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Role of the Physical Examination in the Determination of Etiology of Ischemic Stroke
Correspondence Address: Source of Support: None, Conflict of Interest: None DOI: 10.4103/0028-3886.284386
Keywords: Clinical exam, ischemic stroke, neurologyKey Message: There are key findings in the physical examination of patients with ischemic stroke that have the potential to indicate the etiology of the infarct and/or to help to choose the use of ancillary tests. Therefore, the physical exam continues to be a valuable tool for the clinician.
The determination of the etiology of ischemic stroke (IS) is the initial step in providing specific secondary prevention measures and determining the patient's prognosis. However, it is also a challenge for the physician. A careful medical history and a focused physical examination can be helpful in identifying probable causes of IS and guiding subsequent confirmatory tests. In this review, we summarize the current literature regarding the physical exam in patients with suspected IS. We describe potential findings in the physical examination of the patient with IS and the implications of these findings for the determination of etiology.
References for this review were identified by electronic searches of Medline, Lilacs, Scielo, and searches of references from pertinent papers. No date limit was set, and we included papers published up to January 2019. Publication types were reviews, cohort studies, clinical trials, and case series. We systematically searched and reviewed papers published in English and used the following search terms. First term: “stroke,” “cerebrovascular accident,” “cerebrovascular disease,” “ischemic stroke,” “transient ischemic attack,” “cerebral infarction,” “cerebral thrombosis.” Second term: “clinical exam,” “clinical examination,” “physical exam,” “etiology,” “risk factors,” “infarction subtypes,” “vital signs,” “ophthalmology,” “auscultation,” “palpation,” “percussion.” On the basis of abstracts, one or more authors selected the papers for the review. We did not perform any kind of statistical analysis.
The primary vital signs are the simplest and most important part of the physical examination in any patient, including patients with stroke. The clinician should always take into account the bidirectional relationship between brain injury and vital signs. On one hand, certain alterations in vital signs can indicate specific stroke etiologies. On the other hand, these altered vital signs can be the product of the brain injury regardless of the etiology. Brain lesions affecting the insula are known to produce dysautonomic disorders such as hypertension bursts and arrhythmias.[1] Additionally, the predictable pattern of decline in the neurological status known as rostrocaudal deterioration manifests with alterations in respiratory pattern and frequency along with the changes in blood pressure associated with the Cushing response.[2]
When evaluating the cardiac frequency, one should take into account its regularity and synchrony with the peripheral arterial pulse, since any discrepancy indicates the presence of an arrhythmia. Among stroke patients, the occurrence of any kind of arrhythmia is a probable cause of the initial stroke; it is estimated that up to 35% of the population of >65 years of age have subclinical tachyarrhythmias which increase their stroke risk 2.5 times.[3] By far, the most common arrhythmia associated with IS is nonvalvular atrial fibrillation (AF), although valvular AF in association with rheumatic heart disease continues to be an important cause of stroke in low- and middle-income countries.[4] AF is the cause of IS in approximately 20% of all patients, although some authors believe that this is an underestimation.[5] Due to its intermittent nature, AF can be difficult to detect based solely on clinical grounds, but the assessment of AF during the primary vital signs evaluation is mandatory. Tachycardia and bradycardia at rest are abnormal findings associated with thyroid disease, which in turn can increase the risk of stroke. The presence of hyperthyroidism is associated with the development of AF, and the metabolic alterations secondary to hypothyroidism have been related to atherosclerotic progression and atherothrombotic stroke.[6] The pulse wave product of the ventricular systole propagates at an estimated velocity of 8–10 m/s; as mentioned earlier, this pulse wave should be synchronous and regular regardless of the place where it is measured. To correctly assess the pulse, the clinician's fingertips are positioned in places where a horizontal segment of an artery can be pressed over a bone. The finding of a decreased brachial artery pulse and decreased pulsation of one or both brachial arteries is one of the American College of Rheumatology (ACR) criteria for the classification of Takayasu arteritis, also known as the pulseless disease.[7] Such a decrease in pulse intensity correlates with the slowly progressive occlusive disease affecting the aorta, and its major branches are usually found in the angiogram [Figure 1] and with the severity and location of the resulting ischemia.
