Vascular Medicine & Surgery

Vascular Medicine & Surgery • • • • • • • • • • • Hyperlipidaemia Atheromatous vascular disease Aneurysms Chronic peripheral arterial occlusive disease Acute arterial occlusive disease Amputation Vasospastic disorders Vascular trauma Venous disease Lymphatic disorders Diagnostic radiology in vascular disorders Vascular 1 2 5 7 9 14 16 19 21 23 25 27 Hyperlipidaemia Hyperlipidaemia = abnormally high level of one or more lipoproteins in the plasma Lipoproteins – hydrophobic lipid, encased in phospholipid, cholesterol and apolipoproteins Chylomicrons – transport triglycerides & cholesterol from GI tract to liver FFA & cholesterol released to: VLDV – transports cholesterol & TG to tissues, TG released --> LDL LDL (bad) – cholesterol taken up by the liver & tissues HDL (good) – absorbs cholesterol from cell breakdown & transfers it to VLDL & LDL • Outline the epidemiological link between cholesterol and cardiovascular risk. Main causes Primary Genetic predisposition Secondary Obesity Excess alcohol intake DM Nephrotic syndrome Hypothyroidism Drugs - B-blockers, Thiazides, Corticosteroids, Retinoids, Oral contraceptives, Anti HIV drugs Consequences High cholesterol is major risk factor for atherosclerosis (ideal < 5.2mmol/l) High risk of developing IHD & cerebrovascular disease Signs Xanthomata – yellow deposits on eyelids, cornea & tendons Who to screen CHD or increased risk (e.g. DM, HT) Family history of hyperlipidaemia or CHD < 65yrs Xanthomata (yellow deposits in skin) or Xanthelasmata (eyelids) Corneal Arcus before 50yrs Non medical management Aim for BMI 20-25 Diet with 10% of calories from saturated fats Increase fibre, fresh fruit & veg & omega-3 fatty acids Avoid lier, offal & fish roe (high in cholesterol) Reduce alcohol consumption Increase excercise • Discuss the evidence for using lipid-lowering drugs in secondary prevention of cardiovascular disease. 4s study – 2o prevention trial (existing IHD) using simvastatin 20mg in 4444 volunteers. NNT to prevent 1 fatal MI was 25 (14 for non fatal events) CARE study – 2o prevention with pravastatin 40mg. NNT for fatalities was 91 (38 for non fatal MI) Heart protection study – 2o prevention trial with simvastatin 40mg. NNT for death = 55 Vascular 2 • Lipid Research Clinics Coronary Primary Prevention Trial (LRC-CPPT) – cholestyramine + diet had 19% lower CHD incidence than placebo & diet in those with high cholesterol Outline the issues relating to the use of lipid lowering drugs in primary prevention of cardiovascular disease. WOSCOPS – 1o prevention in Scotland with over 6500 men. Pravastatin 40mg to prevent 1 fatal MI was 142 (55 for all cardiac events) Helsinki Heart study – gemfibrozil (fibrate) on asymptomatic men. CHD incidence 34% lower in drug group Air force / Texas coronary atherosclerosis prevention study – lovastatin V placebo in asymptomatic with normal cholesterol. Drug reduced incidence of coronary events. • Describe the indications for using HMGCoA reductase inhibitors (statins) and fibrates and outline their principal side effects. Statins (e.g. simvastatin, pravastatin, atorvastatin, fluvastatin) Mechanism Statins are heavily hepatoselective Only 5% reaches the systemic circulation due to high 1st pass metabolism Hydroxymethylglutary ê (HMG-CoA reductase) Mevalonate Statins are HMG-CoA reductase inhibitors ê Cholesterol By reducing the plasma cholesterol à increase LDL receptors in the liver à LDL uptake (NB: less effective in familial cases as unable to make the receptors) Evidence & advice Some evidence that statins à regression of atherosclerosis Statins do slow athersclerotic progression à reduces stroke, CVS disease & death Statins should be considered for ALL patients with high risk of CVS disease, irrespective of their cholesterol level BUT are rationed according to priority and are given to Post angine / MI Those with 30% 10yr risk of CVS disease (e.g. DM, HT) with cholesterol > 5mmol/l Should be taken at night Contraindications Active liver disease Pregnancy & Lactation Adverse effects Derangement of LFTs - Should monitor LFTs if any liver disease Diarrhoea Can à myopathy à rhabdomyolysis so REPORT any muscle pains Have a range of interactions (ciclosporin, fibrates, itroconazole, warfarin) Vascular 3 Fibrates (bezafibrate, gemofibrozil) Activate peroxisome proliferator-activated receptor (PPARα) à alters lipoprotein metabolism à promotes VLDL breakdown à lowers triglycerides May also lower glucose (of use in DM) Contraindications Severe hepatic or renal impairment Gallbladder disease Pregnancy Adverse effects Reversible myositis Nausea Predisposes to gallstones Non-specific malaise Impotence Can à rhabdomyolysis Cholestyramine Can be used with statin Binds bile salts preventing enterhepatic recycling à Reduces absorption of cholesterol à Increases LDL receptors à Decreases absorption of ADEK (& absorption of some drugs (digoxin, thiazides) so give at diff times) à liver makes more bile acids from cholesterol store Adverse effects GI mainly – steatorrhoea. Not very palatable Cholesterol absorption inhibitors (ezetemibe) Prevents GI cholesterol absorptions Use with a statin Contraindications Lactation Adverse effects Occasional diarrhoea & abdominal discomfort Vascular 4 Atheromatous vascular disease • Define atherosclerosis and list the risk factors for its development. Atherosclerosis Is arteriosclerosis (thickening & hardening of the artery wall) … …due to atheroma (accumulation of lipid rich material in the intima) Atherogeneisis Damage to blood vessel à Inflammatory response (changes in intima initially, then later media) à Cholesterol rich deposits & growth of smooth muscle & connective tissue (1st degree = fatty streaks) à Plaques (2nd degree) à reduced lumen à poor perfusion & hypoxia à decreased elasticity à increased aneurysm risk à thrombus (3rd degree) Risk factors Increasing age M > F (oestrogen is protective) Family history (genetic predisposition) • High cholesterol Hypertension Smoking Diabetes Distinguish between macrovascular disease and microvascular disease and briefly outline the differences in their clinical presentation (see section on Diabetes). Microvascular – affecting end arteries and capillaries (e.g. retinopathy, nephropathy) Macrovascular – affecting arteries and large arterioles (e.g. atheroscleotic plaque, thrombus, embolus) • List the specific sites where there is a predilection to develop atheroma and explain why such predilections exist. Coronary arteries Leg arteries Mesenteric arteries Cerebral & vertebral • à angina / MI à claudication à ischaemic colitis à cerebral ischaemic