CASE REPORT

Spinal Cord Ischemia Occurring in Association with Induced Hypotension for Colonic Surgery
John C. Drummond, MD, FRCPC,* Roland R. Lee, MD, FACR, and Erik L. Owens, MD
A 19-year-old woman underwent an ileoanal pull-through. Intraoperatively, deepening of anesthesia was associated with reduced bleeding. Therefore, induced hypotension, mean arterial blood pressure 50 to 55 mm Hg, was maintained for 2.5 hours. Postoperatively, the patient was paraplegic with spinal cord infarction on magnetic resonance imaging from T9 to the tip of the conus medullaris. The collateralization of the anterior spinal artery is very variable and it seems likely that in this individual induced hypotension was associated with inadequate blood flow in the distribution of the artery of Adamkiewicz. (Anesth Analg 2012;114:12971300)

nterior spinal artery syndrome has been reported to have occurred in association with profound systemic hypotension1 4 and sporadically after surgery with general anesthesia.2,4 6 It occurs most frequently in procedures in which branches of the aorta supplying the anterior spinal artery (ASA) are inadvertently or deliberately sacrificed.6 9 When hypotension occurring during surgery has been implicated, it has generally been in patients of advanced age, often with established vascular disease. We report herein the occurrence of the anterior spinal artery syndrome in a 19-year-old woman, free of vascular disease, in whom induced hypotension in combination with continuous lumbar epidural anesthesia was used to facilitate colonic surgery.

CASE REPORT
The authors received permission from the patient and her family to publish this case report. A 19-year-old woman (165 cm, 82 kg, body mass index 30.1 kg/m2) was scheduled for an ileoanal pull-through. Her immediate preoperative blood pressure (BP) was 152/89. However, her history did not include hypertension. The patient had developmental delay without other specific diagnosis. Preoperative laboratory examination was unremarkable. Her hemoglobin was 10.0 g/dL. Her only preoperative medication was lansoprazole. (She was not taking oral contraceptives.) She had a history of colonic polyposis, and 3 months previously had undergone a total colectomy and ileostomy. That operation had been accomplished under general anesthesia supplemented with a thoracic epidural placed at the T10-11 level. Preoperative BP on that occasion was 113/81. During that procedure, BP ranged between 90 and 120 systolic. On this occasion, after sedation with 2 mg midazolam, anesthesia was induced with propofol, paralysis was achieved with rocuronium, and the trachea was intubated.
From the Departments of *Anesthesiology, Radiology, and Surgery, University of California, San Diego; and VA Medical Center, San Diego, California. Accepted for publication September 22, 2011. The authors declare no conflicts of interest. Reprints will not be available from the authors. Address correspondence to John C. Drummond, MD, FRCPC, VA Medical Center125, 3350 La Jolla Village Dr., San Diego, CA 92161. Address e-mail to jdrummond@ucsd.edu. Copyright 2012 International Anesthesia Research Society
DOI: 10.1213/ANE.0b013e31823aca2b

