CF
Maceachern, MS Patton, TW Dougall
Department
of Orthopaedic Surgery, Royal Aberdeen Children’s Hospital, Westburn
Correspondence
to:
Mr
M.S. Patton, Department of Orthopaedic Surgery, Royal Aberdeen Children’s
Email: ort085@abdn.ac.uk
SMJ 2008 53(2): 65
Abstract
A
previously fit and well child attended accident and emergency with increasing
pain in his left lower leg after sustaining a laceration to the pre-tibial
border of his left leg at a local swimming pool 2 months previously. X-rays at
time of presentation showed the formation of a Brodie’s abscess. Following
incision, debridement and drainage, samples sent to the laboratory confirmed
histological features consistent with sub-acute osteomyelitis. Microscopy and
Cultures demonstrated Methacillin Resistant Staphylococcus aureus (MRSA) of a
type seen in community acquired infection. Based on this report we would
advocate MRSA being considered as a possible causative organism in acute or
sub-acute osteomyelitis even in an otherwise healthy child with no prior
hospital exposure.
Case
Report
A
7 year old boy presented to accident and emergency with several weeks of
increasing pain above his left ankle, exacerbated by weight bearing. He was
systemically well except for a low grade pyrexia. The affected area was swollen,
warm to touch, but not erythematous. There was acute tenderness over the distal
tibia but no significant restriction in ankle or foot movement.
Approximately
2 months previously, this child had sustained a laceration to the pre-tibial
border of his left leg at a local swimming pool when he fell on a broken tile.
At that time, the wound had been cleaned and dressed and had healed
uneventfully. Radiographs had failed to demonstrate any underlying bony injury
(Figure 1).
Figure 1: Antero-posterior and lateral radiographs of the left leg and
ankle, following initial laceration. No
bony abnormality detected.
On this presentation, the C-Reactive Protein level was 62mg/l (normal <10mg/l) and the Erythrocyte Sedimentation Rate 32mm/hour. A Full Blood Count was normal. Radiographs demonstrated a well circumscribed, centrally placed, solitary, metaphyseal, lytic lesion with a sclerotic margin in the distal tibial metaphysis. The clinical and radiographic features were typical of a sub-acute osteomyelitis of the tibia (Brodie’s abscess) (Figure 2).
Figure 2: Antero-posterior and lateral radiographs of the left leg and ankle, following representation with pain and swelling. Radiographs demonstrate a solitary lytic lesion in the distal tibial metaphysis. Appearances are those of a Brodie’s abscess.
The
bony abscess was de-roofed, curetted and irrigated under a general anaesthesia
and the cavity packed with gentamicin impregnated collagen sponge. Samples sent
to the laboratory confirmed histological features consistent with subacute
osteomylitis. Microscopy and
Cultures demonstrated Methacillin Resistant Staphylococcus aureus (MRSA) of a
type seen in community acquired infection.
The
child was treated with intravenous Vancomycin for 2 weeks and his inflammatory
indexes rapidly returned to normal. The patient developed a rash when switched
to oral Clindamycin and so was subsequently treated with oral Trimethoprim and
Rifampicin at home for a further 6 weeks. At
3 months review, the child was asymptomatic and had returned to normal
activities. Inflammatory indexes were within the normal range and tibial
radiographs suggested gradual obliteration of the metaphyseal cavity.
Discussion
Cases
of acute haematogenous osteomyelitis are now unusual with the annual incidence
reported as 2.9 / 100,000 child population per year in Scotland1. In
80-90% of culture positive cases the causative organism is Staphylococcal aureus.
The remaining 10-20% are accounted for by group A and B streptococcus,
Streptococcus pneumoniae and Pseudomonas aeruginosa (particularly in the foot).
Since childhood immunisation against Haemophylus influenzae type B (HiB) has
become widespread in the UK, this organism very rarely causes infection.
Occasionally other gram-negative organisms are implicated in the neonate4.
Traditionally
MRSA was not considered in the differential diagnosis of causative organisms in
cases of acute, non-hospital acquired, bone infection. Prior to this report
there have been no documented cases of community acquired MRSA (CA-MRSA) leading
to sub-acute osteomyelitis in the UK. However, in Australia, 9% of acute
haematogenous osteomyelitis cases are now due to CA-MRSA infection2 while,
in New Zealand the same organism causes
almost 20% of cases of musculoskeletal infections3. It
is clear that globally, MRSA, must be considered as a possible
pathogen in any bony infection even if the patient has not experienced prior
hospital contact. Furthermore, there has been recent concern about the
cleanliness of public leisure facilities with particular focus on swimming and
spa pools. This was highlighted in 2001 by the British media who reported the
death of a 14 year old boy who contracted MRSA osteomyelitis from an abrasion
sustained to his foot whilst swimming5. Subsequent investigations
have revealed widespread colonisation by MRSA in public buildings.
The
standard treatment of acute osteomyelitis relies on the appropriate use of
antimicrobial therapy alone, with only 20-35% of cases requiring surgical
drainage1,2. Whilst the British Society for Children’s Orthopaedic
Surgery do not advocate routine exploration of an osteomyelitic focus, they
state that surgery is indicated when there is
clinical or radiographical suspicion of a collection of pus, or where
there is a poor response to antibiotic therapy6. The majority of
patients receive initial empirical antibiotic therapy based on the likely
causative organism.
Based
on this report we would advocate MRSA being considered as a possible causative
organism in acute or subacute osteomyelitis even in an otherwise healthy child.
Failure to respond rapidly to standard initial antibiotic therapy should lead to
surgical exploration, tissue culture and the inclusion of an anti-MRSA agent,
such as vancomycin in the therapeutic regime, until full antibiotic
sensitivities are available. As always, advice from an experienced clinical
microbiologist with a musculoskeletal interest is invaluable.
References
[1]
Blyth MJ, Kincaid R, Craigen MA, Bennet GC.
The changing epidemiology of acute and subacute
haematogenous osteomyelitis in children. J Bone Joint
Surg Br 2001;83-B(1):99-102
[2]
Goergens ED, McEvoy A, Watson M, Barrett IR. Acute
osteomyelitis
and septic
arthritis
in children.
Journal of Paediatrics & Child Health
2005;41(1-2):59-62
[3]
Gwynne-Jones
DP, Stott NS. Community-acquired methicillin-resistant
Staphylococcus aureus: a cause of musculoskeletal sepsis in children. Journal
of Pediatric Orthopedics 1999;19(3):413-6
[4]
Steer AC, Carapetis JR. Acute haematogenous osteomyelitis in children:
Recognition and management. Paediatric Drugs 2004;6(6):333-346
[5]
Superbug killed boy. BBC News 12 December, 2001: http://news.bbc.co.uk/1/hi/england/1706247.stm
[6] The Management of Acute Bone and Joint Infection in Childhood: A Guide to Good Practice. British Society for Children’s Orthopaedic’s Surgery. September 2004