Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Toxic Shock Syndrome Clinical Presentation

  • Author: Ramesh Venkataraman, MBBS; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM  more...
 
Updated: Apr 16, 2015
 

History

Although the clinical manifestations of TSS can be diverse, the possibility of toxic shock should be considered in any individual who presents with sudden onset of fever, rash, hypotension, renal or respiratory failure, and changes in mental status.[12]

STSS most commonly occurs in women, usually those who are using tampons, TSS develops within 5 days after the onset of menstruation. The other clinical settings where STSS has been reported include the following:

  • Surgical wound infections
  • Postpartum infections
  • Focal cutaneous and subcutaneous lesions
  • Deep abscesses
  • Empyema
  • Peritonsillar abscess
  • Sinusitis
  • Osteomyelitis

Soft tissue infections from GAS include necrotizing fasciitis, myositis, or cellulitis. The most common initial symptom of patients with streptococcal TSS is diffuse or localized pain that is abrupt and severe. Other manifestations include the following:

  • Influenzalike syndrome
  • Fever
  • Confusion
  • Signs of soft tissue infection

Approximately 20% of patients with STSS have an influenzalike syndrome characterized by the following:

  • Fever
  • Chills
  • Myalgia
  • Nausea
  • Vomiting
  • Diarrhea

The other reported types of infection are pneumonia, unidentified bacteremia, surgical site infection, septic arthritis, thrombophlebitis, meningitis, pelvic infection, and endophthalmitis.

Common presenting symptoms and frequency of STTS are as follows[10] :

  • Pain (44-85%)
  • Vomiting (25-26%)
  • Nausea (20%)
  • Diarrhea (14-30%)
  • Influenzalike symptoms (14-20%)
  • Headache (10%)
  • Dyspnea (8%)

The following risk factors have been reported to be associated with STSS:

  • Patients with HIV, diabetes, cancer, ethanol abuse, and other chronic diseases
  • Patients with a recent history of varicella infection (chicken pox)
  • Patients who used nonsteroidal anti-inflammatory drugs (NSAIDs)
Next

Physical

Fever is the most common presenting sign, although patients in shock may present with hypothermia. Shock is apparent at the time of hospitalization or within 4-8 hours for all patients. Patients become severely hypotensive and do not respond to intravenous fluid administration. Renal dysfunction progresses or persists in all patients, precedes shock in many patients, and is apparent early. Acute respiratory distress syndrome occurs in 55% of patients and requires mechanical ventilation.

A thorough search for possible sites of streptococcal and staphylococcal infection is a must. The surgical wounds should be carefully examined even if no signs of infection are apparent. Vaginal examination and removal of tampon or other foreign body should be done diligently.

Confusion is present in 55% of patients, and coma or agitation may occur. Alteration in mental status disproportionate to the degree of hypotension can occur with or without seizures. Persistent neuropsychiatric sequelae manifested by memory loss, and poor concentration have been reported.

Nearly 50% of patients are normotensive on presentation but become hypotensive within 4 hours.

Approximately 80% of patients have clinical signs of soft tissue infection (eg, localized swelling, erythema), which usually progresses to necrotizing fasciitis or myositis.

Approximately 20% of patients have various clinical presentations, including the following:

  • Endophthalmitis
  • Myositis
  • Perihepatitis
  • Peritonitis
  • Myocarditis

Diffuse scarlatinalike erythema occurs in 10% of patients. Skin manifestations of streptococcal infection include the following (also see images below):

  • Bullae
  • Scarlet fever–like rash
  • Petechiae or maculopapular rashes
  • Desquamation
    Progression of soft tissue swelling to vesicle or Progression of soft tissue swelling to vesicle or bullous formation is an ominous sign and suggests streptococcal shock syndrome. Courtesy of S. Manocha.
    A 46-year-old man presented with nonnecrotizing ce A 46-year-old man presented with nonnecrotizing cellulitis and streptococcal toxic shock syndrome. This patient also had streptococcal pharyngitis. Courtesy of Rob Green, MD.
    A 46-year-old man presented with nonnecrotizing ce A 46-year-old man presented with nonnecrotizing cellulitis and streptococcal toxic shock syndrome. The patient had diffuse erythroderma, a characteristic feature of the syndrome. Courtesy of Rob Green, MD.

Mucosal involvement includes conjunctival/scleral hemorrhage and hyperemia of the vaginal and oropharyngeal mucosa. Petechial hemorrhages (“strawberry tongue”) and ulcerations of mucosal membranes can occur in severe cases.The possibility of STSS should be entertained in any patient who presents with a sudden onset of fever, rash, hypotension, and systemic evidence of toxicity. Five categories of clinical features are needed for the diagnosis (Centers for Disease Control and Prevention, 1990).

