Please respond to this discussion peer post from Taina
Question 6 Compare and contrast the Pathophysiology of Ischemic and Hemorrhagic stroke.
Stroke, also known as CVA (Cerebrovascular accident), or brain attack is defined as interruption of blood flow to the brain. Such interruption can cause brain damage or death if not treated quickly. Stroke is the second leading cause of death and a major contributor to disability worldwide. Cerebral infarction results when an area of the brain loses its blood supply because of vascular occlusion. Causes include: abrupt vascular occlusion (e.g., embolus or thrombi), gradual vessel occlusion (e.g., atheroma), and vessels that are stenosed but not completely occluded.
There is a central core of irreversible ischemia and necrosis or cerebral infarction. The central core is surrounded by a zone of borderline ischemic tissue, the ischemic penumbra. Ischemia in the penumbra is not severe enough to result in structural damage. Prompt restoration of perfusion in the penumbra by injection of thrombolytic agents promotes perfusion and may prevent necrosis and loss of neurologic function. The window of opportunity for protecting the penumbra is about 3 hours (McCance et al., 2023).
Cerebral infarctions are ischemic or hemorrhagic. In ischemic infarcts, the affected area becomes pale and softens 6 to 12 hours after the occlusion (white infarct). Necrosis, swelling around the insult, and mushy disintegration appear by 48 to 72 hours after infarction. There is infiltration of macrophages and phagocytosis of necrotic tissue. The necrosis resolves by about the second week, ultimately leaving a cavity surrounded by glial scarring (McCance et al., 2023).
Per literature by (Pinho et al., 2019), In hemorrhagic infarcts, bleeding occurs into the infarcted area through leaking vessels when the embolic fragments resolve, and reperfusion begins to occur. Hemorrhagic transformation of ischemic infarct (red infarct) may be exacerbated by thrombolytic therapy. Unfortunately, reperfusion can compromise recovery by accelerating the sequence of metabolically damaging events, including oxidative stress (reperfusion injury).
Moreover, (Pinho et al., 2019) state, “Ischemic stroke occurs when there is obstruction to arterial blood flow to the brain from thrombus formation, an embolus associated with atherosclerosis, or hypoperfusion related to decreased blood volume or heart failure. The inadequate blood supply results in ischemia (inadequate cellular oxygen) and can progress to infarction (death of tissue).”
Ischemic strokes are categorized into four types: Thrombotic, Embolic, Lacunar and Hemodynamic. Thrombotic strokes (cerebral thrombosis) arise from arterial occlusions caused by thrombus formation in large or small arteries supplying the brain or intracranial vessels. Conditions causing increased coagulation or inadequate cerebral perfusion (e.g., dehydration, hypotension, prolonged vasoconstriction from malignant hypertension) increase the risk of thrombosis. Cerebral thrombosis develops most often from atherosclerosis and inflammatory disease processes that damage arterial walls. It may take as long as 20 to 30 years for obstruction (stenosis) to develop at the branches and curvatures found in the cerebral circulation. The smooth stenotic area can degenerate, forming an ulcerated area of vessel wall. Platelets and fibrin adhere to the damaged wall, and clots form, gradually occluding the artery. The thrombus may enlarge both distally and proximally in the vessel. Thrombotic strokes occur when portions of the clot detach, travel upstream, and obstruct blood flow, causing acute ischemia (McCance et al., 2023).
Embolic stroke involves fragments that break from a thrombus formed outside the brain usually in the heart, aorta, or common carotid artery. Other sources of embolism include fat, air, tumor, bacterial clumps, and foreign bodies. The embolus usually involves small brain vessels and obstructs at a bifurcation or other point of narrowing, thus causing ischemia. An embolus may obstruct the lumen entirely and remain in place or shatter into fragments and become part of the vessel’s blood flow. Risk factors for an embolic stroke are atrial fibrillation (15% to 25% of strokes), left ventricular aneurysm or thrombus, left atrial thrombus, recent myocardial infarction, rheumatic valvular disease, mechanical prosthetic valve, nonbacterial thrombotic endocarditis, bacterial endocarditis, patent foramen ovale, and primary intracardiac tumors. In persons who experience an embolic stroke, a second stroke usually follows at some point because the source of emboli continues to exist. Embolization is usually in the distribution of the middle cerebral artery (McCance et al., 2023).
Lacunar strokes (lacunar infarcts or small vessel disease) are usually caused by perivascular edema, thickening and inflammation of the arteriolar wall in a deep perforating artery that supplies small penetrating subcortical vessels (small vessel disease). The ischemic lesions (0.5 to 15 mm) or lacunes are predominantly in the basal ganglia, internal capsules, and pons. They are associated with hyperlipidemia, smoking, hypertension, and diabetes mellitus. These strokes represent about 25% of ischemic strokes and, because of the location and small area of infarction, may have pure motor or sensory deficits (McCance et al., 2023).
Hemodynamic stroke (brain hypoperfusion) is associated with systemic hypoperfusion caused by cardiac failure, pulmonary embolism, or bleeding that results in inadequate blood supply to the brain. Stroke may occur more readily if there is carotid artery occlusion. Symptoms usually are bilateral and diffuse (McCance et al., 2023).
