Slipped Capital Femoral Epiphysis (SCFE)

A slipped capital femoral epiphysis is a Salter-Harris type I (occasionally II) separation through the proximal femoral growth plate. It happens under a combination of mechanical overload, obesity being by far the commonest risk factor, and hormonal change: the adolescent growth spurt, and endocrine disorders that weaken the physis.

Which part moves. The epiphysis is held in the acetabulum, so it is really the neck and shaft that displace. The metaphysis moves anteriorly and rotates externally relative to the head, which is why the classic examination finding is obligate external rotation when the hip is flexed.

Why it is high-stakes. First, it hides. The pain is often felt in the thigh or knee rather than the hip, and a mild slip can look almost normal on an AP film, so it is a classic missed diagnosis.

Second, its feared complication, avascular necrosis (AVN) of the femoral head, is driven largely by the initial vascular insult at the moment the slip becomes unstable and by any attempt to reduce it forcefully, rather than by how skilfully it is later pinned. Get the diagnosis early, classify stability correctly and fix in situ, and most children do very well.

Who gets it. The peak age is 10–16 years, at the growth spurt, with a mean of about 12–13 in boys and 11–12 in girls. Boys are affected more often than girls. Incidence is markedly higher in children of African and Pacific Islander ancestry, lowest in East Asian populations, and rising with childhood obesity worldwide.

Risk factors. Obesity is the dominant one. Beyond it, look for:

• Rapid growth, or being tall for age
• Endocrine disorders: hypothyroidism, growth-hormone abnormalities, hypogonadism
• Renal osteodystrophy, and previous radiation
• Femoral retroversion

Where the slip happens. From the epiphysis downward, the growth plate runs through the reserve (resting) zone, the proliferative zone, the hypertrophic zone and the zone of provisional calcification before it meets the metaphyseal primary spongiosa. The hypertrophic zone is the mechanically weakest layer, and in SCFE it is abnormally widened and disorganised under combined hormonal and mechanical influence.

The cleavage plane. The slip propagates as a cleavage through the hypertrophic zone and zone of provisional calcification. Recognising this plane explains both why the slip occurs where it does and why a single screw across the physis arrests it.

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Why the adolescent physis. Around the growth spurt the physis becomes more obliquely or vertically oriented, raising the shear across it, and the reinforcing perichondrial ring thins. Sex-hormone and growth-hormone shifts, plus excess body weight, further reduce its resistance to shear, which is exactly why obesity and endocrinopathy are such strong risk factors.

The blood supply. The femoral head is fed by the retinacular vessels, terminal branches of the medial femoral circumflex artery (MFCA). The MFCA curves around the posterior neck and gives off the posterosuperior retinacular (lateral epiphyseal) vessels, which ascend the posterosuperior femoral neck in a periosteal sleeve that stays attached to the epiphysis. They supply ~80–90% of the head; the artery of the ligamentum teres is only a minor contributor.

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Why AVN is the dominant fear. When the slip occurs the retinacular vessels are stretched, and in an unstable slip they may already be torn or thrombosed. That is why unstable slips carry such a high AVN rate regardless of treatment.

What you are protecting. Any forceful reduction, open or closed, or aggressive dissection along the posterosuperior neck risks tearing these vessels and causing AVN. This is the single reason in situ fixation without reduction is the rule: the posterior periosteum and its vessels are the structures you are protecting.

Three classifications are used, but they are not equal: stability (Loder) predicts the outcome, while Southwick grades the deformity and the temporal labels describe the history.

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Southwick angleTemporal

Southwick (severity) is the lateral epiphyseal–shaft (head–shaft) angle, measured ideally on the frog-leg lateral of both hips. To measure it:

1. Mark the anterior and posterior tips of the capital epiphysis at the physis and join them: the epiphyseal base line.
2. Draw a line perpendicular to that base line.
3. Draw the femoral shaft axis.
4. The angle between the perpendicular and the shaft axis is the head–shaft angle.
5. Subtract the contralateral (normal) hip's head–shaft angle; the difference is the Southwick slip angle. If both hips are slipped, use the normal reference of ~12°.

Mild

Southwick slip angle

Less than 30°

Clinical

Minimal deformity

Moderate

Southwick slip angle

30–50°

Clinical

Some deformity

Severe

Southwick slip angle

Greater than 50°

Clinical

Significant deformity, cam-FAI risk

Severity	Southwick slip angle	Clinical
Mild	Less than 30°	Minimal deformity
Moderate	30–50°	Some deformity
Severe	Greater than 50°	Significant deformity, cam-FAI risk

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Temporal labels describe the history rather than the prognosis: acute (symptoms under 3 weeks), chronic (over 3 weeks), or acute-on-chronic (a chronic slip with an acute exacerbation). They are less useful than Loder stability for predicting outcome.

History. The child limps, with an antalgic or abductor gait, and has groin, thigh or knee pain; the referred knee pain is the classic trap. The critical question is can the child weight-bear?, because the answer decides stability. Ask about endocrine and renal history and a family history of SCFE.

