Diagnostic Tests for Dengue hemorrhagic fever
Dengue hemorrhagic fever Tests: Book Excerpts
Home Diagnostic Testing
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Dengue hemorrhagic fever Diagnosis: Book Excerpts
Diagnostic Tests for Dengue hemorrhagic fever: Online Medical Books
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PURPURA AND ABNORMAL BLEEDING:
DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)
If a coagulation disorder is suspected, consult a hematologist first. Routine diagnostic studies include a CBC, platelet count, sedimentation rate, blood smear for red cell morphology, urinalysis, chemistry panel, coagulation profile, rheumatoid arthritis factor, ANA test, serum protein electrophoresis, VDRL test, EKG, chest x-ray, and flat plate of the abdomen. The coagulation profile should include a platelet count, a bleeding time, a coagulation time, a partial thromboplastin time, and a prothrombin time.
If there is fever, blood cultures should be done. A bone marrow examination and bone marrow culture may be useful. If disseminated intravascular coagulation is suspected, a fibrinogen assay and estimation of fibrin degradation products should be done. Platelet function may be assessed by clot retraction tests. Spleen and liver scans and bone scans may be needed. A CT scan of the abdomen and pelvis may also be necessary. Skin, muscle, and even kidney biopsies are often done to complete the workup.
It can be seen from the above array of diagnostic tests that a hematologist should be consulted at the outset. Various forms of vasculitis may be confirmed by skin or muscle biopsy.
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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
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
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
Purpura:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
Ask the patient when he first noticed the lesion and whether he has noticed other lesions on his body. Does he or his family have a history of bleeding disorders or easy bruising? Find out what medications he’s taking, if any, and ask him to describe his diet. Ask about recent trauma or transfusions and the development of associated signs, such as epistaxis, bleeding gums, hematuria, and hematochezia. Also ask about systemic complaints that may suggest infection, such as a fever. If the patient is female, ask about heavy menstrual flow.
Gender Cue: Purpura is more common in women and particularly in individuals with large areas of subcutaneous fat, such as the breasts, abdomen, buttocks, thighs, and calves.
Inspect the patient’s entire skin surface to determine the type, size, location, distribution, and severity of purpuric lesions. Also inspect the mucous membranes. Remember that the same mechanisms that cause purpura can also cause internal hemorrhage, although purpura isn’t a cardinal indicator of this condition.
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Source: Handbook of Signs & Symptoms (Third Edition), 2006
Purpura:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
Ask the patient when he first noticed the lesion and whether he has noticed other lesions on his body. Does he or his family have a history of a bleeding disorder or easy bruising? Find out what medications he’s taking, if any, and ask him to describe his diet. Ask about recent trauma or transfusions and the development of associated signs, such as epistaxis, bleeding gums, hematuria, and hematochezia. Ask about systemic complaints that may suggest infection, such as fever. If the patient is female, ask about heavy menstrual flow.
Inspect the patient’s entire skin surface to determine the type, size, location, distribution, and severity of purpuric lesions. Inspect the mucous membranes. Remember that the same mechanisms that cause purpura can also cause internal hemorrhage, although purpura isn’t a cardinal indicator of this condition.
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Source: Professional Guide to Signs & Symptoms (Fifth 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
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
Petechiae and Purpura:
Physical examination
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
A. General and vital signs. Does the patient appear toxic or unstable? Considerations would include meningococcemia, Rocky Mountain spotted fever, disseminated intravascular coagulation (DIC), sepsis from Staphylococcus aureus, or thrombotic thrombocytopenic purpura.
