Abstract

Although epidural analgesia reduces the postoperative stress response and provides good pain relief for patients, potential complications associated with the technique may decrease its acceptability for some patients. We describe a 76-year-old female who underwent surgery for carcinoma of the urinary tract. Postoperative epidural analgesia was performed at the postanesthesia care unit. Neither a repeat attempt nor accidental dural puncture was encountered during the procedure. Unfortunately, she sustained neurological impairment of the bilateral lower limbs following an episode of myocardial ischemia during the early postoperative period. When the neurological deficit was recognized following epidural anesthesia, poor puncture technique was the first to be blamed. In fact, a high level of sensory blockade could markedly decrease blood pressure and heart rate, particularly in the presence of hypovolemia, which might lead to impairment of coronary perfusion and result in my ocardial ischemia. Severe systemic hypotension might further lead to hypoperfusion of the spinal cord, most possibly in the mid-thoracic region (T4 to T8) due largely to its relative hypovascularity. Therefore, we recommend that maintaining sufficient circulatory volume of the patient, evaluating and recording the neurological function of the patient and determining the possible risk factors associated with coronary arterial disease are imperative prior to performing an epidural procedure.

Keywords

analgesia, epidural; myocardial ischemia; neurologic manifestations;

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1. Introduction

Epidural analgesia is a well-established method for relieving postoperative pain involving the thorax, abdomen or lower limbs. Potential complications associated with the technique may reduce its acceptability to some patients and the willingness of clinicians to use it. We report an aged female patient who, without evidence of preexisting cardiovascular diseases, sustained an episode of myocardial ischemia followed by paresis of her lower limbs after being given continuous epidural analgesia for postoperative pain at the postanesthesia care unit (PACU).

2. Case Report

A 76-year-old female (height, 155 cm; weight, 66 kg) with history of hypertension underwent right ureterectomy and nephrectomy for transitional cell carcinoma of the right urinary tract under general anesthesia. After an uneventful surgery, she was sent to the PACU for observation with clear consciousness, good orientation and spontaneous breathing. With her informed consent, epidural analgesia was carried out in the PACU. Premedication with midazolam 2 mg and fentanyl 50 μg was given intravenously prior to the procedure. In spite of her thoracic scoliosis (Figure 1), the thoracic epidural space at the T10 level was identified and entered by a 17-gauge Tuohy needle through the left paramedian approach using the loss-of-resistance technique for confirmation. An Arrow flex-tip epidural catheter was advanced smoothly and was secured at the mark of 12 cm on the skin. The length of epidural catheter in the epidural space was 7−8 cm cephalad. Neither a repeat attempt nor accidental dural puncture occurred during the procedure. Aspiration of the catheter was negative and a test dose of 2 mL 2% lidocaine was then given. Fifteen minutes later, progressive bradycardia and hypotension occurred. The ST-T segment of electrocardiography on the monitor was not significantly changed compared with the preoperative 12-lead waveform. The lowest noninvasive blood pressure registered was 70/55 mmHg, which was immediately resolved with volume expansion and vasopressor (ephedrine) administration. The systemic hypotension persisted for about 10 minutes. After taking measures to stabilize the patient’s blood pressure, continuous patient-controlled epidural analgesia (PCEA) was programmed and initiated. The pain control solution consisted of 0.83 μg/mL fentanyl and 0.1% ropivacaine solution with epinephrine 1:600,000 (0.0017 mg/mL). The maintenance infusion rate was 6 mL per hour and an additional 6 mL rescue bolus for breakthrough pain was allowed with a lockout time of 20 minutes.

During the night of postoperative day 1, when the patient experienced progressive chest tightness with cold sweating, and hypotension occurred again, the PCEA program was halted. Electrocardiography showed significant ST segment depression and cardiac enzyme studies revealed elevated values. She was therefore transferred to the cardiac intensive care unit under the tentative diagnosis of postoperative acute myocardial ischemia. Precordial echocardiography demonstrated partial hypokinesia of the left ventricle. As the management for acute myocardial ischemia proceeded with improvement of symptoms and signs, the PCEA program was resumed. On postoperative day 3, she developed profound bilateral lower extremity numbness; after discussion with her family, the PCEA program was terminated. The epidural catheter was promptly removed.

Because of persistent paresis of the lower extremities, particularly severe on the right, a neurologist was consulted and electromyography and a nerve conduction velocity test were performed. The results were compatible with right lumbarsacral radiculopathy. Magnetic resonance imaging (MRI) of the spine was subsequently performed, and demonstrated no compressive lesions, but revealed high signal intensity in the central canal spanning T2 to T9 (Figure 2), with “owl eyes” appearance in the cross section image (Figure 3).

As the MRI study excluded the possibility of compressive lesions on the spinal cord, the patient was treated conservatively with rehabilitation. Unfortunately, her neurological deficit did not improve during the remainder of her hospital stay. Neurological recovery was incomplete on review of the medical record at follow-up and the patient died of sepsis 2 years after the surgery.

