The USPSTF found few data on the accuracy of the ankle-brachial index (ABI) for identifying asymptomatic persons who benefit from treatment of peripheral arterial disease (PAD) or cardiovascular disease (CVD). Conclusion: The USPSTF concluded that the current evidence is insufficient to assess the balance of benefits and harms of screening for PAD and CVD disease risk using the ABI in asymptomatic adults. Commentary: In the last 5 years, various specialties have weighed in on whether or not performing a screening ABI is worthwhile. Some of you may be surprised to know that both the Society for Vascular Surgery and the American College of Cardiology/American Heart Association released practice guidelines saying it is reasonable to obtain a screening ABI in asymptomatic patients, namely those >65-70 years old and in younger patients with atherosclerotic risk factors. 1,2 However, the American Academy of Family Physicians concluded that there was insufficient evidence to assess the balance of benefits and harms of screening for PAD and CVS using the ABI in asymptomatic adults, 3 as did the current review by the USPSTF. By the way, the U.S. Congress mandates that the Agency for Healthcare Research and Quality (AHRQ) supports the operations of the USPSTF. This is an important article because of its practical implications. If an asymptomatic patient is shown to have an abnormal ABI, don't all of us agree that interventions should not be performed for asymptomatic arterial occlusive disease of the lower extremities? I hope and expect that physicians do not obtain ABIs in asymptomatic patients simply as a means to increase revenue via the noninvasive vascular laboratory. Although the SVS practice guidelines delineate reasonable exceptions, I don't see the value of performing an ABI in most patients without suspected arterial claudication, ischemic rest pain, or ischemic tissue loss. Take-home message: Make sure you have a darn good reason for performing screening ABIs in asymptomatic patients so that you don't get accused of being one of those greedy doctors. References: 1. Guidelines Writing Group, Conte MS, Pomposelli FB, Clair DG, Geraghty PJ, McKinsey JF, et al. Society for Vascular Surgery Lower Extremity Guidelines Writing Group. Society for Vascular Surgery practice guidelines for atherosclerotic occlusive disease of the lower extremities: management of asymptomatic disease and claudication.

Introduction : A 51‐year‐old lady with a past medical history of Essential Hypertension, Hypothyroidism, prior Herpes Zoster infection 8 weeks ago was admitted with complaints of abdominal pain, bilateral flank pain, and restlessness. Her initial workup was significant for hyponatremia and hypokalemia. On the 3rd day of admission, she developed acute hypoxemic respiratory failure which led to intubation. At that time, CTA Chest was not done but CT Chest revealed prominent mucous plugging with left side glass ground opacities, Ultrasound of lower extremities revealed right common femoral vein DVT which led to concerns that she may have suffered from Pulmonary Embolism and led to starting Heparin drip. On the 6th day of admission, she developed Acute Encephalopathy, MRI Brain revealed acute infarcts in bilateral cerebral cortices and cerebella, CT Angiogram Head showed acute subarachnoid hemorrhage in the high posterior right parietal lobe, stenosis of the right high cervical internal carotid artery, and irregular, the appearance of the arterial vasculature throughout and CT Angiogram Neck abrupt change in caliber of the right ICA, 1.5 cm distal to the bifurcation with markedly severe narrowing of the majority of the extracranial right ICA throughout its course. A cerebral Angiogram was done which showed diffuse tandem segments of tandem cervical and intracranial portions of the right internal carotid artery and she was given nitroglycerin was administered as a therapeutic intervention. Lumbar Puncture showed WBC 2, RBC 7, Protein 162, Glucose 64, VZV PCR was negative, CSF VZV IgG Antibody positive at 303 IV (>165 IV indicative of current or past infection). Serum VZV IgG Antibody was positive at >4000 IV. Infectious Diseases were consulted after Lumbar Puncture, they initially started Acyclovir but once the Serum VZV IgG Antibody came back much higher than Serum VZV IgG Antibody levels, their assessment was that VZV vasculitis is unlikely and Acyclovir was discontinued. Eventually, the case was discussed at Neuroradiology which led to us getting a repeat MRA Neck without contrast which showed a concentric T1 and T2 hyperintensity along with a small and irregular caliber right cervical ICA consistent with dissection. She eventually completed a 21‐day course of Nimodipine due to underlying Subarachnoid Hemorrhage. Methods : NA Results : NA Conclusions : Our case demonstrates how it can become difficult to ascertain the etiology of stroke in certain patients. Our patient presented with multiple non‐specific symptoms initially and it was later on due to her Acute Encephalopathy that her Strokes and Subarachnoid Hemorrhage were discovered. It is still difficult to pinpoint whether the cause of strokes was dissection or VZV infection. Lumbar Puncture remains an essential tool to complete work up on uncommon etiologies of stroke.