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‘Fast Casts’: Evidence Based and Clinical Considerations for Rapid Ponseti Method

Posted on September 1, 2013 | Comments Off on ‘Fast Casts’: Evidence Based and Clinical Considerations for Rapid Ponseti Method

by April Sutcliffe1, Kolini Vaea2, John Poulivaati2, Angela Margaretpdflrg Evans3,4

The Foot and Ankle Online Journal 6 (9): 2

The Ponseti method of correction of congenital clubfoot is recognized as the preferred management technique for this pediatric deformity. The original method has been subtly modified over time in response to clinical experience and research findings. Most recently, two randomized controlled trials have shown that less time is needed for each serial cast immobilization. Clinical cases from the Kingdom of Tonga are presented to illustrate the clinical use of more rapid plaster cast changes – the ‘fast casts’ modification incorporating increased manual manipulation time, within the Ponseti method. The Pirani score was used to monitor the clubfoot correction between each plaster cast change for each baby. In all feet the Pirani scores reduced sequentially with shorter periods of casting. Shorter duration of cast immobilization – ‘fast casts’ – can be used with many advantages for the clinical setting. Less time in plaster can at least halve the corrective phase of Ponseti management without compromising results. In addition, there are possible benefits for families from distant locations, for babies being less prone to skin irritations, and less difficult day-to-day baby care related to long leg plaster casts. These factors may benefit compliance and overall treatment outcomes.

Key words: clubfoot, Ponseti, pediatric, foot

Accepted: August, 2013
Published: September, 2013

ISSN 1941-6806
doi: 10.3827/faoj.2013.0609.002

Address correspondence to: Department of Podiatry, Lower Extremity and Gait Studies (LEGS) Research Program, La Trobe University, Bundoora, Melbourne, Australia. Email: angela.evans@latrobe.edu.au

1Sydney Children’s Hospital, High Street, Randwick, Sydney, Australia
2Vaiola Hospital, Tonga
3Department of Podiatry, Lower Extremity and Gait Studies (LEGS) Research Program,
La Trobe University, Bundoora, Melbourne, Australia
4Health and Rehabilitation Research Institute, AUT University, Auckland, New Zealand

The Ponseti method has taken the developed world by storm in the last decade, becoming acknowledged as the optimal treatment for congenital clubfoot deformity.[1,2]

Cited as the most significant and potentially debilitating congenital pediatric orthopaedic deformity, talipes equino varus, has littered the pages of historic tomes, medical journals and textbooks alike.[3] The Egyptian boy king, Tutankhamen; the tragic poet, Lord Byron; and celebrated stage and screen actor, Dudley Moore; eponymously all male, were born and/or lived with clubfoot deformity. [4]

Whilst management with splints, binding, and plaster casts has been evident across the hundreds and thousands of years in which clubfoot deformity is referenced, the 20th century saw such conservative measures subsumed by surgical correction, and notably the posterior medial release (PMR). [5-7] The PMR is a joint invasive procedure, which also severs to lengthen, all the soft tissue structures found contracted on the medial and posterior aspects of the infant clubfoot.[8]

In the 21st century, surgical correction of clubfeet has been firmly denounced.[9] Both retrospective concerns and reviews, and prospectively designed studies have shown the poor outcomes, in terms of pain and function, resulting from the PMR and akin surgical procedures.[7]

Simultaneously, the Ponseti method, developed and named after the orthopedic specialist Ignacio Ponseti[10], has been investigated both retrospectively and in many prospective randomized controlled trials (RCTs), and found not only to give the best clinical outcomes, but to also be a more economical management, when compared to surgery – the rare health care setting finding of a ‘win:win’.[11]

Much investigation of Ponseti’s original method has occurred in the last decade.[7,12,13] Whilst it’s superior outcomes for management of congenital clubfoot has met with universal consensus, this has also resulted in considerable refinement of the technique.[11,14,15]

The original Ponseti method

The duration of each serial plaster cast, a fundamental aspect of the basic weekly casts which made up the original Ponseti method[16] now has good evidence for amendment.

