Introduction
Cerebrovascular diseases commonly confront primary care providers. Stroke, the most common serious manifestation of cerebrovascular disease, is the fifth leading cause of death in the United States and a major cause of severe disability. It is the leading cause of hospitalization for neurologic disease. This review addresses many issues in the prevention, diagnosis, and management of cerebrovascular diseases, causing both ischemic and hemorrhagic stroke, that commonly confront primary care physicians.
Epidemiology
The 2022 update of the American Heart Association report “Heart Disease and Stroke Statistics” estimates that the prevalence of stroke in the United States in 2018 was approximately 2.7%, which translates into 7.6 million Americans 20 years of age or greater who had suffered a stroke, nearly 800,000 new or recurrent stroke events yearly and over 160,000 deaths. Age is the most important demographic risk factor, and although the incidence of stroke has fallen in recent years, the lifetime risk of stroke has increased due to the aging of the population. Female sex and African American race confer added risk. The estimated annual direct and indirect cost of stroke in 2017–18 was $52.8 billion.
The falling incidence of stroke since 1999 correlates with improvements in control of cardiovascular risk factors—improved control of hypertension, diabetes mellitus, and hyperlipidemia and lower rates of smoking—and in better stroke preventive treatment of cardiac arrhythmias. This means that primary care physicians are in the most important position to minimize the burden of stroke in the population.
ISCHEMIC STROKE
Ischemic Stroke: Pathology, Pathophysiology, and Stroke Types
Pathophysiology and Classification of Ischemic Stroke
The primary lesion of ischemic stroke is cerebral infarction. With an inadequate supply of blood to cerebral tissue, there is first a reversible loss of tissue function and, given enough time, infarction of tissue with loss of neurons and supportive structures. Ischemia sets off a cascade of events that begins with loss of electrical function and passes through disturbance of membrane channel function with calcium influx, leading to calcium-dependent excitotoxicity, generation of reactive oxygen species, and ultimately completes destruction of cell membranes and lysis of cells at its extreme, leaving a cavitation at the site of infarction.
There are several different mechanisms of vascular occlusion and many diseases that may underlie them ( Boxes 5.1 and 5.2 ).
Embolism
Cardioembolism
Artery-to-artery embolism
Paradoxical embolism
Large vessel disease
Atherosclerotic stenosis of occlusion
Arterial dissection
Small vessel disease
Other identifiable underlying causes
Hypercoagulability etc.
No identified cause despite extensive evaluation
Embolism
Infective endocarditis
Nonbacterial thrombotic (marantic) endocarditis
Embolism of other materials: calcium, fat, air, amniotic fluid, medical devices
Hypercoagulability (see below)
Large vessel disease
Moyamoya disease and moyamoya syndrome
Large vessel vasculitis
Small vessel disease
Small vessel vasculitis
CADASIL a
a Cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy.
and other inherited vasculopathies
Cerebral amyloid angiopathy (more commonly causes hemorrhage)
Hypercoagulability
Hypercoagulability of malignancy
Antiphospholipid antibody syndrome
Inherited and acquired clotting disorders (most commonly cause venous thrombosis)
Hypercoagulability of pregnancy
Sickle cell disease (with or without secondary moyamoya syndrome)
Infections
Infective endocarditis (see above)
Zoster ophthalmicus (an infectious form of vasculitis)
Syphilis
Tuberculosis and angioinvasive fungi (e.g., Aspergillus )
Cerebral venous thrombosis
Embolism is the commonest mechanism of stroke ( Fig. 5.1 ). The great majority of emboli are blood clots generated from the heart ( cardioembolism ) due to cardiac disease. Common cardiac disorders leading to stroke include atrial fibrillation, valvular heart disease, and cardiomyopathy from coronary artery disease with myocardial infarction or hypertension. Less common causes of cardiomyopathy (e.g., viral, drug-induced, infiltrative, hereditary, or idiopathic) leading to low left ventricular ejection fraction, arrhythmia, and intracardiac thrombus formation may also cause embolic strokes. Right-to-left shunting, most commonly from patent foramen ovale or from congenital heart disease, may lead to paradoxical embolism from the venous circulation. Artery-to-artery embolism occurs when a thrombus, usually in association with atherosclerotic plaques or at sites of arterial dissection, is dislodged from a large vessel wall and flows distally to lodge in smaller downstream vessels. Much less common, but important to consider in the right circumstances, material other than thrombus may embolize to cause strokes. Calcium may embolize from calcified atherosclerotic lesions. Fat may embolize after fracture of or surgery on long bones and in the setting of sickle cell crisis. Air may embolize during the placement or removal of intravenous catheters or during open heart and intravascular surgery. Amniotic fluid may embolize in the course of labor and delivery. Finally, intravascular medical devices may embolize when fractured or dislodged.
