STROKE

Adi Putra Siswoyo

Anis Sopiyati

Annis Kurnia R

Astrid Ayu Alaika

Bangun Mulyadi

Danang Tri S

Dewi Ayu

Diyan Dwi Astuti

Dwi Ermawati

Fajar Nur R

DEFINITION

• Stroke is a disease of the brain functional disorder of acute focal or global symptoms and signs the appropriate part of the brain affected, previously without warning, and can recover completely, cured with a disability or death, resulting from interruption of blood flow to the brain due to bleeding or non bleeding (Junaidi Iskandar, 2002).

• Stroke is a clinical syndrome that initial sudden onset, rapid progression, a focal neurological deficit or global and lasting 24 hours or more or the direct cause of death, and solely caused by the interference of non traumatic brain blood circulation (Capita Selekta Medicine, 2000).

ETIOLOGY

• Trombosist• Cerebral Embolism• Ischemia• Cerebral Hemorragic

PATHOPHYSIOLOGY

• Partial or complete occlusion of a cerebral blood vessel resulting from cerebral thrombosis (due to arteriosclerosis) or embolism.

• Ischemia related to decreased blood flow to an area of the brain secondary to systemic disease, such as cardiac or metabolic disease.

• Hemorrhage occurring outside the dura (extradural), beneath the durameter (subdural ), in the subarachnoid space (subarachnoid), or within the brain substance (intracerebral).

• Risk factor include hypertension,TIAs, heart disease, elevated cholesterol, diabetes mellitus, obesity, carotid stenosis, polycythemia, cigarette smoking.

PATHWAY

CLINICAL MANIFESTATION

– Tingling or impaired sensibility and weakness of the limbs, including the face.

– Difficulty speaking or understanding speech, and suddenly became confused

– Impaired vision in one or both eyes– Difficulty walking, staggering or loss of balance– Severe headache with no apparent cause accompanied by nausea

and vomiting– Sudden change of behavior / mental status– Dysarthria

CLASSIFICATION

• Stroke Non Haemorragic

Stroke is caused by the following factors:

a. Stacking of fat in the blood vessels that lead from blood clots.

b. Foreign bodies in the blood vessels of heart

c. The existence of holes in blood vessels leak blood causing blood flow to the brain is reduced.

• Stroke Haemorragic

Stroke is caused by a blood vessel in the brain leaks or ruptures, blood fills the brain cells.

a. High blood pressure can cause blood vessel rupture

b. Consolidation of the blood vessels that cause blood vessel rupture

c. Tumor blood vessels

CLASSIFICATION

Differences Between Stroke Haemorragic and Stroke Non Haemorragic

Symptoms Stroke non Haemorragic

Stroke Haemorragic

Time Suddenly, when have a break

Suddenly, when do activity

Headache Light Great

Convulsions No Yes

Vomitus No Yes

Warning Signs Yes No

• Risk Factors that can be controlled- Hypertension

- Diabetes mellitus

- Smoking

- Heart disease

- Overweight / obesity

- Hypercholesterolaemia and hyperuricaemia

- Carotid artery abnormalities

- Hypercoagulation (simple blood clot)

- Excessive alcohol consumption

- Drug abuse

- Respiratory disorders during sleep (sleep apnea)

- Never get transient ischemic attack (TIA) before.

RISK FACTORS

• Risk Factors that can’t be controlled– Age– Sex– Racial / Ethnic Groups– Abnormalities congenital / hereditary– History of stroke / TIA previous

RISK FACTORS

• Depression• Frozen Blood• Pneumonia• Decubitus

COMPLICATION

• CT-Scan• Angigrafi• EEG• MRI• Brainplan• Ultrasonography dopler• Skuli Rontgenogram• Substraction Digital Angiography• Eshoencephalography• B. mode Ultrasound

RADIOLOGICAL EXAMINATION

• CT-Scan• Angigrafi• EEG• MRI• Brainplan• Ultrasonography dopler• Skuli Rontgenogram• Substraction Digital Angiography• Eshoencephalography• B. mode Ultrasound

RADIOLOGICAL EXAMINATION

CASE

A 38-year-old man had a sudden onset of right-sided weakness and fell to the

ground. On examination in the emergency department, blood pressure was 160/90

mm Hg, and he was alert with dysarthria and reduced speech output. He followed

simple, but not two-step, commands. He had a forced left gaze and right visual field

cut. Strength in the right arm and leg was antigravity only, and sensation was

diminished on that side. Head CT showed a hyperdense left MCA sign. He received

IV t-PA 150 minutes after symptom onset and was admitted to the ICU for monitoring.

The examination remained unchanged over the subsequent 16 hours, but at that

point blood pressure climbed to 190/100 mm Hg and he began to complain of

headache, had episodes of emesis, and became progressively less alert. The right

side became flaccid. Head CT showed a persistent hyperdense left MCA sign as well

as hypodensity in the entire left MCA territory with 8 mm of midline shift, subfalcine

herniation, and compression of the suprasellar cistern.

CRITICAL MANAGEMENT

1. Oxygenation teraphy

Sample Intubation Procedure for Patients With acute Ischemic Stroke at Risk for Elevated Intracranial Pressure

a. Preoxygenation : 100% oxygen for approximately 5 minutes Induction : Etomidate 0.1 mg/kg to, 0.5 mg/kg or thiopental, 1 mg/kg to 5 mg/kg

b. Intubation : Application of cricoid pressure (Sellick maneuver) Laryngoscopy with intubation

c. Confirmation of Placement : With Auscultation, End-Tidal Carbon Dioxide, and Chest X-ray

d. Postintubation : Full ventilatory support (assist control or intermittent mandatory ventilation) Hyperventilation (increase ventilation to lower arterial P CO to 25 mm Hg to 30 mm Hg) if acute neurologic deterioration or suspicion of increased. intracranial pressure is present . Sedation with short-acting agents such as fentanyl, midazolam, or propofol, as needed

2. Hyperosmolar Therapy

Osmotic agents such as mannitol and hypertonic saline lower elevated ICP and can reverse transtentorial herniation, effects that appear to be achieved primarily via extraction of water from the intracellular and interstitial spaces,resulting in temporary brain shrinkage.

Mannitol is typically administered as a bolus at a dose of 0.5 g/kg to 1.0 g/kg every 4 to 6 hours

Monitoring the clearance of mannitol between administrations is most effectively achieved with the osmolal gap (the difference between osmolality and osmolarity, calculated using the formula [2 sodium] + [blood urea nitrogen/3] + [glucose/18]) rather than simple osmolality since only the former correlates well with mannitol levels (Garcia-Morales et al,2004)

Clearance of mannitol between doses should be monitored with the osmolal gap, and urine output should be replaced with isotonic fluids to reduce risk of rebound intracranial hypertension and renal failure.

NCP

Thank You