Informative Essay on Traumatic Brain Injury: Pathophysiology and Treatment

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Introduction

Traumatic brain injury (TBI) is commonly defined as an insult to the brain from an external force that causes temporary or permanent impairment in functional, psychosocial, or physical abilities (Delgado, 2016). It is a significant cause of morbidity and mortality, and the leading cause of death and disability among young adults. Common causes of TBI include motor vehicle accidents, falls, sports injuries, and violence, and it is recognized increasingly in war zone injuries. According to Lozano (2015) “There are many types of TBI which includes concussions, contusions, diffuse axonal injury (DAI), traumatic subarachnoid hemorrhage (tSAH), and Hematoma”. According to (Talsky, 2011) “In the US, approximately 2 million people will sustain a TBI each year, one-quarter of whom will require hospitalization, leading to a conservative estimate of direct and indirect costs of $50 billion to $100 billion annually”. The side effects of a TBI can be mild, moderate, or severe, depending on the degree of harm to the brain (Delgado, 2016). In mild TBI the person is awake; eyes open. Symptoms can include confusion, disorientation, memory loss, headache, and brief loss of consciousness. In moderate TBI the person is lethargic; eyes open to stimulation. Loss of consciousness lasting 20 minutes to 6 hours. Some brain swelling or bleeding causes sleepiness, but still arousable. Whereas in severe TBI the person is unconscious; eyes do not open, even with stimulation. Loss of consciousness lasting more than 6 hours (Talsky, 2011).

Etiology

Ground-level fall
Elevated-level fall
Low-speed motor vehicle collision (< 25 mph)
High-speed motor vehicle collision (> 25 mph)
Blunt trauma
Sports-related
Military-related (blast)Penetrating injury
Acceleration–Deceleration injury
“Shaken Baby” injury (Lozano, 2015)

Briefly explain how TBI is diagnosed.

TBI needs to undergo a systematic yet fast assessment in the emergency room. Cardiovascular and pulmonary function is assessed first. According to (Richardson, 2018) “Next, a speedy assessment of the entire body is performed, followed by a total neurological assessment”. The neurological examination includes an assessment utilizing the Glasgow Coma Scale (GCS). In addition to the GCS, the ability of the pupils to become smaller in bright light is also tested. In patients with large mass lesions or with high intracranial pressure (ICP), one or both pupils may be very wide or ‘blown’ (Richardson, 2018). The presence of a wide or dilated pupil on only one side suggests that a large mass lesion may be present on the same side as the dilated pupil. Brainstem reflexes including gag and corneal (blink) may also be tested (Richardson, 2018).

A computed tomography scan (CT or CAT scan) is the gold standard for the radiological evaluation of a TBI patient. According to (Richardson, 2018) “A CT scan is easy to perform and is an excellent test for recognizing the presence of blood and fractures, which are the most crucial lesions to identify in medical trauma cases”.

Describe the pathophysiology of traumatic brain injury

Traumatic brain injury (TBI) stays one of the main sources of morbidity and mortality among citizens and the military workforce internationally. Despite advances in our knowledge of the complex pathophysiology of TBI, the underlying mechanisms are yet to be fully elucidated (Yun, 2019). While initial brain insult involves acute and irreversible primary damage to the parenchyma, the ensuing secondary brain injuries often progress slowly over months to years, hence providing a window for therapeutic interventions. As per Lee ‘To date, hallmark occasions during deferred optional CNS harm incorporate Wallerian degeneration of axons, mitochondrial brokenness, excitotoxicity, oxidative pressure and apoptotic cell passing of neurons and glia’ (2019). Broad research has been coordinated to the recognizable proof of druggable targets related to these procedures. Moreover, huge exertion has been advanced to improve the bioavailability of therapeutics to CNS by formulating systems for the productive, explicit, and controlled conveyance of bioactive operators to cell targets (Yun, 2019).

