Stroke

Chapter 101


Stroke




Perspective



Background


Stroke is the third leading cause of death in the United States and a leading cause of long-term disability.1 It affects about 795,000 people per year. On average, someone has a stroke every 40 seconds, and someone dies of a stroke every 4 minutes.2 Stroke patients have an in-hospital mortality rate of 5 to 10% for ischemic stroke and 40 to 60% for intracerebral hemorrhage (ICH).3 Only 10% of stroke survivors will recover completely. The remaining survivors will be left with an impairment that will often necessitate rehabilitation.4 The estimated direct and indirect cost of stroke in the United States in 2010 was $73.7 billion.2


Stroke can be defined as any vascular injury that reduces cerebral blood flow (CBF) to a specific region of the brain, causing neurologic impairment. The onset of symptoms may be sudden or stuttering, often with transient or permanent loss of neurologic function. Approximately 87% of all strokes are ischemic in origin, caused by the occlusion of a cerebral vessel.2 Approximately 13% are hemorrhagic strokes caused by the rupture of a blood vessel into the parenchyma of the brain (ICH) or into the subarachnoid space (subarachnoid hemorrhage [SAH]).2 Only ischemic stroke and ICH are discussed in this chapter.


Before the development of interventional strategies, treatment for stroke consisted of stabilization, observation, and rehabilitation. More recently, a better understanding of the pathophysiology of neuronal injury and the introduction of new therapies have led to a shift from observation to early evaluation and treatment. Current interventional treatment regimens include blood pressure (BP) management, anticoagulation, thrombolytic therapy, catheter-based interventions, and surgery. The key to success is early identification and treatment of patients with stroke before neurologic deficits become irreversible.



Epidemiology



Ischemic Stroke


An estimated 610,000 “first-ever” ischemic strokes occur each year in the United States.2 These may result either from in situ thrombosis or embolic obstruction from a more proximal source, usually the heart. In more than one third of these first-ever strokes, no clear cause is identified5–7 (Table 101-1).



Approximately one third of all ischemic strokes are thrombotic in nature. These can be caused by either large- or small-vessel occlusions. Common areas for large-vessel occlusions are cerebral vessel branch points, especially in the distribution of the internal carotid artery. Thrombosis usually results from clot formation in the area of an ulcerated atherosclerotic plaque that forms in the area of turbulent blood flow, such as a vessel bifurcation. A marked reduction in flow results when the stenosis occludes more than 90% of the blood vessel diameter. With further ulceration and thrombosis, platelets adhere to the region. A clot then either embolizes or occludes the artery.


Lacunae, or small-vessel strokes, involve small terminal sections of the vasculature and more commonly occur in African Americans and patients with diabetes and hypertension.5 A history of hypertension is present in 80 to 90% of patients who experience lacunar strokes. The subcortical areas of the cerebrum and brainstem often are involved. The infarcts range in size from a few millimeters to 2 cm and are seen most commonly in the basal ganglia, thalamus, pons, and internal capsule. They may be caused by small emboli or by a process termed lipohyalinosis, which occurs in patients with hypertensive cerebral vasculopathy. Although nearly 20 lacunar syndromes have been described, the most common of these lacunar syndromes are pure motor strokes, pure sensory strokes, or ataxic hemiparesis. Because they are subcortical and well localized, lacunar strokes do not typically cause cognitive impairment, aphasia, or simultaneous sensorimotor findings.


One fourth of all ischemic strokes are cardioembolic in nature.5,6 Embolization of a mural thrombus in patients with atrial fibrillation is the most common mechanism, and patients with atrial fibrillation have an approximate fivefold increased risk for development of a stroke.8 In addition, roughly 45% of all embolic strokes occur as a result of atrial fibrillation.8 Noncardiac sources of emboli may include diseased portions of extracranial arteries, resulting in an artery-to-artery embolus. One common example is amaurosis fugax, in which emboli from a proximal carotid artery plaque embolizes to the ophthalmic artery, causing transient monocular blindness.


