Stop Maligning the Asymptomatic Child’s Flatfoot

Volume 4 | Issue 2 | July-December 2018 | Page: 01-02 | Benjamin Joseph

Authors: Benjamin Joseph [1]

[1] Aster Medcity, Kochi, Kerala, India.

Address for correspondence:
Prof. Benjamin Joseph,
18 H.I.G. Colony, Manipal − 576 104, Karnataka, India
E-mail: bjosephortho@yahoo.co.in

Recently, a lady met me and gave me some very colourful pamphlets about a range of fancy foot wear and shoe inserts for toddlers and young children designed to ’correct’ flatfeet. I asked her why asymptomatic flatfeet need to be treated. I patiently listened to her as she listed several ‘harmful effects of flatfeet’ including a predilection for foot injury, back ache and so on, which, according to her could be avoided by using the shoes and shoe inserts she was promoting. Needless to say, there were no scientific data to support these claims. After she left, I reflected about what the scientific literature had to say about flatfoot and also recollected my personal experience of dealing with flatfeet in young children in my practice.

There has been a long-held notion that flatfeet are bad and that they may interfere with strenuous physical activity. On the basis of this, young men with flatfeet were rejected from recruitment into the armed forces. However, Cowan et al.[1] did a study on army recruits in the USA and could not demonstrate a higher frequency of injuries in those with flatfeet. Esterman and Pilotto[2] did a similar study in Australia and concluded that ’foot shape has little impact on pain, injury and function’. Tudor et al.[3] studied athletic performance in school children with flatfoot and normal arches and documented no difference in performance in 17 different tasks. So it is high time we dispel the erroneous notion that the flatfoot is in some way inferior to feet with a well-formed arch.

Stemming from the belief that flatfoot is undesirable, concerted efforts have been made to ‘treat’ young children with shoe modifications and various types of shoe inserts that elevate the medial longitudinal arch or control the hindfoot valgus. Despite the fact that Wenger et al.,[4] in as early as 1989, demonstrated clearly that shoes and shoe inserts in no way alter the natural history of flatfoot, orthopaedic surgeons continue to prescribe them. This wasteful and meaningless practice needs to stop.

The natural history of asymptomatic flexible flatfoot is that of resolution in the vast majority of children because the arch develops by the age of 6–7 years. This is very evident as at 1 year of age, 95% of children have flatfeet and by the age of 10, the prevalence is as low as 5%. The increase in the tone of muscles that support the arch and spontaneous reduction in joint laxity as the child grows facilitate the arch to develop. Barefoot activity in early childhood also facilitates the arch to develop while shoe-wearing appears to be detrimental to the development of the arch. This was demonstrated in two large cross-sectional surveys, which showed that the prevalence of flatfoot was highest among children who wore closed-toe shoes below the age of 6 years and lowest in the unshod.[5,6] The frequency of flatfoot in children who wore sandals and slippers fell between these two. With this evidence, it seems hardly logical to prescribe shoes for a young child with flatfoot. Instead, we need to spread the message to encourage children to play barefoot outdoors on sand and gravel. We could also encourage school authorities to have sandals rather than shoes as the regulation footwear. These suggestions are perfectly appropriate in the warm climate in India.

In my practice, I have never had parents from the lower socio-economic strata bring a child for the treatment of flatfoot. Every single child brought to me with the complaints of flatfoot has been from an affluent family. Often it has been a paediatrician, or family physician, who referred the child with flatfoot to me. For a long time, I wondered why there was this socio-economic difference in my flatfoot practice. It then dawned on me; the poor child is unshod and in early childhood has played barefoot, and the poor child consequently is unlikely to have flatfoot. Even if the poor child has flatfeet, they cause no pain and the feet function perfectly well. The child’s parents have no access to the internet, so they have never heard anyone maligning their child’s feet. No wonder, I never saw a poor child with flatfoot in my clinic.

