Managment of asymptomatic stenosis==

Bob Brown
*Use ASA as antiplatelet choice
* selective not widespread carotid screening
* CEA in select patients, consider age, general health and life expectancy, surgeon, high grade v. progressive stenosis, CAS in high risk

Carotid Bruits-- Pearls

1. 8.2 % prevalence in age> 75; 40 % of those with ? 50 % stenosis have a bruit
2. Only characteristic of a bruit predictive of stenosis is a diastolic bruit
3. With greater than 75 % stenosis, the stroke risk at one year is 5.5 % with bruit
For 75-94 % stenosis, risk of stroke at one year is 3.7 %
4. In asymptomatic patients, keep in mind cardiac ischemia, risk is increased
5. Risk of noncardiac surgery not higher with bruit
6. Symptomatic VB stenosis confers 6 % risk of GET
7. Asymptomatic intracranial stenosis, carotid stenosis does not increase risk of general anesthesia except CABG

Acute treatment of stroke

Based on Tom Brott lecture-- many obvious guidelines are omitted and only a few of less obvious ones are listed below, based on my own discretion

*treat hypoxia
* treat fever
*cardiac monitoring for 24 hours
*Until more definitive data, cautious approach to treating BP in first 24 hours
* Alteplase guidelines for BP management also apply to other interventional procedures
* In first 24 hours, withholding meds for BP unless BP> 220-120
*Hypovolemia should be corrected
* Hypoglycemia should be corrected
* Beware of AE of angioedema with alteplase
* For arterial therapy, centers are encouraged to define criteria to credential
* ASA dose of 325 is now recommended within 24-48 hours
* Patients possibly needing neurosurgery (cerebellar infarct, major hemispheric infarct) should be transferred to a facility with that capability
* Hydrocephalus due to a cerebellar stroke can be treated with a drain

For hemorrhage:
* Use protamine/vit K to reverse anticoagulation if applicable
* Surgical removal dangerous cerebellar hemorrhage > 3 cm

Metabolic syndrome in stroke

3 or more of following:

*abdominal obesity (> 102 cm in men, 88 in women)
* Elevated TG;s (>150)
* low HDL (< 40 in men, <50 in women)
* BP (>130/85
* FBS elevated glc intolerance or DM ( >110)

WEIGHT LOSS, DIETARY CHANGE, EXERCISE

Management of stroke in diabetics: sec prevention

* independent risk factor for stroke, 2x normal risk
* secondary prevention may reduce microvascular complications more than cardiovascular
* aggressive control with diet, exercise, oral agents and insulin as needed.
* use of ACEI or ARB in HTN
* statin even if lipids are normal

Risk factors to be assessed in stroke

HTN--
Cigarette smoking
dyslipidemia
DM
Metabolic syndrome
? Elevated homocystein
Excess alcohol consumption
Obesity
Physical inactivity
Sleep apnea syndrome esp Obstructive

Hospitalize after TIA?

stratify risk (ABCD(2)) if higher risk, if a candidate for alteplase, if need rapid evaluation, carotid stenosis, AF

Notes Carotid disease accounts for about 11 % of TIA's and short term risk of stroke may be as high as 20 % in 90 days.

Stroke risk after stroke

about 4 % in 90 days based on

IST 3.3 %
Cast 1.6 %
TOAST 5.7 %
nascet 2.3 %

MAY BE HIGHER RISK WITH RAPID RECOVERY

Small vessel pathology AND cerebral blood flow

from Continuum chapter on pathophysiology

Small vessel disease- 20-30 % of total

1.lipohyalinosis is replacement of vessel wall with fibrin and collagen due to to HTN

2.microatheroma is an atheromatous plaque at the origin of a penetrating artery may cause larger subcortical strokes.

3. Fibrinoid necrosis is associated with very high BP leading to necrosis of smooth muscle cells extravasation of plasma proteins which appear as fine granular eosinophilic deposits in the connective tissue of the vessel wall.

