglobin, and hemoglobin electrophoresis. The reticuloendothelioses require liver biopsy. Hemochromatosis is also diagnosed by liver biopsy, but a test for serum iron and iron-binding capacity should also be done. Wilson's disease is diagnosed by serum copper and ceruloplasmin tests. Venography will diagnose hepatic vein thrombosis.
Most physicians prefer to refer the patient with hepatomegaly to a gastroenterologist once the preliminary studies have been done. This would be the most cost-effective approach.
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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
JAUNDICE:
DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)
The basic workup includes a CBC, sedimentation rate, reticulocyte count, red cell fragility test, urinalysis, chemistry panel, VDRL test, EKG, a chest x-ray, and flat plate of the abdomen.
If infectious hepatitis is suspected, a hepatitis profile, febrile agglutinins, Monospot test, cytomegalic virus antibody titer, and leptospirosis antibody titer should be done. If lupoid hepatitis is suspected, a test for antinuclear antibodies and a smooth muscle antibody should be done.
If hemochromatosis is suspected, a serum iron, iron-binding capacity, and ferritin should be done.
If hemolytic anemia is suspected, serum haptoglobins, hemoglobin electrophoresis, and sickle cell preparations may be done.
If obstructive jaundice is suspected, then gallbladder ultrasound should be done to rule out gallstones, and a CT scan of the abdomen may be done to look for GI neoplasm. An upper GI series may assist in finding a primary neoplasm in the GI tract.
ERCP or percutaneous transhepatic cholangiography will assist in determining whether there is definitely obstructive jaundice and whether it is due to a surgically resectable lesion. Peritoneoscopy can also be helpful. An exploratory laparotomy will probably be necessary regardless of whether one performs the above tests. Cholangiopancreatography and endoscopic ultrasonography are two newer methods that may be used to evaluate the biliary tree and pancreatic ducts, especially when a neoplasm is suspected.
Hepatocellular jaundice will often require a needle biopsy of the liver to pin down the diagnosis. Antimitochondrial antibodies will need to be ordered to screen for biliary cirrhosis. An alpha 1-fetoprotein will help diagnose hepatocellular carcinoma. By the time you have reached this point, you have gone to considerable expense in the diagnostic workup. It would be much more prudent to ask for a gastroenterology consultation before ordering all these expensive diagnostic tests.
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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
Hepatomegaly:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
Hepatomegaly is seldom a patient’s chief complaint. It usually comes to light during palpation and percussion of the abdomen.
If you suspect hepatomegaly, ask the patient about his use of alcohol and exposure to hepatitis. Also ask if he’s currently ill or taking any prescribed drugs. If he complains of abdominal pain, ask him to locate and describe it.
Inspect the patient’s skin and sclera for jaundice, dilated veins (suggesting generalized congestion), scars from previous surgery, and spider angiomas (commonly occurring in cirrhosis). Next, inspect the contour of his abdomen. Is it protuberant over the liver or distended (possibly from ascites)? Measure his abdominal girth.
Percuss the liver, but be careful to identify structures and conditions that can obscure dull percussion notes, such as the sternum, ribs, breast tissue, pleural effusions, and gas in the colon. (See Percussing for liver size and position.) Next, during deep inspiration, palpate the liver’s edge; it’s tender and rounded in hepatitis and cardiac decompensation, rocklike in carcinoma, and firm in cirrhosis.
Take the patient’s baseline vital signs, and assess his nutritional status. An enlarged liver that’s functioning poorly causes muscle wasting, exaggerated skeletal prominences, weight loss, thin hair, and edema.
Evaluate the patient’s level of consciousness. When an enlarged liver loses its ability to detoxify waste products, the result is accumulation of metabolic substances toxic to brain cells. As a result, watch for personality changes, irritability, agitation, memory loss, an inability to concentrate and poor mentation, and — in a severely ill patient — coma.
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Source: Handbook of Signs & Symptoms (Third Edition), 2006
Jaundice:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
Documenting a history of the patient’s jaundice is critical in determining its cause. Begin by asking the patient when he first noticed the jaundice. Does he also have pruritus, clay-colored stools, or dark urine? Ask about past episodes or a family history of jaundice. Does he have nonspecific signs or symptoms, such as fatigue, a fever, or chills; GI signs or symptoms, such as anorexia, abdominal pain, nausea, weight loss, or vomiting; or cardiopulmonary symptoms, such as shortness of breath or palpitations? Ask about alcohol use and a history of cancer or liver or gallbladder disease. Has the patient lost weight recently? Also, obtain a drug history. Ask about a history of hepatitis, gallstones, or liver or pancreatic disease.