3. Discussion

Continuous thoracic epidural analgesia is a common method of pain relief after major thoracic and abdominal surgeries. Because of the fear of neurological sequelae, some patients and even clinicians hesitate to accept the technique. A recent prospective study by Scherer et al¹ revealed that in 1071 patients who received thoracic epidural catheterization for postoperative analgesia, the incidence of primary dural puncture, radicular pain syndrome, and respiratory depression were 1.23%, 0.56% and 0.09%, respectively. In an earlier investigation of 4185 patients by Giebler et al,² complications related to thoracic epidural catheterization included dural puncture, unsuccessful catheter placement, postoperative radicular type pain, and peripheral nerve lesions. Although no persisting neurological sequelae occurred in either study, the latter gave a predicted maximum risk of 0.07% for permanent neurological complications. The etiology of paraplegia following epidural analgesia may be due to direct trauma to the spinal cord, compression of the spinal cord from hematoma or abscess, ischemia of the spinal cord secondary to hypotension, spasm of, or trauma to, the anterior spinal artery.³ As described in various case reports, serious neurological sequelae usually result from compression of the spinal cord or nerve roots from an abscess or hematoma,^4,5 unintentional trauma during epidural needle puncture or catheterization,⁶⁻⁸ ischemia or infarction of the spinal cord.^9,10 Here, we report a patient who, after receiving epidural analgesia, had neurological impairment concurrent with an episode of postoperative myocardial ischemia, which in our opinion was the real cause of the incident rather than direct trauma to the spinal cord as many supposed.

Hypotension and bradycardia are two potential manifestations of hemodynamic instability because of sympatholysis resulting from epidural anesthesia or analgesia. Although epidural analgesia has been proved to reduce postoperative myocardial ischemia or infarction,¹¹ a high level of sensory blockade involving segments T1 to T5 will markedly reduce blood pressure and heart rate, particularly in the presence of hypovolemia¹² and thus may impair coronary perfusion and result in myocardial ischemia. Severe systemic hypotension may also lead to hypoperfusion of the spinal cord to varying degrees. In fact, the mid-thoracic region (T4 to T8) is most vulnerable to ischemic damage, as a result of its relative hypovascularity. The spinal MRI of this patient demonstrated high signal intensity in the central canal of the spinal cord with “owl eyes” appearance in the cross section image (Figure 3), which signified spinal cord ischemia or infarction.¹³ The owl eyes appearance is specific for infarction of the anterior horns because of the unique vascular architecture of the spinal cord. This imaging pattern in differential diagnosis could distinguish spinal infraction from intramedullary tumor, myelitis, and demyelination.¹⁴ However, the result of the MRI study of the patient was not compatible with her clinical neurological signs (lumbar-sacral radiculopathy). As she did not feel pain in the back during the epidural procedure and the neurologic symptoms did not develop immediately after the procedure, the possibility of direct traumatic injury was less likely.

Epinephrine is usually added to the epidural local anesthetic-opioid solution to prolong and potentiate the effect of local anesthetic block, but the vasoconstriction effect of epinephrine may decrease epidural arterial and venous blood flow to reduce perfusion. It has been reported that the use of epinephrine at a concentration of more than 1:160,000 (0.00625 mg/mL) with anesthetic solution would cause vasospasm and/or thrombosis of the nutrient arteries to the cord.^9,10 It has been reported that epinephrine, in a dose-related manner, improves the pain-relieving effect and that the minimally effective concentration of epinephrine to maintain relief of dynamic pain is approximately 1.5 μg/mL.¹⁵ Although the concentration of epinephrine in our formula was 1:600,000 (0.0017 mg/ mL), a more serious vasoconstriction effect on the nutrient arteries in the presence of systemic hypotension should be seriously considered. Moreover, spinal cord ischemia can occur in retroperitoneal surgery and the use of epidural local anesthetics immediately after surgery may disguise the true cause of the postoperative neurological deficit.¹⁶⁻¹⁸ We suspected that the lumbar radiculopathy in our patient might be associated with the surgery itself. However, when the neurological deficit was recognized, the epidural procedure was instantly blamed with no time to challenge this initially.

As mentioned above, etiologies of neurologic sequelae are variable. It is better to make a differential diagnosis to determine the true cause as the treatments and outcomes are not quite identical overall (Figure 4). Although there was no solid evidence to substantiate the cause, we considered that the delayed onset of paresis in this patient might result from the surgical factor combined with systemic hypotension rather than from an error in the technique of the epidural procedure. Complications attributed to epidural anesthesia and analgesia may also be due to preexisting neurological or vascular diseases that are not detected preoperatively.

In conclusion, we recommend that it is necessary to determine the circulatory volume status of a patient prior to performing epidural analgesia, while at the same time evaluating and recording neurological function and investigating the possibility of coronary arterial disease.