Hypertensive Encephalopathy and Emergencies

Hypertensive Encephalopathy and Emergencies

1. WELCOME TO MORNING SESSION

2. DR.MD.SAZZAD HOSSAIN SAJAL INTERN DOCTOR MEDICINE DEPARTMENT TMMC&H

3. Hypertensive encephalopathy and Hypertensive Emergencies

4. 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 .

5. 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 )

6. 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).

7. 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.

8. 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

9. 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)

10. 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

11. Treatment:- L owering 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

12. 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)

13. 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)

14. 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.

15. 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.

16. 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

17. 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%

18. 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

19. 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

20. 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

21. 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

22. 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

23. 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)

24. Medications Preferred agents by end organ damage Pulmonary Edema (systolic)— Nicardipine Pulmonary Edema (diastolic)— Esmolol Myocardial ischemia and infarction Nicardipine plus esmolo l 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

25. 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.