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Diseases » Leptospirosis » Diagnosis

Diagnosis of Leptospirosis

Diagnostic Test list for Leptospirosis:

The list of medical tests mentioned in various sources as used in the diagnosis of Leptospirosis includes:

Leptospirosis Diagnosis: Book Excerpts

Tests and diagnosis discussion for Leptospirosis:

The confirmatory microscopic agglutination test (MAT) is too labor intensive and not widely available. Rapid serologic assays have been shown to be sensitive and specific. (Source: excerpt from Leptospirosis: DBMD)

Diagnostic Tests for Leptospirosis: Online Medical Books

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

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

Is there a history of drug ingestion or injection? This will help diagnose drug reactions and serum sickness, which are common and easily discovered in the history. Patients with glucose-6-phosphate dehydrogenase deficiency may develop fever after receiving certain drugs.
Is there a rash? The presence of a rash should make one think of a drug reaction, meningococcemia, the various exanthems, and subacute bacterial endocarditis.
Is there localized pain? If there is a sore throat, obviously streptococcal pharyngitis or a viral URI is likely. If there is headache, meningitis or encephalitis must be considered. If there is chest pain, one should consider a pulmonary infarct, myocardial infarction, or Bornholm disease. If there is abdominal pain, one would consider pyelonephritis, cholecystitis, and appendicitis among the various conditions. If there is joint pain, one should consider rheumatic fever, rheumatoid arthritis, or septic arthritis.
Is there a focal discharge? A productive cough would make one consider pneumonia. A rectal discharge would make one consider a perirectal abscess. A urethral discharge should make one think of gonorrhea.
Are there other localizing signs? Frequency of urination should make one think of pyelonephritis. A productive cough should make one think of pneumonia, whereas jaundice would make one think of hepatitis.

DIAGNOSTIC WORKUP

Routine studies include a CBC, sedimentation rate, chemistry panel, urinalysis, chest x-rays, VDRL test, and tuberculin skin test. Serial blood cultures should be done on all patients. Febrile agglutinins usually should be done. An ASO titer or streptozyme test should be done to exclude rheumatic fever. RNA, ANA, and DNA tests should be done to look for lupus and other connective tissue disease. An HIV antibody titer may need to be ordered.

The next step is to culture any discharge or various body fluids that might be suspect. Thus, a urinalysis and urine culture should be done. A nose and throat culture should be done. A sputum smear and culture may need to be done. The next consideration is to do various serologic tests. A heterophile antibody titer should be done in teenagers. Febrile agglutinin tests may need to be done. Acute and convalescent phase sera for viral studies may need to be done.

Next one should do skin testing. Thus, histoplasmin, coccidioidin, and blastomycin skin testing should be done on patients with a cough. Trichinella skin testing may need to be done, as well as brucellin skin testing. A Kveim test might need to be done for suspected sarcoidosis.

The next step is to do plain x-rays of suspected areas. For instance, x-rays of the teeth may disclose an abscessed tooth. X-rays of the long bones may disclose a metastatic carcinoma.

The next step is contrast x-ray studies of various organ systems. An intravenous pyelogram may show a hypernephroma. A cholecystogram may show gallstones. An upper GI series and barium enema may show chronic pancreatitis or diverticulitis. Angiography may disclose periarteritis nodosa, aortitis or giant cell arteritis.

The next step is to do a CT scan of the abdomen and pelvis. If this is negative, consider a CT scan of the chest and mediastinum. Echocardiography may disclose valvular vegetations or an atrial myxoma.

Next, consider biopsying various organ systems. For instances, a lymph node biopsy may disclose a lymphoma or sarcoidosis. A muscle biopsy may disclose periarteritis nodosa, polymyositis, or trichinella.

Next one should do bone scans and gallium scans for possible metastasis, osteomyelitis, or localized abscesses.

If all these procedures fail to turn up a lesion, then an exploratory laparotomy may need to be done. A fibrin test may indicate Mediterranean fever, or urine for etiocholanolone may also indicate a relapsing type of fever. A urine test for porphobilinogen may diagnose porphyria.

The wisest move is to conduct this investigation with the help of an infectious disease specialist or a specialist in the body organ system most likely suspected of harboring the infection.

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

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

Is there a history of drug ingestion or injection? Of course, the history should reveal that the patient has been on a certain drug or has received certain antitoxins, serums, or vaccines.
Is there a rash? If there is a rash, one should suspect subacute bacterial endocarditis, Rocky Mountain spotted fever, secondary syphilis, rat-bite fever, pemphigus, a drug reaction, lupus erythematosus, dermatomyositis, or typhoid fever. There are other conditions associated with a rash also.
Is there a characteristic pattern to the fever? The various forms of malaria give a characteristic pattern of the fever, as well as undulant fever in Hodgkin's disease.
Is there localized pain? Abdominal pain should suggest a cholecystitis, hepatic abscess, diverticulitis, etc. A sore throat should suggest infectious mononucleosis, leukemia, and subacute thyroiditis. Joint pain should suggest rheumatoid arthritis, rheumatic fever, or gonococcal arthritis. Earache should suggest otitis media or mastoiditis. Chest pain should suggest tuberculosis, pleurisy, or empyema.
Is there a localized discharge? Purulent sputum should suggest pneumonia, tuberculosis, or chronic fungal disease in the lung. A urethral discharge would suggest gonorrhea or Reiter's disease.
Is there a localized mass or swelling? An abdominal mass would suggest hepatic abscess, pancreatic cyst, or diverticular abscess. A flank mass might suggest hypernephroma or perinephric abscess.

DIAGNOSTIC WORKUP

The diagnostic workup is similar to that for acute fever on page 168 .

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

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

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.
Is the hepatomegaly massive? Massive hepatomegaly is associated with Gaucher's disease.
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.
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.
Is there skin pigmentation? The presence of skin pigmentation that is not bilirubin suggests hemochromatosis.
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.
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.

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

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

Infection is the most common cause
–Viral (e.g., influenza, HIV, hepatitis, herpes simplex encephalitis, mononucleosis, adenovirus)
–Bacterial (e.g., pneumonia, endocarditis, tuberculosis, meningitis, pyelonephritis, appendicitis, cholecystitis, cellulitis)
–Lyme disease
–Malaria
–Syphilis
–Tularemia
–Intra-abdominal abscess

Malignancy
–Lymphoma (Hodgkin's and non-Hodgkin's)
–Lymphoproliferative disorders
–Renal cell carcinoma
–Leukemia
–Hepatocellular carcinoma
Rheumatologic disorders
–Temporal arteritis/giant cell arteritis
–Adult-onset Still's disease
–Systemic lupus erythematosus
–Sarcoidosis
–Rheumatoid arthritis
Drug fever
–Often temporally associated with the initiation of a new medicine
–Often associated with a rash (biopsy reveals leukocytoclastic vasculitis)
–Eosinophilia is common

Pulmonary embolism
–Mild fever is often present
–Other findings of thromboembolic disease (e.g., leg swelling, dyspnea) may be present

Osteomyelitis

Occult abscess

Malignant hypothermia

Workup and Diagnosis

Complete history and physical examination
–In most cases, the cause of fever will be suggested during the history and physical
–Note characteristics of the fever, maximum temperature, presence of diurnal variation, and recent travel
Initial laboratory studies may include CBC with differential, electrolytes, BUN/creatinine, glucose, calcium, urinalysis, urine cultures, liver function tests, and ESR
Blood cultures, including thick smear of the blood to evaluate for parasites (e.g., malaria)
Chest X-ray may reveal focus of infection (e.g., pneumonia, tuberculosis, malignancy)
Lumbar puncture for CSF analysis may be indicated
CT scan of chest and abdomen may reveal an occult infection, abscess, or malignancy
Echocardiogram is indicated if suspect infective endocarditis or aortitis (syphilis)
Tagged white cell scans may be used to localize abscess
Bone marrow biopsy may be indicated if leukemia or a myelodysplastic syndrome is suspected

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Rash with Fever: Differential Diagnosis
(In a Page: Signs and Symptoms)

Viral exanthems
–Leading cause of fever and rash in childhood
–Most children present with low-grade fevers, viral prodromal symptoms, and a secondary diffuse exanthem that is usually nonspecific and morbilliform
–Often last only a few days and requires only supportive management
Drug reactions
–Account for a large portion of rashes with associated fever
–Immune complex disease or serum sickness has been reported with many medications
Meningococcemia
–Most common under age 1
–After a brief prodrome; onset is abrupt with spiking fevers, diffuse purpuric lesions, delirium, and death
–DIC and purpura fulminans with secondary necrosis of digits and limbs can occur

Rocky Mountain Spotted Fever
–A fulminant and deadly rickettsial disease transmitted by a tick bite
–Only 60% of patients are aware of tick bite
–Characteristic rash starts acrally on wrists and ankles and spreads toward the trunk
–Initially, pink macules evolve over 10–24 hours into red papules, then purpuric macules and violaceous patches involving most of the body surface area
–Necrosis and DIC may occur
Toxic shock syndrome, Staphylococcus aureus, and streptococcal diseases
–Most cases due to toxin production
–Rapid onset of fever, hypotension with generalized skin (palms and soles common) and mucous membrane erythema (“erythroderma” in case definition), and subsequent multiorgan failure
–Palmar/solar desquamation in 1–3 weeks
–A morbilliform rash and skin “pain” or hyperesthesia is common
–Nonsurgical and surgical wounds are often the source of infection in the more common nonmenstrual variant of TSS

Fifth disease
Measles
Rubella
Parvovirus
Varicella

Workup and Diagnosis

Because of a seemingly endless list of possible etiologies for fever and rash, a focused history and physical exam are essential to a quick, accurate diagnosis
Determine whether the patient appears toxic; age and presence of co-morbid conditions aid diagnosis
If there is any evidence of purpura;
–Quickly consider the diagnosis of RMSF, meningococcemia, or systemic vasculitis
–In the cases of meningococcemia and RMSF, the diagnosis must be made empirically, then later confirmed so that therapy is immediately initiated

Obtain bacterial cultures from any wounds, culture the pharynx if indicated, and consider skin biopsy and culture; blood cultures are indicated in toxic patients; consider immediate lumbar puncture for CSF culture and Gram stain if meningococcemia is suspected

Acute and convalescent antibody titers can confirm RMSF; skin biopsy with immunofluorescnce may demonstrate a vasculitis with visible rickettsial organisms within the endothelium

TSS is often diagnosed by history and examination alone; recent cutaneous injury and nonspecific morbilliform rash in a hypotensive patient in association with the presence of epidermal necrosis on skin biopsy can confirm the diagnosis; wound cultures with growth of staph or strep

» READ BOOK EXCERPT ONLINE »

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

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Fever – Acute: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

Viral infections
–Account for the majority of febrile illnesses (FI) in infancy and childhood
–Upper respiratory infections (e.g., parainfluenza virus)
–Lower respiratory infections (e.g., RSV)
–Non-bacterial gastroenteritis (e.g., rotavirus)
–Aseptic meningitis (e.g., enterovirus)

