Toxic Shock Syndrome: Continuing Professional Development

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EN688 Lillitos P, Harford D, Michie C (2007) Toxic shock syndrome. Emergency Nurse. 15, 6, 28-33. Date of acceptance: October 1 2007


Peter Lillitos MBBS, BSc is senior house officer in emergency care at West Middlesex University Hospital NHS Trust, London

Denise Harford DipEd is a nurse teacher in haematology

Colin Michie FRCPCH, FRIPH, FLS is a consultant senior lecturer in paediatrics both at Ealing Hospital NHS Trust, London

This article has been subjected to double blind peer review


Toxic shock syndrome is outlined, paying particular attention to the important role of nurses in its diagnosis and early management

Key words

  • Bacterial infections
  • Shock
  • Infection control

These key words are based on subject headings from the British Nursing Index.


For related articles visit our online archive at: and search using the key words above

Aims and intended outcomes

By reading this article and completing the Time Outs, readers should be able to:

  • Understand the nature of toxic shock syndrome (TSS)
  • Describe the disease processes underlying the condition
  • Understand the epidemiology of TSS
  • Recognise patients with the symptoms common to TSS
  • Establish how to make a diagnosis of TSS and understand the difficulties in achieving this
  • Recognise the importance of making an early diagnosis and that the initial diagnosis may have to be changed as a patient’s problems evolve
  • Develop an understanding of an initial management of patients with suspected TSS
  • Recognise the importance of education and raising awareness about rare but dangerous conditions such as TSS.


Toxic shock syndrome is a rare condition that is most common in young people, so rare in fact that emergency nurses will probably encounter only one or two cases during their careers, but it can also be fatal (Chesney 1989, Mellish and Cherry 1992).

It can develop after a burn or a traumatic or surgical wound, so A&E nursing staff are likely to be the first healthcare professionals to come into contact with patients with TSS.

The working knowledge of the condition offered by this article is valuable therefore because early diagnosis and treatment can be life saving.

Toxic Shock Syndrome

Toxic shock syndrome results from the production of toxins during the multiplication of Staphylococcus aureus bacteria.

This process of bacterial growth is termed colonisation, but does not necessarily involve invasion of the host, inflammation or production of pus.

Toxic shock syndrome most commonly develops after burns or trauma, when S. aureus bacteria colonise the damaged skin tissue (Chesney 1989).

The first series of TSS cases, reported in the United States, was associated however with tampon use (Chesney 1989, Mellish and Cherry 1992).

Streptococci, another type of bacteria, which can invade muscle or deep tissues, produce toxins similar to those produced by S. aureus. These toxins can lead to the life threatening condition, necrotising fasciitis, often nicknamed in the media the ‘flesh eating bug’.

Necrotising fasciitis meets the US Centers for Disease Control and Prevention’s criteria for TSS but is distinguished in writing from staphylococcal versions by prefixing ‘TSS’ with the letter ‘s’. Most authors accept this use of ‘sTSS’, although some prefer to use the abbreviation ‘TSLS’, which stands for ‘toxic shocklike syndrome’.

Streptococcal TSS is occasionally seen in children following chickenpox, and it was one such case that led to the development of the Isabel computer system, designed to assist emergency department (ED) staff with diagnosis.

Clinical case series (Melish and Cherry 1992) show that a small number of individuals can develop recurrent TSS or sTSS, presumably because they fail to develop antibodies to the toxins.

Because TSS is a syndrome, diagnosis is made when several clinical signs are found together. Its first description (Todd et al 1978), refined by the Centers for Disease Control and Prevention, is outlined in Table 1.

Table 1. Diagnosing TSS

Patients are diagnosed with toxic shock syndrome if they have any five of the following seven signs or symptoms:

  • Fever
  • Rash: usually red and widespread, although often faint
  • Low blood pressure
  • Desquamation, or peeling of the skin
  • Involvement of three or more organ systems, including muscle aches, diarrhoea, vomiting, irritability, drowsiness with no focal neurological signs, inflammation of the conjunctivae or other mucosal surfaces, and biochemical evidence of renal or liver malfunction
  • Negative culture of organisms from blood, cerebral spinal fluid or throat
  • Negative serology for measles, leptospirosis or the tick borne disorder, Rocky Mountain spotted fever

(Centers for Disease Control and Prevention 2005)

Development of TSS

Damaged areas of skin or mucosa become covered or colonised with multiplying bacteria in between 12 and 24 hours, and these colonising bacteria can, in some situations, produce particularly potent toxins known as superantigens.

