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SESSION
DR.MD.SAZZAD HOSSAIN SAJAL
INTERN DOCTOR
MEDICINE
DEPARTMENT TMMC&H
Hypertensive encephalopathy
and
Hypertensive Emergencies
 HYPERTENSIVE
ENCEPHALOPATHY
• Definition:-
• Hypertensive encephalopathy is a rare
condition characterized by high BP and
neurological symptoms, including transient
disturbances of speech or vision,
paraesthesiae, disorientation, fits ,loss of
consciousness and papilloedema.
• Hypertensive encephalopathy is a
neurological dysfunction induced by
malignant hypertension.
• Malignant hypertension is commonly defined
as sustained, elevated arterial blood
pressure, with diastolic levels of 130 mm Hg
or greater and systolic pressure in excess of
200 mm Hg.
(cecil)
 Historical note and terminology
The term “hypertensive encephalopathy” was
introduced by Oppenheimer and Fishberg
(Oppenheimer and Fishberg 1928). They
described essential clinical characteristics of
acute malignant hypertension. Ten years
prior, Volhard was the first to separate clearly
acute hypertension-induced neurologic
dysfunction from a uremic state and
introduced the term “pseudouremia” to refer
to hypertensive encephalopathy (Volhard
1918).
 PATHOGENESIS:-

• The pathogenesis of hypertensive encephalopathy

remains unclear.
• Pathologic findings include purpura in the brain, retinal
hemorrhages, papilledema,and fibrinoid arteriolar lesions
of the glomeruli.
• Diffuse fibrinoid necrosis and thrombotic occlusion of
arterioles cause micro infarctions and petechial
hemorrhages, and these changes lead to distal ischemia.
• Ring hemorrhage around a thrombosed precapillary is the
characteristic microscopic lesion of hypertensive
encephalopathy. Multiple, compacted petechiae can
resemble a hematoma.
 HTN Encephalopathy
• Symptoms • Signs
– Severe headache – Disorientation
– Nausea and vomiting – Focal neurologic
– Visual disturbances defects
– Confusion – Focal or generalized
– focal or generalized seizures
weakness – nystagmus
- irritability and
altered mental status
due to
cerebrovascular
 Investigations:
• - brain often shows haemorrhage
CT scan of the
in and around the basal ganglia; however, the
neurological deficit is usually reversible if the
hypertension is properly controlled.
• Urine for blood, protein and glucose
• Blood urea, electrolytes and creatinine
• Blood glucose
• Serum total and HDL cholesterol
• Thyroid function tests
• 12-lead ECG (left ventricular hypertrophy,
coronary artery disease)
 Diagnosis:-
• Differential diagnosis of hypertensive
encephalopathy include hemorrhagic and
ischemic strokes. Focal neurologic signs
predominate in these other conditions, whereas
mental status changes are characteristic of
hypertensive encephalopathy.
• In increased intracranial pressure from
obstructive hydrocephalus ,brain tumor or
subdural hematoma can elevate blood
pressure and slow the pulse, but
encephalopathy and markedly elevated blood
pressure are absent
 Treatment:-
• Lowering BP too quickly may compromise tissue
perfusion and can cause cerebral damage,
including occipital blindness, and precipitate
coronary or renal insufficiency.
• In hypertensive encephalopathy, a controlled
reduction to a level of about 150/90 mmHg over
a period of 24–48 hours
• Oral Therapy:-
sublingual captopril can
substantially lower the BP within 10 to 30 minutes
in many patients
• Parenteral therapy :- must be given under
careful supervision and in a high dependency
unit-
• Intravenous or intramuscular labetalol (2
mg/min to a maximum of 200 mg),
• intravenous glyceryl trinitrate (0.6–1.2
mg/hr),
• intramuscular hydralazine (5 or 10 mg
repeated at half hourly intervals)
• intravenous sodium nitroprusside
(0.3–1.0
µg/kg body weight/min)
 Control of fits and Seizures:-
• Seizures Can usually be stopped with
intravenous diazepam (10 mg); in
eclamptic patients fosphenytoin (15 to 20
mg phenytoin equivalent per kilogram
intravenously)
• It is important to remember that
rarely hypertensive encephalopathy
may present with primary brainstem
edema with or without occipital
involvement. This so-called
“brainstem hypertensive
encephalopathy” may not respond to
simple blood pressure lowering, and
surgical intervention may be life-
saving.
• Prognosis:-
• Patients with hypertensive encephalopathy
who are promptly treated usually recover
without deficit. However, if treatment is not
administered, the condition can lead to death.
• Hypertensive Emergency

