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SECOND-IMPACT SYNDROME
NEUROLOGIC ATHLETIC HEAD AND NECK INJURIES
0278-5919/98 $8.00
+ .OO
SECOND-IMPACT SYNDROME Robert C. Cantu, MD, FACS, FACSM
If we define a direct fatality as one occurring directly from participation in the skills of a sport as opposed to an indirect fatality, which is one caused by systemic failure as a result of exertion while participating in a sport, head injury is the most frequent direct cause of death in sport.16 Furthermore, injury to the head takes on a singular importance when we realize the brain is neither capable of regeneration nor, unlike many other body parts and organs, of transplantation. Every effort must be made to protect the athlete's head as injury can lead to dementia, epilepsy, paralysis, and death. Over the last 20 years there has been a dramatic decrease in the most serious head injuries-especially the incidence of subdural hematoma-due to multiple factors including rule changes, such as outlawing spear tackling and butt blocking in American football, equipment standards, better conditioning of the neck, and improved on-field medical care. During this same time period, and especially within the last 5 years, there has been a dramatic increase in the literature citations of the second-impact syndrome (SIS) with 17 of 24 citations coming between 1992 and the present. We have no reason, however, to assume the incidence of SIS has increased as the number of cases seen annually in football has remained at one or two. Rather, we believe this condition is better recognized and reported by sports medicine professionals today. Recognition of a head injury is easy if the athlete has lost consciousness. It is much more difficult to recognize the far more frequent head injuries in which there is no loss of consciousness but rather only a transient loss of alertness. More than 90% of all cerebral concussions fall into this most mild category where there has not been a loss of conFrom the Neurosurgery Service and the Service of Sports Medicine, Emerson Hospital, Concord, Massachusetts
CLINICS IN SPORTS MEDICINE VOLUME 17 * NUMBER 1 *JANUARY 1998
37
38
CANTU
sciousness but rather only a brief period of post-traumatic amnesia or loss of mental alertne~s.~, Because the dreaded SIS can occur after a grade 1 concussion, just as it can after more serious head injuries, it becomes very important to recognize all grades of conc~ssion.~~
WHAT IS THE SECOND-IMPACT SYNDROME?
What Saunders and Harbaughls called “the second-impact syndrome of catastrophic head injury” in 1984 was described by Schneider in 1973.19The syndrome occurs when an athlete who sustains a head injury-often a concussion or worse injury, such as a cerebral contusionsustains a second head injury before symptoms associated with the first have lear red.^, 6, l4 Typically, the athlete suffers postconcussion symptoms after the first head injury. These may include headache, labyrinthine dysfunction, visual, motor, or sensory changes or mental difficulty, especially the thought and memory process. Before these symptoms resolve, which may take days or weeks, the athlete returns to competition and receives a second blow to the head. The second blow may be remarkably minor, perhaps only involving a blow to the chest that jerks the athlete’s head and indirectly imparts accelerative forces to the brain. Affected athletes may appear stunned but usually do not lose consciousness and often complete the play. They usually remain on their feet for 15 seconds to 1 minute or so but seem dazed, like someone suffering from a grade 1 concussion without the loss of consciousness. Often, affected athletes remain on the playing field or walk off under their own power. What happens in the next 15 seconds to several minutes sets this syndrome apart from a concussion or even a subdural hematoma. Usually within seconds to minutes of the second impact, the athleteconscious yet stunned-quite precipitously collapses to the ground, semicomatose with rapidly dilating pupils, loss of eye movement, and evidence of respiratory failure. The following five case histories taken from boxing illustrate the SIS. Case 1
A 17-year-old Golden Gloves boxer fought a difficult semifinal bout in a regional tournament. During the 2-day rest period before the final bout, he complained of a severe headache; his mother stated he had literally “eaten” two bottles of aspirin. On the morning of the final bout, he was in an automobile accident and struck his head forcefully. He felt nauseated on the way to the finals bout that evening, and his coach twice tried to pull the car over to the side of the road so the boxer could vomit. During the precompetition examination, the physician asked if there were any problems: The boy and his coach answered “none.” After an uneventful first round and minor head blows during
SECOND-IMPACT SYNDROME
39
the second round, the boxer collapsed in the ring. Shortly thereafter he became decerebrate with fixed dilated pupils. He was intubated and taken to the hospital where, after he received intravenous mannitol and dexamethasone, his condition remained unchanged. Emergency CT scan showed massive brain swelling and a small left frontal subdural hematoma. After conferring with his parents, surgeons performed an emergency craniotomy. After removing the subdural hematoma, surgeons observed massive brain herniation out of the craniotomy defect and performed a decompressive craniectomy. Despite intensive treatment, the boxer's condition did not improve. Two postcraniotomy electroencephalograms were flat, and the patient died of cardiac arrest 1 week after surgery. Case 2
