Toxic shock syndrome history and symptoms
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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
STSS may occur with infection at any site, but most often occurs in association with infection of a cutaneous lesion. Many invasive streptococcal infections have no known portal of entry.2659990. 3890787. Signs of toxicity and a rapidly progressive clinical course are characteristic and the case fatality rate may exceed 50%. NF may follow local blunt or penetrating trauma to the skin. It occurs most commonly in the lower limb, followed by the upper limb.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.10323689. 17697787.
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 [3,4]. 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.17577829. 1457666. 2026891. 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 . wiki.
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 15516429. 9155682.
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 17083018.
- {| class="wikitable sortable" ! | | | |- !diffuse edema |Rapid development of generalized and massive tissue | | |- !effusion |Pleural, pericardial, and peritoneal |
- due to capillary leak from toxin-mediated changes in the vascular endothelium
- hypoalbuminemia | |- ! | | | |} edema [8,19].
- effusions are common [2,8]. These develop [2].
- 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 [2-4,8,40]. In general, an increased percentage of mature and immature neutrophils and increased absolute numbers of lymphocytes and monocytes are observed. The presence of leukemoid reaction is highly predictive of mortality [8]. In one study, patients who died had average WBC count of >75,000 cells/mm3; survivors had average WBC count of 18,000 cells/mm3 [8].
- Hemoconcentration is common; hematocrit levels up to 80 percent have been reported [2,4,5,15,39,40].
- Absence of fever [2,4,8].
- Refractory hypotension and tachycardia
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.