The initial phases of cerebral damage after TBI are described by direct tissue harm and impaired regulation of CBF and metabolism. This ‘ischemia-like’ pattern leads to the accumulation of lactic corrosive because of anaerobic glycolysis, increased membrane permeability, and continuous edema development (Yun, 2019). Since the anaerobic metabolism is inadequate to maintain cellular energy states, the ATP stores deplete and failure of energy-dependent membrane ion pumps occurs. The second phase of the pathophysiological is described by terminal membrane depolarization alongside the excessive release of excitatory neurotransmitters (for example glutamate, aspartate), activation of N-methyl-D-aspartate, α-amino-3-hydroxy-5-methyl-4-isoxazole propionate, and voltage-dependent Ca2+- and Na+-channels (Yun, 2019). The sequential Ca2+-and Na+- influx leads to self-digesting (catabolic) intracellular processes. Ca2+ activates lipid peroxidases, proteases, and phospholipases which in turn increase the intracellular concentration of free fatty acids and free radicals. Furthermore, activation of caspases (ICE-like proteins), translocases, and endonucleases start dynamic basic changes of natural films and the nucleosomal (DNA fracture and restraint of DNA fix) (Yun, 2019). Together, these events lead to membrane degradation of vascular and cell structures and ultimately necrotic or programmed cell death (apoptosis).

What are the signs and symptoms associated with TBI?

The seriousness of manifestations relies upon whether the damage is mild, moderate, or severe. concussion either doesn’t cause unconsciousness or unconsciousness lasts for 30 minutes or less (Alzheimer’s Association, 2020). Mild traumatic brain injury symptoms may include:

Failure to recollect the reason for the damage or occasions that happened preceding or as long as 24 hours after it occurred:

Perplexity and bewilderment.
Trouble recollecting new data.
Migraine.
Unsteadiness.
Foggy vision.
Queasiness and spewing.
Ringing in the ears.
Inconvenience talking intelligently.
Changes in feelings or rest designs (Alzheimer’s Association, 2020)

These side effects regularly show up at the hour of the damage or before long, yet at times may not produce for a considerable length of time or weeks. Mild traumatic brain injury manifestations are generally impermanent and clear up within hours, days, or weeks; be that as it may, once in a while, they can a month ago or more. According to Alzheimer’s Association, (2020). Mild traumatic brain injury causes obviousness enduring over 30 minutes yet under 24 hours, and serve traumatic brain injury causes obviousness for over 24 hours. Side effects of moderate and serve traumatic brain injury are like those of mild traumatic brain injury, yet progressively genuine and longer-enduring.

In all types of, traumatic brain injury cognitive changes are among the most widely recognized, disabling, and long-lasting symptoms that can result directly from the injury. The capacity to learn and recall new data is often affected (Alzheimer’s Association, 2020). Other commonly affected cognitive skills include the ability to focus, arrange thoughts, plan effective strategies for finishing tasks and activities, and make sound decisions.

Outline the medical and surgical treatment of TBI

Medical Treatment

Before a surgical procedure is considered, medical management is typically attempted to reduce ICP. As indicated by (Knot, 2014) ‘Mannitol or hypertonic sodium chloride solution are typically the first-line treatments after pain and agitation have been dealt with and the patient is inappropriate body position as described before’. I.V. administration of hyperosmolar agents, including hypertonic sodium chloride solution and mannitol, makes an osmolar angle, drawing water across the blood-brain barrier and diminishing interstitial volume. This intervention has been shown to decrease ICP and improve CPP in patients with severe TBI (Knot, 2014).

Barbiturates are regularly used to treat ICP. There is no affirmation that barbiturates lessen mortality; it also causes low BP. Phenytoin is recommended to decrease posttraumatic seizures. Levetiracetam can be utilized as another option (Varghese, 2017). Sympathetic storming which includes posturing, dystonia, hypertension, tachycardia, dilatation of the pupils, sweating, hyperthermia, and tachypnea can occur within the first 24 h after injury until several weeks. As per (Varghese, 2017) ‘This can be caused after the cessation of sedatives and narcotics in the ICUs and ought to be treated based on their signs and symptoms by initiating planned medications to reduce the activities of the sympathetic nervous system”. The patients who receive erythropoietin show lower mortality and better neurological result and limited neuronal harm induced by TBI. Naloxone effectively reduces mortality and controls ICP in TBI (Varghese, 2017).

