Vascular Emergencies PDF

Vascular Emergencies Radwa Muhammad Ashour Lecturer of Emergency Medicine  Acute Limb Ischemia  Definiti on Acute Limb Ischemia is a sudden decrease “< 2 weeks” in arterial perfusion of the limb, with a potential thre...

Vascular Emergencies Radwa Muhammad Ashour Lecturer of Emergency Medicine  Acute Limb Ischemia  Definiti on Acute Limb Ischemia is a sudden decrease “< 2 weeks” in arterial perfusion of the limb, with a potential threat to the survival of the limb, requiring urgent evaluation and management.  Etiology Arterial occlusion: 1) Thrombosis (Acute Thrombotic Occlusion) (Thrombosis in Situ) “the most common cause”  Peripheral arterial disease: atherosclerosis  Stent or graft thrombosis  Aneurysmal thrombosis (most commonly popliteal aneurysms)  Vasculitis.  IV Drug use.  Hypercoagulability: thrombophilia.  Etiology Arterial occlusion: 2) Embolism  Cardiac emboli: Atrial fibrillation (most common) - MI  Cholesterol embolism: e.g., blue toe syndrome  Septic emboli (e.g., from endocarditis)  Proximal aneurysms (aortic, popliteal) or atherosclerotic lesions  DVT (paradoxical embolism via a patent foramen ovale)  Etiology Arterial Compression: 1) Compartment syndrome 2) Cast – Tourniquets Arterial Wall injury: 1) Trauma: "leading to transection, dissection"  Dislocations  Crush injury of a limb  Iatrogenic injury at the site of arterial access 2) Aortic dissection  Etiology Peripheral vasoconstriction/vasospasm: (nonocclusive arterial ischemia) If prolonged, arterial thrombosis may be superimposed. 1. Raynaud phenomenon: digital ischemia 2. Shock 3. Administration of vasoactive drugs: as TTT of shock or illicit drug. Venous occlusion: Phlegmasia Alba Dolens  Pathophysiolo gy Depends upon: A. The time course of vessel occlusion. B. The location of the affected vessel(s). C. Presence of Collaterals. Extensive tissue necrosis can develop by approximately 6 hours with complete arterial occlusion  Manageme nt HISTO RY A. Past medical history:  Previous history of claudication.  PAD.  Vascular procedures: vascular repair and arterial bypass.  HTN, DM, Cardiomyopathy, congestive heart failure, renal failure, malignancy, hypercoagulable states, smoking. B. Event History: onset, duration, location, intensity of symptoms.  Manageme nt Examinat ion A. The 6 Ps: ″classic presentation of acute occlusion in patients without underlying occlusive vascular disease‶  Pain: the earliest symptom  Pallor “color changes: pale or mottled skin”  Poikilothermia “cold skin”  Paresthesia  Paralysis  Pulselessness: loss of pulses  Manageme nt Examinat ion B. Signs of chronic insufficiency:  Atrophy of skin and subcutaneous tissues, and muscle.  Evidence of ischemic ulcers. C. Gangrene. D. Vascular evaluation:  Doppler signals: arterial – venous.  Ankle-brachial index (ABI) ratio: Adequate if > 0.9.  Manageme nt Examinat ion E. Neurologic examination:  Compare both sides.  Motor and sensory.  Profound paralysis + complete lack of sensation → irreversible state of ischemia. F. Signs of compartment syndrome: pain on passive movement - hardening of the muscle group.  Manageme nt R u t h e r f o r d ' s c l a s s i fi c a t i o n o f a c u t e limb ischemia  Manageme Investigat nt ion 1) ECG: cardiac source of emboli: cardiac arrhythmias (AF). 2) Laboratory Investigation: 1) CBC, creatinine, electrolytes, and coagulation profile. 2) Blood gas analysis: acidosis “rehydration”. 3) Radiological investigation: “depend on the local resources available” 1) Echocardiography. 2) Arterial duplex: noninvasive but is operator dependent and iliac, and calf vessels can be difficult to image.  Manageme nt Investigat ion 3) Radiological investigation: “depend on the local resources available” 3) CTA: less invasive, quicker and more readily available 4) MRA: less invasive. 5) Digital subtraction angiogram: invasive procedure using intra- arterial contrast but has the potential for therapeutic intervention (thrombolysis and angioplasty)  Manageme nt Tr e a t m e n t 1) Initial management of ALI: 1) Analgesia 2) Anticoagulation: a) IV UFH: 80 IU/Kg IV bolus immediately to all patients “to prevent propagation of thrombosis” then, b) If definitive treatment is deferred:  UFH: 18 IU/Kg/h IVI   Manageme nt Tr e a t m e n t 1) Initial management of ALI: 3) IVF: Why? Dehydrated – contrast - Reperfusion injury. 