Second Impact Syndrome

Etiology

There have been very few confirmed cases of SIS to date; therefore, the exact incidence, risk, and pathophysiology of the condition are unknown. According to the Centers for Disease Control and Prevention, an estimated 1.6 to 3.8 million sports-related concussions occur in the United States each year.[2]While the etiology of a concussion is generally understood, the etiology of a second impact syndrome is not well understood. The generally accepted cause relates to sustaining a second concussion before the brain has a chance to recover from the initial insult fully. The athlete will rapidly develop altered mental status and a loss of consciousness within seconds to minutes of the second hit, resulting in catastrophic neurological injury.[3] The devastating injury results from the dysfunctional cerebral blood flow autoregulation, leading to an increase in intracranial pressure. The pressure rapidly develops and eventually results in brain herniation. The herniation may occur either medially across the falx cerebri or inferiorly through the foramen magnum, resulting in brain stem injury and rapid deterioration and leading to death within 2 to 5 minutes. A recent case report sheds some light on the injury pattern[4]. An athlete returned to hitting drills five days after his initial concussion. He had a routine CT scan on day four but had a persistent severe headache. After getting hit at practice one day later, he collapsed several plays later after complaining of headaches and not being able to feel his legs. A second CT done in a local emergency room demonstrated bilateral but thin subdural hematomas. However, a subsequent MRI demonstrated caudal displacement of midline structures with injury to both thalami resulting in transtentorial herniation.[4]

Epidemiology

A review article in 2016 completed a PubMed search and found only 36 cases reported in 15 publications, with 17 cases meeting the inclusion criteria.[3] The characteristics of an athlete susceptible to a second impact injury were male gender, aged 13 to 24 years, and contact sports like American football, boxing, and hockey. Only 7 of the 17 received a direct blow to the head; the others were thought to have received a blow to the body and the forces transmitted to the head. Computed tomography (CT) demonstrated diffuse cerebral edema with midline shift leading to herniation in 4 of the cases. Additionally, all of the cases had either thin or moderate subdural hematomas, 2 of the cases had a subarachnoid hemorrhage, and 3 suffered an ischemic stroke.

Pathophysiology

Patients who have experienced a concussion show a poorly understood but complex array of neuronal, metabolic, and ionic changes. The mechanism of injury seems to be associated with axonal shearing. This causes rapid depolarization, neurotransmitter release, and ionic shifts where potassium ions leak extracellularly and are replaced with sodium and calcium intracellularly. This results in dysregulation of the cerebral blood flow leading to edema. Thus increased glucose utilization combined with the injury-related decrease in resting cerebral blood flow creates an energy mismatch. [5] All these changes require time and energy for a return to normal neurotransmitter physiology. Generally, this is thought to take about 7 to 10 days but may be longer in younger athletes. Metabolic abnormalities after an initial concussion may leave the brain more susceptible to further injury. [6]

History and Physical

Any athlete who has returned to play after a concussion should be watched carefully, even if they have had an appropriate recovery period and completed a return-to-play protocol. A concussed patient will report any combination of symptoms, including a headache, nausea, memory loss, dizziness, blurry vision, confusion, fatigue, photo- or phonophobia, motor or sensory loss, poor hand-eye coordination, or emotional irritability/lability. On physical examination, the patient may have an altered level of consciousness, retrograde, or post-traumatic amnesia, but generally, difficulty concentrating and balance seem to be consistently impaired. Additionally, there may be sensory or motor abnormalities or visual abnormalities. Unless the player has been knocked out, if they remain on the field of play, they may show signs of ataxia, running in the wrong direction, or slowed reaction time.

As concussions have been more widely recognized and the complications related to insufficient recovery have become better recognized, sideline evaluations have developed. Sideline evaluation of cognitive function is an essential component in assessing this injury. Brief neuropsychological (NP) test batteries that assess attention and memory function are practical and effective. Such tests include the SCAT5, which incorporates the Maddocks' questions, and the Standardised Assessment of Concussion (SAC).[7]

For an athlete who has collapsed with a suspected SIS, a Glasgow coma scale score, pupillary reactivity, deep tendon reflexes, upper/lower extremity clonus, and the presence or absence of a Babinski reflex can be done before transport or upon arrival at the emergency room.  

Due to the challenges of what constitutes a second impact syndrome, the lack of research, and the rapidly progressing nature of the condition, it is challenging to provide sound guidance on an appropriate history and physical exam. Perhaps clinicians should change their mindset and think every concussion they see, especially in male athletes aged 13 to 24, could be a second impact syndrome and observe the injured athlete closely for progressing signs or symptoms.  

Evaluation

Obtaining a thorough history is critical in evaluating a patient with a suspected brain injury. Though the patient will unlikely be able to provide a good history, one should gather as much information from those who may have witnessed the incident. It is essential to determine how the injury occurred, if there is any seizure or concussion history, if alcohol or illicit drug use was involved, whether or not there was any loss of consciousness, any resultant weakness or paresthesias, difficulty walking, or incontinence of the bladder or bowel.

Patients who have experienced significant injury or loss of consciousness, continued symptoms, deterioration in neurologic function, or neurologic deficits should be evaluated with imaging studies. Screening for alcohol or illicit drugs would be recommended. CT is the preferred imaging modality for acute head trauma. It is a more sensitive imaging modality for detecting acute hemorrhage than a nonenhanced CT, provides better delineation of bone, and is more sensitive in detecting acute hemorrhage and identifying any surgically reversible injuries. 

Current guidelines recommend a CT for a suspected skull fracture, intracranial bleeding, or other intracranial disorders based on physical exam findings.[8] Since second impact syndrome injuries generally cause loss of consciousness, it would seem prudent to start with a CT scan of the head. 

Treatment / Management

The management of second impact syndrome is limited due to the limited understanding of the condition, the lack of research, and the controversial nature of the condition. The management of SIS starts with prompt recognition of a sports-related concussion and protecting the athlete until they recover from the initial injury. The current treatment guidelines consist of relative rest, both cognitive and physical, and then a graded return to play. This should be supervised ideally by a team physician with experience in managing concussions and athletic training staff. The athlete should not be cleared to return to full participation until they have completed a return-to-play protocol and the medical staff gives clearance.[5]

Differential Diagnosis

The differential diagnosis of second impact syndrome includes:

• Subarachnoid bleed
• Ischemic stroke
• Subdural hematoma
• Basal skull fracture
• Skull fracture.