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ACUTE OSTEOMYELITIS IN CHILDREN


IDENTIFICATION DATA
Name

Letchumi a/p Paranthaman

Age

1 years old

Sex

Female

R/N

14356/00

This patient is a 1 years old Indian child who was admitted with history of
left thigh pain and swelling for about a week prior to admission. The swelling was
slowly enlarging and very painful. The child refused to walk. There was no history of
trauma; she had a low-grade fever and cough and had been treated by her GP with
paracetamol and antibiotics.
Clinically she was febrile, irritable and slightly dehydrated. The left hip
revealed a diffused swelling, tender and warm. All movements of the left hip and knee
were limited and painful.
Initial blood investigation shown erythrocyte sedimentation rate was
121mm/hr., total white blood cells count was 23000/ mm and hemoglobin level was
10.8 gm%. The blood culture and sensitivity was negative. The plain radiograph
showed extensive lytic lesion over the metaphyseal part of the upper end of the left
femur. There was no obvious soft tissue swelling. There were no other lesions noted
on her left acetabulum. Ultrasound of her left hip showed no evidence of fluid
collection.
A diagnosis of acute osteomyelitis of the left femur was made. Incision and
drainage was done and revealed necrotic tissues with minimal pus collection around
the femur. The tissue was sending for culture and sensitivity .The culture result
showed Staphylococcus aureus.

MANAGEMENT
Intravenous fluid resuscitation was started. Intravenous broad spectrum antibiotic
(cefobid) was given. The antibiotic was continued after the culture tissues result were
available because the organism was sensitive to cefobid and her condition improved.
The intravenous antibiotic was continued for another two weeks followed by four
weeks of oral intake.
DISCUSSION
Osteomyelitis is an infectious process of the bone and its marrow and the term
osteomyelitis is normally refers to infections caused by pyogenic microorganisms but
can be used for granulomatous infections such as tuberculosis, syphilis, viral and
fungal infections (Aprin, 1998). The diagnosis and treatment of osteomyelitis
continue to be a problem. Early diagnosis with prompt and adequate treatment is
essential to reduces the risk of permanent damage and recurrence. Although now day
the mortality of osteomyelitis is relatively rare but the morbidity is still common
despite modern antibiotic and surgical treatment.
Osteomyelitis has commonly been classified based on duration of symptoms,
the mechanism of infection and the type of host response to the infection.
Osteomyelitis has been classified as acute, subacute or chronic, exogenous (cause by
trauma, surgery) or hematogenous, and pyogenic or non pyogenic (Warner, 1991).
Acute hematogenous osteomyelitis is the common type of bone infection and
it is the most common in children. Bacteremia is not necessarily the only etiologic
factor although bacteremia is an almost daily event in childhood, and other etiologic
factors such as a localised trauma or debilitation from chronic illness, malnutrition or
inadequacy of the immune system must be present for the infection to develop
(Morrissy, 1989 and Warner, 1991). Sometimes the exact cause for osteomyelitis
cannot be found.

PATHOPHYSIOLOGY
Organisms
Staphylococcus aureus is still the organism responsible for about 50% to 80%
of all such infections in children between one month to five years of age (Aprin,
1988). The second most common are both group A and group B streptococci and in
neonates Haemophilus influenza is an occasional cause that is often associated with
meningitis. There are increasing numbers of gram negative organism causing
osteomyelitis especially in drug addicts. Salmonella osteomyelitis has long been
associated with hemoglobinopathies (Warner, 1991). The other rare organisms such as
Candida albicans can be cultured in patients with diabetes, immunosuppressed
patients with long term antibiotic therapy and premature infants (Akbar Bonakdarpour, 1983).
Pathology
Osteomyelitis is most common in the long bone, but neonate multiple sites of
infection are relatively common. Metaphysis is a rapid growing area of the long bone
in children and the most frequently site of involvement. The vascular architecture of
the metaphysis where the nutrient capillaries form sharp loops and terminate as end
vessel predispose to infection following bacteremia. In children more than two years
old, the growth plate acts as a barrier that prevents the metaphyseal abscess from
extending directly into the epiphysis, but in children less than two years, some vessels
cross the growth plate and may allow the spread of infection into the epiphysis and
joint.
The infections causes an inflammatory reaction, local ischemic necrosis of the
bone marrow and subsequently abscess formation. As the abscess increased in size,
increases local intramedullary pressure impaired capillary circulation and this causes
more bone to become ischemic. The purulent material passes through the cortex into
the subperiosteal space and form a subperiosteal abscess and later the periosteum may