Perform the physical examination in a room with natural light. Make sure that the orange-yellow hue is jaundice and not due to hypercarotenemia, which is more prominent on the palms and soles and doesn’t affect the sclera. Inspect the patient’s skin for texture and dryness and for hyperpigmentation and xanthomas. Look for spider angiomas or petechiae, clubbed fingers, and gynecomastia. If the patient has heart failure, auscultate for arrhythmias, murmurs, and gallops as well as crackles and abnormal bowel sounds. Palpate the lymph nodes for swelling and the abdomen for tenderness, pain, and swelling. Palpate and percuss the liver and spleen for enlargement, and test for ascites with the shifting dullness and fluid wave techniques. Obtain baseline data on the patient’s mental status: Slight changes in sensorium may be an early sign of deteriorating hepatic function.
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Source: Handbook of Signs & Symptoms (Third Edition), 2006
Hepatomegaly:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
Hepatomegaly is seldom a patient’s reason for seeking care. It usually comes to light during palpation and percussion of the abdomen.
If you suspect hepatomegaly, ask the patient about his use of alcohol and exposure to hepatitis. Also ask if he’s currently ill or taking any prescribed drugs. If he complains of abdominal pain, ask him to locate and describe it.
Inspect the patient’s skin and sclerae for jaundice, dilated veins (suggesting generalized congestion), scars from previous surgery, and spider angiomas (common in cirrhosis). Next, inspect the contour of his abdomen. Is it protuberant over the liver or distended (possibly from ascites)? Measure his abdominal girth.
Percuss the liver, being careful to identify structures and conditions that can obscure dull percussion notes, such as the sternum, ribs, breast tissue, pleural effusions, and gas in the colon. (See Percussing for liver size and position.) Next, palpate the liver’s edge during deep inspiration; it’s tender and rounded in hepatitis and cardiac decompensation, rocklike in carcinoma, and firm in cirrhosis.
Take the patient’s baseline vital signs, and assess his nutritional status. An enlarged liver that’s functioning poorly causes muscle wasting, exaggerated skeletal prominences, weight loss, thin hair, and edema.
Evaluate the patient’s level of consciousness. When an enlarged liver loses its ability to detoxify waste products, metabolic substances toxic to brain cells accumulate. As a result, watch for personality changes, irritability, agitation, memory loss, inability to concentrate, poor mentation, and—in a severely ill patient—a coma.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Jaundice [Icterus]:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
Documenting a history of the patient’s jaundice is critical in determining its cause. Begin by asking the patient when he first noticed the jaundice. Does he also have pruritus, clay-colored stools, or dark urine? Ask about past episodes or a family history of jaundice. Does he have nonspecific signs or symptoms, such as fatigue, fever, or chills; GI signs or symptoms, such as anorexia, abdominal pain, nausea, weight loss, or vomiting; or cardiopulmonary symptoms, such as shortness of breath or palpitations? Ask about alcohol use and a history of cancer or liver or gallbladder disease. Has the patient lost weight recently? Also, obtain a drug history. Ask about a history of hepatitis, gallstones, or liver or pancreatic disease.
Perform the physical examination in a room with natural light. Make sure that the orange-yellow hue is jaundice and not due to hypercarotenemia, which is more prominent on the palms and soles and doesn’t affect the sclera. Inspect the patient’s skin for texture and dryness and for hyperpigmentation and xanthomas. Look for spider angiomas or petechiae, clubbed fingers, and gynecomastia. If the patient has heart failure, auscultate for arrhythmias, murmurs, and gallops. For all patients, auscultate for crackles and abnormal bowel sounds. Palpate the lymph nodes for swelling and the abdomen for tenderness, pain, and swelling. Palpate and percuss the liver and spleen for enlargement, and test for ascites with the shifting dullness and fluid wave techniques. Obtain baseline data on the patient’s mental status: Slight changes in sensorium may be an early sign of deteriorating hepatic function. (See Differential diagnosis: Jaundice, pages 462 and 463.)
