Diseases » Hepatitis X » Diagnosis

Diagnosis of Hepatitis X

Hepatitis X Diagnosis: Book Excerpts

• Ask the Following Questions - HEPATOMEGALY
• Ask the Following Questions - JAUNDICE
• Differential Diagnosis - Hepatomegaly
• Differential Diagnosis - Jaundice
• Differential Diagnosis - Hepatomegaly
• Differential Diagnosis - Jaundice in Infants – Direct
• Differential Diagnosis - Jaundice in Infants – Indirect
• Approach to the Diagnosis - HEPATOMEGALY
• Approach to the Diagnosis - JAUNDICE
• History and physical examination - Hepatomegaly
• History and physical examination - Jaundice
• History and physical examination - Hepatomegaly
• History and physical examination - Jaundice [Icterus]
• History - Hepatomegaly
• History - Jaundice
• Differential Overview - Hepatomegaly
• Differential Overview - Jaundice
• History - Hepatomegaly
• History - Jaundice
• Clinical Features and Diagnosis - Hepatomegaly
• Clinical Features and Diagnosis Unconjugated Hyperbilirubinemia(Neonatal Onset) - Jaundice
• History and physical examination - Hepatomegaly
• History and physical examination - Jaundice [Icterus]
• Approach to the Diagnosis - HEPATOMEGALY
• Approach to the Diagnosis - JAUNDICE

Diagnostic Tests for Hepatitis X: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about diagnostis of Hepatitis X.

HEPATOMEGALY: Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)

1. Is there jaundice? Hepatomegaly with jaundice may make one think of hemolytic anemias; toxic or infectious hepatitis; bile duct obstruction due to stones, carcinoma of the pancreas, or ampulla of Vater; and biliary cirrhosis.
2. Is there fever? Hepatomegaly with fever should make one think of viral hepatitis, infectious mononucleosis, ascending cholangitis, and other infectious diseases.
3. Is there splenomegaly? Hepatomegaly and splenomegaly should make one think of alcoholic cirrhosis, amyloidosis, reticuloendotheliosis, various hemolytic anemias, biliary cirrhosis, and myeloid metaplasia. It should also make one think of various parasitic diseases.
4. Is there an enlarged gallbladder? The presence of hepatomegaly with jaundice and enlarged gallbladder is characteristic of bile duct obstruction due to carcinoma of the pancreas, bile ducts, or ampulla of Vater. The clinician should remember that hydrops of the gallbladder with a common duct stone can mimic the same clinical presentation.
5. Is the splenomegaly massive? Massive splenomegaly is characteristic of Gaucher's disease, kala azar, and myeloid metaplasia. Occasionally, other forms of reticuloendotheliosis may also be associated with massive splenomegaly.
6. Is there another abdominal mass? The presence of another abdominal mass suggests metastatic carcinoma.
7. Is the liver tender? Tenderness of the liver is seen with viral or toxic hepatitis, congestive heart failure, and ascending cholangitis.

DIAGNOSTIC WORKUP

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: Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)

1. Is the jaundice associated with hepatomegaly? There is little or no hepatomegaly associated with hemolytic anemias, pernicious anemia, Gilbert's disease, and Dubin-Johnson syndrome.
2. Is the hepatomegaly massive? Massive hepatomegaly is associated with Gaucher's disease.
3. Is there associated fever, right upper quadrant pain, or a tender liver? These findings would suggest viral hepatitis, cholecystitis, infectious mononucleosis, leptospirosis, ascending cholangitis, hepatic vein thrombosis, and toxic hepatitis.
4. Is the gallbladder enlarged? The finding of an enlarged gallbladder with the jaundice suggests obstructive jaundice, carcinoma of the pancreas, carcinoma of the bowel ducts, or ampulla of Vater.
5. Is there skin pigmentation? The presence of skin pigmentation that is not bilirubin suggests hemochromatosis.
6. Is there splenomegaly? The presence of significant splenomegaly suggests infectious mononucleosis, cirrhosis of the liver, hemolytic anemia, Gaucher's disease, kala azar, or agnogenic myeloid metaplasia.
7. Is there edema and ascites? The presence of edema and ascites suggests alcoholic cirrhosis.