rupture and pus escapes into the adjacent tissues. Damage to the metaphyseal blood
supply, cause by the release of the bacterial toxins and stripping of the periosteum
cause the portions of the bone to become necrotic. The dead bones, which are
separated from the surrounding viable bone by granulation tissue, are call sequestra
and the periosteal responses are to lay down new bone called the involucrum.
Inadequate treatment results in extensive sequestration of the bone and chronic
osteomyelitis.
CLINICAL FEATURES
The clinical diagnosis of osteomyelitis is difficult especially in the early stages
of the disease (Abiri, 1989) due to wide variation of clinical presentation. The
variation in clinical presentation may be due to interaction of the virulence of the
infecting organism, local environment, age of the patient and resistance of the host
(Wedge, 1988). The classical clinical picture is a short history of pain, swelling,
redness, high fever and impaired function of the infected limb. In infant sometime the
only early manifestation may be failure to thrive. The impaired systemic response to
the sepsis may allow the infant to remain apyrexic and normal white cells count
although the ESR is elevated. But usually the infant is septicemic and very ill, and
very difficult to exclude from other common causes of illness such as meningitis or
pneumonia until a large soft tissue abscess is apparent (Apin, 1988). There is frequent
association with minor trauma and the child may be given analgesic and antibiotics
that mask the systemic signs.
INVESTIGATIONS
Haematology
The white blood cell is raised and the differential shifted to the left, which
generally shows a neutrophil leucocytosis, and sometime mild anemia may be present
(Nade, 1993). The erythrocyte sendimentation rate (ESR) may be normal within the

first 48 hours but then raises rapidly and may exceed 100mm/hr and remains elevated
for weeks. Its gradual decline is an indication of a successful response to treatment
(Aprin. 1988).
OBrian, 1982 however found that elevation of temperature, increased ESR
and raised peripheral white cell count are not specific to osteomyelitis and have little
value in arriving to the diagnosis. These findings are more useful in monitoring the
progress of the disease. C-Reactive protein (CRP ) have been found to be more
sensitive than ESR and WBC in monitoring the progress and respond of the disease
towards therapy.(Kallio,1994).CRP are found to increase and decrease more rapidly as
compared to ESR, thus more sensitive in monitoring the therapy and early detection
of complications.
Blood culture and serology
Blood culture is positive in about 50% to 75% of cases. A positive blood
culture can be obtained in 24 hours, but more time is required for determining specific
antibiotic sensitivity.
Bone aspiration can be done to establishing an accurate bacteriological
diagnosis. A negative aspiration should not rule out the diagnosis. Fine needle bone
biopsy (FNBB) has 87% sensitivity and 93% specificity. It accuracy is increased if it
is done under ultrasound guidance. Interpretation of the results of the biopsy should
be done cautiosly and it is not adiagnostic tool. It is however useful in addition to
clinical findings and radiological evidence to arrive into the diagnosis of osteomyelitis
especially in difficult cases (Howard et al , 1994).
Immunological study for detection of antibodies to the teichoic acid cell wall
of Staph. aureus may be helpful for detecting Staphylococcal osteomyelitis. The test is
more sensitive in acute (82%) than in chronic (43%) osteomyelitis. The cell wall of
Staphylococcus aureus has three components, peptidoglycan, teichoic acid and protein

A and the teichoic acid is the major component. The detection and quantification of
teichoic acid antibodies is of great value for early diagnosis of patients with acute
osteomyelitis caused by Staphylococcus aureus and for assessing the clinical response
of patients (Tauzon, 1982). In children younger than three years, H.influenzae type b
is the one of the causes of osteomyelitis and urine should be checked for H.influenzae
type b capsule antigen (Faden and Grossi, 1991).
Radiology
X-ray may show soft tissue swelling, but skeletal changes, such as localized
destruction of bone or periosteal reaction, are not seen for at least 10 to 12 days
(Warner, 1991). Alterations in radiographic density cannot be detected until there is a
decrease of 35 to 50% in bone mineral content (Akbar Bonakdar-pour, 1983).
Radiological diagnosis may be made on the basis of three signs which usually evolve
in the following order (Patton, 1988):1.

Soft tissue swelling with poor definition of local fat plains.

2.

Periosteal new bone formation

3.