Large vessel disease is another common underlying cause of stroke ( Fig. 5.2 ). Large vessel atherosclerotic disease , most commonly in the proximal cervical internal carotid arteries, but also at times in the more distal internal carotid arteries, in the aorta, the vertebral and basilar arteries, or intracranially, may cause strokes. Arterial dissection affecting any of these vessels is the next most common cause of large vessel disease. Arterial dissection is a common cause of stroke in young patients without alternative risk factors and in patients with certain predisposing conditions. The most common cause of arterial dissection is major trauma or minor trauma from vigorous coughing, vomiting, or chiropractic manipulation. Diseases that compromise the integrity of connective tissues may predispose patients to arterial dissection, including fibromuscular dysplasia, Marfan syndrome, vascular Ehlers-Danlos syndrome, and Loeys-Dietz syndrome. Many arterial dissections occur without any apparent provocation and without any of these disorders. Many such patients likely harbor genetic polymorphisms that render them vulnerable to minor traumas of everyday life. The commonest mechanism by which large vessel disease leads to stroke is artery-to-artery embolism so large vessel disease and embolism are overlapping categories defining stroke mechanisms. Large vessel stenosis or occlusion may alternatively lead to low flow in distal branches, typically causing infarction in the border zones of converging perfusion fields ( Fig. 5.3 ).
Small vessel disease typically causes small, deep strokes. Ischemia extends around occluded distal arteries to create oval “little lakes” of infarction, so-called lacunar strokes. Small penetrating arteries, which are most vulnerable to the effects of chronic hypertension and other risk factors, are most commonly affected. Common sites for lacunar infarction that may cause recognizable clinical presentations include the posterior limb ( pure motor hemiplegia and ataxic hemiparesis ) and genu ( clumsy hand-dysarthria ) of the internal capsule, the basis pontis ( pure motor hemiplegia and clumsy hand-dysarthria ), the thalamus ( pure hemisensory and contralateral cerebellar syndrome ) ( Fig. 5.4 ), and the cerebellum. Other sites of deep white matter infarction may cause symptoms that are referable to their locations.
Many other uncommon vascular and hematologic lesions may cause vascular disease with occlusion or embolism leading to strokes. Many of these less common causes of stroke are listed in Box 5.2 .
Pathophysiology: Time Course of Blood Flow Deficit
The progression of cerebral tissue to irreversible infarction depends on the magnitude of the drop in cerebral blood flow and the duration of this drop. With a fall in cerebral blood flow by approximately 50%, the oxygen extraction from perfusing blood is increased to compensate for the drop in flow, and the patient remains asymptomatic. With a further fall in cerebral blood flow, reversible neuronal dysfunction occurs, leading to ischemic symptoms, typically deficits of function corresponding to the location of the ischemia and the topographic representation of function. If flow is restored rapidly enough, neuronal function returns without infarction, and the patient is said to have had a transient ischemic attack . If, on the other hand, flow-causing ischemia lasts long enough, irreversible tissue injury occurs, leading to the pathophysiologic events described above for cerebral infarction or ischemic stroke . The time from the onset of symptoms until the onset of irreversible tissue injury depends, in each area of the brain, on the magnitude and duration of the drop in cerebral blood flow ( Fig. 5.5 ). Infarction occurs earlier, sometimes within minutes, in the core of the lesion, where flow is lowest, and it may occur much later in the periphery of the lesion, where flow is nearer the threshold of reversibility. This understanding of the time course of cerebral infarction leads to the concept of the infarct core surrounded by a periphery of tissue at risk and the penumbra surrounded by a periphery of oligemic tissue that is not at risk of infarction ( Fig. 5.6 ). The delay in the development of infarction depends in large part on the adequacy of collateral circulation, the supply of blood to the peripheral zone of ischemia by alternative vessels that normally perfused adjacent areas. The duration of delay until the completion of infarction varies from minutes to many hours. This provides both an opportunity for urgent therapy to restore blood flow and an imperative to act rapidly before the window of opportunity to minimize the stroke volume closes.