A 19-year-old boxer with the US Marine Corps won the first bout of a camp tournament. He was knocked down in the bout and the next day complained of a headache. The following day he was allowed to box after a limited precompetition examination in which he reported a "slight headache." In the second round, he collapsed after receiving minor blows, experienced a seizure, and became decerebrate with fixed, dilated pupils. At the hospital, an emergency CT scan revealed a small right subdural hematoma and massive brain swelling. The clot was removed surgically, and the swollen brain was observed to herniate from the skull opening. Despite hyperventilation, decompressive craniectomy, and intravenous mannitol, the postsurgical intracranial pressure was impossible to control, and the patient died 6 days later. Case 3
A 17-year-old amateur boxer fought poorly in his first bout in an international tournament. He received several standing 8-counts after being stunned by head blows. Afterward, he was obsessed with boxing again and (in retrospect) exhibited inappropriate obsessive behavior. Six hours later after another boxer's bout was canceled, he boxed again, encouraged by his coach. He again performed poorly, taking several severe hits that included two standing 8-counts, and the referee stopped the bout in the second round. A few minutes later, while the referee was announcing the winner and holding the contestants' hands, the injured boxer collapsed in the center of the ring. He immediately lapsed into a coma with fixed, dilated pupils. Despite medical treatment that included decompression craniotomy, he died the next day. The autopsy showed severe cerebral edema with bilateral uncal herniation. Case 4
A 21-year-old college student prepared for a weekend fraternity smoker-an unofficial boxing match between two inexperienced boxers in which few rules were followed. He trained with an experienced boxer who inflicted head blows and other hits that were of considerable force. Afterward, the college student developed a headache and saw a physician at the student health center. He downplayed the severity of the pain and failed to keep a follow-up appointment.
40
CANTU
Two days later he sparred again in a training session without coaching or corner supervision.After 2 minutes of a light workout, he collapsed in the ring, lapsed into a coma with fixed, dilated pupils, became apenic, and died before medical attention could be obtained. Case 5
A 24-year-old novice boxer fought an extremely hard bout with a ranked boxer and received many forceful blows. During three rounds, he received four standing 8-counts-the fourth terminated the fight. He left the ring unassisted and returned to the dressing room. Within minutes he collapsed into a deep coma. He was taken to the hospital, but despite intensive medical treatment with a ventilator, mannitol, and corticosteroids, he died shortly thereafter. Autopsy revealed massively increased intracranial pressure from edema and vascular congestion and herniation that caused midbrain necrosis. No subdural hematoma was present.
What do these cases have in common? First, five patients had had a concussion with residual cerebral symptoms. In case 5, the patient sustained multiple grade 1 concussive blows in the same bout. Second, all apparently lapsed into a coma with brainstem collapse from brain herniation secondary to massively increased intracranial pressure. The fatal lesion confirmed at surgery or autopsy was massive edema. Though subdural hematomas were present in half of the cases, they were small and of no clinical consequence. These extraordinary brain changes occurred with what appeared to be relatively minor head trauma and were refractory to medical treatment. In short, the findings of the six case studies are consistent with SIS.
PATHOPHYSIOLOGY OF SECOND-IMPACT SYNDROME The pathophysiology of SIS is thought to involve a loss of autoregulation of the brain's blood supply. This loss of autoregulation leads to vascular engorgement within the cranium, which, in turn, markedly increases intracranial pressure and leads to herniation either of the medical surface (uncus) of the temporal lobe or lobes below the tentorium of the cerebellar tonsils through the foramen magnum (Fig. 1). Animal research has shown that vascular engorgement of the brain after a mild head injury is difficult, if not impossible, to control.", l5 The usual time from second impact to brainstem failure is rapid, taking 2 to 5 minutes. Once brain herniation and brainstem compromise occur, ocular involvement and respiratory failure precipitously ensue. Demise occurs far more rapidly than usually seen with an epidural hematoma. MR imaging and CT scan are the neuroimaging studies most likely to demonstrate the SIS. Although MR imaging is the more sensitive to traumatic brain injuries, especially true edema? the CT scan is usually adequate to show bleeding or midline shifts of the brain requiring neurosurgical
SECOND-IMPACT SYNDROME
cerebelli
A
B
Brain stem
\
41
lobe
stem
Figure 1. In second-impact syndrome, vascular engorgement within the cranium increases intracranial pressure, leading to herniation of the uncus of the temporal lobe (arrows) below the tentorium in this frontal section (A), or to herniation of the cerebellar tonsils (arrows) through the foramen magnum in this midsagittal section (B).These changes compromise the brainstem, and coma and respiratory failure rapidly develop. The shaded areas of the brainstem represent the areas of compression.
