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The New Zealand Medical Journal

 Journal of the New Zealand Medical Association, 22-August-2003, Vol 116 No 1180

Necrotising fasciitis in neonates: a multidisciplinary approach
Stanley Loo, Stephen Mills, Michael Muller and Vipul Upadhyay
Necrotising fasciitis is a rare but often fatal condition among neonates. When present it is frequently attributable to secondary infection such as omphalitis, mammitis, balanitis, post-operative complications, fetal scalp monitoring and bullous impetigo. It is important to have a high index of suspicion, since early recognition and aggressive multidisciplinary management offers the best chance for survival.
We report two cases of necrotising fasciitis in neonates who presented to the Starship Hospital, Auckland, and discuss the aetiopathogenesis and management. We believe that a multidisciplinary approach in a tertiary hospital is vital to ensure maximum survival and minimum morbidity. It is likely that these patients will require the treatment of neonatal surgeons, plastic surgeons, infectious disease specialists, intensivists, neonatal anaesthesiologists and an infrastructure that is found in a tertiary paediatric hospital.

Case 1

Baby A was born at term by normal vaginal delivery. He originally presented to a peripheral hospital at ten days of age and four days following a superficial burn to his back. The burn was sustained from a hot water bottle placed against his back for fifteen minutes. Two days later a visiting midwife noted a black streak had developed across the area of redness on his back. One day later the area of blackness was noted to be much larger and so he was referred to the local hospital.
On presentation to the peripheral hospital, Baby A was noted to be dehydrated, unwell and septic with a leucocytosis (29.7 x 109/L) with toxic changes. He was initially resuscitated with fluids, amoxicillin, metronidazole, gentamicin and fresh, frozen plasma, and transferred to the Starship Hospital (Figure 1).
Aggressive debridement of non-viable tissue on his back was undertaken. The resulting defect extended from the gluteal folds up to the interscapular line in both flanks. In the next 48 hours he required further debridement on two occasions, since the non-viable tissue had extended in all directions to include the ischiorectal fossae. A biopsy of normal skin was procured and dispatched to Perth for cultured skin (epithelial autograft culture). The defect was covered with cadaver skin grafts in the interim and cultured skin was used when it arrived from Perth.
Swabs taken from the affected area on admission grew Staphylococcus aureus (sensitive to flucloxacillin) and biopsy of the affected region confirmed necrosis of the fascial layer.
Baby A required total parental nutrition and naso-gastric feeding. A defunctioning colostomy was performed on Day 4 to prevent wound contamination.
Eleven days after admission, Baby A had the cadaveric skin removed, and autologous skin grafts and cultured cell suspension were placed on the defect. With ongoing wound management the skin grafts had a good take and the defect was successfully covered.
Fifty five days after admission to the Starship Hospital, Baby A had a reversal of his colostomy and on Day 62 was discharged back to the referring hospital for convalescence. Follow up two months after discharge revealed that Baby A was doing well with a completely healed wound on his back.

Figure 1. Baby A at presentation to the Starship Hospital. Debridement required removal of all the discoloured area.
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Case 2

Baby B presented seven days after birth to the Starship Hospital. She was born at term at the referring hospital with no reported problems. On Day 3 of life a pustule was noted on the back of her neck, which was pricked with a needle by the midwife. The following day Baby B represented to the referring hospital with cellulitis. Swabs were cultured and she was admitted for treatment with intravenous flucloxacillin. (Cultures later grew methicillin-resistant Staphylococcus aureus and her antibiotic was changed to vancomycin.) Her infection, however, was not controlled and on Day 7 of life she was referred to the paediatric surgical service at the Starship Hospital for incision and drainage of what was thought to be a developing abscess. Clinical findings raised the possibility of necrotising fasciitis and Baby B went for radical debridement of the area. At operation she was noted to have extensive areas of non-viable fascia and subcutaneous tissues but the muscles were viable. These areas underwent extensive debridement and samples were sent for histology and microbiology.
Baby B then required intensive care support and the following day was taken back to the operating theatre by the plastic surgical team for re-debridement and the application of cadaver skin to the defect. Histology at this time confirmed the diagnosis of necrotising fasciitis. Eight days after admission (15 days of life), Baby B was taken back to the operating theatre to remove the cadaver skin graft and place an autologous, split skin graft from her back onto the defect. Five days after the last procedure she had a change of dressing, which revealed a good take for the skin graft. Follow up suggests a good outcome with ongoing follow up planned.