events List the clinical consequences and complications of atheroma. Expansion of the intima à decreases lumen à decreases flow à ischaemia Ulceration of intima à predisposition to thrombus Plaque fissure formation à haemorrhage Loss of vessel elasticity à aneurysm • Discuss ways to modify the atherosclerotic process including general health measures Conservative Avoidance of smoking Diet Weight loss if overweight Exercise Pharmacological Control of blood pressure (reduces risk) Reducing hyperlipidaemia (slows process of atheroscleosis) Control of diabetes (reduces risk) Vascular 5 Aspirin (reduces risk of plaque formation & thrombus risk) • Outline the pathophysiology of vasculitis and discuss the conditions associated with vasculitis including autoimmune disease (SLE, polyarteritis, temporal arteritis), infection, malignancy and haematological disease Vasculitis = inflammatory disorder of blood vessel walls Can affect any organ or tissue Large – Giant cell arteritis, takayasu’s arteritis, polymyaligia rheumatica Medium – polyarteritis nodosa, Kawasaki disease Small ANCA +ve – glomerulonephritis, wegners granulomatosis, microscopic polyangiitis, Churg-Strauss syndrome ANCA -ve – Henoch-Schonlein purpura, cryoglobulinaemia, goodpastures diease May also be secondary to SLE, RA, Hep B & C and HIV NB: ANCA = Ab against neutrophil cytoplasma antigens Features General – fever, malaise, weight loss, arthralgia, myalgia Skin – purpura, ulcers, livedo reticularis, nailbed infarcts, digital gangrene Eyes – episcleritis, ulcers, visual loss ENT – epistaxis, nasal crusting, stridor, deafness Pulmonary – haemoptysis, dyspnoea Cardiac – heart failure, angina / MI GI – pain, malabsorption (due to chronic ischaemia) Renal – HT, haematuria, proteinuria, casts, renal failure (acute or chronic) Neurological – mononeuritis multiplex, sensorimotor neuropathy, stroke, fits, chorea, psychoses, confusion, decreased cognition, change in mood Diagnosis Clinical findings +/- histology Raised ESR & CRP ANCA may be +ve Treatment Large vessel vasculitis: steroids in most cases Medium / small: steroids + cyclophosphamide. Azothioprine may be used as maintainence Vascular 6 Aneurysms Aneurysm – abnormal, permanent dilatation (to above 150% of origional diameter) of an artery or part of the heart • Describe the common sites and relative incidence of atherosclerotic arterial aneurysms. Atherosclerotic –due to thin, fibrous replacement of the media Aorta - 3% of those over 50 Iliac Femoral Popliteal Berry – cerebral arteries. Usually congenital Syphylitic – ascending aorta & arc – due to inflammatory destruction of media à fibrous plaque Mycotic (infective) – can occur anywhere. Are due to bacteria in an infected thrombus • Differentiate true and false aneurysms. True aneurysm = abnormal dilatation of artery. Should be pulsatile & expansile False aneurysm = collections of blood around a vessel wall (e.g. after trauma) that communicate with the vessel lumen. A dissecting aneurysm is not a true aneurysm • Describe the pathophysiology of arterial dissection (dissecting aneurysm) and outline its clinical presentation, medical and surgical treatment, complications and causes of death. Blood forces a passage through a break in the vessel intima à a false channel between laters Thoracic dissection of Aorta presents with: Severe, tearing, central chest pain Radiating to the back and down the arms (mimics MI) Can appear shocked, with neuro signs 2o to loss of blood supply to spine Can à reduced flow to organs / areas supplied by branches of affected vessel Complications Can rupture externally à internal haemorrhage (mediastinal / haemopericardium) Predisposing factors Hypertension (70%) Atherosclerosis Heriditary (e.g. Marfans, ehlers-danlos) • List the symptoms and signs of a rupturing abdominal aortic aneurysm and discuss the differential diagnosis. Severe back pain Radiates to groin & iliac fossa (differential renal colic) Profound shock & Collapse General abdominal tenderness Pulsatile, expansile abdominal mass • Outline an emergent diagnostic and management plan for a rupturing aneurysm. Summon vascular team & anaesthetists & warn theatre Vascular 7 Min 2 large venflons Take bloods – serum amylase, FBC & cross match most important IV infusions but keep systolic < 100. Transfuse with O-neg if required ECG Catheterise (to monitor UO) Prophylactic Abx (ampicillin & flucloxacillin) Surgery involves insertion of a Dacron graft to repair vessel • Discuss the indications, contraindications and risk factors for surgery in chronic asymptomatic abdominal aneurysm. Stable aortic aneurysm Often asymptomatic – discovered incidentally on examination May cause back/abdominal pain <5.5cm can be monitored by regular examination & US. Rupture risk = 1%/yr >6cm have rupture risk of 25%/yr Consider elective repair if: >6cm Expanding at >1cm/yr Symptomatic Operative mortality is 5%. Complications include spinal/mesenteric ischaemia due to dislodged thrombus debris • Describe the presentation, complications and treatment of popliteal aneurysm The most common peripheral aneurysm Associated with others and usually bilateral Presentation Mostly asymptomatic Distal embolisation of sac contents à claudication / digital infarct Acute occlusion & rupture are uncommon Investigations O/E – prominent pulsation in popliteal fossa, often extending proximally. Check distal to look for embolisation Duplex US – to assess size & extent Angiography – to examine arterial tree distal to aneurysm Management If symptomatic do femoral-distal popliteal bypass with ligation of feeding vessels If containing clot repair electively Distal emboli can be treated with thrombolysis at surgery Vascular 8 Chronic peripheral arterial occlusive disease • List the clinical manifestations of chronic peripheral arterial occlusive disease. Usually affects the aorto-iliac / infrainguinal arteries Skin changes Cold, dry skin with lack of hair Venous guttering – due to empty veins Pulses Weak / absent pulses (tissue may be maintained by collaterals) Intermittent claudication Severe cramp in calf on exercise Resolves on resting and never occurs at rest Severe peripheral vascular disease Rest pain – severe & unremitting Night pain – when gravity not aiding flow to legs, prevents sleep, relief on standing Ulceration / necrosis of tissue On examination Slow capillary refill Poor / absent peripheral pulses +ve Buerger’s test – raise legs slowly – poor supply = pallor (angle at which pallor appears & buerger’s angle). Then swing over edge of bed à dusky crimson = reactive hyperaemia ABPI Normal = 1-1.2 Claudication = 0.6-0.9 