The five categories are (1) fever; (2) rash (diffuse macular erythroderma); (3) desquamation (1-2 wk after illness onset, involving palms and soles); (4) hypotension (systolic blood pressure < 90 mm Hg, orthostatic drop in diastolic blood pressure < 15 mm Hg, orthostatic syncope, and dizziness); and (5) evidence of multisystem involvement in 3 or more of the following systems:

  • Gastrointestinal - Vomiting or diarrhea at the onset of illness
  • Muscular - Severe myalgia or creatine kinase (CK) elevation (>2 times normal upper limit)
  • Mucous membrane - Vaginal, oropharyngeal, or conjunctival erythema
  • Renal - BUN or serum creatinine greater than 2 times the upper limit of normal
  • Hepatic - Bilirubin or transaminases greater than 2 times the upper limit of normal
  • Hematological - Platelets less than 100,000
  • Central nervous system - Disorientation or alteration in consciousness without focal signs

Common presenting symptoms and frequency of STTS are as follows[6] :

  • Tachycardia (80%)
  • Fever (70-81%)
  • Hypotension (44-65%)
  • Confusion (55%)
  • Localized erythema (44-65%)
  • Localized swelling and erythema (30-75%)
  • Scarlatiniform rash (0-4%)

The case definition of streptococcal TSS involves the isolation of GAS, hypotension, and multisystem involvement.[13]

The presence of hypotension (systolic pressure < 90 mm Hg in adults or less than fifth percentile for children) is required, along with either (1) the isolation of GAS (S pyogenes) from a normally sterile site (eg, blood, cerebrospinal fluid, pleural fluid) for a definite case or (2) the isolation of GAS (S pyogenes) from a nonsterile site for a probable case.

Additionally, multiorgan involvement, as evidenced by at least 2 of the following, is required for either definite or probable cases:

  • Renal impairment - Creatinine level more than 177 µmol/L for adults or twice upper normal limit for age or more than twice the baseline level for patients with renal disease
  • Coagulopathy - Platelet count less than 100 X 10 6/L or disseminated intravascular coagulation
  • Liver involvement - Alanine aminotransferase, aspartate aminotransferase, or total bilirubin level more than twice normal limit for age or more than twice baseline in patients with chronic liver disease
  • Pulmonary involvement - Adult respiratory distress syndrome or evidence of diffuse capillary leak syndrome
  • Generalized erythematous macular rash
  • Soft tissue necrosis (necrotizing infection, necrotizing myositis, or gangrene)
Previous
Next

Causes

Acquisition of infection

Risk factors for the development of STSS are tampon use, vaginal colonization with toxin-producing S aureus, and lack of serum antibody to the staphylococcal toxin.[14] STSS also has occurred following use of nasal tampons for procedures of the ears, nose, and throat.

The portal of entry for streptococci is unknown in almost one half of the cases. Procedures such as suction lipectomy, hysterectomy, vaginal delivery, and bone pinning have been identified as the portal of entry in many cases. Most commonly, infection begins at a site of minor local trauma, which may be nonpenetrating. Viral infections, such as varicella and influenza, also have provided a portal of entry.

Previous
 
 
Contributor Information and Disclosures
Author

Ramesh Venkataraman, MBBS Consultant, Critical Care Medicine, Apollo Hospitals, India

Ramesh Venkataraman, MBBS is a member of the following medical societies: American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Medical Association, Society of Critical Care Medicine, Indian Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Sat Sharma, MD, FRCPC Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital

Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, World Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Richard B Brown, MD, FACP Chief, Division of Infectious Diseases, Baystate Medical Center; Professor, Department of Internal Medicine, Tufts University School of Medicine

Richard B Brown, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Chest Physicians, American College of Physicians, American Medical Association, American Society for Microbiology, Infectious Diseases Society of America, Massachusetts Medical Society

Disclosure: Nothing to disclose.

Chief Editor

Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM Professor of Critical Care Medicine, Bioengineering, Cardiovascular Disease, Clinical and Translational Science and Anesthesiology, Vice-Chair of Academic Affairs, Department of Critical Care Medicine, University of Pittsburgh Medical Center, University of Pittsburgh School of Medicine

Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM is a member of the following medical societies: American College of Chest Physicians, Association of University Anesthetists, European Society of Intensive Care Medicine, American College of Critical Care Medicine, American Heart Association, American Thoracic Society, Shock Society, Society of Critical Care Medicine

Disclosure: Received income in an amount equal to or greater than $250 from: Masimo<br/>Received honoraria from LiDCO Ltd for consulting; Received intellectual property rights from iNTELOMED for board membership; Received honoraria from Edwards Lifesciences for consulting; Received honoraria from Masimo, Inc for board membership.

