3. Introduction
• Hypertensive encephalopathy is one of the
manifestation of hypertensive crisis
• Hypertensive crises is classified into
o Hypertensive emergency; cerebral infarction,
HTN encephalopathy, ALVHF, aortic dissection
, MI, eclampsia, AKI
o Hypertensive urgency
4. Introduction….cont’d
• Hypertensive encephalopathy was introduced in
1928 by oppenheimer and Fishberg to describe
accelerated and malignant phase of HTN
• It is a less commonly encountered type of
hypertensive emergency
• HTNsive encephalopathy refers to the transient
migratory neurologic symptoms associated with
malignant hypertensive state in hypertensive
emergency
• Clinical symptoms are reversible with prompt
treatment
5. Epidemiology
• About 1billion people have HTN out of which 1-
2% develop HTN emergency
• Hypertensive encephalopathy accounts for 15%
of HE
• Mostly occurs in middle aged individuals who
have a hx of longstanding HTN
• The frequency of hypertensive encephalopathy
in various races corresponds to the frequency of
HTN in general population
• Commoner in men than women
8. Pathophysiology
• The brain sustains blood flow within a narrow
perfusion pressure range without being
affected by fluctuations in systemic arterial
pressure.
• For healthy individuals, the pressure ranges
are 50-150 mm Hg cerebral perfusion pressure
(CPP) or 60 to 160 mm Hg mean arterial
pressure (MAP).
• The CPP = MAP – intracranial pressure (ICP).
9. Pathophysiology…..cont’d
• With increased MAP, cerebral arteriolar
vasoconstriction occurs, with decreased MAP,
arteriolar dilation occurs to keep the CPP
constant.
• This adaptive process maintains brain perfusion
at a constant level despite SBP changes.
• In chronically hypertensive pts, the cerebral
autoregulatory range is gradually shifted to
higher pressures as an adaption to chronic ↑
SBP
10. Pathophysiology…..cont’d
• However, a sudden and severe increase in
arterial pressure can exceed this autoregulatory
mechanism because the arterioles are limited in
their ability to constrict
• The then intracerebral elevated blood pressure
causes a breach in the blood-brain barrier, and
vascular fluid diffuses across the capillary
membranes into the brain parenchyma.
• This leads to the development of cerebral edema,
increased intracranial pressure, and neurologic
deficits, visual deficits, and seizures
11. Management
• It is a medical emergency
• Brief and targeted hx
• Resuscitation
12. Clinical presentation
History
• Pts present with vague neurologic symptoms
of headache, change in mental status,
irrational talk, restlessness, visual
disturbances, seizures, nausea, vomiting,
• May present with symptoms of other end
organ damage from other systems
13. Clinical presentation….cont’d
Examination
• Middle aged, confused or unconscious
• Nervous system reveal altered mental status,
transient nonfocal deficits(nystagmus to
weakness)
• Fundoscopy; features of hypertensive
retinopathy (cotton wool spots, haemorrhage
exudates, papilloedema)
14. • CVS; relative bradycardia, markedly elevated
BP, ± features of long standing HTN
• Chest ; abnormal respiration
16. Treatment
• 2018 ACC/AHA guildlines
• ICU management for continuous monitoring
• Goal of treatment is immediate but controlled
reduction in MAP by 25% within 1-2hrs using
parenteral antihypertensives and an absolute
value of 160/100-110mmhg
• Relieve of raised ICP
• Monitor neurological state, ECG, fluid balance
17. Treatment …..cont’d
• Labetalol: A 20 mg bolus is given initially,
followed by subsequent boluses of 20 to 80
mg intravenously every 10 minutes to a
maximum total dose of 300 mg in a day.
Labetalol can also be given as a continuous
infusion at 0.5 to 2 mg/min.
• Nicardipine: The initial dose is 5 mg/hour, and
the usual maximum dose is 15 mg/hour.
18. Treatment ……cont’d
• Fendolopam: The initial dose of infusion is 0.1
mcg/kg per min, and the dose is titrated at 15-
minute intervals, depending upon the
response.
• Clevidipine: The initial dose is 1 mg/hour, and
the usual maximum dose is 21 mg/hour.
• Sodium nitroprusside: The initial dose is 0.25
to 0.5 mcg/kg/min and the usual maximum
dose is 8 to 10 mcg/kg/min.
19. Treatment …..cont’d
• Elevate head of bed
• Hyperventilate pt
• Iv mannitol 250ml stat, then 250ml 8hrly
• Oral antihypertensives may be started as the
initial IV therapy is tapered and discontinued
after reaching the target BP
22. Follow up
• Discharge on antihypertensives
• Emphasis on importance of adherence
• Lifestyle modifications
• Follow up for reassessment
23. Prognosis
• The prognosis of patients with untreated HE is
poor if not treated promptly
• Before the introduction of antihypertensives,
1 year mortality exceeds 80% and 5 year
mortality was 99%.
• In the modern era of effective
antihypertensive agents, 10 year survival has
improved to 70%
24. Conclusion
• It is a manifestation of hypertensive
emergency requiring prompt and meticulous
treatment
• Brief hx and physical examination should be
done to identify and treat immediately to
prevent dare complications
25. References
• ESC Guidelines on management of
hypertension 2018
• ACC/AHA Guidelines on management of
hypertension 2018
• Cleveland manual of cardiovascular medicine
5th edition
• Braunwald textbook of cardiovascular
medicine 11th edition
• Medscape
The term accelerated and malignant HTN were used to describe the retinal findings with HTN
Accelerated HTN is associated with group 3 of keith wagener barker retinopathy….retinal haemorrge & exudate
Malignant htn is associated with group 4 of kwb retinopathy……..papilloedema
The incidence of HTN encephalopathy being highest in blacks and lowest in whites
Thereby preserving a constant cerebral blood flow and an intact BBB
Headaches are usually anterior and constant in nature
Complications
Failure or late treatment of a hypertensive emergency can result in renal failure, retinopathy, myocardial infarction, and stroke. In particular, without prompt treatment of high blood pressure in patients with encephalopathy, brain edema can progress and lead to status epilepticus, coma, or death. Aggressive treatment of hypertension is not advised and can lead to ischemic conditions in target organs, especially in patients with an adapted autoregulatory mechanism due to chronic hypertension.
The symptoms of hypertensive encephalopathy are insidious. Headache, nausea, and vomiting gradually worsen with time and are followed by non-localizing neurologic symptoms. This is in contrast to the abrupt and focal neurologic symptoms found with ischemic stroke or intracerebral hemorrhage.