Focal bone radiolucency

Bone scan
Technetium-99m bone scan can confirm the diagnosis as early as 24 hours to
49 hours after onset in 90% to 95% of patients (Warner, 1991). Technetium 99mlabelled methylene disphosphonate (99m-Tc-MDP) can be used to differentiate
osteomyelitis from overlying soft tissue lesions. The three phase bone scan shows
well defined increase in uptake in the bone on both the blood pool and the delayed
scan.
The blood pool phase (phase 2) shows the relative vascularity of the area,
whereas the delayed image phase (phase 3) obtained 3 to 4 hour after injection reflects

increased uptake in the skeleton. By contrast with the well defined bone uptake seen
in osteomyelitis, there is rather diffuse uptake in cellulitis and septic arthritis.
Gallium-67-labelled scans and indium-111-labeled leukocyte scans may also be useful
in conjunction with the technetium-99m. Gallium citrate accumulated locally with
white cells has high sensitivity to infectious inflammatory precess but variable and
unpredictable sensitivity to other inflammatory condition and if used 48 hours after
technetium will show both isotopes accumulated in the same region of bone highly
suggestive of infection. The accuracy is 62%. The problem with indium-labeled
leukocyte was the time length to prepare the white cell from the sample of the patient
blood and this is not appropriate in a sick patient. This technique is more accurate and
easier to interpret than Tc-Ga scanning with a reported sensitivity of 83%, specificity
of 86% and accuracy of 83% (April, 1988 and Scoles, 1980). Confirmatory bone scan
should not be necessary if the diagnosis is clinically obvious and under no
circumstances should appropriate treatment be delayed while awaiting such a test.
Bone scan should be reserved in difficult site of involvement, eg, pelvis ,
shoulder or foot. False positive are due to contagious soft tissue infection with
secondary hyperaemia of the surrounding bone (Charles, 1980). Israel, 1987
differiantiate this finding by comparing the ratio of uptake at 24 hours to 4 hours at
the hyperaemic bone. In infected bone, the uptake would last longer than 24 hours.
False negative can be due to previous antibiotic treatment or transition period from
the cold to the hot phase.
Predictive value of cold scan is higher (100%) as compared to hot scan (82%)
in acute osteomyelitis (Tuson and Hoffman, 1994). Cold scan are due to local
ischaemia due to increased intraosseous and subperiosteal pressure. Patient with
clinical findings of osteomyelitis with positive cold scan can safely be diagnosed as
osteomyelitis. Osteomyelitis in bone scan shows uneven distribution of uptake in the
joint with extensive and asymmetrical involvement beyond the joint. Cold scan
indicate severe infection and also associates with severe systemic presentation (Scott
et al, 1990). High positive results bone aspiration from cold spot as compared to the

hot spots on the bone scan (Pennington et al, 1999). Cold scan however can present in
leukamia, metastatic bone disease, avascular necrosis or sickle cell disease.
Ultrasound
The early clinical signs may be minimal, non-specific and difficult to elicit in
an uncooperative child. The primary lesion of osteomyelitis is within the bone, but the
surrounding soft tissues are very soon involved. Ultrasound cannot penetrate dense
bone but it can show early changes in the tissues.
In children with osteomyelitis there were characteristic ultrasound findings
(Howard, 1993): 1.

thickening of the periosteum, with hypo echogenic zones both superficial


and deep to it, giving the appearance of a sandwich.

2.

elevation of the periosteum by more than 2mm ; in severe cases there


were both echoless and moderately echogenic zones between the
periosteum and the cortex

3.

swelling of the overlying muscle or subcutaneous tissue, maximal


nearest to the bone

Magnetic Resonance Imaging (MRI)


In the early stage of osteomyelitis the MRI will show intraosseous and
extraosseous changes. These changes are evident before any that may be seen on
routine x-ray films (Aprin, 1988). In osteomyelitis, the typical finding is a low signal
on T1 images and high intensity signal in T2 images. These findings are due to
increased water content in the marrow due to oedema, hyperaemia and purulent
exudative characteristics of osteomyelitis (Tachdjian, 1990).

TREATMENT

Surgery or antibiotic treatment for acute hematogenous osteomyelitis is


complimentary, in some patients antibiotic alone will cure the disease but in others
prolonged antibiotic alone is doomed to failure without surgical treatment (Warner,
1991).
Nade (1983) proposed the following five principles for treatment of
osteomyelitis: 1.

an appropriate antibiotic will be effective before the pus formation.

2.

antibiotic will not sterilize avascular tissues and purulent material that
must be removed surgically.

3.

if such removal is effective, then antibiotics should prevent their


reformation primary wound closure should be safe.

4.

surgery should not further damage already damage bone, pus removal
allows restoration of continuity between periosteum and cortex and
restores blood flow.

5.

antibiotics should be continued after surgery.

