Hypertensive Encephalopathy is an acute transient disturbance of cerebral function due to sudden rise of blood pressure in cases with severe hypertension.


Due to sudden high rise of blood pressure, there is cerebral arteriolar constriction and consequent cerebral ischaemia. Recently considerable doubt has been thrown regarding cerebral vasospasm. Current thought is that there is multifocal arteriolar constriction and dilatation leading to diffuse micro haemorrhage which may lead to ischaemia. The episode is transitory.


(i) Hypertension.

(ii) Abrupt withdrawal of anti-hypertensive drugs.

(iii) Immune complex nephritis.

(iv) Chronic nephritis.

(v) Toxaemias of pregnancy.

(vi) Phaeochromocytoma.

(vii) Chronic lead poisoning (Lead produces vasoconstriction).

(viii) Intake of food rich in tyramine in patients taking MAO inhibitor.


Onset of Hypertensive Encephalopathy is usually sudden.


(a) Headache.

(b) Vomiting.

(c) Blurring of vision (cortical type).

(d) Speech disturbances.

(e) Paraesthesia.

(f) Convulsion.

(g) Hemiparesis.

(h) Somnolence.

(i) Stupor and coma.


Patient is usually in stupor or in coma. Pupils are dilated but not reacting to light, slight neck rigidity may be present, plantar reflex is extensor on both sides, there may be evidences of hemiparesis which disappears completely after the attack is over.

Blood pressure is always high, in the vicinity of 250/150 mm of Hg. Heart sounds are accentuated.

There may be bradycardia. Ophthalmoscopic examination may reveal hypertensive retinopathy, even early papilloedema. LP shows high CSF pressure (above 180 mm of water) with elevation of protein level and cells (both RBC and WBC).


1.Cerebral haemorrhage

Patient is deeply comatose, all reflexes are lost, stertorous and Cheyne-Stoke’s breathing may be present, lumber puncture shows frank blood, patient progresses downhill and expires within a few hours to few days.

2.Cerebral thrombosis and Embolism

Headache and vomiting are usually absent, hemiplegia is present, BP is not usually so high. Coma is usually absent, LP shows no CSF change.

3.Subarachnoid haemorrhage

Severe occipital headache followed by deep coma, hemiplegia or hemiparesis are not usually present. Neck rigidity is marked Ophthalmoscopic examination shows subhyaloid haemorrhage and pailloedema. LP shows frank blood with increased tension. Prognosis is usually good.


Transient attacks of unconsciousness with tonic and clonic spasms are present. Attack very soon passes off. BP is not high. It usually occurs in children and often recurs

5.Intracranial tumour

Onset is gradual, headache and vomiting are present for a long time, ophthalmoscopic examination may show bilateral papilloedema, bradycardia may develop very insidiously, cranial nerve palsy may be present, X-ray of the skull, cerebral angiography, ventriculography, EEG, brain scan and ECHO encephalography are helpful for diagnosis.

6.Stokes-Adams attack

Transient and recurrent unconsciousness in aged persons may be seen with fixed pulse rate of 36-40 per min and during attack pulse may be absent or markedly slow (such as 20/ min). No neurological signs except transient unconsciousness is present. ECG is diagnostic.


1. Rest in bed in a railed cot with all precautions for unconscious patient. ITU is preferred.

2. Urgent reduction of BP may be done with IV Sodium nitroprusside and then BP should be gradually lowered. In presence of uraemia Hydrallazine, Prazosin or Diazoxide may be used.

3. Diuretics like Frusemide 40 mg IM or 20 mgm IV may be used, and may reduce cerebral oedema. The foramen also help in lowering BP.

4. To reduce intracranial tension-lumber puncture may be done or 50% 50 cc Glucose IV or 50 % 100 cc Sucrose IV may be given. Intravenous Mannitol 25%, 200-400 cc may also be given with good result.

5. For convulsion-Paraldehyde 6-8 cc IM or Phenobarbitone sodium 0.2 mg or Diazepam 10-20 mg IM or IV may be given.

6. After the attack is over the underlying cause should be treated as far as practicable.

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