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Show Editorial Comment The Electrical Stroke A Hazard of the Good Life The movement of electmns creates an electrical current (amperage), which varies directly with electmmotive force (voltage) and indirectly with interposed resistance (ohms). Living without e1ectricitv would be difficult for those of us fortunate eno~gh to control this energy with the flick of a switch. Yet, many people in Third World nations have no or very limited access to this important force that has contributed to man's many successes and advances. Familiarity and easy availability cause complacency and dependency, and nowhere is this better illustrated than when we cannot use electricity after a power outage. So, although we can live without electricity, it is hard and limits our capabilities tremendously. When we utilize electricity without due caution and respect, problems arise. Gans and Glaser (1) describe such a tragic situation in which a 53-yearold male electrician developed right homonymous hemianopia 4 days after being shocked by 220 V of alternating current that "short-circuited." A computerized tomogram demonstrated a hypodense lesion in his left occipital region consistent with a cortical infarct. Unfortunately, but certainly expectedly, morphologic verification is not available. Consequently, questions remain about the exact nature and cause for this man's underlying neuroophthalmologic deficit. Circumstantial evidence, however, incriminates the electrical shock, even though he had hypertension. Damage from electrical shocks has been known since the introduction of this energy. Minor electrical jolts have been experienced at some time by most people exposed to easily accessible electricity, and we teach our children to be careful around electrical outlets and appliances, but often forget to do the same ourselves. Nonlethal and persistent deficits, as described by Gans and Glaser (1), do develop after electrical injuries (2-5). These may be immediate or delayed problems occurring several days after the shock. Addn'ss correspondencl' and reprint requests to Joseph C. Parker, Jr., M.D., Department of Pathology, Truman Medical Center, 2301 Holmes St., Kansas City, MO MIOH, U.S.A. 222 'h 19M Raven Press, New York For example, a few days or weeks following a cutaneous electrical burn, secondary ischemic necrosis may appear due to arterial and arteriolar thromboses superimposed upon previously damaged intima. To create either a physiological response or damage, tissues must be interposed between two conductors to complete an electric circuit. The electric current, which is a movement of ions, can be passed through all tissues to some degree, but moves most easily through nerves and blood vessels which possess the least tissue resistance. The dry cornified skin, on the other hand, acts as a protective insulator which, unlike conductors, has fe\ver free electrons. The ionic movement of electricity may cause immediate tissue alterations through its depolarizing effects and heat generation. The delayed tissue changes are a manifestation of subsequent reactions to initial vascular alterations, in concert \\'ith membrane injuries with delayed lysosomal damage. Even though the exact mechanism for dela~'ed electrical injuries is not clear, delayed neurological and psychiatric features have been recognized (2-5), but not well documented by morphologic studies. These later deficits result from acute disruptions of blood vessels with intimal damage and subsequent thrombotic occlusions. Electrical damage to endothelial surfaces, as well as the vessel wall, provide the potential for further reactive changes, including thrombus formation. This may occur hours, days, or weeks follOWing the initial electrical injury (2-8). Alterations caused by electrical injury vary with the type of current (alternating current versus direct current), the amount of current, its path through the body, duration of flow, tissue resistance or impedance, the electrical charge, and contacted surface area. The current, manifested by movement of electrical charges as a function of time, produces the tissue damage. After entering the body, current spreads radially which lowers the current density per unit area of cross section. Even moderately high currents (300 milliamperes) are not dangerous, unless the heart is in the elec- /,...,--------- EDITORIAL CUMMENT 223 trical pathway. Brain tissue can toll'rate much greater currents than the heart, as dl'monstrated by controlled electroconvulsive shl'Cks with alternating currents between 500 milli,lInpl'rl's and 1 ampere. No recogniZt'd morphologic alterations occur with this therapy. Nervous tissue is damaged by till' l'll'ctrical generation of heat and transfer of electrical energy as electromechanical effects, especi'1l1y following lightning strikes or high-vl)ltagl' shock. These cause immediate eHects, but mav Il',h.i to delayed injuries b~' secondarily producing thrombl)ses and altering the cytosol of cells in the nervous system aHecting neurites, syn,1pses, glia, and myelin. Lesions in the nervous system caused by electrical current may be vascular, parenchymaL or both. Alternating current produces early perivascular hemorrhages (6-8), possibly related to electrical irritation of nervi vasorum and/or vasomotor responses. On the other hand, parenchymal alterations include nuclear pyknosis and neuronal chromatolysis, caused by intracellular electrolytic derangements (6-8). Subsequent glial reactions may occur. Delayed seizures are unusual. Neverthe'less, dementi~, focal neurologic deficits, demyelination, and psychiatric disorders have been described as delayed complications from electrical injury to the nervous system (2-5). Since blood vessels are a primary conductor of electricity in the body, they are susceptible to damage by this force. Earlv vascular lesions include frank disruptions with hemorrhages (7), and, as indicated, the later vascular lesions include thromboses related to the altered intima in previously damaged blood vessels (1,2,6-8). Various stroke syndromes can result (1-7). Benefits from electricity far outweigh its deficits, so, like any energy source, it should be handled knowledgeably and with due caution. Let the user beware. Joseph c. Parker, Jr., M.D. Department of Pathology Truman Medical Center Kansas City, Missouri REFERENCES 1. Gans M, Glaser )S. Homonymous hemianopia following electrical injury. I (lill Neuro-Ophtlzalmo/1986;6:000-000. 2. Alexander L. Electrical injuries to the central nervous system. Met! Clill North Am 1983;22:663-88. 3. Farrell OF. Starr A. Delayed neurological sequelae of electric injuries. Neuroiosy 1968;18:601-6. 4. Langworthy OR. Neurological abnormalities produced by electricity. / NeTt' Mellt Dis 1936;84:13-26. 5. Silversid~s). The neurological sequelae of electrical injury. (all Met! Assoc /1964;91:195-20-1. 6. JaHe RH. Electropathology: a review of the pathologic changes produced by electric currents. Arch Path"l 1928; 5:837-70. 7. Parker jC Jr. Philpot ). Pillow JR. Infantile hematomvelia complicating e1ectro-cardio\'ersion. Arch Pat/wi Lab l\1ed 1985;109:370- J. 8. Zeman W. Thermal eHects and electrical injuries. In: Minckler j, ed. Pathoiosy of the llen'l'l/5 s!lstelll. New York: McGraw-Hili. 1968;1:939-48. , Clill NCllnHll'iItilallll,l!, Vol. 6. No.4. 1986 |