Anesthesia was maintained with desflurane and intermittent doses of fentanyl. After induction of anesthesia, the patient was placed in the lateral position and an epidural catheter was inserted at the L3-4 level and advanced 5 cm into the epidural space. A test dose of 1.5% lidocaine with 1:200,000 epinephrine was administered, followed shortly thereafter by a bolus of 8 mL of 0.25% bupivacaine followed by an infusion of 0.1% bupivacaine with fentanyl, 2 g/mL, (without epinephrine) at 10 mL/h. Her BP decreased from 125/60 to 95/50. The patient was placed in the lithotomy position with the arms at 90 degrees on arm boards. Laparoscopic access was achieved. However, during the course of attempts to mobilize the rectal stump, there was a moderate amount of bleeding and the procedure was converted to an open technique. The ileostomy was taken down and the ileum was connected to the rectum. A loop ileostomy was established. Trendelenburg posture was used intermittently during the procedure. During the first 6 hours of the procedure, her systolic BP was between 110 and 95 mm Hg with the large majority of systolic recordings 100 mm Hg. During the course of that time, her heart rate increased progressively from initial values in the 60 to 70 range to 95 to 100. The latter was interpreted as indicating light anesthesia and the epidural infusion was increased to 24 mL/h. Her BP decreased initially to approximately 85 systolic, and 45 minutes thereafter to 70 to 80 systolic. Her heart rate decreased progressively to 65 bpm. Because blood loss diminished and was more readily controllable, hypotension was maintained. BP, as guided by the mean arterial BPs (MAPs) generated by the noninvasive BP device (NIBPD), was managed to maintain MAPs of 50 to 55 mm Hg. The charted systolic BP was between 70 and 80 systolic, with diastolic pressure between 35 and 25 mm Hg for a period of 2.5 hours. At the conclusion of the procedure, the trachea was extubated and the patient was taken to the recovery area. Total anesthesia time was 11 hours and 5 minutes. Her hemoglobin reached a nadir of 7.5 g/dL in the sixth and seventh hour of the surgical procedure. Two units of packed red blood cells were administered and the final hemoglobin was 9.9. Base excess reached a nadir of 7 at the eighth hour of surgery and was 5 at the conclusion of the procedure. Blood loss, as estimated by the anesthesia team, was 650 mL, and, as estimated by the surgeon, 400
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Figure 1. A, Axial T2-weighted image at the T10 vertebral level showing marked central T2 prolongation and swelling of the spinal cord, consistent with acute/subacute ischemia. B, Axial T2-weighted image at the T12 vertebral level showing marked diffuse T2 prolongation and swelling of the conus, consistent with acute/subacute ischemia.

Figure 2. Axial postcontrast T1-weighted image at the L1-2 level showing swelling and postcontrast enhancement of the distal conus and the ventral roots of the cauda equina, consistent with subacute ischemia.

position sensation at some joints. During the preceding 4 days, motor activity had either not been recorded, or, when charted, had been said to be absent. However, 2 of the pain attending physicians thought, in retrospect, that they had seen the patient move at least one lower extremity during the 2-day period preceding the removal of the epidural catheter. A noncontrast magnetic resonance image (MRI) of the lumbar spine obtained on postoperative day 4 revealed no epidural hematoma. However, increased T2 signal, consistent with an ischemic injury, was evident in the conus medullaris. A repeat MRI of the entire spine and spinal neuraxis (without and with IV contrast) on the seventh postoperative day revealed progression of the injury including significant cord swelling and T2 prolongation consistent with infarction of the cord from the T9 vertebral level through the distal conus at L1-2 (Fig. 1) Postcontrast enhancement of the conus and cauda equina was evident on axial T1-weighted images, again consistent with an ischemic injury (Fig. 2).

mL. In total, 7000 mL crystalloid and 2 U packed red blood cells were administered. Urine output was 650 mL. In the postoperative period, the epidural infusion was continued (0.1% bupivacaine with fentanyl, 2 g/mL, at 12 mL/h) and the patient was followed by the Anesthesia Pain Service. No pharmacologic deep vein thrombosis prophylaxis was administered. Because of persisting complaints of pain on the first postoperative day, a bolus of 10 mL of 0.25% bupivacaine was administered and the epidural infusion was changed to 0.1% bupivacaine with hydromorphone 10 g/mL at 18 mL/h. The sensory level was noted to be T7 on the left and T10 on the right. Later that day, because the patient was unable to assist in transfer to a chair, the infusion was decreased to 14 mL/h. On the second postoperative day, because of the clinical suspicion of a pulmonary embolus, the epidural catheter was removed in anticipation of the administration of anticoagulants. Ultrasound evaluation revealed a clot of uncertain age in one common femoral vein. Cardiac echocardiography examination revealed a patent foramen ovale. Heparin was administered. The pulmonary embolus work up was eventually negative as was a thrombophilia evaluation by a hematologist. On postoperative day 4, the patient was still unable to move her legs. Neurologic evaluation revealed complete loss of motor function below T10 with preservation of

