| ID | 117 |
|---|---|
| Name | CEREBRAL HAEMORRHAGE (IN ACUTE STROKE) |
| Cause | Causes: 1. Rupture of microaneurysms 2. Arteriovenous malformation 3. Rupture of intracerebral arteries (hypertension, atherome-tous degeneration). 4. Other causes- tumour, abscess, anticoagulants & blood discrasias. |
| Signs Symptoms | |
| Diagnosis | |
| Investigations | Investigations for acute stroke:1-2 1. CT/MRI- to know whether the lesion is vascular or else? whether ischaemic or haemorrhagic? whether subarachnoid haemorrhage? 2. Carotid duplex ultrasonography- to detect any significant stenosis of the internal carotid artery. 3. Lumbar puncture (LP) for CSF-to know whether subarachniod haemorrhage? 4. To know underlying vascular disease: (as desired by the consultant physician) ECQ Cardiac ultasound, MRA, Doppler ultrasound, Contrast angiography. 5. To know the risk factors: (as desired by the consultant physician) Complete blood count, Fasting blood glucose, Serum cholesterol, Serologic test for syphilis, Clotting/thrombo-philia screen. Chest X-ray. |
| Management | Management: A. General measures- Careful nursing Regular turning of patient to avoid pressure sores; skin kept dry and clean. Care of airway Oropharyngeal tube with regular suction of secretions if patient is unconscious. Fluid balance Nasogastric feeding if patient cannot swallow; bladder catheterisation if there is incontinence. Physiotherapy Start immediately to prevent joint contractures; to clear chest secretions; to promote recovery of strength and coordination. Speech and occupational therapy Start once acute stage over to assess functional problems and to encourage recovery of skills B. Specific measures - 1. Antihypertensive agents- if there are features of accelerated hypertension and/or signs of end-organ involvement, antihypertensive agents are necessary, otherwise not. 2. Anticoagulant- if there is a clear persisting embolic source (e.g AF. etc). 3. Osmotic diuretics and potent Steroid- to reduce brain oedema if present. 4. Vasodilator- vinpocetine may be used to increase the cerebral blood flow- but role is still doubtfull. 5. Surgery- drainage of the haematoma in cerebral haemorrhage is life saving. C. Continuing management - - Rehabilitation of the patient. - Avoidance of risk factor. |
| Introduction | |
| History | |
| Etiology | |
| Clinical Features | Clinical presentation (of stroke): Majority of patients exhibits- 1. Hemiparesis or hemiplegia 2. Dysphasia, with or without- 3. Hemianaesthesia or homonomous hemianopia. 4. Flaccid paralysis with extensor planter response initially, lateron tone usually increases and reflexes become hyperactive on the affected side. With severe hemisphere damage flaccid hemiplegia, impaired consciousness & papilloedema occur. If stroke affecting the brain stem-Oculomotor palsy, palatal paralysis in same side. Pyramidal and spinothalamic signs in opposite limbs. |
| Preventions | |
| Treatment | |
| Complications | |
| Prognosis | |
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