- Email: [email protected]
Paraplegia in an electrical burn: a case report
Burns (1988)14,(l), 49-50
Printedin
GreatBritain
49
Paraplegia in an electrical burn: a case report S. Kanitkar North
Staffordshire
Royal Infirmary,
Stoke on Trent, UK
A. H. N. Roberts Stoke Mandeville
Hospital,
A ylesbury,
UK
Summary Electrical burns constitute a significant component of burn injuries worldwide. Cason (1981) reported about 150 deaths occurring every year from electrical injuries in the UK. However, spinal cord involvement is a relatively uncommon sequel of electrical injury. A case of paraplegia mainly with motor involvement, following electrical injury, and near complete recovery is reported.
CASE REPORT An Id-year-old man was admitted to hospital following an electrical injury. He had taken a shortcut to his home by jumping over a railway bridge while under the effect of alcohol. In the process, he came into contact with 25 000 volt a.c. overhead cables. On admission he was found to have 27 per cent burns on his head. neck and trunk. Most of these were full thickness or deep dermal in depth. The deepest burn was on the posterior neck with obvious charring of underlying muscle. Escharotomies were performed on the neck. He was intoxicated with alcohol but conscious. About 12 h later, he was noted to have some weakness in both lower limbs. There was increased tone and brisk reflexes. There was also a slight reduction of touch sensation in his lower limbs. X-rays of his cervical spine showed loss of curvature. Subsequent X-rays ruled out any bony injury. X-rays of the dorsal and lumbar spines were normal. Over the next 3 days. his paraplegia progressed and he was transferred to the Stoke Mandeville Burns Unit for joint management at the National Spinal Injuries Centre. He then had a near total paralysis of the lower limbs. Muscle tone was increased and reflexes were brisk. Plantar reflexes were extensor. There was a 0 1988 Butterworth 0305-4179/88/010049-02
6i Co (Publishers) $03~00
Ltd
doubtful loss of proprioception in the toes. and slightly abnormal light touch sensation in the distal lower limbs. His bladder and bowel functions were normal. The burns on his anterior surface were treated by early excision and skin grafting. The posterior cervical muscles were extensively burned and needed excision. Mild depression was treated with appropriate therapy and rigorous physiotherapy was instituted. Two months after injury he had considerable recovery in lower-limb muscles. He was able to walk with support and mobilize independently in a wheelchair, although he still suffered from spasms. Eight months after injury his recovery continues and rehabilitation is progressing well. His major remaining problem is lower motor neurone-type muscular spasm, which makes walking difficult and tiring.
DISCUSSION The effects of electrical current on the body have been well documented. Because electrical current travels along the path of least resistance, nerve tissue is particularly vulnerable. Varghese et al. (1986) in a review of the literature reported an incidence of spinal cord involvement varying between 2 and 27 per cent in various series, although 6 per cent seemed to be a commoner figure in the larger series. Many authors do not mention spinal injury as a complication of electrical injury, and in particular it is not well documented in the burns literature. The onset of spinal cord involvement varies from the time of injury to many weeks after the injury (Jackson et al. 1964; Silversides, 1964). The extent of the injury is also very variable, and
50
Burns (1988) Vol. 14/No. 1
relative sparing of the sensory component has been noted by Holbrook et al. (1970), Christensen et al. (1980) and Varghese et al. (1986). The prognosis varies from total recovery to occasional death (Jackson et al. 1964; Holbrook et al. 1970; Christensen et al. 1980; Varghese et al. 1986). Lightning injury may lead to an interesting phenomenon of keraunoparalysis where transient paralysis is associated with vascular shutdown in an extremity, followed by complete recovery (ten-Duis et al., 1985). The pathophysiology injury is as yet unclear,
of the electrical spinal but the various possible
modes are: 1. Thermal damage within the nerve due to heat production by electrical current. 2. Vascular damage causing thrombosis or haemorrhage. 3. Direct mechanical trauma from fracture or dislocation resulting from intense muscle spasm. 4. ‘Radiation-like’ effect caused by changes in tissue proteins following passage of electrical current which may lead to secondary vascular changes. 5. A build up of electrostatic forces leading to violent tissue disruption in ungrounded victims (Pritchard, 1934). None of these explain the relative sensory sparing of the condition. In the patient reported here, the onset of paralysis was delayed for 12 h, although it is possible that alcohol intoxication masked initial detection due to difficulty in examination. The neurological manifestations progressed for 4-5 days, then reached a plateau and have been recovering since then. Although there was some possible reduced sensation in the first 24 h, the sensory tracts as well as the bladder and