Benjamin Joseph
Aster Medcity, Kochi, Kerala, India
Address for correspondence: Prof. Benjamin Joseph, 18 H.I.G. Colony,
Manipal − 576 104, Karnataka, India
E-mail: bjosephortho@yahoo.co.in

References 

1. Cowan DN, Jones BH, Robinson JR. Foot morphologic characteristics
and risk of exercise-related injury. Arch Fam Med 1993;2:
773-7.
2. Esterman A, Pilotto L. Foot shape and its effect on functioning in Royal
Australian Air Force recruits. Part 1: Prospective cohort study. Mil Med
2005;170:623-8.
3. Tudor A, Ruzic L, Sestan B, Sirola L, Prpic T. Flat-footedness is not a
disadvantage for athletic performance in children aged 11 to 15 years.
Pediatrics 2009;123:e386-92.
4. Wenger DR, Mauldin D, Speck G, Morgan D, Lieber RL. Corrective
shoes and inserts as treatment for flexible flatfoot in infants and
children. J Bone Joint Surg Am 1989;71:800-10.
5. Rao UB, Joseph B. The influence of footwear on the prevalence of flat
foot. A survey of 2300 children. J Bone Joint Surg Br 1992;74:525-7.
6. Sachithanandam V, Joseph B. The influence of footwear on the
prevalence of flat foot. A survey of 1846 skeletally mature persons. J
Bone Joint Surg Br 1995;77:254-7.

How to Cite this Article:  Joseph B |  Stop Maligning the Asymptomatic Child’s Flatfoot | July-
December 2018; 4(2): 01-02.

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10-Year Radiological Follow-Up of Multifocal Recurrent Eosinophilic Granuloma With Vertebra Plana: A Case Report and Review of Literature

Volume 4 | Issue 2 | July-December 2018 | Page: 32-36 | Amit Kumar, Shivam Sinha, Shyam Kumar Saraf, Vineeta Gupta, Deepa Rani, Jyoti Kumari

DOI- 10.13107/ijpo.2018.v04i02.016

Authors: Amit Kumar, Shivam Sinha, Shyam Kumar Saraf, Vineeta Gupta [1], Deepa Rani [2], Jyoti Kumari [3]

 

Departments of Orthopedics, [1] Pediatrics and, [2] Pathology, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh, [3] Department of Pediatrics, All India Institute of Medical Sciences, New Delhi, India

Address of Correspondence
Dr. Amit Kumar,
Department of Orthopaedics, Institute of Medical Sciences, Banaras Hindu University, Varanasi − 221 005, Uttar Pradesh, India.
E-mail: amit2k03@gmail.com

Abstract

Eosinophilic granuloma (EG) is the benign localized form of histiocytosis. Owing to the relative rarity of the condition, diagnosis is often delayed or missed, and many questions remain unanswered, ranging from cause and pathogenesis to therapy. Observation and immobilization are adequate for improvement of the condition in most patients. However, treatment other than simple observation is recommended in patients with symptomatic EG. This article presents a 10-year follow-up study of a 15-year-old girl with a symptomatic multifocal EG treated effectively by monitored chemotherapy and orthosis.
Keywords: Eosinophilic granuloma, langerhans cell histiocytosis, osteochondritis, osteogenesis imperfecta, tuberculosis, vertebra plana

