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1. HYPERTENSIVE CRISES AND PERIPHERAL ARTERIAL DISEASES MUTYABA MICHAEL SEBITOSI

2. Outline Definitions Hypertensive emergency Severe asymptomatic Hypertension Causes of hypertensive crisis Diagnostics Management Special Considerations Differential diagnosis Complications

3. Definitions Hypertensive Crisis : sudden severe elevation of blood pressure above 180/120mmHg. Severe Hypertension : Term used broadly to define a very high blood pressure (>180/120 mmHg) Hypertensive Emergency : Severe elevation in blood pressure above 180/120 mmHg accompanied by acute life-threatening end-organ damage. Severe Assymptomatic Hypertension : Severe elevation in blood pressure above 180/120mmHg in absence of symptoms or evidence of Acute end-organ damage.

4. Malignant Hypertension : A subtype of hypertensive emergency characterized by severely elevated blood pressure accompanied by end-organ damage. Commonly papilledema. Accelerated Hypertension : Refers to subtype of hypertensive emergency characterized by a recent significant increase over baseline blood pressure with end-organ damage. Hypertensive Urgency : Other name for severe asymptomatic hypertension

5. Note: There is potential for end-organ damage even when the BP is below the 180/110-120mmHg.

6. Severe asymptomatic HTN BP ≥180/120 without evidence of end-organ damage (may have mild headache) Assess adherence to prior treatment before aggressively up-titrating regimen to avoid overcorrection of BPs & hypotension Assess cause before treatment; commonly due to pain, anxiety, urine retention, meds (e.g. steroids), OSA, nausea, withdrawal, etc.

7. Hypertensive emergency Refers to a BP ≥180/120 mmHg with evidence of acute end-organ damage. Rate of rise is more often more important than the actual BP. This explains why patients with a prior diagnosis of hypertension tolerate higher levels of BP without symptoms compared to those presenting with hypertension for the first time. There is a characteristic fibrinoid necrosis of the arterioles and small arteries leading to the end organ damage.

8. End-organ damage Neurological : HTN encephalopathy (severe HA, seizure, AMS), PRES, TIA, CVA (SAH, ICH) Occular: Retinopathy , Papilledema, Hemorrhage Respiratory : Pulmonary edema Cardiovascular : MI, Angina, Aortic dissection Hematological : Microangiopathic Hemolytic Anemia Renal : Acute Renal Failure, Hematuria, Proteinuria

9. The most common clinical presentation of hypertensive emergency are: Cerebral infarction (24.5%) Pulmonary Edema (22.5) Hypertensive Encephalopathy (16.3%) Congestive Heart Failure (12%) Less common presentations include intracranial hemorrhage, Aortic Dissection and Ecclampsia

10. Causes of Hypertensive crisis Idiopathic Non-adherence to drugs Secondary hypertension causes including: Pregnancy Hyperthyroidism Pheochromocytoma Renal artery stenosis Use of cocaine or MAOIs Withdrawal of alcohol, beta-blockers, alpha stimulants

11. Diagnostics Physical examination Vitals: Elevated BP and Tachycardia General examination: Edema CVS: tachycardia, added sounds(S4) displaced apex beat due to dilated Cardiomyopathy, Jugular venous distention Respiratory exam: Rales Opthalmologic exam: Nicking of blood vessels, Retinal hemorrhages, Soft exudates and papilledema

12. Diagnostics (Labs) Complete Blood Count Electrolytes BUN LFTs RFTs Urinalysis TSH 24h Vanillylmadellic acid

13. Diagnostics: Imaging Chest radiograph: Cardial enlargement, pulmonary edema other structures Transesophageal electrocardiography Renal angiography Electrocardiogram

14. Management: Severe Asymptomatic Hypertension Floor vs outpatient Management (with close follow up) ↓BP no more than 25-30% over hrs-days; then to goal as outpatient. There is no evidence to support rapid lowering of BP in this case. If hospitalized for non-cardiac reason, worse outcomes with intensifying anti-HTN immediately on admission Oral medication is preferred. IV or high-dose meds are avoided due to increased risk for AKI, stroke and MI due to hypoperfusion