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Hepatomegaly:
Physical examination
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
A. How does a clinician diagnose hepatomegaly?
1. Palpation and percussion. Evaluation of the liver is difficult given its irregular shape and its location within the abdomen. Approach palpation of the right upper quadrant from one of two directions: palpate from below using the fingertips to palpate superiorly or from above with the fingertips hooked over the lower rib. Either method is facilitated by the patient’s deep inspiration. 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. If the margin is not palpated but hepatomegaly is suspected, then attempt direct percussion of both margins.
2. Auscultation. The “scratch method” (gently stroking 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 by Tucker comparing ultrasound to the results of the scratch test found that this test was unreliable and inaccurate (3). Auscultation of the right upper quadrant has been described and several findings can be noted: friction rubs, bruits, and abnormal pulsations.
3. Other associated signs. Associated physical examination findings 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 presence in the setting of hepatomegaly support further diagnostic testing.
B. How accurate is the physical assessment? Palpation of the liver 2 cm below the costal margin correlates with a 50% chance of having hepatomegaly on further diagnostic workup. A 63% chance exists that a palpable liver relates to liver disease (4). The converse is also true: A nonpalpable liver could also be enlarged, therefore, the need for further assessment should be based on clinical context and associated signs. The liver span has classically been measured in the midclavicular line, although some have suggested that the use of the midclavicular line is too inaccurate. Several studies have attempted to establish a new reference point but no consensus has developed. Direct percussion (lightly tapping with index finger) is more accurate in identifying the extent of the margins than indirect percussion. Indirect percussion (heavy tapping of one finger against another finger held against the body firmly) often will not illicit a change over the thin lower margin or detect a change at the upper margin, depending on the contour of the diaphragm and the volume of the lower lungs (2). Nuclear medicine scintigraphy or ultrasound study defines hepatomegaly as greater than 15.5 cm. Studies comparing physical examination to these modalities have not shown physical examination to be accurate or consistent, with high interexaminer differences. Skrainka et al. evaluated liver size estimation by direct percussion, indirect percussion, palpation, and ultrasound. His results demonstrated that experienced clinicians (medicine consultants) accurately assessed liver size compared with ultrasound and that direct percussion measurements correlated the best with liver size in all groups (5).
Testing
A. What are appropriate diagnostic tests in the setting of hepatomegaly? An ultrasound of the right upper quadrant should be obtained, as well as a chest x-ray, and kidney, urinary tract, and bladder studies. Initial laboratory evaluation should include a complete blood count, electrolytes, creatinine, glucose, liver enzyme testing (alanine aminotransferase, aspartame transferase, γ-glutamyl transpeptidase, alkaline phospatase), and true liver function tests (albumin, prothrombin time, partial thromboplastin time and bilirubin). If liver enzymes are elevated, a hepatitis serology panel is added. Nondiagnostic ultrasound or hepatic masses should prompt computed tomography scan. Further differential testing is shown in Table 9.7.
B. Liver biopsy is indicated for unexplained hepatomegaly or jaundice, persistent abnormal liver tests, chronic viral hepatitis, suspected cirrhosis or portal hypertension, primary or secondary malignancy, suspected hemochromatosis, suspected Wilson’s disease, and hepatic dysfunction following liver transplantation.
Diagnostic assessment
How are the physical examination findings used to form a differential diagnosis?
A. Smooth nontender liver: suspect fatty infiltration, congestive heart failure (CHF), portal cirrhosis, primary biliary cirrhosis, lymphoma, portal obstruction, hepatic venous thrombosis, hepatic vein thrombosis, lymphocytic leukemia, amyloidosis, schistosomiasis, or kala-azar.
B. Smooth tender liver: suspect early CHF, acute hepatitis, amoebic abscess, or hepatic abscess.
C. Nodular liver: suspect late portal cirrhosis, tertiary syphilis, hydatid cyst, or metastatic carcinoma.
D. Very hard nodular liver: nearly always indicates metastatic carcinoma.
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Jaundice:
Physical examination
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
The physical examination should focus on the following: Eyes should be examined for icterus or Kayser-Fleischer rings, which are copper-colored rings suggestive of Wilson’s disease. Heart and lung examination revealing S3 gallop or rales is suggestive of congestive heart failure, which leads to passive liver congestion. Ascites, hepatosplenomegaly, venous hum, and tenderness on abdominal examination points to portal hypertension and indicates liver cirrhosis (Chapters 9.2 and 9.9). Suspect pancreatic carcinoma when a nontender, palpable mass is found on upper abdominal examination. Signs of cirrhosis include excoriations, spider nevi, caput medusa, Dupytren’s contracture, gynecomastia, and palmar erythema. Delirium, drowsiness, asterixis, and tremor occur with liver failure.