DIAGNOSTIC WORKUP

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: Differential Diagnosis
(In a Page: Signs and Symptoms)

Right heart failure

• 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

Jaundice: Differential Diagnosis
(In a Page: Signs and Symptoms)

• Viral hepatitis
  –Fatigue, anorexia, fever, nausea, vomiting, dark urine, light-colored (acholic) loose stools, RUQ pain, hepatomegaly, and/or pruritis

• Alcoholic hepatitis
  –Associated with fever, leukocytosis, and AST:ALT ratio >2

• Nonalcoholic steatohepatitis or nonalchoholic fatty liver disease
  –Associated with obesity, diabetes, hyperlipidemia and medications

• Cholecystitis
  –RUQ pain, fever, leukocytosis
  –Female, fertile, fat, forty
  –Murphy's sign: Pain upon palpation of the
  gallbladder while taking a deep breath

• Drugs and toxins
  –Acetaminophen, alcohol, estrogens, isoniazid, chlorpromazine, erythromycin, nitrofurantoin, rifampin

• Gilbert's syndrome
  
  –Decreased conjugation of bilirubin, especially with dehydration, fasting, infection

Sepsis

Malignancy (liver, pancreas, gallbladder/common bile duct, metastatic)

• Liver infiltration
  –Amyloidosis, lymphoma, sarcoidosis, tuberculosis

Total parenteral nutrition (usually requires at least 2 weeks of therapy)

Intravascular hemolysis

• Cholangitis
  –Charcot's triad of fever, RUQ pain, and jaundice

Sickle cell disease
–Chronic hemolysis, hepatic dysfunction

• Autoimmune hepatitis
  –May mimic viral hepatitis
  –Females >> males, often 10–30 years old
  –Associated with autoimmune disease
  (e.g., RA, UC, Sjögren's syndrome, thyroiditis)

Intrahepatic cholestasis of pregnancy
–Pruritus in third trimester
–Resolves after delivery

Hereditary cholestatic disorders (e.g., Dubin-Johnson syndrome, Rotor syndrome)

Physiologic jaundice of newborn

Workup and Diagnosis

• History and physical examination
  –Duration, associated symptoms (e.g., abdominal pain, constitutional symptoms, pruritis), history of alcohol use or hepatotoxic medications, and/or personal/family history of liver disease
  –Jaundice is best seen in the periphery of ocular conjunctivae and oral mucous membranes
  –Yellow skin discoloration may occur with elevated serum carotene level without scleral icterus
  –Evaluate for hepatomegaly, splenomegaly, palpable gallbladder, and signs of chronic liver disease (e.g., gynecomastia, testicular atrophy, palmar erythema, spider telangiectasias)

• Initial laboratory evaluation includes total and unconjugated (indirect) bilirubin (cannot detect jaundice until serum bilirubin >2 mg/dL), AST, ALT, alkaline phosphatase (elevated with hepatocellular damage or cholestasis), albumin, HIV and hepatitis serologies (if risk factors present), reticulocyte count, LDH, haptoglobin (hemolysis), prothrombin time (to evaluate synthetic liver dysfunction or vitamin K deficiency), ANA (autoimmune hepatitis), and possibly antimitochondrial antibodies (primary biliary cirrhosis)
• Abdominal ultrasound or CT scan to evaluate for biliary obstruction, dilated ducts, pancreatic mass, or gallstones
• ERCP if extrahepatic obstruction on imaging tests
• Liver biopsy is generally not necessary

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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

Jaundice in Infants – Direct: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

• Bile duct obstruction
  –Biliary atresia: Represents the most frequent cause for liver transplantation in the pediatric patient; prompt diagnosis is crucial, as patient outcome is better if intervention comes before 60 days of life
  –Choledochal cyst
  –Common bile duct gallstone
  –Choledochocele
  –Bile duct stricture
  –Alagille syndrome
  –Caroli disease
  –Congenital hepatic fibrosis

• Neonatal hepatitis
  –Idiopathic hepatitis: Diagnosis of exclusion that should be made only when other causes are excluded; accounts for 60% of patients with neonatal cholestasis
  –Infections: TORCH, hepatitis B, HIV, E. coli, adenovirus, enterovirus, parvovirus B16, tuberculosis, listeriosis, malaria

• Metabolic disorders
  –α-1 antitrypsin deficiency
  –Cystic fibrosis
  –Hypothyroidism
  –Neonatal iron storage disease
  –Amino acids: tyrosinemia
  –Carbohydrates: Galactosemia, fructosemia
  –Lipids: Niemann-Pick, Gaucher, Wolman, cholesterol ester storage disease
  –Mitochondropathies
  –Bile acid synthetic disorders
  –Peroxisomal: Zellweger syndrome
  –Urea cycle defects
• Toxins
  –Total parenteral nutrition
  –Drugs: Trimethaprim-sulfamethoxazole, anticonvulsants
• Miscellaneous
  –Sepsis/hypoperfusion
  –Erythrophagocytic lymphohistiocytosis
  –Extracorporeal membrane oxygenation
  –Trisomy 17, 18, 21
  –Neonatal lupus erythematosus
  –Donohue syndrome
  –Rotor syndrome
  –Dubin-Johnson syndrome
  –Byler disease (PFIC type 1)
  –Cholestasis of North-American Indians
  –Nielsen syndrome

