Diagnostic Tests for Leptospirosis
Leptospirosis: Diagnostic Tests
The list of diagnostic tests
mentioned in various sources as
used in the diagnosis of Leptospirosis
includes:
Leptospirosis Tests: Book Excerpts
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
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Review excerpts from medical books online, free, without registration,
for more information about the diagnostic tests for Leptospirosis.
FEVER, ACUTE:
DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)
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.
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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
FEVER, CHRONIC:
DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)
The diagnostic workup is similar to that for acute fever on
page 168
.
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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
JAUNDICE:
DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)
The basic workup includes a CBC, sedimentation rate, reticulocyte count, red cell fragility test, urinalysis, chemistry panel, VDRL test, EKG, a chest x-ray, and flat plate of the abdomen.
If infectious hepatitis is suspected, a hepatitis profile, febrile agglutinins, Monospot test, cytomegalic virus antibody titer, and leptospirosis antibody titer should be done. If lupoid hepatitis is suspected, a test for antinuclear antibodies and a smooth muscle antibody should be done.
If hemochromatosis is suspected, a serum iron, iron-binding capacity, and ferritin should be done.
If hemolytic anemia is suspected, serum haptoglobins, hemoglobin electrophoresis, and sickle cell preparations may be done.
If obstructive jaundice is suspected, then gallbladder ultrasound should be done to rule out gallstones, and a CT scan of the abdomen may be done to look for GI neoplasm. An upper GI series may assist in finding a primary neoplasm in the GI tract.
ERCP or percutaneous transhepatic cholangiography will assist in determining whether there is definitely obstructive jaundice and whether it is due to a surgically resectable lesion. Peritoneoscopy can also be helpful. An exploratory laparotomy will probably be necessary regardless of whether one performs the above tests. Cholangiopancreatography and endoscopic ultrasonography are two newer methods that may be used to evaluate the biliary tree and pancreatic ducts, especially when a neoplasm is suspected.
Hepatocellular jaundice will often require a needle biopsy of the liver to pin down the diagnosis. Antimitochondrial antibodies will need to be ordered to screen for biliary cirrhosis. An alpha 1-fetoprotein will help diagnose hepatocellular carcinoma. By the time you have reached this point, you have gone to considerable expense in the diagnostic workup. It would be much more prudent to ask for a gastroenterology consultation before ordering all these expensive diagnostic tests.
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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
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
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:
Physical examination
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
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.
Testing.
In cases of a fever in which the cause is unclear, a number of diagnostic tests may be useful, depending on history and physical examination. These include:
A. Urinalysis with microscopic examination
B. Blood cultures, both aerobic and anaerobic
C. Blood tests: human immunodeficiency virus (HIV), rapid plasma reagent (RPR), antistreptolysin-O (ASO) titer, rheumatoid arthritis (RA) factor, antinuclear antibody (ANA), sedimentation rate, and serum enzymes and chemistries
D. Tuberculosis (TB) skin test
E. Spinal fluid examination
F. Diagnostic imaging: chest film, abdominal ultrasound, abdominal computed tomography (CT), bone scan
G. Biopsies: liver, bone marrow, lymph node, skin, muscle, temporal artery
Diagnostic assessment.
The approach to the febrile patient involves a number of considerations, including the patient’s age, clinical history, risk factors, community illness pattern, and physical presentation. In the family physician’s office, most febrile illnesses are the result of self-limited viral illnesses (e.g., upper respiratory infections). A number of cases of fever will be caused by bacterial infections (e.g., streptococcal pharyngitis or urinary tract infections). The challenge is to select those studies with the highest sensitivity and specificity to increase the probability of a correct diagnosis. When the diagnosis continues to be elusive, repeat the history and the physical examination. Special considerations in specific populations and certain types of fever include:
A. The elderly: 10% of elderly patients will fail to generate a febrile response with pneumonia (1). Fever in the elderly is more likely to indicate a bacterial infection than a fever in younger adults (2).
B. Fever of unknown origin (FUO). An FUO is characterized by the first three criteria listed below:
1. A temperature greater than 38.3°C (101.0°F) on several occasions
2. A duration of 3 weeks
3. Unclear cause after a full physical examination, routine blood tests, cultures, and chest x-ray studies
4. The cause of FUOs will be determined 90% of the time; it will often be a common illness that presents in an unusual manner.
5. Two leading causes of FUO are tuberculosis and infective endocarditis.
6. Other causes include hepatic or subphrenic abscess, neoplasm, and lymphomas such as Hodgkin’s disease.
C. Factitious fever. Factitious fever is a consideration in a patient with a complex emotional disorder. The absence of a normal diurnal pattern, pulse elevation, and diaphoresis may suggest a diagnosis of factitious fever.
