Annals of the MBC - vol. 4 - n' 2 - June 1991

NEUROLOGICAL DISORDERS FOLLOWING ELECTRICAL BURN INJURIES

Lochaitis A., Parker I, Stavropoulou V., PanaVotaki D.

Department of Plastic Surgery and Burns, General Hospital of Attica (K.A.T.), Athens, Greece

SUMMARY. Two cases are described of the infrequent complication of neurological disorders due to progressive spinal cord involvement following electrical injury. The possible mechanisms of this type of damage are discussed.

Introduction

The first recorded case of electrical injury after the discovery of the electrical phenomenon occurred in 1746 when two Dutchmen were injured by the accidental discharge of a L,eyden jar. Since then, the mechanisms by which damage is caused by electric current in the human body have been a matter of controversy. They are still not fully understood but the unfortunately large number of electrical accidents both in the home and at work, comprising 3% of all burn admissions in the USA, makes research in this matter.
At the General District Hospital of Attica a total of 90.5 burn cases were admitted between 1986 and 1988. Of these, 23 were electrical injuries (2.5%) (Fig. 1).  Most were due to 220 V alternating current in household accidents although some were due to high-tension current (above 20,000 V) on building sites or in other related jobs.
The effect of current on the nervous system has been well-documented and its sensitivity to electrical damage is commonly seen. This can take the form of cerebral or spinal cord lesions or peripheral nerve damage.
Over the past 4 years a variety of neurological pictures have emerged from our unit, complicating electrical burns. They range from localized single nerve paresis through multiple peripheral., nerve lesions, localized lesions of the brain such as cerebellar ataxia after, electrical injury through the skull, more generalized brain damage and spinal cord lesions which have in some cases been transient but which in two cases, with delayed onset, left More permanent damage.
In this paper these two cases of progressive spinal cord involvement after electrical injury are presented, partly because of the infrequency of this complication and partly to discuss possible mechanisms of such damage.

Case reports

Case I (Fig. 2)

Fig. 2 Distribution of burns: case I

Fig. 2 Distribution of burns: case I

On August 4 1988 a 32-year-old policeman sustained electrical injury while installing a television aerial which accidentally touched an overhead high tension cable carrying approximately 22,000 V. The patient lost consciousness but recovered on the way to a general hospital in Athens where he was admitted and given shock resuscitation. His general condition was good with no signs of cardiovascular, respiratory or neurological involvement. His burn injury was 25% T13SA and consisted of full-, and partial-thickness burns as shown. Small charred areas on the right side of the neck and right hip suggested the entrance and exit points of the current.
On transfer to the Burns Unit of th.e General Distrct Hospital of At.tica, resuscitation was continued with good response. Escharotomics were carried out on the neck to relieve the extensive oedema which had formed. Neurological examination was negative and X-rays showed no sign of skeletal damage.
Three days later the patient noticed weakness of his right hand when trying to hold a pen or fork but, having occlusive dressing on both arms, did not pay special attention to this initially. This weakness worsened, however, progressing to the left side and the patient was no longer able to feed. himself. Maximum deterioration was approximately 15 days post-burn. Electromyograms of the right arm were negative. During this time weakness of the legs had also increased and, as in the arm, the first ' find ' ings went unnoticed until the patient tried to stand. Characteristically, sensation was retained at all times but reflexes were increased and the Babinski sign was positive.
At 25 days the patient underwent surgery and full-,thickness areas were grafted, After this there was gradual improvement of his quadriparesis and at 6 weeks post-bum he was able to walk a few. steps assisted while upper limb function improved more rapidly than that of the lower limbs.
The patient was discharged after , 8 weeks to continue physiotherapy and neurological follow-up as an out-patient. Improvement has been gradual over the year and although the patient walks well and upper limb function is very good, neurological examination still reveals evidence of spinal cord lesion at the level of C4-C5 involving selective pyramidal tracts with increased reflexes, some clonus and slight spasticity.

Case 2 (Fig. 3)

Fig. 3 Distribution of burns: case 2

Fig. 4 Types of electrical injury.