Workup and Diagnosis

• History
  –Prenatal/perinatal history: Infections, gestational age, birth weight, miscarriages, newborn screen
  –Age of onset, activity level, oral intake, urine output, stool color, emesis, hematemesis, hematochezia, melena, bruising, bleeding, fever, developmental milestones, medications, formula type
• Physical exam: Weight/length, icteris, dysmorphic features, cardiac murmur, ascites, abdominal distension, hepatosplenomegaly, edema, bruising, tone, reflexes
• Labs (initial): Fractionated bilirubin (total, indirect, direct), AST, ALT, GGT, alkaline phosphatase, total protein, albumin, CBC, electrolytes including glucose, PT, PTT, blood/urine culture, U/A
• Labs (directed): Thyroid function tests, serum α-1 antitrypsin level, urine for reducing sugars, serum and urine amino acids, urine organic acids including succinylacetone, infectious serologies, serum iron levels, sweat test, consider Alagille genetic testing
• Ultrasound provides best initial radiographic study for obstruction, hepatosplenomegaly
  
• Hepatobiliary scintigraphy (HIDA scan)
• Percutaneous liver biopsy
  –Histology, virology, electron microscopy for bile duct expansion/paucity, storage disorders
• Exploratory laparotomy and intraoperative cholangiogram to rule out biliary atresia
• Consider X-ray for butterfly vertebrae (for Alagille)

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

Jaundice in Infants – Indirect: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

• Icterus neonatorum (physiologic jaundice)
  –The most common form of indirect jaundice in infants under 14 days of age
  –Caused by increased bilirubin production with transient limited conjugation abilities
• Breast-feeding jaundice
  –Occurs in first week of life in 13% of breast-fed infants
  –Secondary to poor volume intake
• Breast-milk jaundice
  –Occurs in about 2% of breast-fed infants after day 7 of life
  –Secondary to glucuronidase in breast milk
• Hematologic: Hemolysis increases bili load
  –Rh incompatability
  –ABO incompatability
  –Glucose-6-phosphate dehydrogenase (G6PD) deficiency
  –Pyruvate kinase deficiency
  –Hereditary spherocytosis
  –Elliptocytosis
  –Thalassemia
  –Polycythemia
• Extravascular blood
  –Cephalohematoma
  –Trauma
  –Swallowed maternal blood
• Endocrinologic
  –Hypothyroidism
  –Maternal diabetes
• Sepsis
• Metabolic
  –Crigler-Najjar I
  –Crigler-Najjar II (Arias syndrome)
  –Crigler-Najjar III
• Cardiopulmonary
  –Congestive heart failure
  –Patent ductus arteriosus
  –Portal vein thrombosis
• Anatomic
  –Pyloric stenosis
  –Duodenal atresia/stenosis
  –Duodenal web
• Drugs
  –Oxytocin
  –Sulfonamides
  –Ceftriaxone
  –Chuen-Lin
• Lucey-Driscoll syndrome

Workup and Diagnosis

• History
  –Prenatal/perinatal: Pregnancy complications, gestational age, maternal blood type/Rh, drug use, infections, delivery method, delivery intervention, birth weight, newborn screen results, previous miscarriages
  –HPI: Onset of jaundice, feeding tolerance, appropriate weight gain, trauma, evidence of bleeding/bruising, urine output, stool output/diarrhea, emesis, lethargy, drug exposure
  –Diet history: Breast- and/or formula-fed, length of time on each breast, latch strength
  –Family history: Bleeding disorders, perinatal deaths, endocrinopathies

• Physical exam
  –Weight, overall appearance, level of jaundice, fontanelle size, cranial abnormalities, scleral icteris, mucous membranes, cardiac murmurs, hepatosplenomegaly, bruising, bleeding, reflexes, tone, seizures
• Labs: Fractionated bilirubin (total, indirect, direct), CBC with smear, reticulocyte count
• Hemolysis: Blood type/Rh, Coombs, hemoglobin electrophoresis
• Thyroid function tests (check state newborn screen)
• Limited value of imaging unless looking for obstruction or bleeding
• Hearing evaluation if kernicterus likely

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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.

» READ BOOK EXCERPT ONLINE »

Source: Differential Diagnosis in Primary Care, 2007

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

The accurate diagnosis of jaundice is established by the association of other symptoms and the performance of liver function and special diagnostic procedures. For example, jaundice with fever, a prodromal phase of anorexia, malaise, and a tender liver suggests hepatitis. Jaundice with itching suggests xanthomatous or primary biliary cirrhosis. Jaundice and anemia suggest hemolytic anemia. Jaundice, back pain, and an abdominal mass suggest a carcinoma of the pancreas.

When liver functions show only an elevated indirect bilirubin level, Gilbert disease or hemolytic anemia is suggested. A normal urine urobilinogen will make Gilbert disease even more likely. Liver function analyses showing only elevated bilirubin and alkaline phosphatase levels suggest bile duct obstruction by a stone or tumor. Liver function results showing an impressive elevation of the bilirubin, serum aspartate aminotransferase, and serum alanine aminotransferase levels suggest hepatitis.

