Ischemic Versus Hemorrhagic Stroke
The two categories of stroke are ischemic stroke and hemorrhagic stroke. Ischemic stroke pertains to having very little blood supply to provide parts of the brain with enough oxygen and nutrients, while hemorrhagic stroke pertains to too much bleeding within the enclosed cranial cavity.1 These two broad categories can be further subdivided based on different etiologies, clinical courses and outcomes, and treatment strategies which will be discussed in this article.
Stroke is a condition in which there is an acute neurologic insult that occurs as a result of ischemic cerebral infarction (80% of strokes) or brain hemorrhage (20% of stroke). A gross specimen of an infarcted brain will initially appear pale. After a few hours or days, the gray matter becomes congested, which is due to dilated blood vessels. Minute petechial hemorrhages may also be seen. Once the obstructing embolus moves, is lysed, or disperses, recirculation of blood to the infarcted area may cause a hemorrhagic infarction. Edema may form if there is a disruption of the blood-brain barrier. A cause of stroke that is unusual is one that is caused by an occlusion of the veins. This causes a backing up of fluid, resulting in brain edema. It may also cause brain ischemia and hemorrhage into the brain.
There are three subtypes of brain ischemia.2 Thrombosis refers to local obstruction of an artery. This obstruction may be due to arteriosclerosis, dissection, or fibromuscular dysplasia. There is thrombus formation. Embolism pertains to debris formed elsewhere that causes an obstruction. A source of embolism must be found and managed in order to treat the patient because local therapy is only a temporary intervention. Systemic hypoperfusion results from a systemic circulatory problem manifesting itself in the brain and other organs of the body. If a patient has a more general circulatory problem, it may manifest itself in the brain. This may cause stroke due to systemic hypoperfusion.
In brain hemorrhage, there can be bleeding directly into the brain parenchyma, which is called intracerebral hemorrhage. If bleeding occurs in the cerebrospinal fluid within the subarachnoid space, this is known as subarachnoid hemorrhage.
Intracerebral hemorrhage originates in the arterioles and small arteries. As the localized hematoma is formed within minutes or hours, it will continue to grow until its own pressure is enough to limit its spread, or until the hematoma decompresses itself into the ventricular system or cerebrospinal fluid.3-4 Intracerebral hemorrhage is caused by hypertension, trauma, substance abuse (cocaine and methamphetamines) and vascular malformations.3-4 It may also be due to tumors aneurismal rupture, or vasculitis. The clinical manifestations depend upon the site of the lesion. Deficits with limb, motor and/or sensory signs can be caused by a contralateral bleeding into the right putamen and internal capsule region. Difficulty with walking may be due to a bleed into the cerebellum. Clinical signs of aphasia may represent a bleed into the left temporal lobe. A hematoma that is large enough to cause a shift in the intracranial contents will cause headaches, vomiting or even a decreased level of consciousness. These are life-threatening conditions because the hematoma and brain edema may cause damage to brain tissues as it enlarges.
Subarachnoid hemorrhages are due to rupture of arterial aneurysms in the base of the brain or bleeding from vascular malformations. The sudden increase in intracranial pressure is secondary to the outpouring of blood into the cerebrospinal fluid. Death or deep coma will ensue if the bleeding continues. The symptoms are abrupt when compared to intracerebral hemorrhage, including rapid cessation of activity and severe headache. Minor hemorrhage occurs in 30% of patients and they often complain of sudden onset of severe headache. If bleeding occurs into the brain and cerebrospinal fluid, focal neurologic signs may ensue.
Neurologic examination of a stroke victim is assessed using the National Institutes of Health Stroke Scale or the Canadian Neurologic Scale. Once stroke has been identified, it is necessary for healthcare providers to determine whether the causality of stroke is secondary to ischemia or hemorrhage, with the goal of minimizing acute brain injury. This can only be established with the use of radiologic imaging modalities such as a CT-scan or an MRI. Therefore patients should only be transferred to a hospital with these imaging modalities available. A hemorrhagic etiology will necessitate prompt referral to a neurosurgeon for appropriate care. On the other hand, an ischemic etiology may indicate that the patient is a candidate for fibrinolytic therapy. The major concern for fibrinolytic therapy is the risk of inducing intracranial hemorrhage. A review of the inclusion and exclusion criteria for fibrinolytic therapy is tantamount.
Recombinant tissue plasminogen activator therapy should be given immediately to patients diagnosed with ischemic stroke within three hours from the onset of symptoms. The inclusion and exclusion criteria is available at this website: http://circ.ahajournals.org/content/122/18_suppl_3/S818.full.pdf+html
It is necessary to transfer stroke patients to a stroke unit so that they may receive treatment within 3 hours from arrival to the hospital. Stroke unit care should emphasize managing hypertension, glycemic control, temperature regulation and nutritional support. These efforts will increase the stroke patient’s chances of return to their previous quality of life.
- Caplan LR. Intracranial branch atheromatous disease: a neglected understudied, and underused concept. Neurology 1989; 39:1246.
- Caplan LR. Basic pathology, anatomy, and pathophysiology of stroke. In: Caplan’s Stroke: A clinical approach, 4th ed, Saunders Elsevier, Philadelphia 2009. P22.
- Kase CS, Caplan LR. Intracerebral hemorrhage. Lancet 1992; 229:656.
- Kase CS, Caplan LR. Intracerebral hemorrhage, Butterworth-Heinemann Boston 1996.