HYPERTENSIVE ENCEPHALOPATHY.pptx

for undergraduate medical students

1. HYPERTENSIVE ENCEPHALOPATHY DEPARTMENT OF INTERNAL MEDICINE CARDIOLOGY UNIT PRESENTER: AKORGA MEMBER ERYKAH DATE: 19/07/2022

2. OUTLINE Introduction Epidemiology Aetiology Pathophysiology Clinical presentation Investigations Treatment Prognosis Conclusion References

3. Introduction Hypertensive encephalopathy is one of the manifestation of hypertensive crisis Hypertensive crises is classified into Hypertensive emergency; cerebral infarction, HTN encephalopathy, ALVHF, aortic dissection , MI, eclampsia , AKI 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

6. A etiology 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. Pathophysiology

8. Pathophysiology T he 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 E xamination 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

15. Investigations Brain imaging FBC EUCR, Urinalysis CXR ECG Toxicology screening Serum metanephrines

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

20. Complications Nephropathy Retinopathy MI Stroke Status epilepticus Coma Death

21. Differentials S troke Encephalitis Hepatic encephalopathy Uremic encephalopathy

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 5 th edition Braunwald textbook of cardiovascular medicine 11 th edition Medscape

26. THANK YOU