Bacterial infections
–UTIs account for 1.7% of FI in children 5 years and 7.5% in infants <8 weeks
–Pneumonia (e.g., group A streptococcus)
–Bacteremia (2% of FI in all children, highest rates seen in younger infants)
–Meningitis (0.8% of FI in all children)
–In febrile neonates, the overall rate of serious bacterial infections (SBI) is ~13%
Vaccine reaction
- Collagen vascular diseases
  –Kawasaki disease: 3,000 cases per year in the U.S., rates higher in Asia, 80% of cases occur in children <5 years
  –Henoch-Schönlein purpura: Low-grade fever is present in 50% of cases
  –Juvenile rheumatoid arthritis: Incidence 1/10,000
  –SLE
  –Acute rheumatic fever
- Malignancy
  –Leukemia: Most common childhood malignancy; early symptoms include fever, fatigue, pallor, anemia, bone pain
  –Lymphoma
  –Solid tumors (neuroblastoma, sarcoma)
- Inflammatory bowel disease
  –Diarrhea, pain, fever, blood loss
  –Crohn disease, ulcerative colitis
- Tissue injury (trauma, hematoma, burns)
- Drug reaction
- Biologic agents (blood products, gamma-globulin)
- Endocrinologic disorders
  –Thyrotoxicosis
  –Pheochromocytoma
- Genetic diseases
  –Familial Mediterranean fever
- Factitious fever
Workup and Diagnosis
- Physical exam
  –Temperature: Rectal preferred for infants <3 months
  –Vitals: Relative brady- or tachycardia, tachypnea
  –Growth parameters especially if frequent febrile episodes/infections (immunodeficiency)
  –Appearance, irritability, quality of cry, consolability
  –Skin (color, rash, desquamation), conjunctivitis, ocular or nasal discharge, mouth lesions, throat and ear exam
  –Lymphadenopathy, abdominal exam, neuro exam
  –Joint exam (arthritis), muscle tenderness
  - Immunologic workup and/or bone marrow for prolonged fever and/or other clinical evidence
  >>>>

» READ BOOK EXCERPT ONLINE »

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

Fever – Cyclic: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

PFAPA, or Marshall syndrome
–Periodic fever (usually high, 104°F [40°C]), aphthous stomatitis, pharyngitis, and adenitis
–Most common diagnosis for true cyclic fever, usually in children <5 years
–Recurs every 3–4 weeks

Cyclic neutropenia
–Periodic fever, average cycle of 21 days
–Pharyngitis, mouth ulcers, and lymphadenopathy are also noted
–May not be associated with infection

Infectious diseases
–Relapsing fever due to Borrelia recurrentis,
relapses every 10–14 days
–EBV may occur at 6–8 week intervals

Familial Mediterranean fever
–Brief attacks of fever and serositis
–Autosomal recessive disease
–Sephardic Jews, Arabs, Turks, and Armenians commonly affected
–50% have onset before 10 years of age
–May occur in regular 7–28-day intervals
–Amyloidosis is a possible complication

Hyper-IgD and periodic fever syndrome (HIDS)
–High fevers, abdominal pain, cervical lymphadenopathy, sometimes diarrhea and arthritis, in early infancy
–Autosomal recessive, most patients from Western Europe (French, Dutch)
–Cycles may be regular every 14–28 days
- TNF-receptor-associated periodic syndrome (TRAPS) or Hibernian fever
  –Fever, myalgias with migratory pattern, conjunctivitis and rash
  –Autosomal dominant
  –first described in Irish/Scottish individuals but other ethnic groups involved
  –Amyloidosis is a possible complication (25% of untreated individuals)
- Factitious fever
Workup and Diagnosis
- History
  –Age of onset, duration of episodes, duration of symptom-free periods, associated symptoms (pharyngitis, aphthous ulcers)
  –Lymphadenopathy, abdominal pain
  –Family history of cyclic fever, ethnicity
  –Exposure to ticks (woods, camping), travel history
>

» READ BOOK EXCERPT ONLINE »

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

Fever – Recurrent: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

Repeated viral infections
–Most common cause of recurrent febrile episodes in childhood
–Start of day care or change of geographic location may be related

Urinary tract infection (UTI)
–May be self-limited but recur especially if underlying anomaly exists

Epstein-Barr virus (EBV)
–May present with recurrent febrile episodes due to one initial infection

Other specific viral syndromes
–Parvovirus B19
–CMV

Immunodeficiency
–Repeated bacterial infections should lead to investigation of immune status

Dental abscess (non-dental abscesses typically present with prolonged daily fever)
Chronic meningococcemia
Acute rheumatic fever
Inflammatory bowel disease (IBD)
Juvenile rheumatoid arthritis (JRA)
Behçet disease

Tumor necrosis factor receptor-associated periodic syndrome (TRAPS) or Hibernian Fever
–Autosomal dominant disease with fever, myalgias with migratory pattern, conjunctivitis and rash

Familial cold autoinflammatory syndrome or familial cold urticaria
–Rash, fever, arthralgia, and conjunctivitis
–Precipitated by exposure to cold

Muckle-Wells syndrome
–Similar presentation to familial cold urticaria
–Symptoms not triggered by cold

Brucellosis
–Most prevalent around the Mediterranean and Arabic countries, also present in South America and India

Yersiniosis
Typhoid fever
Rat-bite fever
Malaria
Factitious fever

Workup and Diagnosis

History
–Documentation of fever
–Duration of episodes and fever-free intervals
–Symptoms associated with the fever
–Symptoms during the fever-free intervals
–Weight loss
–Recent documented infections, medications
–Travel, animal and insect exposure
–Specific conditions related to episodes (e.g., cold)

Physical exam
–Vitals, growth parameters (failure to thrive can be a presentation of UTI and immunodeficiency)
–Rash (transient pink rash in JRA)
–Ophthalmologic exam: Uveitis (IBD and Behçet), conjunctivitis (TRAPS)
–Hepatosplenomegaly, lymphadenopathy
–Genital ulcers (Behçet)
–Perianal skin tags (IBD)
–Mouth ulcers, pharyngitis
–Arthritis

CBC with differential
ESR or CRP
Urine culture
Blood culture
Serology for EBV, CMV, or Parvovirus B19
Low levels of serum type 1 TNF receptor in TRAPS
Documentation of fever in the office should exclude the possibility of factitious fever

» READ BOOK EXCERPT ONLINE »

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

Fever – Unknown Origin: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

Infections (40%)
–Infectious mononucleosis (EBV, CMV)
–Other systemic viral syndromes (e.g., HIV)
–UTI (e.g., E. coli)
–Osteomyelitis (e.g., staphylococcus)
–Upper and lower respiratory infections (sinusitis, mastoiditis, pneumonia)
–Cat-scratch disease (Bartonella henselae)
–Tuberculosis, nontuberculous mycobacterial infections
–Abscess (abdominal or retroperitoneal)
–CNS infections
–Endocarditis (subacute)
–Salmonellosis
–Lyme disease (Borrelia burgdorferi)
–Leptospirosis
–Congenital syphilis
–Others: Brucellosis, histoplasmosis, leishmaniasis, yersiniosis, Q fever (Coxiella burnetii), Rocky Mountain spotted fever (Rickettsia rickettsii)

Autoimmune diseases (15%)
–Rheumatoid arthritis accounts for 3/4 of FUO due to autoimmune diseases
–Systemic lupus erythematosus
–Rheumatic fever
–Vasculitis (e.g., HSP)
–Sarcoidosis

Neoplastic diseases (7%)
–Leukemia/lymphoma accounts for 80% of
FUO due to malignancies
–Neuroblastoma
–Hepatoma
–Soft tissue sarcoma

Inflammatory bowel disease (3%)
Drugs and nutritional supplements (drug fever)
Factitious fever
Munchausen by proxy
Neurologic disorders
–Familial dysautonomia
–Central thermoregulatory disorder
–Head injury
Hyperthyroidism
Anhidrotic ectodermal dysplasia
Diabetes insipidus
Kikuchi disease

Workup and Diagnosis

History
–Differentiate between FUO and multiple febrile
illnesses that occur in short period of time
–Daily documentation of fever, onset, duration
–Weight loss, diet history, medications, sick contacts
–Animal or tick exposure, travel, foreign contacts
–Immune status, history of transfusion, surgery
–FH of autoimmune or neoplastic diseases

Physical exam
–Vital signs, growth parameters
–Skin (rash, desquamation, jaundice)
–Ophthalmologic exam (conjunctivitis, uveitis)
–Oral lesions
–Cardiologic exam (new onset murmur)
–Abdominal exam (masses, hepatosplenomegaly)
–Testicular exam
–Muscle tenderness, bone tenderness, arthritis
–Lymphadenopathy
–Neurologic exam

Labs
–CBC, ESR, C-reactive protein
–Renal and hepatic function tests, albumin and globulin
–Urinalysis, blood and urine culture
–Viral titers, PPD, cultures for specific organisms, ASO, ANA, bone marrow

Radiographic imaging with plain films, ultrasound, bone scan, CT scan or MRI of specific organ systems as warranted by the history and physical exam

» READ BOOK EXCERPT ONLINE »

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)

» READ BOOK EXCERPT ONLINE »

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

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

There are certain things to remember when a patient with fever is approached. First, a mild elevation up to 100.5°F (38°C) rectally may be normal in some people. Second, one should rule out malingering by the patient or incorrect recording by hospital personnel. Finally, psychogenic disorders must be ruled out.

The duration and severity of the fever are important. If possible, a careful chart of the fever should be made with the patient off all drugs (especially aspirin and steroids). Conditions with intermittent or relapsing fever such as brucellosis, malaria, and Mediterranean fever will be elucidated in this fashion (Table 28).

The association with other symptoms is important. Fever, right upper quadrant pain, and jaundice suggest cholecystitis or cholangitis, whereas fever with right-sided flank pain suggests pyelonephritis. After taking a few moments to jot down the differential before launching into the history and physical examination, one can question and examine the patient more appropriately. The differential diagnosis will also lead to more appropriate use of laboratory testing.

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Source: Differential Diagnosis in Primary Care, 2007

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

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

Fever: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

If the patient’s fever is only mild to moderate, ask him when it began and how high his temperature reached. Did the fever disappear, only to reappear later? Did he experience other symptoms, such as chills, fatigue, or pain?

Obtain a complete medical history, noting especially immunosuppressive treatments or disorders, infection, trauma, surgery, diagnostic testing, and the use of anesthesia or other medications. Ask about recent travel because certain diseases are endemic.

Let the history findings direct your physical examination. Because a fever can accompany diverse disorders, the examination may range from a brief evaluation of one body system to a comprehensive review of all systems. (SeeHow fever develops.)

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Source: Handbook of Signs & Symptoms (Third Edition), 2006

Jaundice: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

Documenting a history of the patient’s jaundice is critical in determining its cause. Begin by asking the patient when he first noticed the jaundice. Does he also have pruritus, clay-colored stools, or dark urine? Ask about past episodes or a family history of jaundice. Does he have nonspecific signs or symptoms, such as fatigue, a fever, or chills; GI signs or symptoms, such as anorexia, abdominal pain, nausea, weight loss, or vomiting; or cardiopulmonary symptoms, such as shortness of breath or palpitations? Ask about alcohol use and a history of cancer or liver or gallbladder disease. Has the patient lost weight recently? Also, obtain a drug history. Ask about a history of hepatitis, gallstones, or liver or pancreatic disease.

Perform the physical examination in a room with natural light. Make sure that the orange-yellow hue is jaundice and not due to hypercarotenemia, which is more prominent on the palms and soles and doesn’t affect the sclera. Inspect the patient’s skin for texture and dryness and for hyperpigmentation and xanthomas. Look for spider angiomas or petechiae, clubbed fingers, and gynecomastia. If the patient has heart failure, auscultate for arrhythmias, murmurs, and gallops as well as crackles and abnormal bowel sounds. Palpate the lymph nodes for swelling and the abdomen for tenderness, pain, and swelling. Palpate and percuss the liver and spleen for enlargement, and test for ascites with the shifting dullness and fluid wave techniques. Obtain baseline data on the patient’s mental status: Slight changes in sensorium may be an early sign of deteriorating hepatic function.

