Peripheral arterial disease Definition Investigations Chronic insufficiency of the arterial blood supply of the limbs due to ABPI: peak systolic doppler ankle to arm pressure ratio stenosis or occlusion of the vessels 1.1-0.9 Normal 0.9-0.5 Intermittent claudication Causes <0.5 Rest pain Atherosclerosis (primary pathological cause) <0.3 Tissue loss Fibromuscular dysplasia >1.1 Calcified arteries (ie DM)à false elevation Vasculitides (Buerger’s disease, Takayasu arteritis) Duplex US Radiation-induced vascular injury CT angiogram/ MR angiogram Digital subtraction angiography DSA Symptoms Intermittent claudication: muscular pain brought on by exercise and Management relieved by rest Conservative: RF management Critical limb ischaemia: pain @ rest > 2w Smoking cessation ** Results in tissue loss (ulcers, gangrene, necrosis) Exercise Pallor of LL Diet modification Reduced temp of LL Burning sensation, paraesthesia Medical 6 Ps are for acute limb ischaemia Antiplatelet (aspirin, clopidogrel) Leriche syndrome: occlusion @ bifurcation of aorta causing classical Cholesterol (statin) triad Control BP Buttock/ thigh claudication Tight glycaemic control Absent/ reduced femoral pulses Symptomatic relief from intermittent claudication Erectile dysfunction Cilostazol: phosphodiesterase inhibitor vasodilator - Rutherford-Fontaine classification I Asymptomatic II Intermittent claudication IIA: claudication distance > 200m IIB: claudication distance < 200m III Rest pain IV Tissue loss Pentoxifylline: xanthine derivative Endovascular Angioplasty ± stenting under local Surgical Bypass procedures if not managed by endovascular (Fem-pop, fendistal, aorto-bifem, axillo-bifem, fem-fem crossover) Synthetic graft (PFTE/ Dacron) or vein graft (GSV) Ø Vein graft better option Amputation RFs Male >55yo Fam hx Smoking ** HTN High cholesterol DM Previous stroke/ MI/ angina Hyperhomocysteinemia DDx Spinal stenosis OA Nerve root entrapment (ie sciatica) Acute LL ischaemia Definition Clinical features: 6Ps (pain, pallor, pulselessness, perishing cold, Abrupt interruption in perfusion that threatens viability of the LL paraesthesia, paralysis) Causes Acute thrombus with pre-existing atherosclerosis (acute-on-chronic ischaemia) Patient has a hx of claudication and usually no obvious source of emboli Embolus 70-80% cardiac source: mural thrombus after MI, arrhythmias, infective endocarditis, prosthetic heart valves, atrial myxoma) Blue toe syndrome: atheroembolic debris resulting in distal small arterial occlusion with blueish discolouration of the distal foot Paradoxical emboli can occur from intracardiac shunts (PFO) or AV malformations Direct arterial trauma Intra-arterial drug injection Aortic dissection Popliteal aneurysm Iatrogenic cause Complications of reperfusion Reperfusion injury Rhabdomyolysis—↑K+, ↑CPK, renal impairment, myoglobinuria Treat with aggressive IV fluids, diuresis with Mannitol, alkalinisation of urine Compartment syndrome—4-compartment fasciotomy Digital Ray—if gangrene extends to forefoot Transmetatarsal—used if several toes are gangrenous Complication Irreversible tissue damage after 6h à limb loss, mortality Management If clear dx on hx and exam, don’t delay treatment Address comorbidities Give O2 IV fluids if dehydrated Bloods—fbc, U&E, coag, troponin, glucose, group and save CXR ECG Analgesia (morphine) Unfractionated heparin: (ensure no contraindications) Stat dose 5000IU then infusion of 1000IU/h; check aPTT in 4-6h (60-90) Definitive treatment depends on severity of ischaemia Petechial haemorrhages, hard musclesà (irreversible) amputation Swollen, tender + loss of f(x)à consider amputation if there are life threatening systemic complications Obvious embolusà urgent embolectomy ± fasciotomy Fogarty catheter Limb still viable à cont IV Heparin + CT angio OR stop Heparin 4h before angiography and then thrombolysis ± angioplasty (if no contraindications to thrombolysis) Types of amputation Below knee amputation Through knee amputation Above knee amputation Definition Abnormal localised dilated of aorta exceeding normal diameter by >50% or >3cm diameter True aneurysm because it contains all 3 layers of the vessel wall Transmural inflammatory △ Abnormal collagen remodelling Loss