Acute Flaccid Paralysis Accompanying West Nile Meningitis Ahmed ...

Adjusting the Therapeutic Threshold: An Evolving Target in Carotid Stenosis Severity?
Staples, AM, DO; Basil, S, OMS3; Heisecke, J, MD; Makdisi, T, MD, FACP
Berkshire Medical Center, Department of Internal Medicine, Pittsfield, MA
Introduction: Carotid stenosis, previously deemed worrisome as it reached severe criteria, is
now increasingly a concern in those with mild to moderate stenosis. Recent studies have shown
that the majority of patients with transient ischemic attacks and minor strokes have a nonsevere
degree of stenosis with ulceration of the carotid atherosclerotic plaques. Ulceration adds
a degree of instability and necessitates further attention.
Case: A 62 year old male with past medical history of atrial fibrillation on Coumadin with
therapeutic INR, hypertension and hyperlipidemia presented to the ER for several recent
episodes of slurred speech, drooling, right-sided facial asymmetry, and confusion, each lasting
5-10 minutes. Patient denied any sensory loss or similar episodes in past. His medications
included Coumadin, Atenolol and Crestor. Physical exam was benign except for an irregularly
irregular heart rhythm. There were no derangements in laboratory data. EKG showed rate
controlled atrial fibrillation. Echocardiogram revealed a LVEF of 50% without mural thrombus.
MRI of the brain showed 3 areas of acute infarction in the territory of the left middle cerebral
artery. MRA of the carotids revealed a 50% left carotid stenosis with an ulcerated plaque. Given
the unilateral pattern and known atrial fibrillation on therapeutic anticoagulation, the ulcerated
carotid plaque was deemed the etiology of his cerebrovascular accident. Left carotid
endarterectomy was performed with Hemashield carotid patch angioplasty, and intraoperative
evidence of ulceration extending through the wall of the internal carotid artery and into the
adjacent soft tissue. The patient was discharged without residual focal neurological deficit.
Discussion: Severe carotid artery stenosis has long been known to be a cause of TIAs and
stroke. However, in the recent past, several cases of TIAs and strokes have been reported in
people with mild to moderate degree stenosis. Further research has shown that 90% of patient
with TIA, amaurosis fugax and minor stroke have stenosis < 50%. Two-thirds of such patients
were found to have a plaque ulceration. Presence of ulceration was directly proportional to the
amount of lipid rich necrotic core and plaque volume. Echolucent plaques, i.e., those with higher
levels of lipid and hemorrhage have been linked to an increased risk of CVA.
Ulceration within a stenotic carotid artery is more prevalent in areas of chronic high shear stress
and sudden changes in intra-arterial pressures as these areas are more prone to plaque
erosion, which in turn cause focal inflammatory changes leading to degradation of plaque wall
and subsequent ulceration. A flow dynamics study further explained that a slipstream flow is
disturbed immediately distal to stenotic area, allowing a backward slipstream to enter the ulcer
in diastole, creating a potential for platelet aggregation. Furthermore, at peak systole, a
whirlpool like circulation was noticed, which had the potential to suck those aggregates from the
ulcer, leading to frequent small embolizations.
Diagnosis can be established with the help of a two-dimensional echo, which can detect
stenosis and an MRA, which detects both stenosis and presence of ulceration. Additionally,
convergent color doppler has been shown to be the best non-invasive and feasible diagnostic
modality for diagnosis of ulcerative lesions with atherosclerotic lesions. Treatment involves
carotid endarterectomy to prevent recurrence of TIAs or stroke. During carotid endarterectomy,
plaque area is cut in full length and not mobilized much due to fear of embolization, thus
explaining the reason for lack of connection between ulceration and symptomatic patients until
recently.