Postoperative paraplegia coincident with single shot spinal anaesthesia.
Paraplegia is a rare but serious complication of spinal anaesthesia. We report an 83-year-old patient who developed anterior spinal artery syndrome resulting in paraplegia some 24 hours after undergoing spinal anaesthesia for a Moore's hemiarthroplasty. Return of neurologic function was documented prior to the onset of paralysis, with magnetic resonance imaging evidence suggestive of spinal cord infarction.
Key Words: spinal anaesthesia, complications, anterior spinal artery syndrome, paraplegia
Paraplegia is a rare but serious complication of neuraxial blockade (1). Paraplegia after spinal anaesthesia has been reported secondary to pressure from haematoma or abscess formation (2), as well as the anterior spinal artery syndrome (3). It has been attributed to the vasoconstrictive effect of additives to local anaesthetics and to thromboembolic events or profound hypotension (4). This case report describes the complication of postoperative paraplegia in an elderly female patient that was associated with the use of single shot spinal anaesthesia.
An 83-year-old female presented for emergency Moore's hemiarthroplasty for a sub-capital fracture of her left femoral neck, following a fall some three days previously. Her preoperative history included depression, peripheral vascular disease, stable ischaemic heart disease and well controlled systemic hypertension (blood pressure [BP] 160/80 mmHg). She also had left leg weakness secondary to left-sided lumbar foraminal stenoses, as well as a 10-packet-year history of smoking. She was not diabetic. A transthoracic echocardiogram performed six months previously had shown normal left ventricular and valvular function. Her medications included ranitidine, perindopril, dipyridamole and aspirin, all of which had been taken up to and including the day of surgery. She lived in assisted hostel accommodation and was usually ambulant with the help of a walking frame. On examination, she was a frail, emotionally depressed woman, with obvious shortening and rotation of her left leg. Neurologically, there was noticeable weakness in her left leg, graded as 3/5, with normal power in her right leg. There was no documented sensory deficit in either leg. Routine full blood examination, urea, creatinine and electrolytes, as well as international normalised ratio (INR) and activated partial thromboplastin time (APTT) were within normal limits. After gaining informed consent, a single shot spinal anaesthetic technique was employed. The 4th-5th lumbar interspace was identified in the right lateral position and plain bupivacaine 0.5% 2.5 ml was easily injected through a 25-gauge pencil-point spinal needle on the first pass. There was no evidence of paraesthesia or blood in the needle on insertion. The procedure lasted 35 minutes in the right lateral position. The patient was monitored with electrocardiography, pulse oximetry, non-invasive BP monitoring every three minutes and apnoea monitoring. She was given midazolam 2 mg intravenously and a single dose of cephazolin 1 g. Her recorded systolic blood pressure was maintained above 140 mmHg at all times. There was no evidence of hypoxia or arrhythmia or altered conscious state. Blood loss was not measured, but was described as "minimal". Preoperatively, her haemoglobin concentration was 96 g/l. On the second postoperative day it had decreased to 92 g/l. She was recovered in the supine position uneventfully and returned to the ward after one hour. In the light of her previous lumbar foraminal stenoses, her lower limb neurologic function was reassessed at regular intervals throughout the night. The return to her pre-operative neurological function was documented at approximately four hours postoperatively. She was assessed again eight hours postoperatively and found to be neurologically similar to her preoperative condition. During the postoperative phase she had four-hourly recording of her vital signs including heart rate, non-invasive BP, respiratory rate and conscious state. Her urine output was not recorded. At no time were significant hypotension, altered conscious state or increased bleeding into her drains documented.
Approximately 24 hours postoperatively, the patient was re-assessed and found to have severe bilateral motor deficits, as well as mildly decreased pinprick sensation in both legs (the right more so than the left) to the level of the T10 dermatome. A prompt neurosurgical opinion was sought, and given the relative paucity of sensory signs, a provisional diagnosis of spinal cord infarction made. A magnetic resonance imaging scan was undertaken, which showed a focal hyperintensity centrally within the spinal cord at the T11/12 level. The signal change in the spinal cord, given the clinical context, was thought most likely to represent a spinal cord infarct. In the light of the diagnosis of the spinal cord infarction, no neurosurgical intervention was considered and supportive therapy was instituted. Six months after the procedure, the patient was still unable to move her legs and was wheelchair bound.
