Streptococcus Associated Toxic Shock

126 Archives ofDisease in Childhood 1992; 67: 126-130 Arch Dis Child: first published as 10.1136/adc.67.1.126 on 1 January 1992. Downloaded from Streptococcus associated toxic shock C Torres-Martinez, D Mehta, A Butt, M Levin Abstract syndrome toxin-I (TSST-1). TSST-1 and other In the past few years, there appears to have enterotoxins are thought to cause the disorder been a change in the spectrum of disease by activating host inflammatory responses, and caused by group A ,-haemolytic streptococcus in particular by triggering release of cyto- (GABHS), and a toxic shock-like syndrome kines." caused by this organism has recently been In the past four years, there have been a described in adults. We report four children number of reports of a toxic shock-like disorder with an acute illness characterised by rapid occurring in both adults and children, which progression of shock, erythematous rash, has been associated not with S aureus but multisystem organ involvement, electrolyte with group A j3-haemolytic streptococcus derangements, and desquamation who fulfil (GABHS).73 Furthermore, there appears to the previously established diagnostic criteria have been an increase in the prevalence of for toxic shock syndrome. Three of the serious invasive disease due to GABHS in many children had extensive cutaneous and soft parts of the world.126 tissue infection and the fourth had peritonitis. In order to illustrate the clinical and patho- All four developed bacteraemia. Treatment logical features of the disease, we report four included aggressive cardiovascular resuscita- children with streptococcus associated toxic tion and antibiotic therapy. Although no shock syndrome and discuss the mechanisms patient died, they suffered multiple and severe involved in its pathogenesis. complications requiring prolonged treatment and hospitalisation. Streptococcal toxic shock syndrome is a separate and clearly defined Patients and methods entity occurring in previously healthy children. Streptococcus associated toxic shock syndrome was diagnosed infourchildren between February 1988 and November 1990. Three were admitted In 1978, Todd and Fishaut described seven to the Hospital for Sick Children, Great children with an acute disease characterised by Ormond Street, London, and one to Guy's http://adc.bmj.com/ fever, mucous membrane hyperaemia, subcut- Hospital, London (table 1). All four cases aneous oedema, desquamating erythroderma fulfilled the diagnostic criteria for staphylococcal and rapid progression to hypotension and multi- toxic shock syndrome,27 but in each case system organ involvement, and which they GABHS was isolated from the blood (table 2). called staphylococcal toxic shock syndrome.' The disorder subsequently became more widely Table 2 Criteria of staphylococcal toxic shock syndrome in children with associated toxic recognised as an illness affecting young women, (TSS) four streptococcus on September 29, 2021 by guest. Protected copyright. shock syndrome which was associated with vaginal colonisation by Staphylococcus aureus and the use of Case No tampons. At least 13% ofcases are not associated 1 2 3 4 with menstruation but with focal staphylococcal Staphylococcal TSS criteria infections and/or colonisation,3 and a significant Temperature >389°C + + + + proportion of these non-menstrual cases are Rash + + + + Desquamation + + + + children. Hypotension + + + + In the past decade, major advances have Multisystem involvement Gastrointestinal - - + + occurred in the understanding of the patho- Muscular + + - + genesis of staphylococcal toxic shock syndrome. Mucous membrane + + + Renal + Infectious Disease Unit, It is now well established that most cases are Haematological - + + Academic Department caused by a number of related enterotoxins Hepatic + + of Paediatrics, Central nervous system - + - + St Mary's Hospital produced by S aureus, the most common of Medical School, which is the 22 kDa protein called toxic shock +, Present; -, absent. South Wharf Road, London W2 INY C Torres-Martinez Table I Clinical characteristics children with streptococcus associated toxic shock M Levin of four syndrome Department of Case Age Sex Clinical Initial Prodromal GABHS Paediatrics, No presentation symptoms period* isolation Guy's Hospital, London I 10 years F Shock, fasciitis Fever, rash 6 days Blood, skin wound D Mehta 2 22 months F Shock, cellulitis Fever, focal swelling 12 hours Blood, builae, nose, skin A Butt 3 13 days F Peritonitis, shock Diarrhoea, rash 3 days Blood, nose, peritoneal fluid 4 10 weeks F cellulitis Fever, focal 18 hours Blood Correspondence to: Shock, swelling Professor Levin. *From onset of symptoms to shock. Accepted 14 August 1991 GABHS, Group A ,1 haemolytic streptococci. Streptococcus associated toxic shock 127 Microorganisms were recovered and identified spite of the decompression of her forearm, the according to standard procedures.28 Antibiotic muscles looked progressively less viable over susceptibility was determined by the disc the next few days. A bone scan suggested an Arch Dis Child: first published as 10.1136/adc.67.1.126 on 1 January 1992. Downloaded from