Another cause of stroke is recent myocardial infarction (MI). Approximately 12 ischemic strokes occur per 1000 nonfatal MI patients within 1 month after the index event. Furthermore, 11 ischemic strokes occur per 1000 nonfatal MI patients in the post-MI hospitalization period. Independent predictors of stroke after acute MI are advanced age, diabetes, hypertension, history of previous stroke, anterior location of index MI, previous MI, atrial fibrillation, heart failure, and nonwhite race.9 The use of aspirin has been shown to reduce the incidence of post-MI stroke by 46%.10


Approximately 3 to 4% of all strokes occur in patients aged 15 to 45 years. Although atherosclerosis is the most common cause in older patients, causative disorders and conditions in younger patients often are uncommon and may be reversible. Pregnancy, the use of oral contraceptives, antiphospholipid antibodies (such as lupus anticoagulant and anticardiolipin antibodies), protein S and C deficiencies, sickle cell anemia, and polycythemia all predispose patients to sludging or thrombosis, thereby increasing the risk of stroke. Fibromuscular dysplasia of the cerebral vasculature also may lead to stroke, and in rare instances prolonged vasoconstriction from a migraine syndrome causes stroke. Recreational drugs such as cocaine, phenylpropanolamine, and amphetamines are potent vasoconstrictors that have been associated with both ischemic and hemorrhagic stroke.


Carotid and vertebral dissections often are associated with trauma but may follow such mild events as turning the head sharply. Carotid and vertebral dissections also are seen more frequently in people with underlying pathology of the vessel wall, such as in fibromuscular dysplasia and connective tissue disorders. Alteration in the vessel intima can lead to vessel stenosis, occlusion, or embolism. The patient may report a minor preceding event such as spinal manipulation, yoga, working overhead, coughing, or vomiting. Presenting manifestations may include headache, facial pain, visual changes, cranial nerve (CN) palsies, pain over the affected vessel, Horner’s syndrome, amaurosis fugax, SAH, or an ischemic stroke. The headache frequently is unilateral and may occur days before onset of the other neurologic symptoms.11 Although angiography has been the standard diagnostic study, dissections are increasingly being diagnosed by less invasive modalities such as ultrasonography, magnetic resonance angiography (MRA), and computed tomography angiography (CTA).12 Medical therapy includes early anticoagulation if SAH is not suspected. If symptoms recur despite anticoagulation, the patient may be eligible for endovascular intervention. Carotid or vertebral dissection is not considered a contraindication to use of tissue plasminogen activator (tPA) in the eligible patient.13 This entity is considered a major cause of stroke in younger patients.11,14,15


A transient ischemic attack (TIA) was historically defined as a neurologic deficit with complete resolution within 24 hours. However, advances in neuroimaging suggest that many such events represent minor stroke with resolved symptoms rather than true TIAs.16 Therefore the American Heart Association (AHA) recommends the following definition: a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction.17


From 200,000 to 500,000 TIAs per year are diagnosed in the United States, and emergency department (ED) visits for TIA occur at a rate of about 1 visit per 1000 population.16 TIAs constitute an important warning sign for the future development of cerebral infarction. Approximately 10% of the patients who experience a TIA will experience a stroke within 3 months of the sentinel event, and one half of these occur within the first 2 days.18



Hemorrhagic Stroke


Spontaneous ICH causes 10 to 15% of all acute strokes, affecting approximately 65,000 patients per year.19 It carries a 30-day mortality rate of up to 50%, with one half of patients dying in the first 2 days. Among survivors, only 1 in 5 are living independently at 6 months.3


The two major underlying causes of ICH are hypertensive vasculopathy (caused by long-standing hypertension) and cerebral amyloid angiopathy (usually found in elders, the result of amyloid deposition in cerebral vessel walls). Hypertensive hemorrhage results from degenerative changes in the small penetrating arteries and arterioles, leading to lipohyalinosis of small, deep penetrating arteries. Such hemorrhages generally occur in the deep regions including basal ganglia and thalamus. The most common sites for hypertensive hemorrhage are listed in Box 101-1. ICH caused by amyloid angiopathy tends to be lobar in nature and to occur more commonly in elders. Specific apolipoprotein E alleles appear to predispose to the development and recurrence of ICH.



