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PERIPHERAL ARTERIAL/Vascular DISEASE.pptx

The document provides a comprehensive overview of peripheral arterial disease (PAD), including its epidemiology, risk factors, clinical presentations, and management strategies. It discusses diagnostic methods such as the ankle-brachial index and various imaging techniques, alongside treatment options ranging from lifestyle modifications to surgical interventions. Key clinical classifications and presentations are detailed, highlighting the importance of correct diagnosis and appropriate therapeutic approaches.

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Dr. Bipin Chaudhary MS Resident-2nd Year COMS-TH Moderator: Dr. Saroj Babu Pradhan PERIPHERAL ARTERIAL DISEASE
Outline of contents: • Introduction • Epidemiology • Aetiology/Risk factors • Clinical Presentation and Assessment • Investigations • Management • Prognosis • Special PAD
LOWER EXTREMITY ARTERIAL ANATOMY
Peripheral Arterial Disease • PAD is a clinical term that denotes an occlusive disease arising from narrowing of the arteries distal to the arch of Aorta • Lack of blood flow to the musculature relative to its metabolism leads to clinical symptoms
Epidemiology • Global Prevalence: 1.52% across all age group (113 Million) • 55 million individuals in southeast Asia • ≈2% of the population aged 40-60 years and • 6% of the population older than 70 years are affected with PAD (claudication) • Men : Women (after 50 yrs) = 3.5 %: 2 %
Risk Factors • Atherothrombosis: thrombus formation on top of existing atherosclerosis • Occurs in multiple arterial bed • Modifiable vs non-modifiable
Risk Factors for PAD: Sex (Male) Age Smoking Hypertension Diabetes Hyperlipidemia Hypercoagulability Hyperchromocysteine CKD Family History Sedentary lifestyle Atherosclerosis Atherothrombosis PAD Ischemic stroke Myocardial infarction
Biomarkers for PAD: *Scottish Heart Health Extended Cohort study (1984-2009) • Homocysteine • NT-proBNP • Expired CO and Cotinine • High sensitivity C-Reactive Protein • Cystatic-C • Lipoprotein-a *Novel cardiovascular biomarkers ass. with PAD: Dakhel et. al. 2022; VASA • 11 other biomarkers: (secretoglobin family 3A member 2, osteoprotegerin, urokinase-type plasminogen activator surface receptor, serum macrophage chemokine ligand 16, matrix metalloproteinase 9, p-selectin, growth differentiation factor 15, elafin, cystatin-B, trefoil factor 3, and fatty acid-binding protein 4)
PAD risk loci and known causal risk factors - UptoDate 2024
Schematic representation of the response to ischemia in PAD:
Clinical Presentation: History 1. Age and sex 2. Limbs affected, Bilateral/unilateral 3. Mode of onset 4. Pain: Intermittent claudication vs Rest pain 5. Effects of heat and cold 6. Paresthesia 7. History of superficial phlebitis 8. Involvement of other arteries 9. Impotence 10. Past Medical, Personal, Family history
Site of Occlusion and Pain Location: • Buttock and hip: Aortoiliac disease: Leriche’s syndrome triad =>claudication, absent femoral pulses and erectile dysfunction • Thigh: aorto-iliac or common femoral artery • Upper two-thirds of the calf: superficial femoral artery • Lower one third of the calf: popliteal artery • Foot claudication: Tibial or peroneal artery
Clinical Presentation: Claudication (Vascular) Pseudoclaudication (Neurologic) Character Cramping, Tightness, Aching Same + tingling, numbness Location Buttock, hip, thigh, calf, foot Along a dermatone Exercise –induced Yes Variable Distance Consistent Variable Occurs with Standing No Yes Action for Relief Stand (A)/leg elevation (V) Sit, Change position Time for Relief <5 minutes >30 minutes
• Boyd’s Classification of Claudication Grades Pain I Pt. walks for a distance, gets pain, continues to walk and the pain disappears II Pt. walks for a distance, gets pain, continues to walk with the pain and limping III Pain compels the patient to take rest IV Pain at Rest (due to involvement of Vasa Nervosum)
Clinical Presentation: Stages Asymptomatic: (20-50%) Without obvious symptomatic complaint (but usually with a functional impairment) Classic intermittent claudication: (10-35%) Reproducible discomfort of a defined group of muscles that is; brought on by walking not present on taking the first step (unlike osteoarthritis) relieved by standing still “Atypical” leg pain: (40-50%) Lower extremity discomfort that is exertional but that does not consistently resolve with rest, consistently limit exercise at a reproducible distance ACC/AHA guidelines (≥50yrs)
Critical limb lschemia: Ischemic rest pain, nonhealing wound, or gangrene Acute limb ischemia: (1-2%)The five “P”s, defined by the clinical symptoms and signs that suggest potential limb jeopardy: Pain Pulselessness Pallor Paresthesis Paralysis ACC/AHA guidelines (≥50yrs)
Examination: • General Examination • Vitals • Systemic Examination
Examination : Palpation Local skin temperature Muscle tone Palpation of the blood vessels: • Absence of pulse signifies arterial obstruction proximal to the area • Pulse intensity: 0-absent 1- diminished 2-normal 3-bounding Artery Landmark Dorsalis pedis Lateral to extensor hallucis longus tendon Posterior Tibial Betn medial malleolus and tendo-Achilles Anterior Tibial Midway betn malleoli, above ankle joint Popliteal Against tibial condyles in popliteal fossa @40◦ Femoral Just below inguinal lig, betn ASIS and Symphysis Radial and Ulnar At wrist Brachial At elbow just medial to bicep tendon Subclavian Just above mid clavicle
Examination: Inspection Change in Colour Signs of ischemia: − Thinning of skin, shininess − Loss of subcutaneous fat − Trophic change/Thickened brittle toe nails with transverse ridges − Ulcerations/necrotic tissue in pressure areas Buerger’s postural test (<20sec to return blood) Capillary filling time Venous filling Atrophy of calf muscles In established gangrene: Extent and colour, Type, Line of demarcation, Limb above Blue toe syndrome
Examination: Characteristics Arterial Ulcer Venous Ulcer Neuropathic Ulcer Location Toe joints, malleoli, shin, heel, pressure points Malleolus, bony prominence, calf Plantar foot, heel, pressure points Appearance Irregular, base dry, necrotic Irregular, red base, exudate Punched out, deep Ulcer within callus Rare No Callus with ulcer Foot temperature Cold Warm Warm Pain Yes, severe Yes, mild No Arterial pulses Absent Present Present Sensation Variable Present Absent (Glove and stocking) Foot deformity No No Often Skin changes Shiny, taut, loss of hair Erythema, stasis, dry Waxy, edematous Reflexes Present Present Absent TASC Working Group