diffusion method in the microbiological labora- avascular right ulna. Antibiotic therapy was tories of the respective hospitals. changed to cefotaxime and clindamycin. Sensation of the right hand disappeared, and three weeks after admission, amputation of the CASE REPORTS right upper limb below the elbow was carried Case I out. Additional amputation of her feet was A previously healthy 10 year old girl experienced avoided, although extensive skin grafting was pain and swelling over both ankles three days necessary. Progressive clinical recovery followed after sustaining a cut below her left knee. She with re-establishment of normal renal, hepatic, subsequendy developed a non-specific macular and pulmonary function. She returned to the erythematous rash and fever and was admitted local hospital five weeks after initial admission. to a local hospital. During the ensuing five days, she became increasingly tachycardic and jaundiced, and blistering areas were noted in Case 2 the right upper limb. A 22 month old girl presented to a local hospital After 24 hours of progressive drowsiness and with a one week history of cough, fever, and hypotension she was transferred to Guy's mild facial swelling. One day before admission, Hospital where, on arrival, she was toxic and she developed multiple red bullae over her lethargic but responsive. Her temperature was trunk and limbs. On admission, she was febrile 39°C, heart rate 150 beats/min, respiratory rate (40 6°C), with a rate of 200 beats/min, and 40/min, and systolic blood pressure 85 mm Hg. blood pressure of 65/40 mm Hg. She had She had red lips and tongue with conjunctival generalised subcutaneous oedema and delayed hyperaemia and mild icterus. A soft 2/6 systolic peripheral perfusion. A presumptive diagnosis murmur was noted. The liver was 2 cm below of septic shock was made and aggressive fluid the right costal margin. Her ankles and wrists resuscitation (in excess of 300 ml/kg) was were intensely swollen. A fine papular general- instituted. Initial antimicrobial therapy included ised rash with desquamation, particularly over flucloxacillin, fusidic acid and gentamicin. the trunk and limbs, was found in conjunction Laboratory investigations recorded haemoglobin with large yellow blisters and necrotic areas over concentration 82 g/l, white cell count 3 5 x 109/1, her right forearm and lateral aspect of her left neutrophils 1 9x 109/1, platelet count 90x 109/1, foot. The pulse in the right radial artery was concentrations of sodium 129 mmol/l, potas- absent, though detectable on Doppler examina- sium 2-7 mmol/l, calcium 1- 86 mmol/l, crea- tion. Initial investigations were as follows: tinine 48 Fmol/l, urea 7-1 mmol/l, albumin 22 haemoglobin concentration 87 g/l, white cell g/l, fibrinogen 4-6 g/l and fibrin degradation count 30x 109/1 with 25 x 109 neutrophils, products >20 [tg/ml, prothrombin time 51 platelet count 251 x 109/l, and erythrocyte sedi- seconds (control 14 second), partial thrombo- http://adc.bmj.com/ mentation rate 45 mm/hour. Biochemical find- plastin time 35 seconds (control 32 seconds), ings showed concentrations of sodium 125 aspartate aminotransferase 152 U/I and creatine mmol/l, urea 22-4 mmol/l, creatinine 175 ,umol/l, phosphokinase 221 U/1. GABHS was grown bilirubin 71 mmol/l and albumin 31 g/l, creatine from blood, fluid from bullae, and her nose. phosphokinase 3108 U/l and aspartate amino- Penicillin was added to her antimicrobial transferase 181 U/1. Urine contained granular therapy. casts and blood cells, and was positive for After resuscitation her condition improved on September 29, 2021 by guest. Protected copyright. myoglobin -and protein (3+), urinary sodium but she continued to be febrile and developed was less than 10 mmol/l. Blood cultures and swelling over her left forearm and calf. She was swabs from the cut below the left knee grew referred to the Hospital for Sick Children with a GABHS. possible diagnosis of necrotising fasciitis. On She was resuscitated with large volumes of arrival she was febrile (39°C) with a heart rate of colloid and required inotropic support with 190 beats/min. She had enlarged and tender dobutamine and dopamine. Despite an adequate lymph nodes in the left cervical chain and central venous pressure, she remained poorly generalised subcutaneous oedema. A left sided perfused; a continuous infusion of prostacyclin cervical mass anterior to the carotid vessels was was introduced as a vasodilator. She was elec- demonstrated on cervical ultrasound and tively ventilated and required full sedation and thoracic computed tomography. A technetium paralysis. High dose penicillin and flucloxacillin white cell scan suggested an inflammatory were started. Her oxygen requirement increased lymphadenitis as there was marked focal uptake over the next few hours and radiological changes of the labelled white cells. A nuclear magnetic consistent with adult respiratory distress syn- resonance scan revealed multifocal soft tissue drome appeared. After resuscitation, her renal lesions in the left side of the neck and extending and hepatic function returned slowly to normal.

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