The utility of ultrasound in showing a unique cause of posterior interosseous nerve syndrome

Dear Editor These ultrasound images (Fig. 1. Images A–D) convey an enlarged posterior interosseous nerve (PIN) with interruption of the PIN course by dislodgement of the distal of two Mitek anchors inserted 5 years previously for a biceps tendon rupture raising suspicion of PIN transection at the level of the distal biceps anchor. Surgical exploration confirmed complete PIN laceration with the most likely mechanism chronic PIN abrasion by the dislodged anchor related to occupational repetitive forearm supination and pronation. A 56-year-old barista, whose work duties involved chronic, repetitive wrist and forearm pronation and supination, presented with a gradual onset (over several weeks) progressive weakness involving right thumb, finger and wrist extension and supination with preservation of strength in extensor carpi radialis longus, brachioradialis and triceps muscles and normal sensation. Right superficial radial sensory amplitude was normal. Electromyography revealed denervation (fibrillation potentials) with no motor units under voluntary control in radial-innervated muscles distal to supinator including extensor digitorum communis. Examination and electromyographic findings were consistent with a PIN syndrome. X-rays showed protrusion of distal Mitek anchor through posterior aspect of radius (Image E). MRI demonstrated increased signal intensity and thickening of the PIN proximal to supinator but visualization within supinator was marred by magnetic susceptibility due to the anchor. Ultrasound showed a normal nerve in the radial tunnel (~2 mm diameter) and an increasingly grossly, swollen abnormal PIN posterior to the proximal radius (6.8 mm diameter). A metallic anchor was seen (Image C) within the substance of the nerve. The anchor had its prong uppermost (ultrasound) and was clearly not in bone. The ultrasound, clinical and electromyographic findings were strongly suggestive of transection of the PIN justifying exploration at the biceps anchor level rather than radial tunnel, which prior to the ultrasound was the favored site for exploration. Surgery confirmed a dislodged distal anchor and a transected, injured and scarred (over 3 cm segment) PIN distal to supinator and superficial radial nerve branches. The prong of the distal anchor was protruding through the radius posterior cortex and deep head of supinator into the PIN giving support to the likely mechanism of injury. The patient underwent a right PIN repair with 4 cm sural nerve graft. At 8 months, there was recovery of supination and improvement in wrist extension and finger extension (MRC grade 3) but ongoing severe thumb extension weakness. PIN syndrome is usually caused by compression most commonly at the “arcade of Frohse” [1]. Injury to the PIN as a complication from biceps tendon repair is an uncommon temporary complication usually noted in the immediate post-operative phase due to poor deployment of the cortical fixation anchor, stretching or pressure of the nerve in a pronator position [2]. Our patient's work duties may have contributed to delayed anchor dislodgement. Imaging modalities such as MRI and sonography help delineate PIN lesion location and etiology. Determination of the lesion is important in complete transections because nerve repair techniques are only useful within 1 year from injury for successful reinnervation of motor endplates [3]. Sonography was able to visualize a markedly swollen PIN associated with the displaced anchor confirming the level of pathology and allowing prompt treatment and opportunity for recovery of muscles innervated by the PIN. In summary, our case shows a unique cause of a transected PIN due to delayed displacement of a biceps tendon anchor. It also demonstrates the benefit of ultrasound in examining peripheral nerves and in this case localizing and determining the etiology of the PIN palsy. A video of the ultrasound can be seen in the supplementary data (Appendix A).