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Show ", 19H6 Raven Press, New York Homonymous Hemianopia Following Electrical Injury Mark Gans, M.D., and JocI S. Glaser, M.D. The clinical spectrum of l'1ectric'll injuries is complex and diverse. Despite the high annual incidence of electrical accidents. little has been reported recently regarding the neurological deficits associated with this form of trauma. The most frequently cited reviews are those of Critchley (1), Langworthy (2), Naville and De Morsier (3), and Silversides (4). These authors have divided the neurological complications into three groups based on the temporal relationship between the shock and the manifestation of clinical signs: immediate, secondary, and delayed. The present case devl'1oped a dense homonymous hemianopia 4 days following an electrical accident. The details of the abovementioned classification, as well as a review of the pathophysiology, will be presented. Key Words: Electrical injury-Homonymous hemianopia. From the Bascom Palmer EYl' Institute, University of Miami School of Medicim', Miami, Fiorida. . Dr. Gans is a recipient of a fellowship grant from the E. A. Baker Foundation, Toronto, Ontario, Canada. Address correspondence and reprint requests to J. S. Glaser, M.D., Bascom Palmer Eye Institute, P.O. Box OlhHHO, Miami. FL 33101, U.S.A. 2/8 Local injury secondary to direct contact with electricity is a well-known phenomenon (1-4). Howeve~, less well understood are the higher level neurological deficits that follow such injuries. We report a case of a right homonymous hemianopia occurring 4 days subsequent to an upper limb electrical injury. A review of the literature and a discussion of the pathophysiology are presented. CASE REPORT A 53-year-old male electrician was working with a set of wires carrying 220 V alternating current (AC) when they suddenly "short-circuited." There was marked blurring of bilateral vision for several minutes, and, once this gradually improved, he had no further acute visual symptoms. The left hand was "burned," but there were no other symptoms at the time. Four days later, on awakening, the patient noted that he could not see objects to the right. There was a history of hypertension for approximately 8 years and kidneY stones 13 years before. Medi~atil~ns included Zyl~prim and Capoten. On examination 4 days postinjury, his blood pressure was 15l1100 and his pulse 68 and regular. There was no meningismus, carotid pulsations were full, and no bruits were heard. Both pupils reacted well to light, and ocular motility was normal without nystagmus. The retinal vasculature was thought to be in keeping with mild hypertensive changes. There was a dense right homonymous hemianopia on confrontation field testing. All cranial nerves were intact, and the remaining neurological and physical exam was within normal limits. Hospital workup included an ultrasound and doppler study of the carotids, without abnormalities. A computerized tomogram (eT) without contrast demonstrated a hypodense lesion in the left occipital region consistent with a cortical infarct (Fig. 1). / .....- ....._----- HOMONYMOUS HEMIANOPIA FOLLOWING INJURY 219 FIG. 1. Noncontrast CT shows a lucency in left occipital cortex (arrow) with no mass effect. On presentation to the Bascom Palmer Eye Institute 6 months following his injury, examination revealed the following: visual acuity was 20/20 in both eyes; there was a dense right homonymous hemianopia on Goldmann field testing (Fig. 2); pupils were 5 mm each, and both reacted briskly to light; ocular motility was normal; the slit-lamp examination was unremarkable; and the fundi demonstrated mild hypertensive changes. DISCUSSION Electricity is governed by three parameters: voltage, resistance, and amperage. These characll'ristics art' related according to Ohm's Law (amperagt' = voltage/resistance). Although the voltage is known in most electrical accidents, the precise amperage and resistance are usually unknown. Skin resistance can range from 1,000 ohms in a sweaty palm to over 1,000,000 ohms in a dry, calloused hand (5-7). The extent of injury is influenced, furthermore, by the nature of the current, i.e., AC versus direct current (DC). AC is more destructive than DC due to the resulting tetanic muscle spasms that can fix the victim to the electrical source, and the sensitivity of the heart and respiratory center to this type of current (8). In fact, household AC (60 Hertz) is most effective in causing ventricular fibrillation (9). There are approximately 1,000 electrically related deaths and 2,400 patients requiring emergency treatment for electrical injuries annually in the U.S. (10,11). Despite this-high incidence, and the 10-44<7c, prevalence of neurological sequelae amongst the survivors (3,8,12), few reports have been presented recently. The neurological consequences of this form of trauma are important, yet poorly understood phenomena. In past reviews, the neurological complications have been classified as immediate, secondary, and delayed (1,4,10,12). Immediate effects can range from a painful sensation at 1 milliampere/60 V AC to loss of consciousness and/or respiratory arrest at over 90 milliampere/60 V AC (6). Typically, lower voltage currents affect cardiac muscle, whereas 1:.