The original method described by Ponseti involves a series of plaster casts changed weekly for a period of five to six weeks, followed by percutaneous elongation of the Achilles tendon and application of a final cast for three weeks. The foot abduction bracing phase, is commenced immediately after the post tenotomy cast is removed.

There is now strong evidence to suggest that accelerated frequency of cast changes has comparable outcomes to those of the original Ponseti method.[17] with the benefit of limiting time spent is casts during the corrective phase of treatment.

The evidence for, and implication of, ‘fast casts’

It was first revealed that casts changed every five days, instead of the originally prescribed seven days, gave the same results – potentially saving ten to 12 days in the initial casting phase.[18] Two more recent RCTs have shown that casts changed twice (even three times) each week attain the same correction as weekly casts. [17, 19]

The halving of the casting phase from an average six weeks to three weeks, without compromising results, has clear advantages. Less time immobilized in plaster casts is intuitively preferable for the baby, and their parents or caregivers. Shorter durations of each corrective cast reduces the likelihood and extent of undetected skin pressure lesions, and at least halves the overall corrective phase, such that babies commence the (virtually) full-time boots and bar phase over three months, at a younger and possibly more amenable age. With the consistently demonstrated and positive correlation between successful use of the maintenance boots and bar, and lessened relapse of clubfoot correction – starting the boots and bar habit earlier within the rapid development that hallmarks infancy – may be more helpful than at first glance considered.[20-22]

How can the notion of ‘fast casts’ be applied clinically, and what are the possible pitfalls as well as benefits?

Illustrative use of the ‘fast casts’ technique

Two cases from Tonga, the country with the world’s highest incidence of congenital clubfoot deformity[23], are included in this review. In Tonga, a pacific island country geographically comprised of numerous islands, clinical use of the ‘fast casts’ method facilitates coordination with the availability of surgical expertise to perform Achilles tenotomies, as well as accelerated progress of babies through the casting stage. Both of the case-study babies were cast and re-cast four times in one week. This is more rapid and intense than might normally occur due to the visit from the off-shore surgeon occurring the following week (the local surgeon has now undertaken training for tenotomy procedures).

Fig 1 Baby J

Figure 1 Baby J, whose data is presented in table 2.

Table1

Table 1 Baby J – left congenital clubfoot. The use of ‘fast casts’ saw this baby’s corrected and ready for the tenotomy procedure after six days (4 casts).

Fig 2 Baby S

Figure 2 Baby S, whose data is presented in table 3.

Table2

Table 2 Baby S – bilateral congenital clubfeet. The use of ‘fast casts’ corrected the cavus and adduction of the clubfoot deformity, but made no change to the equinus component, which required the tenotomy for correction (as indicated by the initial Pirani score).

As the Tables 1 and 2 show, both babies showed consistent correction of their foot deformity with manipulation and casting. (Fig. 1 and 2) The Pirani scores reduced consistently within the initial corrective phase, showing the value of using this demonstrably reliable and objective measure. Further, the initial Pirani scores of 5 and 5.5 respectively, heralded the very likely need for tenotomies.[24] Indeed, the hindfoot scores equaled or approximated the total Pirani scores after the casting phase, signaling the residual equinus aspect of the deformity. It must be stated that similarly to the findings of the clinical trial by Xu et al[17], that these Tongan cases also underwent ‘more rather than less’ manipulation prior to casting. Whilst the effect of manipulation time has not been formally studied, histological investigation directs maintained loading of ligaments to promote the lengthening or ‘uncrimping’ of these structures.[25] Might it be that more attention to, and time spent, carefully manipulating clubfoot correction is able to render cast time less relevant?

Considerations, variations, and further questions

There are many factors to consider when contemplating the use of ‘fast casts’ as part of the Ponseti clubfoot correction method.

Firstly, there is now very good evidence to support shortening cast time[17] for the typical, congenital clubfoot deformity.