Discussion

Necrotising fasciitis is a rare condition in neonates. If it is not suspected and the diagnosis is missed, it can be fatal.1,2 It is frequently attributable to secondary infection such as omphalitis, mammitis, balanitis, postoperative complications, and bullous impetigo,3,4 and may be associated with diabetes mellitus, necrotising enterocolitis, immunodeficiency and septicaemia.3,5 The most common site of involvement in paediatric patients is the abdominal wall followed by the thorax, back, scalp and extremities.3
The initial skin presentation ranges from a minimal rash to erythema, oedema, induration or cellulitis. These lesions spread rapidly. The overlying skin may later develop a violaceous discolouration, peau d’orange appearance, bullae, or necrosis.5,6 Fever and tachycardia may be present. Marked tissue oedema, rapid progression of inflammation and signs of systemic toxicity are diagnostic clues.5,6
Some authors have used ultrasonography, CT and MRI scans in the diagnosis of necrotising fasciitis showing a thickened and swollen fascial layer.7,8 However, we believe it is the clinical presentation and signs at examination, with a high index of suspicion and knowledge of necrotising fasciitis, that reveal the diagnosis.
The initial management of this condition is immediate surgical debridement, as this is the only factor that has shown a decrease in mortality. All non-viable tissue is excised until bleeding viable tissue is seen. This may require drainage of the fascial plane and extensive fasciotomies.
Other measures required in the initial management include high-dose intravenous antibiotics, aggressive fluid resuscitation and analgesia. A combination of penicillin and cephalosporins are recommended for gram-positive bacteria, aminoglycosides for gram-negative bacteria, and clindamycin or metronidazole for anaerobic bacteria.9 Clindamycin has been shown to improve survival of endotoxic shock by modulating the release of inflammatory cytokines. Hyperbaric oxygen has been reported in the literature; its use has not shown a decrease in mortality, but can be an option if anaerobic bacteria are cultured.
In a literature review of 66 neonatal patients with necrotising fasciitis, the mortality rate was noted to be 59%.3 Death usually occurred before surgery or shortly after surgical intervention as a result of bacterial infection with septic shock, disseminated intravascular coagulation and/or multiple organ failure.
Coverage and reconstruction of the defects left from this condition can be significant and complex. The services of a plastic surgical unit should be sought in association with the initial surgical management for coverage of the wound. The principles of wound management in this condition include temporary wound coverage initially, while there is ongoing infection, and then formal reconstruction of the defect once the infection has settled.
In both of the above cases cadaveric skin was used as a temporary cover for the defect.
Formal coverage is usually performed using autologous skin grafts. In rare instances coverage can be performed with tissue flaps. In small defects coverage can be obtained with sheet grafts (Baby B). However, in covering larger defects the skin requires expansion with meshing. In Baby A the meshed graft was enhanced with autologous cell culture suspension.
Cell suspension is a new technique in which autologous skin is cultured and placed in a suspension that can be sprayed onto a defect. This is used in conjunction with widely meshed skin grafts to provide coverage in patients with insufficient autologous skin to cover defects. However, the disadvantage is that it does not provide a dermal layer and therefore the cosmetic result is not as good as a sheet graft. This technique was used in Baby A as there was a large defect.
In conclusion, neonatal necrotising fasciitis is a rare but serious and often fatal condition. A high index of suspicion must be kept if the diagnosis is to be made and treatment commenced. To date, the only predictor to prognosis is the time to surgical debridement.2 It is a condition that requires the services of multiple specialties including surgery, infectious diseases, intensive care, plastic surgery, dietetics, physiotherapy and occupational therapy. Patients with these conditions should therefore be treated in centres that provide these services and early referral from peripheral hospitals to a specialist centre must be encouraged.
Author information: Stanley Loo, Surgical Registrar, Department of Paediatric Surgery, Starship Hospital; Stephen Mills, Consultant Plastic Surgeon, Department of Plastic Surgery; Michael Muller, Consultant Burn Surgeon, South Auckland Burns Service, Middlemore Hospital; Vipul Upadhyay, Consultant Paediatric Surgeon, Department of Paediatric Surgery, Starship Hospital, Auckland
Acknowledgements: We thank Mr G Bartlett and Mr P Morreau for their contributions to this paper.
Correspondence: Dr Vipul Upadhyay, Department of Paediatric Surgery, Starship Hospital, Private Bag 92024, Auckland. Fax: (09) 307 8952; email: vipulu@adhb.govt.nz
References:
  1. Rietveld JA, Pilmore HL, Jones PG, et al. Necrotising fasciitis: a single centre’s experience. NZ Med J 1995;108:72–4.
  2. Bilton BD, Zibari GB, McMillan RW, et al. Aggressive surgical management of necrotizing fasciitis serves to decrease mortality: a retrospective study. Am Surg 1998;64:397–400.
  3. Hsieh WS, Yang PH, Chao HC, Lai JY. Neonatal necrotizing fasciitis: a report of three cases and review of the literature. Pediatrics 1999;103:e53.
  4. Bliss DP Jr, Healey PJ, Waldhausen JH. Necrotising fasciitis after Plastibell circumcision. J Pediatr 1997;131:459–62.
  5. Hung CC, Chang SC, Lin SF, et al. Clinical manifestations, microbiology and prognosis of 42 patients with necrotising fasciitis. J Formos Med Assoc 1996;95:917–22.
  6. Moss RL, Musemeche CA, Kosloske AM. Necrotising fasciitis in children: prompt recognition and aggressive therapy improve survival. J Pediatr Surg 1996;31:1142–6.
  7. Becker M, Zbaren P, Hermans R, et al. Necrotizing fasciitis of the head and neck: role of CT in diagnosis and management. Radiology 1997;202:471–6.
  8. Chao HC, Kong MS, Lin TY. Diagnosis of necrotizing fasciitis in children. J Ultrasound Med 1999;18:277–81.
  9. Brook I. Microbiology of necrotizing fasciitis associated with omphaitis in the newborn infant. J Perinatol 1998;18:28–30.


     
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