B. Skin. Purpura should not blanch or only partially blanch with pressure. Petechiae are generally indicative of a quantitative or qualitative platelet abnormality. These nonpalpable petechiae may be caused by thrombocytopenia, which is either congenital or acquired (Chapter 16.7). The acquired thrombocytopenia can be caused by decreased platelet production as seen with viral infections, B12 or folate deficiency, iron deficiency, or a drug reaction. It is also seen with evidence of platelet destruction as present in ITP, connective tissue disease, leukemia, drugs, DIC, and thrombotic thrombocytopenic purpura. Abnormal platelet function is seen with aspirin ingestion, kidney and liver dysfunction, and in the thrombocytosis seen with myeloproliferative disorders. Significant straining with the Valsalva maneuver can cause petechiae. Lastly, the chronic pigmented purpura are the brown-orange spots occasionally seen on the lower extremities of adults. Schamberg’s disease is the most frequently seen and well known of the group. In these disorders, petechia are often intermixed with the pigmentation.
Ecchymoses are usually associated with coagulation disorders (e.g., in hemophilia, von Willebrand’s disease, anticoagulant usage, DIC, and vitamin K deficiency). Also responsible for ecchymoses are weakened connective tissue with less protection for vessels, as seen in senile purpura; glucocorticoid excess; vitamin C deficiency; and congenital disorders, such as Ehlers–Danlos syndrome.
Palpable purpura are usually secondary to a vasculitis. The causes are many and include hypersensitivity vasculitis to drugs; infections, including viral, rickettsial, and bacterial illnesses; cryoglobulinemias, such as Waldenström’s; and granulomatous causes, such as Wegener’s granulomatosis.
Testing
A. Test selection. Initial laboratory: Complete blood count (CBC), platelet count, peripheral smear, prothrombin time (PT), activated partial thromboplastin time (APTT), and possibly a bleeding time (3). If the lesions appear vasculitic, consider a sedimentation rate and C-reactive protein determination. Serum creatinine and urinalysis can be ordered to screen for renal involvement. In vasculitis, the laboratory findings are often nonspecific and a skin biopsy for histology is employed (2).
B. Significance of test results
1. Isolated thrombocytopenia: most often ITP in nonpregnant women. Without atypical features, no follow-up laboratory study is recommended (4).
2. Isolated, increased APTT: low levels of factors VIII, IX, XI. Follow-up studies: factor VIII level and von Willebrand’s factor assay and activity.
A slightly increased APTT and slightly decreased factor VIII are consistent with von Willebrand’s disease. A very prolonged APTT and very low factor VIII is consistent with an acquired factor VIII inhibitor (3).
3. Thrombocytopenia with increased PT, APTT: consider DIC and liver failure. Follow-up study: d-dimer, fibrinogen, fibrin degradation products.
In newborns with purpura, evaluation for sepsis, serologies for the TORCH syndrome (acronym for Toxoplasmosis, Other infections, Rubella, Cytomegalovirus infection, and Herpes simplex), and coagulation factors are also recommended. Proteins C and S activities are also indicated in purpura fulminans (diffuse ecchymoses that become bullous and necrotic); neutropenia or abnormal neutrophils may indicate leukemia. Other laboratory tests when evaluating vasculitis can include complement levels, antinuclear antibody, and cryoglobulins.
Diagnostic assessment (4)
With petechiae resulting from lone thrombocytopenia, ITP may be difficult to differentiate from pregnancy-induced thrombocytopenia (which tends to be milder), viral infection, or drugs. ITP is designated if no other clinically obvious cause is noted.
Thrombotic-thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS) are seen in many clinical situations, including pregnancy, cancer, infections, chemotherapy, and so on. Signs include the pentad of fever, thrombocytopenia, microangioipathic hemolytic anemia, hemorrhage (including purpura), and neurologic abnormalities. Because of serious consequences, the diagnosis should be considered if thrombocytopenia and fragmented red blood cells are seen on the peripheral smear. TTP-HUS has a normal PT, APTT, and d-dimer as opposed to DIC.
In regard to coagulation factor abnormalities, hemophilia A and B can cause increased bruising and ecchymoses but not nearly as frequently as von Willebrand’s disease. Children being investigated for nonaccidental bruising should be evaluated for coagulation disorders with a CBC, platelet count, PT, APTT, and a bleeding time. With the sudden onset of large ecchymoses and hematomas in an adult with normal platelets, an acquired factor VIII deficiency (autoantibody) should be investigated in cases of a prolonged PT, APTT.