Rest pain = 0.3-0.6 Impending gangrene = <0.3 NB: heavily calcified vessels may à false high readings Exercise test – if not limited by CVS / RS disease Investigations Urine & blood sugar for DM Hb – to exclude anaemia / polycythaemia ESR & CRP – will be raised if inflammatory / mycotic conditions Serum cholesterol – risk factor. ECG – to assess if co-existing cardiac disease Echocardiogram – to confirm valvular lesion, mural thrombus, ventricular aneurysm CXR – bronchial CA common if smoker with end stage vascular disease Doppler US – to show wave forms. Biphasic if normal, monophasic if hardened arteries Duplex US – assesses stenosis based on flow rates Arteriography – if reconstructive surgery is contemplated Angioplasty – dilatation of stenosed segment During slow occlusion collaterals develop to supply the tissue = compensation • Contrast atherosclerotic gangrene in diabetic and non-diabetic patients. Gangrene is death of tissue from poor vascular supply = sign of critical ischaemia Typically around toes & pressure areas on foot Wet gangrene = tissue death + infection (usually pseudomonas) Dry gangrene = no infection Rx with radical debridement + Abx. Vascular 9 • Describe the pathophysiology of intermittent claudication; differentiate claudication from other causes of leg pain. Intermittent claudication is like angina in the leg muscle. At rest blood flow is sufficient, but not during exercise. Spinal canal claudication – leg pulses still present Oesteoartritis – knee pain at rest Peripheral neuropathy – numbness / paraesthesia Popliteal artery entrapment – young person with normal pulses Venous claudication – busrting pain on walking. History of DVT Buerger’s disease – young males, heavy smokers Fibromuscular dysplasia • List criteria to help differentiate venous, arterial, diabetic and infectious leg ulcers. Venous 80% of leg ulcers are due to venous hypertension Pathology Valves in deep veins lose competency à increased pressure in small venules and capillaries à tissue oedema à hydrostatic pressure à decreased flow à impaired tissue oxygenation & poor wound healing Fibrin is extravasated in oedema fluid à cuff around vessels à further impaired oxygenation Inflammatory mediators (due to hypoxia and infection) released into skin & subcutaneous fat à further tissue damage Predisposing factors Venous disease (DVT, Varicose veins, thrombophlebitis) Childbirth Orthopaedic / abdominal surgery Features Normal foot pulses (unless concurrent arterial insufficiency) Varicose veins Brown discolouration (heamosiderin) Pitting oedema Ulcer – usually on lower 1/3 of leg, mostly medial 2o complications Infection Swab ulcers regularly Superficial (pseudomonal & anaerobes) à slough, exudates & odour, If S.aureus = pain & enlarging with slough. Rx topical antiseptics Cellultis – skin & subcut tissue. Pain, oedema, erythema, blistering, long term risk of lymphoedema with destruction of the lymphatics. Rx aggressive IV Abx until improvement, then oral Dermatitis Irritants – exudates, topical antiseptic Allergens – lanolin, Abx, Cream preservatives Should do a patch test Lymphoedema Due to lymph damage, immobility etc Flexion contractures Of foot due to pain & fibrosis à worsens immobility Treatment General – elevation, exercise, compression, nutrition, treat anaemia, social issues Vascular 10 Topical – wash, debride, deslough, antiseptic, antibiotic, dressing & skin care Skin graft – pinch, punch or split skin grafts Systemic – Abx for cellulites, oxypentifyline, antiplatelet, antifibrinolytic, diuretics only if another comorbidity Arterial 5-10% of all ulcers Diagnosis Hx – smoking, rest pain, claudication, other ischaemic disease OE – decreased / absent pulses, decreased dopplers, cool limb, atrophic, hairless, poor capillary refill, painful, punched out Treatment Local – clean & debride, treat infection, stop smoking, graft if possible Surgical – embolectomy, endarterectomy, bypass, amputation Vasculitic Uncommon but may show systemic disease Diagnosis Multiple small painful ulcers on the legs & feet with areas of purple/black necrosis & purpura Histopathology shows vasculitis Aetiology Inflammatory – SLE, rheumatoid, polyarteritis nodosa, HSP, pyoderma gangrenosum Small vessel occlusion – septic emboli, cellular debris, hyperviscosity, Neoplastic Neuropathic Sensory neuropathy à decreased sensation à minor repeated trauma e.g. DM, leprosy, syphilis, paraplegia, motor neuropathy (decreased movement & perfusion) Diabetic Very common & multifactorial (small vessel disease, neuropathy & infection) A combination of sensory (insensitive to pain), motor (keep feet still) and autonomic (decreased perspiration à infection) neuropathy Neoplastic Skin tumour à necrosis à non healing ulcer • Describe the conservative & medical management of arterial occlusive disease Conservative management Decrease risk factors Nicotine à vasospasm, CO reduces O2 carrying capacity, & platelets more “sticky” Regular chiropody for diabetics Supervised exercise à improved walking distances Adapt lifestyle to live with claudication distance Weight loss – less effort for the muscles Raising the heel of the shoe – less work for the muscles Medical management Check for anaemia, treat if appropriate Protect from further atheroscleosis (statin, aspirin / warfarin, control DM) • Describe the operative treatment choices for patients with occlusive disease of the distal aorta and iliac arteries, superficial femoral/popliteal arteries and tibial and peroneal arteries. Vascular 11 Treat the handicap, not the disability – do they need to walk 1 mile!!! Angioplasty – to stretch & fracture the stenosis, allowing more blood to pass through. Less use for blocks over 10cm long (femoral or distal popliteal). Endoluminal stenting – can be placed at same time as angioplasty. Can maintain patency after angioplasty. Has risk of distal embolisation and vessel perforation Thrombolysis – if acute deterioration of chronic claudication. Streptokinase / TPA is infused to the clot à dissolves. Only used if limb is threatened Bypass surgery – only if severely handicapped (limiting claudication / rest pain). Comlications include intimal dissection, distal embolisation, graft thrombosis • Describe the symptoms, signs, investigations, differential diagnosis and treatment of chronic mesenteric vascular occlusive disease. Chronic small bowel ischaemia Follows ingestion of food – as triggers O2 requirement of gut History of severe colicy pain after meals, marked weight loss & fear of eating due to pain Angioplasty is possible if the bowel is viable Chronic large bowel ischaemia Low flow in