of elastin and smooth muscle cells M>F 9:1 4% of males >65yo 95% of AAA are infrarenal Surgery: 50% mortality RFs Same as PVD 10 fold ↑in smoking 50% in poorly controlled HTN Increased expansion and rupture risk a/w smoking and uncontrolled HTN Collagen and elastin defects (ie Marfan’s, EDS) AAA diameter > 5.5cm and expansion rate >0.5cm in 6mo a/w ↑risk of rupture Aortitis (from bacteraemia, endocarditis, mycotic aneurysms) Surveillance guidelines (UK) 3cm-4.4cm Annual USS 4.5cm-5.4cm 3 monthly USS > 5.5cm Surgery Clinical features Most asymptomatic (<50% detected on exam by pulsatile and expansile mass palpated in abdomen) 40% detected incidentally on imaging Symptoms arise from expansion, rupture or peripheral embolism Abdo/ back/ flank pain Distal peripheral embolisation or ischaemia Upper GI bleeding from aortoenteric fistula Syncope or chock with large pulsatile mass, ecchymoses or death from rupture DDx for sudden onset abdo/ back/ flank pain Ischaemic bowel Perforated PUD Pyelonephritis Nephrolithiasis Acute pancreatitis AAA Elective repair Open surgical repair Synthetic (Dacron) graft to repair aneurysm Long midline incision (laparotomy) Aorta clamped below renal arteries where possible to prevent renal ischaemia If iliac arteries not involved: straight graft If iliac arteries involved: bifurcated graft 3-7% mortality Endovascular aneurysm repair (EVAR) Insertion of a stent over aneurysm segment Small groin incisions (vertical/ transverse) Cross clamping of aorta not required Carried out under direct radiological guidance Use high dose nephrotoxic contrast Reduced early mortality High early re-intervention rate if endoleak occurs Ø Requires lifelong surveillance post-op for endoleak Complications of AAA repair Death Haemorrhage—uncontrolled vessels or anastomotic breakdown Myocardial ischaemia (20% of patients) Arrhythmias; cardiac failure Bowel ischaemia (urgent laparotomy if peritonitis) Abdominal compartment syndrome Atelectasis, ARDS, RTI Endoleak (EVAR) Renal dysfunction Limb ischaemia Wound infection Impaired sexual function Graft infection Graft limb occlusion (presents within 30d and may present with acute ischaemic limb) Aortoenteric fistula Endoleak Persistent blood flow into an aneurysmal sac after EVAR Type I Leak at attachment sites of graft Type II Filling of aneurysmal sac by collateral vessels (IMA, Lumbar) Type III Leak through defect in graft Type IV Leak through fabric of graft due to porosity Type V Expansion of aneurysm sac without evidence of leak on imaging Imaging USS 98% accuracy Does not define extent of aneurysm Inadequate for planning repair CT abdo with IV contrast Highly accurate to determine size and extent of aneurysm Relationship of AAA with renal arteries Determine if AAA is leaking Determines suitability or endovascular repair Ruptured AAA Presentation may be delayed if rupture is contained within Management retroperitoneal space Airway A contained leak may initially be haemodynamically stable but can Breathing: 15L 100% O2 via non-rebreather mask proceed rapidly to rupture Circulation: Wide bore IV access x2 + IV fluids Longstanding leak causing aortoenteric fistula can present with high Bloods: fbc, u&e, coag, group and x-match 10u) output HF and GI bleed Request platelets and fresh frozen plasma Sudden onset abdo/ back/ flank pain Urinary cathether to monitor output Sudden collapse with hypotension Allow permissive hypotension to avoid worsening the rupture (don’t Pulsatile abdo mass not always palpable aggressively hydrate) Analgesia Alert vascular surgeon, anaesthetist, theatre, ICU (post-care) + gain consent for surgery à urgent transfer to theatre If not candidate for surgery: analgesia and palliative Based on age, comorbidities, extent of aneurysm, patient’s and family’s wishes CT angiogram to aid dx and plan repair Other aneurysms Thoraco-abdominal Carotid Often asymptomatic Pulsatile neck swelling Chest pain, back pain, acute aortic regurgitation, acute HF May have neurological or pressure symptoms Widened mediastinum on CXR Diagnosed with carotid duplex scan Rupture is rare without pre-existing symptoms 20% mortality with elective repair Iliac Endovascular repair may be used (fenestrated or branched grafts) Mostly