Giant cell arteritis (GCA) is another potential cause of stroke that can be detected through pulse abnormalities. GCA is most commonly associated with retinal ischemia and amaurosis but can also increase the risk of stroke.[8] Pulse abnormalities at the level of the temporal arteries are a part of the ACR criteria for GCA.[9] The temporal arteries can be palpated in front of the tragus and along the mid-portion of the temporal bone.[10] Both sides are usually palpated simultaneously. The absence of a pulse on one side or the presence of pain over the artery suggests temporal arteritis; advanced cases can show thickening or a “string-of-beads appearance” but these are difficult to palpate.
Hypertension (blood pressure values ≥140/90 mmHg) is one of the most important modifiable risk factors for stroke[11] and is present in up to 70% of all stroke patients on arrival.[12] However, these increases in BP are usually transient and resolve spontaneously. Current treatment guidelines[13] recommend the use of antihypertensive medication during the initial 24 h of acute IS only if BP is >220/120 mmHg. Regarding stroke etiology, for certain patients, it is advisable to register BP values in both arms. Differences in the BP values of >20 mmHg between sides are suggestive of subclavian artery stenosis, which can manifest as syncope and vertebral basilar IS [Figure 1]. A difference of ≥10 mmHg in BP values between arms is also a part of the ACR criteria for Takayasu arteritis.[14] Takayasu arteritis, also known as occlusive thromboaortopathy or Martorell syndrome, is a non-atherosclerotic vasculopathy capable of leading to the brain or retinal ischemic injury.[14] In addition to accounting for interbrachial differences, it is also important to assess the effect of different body positions on BP. Orthostatic hypotension, defined as a drop of >20 mmHg systolic, 10 mmHg diastolic, or both when an upright position is assumed,[15] has been linked to the presence of watershed infarction,[16] especially in patients with impaired autoregulation of cerebral blood flow.[17]
Approximately one-third of patients with IS have hyperthermia (body temperature >37.3°C) 4–6 h after the stroke onset. However, when hyperthermia appears after 10–12 h, it is related to a poor outcome.[18] In this regard, most elevations in body temperature are related to concomitant infection but in special populations (known valvular heart disease (VHD), the history of intravenous illegal drug use), fever can indicate the presence of infective endocarditis as the source of emboli.[19] Additional factors supporting this diagnosis are subtle vascular phenomena such as conjunctival hemorrhages, Janeway lesions, and splinter hemorrhages.[20] Fever is also a common symptom accompanying GCA.[21] Spontaneous hypothermia (body temperature <35.0°C) is an ominous sign that confers a higher risk of in-hospital death in patients with stroke; it is more common among patients with hemorrhagic stroke.[22]
Respiration rate and pattern abnormalities are common in rostrocaudal deterioration associated with malignant brain edema in middle cerebral artery infarction.[23] However, these findings are common to all causes of deterioration, and there is not a specific etiology of stroke associated with respiration rate irregularities. Chronic obstructive pulmonary disease (COPD) has been associated with an increased risk of stroke through various mechanisms.[24] Clinical findings of COPD such as diminished breath sounds,[25] increased anterior-posterior chest diameter, and the Hoover sign[26] can be obtained through physical examination alone but the significance of these findings is unclear.