Secondly, the convenience for parents travelling with infants to distant clinics for treatment which necessitates time away from home, work, and family, a common occurrence in developing countries, may be greatly improved.[26-28] If, as on average, a baby requires six casts, the time away from home/work may be reduced from six weeks to two weeks. This could provide great savings for costs incurred whilst living away from home, and time lost from work. In turn, compliance may also benefit.

Thirdly, less time immobilized in plaster is probably advantageous for the baby in terms of reduced skin sore issues, easier bathing, more normal motor development and possibly lessens the risk of osteopenia.[29]

Notable in the current findings on faster casting is the longer manipulation time, (two minutes) specified by Xu, et al., [17], an additional departure from the original Ponseti protocol, and also the long follow up time of this study, as opposed the otherwise similar Malawi trial.[19]

It is important to appreciate that all accelerated casting studies and trials have addressed the typical congenital clubfoot, and that the effects and use in syndromic[11] or complex clubfoot types[30] are unknown.

The application of best available evidence to any health care setting is important, particularly if there are clear benefits to the recipients of this care. The rescheduling of the weekly clubfoot clinic for casting, to at least twice weekly, is now a possible shift in contemporary evidence based practice.

Conclusions

The Ponseti method continues to be the best approach to correction of the typical congenital clubfoot. There is now high-level evidence to support changing casts after three days or less, which greatly reduces the time infants spend immobilized in plaster.

The pre-casting manipulation is important and indications are that more time spent may be beneficial in correcting the clubfoot deformity.

In developing countries where travelling to clinics necessitates time away from home, work, and family, the adoption of ‘fast casts’ can reduce costs to families, and perhaps help to improve compliance and overall outcomes.