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Source: Handbook of Signs & Symptoms (Third Edition), 2006

Colorado tick fever: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

CONFIRMING DIAGNOSIS A history of recent exposure to ticks along with moderate to severe leukopenia, complement fixation tests, or virus isolation confirm the diagnosis.

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

Lassa fever: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

CONFIRMING DIAGNOSIS Isolation of the Lassa virus from throat washings, pleural fluid, or blood confirms the diagnosis.

Recent travel to an endemic area and specific antibody titer support the diagnosis.

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

Relapsing fever: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

CONFIRMING DIAGNOSIS Diagnosis requires demonstration of the spirochetes in peripheral blood smears during febrile periods, using Wright's or Giemsa stain.

Borrelia spirochetes may be more difficult to detect in later relapses because their number declines in the blood. In such cases, injecting the patient's blood or tissue into a young rat and incubating the organism in the rat’s blood for 1 to 10 days commonly allows spirochete identification.

In severe infection, spirochetes are found in the urine and cerebrospinal fluid. Other abnormal laboratory results usually include a white blood cell (WBC) count as high as 25,000/µl, with increases in lymphocytes and erythrocyte sedimentation rate; however, the WBC count may be normal. Because the Borrelia organism is a spirochete, relapsing fever may cause a false-positive test for syphilis in 5% to 10% of cases.

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

Rheumatic fever and rheumatic heart disease: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Diagnosis depends on recognition of one or more of the classic symptoms (carditis, rheumatic fever without carditis, polyarthritis, chorea, erythema marginatum, or subcutaneous nodules) and a detailed patient history. Laboratory data support the diagnosis:

❑ White blood cell count and erythrocyte sedimentation rate may be elevated (during the acute phase); blood studies show slight anemia due to suppressed erythropoiesis during inflammation.

❑ C-reactive protein is positive (especially during acute phase).

❑ Cardiac enzyme levels may be increased in severe carditis.

❑ Antistreptolysin-O titer is elevated in 95% of patients within 2 months of onset.

❑ Electrocardiogram changes aren’t diagnostic; but PR interval is prolonged in 20% of patients.

❑ Chest X-rays show normal heart size (except with myocarditis, heart failure, or pericardial effusion).

❑ Echocardiography helps evaluate valvular damage, chamber size, and ventricular function.

❑ Cardiac catheterization evaluates valvular damage and left ventricular function in severe cardiac dysfunction.

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

Rocky Mountain spotted fever: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

CONFIRMING DIAGNOSIS Diagnosis is usually based on a history of tick bite or travel to a tick-infested area and a positive complement fixation test (which shows a fourfold increase in convalescent antibody titer compared with acute titers). Blood cultures or skin biopsy at the rash site should be performed to isolate the organism and confirm the diagnosis.

Another common but less reliable antibody test is the Weil-Felix reaction, which also shows a fourfold increase between the acute and convalescent sera titer levels. Increased titers usually develop after 10 to 14 days and persist for several months.

Additional recommended laboratory tests consist of a platelet count for thrombocytopenia (12,000 to 150,000/µl) and a white blood cell count (elevated to 11,000 to 33,000/µl) during the second week of illness.

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

Fever [Pyrexia]: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

If the patient’s fever is only mild to moderate, ask him when it began and how high his temperature reached. Did the fever disappear, only to reappear later? Did he experience any other symptoms, such as chills, fatigue, or pain?

Obtain a complete medical history, noting especially immunosuppressive treatments or disorders, infection, trauma, surgery, diagnostic testing, and use of anesthesia or other medications. Ask about recent travel because certain diseases are endemic.

Let the history findings direct your physical examination. (See Differential diagnosis: Fever, pages 338 and 339.) Because fever can accompany diverse disorders, the examination may range from a brief evaluation of one body system to a comprehensive review of all systems. (See How fever develops, page 340.)

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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

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

A. Taking a detailed patient history is critical; include questions relating to travel, animal exposure, occupation, injuries or operations, household members or contacts who are ill, medications, past illnesses, and a complete review of systems.

B. Chills, malaise, myalgia, headache, and fever are common with infectious diseases.

C. The febrile pattern may be helpful in making a diagnosis. Antipyretics, antibiotics, and glucocorticoids affect the fever pattern. Specific patterns of fever are shown in Table 2.4.

Physical examination

A. The examination should include the skin, lymph nodes, eyes, nail beds, heart, lungs, abdomen, joints, nervous system, and genitourinary system, including rectal and bimanual pelvic examinations.

B. Infections will increase the pulse rate approximately 10 beats per minute for each 0.5°C (1.0°F) temperature increase.

C. When fever is present, the respiratory rate will frequently increase above the usual 12 to 14 breaths per minute.

D. Infections with Mycoplasma pneumonia, psittacosis, and typhoid fever are often associated with a relative bradycardia.

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

Rash Accompanied by Fever: History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

History is quite important and should include standard items, such as onset, duration, aggravating factors, relieving factors, and associated symptoms. Additionally, other factors to consider, include:

A. Exposure history. Are any other family members or close contacts ill? Is there a history of exposure to brackish water, mosquitoes, foreign travel, and so forth?

B. Are there any underlying illnesses or a significant possibility of immunologic compromise (e.g., undiagnosed HIV infection)?

Physical examination

A. Examine the lesions and their distribution carefully. Classify the rash as petechial, maculopapular, vesiculobullous, erythematous, or urticarial. Note the distribution of the rash. For instance, rubella and rubeola generally begin on the face and spread to the trunk, whereas RMSF petechiae tend to occur on the ankles and wrists first.

B. Conduct a general physical examination. Areas of particular concern are:

1. Head, eyes, ears, nose, and throat. The presence of Koplik’s spots is pathognomic for rubeola. The discovery of a tick lends support to the diagnosis of RMSF. Sinusitis may represent a source for meningococcemia. Pharyngitis in a young adult with diffuse erythema may be caused by C. haemolyticum. Mucous membrane swelling may indicate early anaphylaxis.

2. Lung examination. Expiratory wheezing, especially in a patient who has recently received medications or contrast dye, can indicate anaphylaxis. Evidence of pneumonia is consistent with psittacosis and mycoplasma.

3. Cardiac examination. Cardiovascular collapse is associated with meningococcemia and other sepsis. A new murmur (Chapters 7.6 and 7.7) may indicate subacute bacterial endocarditis in a patient with subungual or scleral petechiae.

4. Genital examination. Purulent urethral drainage or evidence of pelvic inflammatory disease supports consideration of gonorrhea. A chancre would support a diagnosis of syphilis, although palmar lesions often occur well after healing of the initial chancre.

5. Joint examination and extremities. A petechial rash near the ankles and wrists is suggestive of RMSF. Evidence of joint swelling supports a diagnosis of meningococcemia or gonococcemia. A maculopapular rash may be seen in juvenile rheumatoid arthritis and other rheumatologic conditions as well.

6. Neurologic examination. Evidence of meningitis supports a diagnosis of meningococcemia. Patients with RMSF may also have meningeal signs.

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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

Fever of Unknown Origin: Differential Overview
(Field Guide to Bedside Diagnosis)

Infection

❑ HIV

❑ Tuberculosis

❑ Endocarditis

❑ Osteomyelitis

❑ Malaria

❑ Syphilis

❑ Zoonosis

❑ Typhoid fever

❑ Chronic meningococcemia

Neoplasm

❑ Lymphoma

❑ Liver metastases

❑ Renal cell carcinoma

❑ Atrial myxoma

Collagen-Vascular Disease

❑ Giant cell arteritis

❑ Systemic lupus erythematosus

❑ Vasculitis

❑ Rheumatic fever

❑ Still disease

Other

❑ Drugs

❑ Heat stroke

❑ Factitious

❑ Malignant hyperthermia

❑ Multiple pulmonary emboli

Diagnostic Approach

Fever of unknown origin (FUO), when a fever over 101°F (38.5°C) remains unexplained for longer than 3 weeks, is usually a result of infection (40%), neoplasm (20%), or collagen-vascular disease (20%). It is most commonly caused by an atypical presentation of a common disease. Always document the fever before pursuing the evaluation.

Consider relatively hidden (deep) sites: retroperitoneum (hematoma or infection), bone, dental, sinus, ovary, prostate, subphrenic (following abdominal surgery), renal, spleen, or prostheses. With FUO in a hospitalized patient, consider sequestered sites (e.g., sinuses in intubated patients or implanted hardware), indwelling lines, C. difficile, or drug reactions. With FUO in a neutropenic patient, consider catheters, perianal infections, Candida, and Aspergillus. Cardinal signs may be absent, e.g., meningitis with opportunistic pathogens without meningismus in 63%, and pneumonia without purulent sputum in 92%. Neutropenic fevers are usually due to bacteremia, with fungal organisms becoming predominant after 7 days of unremitting fever. Fever may also be due to the underlying neoplasm, drugs such as antibiotics, or blood products.

Examine for subtle clues:

• Petechial eruptions in meningococcemia and Rocky Mountain Spotted Fever

• Pustular lesions in gonococcemia or staphylococcal sepsis

• Ecthyma gangrenosum in Pseudomonas sepsis

• Splinter hemorrhages, conjunctival hemorrhages, Roth spots, Osler nodes, and Janeway lesions in endocarditis

• Choroidal tubercles in miliary tuberculosis and candidemia

• Splenomegaly in endocarditis, lymphoma, and cirrhosis

• Hepatic bruit or friction rub in subphrenic abscess

• Temporal artery or scalp tenderness or jaw claudication in giant cell arteritis

• Epitrochlear lymphadenopathy in syphilis

Extreme elevations of fever (.40°C) are found in heat stroke, hypothalamic dysfunction, meningitis, midbrain hemorrhage, falciparum malaria, Rocky Mountain Spotted Fever, typhus, sepsis, malignant hyperthermia, and hypernephroma.

Relative bradycardia occurs in salmonellosis (typhoid fever), meningitis with increased intracranial pressure, mycoplasma and legionella pneumonia, factitious fever, tularemia, brucellosis, mumps, hepatitis, and with concomitant beta blockers. Bradycardia in fever may also signal cardiac conduction abnormalities in acute rheumatic fever, Lyme disease, viral myocarditis, or endocarditis with valve ring abscess.

Relapsing fevers (days of fever alternating with days without) occur in brucellosis (fever with physical activity), Hodgkin disease, extrapulmonary tuberculosis, malaria, and Lyme disease. Hectic fever (difference between peak and trough .1.5°C) suggests abscess, pyelonephritis, ascending cholangitis, tuberculosis, lymphoma, and drug reactions. Absence of diurnal variation suggests a central source. Reversal of the diurnal pattern (“typhus inversus”) occurs with disseminated tuberculosis, typhoid fever, polyarteritis nodosa, and salicylate toxicity.

FUO in patients from the developing world include tuberculosis, typhoid, amebic liver abscesses, AIDS, and geographically restricted infections such as malaria, schistosomiasis, brucellosis, kala azar, filariasis, or Lassa fever. They may present after long incubation or latency periods.

When FUO lasts longer than 6 months, consider factitious fever, granulomatous hepatitis, neoplasm, Still disease, infection, collagen-vascular disease, or exaggerated circadian rhythm.

Patients who remain undiagnosed have a good prognosis (83% resolution in 1 year, 4% mortality).

