approach to stroke

1. Stroke

2. • Cerebrovascular disease is caused by one of several
pathophysiologic processes involving the blood vessels of the
brain:
• A) Intrinsic vessel abnormality
• B) Embolism
• C) Inadequate blood flow
• D) Vessel rupture

3. TIA VS STROKE
• TIA is now defined as a transient episode of neurologic
dysfunction caused by focal brain, spinal cord, or retinal
ischemia, without acute infarction. This tissue-based definition
of TIA relies on the absence of end-organ injury as assessed by
imaging or other techniques.

4. • Vital signs — Parameters of particular concern in patients with
stroke include blood pressure, breathing, and temperature.

5. History and Exam
• Last seen normal, or last known well: this is the time of
onset
• –Time of onset is not necessarily when the patient was found
• –Time of onset is not necessarily when there was an abrupt
change if the patient changed from having a mild deficit to a
severe deficit
• –“When was the last time today that Mr. Jones was walking and
talking normally?”

6. What are the symptoms?
• Weakness in face, arm or leg
• Speech difficulty
• Sensory changes
• Vision changes
• Ataxia

7. Describing symptoms
• For weakness, say what the patient can do

8. “Sudden onset…”
• How quickly did symptoms reach maximal severity?
• –Symptom onset is often described as sudden
• –But symptoms often worsen after “sudden onset”
• –“Sudden onset right face and arm numbness” becomes
“Sudden onset right face numbness which got worse over the
next 30 minutes and spread to the right arm”

10. • Previous transient ischemic attack —
• A history of TIA (especially more than one) in the same territory
as the stroke strongly favors the presence of a local vascular
lesion (thrombosis).
• Attacks in more than one vascular territory suggest brain
embolism from the heart or aorta.

11. Activity at the onset or just before the stroke —
• Hemorrhages (ICH and SAH) can be precipitated by sex or other
physical activity, while thrombotic strokes are unusual under
these circumstances.
• Trauma before the stroke suggests traumatic dissection or
occlusion of arteries or traumatic brain hemorrhage.
• Sudden coughing and sneezing sometimes precipitates brain
embolism.
• Similarly, getting up during the night to urinate seems to
promote brain embolism (a matutinal embolus).

12. Associated symptoms
• Fever raises the suspicion of endocarditis and resulting embolic
stroke.
• Headache is typically a feature of hemorrhagic strokes
• Vomiting is common in patients with ICH, SAH, and posterior
circulation large artery ischemia
• Seizures are most often seen in patients with lobar ICH or brain
embolism; they are rare in patients with acute thrombosis.
• Reduced alertness favors the presence of hemorrhage.
Accompanying neurologic signs are suggestive of ICH
• Loss of consciousness is also common in patients with thrombotic
and embolic strokes that are large or involve the posterior circulation
large arteries.

13. Exam
- power
- tone
- reflexes
-sensory
- cerebellar
- cranial nerves

14. • The presence of a neck bruit suggests the presence of occlusive
extracranial disease
• Cardiac findings, especially atrial fibrillation, murmurs, and
cardiac enlargement, favor cardiac-origin embolism.

15. Symptoms and Signs Syndrome
Contralateral hemiparesis (maximal in the leg), urinary incontinence, apathy, confusion, poor judgment,
mutism, grasp reflex, gait apraxia
Anterior cerebral artery (uncommon)
Contralateral hemiparesis (worse in the arm and face than in the leg), dysarthria, hemianesthesia,
contralateral homonymous hemianopia, aphasia (if the dominant hemisphere is affected) or apraxia and
sensory neglect (if the nondominant hemisphere is affected)
Middle cerebral artery (common)
Contralateral homonymous hemianopia, unilateral cortical blindness, memory loss, unilateral 3rd cranial
nerve palsy, hemiballismus
Posterior cerebral artery
Monocular loss of vision (amaurosis) Ophthalmic artery (a branch of the internal carotid artery)
Unilateral or bilateral cranial nerve deficits (eg, nystagmus, vertigo, dysphagia, dysarthria, diplopia,
blindness), truncal or limb ataxia, spastic paresis, crossed sensory and motor deficits*, impaired
consciousness, coma, death (if basilar artery occlusion is complete), tachycardia, labile blood pressure
Vertebrobasilar system
Absence of cortical deficits plus one of the following:
•Pure motor hemiparesis
•Pure sensory hemianesthesia
•Ataxic hemiparesis
•Dysarthria–clumsy hand syndrome
Lacunar infarcts
* Ipsilateral facial sensory loss or motor weakness with contralateral body hemianesthesia or hemiparesis indicates a lesion at the pons or medulla.

16. MX
• Fluids
• Hypoglycemia/Hyperglycemia ((>10 mmol/L)
• Swallowing assessment /ASPIRATION PRECAUTION
• Head and body position
• Fever —Common etiologies of fever, including aspiration
pneumonia and urinary tract infection, should also be excluded.

17. BLOOD PRESSURE MANAGEMENT
• For patients with ischemic stroke who are not treated with
thrombolytic therapy, blood pressure should not be treated
acutely unless the hypertension is extreme (systolic blood
pressure >220 mmHg or diastolic blood pressure >120 mmHg),
• When treatment is indicated, cautious lowering of blood
pressure by approximately 15 percent during the first 24 hours
after stroke onset is suggested.

18. • For patients with acute ICH who present with systolic blood
pressure (SBP) between 150 and 220 mmHg, we suggest
lowering of SBP to a target of 140 mmHg, ideally within the
first one hour of presentation, provided the patient remains
clinically stable. This degree of blood pressure reduction
appears safe in most patients and may improve functional
outcome.

19. • For patients with acute ICH who present with SBP >220 mmHg, we
suggest rapid lowering of SBP to <220 mmHg.
• Thereafter, the blood pressure is gradually reduced (over a period of
hours) to a target range of 140 to 160 mmHg, provided the patient
remains clinically stable.
• Patients who deteriorate clinically during this period may require reduction
of acute antihypertensive therapy. The optimal blood pressure goal is
uncertain, but an SBP of 140 to 160 mmHg is a reasonable target for
patients who remain clinically stable