References

1.           Steinman S, Richards BS, Faulks S, Kaipus K. A comparison of two nonoperative methods of idiopathic clubfoot correction: the Ponseti method and the French functional (physiotherapy) method. Surgical technique. JBJS 2009 91A (Suppl 2): 299-312. [PubMed]
2.           Carroll NC. Clubfoot in the twentieth century: where we were and where we may be going in the twenty-first century. J Pediatr Orthop 2012 21: 1-6. [PubMed]
3.           Dobbs MB, Morcuende JA, Gurnett CA, Ponseti IV. Treatment of idiopathic clubfoot: an historical review. Iowa Orthop J 2000 20: 59-64. [PubMed]
4.           Anand A, Sala D. Clubfoot: Etiology and treatment. Indian J Orthop 2008 42: 22-28.  [PubMed]
5.           Manzone P. Clubfoot surgical treatment: preliminary results of a prospective comparative study of two techniques. J Pediatr Orthop 1999 8: 246-250. [PubMed]
6.           Zionts LE, Zhao G, Hitchcock K, Maewal J, Ebramzadeh E. Has the rate of extensive surgery to treat idiopathic clubfoot declined in the United States? JBJS 2010 A92: 882-889. [PubMed]
7.           Halanski MA, Davison JE, Huang J-C, Walker CG, Walsh SJ, Crawford HA. Ponseti method compared with surgical treatment of clubfoot: a prospective comparison. JBJS 2010 A92: 270–278. [PubMed]
8.           Laaveg S, Ponseti I. Long-term results of treatment of congenital club foot. JBJS 1980 62A:23-31. [PubMed]
9.           Morcuende J, Dolan L, Dietz F, Ponseti I. Radical reduction in the rate of extensive corrective surgery for clubfoot using the Ponseti method. Pediatrics 2004 113: 376-80. [PubMed]
10.         Ignacio Ponseti [Internet]. Wikipedia. [cited 2013 Jan 29]. Available from: http://en.wikipedia.org/wiki/Ignacio_Ponseti 
11.         Dobbs MB, Gurnett CA. Update on clubfoot: etiology and treatment. Clin Orthop and Rel Res  2009 467: 1146-1153. [PubMed]
12.         Niki H, Nakajima H, Hirano T, Okada H, Beppu M. Ultrasonographic observation of the healing process in the gap after a Ponseti-type Achilles tenotomy for idiopathic congenital clubfoot at two-year follow-up. J Orthop Sci 2013 18: 70-75. [PubMed]
13.         Carroll N. Editorial: Clubfoot: What Have We Learned in the Last Quarter Century? J Pediatr Orthop 1997 17: 1-7.  [PubMed]
14.         Rijal R, Shrestha BP, Singh GK, Singh M, Nepal P, Khanal GP, Rai P. Comparison of Ponseti and Kite’s method of treatment for idiopathic clubfoot. Indian J Orthop 2010 44: 202-207. [PubMed]
15.         Andriesse H, Roos EM, Hägglund G, Jarnlo G-B. Validity and responsiveness of the Clubfoot Assessment Protocol (CAP). A methodological study. BMC Musculoskelet Disord 2006 7: 28. [PubMed]
16.         Ponseti I. Clubfoot management. J Pediatr Orthop 2000 20: 699-700.[PubMed]
17.         Xu RJ. A modified Ponseti method for the treatment of idiopathic clubfoot: a preliminary report. J Pediatr Orthop 2011 31: 317-319. [PubMed]
18.         Morcuende J, Abbasi D, Dolan L. Results of an accelerated Ponseti protocol for clubfoot. J Pediatr 2005 25: 623-625. [PubMed]
19.         Harnett P, Freeman R, Harrison WJ, Brown LC, Beckles V. An accelerated Ponseti versus the standard Ponseti method: a prospective randomised controlled trial. JBJS 2011 B93: 404-408. [PubMed]
20.         Garg S, Porter K. Improved bracing compliance in children with clubfeet using a dynamic orthosis. J Children’s Orthopaedics 2009 1: 271-276. [PubMed]
21.         Boehm S, Sinclair M. Foot abduction brace in the Ponseti method for idiopathic clubfoot deformity: torsional deformities and compliance. J Pediatr Orthopaedics 2007 27: 712-716. [PubMed]
22.         Ippolito E, Fraracci L, Farsetti P, Di Mario M, Caterini R. The influence of treatment on the pathology of club foot. CT study at maturity. JBJS 2004 B86: 574-580. [PubMed]
23.         Chapman C, Stott NS, Port RV, Nicol RO. Genetics of club foot in Maori and Pacific people. J Med Genet 2000 37: 680-683. [PubMed]
24.         Shack N, Eastwood D. Early results of a physiotherapist-delivered Ponseti service for the management of idiopathic congenital talipes equinovarus foot deformity. JBJS 2006 88: 1085-1089. [PubMed]
25.         Ponseti I. Treatment of congenital club foot. JBJS 1992 74: 448-454.[PubMed]
26.         Pirani S, Naddumba E, Mathias R, Konde-Lule J, Penny JN, Beyeza T,  Mbonye B, Amone J, Franceschi F.Towards Effective Ponseti Clubfoot Care: The Uganda sustainable clubfoot careproject. Clin Orthop Rel Res 2009 467:1154-1163. [PubMed]
27.         Evans AM, Van Thanh D. A review of the Ponseti method and development of an infant clubfoot program in Vietnam. JAPMA 2009 99: 306-316. [PubMed]
28.         Evans AM. Preliminary evaluation of implementing the Ponseti method for correction of clubfoot in Vietnam. J Children’s Orthop 2010 4: 553-559. [PubMed]
29.         Lourenço AF, Morcuende JA. Correction of neglected idiopathic club foot by the Ponseti method. JBJS 2007 89B: 378-381. [PubMed]
30.         Ponseti IV, Zhivkov M, Davis N, Sinclair M, Dobbs MB, Morcuende JA. Treatment of the complex idiopathic clubfoot. Clin  Orthop Rel Res 2006 451:171-176. [PubMed]

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Acute Multifocal Hematogenous Osteomyelitis in a 13 year-old: A Case Report