Examination: Palpation Capillary, Venous refilling Crossed leg test Cold and warm water test Elevated arm test Allen’s test: for patency of Radial and Ulnar Artery Branham’s test : for AV Fistula Costoclavicular compressive manoeuvre Hyperabduction manoeuvre Gangrenous area: hard vs oedematous/discharge vs crepitus Limb above the gangrenous area Neurologic examination Adson’s test Examination of the lymph Nodes
Examination: • Auscultation for bruits in the abdominal and pelvic regions • Handheld Doppler Device
Examination: • Asymtomatic PAD: most often detected by ABI (should be treated) • Ankle Brachial Index = • ABI is 95% sensitive and 99% specific for PAD − Establishes the diagnosis of PAD − Identifies a population at high risk of CV ischemic events • ABI may be less accurate in diabetic d/t calcinosis • Procedure: Lower extremity systolic pressure Brachial artery systolic pressure
Ankle Brachial Index: ABI≤ 0.90 Diagnostic for PAD ABI= 0.91-1.3 Normal: No further testing Indicated ABI>1.3 Doppler ankle waveforms, Toe Pressure ABI
ABI limitations: 1. Toe Brachial index: Incompressible arteries (TBI≤0.7) 2. Cant define degree of functional limitation 3. Exercise testing Done In patients with claudication but pulses and ABI normal (drop in ABI of 0.2 or in ankle pressure of 20 mmhg)
Clinical Presentation: Classification Fontaine Rutherford Stage Clinical Grade Category Clinical I Asymtomatic 0 0 Asymtomatic IIa Mild Claudication (walking >200m) I 1 Mild claudication IIb Moderate to Severe Claudication (walking <200m) I 2 Moderate Claudication I 3 Severe Claudication III Ischemic Rest/Nocturnal Pain II 4 Ischemic Rest Pain IV Ulceration/Gangrene III 5 Minor Tissue loss III 6 Major Tissue loss Critical limb Ischemia
Classification: Society for Vascular Surgery (SVS)
Classification: Society for Vascular Surgery (SVS)
Clinical Presentation: Classification • GLASS classification: Global Limb Anatomic Staging System • Femoropopliteal segment: Grade 0,1,2,3,4 • Infrapopliteal segment: Grade 0,1,2,3,4 • TASC classification: Trans-Atlantic Inter-Society Consensus (TASC II): (Type A, B, C, or D) • anatomic distribution, • number and nature of lesions (stenosis, occlusion), and • overall success rates of treating using endovascular or surgical means • Bollinger scoring method : 13 infrainguinal segments • Graziani morphologic classification : in pt with Diabetes
Differential Diagnosis: Vascular Aneurysm, dissection, embolism, limb trauma, radiation exposure, vasculitis, popliteal entrapment syndrome, chronic venous disease, Buerger’s disease Neurological Neuro-spinal (disc disease, spinal stenosis, tumour) or neuropathic causes (e.g.: DM, Alcohol abuse) Musculoskeletal Pain derived from the bone, joints, ligaments, tendons and fascial elements of the lower extremity
Investigations: • Lab tests: − CBC, CRP, ESR − RBS − Renal Function − Lipid profiles − Urine RE − Homocysteine, lipoprotein A • ECG • X-ray of limb
Algorithm for vascular testing in symptomatic PAD Chronic limb threatening Ischemia: Rest pain Tissue loss Non-healing ulcer, Gangrene Diagnostic for PAD Referral to vascular specialist -Atypical leg pain -Claudication Measure Ankle Brachial index ABI≤0.90 or >1.3 -Consider consultation with vascular specialist, -Further testing indicated by magnitude of symptoms, Duplex imaging, CTA, MRA, Angiography ABI 0.91 to 1.3 Exercise testing Abnormal post-exercise ABI decreased by ≥20% Normal: post-exercise ABI unchanged or increased © 2024 UpToDate
Segmental Doppler Pressure: • Placement of cuffs at proximal and distal thigh, calf and ankle − At the thigh: aortoiliac or superficial femoral artery disease − At the calf: distal superficial femoral artery, popliteal disease − At the ankle: infra-popliteal disease • Occlusion if decrease in pressure of >20 mmhg in comparison to above levels • In addition a toe pressure of <60% of the ankle pressure indicates digital artery occlusive disease
Plethysmography: • Injecting a standard volume of air into pneumatic cuffs placed at various levels along the extremity • Volume changes in the limb segment below the cuff are translated into pulsatile pressure
Duplex Imaging: • (Doppler+B-Mode) Uses colour doppler system • B-mode imaging information about vessel wall and peak systolic velocity • Ratio of PSV at stenosis to proximal segment of 2=50% obstruction, 4=70% • Provides accurate localization and quantification of lesions • Differentiate Stenosis vs occlusions • Useful in evidence of progression and monitoring vascular reconstructions • Normal is triphasic. • As onstruction increases widening of diastolic peak occurs and flow monophasic
CT Angiography: • Multidetector computed tomography: high resolution, IV contrast inhanced images • For road mapping before surgery -Danae et al. ‘Reporting lower extremity CT angiography’ ElSEVIER
Magnetic Resonance Angiography: • In pts with CI to Standard Contrast Angiography -Abdelzaher et al. ‘Interobserver and inter-modality concordance of MRA and CT angiography
Contrast Angiography: • Remains the Gold Standard • In patients without a contraindications who are expected to undergo revascularization • Complete study of aorta, iliac, femoral, popliteal and run-off vessels is done on both sides
• Isotope technique: IM Technetium 99 via Gamma Camera
Management
Management of Asymptomatic PAD and Claudication • Risk factor Modification − Smoking cessation, Care of feet − Diet/obesity control (BMI<25) • Exercise Therapy • Pharmacological Treatment − Platelet aggregation suppression: Cilostazole (Phosphodiesterase inhibitors) − Antiplatelet therapy − Control risk factors: DM, HTN − Pentoxyphylline (xanthine derivative), statins, Naftidrofuryl • Revascularization by Open surgery or EndoVascularization • Therapeutic Angiogenesis
UpToDate 2024
UpToDate 2024
Risk Factor Modification • Smoking Cessation • Diabetes control: Goal HbA1c<7% each 1% rise in HbA1c ass. With 28% risk for PVD) Metformin or Glitazone Vs Insulin (BARI 2D trial) • Hypertension control: ACE inhibitors Goal: DM: <140/90, CKD: <130/80 • Hyperlipidemia: Diet modification Statins: improve maximal walking distance Niacin or Fibrates
