Vascular Medicine and Surgery Flashcards
HYPERTENSION:
- Outline the levels of hypertension and how they are confirmed
- Describe malignant hypertension and its features
- Discuss pathological consequences of hypertension
- Discuss investigations to exclude secondary causes of hypertension
- Outline common medications used to control hypertension (contraindications and side effects)
- Who to treat
- See table
- ABPM - 2 readings of BP/hour during normal waking hours
- HBPM - 2 readings/day for 7 days. 2 readings should be taken each time, at least 1 minute apart with the pt sat. Readings from the first day are discarded and an average of the rest calculated.
- Malignant hypertension describes BP > 180/120 with signs of end organ damage (papilloedema or retinal haemorrhage). It can present with headaches, seizures, nausea/vomiting, visual disturbance, chest pain, neurological deficit (e.g. stroke, confusion) and signs of end organ damage (papilloedema, retinal haemorrhage, renal dysfunction, ACS/CCF, cerebrovascular event (stroke/haemorrhage)). It requires urgent treatment and referral to secondary care if signs of end organ damage are present.
- Pathological consequences of hypertension - renal damage, ophthalmic damage, CCF, ACS, cerebrovascular incident. If symptoms are experienced they are related to damaged organ e.g. palpitations, angina, new neurology.
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Investigations:
- Endocrine causes: Conn’s/primary hypoaldosteronism (serum aldosterone:renin ratio, hypokalaemia and hypernatraemia), phaechromocytoma (24 hour urine collection, shows increased catecholamines), hyperthyroidism, Cushing’s syndrome, acromegaly (IGF)
- Renal: Renal stenosis (duplex US), U&Es, eGFR
- Pregnancy: Pre-eclampsia (urine dip, doppler US)
- Medications: Steroids, COCP, SSRIs, NSAIDs, EPO
- Coarctation of the aorta - consider in children or young adults.
- OSA
- ALSO, look at CVD risk: Cholesterol, fasting glucose, HbA1c, FBC
- ACEi - First line if < 55. Side effects include dry cough and hyperkalaemia
- Calcium channel blocks - First line if > 55 or black or caribbean orgin. Side effects include ankle oedema, headache
- Beta blockers - Add on therapy. Side effects include cold peripheries and erectile dysfunction
- Thiazide diuretics - Add on therapy. Side effects include gout, hyperglycaemia and hypercalcaemia (but hypocaluria)
- Who to treat
- <80 years with stage 1 hypertension and with end organ damage/10 year cardiovascular risk > 10%
- Stage 2 after confirmation with ABPM or 3 hypertension
- For Stage 3 WITHOUT signs of end-organ damage BP should be repeated in 7 days
HYPERLIPIDAEMIA:
- Outline links between cholesterol and CV risk
- Discuss indications for lipid lowering medications in the prevention of CVD, together with side effects
- Elevated cholesterol levels correlate with increased risk of cardiovascular disease. Elevated cholesterol levels allow for accelerated atherosclerosis
- Indications for lipid lowering medications: Post-MI as secondary prevention, post-stroke as secondary prevention, primary intervention in pts with QRISK score of 10% or >, if lifestyle modifications are ineffective
ATHEROMATOUS AND VASCULITIC VASCULAR DISEASE:
- Name common sites of atherosclerotic arterial aneurysms
- Symptoms, signs and ddx for ruptured AAA
- Emergency treatment of AAA
- Presentation, complications and treatment of popliteal aneurysm
- Pathophysiology of aterial dissection, presentation, management, complications and causes of death
- Differentiate between true and false aneurysm
- Infrarenal aorta, popliteal, iliac artery, femoral
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Ruptured AAA:
- Symptoms: Chest/epigastric/abdo pain with radiation to the back/iliac fossa/groin, syncope/dizziness, nausea/vomiting
- Signs: Shock (tachy, hypotensive, reduced urine output, confusion), pulsatile abdominal mass, reduced/absent pulses below the site of rupture, dullness to percussion in the abdomen.
- Ddx: Diverticulitis, nephrolithiasis, IBS, IBD, appendicitis, ovarian torsion, GI haemorrhage
- Screening for AAA: Single abdominal US for males aged 65. If > 5.5 cm then 2/52 referral to vascular surgery is required for probable intervention. For aorta widths > 3 cm repeat scanning is offered every 12 or 3 months, dependent on size.
