Loss of Consciousness As An Indication For The Need To Transport Following Head Impact in Athletics

by Michael Cendoma, MS, ATC, ACLS
Program Director
Sports Medicine Concepts, Inc
email correspondence mjc@SportsMedicineConcepts.com

    Understanding the neurometabolic injury cascade of concussion is essential to proper concussion management throughout the entire continuum of care.  During the initial stage of acute care of athletes suffering head impact the medical team’s primary objective is to determine the extent of injury and the need for transport to an appropriate medical receiving facility.  While many state concussion guidelines suggest loss of consciousness (LOC) is an immediate indication for transport, many practicing experts do not feel that LOC is, in and of itself, indicative of the need to transport (1).  This brief will use the neurometabolic injury cascade of concussion to describe three potential consequences of head trauma in athletics that can result in LOC.  This brief will also provide a general clinical criteria for the indication for transport secondary to LOC related to head impact in athletics.
    LOC is a clinical sign accounted for by all of the major sport concussion grading systems that became prevalent beginning in the mid-1980s (2).  Concussion grading systems were beneficial in helping medical professionals come to understand the importance of proper sports concussion management, but have since been replaced by a more individualized approach to care and management.  However, reflecting on the seminal grading scale offered by Dr. Cantu in 1986 may help explain why some medical experts do not feel brief LOC is indicative of an immediate need to transport an athlete having suffered a head impact.
    Historically, Dr. Cantu has suggested that amnesia is a more significant indicator of extent of injury than brief LOC (< 1 min) (3).  This argument may be supported by the concept of spreading depression described within the confines of the neurometabolic injury cascade of concussion.  Accordingly, there is an immediate dramatic rise in cellular potassium following head impact which results in rapid depolarization of brain cells across the cerebral cortex.  Athletes exposed to head impact may experience brief LOC during the interval between rapid cellular depolarization and repolarization that is not associated with histological damage or long term consequences (4).  On average cellular potassium concentrations take up to 8 min to return to baseline, but Dr. Cantu’s grading scale defines brief LOC as that lasting less than 1 min.  Therefore, in the absence of any other sequelae, some may be comfortable attributing LOC lasting less than 1 min to spreading depression that is not necessarily indicative of the need for immediate transport of the injured athlete.  Though immediate transport may not be indicated with brief LOC alone, immediate removal from further participation is because the brain remains in a neurometabolic state that leaves it vulnerable to further injury.
    Unfortunately, spreading depression is not the only neurometabolic consequence of head impact that can result in brief LOC.  Second Impact Syndrome (SIS) or vascular congestion syndrome is believed to be attributable to a second exposure to head trauma when the brain is in a neurometabolically vulnerable state characterized by ionic flux, acute metabolic energy crisis, and cerebral blood flow alterations.  The resulting second impact results in rapid edema and a catastrophic rise in intra-cranial pressure. SIS has been associated with a lucid interval without unconsciousness, or a brief LOC followed by a lucid interval (5,6,7).  This may be why many experts and state concussion guidelines call for immediate transport following any LOC.  However, signs and symptoms of SIS, including sudden collapse, dilating pupils, abnormal or non-existent eye movements, and respiratory failure present within a matter of seconds to minutes.  Therefore, multiple signs and symptoms associated with catastrophic neurological injury will quickly overshadow LOC as a single factor determining the need for immediate transport.
    According to the National Center for Catastrophic Sports Injury, acute subdural hemorrhage is a more common cause of death due to head injuries in sports than is SIS (8).  Athletes suffering acute subdural hemorrhage may suffer LOC and become comatose immediately, resulting in an obvious need for transport.  However, symptoms of headache, confusion, behavior change, nausea and vomiting, lethargy, weakness, apathy, and seizures following LOC may present sometime after the athlete suffers brief LOC for which they were not immediately transported.  Signs and symptoms of subdural hemorrhage may present over minutes, hours, or days in a slow-growing subdural hemorrhage. Therefore, athletes who are not transported immediately following brief LOC must be observed for signs and symptoms of hemorrhage and associated rising intra-cranial pressure over time to ensure slower onset signs and symptoms indicating the need to transport are readily identified.
    In cases involving athletes suffering LOC that is either greater than 1 min or less than 1 min with concurrent signs and symptoms of SIS, vascular congestion syndrome, or acute subdural hemorrhage, timely life-saving medical care requires immediate advanced life support (ALS) EMS transport to a regional Level 1 trauma center.  Due to the rapid clinical deterioration associated with these conditions, the need for ALS transport will likely be clear within moments. Immediate ALS transport also seems warranted for athletes with a known recent history of concussion who suffer any LOC, regardless of any other sequelae, simply because it is better to be safe than sorry when there is at least some chance the athlete may still be in a neurometabolic state that leaves them vulnerable to SIS or vascular congestive syndrome even though they may have successfully completed concussion return to play criteria.
    Athletes who suffer brief LOC (< 1 min) and who do not present with a clear indication for the need to transport within moments of injury should be assumed to be in a neurometabolically vulnerable state and removed from further participation.  Additionally, these athletes should be assumed to be at risk of hematoma or edema until otherwise ruled out. Generally, more gradual onset of a subdural hemorrhage provides opportunity for the medical team to observe clinical presentations in time to take life-saving action.  Therefore, once removed from participation the medical staff should conduct serial vital sign measures and monitor the athlete for signs and symptoms indicative of a more gradual subdural hemorrhage using a clinical assessment battery such as Sports Medicine Concepts’ Enhanced Vital Signs Trending Sideline Assessment Report.

 Figure 1.  When to transport suggestions

  • LOC > 1min
  • LOC < 1min with other neurological sequelae
  • LOC < 1min with recent history of concussion
  • Signs and symptoms of SIS
  • Abnormal vital signs trending
  • Apprehension regarding athlete’s condition
    This brief provided clinical criteria for LOC as an indication for the need to transport athletes who suffer head impact.  The clinical criteria is based on the neurometabolic injury cascade of concussion as it relates to spreading depression, Second Impact Syndrome, and subdural hemorrhage.  Knowledge of the neurometabolic injury cascade of concussion can help medical professionals make better decisions regarding LOC as an indication for transport and overall head injury management throughout the entire continuum of care.

References
  1. Cendoma, MJ.  Observations of expert opinion regarding the need to transport following loss of consciousness following head impact in athletics during sports emergency care simulation training. 2018.
  2. Cantu RC. Posttraumatic retrograde and anterograde amnesia: pathophysiology and implications in grading and safe return to play. J Athl Train. 2001;36(3):244-248.
  3. Cantu RC. Guidelines for return to contact sports after a cerebral concussion. Physician Sportsmed. 1986;14(10):75-83.
  4. Giza CC, Hovda DA.  The neurometabolic cascade of concussion. J Athl Train. 2001;36(3):228-235.
  5. Bailes JE, Cantu RC. Head injury in athletes. Neurosurgery. 2001;48(1):26-45.
  6. Junger EC, Newell DW, Grant GA, et al. Cerebral autoregulation following minor head injury. J Neurosurg. 1997;86(3):425-432.
  7. Kelly JP, Nichols JS, Filley CM, et al. Concussion in sports. Guidelines for the prevention of catastrophic outcome. JAMA. 1991;266(20):2867-9.
  8. Mueller F.O. Cantu R.C. Chapel Hill; NC: 2009. National Center for Catastrophic Sports Injury Research 27th Annual Report. Fall 1982 to Spring 2009.

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