Toxic shock syndrome history and symptoms: Difference between revisions

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=== [[Streptococcus|Streptococcal]] [[Toxic shock syndrome|TSS]] ===
=== [[Streptococcus|Streptococcal]] [[Toxic shock syndrome|TSS]] ===
[[Streptococcus|Streptococcal]] [[Toxic shock syndrome|TSS]] may occur with infection at any site, but most often occurs in association with infection of a [[Skin lesions|cutaneous lesion]], specially with local [[blunt trauma]] injury and [[Penetrating wound|penetrating tissue]] trauma that can lead to [[Necrotizing Fasciitis|necrotizing fasciitis]] (NF). [[Necrotising fasciitis|NF]] mostly occurs in the [[lower limb]], followed by the [[upper limb]]. Although the invasive nature of disease is well known, most of the time origin of entry and source of infection can not be identified that lead to a significant problem .<ref name="pmid2659990">{{cite journal |vauthors=Stevens DL, Tanner MH, Winship J, Swarts R, Ries KM, Schlievert PM, Kaplan E |title=Severe group A streptococcal infections associated with a toxic shock-like syndrome and scarlet fever toxin A |journal=N. Engl. J. Med. |volume=321 |issue=1 |pages=1–7 |year=1989 |pmid=2659990 |doi=10.1056/NEJM198907063210101 |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> . The disease should be diagnosed based on the clinical findings primarily. In most cases fatality rate may exceed 50%<ref name="pmid9236481">{{cite journal |vauthors=Kaul R, McGeer A, Low DE, Green K, Schwartz B |title=Population-based surveillance for group A streptococcal necrotizing fasciitis: Clinical features, prognostic indicators, and microbiologic analysis of seventy-seven cases. Ontario Group A Streptococcal Study |journal=Am. J. Med. |volume=103 |issue=1 |pages=18–24 |year=1997 |pmid=9236481 |doi= |url=}}</ref>.  
[[Streptococcus|Streptococcal]] [[Toxic shock syndrome|TSS]] may occur with infection at any site, but most often occurs in association with infection of a [[Skin lesions|cutaneous lesion]], specially with local [[blunt trauma]] injury and [[Penetrating wound|penetrating tissue]] trauma that can lead to [[Necrotizing Fasciitis|necrotizing fasciitis]] (NF). [[Necrotising fasciitis|NF]] mostly occurs in the [[lower limb]], followed by the [[upper limb]]. Although the invasive nature of disease is well known, most of the time origin of entry and source of infection can not be identified that lead to a significant problem<ref name="pmid2659990">{{cite journal |vauthors=Stevens DL, Tanner MH, Winship J, Swarts R, Ries KM, Schlievert PM, Kaplan E |title=Severe group A streptococcal infections associated with a toxic shock-like syndrome and scarlet fever toxin A |journal=N. Engl. J. Med. |volume=321 |issue=1 |pages=1–7 |year=1989 |pmid=2659990 |doi=10.1056/NEJM198907063210101 |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>. The symptoms and signs of [[Toxic shock syndrome|TSS]] develop rapidly, usually in otherwise healthy individuals. The disease should be diagnosed based on the clinical findings primarily. In most cases of [[Necrotizing fasciitis|NF]]-related [[Toxic shock syndrome|TSS]] fatality rate may exceed 50%<ref name="pmid9236481">{{cite journal |vauthors=Kaul R, McGeer A, Low DE, Green K, Schwartz B |title=Population-based surveillance for group A streptococcal necrotizing fasciitis: Clinical features, prognostic indicators, and microbiologic analysis of seventy-seven cases. Ontario Group A Streptococcal Study |journal=Am. J. Med. |volume=103 |issue=1 |pages=18–24 |year=1997 |pmid=9236481 |doi= |url=}}</ref>.  