References 

1. Willman CL, Busque L, Griffith BB, Favara BE, McClain KL, Duncan MH, et al. Langerhans histiocytosis (histiocytosis X): A clonal proliferative disease. New Engl J Med 1994;331:154-60.
2. Lichtenstein L. Histiocytosis X (eosinophilic granuloma of bone ‘Letterer-Siwe disease and Schuller-Christian disease’): Further observations of pathological and clinical importance. J Bone Joint Surg Am 1964;46:76-90.
3. Ladish S, Jaffe ES. The histiocytocis. In: Pizzo PA, Poplack DG, editors. Principles and Practices of Pediatric Oncology. Philadelphia: J. B. Lippincott Company; 1989. p. 491-504.
4. Huvos AG. Bone tumors. Diagnosis, Treatment and Prognosis. 2nd ed. Philadelphia: WB Saunders; 1990.
5. Sweasey TA, Dauser RC. Eosinophilic granuloma of the cervicothoracic junction. J Neurosurg 1989;71:942-4.
6. Nesbit ME Jr. Bone tumours in infants and children. Paediatrician 1972 /73;1:273-87.
7. Tanaka N, Fujimoto Y, Okuda T, Nakanishi K, Sumida T, Manabe H, et al. Langerhans cell histiocytosis of the atlas. A report of three cases. J Bone Joint Surg Am 2005;87:2313-7.
8. Dickinson LD, Farhat SM. Eosinophilic granuloma of the cervical spine. A case report and review of the literature. Surg Neurol 1991;35: 57-63.
9. Bertram C, Madert J, Eggers C. Eosinophilic granuloma of the cervical spine. Spine (Phila Pa 1976) 2002;27:1408-13.
10. Capanna R, Springfield DS, Ruggieri P, Biagini R, Picci P, Bacci G, et al. Direct cortisone injection in eosinophilic granuloma of bone: A preliminary report on 11 patients. J Pediatr Orthop 1985;5:339-42.
11. Garg S, Mehta S, Dormans JP. Langerhans cell histiocytosis of the spine in children long-term follow-up. J Bone Joint Surg Am 2004;86: 1740-50.
12. Bechan GI, Egeler RM, Arceci RJ. Biology of Langerhans cells and Langerhans cell histiocytosis. Int Rev Cytol 2006;254:1-43.
13. Egeler RM, Favara BE, van Meurs M, Laman JD, Claassen E. Differential in situ cytokine profiles of Langerhans-like cells and T cells in Langerhans cell histiocytosis: Abundant expression of cytokines relevant to disease and treatment. Blood 1999;94:4195-201.
14. Seimon LP. Eosinophil granuloma of the spine. J Pediatr Orthop 1981;1:371-6.
15. Brown CW, Jarvis JG, Letts M, Carpenter B. Treatment and outcome of vertebral Langerhans cell histiocytosis at the Children’s Hospital of Eastern Ontario. Can J Surg 2005;48:230-6.
16. Greenlee JD, Fenoy AJ, Donovan KA, Menezes AH. Eosinophilic granuloma in the pediatric spine. Pediatr Neurosurg 2007;43: 285-92.
17. Yeom JS, Lee CK, Shin HY, Lee CS, Han CS, Chang H. Langerhans’ cell histiocytosis of the spine. Analysis of twenty-three cases. Spine 1999;24:1740-9.
18. Plasschaert F, Craig C, Bell R, Cole WG, Wunder JS, Alman BA. Eosinophilic granuloma. A different behaviour in children than in adults. J Bone Joint Surg Br 2002;84:870-2.
19. Levy EI, Scarrow A, Hamilton RC, Wollman MR, Fitz C, Pollack IF. Medical management of eosinophilic granuloma of the cervical spine. Pediatr Neurosurg 1999;31:159-62.
20. Fernández-Latorre F, Menor-Serrano F, Alonso-Charterina S, Arenas- Jiménez J. Langerhans’ cell histiocytosis of the temporal bone in pediatric patients. AJR Am J Roentgenol 2000;174:217-21.
21. Kamimura M, Kinoshita T, Itoh H, Yuzawa Y, Takahashi J, Ohtsuka K. Eosinophilic granuloma of the spine: Early spontaneous disappearance of tumor detected on magnetic resonance imaging. J Neurosurg 2000;93(2 Suppl):312-6.
22. O’Donnell J, Brown L, Herkowitz H. Vertebra plana-like lesions in children: Case report with special emphasis on the differential diagnosis and indications for biopsy. J Spinal Disord 1991;4: 480-5.
23. Egeler RM, Thompson RC Jr, Voûte PA, Nesbit ME Jr. Intralesional infiltration of corticosteroids in localized Langerhans cell histiocytosis. J Pediatr Orthop 1992;12:811-4.
24. Grois N, Pötschger U, Prosch H, Minkov M, Arico M, Braier J, et al. Risk factors for diabetes insipidus in Langerhans cell histiocytosis. Pediatr Blood Cancer 2006;46:228-33.
25. Munn SE, Olliver L, Broadbent V, Pritchard J. Use of indomethacin in Langerhans cell histiocytosis. Med Pediatr Oncol 1999;32:247-9.
26. da Costa CE, Annels NE, Faaij CM, Forsyth RG, Hogendoorn PC, Egeler RM. Presence of osteoclast-like multinucleated giant cells in the bone and nonostotic lesions of Langerhans cell histiocytosis. J Exp Med 2005;201:687-93.
27. Raab P, Hohmann F, Kuhl J, Krauspe R. Vertebral remodelling in eosinophilic granuloma of the spine: A long-term follow-up. Spine 1998;23:1351-4.
28. KasteSC,Rodriguez-GalindoC,McCarvilleME,ShulkinBL.PET-CTin pediatric Langerhans cell histiocytosis. Pediatr Radiol 2007;37:615-22.
29. Lau LM, Stuurman K, Weitzman S. Skeletal Langerhans cell histiocytosis in children: Permanent consequences and health-related quality of life in long term survivors. Pediatr Blood Cancer 2008;50: 607-12. Kumar, et al.: Multifocal recurrent eosinophilic granuloma with vertebra plana : A case report 76

