Injuries to the brachial plexus during mastectomy and axillary dissection are rare. The causes are usuallydirect surgical injuries to the brachial plexus, over-traction during axillary exploration or over manipulation of the upper extremity in order to improve exposure . Traction injury from arm movement during combined mastectomy and latissimusdorsi breast reconstruction was once reported by Wilkinson , with two of the cases being temporary brachial plexus palsy. Here, we report a case of temporary brachial plexus palsy after immediate breast reconstruction with LDF.
Brachial plexus injury as a surgical complication was first reported by Budingerin 1894 who attributed it to the toxic effect of chloroform . In 1899, the English neurosurgeon Victor Horseley reported that brachial plexus injury might be caused by stretching and/or compression of the plexus . The toxicity mechanism was later abandoned while the stretch or compression mechanism was widely speculated, basing these mechanisms on three principal anatomical features. First, its superficial location makes it susceptible to direct damage by surgery. Second, the nerve roots of the brachial plexus are fixed at both their proximal sites of origin (the intervertebral foramina) and the investing fascia, muscles, and other tissues to which they are tethered distally. As a result, force applied between these points increases the likelihood of producing a stretch neuropathy. Third, the space between the first rib and the clavicle is narrow. Thus, fracture and/or displacement of the first rib can directly damage the brachial plexus .
Previous studies,which have attempted to investigate the relationship between arm positioning and brachial plexus neuropathy, failed to show consistent results. Jackson and Keats evaluated the stress caused by various positions on the brachial plexus in 15 cadavers. The study showed that hands-up positioning (defined as abduction of the arm to no more than 90 degrees, anterior flexion of the elbows, and elevation of the elbows six inches above the table) was associated with less tension and compression to the brachial plexus . A prospective study from Kwaan et al.  was about the effect of arm position (arms following abductions to more than 90 degrees and extension) on the tension of brachial plexus. It showed that brachial plexus tension or stretching increased by progressive forearm abduction in nine fresh cadavers. In the present case, the mechanism leading to the brachial plexus injury was mostly probablya stretchingof the nerves. Both arms were in the abduction position with extension and maintained at 90 degrees abduction during the operation which lasted for fourand a half hours. The plexus was under maximum tension in this circumstance. In this procedure the left arm was manipulated to improve exposure of the operating field. Additionally, the patient was returned to the original supine position andher head was not rotated from the lateral decubitus to the supine position at this time. Studies by Kwaanet al.  showed that abduction of the arm was associated with head rotation to the contralateral side which would increase tension on the nerve.
Duration of surgical procedure could also be a risk factor of brachial palsy injury. Upton and McComas reported a double crush syndrome in 1973 . A preexisting subclinical neuropathy may explain the postoperative clinically overt palsy. The periphery of the axons is continuously supplied by axonal flow of nutrients from the cell bodies in the dorsal root ganglion. Any injury that interferes with this nutrient supply can cause damage to the nerve. Such an injury may result from mechanical (nerve entrapment), metabolic (diabetes), or ischemic mechanisms. The injury may be subtle and clinically unrecognized. However, when this nerve is exposed to a second trivial injury like prolonging the operation time or continuous stretching the upper extremity, the combination of these factors may lead to significant nerve damage and clinically overt symptomatology. On the other hand, anesthesia can lead to the unconscious patient sustaining an early nerve pressure palsy which is the most common positioning injury. In our case, general anesthesia was conducted and the surgical procedure lasted for four and ahalf hours, and both arms remained in the abduction position forthe duration of the operation. These risk factors mentioned above could lead to injury to the arms in the hyper-abducted position caused by compression of the brachial plexus on both sides.
Body weight is also linked to the tension of the brachial plexus when in the respective positions of abduction, extension, or the combination of both , and a thinnerperson is more susceptible to brachial plexus neuropathy for nerve tension appears to be less in the heavier individuals . In our case, the patient was fairly thin and weighed 41 kg which may be a contributing cause of her brachial plexus nerve injurydespite reasonable care having been taken while appropriately positioning her. In some certain conditions brachial plexus nerve injury may occur in spite of conventionally accepted positioning and padding .
Diagnosis of brachial plexus nerve injuries is based on clinical examination, myelography, axon reflex testing, and electrophysiologic studies. Electrophysiologic studies can detect changes in nerve function during the perioperative period, but large, prospective trials demonstrating the importance of electrophysiologic studies in the early diagnosis and prevention of brachial plexus neuropathy are lacking . In our patient, the disability of abduction of the left upper extremity was obvious in the first few weeks, but electromyography (EMG) and axillary nerve conduction velocity (NCV) revealed no abnormal findings 15 days later. Symptoms during abduction of the left upper extremity persisted for six months but had completely remitted after conservative treatment.
The overall prognosis of brachial plexus neuropathies is generally good. However, prolonged recovery (up to one year) with residual symptoms sometimes occurs . Hanson et al.  studied 531 cases patients prospectively and the clinical diagnosis of brachial plexus neuropathy was made in 5% (26 of 531) patients. Similarly only 1% (6 of 531) of the patients had persistent symptoms for more than four months. Vahl et a l. , in a prospective study of 1,000 patients, showed that 0.8% (8 of 1,000) patients had symptoms continuing for more than three months. Our patient’s symptoms lasted for more than four months. Six months after discharge, the patient had recovered almost full function of her left arm (summarized in Table 1).
The LDF is one of the most commonly used flap procedures and is believed to result in minimal donor-side morbidity for breast reconstruction after mastectomy . It appears that, despite optimal surgical and anesthetic techniques, brachial plexus neuropathies cannot be avoided . Factors that may reduce the frequency of brachial plexus neuropathies include (1) arm abduction should be limited to less than 90 degrees in supine patients and the hand and forearm kept in full supination; (2) abduction of the arm associated with head rotation to the contralateral side should be avoided; (3) padded arm boards may decrease the risk of neuropathy; (4) postoperative neurologic assessment should be performed in every patient to allow early detection and therapy of nerve lesions [3, 13, 17].