ALPSA Lesions

What it is. An ALPSA lesion (Anterior Labroligamentous Periosteal Sleeve Avulsion) is an avulsion of the anterior labrum and IGHL from the glenoid rim in which the anterior scapular periosteum remains intact but stripped. Because the periosteum holds, the tissue behaves as a sleeve: the labrum slides medially down the glenoid neck and heals there, inferiorly on the neck, scarred into a non-functional position.

How it differs from a Bankart. In a Bankart lesion the periosteum tears, creating a distinct separation: the detached labroligamentous structures float free anterior to the rim and the lesion does not heal, leaving a gap. In an ALPSA the tissue is still present but medialised, and that "medialisation" eliminates the glenoid depth, predisposing the joint to recurrent anterior instability even with minor trauma.

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The labroligamentous complex. The structures involved are the labrum, the inferior glenohumeral ligament and the periosteum:

• Labrum: a fibrocartilaginous bumper that increases glenoid depth by 50%
• Inferior glenohumeral ligament (IGHL): the main static restraint
• Periosteum: the thick anterior scapular periosteum

The mechanism. A forceful anterior dislocation strips the periosteum without rupturing it. The stripped periosteum forms a sleeve, and the labrum and ligament slide medially within it.

The healing trap. Because the tissue remains vascularised through the periosteum and stays in contact with bone, it heals. It heals on the glenoid neck, medial to the rim, so the glenoid concavity is lost (the "flat glenoid") and the chock-block effect is gone. This is what explains the high recurrence rates in untreated ALPSA.

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Biomechanical consequences. Loss of labral height reduces the effective glenoid concavity by up to 50%. Medialised healing elongates the IGHL complex, leaving it effectively lax and reducing its tension; force distribution across the glenohumeral joint is disrupted, and the force required to cause a dislocation is significantly reduced.

The compression-concavity mechanism. The labrum normally creates a chock block that resists humeral head translation. When the labrum is medialised that effect is lost even though the tissue is present, and the joint becomes functionally equivalent to a glenoid with bone loss. This is why a repair without mobilisation fails: the bumper never returns.

Neviaser classification. Neviaser staged the lesion by its age and the state of the tissue, and the distinction is crucial for surgical planning:

Chronic lesions often require a capsular release, anterior and inferior, to gain excursion.

History. The patient reports recurrent instability, often described as a "loose" shoulder, and often gives a history of multiple dislocations. Clicking or catching can occur. The provoking position is abduction and external rotation, the ABER position, and the lesion is common in young patients under 25.

What the history can tell you. The history is identical to Bankart instability. Chronic symptoms suggest an ALPSA rather than an acute Bankart.

Red flags. These warrant urgent imaging and specialist referral:

• First-time dislocation over age 40 (rotator cuff tear risk)
• Neurological symptoms (axillary nerve injury)
• Unable to reduce (locked posterior dislocation)

Findings. The tests and what they show:

The limit of the examination. You cannot clinically distinguish an ALPSA from a Bankart. Imaging is the only differentiator.

The anterior lesion family. A Bankart lesion is a true labral detachment with a floating labrum. A Perthes lesion is a non-displaced periosteal sleeve avulsion. A GLAD lesion is a glenolabral articular disruption, with the focus on the cartilage. Beyond these, consider a HAGL lesion (humeral avulsion of the glenohumeral ligament), a bony Bankart (labrum with an attached bone fragment) and multidirectional instability (global capsular laxity, atraumatic).

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The posterior counterpart. Everything above is anterior. The posterior analogue is the POLPSA (Posterior Labrocapsular Periosteal Sleeve Avulsion), the direct mirror of the ALPSA: in posterior instability the posterior labrum and capsule are stripped with an intact periosteal sleeve and displace and medialise on the posterior glenoid neck, and the same principle applies, mobilise the medialised tissue before fixation. Posterior instability is more often atraumatic or from repetitive loading (linemen, bench-pressing) than a single dislocation, but the labroligamentous-sleeve concept is identical. The related posterior lesions:

• Reverse Bankart: a discrete postero-inferior labral detachment, the posterior equivalent of the Bankart
• Kim lesion: an incomplete, "concealed" avulsion of the postero-inferior labrum (a marginal crack with an intact superficial surface) that must be completed and then repaired
• Reverse Hill-Sachs (McLaughlin) lesion: the anteromedial humeral-head impaction of a posterior dislocation, classically after a seizure or electrocution

The decision. Non-operative treatment has a high failure rate in young patients and is not recommended for athletes. Operative treatment is indicated for recurrent instability. Arthroscopic repair is the gold standard; open repair is rarely needed unless there is massive bone loss. The key is the technical execution of the repair.

Timing. Early repair of an acute lesion is easier because the tissue is not scarred. Chronic repair is equally successful if the lesion is adequately mobilised. Do not delay once the diagnosis is confirmed.

Algorithm

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Arthroscopic repair, step by step.