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Perioperative nerve injuries and paraplegia have long been recognised as a complication of spinal anaesthesia (4). Neurological sequelae may result from injury from the needle itself, epidural abscess or haematoma, local anaesthetic toxicity and infection (2-4).
The incidence of persistent neurological dysfunction or weakness after resolution of spinal anaesthesia ranges from 0% to 0.16%1, but spinal cord infarction is an extremely rare event. It is usually related to periods of hypotension either intra-or postoperatively, in a patient predisposed to atherosclerotic disease. Likewise, it may develop rarely as a thromboembolic event in a patient with cardiovascular disease (1).
The vascular supply to the spinal cord is derived from two sources: arteries from the vertebral system superiorly, and spinal branches of the aorta, subclavian and iliac arteries inferiorly. A single anterior spinal artery arises from branches off both vertebral arteries to supply the anterior two-thirds of the spinal cord. It descends in the anterior median fissure with its corresponding vein. The anterior spinal artery is reinforced by several radicular arteries arising from nearby vessels, as it can be an incomplete vessel. Of these, only six or seven (1) make a substantial contribution, effectively dividing the spinal cord into three separate vascular territories. The largest of these feeder' vessels, the artery of Adamkiewicz (radicularis magna) supplies the cord in the lumbar region. Its origin is variable, usually left-sided (78%) between T8 and L3, with 60% being between T9 and T12 (5). It is here, in a so-called 'watershed' area, that the spinal cord is especially vulnerable to hypotensive or ischaemic insults (6). The less significant posterior spinal arteries arise from the cerebral circulation, most notably the posterior inferior cerebellar arteries, as branches from the vertebral arteries. This branch divides into two separate vessels that run on either side of the spinal cord, being fed by multiple radicular vessels.
Several surgical procedures place the spinal cord at risk of ischaemia due to damage to the artery of Adamkiewicz. Thoracotomies, especially through the left hemithorax, are particularly notable. Prolonged aortic clamp time exceeding 30 to 45 minutes during aortic aneurysm surgery' and left-sided nephrectomy has been implicated, as has splenectomy, pneumonectomy and adrenalectomy. However, it is important to realise that spinal cord infarction has not been described in the recent literature to be associated with hip hemiarthroplasty and spinal anaesthesia. Variations in patient positioning, such as extreme lumbar lordosis, which is very different positioning from that used in this case, have been associated with spinal cord infarction (7). Also, patients with co-existing disease of the vertebral column such as Paget's (8), scoliosis or spondylolisthesis, as well as patients with vasculitides and atheromatous disease are particularly at risk. The typical patient at risk of anterior spinal artery syndrome is an elderly patient with a past history of arteriosclerosis or recent period of hypotension, who presents with a sudden onset of flaccid paralysis, abolished segmental reflexes and minor or patchy sensory disturbance. Vibration and position sense are typically retained. Examination of the cerebrospinal fluid, computerised tomography and other laboratory data are invariably normal (4). A magnetic resonance imaging scan is the investigation of choice (9).
This case illustrates the devastating complication of spinal cord infarction causing postoperative paraplegia in an elderly female patient. Despite the return of preoperative neurological function at approximately four hours, her paralysis was evident by 24 hours. We were able to document the return of normal function after the neuraxial block had regressed, prior to the onset of paralysis. Although several factors may have been responsible for the patient's neurological outcome, it is possible that during the first postoperative day, the patient experienced a period of undetected and prolonged hypotension or a thromboembolic event on the orthopaedic ward, which caused profound spinal cord hypoperfusion resulting in the subsequent spinal cord infarction. However, most reports of spinal cord ischaemia and infarction are associated with intraoperative (10-13) rather than postoperative hypotension (14). These postoperative episodes are typically related to epidural analgesia, not spinal anaesthesia. Whether the use of invasive blood pressure monitoring both during and after the procedure would have altered the outcome in this case is debatable, as is the question of whether routine post-surgical high dependency monitoring should be used for this cohort of patient. Likewise, it is possible to debate the merits of using regional anaesthesia over general anaesthesia in a patient such as the one presented. The patient had documented peripheral vascular disease, as well as stable ischaemic heart disease, so it may be assumed the atherosclerotic process was also present in her spinal arterial system. Aspirin together with dipyridamole has been shown to be efficacious in the treatment of peripheral arterial disease (15) but has not been shown to increase the risk of spinal cord haematoma. It only requires spinal artery ischaemia of two to three minutes' duration before permanent spinal cord damage occurs (16). In this case, once a neurological deficit was suspected clinically, the diagnosis was confirmed with magnetic resonance imaging, but no intervention could be carried out to alleviate the paralysis.
