Posteromedial Bow of Tibia

• Rare; reported as roughly 1 per 1,000 to 1 per several thousand live births in older series (exact incidence uncertain — most evidence is small single-centre cohorts)
• Usually unilateral; the left side is more frequently affected in collated case-series data
• A slight male predominance is reported in pooled literature, though individual series vary
• Sporadic — no Mendelian inheritance pattern and no reproducible familial clustering
• An association with firstborn status has been noted, supporting an intrauterine-packaging mechanism

the two components behave oppositely over time. According to PubMed, Pappas (1984) followed 33 patients and showed that the posterior and medial angular components reduce markedly with growth, but tibial shortening persists and is proportional to the initial bow, with absolute discrepancies of 3.3-6.9 cm at maturity (DOI/PMID 6490868).

the tibia is normally straight in both the sagittal and coronal planes, with a triangular cross-section. Bone remodels throughout childhood in response to physeal growth and mechanical (Heuter-Volkmann) forces, which is why a flexible neonatal angular deformity can correct.

• Posterior + medial diaphyseal angulation — apex posteromedial, concavity anteromedial; initial bow at birth ranges from roughly 25 to 70 degrees
• Normal bone architecture — no narrowed/sclerotic canal, no cystic lesion and no hamartomatous fibrous tissue (these are features of the CPT spectrum, not of posteromedial bow)
• Tibial and fibular shortening present from birth and progressive in absolute terms through growth
• Distal tibial changes can develop — wedging of the distal tibial epiphysis, fibular hypoplasia and valgus inclination of the distal articular surface in some children

the leading hypothesis is intrauterine moulding / packaging (fetal constraint of a dorsiflexed, externally rotated foot pressing the leg posteromedially), supported by the firstborn association, the universal calcaneovalgus foot and prenatal ultrasound detection. It is not a positional deformity in the trivial sense, because the shortening is a true growth disturbance, not just a postural curve.

• Calcaneovalgus foot — almost universal at birth, usually resolves
• Reduced ankle dorsiflexion and sometimes calf/peroneal muscle weakness — may persist into later childhood (Pappas described early posterior soft-tissue fullness evolving into relative muscle atrophy)
• Progressive limb-length discrepancy — the dominant long-term issue

• Bowing noted at birth or early infancy
• May have calcaneovalgus foot noted
• Usually no pain or functional limitation
• Family history (rare but may be present)
• No history of trauma

• Assess posteromedial bowing
• Measure bowing angle
• Evaluate bone structure (should be normal)
• Assess for any cystic changes (should be absent)
• Evaluate medullary canal (should be normal)

• Measure bowing angle accurately
• Assess alignment
• Evaluate for leg length discrepancy
• Assess foot position

• Posteromedial diaphyseal angulation with normal bone architecture — normal cortical thickness, no canal narrowing/sclerosis, no cyst, no pseudarthrosis (these features exclude the CPT spectrum)
• Tibial and fibular shortening, often with fibular hypoplasia distally
• Possible distal tibial epiphyseal wedging and increased lateral distal tibial angle deviation (ankle valgus) over time

• Track the angular bow (AP and lateral interphyseal angles) — expect rapid early correction
• Track the percentage tibial shortening and predict LLD at maturity using the multiplier method — the proportional discrepancy is stable after about 12 months, making prediction reliable
• Follow at 6-12 month intervals in early childhood, then periodically; continue surveillance until skeletal maturity because LLD progresses and ankle deformity can evolve — do NOT discharge once the angle looks better

posteromedial bowing can be detected on antenatal ultrasound (reported from the second trimester); recognising it prenatally allows appropriate parental counselling and avoids misdiagnosis as a skeletal dysplasia or fracture.

