O148-396X/85/1605-0686$02.00/0 NEUROSURGERY Copyright © 1985 by the Congress of Neurological Surgeons Vol. 16, No. 5. 1985 Printed in U.S.A. Intracerebral Hematoma Secondary to Lightning Stroke: Case Report and Review of the Literature Lowell D. Stanley, M.D., and Richard A. Suss, M.D. Division of Neurosurgery (L.D.S.) and Department of Radiology (R.A.S.), The University of Texas Health Science Center at Dallas, Dallas, Texas A young boy sustained a lightning stroke to his head. He was rendered immediately unconscious and hemiplegic. Computed tomography revealed three discrete basal ganglia hematomas. This patient’s management is discussed, and a review of lightning injuries to the central nervous system is presented. (Neurosurgery 16:686-688, 1985) Key words: Basal ganglia, Cerebral hematoma, Computed tomography, Lightning Accidental death due to lightning is an uncommon but spectacular injury. Approximately 300 persons are struck by lightning every year in the U.S. In the past, it was generally believed that lightning injury was nearly uniformly fatal, but recent reviews of the subject indicate that only about one- third of the people struck by lightning die. Although a multi- tude of organ system injuries have been associated with light- ning injury, death usually occurs secondary to respiratory arrest, cardiac arrest, or ventricular fibrillation. We are re- porting a case of direct lightning stroke to the head of a young boy. His clinical course and management and a review of the literature are presented. CASE REPORT On April 8, 1984, an | 1-year-old boy was walking from a soccer field when he sustained what appeared to be a direct lightning stroke to the head, which rendered him immediately unconscious. A medical student witnessed the event, felt the boy to have suffered a cardiac arrest, and immediately began cardiopulmonary resuscitation (CPR). The patient was intu- bated by a paramedic team and CPR was continued until they arrived at a community hospital. On arrival there, the patient had a blood pressure of 120/70 mm Hg, a pulse of 76 beats/minute, and 28 regular, spontaneous respirations per minute. Arterial blood gas analysis showed a pH of 6,93, a PCO, of 58 torr, and a PO, of 47 torr on arrival. Physical examination revealed a comatose child with burns of his head, trunk, and lower extremities. The lower extremities were mottled, and no pedal pulses were palpable. Electrocardiog- raphy (EKG) revealed a normal sinus rhythm except for peaked T waves. The chest roentgenogram revealed bilateral diffuse infiltrates suggesting aspiration. After stabilization, the patient was transferred to Parkland Memorial Hospital in Dallas, Texas. On admission, the patient’s blood pressure and pulse were stable. He was breathing spontaneously. Physical examination revealed a comatose boy with second degree burns on the left parietooccipital scalp, left chest, left abdomen, and both lower extremities. Hemotympanum with perforation was noted on the left. The lungs had bilateral diffuse rhonchi. Good pulses were present in all four extremities. Neurological examination revealed that the pupils were equal and reactive to light, the extraocular muscles were intact. and the bilateral corneal reflexes were intact. The patient had a dense left hemiplegia, but responded purposefully to deep pain on the right. The results of a complete blood count and serum electrolyte 686 determinations were within normal limits. The arterial blood gas results were: pH 7.31; PCO», 61 torr; PO2, 67 torr; and 90% saturation on 100% FIO. The chest x-ray film and EKG were unchanged. Skull films revealed no evidence of skull fracture. Computed tomography of the brain revealed three discrete hematomas in the right basal ganglia without hydro- cephalus or midline shift (Fig. 1). A ventriculostomy was placed for intracranial pressure (ICP) monitoring. The patient was maintained on a ventilator, both for hyperventilation and for management of his aspira- tion pneumonia. The patient was treated with prophylactic phenobarbital. The burns were managed with dressing changes and silver sulfadiazine cream. The ICP remained within normal limits, and on the 5th day the ventriculostomy was removed. The neurological examination was unchanged until Day 7, when the patient would occasionally follow commands and open his eyes to verbal stimuli. On Day 11, he was extubated. By day 12, he was awake with eyes open and speaking a few words. After 22 days in the hospital, the patient was transferred to a rehabilitation center. At discharge, he was awake and alert and speaking with only a mild dysphasia. A severe left hemiparesis remained. Fourteen weeks after the injury, he was reevaluated. He had mild hearing impairment bilaterally, worse on the left. He was ambulatory. The left hemiparesis was improved but still present and was worse in the upper extremity. DISCUSSION Lightning arises when warm updrafts from the earth meet cooler air present in storm clouds, creating large amounts of static electricity. This develops a net positive charge in the upper layers of the cloud and a net negative charge in the lower layers. A potential difference builds up within the cloud and is discharged to earth as lightning (4). This bolt of lightning is estimated to carry 10 to 100 million volts and a current as high as 200,000 amperes. It travels toward the earth at speeds of | to 2 million meters/second (8) and when it strikes can cause temperatures of 15.000 to 60.000°F (18. 