Lesson 1: Acute Arterial Ischaemia Notes PDF

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ShinyBliss

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Universidad CEU San Pablo

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arterial ischaemia vascular system acute occlusive arterial pathology medical notes

Summary

These notes cover acute occlusive arterial pathology, focusing on causes, symptoms, diagnosis, and treatment of acute ischaemic syndromes. The document details causes like embolism and thrombosis, and associated complications. It also touches on vascular traumas and their treatment.

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vascular system: acute occlusive arterial pathology lesson 1 acute occlusive arterial pathology  Qx Emergency: Limb in risk (or even patient´s life) ACUTE ISCHAEMIC SYNDROME  Sudden occlusion of LL blood flow in LL → Important ischaemia distally to obstruction → Massive muscle ischaemia → Muscl...

vascular system: acute occlusive arterial pathology lesson 1 acute occlusive arterial pathology  Qx Emergency: Limb in risk (or even patient´s life) ACUTE ISCHAEMIC SYNDROME  Sudden occlusion of LL blood flow in LL → Important ischaemia distally to obstruction → Massive muscle ischaemia → Muscle necrosis  Hyperpotassaemia + Metabolic Acidosis (lactic and pyruvic acid by anaerobic glycolysis) +/Myoglobinuria → RI (Renal Insufficiency)  +Fq: LL (especially femoral artery) atherosclerosis  Cardiovascular Risk Factor (injury factors): Hypercholesterolemia (↑ LDL) HBP DM Tobacco Produce endothelial dysfunction (vessel wall inflammation) -Endothelial adhesion molecules -Increased vessel permeability -Cytokines release: Attract Monocytes + Lymphocytes T (intima layer vessels) -LDL oxidation (LDL oxidase) atherosclerosis  Cardiovascular Risk Factor (injury factors): Hypercholesterolemia (↑ LDL) HBP DM Produce endothelial dysfunction (vessel wall inflammation) -Endothelial adhesion molecules Obesity -Increased vessel permeability -Cytokines release: Attract Monocytes + Lymphocytes T Tobacco (intima layer vessels) -LDL oxidation (LDKL oxidase) Monocytes Macrophages + LDL oxidase Foam cells (proinflammatory mediators) Fatty streak vessel wall Muscle cells + Foam cells + Lipids (Ch) Fibrous cap acute occlusive arterial pathology  AETIOPATHOGENESIS: 2 main causes EMBOLISM: Thrombus originated distally → migrates and impacts in peripheral artery +Fq origin: Heart (especially Heart Failure – ischaemic cardiopathy-, AF –Atrial Fibrillation-, MS –Mitral Stenosis-). Main vascular disease in UL (Upper Limbs) Site: Main arteries bifurcation THROMBOSIS IN SITU: Thrombus formed locally, normally aftermath of previous atherosclerotic injury +Fq: Chronic arterial ischaemia, By pass or endoprosthesis holders, iatrogenic (percutaneous catheterism), trauma,… acute occlusive arterial pathology  CLINIC: Proximal + dangerous > Distal.  “5P” rule: -Pain -Paraesthesia -Pallor (→ Cyanosis -lividness when chronic- → Extremity swelling W/ prenecrotic blisters → gangrene + Cold extremity) -Pulselessness -Paralysis Rutheford stablished clinic criteria for severity of acute ischaemia acute occlusive arterial pathology  D(x): Clinic  Image: Arteriography (Gold standard) = Location, Extension, Severity, Differentiates between Embolus and Thrombosis in situ USS (Doppler) = Site, Extension and previous arteriosclerosis. Angio-CT Scan + AngioMRI = Higher sensibility + Specificity  TREATMENT: Heparin (emergency) Extremity: Rest and incline. Analgesia for pain Severe (limb viability): Qx (open or endovascular) Embolus suspicion: Arterial embolectomy By pass thrombosis: Mechanical thrombectomy (or intra-arterial fibrinolysis) + angioplasty (or deviation) W/ or W/O stent  PHYSIOTHERAPY: PREVENTS COMPLICATIONS. NO CURE (differently from CHRONIC pathologies)      COMPLICATIONS:  General: Exitus (10-20% by Heart Attack or Arrythmias), Acute Renal Insufficiency (myoglobinuria), Amputation  Local: Compartment syndromes (fasciotomy). Rethrombosis (45% embolus, 55% thrombus) acute occlusive arterial pathology EXTRINSIC ARTERIAL COMPRESSIONS  Young. Infrequent Popliteal Artery Entrapment Syndrome (PAES)     Clinically = Intermittent Claudication PE: Popliteal , Posterior tibial and Dorsalis pedis pulses diminish. Might be normal, but reduced W/ dorsiflexion foot If severe → Qx (myotomy) Artery Endofibrosis Young, Cyclists (endurance sports). Mainly External Iliac (also in common iliac). Treatment: Qx  Repetitive movements in hyperflexion → Distension + Plication external iliac artery → Stenosis, Thrombus (occ dissection)  Clinic occ “buttock pain” misdiagnosed W/ musculoskeletal or neurological injury Thoracic outlet syndrome (TOS)   Compression brachial plexus, subclavian artery or vein in superior thoracic outlet Clinic: Nerve compression = Pain, Paraesthesia + “pin and needles” UL (especially cubital region). Artery compression = Exercise claudication (cold, pallor, numb and paraesthesia in limbs W/ exercise). Vein Compression = Effort Vein Thrombosis  Chronic situations → Subclavian aneurysm  Intermittent compression axillar or subclavian vein → Effort Venous Thrombosis (Paget-Schroetter syndrome)  PE unspecific. Image D(x): Aetiological (cervical rib)  Treatment: Neck and Shoulder girdle strengthening. Occ Qx acute occlusive arterial pathology VASCULAR TRAUMAS  +Fq cause death 1-45 years: Traffic, Work or Domestic Accidents, Violence (arms), Iatrogenic, Fx, Dislocation (elbow, knee). Mainly limbs, especially femoral artery (LL) and brachial artery (UL)  D(x):  Hard Signs: Evident bleeding, Distal pulses absent, Pulsatile or expansive haematoma, Distal neurological signs, Acute ischaemic signs  Soft signs: Hx of bleeding next to vessels, Nonpulsatile haematoma, Reduced peripheral pulses, Dubious neurological injury  TREATMENT: Vital Support (emergency)  1) BLEEDING CONTROL  2) Qx (1st Orthopaedic → 2nd Vascular): Occ amputation

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