Vascular Emergencies. Scott M Surowiec, MD Assistant Professor of Surgery Upstate Vascular and Crouse Hospital September 29, 2015

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1 Vascular Emergencies Scott M Surowiec, MD Assistant Professor of Surgery Upstate Vascular and Crouse Hospital September 29, 2015

Introduction Main vascular emergencies include Ruptured Abdominal Aortic Aneurysm (raaa) Aortic Dissection Acute Limb Ischemia Embolism from Cardiac Source Most Common Thrombosis of Preexisting

2 Introduction Main vascular emergencies include Ruptured Abdominal Aortic Aneurysm (raaa) Aortic Dissection Acute Limb Ischemia Embolism from Cardiac Source Most Common Thrombosis of Preexisting Diseased Vessel Thrombosis of Limb Bypass Graft Thrombosed Dialysis Access Native Arteriovenous Fistula Clotted Arteriovenous Graft Symptomatic Carotid Artery Stenosis Symptoms range from Stroke to Amaurosis Fugax, Hemiparesis, or Speech Deficit Episodes Vascular Trauma

3 Abdominal Aortic Aneurysm Abdominal Aorta with Max Diameter > 3.0 cm Most often affect the segment of aorta below the renal arteries Most AAA produce no symptoms Ruptured AAA aortic rupture is due to the weakening of the aortic wall leading to tearing of the aortic wall, allowing blood to escape outside the confines of the aorta Symptomatic (non-ruptured) AAA refers to any number of symptoms (eg abdominal/back/flank pain, limb ischemia) that can be attributed to the aneurysm. The presence of symptoms increases the risk for rupture

4 Abdominal Aortic Aneurysm PreOp Factors Predict 100% raaa Mortality Age > 76 (odds ratio 2.1) PreOp Creatinine >2 mg/dl (odds ratio 3.7) Blood ph < 7.2 (odds ratio 2.6) SBP at any point < 70 mm Hg (odds ratio 2.7)

303 Ruptured AAA Patients Harborview Medical Center (Seattle) 2002

5 303 Ruptured AAA Patients Harborview Medical Center (Seattle) day mortality 54% for open repair 22% for endovascular repair

6 raaa Initial Management Classic signs and symptoms of rupture: Hypotension Flank/back pain Pulsatile Mass Hemodynamically Unstable Patients, Candidate for Repair Straight to OR Perhaps with stop in CT scanner if endovascular repair possible Hemodynamically Stable, Symptomatic (non-ruptured) ICU monitoring

7 raaa: Initial Mangement 2 Large Bore peripheral IV Permissive Hypotension Indirect evidence from Trauma Population, one observational study Allowing relatively low SBP of may prevent further tearing of the aorta and limit blood loss Pain Control Keep patient comfortable, but consciousness should be maintained In patients who remain severely hypertensive (non-ruptured AAA), short-acting IV beta-blockers (eg. esmolol) can be used Lab Studies 10 Units PRBC should be available for OR FFP, PF24

8 raaa In general, without repair, raaa is uniformly fatal Death occurs usually within hours and certainly within a week of rupture Some patients may be too high risk due to underlying comorbidities that comfort care is appropriate HD unstable patients go straight to OR HD stable patients get CT of Abdomen

9 raaa: Decision for Patient Transfer raaa patients should be treated at a facility where surgical expertise and/or the perioperative resources necessary for major aortic surgery are available For patients who present to a facility where these are not available, transfer to a vascular center is appropriate The number of qualified surgeons in the community experienced with open repair of ruptured AAA is declining If transfer is chosen, the patient and their family should be informed of the potential risk for deterioration during transfer

10 Institutional Factors for EVAR Systems must be in place to support the endeavor: Appropriate Hospital Personnel Rapid Availablilty of High Quality CT Availability of Trained support staff (RN, Scrub Tech, Radiology Tech, Anesthesia) Stock of Available Endovascular Prosthesis Available Vascular Surgeon trained in endovascular techniques