IMA territory Left lower quadrant abdominal pain & bloody diarrhoea. Can be pyrexia, tachycardia, PR bleed & leucocytosis = ischaemic colitis (barium enema shows thumb-printing from submucosa swelling Management Conservative at start – iv fluid & Abx – most will recover Angioplasy & stenting are possible May à gangrene of bowel, peritonitis & hypovolaemic shock Requires resection and colostomy • Describe the clinical presentation, investigation and management of renal artery stenosis. Stenosis of the renal arteries (renovascular disease) can cause hypertension. Renal ischaemia results in reduced pressure in afferent glomerular arterioles à Increase in renin release from juxtaglomerular apparatus à Increase in ATII (potent vasoconstrictor) à Hypertension Renal perfusion pressure is reduced à prolonged nephron transit time à Increased salt and water reabsorption à More concentrated urine, low sodium (+ low creatinine, inulin & PAH clearance) Caused by 2 pathological entities Fibromuscular disease (20-40% of renovascular disease). 4 types: Medial fibroplasia (65-85%) – benign. Never progressive after 40yrs Perimedial fibroplasias (10-15%) – progressive, can à total occlusion Intimal fibroplasias (5-10%) – progressive, can à total occlusion Medial hyperplasia (5%) – young females, elevated BP but normal perfusion. Angioplasty & stenting can help Atherosclerotic renovascular disease Common cause of ischaemic nephropathy 5% under 60yrs, 16% in over 60s Lesion is usually within 1cm of renal artery origin + symptomatic lesions elsewhere in body (peripheral vascular, coronary artery, aneurysms etc) Vascular 12 Consequences include hypertension, Na retention (à oedema), proteinuria & decreased GFR Investigations Radionuclide studies – demonstrate reduced renal perfusion on affected side. Significant stenosis shown by disproportionate fall in uptake on aspirin / captopril administration. Doppler US – very sensitive but time consuming & operator dependent. Gives data on resistance. MR angiography – visualise the renal artery Spiral CT – imaging the arteries but involves radiation and contrast Renal angiography – gold standard Treatment Aims to correct HT & improve renal perfusion and excretory function Transluminal angioplasty will dilate the stenotic region + stent Revascularisation if >75% stenosis If other kidney asymptomatic consider nephrectomy • List the surgically curable causes of hypertension. 2o causes of hypertension include: Renovascular disease (see above) Coarctation of the aorta Endocrine causes Phaeochromocytoma Cushing’s syndrome Conn’s syndrome Raised ICP Toxamia in pregnancy • Describe the principle of measurement of the ankle-brachial pressure index and the limitations of the test Using a doppler probe and sphyg the ankle & brachial systolic pressure are measured >1.3 = abnormal – due to calcification / hardening of vessel walls >0.9 = normal <0.9 = peripheral arterial occlusive disease <0.8 = moderate disease <0.5 = severe disease Limitations Intraobserver variability Systolic BP can vary with stress etc Reading can appear high if calcification of vessel walls Vascular 13 Acute arterial occlusive disease • List the causes of acute arterial occlusion. Embolic or thrombotic disease • Differentiate embolic and thrombotic occlusion. Embolic Vegtations from RF heart valves Thrombus from heart (arrhytmias / valve replacements) Thrombus from atherosclerotic plaques Other rare ones include air, fat & marrow (trauma), amniotic fluid and tumour (mets) Thrombotic Thrombus formation on existing plaque, grafts etc Solid mass of platelets and fibrin mesh forms in alternate layers Becomes pathological when thrombosis > fibrinolysis à decreased lumen Predisposing factors: Endothelial dysfunction (injury, inflammation, atheroma) Change in flow (stasis, slow flow, turbulance = loss of laminar flow) Change in blood coagulability (increased fibrin (acute phase response), increased prothrombin & fibrin (COCP), increased protein C, S and antithrombin 3 (congenital)) Structure In high flow vessels = firm, pale, prominent layers. High fibrin/platelet content In low flow vessels = red, soft, gelatinous, poor layers. High red cell content Possible outcomes Fibrinolysis – total breakdown Propagation – elongation along the vessel Thromboembolism – fragments break off Organisation – replacement by granulation tissue Recannalisation – new vessels bridge occlusion • List the symptoms and signs of acute arterial occlusion. Systemic arterial occlusion Pale Pulseless Perishingly cold Pain Paraesthesia Paralysis If pulmonary embolus (pulmonary artery occlusion) 5% massive – if 60% of flow is blocked à CVS collapse 10% major – middle size arteries 85% minor – asymptomatic / breathless • Outline the initial management of acute arterial occlusion. Heparin – prevents propagation of blockage Give opioid pain relief Check pulses & arrange urgent imaging to detect level & nature of occlusion • Contrast the indications for surgical and medical treatment of acute arterial occlusion. Vascular 14 Medical management Those showing improvement may be treatable with heparin & treatment of the cause. Those with emboli following MI/AF need warfarin Surgical management If existing graft à need graft thrombolysis If stenosis through which wire can be passed à Angioplasty If large embolus à surgical embolectomy If occlusion of popliteal aneurysm à bypass graft NB: the sudden revascularisation can à reperfusion injury with release of toxic metabolites à oedema (can manifest as compartment syndrome) If severe ischaemia & tissue non viable à amputation • Differentiate the symptoms and signs of acute arterial from acute venous occlusion. Venous occlusion (e.g. DVT) Swelling distal to occlusion Pain in calf – worse on standing / walking Warmth Pitting oedema • Describe the natural history of treated and untreated acute arterial occlusion. Ischaemia à coagulative necrosis in the target organ / tissue Complete ischaemia à necrosis within 6 hrs unless sufficient collaterals Changes seen Immediate – poorly defined, pale & swollen 48hrs – pale, yellow, better demarcation à red hyperaemic border 10 days – granulation tissue & organisation à collagenous scarring • Correlate the level of arterial occlusion with the level of tissue demarcation in the lower extremity. Excluding collaterals the level of tissue damage will depend on the level at which the artery is blocked… Iliac / common femoral will compromise the entire leg Deep femoral (profunda femoris) will affect the quad muscles and the femur Superficial femoral / Popliteal will affect all tissue distal to the knee Anterior