Toxic shock syndrome history and symptoms
|
Toxic shock syndrome Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Toxic shock syndrome history and symptoms On the Web |
|
American Roentgen Ray Society Images of Toxic shock syndrome history and symptoms |
|
Risk calculators and risk factors for Toxic shock syndrome history and symptoms |
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 nonmenstrual illness.[1]
clinical manifestations of 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]
This rash can be subtle and fleeting. In postoperative TSS, the erythema may be more intense around the involved surgical wound site. Mucosal involvement includes conjunctival-scleral hemorrhage and hyperemia of the vaginal and oropharyngeal mucosa (picture 3) [56]. In more severe cases, superficial ulcerations occur on the mucous membranes, and petechiae, vesicles, and bullae develop. Patients also have nonpitting edema due to increases in interstitial fluid. Late-onset skin manifestations include a pruritic maculopapular rash that may occur one to two weeks after the disease onset and desquamation of the palms and soles that characteristically begins one to three weeks after illness develops (picture 4). Since desquamation occurs late, this is not be used for acute diagnosis of TSS. In some cases, TSS may not be considered in the differential diagnosis until later when desquamation is observed; this is particularly true in nonmenstrual disease [57]. Some patients also experience loss of hair and nails one to two months following onset of illness, with regrowth by six months.
Multiorgan system involvement — TSS can involve all organ systems. Many patients report diffuse myalgias and weakness as presenting symptoms, which are usually accompanied by an increase in serum concentrations of creatine phosphokinase (CPK). Gastrointestinal symptoms are also common, particularly profuse diarrhea. Both prerenal and intrinsic renal failure can occur and are often accompanied by other metabolic abnormalities including hyponatremia, hypoalbuminemia, hypocalcemia, and hypophosphatemia [58].
Encephalopathy, manifested by disorientation, confusion, or seizure activity, can be a presenting symptom of TSS [59] and is probably due to cerebral edema [60]. Other central nervous system (CNS) findings have been reported in some patients. Persistent neuropsychological sequelae can develop such as headaches, memory loss, and poor concentration [61]. Other findings include pulmonary edema and pleural effusions, depression of myocardial function [62], hepatic dysfunction, and hematologic abnormalities, such as anemia and thrombocytopenia.
Menstrual versus nonmenstrual cases — The clinical presentations of menstrual and nonmenstrual TSS are similar. In one small study, nonmenstrual TSS was associated with earlier onset of rash and fever, more pronounced renal and CNS complications, and less musculoskeletal involvement [63]. Surgical wound sites and cutaneous infections that harbor toxin-producing S. aureus are frequently benign, appearing without obvious purulence [29,63].
In contrast to STSS, Staphylococcus aureus is only rarely (5%) recovered from blood cultures.
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
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".