• CT/MRI — not routinely indicated; reserve for surgical planning or atypical features
• Genetic / NF1 testing — only if NF1 stigmata raise the possibility of an anterolateral (CPT) lesion instead

• Progressive limb-length discrepancy — the dominant problem; mean 3-4 cm, frequently over 2.5 cm, occasionally over 5 cm. NOT a trivial sub-centimetre difference
• Residual angular deformity — uncommon but may persist beyond age 4 if the initial bow was severe
• Persistent reduced ankle dorsiflexion and calf/peroneal weakness
• Ankle valgus from distal tibial wedging / fibular hypoplasia

• Accurate prediction (multiplier method) and correct timing of equalisation
• Circular/hexapod fixation or internal lengthening with adequate stability
• Proactive ankle protection and physiotherapy during distraction

the untreated complication that matters is the progressive discrepancy, not fracture (this condition does not pseudarthrose); the treatment-related complications are those of limb reconstruction.

• At diagnosis — baseline clinical exam, radiographs, document angle, percentage shortening, foot/ankle posture
• 6-12 monthly through early childhood, then periodic review until skeletal maturity
• Each visit: re-measure interphyseal angles and LLD, re-run the multiplier prediction, reassess ankle dorsiflexion
• Do not discharge once the angle improves — the discrepancy and ankle deformity evolve over years

prognosis is excellent — the posteromedial bow remodels spontaneously and substantially, with most correction in the first year and the majority of children needing no angular surgery. A mild residual medial component may remain.

prognosis is guarded without planning — the discrepancy is progressive and proportional to the initial bow:

• Hofmann & Wenger (1981): mean LLD 3.1 cm at follow-up, with 9 of 13 children over 2.5 cm and usually progressing
• Pappas (1984): absolute tibial discrepancy 3.3-6.9 cm at maturity, greater with greater initial bow
• Modern series confirm progressive shortening and frequent need for equalisation (epiphysiodesis or lengthening)

the calcaneovalgus foot resolves, but reduced ankle dorsiflexion may persist and ankle valgus can develop from distal tibial changes.

• Greater initial angular bow (the single best predictor)
• Greater early percentage shortening
• Distal tibial epiphyseal wedging / fibular hypoplasia (predict ankle valgus)

generally good. With appropriate prediction and timely, well-executed equalisation, most patients reach maturity with near-equal leg lengths, neutral alignment and good function; outcomes after lengthening are good in modern series, though at the cost of the morbidity of reconstruction. The key message is that good outcomes depend on surveillance and planning, not on assuming the condition disappears on its own.

According to PubMed, Pappas described enlargement of the posterior soft tissues of the affected leg in early life that evolves into a relative muscle atrophy in later years, together with an initial calcaneovalgus foot and a decrease in ankle motion that does not improve with age (DOI is for the related Shah series; Pappas is PMID 6490868, no DOI indexed). Shah, Doddabasappa and Joseph (2009) likewise recommended following all children to maturity specifically to detect residual muscle weakness alongside limb-length inequality and ankle deformity (DOI).

• At birth the foot sits in calcaneovalgus (dorsiflexed against the shin); this posture resolves, but the underlying posterior-compartment weakness and a fixed reduction in ankle dorsiflexion frequently persist
• The functional consequence is weak plantarflexion / push-off — the child may have difficulty with toe-walking and heel-rise, and a subtly weaker calf on the affected side
• This is distinct from the calcaneovalgus foot itself (a flexible neonatal foot posture that is comprehensively covered as its own entity); here the concern is the leg's posterior musculature and the ankle's motion arc, which are CPMBT-specific and long-lasting

• Compare calf girth side to side; document active and passive ankle dorsiflexion/plantarflexion and single-leg heel-rise as the child matures
• Note that reduced dorsiflexion here is a motion/strength deficit, separate from the later ankle valgus produced by distal tibial wedging and fibular hypoplasia — the two can coexist and should be recorded separately

• Physiotherapy and stretching for the ankle motion arc and calf strength; this is the mainstay and surgery is rarely needed
• A fixed equinus/limited-dorsiflexion contribution should be recognised before any lengthening, because distraction tends to aggravate equinus and valgus — the ankle must be protected (physiotherapy, sometimes temporary foot-frame extension) during reconstruction
• True operative soft-tissue correction (tendo-Achilles or posterior release) is reserved for the rare rigid or functionally limiting deformity