Ischemic Stroke: Diagnostic Imaging
After initial evaluation to establish airway and circulatory stability, a patient presenting with acute onset of a focal neurologic deficit should undergo a rapid, focused history and examination. The history should elicit, as nearly as can be determined, the time the patient was last seen well, relevant details of onset risk factors, medications, and clues of possible relevant illness. A rapid focused examination should record the vital signs, including the heart rate and rhythm, blood pressure (BP), and the presence or absence of fever, and signs of possible endocarditis or other immediately relevant illness. The patient should then proceed immediately to the scanner for urgent brain imaging.
A noncontrast head computed tomography (CT) is, in most institutions, the first study of choice. CT is widely available and can be completed rapidly. The CT is reviewed with special attention to the following: (1) hemorrhage or other alternative nonstroke diagnoses that might explain the presentation, (2) signs of infarction, and (3) evidence of the site of vascular occlusion. Hemorrhage appears as hyperdensity on the head CT. Acute hemorrhage represents an absolute contraindication for intravenous thrombolytic therapy, so it is important to review the images carefully to rule it out. Early in the evolution of an ischemic stroke in the middle cerebral artery territory, the earliest signs of infarction are most commonly in the insula and the deep basal ganglia, especially the putamen. Early signs of infarction include loss of gray-white differentiation due to decreased density in gray matter structures such as the insular cortex ( insular ribbon sign ) or the deep gray matter (loss of putaminal definition). Loss of gray-white differentiation might be seen elsewhere as well. With more time, sulcal effacement due to tissue swelling, other signs of mass effect, and frank hypodensity are seen. The ASPECTS score is a grading scale that is commonly used to standardize communication about the extent of early infarction ( Fig. 5.7 ). Head CT may be normal early after onset of acute ischemic stroke, so the lack of hemorrhage or of an alternative cause for the focal deficit and the lack of a large completed stroke on CT provide adequate imaging to support urgent intravenous thrombolysis with alteplase or tenecteplase.
To plan for possible urgent endovascular thrombectomy, many centers typically add vascular imaging with CT angiography (CTA) to the initial CT study. This adds only a few minutes and offers much needed information. However, care must be taken that this does not delay initiation of treatment with IV thrombolysis.
CTA from the aortic arch to the crown allows the identification of large vessel occlusions that might be amenable to endovascular therapy and allows the endovascular team to plan their approach to therapy. It is important to review the entire study, including the chest, neck, and intracranial arteries, and the arteries outside of the area of the suspected stroke, to avoid errors in diagnosis.
Magnetic resonance imaging (MRI) is more sensitive for the early identification of acute ischemic stroke, yet it is not commonly used as the initial study because it takes longer to complete. However, when there is doubt about the diagnosis of stroke or when the timing of presentation or other aspects of the case demand a clearer early definition of the infarcted core or when iodinated contrast is contraindicated and urgent vascular imaging is needed, MRI may be useful. Diffusion-weighted (DWI) and apparent diffusion coefficient (ADC) sequences are nearly 100% sensitive in identifying acute infarction ( Figs. 5.2 and 5.4 ). MRI lesions that are bright on DWI and dark on ADC without early changes on the fluid attenuated inversion and recovery (FLAIR) are typical of acute strokes imaged less than approximately 6 hours after onset.
Magnetic resonance angiography (MRA) can demonstrate flow or stenosis or occlusion in the arteries of the chest, neck, and head. MRA is more likely than CTA to overestimate loss of flow.
Perfusion imaging to define the core and penumbra can be done with CT or MRI, and these studies are recommended in many cases presenting late and being considered for endovascular thrombectomy.
Diagnostic digital subtraction angiogram (DSA) remains the gold standard for vascular imaging, and DSA will be done urgently before proceeding to endovascular thrombectomy (see Fig. 5.1 ).
Ischemic Stroke: Acute Treatment
Acute treatment of stroke is directed at early reperfusion of tissue at risk with intravenous thrombolysis and/or endovascular thrombectomy and with optimization of hemodynamic status through management of fluid volume, BP, and cardiovascular status.
