Tourniquet Palsy or Residual Block?

Abstract

To the Editor: We describe prolonged neurological deficit in a diabetic patient after upper extremity surgery using a combined general-regional anesthetic technique. This case highlights the difficulty in determining the etiology of perioperative nerve injury and the potential for diabetics to have an increased susceptibility to nerve injury. A 52-year-old diabetic patient (55 kg, 165 cm) with a closed fracture left radius (upper third) underwent open reduction internal fixation under general anesthesia. A left supraclavicular block was performed by the “classical” approach (1). After eliciting paresthesia in the hand, 30 mL of equal volumes of 2% lidocaine with adrenaline (1:200,000) and 0.5% bupivacaine were injected. A tourniquet (inflated 100 mm Hg above the SBP) was maintained continuously for 70 min. Four hours postoperatively sensation to touch and pinprick had returned, but a wrist drop was noticed. Neurological examination revealed paralysis (Medical Research Council (2) Grade 0) (see Table 1) of the muscles supplied by the ulnar, median, and posterior interosseus nerve in the forearm and hand. Shoulder and elbow movements were normal and sensation over the shoulder and arm were preserved. The power was Grade 1 at discharge on the 10th postoperative day, and 3 months later with continued physiotherapy, improvement to Grade 4 has been achieved. He had no abnormal pain in the limb.Table 1: Medical Research Council Grade of Motor Power (2)In this patient, there was a prolonged motor blockade of the forearm and hand while all sensory modalities preserved. These deficits could have been due to a) preoperative injury (3), b) peripheral neuropathy (4), c) faulty positioning (5), d) surgical trauma (6), e) anesthetic nerve block (7), or f) the tourniquet (8). Neurovascular injury in the limb (from the trauma or even prior) was presumably absent as the preoperative neurological examination was normal. In this diabetic patient, an undiagnosed (subclinical) peripheral neuropathy was possible. Brachial plexus injury due to faulty positioning of the arm (by stretching of the neck) should have involved the shoulder function. Direct surgical trauma should have spared the ulnar nerve. Local anesthetic induced complications may be due to direct trauma (the use of sharp needles (9)) and use of epinephrine-containing solutions (10). Perineural (7) injection (distinctly uncomfortable at injection) causing intrinsic compression of the brachial plexus would have also presented with motor symptoms but affected the shoulder. Tourniquet palsies are due to direct extrinsic pressure or axonal hypoxia on the nerves beneath the tourniquet and are related to the cuff pressure and duration of application (11). They are predominantly motor and are well localized to the point of application. These arguments make tourniquet palsy the most likely, although a residual block cannot be completely ruled out. For these complications, electromyography (EMG) and nerve conduction studies (NCS) may have contributed to the diagnosis by identifying the location (etiology) and the presence of peripheral neuropathy (risk factor). But these studies may also be inconclusive (12) or unavailable (in our case, as is in much of the developing world). Additional risk factors of adverse neurological outcomes have been postulated (not been definitely shown). These include the paresthesia method (7), use of regional techniques (in diabetics (13)), tourniquets (in peripheral neuropathies (14)), and the latter two combined (11). For this patient, all these together may have increased the risk. We conclude that tourniquets and nerve blocks should be used with caution in these patients. Naveen Eipe, MD Department of Anesthesia [email protected] Nihar Ranjan Padhi, MS Department of Orthopedics Padhar Hospital Padhar, Madhya Pradesh, India [email protected]