Wallach's Interpretation of Diagnostic Tests: Pathways to Arriving at a Clinical Diagnosis (106 page)
Authors: Mary A. Williamson Mt(ascp) Phd,L. Michael Snyder Md
Embolism is caused by particles of debris or tissue that originate distally (from vessel walls, the heart, or tumors) and travel through the circulation resulting in the blockage of arterial blood flow to the brain. Unlike thrombosis, which involves the local vessel, local therapy in embolic stroke is only temporizing. The source of the embolic fragment must be identified and treated, or additional events may occur. There are four categories of embolic stroke: those with known cardiac source, those with a possible cardiac or aortic source, those with an arterial source, and those with an unknown source (see eBook Figure 4-29). Cerebral embolism is the most common cause of stroke in the elderly.
Clinical Presentation
Embolic stroke should be suspected if the change is sudden with maximal deficit at the onset, if the infarct is large, if there is a known cardiac or large arterial lesion, if the infarct is or becomes hemorrhagic on CT, if there are multiple lesions, and if clinical findings improve quickly. It is more common in patients with strokes of the posterior circulation. Atrial fibrillation, cardiac murmurs, and enlargement are risk factors for embolus of cardiac origin. A possible cardiac source should always be considered even in young patients. If the patient is febrile, septic emboli and endocarditis should be suspected. Small vessel (lacunar) stroke is most commonly seen in patients with hypertension, DM, or polycythemia. Patent foramen ovale is also a risk factor for venous to arterial embolism.
The diagnosis of embolic stroke is primarily made on clinical examination and neuroimaging (MRI and CT scan). Cardiac evaluation with EKG and echocardiography is also helpful. Doppler studies of the large vessels of the neck and aorta may show lesions in these regions. Additional imaging studies to rule out myxoma of the left atrium, fat embolism in fracture of long bones, and air embolism in the neck, chest, or cardiac surgery may be indicated.
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Laboratory tests should be performed to try to determine any underlying disorder and should include blood cultures to rule out bacterial endocarditis, hypercoagulable panel to rule out nonbacterial thrombotic vegetations on heart valves (lupus anticoagulant, anticardiolipin, prothrombin mutation, factor V Leiden mutation), and cardiac enzymes to rule out underlying myocardial infarction with mural thrombus.
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Lumbar puncture with evaluation of the CSF reveals findings similar to cerebral thrombosis. Hemorrhagic infarction develops in one third of patients, usually producing slight xanthochromia. Some patients may have grossly bloody CSF (10,000 RBCs/μL). Septic embolism (e.g., bacterial endocarditis) may cause increased WBC (CSF WBC count ≤200/μL with variable lymphocytes and PMNs), increased RBC (CSF RBC count ≤1,000/μL), slight xanthochromia, increased protein, normal glucose, and negative culture.
References
1. DeRook FA, Comess KA, Albers GW, Popp, RL. Transesophageal echocardiography in the evaluation of stroke.
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2. Jauch EC, Saver JL, Adams HP Jr, et al. Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association.
Stroke.
2013;44:870.
3. Markus HS, Hambley H. Neurology and the blood: haematological abnormalities in ischaemic stroke.
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INTRACEREBRAL HEMORRHAGE
Intracerebral hemorrhage (ICH) is defined as bleeding into the brain parenchyma and has many etiologies (see eBook Figure 4-30).
ICH is the second most common cause of stroke following ischemic stroke. It is the cause of up to 15% of all first time strokes, with a higher incidence in Asians, Hispanics, and African Americans.
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The risk for ICH is increased in patients with hypertension, amyloidosis, vascular malformations, and berry aneurysm. Risk also increases with age, alcohol intake, and African American ethnicity. Etiologies of ICH include hypertensive vasculopathy, septic emboli, brain tumor, infection, vasculitis, bleeding disorders (including anticoagulants), and drugs such as cocaine and amphetamines.
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The diagnosis of intracranial hemorrhage is made by neurologic imaging (CT or MRI).
Lumbar puncture reveals an increased CSF WBC count (15,000–20,000/μL), higher than in cerebral infarct (e.g., embolism, thrombosis). All patients should have a platelet count, PT, and PTT to establish bleeding potential. Tests that may be helpful include an elevated ESR in vasculitis and urinalysis, which may reveal transient glycosuria or concomitant renal disease. Additional tests may be obtained to rule out causes of intracerebral hemorrhage such as leukemia, aplastic anemia, polyarteritis nodosa, SLE, and other coagulopathies.
References
1. Flaherty ML, Woo D, Haverbusch M, et al. Racial variations in location and risk of intracerebral hemorrhage.
Stroke.
2005;36:934.
2. Gebel JM, Broderick JP. Intracerebral hemorrhage.
Neurol Clin.
2000;18:419.
BERRY ANEURYSM (SACCULAR ANEURYSM)
A berry or saccular aneurysm is a rounded dilation of an artery in the brain. The wall of the aneurysm is weaker than the normal vessel and therefore at risk for rupture with increased pressure (see eBook Figure 4-31).
Most subarachnoid hemorrhages are due to ruptured saccular aneurysms. The incidence of saccular aneurysms is approximately 5% among the general population.
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The risk of rupture varies with aneurysm size, and most subarachnoid hemorrhages due to aneurysm rupture occur in the 40- to 60-year-old age group, with a slight increase in women over men. African Americans have a higher incidence than Caucasians.
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Patients with subarachnoid hemorrhage due to aneurysm rupture present with severe headache, nausea, vomiting, vision loss, or loss of consciousness.
Risk factors for saccular aneurysm include smoking, hypertension, genetic diseases (adult dominant polycystic kidney disease, aldosteronism, Ehlers-Danlos syndrome), family history, and sympathomimetic drugs such as phenylpropanolamine and cocaine, and decreased estrogen as is seen in postmenopausal women. A number of studies have looked at the evidence for a candidate gene associated with aneu-rysmal subarachnoid hemorrhage including the elastin gene on chromosome 7q.
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