Clinical manifestations of thrombotic or embolic ischemic stroke vary, depending on the distribution of the artery obstructed. Different sites of vessel obstruction create different occlusion syndromes. Contralateral sensory and motor manifestations occur on the opposite side of the body from the location of the brain lesion because motor tracts originate in the cortex and most cross over in the medulla. Sensory tracts originate in the periphery and cross over in the spinal cord. Ipsilateral manifestations occur on the same side as the brain lesion for tracts that do not cross over (Colasurdo et al., 2024).
According to (Abdu et al., 2021), Hemorrhagic strokes are placed in two categories based on where the bleeding occurs and its cause:
· Intracerebral hemorrhage — Intracerebral hemorrhages are caused by a broken blood vessel located in the brain. Bleeding is from the blood vessels within the brain.
· Subarachnoid hemorrhage — Subarachnoid hemorrhages occur when a blood vessel gets damaged, leading to blood accumulating on the brain’s surface. Bleeding is in the subarachnoid space (the space between the brain and the membranes that cover the brain).
Hemorrhagic stroke (spontaneous intracranial hemorrhage [ICH]) is the third most common cause of CVA. Hemorrhagic stroke can occur within the brain tissue (intraparenchymal) or in the subarachnoid or subdural spaces. The primary cause of intraparenchymal hemorrhagic stroke is hypertension with other causes including tumors; coagulation disorders; trauma; or illicit drug use, particularly cocaine. Hypertensive causes of hemorrhagic stroke evolve over several years. They involve primarily smaller arteries and arterioles, resulting in thickening of the vessel walls and increased cellularity of the vessels. Necrosis may be present with vessel rupture. Microaneurysms in these smaller vessels or arteriolar necrosis may precipitate bleeding. Prevention or control of hypertension reduces the incidence of hemorrhagic stroke (McCance et al., 2023).
The clinical manifestations of hemorrhagic stroke are similar to those for embolic and thrombotic stroke and depend on the location and size of the bleed. Once a deep unresponsive state occurs, the immediate prognosis is grave, and the individual rarely survives. If the person survives, however, recovery of function frequently is possible (Colasurdo et al., 2024).
Individuals experiencing intracranial hemorrhage from a ruptured or leaking aneurysm have one of three sets of symptoms: (1) onset of an excruciating generalized headache with an almost immediate lapse into an unresponsive state; (2) headache, but with consciousness maintained; and (3) sudden lapse into unconsciousness. If the hemorrhage is confined to the subarachnoid space, there may be no local signs. If bleeding spreads into the brain tissue, hemiparesis/paralysis, dysphasia, or homonymous hemianopsia may be present. Warning signs of an impending aneurysm rupture include headache, transient unilateral weakness, transient numbness and tingling, and transient speech disturbance. Such warning signs are often absent. (McCance et al., 2023).
To summarize, an ischemic stroke is when a blood clot or other particles reduce blood flow to part of the brain, depriving it of oxygen. A hemorrhagic stroke occurs when a blood vessel in part of the brain bursts, cutting off the oxygen supply. Per our text, (McCance et al, 2023), “Imaging is used to diagnose the different subtypes of ischemic stroke (i.e., MRI and CT imaging). Treatment of ischemic stroke is focused on (1) restoring brain perfusion in a timeframe that does not contribute to reperfusion injury, (2) counteracting the ischemic cascade pathways, (3) lowering cerebral metabolic demand so that the susceptible brain tissue is protected against impaired perfusion, (4) preventing recurrent ischemic events, and (5) promoting tissue restoration. Intravenous thrombolysis (i.e., recombinant tissue plasminogen activator [rtPA]) given within 3 and up to 4.5 hours of onset of symptoms increases independent ambulation at 6 months when the diagnosis of ischemic stroke has been confirmed and contraindications are eliminated. Diagnosis of hemorrhagic stroke considers the health history, clinical presentation, laboratory tests, and neuroimaging procedures (CT and MRI). Treatment needs to be initiated within 3 to 4 hours of symptom onset for reversibility of brain ischemia. Care in multidisciplinary stroke rehabilitation units appears to be most effective at reducing disability, dependency, and length of hospital stay for all stroke syndromes. Known coagulopathies should be corrected and oral anticoagulation reversed. Hypertension management is individualized. Elevated blood pressure can expand the hematoma, and low blood pressure can contribute to ischemia. Treatment of a hemorrhagic stroke, regardless of cause, is focused on (1) stopping or reducing the bleeding, (2) controlling cerebral edema and intracranial pressure, (3) preventing a rebleed, (4) preventing vasospasm, and (5) promoting tissue restoration and preventing or controlling seizures.”
References
Abdu, H., Tadese, F., & Seyoum, G. (2021). Comparison of ischemic and hemorrhagic stroke in the medical ward of Dessie Referral Hospital, Northeast Ethiopia: A retrospective study. Neurology Research International, 2021, 1–9. https://doi.org/10.1155/2021/9996958
Colasurdo, M., Chen, H., & Gandhi, D. (2024). MR imaging techniques for acute ischemic stroke and delayed cerebral ischemia following subarachnoid hemorrhage. Neuroimaging Clinics of North America. https://doi.org/10.1016/j.nic.2023.12.002
McCance, K. L., Huether, S. E., Rogers, J. L., & Brashers, V. L. (2023). Pathophysiology: The biological basis for disease in adults and children (9th ed.). Elsevier Mosby.
Pinho J, Costa AS, Araújo JM, Amorim JM, Ferreira C. Intracerebral hemorrhage outcome: A comprehensive update. J Neurol Sci. (2019); 398:54–66. doi: 10.1016/j.jns.2019.01.013