Posted on April 29, 2013 | Comments Off on Acute Multifocal Hematogenous Osteomyelitis in a 13 year-old: A Case Report

by M.F. Madu, MD1, T. Klok, MD2, L. Sijbrandy, MD PhD3, J. Bekhof, MD4pdflrg

The Foot and Ankle Online Journal 6 (4): 1

Background: Acute hematogenous osteomyelitis (AHOM) is a serious pyogenic infection that is generally caused by bacteria and is most commonly found in children. A multifocal presentation of the disease is rare, mostly seen in the newborn and only in a small percentage of older children. We report a case of multifocal AHOM in a previously healthy, 13-year old girl, who presented herself with several painful and swollen joints, accompanied by high fever. The history, clinical course, radiologic findings and management rationale are presented in this report.
Methods: A review of the clinical, laboratory, radiological and microbiological data of the patient was done.
Results: Arthrocentesis of a swollen ankle, done under suspicion of septic arthritis, yielded clear and sterile synovial fluid. Magnetic resonance imaging scans of affected joints later confirmed AHOM close to the joint, causing the sterile joint effusion.
Discussion: A lesson to be learned from this case is that in case of a clinically suspected septic arthritis, a negative joint puncture could mean an osteomyelitis close to the joint.

Keywords: AHOM, pediatric, child, acute, multifocal, hematogenous, osteomyelitis, staphylococcal

Accepted: March, 2013
Published: April, 2013

ISSN 1941-6806
doi: 10.3827/faoj.2013.0604.001

Address correspondence to: J. Bekhof, MD, Isala Klinieken, Department of Pediatrics. PO Box 10400, 8000 GK Zwolle, The Netherlands. j.bekhof@isala.nl

1-4Department of Pediatrics, Isala Klinieken, Zwolle, The Netherlands.

Acute hematogenous osteomyelitis (AHOM) is a serious pyogenic infection that is generally caused by bacteria and is most commonly found in children.[1] Usually, antibiotics and the careful use of surgery can effectively treat the disease, but when managed poorly it can be life threatening, or at best, a debilitating and crippling illness.[2] AHOM is frequently caused by S. aureus, which is responsible for over 80-90% of culture positive cases.[5] These cases amount to 20-90% of all cases.[1]

AHOM typically presents with local pain and fever that has lasted for approximately 3 days on presentation in the hospital.[3] It is most commonly found in tubular bones. The femur and tibia are affected in one third of the cases, followed by the humerus.[4,5] Infection of pelvic bones, which was seen in the following case, is rare.[6] Multifocal presentation of acute hematogenous osteomyelitis occurs even less frequently in older children.

hetosteoFig

Figure 1
a. Anterior posterior radiograph of the left ankle, demonstrating soft tissue swelling (arrow) and lytic bone lesions in the distal fibula (arrowheads).
b. Coronal T-1 weighted, fat suppressed magnetic resonance imaging (MRI) scan of the left ankle, showing a large skin and subcutaneous defect (arrow), where incision and drainage of the abscess was performed.
c. The same image after intravenous contrast (gadolinium), showing contrast enhancement in the distal fibula, corresponding with osteomyelitis (arrow). Abscess formation (arrowheads) and edema in the surrounding subcutaneous tissue can be seen.

While a multifocal presentation is common in neonates, where around 50% of the cases involve multiple bones[7], this is unusual in older children, occurring in 6-9% of those cases.[8,9] Multifocal osteomyelitis can also be caused by chronic recurrent multifocal osteomyelitis (CRMO), a rare disease that presents with sterile osteomyelitis with an unclear, presumably autoimmune etiology.[19]

We report an unusual case of multifocal AHOM in a 13-year old girl. The aim of this study is to emphasize that this diagnosis should be considered when a child presents with multifocal bone pain and/or painful joints, resembling a multifocal arthritis.

Case report

A 13 year-old girl was referred to our hospital with several painful joints since two days, accompanied by vomiting and fever. Physical examination showed a swollen right knee and a red, swollen proximal interphalangeal joint of the third digit of the left hand.

