Acute haematogenous osteomyelitis in children
BMJ 2014; 348 doi: https://doi.org/10.1136/bmj.g66 (Published 20 January 2014) Cite this as: BMJ 2014;348:g66
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Thank you for the two rapid comments pointing out a small error in our article. Haemophilus influenza is not sensitive to benzylpenicillin and should be treated instead by cefuroxime or a similar cephalosporin. We apologise for this oversight and will ensure the article is corrected.
Competing interests: No competing interests
A small error crept into this useful review of ostemyelitis in children. Haemophilus influenzae would not be treated with benzylpenicillin and some of the first generation cephalosporins have poor activity against this organism. I suspect this error arose from a misreading of the BOA Blue Book (reference 15) which suggests these antibiotics for the treatment of Kingella kingae infections in their Table 1.
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As a children's orthopaedic specialist, I found this article targeted at a general readership both informative and stimulating. Greater awareness of this easily missed but treatable pathology is much to be desired . However, there is one important factual error in the text which is of practical importance and needs correction.
As the authors suggest, Haemophilus influenza is now a rare cause of osteomylitis in the UK but it must not be forgotten in non immunised children. But, being a Gram negative organism it is not sensitive to Benzylpenicillin and the addition of this antibiotic to cover the organism (as the authors suggest) would be ineffectual.
The cited reference to the BSCOS guidelines is inaccurate. These correctly state Cefuroxime or a similar cephalosporin not Benzylpenicillin should be prescribed when Haemophilis is a possibility.
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Re: Acute haematogenous osteomyelitis in children
Andrea Yeo and Manoj Ramachandran’s informative article (25 Jan) quite correctly stresses “a high index of suspicion” as being “essential for a good outcome” in patient management [1]. Nowhere is this advice more important than in African children where a hot swollen limb or a Brodie’s abscess or a pathological fracture in a child calls for a presumptive clinical diagnosis of Haemoglobinopathy with Salmonella osteomyelitis. Association of enteric fever and its complications with sickle cell disease goes back farther than the “Medline and Google” cut off points of 20 years that the authors used [1], because 80 years ago Lemuel Diggs and R E Ching observed these associations [2]. And when 49 years ago we described from Ghana “skeletal crumbling in sickle cell anaemia complicated by Salmonella typhi infection” [3] our list of cited associations in the literature was not short.
DATA FROM CONSECUTIVE SICKLE CELL DISEASE PATIENTS
Yeo and Ramachandran’s data from cohort studies is helpful but a great deal can be learnt from consecutive sickle cell disease patients living in an unhealthy “microbial mileu”. Of 597 consecutive sickle cell anaemia “SS” phenotype patients seen at the Korlle-Bu Hospital in Accra, 31 (5.2%) had osteomyelitis, while of 606 consecutive sickle cell haemoglobin C disease “SC” phenotype patients 27 ie 4.5% developed osteomyelitis. Other sickle cell disease phenotypes with osteomyelitis were sickle cell beta-Thalassaemia (5 patients), sickle cell Hereditary Foetal Haemoglobin disease “SF” (1 patient), and 1 patient with sickle cell Haemoglobin Korle-Bu “SKorle-Bu” phenotype [4 5]. In this last case osteomyelitis did not arise de novo “but as the result of a shrapnel wound acquired when a bomb exploded” [4, page 248]. There is no statistical difference between incidence of osteomyelitis in the different sickle cell disease phenotypes at the Korle-Bu Hospital Sickle Cell Clinic.
HOW WE MANAGED AFRICAN PATIENTS WITH OSTEOMYELITIS
As 1 in 6 Ghanaian males have G6PD Deficiency [6-8] and its effect on the sickle cell disease patient is hazardous [4 8], and as our best therapeutic agent for salmonella was Chloramphenicol, a drug that caused haemolysis in G6PD Deficiency [9] we used it with great care. Adequate hydration of the patient made the difference between quick improvement and an ominous outcome. Whole blood transfusion was avoided, preferring the bedside partial exchange transfusion by the method I described which any doctor (or indeed nurses) could perform [4, pages 416-417]. A surgeon was always alerted on “Day 1” to stand by for bone curetting as needed.
It can hardly be stressed sufficiently that acute osteomyelitis can be both the cause and the sequel of sickle cell crisis not only in different patients, but also in the same patient at different times. Astute clinical judgment is called for to anticipate both outcomes whose cardinal feature is excruciating pain. Management of pain considered appropriate for others is harmful for sickle cell disease patients. Morphine or Diamorphine was never prescribed for sickle cell disease pain in Ghana, as is the case in the UK with NICE–approved Protocols which I have not ceased to criticize [10-15]. “Pain was adequately controlled but the patient died from the chest syndrome of sickle cell crisis” was not an uncommon lament in the UK [11], as the NCEPOD REPORT of 2008 also laid bare [16].