15. PO: start captopril, labetalol >> hydralazine (unpredict., reflex tachy) & convert to long-acting before discharge OR start long-acting agents

16. Management: Hypertensive Emergency Floor vs ICU Manage in the ICU if patient needs arterial line, anti hypertensive gtt or if severe end organ damage. Continuous cardiac monitoring Frequent assessment of neurological status Monitoring fluid intake and output Excessive BP reduction will cause hypoperfusion. Thus: Reduce by max 25% within 1st hour and no lower than 160/100mmHg within 2-6 hours. Reduce to baseline over 24-48 hours.

17. Management: Hypertensive Emergency Start with short acting titratable IV agents, then transition to oral agents on the floor or discharge. No single drug is recommeded, though IV: labetalol >> hydralazine Rapid acting sublingual or oral medications (nitroglycerin and captopril) may be used if there is no IV access.

18. Disease-process specific considerations Acute LV Failure with Pulmonary Edema Nitroglycerin OR Sodium Nitroprusside. Furosemide. Avoid hydralazine (increased cardiac work) and beta-blockers (decreased cardiac contractility). Acute Coronary Syndromes Nitroglycerin OR Labetalol OR Esmolol. Avoid hydralazine (increased cardiac work).

19. Disease-process specific considerations Aortic Dissection Rapid HR reduction in first 10 minutes to <60. BP reduction to <120-140 mmHg in first 60 min ICU management due need for arterial line. Labetalol OR Esmolol OR Metoprolol OR Nitroglycerin OR Sodium Nitroprusside. Surgery consult Eclampsia/Pre-eclampsia Magnesium sulfate in eclampsia. Nifedipine OR Labetalol OR Hydralazine OR Methyldopa in pre-eclampsia.

20. Disease-process specific considerations Hypertensive Encephalopathy Diagnosis of exclusion after ruling out intracranial pathology. Labetalol OR Hydralazine. Avoid sodium nitroprusside if suspected ICP due to intracerebral shunting. Acute Ischemic Stroke Higher MAP essential to perfusion. BP should not be lowered acutely except at extremes (some clinicians use >220/120). Gradual BP reduction should occur. Thrombolysis contraindicated with extreme hypertension due to risk of bleeding. Lower BP to <185/110 pre-treatment and maintain <185/105 throughout treatment. Labetalol OR Hydralazine OR Enalapril often used.

21. Disease-process specific considerations Acute Intracranial Hemorrhage Systolic BP >220 mmHg can be harmful. Debate exists over target BP, <140 mmHg or <180 mmHg systolic often used. Labetalol OR Esmolol OR Enalapril OR Phentolamine.

22. Management Ambulatory vital monitoring. IV monitoring may be neccesary Diet and Lifestyle modification Follow-up Patient education on warning signs

23. Differential Diagnosis Acute kidney injury Aortic coarctation Aortic dissection Chronic kidney disease Ecclampsia Hyperthyroidism Pheochromocytoma Renal artery stenosis Subarchnoid hemorrhage

24. Complications Renal Failure Vision loss Myocardial Infarction Stroke

25. Questions....?

26. Peripheral Arterial Disease

27. Outline Definition Etiology Risk factors Presentation Diagnosis Management Acute Limb Ischemia

28. Definition PAD refers to tissue damage in the arms and legs arising from a mismatch between blood supply relative to tissue metabolism due to narrowing of the arteries. Peripheral artery disease is usually a sign of extensive arteriosclerosis. The signature feature of PAD is claudication. Which refers to a pain in the limb, normally the calves during walking. The papin is normally relieved by rest.