The general appearance of a patient may provide diagnostic clues to the etiology of stroke. For example, tall and long-limbed individuals may have Marfan's syndrome, while Ehlers-Danlos syndrome features fragile skin and laxity of the joints. Both conditions predispose individuals to cervical artery dissections (CAD) and subsequent IS.[27],[28] An endomorph somatotype with central obesity and a body mass index >30 kg/m2 has also been related to a higher risk of vascular morbidity, metabolic syndrome, atherosclerosis, and stroke.[29],[30]
The finding of skin and hair abnormalities in patients with IS can indicate the presence of a variety of causes of stroke, either through direct mechanisms (an autoimmune disease) or through indirect mechanisms such as increased prevalence of traditional vascular risk factors. Among young patients with stroke (<45 years of age), autoimmune disorders (AD) constitute up to 35% of all stroke causes.[31] AD usually present with multiple cutaneous manifestations.[32] For example, systemic lupus erythematosus (SLE) can produce stroke through multiple mechanisms including vasculitis, hypercoagulable states, and cardioembolism due to Libman–Sacks (LS) endocarditis. SLE hair changes include the presence of alopecia areata[33] and subtle changes in hair diameter in the frontal and temporal areas known as “lupic hair.”[34] Another cutaneous manifestation of SLE is livedo (a persistent violaceous, red or blue pattern on the skin of the trunk, arms, or legs that does not disappear on warming). Livedo may consist of a regular pattern of broken circles (livedo racemosa) or a pattern of unbroken circles (livedo reticularis) [Figure 2] and is usually found in conjunction with antiphospholipid antibody syndrome (AAS).[35]Livedo racemosa is also found in patients with a rare noninflammatory thrombotic vasculopathy called Sneddon syndrome that can cause transient ischemic attacks and infarction.[36]
SLE patients can also exhibit oral or nasopharyngeal ulcers and the classic malar erythema; both cutaneous findings are part of the clinical criteria for the diagnosis of the disease.[37] Red coloration of the skin can also be found in patients with increases in the hematocrit that result in increased blood viscosity that in turn promotes ischemic heart disease and stroke.[38] Such increases in the hematocrit are observed in patients with polycythemia vera or polycythemia secondary to COPD; in these cases, it is also common to find marked conjunctival erythema and injection. Severe injection and subconjunctival hemorrhage (hyposphagma) can indicate the presence of carotid occlusive disease due to the augmentation of the flow rate through the anastomotic pathway between the internal and external carotid arteries.[39] Hyposphagma can also be a sign of an advanced case of carotid-cavernous sinus fistula and is usually accompanied by chemosis, ophthalmoplegia, and retro-orbital pain.[40] While examining the eyes, one may observe xanthelasma palpebrarum, the most common form of cutaneous xanthoma frequently associated with primary or secondary hyperlipidemias and known to increase the risk of stroke [Figure 3].[41] Psoriasis, commonly manifested as psoriatic plaques found on the scalp, elbows, and/or knees, is another inflammatory disease that can cause accelerated atherosclerosis and is associated with a higher risk of AF.[42]
Heart sounds Cardiac auscultation should be performed in all patients with stroke since cardiac emboli are the cause of approximately 20% of strokes. The likelihood of a cardiac source of stroke is increased when cortical or cerebellar infarcts are present, when patients do not have traditional risk factors for atheroma or lacunar infarct and when patients are young. The occurrence of a stroke during a spontaneous Valsalva maneuver suggests the presence of a paradoxical embolism and should prompt the investigation of a thrombotic source in the lower extremities.[43] As mentioned earlier, the most common cardiac abnormalities are AF and VHD. These abnormalities, in conjunction with infectious endocarditis, recent acute myocardial infarction, sick sinus syndrome, dilated cardiomyopathy, and cardiac myxoma, constitute the major cardioembolic sources of stroke.[44] Cardiac auscultation findings associated with AF include variation in the intensity of the first heart sound and absence of a fourth sound that was previously present (while the patient was in sinus rhythm). Atrial flutter may also produce similar findings, except that the rhythm may be regular and rapid venous oscillations may occasionally be visible in the jugular pulse. Since the most common cause of chronic AF is mitral valve disease (MVD),[45] it is always mandatory to auscultate for a systolic murmur over the mitral valve auscultation area of the chest and left axilla. Cranial and orbital auscultation Cranial and orbital bruits result from turbulence in the intracranial or extracranial vessels; they are usually systolic and may originate within the cranium or be transmitted from arteries in the neck. The presence of these bruits frequently indicates atherosclerotic stenosis, but the existence of a carotid-cavernous sinus fistula should always be investigated as well.[40]
