Nurses and the management of Toxic Shock Syndrome

Colin A Michie MA. FRCPCH.LS
    Consultant Senior Lecturer in Paediatrics
    Honorary Consultant Public Health Laboratories Service

Varsha Shah
    Sister, Department of Paediatrics



A recent case review showed that nurses play an important role in diagnosing toxic shock syndrome, or TSS. What is this condition, and how can we improve the care of sufferers? TSS is a rare and potentially fatal condition which may develop in individuals of all ages. The average casualty nurse will probably only ever encounter a single case. However nursing staff will probably be the first to meet the patient with this problem. Some knowledge of toxic shock syndrome is important because early diagnosis and treatment may be life-saving.

What is TSS?

Toxic shock syndrome can only be diagnosed on clinical findings: there is no specific blood test or measurement. The description of TSS was first made in 1978 by James Todd following observations in a series of children with burns and trauma (fully outlined in Table 1). Looking carefully at the table, it is clear that measuring blood pressures in patients with fevers and rashes is particularly important. Toxic shock syndrome develops following exposure to a bacterial toxin. The toxin is usually produced by Staphylococcus aureus or Streptococcal species of bacteria. The toxins are particularly potent and are referred to as superantigens. The bacteria which can make superantigens are commonly found on healthy skin and mucosal surfaces. It is not known why most of these organisms never produce significant amounts of toxin to cause illness.

Who is likely to develop TSS?

Toxic shock syndrome is rare in the first 5 years of life and is less common in Afro-Caribbean races. Higher rates of TSS illness in the USA during the 1980s were associated with the use of a specific type of vaginal tampon during menstruation or certain surgical packs following nasal surgery. This pattern was not seen in the UK: the Public Health Laboratories recorded up to 15 cases a year, with the greatest number in 1990. Although cases are now less numerous, TSS continues to be diagnosed regularly, the majority in hospital casualty departments. Between 2 and 5 deaths annually in the UK are thought to be caused by TSS, although the exact number is difficult to estimate. Most UK cases now follow burns or trauma in children; the numbers of menstrually-related cases has fallen over the last 10 years.

Many early exposures to staphylococcal toxins probably recover without diagnosis or treatment – these are referred to by some as ‘near miss’ TSS. The exact size of this problem is difficult to estimate: it is likely that exposure to toxins without development of clinical symptoms is common.

The typical case

A child with a burn or scald involving less than 5% of body surface area usually recovers without incident. One in every 1000 of such cases will develop fever and malaise 2-3 days following the epidermal damage. This rapidly progresses in a small proportion of children to include a rash, conjunctival injection and diarrhoea within 24 hours. On examination such a child will be found to have tachycardia and hypotension. The hypotension is progressive and often unresponsive to intravenous resuscitation. The first problems nursing staff or parents might notice are fever and drowsiness, perhaps with a rash and diarrhoea. This is toxic shock syndrome.

The toxic shock syndrome toxins stimulate immune cells leading to the release of inflammatory cytokines. It is these cytokines which cause fever and tissue damage. For instance activation of skin T-cells causes a red rash which later peels, activation of gut T-cells leads to diarrhoea, activation of cells in muscles leads to muscle pain and cramps.

With the early use of standard supportive treatments (Table 2) most patients will recover without the need for intensive care or ventilation and should demonstrate no long-term sequelae. There is a possible risk of recurrence present in some 2-5% of cases. Elimination of nasal carriage of Staphylococci is a sensible precaution to reduce recurrence rates.

Why are nurses important in the diagnosis of TSS?

A case series of 68 UK TSS cases complied between 1990 and 2000 has shed some light on who diagnoses TSS. Of this group 43 cases were burn or trauma-related. Examination of the records indicated that the median period of fever before diagnosis was 4 days (range 2-12 days). Some 20 cases were diagnosed by primary carers or parents prior to referral, a further 11 were diagnosed in casualty on arrival. Cases which were burns-related were missed at initial presentation more often than those which were menstrually related. Nursing staff first made 6 of the diagnoses in casualty and a number of diagnoses on the wards.