29. Etiology Atherosclerosis. Swelling or irritation of blood vessels Injury/Trauma to the limbs Changes in muscles or ligaments Radiation exposure

30. Risk factors for PAD Modifiable Smoking High blood pressure High cholesterol Diabetes Obesity Physical inactivity Non-Modifiable Age Family history

31. Common symptoms of PAD Leg pain or cramping especially when walking: Classic claudication: reproducible exertional pain distal to occlusion, relieved by rest. Numbness Coldness Sores Changes in skin color or teture Reduced or absent pulses in the limbs

32. Rutherford Classification

33. Diagnosis of PAD History Physical examination Checking local pulse Local examination of skin texture, temperature, hair or ulcers Labs Doppler Ultrasound MRA CTA Exercise testing: if high suspicion for PAD & normal resting ABIs

34. Doppler US findings

35. Management Optimize CV risk factors (e.g., HTN, DM, HLD, weight loss), formal exercise program, high-intensity statin, smoking cessation CLEVER-RCT: supervised exercise therapy is at least as effective as stenting ERASE-RCT: supervised exercise therapy + revascularization > exercise alone

36. Management Ischemic ulcers Proper wound care (proper fitting breathable shoes, Moisturising creams, Hygiene) Revascularization for appropriate healing depending on ABI

37. Management: Pharmacologic Treatment is not as effective as CAD. Especially the use of vasodilators. Anti-platelets If symptomatic, low dose aspirin <300mg or clopidogrel 75mg qd to decrease risk of MI, CVA and vascular death If asymptomatic, consider low dose aspirin .

38. Management Avoid Dual antiplatelet therapy (DAPT) unless clinically indicated, usually post-revascularization. Anti-coagulation : rivaroxaban 2.5mg BID + Aspirin:decreases adverse cardiac & limb events vs ASA alone . Use with caution as this increases major bleeding, but no fatal bleeding in pts w/ stable PAD in study Thrombolysis : Streptokinase and Ralteplse are effective in acute cases.

39. Management Cilostazol : Start 100mg BID. PDE3 inhibitor with vasodilatory and anti-platelet effects. Adjunct for symptom relief refractory to exercise therapy/smoking cessation. Use in combination with ASA or anti platelet Only AHA/ACC recommended drug to increase exercise capacity Contraindicated in HF. Ie helps relieve symptoms of claudication. Angiogenic growth factors like VEGF and bFGF are being studied. They are also been shown in reduce claudication.

40. Management Revascularisation : Endovascular repair (Percutaneous Transluminal Angioplasty (PTA) vs stent vs Athrectomy) if threatened limb and/or severe symptoms refractory to medical management. Assess benefit of revascularization vs amputation.

41. Complications of PAD Tissue damage: Ulcers Gangrene Amputation secondary to critical limb ischemia Myocardial infarction Stroke

42. Acute Limb Ischemia Sudden decrease in limb perfusion threatening viability. It is the most severe pattern of PAD. It develops over hours to days. It is a surgical emergency that requires immediate consultation with vascular surgery Viable : no immediate threat of tissue loss; audible arterial Doppler signal, intact motor/sensory Threatened : salvage requires prompt intervention; no audible arterial Doppler signal, motor or sensory deficits

43. Etiologies Embolic (e.g., AF, endocarditis, proximal lesion) Thrombosis (e.g., atherosclerosis, APS, HITT) Trauma

44. Precipitating factors Dehydration Hypotension Abnormal posture (i.e. kneeling) Malignancy Hyperviscosity Hypercoagulability

45. Presentation (6Ps) Pain Poikilothermia Pallor Pulselessness Paresthesia (unable to sense light touch) Paralysis

46. Diagnosis Pulse with Doppler ultrasonography Angiography

47. Treatment Urgent Vascular Surgery consult Anti-coagulation ± thrombolytic therapy Endovascular repair

48. Complications After treatment, monitor for: Reperfusion acidosis Hyperkalemia Myoglobinemia (AKI) Compartment syndrome Monitor for other complications like Stroke, MI etc

49. Harrison’s Principles of Internal Medicine Up-to date Medscape

50. The end Questions???