When superantigens come into contact with patients’ cells, they react, with various consequences depending on cell type:

  • Activation of blood vessel muscle cells leads to vasodilation and a fall in blood pressure (BP)
  • Activation of skin lymphocytes causes a nonpurpuric, red rash that later peels
  • Activation of gut lymphocytes leads to diarrhoea
  • Activation of muscle cells leads to muscle pain and cramps.

Toxic shock syndrome most commonly occurs in people under 25 years of age probably because, by the time they are in their twenties, most people have developed protective antibodies to superantigen toxins (Chesney 1989).

In private correspondence with the author this year, the Health Protection Agency claimed that, in the UK, about 15 people develop TSS each year, of whom between two and five die as a result. Most presentations of such patients are at EDs.

Toxic shock syndrome can develop secondary to viral infection, such as influenza or chickenpox, or after surgical procedures, particularly those that involve the nose, because of the propensity of the nasal passages to be colonised with S. aureus. It can also develop in newborn babies.

Although extremely rare in the UK, this is seen most frequently in Japan (Takahashi 2003).


Toxic shock syndrome has a high mortality rate, although most patients who contract it recover without event and with no long term problems.

A small number of patients suffer organ damage or limb loss however as a result of low BP caused by their illness.

This complication can be reduced by early and aggressive hospital based treatment (Table 2) , so early diagnosis is vital, as with any other cause of circulatory collapse.

This and other complications associated with TSS are illustrated by the following case study.

Table 2. Principles of managing TSS

  • Rapid recognition, diagnosis and hospitalisation
  • Investigations including blood tests, swabs, radiographs and echocardiograph
  • Supportive monitoring and therapy, for example with oxygen and intravenous fluids, to maintain blood pressure and support the major organ systems, possibly including intensive care (Bench 2004, Wu 2006)
  • Antimicrobials such as clindamycin or flucloxacillin to remove the source of bacteria creating the toxins; mupirocin or rifampicin to eliminate nasal carriage
  • In early diagnoses, antitoxin therapy with intravenous immunoglobulin
  • Ensure follow up and consider psychological support

Case study

An eightyearold boy attends an ED after accidentally tipping boiling water onto his feet and legs. He has sustained superficial burns to about 5 per cent of his body surface area.

Apart from these injuries, and the pain and emotional distress they have caused, he appears to be in good health. He is admitted for observation and pain relief, and to check his fluid balance. Having received analgesia and appropriate dressings, he feels comfortable and his stay overnight is uneventful.

After 48 hours however, the boy develops a temperature of 39?C and feels generally unwell, with muscle aches in his back and shoulders.

The nurse informs a doctor, who prescribes ibuprofen. Later that day, the boy’s parents tell the nurse that their child has developed a red rash all over his body, and that he has had two bouts of diarrhoea.

The child looks sweaty, has reddened eyes, and is drowsy and difficult to rouse, even though it is daytime. Observations reveal that his pulse rate is 120 beats per minute and his BP has fallen from 109/75 to 80/40.

The doctor starts intravenous fluids and takes blood for analysis. The boy’s BP does not increase however and he becomes less responsive. He appears to have a tender left leg with poor circulation to his toes.

The next day the boy is moved to intensive care for more aggressive management of his low BP and fever. He receives fluids, antibiotics and drugs to increase cardiac output, and has hourly reviews to ensure optimal oxygenation and tissue perfusion. He briefly requires ventilation and, after three days, begins to show signs of improvement. Subsequently, he develops ischaemia of two toes on the left foot, and these require amputation.

After a week back on the ward, his skin rash has started to peel in places, particularly around his fingers and toes.


The boy described in the case study represents the one child in a thousand who deteriorates in this way following this type of burn.

Early administration of antibiotics and fluids in this case may have prevented the need to transfer the child to intensive care, which shows how a lack of awareness of TSS can lead to delays in treatment.

A computer programme, named after a girl called Isabel whose TSS was not diagnosed swiftly, has been developed to help ED staff make early diagnoses and instigate immediate treatment.

A checklist for nurses to consider when caring for children like the boy in the case study is shown in Table 3.

Table 3. Checklist for considering a diagnosis of TSS

To ensure to they do not miss TSS, nurses should:

  • Check blood pressure of patients with diarrhoea, vomiting or drowsiness
  • Remember that TSS can present at any age and in either sex
  • Be wary of a fever or any other of the named symptoms developing in children who have recently sustained burns or trauma
  • Consider a wide differential diagnosis if patients’ diagnoses are difficult
  • Discuss with clinical teams the cases of patients who show signs or symptoms of TSS

Time Out 1

Rehearse with yourself and colleagues methods of recognising and ensuring the airway, breathing and circulation (ABC) of the sick child described in the case study according to. Consider attending resuscitation courses to further your skills in managing acutely unwell children so that, even if you are unsure of a diagnosis of TSS, you will be taking measures to stabilise the child and reduce tissue damage. One?day courses such as Paediatric Life Support or Advanced Paediatric Life Support, both of which are provided by the Advanced Life Support Group, for example concentrate on recognition and management of sick children

Difficulties in diagnosis

Despite the existence of clearly established diagnostic criteria (Table 2) for TSS, its severity and its relation to injuries or menstruation are not easy to assess.