A revolution in acute stroke care began with the publication in 1995 of the NINDS trial of IV tissue-plasminogen activator (tPA alteplase) for acute ischemic stroke. This trial showed a benefit of urgent treatment for selected patients when IV tPA was started within 3 hours of onset, which was defined as the time the patient had last been seen well. A subsequent trial and meta-analyses extended the window for treatment with IV tPA to 4.5 hours in selected patients ( Box 5.3 ). Although beneficial overall many patients, especially those with proximal large vessel occlusions middle cerebral artery, stem, and internal carotid artery), do not respond to IV tPA with early recanalization. Fine-tuning of techniques of urgent endovascular thrombectomy has led to a second revolution in reperfusion therapy for patients with these common large vessel occlusions. All patients presenting within 6 hours of onset with significant functional deficits with a large vessel occlusion, without a large established stroke on CT or MRI, and without contraindications and selected patients up to 24 hours should be considered for endovascular thrombectomy. Selection for late-window (>6 hours) intervention is defined by imaging to confirm the likelihood of recoverable tissue at risk and a small established core infarct. Recent data suggest that many patients with significant areas of established infarction, and hence low ASPECTS scores, may still benefit from urgent endovascular thrombectomy.
Indications for IV thrombolysis
- 1.
Acute ischemic stroke with disabling deficit
- 2.
Onset time within 3–4.5 hours with these added exclusions:
- a.
Age > 80 years
- b.
NIHSS > 25
- c.
Taking oral anticoagulants
- d.
History of both diabetes mellitus and prior stroke
- a.
- 3.
Head CT without well-established infarct, hemorrhage, or alternative explanation for the focal neurologic deficit
- 1.
Absolute contraindications
- 1.
Head CT showing hemorrhage, or well-established infarct, or other diagnosis that contraindicates treatment, such as tumor, abscess
- 2.
Known CNS vascular malformation or tumor (except certain benign tumors, such as small meningiomas)
- 3.
Mild deficit
- 4.
Added exclusions for 3–4.5 hours, use (see above)
- 1.
Relative contraindications a
a In clinical practice where the risk of permanent disability due to stroke is felt to be great, judgments may favor therapy.
- 1.
Bacterial endocarditis
- 2.
Significant trauma within 3 months
- 3.
Stroke within 3 months
- 4.
History of intracranial hemorrahge or symptoms suspicious for SAH
- 5.
Major surgery within 14 days; minor surgery within 10 days, including liver or kidney biopsy, thoracocentesis, lumbar puncture
- 6.
Arterial puncture at noncompressible site within 7 days
- 7.
Gastrointestinal, urologic, or pulmonary hemorrhage within 21 days
- 8.
Known bleeding, diathesis, or hemodialysis
- 9.
aPTT > 40 seconds; INR >1.5; platelet count <100,000/mm 3
- 10.
SBP >185 or DBP >110, despite therapy to lower BP acutely
- 11.
Seizure at onset of stroke b
b This relative contraindication is intended to prevent the treatment of patients with focal deficits due to a cause other than stroke. If the deficit persists after correction of the glucose abnormality or if the rapid diagnosis of a vascular occlusion can be made by CT or MR angiography, then treatment may be indicated.
- 12.
Glucose <50 or >400 mg/dL b
- 1.
Prevention of Ischemic Stroke
While work in the last 25 years has greatly extended our capability to minimize the volume of acute strokes and preserve neurologic function in many cases, we can make our greatest contribution to stroke care and patient health by preventing strokes. The great majority of this care falls ultimately to primary care physicians. Stroke has fallen from the third to the fifth leading cause of death in the United States with a decreasing incidence in the last 25 years. However, the lifetime risk of stroke has increased, due to aging of the population, so the need for vigilance in preventive care has only increased. Success depends on the proper application of the various modalities of therapy, optimizing our choices of antiplatelet and anticoagulant therapies, optimal control of treatable risk factors, and selective referral for surgical therapies, when indicated.
Antiplatelet agents
Except when displaced by anticoagulants or when contraindicated due to bleeding risks, antiplatelet agents should be given for secondary stroke prevention in almost all patients after TIA or ischemic stroke. Low-dose aspirin is the mainstay of such therapy. Doses as low as 30 mg daily have shown success in clinical trials with endpoints including MI and cardiovascular death in addition to stroke. However, some patients with aspirin resistance will respond best to doses from 81 to 325 mg daily. This dose lowers the relative risk of recurrent stroke by approximately 20% per year. Clopidogrel and aspirin combined with dipyridamole confer risk reduction similar to that of aspirin. Clopidogrel may be chosen in patients with sensitivity to aspirin. Ticagrelor, like clopidogrel, blocks platelet P2Y12 receptors; however, it does not require metabolic activation and therefore may offer advantages over clopidogrel, especially in patients who carry the CYP2C19 trait, which limits the activation of the prodrug clopidogrel. Prasugrel is another prodrug that inhibits the platelet P2Y12 receptor. It has some potential pharmacologic advantages over clopidogel. Clinical trials so far suggest a clinical benefit for stroke prevention comparable to that of clopidogrel. Any of these alternatives may be chosen for patients who have events despite proper aspirin use.
