Toxic shock syndrome laboratory findings
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview:
- An elevated/reduced concentration of serum/blood/urinary/CSF/other [lab test] is diagnostic of [disease name]
- Laboratory findings consistent with the diagnosis of toxic shock syndrome (TSS) include leukocytosis, anemia and thrombocytopenia.
- There are no diagnostic lab findings associated with [disease name].
- Additional Sentences:
- Additional Sentence 1: [Test] is usually normal among patients with [disease name].
- Additional Sentence 2: Some patients with [disease name] may have elevated/reduced concentrations of [test], which is usually suggestive of [progression/complication].
Laboratory Findings
The international guideline committee for diagnosis of septic shock recommends obtaining appropriate cultures that may include at least two blood cultures, urine, cerebrospinal fluid, wounds, respiratory secretions, or other body fluid cultures before antimicrobial therapy is initiated. If such cultures do not cause significant delay in antibiotic administration, then other tests that may be done include blood gases, kidney function tests, platelet count, white blood cell count, blood differential, fibrin degradation products, and peripheral smear.
Electrolyte and Biomarker Studies
Baseline tests
- Complete blood count:
- Serum calcium levels - can reflect underlying disease states (e.g, severe hypercalcemia may reflect underlying malignancy or hyperparathyroidism; hypocalcemia can contribute to osteoporosis)
- Serum phosphate and alkaline phosphatase
- Serum 25 (OH) vitamin D levels
- Serum creatinine levels - reflect chronic renal failure which leads to renal osteodystrophy
- Serum magnesium levels - important in calcium homeostasis
- Serum iron and ferritin levels - for excluding hemochromatosis
- Liver function tests (alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transferase, bilirubin) - aids in diagnosing alcoholism
- Thyroid function tests
Serum lactate
●Renal and liver function tests: Elevated blood urea nitrogen (BUN), creatinine, and transaminases are usually due to shock-induced end-organ damage (eg, acute kidney injury, shock liver).
hypo- or hypernatremia, hypo- or hyperkalemia, low urinary sodium concentration, or fractional excretion of sodium <1 percent may indicate hypovolemia.
●Complete blood count and differential:leukocytosis may suggest septic shock. A high hematocrit may suggest hemoconcentration from hypovolemia. A low white blood cell count and especially a bandemia are more worrisome for sepsis in the setting of undifferentiated shock
●Coagulation studies and D-dimer level
●Blood gas analysis-Venous blood gas (VBG) and arterial blood gas analysis (ABG)Hypoxemia may be present as a result of pulmonary edema and pleural effusion
elevated levels of creatine phosphokinase (CPK)
- Renal failure can lead to metabolic abnormalities such as hypocalcemia, hyponatremia, hypoalbuminemia, and hypophosphatemia.
hematologic abnormalities, especially anemia and thrombocytopenia.
leukocytosis, hemoconcentration,
- Profound leukocytosis (leukemoid reaction) consisting of white blood cell (WBC) count >50,000 cells/microL, which can increase to 200,000 cells/microL within 48 hours
- An increased percentage of mature and immature neutrophils and increased absolute numbers of lymphocytes and monocytes
- Leukemoid reaction is highly predictive of mortality
Hematocrit levels up to 80 percent have been reported
due to capillary leak from toxin-mediated changes in the vascular endothelium and ahypoalbuminemia
A diagnosis of probable GAS TSS can be made if GAS is isolated from a normally nonsterile site (eg, throat, vagina, skin lesion) but the patient fulfills the other criteria noted above and no other etiology for the illness is identified.
Recovery of the organism from blood cultures usually takes 8 to 24 hours. Gram stain of involved tissue demonstrating gram-positive cocci in pairs and chains can provide an early diagnostic clue in many cases.....8418347
Bacteremia is common.....3890787
Cultures from mucosal and wound sites should be obtained because S. aureus isolates can be tested for toxin production in research laboratories.acute and convalescent serum can be analyzed for antibody responses to various S. aureus exotoxins. The presence of a strain of S. aureus that produces toxin in a patient who does not have acute phase antibody to the toxin is highly suggestive of TSS.
Polymerase chain reaction (PCR) analysis of peripheral blood T cells from adults with TSS has shown a protracted expansion of TSST-1–reactive Vβ2-positive T cells persisting for 4–5 weeks.
| [null serotyping] | evidence of streptococcal exotoxins |
| [null microscopy and culture (blood, wound, fluid, tissue)] | positive for group A streptococcus or Staphylococcus aureus |
| [null CBC] | leukocytosis with a left shift; anemia; thrombocytopenia with platelets <100 x 10^3/microliter |
| [null prothrombin time] | prolonged in staphylococcal disease in conjunction with DIC |
| [null partial thromboplastin time] | prolonged in staphylococcal disease in conjunction with DIC |
| [null serum BUN and creatinine] | elevated |
| [null urinalysis] | hemoglobinuria |
| [null LFTs] | elevated transaminases and bilirubin |
| [null creatine kinase (CK)] | elevated in necrotizing fasciitis or myositis and in some staphylococcal disease |
| [null serum calcium] | low in streptococcal disease |
| [null serum albumin] | low in streptococcal disease |
| [null serum lactic acid] | elevated in severe sepsis and septic shock |