Risk Factor Modification Anti-platelet Theray: • Aspirin: • Std dose: 75 to 325 mg/day • Clopidogrel: 75 mg/day Start single or both
Exercise Therapy • A daily brisk walking of 45-60 min • Walk until claudication, rest until pain subside and then repeat • Substantial improvement: 80-234% in controlled studies • Condition muscle, extract more blood, increase collateral vessel formation Supervised Exercise Rehabilitation: • For intermittent claudication • Minimum 30 to 45 min. sessions at least 3/week for 12 weeks
Pharmacologic Therapy • Cilostazol: • MOA: Phosphodiesterase III inhibitor; increases cAMP, inhibits smooth muscle cell proliferation and contraction, suppresses platelet aggregation and is a direct arterial vasodilator • Also decreases TG and increases HDL • Dose: 50 mg/day X 1 week then 50 mg BD X 1 week then 100 mg BD
• Review of Phase-3 multicenter, double-blind, parallel-design trials (7 USA+1 UK) • Inclusion: 40 yrs. with symptomatic LL PAD of >6 months with ABI <0.9 • Exclusion: with known systemic/arterial disease, interventions, acute limb ischemia • Exercise treadmill testing, to assess patient response to therapy • Cilostazol in dosages of 50, 100, or 150 mg twice daily on Placebo from 12 to 24 weeks • Result: − Cilostazol therapy increased maximal and pain-free walking distances by 50% and 67%, respectively. − Decreased triglycerides by 15.8% and increased high-density lipoprotein cholesterol by 12.8%
Pharmacologic Therapy • Naftidrofuryl: Serotonin antagonist, promotes vasodilation • Pentoxifylline: • Xanthine derivative; reduces viscocity, decreases platelet aggregation • Course: 400 mg TDS (max 1800 mg/day) x 2-3 months
Surgical Intervention • Interventional Radiology: Endovascular Percutaneous transluminal balloon angioplasty Local fibrinolytic therapy for recent thrombosis: streptokinase 6000 U/hr directly into occlusion Atherectomy Thrombectomy • Surgical Revascularization: Endarterectomy Graft angioplasty Peripheral artery bypass surgery • Laser endovascular ablation for total occlusions
Surgical Repair Options for Aorto-iliac Disaese Endarterectomy: • Opening of diseased segment and removing plaque • Indications: infected cases, small vessel, impotence Aorto-Bifemoral Bypass: • PTFE/Dacron grafts, between infrarenal aorta and b/l Femoral A • End to end anastomosis
Surgical Repair Options for Aorto-iliac Disaese Axillo-Bifemoral Bypass; • Subcutaneous graft between Axillary A. and ipsilateral Femoral A. • Opposite limb vascularizes by femoro-femoral bypass
Surgical Repair Options for Aorto-iliac Disaese Femoro-femoral Bypass: for U/L Iliac A occlusion Obturator bypass: • Graft between Iliac A. and Femoral A. through obturator membrane in infected or distorted groin anatomy
Surgical Repair Options for infra-inguinal disease • Autogenous grafts: Great saphenous, short saphenous, cephalic/basilic vein • Very low success rate with synthetic grafts
EndoVascular Approach • Balloon Angioplasty: insert guidewire and inflate a balloon over the wire • Considered successful if residual stenosis <30%
Endovascular Approach Vs Surgical approach EndoVascular approach Surgical Approach Shorter Hospital stay Less Morbidity Less Interference with daily life Low Patency Rate Longer perioperative stay More complications Bowel/ureteric injury, impotence Superior Patency rate • TASC II recommends angioplasty over Surgery • BASIL (2005 UK) trial favors Surgical Group
Therapeutic Angiogenesis • Gene transfer: 4000 mg naked Plasmid DNA encoding VEGF injected directly in ischemic limbs • Others: stem cells, autologous progenitor cells, growth factors, transcription factors • Used in CLI patints who lack options for endovascular or surgical revascularization
Peripheral Arterial Diseases
Critical Limb Ischemia: Acute vs Chronic Acute limb ischemia: • ‘Sudden decrease in limb perfusion that causes a potential threat to limb viability in pts who present within 2 weeks’ • Manifested by : • Ischemic rest pain • Pulselessness • Pallor • Paresthesia • Paralysis • poikilothermia • Ischemic ulcer/Gangrene
Acute limb ischemia: Etiology Embolus Thrombosis :  Vascular grafts  Atherosclerosis  Thrombosis of aneurysm  Entrapment syndrome  Hypercoagulable state  Low flow rate Cardiac source:  Atrial fibrillation  Myocardial infarction  Endocarditis  Valvular disease  Atrial myxoma  Prosthetic valves Arterial source:  Aneurysm  Atherosclerotic plaque Trauma:  Blunt  Penetrating  Iatrogenic
Acute limb ischemia: Classification Viable Marginally Threatened Immediately Threatened Nonviable Pain Mild Severe Severe Variable Capillary Refill Intact Delayed Delayed Absent Motor Deficit None None Partial Complete Sensory deficit None Minimal Partial Complete Arterial Doppler Audible Inaudible Inaudible Inaudible Venous Doppler Audible Audible Audible Inaudible Treatment Urgent workup Emergency Surgery Emergency Surgery Amputation UpToDate 2024/Rutherford et al.
Acute limb ischemia: Imaging • Angiography: detailed arterial anatomy, distinguish thrombosis and embolism • If threatened extremity; immediate surgical revascularization with intraoperative angiography
Acute limb ischemia: Management • Heparin: IV Heparin bolus 100 U/kg followed by a continuous heparin infusion 15 U/kg/hour with goal PTT 60-80 sec (Refer to specialist) • Revascularization within 6 hrs critical to avoid limb loss
Acute limb ischemia: Management Viable Extremity: Urgent Arteriography to plan surgical or percutaneous revascularization Two methods of Treatment: Embolectomy Vs Intra-Arterial Thrombolysis
Acute limb ischemia: Management Embolectomy: • Under Local/General Anesthesia • The Artery (usually the femoral), exposed and held in slings • Longitudinal or transverse incision; clot removed together with embolus with Fogarty Balloon Catheter • Catheter introduced both proximally and distally • Procedure repeated until bleeding occurs
Acute limb ischemia: Management Intra-arterial Thrombolysis: • 5F catheter passed into occluded vessel; left embedded in clot • Thrombolysis: Tissue plasminogen activator 5 mg bolus with Mechanical spray/suctioning • Abandoned if no progression of dissolution of clot in 24 hrs.