It is reasonable to start the treatment with a combination of antibiotics active


against Staph. aureus and also beta-hemolytic Steptococcus. When the organism is
identified and antibiotic sensitivity is determined, treatment can be continued with a
single appropriate drug (Cole, 1982 and Scoles, 1984). The combination of cloxacillin
and penicillin has been recommended by several authorities (Nade, 1883 and Cole,
1982) and others advocated a combination of sodium fusidate and erythromycin.
Sodium fusidate and erythromycin are drugs of low toxicity, show synergism and
broaden the range of antibiotic coverage (for instance, to include Haemophilus)
(Nade, 1983).
The duration of the antibiotic therapy is controversial. The current trend is
toward a short course intravenous antibiotics, followed by oral antibiotic and
monitoring of serum antibiotic levels. Trueta (1968) recommended prolonged

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antibiotic treatment of patients with acute osteomyelitis, for example, six weeks of
full dosage because inadequate duration of treatment appears to be empirical by some
authors, they recommended that after 10 days it would be reasonable to discontinue
antibiotic therapy if the clinical signs had subsided, the ESR was normal or falling,
and a radiograph showed only local osteoporosis without erosion of the cortex or new
bone formation (Nade, 1983). In general, four to six week of effective antimicrobial
therapy is required for successful treatment of childhood osteomyelitis.
Oral therapy may be used if the following criteria are met (Scoles, 1984):
1.

clinical response to parenteral antibiotic therapy

2.

isolation of a bacterial pathogen that is susceptible to orally


administrated antibiotics.

3.

patient tolerance of an orally administered agent

4.

adequate serum bactericidal activity on oral therapy (peak serum


bactericidal titer greater than 1: 8, trough titer greater than 1:2).

5.

ensurance of patient compliance with drug therapy, usually by


hospitalization

In the early stage of disease, successful response to the treatment is seen


within 24 to 36 hours, with a dramatic fall in temperature and improvement in the
local signs. The white blood cell count falls rapidly provided these is no abscess. The
ESR will probably decline slowly, and return of function in the infected limb is a good
sign of positive response.
Conservative treatment with antibiotics has equeal results with surgical
treatment in subacute osteomyelitis with benign radiological findings. Surgery withy
open surgical debridement should be reserved in patients who do not respond to
antibiotics or radiological features of an aggressive disease or malignant tumour
(Reggie et al, 1996).

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During treatment the affected limb is immobilized to diminish pain,


occasionally some form of the skin traction is required. Protective splintage is
continued in the upper limb until antibiotic therapy is terminated.
Failure to response to treatment after 36 hours probably means that pus is
present in the metaphysis and possibly in the subperiosteal region. Surgical drainage
of any intramedullary or subperiosteum abscess is required in these patients without
further delay.
Two main indications for surgery in the acute hemtogenous osteomyelitis are
(Warner, 1991): 1.

the presence of an abscess requiring drainage.

2.

failure of the patient to improve despite appropriate intravenous


antibiotic treatment.

The bone is exposed at the side of maximum tenderness and swelling, and the
periosteum is incised longitudinally. Pus is evacuated and specimens are obtained for
a gram stain, cultures and tests for antibiotic sensitivity. The objective of the surgery
is to drain any abscess cavity and remove all dead or necrotic material, and if a
subperiosteal abscess is found, several small holes should be drilled through the
cortex into medullary canal. If intramedullary pus is found, then a small window of
bone is removed, the pus is drained, and the necrotic tissue is gently removed
(Warner, 1991). Some authors do not recommend drilling the cortex to explore the
metaphysis in view that pus under pressure is rarely found inside the medulla (Cole,
1982).
They believe that the concept of decompressing the medulla and improving
the blood flow is unlikely to be of much benefit since bone death has already occurred
in the presence of a large subperiosteal abscess. It is, however, worthwhile drilling
any obviously soft tissue areas in the cortex (Aprin, 1988)

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The wound may be loosely closed but provision made for free drainage
through appropriate surgical drains. The value of closed suction drainage with
continous intramedullary irrigation remains to be proved (Aprin, 1988).
PROGNOSIS AND COMPLICATION
Acute hematogenous osteomyelitis is curable provided there is early diagnosis
and prompt treatment with the correct antibiotic for the correct period of time (April,
1988).
The chance of cure is directly related to the following five factors (Nade,
1983): 1.

the virulence of the organism causing the infection, and the resistance of
the host to the spread of the infection.

2.

the choice of the antibiotics used initially these should be the


bactericidal antibiotics most appropriate in treating staphylococcal
infections, given parenterally in adequate dosage.

3.

the site of infection.

4.

the duration of treatment with antibiotics.

5.

a short interval between onset of symptoms and institution of correct


therapy.