Cervical bruits arise from neck arteries, and it is possible to auscultate not only the carotid circulation but also the vertebral and subclavian arteries. Carotid bruits are the result of turbulent flow across the vessel; thus, intrinsic stenosis or, occasionally, arterial tortuosity and kinking can produce them. They are present during systole and are short and high-pitched.[46] The examiner should always ask the patient to hold his or her breath in order to eliminate breathing sounds and place the diaphragm of the stethoscope under the angle of the mandible, being careful not to apply excessive compression that could lead to rupture or dislodgement of the subjacent atherosclerotic plaque.[47] Approximately, 75% of patients with carotid bruit have at least 50% stenosis. However, the ability to detect a bruit decreases in high-grade (90–90%) stenosis, resulting in low overall sensitivity.[48] Supraclavicular bruits during systole are a frequent finding in normal children and in adults with subclavian or vertebral artery stenosis. Supraclavicular auscultation can be used to evaluate vertebral artery occlusive symptoms, arm claudication, or “subclavian steal” in adults with atherosclerosis or compression of the subclavian artery. Both atherosclerosis and compression of the subclavian artery can lead to brachial ischemia and, in rare cases, retrograde embolism toward the vertebral artery. Frequent additional findings are unilateral Raynaud's phenomenon,[49] brittle nails, and digital ulcers. In addition to supraclavicular auscultation, Adson's test (checking for the loss of the radial pulse in the arm by rotating the head to the ipsilateral side with extended neck following deep inspiration) and Wright's test (looking for weakening or disappearance of the radial pulse when the arm is abducted and externally rotated) can be helpful in determining the presence of subclavian artery compression. Eye examination Monocular amaurosis is a well-known symptom of acute retinal ischemia frequently caused by thromboembolic and carotid artery diseases. However, eye symptoms related to carotid artery disease can sometimes have a chronic or subacute course. The resulting syndrome, known as ocular ischemic syndrome (OIS), hypoperfusion/hypotensive retinopathy, or ischemic oculopathy,[50] can be identified by the progressive and painless loss of visual acuity, as well as one or more of the following symptoms: Iris atrophy and neovascularization, secondary glaucoma, peripheral retinal microaneurysms, punctiform retinal hemorrhages, retinal veins dilatation and tortuosity, and papilledema [Figure 4]. These manifestations of OIS are present in 4–18% of patients with severe carotid stenosis or carotid occlusion.[51]
Ophthalmoscopy Ophthalmoscopic observation of cholesterol embolus (Hollenhorst plaque) in a blood vessel of the retina is a sign that indicates an increased risk of subsequent ipsilateral transient ischemic attack or IS.[52] Interestingly, such plaques infrequently correspond to locations of visual field defects in retinal ischemia.[52] Hypertensive retinopathy is a much more common finding in patients with IS that can help distinguish between the reactive rise in BP seen during the first hours after IS and chronic undiagnosed hypertension. The presence of hypertensive retinopathy (which includes microaneurysms, soft exudates, hard exudates, macular edema, intraretinal microvascular abnormalities, venous beading, new vessel formation and, generalized arteriolar narrowing) also predicts the long-term risk of stroke, independent of blood pressure in patients without acute stroke.[53]
Current trends in medical practice tend to place the physical examination in a secondary role when evaluating a patient.[54] Nevertheless, the physical examination of patients continues to provide valuable information, and patients with IS are no exception. Even though the diagnosis of IS cannot be made without the aid of neuroimaging, it is clear that the physical examination can provide helpful indicators regarding the etiology of IS. Information from the physical examination can, thus, lead to better use of diagnostic tools and confirmatory tests, which in turn can reduce the time to etiology-based treatment and/or secondary prevention of IS. We hope that the present review serves as a reminder to all clinicians to not overlook this fundamental tool of the medical profession. Acknowledgements Dr. Thammar Gómez from the Instituto Nacional de Neurologia y Neurocirugia and Dr. Gabriela Calvo Leroux from the Instituto Nacional de Cardiologia in Mexico City provided photographs showed in [Figure 4] from her personal archive to illustrate the present article. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.
[Figure 1], [Figure 2], [Figure 3], [Figure 4]
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