Toxic shock syndrome history and symptoms: Difference between revisions
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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 {| class="wikitable | * diagnostic clues based on signs and symptoms of disease | ||
{| class="wikitable" | |||
! | |||
!diagnostic clues in C. sordellii | |||
!causes | |||
! | |||
|- | |||
!generalized symptoms | |||
|[[hypotension]] | |||
[[tachycardia]] | |||
absence of fever | |||
|generalized toxic-mediated changes | |||
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|- | |||
!diffuse [[edema]] | |||
|generalized | |||
|rapid development of generalized and massive tissue edema due to toxin-mediated changes and increase in [[vascular]] [[permeability]] | |||
| | |||
|- | |||
!effusion | |||
|[[Pleural effusion|pleural]] | |||
[[Pericardial effusion|pericardial]] | |||
[[Peritoneum|peritonea]]<nowiki/>l | |||
|due to [[capillary]] leak from toxin-mediated changes in the vascular endothelium and ahypoalbuminemia | |||
| | |||
|- | |||
!laboratory changes | |||
|[[leukocytosis]] [[hemoconcentration]] | |||
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* 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 | |||
|} | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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
Staphylococcal TSS
Staphylococcal TSS can be devided into 2 major categories based on the disease cause: menstrual and non-menstrual illness.[1] Although these 2 types are pretty much difference 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:
- Hypotension: It usually happens in a rapid onset, with a systolic blood pressure of ≤90 mmHg for adults or less than fifth percentile by age for children <16 years of age. This hypotension can be unresponsive to fluid infusion even large amounts of isotonic intravenous fluids and can persist for several days.
- Skin manifestations: these manifestations are usually due to hypersensitivity reactions. they can be very variable. The initial erythroderma can involves both mucous membranes and skin. It's main characteristics involve diffuse, red, macular rash resembling sunburn that can also involve the palms and soles.[2] It can be fleeting and subtle. Conjunctival-scleral hemorrhage and hyperemia of the vaginal and oropharyngeal mucosa can be found while mucosal involvement is associated with skin manifestations. Superficial ulcerations can also occur on the mucous membranes especially in more advanced forms of the disease. it can lead to petechiae, vesicles, and bullae development. Non-pitting edema can develop as a result of increases in interstitial fluid. Late-onset skin findings include pruritic maculopapular rash and palm/soles desquamation which particularly begins 1-3 weeks after disease beginning. as a matter of late onset characteristic of dequamation, it can not be used as a good diagnostic feature. Hair and nail loss may also occur in some cases one to two months after the onset of disease, with regrowth by six months.
- Multiorgan system involvement: All body organ systems can be involved during disease, which can lead to specific organ related symptoms. Many patients complaint of generalized myalgias and weakness as their primary chief complaints. In these patients, usually elevated levels of creatine phosphokinase (CPK) concentration can be detected. Gastrointestinal complaints are also common, particularly watery diarrhea. Both prerenal and intrinsic renal failure can occur. Renal failure can lead to metabolic abnormalities such as hypocalcemia, hyponatremia, hypoalbuminemia, and hypophosphatemia.[3]
- Encephalopathy: Cerebral edema as a complication of TSS can lead to encephalopathy which is fatal and manifested by disorientation, confusion, or seizure activity[4],[5]. Other central nervous system (CNS) findings may be present rarely in patients for instance persistent neuropsychological sequels can develop such as headaches, memory loss, and poor concentration [6]. Other symptoms that can be found in patients with encephalopathy due to TSS include pleural effusions and pulmonary edema, cardiac dysfunction, hepatic failure, and hematologic abnormalities, especially anemia and thrombocytopenia.[7]
The isolation of S. aureus is not required for the diagnosis of staphylococcal TSS, but isolation of GAS is absolutely necessary for the diagnosis of group A streptococcal causes of TSS
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 disease should be diagnosed based on the clinical findings primarily. In most cases fatality rate may exceed 50%. 9236481.
Patients with 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[9],[10].
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.
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 sordellii
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[11],[12], [13]. 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[14],[15].
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 [16].
- diagnostic clues based on signs and symptoms of disease
| diagnostic clues in C. sordellii | causes | ||
|---|---|---|---|
| generalized symptoms | hypotension
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 | due to capillary leak from toxin-mediated changes in the vascular endothelium and ahypoalbuminemia | |
| laboratory changes | leukocytosis hemoconcentration |
|
References
- ↑ 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.
- ↑ "Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 8th edition - Judith Tintinalli, J. Stapczynski, O. John Ma, David M. Cline, Garth Meckler - Google Books".
- ↑ 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.
- ↑ Barrett JA, Graham DR (1986). "Toxic shock syndrome presenting as encephalopathy". J. Infect. 12 aissue=3: 276–8. PMID 3722844.
- ↑ Smith DB, Gulinson J (1988). "Fatal cerebral edema complicating toxic shock syndrome". Neurosurgery. 22 (3): 598–9. PMID 3362331.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 9.0 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.
- ↑ 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.
- ↑ 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.
- ↑ Spera RV, Kaplan MH, Allen SL (1992). "Clostridium sordellii bacteremia: case report and review". Clin. Infect. Dis. 15 (6): 950–4. PMID 1457666.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.