CEREBRAL OEDEMA AND ITS LINK TO ELEVATED INTRACRANIAL PRESSURE, POST STROKE

 

 

 

 

 

CEREBRAL OEDEMA AND ITS LINK TO ELEVATED INTRACRANIAL PRESSURE, POST STROKE

 

 

 

 

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Injuries and illness related to or affecting the brain may result in swellings of the brain if not properly managed. An acute ischemic stroke may develop some severe complications that would lead to cerebral oedema as a result of blood pressures caused by poor stroke outcomes (Castillo et al. 2004). The complication is life-threatening as it may affect significant brain functions and eventually may lead to fatalities if not given a keen observation by the relevant physicians. Intracranial pressures accompanying a stroke are the primary linkage to the disease as they affect an individual’s blood tissues of the cerebral arteries and resulting in swellings and other adverse health effects and eventualities.

• Stroke is the leading cause of oedema if not clearly and adequately managed. Oedema leads to more deaths of the patients witnessed within the first week, usually four to five days, after a stroke attack. Various blood vessels and tissues of the brain are typically affected by the occurrence. Brain operations are impaired. The severe brain impairment eventually leads to patient death if not attended to with urgency in the first few hours of the occurrence (Thorén et al. 2017).
• An occurrence of an ischemic stroke results in the occlusion of the cerebral blood vessels and the intracranial arteries (Wells et al. 2015). The occlusion causes the sudden loss of circulation of blood in the brain organ, and thereby the blood vessels becoming hollow and thus affecting major brain functioning and activities.
• The insult of the brain by the resultant ischemic stroke poses a risk factor for the onset of cytotoxic oedema, which is accompanied by a brain swelling. The various ions such as those of Na⁺ accumulate in the brain neurons and astrocytes, leading to the blood-brain barrier (BBB) (Stokum et al. 2015). Such an influx of cations if not checked results to the blockage of such tissues. In describing the pathophysiology of cytotoxic oedema, the resultant ischemic stroke often interferes with the production and hormone content of the Adenosine Triphosphate (ATP). Thus if corrective measures are not conducted, the homeostasis process is hindered. The occurrence leads to interference with cations production resulting in the influx. The interactions between the cations and anions further result in organic water production in the brain, causing swellings (Liang et al. 2007). The swellings increase the intracranial pressure in the brain.
• Elevated intracranial pressure (ICP) exerted by the fluids flow in various brain tissues, or surrounding vessels of the affected vessel may lead to the general swelling or oedema. The swelling usually starts to manifest after 24 hours of an occurrence of occlusion and may take a maximum of 4 to 5 days after the incident of the acute ischemic stroke occurrence (Dostovic et al. 2016). Interventions may be taken even after the first 24 hours. However, the case is usually significant and need an urgent response within the early 24 hours in the case of a massive cerebral infarction.
• Following a stroke occurrence, diagnostic measures can be taken to determine if the patient might have developed oedema for appropriate medical treatment to be taken (Powers et al. 2015). Magnetic Resonance Imaging (MRI) scan can be conducted on the patient to determine the swellings and resultant intracranial brain pressures. The treatment is usually complicated as it involves the brain. Removal of the excess fluids through osmotherapy, which may include a surgical process and use of diuretics to reduce the volume of the fluid is a vital treatment method (Walcott, Kahle and Simard, 2012).

 

In conclusion, cerebral oedema results to swellings of the brain, which eventually results in the death of many patients if counteracting measures are not done with immediate effect. Oedema is one of the leading causes of death; hence the risk factors such as ischemic stroke need to be monitored effectively.

 

 

Bibliography

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Dostovic, Z., Dostovic, E., Smajlovic, D., Ibrahimagic, O.C. and Avdic, L., 2016. Brain edema after ischaemic stroke. Medical Archives, 70(5), p.339.

Liang, D., Bhatta, S., Gerzanich, V. and Simard, J.M., 2007. Cytotoxic oedema: mechanisms of pathological cell swelling. Neurosurgical Focus, 22(5), pp.1-9.

Powers, W.J., Derdeyn, C.P., Biller, J., Coffey, C.S., Hoh, B.L., Edward, C. and Jauch, K.C.J., 2015. Acute Ischemic Stroke Endovascular Therapy. Stroke, p.74.

Stokum, J.A., Kurland, D.B., Gerzanich, V. and Simard, J.M., 2015. Mechanisms of astrocyte-mediated cerebral oedema. Neurochemical Research, 40(2), pp.317-328.

Thorén, M., Azevedo, E., Dawson, J., Egido, J.A., Falcou, A., Ford, G.A., Holmin, S., Mikulik, R., Ollikainen, J., Wahlgren, N. and Ahmed, N., 2017. Predictors for cerebral oedema in acute ischemic stroke treated with intravenous thrombolysis. Stroke, 48(9), pp.2464-2471.

Walcott, B.P., Kahle, K.T. and Simard, J.M., 2012. Novel treatment targets for cerebral oedema. Neurotherapeutics, 9(1), pp.65-72.

Wells, A.J., Vink, R., Helps, S.C., Knox, S.J., Blumbergs, P.C. and Turner, R.J., 2015. Elevated intracranial pressure and cerebral edema following permanent MCA occlusion in an ovine model. PLoS One, 10(6).