  • Electrothermal bum - due to arc
  • Flame bum - due to ignition of clothes, etc.
  • Deep thermal bum - due to current conduction along pathway of least resistance in body
  • "Crush" injury. - due to cellular and ischaemic damage from the current

Fig. 3 Distribution of burns: case 2

A 43-year-old Yugoslav working for ' the Greek electrical company in the north accidentally came into contact with high tension cables causing him to be thrown from a height of 4 M.
On admission to the nearest hospital, the patient was conscious and found to have 10% burns, chiefly partial-thickness, of the face, right upper arm and a small area of the left thigh, without any of th ' ese indicating the exact entrance and exit points of the current. He also had a fractured left femur and 8th right ' rib. ECG revealed a right bundle block which quickly righted itself. Neurological examination revealed paresis of the right radial nerve. He was transferred immediately to the Bums Unit of our hospital where the clinical picture was the same.
The follgwing day the patient complained of weakness of both lower limbs which progressed rapidly upwards showing almost complete paraparesis within the next 2 days. Characteristically sensation was fully retained as well as proprioception. Reflexps were again increased and signs for pyramidal damage were positive. Since there was initially some doubt as to whether the neurological picture might in fact.be due to damage to the vertebral column, the patient was then transferred to the Orthopaedic Unit for full, investigations.
Laboratory and radiological investigations were all negative, as was the myelogram and CT scan of the spinal cord, and though his paraparesis remained essentially unchanged the patient began to show increased tendon reflexes in both upper limbs, indicating the continuing progression of hi.S spinal cord lesion.
Immediately after, completion of in ' vestigations the patient was transferred at his request to Yugoslavia, thus making follpw-up of his case impossible.

Discussion

The effects of electric current on the human body have been generally well-documented, though numerous factors are involved which will affect , the type and extent of the damage caused. It is well known that there are basically fou~ types of electrical injury. (Fig. 4):

  1. The electrothermal burn, caused by arcing of the current from the source to the body and usually affecting the skin only in varying depth and extent. This is usually foupd where high-voltage current is involved.
  2. The flame burn, usually caused by ignition of the clothes, again of varying extent and depth.
  3. The deep thermal burn, due to conduction of the current along the pathway of le , ast resistance, causing tissue destruction often.far more serious than surface. burns suggest.
  4. The "crush" type of injury, which can affect. any organ of the body and has been attributed to cellular and ischaernic damage from the current.

With regard to the actual current causing the accident, again there are many factors which will affect.the degree of injury. (Fig. 5):

Fig. 5 Factors affect , ing injury. due to the passage of electric current through the body

  • Type of circuit and current
  • Voltage of circuit
  • Resistance of tissues
  • Amperage of current
  • Pathway of current through the body
  • Duration of contact

1) Type of circuit and current

Experimental studies have shown (Lee and Kolodney, 1987) the importance of the type of ci~Cuit created when current flows through the body. When a voltage is applied across the body the rate of heating of each tissue through which current passes depends not only on the properties of the tissue themselves but also on their arrangement within the circuit.

  •  

If th , e tissues are in series the current density is identical but the fielq strength is differqpt in each tissue and heating is inversely proportional to tissue conductivity. In parallel, as we see in the cross-section of the limb (Fig.6), urrent density varies with each type of tissue, with the layer having the highest conductivity experiencing the highest temperature rise. We can also see (Fig. 7) that current density in differptit areas varies, being most concentrated near the joints and inversely proportional to the cross-sectional area of the limb. Thus the quantity of heating produced in electrical injury. is dependent on tissue conductivity, current density and the relationship of tissues to the current flowing through them.
It should also be remembered that the type of current, alternating or direct, will also affect the injury, low-voltage AC usually causing more damage than the equivalent DC, though high-voltage DC is more frequently fatal.

2) Voltage

Potentials of les , s than 24 V are usually considered safe. High-voltage accidents usually cause devastating injuries. It is interesting to note that all recorded instances of spinal cord damage are from high-voltage circuits.

3) Resistance (Fig. 8)

It is quite well known that tissues offer.yarying resistances to electric current and it has always been i thought that heating is greater in tissues of high resistance (Baxter et al.). However, Lee and Kolodney in an experimental model of the upper limb where tissues are in parallel fou4d that the greatest temperature rise when 4 V was applied was in tissue of lowest resistance.

Fig. 6 Fig. 7 Current density is concentrated at joints
Fig. 6 Fig. 7 Current density is concentrated at joints
Fig. 8 Fig. 8

4) Amperage

This is of extreme importance. Currents of greater than 15 milliamperes are sufficiqnt to cause nerve and muscle stimulation and tetanic contraction and currents of over 60 milliamperes usually cause ventricular fibrillation.