In newborns, a blueberry muffin baby (from extramedullary hematopoiesis) may appear purpuric, and this condition must be differentiated from purpura fulminans secondary to protein C or S deficiency, or sepsis.
Vasculitis causing palpable purpura in children is most common with Henoch–Schönlein purpura. In connective tissue diseases, purpuric lesions are usually a secondary finding.
The causes of purpuric lesions are many. A thorough history and physical examination, along with some basic laboratory studies and an occasional skin biopsy, are all that is needed to establish a likely diagnosis.
References
1. Baselga E, Drolet BA, Esterly NB. Purpura in infants and children. J Am Acad Dermatol 1997;37:673–705.
2. Cuttica RJ. Vasculitis in children: a diagnostic challenge. Curr Probl Pediatr 1997 27:309–317.
3. Loserh JM. Screening and diagnosis of coagulation disorders. Am J Obstet Gynecol 1996;175:778–783.
4. Diagnosis and treatment of idiopathic thrombocytopenic purpura: Recommendations of the American Society of Hematology. The American Society of Hematology ITP Practice Guideline Panel. Ann Intern Med 1997;126:319–326.
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Purpura/Petechiae/Excessive Bleeding:
Diagnostic Approach
(Field Guide to Bedside Diagnosis)
A patient with a suspected bleeding disorder should be questioned about response to trauma, past bleeding problems, for example with surgery or dental extractions, history of transfusion, menstrual history and dietary habits. Absence of abnormal bleeding with surgery, significant trauma, or dental extractions makes an inherited bleeding disorder unlikely.
Petechiae are small capillary hemorrhages resulting from platelet or vascular abnormalities. Petechiae on the lower extremities or mucous membranes are usually caused by thrombocytopenia. Tender, elevated petechiae plus abnormalities in other organs suggests vasculitis. Platelet defect disorders produce petechiae and ecchymoses occurring immediately after local trauma. Bleeding is superficial, occurring in the skin, the mucous membranes, the nose, and the gastrointestinal and genitourinary tracts. Bleeding does not occur with normal platelets until the count falls to less than 50,000, and the threshold for important bleeding is 20,000. Oozing blood around catheters suggests DIC, vitamin K deficiency, or platelet abnormalities.
Large-area bruising occurs with vitamin-K–dependent factor deficiency, but not with hemophilia. Plasma protein disorders produce bleeding in deep tissues, such as joints, muscle, and retroperitoneum. The onset of such bleeding can be delayed for hours after trauma.
Palpable purpura is seen with autoimmune or infectious (e.g., meningococcemia, endocarditis) vasculitis. Infectious emboli have an irregular outline, whereas lesions of leukocytoclastic vasculitis are circular.
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Source: Field Guide to Bedside Diagnosis, 2007
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
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
Purpura:
Physical assessment
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Inspect the patient’s entire skin surface to determine the type, size, location, distribution, and severity of purpuric lesions. Also inspect the mucous membranes. Remember that the same mechanisms that cause purpura can also cause internal hemorrhage, although purpura isn’t a cardinal indicator of this condition.
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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
Purpura and Bleeding:
Diagnostic Approach
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
Age, clinical findings, family history, andscreening tests (CBC with differential, platelet count, analysisof blood smear, PT and aPTT, and standardized Ivy bleeding time)are either diagnostic or narrow diagnostic possibilities in individualspresenting with purpura and bleeding.