22). Lightning can strike an individual by three different mech- anisms—direct stroke. side flash. and step voltage (8, 16). A direct stroke occurs when the lightning bolt contacts a victim directly at his highest point—most commonly the head or an upstretched arm. The current is then transferred to the body and. if the individual is grounded. is dissipated into the ground. A side flash occurs when a tree or other tall object is struck and quickly develops a resistance higher than that of May 1985 Fic. 1. Noncontrast CT shows two deep left hematomas in the putamen and the internal capsule. There was a third, smaller hema- toma between the left caudate nucleus and the anterior limb of the internal capsule on a lower slice of the CT. the surrounding air. The current is then diverted to the air, along the path of least resistance, striking anyone in the immediate vicinity. Step voltage occurs when lightning strikes the ground and a person is standing nearby. A potential difference can develop between his legs, causing a current to flow through the lower extremities and trunk. The heart and brain are usually spared with this injury, but the victims are frequently rendered transiently paraplegic. The direct stroke is associated with the most severe injuries and carries the highest mortality of the three. When lightning strikes an individual, he is usually rendered immediately unconscious for a variable amount of time (18). Cardiorespiratory arrest occurs in the vast majority of cases. The application of a large surge of direct current to the body acts as a defibrillator on the heart. causing a single systole followed by a transient period of asystole. Sinus bradycardia then develops and the normal sinus rhythm usually resumes if adequate ventilation. either spontaneous or artificial. is present. In the absence of adequate oxygenation, ventricular fibrillation may develop. The respiratory arrest is thought to be central in origin and self-limited as well. although some- times it can be quite prolonged. Periods of apnea lasting as long as 3 hours before spontaneous respirations resume have been reported (6). Because of the transient nature of the cardiorespiratory arrest. prompt and sustained artificial life support are strongly advocated. Experimentally. survival can be improved by 20% with the use of artificial respiration alone (10). The aggressive support of lightning stroke victims who appear “dead” has significantly improved the mortality of these accidents (9. 18. 20, 23. 24). LIGHTNING STROKE 687 Depending on the site of entry and the path of the current, virtually any organ system can be injured by lightning. In addition to cardiac arrest, cardiac involvement ranging from minor EKG changes and arrhythmias to actual myocardial damage resulting in acute congestive failure can occur (3, 11. 22). At the time of lightning strike, an intense systemic vasoconstriction occurs (2, 7). As a result, many patients present with cyanotic, pulseless extremities, complaining of paraesthesias or anesthesia of the involved extremity. In the great majority of cases, this vasoconstriction resolves, but close observation is important as these extremities sometimes progress to develop gangrene, which occasionally requires amputation. Burns associated with lightning injuries can be quite severe and thus carry many of the same management problems as severe burns of different causes. Other injuries reported to be related to lightning injury include cataracts, retinal damage, isolated cochlear nerve involvement, rupture of the tympanic membrane, and muscular damage resulting in myoglobinuria, which may secondarily cause renal damage (17, 23). Involvement of the central nervous system with lightning injuries is common. One review of the literature found that unconsciousness occurred in 75% of the victims This period of unresponsiveness is usually transient, the only resid- ual neurological deficit commonly being a retrograde amnesia (5, 18). Transient paralysis, much more common in the lower than the upper extremities, frequently occurs and is probably related to the electrical current flow through the spinal cord. Only rarely do these deficits persist. The syndrome of inap- propriate antidiuretic hormone secretion, seizures, and cere- bellar ataxia have all been reported after lightning injury, as has death from diffuse cerebral edema, but it is difficult to sort out the direct effects of lightning vs. secondary effects from anoxic injury (9, 12. 13. 16). There have been three reports of intracranial hematoma associated with lightning. In the first, a subdural hematoma was found in a motorcyclist struck while riding (22). In the second, an epidural hematoma developed in a patient found unconscious on a cement floor—he also had sustained a skull fracture (15). Both of these patients had evidence of a second- ary traumatic cause for their intracranial hemorrhages. The third report, by Mann et al., involved a 20-year-old man struck in the head by lightning while fishing (14). He was rendered immediately unconscious. Examination revealed a left hemotympanum and a right hemiparesis. Routine skull films were interpreted as normal. Computed tomography (CT) demonstrated several deep intracerebral hemorrhages as well as subarachnoid and intraventricular blood. Although some early reports of persistent hemiparesis in the pre-CT era could have involved intracranial bleeding, our case and the third case described above seem to be the first two reports of a documented intracerebral hematoma without evidence of a traumatic cause other than the lightning strike. A