42
CANTU
intervention. This is important because CT scanning is cheaper, more widely available, and more quickly performed than MR imaging. INCIDENCE
Although the precise incidence per 100,000 participants is not known because the precise population at risk is unknown, the SIS is more common than previous reports have suggested. Between 1980 and 1993, the National Center for Catastrophic Sports Injury Research in Chapel Hill, NC, identified 35 probable cases among American football players alone. Necropsy or surgery and MR imaging findings confirmed 17 of these cases. An additional 18 cases, though not conclusively documented with necropsy findings, most probably are cases of second impact syndrome. Careful scrutiny excluded this diagnosis in 22 of 57 cases originally suspected" SIS is not confined to American football players. Head injury reports of athletes in other sports almost certainly represent the syndrome but do not label it as such. Fekete,7 for example, described a 16-year-old high school hockey player who fell during a game, striking the back of his head on the ice. The boy lost consciousness and afterward complained of unsteadiness and headaches. While playing in the next game 4 days later, he was checked forcibly and again fell striking his left temple on the ice. His pupils rapidly became fixed and dilated, and he died within 2 hours while in transit to a neurosurgical facility. Necropsy revealed contusions of several days' duration, an edematous brain with a thin layer of subdural and subarachnoid hemorrhage, and bilateral herniation of the cerebellar tonsils into the foramen magnum. Though Fekete did not use the label "second-impact syndrome," the clinical course and necropsy findings in this case are consistent with the SIS. Other cases include an 18-year-old male downhill skier described by McQuillen and ass~ciates,'~ who remains in a persistent vegetative state, and a 17-year-old football player described by Kelly and coworkers.'O who died. Such cases indicate that the brain is vulnerable to accelerative forces in a variety of contact and collision sports. Therefore, physicians who cover athletic events, especially those in which head trauma is likely, must understand the SIS and be prepared to initiate emergency treatment. PREVENTION OF SUDDEN-IMPACT SYNDROME
For a catastrophic condition that has a mortality rate approaching 50% and a morbidity rate nearing loo%, prevention takes on the utmost importance. An athlete who is symptomatic from a head injury must not participate in contact or collision sports until all cerebral symptoms have subsided, and preferably not for at least 1 week after. Whether it takes days, weeks, or months to reach the asymptomatic state, the athlete
SECOND-IMPACT SYNDROME
43
must never be allowed to practice or compete while still suffering postconcussion symptoms. Coaches, players, and parents as well as the physician and medical team must understand this. Files of the National Center for Catastrophic Sport Injury Research include cases of young athletes who did not report their cerebral symptoms. Fearing they would not be allowed to compete and not knowing they were jeopardizing their lives, they played with postconcussional symptoms and tragically developed SIS.
MALIGNANT BRAIN EDEMA SYNDROME
This condition is found in athletes in the pediatric age range and consists of rapid neurologic deterioration from an alert conscious state to coma and sometimes death, minutes to several hours after head trauma.17,2o Although this sequence in adults almost always is caused by an intracranial clot, in children pathology studies show diffuse brain swelling with little or no brain injury.20Rather than true cerebral edema, Langfitt and colleagues12,l3 have shown that the diffuse cerebral swelling is the result of a true hyperemia or vascular engorgement. Prompt recognition is extremely important because there is little initial brain injury, and the serious or fatal neurological outcome is secondary to raised intracranial pressure with herniation. Prompt treatment with intubation, hyperventilation, and osmotic agents has helped to reduce the mortality.’, *
CONCLUSION
As you can see from the preceding description, the malignant brain edema syndrome occur in the pediatric age group after a first head injury and thus, unlike the SIS, is not preventable. Prompt recognition and treatment is thus vital. On the other hand, the SIS is preventable. Because the consequences of this syndrome are so catastrophic and because SIS is more common than previously thought and is not confined to football players, physicians covering all collision or contact sports must be aware of the syndrome, its prevention, and its immediate treatment. In addition, educating athletes and their parents about this condition and its prevention cannot be overemphasized.
