Anterior Interosseous Nerve Palsy After Cardiopulmonary Resuscitation in a Resuscitator with Undiagnosed Muscle Anomaly

Abstract

Techniques for cardiopulmonary resuscitation (CPR) are now widely taught, not only to medical staff but also to the general public. At the same time, risks to the administrator of CPR, such as infection, postraumatic disorder, and myocardial ischemia (1–3) have also been reported. We report a case of anterior interosseous nerve (AIN) palsy after administration of CPR in a resuscitator with undiagnosed muscle anomaly. Case Report A 38-yr-old fisherman was admitted to the hospital with an inability to move the fingers of his right hand. He had performed unassisted CPR on a 70-yr-old man with cardiac failure for a period of 30 min. He had noticed dull pain over the right forearm during the procedure. The next morning he could not pinch powerfully between the thumb and index finger. On admission, he described dull pain and tenderness over the flexor muscles of the right forearm and the inability to pinch powerfully between the thumb and index finger to form a perfect “O” figure. The patient presented with a subcutaneous soft tissue mass on the volar aspect of the right wrist and along the forearm. The mass was chicken-egg size, elastic and soft, with clear margins, and not manifesting tenderness or signs of inflammation. Flexion of the interphalangeal joint of the thumb, index finger, and middle finger was weak, but the sensory examination and radiograph findings on the hand and forearm were normal. According to the diagnosis of AIN palsy, the patient was treated conservatively for 6 wk, but with no effect. Therefore, exploratory surgery was performed. The surgical examination showed that the flexor tendons of the thumb, index finger, and middle finger were normal. However, an anomalous muscle that originated from the radiocarpal aponeurosis lay on the volar side of the wrist and along the forearm, and its tendon was inserted reversibly over the proximal third of the radius and the tendinous area of the flexor muscles (Fig. 1). A subcutaneous soft tissue mass corresponded with the edematous belly of the anomalous muscle. The proximal part of the AIN was constricted by the fibrous band from the anomalous tendon and flexor muscles (Fig. 1). On the constricted site, the nerve was slightly swollen and edematous, with limited mobility, and kinked by flexion of the elbow. The AIN was freed from compression by the removal of the anomalous tendon and the fibrous band. Six weeks after the operation, flexion of the interphalangeal joint of the thumb and index finger was strengthened, and 6 mo later the powerful pinch was fully recovered.Figure 1: Intraoperative findings of patient’s right forearm. The anterior interosseous nerve is compressed by the fibrous band from the anomalous tendon and flexor muscles.Discussion The AIN is derived from the median nerve at the elbow and passes through the narrow space between muscles of the pronators and flexors of fingers and their fibrous band. It supplies the pure motor function to the flexor muscles of the thumb, the index and middle fingers, and to the pronator quadratus muscle. In this narrow space, the AIN is easily entrapped by a fibrous band (4,5), which results in entrapment neuropathy with the frequent flexion of the elbow. In general, the patient is treated conservatively and surgical exploration is only performed if the patient does not recover well under conservative treatment (4). In the present case, an anomalous palmaris longus muscle compressed the nerve. This muscle is known as the most variable muscle of the upper extremity (6) and causes nerve entrapment neuropathies of the ulnar and median nerves (7,8). The patient was a resuscitator and prolonged performance of chest compression induced AIN palsy. Schuurman et al. (9) reported four cases of effort-related median nerve compression resulting from a reversed palmaris longus muscle hypertrophy and an increased intracompartmental volume that leads to abnormal compartmental pressure increase during muscle activity (10). It is believed that the anomalous muscle increased in volume during exercise, causing local pressure on the AIN. The affected patient’s occupation as a fisherman required forearm muscle exertion while hauling in nets and was another factor promoting muscle hypertrophy with induction of a condition susceptible to nerve palsy. Peripheral neuropathies have various etiologies such as compression, stretch, ischemia, and direct nerve injury (11). The present palsy probably resulted from nerve ischemia by local compression to the AIN. The CPR technique requires too much effort to be continued for prolonged periods. Because our patient performed chest compressions for about 30 minutes without help, repetitive contraction and stretch of the arm muscles probably induced the nerve palsy. Clinicians should be aware of the effort-related nerve palsy (associated with the presence of muscle anomaly) after excessive muscle exertion such as CPR.