In cases in which obstruction versus parenchymal disease remains a dilemma after routine tests, several newer procedures have been developed that may help avoid an exploratory laparotomy. ERCP, cutaneous transhepatic cholangiography, and peritoneoscopy are very useful in these cases. CT scans and ultrasonography are also valuable. The old steroid whitewash is still useful. This is done by administering 20 mg of prednisone daily for 5 days and monitoring the bilirubin level. A positive test, indicating parenchymal diseases, is considered a drop of the bilirubin to one half its original value or more. Exploratory laparotomy may be necessary despite an extensive workup.

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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.

» READ BOOK EXCERPT ONLINE »

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.

» READ BOOK EXCERPT ONLINE »

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: 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

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

 A. Does the patient have exposure risk to alcohol, drugs, toxins, or medications? A history of nonprescription and prescription drugs and potential chemical toxins at home or work must be elicited.

 B. Recent trauma can result in hemolysis. Pruritus, dark urine, and clay-colored stools suggest cholestasis. If the patient presents with right upper quadrant pain and nausea following a fatty meal, think cholelithiasis. A fever with right upper quadrant pain suggests cholangitis or, with a history of exposure, hepatitis. Jaundice, vague epigastric discomfort, and weight loss suggest pancreatic cancer. A family history of liver disease points to a hereditary cause (e.g., Gilbert’s or Wilson’s syndromes).

C. Is the jaundice acute or chronic? Acute onset of jaundice suggests a viral hepatitis, acute liver failure, or an acute biliary tract obstruction. Gradual onset of jaundice points to chronic liver failure, alcohol toxicity, or malignancy. A lifelong history of jaundice suggests an inherited metabolic or hemolytic cause.

Physical examination

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.

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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

Jaundice: Differential Overview
(Field Guide to Bedside Diagnosis)

Conjugated

❑ Viral hepatitis

❑ Gallstone obstruction

❑ Drugs

❑ Carotinemia

❑ Alcohol-induced hepatitis

❑ Cirrhosis

❑ Pregnancy (cholestatic)

❑ Postoperative

❑ Metastatic cancer

❑ Pancreatic cancer

❑ Ampullary carcinoma

❑ Hepatoma

❑ Sclerosing cholangitis

❑ Primary biliary cirrhosis

❑ Leptospirosis

❑ Hepatic vein obstruction (Budd-Chiari)

❑ Hemochromatosis

Unconjugated

❑ Hemolysis

❑ Gilbert syndrome

❑ Sepsis

Diagnostic Approach

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: 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.

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

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

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 pancreatic disease.

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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

May be dueto hepatitis viruses (A, B, C, D, E), and liver may be enlarged.

Other viruses that also may producehepatomegaly include Epstein-Barr virus, herpes simplex virus, rubellavirus, cytomegalovirus, and HIV.

See Chap.36, Jaundice, and Chap.53, Recurrent Infection.

Bacterial

A number of bacterial infections may causehepatomegaly. They include septicemia, endocarditis, brucellosis,leptospirosis, cat scratch disease, tuberculosis, and liver abscess.See Chap. 7, Cardiac Failure; Chap. 10, Cough; Chap. 21, Fever; and Chap. 42, Neck Masses.

Other Infections

Rickettsial (Rocky Mountain spotted fever),fungal (histoplasmosis, coccidioidomycosis), and parasitic (malaria,amebiasis, toxoplasmosis, ascariasis, schistosomiasis, toxocariasis)infection also may produce hepatomegaly. See Chap. 10, Cough; Chap. 14, Diarrhea; Chap. 21, Fever; Chap. 36, Jaundice;, and Chap. 60, Skin Lesions and Rashes.

Toxic

Certain drugs may cause hepatic injury andhepatomegaly. See Chap. 36, Jaundice.

Autoimmune

Autoimmune hepatitis also may cause hepatomegaly.See Chap. 36, Jaundice.

Cholangitis

Enlarged tender liver and jaundice may occurwith cholangitis. See Chap. 36,Jaundice.

Hemolytic Anemia

Virtually any hemolytic anemia [see Chap. 45, Pallor (Anemia)] cancause hepatomegaly as well as splenomegaly as result of extramedullaryhematopoiesis; however, this is usually seen in infants.

Cardiac Disorders

Moderate-to-severe cardiac failure may producehepatomegaly. Other causes of hepatomegaly include pericardial disease(e.g., constrictive pericarditis and cardiac tamponade).

Trauma

Trauma toliver can produce tender enlarged liver. Hypotension and shock mayoccur with significant bleeding.

Serum aspartate aminotransferase >200U/L and alanine aminotransferase >100 U/Lindicate probable hepatic injury.

CT should be performed to determinelocation and extent of liver injury.

Bile Duct Obstruction

See Chap.36, Jaundice, for discussion of biliary atresiaand Caroli disease.

Vascular Disorders

See Chap.36, Jaundice, for discussion of Budd-Chiari syndromeand venoocclusive disease.

