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__NOTOC__
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{{Toxic shock syndrome}}
{{CMG}}
{{CMG}},{{AE}}{{MIR}}
==Overview''':'''==
==Overview''':'''==
:An elevated/reduced concentration of serum/blood/urinary/CSF/other [lab test] is diagnostic of [disease name]
[[Laboratory findings template|Laboratory finding]]<nowiki/>s consistent with the diagnosis of [[toxic shock syndrome]] (TSS) include [[leukocytosis]], [[anemia]] and [[thrombocytopenia]]. A positive [[blood culture]] is diagnostic for [[Streptococcus|Streptococcal]] TSS, although in other causes of TSS [[blood culture]] doesn't have a high value.
: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==
==Laboratory Findings==
The international guideline committee for diagnosis of septic shock recommends obtaining appropriate [[culture]]s 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]].
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. In [[Toxic shock syndrome|TSS]] patients, [[blood culture]] for [[staphylococcus]] is not diagnostic, although blood culture for [[Streptococcus|streptococcal]] TSS is highly diagnostic.


===Electrolyte and Biomarker Studies===
=== Primary General Electrolyte and Biomarker Studies<ref name="pmid8418347">{{cite journal |vauthors= |title=Defining the group A streptococcal toxic shock syndrome. Rationale and consensus definition. The Working Group on Severe Streptococcal Infections |journal=JAMA |volume=269 |issue=3 |pages=390–1 |year=1993 |pmid=8418347 |doi= |url=}}</ref><ref name="pmid3890787">{{cite journal |vauthors=Adams EM, Gudmundsson S, Yocum DE, Haselby RC, Craig WA, Sundstrom WR |title=Streptococcal myositis |journal=Arch. Intern. Med. |volume=145 |issue=6 |pages=1020–3 |year=1985 |pmid=3890787 |doi= |url=}}</ref> ===
====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|creatine phosphokinase (CPK)]]
* [[Renal failure]] can lead to [[Metabolic Control Analysis|metabolic abnormalitie]]<nowiki/>s such as [[hypocalcemia]], [[hyponatremia]], [[hypoalbuminemia]], and [[hypophosphatemia]].
[[CBC|hematologic abnormalities]], especially [[anemia]] and [[thrombocytopenia]].
 
[[bacteremia]],  
 
[[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 [[Neutrophil|neutrophils]] and increased absolute numbers of [[Lymphocyte|lymphocytes]] and [[Monocyte|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.
{| class="wikitable"
{| class="wikitable"
|[null serotyping]
! align="center" style="background:#4479BA; color: #FFFFFF;" |Laboratory Tests
|evidence of streptococcal exotoxins
! align="center" style="background:#4479BA; color: #FFFFFF;" |Result
|}
|-
{| class="wikitable"
| rowspan="4" align="center" style="background:#DCDCDC;"|[[Complete blood count]] (CBC)
|[null microscopy and culture (blood, wound, fluid, tissue)]
|[[Leukocytosis]] with a left shift
|positive for group A streptococcus or Staphylococcus aureus
|-
|[[Hematocrit]] levels up to 80 percent have been reported
|-
|[[Thrombocytopenia]] with [[Platelet|platelets]] <100 x 10^3/microliter
|-
|[[Anemia]]
|-
|align="center" style="background:#DCDCDC;"|Blood culture
|[[Bacteremia]]
|-
| rowspan="2" align="center" style="background:#DCDCDC;"|[[Renal function tests]]
|Elevated serum [[BUN]] and [[creatinine]]
|-
|[[Urine appearance|Urine Analysis]]: [[Hemoglobinuria]]
|-
| rowspan="2" align="center" style="background:#DCDCDC;"|[[Liver function tests|Liver Function Tests]]
|Elevated [[Transaminase|transaminases]] and [[bilirubin]]
|-
|[[Hypoalbuminemia]]
|-
|align="center" style="background:#DCDCDC;"|Serum [[lactic acid]]
|[[Lactic acidosis|Hyper lactic acidosis]]
|-
| rowspan="3" align="center" style="background:#DCDCDC;"|Metabolic tests
|[[Hypocalcemia]]
|-
|[[Hyponatremia]]
|-
|-
|[null CBC]
|[[Hypophosphatemia]]
|leukocytosis with a left shift; anemia; thrombocytopenia with platelets <100 x 10^3/microliter
|-
|-
|[null prothrombin time]
| rowspan="2"v align="center" style="background:#DCDCDC;"|Blood gas analysis:
|prolonged in staphylococcal disease in conjunction with DIC
Venous blood gas (VBG) and arterial blood gas analysis (ABG)
|[[Hypoxemia]] may be present as a result of [[pulmonary edema]] and [[pleural effusion]]
[[Metabolic acidosis]]
|-
|-
|[null partial thromboplastin time]
| align="center" style="background:#DCDCDC;"|[[Creatine phosphokinase|Creatine phosphokinase (CPK)]]
|prolonged in staphylococcal disease in conjunction with DIC
|Elevated
|}
 