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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

Rheumatic fever and rheumatic heart disease: Diagnosis
(Handbook of Diseases)

Recognition of one or more classic signs or symptoms (carditis, polyarthritis, chorea, erythema marginatum, or subcutaneous nodules) and a detailed patient history allow diagnosis. The following laboratory data support the diagnosis:

❑ White blood cell count and erythrocyte sedimentation rate may be elevated (during the acute phase); blood studies show slight anemia from suppressed erythropoiesis during inflammation.

❑ C-reactive protein is positive (especially during the acute phase).

❑ Cardiac enzyme levels may be increased in those with severe carditis.

❑ Antistreptolysin O titer is elevated in 95% of patients within 2 months of onset. (Rising antiDNase B test results can also detect recurrent streptococcal infection.)

❑ Electrocardiography changes aren’t diagnostic, but the PR interval is prolonged in 20% of patients.

❑ Chest X-rays show normal heart size (except with myocarditis, heart failure, or pericardial effusion).

❑ Echocardiography helps evaluate valvular damage, chamber size, and ventricular function.

❑ Cardiac catheterization evaluates valvular damage and left ventricular function in those with severe cardiac dysfunction.

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Source: Handbook of Diseases, 2003

Fever: History
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

If the patient’s fever is mild to moderate, ask him when it began and how high his temperature reached. Did the fever disappear, only to reappear later? Did he experience any other symptoms, such as chills, fatigue, or pain?

Obtain a complete medical history, noting immunosuppressive treatments or disorders, infection, trauma, surgery, diagnostic testing, and use of anesthesia or other medications. Ask about recent travel because certain diseases are endemic.

Physical examination

Let the history findings direct your physical examination. Because fever can accompany diverse disorders, the examination may range from a brief evaluation of one body system to a comprehensive review of all systems. (See How fever develops, pages 148.) Assess vital signs and evaluate the patient for complications related to the fever such as dehydration, body aches, fatigue, anorexia, and seizure activity.

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Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007

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

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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

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

Common Causes

Infectious

Infectious causes of acute fever are listedbelow and discussed in other chapters.

Respiratorytract

Upperrespiratory tract infection (common cold)

Pharyngitis

Tonsillitis

Otitis media

Herpes gingivostomatitis

Herpangina

Sinusitis

Croup

Bronchiolitis

Bronchitis

Pneumonia (viral, bacterial, mycoplasma)

Pertussis

Gastrointestinal

Gastroenteritis

Appendicitis

Hepatitis

Genitourinary

Urinary tract infection (includingpyelonephritis)

Sexually transmitted diseases

Musculoskeletal

Septic arthritis

Osteomyelitis

Myositis

Central nervous system

Meningitis(viral, bacterial)

Viral encephalitis

Infections associated with prominentrash

Roseola

Hand-foot-mouth syndrome

Varicella

Erythema infectiosum (parvovirus B19)

Measles

Scarlet fever

Meningococcemia

Rocky Mountain spotted fever

Other

Viral illnesses

Septicemia/bacteremia

Infectious mononucleosis

Lymphadenitis

Cellulitis/abscess

Cat scratch disease

Dental abscess

Periorbital cellulites

Parotitis

Noninfectious

Drug Reactions

Hypersensitivityreactions are responsible for most cases of drug fever.

Although fever can occur without otherfindings, urticarial rash and peripheral eosinophilia make diagnosismore likely.

Vaccine Reactions

Reactionsto acellular pertussis vaccine can produce fever but are uncommon.

Within 7–10 days after administrationof live measles vaccine or measles, mumps, rubella (MMR) vaccine,fever can occur and is often associated with macular or papular rash.

Trauma

Crush injuries and fractures of large bonescan cause fever due to large amount of tissue damage and releaseof inflammatory mediators.

Burns

Fever may occur with severe burns, even inabsence of infection, because of fluid losses and resetting of thermoregulatorycenter. Severe sunburn also may cause fever.

Kawasaki Disease

Definedas vasculitis of unknown cause that usually occurs in children <5yrs of age.

Diagnostic criteria are absence ofany other disease process and presence of fever for ≥5 days associatedwith 4 of 5 signs:

Bilateral conjunctival injection

Cervical lymphadenopathy

Macular or papular rash primarily ontrunk

Mucous membrane involvement with dry,fissured lips, strawberry tongue, or pharyngeal injection

≥1 change in extremities, includingpalmar erythema, edema, and periungal or generalized desquamation

Lab findings include leukocytosis,pyuria, proteinuria, spinal fluid pleocytosis, elevation in serumaminotransferases, and increased erythrocyte sedimentation rate.

Chest radiograph may show small pleuraleffusions.

Platelet count may be normal at onset,but thrombocytosis usually occurs during second week of illness.

Complications include coronary arteryaneurysms, myocarditis, and myocardial infarction.

2-D echocardiography may reveal coronaryartery aneurysms within 1–2 cm of origin of coronary arteriesfrom aorta.

Uncommon Causes

Infectious

Many infections in this category, as listedbelow, are discussed in other chapters.

Respiratorytract

Viral(hantavirus pulmonary syndrome)

Bacterial [supraglottitis,bacterial tracheitis, abscess (peritonsillar, retropharyngeal, lateral pharyngeal),tuberculosis, actinomycosis, nocardiasis, Legionella]

Fungal (aspergillosis, blastomycosis,histoplasmosis, coccidioidomycosis)

Parasitic (P. carinii)

Gastrointestinal

Amebiasis

Pancreatitis

Cholecystitis

Cholangitis

Peritonitis

Intraabdominal abscess

Genitourinary

Epididymitis

Orchitis

Abscesses (perinephric, tuboovarian)

Cardiac

Acute rheumatic fever

Myocarditis

Pericarditis

Endocarditis

Central nervous system (brain abscess)

Other

Viral (HIV, rabies)

Bacterial [staphylococcalscalded skin syndrome, toxic shock syndrome, orbital cellulitis/abscess,Borrelia (relapsing fever), brucellosis, leptospirosis, plague,psittacosis (ornithosis), rat-bite fever, syphilis, tularemia, tetanus]

Fungal (disseminated histoplasmosis,nonpulmonary blastomycosis)

Parasitic [malaria, ascariasis,toxocariasis (visceral larva migrans, ocular larva migrans), toxoplasmosis,trichinosis]

Rickettsial [endemic typhus(murine), epidemic typhus (louse-borne typhus), Q fever, rickettsialpox, ehrlichiosis]

Hantavirus Pulmonary Syndrome

Can occurafter exposure to infected rodents (most commonly, deer mouse),their saliva, or excreta.

Characterized by acute onset of fever,headache, myalgia, cough, vomiting, and diarrhea followed by developmentof hypotension and noncardiogenic pulmonary edema. Leukocytosiswith immature granulocytes, thrombocytopenia, and elevated Hct arefrequent findings.

Reverse-transcriptase polymerase chainreaction or enzyme immunoassay can detect viral antigen from clinicalsamples. Diagnosis also can be confirmed serologically.

Borrelia (Relapsing Fever)

Caused byspirochetes of Borrelia. Infected ticks (Ornithodoros species) andlice (P. humanus) are sources of human infections. Most cases inU.S. are transmitted by ticks, which become infected by feedingon rodents and other small mammals.

Incubation period of 7–10days is followed by fever, headache, chills, myalgia, and arthralgia,which may last up to 1 wk. Transient macular rash, petechiae ofskin, jaundice, and hepatosplenomegaly may occur.

Complications include pneumonia, myocarditis,and meningitis. After 5- to 10-day interval, relapse occurs withfever and same clinical findings as described above.

Spirochetes can be seen by dark-fieldmicroscopy and in Wright-stained smears of peripheral blood. Positiveblood culture is also diagnostic.

Brucellosis

Transmittedby direct contact with infected animals (goats, sheep, cows, swine)or by ingestion of contaminated milk or milk products produced bythem.

Onset can be acute or insidious, withfever, headache, abdominal pain, arthralgia, myalgia, weight loss,lymphadenopathy (especially cervical and axillary), and hepatosplenomegaly.Prolonged fever without any other findings sometimes occurs.

Complications include meningitis, osteomyelitis,and endocarditis.

Organism can sometimes be culturedfrom blood, urine, spinal fluid, bone marrow, or lymph node. Ifthese cultures are negative, diagnosis depends on serologic findings.Serum agglutination test with antibody titer ≥1:160 or 4-foldincrease in agglutination titer on serial samples is diagnostic.

Leptospirosis

L. interrogansinfects humans through contact with animal urine in contaminated foodor water. Incubation period is 2–20 days.

Acute illness usually consists of fever,headache, chills, malaise, myalgia, vomiting, lymphadenopathy, andabdominal pain. Hepatic (hepatomegaly, jaundice, liver failure),renal (azotemia, renal failure), and CNS dysfunction (aseptic meningitis,alteration in consciousness) may follow.

Diagnosis confirmed by positive blood,urine, or spinal fluid cultures; 4-fold increase in serial agglutinationtiters; or visualization of spirochete by dark-field microscopyof urine.

Plague

Y. pestisis responsible for plague. Most common form is bubonic plague, whichis usually transmitted by bites of infected fleas and uncommonlyby contact with infected tissues and fluids of wild rodents (e.g.,prairie dogs, ground squirrels, chipmunks, hares, rabbits, and rats).

Characterized by fever and painfulregional adenopathy, usually involving cervical, inguinal, or axillarylymph nodes (buboes).

Less common forms include pneumonicplague (cough, fever, dyspnea, hemoptysis), septicemic plague (fever,hypotension, coagulopathy), and meningeal plague (fever, headache,photophobia, seizures).

Positive fluorescent antibody testof sputum, lymph node aspirate, blood, or spinal fluid is presumptiveevidence of infection. Serologic tests also may confirm diagnosis.Positive sputum, lymph node, blood, or spinal fluid cultures aredefinitive.

Psittacosis (Ornithosis)

C. psittacicauses psittacosis, which is transmitted from parrots and otherrelated species (parakeets, finches, cockatoos), and ornithosis,which is acquired from turkeys, pigeons, ducks, chickens, and otherfowl. Transmission is by inhalation of organisms from infected bird'senvironment. Incubation period is usually 1–2 wks.

Affected individuals have acute respiratorytract infection with fever and nonproductive cough.

Chest radiograph usually shows interstitialpneumonia. Usual method of diagnosis is serologic, with 4-fold increasein complement fixation antibody titer. With compatible clinicalpicture, single complement fixation titer ≥1:32 is also considereddiagnostic.

Rat-Bite Fever

May followrodent bite, usually that of rat.

2 different organisms, S. moniliformis,which is more common in U.S., and S. minus, which is more commonin Japan, can cause this infection.

Clinical features include fever, chills,headache, muscle pain, and rash (macular, papular, or petechial).

Migratory polyarthritis/arthralgiasoccur in some cases of S. moniliformis infection. Complicationsinclude pneumonia, meningitis, myocarditis, pericarditis, endocarditis,and soft tissue or solid organ abscesses. Positive culture fromsite of bite, blood, or joint fluid confirms diagnosis.

With S. minus infection, the bite maybe followed by ulceration, lymphadenopathy, and rash composed ofpurple or red plaques. Diagnosis of S. minus may be confirmed byobservation of organisms by dark-field microscopy in wet mountsof blood, exudate of lesion, and lymph nodes.

Syphilis

T. pallidumcauses syphilis, which may be congenital or acquired. See Chap. 36, Jaundice, fordiscussion of congenital syphilis.

Acquired syphilis almost always occursby sexual transmission.

Incubation period is 10–90days.

In primary stage, ≥1 painless ulcer(chancres) occurs on skin or mucous membranes at site of inoculation,usually on genitalia.