4. Charcot-Brouchard aneurysms are areas of focal dilations in the wall that thrombose and occlude the vessel



CBF

Main factors of tissue outcome are regional CBF and duration of occlusion.

Local tissue perfusion pressure, which is main factor accounting for outcome, depends on collaterals, on arterial blood pressure, and inversely correlates with local tissue pressure, which is due partly to edema.



Thresholds:

studied in carotid clamping surgeries decades ago, reversible ischemia occurred with loss of CBF to 30-50 % of normal, and permanent with less than 30 % perfusion pressure. Higher CBF values required a longer time to infarct. EEG slows at CBF<23 flat at 15.

High and low risk cardiac conditions for stroke

from Continuum 2008 chapter on pathophys

High risk for stroke-- atrial fibrillation with structural disease, sustained atrial flutter, sick sinus syndrome, left atrial thrombus, left atrial/ appendage thrombus, left atrial myxoma, mitral stenosis, mechanical valve, infective endocarditis, non-infective endocarditis, left ventricular myxoma, recent anterior MI, dilated cardiomyopathy , left intraventricular thrombus

Low or uncertain risk for stroke
Lone AF, PFO, ASA, spontaneous atrial contrast, MVP, calcific aortic stenosis, fibroelastoma, Giant Lambel excrescence, akinetic or dyskinetic ventricular wall segment, Subaortic hypertrophic cardiomyopathy, congestive heart failure , ventricular aneurysm,






also see http://strokenotes.blogspot.com/2007/02/treatment-of-cardiac-problems-in-stroke.html

Minutiae of pathophysiology of acute stroke

from corresponding chapter in Continuum late 2008
1. Occlusive infarcts are divided into "white" and "red", the latter of which corresponds to hemorragic transformation due to leaky blood cells into dying brain and are not equivalent to parenchymal hematoma due to vessel burstage. Hemorrhagic transformation occurs in up to 80 %.
2. Pathological stages (garcia, 1998) first 24 hours-- lesion barely visible. Swelling peaks days 3-5. Between days 5-10, the infarcted tissue become sharply demarcated from unaffected brain tissue. The fourth stage , lasting weeks to months, is liquefaction necrosis.

3. Mechanism for low flow stroke may be due to decreased cardiac output, systemic hypotension, increased metabolic demands of tissue (fever, acidosis), or steal of flow from affected to unaffected areas (Alexcandrov, Stroke, 2007). Caplan wonders whether low flow may potentiate emboli due to impaired clearance of emboli with low flow states.

4.

Mechanisms of neuronal damage in stroke

necrosis
apoptosis
excitotoxicity
inflammation
periinfarct depolarization
acidosis
free radical formation

Accurate diagnosis of TIA would reduce incidence by 33 % annually (from 180,000) and commensurately increase number of strokes by 7 % (from 820,000 in US annually).

Continuum Acute Stroke

Notes on a few minutiae in the book that were not at first transparently obvious to me (not that is a criterion).
from "Diagnosis" chapter
1. The presence of early infarct changes (EIC) on CT were not independently associated with adverse outcome in the NINDS trial and should not preclude thrombolysis (Patel, 2001).
2. Another study found interobserver agreement "moderate to poor" on the presence of EIC's and increased outcome of poor results in their presence (Wardlaw and Meilke, 2005).
3. Clearly delineated hypodensity and mass effect is "incompatible" with three hour window.
4. Six percent of patients with brain tumors presenting to ER's had symptoms of less than 1 day duration (Snyder, 1993).
5. The critical glucose number bandied around for "hypoglycemia" is 45.
6. Chest pain as part of a stroke syndrome mimicking MI is reported after stroke of the thalamus, lateral medulla, and corona radiata.
7.

Lack of utility of bariatric chamber in stroke

A Cochrane review of the subject 2.5 yrs ago found no evidence to support its use (Stroke 2006;37;1953-1954)