BOX 101-1   Most Common Sites for Hypertensive Intracranial Hemorrhage



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Other factors leading to ICH include underlying vascular malformations, including arteriovenous malformations (AVMs) and aneurysms, drug intoxication (particularly sympathomimetics, such as cocaine), malignant hypertension, saccular aneurysms, blood dyscrasias, venous sinus thrombosis, hemorrhagic transformation of an ischemic stroke, moyamoya disease, and tumors. High-risk features for such secondary forms of ICH include lobar location, presence of intraventricular blood, and younger age.20



Principles of Disease



Pathophysiology


The cerebral vasculature supplies the brain with a rich flow of blood that contains the critical supply of oxygen and glucose necessary for normal brain function. When a stroke occurs, there are immediate alterations in CBF and extensive changes in cellular homeostasis. The normal CBF is approximately 40 to 60 mL/100 g of brain per minute. When CBF drops below 15 to 18 mL/100 g of brain per minute, several physiologic changes occur. The brain loses electrical activity, becoming electrically “silent,” although neuronal membrane integrity and function remain intact. Clinically, the areas of the brain maintaining electrical silence manifest a neurologic deficit, even though the brain cells are viable. When CBF is below 10 mL/100 g of brain per minute, membrane failure occurs, with a subsequent increase in the extracellular potassium and intracellular calcium and eventual cell death. The ischemic penumbra is the area of the brain surrounding the primary injury, which is preserved by a tenuous supply of blood from collateral vessels. This border zone of neuronal tissue is the area of greatest interest to investigators for possible salvage in both ischemic and hemorrhagic stroke. In ischemic stroke, the duration of occlusion plays a critical role in neuronal survival.21 Increasing the duration of occlusion increases both the irreversibility of deficits and the amount of cerebral infarction. Thus, ischemic stroke trials typically focus on the first few hours after symptom onset.


In ICH, acute vessel rupture is most often caused by underlying small vessel disease, as noted earlier, and causes injury by several mechanisms. First, there is mass effect from the hematoma itself, followed by activation of the coagulation cascade, release of inflammatory cytokines, and blood-brain barrier (BBB) disruption. This leads to perihematomal edema formation and secondary brain injury. Finally, continued bleeding, or hematoma expansion, occurs in many patients—either continued bleeding from the primary source or secondary bleeding at the periphery of the hemorrhage.19



Anatomy and Physiology


Blood is supplied to the brain by the anterior and posterior circulations. The anterior circulation originates from the carotid system and perfuses 80% of the brain including the optic nerve, retina, and frontoparietal and anterior-temporal lobes. The first branch off the internal carotid artery is the ophthalmic artery, which supplies the optic nerve and retina. As a result, the sudden onset of painless monocular blindness (amaurosis fugax) identifies the stroke as involving the anterior circulation (specifically the ipsilateral carotid artery) at or below the level of the ophthalmic artery. The internal carotid arteries terminate by branching into the anterior and middle cerebral arteries at the circle of Willis.


The anterior cerebral artery supplies the basal and medial aspects of the cerebral hemispheres and extends to the anterior two thirds of the parietal lobe. The middle cerebral artery feeds the lenticulostriate branches that supply the putamen, part of the anterior limb of the internal capsule, the lentiform nucleus, and the external capsule. Main cortical branches of the middle cerebral artery supply the lateral surfaces of the cerebral cortex from the anterior portion of the frontal lobe to the posterolateral occipital lobe.


Although the posterior circulation is smaller and supplies only 20% of the brain, it supplies the brainstem (which is critical for normal consciousness, movement, and sensation), cerebellum, thalamus, auditory and vestibular centers of the ear, medial temporal lobe, and visual occipital cortex. The posterior circulation is derived from the two vertebral arteries that ascend through the transverse processes of the cervical vertebrae. The vertebral arteries enter the cranium through the foramen magnum and supply the cerebellum by the posterior inferior cerebellar arteries. They join to form the basilar artery, which branches to form the posterior cerebral arteries.


The extent of injury in either an anterior or a posterior stroke depends on both the vessel involved and the presence of collateral blood flow distal to the vessel occlusion. A patient with excellent collateral blood flow from the contralateral hemisphere may have minimal clinical deficits despite a complete carotid occlusion. By contrast, a patient with poor collateral flow may have hemiplegia with the same lesion.