Acute limb ischemia: Management Threatened Extremity: • Irreversible changes can occur within 4-6 hrs of ischemia • Emergent surgical revascularization • Embolectomy is often all that is required to relieve occlusion • Intraoperative completion Arteriogram after embolectomy • Intraoperative thrombolytic therapy for small emboli in distal runoff vessels • Fasciotomy may be required to prevent Compartment Syndrome
Acute limb ischemia: Management Non-Viable Extremities: • Prompt amputation • Arteriography is usually not necessary • Delay in amputation may result in infection, myoglobinuria, ARF, hyperkalaemia
Amputation Indications Dead Limb: -Gangrene Deadly Limb: -Wet gangrene -Spreading cellulitis -Arteriovenous Fistula -Other (e.g. malignancy) “Dead loss” limb: -Severe rest pain with unreconstructable critical limb ischemia -Paralysis -Other (e.g. contracture, trauma) Site Selection Upper Limb: A/E= 20 cm from Acromion B/E= 18 cm from Olecranon Lower Limb: A/K= 12 cm from joint line B/K= 14 cm from joint line
Amputation levels (upper limbs) • Hand & Partial–Hand - Finger, thumb, palm below wrist • Wrist Disarticulation • Trans-Radial (Below Elbow) • Trans-Humeral (Above Elbow) • Shoulder Disarticulation • Forequarter Amputation - At shoulder level; both shoulder blade and collar bone are removed
Amputation levels (lower limbs) • Foot Amputations • Amputations of greater toes and other toes • Ankle disarticulation: Syme’s Operation • Lisfranc’s operation: Tarso-Metatarsals • Chopart’s operation: Mid-Tarsals • TransTibial • Knee Disarticulation • Trans-femoral • Hip Disarticulations
Chronic Limb Ischemia • Definition: Decrease in limb perfusion that causes a potential threat to limb viability in patients who present >2 weeks of rest pain, ulcer or tissue loss, characterized by ABI<0.4 Ankle systolic pressure: <50 mmhg Toe systolic pressure: <30 mmhg • Seen when two or more levels of arterial tree occluded
Chronic Limb Ischemia: Management • Management: Imaging: duplex, CTA, MRA, Angiography Risk factor reduction Wound care: conservative Prostaglandins E1??- no long term benefit at 6 months Catheter based intra-arterial thrombolytic therapy (acute thrombosis over old occlusion) Revascularization: Angioplasty Vs Bypass Surgery ACC/AHA guideline for PAD recommends: • Life expectancy <2 years or do not have autogenous vein: Balloon Angioplasty • Life expectancy >2 years and have autogenous vein conduit: Bypass Surgery
Prognosis • Framingham study: 1.6% of patients with claudication reached amputation stage after 8.3 years of f/u • Predicted mortality for patients with claudication: (CVS cause) • 30% at 5 years f/u • 50% at 10 years • 70% at 15 years
Thromboangiitis Obliterans/Buerger’s disease • Nonatherosclerotic, segmental inflammation of small and medium sized arteries, vein of upper and lower extremities  More common in men 25-40 years of age  Correlates with cigarette smoking, HLAB5 and A9 antigens  Rest pain, ischemic ulcerations  Disease of Exclusion  Colour Duplex: serpiginous or corkscrew collaterals at the site of occlusion with normal arterial wall
Thromboangiitis Obliterans/Buerger’s disease Olin Criteria for Diagnosis: • Age <45 years • Current/recent hx of Tobacco Use • Presence of distal extremity ischemia (non-invasive vascular testing) • Exclusion of Autoimmune Dx, Hypercoagulability, Diabetes • Exclusion of Proximal source of emboli by ECHO/Arteriography • Consistent arteriographic findings
Buerger’s disease: Treatment  Tobacco cessation  Active Vs Passive Vascular exercise  Analgesics and position, care of feet  Intra-arterial streptokinase (bolus 10000 U f/b 5000 U/Hour)  Meds: − Prostaglandins, − Anti-platelets, − Vasodilators, − Pentoxyphylline − Niftidrofuryl
Buerger’s disease: Treatment  Sympathectomy: ↓vasomotor tone, abolish pain impulse Nakata et al reported ulcer healing in 58% and relief of rest pain in 64% Contraindicated in Intermittent Claudication by stealing blood from muscle to skin Surgical Sympathectomy oLumbar: L1,L2, L3, L4 removed (Temporary) − Open vs Lap Extraperitoneal vs Transperitoneal route oCervical: T1, T2, T3 removed − Approach: Supraclavicular, Axillary, Posterior, Transthoracic (lap) Chemical Sympathectomy: Under LA, Fluoroscopic/USG guidance on lateral position 5 ml Phenol in water (1:16) injected beside bodies of 2nd and 4th vertebrae
Buerger’s disease: Treatment  Omental Transposition:  Omentum: Rich Vascular supply  Causes Neo-vascularization, Increases lymphatic drainage  Procedure: omentum mobilized-Subfascial Tunneling from inferior end to inguinal incisionDistal end of pedicle is fixed to Gastrocnemius with catgut.  Surgical: AV fistula creation proximal to block Amputation (gangrene, severe infection)
Raynaud’s Disease • Episodic reversible vasospastic disorder of small cutaneous arteries in fingers and toes in response to cold or stress (may involve nose, ears and tongue) • Cause: Exaggerated SNS stimulation • Occurs in women 15-40 yrs of age • Raynaud’s Disease: Primary Raynaud’s Phenomena (cause: Unknown) • Raynaud’s Syndrome: Secondary Raynaud’s Phenomena due to to collagen diseases: RA, scleroderma, SLE, Sjogrens, MS • Phase 1: Vasospasm phase: Pallor/blanching of hands and fingers with throbbing, aching pain, numbness, tingling • Phase 2: Venous pooling: Cyanosis due to deoxygenated blood • Phase 3: Hyperaemic phase: Erythematous swelling
Raynaud’s Disease • Tx: smoking cessastion, no meds with vasoconstrictive effect, avoid cold, avoid constrictive clothes • Meds: Calcium-Channel Blockers vasodilators, vascular smooth muscle relaxants • Botox • Surgery: Sympathectomy
References • Bailey and Love’s Short Practice of Surgery 28th Edition • Sabiston Textbook of Surgery 21st edition • Uptodate 2024
PERIPHERAL ARTERIAL/Vascular DISEASE.pptx

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PERIPHERAL ARTERIAL/Vascular DISEASE.pptx

  • 1.
    Dr. Bipin Chaudhary MSResident-2nd Year COMS-TH Moderator: Dr. Saroj Babu Pradhan PERIPHERAL ARTERIAL DISEASE
  • 2.
    Outline of contents: •Introduction • Epidemiology • Aetiology/Risk factors • Clinical Presentation and Assessment • Investigations • Management • Prognosis • Special PAD
  • 3.