Patients with [[Streptococcal infections|GAS]]-associated NF may have only subtle signs of severity at initial presentation and can therefore be difficult to differentiate from a simple [[cellulitis]]. Severe pain and tenderness that is disproportionate to the physical findings are the clinical hallmark that differentiates NF from more superficial infection. Tense edema and the development of bullae that seem bluish as the disease progresses are also useful signs, but are often late signs and indicate significant tissue necrosis. Several studies have reported that patients with NF often have a history of recent blunt trauma<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>,<ref name="pmid17697787">{{cite journal |vauthors=Nuwayhid ZB, Aronoff DM, Mulla ZD |title=Blunt trauma as a risk factor for group A streptococcal necrotizing fasciitis |journal=Ann Epidemiol |volume=17 |issue=11 |pages=878–81 |year=2007 |pmid=17697787 |pmc=4029051 |doi=10.1016/j.annepidem.2007.05.011 |url=}}</ref>.  
Patients with [[Streptococcal infections|GAS]]-associated [[Necrotizing fasciitis|NF]] may present with non-specific signs of disease when they primarily administered. This can make it difficult to differentiate their disease from a simple [[cellulitis]]. [[Necrotizing fasciitis|NF]] can cause severe pain and local [[tenderness]] which is disproportionate to other physical findings; this can be used as a clinical hallmark for differentiating [[Necrotizing fasciitis|NF]] from other superficial infections. Late signs that present themselves with disease progression include [[Edema|tense edema]] and bullae development that seem bluish. Edema and bluish bullae indicate significant [[Necrosis|tissue necrosis]] and severity of the disease.<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>,<ref name="pmid17697787">{{cite journal |vauthors=Nuwayhid ZB, Aronoff DM, Mulla ZD |title=Blunt trauma as a risk factor for group A streptococcal necrotizing fasciitis |journal=Ann Epidemiol |volume=17 |issue=11 |pages=878–81 |year=2007 |pmid=17697787 |pmc=4029051 |doi=10.1016/j.annepidem.2007.05.011 |url=}}</ref>.  


who reported that skeletal muscle injury resulted in increased cellular vimentin expression, which enhanced binding of GAS to skeletal muscle cells. The case fatality rate of GAS-associated NF is 30% to 50%, and most deaths occur in the first 48 hours after presentation, reflecting the rapidly progressive nature of the disease and between 30% and 50% of patients with GAS-associated NF develop STSS.
[[Toxic shock syndrome|Toxic shock syndrom]]<nowiki/>e signs and symptoms are exactly like [[Staphylococcal]] [[Toxic shock syndrome|TSS]] and include [[fever]], [[hypotension]], and skin manifestations (as mentioned before). Also non-specific signs like [[chills]], [[malaise]], [[Sore Throat|sore throat]], [[fatigue]], [[Myalgia|myalgias]], [[headache]], [[abdominal pain]], [[diarrhea]], [[vomiting]] and [[Orthostatic hypotension|orthostatic]] [[hypotension]] with [[dizziness]] or [[syncope]] may be seen.
 
Clinical manifestations of toxic shock syndrome include fever, hypotension, and skin manifestations. Additional symptoms and signs include chills, malaise, headache, sore throat, myalgias, fatigue, vomiting, diarrhea, abdominal pain, and orthostatic dizziness or syncope.
 
The symptoms and signs of TSS develop rapidly, usually in otherwise healthy individuals. The median interval between the onset of menstruation and TSS in menstrual cases is two to three days


=== [[Clostridium|Clostridium sordellii]] [[Toxic shock syndrome|TSS]] ===
=== [[Clostridium|Clostridium sordellii]] [[Toxic shock syndrome|TSS]] ===
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Disease primary symptoms include nonspecific symptoms that may be misdiagnosed with [[viral infections]] like flu and may include [[Nausea and vomiting|nausea]], [[Nausea and vomiting|vomiting]], [[lethargy]], [[influenza-like symptoms]], and [[abdominal tenderness]]<ref name="pmid15516429">{{cite journal |vauthors=Wiebe E, Guilbert E, Jacot F, Shannon C, Winikoff B |title=A fatal case of Clostridium sordellii septic shock syndrome associated with medical abortion |journal=Obstet Gynecol |volume=104 |issue=5 Pt 2 |pages=1142–4 |year=2004 |pmid=15516429 |doi=10.1097/01.AOG.0000142738.68439.9e |url=}}</ref>,<ref name="pmid9155682">{{cite journal |vauthors=Bitti A, Mastrantonio P, Spigaglia P, Urru G, Spano AI, Moretti G, Cherchi GB |title=A fatal postpartum Clostridium sordellii associated toxic shock syndrome |journal=J. Clin. Pathol. |volume=50 |issue=3 |pages=259–60 |year=1997 |pmid=9155682 |pmc=499826 |doi= |url=}}</ref>.  
Disease primary symptoms include nonspecific symptoms that may be misdiagnosed with [[viral infections]] like flu and may include [[Nausea and vomiting|nausea]], [[Nausea and vomiting|vomiting]], [[lethargy]], [[influenza-like symptoms]], and [[abdominal tenderness]]<ref name="pmid15516429">{{cite journal |vauthors=Wiebe E, Guilbert E, Jacot F, Shannon C, Winikoff B |title=A fatal case of Clostridium sordellii septic shock syndrome associated with medical abortion |journal=Obstet Gynecol |volume=104 |issue=5 Pt 2 |pages=1142–4 |year=2004 |pmid=15516429 |doi=10.1097/01.AOG.0000142738.68439.9e |url=}}</ref>,<ref name="pmid9155682">{{cite journal |vauthors=Bitti A, Mastrantonio P, Spigaglia P, Urru G, Spano AI, Moretti G, Cherchi GB |title=A fatal postpartum Clostridium sordellii associated toxic shock syndrome |journal=J. Clin. Pathol. |volume=50 |issue=3 |pages=259–60 |year=1997 |pmid=9155682 |pmc=499826 |doi= |url=}}</ref>.  