Clinical Features



Ischemic Stroke


The signs and symptoms of an ischemic stroke may appear suddenly and without warning or may have a stuttering, insidious onset. Disruption of the flow to one of the major vascular limbs of the cerebral circulation will result in physiologic disruption to the anatomic area of the brain supplied by that blood vessel. Ischemic strokes can be classified as anterior or posterior circulation strokes depending on the vasculature involved. The presence of neurologic deficits is highly dependent on collateral flow. In addition to the vascular supply involved, ischemic strokes can be further described by the temporal presentation of their neurologic deficits. A “stroke in evolution” is one in which focal neurologic deficits worsen over the course of minutes or hours. Approximately 20% of anterior circulation strokes and 40% of posterior circulation strokes will show evidence of progression. Anterior circulation strokes may progress within the first 24 hours, whereas posterior strokes may progress for up to 3 days. Propagation of thrombus is postulated as a likely mechanism for progression. With anterior circulation strokes (involving variously and primarily the carotid, anterior, and middle cerebral arteries), the clinical presentation rarely includes complete loss of consciousness unless the lesion occurs in the previously unaffected hemisphere of a patient who has experienced a previous contralateral stroke. Occlusions in the anterior cerebral artery mainly affect frontal lobe function. The patient has altered mentation coupled with impaired judgment and insight, as well as the presence of primitive grasp and suck reflexes on physical examination. Bowel and bladder incontinence may be features of anterior cerebral artery stroke. Paralysis and hypesthesia of the lower limb opposite the side of the lesion are characteristic. Leg weakness is more pronounced than arm weakness in anterior cerebral distribution stroke. Apraxia or clumsiness in the patient’s gait also may be noted.


Marked motor and sensory disturbances are the hallmarks of occlusion of the middle cerebral artery. They occur on the side of the body contralateral to the side of the lesion and usually are worse in the arm and face than the leg. Such disturbances may involve only part of an extremity or the face but almost always are accompanied by numbness in the same region as that of the motor loss. Hemianopsia, or blindness in one half of the visual field, occurs ipsilateral to the lesion. Agnosia, or the inability to recognize previously known subjects, is common, and aphasia may be present if the lesion occurs in the dominant hemisphere. Patients often have a gaze preference toward the affected hemisphere because of disruption of the cortical lateral gaze centers. The clinical aphorism is that a patient looks at a destructive lesion (stroke) but away from an irritative lesion (seizure focus).


Aphasia, a disorder of language in which the patient articulates clearly but uses language inappropriately or understands it poorly, also is common in dominant-hemisphere stroke. Aphasia may be expressive, receptive, or a combination of both. Wernicke’s aphasia occurs when the patient is unable to process sensory input such as speech and thus fails to understand verbal communication (receptive aphasia). Broca’s aphasia refers to the inability to communicate verbally in an effective way, even though understanding may be intact (expressive aphasia). Aphasia should be distinguished from dysarthria, which is a motor deficit of the mouth and speech muscles; the dysarthric patient articulates poorly but understands words and word choices. Aphasia is important to recognize because it usually localizes a lesion to the dominant (usually left) cerebral cortex in the middle cerebral artery distribution. Aphasia and dysphasia are terms that are used interchangeably but must be distinguished from dysphagia, which is difficulty in swallowing.


Pathology in the vertebrobasilar system (i.e., posterior circulation strokes) can cause the widest variety of symptoms and as a result may be the most difficult to diagnose. The symptoms reflect CN deficits, cerebellar involvement, and involvement of neurosensory tracts. The brainstem also contains the reticular activating system, which is responsible for mediating consciousness, and the emesis centers. Unlike those with anterior circulation strokes, patients with posterior circulation stroke can have loss of consciousness and frequently have nausea and vomiting. The posterior cerebral artery supplies portions of the parietal and occipital lobes, so vision and thought processing are impaired. Visual agnosia, the inability to recognize seen objects, may be a feature, as may alexia, the inability to understand the written word. A third nerve palsy may occur, and the patient may experience homonymous hemianopsia. One of the more curious facets of this syndrome is that the patient may be unaware of any visual problem (visual neglect). Vertigo, syncope, diplopia, visual field defects, weakness, paralysis, dysarthria, dysphagia, spasticity, ataxia, or nystagmus may be associated with vertebrobasilar artery insufficiency. Posterior circulation strokes also demonstrate crossed deficits, such as motor deficits on one side of the body and sensory loss on the other. In anterior circulation strokes, by contrast, abnormalities are always limited to one side of the body.


