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DR.MD.SAZZAD HOSSAIN SAJALINTERN DOCTOR

MEDICINE DEPARTMENTTMMC&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 terminologyThe 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– Severe headache– Nausea and vomiting– Visual disturbances– Confusion– focal or generalized weakness

- irritability and altered mental status due to cerebrovascular spasm

• Signs– Disorientation– Focal neurologic defects– Focal or generalized seizures– nystagmus

Investigations:-• CT scan of the brain often shows

haemorrhage 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, oftensevere, elevations in blood pressure, accompanied by rapidly progressivetarget 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%– Acute renal failure……………………………………9%

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 hypertensive retinopathy

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

Treatment• 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.