Testing
A. Laboratory tests. Laboratory assays measure bilirubin as indirect (unconjugated) and direct (conjugated) fractions. An elevated indirect bilirubin level is consistent with overproduction of bilirubin or decreased uptake, transport, or conjugation by the hepatocyte. Elevation of direct bilirubin points to decreased excretion or transport by the biliary system (3). Transaminase levels (aspartate aminotransferase and alanine aminotransferase) increase from hepatocellular necrosis or inflammation from the release of aspartate aminotransferase from lysed hepatocytes. Hepatocyte damage and cholestasis increase alkaline phosphatase levels. γ-Glutamyl transpeptidase levels increase in cholestasis and alcohol abuse. Pancreatitis, pancreatic carcinoma, or common bile duct stones elevate amylase levels. With hepatocellular damage, coagulation studies can be prolonged. Antimitochondrial antibodies are present in primary biliary cirrhosis. Hepatitis B serologic tests are summarized in Table 9.8. Hepatitis A IgM antibody detects acute stage hepatitis A and IgG detects chronic stage hepatitis A. Anti-hepatitis C virus indicates hepatitis C infection. Hepatitis D only occurs with hepatitis B infection and is detected by anti-hepatitis D (4).
B. Diagnostic imaging has limited uses. Plain films of the abdomen rarely provide useful information. Cholelithiasis or pancreatic mass are best detected by ultrasound. Magnetic resonance imaging or computed tomography scans are used to examine the liver, pancreas, biliary tree, and suspected obstruction not identified by ultrasound. Hepatoiminodiacetic acid scanning is useful in a patient with suspected acute cholecystitis. Percutaneous transhepatic cholangiography and endoscopic retrograde cholangiopancreatography are used if obstructive jaundice is suspected to show the cause, location, and extent of involvement (5).
C. Other tests. Percutaneous liver biopsy is not indicated in the routine workup of jaundice but may prove useful in diagnosing the cause of jaundice when the above-mentioned tests are inconclusive. Iron levels are increased in hemochromatosis. Copper levels are increased in Wilson’s disease.
Diagnostic assessment
The patient’s history and associated symptoms guide the initial differential diagnosis of jaundice. Physical examination further narrows the causative choices and analysis of hepatic enzyme levels and viral serologies should confirm the initial diagnosis. Imaging studies play a limited role, except in suspected cases of malignancy or biliary obstruction.
Most patients have acute viral hepatitis as the cause of jaundice. Consultation is indicated when testing is inconclusive, when a surgical cause is suspected, or as needed for treatment.
References
1. Scharschmidt BF, Goldberg HI, Schmid R. Approach to the patient with cholestatic jaundice. N Engl J Med 1983;308:1515.
2. Lucas WB, Chuttani R. Pathophysiology and current concepts in the diagnosis of obstructive jaundice. Gastroenterologist 1995;3:105–118.
3. Fevery J, Blanckaert N. What can we learn from analysis of serum bilirubin?
J Hepatol 1986;2:113–121.
4. Bakerman S. ABC’s of interpretive laboratory data, 3rd ed. Myrtle Beach, SC: Interpretive Data, Inc., 1994:279–286.
5. Barloon TJ, Bergus GR, Weissman AM. Diagnostic imaging to identify the cause of jaundice. Am Fam Physician 1996;54:556–562.
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Hepatitis:
Physical examination
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
A. General examination. Common findings in viral, alcoholic, or drug-induced hepatitis include fever, jaundice, scleral icterus, weight loss, muscle tenderness or weakness, and a palpable tender liver. Ecchymosis or petechiae indicates significant clotting factor abnormalities and, coupled with a small liver which diminishes in size, is suggestive of severe hepatitis or impending hepatic failure.