How to Cite this Article:  Kumar A, Sinha S, Saraf SK, Gupta V, Rani D, Kumari J | Year Radiological Follow-Up of Multifocal Recurrent Eosinophilic Granuloma With Vertebra Plana: A Case Report and Review of Literature | July-December 2018; 4(2): 32-36.
 

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The Role of Imaging in Diagnosis and Management of Congenital High Scapula (Sprengel’s Deformity): Case Report and Review

Volume 4 | Issue 2 | July-December 2018 | Page: 27-31 | Nada Garrouche, Saida Jerbi, Nedra Chouchane, Wassia Kessomtini, Hssine Hamza

DOI- 10.13107/ijpo.2018.v04i02.015

Authors: Nada Garrouche, Saida Jerbi, Nedra Chouchane, Wassia Kessomtini [1], Hssine Hamza

Departments of Radiology and, [1] Physical Medicine Rehabilitation, Taher Sfar University Hospital, Mahdia- Tunisia

Address of Correspondence
Dr. Nada Garrouche,
Rue Habib Zine el Abidine n°200 (7) Sahloul 2 Sousse 4054-Tunisia.
E-mail: nadagarrouche@yahoo.fr

Abstract

Sprengel’s deformity is the congenital failure of descent of the scapula. The diagnosis is based on a clinical examination and radiological procedures. Volume rendering three-dimensional computed tomography reconstructions analyze the precise topography and spatial proportions of examined bone structures. It enables an optional rotation of visualized bone structures to clarify the anatomical abnormalities. Ultrasound and magnetic resonance are useful in prenatal management and for the diagnosis of concomitant abnormalities. In this paper, we report our imaging experience from one child with Sprengel’s deformity and discuss the importance of imaging techniques with a particular focus on the role of three-dimensional reconstructions.
Keywords: Congenital high scapula, CT, MRI, Sprengel’s deformity, ultrasound, volume rendering 3D-CT