References 1. Bowers SA, Marchall L F Outcome in 200 consecutive cases of severe head injury treated in San Diego County: A prospective analysis. Neurosurgery 6:237, 1980 2. Bruce DA, Alavi A, Bilaniuk L, et al: Diffuse cerebral swelling following head injuries in children: The syndrome of “malignant brain edema.” 54:170-178, 1981
44
CANTU
3. Cantu RC: Guidelines for return to contact sports after a cerebral concussion. Physician and Sportsmedicine 14:10, 1986 4. Cantu RC: Minor head injuries in sports. In Dyment PG (ed): Adolescent Medicine: State of the Art Reviews. Philadelphia, Hanley & Belfus, 1991 5. Cantu RC: Second impact syndrome: immediate management. Physician and Sportsmedicine 2055, 1992 6. Cantu RC, Voy R: Second impact syndrome a risk in any contact sport. Physician and Sportsmedicine 2327, 1995 7. Fekete JF: Severe brain injury and death following rigid hockey accidents: The effectiveness of the ”safety helmets” of amateur hockey players. Can Med Assoc J 99:1234, 1968 8. Gentry LR, Godersky JC, Thompson B, et al: Prospective comparative study of intermediate field MR and CT in the evaluation of closed head trauma. Am J Neuroradiol 150:673, 1988 9. Jenkins A, Teasdale G, Hadley DM, et al: Brain lesions detected by magnetic resonance imaging in mild and severe head injuries. Lancet iik445, 1986 10. Kelly JP, Nichols JS, Filley CM, et al: Concussion in sports: Guidelines for the prevention of catastrophic outcome. JAMA 226:2867, 1991 11. Langfitt TW, Weinstein JD, Kassell NF: Cerebral vasomotor paralysis produced by intracranial hypertension. Neurology 15622, 1965 12. Langfitt TW, Kassell NF: Cerebral vasodilations produced by brainstem stimulation: Neurogenic control vs autoregulation. Am J Physiol 215:90, 1978 13. Langfitt TW, Tannenbaum HM, Kassell NF: The etiology of acute brain swelling following experimental head injury. J Neurosurg 24:47, 1966 14. McQuillen JB, McQuillen EN, Morrow P: Trauma, sports, and malignant cerebral edema. Am J Forensic Med Pathol 9:12, 1988 15. Moody RA, Ruamsuke S, Mullen SF: An evaluation of decompression in experimental head injury. J Neurosurg 29586, 1968 16. Mueller FO, Blyth CS: Survey of catastrophic football injuries: 1977-1983. Physician and Sportsmedicine 13:75, 1985 17. Pickles W: Acute general edema of the brain in children with head injuries. N Engl J Med 242607, 1950 18. Saunders RL, Harbaugh RE: Second impact in catastrophic contact-sports head trauma. JAMA 252538, 1984 19. Schneider RC: Head and neck injuries in football. Baltimore, Williams & Wilkins, 1973 20. Schnitker MT A syndrome of cerebral concussion in children. J Pediatr 35557, 1949
Address reprint requests to Robert C. Cantu, MD, FACS, FACSM Service of Sports Medicine Emerson Hospital Concord, MA 01742
0278-5919/98 $8.00
+ .OO
SECOND-IMPACT SYNDROME Robert C. Cantu, MD, FACS, FACSM
If we define a direct fatality as one occurring directly from participation in the skills of a sport as opposed to an indirect fatality, which is one caused by systemic failure as a result of exertion while participating in a sport, head injury is the most frequent direct cause of death in sport.16 Furthermore, injury to the head takes on a singular importance when we realize the brain is neither capable of regeneration nor, unlike many other body parts and organs, of transplantation. Every effort must be made to protect the athlete's head as injury can lead to dementia, epilepsy, paralysis, and death. Over the last 20 years there has been a dramatic decrease in the most serious head injuries-especially the incidence of subdural hematoma-due to multiple factors including rule changes, such as outlawing spear tackling and butt blocking in American football, equipment standards, better conditioning of the neck, and improved on-field medical care. During this same time period, and especially within the last 5 years, there has been a dramatic increase in the literature citations of the second-impact syndrome (SIS) with 17 of 24 citations coming between 1992 and the present. We have no reason, however, to assume the incidence of SIS has increased as the number of cases seen annually in football has remained at one or two. Rather, we believe this condition is better recognized and reported by sports medicine professionals today. Recognition of a head injury is easy if the athlete has lost consciousness. It is much more difficult to recognize the far more frequent head injuries in which there is no loss of consciousness but rather only a transient loss of alertness. More than 90% of all cerebral concussions fall into this most mild category where there has not been a loss of conFrom the Neurosurgery Service and the Service of Sports Medicine, Emerson Hospital, Concord, Massachusetts
CLINICS IN SPORTS MEDICINE VOLUME 17 * NUMBER 1 *JANUARY 1998
37
38
CANTU
sciousness but rather only a brief period of post-traumatic amnesia or loss of mental alertne~s.~, Because the dreaded SIS can occur after a grade 1 concussion, just as it can after more serious head injuries, it becomes very important to recognize all grades of conc~ssion.~~
WHAT IS THE SECOND-IMPACT SYNDROME?