B. Chronic liver disease results in progressive liver dysfunction, fluid retention, and portal hypertension. The liver plays a key role in the detoxification of endogenous hormones, drugs, and ingested substances. Abnormalities in estrogen metabolism have often been considered the cause of peripheral stigmata such as spider angiomata, palmar erythema, gynecomastia, parotid enlargement, and testicular atrophy.
C. Does the abdominal examination reveal hepatosplenomegaly? Modest enlargement of the liver occurs in acute viral and chronic hepatitis, whereas marked enlargement (>10 cm below the costal margin) is seen in alcoholic hepatitis. Ascites, prominent abdominal collateral veins, bruits, rubs, abdominal masses, or a palpable gallbladder can also indicate hepatitis, whereas a small liver can indicate cirrhosis.
Testing
Laboratory tests differentiate between hepatocellular disorders (e.g., viral hepatitis) and cholestatic syndromes (e.g., primary biliary cirrhosis and bile duct obstruction).
A. Liver function tests (LFTs)
1. Elevated alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are nonspecific indicators of hepatocellular damage and do not distinguish viral from drug-induced hepatitis. Alcoholic liver disease is suggested when the AST:ALT ratio is greater than 2:1.
2. Total serum bilirubin is not a sensitive indicator of hepatic dysfunction. Hepatitis impairs the excretion phase of bilirubin metabolism, resulting in an elevated direct (conjugated) bilirubin greater than 0.1 mg/dl.
3. γ-Glutamyl transpeptidase (GGT) is a very sensitive indicator for minimal hepatocellular damage. Elevations are seen in alcoholic liver disease before other LFTs are abnormal.
4. Alkaline phosphatase indicates cholestasis or obstruction. Approximately 75% of patients with prolonged cholestasis have alkaline phosphatase values increased fourfold or greater.
5. Immunoglobulins (IgA, IgG, IgM) in acute hepatitis are normal or minimally increased. A moderate increase is seen in chronic active or autoimmune hepatitis. Indices are useful in monitoring response to immunotherapy.
6. Circulating autoantibodies (e.g., antinuclear, smooth muscle, liver-kidney microsomal) may be seen in autoimmune hepatitis.
B. Hepatitis serology. Serologic testing (anti-HDV, anti-HCV) is now available for each type, except hepatitis E virus (HEV) (5) (Fig. 9.1). Hepatitis G virus (HGV) and GB virus C (GBV-C) are the most recently discovered hepatitis viruses (2). HGV is present in asymptomatic blood donors and, although it is thought to cause chronic hepatitis, no causal relationship between HGV and hepatitis has been convincingly established (3).
C. Radiologic and diagnostic procedures
1. Abdominal films are useful in detecting splenomegaly.
2. Ultrasound is helpful in detecting gallstones in patients with jaundice and in detecting mass lesions (tumors or liver abscesses).
3. Abdominal computerized tomography aids in the diagnosis of mass lesions of the liver and abnormalities of the gallbladder.
4. Percutaneous needle biopsy of the liver permits an accurate diagnosis of diffuse parenchymal disorders such as hepatitis, drug reaction, cirrhosis, and liver tumors.
Diagnostic assessment
Viral hepatitis can be diagnosed by a thorough history and serology used in tandem. Individual susceptibility to hepatic injury in drug-induced hepatitis can be affected by genetic factors, age, gender, nutritional status, exposure to other drugs and chemicals, systemic disease, and other factors (4). Liver injury produced by drugs is either cytotoxic (hepatocellular), cholestatic, or a combination of the two. Knowledge of these mechanisms is extremely important in diagnosing the inciting agent. Alcoholic hepatitis is identified by the history coupled with the typical laboratory abnormalities. Chronic hepatitis requires elevated LFTs for at least 6 months and can result from infection with HBV or HCV, alcoholic liver disease, drug toxicity, or autoimmune causes. Liver biopsy is required for accurate assessment and classification of chronic hepatitis. Although effective vaccines are available for HAV and HBV and have yielded protection for decades, vaccines for HCV and HEV are only in early development and no vaccine exists for HDV.
References
1. Schiff ER, Sorrell MF, Maddrey WC. Diseases of the liver, 8th ed. Philadelphia:
Lippincott Williams & Wilkins, 1999:234–235, 919–921.
