Definition
CVA / CVD / Stroke: Clinical syndrome characterized by signs / symptoms of focal or global loss of cerebral function which last for more than 24 hours or leading to death with no apparent cause other than that of vascular origin
Classification
Type:
Ischemic / Infark stroke Bleeding Stroke
Clinical Course:
TIA (Transient Ischemic Attack) Neurological deficits lasts for fewer than 24 hours RIND (Reversible Ischemic Neurologial Deficit Neurological deficits lasts from 24 hours since 3 weeks PRIND (Progressive RIND) : more than 3 weeks
Progressive Stroke / Stroke in Evolution Symptoms are gettin worse Complete Stroke Neurological deficits remain the same since the onset of the disease
Clinical Manifestation
Based on the lesion site (of the artery)
Based on artery that supplies the brain region
SAH
+++ +++
Meningeal Sign
Paresis of N III & IV Weakness
+
+ Plegi
+++
+++ Paresis
Hypertension
Cerebrospinal fluid
++
>1000
+
>25000
Retinal Bleeding
Meningeal Sign Location CT SCAN Prognosis
+
+ Cortical / subcortical Hyperdense mortality
Why at sleep? While sleeping, the heart pumps the blood within the blood vessels slower than at activity. This cause the mean arterial pressure is also decreasing and when the thrombotic or emboli occured and ischemia process is developing, it is gettin worse because the cardovascular system is not adequate to mantain the normal cerebral blood flow
Pathophysiology of CVA
Cerebral Blood Flow determined by: 1. Extrinsic Factors
Systemic Blood Pressure Cardiac Output (the ability of the Heart to pump the blood to the systemic circullation) The quality of caroticovertebral Arteries Blood Viscosity
2. Intrinsic Factors
Cerebral Arteries Autoregulation Regional Biochemistry Factors
Pathophysiology - Infark
N CBF = 50 60 ml/min ; aerob metablism (36 ATP) 18 20 ml / 100g / min: Neuronal electrical activity
10ml / 100g / min: Anaerobic metabolism (2ATP) +Lactate: Deprived Na K ATPase channel function (Na Intracell & K Extracell) caused (1) edema of the brain (2) NMDA depolarisation that lead to: 1. Cell necrosis (<5ml) 2. Activation of Glutamate cascade (Ca extracell influx cause catastrophic membrane cell injury and acceleration of cell apoptosis) which all leads to (1) Cognitive deficit and neurological impairment, cell death, and (2) activation of PFE (proteinase, Fosfolipase, Endonuklease)
Pathophysiology Bleeding
AVM / Aneurysm / Hypertension cause the blood vessel to RUPTURE, lead to an increased intracranial pressure ICP symptoms perivascular bleeding edema
Unmodifiable
Risk Factors
Male > Female Age >50 y o more susceptible to CVA Race white skin > black skin, hereditary
Radiology
Thorax Photo: Cardiomegaly; Tumour; TB; etc ECG MRI / CT: GOLD STANDARD
Head CT: Initial Assess ( Bleeding > Infarct) MRI : to assess infarct stroke, brain stem origin
LP
Topical Diagnoses
Carotis vascular origin
ICA: Blindness; dysphagia; contralat hemiparesis ACA: Mental disorder; seizures; urine incontinence; hemiparesis contralateral (leg> arm) MCA: Hemi / hyperesthesia; Aphasia; Spatial disorder; Hemiparesis contralateral (leg=arm / leg<<arm&face) Double hemisphere: Hemiplegic duplex; disphagia; dysartria; emotional disorder; pseudobulbar paralysis
Dx Etiology DD
1. Tumor 2. Trauma 3. Infeksi 4. Stroke 5. Metabolic (Hypoglicemia) 6. Todds Paralysis 7. Multiple Scerosis 8. CP 9. Toxin 10.HT encephalopathy
Therapy
B1-B6 1. B1 Breathing
Free the airway: tilt/oblique position; O2; ETT;etc
2. 3. 4. 5. 6.
Anti Platelet Aggregtion RIND (progressive) IVFD Anti Platelet Aggregation Phentoxyphilline Metabolit Ativator Neuroprotectant + Neurotropic Rehab + avoid risk fx Complete Stroke +CCB