References 

1. Cho TJ, Choi IH, Chung CY, Hwang JK. The Sprengel deformity. Morphometric analysis using 3D-CT and its clinical relevance. J Bone Joint Surg Br 2000;82:711-8.
2. Dilli A, Ayaz UY, Damar C, Ersan O, Hekimoglu B. Sprengel deformity: Magnetic resonance imaging findings in two pediatric cases. J Clin Imaging Sci 2011;1:13.
3. Horwitz AE. Congenital elevation of the scapula–Sprengel’s deformity. Am J Orthop Surg 1908;s2-6:260-311.
4. Grogan DP, Stanley EA, Bobechko WP. The congenital undescended scapula. Surgical correction by the Woodward procedure. Bone Joint J 1983;65:598-605.
5. Gonen E, Simsek U, Solak S, Bektaser B, Ates Y, Aydin E. Long-ter results of modified Green method in Sprengel’s deformity. J Chil Orthop 2010;4:309-14.
6. Bindoudi A, Kariki EP, Vasiliadis K, Tsitouridis I. The rare Sprengel deformity: Our experience with three cases. J Clin Imaging Sci 2014;4:55.
7. Siu KK, Ko JY, Huang CC, Wang FS, Chen JM, Wong T. Woodwar procedure improves shoulder function in Sprengel deformity. Chang Gung Med J 2011;34:403-9.
8. Nakamura N, Inaba Y, Machida J, Saito T. Use of glenoid inclination angle for the assessment of unilateral congenital high scapula. J Pediatr Orthop B 2016;25:54-61.
9. Stein-Wexler R. The Shoulder: Congenital and Developmental Conditions. Pediatric Orthopedic Imaging. Berlin Heidelberg: Springer; 2015. p. 129-39.
10. Greitemann B, Rondhuis JJ, Karbowski A. Treatment of congenital elevation of the scapula: 10 (2–18) year follow-up of 37 cases of Sprengel’s deformity. Acta Orthop Scand 1993;64:365-8.
11. Füllbier L, Tanner P, Henkes H, Hopf NJ. Omovertebral bone associated with Sprengel deformity and Klippel-Feil syndrome leading to cervical myelopathy. J Neurosurg Spine 2010;13:224-8.
12. Chinn DH. Prenatal ultrasonographic diagnosis of Sprengel’s deformity. J Ultrasound Med 2001;20:693-7.
13. Cavendish ME. Congenital elevation of the scapula. J Bone Joint Surg Br 1972;54:395-408.
14. Rockwood CA. Rockwood and Matsen’s the shoulder. Elsevier; 2017.
15. van der Molen AJ, Prokop M, Galanski M, Schaefer-Prokop CM. Spiral and Multislice Computed Tomography of the Body. Stuttgart, New York: Georg Thieme Verlag; 2003.
16. Yuksel M, Karabiber H, Yuksel KZ, Parmaksiz G. Diagnostic importance of 3D CT images in Klippel-Feil syndrome with multiple skeletal anomalies: A case report. Korean J Radiol 2005;6:278-81.
17. Rasul ME, Reddy AV. The sprengel deformity. Int J Res Med Sci 2015;3:3869-71.
18. Rockwood CA. The shoulder. Vol. 1, Ch. 3, Elsevier Health Sciences;2009. p. 120-4.
19. Andrin J, Macaron C, Pottecher P, Martz P, Baulot E, Trouilloud P, et al. Determination of a new computed tomography method for measuring the glenoid version and comparing with a reference method. Radio-anatomical and retrospective study. Int Orthop 2016;40:525-9.
20. Friedman RJ, Hawthorne KB, Genez BM. The use of computerized tomography in the measurement of glenoid version. J Bone Joint Surg Am 1992;74:1032-7.
21. Nyffeler RW, Jost B, Pfirrmann CW, Gerber C. Measurement of glenoid version: conventional radiographs versus computed tomography scans. J Shoulder Elbow Surg 2003;12:493-6.
22. Hamner DL, Hall JE. Sprengel’s deformity associated witmultidirectional shoulder instability. J Pediatr Orthop 1995;15: 641-3.
23. Guillaume R, Nectoux E, Bigot J, Vandenbussche L, Fron D, Mézel A, et al. Congenital high scapula (Sprengel’s deformity): Four cases. Diagn Interv Imaging 2012;93:878-83.
24. Wada A, Nakamura T, Fujii T, Takamura K, Yanagida H, Yamaguchi T, et al. Sprengel deformity: Morphometric assessment and surgical treatment by the modified green procedure. J Pediatr Orthop 2014;34:55-62.
25. Woodward JW. Congenital elevation of the scapula. J Bone Joint Surg Am 1961;43:219-28.

How to Cite this Article:  Garrouche N, Jerbi S, Chouchane N, Kessomtini W, Hamza H The Role of Imaging in Diagnosis and Management of Congenital High Scapula (Sprengel’s Deformity): Case Report and Review | July-December 2018; 4(2): 27-31.

 

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Amputation Following Meningococcal Septicaemia in Children: the Surgical Management of the Residual Limb

Volume 4 | Issue 2 | July-December 2018 | Page: 20-26 | Brigid M. Aherne, Fergal P. Monsell

DOI- 10.13107/ijpo.2018.v04i02.014

Authors: Brigid M. Aherne, Fergal P. Monsell [1]

 

Medical Student, University of Bristol, [1] Consultant Orthopaedic Surgeon, Bristol Royal Hospital for Children, Bristol, England, United Kingdom.