asymptomatic Rupture may be missed as acute abdomen or renal colic Femoral Presents with pulsatile groin swelling ± LL ischaemia Visceral Splenic artery aneurysms most common Popliteal Mostly asymptomatic but bilateral Can cause acute limb ischaemia Varicose veins Tortuous dilated segments of veins a/w venous HTN caused by Management incompetent valves Conservative Usually superficial branches of the long and short saphenous system Leg elevation Exercise RFs Weight loss Advancing age Pregnancy Medical Prolonged standing Pelvic masses Compression stockings Elevated BMI Previous DVT Sclerotherapy—laser, foam Smoking Ligamentous laxity Topical agents for skin △s Sedentary lifestyle LL trauma High oestrogen levels Surgical Symptoms Radiofrequency ablation Pain Laser ablation Heaviness of leg Local stab avulsions: open ligation ± GSV stripping Oedema (worse in evening and hot weather) Dry skin Indications for surgery Tightness Cosmetic Itching Symptomatic Prevent complications Complications Stasis dermatitis/ eczema Complications of surgery Phlebitis Nerve injury resulting in area of pain/ paraesthesia/ numbness Lipodermatosclerosis—fibrosing dermatitis of subcut tissue DVT Skin pigmentation due to haemosiderin deposition Recurrence Ulceration Bruising/ haematoma Bleeding Bleeding Wound infection Dx and investigations Typically a clinical dx Always examine the abdomen to assess for an abdo/ pelvic mass Trendelenburg test and Perthes test to clinically identify points of incompetence USS duplex of superficial and deep veins Virchow’s triad – factors contributing to thrombosis 1. Stasis of blood flow 2. Endothelial injury 3. Hypercoaguability DVT Complications of DVT PE Chronic venous insufficiency Venous gangrene RFs for DVT “THROMBOSIS” Trauma, travel Hormones (OCP, HRT) Road traffic accidents (fractures) Operations Malignancy Blood disorders (Factor V Leiden, protein c/s deficiency, antithrombin def) Obesity, old age, ortho surgery Serious illness (prolonged hospital stay) Immobilisation, inadequate hydration Smoking Clinical features Limb swelling Pain Warmth Erythema Homan’s sign—calf pain on dorsiflexion (unreliable and should not be performed due to risk of embolisation) May have mild pyrexia and tachycardia May be asymptomatic Dx and investigations D-dimers: sensitive but not specific Duplex scan: investigation of choice for DVT CT pulmonary angiogram: best for suspected PE Prophylaxis Prophylactic LMWH TEDS Mobilisation Hydration Smoking cessation Stop OCP 4-6w pre-op Wells score – probability of developing a DVT Active malignancy +1 Paralysis, paresis, recent plaster immobilisation of LL +1 Localised tenderness along deep venous system +1 Entire leg swollen +1 Calf swelling >3cm and larger than asymptomatic side +1 Pitting oedema +1 Collateral superficial veins +1 Previously documented DVT +1 Alternative dx equally as likely as DVT -2 ≥2: DVT likely < 2: DVT unlikely Treatment Uncomplicated DVT Therapeutic LMWH then switch to warfarin for 3-6mo Complicated DVT IV unfractionated heparin/ LMWH while converting to warfarin Thrombolysis/ thrombectomy if severe thrombosis IVC filter Inserted percutaneously via jugular/ fem vein to catch and prevent PE Used in recurrent PE despite treatment/if anticoag contraindicated/ anticoag cannot be used during major surg Risks of IVC placement: air embolism, arrhythmia, pneumo/haemothorax, IVC obstruction, bleeding Thrombolysis Streptokinase, urokinase, recombinant tPA Administered via catheter as a low dose intra-arterial infusion Indications Acute limb ischaemia Venous thrombosis Acute surg graft occlusions Thrombosed popliteal artery aneurysm Contraindications Bleeding disorders Current peptic ulcer Recent haemorrhagic stroke Recent major surg Evidence of muscle necrosis—may cause reperfusion injury Contraindications Allergy Catheter leak, occlusion Bruising Major bleed/ stroke Carotid artery disease Cerebrovascular accident—rapidly developing neurological deficit Management lasting >24h Medical Antiplatelet agents—aspirin, plavix Transient ischaemic accident—acute episode of focal neurological Anticoag—use in non-cardiac emboli is controversial deficit that resolves within 24h Smoking cessation BP control Carotid artery stenosis occurs