During secondary stage, which occurs1–2 mos later, generalized macular or papular rash appears,usually involving palms and soles. Fever, malaise, headache, arthralgia,generalized adenopathy, splenomegaly, and condyloma lata also canoccur.

Tertiary stage occurs several yearsto decades later and is characterized by aortitis or gummatous changesof skin, bones, or viscera.

Neurosyphilis can occur at any stage.

Nontreponemal reagin antibody test(rapid plasma reagin card test) and VDRL slide test, which measureimmunoglobulins directed against cardiolipin antigen, are usefulscreening tests.

Any positive test result should beconfirmed by 1 treponemal test.

Specific treponemal antibody serologictests include fluorescent treponemal antibody absorption test (FTA-ABS),which usually remains positive for life, even with successful therapy.

Microscopic dark-field exam of lesionscraping or lymph node aspirate that shows spirochetes or positivedirect fluorescent antibody test of lesion exudate or tissue isalso diagnostic.

Diagnosis of CNS involvement is establishedby positive CSF VDRL or FTA-ABS tests. CSF pleocytosis and increasedCSF protein concentration also may be found.

Tularemia

Source ofinfection with F. tularensis is infected animal or carcass, usuallyrabbit. Infection is acquired by ingestion of contaminated meator water, handling infected animals, or bites by dog ticks or deerflies that have come into contact with infected animal.

Fever, chills, headache, and myalgiaare usual findings. Common presentation is ulceroglandular syndromewith painful, swollen, ulcerating papule and inflamed lymph nodesthat may drain spontaneously.

Other syndromes are glandular (absenceof skin or mucous membrane involvement); oculoglandular (conjunctivitisand preauricular lymph node involvement); oropharyngeal (exudativepharyngitis); typhoidal (fever and hepatosplenomegaly); and pneumonic(cough).

Positive culture or 4-fold increasein serum agglutinin titer is diagnostic.

Malaria

Sporozoaof genus Plasmodium cause malaria, which occurs in many tropicaland subtropical countries. Bite by infected female Anopheles mosquitotransmits infection. 4 known types of malaria are caused by differentspecies and have the following incubation periods:

P. falciparum,9–14 days

P. vivax, 12–17 days

P. ovale, 16–18 days

P. malariae, 18–40 days

P. falciparum and P. vivax infectionsare most common, whereas P. falciparum infection is most serious.Mixed infections with more than 1 type also occur.

Typical symptoms are fever with chills,sweats, and headache. Fever usually occurs every other day withP. vivax, P. falciparum, and P. ovale infections, and every thirdday with P. malariae infection. Vomiting, diarrhea, cough, and abdominalpain are other manifestations. Significant hemolysis produces pallorand jaundice. Hepatosplenomegaly may occur with chronic infection.

Clinical syndromes that may occur withP. falciparum infection include

Febrile illness without specific or localizingsigns

Severe anemia

Respiratory failure ± pulmonaryedema

Renal failure secondary to acute tubularnecrosis

Cerebral malaria with seizures andalteration of consciousness

Vascular collapse and shock associatedwith adrenal insufficiency

P. vivax and P. ovale may cause anemiaand hypersplenism, whereas nephrotic syndrome may be associatedwith P. malariae infection. Any type can cause congenital malaria,which is characterized by fever, irritability, and lethargy.

Analysis of thick and thin blood smearsusing Wright or Giemsa stain identifies parasite and confirms diagnosis.

Ascariasis

Infectionwith roundworm A. lumbricoides is usually asymptomatic, but diarrhea, vomiting,and abdominal pain sometimes occur. Larval migration through lungcan cause transient pneumonitis associated with fever and eosinophilia.

Adult worms, which are whitish brownin color and 15–30 cm (males) or 20–40 cm (females)long, sometimes pass through rectum.

Identification of ova by microscopicidentification of stool or adult worm is diagnostic.

Toxocariasis (Visceral Larva Migrans, Ocular Larva Migrans)

Dog roundwormT. canis and cat roundworm T. cati cause toxocariasis.

Ingestion of infective eggs from soilcauses human infection, which is most common in toddlers.

Although infection can be asymptomatic,with eosinophilia as its only manifestation, other findings includefever, cough, macular or papular rash, and hepatosplenomegaly. Pneumonia,myocarditis, and encephalitis are rare complications. Ocular invasionusually occurs without other evidence of infection.

Enzyme immunoassay for serum Toxocaraantibodies available through CDC is both sensitive and specificfor visceral larva migrans and less sensitive for ocular larva migrans.Liver biopsy also may detect larvae, but yield is low.

Trichinosis

Infectionwith nematode T. spiralis is acquired by eating undercooked meat(usually pork) containing encysted larvae.

Fever, diarrhea, vomiting, and abdominalpain follow in 1–7 days. During next 2–8 wks,fever, myalgia, urticarial rash, and hemorrhages (conjunctival andsubungual) may develop. Eosinophilia as high as 70% alsomay occur. Most serious complication is myocarditis.

Identification of larvae in suspectmeat is fastest way to diagnose. Diagnosis also can be made by visualizinglarvae in muscle biopsy or by increase in paired acute and convalescentantibody titers.

Endemic Typhus (Murine)

Murine typhuscaused by R. mooseri is primarily infection of rats. Transmissionto humans occurs by bite of infected rat or inhalation of infectedrat excreta 1–2 wks after exposure. Infection occurs insoutheastern U.S. and is more common during summer months.

Fever, headache, and myalgia are usualfindings. Macular or papular rash occurs about 1 wk into illness,which lasts 2–3 wks.

Diagnosis is usually confirmed by serologictests.

Epidemic Typhus (Louse-Borne Typhus)

Humans areonly known reservoir of R. prowsekii, which causes epidemic typhus.

Infection is transmitted by infectedbody louse feces, usually through skin abrasion. Crowding, poorpersonal hygiene, and poverty are factors that contribute to itsoccurrence.

Usual incubation period is 1–2wks.

Begins with sudden onset of fever,chills, headache, and myalgia. Macular or papular rash appears in3–7 days and is followed by petechial or hemorrhagic rash.Face, palms, and soles are usually spared. In severe cases pneumonia,renal failure, and alteration in consciousness may occur.

Diagnosis may be confirmed by isolationof organism, visualization of rickettsiae in tissues, detectingrickettsiae by polymerase chain reaction, or by serologic testing.

Q Fever

Caused byC. burnetii, which infects cattle, sheep, goats, and rodents.

Human infection follows inhalationof infected dust from exposure to hides or products of conceptionof these animals.

Incubation period is 10–20days.

Acute onset of fever, chills, headache,and weakness are characteristic. Hepatosplenomegaly and weight lossoften occur. Persistent cough may signify pneumonia. High, spikingfever may continue for 1–3 wks, with gradual resolution.Major manifestations of chronic disease are hepatitis and endocarditis.

Immunofluorescence, complement fixation,enzyme immunoassay, and immune adherence hemagglutination antibodytests are used diagnostically.

Rickettsial Pox

Definedas mild illness caused by R. akari.

House mice harbor this organism, whichis transmitted to humans by mites.

Incubation period is 2–7 daysfollowing attachment of infected mite.

Mite bite produces red papule, whichforms vesicle that ulcerates. Fever, headache, chills, sweats, myalgia,and papular/vesicular eruption follow in 1–3 days.

During acute stage, organism may beisolated from blood. Serologic tests are also diagnostic.

Ehrlichiosis

Consistsof at least 2 distinct diseases: human monocytic ehrlichiosis causedby E. chaffeensis and human granulocytic ehrlichiosis caused byan unnamed Ehrlichia species. Both are transmitted by tick vectors.

Both resemble Rocky Mountain spottedfever, with fever, headache, malaise, chills, and myalgia. Macularor papular rash that occasionally can be petechial occurs commonlywith monocytic form and rarely with granulocytic form.

Lab findings include anemia, thrombocytopenia,increased liver aminotransferases, and CSF pleocytosis with predominanceof lymphocytes.

Diagnosis may be confirmed by serologicmethods or by polymerase chain reaction of DNA from a clinical sample.

Noninfectious

Many uncommon noninfectious causes, as listedbelow, are discussed in other chapters.

Respiratory

Pulmonaryinfarction

Pulmonary embolism

Gastrointestinal

Intestinal obstruction

Inflammatory bowel disease

Cardiac (postpericardiotomy syndrome)

Hematologic

Intravascular hemolysis

Bleeding into closed space

Endocrine

Thyrotoxicosis

Diabetes insipidus

Central nervous system

Intracranialinjury and hemorrhage

Spinal cord injury

Hypothalamic and brain stem lesions

Status epilepticus

Neoplasia

Leukemia

Lymphoma

Neuroblastoma

Pheochromocytoma

Connective tissue disorders

Juvenile rheumatoidarthritis

Systemic lupus erythematosus

Polyarteritis nodosa

Polymyositis

Dermatomyositis

Mixed connective tissue disease

Poisonings

Atropine

Cocaine

Salicylate

Lysergic acid diethylamide

Hydrocarbons

Organophosphates

Tricyclic antidepressants

Amphetamines

Phenothiazines

Other

Spider bites (black widow, brown recluse)

Stevens-Johnson syndrome

Heat-related illness

Serum sickness

Anhidrotic ectodermal dysplasia

Familial dysautonomia

Sarcoidosis

Familial Mediterranean fever

Factitious fever

Central Nervous System

Increasedtemperature may occur with intraventricular hemorrhage as well assubdural hematoma or effusion. CT is diagnostic.

Absence of effective control mechanismsof temperature regulation sometimes results from spinal cord injury.In such cases, significant increase in environmental temperatureproduces hyperpyrexia.

Any hypothalamic or brainstem lesionmay damage hypothalamic temperature-regulating center and producehyperpyrexia. Hypoxic-ischemic encephalopathy and brain tumors arecommon examples.

Prolonged status epilepticus may resultin autonomic changes with associated increase in temperature.

Neoplasia

Fever in children with cancer usually occursbecause of underlying disease process, infection, or effects oftreatment. Important factor in determining risk of serious infection,especially bacterial infection, is neutropenia (absolute neutrophilcount <500 cells/mm³).

Other

Spider Bites

Bite ofbrown recluse spider (L. reclusa) can cause severe local reaction,with fever, pain, and swelling followed by blister formation andnecrosis. Spider is brown, 10–15 mm long, with 6 eyes arrangedin an arc.

Female black widow spider (L. mactans)has red ventral spot and variable red dorsal spots. Usual lengthis about 2 cm, and bite produces twin red fang marks in skin. Injectionof venom produces pain and swelling at site of bite. Vomiting, fever,and intense abdominal pain may occur within 30 mins.

History and identification of spiderconfirm diagnosis.

Serum Sickness

Occurs 1–2wks after exposure to animal serum (e.g., diphtheria antitoxin;botulism antitoxin types A, B, and E; and antivenoms for snake orspider bites). Accelerated reaction may occur within 1–5days in individuals who have had previous exposure.

Clinical manifestations include fever;macular, papular, erythematous, or urticarial rash; localized orgeneralized adenopathy; hepatosplenomegaly; vomiting; abdominalpain; arthralgia or arthritis; and generalized edema. Usually self-limitedillness and lasting few days to few weeks.

Factitious Fever

Sometimes parent or guardian fabricates andreports persistent fever in child. Clues to this diagnosis are

Lack oftachycardia, flushing, sweating, or warm skin at time of fever

Rapid appearance and disappearanceof high fever in child who is otherwise well

Absence of fever when nurse or physiciantakes temperature

Wide discrepancy between oral and rectaltemperatures when taken simultaneously.

In any of these situations, consider Munchausensyndrome by proxy.

