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Small vessel disease affects the intracerebral arterial system. A stroke due to impedimenta of these vessels is referred to as a lacunar infarction. Lacunar infarctions are small (0 2 to 15 millimeter in diameter) noncortical infarctions caused by occlusion of a single penetrating branch of a large cerebral arterial blood vessel. Lacunar stroke has 5 classic syndromes and motor stroke is the most syndrome. The typical presentation is hemiparesis of face, arm or leg of one side. Clinical symptoms of stroke are slurred speech, right hand numbness, weak right mitt grip, and right sided facial palsy.(health direct, 2014)and most common among ischemic strokes (Rathore, Hinn, Cooper, Tyroler, & Rosamond, 2002).
Mechanisms of ischemic cell injury and death
There is progressive vasoconstriction of arterioles until the BP exceeds the upper limit of auto regulation, followed by breakthrough vasodilation, increase in cerebral blood flow, blood-brain barrier dysfunction, and cerebral oedema(Rodriguez-Yanez et al., 2006). Cerebral ischemia results in severely ischemic tissue with failure of electrical activity and ionic pumps (Rodriguez-Yanez et al., 2006) There is increase in the release of the excitatory amino acid glutamate due to electrical failure. (Rodriguez-Yanez et al., 2006) . Glutamate receptors are activated as a result and cause the opening of ion channels that allow potassium ions to leave the cell and sodium and calcium ions to enter. This has a number of physiological effects.
The above events end in cell death, including depletion of ATP, changes in ionic concentrations of sodium, potassium, and calcium, increased lactate, acidosis, accumulation of oxygen free radicals, intracellular accumulation of water, and activation of proteolytic processes.(Deb, Sharma, & Hassan, 2010). Surrounding this is the penumbra(Rodriguez-Yanez et al., 2006)
Different cellular signaling pathways respond to calcium levels. The inflow of calcium resulting from glutamate receptor stimulation leads to their activation.
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Nitric oxide is a significant signaling molecule in the body and is essential at normal physiologic levels. One advantage is that , endothelial nitric oxide synthase results in the production of low levels of nitric oxide that leads to vasodilation and increase blood flow(Lu & Liu, 2001) Moreso, nitric oxide is a free radical and reacts directly with cellular components injuring them. (Lu & Liu, 2001) In addition, DNA repair enzymes are activated as a result and consume vital energy needed for other processes. Furthermore, DNA injury also may activate the process of apoptosis, leading to cell death. Reactive oxygen species, which a normal by product of oxidative metabolism is produced, and increased during ischemia. These reacts with and damage cellular components. Furthermore, plasma membrane injury of a cell can result in the inability to control ion influx causing mitochondrial failure. In addition this leads to reactive oxygen species including calcium influx and other factors, which can also permeabilize the mitochondrial membrane. Also the injury of plasma membrane leads to metabolic failure as well as the release of initiators of apoptosis and DNA damage. In addition metabolic failure results in the depletion of cellular ATP levels. Hence ATP is required for nuclear condensation and DNA degradation in the final stages of apoptosis]. In the absence of ATP, cell death occurs by necrosis.
The inflammatory pathway components are activated by release of by products from cellular damage and death by necrosis. (Kamel & Iadecola, 2012). The inflammation role during ischemia is mixed, having both positive and negative effects (del Zoppo, Becker, & Hallenbeck, 2001).(Snider, Gottron, & Choi, 1999) Firstly during inflammation process blood flow to the ischemic region is increased, delivering vital glucose and oxygen to cells. Contrary ,more calcium is delivered to the area due to increased blood flow, resulting in increased tissue damage.
In addition, leukocytes migrate to damaged tissue during the inflammation process (Macrez et al., 2011). The leukocytes remove damaged and necrotic tissue at the same time releasing cytokines to attract additional inflammatory cells. These cytokines can accumulate to toxic levels under severe inflammatory conditions.
Necrosis and apoptosis
Cell death by necrosis or by apoptosis occurs following cerebral ischemia or stroke. Cellular chromatin becomes uniformly compacted, the endoplasmic reticulum is dilated, and ribosomes are dispersed in early stages (Snider et al., 1999; Ueda & Fujita, 2004). In later stages, swelling of the cell and mitochondria is followed by rupture of the nuclear, organelle, and plasma membranes, resulting in the influx of cellular material into the surrounding environment. This influx of material results in the stimulation of inflammatory processes within the brain.
During early stages of apoptosis the chromatin and the contents of the cytoplasm condense whilst the mitochondria and other organelles remain intact. In later stages, the nucleus is broken into discrete fragments and the entire contents of the cell are divided into membrane bound bodies that are subsequently phagocytosed by macrophages. Apoptosis can be initiated by three pathways,(Ueda & Fujita, 2004) The three pathways that initiate apoptosis are mitochondrial permeabilization, death receptor (Fas) pathway and endoplasmic reticulum stress (Ueda & Fujita, 2004).
SMOKING AND HYPERTENSION
Smoking increases the risk of stroke by promoting atherosclerosis and increasing the levels of blood-clotting factors, such as fibrinogen. (Oksala et al., 2007)In addition smoking also increases the damage that results from stroke by weakening the endothelial wall of the cerebrovascular system. (Ambrose & Barua ,2004). Smoking increases the risk of high blood pressure which is a direct cause of ischemic stroke(Oksala et al., 2007). In addition, smoking more than 15 or more cigarettes increases the risk of hypertension(Bowman, Gaziano, Buring, & Sesso, 2007). Furthermore, cigarette smoking induces arterial stiffness furthering the risk of stroke(Jatoi, Jerrard-Dunne, Feely, & Mahmud, 2007).
