% vol = 14 number = 2 prevlink = 90 nextlink = 96 titolo = "PERMANENT PARAPLEGIA IN AN ELECTRICAL BURN PATIENT FOLLOWING SPINAL ANAESTHESIA (CASE REPORT AND REVIEW)" volromano = "XIV" data_pubblicazione = "june 2001" header titolo %>
SUMMARY. Spinal anaesthesia is frequently used in the reconstruction of burned lower extremities and presents well-known complications. Neurological damage following spinal anaesthesia is sometimes irreversible; though rare, it is occasionally seen. We present a case report of permanent motor paraplegia in an electrical burn patient who was operated on for stump revision 6 months post-injury. Neurological examination and EMG suggested a cauda equina/conus lesion due to spinal anaesthesia. The pathophysiology of electrical spinal injury is still unclear. In conclusion, when spinal anaesthesia is performed on high-tension electrical injury patients, hidden and delayed neurological damage must be considered.
Many anaesthesia techniques have been described for burn patients. Surgical procedures such as debridement, grafting, and reconstruction may be performed early and repeatedly. The special needs of these critically injured patients must be recognized. Spinal anaesthesia is frequently used in the reconstruction of burned lower extremities. Patients surviving high-voltage electrical injury may have hidden and delayed sequelae.1-5 The pharmacokinetic and pharmacodynamic effects of anaesthetic agents are therefore important in the victims of electrical burns.
Spinal anaesthesia (SA) has a number of well-recognized complications. Neurological damage following SA is sometimes irreversible; though rare, it is still occasionally seen.6-8 Several aetiological factors have been suggested: chemical or bacteriological contamination, disinfectants, preservatives, local anaesthetics, acidic solutions, bleeding, pre-existing pathology, hypotension, mechanical damage to the nerves, epinephrine, or pre-existing spinal stenosis.6,7,9
We present a case report of permanent motor paraplegia in an electrical burn patient. This may help to inform surgeons and anaesthesiologists involved as regards the toxicity of anaesthetic agents in such patients.
A 38-yr-old man was injured in May 1998 by a 25,000-volt shock from a high-tension line and was admitted to our hospital for treatment of his electrical injury. He was unconscious on admission to our Burn Centre. On admission, circulation of both feet was disrupted and fasciotomy was performed in both legs. Physical examination revealed full-thickness burns in the right forearm and both feet; the muscles in the fasciotomy sites were necrotic. Laboratory findings, ECG, and computerized tomography were normal. The entrance and exit wounds were respectively in the right forearm and both feet. Both dorsalis pedis and tibialis posterior arteries in both feet were found to be occluded on angiogram. An irreversible muscle injury and necrosis were observed 7 days post-injury. The patient therefore underwent surgery, and amputation of both legs below the knee was performed. Six months later the patient was admitted to our burn centre because of a fistula in the right stump. Stump revision and fistula extirpation were performed under spinal anaesthesia. After intravenous infusion, spinal anaesthesia was performed in a sitting position with a 25-gauge needle at L2-L3. A total amount of 4 cc prilocaine 2% with epinephrine 1:100,000 was administered to produce L1 level. The surgical procedure terminated 1 h after spinal anaesthesia. On arrival in the post-anaesthesia care unit, the patient presented L1 sensory level and was unable to move either lower extremity. Three hours after elimination of the drug, spinal anaesthesia paralysis had not returned. A neurosurgical and anaesthesia consultation was obtained. Magnetic resonance imaging and EMG were planned. A booster dose of i.v. 2500 mg methylprednisolone, followed by 432 mg/h methylprednisolone, was administered. Neurological examination revealed pathological patellar and deep tendon reflexes, decreased pain, sensation and pinprick reflexes, and urinary retention. There was no magnetic resonance imaging evidence of cord disease. EMG revealed bilateral total denervation of the quadriceps femoris and biceps femoris. No response was detected when the femoral nerve was stimulated. Neurological examination and EMG suggested a cauda equina/ conus lesion. After two years follow-up no significant motor or functional improvements were noted.
Electrical injury may cause cerebral injury, spinal cord lesion, peripheral nervous system involvement, and neuropsychological sequelae. Only a few reports are available that present the complications of spinal anaesthesia in electrical burn patients. The onset of spinal cord involvement may vary from the time of injury to many weeks after the injury.5 The extent of the injury is variable, and the prognosis varies from total recovery to occasional death.10 The spinal form may resemble either progressive muscular atrophy, amyotrophic lateral sclerosis, or transverse myelitis.1 The upper-motor-neuron type of motor deficit is seen most often, with lower parts or functions being affected more commonly. Therefore paraplegia, quadriplegia, impotence, and bladder dysfunction consequently have been described.1 The pathophysiology of electrical spinal injury is still unclear; possible explanations are:
Neurological deficits after spinal anaesthesia have been attributed to needle-catheter-induced trauma, spinal stenosis (possibly combined with hypotension) leading to cord ischaemia, or direct cord drug toxicity.6,7
Neurological damage after spinal anaesthesia with local anaesthetics is well known and Kane8 has defined three types of sequelae following spinal anaesthesia:
Type 1: Aseptic meningitis symptoms starting within 24 h. Recovery is complete in one week.
Type 2: The cauda equina syndrome, with urinary and faecal incontinence, perineal sensory loss, and motor weakness in the legs. The onset is immediately after recovery from spinal anaesthesia. The symptoms may either be permanent or show regression within weeks.
Type 3: Adhesive arachnoiditis, with progressive weakness and sensory loss in the legs. The symptoms start weeks after spinal anaesthesia and may lead to paraplegia and, in severe cases, to death.
Our patient can be placed in the second group. Neurological toxicity to prilocaine has not been reported before. Also, vasoconstrictive agents such as epinephrine could decrease the blood flow to pre-injured spinal cord.
Paraplegia in electrically injured patients following spinal anaesthesia has not been reported in the literature regarding burns. This seems unlikely to be solely relevant only in the case presented here. No paraesthesia was elicited during needle or catheter placement. There was no magnetic resonance imaging evidence of cord disease. In our opinion, the most likely explanation may be that the electrical injury caused cellular damage not recognized by clinical examination and conventional laboratory measurements, together with sensitivity to spinal anaesthesia. In conclusion, when spinal anaesthesia is performed in high-tension electrical injury patients, hidden and delayed neurological damage must be considered.
RESUME. La technique de la rachianesthésie est employée fréquemment dans la reconstructioon des extrémités inférieures brûlées, mais elle présente certaines complications bien connues. Les dommages neurologiques après lemploi de la rachianesthésie, quelquefois irréversibles, sont rares mais peuvent se vérifier. Les Auteurs présentent un cas de paraplégie motrice permanente dans un patient atteint de brûlures électriques opéré pour des problèmes au moignon six mois après lincident. Lexamen neurologique et lélectromyographie indiquaient la possibilité dune lésion de la cauda equina/conus causée par la rachianesthésie. La pathophysiologie des lésions spinales électriques est incertaine. Les Auteurs concluent que lorsquon effectue la rachianésthesie dans les patients atteints de lésions électriques causées par la haute tension, il faut considérer la possibilité de lexistence dissimulée ou retardée de dommages neurologiques.
<% riquadro "This paper was received on 26 February 2001.