bowel function have been almost totally spared. As the patient survived, no histology of the spinal cord was available to determine the cause of the injury. In conclusion, spinal cord damage is an important complication of high-voltage electrical injury and hence should be looked for. It can appear immediately or following a variable interval. Following diagnosis. early specialist treatment of both conditions is necessary and is best carried out in a hospital with both burns and spinal injuries units. The presentation may vary in intensity. Complete recovery can take place. Although this is not the rule, this is a reassuring thought for the patient and the treating team. REFERENCES Cason J. S. (1981) Treatment of Burns. London: Chapman and Hall, p. 205. Christensen J. A., Sherman R. T., Balis G. A. et al. (1980) Delayed neurologic injury secondary to high voltage current with recovery. J. Trauma 20, 166. Holbrook L. A., Beach F. X. and Silver J. R. (1970) Delayed myelopathy: a rare complication of severe electrical burns. Br. Med. J. 4, 659. Jackson F. E.. Martin R. and Davis R. (1964) Delayed quadriplegia following electrical burn. Proc. Ann. C/in. Spinal Cord Injury Conf. 13, 40.
Pritchard E. A. B. (1934) Changes in central nervous system due to electrocution. Lancet i, 1163. Silvkrsides J. (1964) The neurological sequelae of electrical iniurv. Can. Med. Assoc. J. 91. 195. ten-Duis H: J.: Klasen H. J. and Reenalda P. E. (1985) Keraunoparalysis, a ‘specific’ lightning injury. Burns 12, 54.
Varghese G., Mani M. M. and Redford J. B. (1986) Spinal cord injuries following electrical accidents. Paraplegia 24, 159. Paper accepted 31 July 1987.
Corresportdcnce.shouldhe crddressedto: Mr A. H. N. Roberts. Consultant Plastic Surgeon, Stoke Mandcvillc Hospital, Aylcshury. Bucks, UK.
Printedin
GreatBritain
49
Paraplegia in an electrical burn: a case report S. Kanitkar North
Staffordshire
Royal Infirmary,
Stoke on Trent, UK
A. H. N. Roberts Stoke Mandeville
Hospital,
A ylesbury,
UK
Summary Electrical burns constitute a significant component of burn injuries worldwide. Cason (1981) reported about 150 deaths occurring every year from electrical injuries in the UK. However, spinal cord involvement is a relatively uncommon sequel of electrical injury. A case of paraplegia mainly with motor involvement, following electrical injury, and near complete recovery is reported.
CASE REPORT An Id-year-old man was admitted to hospital following an electrical injury. He had taken a shortcut to his home by jumping over a railway bridge while under the effect of alcohol. In the process, he came into contact with 25 000 volt a.c. overhead cables. On admission he was found to have 27 per cent burns on his head. neck and trunk. Most of these were full thickness or deep dermal in depth. The deepest burn was on the posterior neck with obvious charring of underlying muscle. Escharotomies were performed on the neck. He was intoxicated with alcohol but conscious. About 12 h later, he was noted to have some weakness in both lower limbs. There was increased tone and brisk reflexes. There was also a slight reduction of touch sensation in his lower limbs. X-rays of his cervical spine showed loss of curvature. Subsequent X-rays ruled out any bony injury. X-rays of the dorsal and lumbar spines were normal. Over the next 3 days. his paraplegia progressed and he was transferred to the Stoke Mandeville Burns Unit for joint management at the National Spinal Injuries Centre. He then had a near total paralysis of the lower limbs. Muscle tone was increased and reflexes were brisk. Plantar reflexes were extensor. There was a 0 1988 Butterworth 0305-4179/88/010049-02
6i Co (Publishers) $03~00
Ltd
doubtful loss of proprioception in the toes. and slightly abnormal light touch sensation in the distal lower limbs. His bladder and bowel functions were normal. The burns on his anterior surface were treated by early excision and skin grafting. The posterior cervical muscles were extensively burned and needed excision. Mild depression was treated with appropriate therapy and rigorous physiotherapy was instituted. Two months after injury he had considerable recovery in lower-limb muscles. He was able to walk with support and mobilize independently in a wheelchair, although he still suffered from spasms. Eight months after injury his recovery continues and rehabilitation is progressing well. His major remaining problem is lower motor neurone-type muscular spasm, which makes walking difficult and tiring.
