Comment on the three discussion posts below (1 paragraph for each, support your response with a rationale and cite the source)

DISCUSSION 1:
All organs and bodily functions are dependent on the brain. The brain is extremely important is it controls, coordinates process information. When our brain is free from injury it enables us to think, feel, remember precious memories, connect with our environment and all the things that make us human. It is imperative that we protect our brains from injury by wearing seatbelts, helmets, and be vigilant in our daily lives, because a traumatic brain injury can alter our lives tremendously.

Traumatic brain injuries caused by car accidents, falls, and unintentional blunt trauma leaves the brain injured resulting in a change in the way the brain functions (McCance et al. 2019). As far as severity traumatic brain injury falls into three categories mild, moderate, and severe and can be determined by Glasgow coma scale (McCance et al. 2019).

According to the CDC mild TBI and concussions are still very serious. Pay attention to signs around a week or two after injury. Observe for signs an symptoms such as bothered by light, poor balance, fatigue, irritability, emotional changes, sleep disturbances and over sleeping (CDC, 2022).

“The Glasgow Coma Score (GCS) is scored between 3 and 15, with 3 being the worst and 15 the best (McCance et al. 2019). It is composed of the sum of three parameters: Best Eye Response, Best Verbal Response, and Best Motor Response. Mild Brain Injury, 13 or higher; Moderate Brain Injury, 9 to 12; Severe Brain Injury, 8 or less” (McCance et al., 2019).

DISCUSSION 2:

Traumatic brain injury is a leading cause of death & disability all over the world. The early diagnosis via CT Brain & the active medical management has improved tremendously in the last decade.(Ahmad, 2019). Traumatic brain injury (TBI) is a complex disease, with a variety of precipitating causes that affect the location and severity of injury and influence the course of recovery. It can simply be defined as an injury to the brain that occurs as a result of a bump or blow to the head or from blunt or penetrating trauma. During the impact, the brain crashes back and forth within the skull resulting in bruising, bleeding, and the shearing of nerve fibers known as axons The outcomes of TBI patients can vary depending on the area and the extent of the brain affected. .TBI can be mild, moderate or severe.

Mild traumatic brain injury (MTBI)

Characterized by a blow to the head, transient confusion or feeling dazed or disoriented, and one or more of these conditions: (1) loss of consciousness for up to 30 minutes, (2) loss of memory for events immediately before or after the accident, and (3) focal neurologic deficit(s) that may or not be transient.Loss of consciousness does not have to occur for a person to be diagnosed with MTBI.No evidence of brain damage on a CT or MRI imaging scan.Includes a wide array of physical and cognitive problems that range from headache and dizziness to changes in behavior. Symptoms usually resolve within 72 hours. Symptoms may persist and last days, weeks, or months. Persistent symptoms following MTBI are also referred to as post-concussion syndrome.

Moderate TBI is characterized by a period of loss of consciousness (LOC) for 30 minutes to 6 hours and a GCS score of 9 to 12. Often but not always, focal or diffuse brain injury can be seen with a diagnostic CT or MRI scan. Post-traumatic amnesia (memory loss) may last up to 24 hours. May occur with either closed or open brain injury. A short acute or critical care stay may be needed for close monitoring and to prevent secondary injury from brain edema, intracranial bleeding, or inadequate cerebral

Severe A severe TBI is defined by a GCS score of 3 to 8 and loss of consciousness for longer than 6 hours.Focal and diffuse damage to the brain, cerebrovascular vessels, and/or ventricles is common. Both open and closed head injuries can cause severe TBI, and injury can be focal or diffuse. Patients with severe TBI require management in critical care, including monitoring of hemodynamics, neurologic status, and possibly intracranial pressure (ICP). Patients with severe TBI are also at high risk for secondary brain injury from cerebral edema, hemorrhage, reduced perfusion, and the biomolecular cascade. Symptoms include Repeated vomiting or nausea, Convulsions or seizures Not being able to wake up from sleep, Larger than normal pupil (dark center) of one or both eyes. This is called dilation of the pupil. Slurred speech, Weakness or numbness in the arms and legs Loss of coordination, Increased confusion, restlessness, or agitation.

The most common causes of TBI in the United States are falls and motor vehicle crashes, followed by colliding with a stationary or moving object . Alcohol and drugs are significant contributing factors to the causes of TBI. Cognitive impairment is a common and disabling consequence of traumatic brain injury (TBI) but its impact on health-related quality of life is not well understood. (Gorgoraptis et al., 2019)

DISCUSSION 3

Increased intracranial pressure (IICP) is the result of extra pressure on intracranial content, this extra pressure can be the result of a tumor, edema, excess cerebral spinal fluid (CSF) or a hemorrhage. There are four stages of intracranial hypertension, each getting progressively worse and ultimately result in death when not properly treated/addressed.

Stage 1: the body compensates for the increased ICP through vasoconstriction and external compression of the venous system. As a result of the body’s compensation, so the patient will be awake and alter, pupils equal and reactive, beathing would be within normal limits, the blood pressure might be slight increased but close to normal range, pulse would be within normal range. Any continuing problems might cause some fluctuation in pressure which may take a little bit to return to the patient’s baseline, this slight change can be found with proper ICP monitoring (McCance et al., 2019). Finding the root cause of the ICP is important different tests can be done to help identify idiopathic intracranial hypertension (IIH), in a study done by Paterson et al. (2018) they found that measuring the optic nerve sheath diameters done with an ultrasound or MRI predicted increased ICP; however, the ultrasound is highly dependent on the operator and technique used while the MRI was less dependent on this.

Stage 2: there is a continuation of the expansion of the intracranial content which leads to the body not being able to compensate anymore. In this stage there are oxygenation to the brain cells are starting to be compromised, the body is still trying to compensate but with the arterial vasoconstriction not just venous. The patient’s vital signs for the most part continue to be relatively normal as what is presented in stage one; however, there is the additional presentation of an altered mental status with episodes of confusion, restlessness, and drowsiness. There might also be a slight pupillary or breathing changes. Stage two is the best stage to act with any medical or surgical interventions (McCance et al., 2019).

Stage 3: This is where the compensation that body is trying to do gets too much as the IICP continues to progress and mental status as well as vital signs are starting to be significantly altered, this stage only starts to occur when the body has exhausted everything it can do. The alterations in the condition a switch from arterial vasoconstriction to arterial pressure also brain tissues are becoming hypoxic and hypercapnia. A patient will have a number of changes in their symptoms there will be a reduced level or central neurogenic hyperventilation, the blood pressure systolic and diastolic will broaden, the heart rate will decrease, and the pupils will become small and be sluggish to react. Any surgical or medical intervention is very important at this point to help reduce progression to stage 4 (McCane et al., 2019).

Stage 4: This is the last stage prior to the death of the patient. The greatest cause for such a change in the patient’s status is the pressure is so great within the intracranial cavity that it causes a herniation of the brain tissues. The herniation greatly affects the oxygen levels to the brain as well as affects blood flow causing more tissue death. Surgical or medical intervention can be done but is typically the outcome is very grave. According to Esnault et al (2018) “hypocapnia induces cerebral vasoconstriction leading to a decrease in cerebral blood flow, which might precipitate cerebral ischemia” (pg 405). During this point the patients’ symptoms is that they have entered coma, pupils are either unequal or dilated and fixed, breathing progresses from Cheyne- Stokes to central neurogenic hyperventilation apneustic or ataxic, blood pressure continues to be wide until the patient is closer to death to which the systolic rapidly decreases, overall the heart rate will decreased (McCance et al., 2019).