Address of Correspondence
Mr. Fergal P. Monsell,
Bristol Royal Hospital for Children, Upper Maudlin St, Bristol BS2 8BJ, England, United Kingdom.
E-mail: Fergal.Monsell@UHBristol.nhs.uk

Abstract

Background: Meningococcal septicaemia is a potentially life-threatening disease and remains the most common infective cause of mortality in the UK. Improvements in healthcare have led to early recognition and treatment, and a decrease in mortality. As more children now survive the initial acute illness, the long-term musculoskeletal consequences have become more prevalent. These include growth plate injury, tissue loss and amputation. Patients with limb loss present specific difficulties due to the effect of remaining longitudinal growth on the function of the residual limb, and often require surgical treatment that continues throughout childhood.
Patients and Methods: This case series reviews the histories of 13 children who underwent amputation as a complication of meningococcal septicaemia. All patients attend a specialist clinic and our experience in the management of the residual limb is described.
Results: Thirteen patients, with a mean age of 16 months at the onset of meningococcal septicaemia, required amputation in the management of the skeletal consequences of the infection. Revision surgery was necessary for all 13 patients and involved management of bone overgrowth, growth arrest, scar and soft tissue contracture, neuroma development, and infection. The details of our approach to each of these complications is described.
Conclusion: Due to improvements in diagnosis and initial management, a significant proportion of patients are surviving infantile meningococcal septicaemia. Many develop musculoskeletal consequences including amputation, and this case series serves to increase knowledge in the complex managements of the residual limb in these patients.
Keywords: Amputation, meningococcal septicaemia, residual limb

References 

1. Paize F, Playfor SD. Improvements in the outcome of children with meningococcal disease. Crit Care 2007;11:172.
2. Maat M, Buysse CM, Emonts M, Spanjaard L, Joosten KF, De Groot R, et al. Improved survival of children with sepsis and purpura: Effects of age, gender, and era. Crit Care 2007;11:R112.
3. Nectoux E, Mezel A, Raux S, Fron D, Maillet M, Herbaux B. Meningococcal purpura fulminans in children: I. Initial orthopedic management. J Child Orthop 2010;4:401-7.
4. de Kleijn ED, Hazelzet JA, Kornelisse RF, de Groot R. Pathophysiology of meningococcal sepsis in children. Eur J Pediatr 1998;157:869-80.
5. Davies MS, Nadel S, Habibi P, Levin M, Hunt DM. The orthopaedic management of peripheral ischaemia in meningococcal septicaemia in children. J Bone Joint Surg Br 2000;82:383-6.
6. Belthur MV, Bradish CE, Gibbons PJ. Late orthopaedic sequelae following meningococcal septicaemia. J Bone Joint Surg Br 2005;87:236-40.
7. Booy R, Habibi P, Nadel S, de Munter C, Britto J, Morrison A, et al. Reduction in case fatality rate from meningococcal disease associated with improved healthcare delivery. Arch Dis Child 2001;85:386-90.
8. Monsell FP, McBride AR, Barnes JR, Kirubanandan R. Angular deformity of the ankle with sparing of the distal fibula following meningococcal septicaemia: A case series involving 14 ankles in ten children. J Bone Joint Surg Br 2011;93:1131-3.
9. Monsell F. The skeletal consequences of meningococcal septicaemia. Arch Dis Child 2012;97:539-44.
10. Nectoux E, Mezel A, Raux S, Fron D, Klein C, Herbaux B. Meningococcal purpura fulminans in children. II: Late orthopedic sequelae management. J Child Orthop 2010;4:409-16.
11. Park DH, Bradish CF. The management of the orthopaedic sequelae of meningococcal septicaemia: Patients treated to skeletal maturity. J Bone Joint Surg Br 2011;93:984-9.
12. Buysse CM, Oranje AP, Zuidema E, Hazelzet JA, Hop WC, Diepstraten AF, et al. Long-term skin scarring and orthopaedic sequelae in survivors of meningococcal septic shock. Arch Dis Child 2009;94:381-6.
13. Nogi J. Physeal arrest in purpura fulminans − A report of 3 cases. J Bone Joint Surg Am 1989;71:929-31.
14. Wheeler JS, Anderson BJ, De Chalain TM. Surgical interventionsin children with meningococcal purpura fulminans − A review of 117 procedures in 21 children. J Pediatr Surg 2003;38: 597-603.
15. Grogan DP, Love SM, Ogden JA, Millar EA, Johnson LO. Chondro-osseous growth abnormalities after meningococcemia − A clinical and histopathological study. J Bone Joint Surg Am 1989;71:920-8.

