Introduction
Traumatic Brain Injury (TBI) is a disease that interferes with the standard functions of the brain due to penetrative or non-penetrative damage to the head. It is among the most complicated illnesses affecting the most complex body organ and has an occurrence rate higher than that of other ailments. This paper delves into the pathophysiology, clinical manifestations, diagnosis and treatment of traumatic brain injury.
Pathophysiology of Traumatic Brain Injury
The most common incidences that result in TBI include falls, violent activities, vehicle collisions, sports injuries, and explosive blasts (Prins, Greco, Alexander, & Giza, 2013). The disease can be fatal or result in permanent disability of the affected victim. TBI is caused by a rapid movement of the brain within the skull arising from a traumatic incident such as a blow or blast waves (Madikians and Giza, 2006). The events are categorized as impact or non-impact based on whether the patient was in direct contact with the object that caused the injury. For instance, the traumatic brain damage arising from a severe blow on the head falls under the impact class while that of waves from a blast is a non-impact.
Traumatic brain injury occasions the neural dysfunction and death of cells due to the biomechanical load exerted on the brain thereby leading to an ionic influx and intemperate release of glutamate and aspartate neurotransmitters (Madikians and Giza, 2006). Consequently, there are notable variations of the cerebral metabolism and blood flow resulting in brain dysfunction. The cerebral hemodynamic alterations are dependent on the nature of the injury and the extent of its severity. Traumatic brain injury patients may get cerebral hyperperfusion during the onset of the damage (Prins et al., 2013).
Clinical Manifestations of Traumatic Brain Injury
The clinical manifestations of a traumatic brain injury differ based on the extremity of the damage and the part of the brain that is affected. They are classified as mild or severe and may develop immediately after the injury or later. The mild symptoms are categorized into physical, sensory and cognitive signs. The physical clinical manifestations in a mild traumatic brain injury include; the loss of mental alertness ranging from seconds to a few minutes, consciousness with a state of disorientation and being stunned, fatigue accompanied by nausea and dizziness that may lead to loss of balance (Prins et al., 2013). The patient may also experience speech problems, headache, have difficulties in sleeping or sleep longer than usual. Individuals with a less severe TBI encounter sensory issues such as blurry vision, unpleasant taste in the mouth, variations in the capability to smell, ringing in the ears and susceptibility to light or sound (Prins et al., 2013). The cognitive symptoms evident in patients include the inability to concentrate, feeling of depression and mood variations (Prins et al., 2013).
The physical symptoms of a severe traumatic brain injury include loss of consciousness ranging from a couple of minutes to hours, constant headaches, incapacity to wake up from sleep, repetitive vomiting, and the presence of a clear fluid flowing from the nose or ears (Madikians and Giza, 2006). A patient may also experience seizures, enlargement of the eyes' pupils, lost coordination and inability to feel the fingers and toes. An individual with severe TBI presents cognitive symptoms such as extreme confusion, mumbled speech, perturbation, and may go into a coma (Madikians and Giza, 2006).
Diagnosis and Laboratory Tests for Traumatic Brain Injury
The differential diagnosis of traumatic brain injury is conducted using various tests namely; Glasgow Coma Scale (GCS), Cognition and Neuropsychological evaluation, measuring the level of TBI and imaging (Dash & Chavali, 2018).
The brain trauma indicator is a laboratory test that is undertaken in the diagnosis of the disease and uses blood as the specimen. The healthcare provider assesses the level of two proteins, Ubiquitin C-terminal Hydrolase-L1 (UCH-L1) and Glial Fibrillary Acidic Protein (GFAP) which are released into the blood from the brain upon the occurrence of a TBI (Mondello, Muller, Jeromin, Streeter, Hayes, & Wang, 2011). If the evaluation reveals the presence of the proteins in high levels, a diagnosis of a traumatic brain injury with intracranial lesions is made.
Treatment of Traumatic Brain Injury
The mode of treatment adopted in the management of traumatic brain injury is dependent on the level of severity. An individual diagnosed with a mild TBI requires no complex treatment other than getting enough rest and using pain relievers from over-the-counter to ease a headache (Dash & Chavali, 2018). However, the patient must be observed strictly both at home and through follow-up assessments by the doctor to take note of continuing or new symptoms. Children and young adults who experience a concussion through sports should avoid sporting activities until a medical practitioner gives a green light.
Individuals with average to acute traumatic brain injury must receive immediate emergency care to ascertain the adequacy of oxygen and blood supply, avert further injuries to the head and maintain blood pressure levels (Galgano, Toshkezi, Qiu, Russell, Chin, & Zhao, 2017). The individual may require emergency surgery to eliminate clotted blood arising from bleeding in the brain, restore skull fractures and ease pressure in the head. There are various medications available for use in the management of traumatic brain injury symptoms, namely;
Anticoagulants: A TBI may cause bleeding in the brain region, thus resulting in the formation of blood clots that hinder the normal flow of blood around the body. The medication is used to prevent clotting of blood, thus avoiding further crisis.
Anesthetic drugs such as propofol and thiopental are used in the management of TBI by permitting the speedy control of the airway while averting additional intracranial pressure and offering hemodynamic stability (Galgano et al., 2017).
Vasopressors: Medical practitioners use these drugs to control blood and cerebral perfusion pressure. An example of the medication is norepinephrine, which is used to increase blood pressure by narrowing the blood vessels (Galgano et al., 2017).
Conclusion
Traumatic Brain Injury is a disease caused by damage to the head. The illness leads to brain dysfunction by altering cerebral metabolism and blood flow and has symptoms such as unconsciousness, seizures, persistent headache, and loss of memory among others. The diagnosis of TBI can be done through a blood test to check for the presence of proteins which are released by the brain upon an injury. The management of TBI uses various treatment measures depending on the extent of the damage.
References
Dash, H. H., & Chavali, S. (2018). Management of traumatic brain injury patients. Korean Journal of Anesthesiology, 71(1), 12-21. http://doi.org/10.4097/kjae.2018.71.1.12
Galgano, M., Toshkezi, G., Qiu, X., Russell, T., Chin, L., & Zhao, L.-R. (2017). Traumatic Brain Injury: Current Treatment Strategies and Future Endeavors. Cell Transplantation, 26(7), 1118-1130. http://doi.org/10.1177/0963689717714102
Madikians, A. and Giza, C. (2006). A Clinician's Guide to the Pathophysiology of Traumatic Brain Injury. Indian Journal of Neurotrauma (IJNT), 3(1), pp.9-17.
Mondello, S., Muller, U., Jeromin, A., Streeter, J., Hayes, R. L., & Wang, K. K. (2011). Blood-based diagnostics of traumatic brain injuries. Expert Review of Molecular Diagnostics, 11(1), 65-78. http://doi.org/10.1586/erm.10.104
Prins, M., Greco, T., Alexander, D., & Giza, C. C. (2013). The pathophysiology of traumatic brain injury at a glance. Disease Models & Mechanisms, 6(6), 1307-1315. http://doi.org/10.1242/dmm.011585
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