An unpublished study of TSS cases in the UK by author Colin Michie suggests reasons for this and illustrates some of the problems that can occur in diagnoses.

In this study, 68 cases of TSS between 1990 and 2000 were reviewed. Examination of the patients’ clinical records showed that 43 were burn or trauma related and that the median period of fever before diagnosis was four days, with a range of between two to 12 days.

Cases of TSS that were burn related were missed at initial presentation more often than those related to menstruation.

Twenty cases were diagnosed by primary carers or parents before referral, and 11 cases were diagnosed on the patients’ arrival in ED. Of these, nursing staff made six of the diagnoses as well as several of the remaining 37 diagnoses on the wards.

The study identifies the causes of a number of difficulties with diagnosing TSS and these are listed in Table 4.

Table 4. Why diagnosing TSS is difficult

  • Slow development or delay in the appearance of all the signs; blood pressure for example often drops late in the illness
  • Blood pressure is not always recorded
  • Confusion when making a first diagnosis, often involving ‘fever and rash’, is not resolved
  • Inadequate compilation of clinical data
  • Toxic shock syndrome is rare, and few nursing and medical staff are aware of it

Improvements in management

The study showed that BP had been recorded for only 23 of the 68 patients involved, and that 17 of the recordings had been carried out by nurses. This highlights the importance for nurses, not only of measuring BP, but also of checking it regularly to avoid missing any deterioration.

Eighteen patients had poor ‘data integration’, as a result of which reported clinical findings were not collated to enable adequate diagnoses.

While single initial diagnoses were recorded for most of the patients in the study, they were not reconsidered or reviewed when new clinical information emerged, a problem that can be avoided if nursing and medical records are kept on single sheets of paper for each patient.

Toxic shock syndrome can resemble other, mostly infective, conditions. In Table 5, these are listed in decreasing order of frequency of occurrence.

Several diagnostic challenges arise when the syndrome definitions listed in Table 1 are used in conjunction with a long differential diagnosis, or list of possible diagnoses.

Some patients with TSS may not fulfil five of the criteria as recommended.

In the study, some patients were diagnosed retrospectively, for example once they had developed desquamation, which is usually a late sign, at one to two weeks after the onset of signs and symptoms. At this stage however, children have usually recovered, illustrating the difficulty of diagnosing rare conditions at initial presentation.

Clinical signs differed both in their sequence and in the speed at which they appeared. For example, children tend to present initially with drowsiness or irritability with fever, whereas older children and young adults are more often first described as having ‘flu like illness’ accompanied by rash.

Toxic shock syndrome can be confused with sepsis syndrome, once called ‘septic shock’, which is similar in the early stages but is caused by the body’s own immune response to bacteria multiplying in the bloodstream.

In sepsis syndrome, bacterial products such as bacterial cell walls cause inflammation to develop rapidly but without the involvement of bacterial superantigens.

Low BP is common to both sepsis syndrome and TSS however, and it is this that causes damage to the limbs, digits, brain, kidneys and heart.

Regardless of possible diagnoses therefore, initial management is always the same: measurement and recording of BP, oxygen saturation and other vital signs, followed by immediate resuscitation for shock.

Table 5. Conditions that resemble TSS

  • Gastroenteritis
  • Septicaemia, for example pneumococcal, meningococcal or haemophiliac
  • Scarlet fever
  • Viral encephalopathy
  • Urinary tract infection
  • Septic abortion
  • Haemorrhagic shock syndrome
  • Streptococcal TSS
  • Measles
  • Leptospirosis
  • Reactions, such as pneumonia or hypersensitivity, to drugs
  • Acute systemic lupus erythematosus
  • Acute rheumatoid arthritis
  • Tick borne disorders including typhus and Rocky Mountain spotted fever

Time Out 2

Practise measuring blood pressures in paediatric patients and check these are always recorded in the notes. What are the normal BP values for children of different ages?


The causes of TSS are bacteria and their toxins, and the effects promote inflammatory changes that compromise many organ systems.

Management principles are therefore:

  • To block the effects of the toxin and remove bacteria that might synthesise more toxin
  • To support the major organ systems, especially cardiovascular, renal and respiratory.

