Diagnosis of Reye's Syndrome

• Inflammatory disorders, resulting in tender hepatomegaly
  –Hepatitis (viral or drug-induced): Associated with jaundice, fever, nausea, vomiting, fatigue, diarrhea, weight loss
  –Alcoholic liver disease: Associated with liver failure and portal hypertension (e.g., caput medusae, spider angiomata, hemorrhoids, testicular atrophy, ALT is more than two times higher than AST)
• Infiltrative disorders
  –Fatty liver (NASH): Predisposing factors include middle age, obesity, female gender, diabetes, and hyperlipidemia
  –Sarcoidosis: Associated with cough, hilar lymphadenopathy; more common in blacks, women, ages 30–40
  –Hemochromatosis: Iron overload resulting in bronzed skin color, diabetes, abnormal iron panel
  –Wilson's disease: Copper excess resulting in liver failure, lenticular degeneration, and Kayser-Fleischer rings in cornea
• Neoplasms present with focal enlargement, arterial bruit and/or hepatic rub, and constitutional symptoms (e.g., fever, night sweats, weight loss)
  –Metastatic cancer is more common than primary liver cancers (colon, lung, breast)
  –Hepatocellular carcinoma is most common primary liver cancer (often due to chronic hepatitis or cirrhosis)
  –Hepatic adenoma or hepatic cysts
  –Leukemia/lymphoma

• Liver abscess
• Less common causes (“zebras”) include tricuspid regurgitation, Budd-Chiari syndrome, schistosomiasis, amyloidosis, kala-azar (visceral leishmaniasis), and HIV/AIDS

Workup and Diagnosis

• History should include past medical history, alcohol and drug use, medications (including herbal remedies), family history of liver disease, and presence of constitutional symptoms
• Physical exam should include palpation of liver surface for tenderness, consistency, nodularity, pulsations, bruits, rubs; skin examination (e.g., for jaundice, spider angiomata); cardiac exam; lymphadenopathy
• Liver function tests (ALT, AST, GGTP, albumin) and coagulation tests (PT/PTT/INR) to assess liver function
• Hepatitis serologies may be indicated, including hepatitis A, B, and C; CMV; and EBV
• Ultrasound will discriminate solid masses from cysts
• Abdominal CT to evaluate masses and fatty liver
• Doppler ultrasound to determine blood flow
• MRI of abdomen is useful to diagnose excess deposition of iron (hemochromatosis) or copper (Wilson's disease)
• Radionuclide scanning to characterize inflammatory and neoplastic lesions
• Angiography is the gold standard to differentiate hemangioma from solid tumor
• Iron panel (hemochromatosis) and ceruloplasmin (Wilson's disease)
• Consider gastroenterology consultation

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Source: In a Page: Signs and Symptoms, 2004

Hepatomegaly: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

• Inflammation
  –Most common infections: EBV; hepatitis A, B, C; CMV; TORCH
  –Less common infections: HIV, malaria, amebiasis, tuberculosis, toxocariasis, Borrelia burgdorferi
  –Drugs: Acetaminophen (commonly used in overdoses among adolescents), NSAIDs, isoniazid, sodium valproate, propothiouracil, halothane
  –Toxins: Tyrosinemia, galactosemia, vitamin A toxicity
  –Autoimmune hepatitis
  –Systemic lupus erythematosus

• Inappropriate storage
  –Glycogen storage diseases I–V
  –Lipids: Gaucher disease, Wolman disease, Niemann-Pick disease
  –Fat: Fatty acid oxidation defects, mucopolysaccharidoses
  –Metals: Wilson disease (copper), hemochromatosis (iron)
  –Abnormal proteins: α-1 antitrypsin deficiency (store abnormal protein product)
  –Peroxisomal disease: Zellweger
  –Mucopolysaccharidoses, types I–IV

