Cardiac sources of embolism can be evaluated as part of the work up with EKG monitoring and echocardiogram. Management
Pulse oximetry can guide the use of supplemental oxygen to maintain oxygen saturation greater than 94%. Hyperoxia should be avoided as may be detrimental in stroke. Hypertension is common in an acute ischemic stroke. A low BP is uncommon and may indicate symptoms exacerbation of a previous stroke due to poor perfusion. Blood pressure of 220/120 mmHg should receive treatment. There is a consensus approach of allowing permissive hypertension up to 220/120 mmHg for patients that are not candidates for thrombolysis. [21]
However, for a patient that is a potential candidate for alteplase, attempt to control BP should be made immediately as goal BP for initiation of IV alteplase is 185/110 mmHg. Usually, titratable short-acting intravenous hypotensive agents are recommended to avoid dropping the BP too much once the patient is at goal. Hypotensive agents that can be options include labetalol, nicardipine, clevidipine, hydralazine, enalaprilat. [21]
For the patients that present within the therapeutic window, the decision to treat with intravenous recombinant tissue plasminogen (less than 4.5 hours from symptom onset) or endovascular treatment with mechanical thrombectomy should be made. Initiation of IV alteplase treatment in the 3 to 4.5-hour window is the current recommendation for patients less than 80 years of age, no history of both diabetes mellitus and prior stroke, use of anticoagulants, and NIHSS score of less than 25. Only patients with disabling symptoms are considered eligible for thrombolytic treatment.
Sneddons syndrome is a form of arteriopathy characterized by several symptoms, including:

Severe, transient neurological symptoms or stroke
Livedo reticularis, or livedo racemosa

Signs and symptoms
Sneddons syndrome generally manifests with stroke or severe, transient neurological symptoms, and a skin rash (livedo reticularis). Livedo reticularis appears as a bluish-purple, netlike mottling of the skin. Sneddons syndrome may instead present with livedo racemosa, which involves larger, less organized patches of bluish-purple mottling of the skin. Both are generally found first in the extremities, both worsen in cold and either may occur without Sneddons Syndrome or any other systemic disease.Sneddons Syndrome can be characterized by: transient amnesia, transient aphasia, palsy, headaches, hypertension, transient ischemic attacks (TIA), stroke, coronary disease and dementia. The skin manifestations may precede the neurologic symptoms by years. Pathogenesis
Sneddons syndrome is a progressive, noninflammatory arteriopathy leading to the characteristic skin condition and to cerebrovascular problems, including stroke, transient ischemic attack (TIA), severe but transient neurological symptoms thought to be caused by cerebral vasospasm, coronary disease and early-onset dementia. Progressive compromise of arterial linings in Sneddons produces clotting, for which high-dose warfarin is most commonly prescribed, and can also cause the development of systemic arterial plaque when cholesterol levels are normal. Diagnosis
There are no diagnostic tests on which all Sneddons patients will have abnormal results, although brain MRI and skin biopsy are often abnormal. The diagnosis is based on a detailed history and physical examination. About 40-60% of patients with the syndrome test positive for antiphospholipid antibodies.