– Hypertensive emergencies are acute, often

severe, elevations in blood pressure,
accompanied by rapidly progressive
target organ dysfunction, such as myocardial
or cerebral ischemia or infarction, pulmonary
edema, or renal failure.
– BP should be controlled within hours and
requires
admission to a critical care setting
• End-Organ Damage (% of cases)
– Cerebral infarction……………………………………
24%
– Hypertensive encephalopathy……………………16%
– Intracranial hemorrhage……………………………4.5%
– Acute aortic dissection………………………………2%
– myocardial infarction…12%
– Pulmonary edema with respiratory
failure…………22%
– Severe eclampsia/HELLP
syndrome………………2%
– Acute congestive heart
failure……………………14%
 Pathophysiology

• Hypertensive Emergency
– Failure of normal autoregulatory function
– Leads to a sharp increase in systemic vascular
resistance
– Endovascular injury with arteriole necrosis
– Ischemia, platelet deposition and release of
vasoactive substances
– Further loss of autoregulatory mechanism
– Exposes organs to increased pressure
 Clinical feature
• hypertensive emergency is a critically ill patient
who presents with a blood pressure above 220/140
mm Hg,
• headaches,
• confusion,
• blurred vision,
• nausea and vomiting,
• seizures,
• pulmonary
edema,
• oliguria
and
• grade 3 or
grade 4
hypertensi
 Diagnosis and Recognition
• Presentation
– Always present with a new onset symptom
• Take a good history
– History of HTN and previous control
– Medications with dosage and compliance
– Illicit drug use, OTC drugs
 Diagnosis and Recognition
• Physical
– Confirm BP in more than one extremity
– Ensure appropriate cuff size
– Pulses in all extremities
– Lungs examination—look for pulmonary edema
– Cardiac—murmurs or gallops, angina, EKG
– Renal—renal artery bruit, hematuria
– Neurologic—focal deficits, HA, altered MS
– Fundoscopic exam—retinopathy, hemorrhage
 Diagnosis and Recognition
• Laboratory/Radiologic evaluations
– BUN
– CBC with smear (hemolytic anemia)
– Urine (proteinuria, hematuria)
– S. creatinin
– ECG to look for ischemia
– CXR to look for pulmonary edema if dyspnea
– Head CT for evaluation of stroke
– MRI chest if unequal pulses and wide
mediastinum to look for aortic dissection
 Treatmen
• t
Hypertensive Emergency
– Goal: Lower DBP by 10-15% in 30-60 min
– controlled reduction to a level of about 150/90 mmHg
over a period of 24–48 hours is ideal
– Initiate oral therapy and IV medications down
• Intravenous or intramuscular labetalol (2 mg/min to a
maximum of 200 mg),
• intravenous glyceryl trinitrate (0.6–1.2 mg/hr),
• intramuscular hydralazine (5 or 10 mg aliquots repeated
at half hourly intervals)
• intravenous sodium nitroprusside (0.3–1.0 µg/kg body
weight/min)
 Medications
• Preferred agents by end organ damage
– Pulmonary Edema (systolic)—Nicardipine
– Pulmonary Edema (diastolic)—Esmolol
– Myocardial ischemia and infarction
Nicardipine plus esmolol
Nitroglycerin plus
labetalol Nitroglycerin
plus esmolol

– Hypertensive Encephalopathy—
Labetolol
– Acute Aortic Dissection—Labetolol
– Eclampsia—Labetolol or Nicardipine
– Acute kidney injury
Fenoldopam
Nicardipine
– Sympathetic Crisis/Cocaine—Verapamil
or Diltiazem
 References
• Davidson’s principles and practice of
medicine
• Kumar & Clark's Clinical Medicine, 7th Edition
• Goldman's Cecil Medicine, 24th
• CURRENT Medical Diagnosis and Treatment
2015
• www.wekipidea.com
• Flanigan, J. and Vitberg, D. “Hypertensive Emergency
and Severe Hypertension: What to Treat, Who to Treat,
and How to Treat.” The Medical Clinics of
North America. Vol 90 (2006) pp. 439-451.