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  2. 2. OUTLINE • Introduction • Epidemiology • Aetiology • Pathophysiology • Clinical presentation • Investigations • Treatment • Prognosis • Conclusion • References
  3. 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. 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. 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
  6. 6. Aetiology • Non compliance with medications • Withdrawal from antihypertensive agents (clonidine) • Sympathomimetics (cocaine, amphetamines, phencyclidine) • Pheochromocytoma • Renal parenchymal dxs; AGN, HUS,SLE, tubulointerstitial nephritis • Renovascular dxs • Collagen vascular disease
  7. 7. Pathophysiology
  8. 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. 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. 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. 11. Management • It is a medical emergency • Brief and targeted hx • Resuscitation
  12. 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. 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. 14. • CVS; relative bradycardia, markedly elevated BP, ± features of long standing HTN • Chest ; abnormal respiration
  15. 15. Investigations • Brain imaging • FBC • EUCR, Urinalysis • CXR • ECG • Toxicology screening • Serum metanephrines
  16. 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. 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. 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. 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
  20. 20. Complications • Nephropathy • Retinopathy • MI • Stroke • Status epilepticus • Coma • Death
  21. 21. Differentials • Stroke • Encephalitis • Hepatic encephalopathy • Uremic encephalopathy
  22. 22. Follow up • Discharge on antihypertensives • Emphasis on importance of adherence • Lifestyle modifications • Follow up for reassessment
  23. 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. 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. 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
  26. 26. THANK YOU

Editor's Notes

  • 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.