Second Impact Syndrome

What is Second Impact Syndrome?

When a concussion (mild traumatic injury) is not fully recovered, but sustain a second minor trauma, then autoregulation of the brain become lost. The consequences of this lead to intracranial and cerebral perfusion pressure mismanagement and clinically termed as second impact syndrome (SIS). This condition is rare, but the probability of a fatal outcome is higher.

Before we discuss much Second Impact Syndrome, a detail note of concussion helps to understand the topic better. A concussion can be defined as an abrupt and temporary loss of consciousness and leads to a short-term amnesia after receiving a direct hit to the head. Athletes mostly affected with this type of syndrome^1,2.

Predominance

Young athletes, who especially participate in sports like boxing, football, baseball, skiing and hockey. It is always advised, if any athlete has undergone a mild traumatic injury (concussion), he/she should not be back to the field before complete curing of the initial head injury¹.

Symptoms

Immediate loss of consciousness after getting a blow to the brain is the initial symptom and certain symptoms usually, arises after or within four weeks of the initial symptom. The included symptoms are:

• Headache
• Dizziness
• Fatigue
• Insomnia
• Irritability
• Alcohol intolerance
• Difficulty in concentrate
• Intellectual difficulties or temporary loss of memory without involvement of the impaired nervous system functionality

Depending upon the complexity and recovery period, a concussion can be classified into two types – simple and complex concussions. The recovery period of simple concussion is less than ten days, but complex concussions take more than ten days to recover and some additional symptoms like seizures, headache due to little mental exertion, destruction of cognition, or confusion also may arise. The duration of  concussive amnesia depends upon the extent of loss of consciousness and the head injury severity.

In the case of true SIS, the included symptoms are dilation of the pupil, eye movement cessation, unconsciousness, respiratory failure and death^2,5.

Pathophysiology

The endurance of initial concussion may inflate cerebral edema, responsible for the loss of consciousness, headache, impairment of memory and confusion. Autoregulatory mechanisms of the brain can able to balance the increased stress arise due to mechanical and physiological force and also provide protection against large inflammation . The symptoms of SIS occur due to sudden blow on the head causes limited cerebral blood flow and thus enhance lactate accumulation and intracellular acidosis.

Subsequently, this leads to alteration of the cerebral metabolism and that usually lasts for ten days. Gradually protein synthesis and oxidative capacity become decreased and the outcome is a loss of consciousness. Ionic flux, sudden alteration of metabolic reaction and cerebral blood flow develop immediately after onset of an initial concussion. There is an enhanced potassium concentration in the extracellular brain chamber, which follows hypermetabolism during initial 10 days after a concussion.

Therefore, in this instance, second offensive brain injury even less intense can enhance susceptibility towards mortality due to all these pathophysiological alterations. For different research, researchers suggested that the autoregulatory mechanism of the brain at the intracranial and cerebral perfusion pressures become lost after receiving the second impact. In severe secondary impact causes cerebral edema pursue by brain herniation and death can occur within 2 to 5 minutes^3,4,5.

Immediate Clinical Workflow Subsequent Brain Injury

Breathing, airway and blood circulation need to check and if require provide medical aids immediately at the emergency clinical setup. Patient need to through check up for cervical spine or spinal cord injury even absence of severe sign and symptoms.

Caregivers need to ask about posterior midline pain and monitor for development of any tenderness, weakness in the limbs, paresthesias, consciousness become down or a further sign of injury. A detail medical history requires preparing by discussing with patient or attainder.

Vital information includes how the injury happened, loss of consciousness, prior history of concussions, past report of seizure attack, transitory weakness or paresthesias, walking difficulty, incontinence of bowel or bladder, and drug or alcohol use. A detailed general physical examination needs to be performed with particular concentration on the neurological examination⁵.

Diagnosis

After providing emergency medical assistance following imaging diagnosis is required to confirm the patient’s safety.

Magnetic Resonance Imaging (MRI) – MRI can identify acute intracranial hemorrhage and detect surgically reversible injury.

Computed Tomography (CT) Scan – CT scan of the head helps to detect detail brain alterations if any after an injury. Computed Tomography much more sensitive than the MRI. CT scan can evaluate intraparenchymal structures, extra-axial, subarachnoid or intraventricular bleeding, loss of the grey-white junction induced cerebral inflammation, and shifting of the midline.

Finding of any autonomic abnormality requires consultation with a neurosurgeon ^5,6,7.

Treatment

• The resultant of true Second Impact Syndrome is death within few minutes due to the onset of brain herniation. In that case, no treatment can manipulate the situation, but for confirming the fatal outcome affected the individual need to shift emergency department.
• Any suspected case require immediate stabilization by providing particular importance on airway management and also require consultation with a neurosurgeon.
• The clinician also prefers to provide quick intubation and mannitol or suitable hypertonic saline administration to minimize the chance of morbidity, as administration of these may provide intracranial pressure lowering effect ^5,8,9.

References

1. Second Impact Syndrome; BrainandSpinalCord.org; http://www.brainandspinalcord.org/second-impact-syndrome/
2. Ropper A, Gorson H. Concussion. N Engl J Med. 2007;356:166–172.
3. DeSalles AA, Kontos HA, Ward JD, Marmarou A, Becker DP. Brain tissue pH in severely head-injured patients: A report of three cases. Neurosurgery. 1987;20:297–301.
4. Kawamata T, Katayama Y, Hovda D, Yoshino A, Becker D. Administration of excitatory amino acid antagonists via microdialysis attenuates the increase in glucose utilization seen following concussive brain injury. J Cereb Blood Flow Metab. 1992;12:12–24.
5. Tareg Bey, Brian Ostick; Second Impact Syndrome; West J Emerg Med. 2009 Feb; 10(1): 6–10
6. McCrory P, Berkovic S, Cordner S. Deaths due to brain injury among footballers in Victoria, from 1968 to 1998. Med J Aust. 2000;172:217–220.
7. Doezema D, King J, Tandberg D, et al. Magnetic resonance imaging in minor head injury. Ann Emerg Med. 1991;20:1281–1285.
8. Scheid R, Walther K, Guthke T, Preul C, von Cramon DY. Cognitive sequelae of diffuse axonal injury. Arch Neurol. 2006;63:418–424.
9. Wakai A, Roberts I, Schierhout G. Mannitol for acute traumatic brain injury. Cochrane Database of Systematic Reviews. 1998;(Issue 1) Art. No.: CD001049.