Dual antiplatelet therapy for long-term use was tested in three trials and found to confer no long-term advantage over single-agent therapy. However, after TIA and nondisabling stroke, the greatest risk of recurrent stroke occurs in the first couple of weeks after the event. Dual antiplatelet therapy with combined aspirin and clopidogrel has been found in two large trials to confer lasting benefit if given for the first 3 weeks after TIA or a small stroke. The second of these trials gave aspirin for 3 months with no benefit over the 3-week regimen and a higher rate of adverse hemorrhagic effects.
Anticoagulants
Many clinical situations call for anticoagulation rather than antiplatelet therapy ( Box 5.4 ). The mainstay of oral anticoagulation was for many years warfarin. Since 2009 several new oral anticoagulants have been shown to be equivalent to warfarin, and in some cases safer, and they are more convenient, since they do not require INR monitoring.
Mechanical heart valve prosthesis
Atrial fibrillation (see also Box 5.5 )
Intracardiac thrombus
Hypercoagulable states
Cerebral venous sinus thrombosis
For nonvalvular atrial fibrillation (AF), stroke risk depends on the presence of other risk factors. This risk is commonly estimated based on the CHADS 2 VA 2 Sc score ( Box 5.5 ). Patients with a true lone AF CHADS 2 score 0–1 may not benefit from anticoagulation; those with scores ≥2 do benefit. Age is not a contraindication to anticoagulation. Although age does confer greater risk of hemorrhage from anticoagulant use, the proportional increase of stroke risk with age is yet greater, so the relative benefit of anticoagulation increases with age.
| CONDITION | POINTS |
|---|---|
| C—Congestive heart failure | 1 |
| H—Hypertension | 1 |
| A 2 —Age ≥75 years | 2 |
| DDiabetes mellitus | 1 |
| S 2 —Prior stroke or TIA or other thromboembolism | 2 |
| V—Vascular disease CAD, PAD, aortic plaque) | 1 |
| A—Age 65–74 years | 1 |
| Sc—Sex category (female) a | 1 |
a A point is given for female sex only if at least one other point is given. CAD , Coronary artery disease; PAD , peripheral artery disease.
The three factor Xa inhibitors, apixaban, rivaroxaban, and edoxaban, and the direct thrombin inhibitor dabigatran have all been shown to be roughly equivalent (noninferior) to warfarin for stroke prevention in AF. All may serve as appropriate substitutes. We typically choose apixaban based on the low risk of adverse effects and the favorable pharmacokinetics for twice daily dosing. Several studies suggest that rivaroxaban and apixaban may substitute for cancer-associated hypercoagulability. So far, studies comparing warfarin to the newer agents have not been promising in patients with antiphospholipid antibody syndrome; therefore we continue to recommend warfarin for that indication. Warfarin also remains the recommended anticoagulant for protection in patients with mechanical heart valve prostheses.
The 2017 COMPASS trial of low-dose rivaroxaban plus rivaroxaban versus aspirin alone is the first trial to show a benefit of anticoagulation in patients outside of the indications discussed previously. In this study, rivaroxaban 2.5 mg twice daily plus aspirin 100 mg daily was superior to rivaroxaban alone 5 mg twice daily and to aspirin alone 100 mg daily for primary prevention of stroke in patients with coronary or peripheral atherosclerotic vascular disease. This benefit came with a small increased risk of major bleeding.
Risk Factor Management
The major decline in the incidence of stroke in recent decades correlates with major improvements in the management of vascular risk factors, including smoking cessation and control of hypertension, hypercholesterolemia, and diabetes mellitus. Therefore it is most important to address all of these conditions for both primary and secondary stroke prevention. High-intensity statins with a goal LDL <70 are recommended for secondary stroke prevention in patients with atherosclerotic risk factors. It is also very important to encourage and support healthy lifestyles, including weight reduction, healthy diet, and regular exercise. We also recommend screening for obstructive sleep apnea and treatment of affected patients.
Surgical Therapies for Ischemic Stroke Prevention
Carotid endarterectomy . Patients with symptomatic stenosis of the cervical internal carotid artery of ≥50% benefit from carotid endarterectomy (CEA) if surgeons maintain low surgical risk. Endovascular placement of carotid artery stents (CAS) may be an alternative to CEA in selected patients. Studies from approximately 20 years ago found benefit of CEA in patients with asymptomatic carotid stenosis. However, a fall in the risk of stroke since these studies were done has raised doubt concerning the benefit of CEA or CAS in asymptomatic patients. This issue is currently under investigation in a large clinical trial. Until this issue is settled we recommend consultation with a vascular neurologist to help with optimal patient selection for CEA or CAS.