DISCUSSION The effects of electrical current on the body have been well documented. Because electrical current travels along the path of least resistance, nerve tissue is particularly vulnerable. Varghese et al. (1986) in a review of the literature reported an incidence of spinal cord involvement varying between 2 and 27 per cent in various series, although 6 per cent seemed to be a commoner figure in the larger series. Many authors do not mention spinal injury as a complication of electrical injury, and in particular it is not well documented in the burns literature. The onset of spinal cord involvement varies from the time of injury to many weeks after the injury (Jackson et al. 1964; Silversides, 1964). The extent of the injury is also very variable, and
50
Burns (1988) Vol. 14/No. 1
relative sparing of the sensory component has been noted by Holbrook et al. (1970), Christensen et al. (1980) and Varghese et al. (1986). The prognosis varies from total recovery to occasional death (Jackson et al. 1964; Holbrook et al. 1970; Christensen et al. 1980; Varghese et al. 1986). Lightning injury may lead to an interesting phenomenon of keraunoparalysis where transient paralysis is associated with vascular shutdown in an extremity, followed by complete recovery (ten-Duis et al., 1985). The pathophysiology injury is as yet unclear,
of the electrical spinal but the various possible
modes are: 1. Thermal damage within the nerve due to heat production by electrical current. 2. Vascular damage causing thrombosis or haemorrhage. 3. Direct mechanical trauma from fracture or dislocation resulting from intense muscle spasm. 4. ‘Radiation-like’ effect caused by changes in tissue proteins following passage of electrical current which may lead to secondary vascular changes. 5. A build up of electrostatic forces leading to violent tissue disruption in ungrounded victims (Pritchard, 1934). None of these explain the relative sensory sparing of the condition. In the patient reported here, the onset of paralysis was delayed for 12 h, although it is possible that alcohol intoxication masked initial detection due to difficulty in examination. The neurological manifestations progressed for 4-5 days, then reached a plateau and have been recovering since then. Although there was some possible reduced sensation in the first 24 h, the sensory tracts as well as the bladder and
bowel function have been almost totally spared. As the patient survived, no histology of the spinal cord was available to determine the cause of the injury. In conclusion, spinal cord damage is an important complication of high-voltage electrical injury and hence should be looked for. It can appear immediately or following a variable interval. Following diagnosis. early specialist treatment of both conditions is necessary and is best carried out in a hospital with both burns and spinal injuries units. The presentation may vary in intensity. Complete recovery can take place. Although this is not the rule, this is a reassuring thought for the patient and the treating team. REFERENCES Cason J. S. (1981) Treatment of Burns. London: Chapman and Hall, p. 205. Christensen J. A., Sherman R. T., Balis G. A. et al. (1980) Delayed neurologic injury secondary to high voltage current with recovery. J. Trauma 20, 166. Holbrook L. A., Beach F. X. and Silver J. R. (1970) Delayed myelopathy: a rare complication of severe electrical burns. Br. Med. J. 4, 659. Jackson F. E.. Martin R. and Davis R. (1964) Delayed quadriplegia following electrical burn. Proc. Ann. C/in. Spinal Cord Injury Conf. 13, 40.
Pritchard E. A. B. (1934) Changes in central nervous system due to electrocution. Lancet i, 1163. Silvkrsides J. (1964) The neurological sequelae of electrical iniurv. Can. Med. Assoc. J. 91. 195. ten-Duis H: J.: Klasen H. J. and Reenalda P. E. (1985) Keraunoparalysis, a ‘specific’ lightning injury. Burns 12, 54.
Varghese G., Mani M. M. and Redford J. B. (1986) Spinal cord injuries following electrical accidents. Paraplegia 24, 159. Paper accepted 31 July 1987.
Corresportdcnce.shouldhe crddressedto: Mr A. H. N. Roberts. Consultant Plastic Surgeon, Stoke Mandcvillc Hospital, Aylcshury. Bucks, UK.