The hallmark sign. Obligate external rotation with hip flexion is the Drehmann sign. As you flex the hip it is forced into external rotation, because the anteriorly displaced metaphysis drives against the anterior acetabulum: it is, in effect, the slip made visible on examination.

The rest of the examination. Internal rotation is lost, a severe slip gives apparent limb shortening, and you should look for a Trendelenburg gait. Always examine the other hip.

The pathway is the same in principle for every slip: confirm stability, fix in situ, then decide about the other hip. The urgency differs sharply with stability.

Prognosis and timing. The prognosis of a stable slip is excellent; that of an unstable slip is guarded because of its high AVN risk. The ~24-hour window for an unstable slip is not universal practice: units vary between emergency fixation within 24 hours and planned-urgent surgery once the synovitis has settled, the approach Aronsson and Loder recommended with preoperative bed rest.

Screw technique. The child lies supine on a fracture table with fluoroscopy. Enter the anterolateral femur, below the vastus lateralis ridge, so that the screw lines up with the centre of the epiphysis on the lateral view.

• Aim for the centre of the epiphysis on both AP and lateral, perpendicular to the physis
• Cross the physis with at least five threads in the epiphysis
• End the tip within ~5 mm of the subchondral bone: close enough for purchase, never through it
• Confirm no joint penetration on live fluoroscopy through a full arc, the approach-withdrawal manoeuvre

One screw. A single screw is sufficient for almost all slips; extra screws add AVN risk without adding stability. Practice still varies over single versus two screws for unstable slips, and over screws versus smooth pins in the very young.

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Severe slips. For a severe slip (greater than ~50–60°) with significant cam-FAI, the safest default remains in situ pinning now and deformity correction later. The options for the residual deformity:

• An intertrochanteric (Imhauser) flexion-rotation osteotomy, away from the physis, with lower AVN risk
• An osteochondroplasty of the metaphyseal prominence
• Only in expert hip-preservation centres, a modified Dunn: surgical hip dislocation with anatomical realignment and an MFCA-protecting retinacular flap

The other hip. The contralateral slip risk is 20–40%. Offer prophylactic fixation more readily when:

• The child is young; chronological age under ~13 is the strongest predictor
• There is an endocrine or renal cause
• The contralateral physis is widened
• Follow-up is unreliable
• The posterior sloping angle is high

The posterior sloping angle (PSA). It is measured on the frog-leg or cross-table lateral of the currently unaffected hip, as the angle between the physis and a line perpendicular to the femoral-neck/shaft axis: how far the physis slopes posteriorly. A PSA above roughly 14° is associated with a markedly higher risk of a subsequent contralateral slip and tips the balance toward prophylactic fixation; a low PSA is reassuring.

If you do not pin it. Counsel the family and monitor to skeletal maturity. It is a shared, individualised decision.

What decides the long-term hip. AVN, when it occurs, is the principal driver of a poor long-term hip, and its risk rises steeply with any reduction attempt. Cam-FAI from residual deformity is the slower, later cause of osteoarthritis, even in mild slips; severe slips drive cam-FAI and early osteoarthritis and may need later deformity correction.

Chondrolysis. It is acute loss of articular cartilage, defined radiographically as joint-space narrowing to under ~3 mm (or under 50% of the contralateral hip), and it presents with progressive pain and a globally stiff, restricted hip. The classic and avoidable cause is persistent intra-articular screw penetration, which is why the full-arc fluoroscopic check is mandatory.

Chondrolysis without penetration. It can also occur idiopathically, without any pin penetration, and is associated with severe slips and prolonged spica immobilisation. Management is to confirm there is no retained intra-articular hardware, then NSAIDs, analgesia and physiotherapy to maintain motion; it is often partly self-limiting but can leave permanent stiffness.

Endocrine or atypical SCFE. Suspect an endocrine cause if the slip is bilateral, or the child is younger than usual, short, or has delayed puberty. Screen for hypothyroidism, growth-hormone deficiency, hypogonadism and renal osteodystrophy, and lower the threshold for prophylactic contralateral fixation.

Reducing the unstable slip. The classical doctrine is no forced reduction. Loder's 1993 series found no demonstrable association between early reduction and AVN, though its small numbers limit that analysis. Modified-Dunn series report anatomical realignment with low AVN, but only in expert centres; elsewhere AVN climbs steeply, and there is no randomised comparison. Outside high-volume units, in situ pinning is the safe default.

Capsular decompression. Some argue that urgent decompression of the tense haemarthrosis in an unstable slip relieves tamponade on the retinacular vessels and lowers AVN. The evidence is conflicting and it is not universally adopted.

Late or missed SCFE. A chronic healed slip may present years later with cam-FAI and early osteoarthritis. Correct the mechanics with an osteotomy or osteochondroplasty, but avoid osteotomy through the old slip site, which carries a high AVN risk even years on.

Everything below condenses SCFE for revision and viva practice: worked vivas, a one-screen cheat sheet and the evidence base.