• Infiltration
  –Hepatoblastoma
  –Hepatocellular carcinoma
  –Hemangioma
  –Histiocytosis
  –Extramedullary hematopoiesis
  –Chronic granulomatous disease
• Vascular congestion
  –Congestive heart failure
  –Budd-Chiari syndrome
  –Veno-occlusive disease
  –Suprahepatic web
• Biliary obstruction
  –Biliary atresia represents the most common cause of pediatric liver transplantation
  –Alagille syndrome
  –Cystic fibrosis
  –Primary sclerosing cholangitis
  –Inspissated bile syndrome
• Miscellaneous
  –Reye syndrome, bile acid synthetic disorder

Workup and Diagnosis

• History
  –Abdominal pain, fever, melena, weight loss, medications, age at onset, diarrhea, vomiting, hematemesis, bleeding, bruising, fatigue
  –Exposure to blood products
  –Nutrition history (neonatal formula)
  –Travel history to endemic infectious areas
  –Family history of liver disease, maternal HBV, HCV

• Physical exam
  –Height, weight
  –Liver size, margin, firmness, nodularity, tenderness
  –Ascites, jaundice/scleral icterus
  –Cataracts; Kayser-Fleischer rings (Wilson); posterior embryotoxin (Alagille)
  –Cardiac exam for murmurs; splenomegaly; tone and strength development; hemangiomas/xanthomas

• Labs
  –CBC, ALT, AST, fractionated bilirubin, alkaline phosphatase, total protein, albumin, globulin fraction, PT, U/A
  –Hepatitis serologies, EBV, TORCH titers, plasma amino acids/urine organic acids for metabolic disease
  –Serum AAT with protease inhibitor typing
  –Ceruloplasmin (decreased in Wilson disease)
  –ANA/anti-smooth muscle antibody/anti-liver kidney microsomal antibody, IgG for autoimmune hepatitis

• Ultrasound for echotexture and masses
  –Consider nuclear study/CT for obstruction
• Liver biopsy in chronic disease (>3 months) or to elucidate etiology

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Source: In A Page: Pediatric Signs and Symptoms, 2007

HEPATOMEGALY: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

The clinical picture will help to distinguish many causes of hepatomegaly. Shortness of breath, pitting edema, and hepatomegaly suggest CHF. Chronic cough, wheezing, jugular vein distention, hepatomegaly, and pitting edema suggest pulmonary emphysema and cor pulmonale. Fever, tender hepatomegaly, and jaundice suggest viral hepatitis or cholangitis. Hepatomegaly and ascites with a history of heavy alcohol intake suggest alcoholic cirrhosis. Hepatomegaly with gross or occult blood in the stool would suggest metastatic neoplasm of the GI tract. Asymptomatic hepatomegaly is probably related to congenital cystic disease, metastasis, or alcoholism.

The initial workup will involve a CBC, urinalysis, sedimentation rate, chemistry panel, amylase and lipase levels, and a flat plate of the abdomen. If viral hepatitis is suspected a hepatitis profile should be done. If CHF is suspected, a circulation time and spirometry is an inexpensive method of confirming the diagnosis. A chest x-ray and ECG need to be ordered also. If obstructive jaundice is suspected, endoscopic retrograde cholangiopancreatography may be done but a CT scan of the abdomen should probably done first. A CT scan of the abdomen will also identify primary and metastatic carcinoma of the liver. The many infectious diseases that are associated with hepatomegaly will need antibody titers, blood smears, or skin tests to reveal the diagnosis. Hemolytic anemias require blood smears, sickle cell prep, serum haptoglobins, and hemoglobin electrophoresis to get a definitive diagnosis. Amebic abscess can be elucidated by a CT scan but an antibody titer will assist in the definitive diagnosis. Venography will reveal hepatic vein thrombosis.

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Source: Differential Diagnosis in Primary Care, 2007

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

Reye's syndrome: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

A history of a recent viral disorder with typical clinical features strongly suggests Reye’s syndrome. An increased serum ammonia level, abnormal clotting studies, and hepatic dysfunction confirm it. Testing serum salicylate level rules out aspirin use. Absence of jaundice despite increased liver aminotransferase levels rules out acute hepatic failure and hepatic encephalopathy.

