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Health Alterations and High Dependancy Nursing Essay

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Updated: Sep 11th, 2021

Brain Injuries

Traumatic brain injury is just one of the causes of raised intracranial pressure (ICP), which is an evident indicator of it (Stocchetti et al. 2007, p. 1339-1346). There are a few factors that may be used to diagnose a rise of intracranial pressure. The most significant signs and symptoms that point towards this phenomenon are ocular palsies, papilledema, headache, and nausea with vomiting. The fact that the patient was behaving aggressively and did not respond to commands indicates altered level of consciousness. This indirectly suggests ICP increase. Clinical deterioration in neurological status is considered to be a sign of increased ICP as well. Papilledema is also secondary to the ICP increase. It can be seen with ophthalmoscope, during dilated fundus examination that may demonstrate disk hyperemia, small hemorrhages and subtle edema of the nerve fiber layer, and obliteration of spontaneous venous pulsation that is usually present in healthy individuals. Cushing’s triad is especially suggestive of high ICP. It includes increased systolic blood pressure, widened pulse pressure, bradycardia, as well as abnormal respiratory pattern. The most common respiratory pattern that suggests high ICP is Cheyne-Stokes respiration. The breathing is rapid for a period, and then absent for a period. Some other signs of increased ICP may include papillary dilatation, abducens (VI cranial nerve) palsies, if the high level of ICP had caused displacement of brain tissue. The abducens paralysis will cause the inward turning of the eye, leading to double vision. There are also a few invasive methods that can help diagnose high ICP. One of them is intraventricular monitoring using ventricular catheter. The pressure is measured in mmHg. Other widely used devices are Richmond screw and Becker bolt along with subdural fluid filled catheter (Stullken 2002, pp. 494-500).

The screw and bolt are used extradurally, whereas the catheter is in the subdural space, connected to arterial pressure monitoring system. There is also a common instrument, used subdurally, extradurally, or even extracutaneously. It is called the Ladd device. The measurement is done using to fiber optic system that detects distortion of a tiny mirror within a balloon system. Likewise, there is a mechanically coupled surface monitoring device called “cardio search pneumatic sensor” that can be used subdurally or extradurally, but it is not very common. Any registered ICP level that exceeds 20 mmHg is considered to be pathologic. An increase of ICP over 40 mmHg usually implies to some sort of neurological dysfunction, observed during head trauma, such as altered consciousness, respiration problems, pupil dilation, whereas ICP over 60 mmHg is fatal. Electroencephalogram (EEG) may also suggest that we are dealing with high ICP, as the impairment of brain’s electrical activity will display an abnormal EEG (Grabois & Young 2001, pp. 13).


Over the next six hours there are three priority interventions that should be performed. As the patient’s GCS score is 8, she is considered to be in a severe coma state. Remaining in the same position for a lengthy period of time will cause decubitus, or pressure sores. The development of a pressure ulcer is of great significance to the life-long rehabilitative management of the person with a central nervous system injury, and may indeed delay and repeatedly interfere with that process (Sheerin & de Frein 2007, p. 447 – 500). They appear in places that are subject to constant pressure, such as ischial tuberosity, trochanteric, sacral regions, as well as malleolar, heel, patellar, and pretibial locations. Such pressure, just above the pressure of capillary filling, for over 2 hours can cause tissue damage due to ischemia. Therefore, the patient’s positioning in bed must be changed at least every 2 hours in order to prevent decubitus. This will supply sufficient blood flow to the risk areas of pressure sores, and prevent ulceration of the skin. The patient’s skin should also be clean and free of urine and feces. In order to prevent dermal infection, ethanol should be used for treating the skin. Likewise, massage, as well as the inflatable raft and the vacuum mattress would be a good physiotherapy that would prevent pressure sores, intensifying the blood flow and eliminating ischemia (Sheerin & de Frein 2007, p. 447 – 500). The above aspect is related to nursing responsibilities. One of the indicators that will show us that there is no disposition towards decubitus is the skin color and texture. It should always stay homogeneous and smooth. Another evaluation criterion would be the absence of cutaneous ulceration in places of decubital risk. Because severe head injury results in significant metabolic changes, the organism’s requirement for protein, and non-protein calories, micronutrients goes up. Thus, a responsibility of nursing would be the efficient supply of carbohydrates, fats, proteins, vitamins, as well as care of the oral cavity.

