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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 1Baby 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.
![]() Case 2Baby 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.
DiscussionNecrotising 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:
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