2. Blum HE. Update hepatitis A-G. Digestion 1997;58(Suppl 1):33–36.
3. Zimmerman HJ. General aspects of drug-induced liver disease. Gastroenterol Clin North Am 1995;24:739–757.
4. Kools AM. Hepatitis A,B,C,D, and E. Update on testing and treatment. Postgrad Med 1992;91:109–114.
5. Schiff ER. Update in hepatology. Ann Intern Med 1999;130:52–59.
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Hepatomegaly:
Diagnostic Approach
(Field Guide to Bedside Diagnosis)
The mean liver span is 10.5 cm in men and 7 cm in women. Larger span
correlates with greater height. A span 2 to 3 cm larger or smaller than these values is considered abnormal. The liver may be palpable but not enlarged (normal span) with emphysema, right-sided pleural effusion, Riedel lobe, and thin body habitus.
An hepatic arterial bruit is heard with alcoholic hepatitis or cancer, either primary or metastatic. A friction rub may be heard with perihepatitis, metastatic cancer, or after liver biopsy.
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Source: Field Guide to Bedside Diagnosis, 2007
Jaundice:
Diagnostic Approach
(Field Guide to Bedside Diagnosis)
Jaundice becomes clinically apparent when the bilirubin level reaches 2 to 2.5 mg/dL. Scleral elastin has a high affinity for bilirubin, and with a white background, it is a sensitive indicator of jaundice. Biliary obstruction gives a greenish skin tint due to accumulation of biliverdin. Hemolysis gives a lemon-yellow tint when observed in natural light. An orange-yellow color is more consistent with hepatocellular disease. Pseudojaundice may be found in black patients with pigmented sclera, with carotinemia, with uremia (a sallow yellowish pallor), and with quinacrine (a yellow-green color).
Dark urine with green foam confirms a conjugated hyperbilirubinemia and excludes hemolysis or a conjugating defect. Unconjugated bilirubin is tightly bound to albumin, which prevents glomerular filtration.
Courvoisier law states: “In a jaundiced patient, a palpable gallbladder indicates that the jaundice is not due to stones.” Painless jaundice usually suggests a gradual process, as is found in intrahepatic cholestasis. The liver in this case is usually enlarged, smooth, and nontender. A patient with hepatocellular disease appears more ill than one with obstruction. Fluctuating jaundice occurs with gallstones, ampullary carcinoma, or toxins.
Anorexia, nausea, vomiting, or weight loss within 2 weeks of the appearance of jaundice suggests acute hepatitis or gallstones. Appearance more than 2 weeks prior suggests malignant biliary obstruction, chronic hepatitis, or toxin exposure (e.g., alcohol). Generalized pruritus suggests biliary obstruction, either extrinsic due to tumor, or canalicular due to drug-induced intrahepatic cholestasis.
Ascites with jaundice is an ominous sign, signifying decompensated cirrhosis with portal hypertension or malignancy with liver metastases. In portal hypertension, veins are engorged radially away from the umbilicus. In inferior vena cava obstruction, flow occurs upward over the abdominal wall. A harsh hepatic bruit may occur with malignancy, alcoholic hepatitis, or hemangioma. Splenomegaly without hepatomegaly occurs with hemolysis or portal vein occlusion.
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Source: Field Guide to Bedside Diagnosis, 2007
Hepatomegaly:
Physical assessment
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Inspect the patient’s skin and sclerae for jaundice, dilated veins (suggesting generalized congestion), scars from previous surgery, and spider angiomas (often occurring in cirrhosis). Next, inspect the contour of his abdomen. Is it protuberant over the liver or distended (possibly from ascites)? Measure his abdominal girth.
Percuss the liver, but be careful to identify structures and conditions that can obscure dull percussion notes, such as the sternum, ribs, breast tissue, pleural effusions, and gas in the colon (See Percussing for liver size and position.) Next, during deep inspiration, palpate the liver’s edge; it’s tender and rounded in hepatitis and cardiac decompensation, rocklike in carcinoma, and firm in cirrhosis.
Take the patient’s baseline vital signs, and assess his nutritional status. An enlarged liver that’s functioning poorly causes muscle wasting, exaggerated skeletal prominences, weight loss, thin hair, and edema.