Another intervention should be aimed towards combating the high ICP, which was 28 mmHg during assessment in the intensive care unit, and should not exceed 10 (Lee et al. 2003, pp. 513). In order to do this, osmotherapy is required. Such medications as mannitol, glycerol, and urea must be administered. Mannitol is the osmotic agent currently in use. Mannitol’s effectiveness in reducing ICP has been shown. Osmotic therapy using mannitol reduces ICP by mechanisms that remain unclear. Mannitol is thought to decrease brain volume by decreasing overall water content, to reduce blood volume by vasoconstriction and to reduce cerebrospinal fluid (CSF) volume by decreasing water content. Mannitol may also improve cerebral perfusion by decreasing viscosity or altering red blood cell rheology. Lastly, mannitol may exert a protective effect against biochemical injury. The most common complications of therapy are fluid and electrolyte imbalances, cardiopulmonary edema and rebound cerebral edema. Nursing care of the patient receiving mannitol requires vigilant monitoring of electrolytes and overall fluid balance, and observation for the development of cardiopulmonary complications in addition to neurologic assessment (Davis & Lucatorto 2002, p. 170-174). A rebound phenomenon occurs in 12% of the patients treated with mannitol and 34% of the glycerol treated ones (Node & Nakazawa 2001, p. 359-363). Mannitol is an osmotic diuretic that works through drawing water across the ependyma of the ventricles, decreasing the amount of fluid within the ventricles, lowering the ICP. It also reduces blood viscosity, which causes a reflex vessel diameter decrease to maintain cerebral blood flow through autoregulation. This decrease in vessel diameter contributes to decreasing total cerebral fluid volume and pressure. Hypertonic 3% saline has the same action mechanism as the mannitol, and it also increases cardiac output, although its adverse effects include electrolyte abnormalities, cardiac failure, bleeding diathesis, and phlebitis (Qureshi & Suarez 2000, p. 3301-3313). Once the water will be transferred from the ventricles into the blood stream, the ICP will decrease. Such intervention is a prerogative of medicine. We will be able to observe the lowering of ICP using a ventricular catheter monitoring device, as ventricular pressure monitoring is indicated in the guidelines of the Brain Trauma Foundation (Akopian et al. 2007, 447-450).

This will be the first evaluation criteria. The second one would be the increase of GCS with recovery of consciousness. We will be able to see this when the patient will start coming out of coma. Her eyes will start opening in response to painful stimuli, then voice, then will open spontaneously. The verbal function will also be restored. The initial incomprehensive sounds will give away to inappropriate words. Following this, the speech ability will improve to being confused and disoriented. Subsequently, the patient’s verbal function will become oriented, and she will be able to converse normally. The motor function will also undergo changes. The soporose person’s reaction to pain will shift from withdrawing to localizing the algetic stimuli. Sooner or later the patient’s motor function will improve to the point, where she will be able to obey commands.

The assessment in the intensive care unit had revealed low diastolic blood pressure. The doctor’s task would be to increase it. One of the ways to do this would be to give the patient catecholamines or their closest equivalents. Phenylephrine or Neo-Synephrine is a powerful vasopressor. As it is an alpha-adrenergic receptor agonist, it imitates the action of norepinephrine upon adrenal receptors. Therefore, it would activate post-synaptic adrenal receptors in the blood vessels, especially in arterioles and capillary veins. This would cause the myocytes in the microvasculature to contract, increasing vascular resistance, and pushing out all the blood into the great vessels. Consequently, this would lead to an increase of arterial blood pressure. Phenylephrine will also activate alpha adrenal receptors of cardial ventricle’s myocardium. This will cause an increase of the stroke volume. All this should help conquer hypotension. The increased blood pressure will lead to activation of baroreceptors in the aortic arch that will result in reflectory bradycardia, thus, the cardiac output will fall (Farley 2002, pp. 8). This is a positive fact, as the pulse rate during assessment was 100 beats/minute. The arterial blood pressure must be measured frequently. An increase of blood pressure and lowering of the heart rate are the two criteria that will indicate the intervention’s success.


Akopian G, Gaspard D. J, Alexander M. 2007, “Outcomes of blunt head trauma without intracranial pressure monitoring”, Am Surg, vol. 73, no. 5, pp. 447-450.

Davis M, Lucatorto M. 2002, “Mannitol revisited”, Neurosci Nurs, vol. 26, no.2, pp. 170-174.

Farley, D. 2002. ‘Head injuries require quick, skilled care’, FDA Consumer.

Grabois, E, Young, M.E. 2001. ‘Managed care experiences of persons with disabilities’, The Journal of Rehabilitation, vol. 67, no. 3, pp. 13.

Node Y, Nakazawa S. 2001, “Clinical study of mannitol and glycerol on raised intracranial pressure and on their rebound phenomenon”, Adv Neurol, vol. 52, pp. 359-363.

Qureshi AI, Suarez JI. 2000, “Use of hypertonic saline solutions in treatment of cerebral edema and intracranial hypertension”, Crit Care Med, vol. 28, no. 9, pp. 3301-3313.

Sheerin F, de Frein R. 2007, “The occipital and sacral pressures experienced by healthy volunteers under spinal immobilization: a trial of three surfaces”, J Emerg Nurs, vol. 33, no.5, pp. 447-450.

Stocchetti N, Colombo A, Ortolano F, Videtta W, Marchesi R, Longhi L, Zanier ER. 2007, “Time course of intracranial hypertension after traumatic brain injury”, J Neurotrauma, vol. 24, no. 8, pp. 1339-1346.

Stullken EH Jr, Sokoll. 2002, “Anesthesia and subarachnoid intracranial pressure”, Anesth Analg, vol. 54, no. 4, pp. 494-500.

Lee, M, Jung, B, Chung, S, Bae, O, Lee, J, Park, J, Yang, J, Lee, H, Chung, J. 2003. ‘Arsenic-induced dysfunction in relaxation of blood vessels. Environmental Health Perspectives’ vol. 111, no. 4, pp. 513.

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