Interscalene brachial plexus block has been widely used for upper limb surgery.1 Neurological complications related to this technique include total spinal anesthesia,2 bilateral epidural blockade,3 and permanent motor neuron damage.4 Other frequent side effects are hoarseness, Horner’s syndrome, or phrenic nerve palsy.5 We report a case of quadriparesis of delayed onset after an interscalene block and general anesthesia in a seated position.
A 71-yr-old woman (68 kg, 169 cm) was scheduled for outpatient arthroscopic rotator cuff repair of the right shoulder in a seated position. Her medical history was significant only for hypertension that was treated with nifedipine. She took no other medication. Her baseline arterial blood pressure was 128/78 mm Hg (mean 94). Midazolam 1 mg was given before performing a brachial plexus block with Winnie’s interscalene technique. The brachial plexus was identified using a stimulator (1 mA initially, then decreased to 0.5 mA) at a depth of 2 cm by observing the ipsilateral shoulder abduction and elbow flexion. Ropivacaine 15 mL 0.5% and 15 mL mepivacaine 1% were injected with a 35-mm needle and with a direction of 15-degrees caudal, checking each 5 mL that blood was not aspirated. There was no pain during injection and, after 15 min, a complete motor and sensory block of the entire right upper extremity was obtained. The patient remained conscious and did not present any adverse events before surgery.
Thirty minutes later, general anesthesia was induced (propofol 2.5 mg/kg and alfentanil 20 μg/kg). A laryngeal mask (no. 4) was placed, and ventilation was maintained with intermittent positive pressure ventilation. Sevoflurane 2% was used for maintenance. No muscle relaxants were administered. The patient was seated upright at 90 degrees during surgery, and standard monitoring was used (electrocardiogram, noninvasive arterial blood pressure cuff on left arm, pulse oximetry, and capnography). The duration of the procedure was 80 min. Her mean arterial blood pressure was kept between 60 and 69 mm Hg for approximately 20 min and between 70 and 79 mm Hg for the remaining 60 min. No drugs were administrated perioperatively to either increase or decrease the blood pressure. There were no intraoperative complications. The patient was transferred to the recovery room. Her mean arterial blood pressure in the recovery room was between 90 and 99 mm Hg.
Two hours later, she demonstrated weakness in both legs when she tried to walk and required assistance to return to a seated position. Physical examination revealed weakness in her bilateral lower extremities and in the left arm (III/V), with decreased thermalgesic sensitivity. Her right arm had a complete motor and sensory block. In addition, bilateral ptosis was evident. She did not have any other neurologic, respiratory, or hemodynamic derangements, and she remained fully alert and oriented. At that time, we suspected central extension of the blockade, and the patient was admitted to the hospital for neurological follow-up with the neurology department. An electromyogram of the lower and upper extremities and a craneocervical T1-2 magnetic resonance imaging (MRI) were performed to exclude other possible causes of quadriparesis. Both diagnostic procedures were normal. The neurology consultation diagnosis was a suspicion of prolonged local anesthesia effect.
The following morning, she was still experiencing quadriparesis (III/V) and bilateral ptosis. She was able to move her left arm against gravity. Thermalgesic sensitivity was still reduced in all extremities. She completely recovered by 72 h after the brachial plexus blockade, without any treatment and without any special sequence of offset of symptoms. She was finally discharged on the fifth postoperative day.
Although many adverse events have been described after an interscalene brachial plexus block,6,7 central extension of the block is rare and a delayed presentation rarer still. Diverse cases of postoperative quadriparesis associated with different symptoms have been reported. The proposed pathophysiological causes referred to, by different authors, include the following.
In the case of delayed epidural or intradural anesthesia, Norris et al.8 proposed two anatomical explanations via injection into a dural cuff into the subepineural space. We suggest a third mechanism, based on the studies of Reina et al.9,10 Epidural fat may influence distribution of the drugs and could act as a reservoir of lipophilic substances. A slow spread can occur from this epidural fat to the epidural or intradural space, producing a delayed and prolonged block. Other less likely causes include: subdural blockade,11 complete spinal block,12–14 and an intraarterial injection of the local anesthetic in the vertebral artery, which can produce a “locked-in syndrome.”15,16 Also, cases of quadriparesis have been described after exposure to nitrous oxide in patients with cobalamin deficit17 and after continuous, concomitant, and prolonged infusion of cisatracurium and methylprednisolone.18 Finally, intraoperative hypotension may lead to ischemia of the spinal cord.19–21 If this occurs, MRI is diagnostic. Edema can be detected with T2-weighted MRI, but diffusion weighted imaging is more sensitive for the detection of spinal cord injury in the first several hours after injury.22
We excluded most of the described causes. It was not a complete spinal block because our patient was fully alert and oriented, hemodynamically stable, breathing spontaneously, and the appearance of symptoms did not occur immediately after the interscalene block. A subdural block was unlikely because of the symmetric symptomatology and the absence of cardiopulmonary symptoms. Intraneural injection was also unlikely because it is associatedwith high resistance and pain during injection. The controlled deliberated hypotension used and the seated position might have contributed to spinal cord hypoperfusion. All of the mechanisms of compression ischemia that produce neurologic disorders and an epidural hematoma23,24 would be visible on imaging studies (computed tomography scans and MRI), which were negative in our patient.
In conclusion, we were in the presence of a retarded central extension of the blockade, probably of multifactorial cause. Bilateral ptosis is more easily explained by a delayed partial intradural progression against a bilateral epidural block. Moreover, the appearance of symptoms, hemodynamic and respiratory stability, and the fact that our patient was conscious justify this diagnosis over that of total spinal anesthesia. The puncture of a dural cuff, which can be extended as far as 8 cm beyond the intervertebral foramen, was the presumed mechanism and might be favored by placing the needle at a depth of 2 cm in this nonobese patient.25 The most remarkable aspect of our case was the duration of the symptoms (more than 72 h). Another possible mechanism causing the symptoms to persist for an extended period, but not as long as 72 h, was an accumulation of the anesthetic in the epidural fat and a slow spread to the epidural and intradural space. Finally, hypoperfusion of the spine in this hypertensive patient could have also contributed to the duration of the block. Diffusion weighted imaging is the best method for detecting cord edema in the first postoperative hours and could have helped us in this case.
Postoperative quadriparesis, although infrequent, can occur through different mechanisms. Central progression of an interscalene block can produce acute or subacute quadriparesis, depending on how the local anesthetic spreads, through direct puncture or by extension from dural cuffs, and to where the anesthetic spreads, to the epineurium or epidural fat. An ultrasound-guided block may help to reduce neurological complications. The symptomatology and the imaging enabled us to refine the differential diagnoses and to exclude the causes of neurologic compromise.
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