Evaluate the patient’s level of consciousness. When an enlarged liver loses its ability to detoxify waste products, the result is accumulation of metabolic substances toxic to brain cells. As a result, watch for personality changes, irritability, agitation, memory loss, inability to concentrate and poor mentation, and — in a severely ill patient — coma.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Jaundice:
Physical assessment
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Perform the physical examination in a room with natural light. Make sure that the orange-yellow hue is jaundice and not due to hypercarotenemia, which is more prominent on the palms and soles and doesn’t affect the sclerae. Inspect the patient’s skin for texture and dryness and for hyperpigmentation and xanthomas. Look for spider angiomas or petechiae, clubbed fingers, and gynecomastia. If the patient has heart failure, auscultate for arrhythmias, murmurs, and gallops. For all patients, auscultate for crackles and abnormal bowel sounds. Palpate the lymph nodes for swelling and the abdomen for tenderness, pain, and swelling. Palpate and percuss the liver and spleen for enlargement, and test for ascites with the shifting dullness and fluid wave techniques. Obtain baseline data on the patient’s mental status: Slight changes in sensorium may be an early sign of deteriorating hepatic function.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Hepatomegaly:
Diagnostic Approach
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
Normal vs Enlarged Liver
First step in diagnosis is to decide whetherliver is enlarged. Because palpation of liver edge can be misleadingdue to displacement by other organs or unusual contour, liver spanshould be measured. Once it is established that liver is enlarged,specific cause needs to be determined.
Clinical Presentations
Hepatomegaly can occur as isolated findingwith or without splenomegaly, with jaundice, with significant increasein serum aminotransferases, in association with systemic disorders,with persistent vomiting and altered consciousness, or with progressiveneurologic deterioration (Boyle, 1996).
Enlarged Liver as Isolated Finding with or without Splenomegaly
Diagnostic possibilities include
Mass (tumor,cyst, abscess)Congenital hepatic fibrosisHepatic outflow obstructionFatty liverMetabolic disease (tyrosinemia, Gaucherdisease type I, Niemann-Pick disease type B, glycogen storage diseasetype IV, Wolman disease, cholesterol ester disease) Jaundice
Disorders causing hepatomegaly and jaundiceare discussed in Chap. 36, Jaundice.
Increased Serum Aminotransferase Levels
When hepatomegaly and increased serum aminotransferaselevels are found, several disorders should be considered:
HepatitisA, B, C, and DDrug-induced hepatitisAutoimmune hepatitisAlpha1-antitrypsindeficiencyWilson diseaseSclerosing cholangitis Association with Systemic Disorders
Hepatomegaly may occur with the followingsystemic disorders:
CardiacfailureSystemic infectionDiabetes mellitusCystic fibrosisConnective tissue diseasesHematologic disorders (sickle celldisease, leukemia)SarcoidosisInflammatory bowel diseaseHistiocytoses Persistent Vomiting and Altered Consciousness
Disorders that cause persistent vomiting,alteration in consciousness, and hepatomegaly include
Fulminanthepatic failureReye syndromeMetabolic disordersUrea cycledefectsFatty acid oxidation disordersOrganic acidemiasRespiratory chain defectsDisorders of gluconeogenesisCarbohydrate metabolism disorders (glycogenstorage diseases I and III, hereditary fructose intolerance) Progressive Neurologic Deterioration
Disorders that cause progressive neurologicdeterioration and hepatomegaly include
Lysosomalstorage diseases (Gaucher disease, Niemann-Pick disease, GM-1 gangliosidosis,mucopolysaccharidoses)Wilson diseaseZellweger syndrome Lab Tests
If hepatomegalyor hepatosplenomegaly occurs without jaundice, several tests should beconsidered initially:CBC and differentialReticulocyte countLiver function tests including serumaspartate aminotransferase, alanine aminotransferase, alkaline phosphatase,total protein, albumin, fractionated bilirubinsedimentation rateSerum alpha1-antitrypsinand Pi phenotypeSerum ceruloplasminProthrombin and activated partial thromboplastintimesUAUrine for reducing sugars Selection of radiographic imaging procedures(e.g., abdominal U/S and CT) depends on suspected diagnosis.Percutaneous liver biopsy is diagnostic of many disorders.In children with hepatomegaly and jaundice,see Chap. 36, Jaundice.In children with another type of presentation,refer to possible causes in each category. Investigations shouldbe tailored to suspected diagnosis.
