Autonomic hyperreflexia (AH) may occur in up to 85% of patients with spinal lesions above the level of T6 . Distention of the bladder, rectum, or cervix; onset of uterine contractions; and surgical stimulation may trigger sympathetic and parasympathetic afferents below the level of the lesion that are not inhibited by supraspinal centers. This can lead to extensive sympathetic stimulation of the cardiovascular system and of the neurologically isolated adrenal medulla . Clinical manifestations of AH include marked hypertension, bradycardia, cardiac dysrhythmias, headache, piloerection, sweating, and flushing above the level of the lesion . The severe hypertension may lead to seizures or fatal cerebral hemorrhage .
In the anesthetic literature, the focus of management of perioperative AH has been limited almost exclusively to the intraoperative period or pregnancy. Accordingly, there is a paucity of information on management strategies for AH in general surgical patients during the immediate postoperative period. There are only two reports in the anesthetic literature that document the occurrence of AH in the postanesthesia care unit. Both occurred during recovery from tetracaine spinal anesthesia in patients with lesions at T4 and T11 after urological surgery .
We describe a case in which AH occurred in the postoperative period in a quadriplegic patient after major urology surgery. This case illustrates the prophylactic and therapeutic use of epidural blockade in AH.
A 27-yr-old man was scheduled for urinary diversion to treat a neurogenic bladder. He had become quadriplegic after a diving accident 2 yr earlier prior after complete transection of his spinal cord at the level of C5. On occasion over the past few months, the patient experienced signs and symptoms suggestive of AH, including facial flushing, sweating, and headache, but there was no documented hypertension.
On preoperative examination, the patient had sensory loss below T4 and complete motor loss below C5-6. There was no respiratory or cardiovascular compromise. Arterial blood pressure was 100/60 mm Hg, heart rate was 75 bpm (normal sinus rhythm), and respiratory rate was 14 breaths/min. After placement of routine monitors, the right radial artery was cannulated for continuous blood pressure monitoring. An epidural catheter was placed at L1-2. A test dose of 2 mL of 2% lidocaine was administered to test for inadvertent spinal anesthesia. After receiving 1000 mL of crystalloid, general anesthesia was induced with propofol 150 mg and fentanyl 150 [micro sign]g. The trachea was intubated with an 8.5 endotracheal tube after initiating paralysis by rocuronium 0.5 mg/kg without hemodynamic compromise. Anesthesia was maintained with a mixture of nitrous oxide, 40% oxygen, and 0.2%-1.5% isoflurane. A bolus dose of 10 mL of bupivacaine 0.25% was administered epidurally before incision and was repeated 30 min before the end of surgery. The urinary diversion procedure was completed within 140 min. No intraoperative problems were encountered, and the patient was extubated before transfer to the recovery room.
Postoperatively, an epidural infusion of 0.1% bupivacaine with fentanyl 4 [micro sign]g/mL was administered at a rate of 5 mL/h. Six hours after surgery, the patient experienced sweating, headache, pelvic pain, leg spasm, and facial flushing, accompanied by hypertension (180/110 mm Hg from previous baseline of 100/70 mm Hg). There was no evidence of bladder (urinary diversion) or rectal impaction. This AH crisis was treated successfully with 180 mg of lidocaine 2% with adrenaline 1:200,000 administered in 60-mg aliquots epidurally over 6 min.
After 12 min, there was complete resolution of symptoms, with blood pressure returning to 110/70 mm Hg. The epidural infusion rate was increased to 8 mL/h. The patient experienced no further episodes of AH, and subsequent investigation showed no evidence of urinary tract infection or bowel distention. The epidural catheter was removed on the third postoperative day, after which the patient had a comfortable recovery.
AH is a potentially life-threatening complication in patients with high spinal cord injury that may present during labor and delivery or postoperatively. The use of either deep general anesthesia  or neuraxial blockade  to attenuate or prevent intraoperative AH has been documented in the literature, but therapy has focused almost exclusively on the intraoperative period or active labor.
A range of stimuli can trigger a mass autonomic response, but bladder distention or bowel distention, uterine contractions, acute abdominal pathology, handling of bowel or bladder manipulations during surgery, and urinary tract infection are the most common . Cutaneous and proprioceptive stimuli are less commonly implicated . These triggers may occur intraoperatively or in the immediate postoperative period. The fact that these noxious stimuli are still capable of triggering AH in the postoperative period tends to be forgotten once surgery has been completed.
Although epidural anesthesia has been used to treat AH in pregnancy  and in the immediate postpartum period , its use has not been extended to patients with chronic spinal cord lesions undergoing major abdominal or pelvic surgery. In a recent review article on anesthesia for chronic spinal cord lesions , epidural anesthesia alone or in combination with general anesthesia was not included in the management strategy for patients undergoing high-risk general surgery. One reason for its omission may be due to the difficulty in determining the level of blockade and, thus, monitoring continuing therapy.
In some patients, the level of blockade may be determined by observing the level at which spastic paresis become flaccid, the disappearance of ankle or knee reflexes, temperature changes in the lower limbs, or the ability to elicit muscle spasm to ethyl chloride spray . However, vigilance is necessary for the early recognition of inadvertent spinal anesthesia.
AH may be triggered by afferent impulses (noxious stimuli) reaching the isolated spinal cord caudal to the level of spinal cord damage. Spinal sites below this are uninhibited by higher centers leading to sympathetic hyperactivity. Perioperatively, epidural anesthesia with local anesthetic and opioids blocks the afferent and efferent nerves and hence attenuates potential triggering impulses for AH .
The rationale for using elective epidural infusions in combination with general anesthesia in both the intraoperative and postoperative periods in patients with high spinal cord lesion undergoing major abdominal or pelvic surgery is to attenuate the risk of developing AH during this physiologically stressful time; to reduce the stress response to surgery; to ensure perioperative analgesia; and to enhance treatment of a severe hypertensive crisis secondary to AH on the ward.
Alternative therapies for patients at risk of AH in the perioperative period include a variety of pharmacological interventions, including the use of an IV ganglion blockade, hydralazine, alpha-blockade, calcium channel blockade, or nitrate derivative infusions, and may necessitate transfer to an intensive care unit setting for drug delivery.
Opioids may block noxious impulses at the posterior horn cells . Using epidural opioids alone to prevent AH in labor has been reported, with mixed results. Fentanyl was ineffective , but meperidine  controlled AH, perhaps because of its local anesthetic action. Whether the use of combined local anesthetic and opioid offers additional protection in these patients is unclear.
For patients with high spinal cord lesions without severe respiratory compromise undergoing high risk surgery (abdominal or pelvic) for AH, the beneficial use of continuous intraoperative and postoperative epidural anesthesia with local anesthetic and opioid requires further investigation.
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