  • 4.
    Peripheral Arterial Disease •PAD is a clinical term that denotes an occlusive disease arising from narrowing of the arteries distal to the arch of Aorta • Lack of blood flow to the musculature relative to its metabolism leads to clinical symptoms
  • 5.
    Epidemiology • Global Prevalence:1.52% across all age group (113 Million) • 55 million individuals in southeast Asia • ≈2% of the population aged 40-60 years and • 6% of the population older than 70 years are affected with PAD (claudication) • Men : Women (after 50 yrs) = 3.5 %: 2 %
  • 6.
    Risk Factors • Atherothrombosis:thrombus formation on top of existing atherosclerosis • Occurs in multiple arterial bed • Modifiable vs non-modifiable
  • 7.
    Risk Factors forPAD: Sex (Male) Age Smoking Hypertension Diabetes Hyperlipidemia Hypercoagulability Hyperchromocysteine CKD Family History Sedentary lifestyle Atherosclerosis Atherothrombosis PAD Ischemic stroke Myocardial infarction
  • 8.
    Biomarkers for PAD: *ScottishHeart Health Extended Cohort study (1984-2009) • Homocysteine • NT-proBNP • Expired CO and Cotinine • High sensitivity C-Reactive Protein • Cystatic-C • Lipoprotein-a *Novel cardiovascular biomarkers ass. with PAD: Dakhel et. al. 2022; VASA • 11 other biomarkers: (secretoglobin family 3A member 2, osteoprotegerin, urokinase-type plasminogen activator surface receptor, serum macrophage chemokine ligand 16, matrix metalloproteinase 9, p-selectin, growth differentiation factor 15, elafin, cystatin-B, trefoil factor 3, and fatty acid-binding protein 4)
  • 9.
    PAD risk lociand known causal risk factors - UptoDate 2024
  • 10.
    Schematic representation ofthe response to ischemia in PAD:
  • 11.
    Clinical Presentation: History 1.Age and sex 2. Limbs affected, Bilateral/unilateral 3. Mode of onset 4. Pain: Intermittent claudication vs Rest pain 5. Effects of heat and cold 6. Paresthesia 7. History of superficial phlebitis 8. Involvement of other arteries 9. Impotence 10. Past Medical, Personal, Family history
  • 12.
    Site of Occlusionand Pain Location: • Buttock and hip: Aortoiliac disease: Leriche’s syndrome triad =>claudication, absent femoral pulses and erectile dysfunction • Thigh: aorto-iliac or common femoral artery • Upper two-thirds of the calf: superficial femoral artery • Lower one third of the calf: popliteal artery • Foot claudication: Tibial or peroneal artery
  • 13.
    Clinical Presentation: Claudication (Vascular)Pseudoclaudication (Neurologic) Character Cramping, Tightness, Aching Same + tingling, numbness Location Buttock, hip, thigh, calf, foot Along a dermatone Exercise –induced Yes Variable Distance Consistent Variable Occurs with Standing No Yes Action for Relief Stand (A)/leg elevation (V) Sit, Change position Time for Relief <5 minutes >30 minutes
  • 14.
    • Boyd’s Classificationof Claudication Grades Pain I Pt. walks for a distance, gets pain, continues to walk and the pain disappears II Pt. walks for a distance, gets pain, continues to walk with the pain and limping III Pain compels the patient to take rest IV Pain at Rest (due to involvement of Vasa Nervosum)
  • 15.
    Clinical Presentation: Stages Asymptomatic:(20-50%) Without obvious symptomatic complaint (but usually with a functional impairment) Classic intermittent claudication: (10-35%) Reproducible discomfort of a defined group of muscles that is; brought on by walking not present on taking the first step (unlike osteoarthritis) relieved by standing still “Atypical” leg pain: (40-50%) Lower extremity discomfort that is exertional but that does not consistently resolve with rest, consistently limit exercise at a reproducible distance ACC/AHA guidelines (≥50yrs)
  • 16.
    Critical limb lschemia:Ischemic rest pain, nonhealing wound, or gangrene Acute limb ischemia: (1-2%)The five “P”s, defined by the clinical symptoms and signs that suggest potential limb jeopardy: Pain Pulselessness Pallor Paresthesis Paralysis ACC/AHA guidelines (≥50yrs)
  • 17.
    Examination: • General Examination •Vitals • Systemic Examination
  • 18.
    Examination : Palpation Localskin temperature Muscle tone Palpation of the blood vessels: • Absence of pulse signifies arterial obstruction proximal to the area • Pulse intensity: 0-absent 1- diminished 2-normal 3-bounding Artery Landmark Dorsalis pedis Lateral to extensor hallucis longus tendon Posterior Tibial Betn medial malleolus and tendo-Achilles Anterior Tibial Midway betn malleoli, above ankle joint Popliteal Against tibial condyles in popliteal fossa @40◦ Femoral Just below inguinal lig, betn ASIS and Symphysis Radial and Ulnar At wrist Brachial At elbow just medial to bicep tendon Subclavian Just above mid clavicle
  • 19.
    Examination: Inspection Change inColour Signs of ischemia: − Thinning of skin, shininess − Loss of subcutaneous fat − Trophic change/Thickened brittle toe nails with transverse ridges − Ulcerations/necrotic tissue in pressure areas Buerger’s postural test (<20sec to return blood) Capillary filling time Venous filling Atrophy of calf muscles In established gangrene: Extent and colour, Type, Line of demarcation, Limb above Blue toe syndrome
  • 20.
    Examination: Characteristics Arterial UlcerVenous Ulcer Neuropathic Ulcer Location Toe joints, malleoli, shin, heel, pressure points Malleolus, bony prominence, calf Plantar foot, heel, pressure points Appearance Irregular, base dry, necrotic Irregular, red base, exudate Punched out, deep Ulcer within callus Rare No Callus with ulcer Foot temperature Cold Warm Warm Pain Yes, severe Yes, mild No Arterial pulses Absent Present Present Sensation Variable Present Absent (Glove and stocking) Foot deformity No No Often Skin changes Shiny, taut, loss of hair Erythema, stasis, dry Waxy, edematous Reflexes Present Present Absent TASC Working Group
  • 21.
    Examination: Palpation Capillary, Venousrefilling Crossed leg test Cold and warm water test Elevated arm test Allen’s test: for patency of Radial and Ulnar Artery Branham’s test : for AV Fistula Costoclavicular compressive manoeuvre Hyperabduction manoeuvre Gangrenous area: hard vs oedematous/discharge vs crepitus Limb above the gangrenous area Neurologic examination Adson’s test Examination of the lymph Nodes
  • 22.