Toxic shock syndrome was therefore not an easy diagnosis to make: what explanations can be offered? If analysed logically two problems became evident. Firstly only 23 of the 68 patients had a blood pressure reading checked on initial presentation to medical services. Of these 17 blood pressures were recorded by the nursing staff, so this initial check by nurses was critical. A number of cases in the series clearly had delays in diagnosis because a blood pressure measurement was not taken and documented. Secondly there was a clear difficulty in what has been defined as data integration. That is, the reported findings were not gathered together into an appropriate diagnosis or differential diagnosis (18 cases). In the majority of cases a single initial diagnosis was recorded, and this was not subsequently reconsidered with updated observations or results. In several of the menstrually-related cases the diagnosis of TSS was suggested by nursing staff.

Several other conditions may resemble TSS – a differential diagnosis includes the disorders outlined in Table 3. In some situations it may be difficult to distinguish between these. One common confusion is with septic shock, as these problems may appear similar in their early stages. Septic shock however is caused by multiplying bacteria, and not mainly by bacterial superantigen toxins. A number of challenges arise when using syndrome definitions such as that in Table 1, together with a long differential diagnosis as in Table 3. Some patients may not quite fulfil all the criteria, or treatment may arrest the development of the disorder. In these situations a diagnosis of TSS cannot be applied. A proportion of cases is diagnosed retrospectively, once they develop skin desquamation (usually a late sign). Patients differ in the sequence and speed with which they show clinical signs. For instance children tend to present initially with drowsiness or irritability with fever; adults more often first describe a ‘flu-like illness which is accompanied by a rash.

In order to remedy these two major correctable difficulties in recognising TSS it is important to educate all health service staff and the public about TSS. The fact that relatively small burns or collections of pus following trauma may result in serious illness needs to be remembered. Practical clinical points to help develop better practice are outlined in Table 4. The value of nurses in making the diagnosis of this acute medical condition, and in particular accurately measuring blood pressure, cannot be underestimated, as demonstrated in this survey.

Management: principles and recommendations

The principles of treatment are to block the effects of the toxin, to remove bacteria which might synthesise more toxin while at the same time supporting the patient. Specifically this will involve support for the cardiovascular, renal and respiratory systems as with any other patient with shock. In practice providing mask oxygen, intravenous resuscitation, intravenous immunoglobulin and clindamycin will be sufficient (see Table 3). Clindamycin is the preferred antibiotic because it blocks further toxin production by bacteria. Intravenous immunoglobulin neutralises toxin and its effects and can result in a rapid improvement in the illness.

It remains difficult to explain why a particular individual develops TSS while others do not. The prediction of long-term complications remains impossible with the limited patient data currently available. Collection of case data in both active and passive surveillance is important, and is an aim of the Public Health Laboratory Service. The value of such collections has been well proven in other areas such as in vaccination and drug reactions. We need to ensure that all cases are well documented; the survey described earlier demonstrated that nursing notes were often more detailed and valuable than other clinical records.


TSS may be difficult to diagnose, but a better awareness of this condition, and skill in measuring the blood pressure in sick patients will save lives and reduce morbidity. TSS may be rare, but nurses have an important role in its diagnosis and management!


The authors would like to acknowledge the assistance of the Toxic Shock Syndrome Information Service and staff in the Ealing Paediatric Department for their advice and recommendations for this script. Sections of this review have been used in other scripts prepared by the authors.

Table 1: How to diagnose toxic shock syndrome (after the Centre for Disease Control, USA, 1990). To have TSS a patient must have 5 of the following:

  1. 1.   Fever
  2. 2.   Rash (usually red and widespread, may be faint)
  3. 3.   Low blood pressure
  4. 4.   Desquamation (peeling of the skin)
  5. 5.   Involvement of 3 or more organ systems(This includes presentation with diarrhoea and vomiting, irritability and drowsiness with no focal neurological signs, muscle aches, inflammation of the conjunctivae or other mucosal surfaces, biochemical evidence of renal or liver malfunction.)
  6. 6.   Negative culture of organisms from blood, CSF or throat, negative serology for measles, leptospirosis or Rocky Mountain spotted fever.