Neoplasia

Primary hepatic tumors are discussed in Chap. 1, Abdominal Masses.Leukemia, lymphoma, neuroblastoma, and Wilms tumor are discussedin Chap. 1, Abdominal Masses,and Chap. 38, Lymphadenopathy.

Metabolic Disorders

All metabolic disorders listed below arediscussed in other chapters, except glycogen storage diseases, Wolmandisease, and cholesterol ester disease.

Disordersof carbohydrate metabolism

Galactosemia

Hereditary fructose intolerance

Glycogen storage disease

Glycogen storagedisease type I

Glycogen storage disease type III

Glycogen storage disease type IV

Glycogen storage disease type VI

Disorders of amino acid metabolism

Tyrosinemia

Urea cycle defects

Disorders of lysosomal storage

Mucopolysaccharidoses

Lipidoses

Gaucher disease (types I, II, III)

Niemann-Pick disease (types A, B, C)

GM-1 gangliosidosis

GM-2 gangliosidosis (Sandhoff disease)

Glycoprotein disorders

Fucosidosis(types I, II)

Sialidosis type II

Wolman disease and cholesterol esterdisease

Disorders of fatty acid oxidation

Disorders of bile acid synthesis andtransport

Alpha₁-antitrypsindeficiency

Wilson disease

Reye syndrome

Zellweger syndrome

Disorders of Carbohydrate Metabolism

Glycogen Storage Disease

Principal forms of glycogen storage diseaseassociated with hepatomegaly include types I, III, IV, and VI.

Glycogen Storage Disease Type I

Type Iais caused by deficiency in enzyme glucose-6-phosphatase, which catalyzes conversionof glucose-6-phosphate to glucose. Gene locus has been mapped tochromosome 17q21.

Type Ib is caused by deficiency inglucose-6-phosphate transport protein and gene locus has been localizedto chromosome 11q23.

Genetic transmission of both typesis autosomal-recessive.

Hypoglycemia and lactic acidosis canoccur after brief fasting, while hepatomegaly is usually noted by3–4 mos of age. Other findings include hyperuricemia andhyperlipidemia. There is no significant increase in blood glucoseafter glucagon administration.

Diagnosis can be confirmed by liverbiopsy and enzyme assay or by molecular genetic analysis.

Glycogen Storage Disease Type III

Autosomal-recessivedisorder caused by deficiency of glycogen debranching enzyme amylo-1,6-glucosidase.Gene locus has been mapped to 1p21.

Type IIIa involves both liver and muscle,while type IIIb involves only liver.

Clinical features include hepatomegaly,cardiomyopathy, muscle weakness, poor growth, hypoglycemia, andhyperlipidemia.

Diagnosis is confirmed by enzyme assayof liver and muscle tissue.

Glycogen Storage Disease Type IV

Deficiencyof glycogen branching enzyme results in hepatomegaly and failureto thrive, with onset usually in first few months of life. Autosomal-recessivedisorder with gene locus mapped to chromosome 3p12.

In most cases, progressive liver dysfunctionand cirrhosis occur. Some children also have hypotonia and weakness,with muscle atrophy and decreased or absent deep tendon reflexes.A few also develop cardiomyopathy.

Demonstration of deficient branchingenzyme activity in liver, muscle, cultured fibroblasts, or leukocytesis diagnostic.

Glycogen Storage Disease Type VI

Deficientenzyme in this autosomal-recessive disorder is liver phosphorylase.Gene locus has been mapped to chromosome 14q21-q22.

In early childhood, hepatomegaly andpoor growth occur. Hypoglycemia and hyperlipidemia also can occurbut are usually mild. Heart and skeletal muscle are unaffected.

Liver biopsy with enzyme assay is diagnostic.

Disorders of Lysosomal Storage

Wolman Disease and Cholesterol Ester Disease

Deficiencyin enzyme activity of lysosomal acid lipase occurs in both of theseautosomal-recessive disorders. Gene locus has been mapped to chromosome10q24-25. Cholesterol esters and triglycerides accumulate in histiocyticfoam cells of most visceral organs.

Wolman disease presents in neonatalperiod with persistent vomiting, steatorrhea, failure to thrive,and hepatosplenomegaly. There is diffuse punctate calcificationin adrenal gland. Death usually occurs in infancy.

Cholesterol ester storage disease isless severe than Wolman disease and has later onset. Hepatomegalymay be only physical finding. Adrenal calcification does not occur.Individuals with this disease are at risk for premature atherosclerosis.

Enzyme assay of peripheral lymphocytesor cultured fibroblasts is diagnostic.

Systemic Disorders

Obesity

Hepatomegaly with fat accumulation in livermay occur in obese children. Serum bilirubin is usually normal,whereas serum aminotransferases and alkaline phosphatase may beincreased.

