The Impact Of TBI On The Sufferer

The Impact Of TBI On The Sufferer

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The Impact Of TBI On The Sufferer

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The Impact Of TBI On The Sufferer

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Identify and discuss two (2) signs or symptoms of clinical deterioration associated with the presenting problem, from chosen case study. This discussion should consider the potential impact of case study data (e.g. pathology results, past medical history) on the health status of the patient in the chosen case.

Traumatic brain injury (TBI) refers to a complex injury that generally manifests in the form of a broad spectrum of disabilities and associated symptoms. The impact of TBI is usually devastating on the sufferers. TBI is commonly defined as disruption of the brain’s normal function that is caused due to a blow, bump or jolt to the head (Barlow, 2013). The severity of symptoms usually depend on the brain part that is affected. The case study is about a flight engineer James Parson, who has been admitted to the High Dependency Unit, 46 hours ago. He was involved in an altercation with some men during which he suffered a punch in the face, lost consciousness, and hit the pavement. This essay aims to discuss the pathophysiology of his presenting complaints and symptoms, and identify the key priority areas for intervention.
Primary diagnosis and pathophysiology- Traumatic brain injury is usually diagnosed by neurologic examination that detects presence of lesions or response of a patient to the Glasgow Coma Scale (Brown et al., 2015, p.179). Two signs and symptoms observed in the patient are an elevated heart rate, and an increased intracranial pressure. Forces that have been found to play an essential role in the onset of TBI include rotational, angular, and translational and shear forces (Hansen et al., 2013, p.110). The first stage of the cerebral injury is characterized by damage of direct tissues and an impaired regulation of metabolism and CBF (Huether & McCance, 2015, p.312). This resulted in an accumulation of lactic acid, following anaerobic glycolysis and increased the membrane permeability, thereby causing oedema formation (Carpenter, Jalloh & Hutchinson, 2015, p.112). Research evidences have supported the association between traumatic brain injury with tachycardia and catecholamine-induced hypertension (Kinoshita, 2016, p.29). Local release of the neurotransmitter norepinephrine from the sympathetic myocardial nerve terminals resulted in tachycardia, characterized by changes in the ECG, and dysfunction of the heart chambers (Algattas & Huang, 2013, p.312).
An increase in the intracranial pressure can be attributed to an elevation in the pressure of the cerebrospinal fluid surrounding the brain and the spinal cord. This increased ICP is often considered as a serious medical complication owing to the damage that it exerts on the spinal cord and the brain, by pressing on essential neuronal structures and restricting the blood flow. The head injury might have contributed to the condition by causing bleeding in the brain tissue and the meninges layer that surrounds the brain. These created adverse effects on the client’s heart and resulted in tachycardia. ICP refers to the pressure present inside the skull, in the CSF and the brain and the normal values of ICP range from 5-15 mmHg. One of the major dangers associated with an increase in ICP is related to the onset of ischemia that occurs due to a reduction in the cerebral perfusion pressure (Romner & Grände, 2013, p.185). Head injury is associated with a restricted volume of blood, CSF, extra tissue, or edema that often adds to the intracranial contents (Forbes & Watt, 2015, p.159). Death or clinical deterioration might soon follow due to an increase in ICP that results in a shift of intracranial contents, compromises cerebral perfusion or distorts the vital brainstem centre (Hawthorne & Piper, 2014, p.121). Past medical history of James of smoking and alcoholism also increased the risk of suffering TBI.
Priority of clinical care- Reducing intracranial pressure is a major clinical care priority. One of the most devastating effect of the brain injury on James was an elevated ICP (21mmHg), which has the likelihood of causing severe damage, if not checked. High ICP would result in cerebral oedema and intracranial hematoma, thus crushing the brain tissue, restricting blood supply and causing hydrocephalus.
Nursing intervention and goals- The first intervention is given below:
Specific- Improve oral health
Measurable- Improve oral health in the patient. This will be measured by recording the baseline data of the patients.
Achievable- Maintain the lips and oral mucosa clean, moist, soft and intact, and keep the teeth free from any debris or plaque. Prevent infection and oral discomfort. The nurse will determine the frequency of mouth care at an interval of 4-6 hours. Oral rinses will be used. Saline, effervescent ascorbic acid and Chlorhexidine can be used for the purpose. Proper toothbrushes, dental floss and foam swabs will be put to practice.
Relevance- Oral rinses are liquid solutions that will swish around the mouth of the affected including the gums, tongue and teeth and provide moisture to the oral tissue. They are not invasice and are an effective method of breaking the inflammatory and microbiologic cascade that leads to the development of periodontal disease (van der Maarel?Wierink et al., 2013, p.4). However, alcohol present in the mouthwashes might bring in a burning sensation in the patient’s mouth, aggravating the inflammation (if any) (Gupta et al., 2014, p.109). Nurses should assess the products prior administration. Chlorhexidine will not prove effective in dental plaque removal. High content of citric acid in ascorbic acid might lead to decay of the teeth enamel (Herrera, 2013, p.17). Thus, it should be used only if patient is edentulous.