D. Drug fever. Drugs are an important cause of noninfectious fever (3).
1. This is a diagnosis of exclusion and requires the fever to coincide with the prescribing of the drug and the resolution of the fever on discontinuing the medication.
2. Drug-associated fevers can be high and take several days to resolve.
3. Among the medications causing a fever are diphenylhydantoin, carbamazepine, histamine-2 (H2) blockers, methyldopa, allopurinol, sulfonamides, cephalosporins, and isoniazid.
E. Postoperative fever. The temporal relationship of the fever to the surgery may provide a clue to the primary source of the infection (4).
1. If fever duration is less than 48 hours, consider atelectasis of the lung.
2. If duration is more than 3 days, consider urinary tract infection or infected intravascular device.
3. If fever has been present more than 5 days, consider wound infection, intraabdominal abscess, or empyema.
F. Hyperthermia. A disruption of thermoregulation can result from excessive heat production, inadequate heat dissipation, or hypothalamus malfunction (5).
References
1. Harper C, Newton P. Clinical aspects of pneumonia in the elderly veterans. J Am Geriatr Soc 1989;37:867–872.
2. Mellors JW, Horwitz RI, Harvey MR, et al. A simple index to identify occult bacterial infection in adults with unexplained fever. Arch Intern Med 1987;147:666–671.
3. Mackowiak PA, ed. Fever: basic mechanisms and management. New York: Raven Press, 1991:239.
4. Mackowiak PA, ed. Fever: basic mechanisms and management. New York: Raven Press, 1991:245.
5. Simon HB. Hyperthermia. N Engl J Med 1993;329(7):483–487.
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Rash Accompanied by Fever:
Physical examination
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
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.
Testing
should be directed by illnesses suspected, with life-threatening illnesses being tested for on reasonable suspicion. A complete blood count is generally useful, although life-threatening sepsis often presents without significant elevation of white blood count. In general, a blood culture should be obtained in all patients with petechial rashes and in those with signs of cardiovascular collapse.
Diagnostic assessment
Based on history and physical examination, the likelihood of various illnesses can be assessed. Patients who appear toxic should be treated as septic until initial laboratory and culture results can be evaluated (4).
References
1. Schlossberg D. Fever and rash. Infect Dis Clin North Am 1996;10(1):101–110.
2. Drolet BA, Baselga E, Esterly NB. Painful, purpuric plaques in a child with fever. Arch Dermatol 1997;133(12):1500–1501.
3. Anonymous. Fever, nausea, and rash in a 37-year-old man [clinical conference]. Am J Med 1998;104(6):596–601.
4. Dellinger RP. Current therapy for sepsis. Infect Dis Clin North Am 1999;13(2):
495–509.
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Jaundice:
Physical examination
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
The physical examination should focus on the following: Eyes should be examined for icterus or Kayser-Fleischer rings, which are copper-colored rings suggestive of Wilson’s disease. Heart and lung examination revealing S3 gallop or rales is suggestive of congestive heart failure, which leads to passive liver congestion. Ascites, hepatosplenomegaly, venous hum, and tenderness on abdominal examination points to portal hypertension and indicates liver cirrhosis (Chapters 9.2 and 9.9). Suspect pancreatic carcinoma when a nontender, palpable mass is found on upper abdominal examination. Signs of cirrhosis include excoriations, spider nevi, caput medusa, Dupytren’s contracture, gynecomastia, and palmar erythema. Delirium, drowsiness, asterixis, and tremor occur with liver failure.
Testing
A. Laboratory tests. Laboratory assays measure bilirubin as indirect (unconjugated) and direct (conjugated) fractions. An elevated indirect bilirubin level is consistent with overproduction of bilirubin or decreased uptake, transport, or conjugation by the hepatocyte. Elevation of direct bilirubin points to decreased excretion or transport by the biliary system (3). Transaminase levels (aspartate aminotransferase and alanine aminotransferase) increase from hepatocellular necrosis or inflammation from the release of aspartate aminotransferase from lysed hepatocytes. Hepatocyte damage and cholestasis increase alkaline phosphatase levels. γ-Glutamyl transpeptidase levels increase in cholestasis and alcohol abuse. Pancreatitis, pancreatic carcinoma, or common bile duct stones elevate amylase levels. With hepatocellular damage, coagulation studies can be prolonged. Antimitochondrial antibodies are present in primary biliary cirrhosis. Hepatitis B serologic tests are summarized in Table 9.8. Hepatitis A IgM antibody detects acute stage hepatitis A and IgG detects chronic stage hepatitis A. Anti-hepatitis C virus indicates hepatitis C infection. Hepatitis D only occurs with hepatitis B infection and is detected by anti-hepatitis D (4).