5) Pathway (Fig. 9)

It is generally observed that where the current passes from hand to hand the mortality rate is high, about 60%, whereas in the head to foot. pathway it is only about 20%. There is an increase of spinal cord injury. usually between the levels of C4-C5 when the current passes from hand to hand.

Fig. 9 Current lines through body if current passes arm-to-arm

Fig. 9 Current lines through body if current passes arm-to-arm

6) Duration of contact

The longer the duration of contact the greater the damage.
Spinal cord involvement (Fig. 10) is one of the less common neurological complications and statistics vary as to the frequency of its appearance. Panze (1930), Hyslop (1949), Silversides (1964) and Jackson (1964) all described such cases. Varghese et al. (1986) described 5 cases of spinal cord injury, out of I 16 patients with electrical injury. (4.3%). Others place this incidence much lower, though possibly some milder cases go unrecognized or are attributed to limb weakness from generalized immobilization and prolonged bed rest. The two cases presented here amongst 23 electrical bums admitted during the past three years represent a percentage of 8.~%.
Appearance of neurological disorders of this type can be immediate but usually varies from a few,days to a few weeks after.injury, although it has been noted up to two years afterwards (Levine et al., 1975; Farrell et al., 1986). Prognosis would seem to be related to the delay of o.nset, being worse when this is considerable, varying from complete recovery to, very rarely, death. Jackson et al. (1964), Holbrook et al. (1970), Christensen et al. (1980) and Varghese et al. (1986) have described 40 cases of delayed onset spinal cord involvement where partial recovery was seen in only two patients, while in 27 cases, where the onset was immediate, complete recovery was 100%.
In both our cases there was a small delay in onset, which was after.three days in the'first. case and after 24 hours in the second. Reasonably good recovery is present in Case I which is still progressing a year later. Unfortunately Case 2 transferred from hospital to his home country before. the outcome of his progressive neurological lesion was known.
Most authors describe these spinal lesions as predominantly motor, taking varying forms. Panze in 1931 described it as "spinal atrophic paralysis" and it can take a form consistent with ascending paralysis, transverse myelitis or amyotrophic lateral sclerosis.
Taking into consideration the factors affecting injury. when electric current passes through the body, as already described, the necessity of find , ing an explanation for the cause of injury. now arises. This can be summarized as follows (Fig. 11):
Trauma. The possibility of direct trauma to the spinal cord, caused either by the patient being thrown by the current or by violent tetanic muscle spasms, cannot be ruled out even where there are no radiological find , ings. However, in this case, one would expect the onset to be immediate, while in our cases it was not. But if we. consider that the artery walls also contain muscle there is a possibility (Petty, 1986) that tetanic contraction of this muscle tissue in small arteries supplying the spinal cord and its roots could cause a delayed atrophy to the nervous system due to impaired blood supply.
Heating. This is caused by the dissipation of electricity in nerve tissue, which would seem to be a proliferative angiopathy in the vessels surrounding the spinal cord. A recent theory of Robson et al. is that heating causes injury, to the cell which responds by producing inflammatory mediators, chiefly Jn the form of thrOmboxane A2, which cause deterioration, ischaernia and cell death.
Irradiation type injury. This explanation attributes injury, to the direct effect , of thp current on the cord which causes changes in the DNA and enzyme systems of nerve cells affecting mitosis which results in the formation of abnormal proteins in the endothelial cells of th , e vessels. These changes are similar to those seen after irradiation. The abnormal cells proliferate within the vessels causing interference with blood flow.

Fig. 11 Mechanisms of injury. to spinal cord

  • Direct trauma
  • Thermal damage
  • Vascular damage
  • "Irradiation type" changes of DNA and enzyme systems
  • Electrogenic breakdown of cells

Electrogenic breakdown of cells. In this complication where neuropathy often , has a delay in onset either of as in our cases, or even years, other mechanisms of damage must be considered. For instance, myoglobulin from muscle rupture is usually released after.electrical injury, and histology shows the adjacent coexistence of normal and damaged cells, a phenomenon difficult to explain by thermal mechanisms alone. There is evidence too, from some reports such as that of Lee et al. (1982), that local electrical fiel0s can be sufficipnt to cause breakdown of cell membranes and thus lysis of the cells with all the pathophysiological consequences. They also suggest that long cells, such as nerve cells, are perhaps more vulnerable and that they are most susceptible when arranged in parallel to the passing current. Small perfora , tions in cell membranes caused by the field are suffici.e.nt to upset the delicate balance between intra- and extracellular environment and will eventually lead to destruction of the cell. Both the increased myoglobulin levels and the derivatives of membrane phospholipids after.electrical injury. Would tend to substantiate this theory of cell rupture after electrical trauma.