What Saunders and Harbaughls called “the second-impact syndrome of catastrophic head injury” in 1984 was described by Schneider in 1973.19The syndrome occurs when an athlete who sustains a head injury-often a concussion or worse injury, such as a cerebral contusionsustains a second head injury before symptoms associated with the first have lear red.^, 6, l4 Typically, the athlete suffers postconcussion symptoms after the first head injury. These may include headache, labyrinthine dysfunction, visual, motor, or sensory changes or mental difficulty, especially the thought and memory process. Before these symptoms resolve, which may take days or weeks, the athlete returns to competition and receives a second blow to the head. The second blow may be remarkably minor, perhaps only involving a blow to the chest that jerks the athlete’s head and indirectly imparts accelerative forces to the brain. Affected athletes may appear stunned but usually do not lose consciousness and often complete the play. They usually remain on their feet for 15 seconds to 1 minute or so but seem dazed, like someone suffering from a grade 1 concussion without the loss of consciousness. Often, affected athletes remain on the playing field or walk off under their own power. What happens in the next 15 seconds to several minutes sets this syndrome apart from a concussion or even a subdural hematoma. Usually within seconds to minutes of the second impact, the athleteconscious yet stunned-quite precipitously collapses to the ground, semicomatose with rapidly dilating pupils, loss of eye movement, and evidence of respiratory failure. The following five case histories taken from boxing illustrate the SIS. Case 1
A 17-year-old Golden Gloves boxer fought a difficult semifinal bout in a regional tournament. During the 2-day rest period before the final bout, he complained of a severe headache; his mother stated he had literally “eaten” two bottles of aspirin. On the morning of the final bout, he was in an automobile accident and struck his head forcefully. He felt nauseated on the way to the finals bout that evening, and his coach twice tried to pull the car over to the side of the road so the boxer could vomit. During the precompetition examination, the physician asked if there were any problems: The boy and his coach answered “none.” After an uneventful first round and minor head blows during
SECOND-IMPACT SYNDROME
39
the second round, the boxer collapsed in the ring. Shortly thereafter he became decerebrate with fixed dilated pupils. He was intubated and taken to the hospital where, after he received intravenous mannitol and dexamethasone, his condition remained unchanged. Emergency CT scan showed massive brain swelling and a small left frontal subdural hematoma. After conferring with his parents, surgeons performed an emergency craniotomy. After removing the subdural hematoma, surgeons observed massive brain herniation out of the craniotomy defect and performed a decompressive craniectomy. Despite intensive treatment, the boxer's condition did not improve. Two postcraniotomy electroencephalograms were flat, and the patient died of cardiac arrest 1 week after surgery. Case 2
A 19-year-old boxer with the US Marine Corps won the first bout of a camp tournament. He was knocked down in the bout and the next day complained of a headache. The following day he was allowed to box after a limited precompetition examination in which he reported a "slight headache." In the second round, he collapsed after receiving minor blows, experienced a seizure, and became decerebrate with fixed, dilated pupils. At the hospital, an emergency CT scan revealed a small right subdural hematoma and massive brain swelling. The clot was removed surgically, and the swollen brain was observed to herniate from the skull opening. Despite hyperventilation, decompressive craniectomy, and intravenous mannitol, the postsurgical intracranial pressure was impossible to control, and the patient died 6 days later. Case 3
A 17-year-old amateur boxer fought poorly in his first bout in an international tournament. He received several standing 8-counts after being stunned by head blows. Afterward, he was obsessed with boxing again and (in retrospect) exhibited inappropriate obsessive behavior. Six hours later after another boxer's bout was canceled, he boxed again, encouraged by his coach. He again performed poorly, taking several severe hits that included two standing 8-counts, and the referee stopped the bout in the second round. A few minutes later, while the referee was announcing the winner and holding the contestants' hands, the injured boxer collapsed in the center of the ring. He immediately lapsed into a coma with fixed, dilated pupils. Despite medical treatment that included decompression craniotomy, he died the next day. The autopsy showed severe cerebral edema with bilateral uncal herniation. Case 4
A 21-year-old college student prepared for a weekend fraternity smoker-an unofficial boxing match between two inexperienced boxers in which few rules were followed. He trained with an experienced boxer who inflicted head blows and other hits that were of considerable force. Afterward, the college student developed a headache and saw a physician at the student health center. He downplayed the severity of the pain and failed to keep a follow-up appointment.