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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
Jaundice:
Diagnostic Approach: Unconjugated Hyperbilirubinemia
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
Most commoncauses of neonatal unconjugated hyperbilirubinemia are physiologic jaundiceand breast-feeding–related jaundice.Diagnostic tests should be performedinNeonateswho become clinically jaundiced during first 24 hrs of lifeTerm bottle-fed infants whose maximumserum bilirubin exceeds 12 mg/dLTerm breast-fed infants whose maximumserum bilirubin exceeds 15 mg/dLPreterm infants Certain tests should be performed initially:Maternal andinfant blood groups and Rh typesUnconjugated and conjugated serum bilirubinCBC and differentialReticulocyte countDirect Coombs testAnalysis of blood smear If jaundice persists, red cell G6PDactivity and T4 and TSH levels should bedetermined.If diagnosis remains uncertain, moreextensive studies for rarer forms of hemolytic disease and enzymeassay for uridine diphosphate glucuronyl transferase activity shouldbe considered. Tests for hepatocellular disease need to be performedonly when there is significant increase in conjugated bilirubin.In infancy and childhood, most commoncause of unconjugated hyperbilirubinemia is hemolytic anemia [see Chap. 45, Pallor (Anemia)].
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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
Hepatomegaly:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
Hepatomegaly is seldom a patient's chief complaint. It usually comes to light during palpation and percussion of the abdomen.
If you suspect hepatomegaly, ask the patient about his use of alcohol and exposure to hepatitis. Also ask if he's currently ill or taking any prescribed drugs. If he complains of abdominal pain, ask him to locate and describe it.
Inspect the patient's skin and sclera for jaundice, dilated veins (suggesting generalized congestion), scars from previous surgery, and spider angiomas (commonly occurring in cirrhosis). Next, inspect the contour of his abdomen. Is it protuberant over the liver or distended (possibly from ascites)? Measure his abdominal girth.
Percuss the liver, but be careful to identify structures and conditions that can obscure dull percussion notes, such as the sternum, ribs, breast tissue, pleural effusions, and gas in the colon. (See Percussing for liver size and position.) Next, during deep inspiration, palpate the liver's edge; it's tender and rounded in hepatitis and cardiac decompensation, rocklike in carcinoma, and firm in cirrhosis.
Take the patient's baseline vital signs, and assess his nutritional status. An enlarged liver that's functioning poorly causes muscle wasting, exaggerated skeletal prominences, weight loss, thin hair, and edema.
Evaluate the patient's level of consciousness. When an enlarged liver loses its ability to detoxify waste products, the result is accumulation of metabolic substances toxic to brain cells. As a result, watch for personality changes, irritability, agitation, memory loss, an inability to concentrate and poor mentation, and—in a severely ill patient—decreased level of consciousness.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
Jaundice [Icterus]:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
Documenting a history of the patient's jaundice is critical in determining its cause. Begin by asking the patient when he first noticed the jaundice. Does he also have pruritus, clay-colored stools, or dark urine? Ask about past episodes or a family history of jaundice. Does he have nonspecific signs or symptoms, such as fatigue, a fever, or chills; GI signs or symptoms, such as anorexia, abdominal pain, nausea, weight loss, or vomiting; or cardiopulmonary symptoms, such as shortness of breath or palpitations? Ask about alcohol use and a history of cancer or liver or gallbladder disease. Has the patient lost weight recently? Also, obtain a drug history. Ask about a history of hepatitis, gallstones, or liver or pancreatic disease.
Perform the physical examination in a room with natural light. Make sure that the orange-yellow hue is jaundice and not due to hypercarotenemia, which is more prominent on the palms and soles and doesn't affect the sclera. Inspect the patient's skin for texture and dryness and for hyperpigmentation and xanthomas. Look for spider angiomas or petechiae, clubbed fingers, and gynecomastia. If the patient has heart failure, auscultate for arrhythmias, murmurs, and gallops as well as crackles and abnormal bowel sounds. Palpate the lymph nodes for swelling and the abdomen for tenderness, pain, and swelling. Palpate and percuss the liver and spleen for enlargement, and test for ascites with the shifting dullness and fluid wave techniques. Obtain baseline data on the patient's mental status: Slight changes in sensorium may be an early sign of deteriorating hepatic function.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
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