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* [[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. | * [[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.<ref name="urlTintinallis Emergency Medicine: A Comprehensive Study Guide, 8th edition - Judith Tintinalli, J. Stapczynski, O. John Ma, David M. Cline, Garth Meckler - Google Books">{{cite web |url=https://books.google.com/books?id=FNKLCgAAQBAJ&q=It%27s+main+characteristics+involve+diffuse,+red,+macular+rash+resembling+sunburn+that+can+also+involve+the+palms+and+soles.&dq=It%27s+main+characteristics+involve+diffuse,+red,+macular+rash+resembling+sunburn+that+can+also+involve+the+palms+and+soles.&hl=en&sa=X&ved=0ahUKEwjlq-LXoODTAhVF7CYKHQ3aDkoQ6AEIJzAA |title=Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 8th edition - Judith Tintinalli, J. Stapczynski, O. John Ma, David M. Cline, Garth Meckler - Google Books |format= |work= |accessdate=}}</ref> | * [[Skin Changes|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.<ref name="urlTintinallis Emergency Medicine: A Comprehensive Study Guide, 8th edition - Judith Tintinalli, J. Stapczynski, O. John Ma, David M. Cline, Garth Meckler - Google Books">{{cite web |url=https://books.google.com/books?id=FNKLCgAAQBAJ&q=It%27s+main+characteristics+involve+diffuse,+red,+macular+rash+resembling+sunburn+that+can+also+involve+the+palms+and+soles.&dq=It%27s+main+characteristics+involve+diffuse,+red,+macular+rash+resembling+sunburn+that+can+also+involve+the+palms+and+soles.&hl=en&sa=X&ved=0ahUKEwjlq-LXoODTAhVF7CYKHQ3aDkoQ6AEIJzAA |title=Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 8th edition - Judith Tintinalli, J. Stapczynski, O. John Ma, David M. Cline, Garth Meckler - Google Books |format= |work= |accessdate=}}</ref> 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. | ||
Late-onset skin | |||
Multiorgan system involvement | * 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 and are often accompanied by other metabolic abnormalities including hyponatremia, hypoalbuminemia, hypocalcemia, and hypophosphatemia. | ||
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. | * 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]. | * 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. | In contrast to STSS, Staphylococcus aureus is only rarely (5%) recovered from blood cultures. | ||
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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 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] 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 and are often accompanied by other metabolic abnormalities including hyponatremia, hypoalbuminemia, hypocalcemia, and hypophosphatemia.
- 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".