Surgical Management

Surgical evacuation is done on patients having a GCS score ≤8 with a huge lesion on non-contrast head CT scan. Depressed skull fractures are open or complicated and need surgical repair (Varghese, 2017). The available surgical options to control increased intracranial pressure and to limit secondary brain damage in the setting of severe traumatic brain injury (TBI) include decompressive craniectomy, cisternostomy, and other methods to divert cerebrospinal fluid (CSF) such as placement of an external ventricular drain (Giammattei, 2018).

Decompressive craniectomy (DC) had been used to control ICP associated with abnormal conditions, including intracranial neoplasm, ischemic disease, and diffuse edema from TBI (Moon,2017). The benefit of DC in the treatment of malignant infarction had been proved by previous studies. Although DC in TBI reduces ICP by evacuating hematoma and providing wider space for the brain, its improvement for the clinical outcome is not clear. DC must be extensive at all times because the benefits of DC are directly affected by surgical technique and the degree of decompression achieved (Moon,2017). According to Moon (2017), “Two main techniques widely used for DC in TBI are unilateral frontotemporoparietal craniectomy and bifrontal craniectomy”. Unilateral frontotemporoparietal craniectomy is especially useful for unilateral localized lesions, including traumatic hematoma, and brain swelling due to middle cerebral artery (MCA) infarction(Moon,2017).

The cisternostomy as a procedure can be either an outflow corridor for the cerebrospinal fluid (CSF) from the ventricular system to the cisternal subarachnoid space or an inflow corridor for the atmospheric pressure to be opened on the basal cistern and equalize cisternal and external pressure aiming for brain relaxation. As indicated by (Hoz, 2018) classify cisternostomy into two broad categories such as outflow corridor and inflow corridor. With the outflow corridor when the cisternostomy procedure provides a drainage pouch for the ventricular CSF and/or closed fluid-containing compartments. Theoretically, the inflow cisternostomy can be categorized into convexity and basal cisternostomy and the last can be partitioned into supratentorial and infratentorial, however, the ongoing proof considers the basal supratentorial cisternostomy is the cisternostomy appropriate.

External ventricular drains (EVDs) are generally utilized in neurosurgery in various conditions however frequently in the management of traumatic brain injury (TBI) to monitor and/or control intracranial pressure (ICP) by occupying cerebrospinal fluid (CSF). According to (Chau, 2019) ‘Their clinical viability, when utilized as a therapeutic ICP- lowering procedure in contemporary practice, stays vague’. No consensus has been reached regarding the drainage strategy and the optimal timing of insertion (Chau, 2019).

Three (3) classes of medications TBI

In 2008 a retrospective analysis was conducted on medications prescribed to brain injury patients. Charts of patients examined in the Raymond J. Greenwald Rehabilitation Center at the SUNY State College of Optometry from the years 2000 to 2003 were reviewed. As indicated by (Kapoor, 2008) ‘ The 4 most common classes of medication taken by TBI patients anti-anxiety/antidepressants (42.5%), anticonvulsants (26.9%), opiate/combination analgesics (23.8%), and cardiac/antihypertensive (23.1%). However, the top three (3) classes of medication used for patients with Traumatic Brain Injury will be elaborated on.

Anti-depressant

Anti-depressant medications are thought to work by affecting the levels of the brain’s natural chemical messengers, called neurotransmitters, and adjusting the brain’s response to them. Examples include citalopram, amitriptyline, paroxetine, and sertraline (CEMM Virtual Library, 2018).

Anti-depressants treat disorders such as:

Anxiety
Bulimia (eating disorder)
Obsessive-compulsive disorder
Panic disorders (CEMM Virtual Library, 2018).

Some possible side effects of Anti-depressants are:

Blurred vision
Cardiac palpitations
Confusion
Constipation
DizzinessDrowsiness (CEMM Virtual Library, 2018).

Anti-convulsant

Anti-convulsant medications are used to suppress the rapid and excessive firing of neurons that start a seizure (CEMM Virtual Library, 2018). Anti-convulsants can sometimes prevent the spread of a seizure within the brain and offer protection against possible excitotoxic (excessive stimulation by chemicals in the nervous system) effects that may result in brain damage (CEMM Virtual Library, 2018). Examples include sodium valproate, gabapentin, topiramate, and carbamazepine.

