We are reporting a case of spinal cord infarction that occurred after epidural anesthesia. There are few similar case reports in the English literature. Spinal cord infarction accounts for only 0.3–1% of stroke cases and therefore has a low incidence relative to other types of stroke . Some studies have reported that age, hypertension, diabetes, obesity, a history of cerebral infarction, and atherosclerotic lesions are risk factors for spinal cord infarction [1, 2]. Other studies have reported the roles of aortic disease and related surgical treatments, as well as spinal disease and related surgical treatments, as risk factors for spinal cord infarction [3, 4]. Although epidural anesthesia is widely used for intraoperative and postoperative analgesia, it can lead to several complications, of which permanent nerve damage is the most severe. Epidural hematoma after epidural anesthesia is a typical nerve complication. While spinal cord infarction as observed in this case is rare, it should still be taken into consideration.
Concerning the cause of spinal cord infarction after anesthesia and surgery, there are few reports in the literature. Some reports have assumed that spinal cord ischemia following epidural anesthesia was associated with intraoperative hypotension [5, 6], toxicity from local anesthesia , or vasospasm related to the administration of a local epinephrine-containing anesthetic [5,6,7]. However, no clear associations have been demonstrated in either case. Another study noted that in elderly patients and those with abnormal spine anatomy, an excessive anesthetic agent volume may cause spinal cord compression . Furthermore, a study of neurological complications after epidural and spinal anesthesia estimated that spinal cord infarction occurred in approximately five per million patients . Four of these five patients were reported to have anatomical abnormalities, such as lumbar spine stenosis and subarachnoid cysts. Therefore, the authors suggested that these spinal abnormalities are associated with neurological complications after epidural/spinal anesthesia . One prior case report showed that spinal cord infarction developed due to severe disc herniation without anesthesia or surgery . Thus, compression to the spinal cord may be an important factor. In our case, the spinal cord infarction occurred at the narrowest area of the spinal cord. This area was narrowed due to the ossification of the yellow ligament and became narrower by the tip of the epidural puncture tube. The small vessels around the narrow spinal cord might have been compressed, causing the infarction. Therefore, patients who complain of numbness and/or weakness of the lower limbs, intermittent claudication, etc. should undergo preoperative MRI examinations of the spinal cord. Some studies have examined paralysis after aortic surgery . The patient in our case underwent soft tissue surgery in the lower abdomen, and the relationship between this abdominal surgery and the patient’s spinal cord infarction may have been negative. In our patient, the causal relationship between epidural anesthesia and spinal cord infarction is still not clear. However, it is unique that her clinical symptoms occurred after anesthesia and surgery. Based on this presentation, anesthesiologists and surgeons must recognize that spinal cord infarction may occur after combined general and epidural anesthesia or surgery.
Concerning the treatment of spinal cord infarction, conservative treatments are usually chosen. In this patient, the motor and sensory deficits were clinically distinct, indicating the infarction of three spinal arteries (one anterior and two posterior). A surgical intervention would have been difficult, and the standard drug therapy is aspirin, based on the consensus recommendation for the acute treatment of ischemic stroke at any site. However, no direct studies have examined the efficacy of drug therapy in spinal cord infarction.
Yellow ligament ossification frequently occurs in middle-aged people and is thought to particularly affect the lower thoracic spine because it often occurs at T10/11 and T11/12 . Numbness and pain in the lower extremities are common symptoms of this condition. In this case, MRI revealed ossification of the yellow ligaments at the T11/12 spinal level, with the accompanying findings of thoracic spinal cord compression. The site of spinal cord infarction was also consistent with the location of epidural catheter insertion. Although the patient in this case did not present with clinical symptoms of thoracic canal stenosis, such as numbness or weakness of the lower extremities, prior to surgery, the onset of spinal cord infarction may have occurred simultaneously with the insertion of the catheter into a site where spinal stenosis was already present.
A preoperative examination with a focus on yellow ligament ossification may be necessary in middle-aged patients undergoing lower abdominal surgery with epidural anesthesia. A preoperative plain chest radiography evaluation of spinal ossification and an evaluation of lower extremity symptoms may be important for reducing the incidence of spinal cord infarction related to epidural anesthesia. When administering epidural anesthesia to patients with a spinal disease, lower thoracic spine catheterization might have to be avoided. Spinal cord infarction in cases of suspected spinal disease may be prevented by preoperatively identifying spinal lesions via a CT or MRI evaluation.