4) Simple measures to improve existing perfusion:  Keep the foot dependent.  Avoid pressure over heel.  Avoid extremes of temperature.  Correct hypotension – hypoxia.  Manageme nt Tr e a t m e n t 1) Initial management of ALI: 5) Correct associated cardiac condition: CHF – AF. 6) Refer to vascular specialist urgently if not available.  Manageme nt Tr e a t m e n t 2) Definitive management: Endovascular treatment: Catheter Directed Thrombolysis Indications:  Grade I or II(a).  Recent acute thrombosis.  No contraindication of thrombolytics.  Manageme nt Tr e a t m e n t 2) Definitive management: Open surgical techniques: Indications:  Immediate surgical revascularization: Grade II (b) or Grade I – II (a) if thrombolysis is not possible or contraindicated.  Acute Embolism: catheter embolectomy under local Anesthesia.  Manageme nt Tr e a t m e n t 2) Definitive management: Open surgical techniques: Options: 1) Balloon catheter thrombectomy 2) Bypass procedures to direct blood flow beyond the occlusion 3) Endarterectomy with or without patch angioplasty 4) Intraoperative isolated limb thrombolysis.  Manageme nt Tr e a t m e n t 2) Definitive management: In Grade III: “Irreversible”  Revascularization: reperfusion injury.  Amputation.  Manageme nt Tr e a t m e n t 3) Risk Factor Management: Blood pressure control. Blood sugar control. Antiplatelet therapy. Statin Therapy. Exercise. Smoke cessation.  Aortic Aneurysm  Definiti on Enlarged aortic diameter > 4.5 cm (Thoracic Aortic Aneurysm) - > 3cm (Abdominal Aortic Aneurysm). Types/ Sites  Risk Factors 1) Positive family history. 2) Medical history: CAD – PVD. 3) Smoking. 4) Older age 65-70 y.  Presentati on Thoracic Aortic Aneurysm: 1) Asymptomatic. 2) If compressing recurrent laryngeal nerve: hoarseness of voice. 3) If associated with bicuspid aortic valve: acute aortic insufficiency. 4) If Ruptured: Chest or back pain in an acutely ill / hypotensive patient.  Presentati on Abdominal Aortic Aneurysm: 1) Asymptomatic. 2) If rapidly expanding: pulsating abdominal mass, impingement of duodenum or ureter, thrombosis “may → acute limb ischemia”. 3) If Ruptured:  Abdominal, back, or flank Pain.  GIT Bleeding (Aorto-enteric fistula)  syncope  Heart failure (if ruptured into IVC)  Presentati on Abdominal Aortic Aneurysm: 3) If Ruptured:  Classical Triad: abdominal pain – hypotension – pulsatile abdominal mass.  Retroperitoneal rupture: Cullen sign – grey turner sign.  Painless hematuria. Any patient > 50 y presenting with abdominal, flank, or back pain especially with hematuria or unexplained syncope or hypotension  Investigati on Thoracic Aortic Aneurysm: 1) CXR:  Widening of the mediastinum  Enlargement of the aortic knob  Displacement of the trachea from midline  Other features: displaced aortic calcification, aortic kinking, and opacification of the aorticopulmonary window  Investigati on Thoracic Aortic Aneurysm: 2) Transesophageal echocardiography. Thoracic/Abdominal Aortic Aneurysm: 3) Bedside Ultrasonography “POCUS”. “modality of choice in unstable patient” 4) CTA.  Treatment Asymptomatic Thoracic Aortic Aneurysm: Follow up Unstable Thoracic Aortic Aneurysm: As AD  3-5.5 → follow up Asymptomatic Abdominal Aortic Aneurysm:  > 5.5 → surgical repair  Treatment Ruptured Abdominal Aortic Aneurysm:  ABC  Pain control  Aim: permissive hypotension (SBP: 80-100 mmHg)  Immediate surgical intervention: operative or endovascular repair.  Transfer hypotensive patient to OR shouldn’t be delayed by prolonged attempts at resuscitation in ED.  In Cardiac arrest: ED Thoracotomy & Aortic Cross Clamp  Acute Aortic Syndrome  Definiti on Disruption of Aortic wall intima that allow column of blood to travel and split Aortic media creating a false lumen. Classificati on Svensson Classification Classificati on  Risk Factors HTN “70%” Family history. Old age. Drug abuse: cocaine. Aortic disease: bicuspid Aortic Valve – coarctation of Aorta – Annulo-aortic ectasia. Vasculitis: Giant cell arteritis. Connective tissue disease: Ehlers-Danlos Syndrome – Marfan Syndrome. Iatrogenic: cardiac surgery – Angiography – Catheterization.  