DISCUSSION
The injury that occurred, as delineated by MRI, is most consistent with ischemia in the distribution of the arteria radicularis magna (ARM), also known as the artery of Adamkiewicz. There is some uncertainty as to the timing of the onset of paraplegia. However, the patient and the family asserted that there was no movement at any time postoperatively and the medical records did not confirm the presence of any motor function postoperatively. It seems likely that the paraplegia was present from the time of surgery and was not appreciated because of the epidural administration of local anesthetic. The etiology cannot be defined with certainty. It is highly unlikely that the surgical procedures to which the patient was submitted resulted in the sacrifice of vessels of aortic or internal iliac origin that might have been contributing to the spinal cords blood supply. Local anesthetic in the epidural space has occasionally been suspected of causing an adhesive arachnoiditis and paraplegia. However, the extensive imaging studies that were performed gave no evidence of this phenomenon. Imaging also excluded epidural hematoma. Other etiologic possibilities include a spontaneous thrombosis of the ARM or embolization to that vessel. However, embolism of atherosclerotic debris seems unlikely in a 19 year old. A patent foramen ovale was present, making paradoxical embolism of venous

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origin a remote possibility. With respect to thrombosis, although both surgery and cancer (adenocarcinoma was noted in a polyp in the earlier colectomy specimen) are associated with hypercoagulability, no specific thrombotic diathesis was identified. The most obvious predisposing factor is the relative hypotension that occurred during the surgical procedure. There is some uncertainty as to the precise BP during the 2.5-hour period of hypotension. The responsible anesthesiologist reported that MAP, as displayed by the NIBPD, was 50 to 55 mm Hg. Only systolic and diastolic values were entered on the anesthesia record, and MAPs calculated (MAP 1/3 [systolic diastolic] diastolic) from those data during the same period were somewhat lower, i.e., 45 mm Hg (75/30). However, in general, the mean values generated by NIBPDs are perceived to be more accurate. Whatever the exact MAP, patient positioning may have exacerbated the effects of hypotension. BP was measured at the arm, with the arms abducted to 90 degrees, and Trendelenburg positioning was used to facilitate surgical access to the lower abdomen. The lumbosacral enlargement of the patients spinal cord may therefore have been somewhat higher than the arm, thereby resulting in somewhat lower pressures at that level than those recorded by the arm cuff. It is also possible that the impact of the relatively low MAP may have been compounded by somewhat higher-than-normal local pressures within the neuraxis during that period of time. There were no obvious anatomical abnormalities of the spinal canal, i.e., the patient did not have either congenital or degenerative spinal stenosis and did not have an unusual accumulation of fat in the epidural space. However, diversion of blood to the epidural venous plexus might have occurred because of pressure from surgical packs and/or retractors on the iliac veins or the lower portion of the interior vena cava. In addition, during the period of hypotension, there was an ongoing epidural infusion at a rate of 24 mL/h, although the contribution therefrom is likely to have been minimal. Although bolus injections of local anesthetic in the epidural space have been observed to produce significant transient increases in cerebrospinal fluid pressure, it seems unlikely, in the face of the typically widely patent intervertebral foramina in a young adult, that significant pressure increases would occur as a result of a continuous infusion. Epinephrine is unlikely to have contributed to flow reduction. Epinephrine was administered with the initial test dose of local anesthetic but none was used thereafter. Whether it was ischemia related to hypotension, with or without the influence of relatively increased pressure in the epidural space, or whether relatively low flow in the distribution of the ARM predisposed to thrombosis, hypotension seems likely to have had a role. Episodic hypotension, occurring as a result of both anesthesia and cardiovascular events, has been implicated on several other occasions as a cause of ischemic spinal cord injury, usually in the distribution of the ASA. However, the present patient, at age 19 years, is by far the youngest surgical patient reported. A portion of the central nervous systems tolerance for hypotension is a function of collateral blood supply, with many regions of the