11 raaa: Decision for Comfort Care Some patients may refuse AAA repair Some patients already refused (ask them) Factors associated with Increased mortality following open raaa repair: SBP < 80 Age > 80 Cardiac Arrest Loss of Consciousness Creatinine > 1.3 Heart Disease Female Gender Hgb < 9.0 on admission Patients who will not undergo repair are kept pain-free and allowed to expire (avg time to death 7 hours; another study median survival 2.2 hours)

12 raaa: Summary Get to Major Vascular Center ASAP Bring films (CT on CD) if possible (Endovascular Repair) Permissive Hypotension (SBP ) is OK Ask patient if they knew about aneurysm and if they want it repaired 2 large bore IV Type and Cross 10 Units PRBC 50/50 survival If patient makes it to Vascular Center Overall 85% mortality (role of screening high risk populations)

13 Aortic Dissection Relatively uncommon (65% men, mean age 63) Catastrophic Severe chest pain and acute hemodynamic compromise Early and accurate diagnosis and treatment are critical to survival Primary event is a tear in the aortic intima Degeneration of the aortic media Blood passes into the aortic media through the tear

14 Aortic Dissection: Clinical Manifestations Severe, sharp, tearing posterior chest of back pain, or anterior chest pain Painless dissection is relatively uncommon Syncope is associated with worse outcome (due to cardiac tamponade and stroke) Hypertension more common in those with a distal (type B) Dissection Pulse deficit present in 19-30% of Type A Dissections and 9-21% of Type B Dissections

15 Aortic Dissection Propagation of the dissection can occur both proximal and distal Can lead to: Coronary Ischemia Stroke Spinal Ischemia Visceral Ischemia Aortic Regurgitation Cardiac Tamponade

16 Aortic Dissection Risk Factors Hypertension Atherosclerosis Aortic Aneurysm (esp Ascending Aorta) Inflammatory diseases that cause a vasculitis Giant cell arteritis Takayasu arteritis Rheumatoid arthritis Syphilitic aortitis Collagen Disorders Marfan Syndrome Ehlers-Danlos Syndrome Others (bicuspid aortic valve, aortic coarct, CABG, trauma, crack cocaine)

17 Aortic Dissection: Types Stanford Type A Dissection: Involves Ascending Aorta Stanford Type B Dissection: All other dissections Ascending dissections are twice as common as Descending Dissections Intimal Tear Without Hematoma Aortic Intramural Hematoma Penetrating Atherosclerotic Ulcer

18 Aortic Dissection: Diagnosis Abrupt onset of pain with sharp, tearing, or ripping character Mediastinal widening on CXR A variation in pulse and/or BP between arms CTA of Chest most commonly used study

19 Aortic Dissection: Chest CTA

20 Aortic Dissection: Acute Management Pain Control (morphine) BP Management (get BP to ) IV Beta Blocker (esmolol) to get HR < 60 ; SBP < 120 Avoid Hydralazine as it can increase aortic shear stress Evaluate hypotension (blood loss, tamponade, valve dysfunction, LV Systolic Dysfunction If unstable bedside TEE If stable CTA Chest Abd Pelvis

21 Aortic Dissection: Definitive Management Type A Dissection: Emergent OR Concurrent hemorrhagic stroke relative contraindication Type B Dissection: Medical Treatment with OR for complications Spontaneous healing of the dissection is uncommon Occlusion of major branch vessel Persistent hypertension or pain Propagation of dissection Aneurysmal Expansion Aortic Rupture

22 Acute Limb Ischemia: Etiology Arterial Emboli Paradoxical Embolism Arterial Thrombosis Arterial Trauma

23 Acute Limb Ischemia: Risk Factors Atrial Fibrillation Recent Myocardial Infarction Aortic Atherosclerosis Large vessel aneurysm disease Prior lower extremity revascularization Risk factors for aortic dissectin Arterial trauma DVT (paradoxical embolism)