=== Specialized Laboratory Tests<ref name="pmid7069224">{{cite journal |vauthors=Davis JP, Osterholm MT, Helms CM, Vergeront JM, Wintermeyer LA, Forfang JC, Judy LA, Rondeau J, Schell WL |title=Tri-state toxic-shock syndrome study. II. Clinical and laboratory findings |journal=J. Infect. Dis. |volume=145 |issue=4 |pages=441–8 |year=1982 |pmid=7069224 |doi= |url=}}</ref> ===
{| class="wikitable"
|-
|-
|[null serum BUN and creatinine]
! align="center" style="background:#4479BA; color: #FFFFFF;" |Laboratory Tests
|elevated
! align="center" style="background:#4479BA; color: #FFFFFF;" |Result
|-
|-
|[null urinalysis]
|align="center" style="background:#DCDCDC;"|Blood microscopy and culture (blood, wound, fluid, tissue)
|hemoglobinuria
|Positive for group A [[streptococcus]] or [[Staphylococcus aureus]]
|-
|-
|[null LFTs]
| align="center" style="background:#DCDCDC;"|[[Prothrombin time]]
|elevated transaminases and bilirubin
|Prolonged in [[Staphylococcus|staphylococcal]] disease in conjunction with [[DIC]]
|-
|-
|[null creatine kinase (CK)]
| align="center" style="background:#DCDCDC;"|[[Partial thromboplastin time]]
|elevated in necrotizing fasciitis or myositis and in some staphylococcal disease
|Prolonged in [[staphylococcal]] disease in conjunction with [[DIC]]
|-
|-
|[null serum calcium]
| align="center" style="background:#DCDCDC;"|[[Creatine kinase|Creatine kinase (CK)]]
|low in streptococcal disease
|Elevated in [[necrotizing fasciitis]] or [[myositis]] and in some [[Staphylococcus|staphylococcal]] disease
|-
|-
|[null serum albumin]
| align="center" style="background:#DCDCDC;"|[[Polymerase chain reaction|Polymerase chain reaction (PCR)]]
|low in streptococcal disease
|Protracted expansion of TSST-1–reactive Vβ2-positive T cells persisting for 4–5 weeks
|-
|-
|[null serum lactic acid]
| align="center" style="background:#DCDCDC;"|Serotyping
|elevated in severe sepsis and septic shock
|Evidence of [[Streptococcus|streptococcal]] [[Exotoxin|exotoxins]]
|}
|}


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Latest revision as of 00:27, 30 July 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1],Associate Editor(s)-in-Chief: Mahshid Mir, M.D. [2]

Overview:

Laboratory findings consistent with the diagnosis of toxic shock syndrome (TSS) include leukocytosis, anemia and thrombocytopenia. A positive blood culture is diagnostic for Streptococcal TSS, although in other causes of TSS blood culture doesn't have a high value.

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. In TSS patients, blood culture for staphylococcus is not diagnostic, although blood culture for streptococcal TSS is highly diagnostic.

Primary General Electrolyte and Biomarker Studies[1][2]

Laboratory Tests Result
Complete blood count (CBC) Leukocytosis with a left shift
Hematocrit levels up to 80 percent have been reported
Thrombocytopenia with platelets <100 x 10^3/microliter
Anemia
Blood culture Bacteremia
Renal function tests Elevated serum BUN and creatinine
Urine Analysis: Hemoglobinuria
Liver Function Tests Elevated transaminases and bilirubin
Hypoalbuminemia
Serum lactic acid Hyper lactic acidosis
Metabolic tests Hypocalcemia
Hyponatremia
Hypophosphatemia
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

Metabolic acidosis

Creatine phosphokinase (CPK) Elevated

Specialized Laboratory Tests[3]

Laboratory Tests Result
Blood microscopy and culture (blood, wound, fluid, tissue) Positive for group A streptococcus or Staphylococcus aureus
Prothrombin time Prolonged in staphylococcal disease in conjunction with DIC
Partial thromboplastin time Prolonged in staphylococcal disease in conjunction with DIC
Creatine kinase (CK) Elevated in necrotizing fasciitis or myositis and in some staphylococcal disease
Polymerase chain reaction (PCR) Protracted expansion of TSST-1–reactive Vβ2-positive T cells persisting for 4–5 weeks
Serotyping Evidence of streptococcal exotoxins

References

  1. "Defining the group A streptococcal toxic shock syndrome. Rationale and consensus definition. The Working Group on Severe Streptococcal Infections". JAMA. 269 (3): 390–1. 1993. PMID 8418347.
  2. Adams EM, Gudmundsson S, Yocum DE, Haselby RC, Craig WA, Sundstrom WR (1985). "Streptococcal myositis". Arch. Intern. Med. 145 (6): 1020–3. PMID 3890787.
  3. Davis JP, Osterholm MT, Helms CM, Vergeront JM, Wintermeyer LA, Forfang JC, Judy LA, Rondeau J, Schell WL (1982). "Tri-state toxic-shock syndrome study. II. Clinical and laboratory findings". J. Infect. Dis. 145 (4): 441–8. PMID 7069224.


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