Age
Neonates,especially preterm infants, have some features that may predisposeto purpura and bleeding. They have increase in capillary fragilityand decrease in platelet aggregation. Concentrations of vitaminK–dependent clotting factors are lower than adult normalvalues.Diagnostic approach to purpura andbleeding depends on whether neonate is well or ill and whether plateletcount is normal or decreased.In well neonate with normal platelet count,most common disorders that cause bleeding are trauma, vitamin Kdeficiency, Factor VIII or IX deficiency, and in utero exposureto drugs taken by mother (e.g., acetylsalicylic acid, phenytoin,or coumadin).In well neonate with decreased plateletcount, most common disorders are alloimmune thrombocytopenia andmaternal autoimmune thrombocytopenia.In ill neonate, common causes of bleedingand purpura are severe birth trauma, septicemia, and DIC. Othercauses include congenital infection (herpes simplex, cytomegalovirus,rubella, toxoplasmosis, syphilis), congenital leukemia, and osteopetrosis. In infancy, childhood, and adolescence,most common causes of purpura and bleeding are accidental trauma,child abuse, Henoch-Schönlein purpura, idiopathic thrombocytopenicpurpura, leukemia, infection, and Factor VIII and IX deficiencies. Clinical Findings
Typically,individuals with loss of vascular integrity have superficial bleedingwith purpura. Diagnosis of loss of vascular integrity depends onclinical recognition of vascular disorder and absence of plateletor coagulation disorder.Individuals with thrombocytopenia orplatelet dysfunction usually have purpura and superficial bleedingof mucous membranes including epistaxis and GI tract bleeding. Alsomay have hematuria, menorrhagia, and intracranial bleeding. Normalplatelet count with prolonged bleeding time suggests qualitativeplatelet defect.Individuals with Factor VIII or IXdeficiency, which are most common coagulation disorders, have recurrentbruising and bleeding into joints and muscle. Family History
Positivefamily history may help confirm diagnosis.As general rule, genetically transmitteddisorders usually have their onset in infancy with appearance ofrecurrent purpura and bleeding.Acquired disorders are usually acute,variable in time of onset, and typically associated with infection,drug reactions, malignancy, or immunologic disorders. Screening and Diagnostic Tests
A plateletcount of <150,000/mm3 isabnormal. Bleeding is rare with platelet count of >30,000/mm3.Large platelets are usually seen on blood smear in disorders inwhich thrombocytopenia is due to increased platelet destruction.Normal-sized platelets are usually seen in disorders in which thrombocytopeniais due to decreased production. When thrombocytopenia is associatedwith neutropenia or pancytopenia, bone marrow aspirate should beperformed searching for evidence of aplastic anemia, leukemia, orother malignancies.With normal platelet count but abnormalbleeding time, most likely diagnoses are von Willebrand disease,aspirin ingestion, qualitative defect in platelet function, anduremia. Tests for renal function, vWF antigen, vWF ristocetin cofactor,and platelet function should be considered.Possible causes of prolonged PT includeFactor VII deficiency, mild vitamin K deficiency, and liver disease.Prolonged aPTT may be caused by FactorVIII, IX, XI, and XII deficiencies; von Willebrand disease; andpresence of circulating anticoagulant. There is no clinical bleedingwith Factor XII deficiency.Possible causes of prolonged PT andaPTT include liver disease, DIC, vitamin K deficiency, congenitalfactor deficiencies (II, V, and X), and fibrinogen disorders (afibrinogenemia,hypofibrinogenemia). Liver function tests should be performed withsuspected liver disease. Otherwise, thrombin time, serum fibrinogen,fibrin split products, and assays for Factors II, V, and X shouldbe performed as indicated. Serum fibrinogen is decreased in congenitalafibrinogenemia, DIC, and sometimes in severe liver disease. >
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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
Purpura:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
Ask the patient when he first noticed the lesion and whether he has noticed other lesions on his body. Does he or his family have a history of bleeding disorders or easy bruising? Find out what medications he's taking, if any, and ask him to describe his diet. Ask about recent trauma or transfusions and the development of associated signs, such as epistaxis, bleeding gums, hematuria, and hematochezia. Also ask about systemic complaints that may suggest infection, such as a fever. If the patient is female, ask about heavy menstrual flow.
Inspect the patient's entire skin surface to determine the type, size, location, distribution, and severity of purpuric lesions. Also inspect the mucous membranes. Remember that the same mechanisms that cause purpura can also cause internal hemorrhage, although purpura isn't a cardinal indicator of this condition.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
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
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