PFO closure . Patent foramen ovale (PFO) is a very common and usually benign condition with estimates of approximately 25% in the general population, depending on the mode of assessment. When patients with no or few vascular risk factors have embolic strokes and are found to have PFO the questions arise: Is the PFO related to the stroke? As a conduit for paradoxical embolism or by another mechanism? Will closure of the PFO lower the risk of recurrent stroke? And is it safe? There is good evidence that paradoxical embolism is a cause of stroke in many otherwise low-risk patients. The RoPE score is a useful tool to estimate the attributable risk in a particular patient. Initial trials of device closure for presumed symptomatic PFO suggested that the procedure can be done safely; however, they failed to establish clear benefit. More recent trials have shown benefit. Consultation with a vascular neurologist and interventional cardiologist with experience in this procedure is now recommended in patients with embolic stroke or TIA without apparent alternative cause and PFO.
External carotid-internal carotid (EC-IC) bypass and indirect surgical revasculariztion procedures . Controlled trials of EC-IC bypass for carotid occlusion have not shown benefit. However, in expert surgical hands, and in patients with cervical or intracranial vascular stenoses with high risk of stroke, especially in moyamoya syndrome, such procedures may be beneficial. This therapy remains unvalidated, and we recommend that symptomatic patients with such vascular occlusions be evaluated by neurologists and surgeons with expertise in this area.
Intracranial stenting . Studies of the placement of intracranial arterial stents in patients with symptomatic intracranial stenoses have not shown benefit. In fact, these studies have shown an excess of events in surgically treated patients. We currently treat such patients according to the protocol used in the medical arm of the SAMMPRIS trail, saving the option of intervention for exceptional patients with demonstrated higher risk.
Future Directions
Advances in recent decades in medical and surgical therapy have had a major impact on stroke care. The most important interventions continue to be the optimal application of available medical therapies for primary and secondary stroke prevention, that is, those interventions introduced and maintained by primary care physicians. Expertise is available to properly select patients for surgical therapies. Since 1995 there has been a revolution in the management of acute stroke which has led to the development of effective thrombolytic and endovascular therapies that can in many cases minimize the disability from strokes. The availability of these therapies has prompted the development of enhanced systems of stroke care to maximize patients’ access to advanced care.
Future refinements of stroke care will fine-tune the development of revascularization therapies and the systems of care to make them as accessible as possible. Further advances in vascular imaging will add to our understanding of cerebrovascular disease and to the most precise diagnosis and best management of patients. Neuroprotection, the use of drugs that protect neurons from ischemia and minimize stroke size or allow greater time for the application of reperfusion therapies, remains an unmet goal, and efforts to find such agents should continue. Genetic studies and studies of basic pathophysiology will help us to understand the basic mechanisms of cerebrovascular disorders and will, we anticipate, lead to improved therapies to allow us to further reduce the burden of ischemic stroke.
HEMORRHAGIC STROKE
Hemorrhagic Stroke: Pathology, Pathophysiology, and Types of Hemorrhage (Differential Diagnosis)
Pathophysiology and Classification of Hemorrhagic Stroke
The primary lesion of hemorrhagic stroke is extravascular blood that has escaped from the intravascular compartment to the brain or surrounding compartments. With escape of blood into these tissues, there may be displacement of normal structures, mass effect with elevation of intracranial pressure (ICP), and resultant compromise of cerebral perfusion, inflammation, release of bioactive substances with toxic effects, such as iron and endothelin, tissue edema, and swelling and herniation of cerebral contents outside of their normal containing boundaries, and vasospasm. Elevation of ICP, local edema, herniation, and vasospasm may compromise cerebral perfusion and lead to secondary infarction. These processes may ultimately lead to destruction of cerebral tissue and cavitation however if mitigated may result in reversible injury to tissues.
It is clinically useful to classify hemorrhagic strokes into the tissue compartments into which the bleeding occurs. Hemorrhage may occur in the parenchyma of the brain or spinal cord, within the brain’s ventricles, or in the subarachnoid space. (Hemorrhage may also occur within the subdural or epidural spaces; however, we do not classify such hemorrhages as strokes.) Many different vascular lesions and disorders may underlie hemorrhage into each of these locations ( Boxes 5.6 and 5.7 ).
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