in 10% of people 80-89yo Tight glucose control Statin Clinical features CVA Surgical/ endovascular Completed stroke Carotid endarterectomy/ carotid stent Stroke in evolution—progressive neurological deficit over days and 50-99% stenosis with recent TIA/ CVA weeks Consideration of intervention if asymptomatic but >70% FAST criteria stenosis in younger patients and low interventional risk Facial droop Contraindications Arms: can they raise them and keep them elevated Ø Severe neuro deficit after cerebral infarction Slurred speech? Ø Occluded carotid artery Time: call for help if any of these signs are present Ø Severe comorbidities TIA Cab gave a transient △ in facial expression, drooping of corner of mouth, dribbling Amaurosis fugax Transient mono-ocular visual loss Like a curtain coming down over eye Cerebral hypoperfusion Dx and investigations Carotid duplex scan—difficult if vessels are calcified Carotid MR angiography Cranial CT/ MR angiography Cardiac echo/ telemetry—useful to exclude cardiac cause of embolic stroke Carotid endarterectomy Can be performed under GA/ LA Incision along ant border of SCM muscle Shunting of carotid artery following clamping can allow for ongoing cerebral perfusion during surgery Endarterectomy is mos commonly closed with a synthetic patch Post op Observe for haematoma that may compromise airway Antiplatelet therapy Monitor BP Complications CVA: increased risk in stenting vs endarterectomy MI: increased risk in endarterectomy us stenting Death Wound haematoma (in endarterectomy)à cause airway obstruction Recurrent stenosis Cranial nerve injury Vagus: vocal cord paralysis, dysphagia Hypoglossal: deviation of tongue Leg ulcer Causes Venous Arterial Mixed arterial and venous Neuropathy DM Vasculitic—Buerger’s disease, Takayasu’s arteritis Malignancy (consider if ulcer doesn’t heal with adequate medical management) Infection Lymphoedema Site Edges Depth Size Base Margin Cause Surrounding features Management Features Ulceration Infection Sensory neuropathy Poorly healing wounds Arterial Distally (digits) Punched out, well defined Deep Small Necrotic Regular Arterial insufficiency Pallor, hairloss, trophic △s, onychogryphosis, cool, weak/ absent pulses, prolonged capillary refill Treat as chronic PVD with critical limb ischaemia Venous Medial gaiter region Sloped Superficial, shallow Large Granulation tissue Irregular Venous HTN Oedema, haemosiderin, lipodermatisclerosis, varicose veins 4 layered profone dressing Elevation Venous support stockings Skin graft Abx if infected Varicose veins surgery if possible after ulcer has healed to reduce recurrence rate Diabetic foot Investigations ABPI/ toe pressures Duplex USS CT angio/ MR angio if co-existing arterial disease suspected Blood glucose level, HbA1c, renal function, BP Aetiology Small and medium vessel disease Sensory neuropathy resulting in unnoticed tissue damage Autonomic neuropathy resulting in reduced sweating, which leads to dry cracked skin and infection RFs Previous ulcers Diabetic neuropathy Stocking distribution Charcot’s joints Associated peripheral arterial disease Calcified peripheral arteries Falsely elevated ABPI Calluses Living alone Evidence of other diabetic complications (ie renal/ visual impairment) Clinical features Ulcers on pressure points Evidence of sensory loss If arterial disease is present, foot may be cool with reduced/ absent pulses Secondary infection of ulcer ± cellulitis Falsely elevated ABPI due to calcified vessels Toe pressures is more useful in determining perfusion Management Best done at a specialist multidisciplinary clinic Regularly inspect feet Appropriately fitted footwear and avoid walking barefoot Chiropodist for debriding calluses and nail care If infected ulcer, Broad spectrum abx ± debridement of dead tissue ± amputation of non-viable digits if adequate arterial supply for healing amputation X-ray/ MRI to rule out osteomyelitis Consider revascularisation if significant arterial disease Consider amputation if no response to medical/ other surgical treatments Neuropathic ulcers Caused by trauma unnoticed by patient Punched out appearance Located over pressure points/ calluses Surrounded by inflammatory tissue Frequently painless due to neuropathy