40
CANTU
Two days later he sparred again in a training session without coaching or corner supervision.After 2 minutes of a light workout, he collapsed in the ring, lapsed into a coma with fixed, dilated pupils, became apenic, and died before medical attention could be obtained. Case 5
A 24-year-old novice boxer fought an extremely hard bout with a ranked boxer and received many forceful blows. During three rounds, he received four standing 8-counts-the fourth terminated the fight. He left the ring unassisted and returned to the dressing room. Within minutes he collapsed into a deep coma. He was taken to the hospital, but despite intensive medical treatment with a ventilator, mannitol, and corticosteroids, he died shortly thereafter. Autopsy revealed massively increased intracranial pressure from edema and vascular congestion and herniation that caused midbrain necrosis. No subdural hematoma was present.
What do these cases have in common? First, five patients had had a concussion with residual cerebral symptoms. In case 5, the patient sustained multiple grade 1 concussive blows in the same bout. Second, all apparently lapsed into a coma with brainstem collapse from brain herniation secondary to massively increased intracranial pressure. The fatal lesion confirmed at surgery or autopsy was massive edema. Though subdural hematomas were present in half of the cases, they were small and of no clinical consequence. These extraordinary brain changes occurred with what appeared to be relatively minor head trauma and were refractory to medical treatment. In short, the findings of the six case studies are consistent with SIS.
PATHOPHYSIOLOGY OF SECOND-IMPACT SYNDROME The pathophysiology of SIS is thought to involve a loss of autoregulation of the brain's blood supply. This loss of autoregulation leads to vascular engorgement within the cranium, which, in turn, markedly increases intracranial pressure and leads to herniation either of the medical surface (uncus) of the temporal lobe or lobes below the tentorium of the cerebellar tonsils through the foramen magnum (Fig. 1). Animal research has shown that vascular engorgement of the brain after a mild head injury is difficult, if not impossible, to control.", l5 The usual time from second impact to brainstem failure is rapid, taking 2 to 5 minutes. Once brain herniation and brainstem compromise occur, ocular involvement and respiratory failure precipitously ensue. Demise occurs far more rapidly than usually seen with an epidural hematoma. MR imaging and CT scan are the neuroimaging studies most likely to demonstrate the SIS. Although MR imaging is the more sensitive to traumatic brain injuries, especially true edema? the CT scan is usually adequate to show bleeding or midline shifts of the brain requiring neurosurgical
SECOND-IMPACT SYNDROME
cerebelli
A
B
Brain stem
\
41
lobe
stem
Figure 1. In second-impact syndrome, vascular engorgement within the cranium increases intracranial pressure, leading to herniation of the uncus of the temporal lobe (arrows) below the tentorium in this frontal section (A), or to herniation of the cerebellar tonsils (arrows) through the foramen magnum in this midsagittal section (B).These changes compromise the brainstem, and coma and respiratory failure rapidly develop. The shaded areas of the brainstem represent the areas of compression.