The patient was not severely ill with a non-febrile temperature. Blood tests showed a slight elevation of inflammatory and hematological markers: erythrocyte sedimentation rate (ESR) 24 mm/hour, C-reactive protein (CRP) 31 mg/l, serum ferritin 160μg/l, leukocyte count 12.6*109/l, neutrophil count 10.3*109/l.

The working diagnosis was reactive arthritis. The differential diagnosis consisted of juvenile idiopathic arthritis and septic arthritis, although low levels of inflammatory markers and a non-critically ill patient made these diagnoses unlikely. Diclofenac 50 mg was prescribed and the patient was sent home.

Over the next week, joint pain had not subsided and the right shoulder and right side of the pelvis were now involved. Furthermore, during the nighttime, the patient had developed a fever in excess of 40 degrees Celsius (104 degrees Fahrenheit), with a normal temperature during the day. Physical examination showed a swollen, warm and red area superior of the left lateral malleolus, as well as swollen digits 2 and 3 of the left hand. In addition, a painful area on the right iliac crest and slightly swollen knees were seen. Blood tests showed rising inflammatory markers (ESR 90 mm/hour, CRP 158 mg/l, serum ferritin 279 μg/l) and a rising leukocyte (15.2*109/l) and neutrophil count (11.6*109/l). Under suspicion of septic arthritis or osteomyelitis, the patient was admitted to the pediatric ward for further examination and treatment. A blood culture was done and the orthopedic surgeon performed a joint puncture of the ankle, which yielded clear liquid. The patient was treated with indomethacin and intravenous amoxicillin/clavulanic acid 2000/200mg three times daily. Three days after admittance, results of the joint puncture and blood culture were available. No bacterial growth was detected in the synovial fluid. The blood culture was positive for Staphylococcal aureus, after which antibiotics were switched to intravenous flucloxacillin 1000mg, four times daily.

In the meantime, her body temperature had dropped to normal levels; however an increase in pain and swelling of the left ankle was reported, with accompanying rising inflammatory markers (ESR 98 mm/hour, CRP 178 mg/l, neutrophil count 16.1*109/l and leukocyte count 18.7*109/l). Ultrasound of the left ankle showed a fluctuating, hypodense lesion, cranial to the lateral malleolus. Since an abscess was suspected, an incision was performed, after which a large amount of pus was drained. The periosteum had been damaged and underlying bone was visible, but still firm. The wound was thoroughly cleansed and was allowed to heal by second intention.

Further radiological evaluation was performed. Ultrasound of the pelvis showed a fluid collection lateral of the right anterior superior iliac spine (ASIS). Magnetic resonance imaging (MRI) scans of the pelvis showed bone edema in the right ASIS, and high signal intensity after intravenous contrast injection, corresponding with osteomyelitis. Pathological fluid pockets were seen in the soft tissue surrounding the affected bone, with capsular enhancement after contrast injection, corresponding with multiple micro-abscesses. MRI scans of the left ankle showed bone edema in the distal fibula and high signal intensity after intravenous contrast injection, corresponding with osteomyelitis. Pathological fluid pockets with capsular enhancement after contrast injection were also seen, pointing to micro-abscesses in the soft tissue surrounding the distal fibula. (Fig. 1)

Since multiple sites were affected, the presumptive diagnosis was multifocal acute hematogenous osteomyelitis.

Pain and limitation of range of motion gradually decreased over the next six days, with blood tests showing ever decreasing inflammatory markers (ESR 54 mm/hour and CRP 9 mg/l) and leukocyte and neutrophil numbers within the normal range. Three weeks after the onset of symptoms, the patient was discharged from our hospital with oral antibiotic therapy consisting of oral clindamycin 450 mg four times per day, which was to be continued for 4 weeks. At the outpatient clinic she showed complete recovery after 6 weeks.