Heightened awareness of altered neurology in patients presenting after neuraxial blockade should lead to prompt evaluation, with the findings documented to enable further consultation and intervention without delay (17).
I would like to thank Drs Craig McCutcheon and Rowan Thomas, Consultant Anaesthetists, and Dr Kit Lee, Consultant Radiologist, for their assistance in proof reading the manuscript.
Accepted for publication on March 20, 2007.
(1.) Cheshire WP, Santos CC, Massey EW Howard JF Jun Spinal cord infarction: etiology and outcome. Neurology 1996; 47:321-330.
(2.) Horlocker TT. Complications of spinal and epidural anesthesia. Anesthesiol Clin North America 2000; 18:461-485.
(3.) Hong DK, Lawrence HM. Anterior Spinal Artery Syndrome following total hip arthroplasty under epidural anaesthesia. Anaesth Intensive Care 2001; 29:62-66.
(4.) Horlocker TT, Wedel DJ. Neurologic complications of spinal and epidural anesthesia. Reg Anesth Pain Med 2000; 25:83-8.
(5.) Cardiac Anesthesia, 4th Ed. Kaplan Reich Konstadt. Saunders. p. 838-839.
(6.) Weinberg L, Harvey WR, Marshall RJ. Post-operative paraplegia following spinal cord infarction. Acta Anaesthesiol Scand 2002; 46:469-472.
(7.) Roberts DRD, Roe J, Baudouin C. Hyperlordosis as a possible factor in the development of spinal cord infarction. Br J Anaesth 2003; 90:797-800.
(8.) Herzberg L, Bayliss E. Spinal-cord syndrome due to non-compressive Paget's disease of bone: a spinal-artery steal phenomenon reversible with calcitonin. Lancet 1980; 2:13-15.
(9.) Gass A, Back T, Behrens S, Maras A. Magnetic resonance imaging of spinal cord infarction. Neurology 2000; 54:2195.
(10.) Harrison PD. Paraplegia following epidural analgesia. Anaesthesia 1975; 30:778-782.
(11.) Bhuiyan MS, Mallick A, Parsloe M. Post-thoracotomy paraplegia coincident with epidural anaesthesia. Anaesthesia 1998; 53:580-588.
(12.) Djurberg H, Haddad M. Anterior Spinal Artery Syndrome: paraplegia following segmental ischaemic injury to the spinal cord after oesophagectomy. Anaesthesia 1995; 50:345-348.
(13.) Walker WE. Paraplegia associated with thoracotomy. Ann Thorac Surg 1990; 50:178.
(14.) Crystal Z, Katz Y. Postoperative epidural analgesia and possible transient anterior spinal artery syndrome. Reg Anesth Pain Med 2001; 26:274-277.
(15.) Aronow WS. Antiplatelet therapy in peripheral arterial disease. Curr Drug Targets Cardiovasc Haematol Disord 2004; 4:265-267.
(16.) Lee JA, Atkinson RJ, Wah MJ. Lumbar puncture and spinal analgesia. New York: Churchill Livingstone, 1985.
(17.) Aromaa U, Lahdensuu M, Cozanitis DA. Severe complications associated with epidural and spinal anaesthesias in Finland 1987-93. A studybased on insurance claims. Acta Anaesthesiol Scand 1997; 41:445-452.
B. W. LAFERLITA
Department of Anaesthesia, St. Vincent's Hospital, Melbourne Victoria, Australia
* M.B., B.S., F.A.N.Z.C.A., Staff Anaesthetist.
Address for reprints: Dr B. W LaFerlita, Department of Anesthesia, St. Vincent's Hospital, Melbourne, Vic. 3065.
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|Publication:||Anaesthesia and Intensive Care|
|Article Type:||Clinical report|
|Date:||Aug 1, 2007|
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