Abnormal test results may include:

❑Liver function studies: aspartate aminotransferase and alanine aminotransferase elevated to twice normal levels; bilirubin level usually normal

❑Liver biopsy: fatty droplets uniformly distributed throughout cells

❑Cerebrospinal fluid (CSF) analysis: white blood cell count less than 10/µl; with coma, increased CSF pressure.

❑Coagulation studies: prothrombin time and partial thromboplastin time prolonged

❑Blood values: serum ammonia levels elevated; serum glucose levels normal or, in 15% of cases, low; serum fatty acid and lactate levels increased.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

Viral hepatitis: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

A hepatitis profile, which identifies antibodies specific to the causative virus and establishes the type of hepatitis, is routine in suspected viral hepatitis.

❑ Type A: Detection of an antibody to hepatitis A confirms the diagnosis.

❑ Type B: The presence of HBsAg and hepatitis B antibodies confirms the diagnosis.

❑  Type C: Diagnosis depends on serologic testing for the specific antibody 1 or more months after the onset of acute hepatitis. Until then, the diagnosis is established primarily by obtaining negative test results for hepatitis A, B, and D.

❑ Type D: Detection of intrahepatic delta antigens or immunoglobulin (Ig) antidelta antigens in acute disease (or IgM and IgG in chronic disease) establishes the diagnosis.

❑ Type E: Detection of hepatitis E antigens supports the diagnosis; however, the diagnosis may also be determined by ruling out hepatitis C.

❑ Type G: Detection of hepatitis G antigen supports the diagnosis but doesn’t clearly implicate infection; the patient may be otherwise asymptomatic.

Additional findings from liver function studies support the diagnosis:

❑ Serum aspartate aminotransferase and serum alanine aminotransferase levels are increased in the prodromal stage of acute viral hepatitis.

❑ Serum alkaline phosphatase levels are slightly increased.

❑ Serum bilirubin levels are elevated. Levels may continue to be high late in the disease, especially in severe cases.

❑ Prothrombin time is prolonged (more than 3 seconds longer than normal indicates severe liver damage).

❑ White blood cell counts commonly reveal transient neutropenia and lymphopenia followed by lymphocytosis.

❑ Liver biopsy is performed if chronic hepatitis is suspected; however, it’s performed for acute hepatitis only if the diagnosis is questionable.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

Nonviral hepatitis: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Diagnostic findings include elevations in serum aspartate aminotransferase and alanine aminotransferase, total and direct bilirubin (with cholestasis), alkaline phosphatase, white blood cell (WBC) count, and eosinophil count (possible in drug-induced type). Liver biopsy may help identify the underlying pathology, especially infiltration with WBCs and eosinophils. Liver function tests have limited value in distinguishing between nonviral and viral hepatitis.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

Hepatic encephalopathy: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

CONFIRMING DIAGNOSIS Clinical features, a history of liver disease, and elevated serum ammonia levels in venous and arterial samples confirm hepatic encephalopathy.

Other supportive laboratory values include an EEG that slows as the disease progresses, an increase in spinal fluid glutamine, elevated bilirubin, and prolonged prothrombin time. Recently, evoked potential testing has been advocated as a more specific indicator of encephalopathy, but its benefit over an EEG isn’t yet clear.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

Fatty liver: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Typical clinical features — especially in patients with chronic alcoholism, malnutrition, poorly controlled diabetes mellitus, or obesity — suggest fatty liver.

CONFIRMING DIAGNOSIS A liver biopsy confirms excessive fat in the liver. These liver function tests support this diagnosis:

❑ Albumin: somewhat low

❑ Globulin: usually elevated

❑ Cholesterol: usually elevated

❑ Total bilirubin: elevated

❑ Alkaline phosphatase: elevated

❑ Transaminase: usually low (less than 300 U)

❑ Prothrombin time: possibly prolonged.

Other findings may include anemia, leukocytosis, elevated white blood cell count, albuminuria, hyperglycemia or hypoglycemia, and iron, folic acid, and vitamin B₁₂ deficiencies.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

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

Hepatitis: History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

Patients may complain of anorexia, fever, arthralgia, malaise, vomiting, diarrhea, or chills. Complaints of dark urine or jaundice are highly suggestive of hepatitis. As these symptoms are seen in many types of hepatitis, specific questions help categorize the cause.

