Infantile Blount’s Disease: A case report of 3 years old child

Dr. SUMERA AKRAM Dr. MUHAMMAD AHMED KHAN

DHQ Hospital Zhob, Balochistan, Pakistan CMH Zhob, Balochistan, Pakistan

INTRODUCTION CASE DISCUSSION CONCLUSION

Blount’s disease is a growth disorder of bones
that results in internal rotation and bowing of
proximal tibia along with beaking at its
posteromedial end.
Named after American orthopedic surgeon
“Walter Putnam Blount” who first described this
condition. Other names ‘tibia vara’,
‘osteochondrosis deformans tibiae’ or
Mau-Nilsonne Syndrome.
PREVALENCE: Blount’s disease once thought a
rare entity has increased in incidence worldwide
since obesity is also on the rise. Exact
prevalence is still unknown.139 cases of Blount’s
disease have been studied in Ghana from 2010
to 2018 out of which 90% of cases belonged to a
particular tribe known as “Akan Tribe”. There is a
positive family history in 14% to 45% of infantile
Blount’s disease cases.
Etiology is multi-factorial with following
PREDISPOSING FACTORS :
1. obesity
2. early walking
3. M>F
4. African, Afro-American race
5. latent varus
6. increased pressure on growth plate due to
infection, trauma or osteonecrosis
7. possibly nutrition.
A three years old girl was brought by her mother in the TYPES of Blount‘s disease: The clinicians
outpatient department of District Headquarter Hospital Zhob with 1. Infantile/ early-onset arises before the age of 4 years usually bilateral and should adopt a high
complaint of progressive bowing of both lower limbs for last one severe index of suspicion
year. 2. juvenile develops., between 4-10 years of age for cases of genu
3. adolescent type/ late-onset develops after 10 years of age. Unilateral and varum with typical
Born by SVD at birthweight of 3.5kg, with uneventful prenatal less severe radiological
and postnatal history, she remained well till first two years of her RADIOLOGIC CLASSIFICATION: findings in children
life until her mother noticed the bowing of her legs. She had (Langenskiold radiographic classification) >3 years old, in
been exclusively breastfed for 8 months. Weaning was 4. Stage 1- medial metaphyseal beaking order to diagnose
introduced late and lacked diversity of solid foods. Milestones 5. Stage 2- saucer shape defect of medial metaphyses the infantile
achieved at appropriate age. She started walking without 6. Stage 3- saucer deepens into step Blount’s disease
support at 11 months of age. Family history is insignificant in 7. Stage 4- slopping of epiphysis over medial beak and to prevent
terms of bone pathologies, developmental disorders or 8. Stage 5- double epiphysis irreversible
metabolic diseases. She had been treated as a case of 9. Stage 6- medial physeal bony bar outcomes in the
suspected rickets during the last years and prescribed calcium affected cases.
and vitamin D supplements multiple times with no benefit.
On the day of her presentation her height was 90cms (at 10th
centile), weight was 17 kgs (at 90th centile), and BMI (body
mass index) was 20.9 (obese).
MANAGEMENT of Blount’s disease depends upon age of presentation and
No features of skeletal dysplasias, syndromic facies or any
severity of disease.
finding of metabolic disorders were noted.
• early stage I or II: Conservative management with bracing.
• Refractory cases/ severe disease: proximal tibial osteotomy followed by
Marked bowing of lower limbs observed at the level of tibia with
difficulty walking. There was no frontal bossing, wide wrist,
immobilization through casts, pins, external and internal fixations.
Management of severe and neglected cases can be challenging and may
REFERENCES
rachitic rosary and alopecia. Normal neurological exam. No
require multidisciplinary approach by a pediatric orthopedic surgeon, 1. Hollman F, Vroeman P. Infantile Blount’s disease: histopathological changes in the
hepatosplenomegaly. Rest of systemic examination was normal. proximal tibial metaphysic, comparison between medial and lateral specimens. Int J
pediatrician, metabolic disorder specialist, rehab specialist and orthotist. Pediatr Res 2016; 2: 025.
She has been advised roentgenograms, basic metabolic panel,
2. Jansen N, Hollman F, Bovendeert F, Moh P, Stegmann A, Staal HM. Blount disease
serum calcium, phosphate, vitamin D (25-hydroxy vitamin D)
• PROGNOSIS is good with early diagnosis and timely management. Early and familial inheritance in Ghana, area cross-sectional study. BMJ Pediatrics Open
and alkaline phosphatase levels. 2021; 5: e001052. Doi: 10.1136/bmjpo-2021-001052.
stages are usually reversible on their own. Untreated and neglected cases 3. Blount WP. Tibia vara osteochondrosis deformans tibiae. J Bone Joint Surg 1937;
can have lifelong gait deformities, short stature, limb length discrepancies 19: 1-29.
X-rays of lower limbs showed tibia in varus with a peculiar beak
and arthritis of knees. 4. Thompson GH, Carter JR. Late onset tibia vara (Blount’s disease). Clin Orthop
at metaphysis and raised metaphyseal-diaphyseal angle (>16 Relat Res 1990; 255: 24-35.
DIFFERENTIAL DIAGNOSIS: Physiological bowing, rickets, trauma, infection,
degrees). No features of rickets were noted in x rays of wrist 5. Schoenecker PL, Meada WC, Pierron RL. Blount’s disease: a retrospective review
fibrocartilaginous dysplasia. and recommendations for treatment. J Pediatr Orthop 1985: 5: 181-6.
joint.

Serum calcium and vitamin D (25-hydroxy vitamin D) were

normal. Serum alkaline phosphatase level was raised (832U/L)
(In literature 15 cases of Blount’s disease in Nigeria showed
significant increase in serum alkaline phosphatase as compared
to control group. The differentiation from rickets is mainly on the
basis of x-rays).

Keeping in view the typical history, examination and radiological

findings diagnosis of Infantile Blount’s disease was made.The
patient was then referred to orthopedic department of tertiary
care hospital for management of Blount’s disease.

CONTACT
Dr. sumera akram
Email: sumera_ak@yahoo.com
Phone: 03216974646