How to Cite this Article:  Aherne BM, Monsell FP | Amputation Following Meningococcal Septicaemia in Children: the Surgical Management of the Residual Limb | July-December 2018; 4(2): 20-26.
 

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The Role of Pirani Scoring in Predicting the Frequency of Casting and the Need for Percutaneous Achilles Tenotomy in the Treatment of Idiopathic Clubfoot Using the Ponseti Method

Volume 4 | Issue 2 | July-December 2018 | Page: 15-19 | Chukwuemeka O. Anisi, Joseph E. Asuquo, Innocent E. Abang, Michael E. Eyong, Onyebuchi G. Osakwe, Ngim E. Ngim

DOI- 10.13107/ijpo.2018.v04i02.013

Authors: Chukwuemeka O. Anisi, Joseph E. Asuquo, Innocent E. Abang, Michael E. Eyong [1], Onyebuchi G. Osakwe, Ngim E. Ngim

Departments of Orthopaedics and Traumatology, University of Calabar, Cross River State, Nigeria. [1] Departments of Paediatrics, University of Calabar, Cross River State, Nigeria.

Address of Correspondence
Dr. Chukwuemeka Okechukwu Anisi,
Department of Orthopaedics and Traumatology, University of Calabar Teaching Hospital, PMB 1278-Calabar, Cross River State, Nigeria.
E-mail: iall4him@yahoo.co.uk

Abstract

Background: The Pirani scoring system is a simple tool widely used for grading the severity of clubfoot. This study was designed to objectively assess its value in predicting the total number of casts required, and the need for percutaneous Achilles tenotomy to achieve correction of the idiopathic clubfoot treated by the Ponseti method. Patients and Methods: All patients with idiopathic clubfoot, who attended our clubfoot clinic between January, 2013 and December, 2015, were prospectively studied. Each clubfoot was scored at presentation and at each visit by the first and second authors, using the Pirani scoring system. All patients were treated by the first and second authors by weekly stretching and cast application following the Ponseti treatment protocol until correction was achieved (with or without percutaneous Achilles tenotomy). Chi-square tests were applied to establish any existing relationship between the Pirani scores and the need for percutaneous tenotomy as well as the number of casts required to achieve correction.
Results: A total of 69 patients with 108 idiopathic clubfeet wer recruited into the study. In that, 14 patients defaulted, leaving the study with 81 clubfeet belonging to 55 patients. The median total Pirani score (TPS), midfoot contracture score and hindfoot contracture score at presentation were 4.0, 2.0 and 2.0, respectively. A total of 57 (70.4%) feet required percutaneous Achilles tenotomy to achieve correction. The average number of casts (including casts after tenotomy) required to achieve correction was 4.9 (2–10). The average number of casts required to achieve correction was 4.1 (2–10) for the no tenotomy group and 5.4 (3–10) for the tenotomy group. Statistically significant relationship was established between the TPS and number of casts required to achieve correction for both the tenotomy group (P=0.039) and no tenotomy group (P=0.05).
Conclusion: High Pirani scores were associated with increased number of casts and percutaneous Achilles tenotomy for the correction of idiopathic clubfoot using the Ponseti method.
Keywords: Achilles tenotomy, clubfoot, idiopathic, Pirani scoring system, Ponseti method