Time- 48 hours
The second intervention is given below:
Specific- Collaborative care (Dietician)
Measurable- Good nutritional status and ICP
Achievable- A dietician would formulate a low energy diet for James and encourage him to embark on the diet for therapeutic benefit.
Relevance- Evidences suggest that a fluid restricted and low salt diet lead to rapid weight loss and help in managing intracranial hypertension (Markey et al., 2016, p.79). TBI has often been related to increased expenditure of energy, following an injury. Furthermore, it is also accompanies by an increase in the blood glucose levels. Feeding James appropriately will help him to attain the basic levels of calorie and reduce mortality chances. He might face the risks of ventilator related pneumonia (Carney et al., 2017, p.14). This adverse risk will be prevented by subjecting James to trans-gastric jejunal feeding.
Time- 72 hours
The third collaborative intervention is given below:
Specific- The physician will help to deliver supplemental oxygen
Measurable- oxygen saturation levels 95-100%
Achievable- The levels of saturated oxygen will determine the impacts of the therapy
Relevance- Repetitive hyperbaric oxygen therapy (HBOT) have shown improvement in outcomes in TBI patients (Boussi-Gross et al., 2013, e.79995). However, continuous oxygen therapy can lead to pulmonary oxygen toxicity and ocular side effects. An ocular examination by an ophthalmologist would be required. Toxicity will be managed by removing the mask from the patient and reducing partial oxygen pressure below 0.6 bar.
Time- 60 hours
Thus, it can be concluded that the patient James manifests a range of signs and symptoms following the traumatic brain injury, which needs to be addressed for reducing his deterioration. While increased intracranial pressure and tachycardia are the primary priorities that should be immediately taken care of, a constant monitoring of the patient will also need to be maintained for noting any other changes in his vital signs and neurological functioning. Following the application of the aforementioned three interventions, his ICP is expected to reduce to levels near 17 mmHg, thereby lowering the associated symptoms of headache, vomiting, decreased mental abilities, and confusion.
Algattas, H., & Huang, J. H. (2013). Traumatic brain injury pathophysiology and treatments: early, intermediate, and late phases post-injury. International journal of molecular sciences, 15(1), 309-341.
Barlow, K. M. (2013). Traumatic brain injury. In Handbook of clinical neurology (Vol. 112, pp. 891-904). Elsevier.
Boussi-Gross, R., Golan, H., Fishlev, G., Bechor, Y., Volkov, O., Bergan, J., … & Efrati, S. (2013). Hyperbaric oxygen therapy can improve post concussion syndrome years after mild traumatic brain injury-randomized prospective trial. PloS one, 8(11), e79995.
Brown, D., Edwards, H., Seaton, L., & Buckley, T. (2015). Lewis’s Medical-surgical Nursing: Assessment and Management of Clinical Problems. Elsevier Health Sciences, 158-275. (179)
Carney, N., Totten, A. M., O’reilly, C., Ullman, J. S., Hawryluk, G. W., Bell, M. J., … & Rubiano, A. M. (2017). Guidelines for the management of severe traumatic brain injury. Neurosurgery, 80(1), 6-15.
Carpenter, K. L., Jalloh, I., & Hutchinson, P. J. (2015). Glycolysis and the significance of lactate in traumatic brain injury. Frontiers in neuroscience, 9, 112.
Forbes, H., & Watt, E. (2015). Jarvis’s Physical Examination and Health Assessment. Elsevier Health Sciences, 158-223.
Gupta, D., Bhaskar, D. J., Gupta, R. K., Karim, B., Jain, A., Singh, R., & Karim, W. (2014). A randomized controlled clinical trial of Ocimum sanctum and chlorhexidine mouthwash on dental plaque and gingival inflammation. Journal of Ayurveda and integrative medicine, 5(2), 109.
Hansen, K., Dau, N., Feist, F., Deck, C., Willinger, R., Madey, S. M., & Bottlang, M. (2013). Angular Impact Mitigation system for bicycle helmets to reduce head acceleration and risk of traumatic brain injury. Accident Analysis & Prevention, 59, 109-117.
Hawthorne, C., & Piper, I. (2014). Monitoring of intracranial pressure in patients with traumatic brain injury. Frontiers in neurology, 5, 121.
Herrera, D. (2013). Chlorhexidine mouthwash reduces plaque and gingivitis. Evidence-based dentistry, 14(1), 17.
Huether, S. E., & McCance, K. L. (2015). Understanding Pathophysiology-E-Book. Elsevier Health Sciences, 307-422.
Kinoshita, K. (2016). Traumatic brain injury: pathophysiology for neurocritical care. Journal of intensive care, 4(1), 29.
Markey, K. A., Mollan, S. P., Jensen, R. H., & Sinclair, A. J. (2016). Understanding idiopathic intracranial hypertension: mechanisms, management, and future directions. The Lancet Neurology, 15(1), 78-91.
Romner, B., & Grände, P. O. (2013). Traumatic brain injury: Intracranial pressure monitoring in traumatic brain injury. Nature Reviews Neurology, 9(4), 185.
van der Maarel?Wierink, C. D., Vanobbergen, J. N., Bronkhorst, E. M., Schols, J. M., & de Baat, C. (2013). Oral health care and aspiration pneumonia in frail older people: a systematic literature review. Gerodontology, 30(1), 3-9.

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