A focused neurologic examination should assess level of consciousness, speech, CN function, motor and sensory function, and cerebellar function. Level of consciousness and fluency of speech can be rapidly assessed in a dialogue with the patient to determine the presence of dysarthria or aphasia. The head should be evaluated for signs of trauma. Pupillary size and reactivity and extraocular movements provide important information about brainstem function, particularly CN III through CN VI; an abnormal third nerve function may be the first sign of tentorial herniation. Gaze preference suggests brainstem or cortical involvement. Central facial nerve weakness from a stroke should be distinguished from the peripheral causes of CN VII weakness. With a peripheral lesion, the patient is unable to wrinkle the forehead. Assessment of facial sensation, eyebrow elevation and squinting, smiling symmetry, gross auditory acuity, gag reflex, shoulder elevation, sternocleidomastoid strength, and tongue protrusion complete the CN evaluation.


Motor and sensory testing is performed next. Muscle tone can be assessed by moving a relaxed limb. Proximal and distal muscle group strength is assessed against resistance. Pronator drift of the arm is a sensitive sign of motor weakness and can be tested simultaneously by having the patient sit with eyes closed and arms outstretched, with palms toward the ceiling, for 10 seconds. Asymmetrical sensation to pain and light touch may be subtle and difficult to detect. Double simultaneous extinction evaluation tests for sensory neglect and can be easily performed by simultaneously touching the right and left limbs. The patient may feel both the right and left sides being touched individually but may not discern touch on one side when both are touched simultaneously. Similarly, the ability to discern a number gently scratched on a forearm, graphesthesia, is another easily tested cortical parietal lobe function. These tests can help differentiate a pure motor deficit of a lacunar stroke from a sensorimotor middle cerebral artery deficit.


Cerebellar testing and the assessment of reflexes and gait complete the examination. Finger-to-nose and heel-to-shin evaluations are important tests of cerebellar functions. Asymmetry of the deep tendon reflexes or unilateral Babinski’s sign may be an early finding of corticospinal tract dysfunction. Gait testing is commonly omitted yet is one of the most informative parts of the neurologic examination. Observing routine ambulation and heel-to-toe walking can assess for subtle ataxia, weakness, or focal cerebellar lesions.


The National Institutes of Health Stroke Scale (NIHSS) is a useful and rapid tool for quantifying neurologic deficit in patients with stroke and can be used in determining treatment options22 (Box 101-2). NIHSS scores have been shown to be reproducible and valid and to correlate well with the amount of infarcted tissue on CT scan.23,24 The baseline NIHSS score can identify patients who are appropriate candidates for fibrinolytic therapy as well as those at increased risk for hemorrhage. In addition, it has been used as a prognostic tool to predict outcome and is currently being used by some stroke centers to stratify patients for entry into treatment trials.22



BOX 101-2


National Institutes Of Health (NIH) Stroke Scale Scoring Form



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EOM, extraocular movement; L, left; NLF, nasolabial fold; R, right; UMN, upper motor neuron.


Modified from online document. Massachusetts General Hospital Stroke Service. NIH stroke scale materials. Scoring form. Available at http://www2.massgeneral.org/stopstroke/pdfs/scoring_form.pdf. Accessed March 6, 2013.



Hemorrhagic Stroke


The classic presentation of ICH is the sudden onset of headache, vomiting, severely elevated BP, and focal neurologic deficits that progress over minutes. Similar to ischemic stroke, ICH is often associated with a motor and sensory deficit contralateral to the brain lesion. Almost 40% of patients will demonstrate significant growth in hemorrhage volume within the first few hours.25


Although headache, vomiting, and coma are common, many patients do not have these findings, and the clinical presentation can be identical to that of patients with ischemic stroke; the two cannot reliably be differentiated in the absence of neuroimaging (Table 101-2).



Ongoing assessment of airway and mental status is of paramount importance in patients with ICH because precipitous deterioration is always a possibility. Emergency airway management requires careful judgment. On the one hand, airway control can prevent aspiration, hypoxia, and hypercarbia; on the other, sedation and paralysis can make it difficult to follow the neurologic examination, which can help monitor for hemorrhage expansion, elevated intracranial pressure (ICP), seizure activity, and brainstem herniation.


As with ischemic stroke, a careful neurologic examination is important in localizing the region and extent of injury. Baseline NIHSS and Glasgow Coma Scale (GCS) scores can be used to assess stroke severity, although the GCS score may be more feasible to follow for neurologic deterioration (Box 101-3). In addition, serial examinations can detect early changes that may suggest ongoing bleeding during the acute phase.