References 

1. Solomon L,Warwick D, Selvadurai N.Appley’s Systemof Orthopaedics and Fractures. 9th ed. London: Hodder Arnold; 2010. p. 591-5.
2. Canale ST, Beaty JH. Congenital anomalies of the lower limb. Campbell’s Operative Orthopaedics. 11th ed. Philadelphia: Mosby Elsevier 2007. p. 937-55.
3. Ngim NE, Okokon E, Ikpeme IA, Udosen MA, Iya J. Profile of congenital limb anomalies in Calabar. Asian J Med Sci 2013;4:58-61.
4. Adewole AO, Giwa SO, Kayode MO, Shoga MO, Balogun RA. Congenital clubfoot in a teaching hospital in Lagos, Nigeria. Afr J Med Sci 2009;38:203-6.
5. Omololu B, Ogunlade SO, Alonge TO. Pattern of congenital orthopaedic malformations in an African Teaching Hospital. West Afr J Med 2005;24:92-5.
6. Adewole AO, Williams OM, Kayode MO, Shoga MO, Giwa SO. Early experience with Ponseti clubfoot management in Lagos, Nigeria. East Cent Afr J Surg 2014;19:72-7.
7. Ponseti IV. Current concept review. Treatment of congenital clubfoot. J Bone Joint Surg 1992; 74:448-54.
8. Sud A, Tiwari A, Sharma D, Kapoor S. Ponseti’s vs Kite’s methods in the treatment of clubfoot − A prospective randomized study. Int Orthop 2008;32:409-13.
9. Morcuende JA, Dolan LA, Dietz FR, Ponseti IV. Radical reduction in the rate of extensive corrective surgery for clubfoot using the Ponseti method. Pediatrics 2004;113:376-80.
10. Morcuende JA, Abbasi D, Dolan LA, Ponseti IV. Results of an accelerated Ponseti protocol for clubfoot. J Pediatr Orthop 2005; 25:623-6.
11. Adegbehingbe OO, Oginni LM, Ogundele OJ, Ariyibi AL, Abiola PO, Ojo OD. Ponseti clubfoot management: Changing surgical trends in Nigeria. Iowa Orthop J 2010;30:7-14.
12. Ponseti IV. Current concept review. Treatment of congenital clubfoot. J Bone Joint Surg 1992;74:448-54.
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How to Cite this Article:  Anisi CO, Asuquo JE, Abang IE, Eyong EM, Osakwe OG, Ngim E | The Role of Pirani Scoring in Predicting the Frequency of Casting and the Need for Percutaneous Achilles Tenotomy in the Treatment of Idiopathic Clubfoot Using the Ponseti Method | July-December 2018; 4(2): 15-19.

 

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Predicting the Need for Tenotomy in the Management of Idiopathic Clubfoot by the Ponseti Method

Volume 4 | Issue 2 | July-December 2018 | Page: 11-14 | Ranjit V. Deshmukh, Aditi A. Kulkarni

DOI- 10.13107/ijpo.2018.v04i02.012

Authors: Ranjit V. Deshmukh, Aditi A. Kulkarni [1]

 

Departments of Orthopedics, [1] Research, Deenanath Mangeshkar Hospital and Research Center, Pune, Maharashtra, India.

Address of Correspondence
Dr. Ranjit V. Deshmukh,
Department of Orthopedics, Deenanath Mangeshkar Hospital and Research Center, Erandwane, Pune − 411 004, Maharashtra, India.
E-mail: drranjitdeshmukh@gmail.com

Abstract

Purpose: The aim of this study was to determine the role of Pirani scoring system for predicting the treatment of idiopathic clubfoot with the Ponseti technique.
Materials and Methods: A retrospective study was conducted. The records of 132 idiopathic clubfeet of patients treated by the Ponseti method and scored by the Pirani system between May 2007 and September 2015 were analyzed.
Result: Of the 132 feet, 101 (76.5%) feet of the patients required tenotomy. The mean number of casts required was significantly higher (P=0.033) for the group that required tenotomy (5.53 ± 1.6 casts) than the group that did not require tenotomy (4.87 ± 0.9 casts).
Conclusion: The initial Pirani score is predictive of the number of casts that may be required and the need for a tenotomy of the Achilles tendon.
Keywords: Casting, Clubfoot, Congenital talipes equinovarus, Pirani scoring, Ponseti, Tenotomy

References 

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How to Cite this Article:  Deshmukh RV, Kulkarni AA | Predicting the Need for Tenotomy in the Management of Idiopathic Clubfoot by the Ponseti Method | July-December 2018; 4(2): 11-14.

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