Table 2: Management of toxic shock syndrome

  1. 1.   Rapid recognition, diagnosis and hospitalisation
  2. 2.   Investigation (including blood tests, swabs, radiographs and echocardiograph)
  3. 3.   Supportive therapy and monitoring (e.g. oxygen, intravenous fluids to maintain blood pressure, routines to support major organ systems)
  4. 4.   Antimicrobials (remove the source of bacteria making the toxin, treat with clindamycin or flucloxacillin; eliminate nasal carriage with rifampicin or mupirocin)
  5. 5.   Anti-toxin therapy (intravenous immunoglobulin if the diagnosis is made early)
  6. 6.   Ensure follow-up, consider psychological support, check an echocardiograph

Table 3: Conditions to consider in a differential diagnosis of staphylococcal TSS, with the most common disorders first:

  1. Gastroenteritis
  2. Septicaemia (e.g. pneumococcus, meningococcus, haemophilus)
  3. Scarlet fever (and staphylococcal scarlet fever)
  4. Viral encephalopathy
  5. Urinary tract infection
  6. Septic abortion
  7. Haemorrhagic shock syndrome
  8. Streptococcal TSS
  9. Measles
  10. Leptospirosis
  11. Drug reactions
  12. Acute systemic lupus erythematosus
  13. Rheumatoid arthritis
  14. Tick-borne disorders including typhus and Rocky Mountain spotted fever (rare)
  15. Arcanobacterium haemolyticum-induced pharyngitis (rare)

Table 4: How to improve clinical practice:

  1. 1.   Always check the blood pressure of a patient with diarrhoea, vomiting or drowsiness
  2. 2.   Remember that toxic shock syndrome may present at any age and in either sex
  3. 3.   If diagnosis is difficult, stand back and consider a wide differential diagnosis
  4. 4.   Discuss all problematic patients with others

Further reading

Useful websites:

(Public Health Laboratories) MMWR weekly report (Infectious diseases Society, USA) (Staphylococcal sequence gene base) for Genomic Research) (Adhesion of Staphylococci) (Toxic Shock Syndrome Information Service)


Mellish ME. Staphylococcal Infections In Feigin RD, Cherry JD eds.

Paediatric Infectious Diseases. Philadelphia: WB Saunders and Company, 1992:

1240-1267; 1277-1295

European Conference on Toxic Shock Syndrome. Editors: J Arbuthnott B Furman.

1997. Royal Society of Medicine Press Ltd.

Papers (please contact the author for further references if required):

Bordage G. Why did I miss the Diagnosis? Some cognitive explanations and educational implications. Acad Med 1999; 74: S138-142.

Chesney PJ. Clinical aspects and spectrum of illness of toxic shock syndrome: overview. Rev Infec Dis. 1989;11: S1-7.

Dinges MM, Orwin PM, Schlievert PM. Exotoxins of Staphylococcus aureus. Clin Microbiol Rev. 2000;13: 16-34.

Lindberg E, Nowrouzian F, Adlerbert I, Long-time persistence of superantigen-producing Staphylococcus aureus strains in the intestinal microflora of healthy infants. Ped Red 2000;48741-747.

McKenny D, Kimberly L. Pouliiot, Ying Wang, Vivek Murthy, Martina Ulridch, Gerd D�ring, Jean C. Lee, Donald A. Goldmann Gerald B. Pier. Broadly Protective Vaccine for Staphylococcus aureus Based on an in Vivo-Expressed Antigen. Science 1999; 284: 1523-1527.

Michie C.A., Cohen J. Clinical significance of superantigens. Trends in Microbiology. 1998; 6: 61-65.

Michie C.A., Bowes A., McAllister M. Toxic Shock Syndrome, Superantigen activity and burns. Ped Res 1998; 43: 152A.

Parsonnet J. Nonmenstrual toxic shock syndrome: new insights into diagnosis, pathogenesis, and treatment. Curr Clin Top Infect Dis. 1996; 16: 1-20

Todd J, Fishaut M, Kapral F, Welch T. Toxic-shock syndrome associated with phage-group-I Staphylococci. Lancet. 1978 Nove25;2(8100):1116-8.

Colin A Michie
Consultant Senior Lecturer in Paediatrics
R&D Director