PROGNOSIS IS GOOD EVEN IN SICKLE CELL DISEASE PATIENT
The prognosis is good if, as advised above, there is a high index of suspicion: Black child with hot swollen tender limb? Then suspect sickle cell disease unless otherwise proven, and culture for Salmonella typhi same time as electrophoresis and G6PD quantification tests are requested, remembering that the raised reticulocytosis in the haemoglobinopathic patient can mask the enzyme deficiency. With prompt action on the lines indicated above, the children we described in 1965 made a remarkable recovery and the shattered bones healed completely, demonstrated by X-rays [3]. Inefficient management can lead to chronic osteomyelitis with limb deformities.
Conflict of Interest: None declared
Felix I D Konotey-Ahulu MD(Lond) FRCP(Lond) FRCP(Glasg) DTMH(L’pool) FGA FGCP FWACP FTWAS - Kwegyir Aggrey Distinguished Professor of Human Genetics, University of Cape Coast, Ghana and Consultant Physician Genetic Counsellor in Sickle Cell and Other Haemoglobinopathies, 9 Harley Street, Phoenix Hospital Group, London W1G 9AL
Email: www,konotey-ahulu.com
1 Yeo Andrea, Ramachandran Manoj. Acute haematogenous osteomyelitis in children. BMJ 2014; 348: g66 & doi:10.1136/bmj.g66
2 Diggs LW, Ching RE. Pathology of sickle cell anemia. Southern Medical Journal 1934; 27: 839-845.
3 Konotey-Ahulu FID, Kuma Eunice. Skeletal crumbling in sickle cell anaemia complicated by Salmonella Typhi infection. British Journal of Clinical Practice 1965; 19: 575-578.
4 Konotey-Ahulu FID. The Sickle Cell Disease Patient. Natural History from a clinico-epidemiological study of the first 1550 patients of Korle-Bu Hospital Sickle Cell Clinic. The Macmillan Press Ltd, London and Basingstoke 1991, 1992 and T-A’D Company, Watford 1996 [www.chaplinmultimedia.co.uk]
5 Konotey-Ahulu FID, Gallo E, Lehmann H, Ringelhann Bela. Haemoglobin Korle- Bu (alpha 2, beta 2, 73 Aspartic acid Asparagine), showing one of the two amino acid substitutions of Haemoglobin C Harlem. J Med Genetics 1968; 5: 107-111.
6 Ringelhann Bela, Dodu SRA, Konotey-Ahulu FID, Lehmann H. A survey for haemoglobin variants, thalassaemia, and Glucose-6 Phosphate Dehydrogenase Deficiency in Northern Ghana. Ghana Medical Journal 1968; 7: 120-124.
7 Owusu SK. Absence of glucose-6 phosphate dehydrogenase in red cells of an African. BMJ 1972; 4: 25-26.
8 Acquaye CTA, Gbedemah KA, Konotey-Ahulu FID. Glucose-6 phosphate dehydrogenase deficiency in sickle cell disease patients in Accra. Ghana Med J 1977; 16: 4-9.
9 Luzzatto L. G6PD deficiency frequency and sickle cell anaemia association on the African continent. INSERM 1975; 44: 229
10 Konotey-Ahulu FID. Morphine for painful crises in sickle cell disease. BMJ 1991; 302: 1604 www.bmj.com/cgi/reprint/302/6792/1604-c.pdf
11 Konotey-Ahulu FID. Opiates in sickle cell crisis? Lancet 1998; 351: 1438
12 Konotey-Ahulu FID. Opiates for sickle cell crisis. Lancet 1998; 352: 651-652
13 Konotey-Ahulu FID. Opiates for pain in dying patients and in those with sickle cell disease. www.bmj.com/cgi/eletters/335/7622/685#177986 BMJ 11 Oct 2007 Rapid Response
14 Konotey-Ahulu FID. Poor care for sickle cell disease patients: This wake-up call is overdue. BMJ Rapid Response May 28 2008 336: 1152 to Susan Mayor “Enquiry shows poor care for patients with sickle cell disease” 2008 on National Confidential Enquiry into Patient Outcome and Death (NCEPOD) REPORT “SICKLE: A Sickle Crisis?” www.bmj.com/cgi/eletters/336/7654/1152a#196224 [
15 Konotey-Ahulu FID. Inquest into diamorphine deaths: Does NCEPOD sickle patients report warrant a similar inquest? BMJ Rapid Response March 25 2009
www.bmj.com/cgi/eletters/338/mar03_3/b903#210208
16 NCEPOD (National Confidential Enquiry into Patient Outcome and Death) Report 2008. SICKLE: A Sickle Crisis? www.info@ncepod.org “Nine out of the 19 patients with sickle cell disease who had pain on admission and who then died had been given excessive doses of opiods” Susan Mayor BMJ 2008; 336: 1152.
Competing interests: No competing interests