Dr Farzadfard

Stroke types  Infarcts  Artery  Vein  Hemorrhages  ICH  IVH  SAH

Presentation Abrupt Onset Fit the distribution of a single vascular territory early decrease in level of consciousness, nausea and vomiting, headache, and accelerated hypertension are more common with hemorrhages. Subarachnoid hemorrhages classically present as a bursting very severe headache (‘‘the worst headache of my life’’), and are often accompanied by stiff neck, decreased consciousness, nausea and vomiting

Signs and symptoms characteristic of the various arterial territories Middle cerebral – contralateral loss of strength and sensation in the face, arm, and to a lesser extent leg. Aphasia if domi­nant hemisphere, neglect if non-dominant. Anterior cerebral – contralateral loss of strength and sensation in the leg and to a lesser extent arm. Posterior cerebral – contralateral visual field deficit. Possibly confusion and aphasia if dominant hemisphere. Penetrating (lacunar syndrome) – contralateral weakness or sensory loss (usually not both) in face, arm, and leg. No aphasia, neglect, or visual loss. Possibly ataxia, dysarthria. Vertebral (or posterior inferior cerebellar) – truncal ataxia, dysarthria, dysphagia, ipsilateral sensory loss on the face, and contralateral sensory loss below the neck. Basilar – various combinations of limb ataxia, dysarthria, dysphagia, facial and limb weakness and sensory loss (may be bilateral), pupillary asymmetry, disconjugate gaze, visual field loss, decreased responsiveness

DIAGNOSIS History Exam presence of comorbidities Absence of seizures or other stroke mimics Imaging

Differential diagnosis  Seizures  Migraine  Syncope  Hypoglycemia  Metabolic encephalopathy  Drug overdose  Central nervous system tumor  Herpes simplex encephalitis (HSE)  Subdural hematoma

 Peripheral compression neuropathy  Bell’s palsy (peripheral seventh nerve palsy)  Benign paroxysmal positional vertigo (BPPV)  Conversion disorder

What to do first  O2 via nasal cannula  Intubation may be necessary  Consider putting the head of the bed flat  Consider normal saline bolus

All patients  brain CT (brain MRI could be considered at qualified centers)  electrocardiogram  blood glucose  serum electrolytes  renal function tests  complete blood count, including platelet count  PT, INR,PTT

Selected patients  hepatic function tests  toxicology screen  blood alcohol determination  pregnancy test  oxygen saturation or arterial blood gas tests (if hypoxia is suspected)  chest radiography (if lung disease or aortic dissection are suspected)  lumbar puncture (if subarachnoid hemorrhage is suspected and CT is negative for blood)  electroencephalogram (if seizures are suspected)

Do not treat hypertension acutely unless:  (1) the patient was treated with TPA  (2) the patient has acute hypertensive end organ damage (congestive heart failure, myocardial infarction, hyperten­sive encephalopathy, dissecting aortic aneurysm, etc.)  (3) systolic or diastolic pressures are above 220 or 120 mm Hg

Proven acute medical treatment for ischemic stroke  tissue plasminogen activator (rt-PA)  Age 18 or older  Clinical diagnosis of ischemic stroke causing a measurable neurological deficit  Onset of stroke symptoms well established to be less than 180 minutes (3 hours) before treatment would begin  aspirin with 48 hours of stroke onset Clopidogrel (Plavix) 375 mg, and then aspirin 81mg and clopidogrel 75mg once daily for the first few days  In patients who :  while already on antiplatelet therapy  have a fluctuating neurological course  have a heavy burden of atherosclerotic risk factors or atherosclerotic lesions

Based on the NINDS rt-PA study, the requirements for administering rt-PA include  a CT scan of the head, which is negative for hemorrhageCT  a serum glucose level between 50 and 400 mg/dL  INR less than 1.7 INR  platelet count more than 100,000 per cubic mL  systolic blood pressure less than 185 mmHg systolic  no recent major procedures, traumas, or stroke

Later head CT (day 2) revealing hypodensity within the left MCA distribution

Acute anticoagulant therapy  patients with a cardioembolic condition at high risk for recurrence (thrombus on valves, or mural thrombus),  documented large-artery (ICA, MCA, or basilar artery ) occlusive clot at risk for distal embolism  arterial dissection  venous thrombosis

Treat  HYPERGLYCEMIA  HYPERTHERMIA

DVT prophylaxis  Heparin 5000 units SC every 12 hours  Enoxaparin (Lovenox, Clexane) 40 mg SC once daily  Dalteparin (Fragmin) 5000 units SC once daily  Sequential compression devices (non-drug)  Compression (TED) stockings

TIA  brief episode of neurologic dysfunction caused by focal brain or retinal ischemia  The causes are the same as for ischemic stroke  the management is similar to that for acute ischemic stroke  Observe the patient for 24 hours  Start daily antiplatelets  EKG  Cardiovascular risk-factor evaluation of blood pressure, lipids, and fasting glucose

Intracerebral hemorrhage  Spontaneous bleeding into the brain parenchyma or ventricles from a ruptured artery, vein, or other vascular structure

Etiology  Hypertension (most common)  Amyloid angiopathy  Drugs  Vascular malformation  Cerebral vein thrombosis  Tumor  Trauma

Initial assesment of ICH  History and physical exam  Glasgow coma scale (GCS) and brainstem reflexes if comatose, NIHSS score if awake.  Measure blood pressure  Oxygen saturation  Brain CT  Check platelet count, INR, and PTT, and urine drug screen  EKG

HEMATOMA ENLARGEMENT  blood pressure levels be maintained below a mean arterial pressure of 130 mm Hg  WARFARIN (COUMADIN)-RELATED INTRACEREBRAL HEMORRHAGE  Goal: normal INR using fresh frozen plasma (FFP) 20 mL/kg and vitamin K  Activated factor VII  HEPARIN-RELATED INTRACEREBRAL HEMORRHAGE  Stop heparin  CT brain immediately  INR, PTT, platelets, CBC, fibrinogen, thrombin time, D-dimers  Type and cross  Give protamine: 25mg initial dose; check stat PTT 10 minutes later and if increased give 10mg additionally; repeat until PTT normal

Subarachnoid hemorrhage  The worst headache of my life  ‘‘Thunder-clap headache  Headache is sometimes associated with focal neurologic symptoms

DIAGNOSIS OF SUBARACHNOID HEMORRHAGE  CT of the head without contrast  If head CT is normal, but you have a high clinical suspicion for SAH, you must do a lumbar puncture, because CT can miss small or subtle SAHs, especially if more than 72 hours has passed since the ictus

DIAGNOSIS OF INTRACRANIAL ANEURYSMS  Digital subtraction angiography (DSA)  CT angiography  MRA

CAUSES OF SAH OTHER THAN INTRACRANIAL ANEURYSM  Perimesencephalic SAH  Arteriovenous malformation (AVM)  Arterial dissection (vertebral artery usually)  Arteriovenous fistula  Pituitary apoplexy  Cocaine  Trauma  Vasculitis

GOALS  Prevention of rebleeding  Blood pressure control may be important before definitive treatment to reduce rebleeding  Bed rest in ICU with monitoring  Treatment of the aneurysm itself: clip or coil  Prevention and treatment of complications: hydrocephalus, seizure, vasospasm, hyponatremia, infections, and DVTs.