Diagnostic Approach: Acute Fever

Most acutefevers are caused by infection, usually viral or bacterial.

Common infections should be consideredbefore less common ones, unless clinical findings suggest otherwise.

Best guide to accurate diagnosis ishistory and physical exam.

Clinical Findings

Age of child,height of fever, compromised host defenses, and associated findings (e.g.,rash, painful extremity, abdominal pain, jaundice, generalized lymphadenopathy,hepatomegaly, or splenomegaly) are important factors in diagnosisof any child who presents with fever.

Important historical information includesany history of contact with other ill individuals, foreign travel,previous immunizations, drug exposure, history of pica, and exposureto animals or birds.

History of pica suggests toxoplasmosis or toxocariasis(visceral larva migrans).

History of tick exposure suggests RockyMountain spotted fever, relapsing fever, or Lyme disease.

History of exposure to animals or birdssuggests diseases caused by rats (plague, rat-bite fever, leptospirosis);hamsters (lymphocytic choriomeningitis encephalitis); rabbits (tularemia);cattle, goats, and dogs (brucellosis); cats (cat scratch disease,toxoplasmosis); and birds (psittacosis).

Age

Risk ofserious bacterial illness (e.g., septicemia and meningitis) varieswith age and is greatest during immediate neonatal period, especiallyin premature infants.

Clinical findings may be nonspecific,including poor feeding, decreased activity, fever, or hypothermia.

In such infants, CBC with differentialand blood, urine, and spinal fluid cultures should be performed.

Gram-stained smear of spinal fluidshould be performed and antigen studies considered.

Chest radiograph should be performedwith history of respiratory symptoms.

Stool culture should be performed withhistory of diarrhea.

Height of Fever

In infants,incidence of serious bacterial infection is higher in those withrectal temperature >41°C compared with those withlower temperature.

Preschool and school-aged childrenoften have high fever that persists for several days and is notassociated with localizing findings. Such children do not appearvery ill and usually have self-limited viral infections.

Continued observation with close follow-upusually clarifies many of these problems.

Whatever the height of fever, assessmentof toxicity and level of functioning is crucial in diagnosis andmanagement.

Compromised Host Defenses

Children with impaired host defenses dueto primary or secondary immunodeficiency disorders are at risk fordevelopment of serious infection caused by wide range of infectiveagents, including bacteria (S. aureus, gram-negative enteric organisms),viruses (cytomegalovirus, VZV), protozoa (P. carinii), and fungi(Candida and Aspergillus species).

Associated Physical Findings

Fever and Rash

Macularor papular rashes occur with viral infection (enteroviruses, herpesvirus6, measles virus, rubella virus, parvovirus B19, Epstein-Barr virus),bacterial infection (scarlet fever, meningococcemia, toxic shocksyndrome, typhoid fever, rat bite fever, leptospirosis), rickettsialinfection (Rocky Mountain spotted fever), Kawasaki disease, anddrug reactions (most commonly penicillins and sulfonamides).

Erythematous rashes occur with viralinfection (parvovirus B19), bacterial infection (scarlet fever,toxic shock syndrome, staphylococcal scalded skin syndrome), Kawasakidisease, and reactions to same drugs causing macular or papularrashes.

Petechial and purpuric rashes occurwith congenital viral infection (rubella virus, cytomegalovirus),other viral infection (enteroviruses, Epstein-Barr virus, arboviruses),bacterial infection (group A Streptococcus, N. meningitidis, S.pneumoniae, N. gonorrhoeae, S. aureus, H. influenzae type b, P. aeruginosaand other gram-negative enteric bacteria), rickettsial infection(Rocky Mountain spotted fever), and parasitic infection (toxoplasmosis).

Vesicular rashes occur with viral infection(herpes simplex virus, varicella-virus infection, enteroviruses)and bacterial infection (bullous impetigo, staphylococcal scaldedskin syndrome).

See Chap.60, Skin Lesions and Rashes.

Fever and Painful Extremity

Infectiousor inflammatory causes

Cellulitis

Septic arthritis

Osteomyelitis

Transient synovitis

Skin/soft tissue abscess

Thrombophlebitis

Acute rheumatic fever

Vaccine immunization

Other causes

Neoplasia (leukemia, osteogenic sarcoma,Ewing sarcoma, metastatic neuroblastoma)

Collagen vascular disease (juvenilerheumatoid arthritis, systemic lupus erythematosus)

Kawasaki disease

Serum sickness

Arthritis associated with inflammatorybowel disease

See Chap.37, Limp.

Fever and Abdominal Pain

Infectiousand inflammatory causes

Nonspecific viral illness

Gastroenteritis

Urinary tract infection

Pneumonia

Appendicitis

Intraabdominal abscess

Hepatitis

Peritonitis

Cholecystitis

Cholangitis

IBD

Pelvic inflammatory disease

Pancreatitis

Generalized vasculitis

Other causes

Neoplasia (leukemia, Hodgkin disease,non-Hodgkin lymphoma, neuroblastoma, hepatic malignancies)

Diabetic ketoacidosis

Black widow spider bite

See Chap.2, Abdominal Pain.

Fever and Jaundice

Most commoncause of fever and unconjugated hyperbilirubinemia in neonates is septicemia.Causes of fever and conjugated hyperbilirubinemia in neonates include

Viral infection(rubella virus, cytomegalovirus, herpes simplex virus, VZV, enteroviruses,hepatitis B virus)

Bacterial infection (septicemia, syphilis)

In infancy and childhood, fever andconjugated hyperbilirubinemia may be due to

Viral infection (hepatitis A, B, C,D, E; enteroviruses; herpes simplex virus; Epstein-Barr virus; cytomegalovirus

Bacterial infection (septicemia, cholecystitis,cholangitis, liver abscess, leptospirosis, brucellosis)

Rickettsial infection (Q fever)

Fungal infection (histoplasmosis)

Parasitic infection (amebiasis, malaria,visceral larval migrans)

Drug reactions

Neoplasia (hepatic malignancies, non-Hodgkinlymphoma)

See Chap.36, Jaundice.

Fever and Generalized Lymphadenopathy

Infectiouscauses

Viralinfection (rubella virus, measles virus, Epstein-Barr virus, cytomegalovirus, VZV,hepatitis A virus, HIV)

Bacterial infection (pyogenic infectionfrom S. aureus, group A Streptococcus, H. influenzae type b, S.pneumoniae; tuberculosis; brucellosis; tularemia; salmonellosis;leptospirosis; syphilis)

Fungal infection (histoplasmosis)

Parasitic infection (toxoplasmosis,malaria)

Noninfectious causes

Neoplasia(leukemia, non-Hodgkin lymphoma, metastatic neuroblastoma)

Langerhans histiocytosis

Collagen vascular disease (juvenilerheumatoid arthritis, systemic lupus erythematosus)

Drug reactions

Serum sickness

Chronic granulomatous disease

Sarcoidosis

See Chap.38, Lymphadenopathy.

Fever with Hepatomegaly, Splenomegaly, or Hepatosplenomegaly

Causes offever and hepatomegaly

Hepatitis (A, B, C, D, E)

Primary liver abscess

Amebiasis

Primary liver malignancies

Causes of fever and splenomegaly

Viral infection(rubella virus, cytomegalovirus, herpes simplex virus, enteroviruses, Epstein-Barrvirus)

Bacterial infection (septicemia, endocarditis,tularemia, plague, salmonellosis, splenic abscess)

Rickettsial infection (Rocky Mountainspotted fever)

Parasitic infection (malaria, toxoplasmosis)

Infectious causes of fever and hepatosplenomegaly

Viral infection(rubella virus; herpes simplex virus; cytomegalovirus; VZV; enteroviruses;Epstein-Barr virus; hepatitis A, B, C, D, E)

Bacterial infection (septicemia, endocarditis,brucellosis, tuberculosis, syphilis, leptospirosis, relapsing fever)

Fungal infection (histoplasmosis, coccidioidomycosis)

Parasitic infection (visceral larvalmigrans, toxoplasmosis, Chagas disease)

Other causes of fever and hepatosplenomegaly

Neoplasia(leukemia, Hodgkin disease, non-Hodgkin lymphoma, neuroblastoma)

Langerhans histiocytosis

Collagen vascular disease (juvenilerheumatoid arthritis, systemic lupus erythematosus)

See Chap.30, Hepatomegaly and Chap. 62, Splenomegaly.

Fever without Localizing Signs

Most childrenwith fever and no apparent focus of infection have self-limitedviral infection that resolves without treatment and has no sequelae.

Small percentage of children with acuteonset of fever ≥39°C and no localizing signs, especiallyat 3–36 mos, may have urinary tract infection, bacteremia,or meningitis.

In infants <1 mo of age, commoncauses of septicemia and meningitis are group B Streptococcus andgram-negative enteric bacteria, commonly E. coli. Much less commonis infection with L. monocytogenes.

At 1–3 mos of age, most commoncauses of septicemia and meningitis are S. pneumoniae, group B Streptococcus,and N. meningitidis.

In children >3 mos of age,S. pneumoniae, N. meningitidis, and Salmonella species (usually occurringwith gastroenteritis) cause most bacterial infections that occurwithout a focus.

Diagnostic and management approachto child with fever without apparent focus of infection dependson age, exposure history, usual pathogens, and severity of illness.

See references at end of chapter forfurther information.

Lab Findings

Lab tests(cultures and radiographs most commonly) are used to confirm diagnostic impressionof infection.

WBC and differential may suggest bacterialor viral infection, but they are not diagnostic. WBC count >20,000/mm³ withpredominance of neutrophils (>70%) or <5,000/mm³ withlarge number of band forms (>5%–10%)suggests bacterial infection. Although similar WBC counts sometimeoccur with viral infections, in such cases there is usually predominanceof lymphocytes and few band forms.

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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

Fever [Pyrexia]: History and physical examination
(Nursing: Interpreting Signs and Symptoms)

If the patient's fever is only mild to moderate, ask him when it began and how high his temperature reached. Did the fever disappear, only to reappear later? Did he experience other symptoms, such as chills, fatigue, or pain?

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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

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

There are certain things to remember when a patient with fever is approached. First, a mild elevation up to 100.5^∘F (38^∘C) rectally may be normal in some people. Second, one should rule out malingering by the patient or incorrect recording by hospital personnel. Finally, psychogenic disorders must be ruled out. The duration and severity of the fever are important. If possible, a careful chart of the fever should be made with the patient off all drugs (especially aspirin and steroids). Conditions with intermittent or relapsing fever such as brucellosis, malaria, and Mediterranean fever will be elucidated in this fashion (see Table 28). The association with other symptoms is important. Fever, right upper quadrant pain, and jaundice suggest cholecystitis or cholangitis, whereas fever with right-sided flank pain suggests pyelonephritis. After taking a few moments to jot down the differential before launching into the history and physical examination, one can question and examine the patient more appropriately. The differential diagnosis will also lead to more appropriate use of laboratory testing.

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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

Fever - Case 11-1: 18-Month-Old Girl: I. History of Present Illness
(Pediatric Complaints and Diagnostic Dilemmas)

An 18-month-old girl presented with a 1-day history of fever to 38.0°C and cough. While in the examination room, she had tonic flexion of her upper extremities and eye deviation to the left. This episode lasted 10 minutes and resolved spontaneously. Mild perioral cyanosis developed just before the end of the seizure. Afterward, the child was tired and irritable. There was no history of rash, eye pain, neck pain, or emesis. There were no alterations in gait or balance. There was no antecedent witnessed trauma. The only pet was a recently acquired goldfish. Several children at her daycare center had had symptoms of upper respiratory tract infection. The remainder of the review of systems was unremarkable.