Additional Contributors

Cory Franklin, MD Professor, Department of Medicine, Chicago Medical School at Rosalind Franklin University of Medicine and Science; Director, Division of Critical Care Medicine, Cook County Hospital

Cory Franklin, MD is a member of the following medical societies: New York Academy of Sciences, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous coauthors Godfrey Harding, MD, FRCP(C), and Ken Dolynchuk, MD, PhD, FRCSC, to the development and writing of this article.

References
  1. Todd J, Fishaut M, Kapral F. Toxic-shock syndrome associated with phage-group-I Staphylococci. Lancet. 1978 Nov 25. 2(8100):1116-8. [Medline].

  2. Shands KN, Schmid GP, Dan BB. Toxic-shock syndrome in menstruating women: association with tampon use and Staphylococcus aureus and clinical features in 52 cases. N Engl J Med. 1980 Dec 18. 303(25):1436-42. [Medline].

  3. Davis JP, Chesney PJ, Wand PJ. Toxic-shock syndrome: epidemiologic features, recurrence, risk factors, and prevention. N Engl J Med. 1980 Dec 18. 303(25):1429-35. [Medline].

  4. Ellies E, Vallée F, Mari A, Silva S, Bauriaud R, Fourcade O, et al. [Toxic shock syndrome consecutive to the presence of vaginal tampon for menstruation regressive after early haemodynamic optimization and activated protein C infusion]. Ann Fr Anesth Reanim. 2009 Jan. 28(1):91-5. [Medline].

  5. Cone LA, Woodard DR, Schlievert PM. Clinical and bacteriologic observations of a toxic shock-like syndrome due to Streptococcus pyogenes. N Engl J Med. 1987 Jul 16. 317(3):146-9. [Medline].

  6. Stevens DL, Tanner MH, Winship J. Severe group A streptococcal infections associated with a toxic shock- like syndrome and scarlet fever toxin A. N Engl J Med. 1989 Jul 6. 321(1):1-7. [Medline].

  7. Lappin E, Ferguson AJ. Gram-positive toxic shock syndromes. Lancet Infect Dis. 2009 May. 9(5):281-90. [Medline].

  8. Davies HD, McGeer A, Schwartz B. Invasive group A streptococcal infections in Ontario, Canada. Ontario Group A Streptococcal Study Group. N Engl J Med. 1996 Aug 22. 335(8):547-54. [Medline].

  9. Eriksson BK, Andersson J, Holm SE. Epidemiological and clinical aspects of invasive group A streptococcal infections and the streptococcal toxic shock syndrome. Clin Infect Dis. 1998 Dec. 27(6):1428-36. [Medline].

  10. Stevens DL. Invasive group A streptococcus infections. Clin Infect Dis. 1992 Jan. 14(1):2-11. [Medline].

  11. Demers B, Simor AE, Vellend H. Severe invasive group A streptococcal infections in Ontario, Canada: 1987-1991. Clin Infect Dis. 1993 Jun. 16(6):792-800; discussion 801-2. [Medline].

  12. Matsuda Y, Kato H, Ono E, Kikuchi K, Muraoka M, Takagi K, et al. Diagnosis of toxic shock syndrome by two different systems; clinical criteria and monitoring of TSST-1-reactive T cells. Microbiol Immunol. 2008 Nov. 52(11):513-21. [Medline].

  13. The Working Group on Severe Streptococcal Infections. Defining the group A streptococcal toxic shock syndrome. Rationale and consensus definition. JAMA. 1993 Jan 20. 269(3):390-1. [Medline].

  14. Park JS, Kim JS, Yi J, Kim EC. [Production and characterization of anti-staphylococcal toxic shock syndrome toxin-1 monoclonal antibody]. Korean J Lab Med. 2008 Dec. 28(6):449-56. [Medline].

  15. Kalyan S, Chow AW. Staphylococcal toxic shock syndrome toxin-1 induces the translocation and secretion of high mobility group-1 protein from both activated T cells and monocytes. Mediators Inflamm. 2008. 2008:512196. [Medline].

  16. Dixit S, Fischer G, Wittekind C. Recurrent menstrual toxic shock syndrome despite discontinuation of tampon use: Is menstrual toxic shock syndrome really caused by tampons?. Australas J Dermatol. 2012 Aug 17. [Medline].

  17. Kaul R, McGeer A, Norrby-Teglund A. Intravenous immunoglobulin therapy for streptococcal toxic shock syndrome--a comparative observational study. The Canadian Streptococcal Study Group. Clin Infect Dis. 1999 Apr. 28(4):800-7. [Medline].