variety of neuropathological changes have been described with lightning injury. The most consistent findings include petechial hemorrhages and subarachnoid blood, fissuring and splitting apart of the cortical layers, and a dilatation of the subarachnoid space surrounding blood vessels (1, 21). Expla- nations for these findings have been the subject of much speculation over the last 50 years. Four theories as to their pathogenesis are generally entertained (19). The first incrim- inates the heating effect of lightning stroke. Extremely high temperatures can be present when lightning strikes. Cerebro- spinal fluid temperatures as high as 145°F have been recorded 4 to 5 hours after legal electrocution (19). Gas bubbles, from heating of the cerebrospinal fluid, are said to play a role in the pathogenesis of the characteristic dilatation of the sub- 688 STANLEY AND SUSS arachnoid spaces. The second theory suggests that the direct electrolytic effect of a current passing through tissue is respon- sible for the lesions. Third, the direct mechanical effect of a strong current striking the head is thought by some to con- tribute to the majority of the abnormalities found. Finally. electrostatic forces between molecules that have obtained like charges from the negatively charged lightning current have been suggested to be responsible for the pathological changes. The patient described in this report sustained intracerebral hematomas in three separate areas of the basal ganglia on one side. His CT findings are remarkably similar to those de- scribed in the report by Mann et al. Although both thermal and direct mechanical effects are plausible explanations for these findings, another explanation might involve the acute vasomotor changes that occur with lightning injury. The intense vasoconstriction has been described. There have been many reports of an acute rise in the systemic blood pressure, although this is not a consistent finding (10, 12, 23, 24). The CT findings are consistent with hypertensive hemorrhage, and certainly an acute rise in systolic blood pressure could have caused these patients’ lesions. Lightning strike is a very complex and poorly understood form of trauma. When evaluating a patient struck by light- ning, one must be aware of the pathophysiology involved and of the variety of injuries that can occur. In addition to the immediate direct effects commonly associated with lightning injury, secondary lesions such as fractures associated with falls, renal damage secondary to myoglobinuria, and gangrene arising from the intense vasoconstriction have all been well documented. Intracerebral hematoma demonstrates yet another impor- tant and perhaps not uncommon form of secondary injury that should not be overlooked in the evaluation and manage- ment of these patients, Although most reports in the literature remark on the transient nature of the neurological findings associated with lightning injury, it is emphasized that actual intracranial damage can occur and that further evaluation is often indicated, CT findings, as demonstrated by this patient, may have an important bearing on patient management. ACKNOWLEDGMENTS The authors thank Doctor Duke Samson for his encourage- ment and advice and Ms, Jolene Jackson and Ms. Vicki Rankin for their secretarial assistance. Received for publication, November 7, 1984; accepted, December 7, 1984, Reprint requests: Lowell D. Stanley, M.D., Department of Surgery, Division of Neurosurgery, The University of Texas Health Science Center at Dallas. 5323 Harry Hines Boulevard, Dallas, Texas 75235. REFERENCES 1. 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JAMA 238:1045-1046, 1977. 17, Noel LP, Clarke WN, Addison D: Ocular complications of lightning. J Pediatr Ophthamol Strabismus 17:245-246, 1981. 18. Peters WJ: Lightning injury. Can Med Assoc J 128:148-150, 1983. 19. Pritchard AB: Changes in the central nervous system due to electrocution. Lancet 1:1163-1167, 1934, 20. Ravitch MM, Lane R, Safar P, Steichen FM, Knowles P: Light- ning stroke. N Engl J Med 264:36-38, 1961. 21. Silversides J: Neurological sequelae of electrical injury. Can Med Assoc J 91:195-204, 1964. 22. Strasser EJ, Davis RM, Menchey MJ: Lightning injuries. J Trauma 17:316-319, 1977. 23. Taussig HB: “Death” from lightning—and the possibility of living again. Ann Intern Med 68:1345-1353, 1968. 24, Tribble CG, Persing JA, Morgan RF, Kenney JG, Edlich RF: Lightning injury. Curr Concepts Trauma Care 7:5-10, 1984. COMMENT The authors present an interesting vignette of an uncom- mon neurological disease and thoughtfully review the perti- nent literature. The precise mechanism of the multiple he- matomas is, as stated, uncertain. I am skeptical about the role of acute vasoconstriction in causing hypertension-induced bleeding. It is my anecdotal impression, weakly supported by the literature (1), that intracerebral hematomas resulting from acute hypertension (e.g., eclampsia, amphetamine use) are not limited in location to those areas that are classically involved in chronic hypertension. Acute hypertension-related hemorrhage seems to involve more frequently the cortex, especially the insular cortex, and to result in lobar hematomas. Thus, the location of the hematomas in this patient, scattered in the basal ganglia, may not offer strong support for the pathogenetic hypothesis of the authors. Robert G. Hart, M.D. San Antonio, Texas 1. Harrington H, Heller HA, Dawson D, Caplan L, Rumbaugh C: Intracerebral hemorrhage and oral amphetamine. Arch Neurol 40:503-507, 1983.