II. Past Medical History

She was born at term after an uncomplicated pregnancy. She had not previously required hospitalization. Her immunizations were up to date and included the pneumococcal conjugate vaccine. She had received supplemental iron starting at 12 months of age for treatment of “anemia.” The maternal grandmother had type 2 diabetes treated with glyburide, a sulfonylurea oral hypoglycemic agent. There was no family history of febrile seizures, but one relative supposedly had a seizure and drowned while swimming. The family was not able to provide further details.

III. Physical Examination

T, 39.1°C; RR, 26/min; HR, 132 bpm; BP, 97/53 mm Hg; SpO₂, 98% in room air

Weight, 25th percentile

The child was crying and seemed mildly disoriented. There were no bruises or abrasions on her face or scalp. Her tympanic membranes were mildly erythematous but mobile. There was copious purulent nasal discharge. The neck was difficult to assess due to the child 's lack of cooperation. While yelling and screaming, she was able to arch her back and neck without apparent limitation. There was no cervical lymphadenopathy. The heart and lung sounds were normal. The abdomen was soft without organomegaly. There were no focal neurologic deficits, but the child appeared groggy and irritable and was slow to respond to her mother 's voice. Several hyperpigmented macules were noted on her skin as her clothes were removed for the lumbar puncture (Fig. 11-1).

IV. Diagnostic Studies

A complete blood count revealed the following: 15,500 white blood cells (WBCs)/mm ³ (61% segmented neutrophils, 22% lymphocytes, 15% monocytes, and 2% eosinophils); hemoglobin, 12.1 g/dL; and 282,000 platelets/mm ³. Serum electrolytes, calcium, and glucose were normal. Urinalysis revealed no WBCs or nitrites. Lumbar puncture revealed 2 WBCs and 19 red blood cells per cubic millimeter. No bacteria were visualized on Gram staining. The cerebrospinal fluid (CSF) protein and glucose concentrations were normal. Blood and CSF cultures were subsequently negative.

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Source: Pediatric Complaints and Diagnostic Dilemmas, 2003

Fever - Case 11-4: 7-Month-Old Girl: I. History of Present Illness
(Pediatric Complaints and Diagnostic Dilemmas)

A 7-month-old Japanese girl developed fever to 38.9°C associated with cough, rhinorrhea, and loose stools. Over the next few days, the respiratory symptoms and diarrhea resolved, but her fever persisted. Six days before admission, she was evaluated by her primary pediatrician and diagnosed with cellulitis involving the labia majora. She was treated with cephalexin, an oral first-generation cephalosporin. She presented to the emergency department because of continued fevers and worsening cellulitis and was admitted for intravenous antibiotic therapy and additional evaluation.

II. Past Medical History

Her birth history was remarkable for unconjugated hyperbilirubinemia. Her bilirubin level peaked at 16 mg/dL and returned to normal without phototherapy. Two months before admission, she developed otitis media that resolved after treatment with a 10-day course of amoxicillin. Cephalexin was her only medication at the time of admission. She had received all of the appropriate immunizations, including three doses of the heptavalent pneumococcal conjugate vaccine. The family history was remarkable for hepatitis A in the maternal grandmother approximately 2 months earlier.

III. Physical Examination

T, 40.3°C; RR, 50/min; HR, 160 bpm; BP, 104/60 mm Hg; SpO₂, 98% in room air

Weight, 75th percentile

Examination revealed an ill but not toxic-appearing infant. The anterior fontanel was open and flat. Tympanic membranes were mildly erythematous but had normal mobility bilaterally. There were no oropharyngeal lesions. Capillary refill was brisk. The heart and lung sounds were normal. The spleen was palpable just below the left costal margin. Examination of the genitalia revealed significant erythema and induration of the left labia majora with mild fluctuance. There was no crepitus. There were no other skin lesions.

IV. Diagnostic Studies

The WBC count was 3,100/mm³, with 2% segmented neutrophils, 28% monocytes, and 70% lymphocytes. The absolute neutrophil count (ANC) was 62 cells/mm ³. Hemoglobin was 12.3 mg/dL, and platelets were 337,000/mm³. A repeat complete blood count produced similar results. Lactate dehydrogenase and uric acid concentrations were normal. Urinanalysis did not reveal pyuria or hematuria. Blood and urine cultures were obtained.

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Source: Pediatric Complaints and Diagnostic Dilemmas, 2003

Jaundice - Case 15-1: 14-Day-Old Boy: I. History of Present Illness
(Pediatric Complaints and Diagnostic Dilemmas)

A 14-day-old, full-term male infant was transferred from a local community hospital for further evaluation and management of sepsis and hyperbilirubinemia. He had been discharged home from the well-baby nursery on the fourth day of life with a bilirubin concentration of 16.7 mg/dL. Two days later, his bilirubin level was 19.4 mg/dL and he was admitted for phototherapy. Within 48 hours after admission, he developed emesis and temperature instability. A blood culture and lumbar puncture were performed, and ampicillin and gentamicin were started. Additional bilirubin measurements revealed the direct fraction to be 5.2 mg/dL. An ultrasound study, performed to assess hepatomegaly, revealed a nondilated biliary system, small gall bladder, and diffuse hepatic enlargement. A nuclear medicine liver scan did not show bile excretion after 4 hours, prompting initiation of phenobarbital therapy.

The baby continued to receive breast milk feedings (with nasogastric tube supplementation required because of poor oral intake) until he experienced blood-tinged emesis. Coagulation studies at that time revealed the prothrombin time (PT) to be greater than 50 seconds and the partial thromboplastin time (PTT) to be greater than 200 seconds; for this reason, vitamin K and a dose of fresh-frozen plasma were given. By report, the baby 's abdomen was soft and his stool quantity and quality were unremarkable. Transfer to a tertiary care center was arranged.

II. Past Medical History

The baby was born to a 27-year-old gravida 1 parity 0 mother with unremarkable prenatal laboratory values. Delivery was via cesarean section at 37 weeks because of breech presentation. The baby 's birth weight was 3.04 kg. He was discharged with his mother on the fourth day of life and was breast-feeding every 3 hours.

III. Physical Examination

T, 36.4°C; RR, 48/min; HR, 140 bpm; BP, 83/50 mm Hg

Weight, 2.7 kg

Physical examination revealed a 2-week-old term boy who was listless but arousable. His skin demonstrated a yellow-green jaundice but no petechiae, rash, or bruising. He was nondysmorphic and normocephalic, with an open, flat fontanel. His pupils were equal, round, and reactive with red reflexes present bilaterally. Mucous membranes were yellow-pink and slightly dry. His respirations were slightly rapid but otherwise unlabored with clear breath sounds bilaterally. The heart examination was normal. The abdomen was soft and nondistended, with a smooth, firm liver edge palpable 3 cm below the right costal margin. Examinations of the genitalia and extremities were normal. His tone, power, and primitive reflexes all appeared to be within normal limits.

IV. Diagnostic Studies

A complete blood count revealed the following: white blood cells (WBCs), 9,400/mm ³ (1% band forms, 41% segmented neutrophils, and 45% lymphocytes); hemoglobin, 16.0 g/dL; and platelets, 66,000/mm ³. PT and PTT were markedly prolonged at 50 and 112 seconds, respectively. Fibrinogen was 127 mg/dL, and fibrin split products were negative. Serum bicarbonate was 17 mEq/L, but the remainder of the serum electrolytes, calcium, magnesium, and phosphorus were normal. Serum glucose was 52 mg/dL. A hepatic function panel revealed the following: alanine aminotransferase (ALT), 115 U/L aspartate aminotransferase (AST), 126 U/L; alkaline phosphatase, 730 U/L; γ-glutamyl transferase (GGT), 55 U/L; and albumin, 3.5 mg/dL. The unconjugated bilirubin concentration was 13.1 mg/dL, and the conjugated bilirubin was 5.9 mg/dL.

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Source: Pediatric Complaints and Diagnostic Dilemmas, 2003

Jaundice - Case 15-3: 2-Month-Old Boy: I. History of Present Illness
(Pediatric Complaints and Diagnostic Dilemmas)

A 2-month-old male infant was admitted for further evaluation of his jaundice and poor growth.

II. Past Medical History

The baby was born via spontaneous vaginal delivery after an uncomplicated, full-term pregnancy and weighed 3.0 kg at birth. On the second day of life, he was transferred to the special care nursery because of hypoglycemia requiring intravenous dextrose. A sepsis evaluation was performed, and the baby received 7 days of ampicillin and gentamicin. On the third day of life, his total bilirubin level was noted to be 18.6 mg/dL (with a direct bilirubin concentration of 2.8 mg/dL), and he received phototherapy for 4 days. His complete blood count, blood type and antibody screen, abdominal ultrasound, and state newborn screen were all normal. The birth hospital reported that the baby was taken home on the ninth day of life against medical advice; his prefeed blood sugar measurement that day was 33 mg/dL.

The baby had been seen by his pediatrician three times for weight and bilirubin checks; blood sugar measurements at those visits were described as “borderline.” His feeding regimen was about 2.5 ounces every 3 hours of cow's milk formula. Because of poor growth and persistent hyperbilirubinemia, he was referred to the hospital 's gastroenterology clinic and subsequently admitted for additional evaluation.

III. Physical Examination

T, 37.3°C; RR, 24/min; HR, 140 bpm; BP, 96/60 mm Hg

Weight, 3.6 kg (less than 3rd percentile); length, 52 cm (less than 3rd percentile); head circumference, 38 cm (10th percentile)

Physical examination revealed a cachectic, somewhat icteric 2-month-old boy in no apparent distress. There was scleral icterus and a 5 × 5 cm anterior fontanel; the oropharynx was clear, with moist mucous membranes. His neck was supple without lymphadenopathy or masses. Breath sounds were clear and unlabored. His pulse was regular, and there was no murmur. The abdomen was soft, nontender, and nondistended; the liver edge was palpable just below the right costal margin, and a small umbilical hernia was present. The testes were palpable (but not fully descended) bilaterally; the penis appeared small, with a stretched penile length of 2.0 cm. The baby appeared alert with grossly normal tone and reflexes. The remainder of the examination was unremarkable.

IV. Diagnostic Studies

Serum electrolyte measurement revealed the following: sodium, 131 mEq/L; potassium, 4.1 mEq/L; chloride, 100 mEq/L; bicarbonate, 22 mEq/L; BUN, 14 mg/dL; creatinine; 0.2 mg/dL; and glucose, 50 mg/dL. The complete blood count revealed 8,000 WBCs/mm ³ with 5% band forms, 30% segmented neutrophils, and 52% lymphocytes. The hemoglobin was 9.2 g/dL, and the reticulocyte count was 1.7%. The total bilirubin measured 10.5 mg/dL; the direct and unconjugated bilirubin levels were 1.5 and 9.0 mg/dL, respectively. Serum albumin was normal. ALT was 46 U/L, AST was 87 U/L, and GGT was 125 U/L.

Abdominal ultrasound examination of the liver revealed normal size, slightly increased echogenicity, and a small, nondistended gall bladder without biliary dilatation. The spleen and kidneys were normal. A sweat test was attempted, but an insufficient amount of sweat was obtained to properly interpret the test.

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Source: Pediatric Complaints and Diagnostic Dilemmas, 2003

Jaundice - Case 15-4: 6-Week-Old Girl: I. History of Present Illness
(Pediatric Complaints and Diagnostic Dilemmas)

A 6-week-old, full-term female infant was brought to the hospital by her mother because of persistence of scleral icterus. The infant had been seen during the first week of life after the mother noted she “looked yellow.” At that time, she was otherwise doing well and the pediatrician diagnosed physiologic jaundice. At 2 weeks of age, the baby began having blood-tinged stools. She was changed first from cow 's milk to soy milk formula, and then to an elemental formula, after which the bleeding resolved.