B. Diagnostic imaging has limited uses. Plain films of the abdomen rarely provide useful information. Cholelithiasis or pancreatic mass are best detected by ultrasound. Magnetic resonance imaging or computed tomography scans are used to examine the liver, pancreas, biliary tree, and suspected obstruction not identified by ultrasound. Hepatoiminodiacetic acid scanning is useful in a patient with suspected acute cholecystitis. Percutaneous transhepatic cholangiography and endoscopic retrograde cholangiopancreatography are used if obstructive jaundice is suspected to show the cause, location, and extent of involvement (5).
C. Other tests. Percutaneous liver biopsy is not indicated in the routine workup of jaundice but may prove useful in diagnosing the cause of jaundice when the above-mentioned tests are inconclusive. Iron levels are increased in hemochromatosis. Copper levels are increased in Wilson’s disease.
Diagnostic assessment
The patient’s history and associated symptoms guide the initial differential diagnosis of jaundice. Physical examination further narrows the causative choices and analysis of hepatic enzyme levels and viral serologies should confirm the initial diagnosis. Imaging studies play a limited role, except in suspected cases of malignancy or biliary obstruction.
Most patients have acute viral hepatitis as the cause of jaundice. Consultation is indicated when testing is inconclusive, when a surgical cause is suspected, or as needed for treatment.
References
1. Scharschmidt BF, Goldberg HI, Schmid R. Approach to the patient with cholestatic jaundice. N Engl J Med 1983;308:1515.
2. Lucas WB, Chuttani R. Pathophysiology and current concepts in the diagnosis of obstructive jaundice. Gastroenterologist 1995;3:105–118.
3. Fevery J, Blanckaert N. What can we learn from analysis of serum bilirubin?
J Hepatol 1986;2:113–121.
4. Bakerman S. ABC’s of interpretive laboratory data, 3rd ed. Myrtle Beach, SC: Interpretive Data, Inc., 1994:279–286.
5. Barloon TJ, Bergus GR, Weissman AM. Diagnostic imaging to identify the cause of jaundice. Am Fam Physician 1996;54:556–562.
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Fever of Unknown Origin:
Diagnostic Approach
(Field Guide to Bedside Diagnosis)
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:
Diagnostic Approach
(Field Guide to Bedside Diagnosis)
Jaundice becomes clinically apparent when the bilirubin level reaches 2 to 2.5 mg/dL. Scleral elastin has a high affinity for bilirubin, and with a white background, it is a sensitive indicator of jaundice. Biliary obstruction gives a greenish skin tint due to accumulation of biliverdin. Hemolysis gives a lemon-yellow tint when observed in natural light. An orange-yellow color is more consistent with hepatocellular disease. Pseudojaundice may be found in black patients with pigmented sclera, with carotinemia, with uremia (a sallow yellowish pallor), and with quinacrine (a yellow-green color).
Dark urine with green foam confirms a conjugated hyperbilirubinemia and excludes hemolysis or a conjugating defect. Unconjugated bilirubin is tightly bound to albumin, which prevents glomerular filtration.
Courvoisier law states: “In a jaundiced patient, a palpable gallbladder indicates that the jaundice is not due to stones.” Painless jaundice usually suggests a gradual process, as is found in intrahepatic cholestasis. The liver in this case is usually enlarged, smooth, and nontender. A patient with hepatocellular disease appears more ill than one with obstruction. Fluctuating jaundice occurs with gallstones, ampullary carcinoma, or toxins.
Anorexia, nausea, vomiting, or weight loss within 2 weeks of the appearance of jaundice suggests acute hepatitis or gallstones. Appearance more than 2 weeks prior suggests malignant biliary obstruction, chronic hepatitis, or toxin exposure (e.g., alcohol). Generalized pruritus suggests biliary obstruction, either extrinsic due to tumor, or canalicular due to drug-induced intrahepatic cholestasis.
Ascites with jaundice is an ominous sign, signifying decompensated cirrhosis with portal hypertension or malignancy with liver metastases. In portal hypertension, veins are engorged radially away from the umbilicus. In inferior vena cava obstruction, flow occurs upward over the abdominal wall. A harsh hepatic bruit may occur with malignancy, alcoholic hepatitis, or hemangioma. Splenomegaly without hepatomegaly occurs with hemolysis or portal vein occlusion.
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Source: Field Guide to Bedside Diagnosis, 2007
Fever:
Physical assessment
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Begin by taking your patient’s vital signs. 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 Taking an accurate temperature.)