 A. Viral hepatitis. Does the patient have exposure to blood (transfusions before 1990, tattoos, body piercing, shared razor, needlestick, sharing needles, intranasal cocaine use)? Hepatitis B is most commonly transmitted via contaminated blood or sexually via risky sexual behaviors (anal intercourse, prostitution, multiple sexual partners). Hepatitis A and E are transmitted via the fecal-oral route. Does the patient have a history of travel to developing countries, raw shellfish ingestion, or work in an institution or daycare?

 B. Drug-induced hepatitis. Does the patient use prescription or over-the-counter medication? The drugs most often associated with hepatitis are anesthetics (halothane), neuropsychotropics (chlorpromazine, haloperidol, tricyclics), anticonvulsants (phenytoin), analgesics (acetaminophen, ibuprofen), antigout (allopurinol), hormonal derivatives and drugs used in endocrine disease (glipizide, tamoxifen, anabolic steroids, oral contraceptives), antimicrobials (tetracyclines), cardiovascular drugs (amiodarone, procainamide), antineoplastic (cisplatin), vitamin A, propoxyphene, cimetidine, and ferrous sulfate.

 C. Alcoholic hepatitis. Could the patient be an alcoholic? Inquire about quantitative alcohol intake and obtain a history from both patient and family members. Use the CAGE questionnaire to help identify individuals at high risk. Inquire about alcohol-associated illnesses (pancreatitis) and motor vehicle citations.

 D. Chronic hepatitis. Has the patient ever been jaundiced or diagnosed with hepatitis before (Chapter 9.10)? Has the patient had elevated liver enzymes for at least 6 months? The most common cause of chronic hepatitis and cirrhosis is alcohol. Viral hepatitis B and C often cause chronic hepatitis, cirrhosis, or hepatocellular carcinoma. Other causes of chronic hepatitis are drug-induced, Wilson’s disease, and α₁-antitrypsin deficiency.

E. Autoimmune hepatitis. Is there a history of arthritis, amenorrhea, or rash? Mediated by the deposition of circulating immune complexes, this disease is also referred to as “chronic active hepatitis.” It is more common in female patients and adolescents; prior hepatitis B virus (HBV) or hepatitis C virus (HCV) infection is a triggering factor.

Physical examination

 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.

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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000

Hepatomegaly: History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

 A. Does the patient have known risk factors for liver disease (Table 9.5)?

 B. Does the patient have symptoms associated with liver disease (Table 9.6)?

Physical examination

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).

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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000

Hepatomegaly: Differential Overview
(Field Guide to Bedside Diagnosis)

❑ Acute hepatitis

❑ Chronic hepatitis

❑ Cirrhosis

❑ Right heart failure

❑ Fatty liver

❑ Hepatocellular carcinoma

❑ Metastatic cancer

❑ Lymphoma/leukemia

❑ Liver cysts

❑ Hepatic vein obstruction (Budd-Chiari)

❑ Primary biliary cirrhosis

❑ Hemochromatosis

❑ Amyloidosis

❑ Gaucher

Diagnostic Approach

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

Reye's syndrome: Diagnosis
(Handbook of Diseases)

Early diagnosis and treatment improves chances of recovery. A history of a recent viral disorder with typical signs and symptoms strongly suggests Reye’s syndrome. An increased serum ammonia level, abnormal clotting studies, and hepatic dysfunction confirm it.

Testing the serum salicylate level rules out aspirin overdose. Absence of jaundice, despite increased liver transaminase levels, rules out acute hepatic failure and hepatic encephalopathy.

Abnormal test results may include the following:

❑ Liver-function studies show aspartate aminotransferase and alanine aminotransferase levels elevated to twice normal; bilirubin level is usually normal.

❑ Liver biopsy reveals fatty droplets uniformly distributed throughout cells.

❑ Cerebrospinal fluid (CSF) analysis reveals a white blood cell count of less than 10; with coma, CSF pressure increases.