    Examination: • Auscultation forbruits in the abdominal and pelvic regions • Handheld Doppler Device
  • 23.
    Examination: • Asymtomatic PAD:most often detected by ABI (should be treated) • Ankle Brachial Index = • ABI is 95% sensitive and 99% specific for PAD − Establishes the diagnosis of PAD − Identifies a population at high risk of CV ischemic events • ABI may be less accurate in diabetic d/t calcinosis • Procedure: Lower extremity systolic pressure Brachial artery systolic pressure
  • 24.
    Ankle Brachial Index: ABI≤ 0.90 Diagnosticfor PAD ABI= 0.91-1.3 Normal: No further testing Indicated ABI>1.3 Doppler ankle waveforms, Toe Pressure ABI
  • 25.
    ABI limitations: 1. ToeBrachial index: Incompressible arteries (TBI≤0.7) 2. Cant define degree of functional limitation 3. Exercise testing Done In patients with claudication but pulses and ABI normal (drop in ABI of 0.2 or in ankle pressure of 20 mmhg)
  • 26.
    Clinical Presentation: Classification FontaineRutherford Stage Clinical Grade Category Clinical I Asymtomatic 0 0 Asymtomatic IIa Mild Claudication (walking >200m) I 1 Mild claudication IIb Moderate to Severe Claudication (walking <200m) I 2 Moderate Claudication I 3 Severe Claudication III Ischemic Rest/Nocturnal Pain II 4 Ischemic Rest Pain IV Ulceration/Gangrene III 5 Minor Tissue loss III 6 Major Tissue loss Critical limb Ischemia
  • 27.
    Classification: Society forVascular Surgery (SVS)
  • 28.
    Classification: Society forVascular Surgery (SVS)
  • 29.
    Clinical Presentation: Classification •GLASS classification: Global Limb Anatomic Staging System • Femoropopliteal segment: Grade 0,1,2,3,4 • Infrapopliteal segment: Grade 0,1,2,3,4 • TASC classification: Trans-Atlantic Inter-Society Consensus (TASC II): (Type A, B, C, or D) • anatomic distribution, • number and nature of lesions (stenosis, occlusion), and • overall success rates of treating using endovascular or surgical means • Bollinger scoring method : 13 infrainguinal segments • Graziani morphologic classification : in pt with Diabetes
  • 30.
    Differential Diagnosis: Vascular Aneurysm, dissection,embolism, limb trauma, radiation exposure, vasculitis, popliteal entrapment syndrome, chronic venous disease, Buerger’s disease Neurological Neuro-spinal (disc disease, spinal stenosis, tumour) or neuropathic causes (e.g.: DM, Alcohol abuse) Musculoskeletal Pain derived from the bone, joints, ligaments, tendons and fascial elements of the lower extremity
  • 31.
    Investigations: • Lab tests: −CBC, CRP, ESR − RBS − Renal Function − Lipid profiles − Urine RE − Homocysteine, lipoprotein A • ECG • X-ray of limb
  • 32.
    Algorithm for vasculartesting in symptomatic PAD Chronic limb threatening Ischemia: Rest pain Tissue loss Non-healing ulcer, Gangrene Diagnostic for PAD Referral to vascular specialist -Atypical leg pain -Claudication Measure Ankle Brachial index ABI≤0.90 or >1.3 -Consider consultation with vascular specialist, -Further testing indicated by magnitude of symptoms, Duplex imaging, CTA, MRA, Angiography ABI 0.91 to 1.3 Exercise testing Abnormal post-exercise ABI decreased by ≥20% Normal: post-exercise ABI unchanged or increased © 2024 UpToDate
  • 33.
    Segmental Doppler Pressure: •Placement of cuffs at proximal and distal thigh, calf and ankle − At the thigh: aortoiliac or superficial femoral artery disease − At the calf: distal superficial femoral artery, popliteal disease − At the ankle: infra-popliteal disease • Occlusion if decrease in pressure of >20 mmhg in comparison to above levels • In addition a toe pressure of <60% of the ankle pressure indicates digital artery occlusive disease
  • 34.
    Plethysmography: • Injecting astandard volume of air into pneumatic cuffs placed at various levels along the extremity • Volume changes in the limb segment below the cuff are translated into pulsatile pressure
  • 35.
    Duplex Imaging: • (Doppler+B-Mode)Uses colour doppler system • B-mode imaging information about vessel wall and peak systolic velocity • Ratio of PSV at stenosis to proximal segment of 2=50% obstruction, 4=70% • Provides accurate localization and quantification of lesions • Differentiate Stenosis vs occlusions • Useful in evidence of progression and monitoring vascular reconstructions • Normal is triphasic. • As onstruction increases widening of diastolic peak occurs and flow monophasic
  • 36.
    CT Angiography: • Multidetectorcomputed tomography: high resolution, IV contrast inhanced images • For road mapping before surgery -Danae et al. ‘Reporting lower extremity CT angiography’ ElSEVIER
  • 37.
    Magnetic Resonance Angiography: •In pts with CI to Standard Contrast Angiography -Abdelzaher et al. ‘Interobserver and inter-modality concordance of MRA and CT angiography
  • 38.
    Contrast Angiography: • Remainsthe Gold Standard • In patients without a contraindications who are expected to undergo revascularization • Complete study of aorta, iliac, femoral, popliteal and run-off vessels is done on both sides
  • 39.
    • Isotope technique:IM Technetium 99 via Gamma Camera
  • 40.
  • 41.
    Management of AsymptomaticPAD and Claudication • Risk factor Modification − Smoking cessation, Care of feet − Diet/obesity control (BMI<25) • Exercise Therapy • Pharmacological Treatment − Platelet aggregation suppression: Cilostazole (Phosphodiesterase inhibitors) − Antiplatelet therapy − Control risk factors: DM, HTN − Pentoxyphylline (xanthine derivative), statins, Naftidrofuryl • Revascularization by Open surgery or EndoVascularization • Therapeutic Angiogenesis
  • 42.
  • 43.
  • 44.
    Risk Factor Modification •Smoking Cessation • Diabetes control: Goal HbA1c<7% each 1% rise in HbA1c ass. With 28% risk for PVD) Metformin or Glitazone Vs Insulin (BARI 2D trial) • Hypertension control: ACE inhibitors Goal: DM: <140/90, CKD: <130/80 • Hyperlipidemia: Diet modification Statins: improve maximal walking distance Niacin or Fibrates
  • 45.
    Risk Factor Modification Anti-plateletTheray: • Aspirin: • Std dose: 75 to 325 mg/day • Clopidogrel: 75 mg/day Start single or both
  • 46.