central nervous system being supplied by potentially overlapping vascular distributions. However, the collateral input to the ASA system is very variable and, in some individuals, relatively limited. The cadaver dissections of Dommisse10 revealed that the number of segmental medullary vessels supplying the ASA varied between 2 and 17. The ARM usually arises from the aorta between T8 and L1 and enters the spinal canal via an intervertebral foramen on the left side. The ARM typically makes a hairpin turn in the caudad direction and delivers blood to the spinal cord below its level of access. The blood supply to the spinal cord above the level of entry of the ARM is typically provided by blood flowing in a caudal direction from more cephalad regions of the cord. The ASA is typically of very small caliber immediately cephalad to the entry point of the ARM (and is sometimes discontinuous11). Accordingly, there is relatively little potential for collateral flow from the ASA cephalad to the ARMs entry point to the lumbosacral enlargement to which the latter usually supplies blood. Furthermore, the ARM is functionally an end artery in some patients. There may be collateral supply to that distribution via vessels of low aortic or internal iliac origin that travel along the roots of the cauda equina to reach the conus medullaris. However, those vessels are present in as few as 40% of adults10 and are thought, when present, only to become important collateral pathways when gradually progressive vascular disease has limited flow to the ASA via other vessels.8,11 Although the possibility of embolization, paradoxical or otherwise, has been acknowledged, it seems somewhat more likely that the present patient was an individual who was, as a result of normal congenital anatomical variation, more vulnerable in the caudal ASA distribution. It is possible that that vulnerability may have been compounded by local increases in spinal canal pressure related to some diversion of venous blood to the epidural venous plexuses. This patient should serve as a reminder that, although induced hypotension may be an adjunct to reducing blood loss and improving surgical visualization, the cost-benefit ratio should be considered carefully. Despite once common assertions that induced hypotension in the range of 50 to 55 mm Hg is well tolerated in normotensive adults, some individuals may be unpredictably intolerant of that degree of hypotension even though it may be well sustained by many others.
DISCLOSURES

Name: John C. Drummond, MD, FRCPC. Contribution: This author wrote the manuscript. Attestation: John C. Drummond approved the final manuscript. Name: Roland R. Lee, MD, FACR. Contribution: This author analyzed the radiologic images and helped write the manuscript. Attestation: Roland R. Lee approved the final manuscript. Name: Erik L. Owens, MD. Contribution: This author helped write the manuscript. Attestation: Erik L. Owens approved the final manuscript. This manuscript was handled by: Gregory J. Crosby, MD.
ACKNOWLEDGMENTS

The authors are grateful to the patient and her family for permission to publish this case report.

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REFERENCES 1. Silver JR, Buxton PH. Spinal stroke. Brain 1974;97:539 50 2. Singh U, Silver JR, Welply NC. Hypotensive infarction of the spinal cord. Paraplegia 1994;32:314 22 3. Tuncel G, Ozalp G, Canoler O, Cakmak H, Ergeneci A, Kadiogullari N. Anterior spinal artery syndrome after thoracic surgery. J Coll Physicians Surg Pak 2005;15:819 20 4. Hobai IA, Bittner EA, Grecu L. Perioperative spinal cord infarction in nonaortic surgery: report of three cases and review of the literature. J Clin Anesth 2008;20:30712 5. Hong DK, Lawrence HM. Anterior spinal artery syndrome following total hip arthroplasty under epidural anaesthesia. Anaesth Intensive Care 2001;29:62 6 6. Linz SM, Charbonnet C, Mikhail MS, Vadehra N, Zelman V, Katz RL, Thangathurai D. Spinal artery syndrome masked by postoperative epidural analgesia. Can J Anaesth 1997;44:1178 81 7. Zornow MH, Drummond JC. Intraoperative somatosensory evoked responses recorded during onset of the anterior spinal artery syndrome. J Clin Monit 1989;5:2435

8. Plecha EJ, Seabrook GR, Freischlag JA, Towne JB. Neurologic complications of reoperative and emergent abdominal aortic reconstruction. Ann Vasc Surg 1995;9:95101 9. Shine TS, Harrison BA, De Ruyter ML, Crook JE, Heckman M, Daube JR, Stapelfeldt WH, Cherry KJ, Gloviczki P, Bower TC, Murray MJ. Motor and somatosensory evoked potentials: their role in predicting spinal cord ischemia in patients undergoing thoracoabdominal aortic aneurysm repair with regional lumbar epidural cooling. Anesthesiology 2008;108:580 7 10. Dommisse GF. The blood supply of the spinal cord: a critical vascular zone in spinal surgery. J Bone Joint Surg Br 1974;56:22535 11. Lazorthes G, Gouaze A, Zadeh JO, Santini JJ, Lazorthes Y, Burdin P. Arterial vascularization of the spinal cord: recent studies of the anastomotic pathways. J Neurosurg 1971;35:253 62

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