tibial will affect the dorsiflexors of the foot and the toes Posterior tibial will affect the medial compartment Peroneal will affect the lateral/posterior aspect of the leg Vascular 15 Amputation • List the types of amputation of the lower limb and contrast their rehabilitation potential. Hip disarticulation Rarely required but indicated if tissue necrosis / infection above level for AKA. Femur is removed from acetabulum Above Knee (AKA) Bone transacted 12-15cm above knee joint (2/3 distal along bone) Fishmouth flaps fashioned Myodesis (suturing muscle to bone) prevents bone dislocation within stump & improves healing May stand at 48hrs and use pylon after 8 days Gritti-stokes Popular in vascular patients à longer lever better for wheelchair dependent Less muscle removed & femur transacted at 30o at level of adductor tubercle Through knee Lower healing rate than Gritti-stokes à wide stump (cosmetically ugly) and prosthesis fitting is difficult Below Knee (BKA) Weight bearing on patella tendon with PTB prosthesis Good knee function essential – not suitable for non-ambulant patient Uses a skew flap method à rounder stump with shorter rehab Tibia transacted 8-10cm distal to tibial tuberosity & fibula 2cm closer May stand at 48 hrs and use PAM aid when scar is sound Transmetatarsal Useful in DM / when several gangrenous toes Control of sepsis is essential Long plantar flap essential for good healing Bone transection at mid-tarsal level Ray Distal localised gangrene extending into forefoot / infection extending beyond proximal phalanx Useful in DM patients when infection tracks up a tendon sheath Digital If dry demarcated gangrene many autoamputate Divide through healthy tissue If viability / infection in doubt leave wound open • List the indications for amputation and discuss the clinical and laboratory methods for selection of amputation site. Indications Life saving (rare) Moist gangrene, spreading infection to viable tissue à systemic infection Extensive tissue necrosis following trauma (tetanus toxoid. Give penicillin / metronidazole if open wound) Uncontrolled sepsis (diabetic foot) à systemic infection Vascular Rest pain / non healing ulceration in non-reconstructable disease Extensive gangrene with loss of function Level of amputation Angiography to establish what level has sufficient perfusion to allow healing Doppler - BKA has reasonable chance of healing if Doppler ACP > 50mmhg Level may be improved by treating a reconstructable lesion (angioplasty / stent / bypass / profundaplasty / sypathectomy) Vascular 16 Pre-op care Restore Hb, fluid & electrolyte levels Ensure adequate DM control X-match blood CXR Pain relief + Abx + treat limb with antiseptic to minimise infection Post-op care Control pain with opiates via PCA OR sciatic / femoral nerve block Regular physiotherapy to prevent muscle atrophy / contractures Early rehab on temporary limb aid • Outline the typical symptoms of phantom limb pain and list the available drug treatments. Phantom limb pain – pain appearing to come from where an amputated limb used to be – is often excruciating (burning, aching, 'as if the hand is being crushed in a vice,') and almost impossible to treat Damage to nerve endings is often important: subsequent erroneous regrowth can lead to abnormal and painful discharge of neurons in the stump, and may change the way that nerves from the amputated limb connect to neurons within the spinal cord. There is also evidence for altered nervous activity within the brain as a result of the loss of sensory input from the amputated limb. Can be helped with regular analgesia or low dose diazepam (2mg) / TCAs TENS can also be used • Outline the rehabilitation of a patient with a below- or above-knee amputation including fitting of artificial limbs. Rehabilitation starts before surgery! Psychologic counseling may be indicated. Rehabilitation team & patient decide if a prosthesis or a wheelchair will be needed. Immediate post-op Flexion contracture of the hip or knee, which may develop rapidly after surgery, can make the fitting and use of a prosthesis difficult. Exercises for general conditioning, stretching of the hip and knee, and strengthening of all extremities are started as soon as the patient is medically stable Elderly amputees should begin standing and balancing exercises with parallel bars as soon as possible Unilateral amputation: Ambulation requires a 10 to 40% increase in energy expenditure after below-theknee amputation and a 60 to 100% increase after above-the-knee amputation. Below knee have a better rehabilitation prognosis as less adaptation is required from normal gait Bilateral amputation: Not unusual for diabetics / peripheral vascular disease. Functional prognosis depends on whether the amputations are AKA or BKA Bilateral below-the-knee amputees with well-fitting prostheses may be able to walk without canes or crutches. Bilateral above-the-knee amputees with prostheses probably can walk only with two canes or crutches. Most elderly patients with bilateral above-the-knee amputations do not have the necessary energy or strength to ambulate with prostheses. Stump Conditioning and Prostheses Vascular 17 Stump conditioning promotes the natural process of stump shrinking that must occur before a prosthesis can be used. After only a few days of conditioning, the stump may have shrunk greatly. An elastic stump shrinker or elastic bandages worn 24 hours/day can help taper the stump and prevent edema. Early ambulation with a temporary prosthesis enables the amputee to be active, accelerates stump shrinkage, prevents flexion contracture, and reduces phantom limb pain. The socket of the pylon, which is made of plaster of paris (calcium sulfate hemihydrate), should fit the stump snugly The permanent prosthesis should be lightweight and meet the needs and safety requirements of the patient. If the prosthesis is made before the stump stops shrinking, adjustments may be needed to satisfy the patient and to produce a good gait pattern. Therefore, manufacture of a permanent prosthesis is generally delayed a few weeks to allow shrinkage of the stump. Care of the stump and prosthesis: Patients must learn to care for their stump. The prosthesis should be removed before going to bed At bedtime, the stump should be inspected thoroughly (with a mirror if inspected by the patient), washed with mild soap and warm water, dried thoroughly, then dusted with talcum powder. If the skin of the stump is too dry, lanolin or petrolatum may be applied. If the stump sweats excessively, an unscented antiperspirant may be applied. If the skin is inflamed, the