Discussion

Diagnosis of multifocal AHOM can present a challenge because of the atypical presentation and similarity to septic arthritis, juvenile idiopathic arthritis and/or reactive arthritis. When AHOM presents in the pelvis, diagnosis can be especially difficult because pain is referred to the hip, thigh or abdomen because of the deep localization of the infection.[10] In one study, only 12 out of 82 patients suffering from pelvic AHOM were admitted with the correct diagnosis.[11]

Presenting clinical features of AHOM are pain, fever and in pelvic AHOM, limping. Laboratory findings include elevated inflammatory markers (ESR and CRP), which are found in over 90% of cases.[12] Peripheral white cell count is not a very reliable indicator of AHOM[1], however, white cell count should be performed, as leukemia is a differential diagnosis of AHOM. In this case, septic arthritis, juvenile idiopathic arthritis and reactive arthritis as well as leukemia were considered. Based on the not very ill patient and elevated inflammatory markers, the working diagnosis was reactive arthritis. Leukemia could be ruled out easily, based on the white cell count and differentiation, which is routinely performed in our hospital in similar cases.

Two important imaging modalities in the diagnosis of AHOM are bone scintigraphy and magnetic resonance imaging (MRI). These techniques are complementary. Hot spots on bone scintigraphy can guide high-resolution imaging modalities such as MRI, which have a limited field of view compared to a bone scan[10], but a higher sensitivity and specificity (93% and 96%).[13] Initial MRI is recommended in clearly localized disease, initial bone scintigraphy in diffuse, not clearly localized disease.[10] Since in this case, although disease was multifocal, symptoms were clearly localized, an indication for initial MRI scanning was present.

Bone or abscess aspiration to confirm the diagnosis is strongly recommended by experts. However, this is becoming increasingly controversial because of the high sensitivity and specificity of radiologic techniques to diagnose AHOM and S. aureus as causative pathogen in the majority of cases. Steer, et al., recommend incision and drainage when certain criteria are met, such as delayed presentation, an immunocompromised patient, abscess formation, underlying malignancy or delayed response to antibiotics.[1] In this case, abscess formation was a reason for incision and drainage of the ankle abscesses, which served as a combined interventional and diagnostic approach. Arthrocentesis of the ankle joint, performed under suspicion of septic arthritis yielded sterile synovial fluid.

A lesson to be learned from this is that AHOM close to a joint can clinically mimic septic arthritis. Therefore, when arthrocentesis is performed in case of a clinically suspected septic arthritis and sterile fluid is obtained, the clinician should consider osteomyelitis close to the joint.

Antibiotic therapy is initially based on the most likely pathogen causing AHOM in children, which is S. aureus. Single β-lactamase-resistant penicillins such as flucloxacillin have shown their effectiveness against methicillin-susceptible staphylococci and streptococci.[14] After identification of the organism, antimicrobial therapy can be changed according to bacterial susceptibility. When blood/bone culture turns out negative, empirical antibiotic therapy can be continued, as long as clinical response is observed. Duration of antibiotic therapy in AHOM differs from that in adults. Adults are usually treated with prolonged intravenously therapy (mostly six weeks). Children can be treated for shorter courses and with parenteral-oral sequential therapy[1], in which intravenous administration is followed by oral continuation of antibiotic therapy. The efficacy and safety of this regimen has been proven in numerous studies, some of which measuring bone concentrations of oral antimicrobials.[15,16] The total duration of therapy and timing of the switch to oral therapy differs greatly between studies, but generally, intravenous therapy for 3-7 days and further continuation of oral therapy for 3-4 weeks is most common[17,18], although this has never been thoroughly tested in a randomized controlled trial.[19]

Conclusion

In our opinion, two important lessons can be learned from the aforementioned case. Firstly, alternative diagnoses such as multifocal AHOM should be considered when patients present with atypical symptoms, including bone or joint pain and fever. Secondly, when arthrocentesis is performed under suspicion of septic arthritis and sterile synovial fluid is obtained, this can very well mean AHOM close to the apparently symptomatic joint. This case underscores the importance of careful consideration of different etiological entities and multidisciplinary diagnosis and treatment when a patient presents with atypical symptoms and signs.