Cold spot on bone scan in children with a painful, inflammed limb gives a
poorer prognosis because of the more aggressive nature of infection it associates with
(Pennigton et al ,1999).
Cole and co-workers observed that the prognosis for cure is much worse in
patients diagnosed late (25%) than in patients diagnosed early, in whom the cure rate
was 92% in their series (Cole, 1982). The risk of recurrence is below 4% after one
year following treatment (Gillespie, 1981). Involvement of an adjacent joint is
common in neonate because of the anatomy of the vasculature of this age group and
the intracapsular position of the physis. This causes irreversible damage to the physis

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and joint. Damaged to the physis can result in overgrowth or growth retardation
leading to the leg length discrepancy and angular deformity (Aprin, 1988).
Pathological fracture may be caused by resorption of bone either in the acute
phase or following surgery and decompression by drill holes through the cortex.
Preventive splint or cast for an appropriate period of 2 to 3 months is indicated.
REFERENCES
1.

Abiri MM., Kirpekar M. and Ablow RC. : Osteomyelitis : Detection with


US. Radiology (1989), 172: 509-511

2.

Akbar Bonakdar-pour and Gaines VD. : The radiology of osteomyelitis.


Clin. Orthop. (1983), 14: 21

3.

Aprin H. and Dee R. : Bone and joint infections. Principles of Orthopaedic


Practice. McGraw-Hill Book Co. (1988), Chap 22: 294-316

4.

Cole WD., Dalziel RE. and Leitl S.: Treatment of acute osteomyelitis in
children. J.Bone and Joint Surg. (1982), 64B: 218-223

5.

Gillespie WJ. and Mayo KM. : The management of acute haematogenous


osteomyelitis in the antibiotics era: A study of outcome. J.Bone and Joint Surg.
(1981), 63B: 126-131

6.

Howard C.B , Einhorn M,Dagan R,Yagupski P : Fine neddle bone biopsy to


diagnose osteomyelitis. J Bone Joint Surg 1994,76 B:311-4.

7.

Faden H. and Grossi M. : Acute osteomyelitis in children. Reassessment of


the etiologic agents and their clinical characteristics. Am. J. Dis. Child. (1991),
145: 65-69

14

8.

Howard CB., Einhorn E., Dagan R. and Nyska M. : Ultrasound in


diagnosis and management of acute haemogenous osteomylitis in children.
J.Bone and Joint Surg. (1993), 75B: 79-82

9.

Kallio L.U, Kallio M.J.T, Eskola J : Serum Creactive protein,Erythrocyte


Sedimentation Rate and White Blood Cell Count in Acute Haemetogenous
Osteomyelitis of children.Paediatric 93:59-62,1994.

10.

Morrissy RT. And Haynes Dw. : Acute hematogenous osteomyelitis : A


model with trauma as an etiology. J.Pediatric Orthop. (1989), 9: 447-456

11.

Nade S.: Acute haematogenous osteomyelitis in infancy and childhood. J.


Bone and Joint Surg. (1983), 65B: 109-119

12.

OBrian T , Mc Manus F , Mac Auley PH :

Acute haematogenous

osteomyelitis.J Bone Joint Surg 1982 ;64-B:109-19.


13.

Ogden JA : Changing patterns of proximal femoral vascularity .J Bone Joint


Surg 1974:56:941-50

14.

Patton JT.: Osteomyelitis : Radiological evaluation. Current Orthop. (1988),


2. : 69-75

15.

Pennington W.T, Mott M.P, Thometz J.G, Sty J.R : Photophenic bone scan
osteomyelitis :Aclinical prespective. J.Paed.Orthop,1999 19: 695-698.

16.

Reggie C.H, Lawton L, Carey T : Subacute haemategenous osteomyelitis


:Are biopsy and surgery always indicated ? J Paeds Orthop 16:220-223,1996

17.

Scoles PV, Hilty MD. and Sfakianakis GN. : Bone scan patterns in Acute
osteomyelitis. Clin. Orthop. (1980), 153: 210-217

15

18.

Scoles PV. and Aronoff SC. : Current concept review : Antimicrobial therapy
of childhood skeletal infections. J. Bone and Surg. (1984), 66A: 1487-1492

19.

Tuazon CU.: Teichoic acid antibodies in osteomyelitis and septic arthritis


caused by Staphylococcus aureus. J.Bone and Joint Surg. (1982), 64A: 762765

20.

Tuson C.E,Hoffman E.B : Isotope bone scanning for acute osteomyelitis and
septic athritis in children .

21.

Warner WC. Jr.: Osteomyelitis. Campbells operative orthopaedics, edited by


Crenshaw AH, eight edition. Mosby Year Book. (1991), Chap. 4: 131-150

22.

Wedge JH. :. Osteomyelitis: Clinical Presentation. Current Orthop. (1988), 2:


65-68.

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