Pathophysiolo gy AD can propagate in variety of direction I. Into Aortic Root: “Ascending Ao.” 1) Aortic Regurgitation. 2) Cardiac Tamponade. 3) Rt Hemothorax. 4) Coronary artery blockage (RCA).  Pathophysiolo gy AD can propagate in variety of direction II. Into origin of arteries: “Ao. Arch” 1) Compression of pulmonary artery/trunk. 2) Carotid artery occlusion: stroke. 3) Subclavian artery occlusion: acute limb ischemia. 4) Mediastinal hematoma.  Pathophysiolo gy AD can propagate in variety of direction III. Into origin of arteries: “abdominal aorta” 1) Celiac/mesenteric artery occlusion: mesenteric ischemia. 2) Renal artery occlusion: renal failure, hematuria. 3) Spinal artery occlusion: paralysis – paresis.  Pathophysiolo gy AD can propagate in variety of direction III. Into spaces: 1) Pleura: rt hemothorax “ascending aorta” – lt hemothorax “descending aorta” 2) Mediastinum. 3) Esophagus “aorto-esophageal fistula” 4) Retroperitoneal “abdominal aorta” IV. Into aortic lumen.  Presentati on  Pain: severe abrupt chest or back pain “interscapular”, tearing, sharp, may be migratory.  Painless syncope.  BP: asymmetric.  HR: Pulse deficit – asymmetric.  presentation of propagation: limb ischemia – ischemic stroke.  Investigati on  ECG: inferior/posterior STEMI “RCA” - LVH  Laboratory Investigation: D-Dimer: 90% sensitivity.  Radiological Investigation: 1) Transthoracic echocardiography: enlarged aortic root 2) CXR  Investigati on  Radiological Investigation: 3) CTA: diagnostic test of choice. 4) Triple rule out CT angiography (TROCT): CTCA, CTPA, CTAo  Treatment  Goal: SBP 100-120, HR < 60.  Medical Treatment: 1. IV ẞ-Blocker: labetalol 10-20 mg IV bolus → Repeat 20-80 mg / 10 min upto 300 mg. 2. IV CCB: if BB is contraindicated 3. Nitroprusside: may be added after BB to achieve BP goal. 4. Hypotensive: IVF – vasopressor.  Treatment  Surgical Treatment: 1. Type A AD: surgical repair with prosthetic graft. 2. Type B AD: medical management – surgical repair if rupture, progression, hemodynamic instability, uncontrolled HTN despite maximal medical treatment.  Deep Venous Thrombosis  Definiti on Thrombosis in deep venous system most commonly in deep veins of the legs. Pathophysiolo gy  Presentati on  Asymptomatic.  Erythema.  Nonspecific.  warmth.  Unilateral limb swelling.  Distended collateral veins.  Pain – tenderness.  Homans sign: pain in calf or posterior knee with passive dosiflexion of foot.  Presentati on  Signs at foot, ankle: Calf vein thrombosis.  Signs at lower 1/3 of the thigh, leg, ankle, foot: femoral-popliteal vein.  Signs at one lower limb: iliofemoral vein.  Signs at both lower limbs: IVC.  Presentati on  Phlegmasia Alba Dolens (Painful white leg): massive iliofemoral thrombosis and arterial vasospasm.  Presentati on  Phlegmasia Cerula Dolens (Painful blue leg): massive iliofemoral thrombosis with acute massive edema, pain, and cyanosis.  Phlegmasia Cerula / Alba Dolens Inflam Pai Blu Wh Diagnostic Algorithm  Wells pretest  Treatment  Immediate anticoagulation: 1. UFH: (in renal failure) Dose: 80 IU/Kg bolus then 18 IU/kg/h. 2. LMWH: Enoxaparin: 1mg/kg/12h SC or 1.5 mg/kg/24h. 3. Factor Xa inhibitors. 4. Oral Anticoagulant:  Warfarin  New Oral anticoagulant: Rivaroxaban – Apixban.  Treatment  Thrombolysis: in massive iliofemoral DVT, phlamesia Cerula dolens.  IVC Filter:  Contraindication to or complication of anticoagulation.  Propagation of DVT despite adequate anticoagulation with warfarin and heparin.  Recurrent DVT on heparin.  Free floating nonadherent iliofemoral DVT > 5 cm.  Massive clot burden  Treatment  Long-term anticoagulation:  For 3 months: 1st episode provoked DVT with major transient risk factor.  For 6-12 month: if persistent major risk factor.  For life: unprovoked proximal, recurrent, provoked with minor risk factor.