Anticonvulsants treat different types of seizures such as:

Absence seizures (formerly called petit mal seizures)
Acute seizures
Bipolar disorders
Corticofocal seizures
Generalized tonic-clonic seizures (CEMM Virtual Library, 2018).

Some possible side effects of Anti-convulsant are:

Alopecia (hair loss)
Amnesia (memory loss)
Nausea
Nystagmus (rapid, involuntary eye movements)
Tremor
Vomiting
Weight gain (CEMM Virtual Library, 2018).

Opiate/Combination analgesics

Pain management medications are used to control pain stemming from TBI, and the symptoms and effects related to the injury (CEMM Virtual Library, 2018). Examples include acetaminophen, ibuprofen, and naproxen sodium.

Opiate/Combination analgesics usually treat symptoms such as:

Arthralgia (joint pain)
Fever
Headache
Mild to moderate pain
Myalgia (muscle pain)

Some possible side effect of Opiate/Combination analgesics are:

Burning sensation
Constipation
Dizziness
Gastrointestinal irritation and bleeding
Heartburn
Nausea (CEMM Virtual Library, 2018).

What are the nursing considerations/management for this patient?

Effective nursing management strategies for traumatic brain injury are still an amazing issue and a difficult task for neurologists, neurosurgeons, and neuro nurses. According to (Varghese, 2017) ‘Nurses are the health professionals who see the full effect of TBI and have what it takes that can alter the course of a patient’s recovery; it is significant for nurses to have a valuable resource with evidence-based”.

Temperature management

Hypothermia reduces ICP (40%) and cerebral blood flow (CBF, 60%), has effects on cerebral metabolism, and improves results for 3 months after injury. Hence, it limits secondary brain injury. Normothermia ought to be maintained with the utilization of antipyretic medication, surface cooling devices, or even endovascular temperature management catheters (Varghese, 2017).

Nutrition

Patients following damage may encounter a systemic and cerebral hypermetabolic state. Early enteral feeding should be initiated within 72 h of damage. By day 7 of postinjury, these patients ought to be given full caloric substitution (Varghese, 2017). After TBI, early initiation of nutrition is recommended.

Fluid therapy

Fluid therapy helps in restoring vascular capacity, tissue perfusion, and cardiac flow rate (Varghese, 2017). Hypertonic saline can be used for patients with complications of TBI and systemic shock.

Hyperventilation

Hyperventilation reduces PaCO2, CBF, and ICP through cerebral autoregulation. It can be used only if ICP >30 mmHg and CPP 70 mmHg but higher ICP >40 mmHg (Varghese, 2017).

Glucose management

Extremes of very high or low blood glucose levels should be managed accordingly. A target range of up to 140 mg/dL or possibly even 180 mg/dL may be appropriate (Varghese, 2017). Patients with hyperglycemia should be managed with insulin protocol in cases with values>200 mg/dl for improving the outcome.

Care Plan

A care plan for this patient offers a critically important basis for the person and his family to fully appreciate the seriousness of the acquired impairments, likely complications, implications for independence and quality of life, and long-term care needs, whether for clinical or litigation purposes. Two actual and one potential diagnosis for this patient includes:

Conclusion

In conclusion, Traumatic Brain Injury is a major health issue that affects the anatomy and functions of the brain. It’s as sudden damage to the brain caused by a blow or jolt to the head. Common causes include car or motorcycle crashes, falls, sports injuries, and assaults. Injuries can range from mild concussions to severe permanent brain damage. While treatment for mild TBI may include rest and medication, severe TBI may require intensive care and life-saving surgery. Those who survive a brain injury can face lasting effects on their physical and mental abilities as well as emotions and personality. Most people who suffer moderate to severe TBI will need rehabilitation to recover and relearn skills. TBI typically affects all aspects of a patient’s future life: domestic, recreational, vocational, social, and personal. Safety precautions in daily activities may help to avoid TBI.

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