In children with suspected TSS, BP should be measured after history taking and examination. Appropriate initial investigations, including blood tests, swabs, radiographs and echocardiographs to rule out cardiac causes of shock, should then be carried out. Supportive oxygen therapy and intravenous fluid therapy are essential to maintain BP. The child must then be monitored closely to evaluate progress or detect deterioration quickly.

Antibiotics must be given to remove the bacteria making the toxin, with clindamycin or flucloxacillin often being used initially until the causative organism is identified (Mellish and Cherry 1992), although elimination of nasal carriage of the bacteria with mupirocin or rifampicin can also be considered (Wu 2006).

Some cases of TSS are caused by antibiotic resistant organisms such as meticillin resistant S. aureus so, depending on the first culture samples, the initial antibiotic may have to be changed. As a result, many people with TSS require admission to intensive care for respiratory support through ventilation.

In such patients, immunoglobulins, which include antibodies that bind to superantigens to stop them activating cells, can be of value, so antitoxin therapy with intravenous immunoglobulin can be recommended when diagnoses are made early.

Staff must make sure that children on this therapy are reviewed regularly to ensure that they do not develop allergic reactions to the immunoglobulin treatment (Bench 2004).

In addition to these clinical measures, psychological support should be given to patients and their families.

Time Out 3

Look up the Isabel website (Table 6) to find if it can help you with diagnosis of patient conditions. Are there other websites you can use to help you recognise this condition?

Advances in analysis

As bacterial gene analysis advances and the knowledge of how bacterial toxins are produced in the body grows, specific antitoxin therapies and vaccines may come into use.

The concept of ‘switching off’ the genes responsible for inducing inflammation may also eventually yield new therapies. In molecular studies, there is now a focus on furthering understanding of the ‘inflammatory cascade’, during which toxins activate proinflammatory genes that in turn set other proinflammatory mechanisms into action.

Greater knowledge of these staged mechanisms will enable effective interventions to prevent the next stage of the process. Meanwhile, early goal directed therapy, the protocol for the early management for septic shock, is helping to reduce morbidity and mortality from this condition, and a similar protocol could be employed for TSS.

To further understand this rare but serious condition, more information on individual incidences is needed. It is still difficult for example to explain why some people develop TSS while others do not.

Investigations into improved methods of predicting long term complications in these patients, and better ways to start treatment earlier, are needed.

For the present, awareness of TSS among the healthcare staff most likely to come into contact with patients who have the condition must be raised. The ability of such staff to detect shock must be improved, and the importance of ensuring that all cases of TSS are well documented should be emphasised (Rivers 2006).


Toxic shock syndrome is a serious and potentially life threatening condition, but can be difficult to diagnose. Therefore, greater awareness of the condition could save lives and reduce morbidity.

Among healthcare professionals, nurses are most often involved in initial management of patients with TSS, so it is essential that they are aware of the condition and the actions they need to take if they suspect its diagnosis.

Nurses need to consider a diagnosis of TSS for all patients who present with malaise, drowsiness or gastroenteritis, and ensure that their vital signs, particularly their BPs, are monitored closely. This can improve significantly the outcome of patients who have developed TSS.

Table 6. Useful websites


The authors would like to acknowledge the assistance of surgical staff nurses in the department of surgery at Ealing Hospital, London, Dee Hughes and Linda Butler for their review, advice and recommendations.


Bench S (2004) Clincal skills: assessing and treating shock: a nursing perspective. British Journal of Nursing. 13, 12, 715721.

Centers for Disease Control and Prevention (2005) Toxic Shock Syndrome. dbmd/diseaseinfo/toxicshock_t.htm (Last accessed September 21 2007).

Chesney PJ (1989) Clinical aspects and spectrum of illness of toxic shock syndrome: an overview. Reviews of Infectious Diseases. 11, Supplement 1, 17.

Mellish ME, Cherry JD (1992) Staphylococcal infections. In Feigin RD (ed) Pediatric Infectious Diseases. WB Saunders and Company, Philadelphia PA.

Rivers E (2006) The outcome of patients presenting to the emergency department with severe sepsis or septic shock. Critical Care. 10, 4, 154.

Takahashi N (2003) Neonatal toxic shock syndromelike exanthematous disease (NTED). Pediatrics International. 45, 2, 233237.

Todd J, Fishaut M, Kapral F, Welch T (1978) Toxicshock syndrome associated with phagegroupI Staphylococci. The Lancet. 2, 8100, 11161118.

Wu CC (2006) Possible therapies of septic shock: based on animal studies and clinical trials. Current Pharmaceutical Design.12, 27, 35353541.

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