Diabetes Mellitus

Liver may be enlarged in individuals withdiabetes mellitus because of fat accumulation or increased glycogenstores. Hepatomegaly is reversible with improved control of bloodglucose concentration.

Cystic Fibrosis

Several liver and biliary tract complicationsmay occur with cystic fibrosis, including fat accumulation, focaland multilobular biliary cirrhosis, portal hypertension, and cholelithiasis.

Malnutrition

Massive hepatomegaly may occur with kwashiorkordue to fat accumulation in liver.

Connective Tissue Diseases

Hepatomegaly and splenomegaly may occur withjuvenile rheumatoid arthritis, systemic lupus erythematosus, andmixed connective tissue disease.

Histiocytoses

Hepatosplenomegaly may occur in each of thethree classes of histiocytoses. See Chap.38, Lymphadenopathy.

Total Parenteral Nutrition

Effect onliver depends on age of child. Cholestasis is main response in infants, whereasolder children develop fat accumulation and hepatitis. In both agegroups, end-stage liver disease may occur; however, pathogenesisis unknown.

First clinical indication may be hepatomegalyafter 2–3 wks of parenteral nutrition. Increase in serumbile acid and direct bilirubin concentrations follows. Serum aminotransferaseand alkaline phosphatase concentrations increase days to weeks later.

Diagnostic Approach

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 fibrosis

Hepatic outflow obstruction

Fatty liver

Metabolic 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 D

Drug-induced hepatitis

Autoimmune hepatitis

Alpha₁-antitrypsindeficiency

Wilson disease

Sclerosing cholangitis

Association with Systemic Disorders

Hepatomegaly may occur with the followingsystemic disorders:

Cardiacfailure

Systemic infection

Diabetes mellitus

Cystic fibrosis

Connective tissue diseases

Hematologic disorders (sickle celldisease, leukemia)

Sarcoidosis

Inflammatory bowel disease

Histiocytoses

Persistent Vomiting and Altered Consciousness

Disorders that cause persistent vomiting,alteration in consciousness, and hepatomegaly include

Fulminanthepatic failure

Reye syndrome

Metabolic disorders

Urea cycledefects

Fatty acid oxidation disorders

Organic acidemias

Respiratory chain defects

Disorders of gluconeogenesis

Carbohydrate 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 disease

Zellweger syndrome

Lab Tests

If hepatomegalyor hepatosplenomegaly occurs without jaundice, several tests should beconsidered initially:

CBC and differential

Reticulocyte count

Liver function tests including serumaspartate aminotransferase, alanine aminotransferase, alkaline phosphatase,total protein, albumin, fractionated bilirubin

sedimentation rate

Serum alpha₁-antitrypsinand Pi phenotype

Serum ceruloplasmin

Prothrombin and activated partial thromboplastintimes

UA

Urine 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: Clinical Features and Diagnosis: Unconjugated Hyperbilirubinemia(Neonatal Onset)
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)

Increased Bilirubin Production

Physiologic

Physiologicjaundice is most common cause of jaundice in newborns. Certain mechanismsproduce physiologic jaundice:

Decrease in life span of red cells (70–80days)

Increase in number of red cells incirculation (normal hematocrit range in newborns, 45–65%)

Increase in blood volume of newborns(85–90 mL/kg)

Enhanced enterohepatic circulationsecondary to diminished intestinal motility

Decrease in activity of enzyme uridinediphosphate glucuronyl transferase, which catalyzes conjugationof bilirubin with glucuronic acid

In term infants, jaundice appears after24 hrs of age, peaks at 2–4 days of age, and resolves at1–2 wks of age.

In preterm infants, maximum serum bilirubinis usually 3–5 mg/dL higher than in term infants.It peaks at 5–7 days of age and usually returns to normalby 2 mos. Maisels and Gifford (1986) reported that ninety-seventhpercentile for maximum serum bilirubin concentration is 12.4 mg/dLfor bottle-fed infants and 15.7 mg/dL for breast-fed infants.

Diagnosis of physiologic jaundice isone of exclusion.

Hemolytic Anemia

Isoimmunization

ABO incompatibilityis most common cause of isoimmunization in newborns. Potential ABOincompatibility exists with type O mother and type A or B infant.Serum bilirubin varies with degree of hemolysis, which is usuallymild. Direct Coombs test is usually positive.

Rh isoimmunization is uncommon nowbecause anti-D immune globulin can be given to Rh-negative motherafter delivery of her infant or after an abortion. Otherwise, Rhisoimmunization can be anticipated by prenatal Rh testing and monitoredwith serial amniocenteses during pregnancy. Intrauterine transfusioncan be performed if necessary.

If not recognized prior to delivery,Rh incompatibility may cause anemia, jaundice, hepatosplenomegaly,and cardiac failure at birth or in first 24 hrs of life. Positivedirect Coombs test of infant's blood indicates that maternalimmunoglobulin G (IgG) has crossed placenta and attached to infant'sred cell antigens.