Conclusion

The presentation of su , ch cases is not new but a study of the literature reveals that cases of spinal cord damage following electrical injury, are uncommon. Infact, it is a complication which sometimes tends to be overlooked, especially when the localized thermal damage is either so insignificapt that it would not be expected or so serious that all efforts are concentrated in that direction. In our first, case, although upper limb weakness was soon evident, lower limb deficit , was not really seen until the patient tried to ambulate. In the second case the neurological problem was quickly obvious since paraparesis developed quickly.
On reviewing the physics involved in the application of an , electric current to the body and also the possible pathophysiological mechanisms which can explain such injury, it is obvious that research in this fielO is far from complete. The variations in onset times for this complication are not entirely explicable nor the selective areas which are usually affectpd. The retention of sensation seems to be a fairly common characteristic present in both of our cases, showing selective preservation of the relative tracts.
Since the exact cause of the damage still remains in doubt, so does the treatment or possible prevention of the development of this often. very serious complication.

RESUME. Deux cas sont présentés de la complication peu fréqpente de troubles neurologiques dus a la déterioration progressive de la moelle épiniére aprés une brillure électrique. Les mécanismes qui peuvent causer ce type de dommage sont discutés.

BIBLIOGRAPHY

  1. Baxter C.R.: Present concepts in the management of rn~ajor electrical injury, Surg. Clinics of North America, 50: 1401-1418, 1970
  2. Christensen J.A., Sherman R.T., Balis G.A., Wuamett J.D.: Delayed neurologic injury. secondary to high-voltage current, with recovery. J. of Trauma, 20, 12: 166-168.
  3. Critchley M.: Neurological effect,§ of lightning and electricity.Lancet: 68-72, 1934.
  4. Duis H.J., Klasen H.J., Reenalda P.E.: Keraunoparalysis, a "specific". lightning injury, Bums, 12: 54-57, 1985.
  5. Farrell D.F., Starr A.: Delayed neurological sequelac of electrical injuries. Neurology, 18: 601-606, 1968.
  6. Holbrook L.A. et al.: Delayed myelopathy: a rare complication of seyCre electrical bums. Br. Med. J., 4: 659-666, 1970.
  7. Jackson F.E., Martin R., David R.: Delayed quadriplegia following electrical bum. Military Medicine: 601-605, 1965.
  8. Kanitkar S., Roberts A.H.N.: Paraplegia in an electrical bum::i a case report. Burns, 14: 49-50, 1988.
  9. LangwWhy O.R.: Neurological abnormalities produced by: electricity. Journal of Nervous and Mental Disease, 84: 13-26, 1929.
  10. Lee R.C., Kolodney M.: Electrical injury. mechanisms: dynamics of thermal response. Plast. and Recon. Surg., 80, 5, Nov. 1987.
  11. Lee R.C., Kolodney M.: Electrical injury. mechanisms: electrical breakdown of cell membranes. Plast. and Recon. Surg., 80, 5, Nov. 1987.
  12. Levine N.S., Atkins A., McKeel D.W. Jr. et al.: Spinal cord injury. following electrical accidents: case reports. J. Trauma, 15: 459-463, 1975.
  13. Petty P.G., Parking G.: Electrical injury. to the central nervous system. Neurosurgery, 19, 2, 1986.
  14. Robson M.C., Murphy R.C.: A new explanation for progressive tissue loss in electrical injuries. Plast. and Recon. Surg., 7 5: 43 1, 1984.
  15. Silversides J.: The neurological sequelae of electrical injury, Canad. Med. Assoc. J., 91: 195-204, 1964.
  16. Varghese G., Mani M.M., Redford. J.B.: Spinal cord injuries following electrical accidents. Paraplegia, 24: 156-166, 1986.

 

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