irritant must be removed immediately, and talcum powder or a low-potency corticosteroid cream or ointment applied. If the skin is broken, the prosthesis should not be worn until the wound has healed. The stump sock should be changed daily, and mild soap may be used to clean the inside of the socket. Standard prostheses are neither waterproof nor water-resistant. Therefore, if even part of the prosthesis becomes wet, it must be dried immediately and thoroughly; heat should not be applied. For elderly persons who swim or prefer to shower with a prosthesis, a prosthesis that can tolerate immersion can be made. Vascular 18 Vasospastic disorders Vasospasm – sudden decrease in the lumen of a vessel due to contraction of smooth muscle in the wall à decreased blood flow & increased systemic vascular resistance • List the underlying diseases or disorders associated with vasospastic changes in the extremities. Reynaud’s syndrome & disease Acrocyanosis • Specify and explain the defining clinical characteristics of Raynaud’s disease or phenomenon, including the rapidity of onset, colour changes and sensory alteration. Peripheral digital ischaemia due to spasm of the digital arteries Precipitated by cold (or emotion), relieved by heat Usually bilateral – fingers most commonly affected Skin pallor à cyanosis On return of flow à redness 2o to hyperaemia Can get numbness, burning and pain during reperfusion If severe can à tissue infarction & digital loss • List the clinical and investigational features that may distinguish primary from secondary Raynaud’s disease. Primary has no identifiable cause (= diagnosis of exclusion) = Raynaud’s disease Prevalence 3-20%, F:M = 9:1, some FH Secondary (Raynaud’s phenomenon) can be due to: Connective tissue disorders SLE, systemic sclerosis, RA Occupation Using vibrating tools Obstructive Thoracic outlet obstruction, buerger’s disease, atheroma Haematological Thrombocytosis, polycythaemia rubra vera Drugs Beta blockers Others Hypothyroidism • List the laboratory investigations used to assess vasospastic disorders. All vasoactive treatments should be stopped 24 hrs before the test Doppler finger pressures – digital systolic BP changes after local cooling at 15oC. A fall of > 30mmHg = significant Screening – FBC, U&E, urinalysis (look for chronic disease), TFTs, plasma viscosity, rheumatoid factor, autoantibody screen No investigations required if history of vibration white finger • Describe the medical and surgical approach to vasospastic disorders. Mainly treatment is conservative Reassurance, explanation & support. Avoid exposure to cold Vascular 19 Stop smoking Medical (Drug therapy) Vasodilators are of little benefit Ca2+ channel blockers (nifedipine / amilodipine) – but SE may limit usage Iliprost infusion – IV over 48-72 hours Surgical = Sypathectomy Confined to superficial lesions Lumbar – open / chemical (phenol / alcohol) for foot symptoms. Short lived effect Cervical – endoscopic technique, poor response rate, high relapse rate • Describe anatomical mechanisms responsible for producing thoracic outlet compression syndromes. Thoracic outlet obstruction = symptoms relating to compression of neurovascular bundle as it leaves the chest, in the area enclosed by the first rib, clavicle and scalenus anterior Symptoms Neural (95%), arterial and venous (remaining 5%) symptoms Exacerbated by elevation of the limb Pain, paresthesiae, weakness & arm claudication • List the investigations for thoracic outlet syndrome. History & examination Upper limb pulses, BP in both arms (elevated & at sides), wrist Doppler pressures Roos test – arm abducted to 90o, hands up, elbows braced backwards, chin elevated, hands clenched & released for 1-2 mins. +ve test of pain or weakness in hand or forearm Adson’s test – pulse diminishes / absent on elevation / abduction of arm (whilst head turned to contralateral side). Less reliable than roos test Allen’s test – assessment of integrity of palmar arch & dominant vessel (radial / ulnar) Phalen’s test, Tinel’s test – to exclude carpal tunnel syndrome Investigations C-spine & thoracic outlet X-rays Wrist Doppler pressure Duplex scan of outlet vascular bundle CT/MRI scan to exclude fibrous bands / ribs Angiography to exclude a more proximal arterial lesion • List the surgical principles for correction of thoracic outlet syndrome. Mild cases – conservative Surgery – if bearable pain or significant loss of function, major lifestyle changes, arterial / venous complications Excision of the 1st rib will improve symptoms in >90% Vascular 20 Vascular trauma • In a patient with recent trauma, outline the physical findings and diagnostic plan for suspected arterial injury. Closed injury Artery is injured by external compression (e.g. crush injury / fracture with displacement / joint dislocation / tight cast with post traumatic oedema) Open / penetrating injury From gunshot, stabbing, penetration by bone splinters, iatrogenic injury “Hard signs” – require intervention without imagaing Pulsatile bleeding Expanding haematoma Absent distal pulses Cold, pale limb Palpable thrill Audible bruit “Soft” signs – require further tests Peripheral nerve deficit History of moderate haemorrhage at scene of accident Weak but palpable pulse Injury proximal to a major artery Diagnosis Pulse Oximetry - A reduction in oximeter readings from one limb, as compared to another is suggestive of, but neither confirms nor excludes a significant vascular injury. It is thereful essentially an unhelpful test. Doppler Ultrasound - The diagnosis of a significant (ie. requiring intervention) vascular injury has been shown to be related to the presence or absence of a palpable pulse. The presence of a doppler signal in a pulseless limb only gives a false sense of security and does not imply a less severe or less urgent injury pattern. A diminished, but palpable pulse is a soft sign of vascular injury. Similarly, a reduction in the ankle-brachial pressure index (ABPI) in the presence of a palpable pulse does not indicate the presence of a vascular injury requiring intervention. Doppler ultrasound is therefore adds little to careful clinical examination. Duplex Ultrasound - Duplex imaging is a non-invasive examination combining Bmode and Doppler ultrasound. It requires an experienced operator and is more operator-dependent. Duplex can detect intimal tears, thrombosis, false aneurysms and arteriovenous fistulae. Its place in the assessment of vascular injury is as yet not completely definded, but it has a high sensitivity and may be appropriate for use as a screening tool. Angiography – see below • List the indications