The baby had lately been acting well, taking her feedings without difficulty, and making a normal number of wet diapers. There was no recent history of emesis, excessive fussiness, bleeding, or bruisability. The mother did report that the baby 's stools had become increasingly white and pasty.

II. Past Medical History

The child was born by an uncomplicated, repeat cesarean section at 38 weeks. Her birth weight was 3.6 kg. Her hospital stay was unremarkable, and she was discharged home with her mother on the third day of life.

The infant had a healthy 3-year-old brother. There was no family history of jaundice, liver disease, anemia, or familial blood disorders.

III. Physical Examination

T, 37.0°C; RR, 32/min; HR, 136 bpm; BP, 88/60 mm Hg

Weight, 4.1 kg (10th to 25th percentile); length, 56 cm (25th to 50th percentile)

On examination, the infant was resting quietly in her mother's arms and was observed to have a mild “muddy” jaundice in her face. She was nondysmorphic and normocephalic, with an open, flat fontanel. Scleral icterus was pleasant. There was no nasal discharge or flaring. The oropharynx was clear, with moist mucous membranes. The lung and cardiac examinations were normal. Her abdomen was soft and nondistended, and a smooth, firm liver edge palpable 2 cm below the right costal margin. The genitourinary, extremity, and neurologic examinations were all normal.

IV. Diagnostic Studies

The complete blood count revealed the following: 6,900 WBCs/mm³ (43% segmented neutrophils and 48% lymphocytes); hemoglobin, 9.2 g/dL; and 332,000 platelets/mm ³. Total bilirubin was 9.5 mg/dL, and the direct bilirubin concentration was 8.4 mg/dL. ALT and AST were 267 and 288 U/L, respectively. Albumin was 3.2 g/dL, and the alkaline phosphatase was 641 U/L. Serum electrolytes, BUN, creatinine, and glucose were normal. Calcium was also normal. Urinanalysis revealed a specific gravity of 1.015 and 1+ blood but no nitrites, leukocyte esterase, protein, or urobilinogen.

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Source: Pediatric Complaints and Diagnostic Dilemmas, 2003

Jaundice - Case 15-6: 5-Week-Old Girl: I. History of Present Illness
(Pediatric Complaints and Diagnostic Dilemmas)

A 5-week-old girl was referred to the hospital for evaluation of her jaundice and poor weight gain. Her father stated that she had been “yellow her whole life,” starting before she left the newborn nursery. Except for some nasal congestion, the baby seemed to be acting and sleeping normally. She had been feeding on cow 's milk formula, taking 2 to 3 ounces every 3 hours, and made five to six wet diapers per day. The father described the baby 's stool output as two to four “loose” and “pasty” bowel movements per day. There was no history of fever, emesis, diarrhea, travel, or unusual exposures.

II. Past Medical History

The baby weighed 3.25 kg at birth; she was the product of a full-term gestation, delivered via cesarean section to a mother with a history of osteoporosis and back pain. The mother took no medications and denied use of drugs or alcohol. The baby was discharged home with her mother on the second day of life. She lived at home with both parents. There was no family history of cystic fibrosis, cardiac or gastrointestinal disease, or other pediatric illnesses.

III. Physical Examination

T, 37.2°C; RR, 28/min; HR, 120 bpm; BP, 80/56 mm Hg

Weight, 3.35 kg (5th percentile); length, 51 cm; head circumference, 36 cm

The infant appeared small but comfortable in her father's lap. She had an open, flat fontanel and a broad forehead; equal and round pupils; and scleral icterus. The oropharynx was clear with moist mucous membranes. Respirations were clear and unlabored. Cardiac examination revealed a II/VI systolic murmur that was loudest at the left sternal border; the rate, rhythm, and distal pulses were all normal. Her abdomen was soft and nondistended, with a smooth liver edge palpable 3 cm below the right costal margin; no spleen or other masses were appreciated. The genitourinary, extremity, and neurologic examinations were all normal.

IV. Initial Diagnostic Studies

A complete blood count revealed the following: 16,700 WBCs/mm³ (31% segmented neutrophils and 61% lymphocytes); hemoglobin, 9.6 g/dL; and 625,000 platelets/mm ³. The BUN and creatinine concentrations were 26 and 1.1 mg/dL, respectively. Serum electrolytes were normal. The total bilirubin concentration was 11.0 mg/dL; unconjugated and conjugated bilirubin were 8.0 and 3.1 mg/dL, respectively. The remainder of the hepatic function panel was as follows: ALT, 190 U/L; AST, 94 U/L; albumin, 3.0 mg/dL; and alkaline phosphatase, 450 U/L. Blood and urine cultures were obtained and were negative. Evaluations for toxoplasmosis, rubella, cytomegalovirus, and HIV were also negative.

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Source: Pediatric Complaints and Diagnostic Dilemmas, 2003

Jaundice: Jaundice - DIAGNOSIS
(The 5-Minute Pediatric Consult)

Approach to the patient:

Step 1: Determine if the hyperbilirubinemia is unconjugated or conjugated.
Step 2: If unconjugated hyperbilirubinemia:
- Obtain CBC and indices.
- Reticulocyte count
- Coombs test: If Coombs test is positive, the diagnosis is isoimmune; if Coombs test is negative, then consider polycythemia, extravascular bleed, or RBC structural or enzyme defects.
Step 3: If conjugated hyperbilirubinemia:
- Alanine aminotransferase (ALT), aspartate aminotransferase (AST), γ-glutamyltranspeptidase (GGT)
- PT/PTT/International normalized ratio
- Ultrasound of the liver/pancreas/gallbladder and biliary tree
- Rule out those etiologies of conjugated hyperbilirubinemia that may adversely affect the outcome if diagnosis is delayed (biliary atresia, tyrosinemia, galactosemia, inborn error of bile acid synthesis, hereditary fructose intolerance, panhypopituitarism).

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Source: The 5-Minute Pediatric Consult, 2008

Fever and Neutropenia: Diagnosis
(Pediatric Infectious Disease)

Due to the risk for life-threatening infection in the patient with fever and neutropenia, current practice suggests that patients meeting the above definitions be admitted to the hospital.

Cultures of the blood, urine, and if possible, induced sputum should be obtained. Chest radiographs are also suggested, especially if respiratory symptoms are present.

» READ BOOK EXCERPT ONLINE »

Source: Pediatric Infectious Disease, 2004

Outpatient Evaluation of Fever: Diagnosis
(Pediatric Infectious Disease)

Studies have suggested that even a negative full diagnostic workup, including complete blood count, urinalysis, stool Gram stain, and lumbar puncture, will miss a percentage of neonates who ultimately have a serious bacterial infection, including bacteremia and urinary tract infections.

» READ BOOK EXCERPT ONLINE »

Source: Pediatric Infectious Disease, 2004

» Next page: Signs of Leptospirosis

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TREATMENTS & RESEARCH

Dr. Huntley's Diagnosis Checklist

Diagnosis of Leptospirosis

Diagnostic Test list for Leptospirosis:

Leptospirosis Diagnosis: Book Excerpts

Tests and diagnosis discussion for Leptospirosis:

Diagnostic Tests for Leptospirosis: Online Medical Books

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

DIAGNOSTIC WORKUP

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

DIAGNOSTIC WORKUP

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

DIAGNOSTIC WORKUP

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

Workup and Diagnosis

Rash with Fever: Differential Diagnosis (In a Page: Signs and Symptoms)

Workup and Diagnosis

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

Workup and Diagnosis

Fever – Acute: Differential Diagnosis (In A Page: Pediatric Signs and Symptoms)

Workup and Diagnosis

Fever – Cyclic: Differential Diagnosis (In A Page: Pediatric Signs and Symptoms)

Workup and Diagnosis

Fever – Recurrent: Differential Diagnosis (In A Page: Pediatric Signs and Symptoms)

Workup and Diagnosis

Fever – Unknown Origin: Differential Diagnosis (In A Page: Pediatric Signs and Symptoms)

Workup and Diagnosis

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

Workup and Diagnosis

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

Workup and Diagnosis

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

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

Fever: History and physical examination (Handbook of Signs & Symptoms (Third Edition))

Jaundice: History and physical examination (Handbook of Signs & Symptoms (Third Edition))

Colorado tick fever: Diagnosis (Professional Guide to Diseases (Eighth Edition))

Lassa fever: Diagnosis (Professional Guide to Diseases (Eighth Edition))

Relapsing fever: Diagnosis (Professional Guide to Diseases (Eighth Edition))

Rheumatic fever and rheumatic heart disease: Diagnosis (Professional Guide to Diseases (Eighth Edition))

Rocky Mountain spotted fever: Diagnosis (Professional Guide to Diseases (Eighth Edition))

Fever [Pyrexia]: History and physical examination (Professional Guide to Signs & Symptoms (Fifth Edition))

Jaundice [Icterus]: History and physical examination (Professional Guide to Signs & Symptoms (Fifth Edition))

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

Physical examination

Rash Accompanied by Fever: History (The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

Physical examination

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

Physical examination

Fever of Unknown Origin: Differential Overview (Field Guide to Bedside Diagnosis)

Diagnostic Approach

Jaundice: Differential Overview (Field Guide to Bedside Diagnosis)

Diagnostic Approach

Rheumatic fever and rheumatic heart disease: Diagnosis (Handbook of Diseases)

Fever: History (Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

Physical examination

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

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

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

Common Causes

Infectious

Noninfectious

Drug Reactions

Vaccine Reactions

Trauma

Burns

Kawasaki Disease

Uncommon Causes

Infectious

Hantavirus Pulmonary Syndrome

Borrelia (Relapsing Fever)

Brucellosis

Leptospirosis

Plague

Psittacosis (Ornithosis)

Rat-Bite Fever

Syphilis

Tularemia

Malaria

Ascariasis

Toxocariasis (Visceral Larva Migrans, Ocular Larva Migrans)

TREATMENTS &
RESEARCH

Dr. Huntley's
Diagnosis
Checklist

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

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

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

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

Rash with Fever: Differential Diagnosis
(In a Page: Signs and Symptoms)

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

Fever – Acute: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

Fever – Cyclic: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

Fever – Recurrent: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

Fever – Unknown Origin: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

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

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

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

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

Fever: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

Jaundice: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

Colorado tick fever: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Lassa fever: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Relapsing fever: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Rheumatic fever and rheumatic heart disease: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Rocky Mountain spotted fever: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Fever [Pyrexia]: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

Jaundice [Icterus]: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

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

Rash Accompanied by Fever: History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

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

Fever of Unknown Origin: Differential Overview
(Field Guide to Bedside Diagnosis)

Jaundice: Differential Overview
(Field Guide to Bedside Diagnosis)

Rheumatic fever and rheumatic heart disease: Diagnosis
(Handbook of Diseases)

Fever: History
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

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

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

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

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

Fever [Pyrexia]: History and physical examination
(Nursing: Interpreting Signs and Symptoms)

Jaundice [Icterus]: History and physical examination
(Nursing: Interpreting Signs and Symptoms)

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

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

Fever - Case 11-1: 18-Month-Old Girl: I. History of Present Illness
(Pediatric Complaints and Diagnostic Dilemmas)

Fever - Case 11-4: 7-Month-Old Girl: I. History of Present Illness
(Pediatric Complaints and Diagnostic Dilemmas)