Disease progression to the [[shock]] and severe symptoms occurs within hours. The [[nature]] of disease which starts with nonspecific symptoms and its rapid progression toward shock make in really hard to diagnose it in early stages; that may be the reason of disease's high [[mortality]] <ref name="pmid17083018">{{cite journal |vauthors=Aldape MJ, Bryant AE, Stevens DL |title=Clostridium sordellii infection: epidemiology, clinical findings, and current perspectives on diagnosis and treatment |journal=Clin. Infect. Dis. |volume=43 |issue=11 |pages=1436–46 |year=2006 |pmid=17083018 |doi=10.1086/508866 |url=}}</ref>.  
Disease progression to the [[shock]] and severe symptoms occurs within hours. The [[nature]] of disease which starts with nonspecific symptoms and its rapid progression toward shock make in really hard to diagnose it in early stages; that may be the reason of disease's high [[mortality]] <ref name="pmid17083018">{{cite journal |vauthors=Aldape MJ, Bryant AE, Stevens DL |title=Clostridium sordellii infection: epidemiology, clinical findings, and current perspectives on diagnosis and treatment |journal=Clin. Infect. Dis. |volume=43 |issue=11 |pages=1436–46 |year=2006 |pmid=17083018 |doi=10.1086/508866 |url=}}</ref>.
 
* diagnostic clues based on signs and symptoms of disease  
* diagnostic clues based on signs and symptoms of disease  
{| class="wikitable"
{| class="wikitable"
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* [[Hematocrit]] levels up to 80 percent have been reported
* [[Hematocrit]] levels up to 80 percent have been reported
|}
|}
* TSS different causes and their symptoms
{| class="wikitable"
{| class="wikitable"
!
!
!type
!type
!main history
!symptoms
!symptoms
|-
|-
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|menstural
|menstural
non-menstural
non-menstural
|
|[[hypotension]]
|hypotension


[[Skin Changes|Skin manifestations]]: [[erythroderma]]
[[Skin Changes|Skin manifestations]]: [[erythroderma]]
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|-
|-
|[[Streptococcus|Streptococcal]] [[Toxic shock syndrome|TSS]]
|[[Streptococcus|Streptococcal]] [[Toxic shock syndrome|TSS]]
|simple GAS-related TSS
|[[Necrotizing Fasciitis|GAS-related NF]]
Necrotizing Fascitis related
|skin and [[Skin lesions|cutaneous lesion]]<nowiki/>s:
|
* [[Necrotizing Fasciitis|necrotizing fasciitis]] (NF)
|
* [[Edema|tense edema]] and bluish bullae with disease progression
General Shock Signs: [[fever]], [[hypotension]], [[chills]], [[malaise]], [[Sore Throat|sore throat]], [[fatigue]], [[Myalgia|myalgias]], [[headache]], [[abdominal pain]], [[diarrhea]], [[vomiting]] and [[Orthostatic hypotension|orthostatic]] [[hypotension]] with [[dizziness]] or [[syncope]]
|-
|-
|[[Clostridium|Clostridium sordellii]] [[Toxic shock syndrome|TSS]]
|[[Clostridium|Clostridium sordellii]] [[Toxic shock syndrome|TSS]]
| -
| -
|
|nonspecific primary symptoms that may be misdiagnosed with [[viral infections]] like [[flu]] ([[Nausea and vomiting|nausea]], [[Nausea and vomiting|vomiting]], [[lethargy]], [[influenza-like symptoms]], and [[abdominal tenderness]])
|
 
[[skin infection]], [[bacteremia]], and organ specific infections such as [[pneumonia]], [[empyema]], [[endocarditis]], [[septic arthritis]], and [[surgical site infection]]
|}
|}



Revision as of 17:08, 10 May 2017

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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

Toxic shock syndrome (TSS) is characterized by sudden onset of fever, chills, vomiting, diarrhea, muscle aches and rash. It can rapidly progress to severe and intractable hypotension and multisystem dysfunction. Desquamation, particularly on the palms and soles can occur 1-2 weeks after onset of the illness.