1. Diagnostic arthroscopy. Confirm the diagnosis. Probe the labrum: it may feel "healed" but it lacks bumper function.
2. Mobilisation, the critical step. Use an elevator or shaver to detach the scarred labrum from the glenoid neck, and release anteriorly and inferiorly, around the corner. "Float the labrum": it must rise to the rim effortlessly.
3. Preparation. Decorticate the glenoid rim to create a bleeding bed.
4. Fixation. Suture anchors on the face, at the articular margin.
5. Shift. Tension the tissue superiorly and laterally to restore the bumper.

Failure to mobilise turns this into a non-anatomical plication.

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Pearls. The 5 o'clock portal is essential for the inferior release. Switch to the anterosuperior portal to view the reduction of the drive-through sign. Use 3 or more anchors for robust fixation, and if the tissue is poor, incorporate the capsule (Bankart repair plus capsular shift).

Recurrence is the most common complication, and is often due to failure to mobilise the lesion fully. Stiffness follows excessive tightening (overtensioning). The axillary nerve is at risk during the inferior dissection. Infection is rare.

Hardware and chondrolysis. Anchors can loosen. Placing anchors on the articular face is necessary for an ALPSA repair, but they must not be prominent: metal or hard PEEK anchors that sit proud can destroy the humeral head cartilage (chondrolysis). Use soft anchors, or ensure that knotless anchors are countersunk.

The protocol. Rehabilitation is identical to that after a Bankart repair:

Sling removal criteria.

• No pain at rest
• Control of the scapula
• Ability to perform activities of daily living at waist level

Contact progression.

• 4 months: non-contact drills (passing, catching)
• 5 months: controlled contact (pad work)
• 6 months: unrestricted contact (tackling)

Return to sport criteria.

• Full, pain-free range of motion
• Symmetrical strength (external rotation, internal rotation, abduction)
• Psychological readiness (ACL-RSI or a similar scale)
• Completion of sport-specific training drills
• No apprehension in the apprehension position

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Recurrence. The recurrence rate is higher than for a discrete Bankart even after arthroscopic repair: 19.2% (5/26) versus 7.4% (5/67) at a mean 47 months (P = .05, Level IV). Proper mobilisation of the medialised lesion is necessary but does not, on the available evidence, bring the failure rate down to that of a discrete Bankart. Without mobilisation, recurrence rates are significantly higher still.

Why. ALPSA patients arrive after significantly more instability events, a mean of 12.3 dislocations or subluxations versus 4.9, so the lesion is a marker of a more damaged shoulder as well as a harder repair. That is the honest reading: the medialisation is part of the problem rather than the whole of it.

Other outcomes. Return to sport is high (greater than 85%). A long-term risk of arthritis exists because of the initial cartilage damage, and a GLAD component often co-exists.

Prognostic factors.

• Age: younger patients have a higher recurrence risk
• Bone loss: significant glenoid bone loss requires a Latarjet, by the thresholds in Imaging (typically over 25%)
• Hyperlaxity: a Beighton score greater than 5 increases the failure risk
• Sport: collision athletes have a higher recurrence

Keep the ALPSA in proportion: bone loss outranks it, and by a wide margin. Across 194 arthroscopic Bankart repairs, significant bone defects, an inverted-pear glenoid or an engaging Hill-Sachs, raised recurrence to 67% versus 4% without, and to 89% in contact athletes with bone loss. The authors identified those bony defects, not the soft-tissue pattern, as the dominant driver of arthroscopic repair failure, and recommended bony reconstruction where glenoid loss is significant.

The practical consequence for a medialised chronic lesion is that recognising and mobilising the ALPSA is necessary but is the smaller half of the assessment. Quantify the glenoid bone loss and characterise the Hill-Sachs before committing to a soft-tissue repair: a beautifully mobilised ALPSA repaired over an inverted-pear glenoid still fails most of the time. The evidence is a retrospective case series that predates the glenoid-track concept, so use it for the magnitude of the effect rather than as a modern decision rule.

• No ALPSA-specific society guideline exists — it is a lesion subtype rather than a stand-alone diagnosis, so management follows the broader anterior shoulder instability literature (ISAKOS, AAOS, BOA-BESS and shoulder-society instability working groups) on labral repair and bone-loss thresholds.
• Epidemiology: ALPSA is over-represented in chronic, recurrent instability and in collision/contact athletes worldwide (rugby, American football, AFL, wrestling, ice hockey), reflecting the repeated dislocations that drive the medialised, scarred lesion.
• Standard of care: Recognition of the medialised lesion and mobilisation (takedown and float to the rim) before fixation is a universally expected technical standard; an "in-situ" repair that fixes the labrum on the neck is regarded internationally as a technical error and a cause of revision.
• Bone-loss integration: Across guidelines the decision is increasingly driven by quantified glenoid bone loss and the glenoid track (subcritical/critical thresholds, off-track Hill-Sachs), so a chronic ALPSA with significant bone loss may need a bony procedure (Latarjet) rather than soft-tissue repair alone.
• Practice variation reflects access to MR arthrography/CT arthrography for diagnosis and to bony-augmentation options, not disagreement on the mobilisation principle.