Toxic Shock Syndrome Clinical Presentation

  • Author: Ramesh Venkataraman, MBBS; Chief Editor: Michael R Pinsky, MD, CM, FCCP, FCCM   more...
 
Updated: Jul 16, 2010
 

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)
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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:
  • Bullae
  • Scarlet fever–like rash
  • Petechiae or maculopapular rashes
  • Desquamation
  • 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, as follows (Centers for Disease Control and Prevention, 1990):
  • Fever
  • Rash - A diffuse macular erythroderma
  • Desquamation - Occurs 1-2 weeks after onset of illness, involving palms and soles
  • Hypotension (systolic blood pressure < 90 mm Hg, orthostatic drop in diastolic blood pressure < 15 mm Hg, orthostatic syncope, and dizziness)
  • 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%)
  • Case definition of streptococcal TSS (Working group definition, JAMA 1993)
    • Isolation of GAS (S pyogenes) from a normally sterile site, eg, blood, cerebrospinal fluid, pleural fluid (definite case), or nonsterile site (probable case) and hypotension (systolic pressure £90 mm Hg in adults or less than fifth percentile for children)
    • Multiorgan involvement, as evidenced by at least 2 of the following:
      • 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 106/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)
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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.[13] 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.
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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, Indian Medical Association, and Society of Critical Care Medicine

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, and World Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Cory Franklin, MD  Professor, Department of Medicine, 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 and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

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, and Massachusetts Medical Society

Disclosure: Nothing to disclose.

Eleftherios Mylonakis, MD  Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital

Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Chief Editor

Michael R Pinsky, MD, CM, FCCP, FCCM  Professor of Critical Care Medicine, Bioengineering, Cardiovascular Disease and Anesthesiology, Vice-Chair, Academic Affairs, University of Pittsburgh School of Medicine, University of Pittsburgh Medical Center

Michael R Pinsky, MD, CM, FCCP, FCCM is a member of the following medical societies: American College of Chest Physicians, American College of Critical Care Medicine, American Heart Association, American Thoracic Society, Association of University Anesthetists, Shock Society, and Society of Critical Care Medicine

Disclosure: LiDCO Ltd Honoraria Consulting; iNTELOMED Intellectual property rights Board membership; Edwards Lifesciences Honoraria Consulting; Applied Physiology, Ltd Honoraria Consulting; Cheetah Medical Consulting fee Consulting

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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.
 
 
 
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