History and symptoms of patients vary based on the organism responsible for the shock.

History and Symptoms

Staphylococcal TSS

Staphylococcal TSS can be divided into 2 major categories based on the disease cause: menstrual and non-menstrual illness.[1] Although these 2 types are different from each other in the terms of cause and pathogenesis, their clinical manifestations are pretty much the same.

Clinical manifestations of Staphylococcal TSS include a variety of shock symptoms, and hypersensitivity that is associated with the disease:

Streptococcal TSS

Streptococcal TSS may occur with infection at any site, but most often occurs in association with infection of a cutaneous lesion, specially with local blunt trauma injury and penetrating tissue trauma that can lead to necrotizing fasciitis (NF). NF mostly occurs in the lower limb, followed by the upper limb. Although the invasive nature of disease is well known, most of the time origin of entry and source of infection can not be identified that lead to a significant problem[8],[9]. The symptoms and signs of TSS develop rapidly, usually in otherwise healthy individuals. The disease should be diagnosed based on the clinical findings primarily. In most cases of NF-related TSS fatality rate may exceed 50%[10].

Patients with GAS-associated NF may present with non-specific signs of disease when they primarily administered. This can make it difficult to differentiate their disease from a simple cellulitis. NF can cause severe pain and local tenderness which is disproportionate to other physical findings; this can be used as a clinical hallmark for differentiating NF from other superficial infections. Late signs that present themselves with disease progression include tense edema and bullae development that seem bluish. Edema and bluish bullae indicate significant tissue necrosis and severity of the disease.[9],[11].

Toxic shock syndrome signs and symptoms are exactly like Staphylococcal TSS and include fever, hypotension, and skin manifestations (as mentioned before). Also non-specific signs like chills, malaise, sore throat, fatigue, myalgias, headache, abdominal pain, diarrhea, vomiting and orthostatic hypotension with dizziness or syncope may be seen.

Clostridium sordellii TSS

This is a rare cause of TSS but maybe the most dangerous cause with a rapid onset. There are a variety of symptoms include skin infection, bacteremia, and organ specific infections such as pneumonia, empyema, endocarditis, septic arthritis, and surgical site infection[12],[13], [14]. C. sordellii toxic shock is characterized by rapid occurrence of severe disease symptoms with shock; in these cases TSS mostly occurs in previously healthy individuals. 2801850. The clinical presentation generally consists of specific infection related manifestations including profound leukocytosis, hemoconcentration, edema, effusions,and followed by multiorgan failure and shock.

Disease primary symptoms include nonspecific symptoms that may be misdiagnosed with viral infections like flu and may include nausea, vomiting, lethargy, influenza-like symptoms, and abdominal tenderness[15],[16].

Disease progression to the shock and severe symptoms occurs within hours. The nature of disease which starts with nonspecific symptoms and its rapid progression toward shock make in really hard to diagnose it in early stages; that may be the reason of disease's high mortality [17].

  • diagnostic clues based on signs and symptoms of disease
diagnostic clues in C. sordellii causes
generalized symptoms hypotension

tachycardia

absence of fever

generalized toxic-mediated changes
diffuse edema generalized rapid development of generalized and massive tissue edema due to toxin-mediated changes and increase in vascular permeability
effusion pleural

pericardial

peritoneal

due to capillary leak from toxin-mediated changes in the vascular endothelium and ahypoalbuminemia
laboratory changes leukocytosis hemoconcentration
  • TSS different causes and their symptoms
type symptoms
Staphylococcal TSS menstural

non-menstural

hypotension

Skin manifestations: erythroderma

Conjunctival-scleral hemorrhage and hyperemia of the vaginal and oropharyngeal mucosa

Streptococcal TSS GAS-related NF skin and cutaneous lesions:

General Shock Signs: fever, hypotension, chills, malaise, sore throat, fatigue, myalgias, headache, abdominal pain, diarrhea, vomiting and orthostatic hypotension with dizziness or syncope

Clostridium sordellii TSS - nonspecific primary symptoms that may be misdiagnosed with viral infections like flu (nausea, vomiting, lethargy, influenza-like symptoms, and abdominal tenderness)

skin infection, bacteremia, and organ specific infections such as pneumonia, empyema, endocarditis, septic arthritis, and surgical site infection