References

1.  Steer AC. Carapetis JR. Acute hematogenous osteomyelitis in Children: Recognition and Management. Pediatr Drugs 2004 6: 333-346. [PubMed]
2.  Mollan R, Piggot J. Acute osteomyelitis in children. JBJS  1977 59B: 2-7. [PubMed]
3.  Karwowska A, Davies HD, Jadavji T. Epidemiology and outcome of osteomyelitis in the era of sequential intravenous-oral therapy. Pediatr Infect Dis  1998 17: 1021-1026. [PubMed]
4.  Tröbs R, Möritz R, Bühligen U, Bennek J, Handrick W, Hörmann D, Meier T. Changing pattern of osteomyelitis in infants and children. Pediatr Surg Int 1999 15: 363-372.
5.  Craigen MAC, Watters J, Hackett JS. The changing epidemiology of osteomyelitis in children. JBJS 1992 74B: 541-545. [PubMed]
6.  Corti N, Sennhauser FH, Nadal D, Stauffer UG, Nadal D. Fosfomycin for the initial treatment of acute hematogenous osteomyelitis. Arch Dis Child 2003 88: 512-516. [PubMed]
7.  Nelson JD. Acute osteomyelitis in children. Infect Dis Clin North Am 1990 4: 513-522. [PubMed]
8.  Nixon G. Acute hematogenous osteomyelitis. Pediatr Ann 1976 5: 64-81. [PubMed]
9.  Labbé JL, Peres O, Leclair O, Goulon R, Scemama P, Jourdel F, Menager C, Duparc B, Lacassin F.  Acute osteomyelitis in children: the pathogenesis revisited? Orthopaedics Traum Surg Res 2010 96 268-275. [PubMed]
10.  Weber-Chrysochoou C, Corti N, Goetschel P, Altermatt S, Huisman TA, Berger C. Pelvic osteomyelitis: a diagnostic challenge in children. J Ped Surg 2007 42 553-557. [PubMed]
11.  Mustafa MM, Sáez-Llorens X, McCracken GH Jr, Nelson JD. Acute hematogenous pelvic osteomyelitis in infants and children, Pediatr Infect Dis  1990 9: 416-421. [PubMed]
12.  Unkila-Kallio L, Kallio MJT, Eskola J, Peltola H. Serum C-reactive protein, erythrocyte sedimentation rate and white blood cell count in acute hematogenous osteomyelitis in children. Pediatrics 1994 93: 59-62.  [PubMed]
13.  Davidson D, Letts M, Khoshhal K. Pelvic osteomyelitis in children: a comparison of decades from 1980-1989 with 1990- 200. J Pediatr Orthop 2003 23: 514- 521. [PubMed]
14.  Krogdstad P, Smith AL. Osteomyelitis and septic arthritis, Textbook of pediatric infectious diseases. 4th Edition. Philadelphia (PA), WB Saunders, 1998.
15.  Bryson YJ, Connor JD, LeClerc M, Giammona ST.
High dose oral dicloxacillin treatment of acute staphylococcal osteomyelitis in children. J Pediatr 1979 94: 673-675. [PubMed]
16.  Feigin RD, Pickering LK, Anderson D, Keeney RE, Shackleford PG. Clindamycin treatment of osteomyelitis and septic arthritis in children. Pediatrics 1975 55: 213-223. [PubMed]
17.  Peltola H, Unkila-Kallio L, Kallio MJ. Simplified treatment of acute staphylococcal osteomyelitis of childhood, Pediatrics 1997 99: 846-850. [PubMed]
18.  Syrogiannopolous GA, Nelson JD. Duration of antimicrobial therapy for acute suppurative osteoarticular infections.  Lancet 1988 I (8575-6): 37-40. [PubMed]
19.  Ferguson PJ, Sandu M. Current understanding of the pathogenesis and management of chronic recurrent multifocal osteomyelitis. Curr Rheumatol Rep 2012 14: 130-141. [PubMed]

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