Minor group antibodies against otherRh antigens and Lewis, Kell, and Duffy systems also may cause hemolysis.

Red Cell Enzyme Defects

Glucose-6-Phosphate Dehydrogenase Deficiency

X-linkeddisorder that is most common red cell enzyme deficiency.

Incidence among African-American malesis about 10%, but hemolysis is unusual except with infectionor exposure to certain drugs (e.g., sulfonamides).

In some infants, jaundice may occurwithout exposure to known hemolytic agents.

Quantitative assay of enzyme in redcells confirms diagnosis [see Chap. 45, Pallor (Anemia)].

Pyruvate Kinase Deficiency

Second mostcommon red cell enzyme deficiency.

May present in neonatal period withhemolytic anemia and jaundice.

Assay of enzyme in red cells confirmsdiagnosis [see Chap.45, Pallor (Anemia)].

Other Enzyme Defects

Hemolyticanemia and jaundice also can occur with deficiencies of certainred cell enzymes:

Hexokinase

Glucose phosphate isomerase

Phosphofructokinase

Triose phosphate isomerase

Glyceraldehyde-3-phosphate dehydrogenase

Phosphoglycerate kinase

2,3-Bisphosphoglycerate mutase

Pyrimidine-5′-nucleotidase

Measuring concentration of deficientenzyme in red cells confirms diagnosis.

Red Cell Membrane Defects

Hereditary Spherocytosis

Most commonred cell membrane defect.

Usual manifestations are hemolyticanemia, mild jaundice, and splenomegaly. Blood smear shows densemicrospherocytes.

Positive incubated osmotic fragilitytest result confirms diagnosis [see Chap. 45, Pallor (Anemia)].

Hereditary Elliptocytosis

May produce hemolytic anemia and mild jaundicein neonatal period. Presence of elliptocytes on blood smear confirmsdiagnosis [see Chap.45, Pallor (Anemia)].

Hereditary Stomatocytosis

Stomatocytesare red cells with slit-like area of pallor in their center.

In some cases severe hemolysis canproduce jaundice and splenomegaly.

Presence of stomatocytes on blood smearis diagnostic [see Chap.45, Pallor (Anemia)].

Infantile Pyknocytosis

Transientabnormality of erythrocyte morphology whose cause is unknown.

Hemolytic anemia usually peaks at 3–4wks of age.

Diagnostic blood smear shows densespiculated red cells called pyknocytes.

Spontaneous resolution occurs in afew months as soon as normal red cells replace abnormal ones.

Septicemia

May cause hemolysis with increase in unconjugatedbilirubin and jaundice. Resolution occurs with successful treatmentof septicemia.

Polycythemia

During first2 days of life, about 5% of newborns have polycythemia,which is defined as a venous Hct >65%.

Possible causes include delayed clampingof umbilical cord, maternal-fetal or twin-twin transfusion, intrauterinehypoxia, and maternal diabetes mellitus. Destruction of larger redcell mass than normal leads to unconjugated hyperbilirubinemia.

Enclosed Hematoma

Birth trauma may produce large cephalohematoma,subdural hematoma, or sequestered blood in abdomen or chest. Destructionof red cells produces increase in unconjugated bilirubin that usuallyresolves by 1–2 wks of age.

Decreased Bilirubin Uptake, Storage, or Metabolism

In addition to causes discussed below, unconjugatedhyperbilirubinemia due to decreased bilirubin uptake, storage, ormetabolism can have physiologic or septicemic causes.

Hypoxia and Acidosis

May contribute to increase in serum bilirubinconcentration because of decreased binding of bilirubin with albumin.

Hypoalbuminemia

If serum level of albumin is decreased, lessis available to bind bilirubin, and jaundice may occur.

Increased Serum Fatty Acids

Primary metabolic products of intravenousfat emulsions are free fatty acids. In high concentration, theycan block binding of bilirubin and albumin, which leads to higherserum bilirubin concentration.

Drugs

Sulfonamides and ceftriaxone displace bilirubinfrom secondary albumin-binding sites, which can lead to increasein serum bilirubin concentration.

Hypothyroidism

Althoughjaundice may be one presenting sign of primary hypothyroidism inneonates, pathogenesis is unclear.

Clinical features of hypothyroidismare discussed in Chap. 23, GrowthDeficiency: Weight and Height.

Low thyroxine (T₄)and high TSH serum levels confirm diagnosis.

Jaundice resolves with proper treatmentof hypothyroidism.

Lucey-Driscoll Syndrome (Transient Familial Neonatal Hyperbilirubinemia)

Rare disorderthat occurs during first few days of life.

In many cases, kernicterus developsunless exchange transfusions are performed. Serum bilirubin levelcan reach ≥60 mg/dL in untreated infants.

Unidentified inhibitor of uridine diphosphateglucuronyl transferase has been found in maternal and infant serum.