    Exercise Therapy • Adaily brisk walking of 45-60 min • Walk until claudication, rest until pain subside and then repeat • Substantial improvement: 80-234% in controlled studies • Condition muscle, extract more blood, increase collateral vessel formation Supervised Exercise Rehabilitation: • For intermittent claudication • Minimum 30 to 45 min. sessions at least 3/week for 12 weeks
  • 47.
    Pharmacologic Therapy • Cilostazol: •MOA: Phosphodiesterase III inhibitor; increases cAMP, inhibits smooth muscle cell proliferation and contraction, suppresses platelet aggregation and is a direct arterial vasodilator • Also decreases TG and increases HDL • Dose: 50 mg/day X 1 week then 50 mg BD X 1 week then 100 mg BD
  • 48.
    • Review ofPhase-3 multicenter, double-blind, parallel-design trials (7 USA+1 UK) • Inclusion: 40 yrs. with symptomatic LL PAD of >6 months with ABI <0.9 • Exclusion: with known systemic/arterial disease, interventions, acute limb ischemia • Exercise treadmill testing, to assess patient response to therapy • Cilostazol in dosages of 50, 100, or 150 mg twice daily on Placebo from 12 to 24 weeks • Result: − Cilostazol therapy increased maximal and pain-free walking distances by 50% and 67%, respectively. − Decreased triglycerides by 15.8% and increased high-density lipoprotein cholesterol by 12.8%
  • 49.
    Pharmacologic Therapy • Naftidrofuryl:Serotonin antagonist, promotes vasodilation • Pentoxifylline: • Xanthine derivative; reduces viscocity, decreases platelet aggregation • Course: 400 mg TDS (max 1800 mg/day) x 2-3 months
  • 50.
    Surgical Intervention • InterventionalRadiology: Endovascular Percutaneous transluminal balloon angioplasty Local fibrinolytic therapy for recent thrombosis: streptokinase 6000 U/hr directly into occlusion Atherectomy Thrombectomy • Surgical Revascularization: Endarterectomy Graft angioplasty Peripheral artery bypass surgery • Laser endovascular ablation for total occlusions
  • 51.
    Surgical Repair Optionsfor Aorto-iliac Disaese Endarterectomy: • Opening of diseased segment and removing plaque • Indications: infected cases, small vessel, impotence Aorto-Bifemoral Bypass: • PTFE/Dacron grafts, between infrarenal aorta and b/l Femoral A • End to end anastomosis
  • 52.
    Surgical Repair Optionsfor Aorto-iliac Disaese Axillo-Bifemoral Bypass; • Subcutaneous graft between Axillary A. and ipsilateral Femoral A. • Opposite limb vascularizes by femoro-femoral bypass
  • 53.
    Surgical Repair Optionsfor Aorto-iliac Disaese Femoro-femoral Bypass: for U/L Iliac A occlusion Obturator bypass: • Graft between Iliac A. and Femoral A. through obturator membrane in infected or distorted groin anatomy
  • 54.
    Surgical Repair Optionsfor infra-inguinal disease • Autogenous grafts: Great saphenous, short saphenous, cephalic/basilic vein • Very low success rate with synthetic grafts
  • 55.
    EndoVascular Approach • BalloonAngioplasty: insert guidewire and inflate a balloon over the wire • Considered successful if residual stenosis <30%
  • 56.
    Endovascular Approach VsSurgical approach EndoVascular approach Surgical Approach Shorter Hospital stay Less Morbidity Less Interference with daily life Low Patency Rate Longer perioperative stay More complications Bowel/ureteric injury, impotence Superior Patency rate • TASC II recommends angioplasty over Surgery • BASIL (2005 UK) trial favors Surgical Group
  • 57.
    Therapeutic Angiogenesis • Genetransfer: 4000 mg naked Plasmid DNA encoding VEGF injected directly in ischemic limbs • Others: stem cells, autologous progenitor cells, growth factors, transcription factors • Used in CLI patints who lack options for endovascular or surgical revascularization
  • 58.
  • 59.
    Critical Limb Ischemia:Acute vs Chronic Acute limb ischemia: • ‘Sudden decrease in limb perfusion that causes a potential threat to limb viability in pts who present within 2 weeks’ • Manifested by : • Ischemic rest pain • Pulselessness • Pallor • Paresthesia • Paralysis • poikilothermia • Ischemic ulcer/Gangrene
  • 60.
    Acute limb ischemia:Etiology Embolus Thrombosis :  Vascular grafts  Atherosclerosis  Thrombosis of aneurysm  Entrapment syndrome  Hypercoagulable state  Low flow rate Cardiac source:  Atrial fibrillation  Myocardial infarction  Endocarditis  Valvular disease  Atrial myxoma  Prosthetic valves Arterial source:  Aneurysm  Atherosclerotic plaque Trauma:  Blunt  Penetrating  Iatrogenic
  • 61.
    Acute limb ischemia:Classification Viable Marginally Threatened Immediately Threatened Nonviable Pain Mild Severe Severe Variable Capillary Refill Intact Delayed Delayed Absent Motor Deficit None None Partial Complete Sensory deficit None Minimal Partial Complete Arterial Doppler Audible Inaudible Inaudible Inaudible Venous Doppler Audible Audible Audible Inaudible Treatment Urgent workup Emergency Surgery Emergency Surgery Amputation UpToDate 2024/Rutherford et al.
  • 62.
    Acute limb ischemia:Imaging • Angiography: detailed arterial anatomy, distinguish thrombosis and embolism • If threatened extremity; immediate surgical revascularization with intraoperative angiography
  • 63.
    Acute limb ischemia:Management • Heparin: IV Heparin bolus 100 U/kg followed by a continuous heparin infusion 15 U/kg/hour with goal PTT 60-80 sec (Refer to specialist) • Revascularization within 6 hrs critical to avoid limb loss
  • 64.
    Acute limb ischemia:Management Viable Extremity: Urgent Arteriography to plan surgical or percutaneous revascularization Two methods of Treatment: Embolectomy Vs Intra-Arterial Thrombolysis
  • 65.
    Acute limb ischemia:Management Embolectomy: • Under Local/General Anesthesia • The Artery (usually the femoral), exposed and held in slings • Longitudinal or transverse incision; clot removed together with embolus with Fogarty Balloon Catheter • Catheter introduced both proximally and distally • Procedure repeated until bleeding occurs
  • 66.
    Acute limb ischemia:Management Intra-arterial Thrombolysis: • 5F catheter passed into occluded vessel; left embedded in clot • Thrombolysis: Tissue plasminogen activator 5 mg bolus with Mechanical spray/suctioning • Abandoned if no progression of dissolution of clot in 24 hrs.