for arteriography in a patient with a possible arterial injury to the extremities. Indications To confirm extent of injury in stable patient with equivocal signs If patient without hard signs but strong suspicion of vascular injury If ABPI < 0.9 and normal vascular examination Will show if ischaemia is due to spasm, intimal tear or arterial disruption. Partial tears can be stented endovascularly at the same time NB: ONLY EVER in a stable patient NB: Any patient with obvious vascular injury (hard signs) mandates immediate surgical exploration with or without intraoperative angiography. Vascular 21 • Differentiate the pathophysiology, findings and treatment in the following types of arterial injury: Spasm - can occur from any injury to vessel. Intimal tear and/or dissection – the artery is stretched & intimal layer tears (but adventicia remains in tact). Intima then buckles & causes a local stenosis. May à thrombosis or dissection Transection (full thickness tear) – all the layers of the artery are divided. May be partial or complete. Partial bleed copiously, complete à spasm with little blood loss False (pseudo) aneurysm – Most commonly occurs following catheterisation of femoral artery. Blood leaks from the artery is contained by the connective tissue. It is pulsatile & expansile as it communicates with the artery. Diagnosis can be confirmed by doppler ultrasound. If left it will thrombose spontaneously or enlarge & rupture. May respond to ultrasound guided compression therapy or require suturing of puncture site or vein patching Arterio - venous fistula - Often presents several weeks after the injury. Patient complains of a swollen limb with dilated superficial veins & machinery type bruit often present throughout cardiac cycle. Diagnosis can be confirmed by angiography. Fistula can be divided an both the vein and artery sutured. Flap of fascia can be interposed between vessels to reduce risk of recurrence Vascular 22 Venous disease • Differentiate primary and secondary varicose veins Varicose veins – abnormally dilated, elongated and tortuous superficial veins Most cases are primary = idiopathic 1o valve defect Familial tendance F:M = 2:1 (increased during pregnancy) Secondary Previous DVT – recannalised vessels but valves remain incompetent Increased venous pressure – due to pelvic tumour / gravid uterus Congenital valve malfunction Arteriovenous fistula (congenital / trauma) = pulsating Severe tricuspid incompetence = pulsating • Outline the normal venous physiology and describe the roles of superficial, deep and perforating veins and venous valves in the scheme of venous blood flow. Long saphenous vein runs medially, anterior to medial malleolus to common femoral vein via cribriform fascia Short saphenous vein runs from posterior calf, enters popliteal vein in popliteal fossa Perforators between deep & superficial veins SFJ - 2.5cm inferior/lateral to pubic tubercle Sapheno-popliteal (behind knee) Mid-thigh perforators 3 x medial calf perforators Calf muscle contracts – deep vein is squeezed empty Relaxation allows the vein to fill from below (due to valves) & from superficial perforators • Discuss common presenting features of varicose veins Most people will consult for cosmetic purposes Dragging feeling after upright work Restless legs Ankle swelling Pruritis “Bruising” – haemosiderin deposits due to breakdown of static blood Complications – see below • Discuss the complications of untreated varicose veins Haemorrhage (can be fatal) Superficial thrombophlebitis: tender, warm, red thickening along vein. Pt.pyrexial, unwell, serious complications unusual Lipodermatosclerosis: calf skin induration, inflammation, pigmentation. Maybe mistaken for cellulitis, thrombophlebitis. Eventually skin stiff, shiny, pigmented, firm/indurated Vascular 23 Venous eczema: red, weepy, scaly, rash, near varicosities Venous ulceration: result of sustained venous hypertension • Describe the use of the venous Doppler and Duplex-scanning test in diagnosing venous valvular incompetence. Examination – always standing as veins fill Inspect medial gaitor area for deep venous insufficiency (haemosiderosis, venous eczema, lipodermatosclerosis) Inspect territory of short & long saphenous for varicose veins Auscultate Saphena varix = prominent dilatation @ SFJ = thrills on coughing Tap test – fingers over SFJ & distal veins. Tap proximal. If felt distal = incompetent valves Trendelenburg test – leg elevated & milked to empty superficial veins. Apply pressure over the SFJ with fingers. Ask the patient to stand (maintaining pressure) to see if vein fills. If vein doesn’t fill level of incompetence is SFJ Tourniquet test – similar to trendelenburg test but uses a tourniquet to apply pressure at different levels. Moving the tourniquet down (mid thigh, above knee, below knee) to find level of problem. Is very unreliable Doppler – used to diagnose reflux. Place the Doppler probe over the SFJ and squeeze the calf. If double “woosh” heard then SFJ is incompetent. Can repeat in popliteal fossa (find arterial pulse then reduce pressure until not heard) Duplex – can accurately map veins & diagnose valvular & perforator incompetence Venography – inject contrast to foot & map progress up the leg • Outline the management of varicose veins; discuss the use of support stockings and the indications for surgery. Education Avoid prolonged standing, lose weight, regular walks (exercise aids calf pump & return) Wear support stockings (compliance problems) Advise skin care Injection Sclerotherapy Esp for those below the knee. Sclerosant is injected at multiple sites & vein compressed for several weeks to prevent thrombosis – granulation tissue obliterated the lumen Surgery Choices based on vein anatomy & surgeon’s preference Options include stripping, saphenofemoral ligation etc Bandage legs tightly & elevate for 24hrs, encourage regular walking Vascular 24 Lymphatic disorders • Define lymphoedema. Chronic, non-pitting oedema Swelling of the subcutaneous tissues Caused by the obstruction of the lymphatic drainage May arise from surgery, radiation, tumour etc Most commonly affects the legs Progressive with age • Differentiate primary from secondary lymphoedema. Primary – presents early in life & is inherited deficiency of lymph vessels (e.g. Milroy’s disease) Secondary – obstruction of vessels Most frequently seen after lymph node dissection, surgery and/or radiation therapy, May also be associated with accidents or certain diseases or problems that may inhibit the lymphatic system from functioning properly. In tropical areas of the world, a common cause is filariasis (parasitic infection) • Explain the pathophysiology of lymphoedema and describe it. When the lymphatic system is unable to drain the excess tissue fluid A large amount of protein rich fluid collects in the affected area à tissue channels increase in size or number à reduced O2 to tissues à affects wound healing & provides culture medium for infection à cellulitis, lymphangitis, lymphadenitis & skin ulcers Left untreated can à lypmhangiosarcoma Staging Stage 0 (latent): some damage but not yet apparent. Lypmh removal still adequate - Lymphedema is not present. Stage 1 (spontaneously reversible): still at the "pitting" stage. Limb is more affected as day progresses & eases over night Stage 2 (spontaneously irreversible): Tissue has spongy consistency and is "non pitting". Fibrosis marks the beginning of the hardening of the limbs and increasing size. Stage 3 (lymphostatic elephantiasis): Swelling is irreversible & over a large area. Tissue is hard (fibrotic) and unresponsive Grading Grade 1 (mild edema): Involves the distal parts. The difference in circumference is less than 4 cm, and other tissue changes are not yet present. Grade 2 (moderate oedema): Involves an entire limb / quadrant of the trunk. Circumference 4-6cm. Tissue changes, such as pitting, are apparent. The patient may experience erysipelas. Grade 3a (severe oedema): One limb and its trunk quadrant. Circumference >6 cm. Significant skin alterations, such as cornification or keratosis, cysts and/or fistulae, are present. Grade 3b (massive oedema): The same symptoms as Stage 3a except that two or more extremities are affected. Grade 4 (gigantic edema): Also known as elephantiasis. In this stage of lymphedema, the affected extremities are huge due to almost complete blockage of the lymph channels. Elephantiasis may also affect the head and face. Vascular 25 • Outline the treatment of recurrent lymphoedema. Complete Decongestive Therapy (CDT) - consists of manual lymphatic drainage (MLD = milking fluid back to central circulation), short stretch compression bandaging, therapeutic exercise, and skin care. Sequential Gradient Pump Therapy – a mechanical massage often used befroe MLD to help break up fibrotic (hard) tissue. Compression bandaging - During activity, whether exercise or daily activities, the shortstretch bandages enhance the pumping action of the lymph vessels by providing increased resistance for them to push against. This encourages lymphatic flow and helps to soften fluid-swollen areas. Skin care – due to increased risk for infections of the affected areas. Thorough but gentle cleansing followed by moisturizing. Education - about the signs and symptoms of infections is also important, since awareness is the key to early identification and treatment. Untreated infections can further damage the already impaired lymphatic system and lead to more severe lymphedema and skin ulcers. Surgical techniques Excisional techniques include: Circumferential excision of the lymphedematous tissue followed by skin grafting (Charles technique) Longitudinal removal of the affected segment of skin and subcutaneous tissue and primary closure (Homans technique) Excision of subcutaneous tissue and tunneling of a dermal flap through the fascia into a muscular compartment of the leg (Thompson technique). Physiological techniques include: Lympholymphatic anastomosis (autologous lymphatic grafts to bridge obstructed lymphatic segments) Lymphovenous shunt (anastomosis of lymphatic channels to veins) Lymphangioplasty enteromesenteric flap omental transfer (pedicled portion of omentum transposed to the affected limb). Vascular 26 Diagnostic radiology in vascular disorders • Describe the indications for arteriogram and venogram. Arteriogram Symptoms of severe IC (lifestyle limiting), critical ischaemia or deterioration Conservative management failed When surgery or PTA would be appropriate NB: But beware anticoagulation and CRF Venogram Confirmation of venous patency Confirmation / exclusion of venous occlusion (esp in the deep veins of lower limbs) Investigation of a DVT Demonstration of venous anatomy prior to a further procedure • List the risks and complications of angiographic studies and describe their management. General complications Local anaesthesia Contrast media Radiation rare Allergy – ALWAYS have crash box on standby Nephrotoxic (?Gd, CO2) – assess U&E before starting 0.04% life threatening Metformin can à lactic acidosis with iodine (stop for 48 hrs before & after) V rare + long term Dose >8 mSv 150 CXR 4x annual background Specific complications for PTA Arterial access not uncommon 1-5% Haematoma 2-3% local/Retroperitoneal Large sheaths, obesity, INR + hypertension Press, resuscitate + summons help False aneurysm AV fistulae Dissection Infection Technique itself Distal Embolisation 2% - “PAT” Thrombosis 1% - heparin Dissection – flow limiting ?stent Rupture – covered stent/ surgery Spasm (esp Tibial) common -GTN Interventional aftercare Infrainguinal digital compression of CFA Minimum 10 min 1/4 hrly BP, pulse and groin obs for 4 hr Then 4 hrly obs for 8 hr Up to 12 hr strict bed rest NB: Beware of retroperitoneal haematoma!!! • List the common insertion sites for arterial catheter studies. Vascular 27 Infrainguinal CFA puncture (SFA direct) Antegrade (SFA and below) Retrograde (Iliacs and above) • Define and discuss transluminal angioplasty as used in coronary, visceral and peripheral vascular arterial beds. Percutaneous Transluminal angioplasty Revascularise limbs or organs Can be used on Iliac, femoral, popliteal and tibial vessels and renal, coronary, mesenteric, subclavian and carotid Dilate stenoses & open short occlusions Prognostic factors for PTA success Length of stenosis >10 cm v poor Nature of stenosis – eccentric plaque, ca2+ Run off vessels Continued smoking Diabetes Subintimal Percutaneous Extraluminal angioplasty “Intentional creation of a dissection within the subintimal plane” Where? Femoro-popliteal segment and tibials. Occasionally Iliacs When? Chronic occlusions >3/12 old How? Antegrade approach, Tapered hydrophilic catheter and wire Indications for SiPTA Long mature occlusions Critical Limb ischaemia - To get healing of ulcers and trophic changes.. Long term patency not issue Short distant Claudicants Reasonable patencies have been seen ?surveillance duplex and reintervention. • List the indications for pulmonary arteriogram. Suspected PE (esp if intermediate / low probability) – may use CTPA instead Evaluation of pulmonary hypertension Aquired aneurysms Acquired / congenital AV malformations Fistulae of the pulmonary artery Vascular 28