Inhibitory effect declines by about2 wks of age.

Crigler-Najjar Syndrome (Types I and II)

Autosomal-recessivedisorder that is caused by deficiency in enzyme activity of uridinediphosphate glucuronyl transferase, whose gene locus has been mappedto chromosome 2q37. Because of severe decrease in enzyme activityin type I, severe jaundice occurs.

Hyperbilirubinemia is milder in typeII because of less severe decrease in enzyme activity. Distinguishingcharacteristic is decrease in serum bilirubin seen in type II afteradministration of phenobarbital compared to no response in typeI.

Liver biopsy with enzyme assay is confirmatory.

Increased Enteropathic Circulation

In addition to causes discussed below, unconjugatedhyperbilirubinemia due to increased enteropathic circulation canhave physiologic causes.

Breast-Feeding–Related Jaundice

When itoccurs as early as 2–4 days of age, it is called breast-feeding–associatedjaundice. When it occurs later (4–7 days of age), it hasbeen called breast milk jaundice syndrome. Overlap occurs betweenthese 2 entities, and evidence to support 2 distinct conditionsis meager.

Mechanisms thought to explain jaundiceassociated with breast-feeding are decreased caloric intake andincrease in enterohepatic circulation of bilirubin.

Evidence for inhibitory substancesin breast milk is conflicting.

Intestinal Obstruction

Contributesto delay in bowel transit time that allows more time for bilirubindeconjugation and reabsorption.

Unconjugated hyperbilirubinemia mayoccur with pyloric stenosis, duodenal or ileal atresia, Hirschsprungdisease, and meconium ileus.

Jaundice resolves with proper treatmentof the basic lesion.

Clinical Features and Diagnosis: Unconjugated Hyperbilirubinemia(Postneonatal Onset)

In addition to hemolytic anemia and Gilbertsyndrome, septicemia may cause unconjugated hyperbilirubinemia.

Increased Bilirubin Production

Hemolytic Anemia

Any hemolytic anemia may produce unconjugatedhyperbilirubinemia. See Chap.45, Pallor (Anemia).

Decreased Bilirubin Uptake, Storage, or Metabolism

Gilbert Syndrome

Onset ofthis disorder, which may be transmitted as autosomal-dominant or-recessive trait, is generally in childhood or adolescence.

Uridine diphosphate glucuronyl transferaseactivity is <50% of normal, which results in mild,fluctuating unconjugated hyperbilirubinemia. Illness, fasting, andstress can exacerbate jaundice. Remainder of liver function testsare normal and there is no hemolysis.

Administration of phenobarbital candecrease serum bilirubin level.

Diagnostic Approach: Unconjugated Hyperbilirubinemia

Most commoncauses of neonatal unconjugated hyperbilirubinemia are physiologic jaundiceand breast-feeding–related jaundice.

Diagnostic tests should be performedin

Neonateswho become clinically jaundiced during first 24 hrs of life

Term bottle-fed infants whose maximumserum bilirubin exceeds 12 mg/dL

Term breast-fed infants whose maximumserum bilirubin exceeds 15 mg/dL

Preterm infants

Certain tests should be performed initially:

Maternal andinfant blood groups and Rh types

Unconjugated and conjugated serum bilirubin

CBC and differential

Reticulocyte count

Direct Coombs test

Analysis 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

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 be 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

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

The accurate diagnosis of jaundice is established by the association of other symptoms and the performance of liver function and special diagnostic procedures. For example, jaundice with fever, a prodromal phase of anorexia, malaise, and a tender liver suggests hepatitis. Jaundice with itching suggests xanthomatous or primary biliary cirrhosis. Jaundice and anemia suggest hemolytic anemia. Jaundice, back pain, and an abdominal mass suggest a carcinoma of the pancreas. When liver functions show only an elevated indirect bilirubin level, Gilbert disease or hemolytic anemia is suggested. A normal urine urobilinogen will make Gilbert disease even more likely. Liver function analyses showing only elevated bilirubin and alkaline phosphatase levels suggest bile duct obstruction by a stone or tumor. Liver function results showing an impressive elevation of the bilirubin, serum aspartate aminotransferase, and serum alanine aminotransferase levels suggest hepatitis. In cases in which obstruction versus parenchymal disease remains a dilemma after routine tests, several newer procedures have been developed that may help avoid an exploratory laparotomy. Endoscopic retrograde cholangiopancreatography (ERCP), cutaneous transhepatic cholangiography, and peritoneoscopy are very useful in these cases. Computed tomography (CT) scans and ultrasonography are also valuable. The old steroid whitewash is still useful. This is done by administering 20 mg of prednisone daily for 5 days and monitoring the bilirubin level. A positive test, indicating parenchymal diseases, is considered a drop of the bilirubin to one half its original value or more. Exploratory laparotomy may be necessary despite an extensive workup.

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Source: Differential Diagnosis in Primary Care, 2007

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