24 Acute Limb Ischemia: Presentation Without underlying vascular disease: No collaterals Rapid onset of symptoms 6 P s : paresthesia, pain, pallor, pulselessness, poikilothermia, paralysis With occlusive vascular disease: Slower onset Gradually increasing symptoms in a patient with a history of chronic ischemia is indicative of arterial thrombosis Sudden return of symptoms similar to those prior to revascularization

Acute Limb Ischemia: Blue Toe Syndrome Small vessel occlusion Embolic occlusion of digital arteries Sudden appearance of cool, painful, cyanotic

25 Acute Limb Ischemia: Blue Toe Syndrome Small vessel occlusion Embolic occlusion of digital arteries Sudden appearance of cool, painful, cyanotic toe(s) Identification and eradication of embolic source Presence of strong pedal pulses Bilateral disease indicates disease above aortic bifurcation

26 Acute Limb Ischemia: Clinical Categories Viable Limb No sensory loss or muscle weakness Arterial and venous doppler signals are audible Marginally viable No or minimal sensory loss No muscle weakness Arterial doppler signals frequently inaudible Salvageable if treated promptly Immediately Threatened Have sensory loss Rest pain Muscle Weakness Salvageable with immediate revascularization Irreversible Ischemia Major tissue loss Permanent nerve damage No arterial or venous doppler signals Will require major amputation Revascularization may be needed to permit healing of amputation

27 Acute Limb Ischemia: Initial Management Anticoagulation Immediate intravenous heparin bolus followed by a continuous heparin infusion Prevents further propagation of thrombus and inhibits distal thrombosis Time is crucial Do not delay while waiting for diagnostic procedures to be performed

28 Acute Limb Ischemia: Definitive Management Viable Extremity: Intraarterial Thrombolysis Embolectomy for proximal embolus Threatened Extremity Emergent surgical revascularization Majority of these patients have had an embolic event The time to successfully dissolve embolus is usually too long Fasciotomy may be required to prevent compartment syndrome Oral anticoagulation used to prevent recurrent embolism Nonviable Extremity Prompt Amputation Preserve as many joints as possible

29 Acute Limb Ischemia: Results Acute limb ischemia is associated with rates of limb loss as high as 30% In-hospital mortality rates are as high as 20% Cardiopulmonary complications account for the majority of the deaths

30 Thrombosed Hemodialysis Access

31 Thrombosed Hemodialysis Access

32 Thrombosed Hemodialysis Access

33 Thrombosed Hemodialysis Access

34 Thrombosed Hemodialysis Access

35 Symptomatic Carotid Artery Stenosis Focal neurologic symptoms that are sudden in onset and referable to the appropriate carotid artery distribution Transient monocular blindness Hemiparesis of one arm or one leg or face Loss of speech episode Vertigo and Syncope are not generally caused by carotid stenosis Patients with these symptoms should be considered asymptomatic if they are found to have a carotid artery stenosis

36 Symptomatic Carotid Artery Stenosis Randomized controlled trials have established carotid endarterectomy as safe and effective for reducing the risk of ischemic stroke in patients with symptomatic carotid artery atherosclerosis CEA recommended Symptoms Carotid stenosis 70-99% Life expectancy 5 years Surgically accessible carotid lesion Absence of clinically significant carotid, pulmonary, or other disease No prior ipsilateral endarterectomy

37 Symptomatic Carotid Artery Stenosis NASCET Trial (mid-1980s) 659 patients with hemispheric or retinal TIA within 120 days and a stenosis of percent Lower risk of any ipsilateral stroke (9% vs 26%) Lower risk of major or fatal ipsilateral stroke (2.5% vs 13.1%) Lower risk of any major stroke or death (8% vs 19%)

Acute arterial embolism

Acute arterial embolism Definition Thrombus come from heart or blood vessel or other embolus such as tumor,air gas or fat flow with blood stream and occlude distal limb or visceral arteries which causes