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Jaundice:
Physical assessment
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Perform the physical examination in a room with natural light. Make sure that the orange-yellow hue is jaundice and not due to hypercarotenemia, which is more prominent on the palms and soles and doesn’t affect the sclerae. Inspect the patient’s skin for texture and dryness and for hyperpigmentation and xanthomas. Look for spider angiomas or petechiae, clubbed fingers, and gynecomastia. If the patient has heart failure, auscultate for arrhythmias, murmurs, and gallops. For all patients, auscultate for crackles and abnormal bowel sounds. Palpate the lymph nodes for swelling and the abdomen for tenderness, pain, and swelling. Palpate and percuss the liver and spleen for enlargement, and test for ascites with the shifting dullness and fluid wave techniques. Obtain baseline data on the patient’s mental status: Slight changes in sensorium may be an early sign of deteriorating hepatic function.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Fever:
Diagnostic Approach: Acute Fever
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
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 causesCellulitisSeptic arthritisOsteomyelitisTransient synovitisSkin/soft tissue abscessThrombophlebitisAcute rheumatic feverVaccine immunization Other causesNeoplasia (leukemia, osteogenic sarcoma,Ewing sarcoma, metastatic neuroblastoma)Collagen vascular disease (juvenilerheumatoid arthritis, systemic lupus erythematosus)Kawasaki diseaseSerum sicknessArthritis associated with inflammatorybowel disease See Chap.37, Limp. Fever and Abdominal Pain
Infectiousand inflammatory causesNonspecific viral illnessGastroenteritisUrinary tract infectionPneumoniaAppendicitisIntraabdominal abscessHepatitisPeritonitisCholecystitisCholangitisIBDPelvic inflammatory diseasePancreatitisGeneralized vasculitis Other causesNeoplasia (leukemia, Hodgkin disease,non-Hodgkin lymphoma, neuroblastoma, hepatic malignancies)Diabetic ketoacidosisBlack 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 includeViral 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 toViral infection (hepatitis A, B, C,D, E; enteroviruses; herpes simplex virus; Epstein-Barr virus; cytomegalovirusBacterial infection (septicemia, cholecystitis,cholangitis, liver abscess, leptospirosis, brucellosis)Rickettsial infection (Q fever)Fungal infection (histoplasmosis)Parasitic infection (amebiasis, malaria,visceral larval migrans)Drug reactionsNeoplasia (hepatic malignancies, non-Hodgkinlymphoma) See Chap.36, Jaundice. Fever and Generalized Lymphadenopathy
InfectiouscausesViralinfection (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 causesNeoplasia(leukemia, non-Hodgkin lymphoma, metastatic neuroblastoma)Langerhans histiocytosisCollagen vascular disease (juvenilerheumatoid arthritis, systemic lupus erythematosus)Drug reactionsSerum sicknessChronic granulomatous diseaseSarcoidosis See Chap.38, Lymphadenopathy. Fever with Hepatomegaly, Splenomegaly, or Hepatosplenomegaly
Causes offever and hepatomegalyHepatitis (A, B, C, D, E)Primary liver abscessAmebiasisPrimary liver malignancies Causes of fever and splenomegalyViral 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 hepatosplenomegalyViral 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 hepatosplenomegalyNeoplasia(leukemia, Hodgkin disease, non-Hodgkin lymphoma, neuroblastoma)Langerhans histiocytosisCollagen 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:
Diagnostic Approach: Unconjugated Hyperbilirubinemia
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
Most commoncauses of neonatal unconjugated hyperbilirubinemia are physiologic jaundiceand breast-feeding–related jaundice.Diagnostic tests should be performedinNeonateswho become clinically jaundiced during first 24 hrs of lifeTerm bottle-fed infants whose maximumserum bilirubin exceeds 12 mg/dLTerm breast-fed infants whose maximumserum bilirubin exceeds 15 mg/dLPreterm infants Certain tests should be performed initially:Maternal andinfant blood groups and Rh typesUnconjugated and conjugated serum bilirubinCBC and differentialReticulocyte countDirect Coombs testAnalysis of blood smear If jaundice persists, red cell G6PDactivity and T4 and TSH levels should bedetermined.If diagnosis remains uncertain, moreextensive studies for rarer forms of hemolytic disease and enzymeassay for uridine diphosphate glucuronyl transferase activity shouldbe considered. Tests for hepatocellular disease need to be performedonly when there is significant increase in conjugated bilirubin.In infancy and childhood, most commoncause of unconjugated hyperbilirubinemia is hemolytic anemia [see Chap. 45, Pallor (Anemia)].
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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
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?
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. (See How fever develops.)
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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 - Case 11-1: 18-Month-Old Girl:
III. Physical Examination
(Pediatric Complaints and Diagnostic Dilemmas)
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:
III. Physical Examination
(Pediatric Complaints and Diagnostic Dilemmas)
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:
III. Physical Examination
(Pediatric Complaints and Diagnostic Dilemmas)
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:
III. Physical Examination
(Pediatric Complaints and Diagnostic Dilemmas)
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:
III. Physical Examination
(Pediatric Complaints and Diagnostic Dilemmas)
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:
III. Physical Examination
(Pediatric Complaints and Diagnostic Dilemmas)
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
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