Swan Neck Deformity (SND) is a common hand abnormality that significantly impairs finger function. The deformity is defined by a characteristic posture where the proximal interphalangeal (PIP) joint, or the middle knuckle, is hyperextended, bending backward beyond its normal range of motion. Simultaneously, the distal interphalangeal (DIP) joint, the joint closest to the fingertip, is held in a flexed position. This configuration creates an “S” shape in the finger, visually resembling the neck of a swan. This mechanical imbalance makes it difficult to fully bend the finger, interfering with grasping or pinching objects.
Primary Cause Inflammatory Arthritis
Inflammatory arthritis, particularly Rheumatoid Arthritis (RA), is the most frequent systemic cause leading to the development of Swan Neck Deformity. Chronic inflammation targets the joint capsule and surrounding ligaments, causing them to weaken and stretch out over time. The most affected structure is the volar plate, a strong band of fibrocartilage on the palm-side of the PIP joint that normally prevents hyperextension.
As the volar plate loses integrity and becomes lax, the PIP joint becomes unstable and hyperextends. This initial hyperextension disrupts the balance of the finger’s extensor mechanism, forcing the DIP joint into a flexed position. The disease can also affect the metacarpophalangeal (MCP) joints, sometimes causing them to shift, which further contributes to the mechanical imbalance. Psoriatic Arthritis is another inflammatory condition that similarly contributes to this progressive joint deformity through chronic inflammation and subsequent tissue damage.
Connective Tissue Disorders and Joint Instability
Systemic conditions affecting connective tissues can cause Swan Neck Deformity by creating inherent structural weakness, independent of joint inflammation. These disorders involve genetic mutations that result in the production of faulty structural proteins. Ehlers-Danlos Syndrome (EDS), for example, is often caused by defects in collagen synthesis, leading to hypermobility and extreme joint laxity.
The resulting tissue fragility means that the volar plate and other ligaments are congenitally weak and overly elastic. Due to normal stresses, this compromised volar plate breaks down prematurely, allowing the PIP joint to hyperextend. Marfan syndrome, which results from a mutation in the FBN1 gene, similarly causes generalized ligamentous laxity. In these conditions, the deformity arises from a breakdown of inherent tissue strength rather than from an autoimmune destructive process.
Localized Trauma and Muscular Imbalance
Causes of Swan Neck Deformity can be highly localized, resulting from an acute event or chronic mechanical disruption within the hand. Direct trauma, such as a poorly healed fracture or an injury that severs the flexor tendon, can instantly destabilize the joint complex. An untreated injury to the fingertip, commonly known as Mallet Finger, frequently progresses into this deformity.
Mallet Finger involves a ruptured extensor tendon at the DIP joint, causing the fingertip to droop into permanent flexion. This DIP flexion creates a mechanical imbalance that increases tension on the extensor mechanism at the PIP joint, pulling it into hyperextension. Nerve damage, such as Ulnar nerve palsy, can also cause an imbalance in the small intrinsic muscles of the hand. This muscular imbalance leads to an intrinsic contracture, where shortened muscles exert an excessive pull on the extension mechanism, contributing to PIP joint hyperextension.