  18. Stevens DL. The flesh-eating bacterium: what's next?. J Infect Dis. 1999 Mar. 179 Suppl 2:S366-74. [Medline].

  19. Breshears LM, Schlievert PM, Peterson ML. A disintegrin and metalloproteinase 17 (ADAM17) and epidermal growth factor receptor (EGFR) signaling drive the epithelial response to Staphylococcus aureus toxic shock syndrome toxin-1 (TSST-1). J Biol Chem. 2012 Sep 21. 287(39):32578-87. [Medline]. [Full Text].

  20. Norrby-Teglund A, Muller MP, Mcgeer A. Successful management of severe group A streptococcal soft tissue infections using an aggressive medical regimen including intravenous polyspecific immunoglobulin together with a conservative surgical approach. Scand J Infect Dis. 2005. 37(3):166-72. [Medline].

  21. Rodríguez A, Rello J, Neira J, Maskin B, Ceraso D, Vasta L. Effects of high-dose of intravenous immunoglobulin and antibiotics on survival for severe sepsis undergoing surgery. Shock. 2005 Apr. 23(4):298-304. [Medline].

  22. Karauzum H, Chen G, Abaandou L, et al. Synthetic human monoclonal antibodies toward staphylococcal enterotoxin B (SEB) protective against toxic shock syndrome. J Biol Chem. 2012 Jul 20. 287(30):25203-15. [Medline]. [Full Text].

  23. [Guideline] Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the infectious diseases society of America. Clin Infect Dis. 2014 Jul 15. 59(2):147-59. [Medline].

  24. Barclay L. IDSA: skin and soft tissue infections guidelines updated. Medscape Medical News. Available at http://www.medscape.com/viewarticle/827399. Accessed: August 22, 2014.

  25. [Guideline] Dellinger RP, Levy MM, Rhodes A, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med. 2013 Feb. 41(2):580-637. [Medline].

 
Previous
Next
 
Description of M proteins and streptococcal toxins.
Group A streptococci cause beta hemolysis on blood agar.
Group A streptococci on Gram stain of blood isolated from a patient who developed toxic shock syndrome. Courtesy of T. Matthews.
This schematic shows interaction among T-cell receptor, superantigen, and class II major histocompatability complex. The binding of superantigen to class II molecules and T-cell receptors is not limited by antigen specificity and lies outside the normal antigen binding sites.
Progression of soft tissue swelling to vesicle or bullous formation is an ominous sign and suggests streptococcal shock syndrome. Courtesy of S. Manocha.
A 46-year-old man presented with nonnecrotizing cellulitis and streptococcal toxic shock syndrome. The leg was incised to exclude underlying necrotizing infection. Courtesy of Rob Green, MD.
A 46-year-old man presented with nonnecrotizing cellulitis and streptococcal toxic shock syndrome. This patient also had streptococcal pharyngitis. Courtesy of Rob Green, MD.
A 46-year-old man presented with nonnecrotizing cellulitis and streptococcal toxic shock syndrome. The patient had diffuse erythroderma, a characteristic feature of the syndrome. Courtesy of Rob Green, MD.
A 46-year-old man presented with nonnecrotizing cellulitis and streptococcal toxic shock syndrome. The patient had diffuse erythroderma, a characteristic feature of the syndrome. The patient improved with antibiotics and intravenous gammaglobulin therapy. Several days later, a characteristic desquamation of the skin occurred over palms and soles. Courtesy of Rob Green, MD.
A 58-year-old patient presented in septic shock. On physical examination, progressive swelling of the right groin was observed. On exploration, necrotizing cellulitis, but not fasciitis, was present. The cultures grew group A streptococci. The patient developed severe shock (toxic shock syndrome). The CT scanning helped evaluate the extent of infection and exclude other pathologies, such as psoas abscess, osteomyelitis, and inguinal hernia.
A 58-year-old patient presented in septic shock. On physical examination, progressive swelling of the right groin was observed. On exploration, necrotizing cellulitis, but not fasciitis, was present. The cultures grew group A streptococci. The patient developed severe shock (toxic shock syndrome). The CT scanning helped evaluate the extent of infection and exclude other pathologies, such as psoas abscess, osteomyelitis, and inguinal hernia.
A 58-year-old patient presented in septic shock. On physical examination, progressive swelling of the right groin was observed. On exploration, necrotizing cellulitis, but not fasciitis, was present. The cultures grew group A streptococci. The patient developed severe shock (toxic shock syndrome). The CT scanning helped evaluate the extent of infection and exclude other pathologies, such as psoas abscess, osteomyelitis, and inguinal hernia.
Necrotizing cellulitis of toxic shock syndrome.
Soft tissue infection secondary to group A streptococci, leading to toxic shock syndrome.
Extensive debridement of necrotizing fasciitis of the hand.
The hand is healing following aggressive surgical debridement of necrotizing fasciitis of the hand (see Image 15).
Necrosis of the little toe of the right foot and cellulitis of the foot secondary to group A streptococci.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.