Diabetes increases the likelihood of large and small artery occlusive disease and ischemic stroke(Karapanayiotides, Piechowski-Jozwiak, van Melle, Bogousslavsky, & Devuyst, 2004)
Individuals with siblings who suffered stroke have an increased risk of suffering from stroke (Kasiman, April 2012) More so, Family history of stroke is an independent risk factor for ischemic stroke with onset before age 70 years.(Jood, Ladenvall, Rosengren, Blomstrand, & Jern, 2005)
High blood pressure is a common symptom on patients with ischaemic stroke caused by small-vessel disease (He et al., 2013) In addition, high blood pressure, is the single most important risk factor for stroke. It causes about 50 per cent of ischemic strokes(Robinson & Potter, 2004).
Significant number of patients with lacunar stroke as compared with other types of stroke are hypertensive and currently smoking..(Woo et al., 1999) According to research patients with lacunar infarcts more frequently had hypertension and diabetes(Chamorro et al., 1991), According to research done about 39 percent of strokes were attributable to smoking (Li, Engstrom, Hedblad, Berglund, & Janzon, 2005).
Diagnosis and Treatment
CT scan is diagnostic tool for lacunar infarction as it shows a clinical syndrome that is consistent with the location of a small noncortical infarct CT has low sensitivity for detecting lacunes (30 to 44 percent) at initial stage of stroke. Clinical signs and symptoms are significant in diagnosing stroke.
Patient presented after three days post stoke hence does not meet criteria for thrombolytic Antiplatelet agent Asprin is the drug of choice.
The initial assessment is to ensure medical stability, with particular attention to airway, breathing, and circulation (Jauch et al., 2013). In addition, reversing any conditions that are contributing to the patient's problem. Furthermore determining if patients with acute ischemic stroke are candidates for thrombolytic therapy and moving toward uncovering the pathophysiologic basis of the patient's neurologic symptoms (Jauch et al., 2013). The history and physical examination should be used to distinguish between other disorders in the differential diagnosis of brain ischemia example drug toxicity can mimic acute ischemia(Jauch et al., 2013). . Brain imaging with CT excludes other potentially life-threatening diagnoses such as intracerebral hemorrhage or subdural hematoma. Noncontrast head CT is the initial imaging modality for most patients presenting with an acute stroke syndrome(Wardlaw et al., 2004).
Ischemia in different vascular territories presents with specific syndromes, some of which provide a clue to the underlying stroke pathophysiology .The history should focus upon the time of symptom onset, the course of symptoms over time, possible embolic sources, items in the differential diagnosis, and concomitant diseases. National Institutes of Health Stroke Scale is used to provide a structured, quantifiable neurologic examination (Goldstein & Samsa, 1997)
The following tests should be done for evaluation, electrocardiogram, complete blood count including platelets, cardiac enzymes and troponin, serum electrolytes, urea nitrogen, creatinine prothrombin time and international normalized ratio (INR) and activated partial thromboplastin time(Broderick et al., 2007).
The ECG and cardiac monitoring are important for the detection of chronic or intermittent arrhythmias that predispose to embolic events and for detecting indirect evidence of atrial/ventricular enlargement that may predispose to thrombus formation(Jauch et al., 2013)
Intravascular volume deficit is common in acute stroke, and may worsen cerebral blood flow (Rodriguez et al., 2009). Isotonic saline without dextrose is the agent of choice for intravascular fluid repletion and maintenance fluid therapy (Burns, Green, Metivier, & DeFusco, 2012).
Hyperglycemia may augment brain injury by several mechanisms including increased tissue acidosis from anaerobic metabolism, free radical generation, and increased blood brain barrier permeability (Lindsberg & Roine, 2004). The American Heart Association/American Stroke Association guidelines for acute ischemic stroke recommend treatment for hyperglycemia to achieve serum glucose concentrations in the range of (7.8 to 10 mmol/L)(Jauch et al., 2013).
Dysphagia is s a major risk factor for developing aspiration pneumonia(Martino et al., 2005). Keep patient nil by mouth and assess for swallowing function prior to administering oral medications or food(Jauch et al., 2013)
Patients to be admitted in a stroke unit for better outcome(Meretoja et al., 2010). According to research, care provided by dedicated multidisciplinary stroke units in the acute or rehabilitation phase of stroke is associated with reduced mortality and improved functional outcomes (Meretoja et al., 2010) .
The arterial blood pressure is elevated mostly due to chronic hypertension, an acute sympathetic response, or to other stroke-mediated mechanisms(Qureshi, 2008) The acutely elevated blood pressure is necessary to maintain brain perfusion in borderline ischemic areas(Aiyagari & Gorelick, 2009) Guidelines recommend that blood pressure not be treated acutely unless the hypertension is extreme (systolic blood pressure >220 mmHg or diastolic blood pressure >120 mmHg)(Jauch et al., 2013).
Patient should consider quitting smoking Cigarette smoking is associated with an increased risk for all stroke subtypes and has a strong, dose-response relationship for both ischemic stroke and subarachnoid haemorrhage (Anthonisen et al., 2005) Nicotine is a potent psychoactive drug that causes physical dependence and tolerance(Stead & Lancaster, 2012). In the absence of nicotine, a smoker develops cravings for cigarettes and symptoms of the nicotine withdrawal syndrome(Stead & Lancaster, 2012). Clinicians should offer smokers both behavioral and pharmacologic therapy, as these treatments in combination are found to most effectively promote abstinence (Stead & Lancaster, 2012)
Medical complications of acute ischemic stroke are common and often lead to poor clinical outcomes(Indredavik, Rohweder, Naalsund, & Lydersen, 2008). Lacunar infarcts have a better clinical outcome(Jackson & Sudlow, 2005).