References

  1. Wharton M, Chorba TL, Vogt RL, Morse DL, Buehler JW (1990). "Case definitions for public health surveillance". MMWR Recomm Rep. 39 (RR-13): 1–43. PMID 2122225.
  2. "Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 8th edition - Judith Tintinalli, J. Stapczynski, O. John Ma, David M. Cline, Garth Meckler - Google Books".
  3. Chesney RW, Chesney PJ, Davis JP, Segar WE (1981). "Renal manifestations of the staphylococcal toxic-shock syndrome". Am. J. Med. 71 (4): 583–8. PMID 7282746.
  4. Barrett JA, Graham DR (1986). "Toxic shock syndrome presenting as encephalopathy". J. Infect. 12 aissue=3: 276–8. PMID 3722844.
  5. Smith DB, Gulinson J (1988). "Fatal cerebral edema complicating toxic shock syndrome". Neurosurgery. 22 (3): 598–9. PMID 3362331.
  6. Rosene KA, Copass MK, Kastner LS, Nolan CM, Eschenbach DA (1982). "Persistent neuropsychological sequelae of toxic shock syndrome". Ann. Intern. Med. 96 (6 Pt 2): 865–70. PMID 7091958.
  7. Olson RD, Stevens DL, Melish ME (1989). "Direct effects of purified staphylococcal toxic shock syndrome toxin 1 on myocardial function of isolated rabbit atria". Rev. Infect. Dis. 11 Suppl 1: S313–5. PMID 2928649.
  8. Stevens DL, Tanner MH, Winship J, Swarts R, Ries KM, Schlievert PM, Kaplan E (1989). "Severe group A streptococcal infections associated with a toxic shock-like syndrome and scarlet fever toxin A". N. Engl. J. Med. 321 (1): 1–7. doi:10.1056/NEJM198907063210101. PMID 2659990.
  9. 9.0 9.1 Adams EM, Gudmundsson S, Yocum DE, Haselby RC, Craig WA, Sundstrom WR (1985). "Streptococcal myositis". Arch. Intern. Med. 145 (6): 1020–3. PMID 3890787.
  10. Kaul R, McGeer A, Low DE, Green K, Schwartz B (1997). "Population-based surveillance for group A streptococcal necrotizing fasciitis: Clinical features, prognostic indicators, and microbiologic analysis of seventy-seven cases. Ontario Group A Streptococcal Study". Am. J. Med. 103 (1): 18–24. PMID 9236481.
  11. Nuwayhid ZB, Aronoff DM, Mulla ZD (2007). "Blunt trauma as a risk factor for group A streptococcal necrotizing fasciitis". Ann Epidemiol. 17 (11): 878–81. doi:10.1016/j.annepidem.2007.05.011. PMC 4029051. PMID 17697787.
  12. Foroulis CN, Gerogianni I, Kouritas VK, Karestsi E, Klapsa D, Gourgoulianis K, Petinaki E (2007). "Direct detection of Clostridium sordellii in pleural fluid of a patient with pneumonic empyema by a broad-range 16S rRNA PCR". Scand. J. Infect. Dis. 39 (6–7): 617–9. doi:10.1080/00365540601105798. PMID 17577829.
  13. Spera RV, Kaplan MH, Allen SL (1992). "Clostridium sordellii bacteremia: case report and review". Clin. Infect. Dis. 15 (6): 950–4. PMID 1457666.
  14. Buchman AL, Ponsillo M, Nagami PH (1991). "Empyema caused by Clostridium sordellii, a rare form of pleuropulmonary disease". J. Infect. 22 (2): 171–4. PMID 2026891.
  15. Wiebe E, Guilbert E, Jacot F, Shannon C, Winikoff B (2004). "A fatal case of Clostridium sordellii septic shock syndrome associated with medical abortion". Obstet Gynecol. 104 (5 Pt 2): 1142–4. doi:10.1097/01.AOG.0000142738.68439.9e. PMID 15516429.
  16. Bitti A, Mastrantonio P, Spigaglia P, Urru G, Spano AI, Moretti G, Cherchi GB (1997). "A fatal postpartum Clostridium sordellii associated toxic shock syndrome". J. Clin. Pathol. 50 (3): 259–60. PMC 499826. PMID 9155682.
  17. Aldape MJ, Bryant AE, Stevens DL (2006). "Clostridium sordellii infection: epidemiology, clinical findings, and current perspectives on diagnosis and treatment". Clin. Infect. Dis. 43 (11): 1436–46. doi:10.1086/508866. PMID 17083018.


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