42
CANTU
intervention. This is important because CT scanning is cheaper, more widely available, and more quickly performed than MR imaging. INCIDENCE
Although the precise incidence per 100,000 participants is not known because the precise population at risk is unknown, the SIS is more common than previous reports have suggested. Between 1980 and 1993, the National Center for Catastrophic Sports Injury Research in Chapel Hill, NC, identified 35 probable cases among American football players alone. Necropsy or surgery and MR imaging findings confirmed 17 of these cases. An additional 18 cases, though not conclusively documented with necropsy findings, most probably are cases of second impact syndrome. Careful scrutiny excluded this diagnosis in 22 of 57 cases originally suspected" SIS is not confined to American football players. Head injury reports of athletes in other sports almost certainly represent the syndrome but do not label it as such. Fekete,7 for example, described a 16-year-old high school hockey player who fell during a game, striking the back of his head on the ice. The boy lost consciousness and afterward complained of unsteadiness and headaches. While playing in the next game 4 days later, he was checked forcibly and again fell striking his left temple on the ice. His pupils rapidly became fixed and dilated, and he died within 2 hours while in transit to a neurosurgical facility. Necropsy revealed contusions of several days' duration, an edematous brain with a thin layer of subdural and subarachnoid hemorrhage, and bilateral herniation of the cerebellar tonsils into the foramen magnum. Though Fekete did not use the label "second-impact syndrome," the clinical course and necropsy findings in this case are consistent with the SIS. Other cases include an 18-year-old male downhill skier described by McQuillen and ass~ciates,'~ who remains in a persistent vegetative state, and a 17-year-old football player described by Kelly and coworkers.'O who died. Such cases indicate that the brain is vulnerable to accelerative forces in a variety of contact and collision sports. Therefore, physicians who cover athletic events, especially those in which head trauma is likely, must understand the SIS and be prepared to initiate emergency treatment. PREVENTION OF SUDDEN-IMPACT SYNDROME
For a catastrophic condition that has a mortality rate approaching 50% and a morbidity rate nearing loo%, prevention takes on the utmost importance. An athlete who is symptomatic from a head injury must not participate in contact or collision sports until all cerebral symptoms have subsided, and preferably not for at least 1 week after. Whether it takes days, weeks, or months to reach the asymptomatic state, the athlete
SECOND-IMPACT SYNDROME
43
must never be allowed to practice or compete while still suffering postconcussion symptoms. Coaches, players, and parents as well as the physician and medical team must understand this. Files of the National Center for Catastrophic Sport Injury Research include cases of young athletes who did not report their cerebral symptoms. Fearing they would not be allowed to compete and not knowing they were jeopardizing their lives, they played with postconcussional symptoms and tragically developed SIS.
MALIGNANT BRAIN EDEMA SYNDROME
This condition is found in athletes in the pediatric age range and consists of rapid neurologic deterioration from an alert conscious state to coma and sometimes death, minutes to several hours after head trauma.17,2o Although this sequence in adults almost always is caused by an intracranial clot, in children pathology studies show diffuse brain swelling with little or no brain injury.20Rather than true cerebral edema, Langfitt and colleagues12,l3 have shown that the diffuse cerebral swelling is the result of a true hyperemia or vascular engorgement. Prompt recognition is extremely important because there is little initial brain injury, and the serious or fatal neurological outcome is secondary to raised intracranial pressure with herniation. Prompt treatment with intubation, hyperventilation, and osmotic agents has helped to reduce the mortality.’, *
CONCLUSION
As you can see from the preceding description, the malignant brain edema syndrome occur in the pediatric age group after a first head injury and thus, unlike the SIS, is not preventable. Prompt recognition and treatment is thus vital. On the other hand, the SIS is preventable. Because the consequences of this syndrome are so catastrophic and because SIS is more common than previously thought and is not confined to football players, physicians covering all collision or contact sports must be aware of the syndrome, its prevention, and its immediate treatment. In addition, educating athletes and their parents about this condition and its prevention cannot be overemphasized.
References 1. Bowers SA, Marchall L F Outcome in 200 consecutive cases of severe head injury treated in San Diego County: A prospective analysis. Neurosurgery 6:237, 1980 2. Bruce DA, Alavi A, Bilaniuk L, et al: Diffuse cerebral swelling following head injuries in children: The syndrome of “malignant brain edema.” 54:170-178, 1981
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Address reprint requests to Robert C. Cantu, MD, FACS, FACSM Service of Sports Medicine Emerson Hospital Concord, MA 01742