Hypertensive encephalopathy,
eclampsia,
and
reversibile posterior
leukoencephalopathy
Introduction
• Oppenheimer and Fishberg, 1928
• Hypertensive emergency:
– Severe elevation of blood pressure
that precipitates end organ damage
• Acute pulmonary edema, congestive heart failure, ischemic
chest pain, retinopathy, papilledema, retinal hemorrhagies,
aortic dissection, rapid deterioration of renal function,
hypertensive encephalopathy
• Hypertensive urgency:
– Severe elevation of blood pressure
without end organ involvement
Introduction
• Hypertensive encephalopathy and
eclampsia
– are similar syndromes that share a common
pathophysiology
• Clinical presentation
• Imaging findings
• theraphy
Cerebral autoregulation
CBF = CPP / CVR
CPP = MAP - ICP
Hypertensive encephalopathy-epidemiology
• Rare even in patients with severe
elevation of blood pressure
– Usually in previously normotensive individuals
– But also in chronically hypertensive patients
– Sympathomimetic drugs (cocaine,
amphetamine, MAO inhibitors)
Hypertensive encephalopathy-presentation
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•
•
•
•
•
•
Headache
Nausea
Vomiting
Visual obscuration (blurring to blindness)
Seizures
Aleteration in the level of consciousness
Hyperreflexia
(Phillips et al., 2002)
Eclampsia - presentation
• Similar to that of hypertensive
encephalopathy
• Association with pregnancy
• 20th week of getation – 2nd week after
parturition
• Lower blood pressures
• Peripheral edema and proteinuria
Normal perfusion pressure breakthrough
• Patients with severe carotid stenosis who
undergo carotid endarterectomy and
carotid stenting
Hypertensive encephalopathy-diagnosis I.
• Hypertension as a result of acute stroke vs.
Neurological symptoms due to hypertension
– Hypertensive encephalopathy is rare:
• Hypertensive crisis is rare (1%)
• premorbide hystory of hypertension is rare in patients who
develop hypertensive encephalopathy
– Symptom onset
• Acute and definitive vs. Subacute and progressive
– Symptoms distribution
• Focal vs. Global
• Retinal arteriolar spasms, papilledema, retinal hemorrhages
Hypertensive encephalopathy-diagnosis II.
• Imaging studies
– CT: low density changes in posterior regions of the brain
– MR more sensitive and specific
• Lesions hyperintense on T2 and hypointense on T1
• Predominantly vertebrobasilar circulation (occipital
lobes, cerebellum, brain stem),
but also deep white matter and basal ganglia
• Usually bilateral and symmetrical, white and gray
matter involvement
• The transient nature of these findings:
“reversible posterior leukoencephalopathy (RPLE)”
Hypertensive encephalopathy-diagnosis III.
• Imaging studies
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–
–
–
dwMRI
Acute diffusion coeficient (increased)
SPECT (increased flow and increased trcer uptake)
Lumbar puncture
• Oppening pressure
• Neutrophilic pleocytosis
– TCD (elevated arterial flow velocities)
Pathophysiology
• Breakthrough of normal cerebral
autoregulation
– Extravasation of fluids and proteins
• Vertebrobasilar system more vulnerable due to
less robust sympathetic innervation
• Reflex vasoconstriction
– Hypoperfusion and ischemia
• Angiografic studies showing vasospasm
• Permanent infarction in some cases
Theraphy I.
• Reduction of MAP within minutes, but no
more than 20-25% during the first 1-2h,
with further reduction over the hours to
days (Chobanian et al., 2003):
• Treatment of end organ damage
• Monitoring (Arterial line)
• Intensive care unit
Therapy II.
• Antihypertensive agent:
– Rapid and predictable onset
– Easy to titrate
– Patients premorbid BP
– Duration of hypertensive emergency
– Concomitant medical disease
– Extent of neurological involvement (rised ICP)
Therapy III.
• Vasodilators
– Sodium nitropruside
initial
titrate
0.5-1mcg/kg/min
as needed
– Nicardipine
5 mg/h
at 5–15min
– Fenoldopam
0.03 mcg/kg/min
0.05 mcg/kg/min
– Nitroglycerin
5 mcg/min
– Enalpril
1.25 mg/6h
– Diazoxide
1-3 mg/kg
increments 5 mcg/min
at 5 – 15 min
Therapy IV.
• Adrenergic inhibitors
initial
titrate
– Labetalol
20 mg
– Urapidil
10-50 mg
2-9mg/min
– Phentolamin
5-10 mg
0.2-5mg/min
• Drugo
– Magnesium i.v.
40-80 mg at 10 min
Therapy V.
• Antiepileptic drugs
– Benzodiazepines
– Phenitoin
– Magnesium
Prognosis
• Generally complete recovery
• Mortality rate 5%
Primer 1: hipertenzivna encefalopatija
Primer 2: eklampsija
Primer 3: normal perfusion pressure breakthrough