BOX 101-3   Glasgow Coma Scale




Poor prognostic indicators for patients with ICH include a decreased level of consciousness on arrival, intraventricular hemorrhage, and large ICH volume, all of which can be assessed in the ED. The ABC/2 technique is a quick and accurate method of measuring ICH volume at the bedside26 (Fig. 101-1). One validated tool to predict outcome is the ICH score (Box 101-4)21: Patients are given 0 to 2 points for GCS score, 1 point for age over 80, 0 to 2 points for ICH volume, 1 point for presence of intraventricular blood, and 1 point for hemorrhage location. This score has been shown to predict short- and long-term mortality.



BOX 101-4


Intracerebral Hemorrhage (ICH) Score


Predicting Mortality after Acute ICH



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Adapted from Hemphill JC, et al: The ICH Score. Stroke 32:891-897, 2001.




Differential Considerations



Ischemic Stroke


Extra-axial collections of blood secondary to trauma can mimic stroke. An epidural or subdural hematoma can cause an altered mental status, focal neurologic signs, and rapid progression to coma. Elders, who represent the age group at highest risk for stroke, can be victims of recurrent falls that lead to chronic subdural hematomas. Carotid dissection may occur after neck trauma or sudden hyperextension and may be associated with focal neurologic signs and symptoms, as with an aortic dissection that extends into the carotid arteries. The diagnosis is supported by a compatible history or relevant findings on computed tomography (CT) imaging or magnetic resonance imaging (MRI).


Other structural lesions that may cause focal neurologic signs include brain tumors and abscesses. Air embolism should be suspected in the setting of marked atmospheric pressure changes, such as in scuba diving or during medical procedures or injuries that may allow air into the vascular system. Seizures, altered mental status, and focal neurologic findings also may be manifestations of air embolism.


Metabolic abnormalities also can mimic stroke syndromes. Hypoglycemia often is responsible for an altered mental status and is a well-known cause of sustained focal neurologic symptoms that can persist for several days. Wernicke’s encephalopathy causes ophthalmoplegia, ataxia, and confusion that can be mistaken for signs of cerebellar infarction.


Migraine may present with focal neurologic findings, with or without headache. A seizure followed by Todd’s postictal paralysis may mimic stroke. Bell’s palsy, labyrinthitis, vestibular neuronitis, peripheral nerve palsy, and demyelinating diseases may all mimic stroke. Ménière’s disease may be difficult to distinguish from a posterior circulation stroke or TIA. Dizziness, vertigo, hearing loss, and tinnitus in Ménière’s disease are common, whereas difficulties with vision or speech or other focal symptoms are uncommon.


Like stroke, giant cell arteritis is a disease of elders. It may cause severe headache, visual disturbances, and, rarely, aphasia and hemiparesis. Other symptoms include intermittent fever, malaise, jaw claudication, morning stiffness, and myalgias. The diagnosis should be suspected in patients with a very high erythrocyte sedimentation rate (ESR) and is confirmed by temporal artery biopsy. Collagen vascular diseases such as polyarteritis nodosa, lupus, and other types of vasculitis may cause stroke syndromes.


Venous sinus thrombosis is another cause of focal neurologic symptoms that most commonly affects the superior sagittal sinus and lateral sinuses (see Chapter 105). The diagnosis of cerebral venous thrombosis can be difficult because of the nonspecific nature of symptoms, as well as the variable time frame of symptom onset (from hours to a few weeks). Patients may have generalized headaches, nausea, vomiting, paresis, visual disturbances, depressed level of consciousness, seizures or even symptoms generally ascribed to psychiatric disorders (such as depression).27 Depending on the location of the thrombus, physical examination of the patient may reveal papilledema, proptosis, or palsies of CNs III, IV, and VI, as well as other focal neurologic signs and symptoms.27 Multiple risk factors predisposing affected patients to venous sinus thrombosis are recognized, including trauma, infectious processes, hypercoagulable states, low-flow states, compression of the venous sinus, dehydration, various drugs (such as androgens, “ecstasy,” and oral contraceptives), and pregnancy or the postpartum state.

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Jul 26, 2016 | Posted by in ANESTHESIA | Comments Off on Stroke

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