~,n 20120 ~n 20/20 FIG. 2. Goldmann perimetry demonstrates a congruous right homonymous hemianopia (12e, 14e, and V4e stimuli). I Clill NClIro-"I,hthallllol. Vol. 6, No.4. 1986 220 M. GANS AND f. S. GLASER TABLE 1. Hemispheric deficits from indirect electrical contact Author Age Contact Delay Deficit Critchley (13) 26 Hand 9 mo Right hemiparesis/aphasia Haase and Luhan (14) 45 Limb 3 wk Right hemiplegia Langworthy (2) 53 Hand 1 day Right hemiplegia Present case 53 Hand 4 days Right homonymous hemianopia higl1l'r voltages C,luse either centrill or peripheral neurogenic respiratl)ry paralysis. Other immediate signs include agitation, confusion, amnesia, tinnitus, visual blurring, weakness, tremors, complete motor paralysis, and hypesthesia (l,4,6). Secondary neurological effects are those occurring within an arbitrarily defined period of 5 days subsequent to the injury (4). These effects include paraplegia, trunk and extremity pain, and autonomic disturbances (edema, cyanosis, peripheral artery spasm, and Horner's syndrome) (1,2,4,10). Although these deficits can persist for some time, the natural history is one of resolution within days. As in the above two groups, the delayed sequelae of electrical injury span a wide clinical spectrum. Spinal cord injury at the level of C4-C8 appears to be the most common complication (1,2,4,6). This is due most likely to the frequent hand-to-hand electrical accident, with resultant electrical transmission through the spinal cord. Less well understood, and more relevant to our case, are the remote effects of electricity on the central nervous system (CNS). Table 1 lists the reported cases of delayed cerebral injury due to indirect electrical contact. Critchley (13) reported a 26-year-old man whose right hand came into contact with a circuit of unknown voltage. Two fingers were burned slightlv, the right arm was paralyzed temporarily, and the patient was unable to speak for 30 min. These deiicits resolved completely, and he remained well for 9 months. After 9 months, he developed a right hemiplegia with aphasia. Cerebrospinal tluid was Wassermann negative. Haase and Luhan's (14) case involved a 45-warold man shocked by a high-voltage transfo'rmer who experienced no immediate symptoms. HI:' continued his normal daily activities for the next 18 days, although personality changes were noted by the family during this period. On the 19th dav, the patient suddenly lost consciousness and was noted to have a right hemiplegia. He remained unresponsive for I year and then died. Autopsy revealed occlusion of the basilar artery with secondary encephalomalacia of the rostra'l end of the pons and of the thalamus. Langworthy (2) discussed a 53-year-old hypertensive man who made brief contact through his right hand with a 220-V current. Immediately following the accident, he was neurologically intact, However, the patient awoke the next morning with a left hemiplegia. Although other cerebral injuries are reported (4,15), these are characterized by direct cranial contact with the source of electricity. Other neurological syndromes have included isolated cases of secondary Parkinsonism, fifth, seventh, and eighth cranial nerve dysfunction, and optic disc edema (1,2,6,16). There is no clear relationship between epilepsy and previous electrical injury. In earlv animal experiments, passing current from for~foot to forefoot generated no current in the brain (17). Yet definite pathological changes in the brain have been noted in \'ictims of electrical shock to the extremities. Alexander describes findings in two patients ''\'ho died from peripheral contact with electricity: "incomplete perivascular necrosis ... and demvelination in the convolutional and central white matter of the brain with swelling of the oligodendroglia and of the macroglial astroc!