❑ Coagulation studies result in prolonged prothrombin and partial thromboplastin times.

❑ Blood values show elevated serum ammonia levels; normal or, in 15% of cases, low serum glucose levels; and increased serum fatty acid and lactate levels.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Diseases, 2003

Hepatitis, viral: Diagnosis
(Handbook of Diseases)

In suspected viral hepatitis, a hepatitis profile is routinely performed. This study identifies antibodies specific to the causative virus, establishing the type of hepatitis as follows:

❑ Type A: Detection of an antibody to hepatitis A confirms the diagnosis.

❑ Type B: The presence of HBsAg and hepatitis B antibodies confirms the diagnosis.

❑ Type C: The diagnosis depends on serologic testing for the specific antibody 1 or more months after the onset of acute hepatitis. Until then, the diagnosis is established primarily by obtaining negative test results for hepatitis A, B, and D.

❑ Type D: Detection of intrahepatic delta antigens or immunoglobulin (Ig) M antidelta antigens in acute disease (or IgM and IgG in chronic disease) establishes the diagnosis.

❑ Type E: Detection of hepatitis E antigens supports the diagnosis; the diagnosis may also be determined by ruling out hepatitis C.

❑ Type G: Detection of hepatitis G antigen supports diagnosis; the patient may be otherwise symptomless.

Additional findings from liver function studies support the diagnosis:

❑ Serum aspartate aminotransferase and serum alanine aminotransferase levels are increased in the prodromal stage of acute viral hepatitis.

❑ Serum alkaline phosphatase levels are slightly increased.

❑ Serum bilirubin levels are elevated. Levels may continue to be high late in the disease, especially in severe cases.

❑ Prothrombin time (PT) is prolonged (more than 3 seconds longer than normal indicates severe liver damage).

❑ White blood cell counts commonly reveal transient neutropenia and lymphopenia followed by lymphocytosis.

❑  Liver biopsy is performed if chronic hepatitis is suspected. (It’s performed for acute hepatitis only if the diagnosis is questionable.)

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Source: Handbook of Diseases, 2003

Hepatitis, nonviral: Diagnosis
(Handbook of Diseases)

Diagnostic findings include elevations in serum aspartate aminotransferase, alanine aminotransferase, both total and direct bilirubin (with cholestasis), and alkaline phosphatase levels; white blood cell (WBC) count; and eosinophil count (possible in the drug-induced type).

A liver biopsy may help identify the underlying pathology, especially infiltration with WBCs and eosinophils. Liver function tests have limited value in distinguishing between nonviral and viral hepatitis.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Diseases, 2003

Hepatic encephalopathy: Diagnosis
(Handbook of Diseases)

Clinical features, a positive history of liver disease, and elevated serum ammonia levels in venous and arterial samples confirm hepatic encephalopathy. Other supportive test results include an EEG that slows as the disease progresses, an elevated bilirubin level, and prolonged prothrombin time.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Diseases, 2003

Fatty liver: Diagnosis
(Handbook of Diseases)

Typical clinical features — especially in patients with chronic alcoholism, malnutrition, poorly controlled diabetes mellitus, or obesity — suggest fatty liver. A liver biopsy confirms excessive fat in the liver. The following findings on liver function tests support this diagnosis:

❑ albumin — somewhat low

❑ globulin — usually elevated

❑ cholesterol — usually elevated

❑ bilirubin — elevated

❑ alkaline phosphatase — elevated

❑ transaminase — usually low (less than 300 units)

❑ prothrombin time — possibly prolonged.

Other findings may include anemia, leukocytosis, albuminuria, hyperglycemia or hypoglycemia, and deficiencies of iron, folic acid, and vitamin B₁₂.

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Source: Handbook of Diseases, 2003

Hepatomegaly: History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Hepatomegaly is seldom a patient’s chief complaint. It’s usually discovered 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.

» READ BOOK EXCERPT ONLINE »

Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Hepatomegaly: Clinical Features and Diagnosis
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)

Infection/Inflammation

Hepatitis

Viral