A 63 YO M underwent arthroscopic rotator cuff repair with GETA and Peripheral Nerve block and catheter placed via ultrasound guidance. The surgery lasted aproximately three hours and was performed in the beach chair position. After the completion of surgery, the patient was extubated and transported to the PACU in good condition. The patient was a diabetic on 60 units bid of levemir, and glipizide. He also had OSA and used CPAP at home, and had high blood pressure. His preoperative blood sugar was 253 mg/dl, for which he was instructed to take 20 units of levemir.
In the PACU, the patient did very well, with no pain. Upon getting up for discharge home, it was discovered that the patient could not stand or walk. After investigation into the cause of this it was recognized that the patient had weakness in his feet with decreased sensation as well. The distribution of his defect was in the sciatic distribution and was bilateral. He was admitted for observation. His deficit improved somewhat the following day, and was remarkably better on POD 2, although the patient still had significant sensory deficits in a stocking like distribution up to just below the malleoli.
The differential for post operative nerve dysfunction is usually related to compression or stretch of a nerve, or ischemia. In this case there was no obvious proximate cause for bilateral sciatic nerve dysfunction, particularly in a distal location. However, this case highlights that patients with pre existing diabetes, the risk for post operative distal neuropathy is heightened. Peripheral Diabetic neuropathy is present in an estimated 4 to 8% of the diabetics. However, some estimate that all diabetics with chronic ongoing diabetes have dysfunction if tested using nerve conduction studies. In this case, it is likely that the patient had poor blood glucose control (as evidenced by his preoperative blood glucose of 250 mg/dl). Although, the patient denied any peripheral neuropathy, it is likely that he was unaware of this.
By putting the patient in the semi-fowler (beach chair) position, it is possible that compression of the sciatic nerve occurred at the ischial tuberosity. The surgeon did take precautions to off load this area of the sciatic nerve by rotating the bed into slight trendelenburg after sitting the patient upright, and providing a bend at the knees to reduce stretch. However, after surgery, the patient was taken to recovery where he remained for two hours in a sitting position with no knee bend and no trendelenburg.
Perioperative Peripheral Nerve Injuries (PPNI) constitute 15% of total claims made, making it the 3rd most common common of litigation. The overall incidence was found to be 0.14% in one study that did not include regional anesthesia.
While, it is not at all common to find a sciatic nerve palsy after shoulder surgery, in patients with pre existing neuropathy, a double crush injury can occur. This theory proposes that two minor injuries to a nerve can be more than additive when they are combined together in one nerve. In this paradigm, pre existing nerve damage along the nerve due to a chronic condition such as diabetes may be subclinical. Then, an otherwise benign insult occurs to this nerve, and the nerve with little reserve is pushed over the edge to the point that now the patient has a full blown neurologic deficit.
In this case the patient had a stocking distribution peripheral neuropathy, with sensory being more severe than motor. It may be wise in some instances to order EMG and NCS to better evaluate the nature of the nerve damage. However, these studies add expense and logistical issues to the patient's care. EMGs involve a neurologist placing needles into the muslces and measuring motor unit activity both at rest and with voluntary movement. Most PPNIs involve axonal damage resulting in reduced numbers of functioning axons which is easily detected during EMG. Another potential finding is abnormal spontaneous activity (fibrillations potentials). These take 1 to 4 weeks to develop after nerve injury and if present a day or two after surgery indicate pre existing nerve damage.
NCS measure the velocity of nerve impulses in nerves and can localize nerve damage if it exists. The compound sensory action potential will be reduced in sensory axonal degeneration if the electrodes overlie the affected portion of the nerve. In demyelination, there is focal slowing of sensory conduction or sensory and motor conduction across the injured portion of the nerve (proportional to the severity of the demyelination). NCSs are able to reveal the presence of a subclinical neuropathy predisposing nerves to injury and may also suggest the underlying pathological process (axon loss vs demyelination), which has implications for the clinical course and prognosis.
NCSs and EMG are complementary and can help to determine whether a lesion is complete or incomplete; determine the basis of the clinical deficit; localize the lesion; define the severity and age of the lesion; and guide prognosis and course of recovery.
Fortunately, the patient in the above case demonstrated significant improvment in his peripheral nueropathy by POD 2. Therefore, it was felt that he could follow up with his primary care physician who then could work with him on lifestyle changes and better managment of blood glucose levels to avoid further damage to his peripheral nerves. No further studies were ordered.