·tes throughout the white matter and with compression l)f the cortical gray ribbon with corresponding defl1rmities of the cortical ganglion cells ... " (18). Ale:\ander felt that these changes were nonfatal, and that the cause of death was due to a generalized arterial vasoconstriction folkH\' ed b,' cardiac arrest (18), Although no specific cases are cited, Langworth!' (2) feels that pre-existing h!'Pertension in the presence of AC increases susceptibility for these CNS lesions. Although admitting that the "mechanisms by which electrical currents applied to skin surfaces Cduse injury to nervous structures remote from the site of application are not clear," Farrell and Starr (10) proposed that an electrically induced progressive vasculopathy, predominantly affecting endothelial cells, was the potential source of thrombosis formation, with subsequent alteration in blood tlow. In his discussion of eNS pathology follOWing electrical injury, Silversides (4) states that unexplained cortex fissuring is seen, with scattered splitting of cortical layers. Although not precisely explaining the etiology of these lesions, HOMONYMOUS HEMIANOPIA FOLLOWING INJURY 221 Silversides discounts the thermaL electrolytic, and mechanical effects of current as adequate causes. However, he does find some merit in Pritchard's hypothesis (4). Pritchard proposed that it is the electrostatic charges developed mostly within the cerebrospinal fluid pathways that can account for the CNS changes. It is not clear from this discussion why there should be a delay in the onset of neurological signs. No other adequate hypothesis explaining either the etiology of associated electrical CNS lesions, or the time of the delay of neurological signs, was noted in the literature. From the above, it is clear that there are incidents of CNS deficits remote from the point of electrical contact. Regarding our case, the latency of 4 days from the injury to the presentation of a field defect and an occipital lesion on CT scan leads us to speculate on the causal relation. Admittedly, our 53-year-old hypertensive patient was at some risk for an isolated homonymous hemianopia; however, the temporal aspects of this case cannot be ignored. Possibly, chronic hypertension increases the risk for ischemic events secondary to vasomotor changes, including those induced by electrical current (2). In summary, we present a 53-year-old hypertensive man who, 4 days subsequent to an electrical accident, developed a cortical homonymous hemianopia with a corresponding focal lesion evident on CT scan. From the literature, it is evident that electrical injury is followed frequently by neurological deficits, even remote from the peripheral site of contact. REFERENCES 1. Critchley M. Neurological effects of lightning and electricity. Lallcet 1934;1 :68-72. 2. Lmgworthy OR. Neurological abnormalities produced by l·lectricity. / NcrI' Mellt Dis 1936;84:13-26. 3. Naville F, De Morsier G. Symptomes neurologiques consecutifs aux electrocutions industrielles. Rei' Neurol (Paris) 1932;1:337-55. 4. Silversides J. The neurological sequelae of electrical injury. Call Med Assoc /1964;91:195-204. 5. Christensen JA, Sherman RT, Balis GA. Wuamett JA. Delayed neurologic injury secondary to high-voltage current with recovery. / Trauma 1980;20:166-8. 6. Hyslop GH. The effects of electric shock on the nervous system, In: Brock S, ed. hlluries of the braill and spinal cord. 4th ed. New York: Springer Publishing Co., 1960:680-95. 7. Thompson JC Ashwal S. Electrical injuries in children. Am / Dis Child 1983;137:231-5. 8. Solem L, Fischer RP, Strate RG. The natural history of elec-trical injury. / Tral/ma 1977;17:487-92. . 9. Halperin OS, Oberhausli j. Rouge Jc. Cardiac and neurological impairments following electric shock in a young child. Hell' Paediatr Acta 1983;38:159-66. 10. Farrell OF, Starr A. Delayed neurological sequelae of electrical injuries. Nel/rology 1968;18:601-6. 11. Walsh FB, Hoyt WF. Clillical Nel/yo-Ophthalmology, Vol. 3. 3rd ed. Baltimore: Williams and Wilkins, 1969:2484-9. 12. DiVincenti FC Moncrief JA, Pruitt BA Jr. Electrical injuries: a review of 65 cases. / Tral/ma 1969;9:497-507. 13. Critchley M. Industrial electrical accidents in their neurological aspect. / State Med 1932;40:459-70. 14. Haase E, Luhan JA. Protracted coma from delayed thrombosis of basilar artery follOWing electrical injury. Arch Nel/roI1959;1:195-202. 15. Tamler E. Electric cataract. Am / Ophthalmol 1962;54:865-6. 16. Bainbridge W. Optic atrophy, with retinal changes caused by high-tension current. Br Med /1930;2:955-6. 17. Sances A, Larson Sj. Mvklebust j. Cusick JF. Electrical injuries. Surg Glfnecol Obste't 1979;149:97-107. 18. Alexander L. Clinical and neuropathological aspects of electrical injuries. / Illd Hl/giene Toxicol 1938;20:191-243. I Clm NCIIYO'0l'hthallllol, Vol. 6. No.4. 1986 |