  • 67.
    Acute limb ischemia:Management Threatened Extremity: • Irreversible changes can occur within 4-6 hrs of ischemia • Emergent surgical revascularization • Embolectomy is often all that is required to relieve occlusion • Intraoperative completion Arteriogram after embolectomy • Intraoperative thrombolytic therapy for small emboli in distal runoff vessels • Fasciotomy may be required to prevent Compartment Syndrome
  • 68.
    Acute limb ischemia:Management Non-Viable Extremities: • Prompt amputation • Arteriography is usually not necessary • Delay in amputation may result in infection, myoglobinuria, ARF, hyperkalaemia
  • 69.
    Amputation Indications Dead Limb: -Gangrene Deadly Limb: -Wetgangrene -Spreading cellulitis -Arteriovenous Fistula -Other (e.g. malignancy) “Dead loss” limb: -Severe rest pain with unreconstructable critical limb ischemia -Paralysis -Other (e.g. contracture, trauma) Site Selection Upper Limb: A/E= 20 cm from Acromion B/E= 18 cm from Olecranon Lower Limb: A/K= 12 cm from joint line B/K= 14 cm from joint line
  • 70.
    Amputation levels (upperlimbs) • Hand & Partial–Hand - Finger, thumb, palm below wrist • Wrist Disarticulation • Trans-Radial (Below Elbow) • Trans-Humeral (Above Elbow) • Shoulder Disarticulation • Forequarter Amputation - At shoulder level; both shoulder blade and collar bone are removed
  • 71.
    Amputation levels (lowerlimbs) • Foot Amputations • Amputations of greater toes and other toes • Ankle disarticulation: Syme’s Operation • Lisfranc’s operation: Tarso-Metatarsals • Chopart’s operation: Mid-Tarsals • TransTibial • Knee Disarticulation • Trans-femoral • Hip Disarticulations
  • 72.
    Chronic Limb Ischemia •Definition: Decrease in limb perfusion that causes a potential threat to limb viability in patients who present >2 weeks of rest pain, ulcer or tissue loss, characterized by ABI<0.4 Ankle systolic pressure: <50 mmhg Toe systolic pressure: <30 mmhg • Seen when two or more levels of arterial tree occluded
  • 73.
    Chronic Limb Ischemia:Management • Management: Imaging: duplex, CTA, MRA, Angiography Risk factor reduction Wound care: conservative Prostaglandins E1??- no long term benefit at 6 months Catheter based intra-arterial thrombolytic therapy (acute thrombosis over old occlusion) Revascularization: Angioplasty Vs Bypass Surgery ACC/AHA guideline for PAD recommends: • Life expectancy <2 years or do not have autogenous vein: Balloon Angioplasty • Life expectancy >2 years and have autogenous vein conduit: Bypass Surgery
  • 74.
    Prognosis • Framingham study:1.6% of patients with claudication reached amputation stage after 8.3 years of f/u • Predicted mortality for patients with claudication: (CVS cause) • 30% at 5 years f/u • 50% at 10 years • 70% at 15 years
  • 75.
    Thromboangiitis Obliterans/Buerger’s disease •Nonatherosclerotic, segmental inflammation of small and medium sized arteries, vein of upper and lower extremities  More common in men 25-40 years of age  Correlates with cigarette smoking, HLAB5 and A9 antigens  Rest pain, ischemic ulcerations  Disease of Exclusion  Colour Duplex: serpiginous or corkscrew collaterals at the site of occlusion with normal arterial wall
  • 76.
    Thromboangiitis Obliterans/Buerger’s disease OlinCriteria for Diagnosis: • Age <45 years • Current/recent hx of Tobacco Use • Presence of distal extremity ischemia (non-invasive vascular testing) • Exclusion of Autoimmune Dx, Hypercoagulability, Diabetes • Exclusion of Proximal source of emboli by ECHO/Arteriography • Consistent arteriographic findings
  • 77.
    Buerger’s disease: Treatment Tobacco cessation  Active Vs Passive Vascular exercise  Analgesics and position, care of feet  Intra-arterial streptokinase (bolus 10000 U f/b 5000 U/Hour)  Meds: − Prostaglandins, − Anti-platelets, − Vasodilators, − Pentoxyphylline − Niftidrofuryl
  • 78.
    Buerger’s disease: Treatment Sympathectomy: ↓vasomotor tone, abolish pain impulse Nakata et al reported ulcer healing in 58% and relief of rest pain in 64% Contraindicated in Intermittent Claudication by stealing blood from muscle to skin Surgical Sympathectomy oLumbar: L1,L2, L3, L4 removed (Temporary) − Open vs Lap Extraperitoneal vs Transperitoneal route oCervical: T1, T2, T3 removed − Approach: Supraclavicular, Axillary, Posterior, Transthoracic (lap) Chemical Sympathectomy: Under LA, Fluoroscopic/USG guidance on lateral position 5 ml Phenol in water (1:16) injected beside bodies of 2nd and 4th vertebrae
  • 79.
    Buerger’s disease: Treatment Omental Transposition:  Omentum: Rich Vascular supply  Causes Neo-vascularization, Increases lymphatic drainage  Procedure: omentum mobilized-Subfascial Tunneling from inferior end to inguinal incisionDistal end of pedicle is fixed to Gastrocnemius with catgut.  Surgical: AV fistula creation proximal to block Amputation (gangrene, severe infection)
  • 80.
    Raynaud’s Disease • Episodicreversible vasospastic disorder of small cutaneous arteries in fingers and toes in response to cold or stress (may involve nose, ears and tongue) • Cause: Exaggerated SNS stimulation • Occurs in women 15-40 yrs of age • Raynaud’s Disease: Primary Raynaud’s Phenomena (cause: Unknown) • Raynaud’s Syndrome: Secondary Raynaud’s Phenomena due to to collagen diseases: RA, scleroderma, SLE, Sjogrens, MS • Phase 1: Vasospasm phase: Pallor/blanching of hands and fingers with throbbing, aching pain, numbness, tingling • Phase 2: Venous pooling: Cyanosis due to deoxygenated blood • Phase 3: Hyperaemic phase: Erythematous swelling
  • 81.
    Raynaud’s Disease • Tx:smoking cessastion, no meds with vasoconstrictive effect, avoid cold, avoid constrictive clothes • Meds: Calcium-Channel Blockers vasodilators, vascular smooth muscle relaxants • Botox • Surgery: Sympathectomy
  • 82.
    References • Bailey andLove’s Short Practice of Surgery 28th Edition • Sabiston Textbook of Surgery 21st edition • Uptodate 2024