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Treatment:
- Summon senior help and vascular surgeons
- Take bloods for ABG, G&S, cross match, clotting scnreen, U&Es.
- Perform ECG, urine dip
- Abdominal USS may be performed in the emergency department
- Insert 2 large bore cannula and give O rhe- blood (if not yet cross matched), ensuring systolic BP remains < 100mmHg
- Provide prophylactic abx
- Surgical repair: Endovascular aneurysm repair (EVAR)
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Popliteal aneurysm:
- Presentation: Asymptomatic with detection as an incidental finding, pulsatile popliteal mass
- Complications: Distal thromboembolism, rupture and subsequent haemorrhage, local compression effects
- Treatment: Reserved for symptmatic aneurysms and asymptomatic aneurysms with a diameter > 2cm. Endovascular insertion of a covered stent or open surgical repair.
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Arterial dissection:
- Pathophysiology: An intimal for entry of blood into the tunica media. This leads to interuption of the vessel layers and the creation of a true and false lumen.
- Presentation: Sudden onset sharp/stabbing chest pain with radiation to the back, dyspnoea, collapse, signs of shock, reduced/absent pulses
- Management (by Stanford classification):
- Type A (ascending aorta): Requires surgical repair. Endovascular repair (guide wires and catheters) is not yet validated. Beta blockers1 and analgesia2 should be initiated at presentation.
- Type B (ascending aorta now involved): Can be managed medically. Aims to keep BP and HR low1, through use of beta blockers, and provision of analgesia. Endovascular stent-graft repair can then be performed after the acute phase (14/7)
- Complications: Cardiac tamponade (raised JVP, muffled heart sounds and hypotension), aortic regurgitation (diastolic murmur, wide pulse pressure, CCF signs), MI
- Causes of death: Exsanguination
- False aneurysm/pseudoaneurysm: Breach of the vessel wall such that blood leaks through the vessel wall but is contained by the tunica adventitia, with direct communication existing between the vessel lumen and the aneurysm. The risk of rupture is higher than that of a true aneurysm.
1: Use of beta blockers in dissection is to achieve a HR < 60 bpm and systolic BP < 120 mmHg
2: Opioid analgesia should be used. Morphine also causes vasodilation and reduced HR by increasing vagal tone
CHRONIC PERIPHERAL ARTERIAL OCCLUSIVE DISEASE:
- List manifestations, investigations and management of PAD
- Differentiate between ischaemic rest pain and neuropathy
- Contrast gangrene in diabetic and non-diabetic patients
- Intermittent claudication vs other causes of leg pain
- List criteria to differentiate leg ulcers
- Radiological and surgery treatment choices for pts with oclusive arterial disease according to the affected vessel
- Symptoms, signs, investigations, ddx and treatment of chronic mesenteric vascular occlusive disease
- Clinical presentation, investigation and management of renal artery stenosis
- Surgical and radiologically curable causes of hypertension (?)
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Peripheral arterial disease (PAD)
- Manifestations: Intermittent claudication, reduced peripheral pulses, cold peripheries, hair loss, ulceration, pallor
- Investigations: clinical examination, ABPI, doppler scan, duplex US, angiography (CT, catheter or MR)
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Management:
- Medical: Statin, antiplatelet, vasodilator
- Endovascular: Angioplasty and stenting
- Surgical: Bypass graft
- Ischaemic rest pain: Associated with PAD hence preceeding symptoms of intermittent claudication/pallor/reduced pulses etc. Nocturnal rest pain may be relieved by ‘hanging’ legs over the bed. Neuropathy: Described as a tingling/burning sensation. Glove and stocking distribution. May have associated sensory loss and risk factors, such as DM.
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Gangrene
- Dry gangrene - due to arterial occlusion
- Wet gangrene - due to venous occlusion or bacterial colonisation of a pre-existing injury (NOTE that DM leads to immunocompromise and hence pts are more prone to wet gangrene)
- Causes of leg pain: Intermittent claudication, MSK, injury, cauda equina, spinal stenosis
- Key Qs: Onset, activities preceeding onset, precipitating/relieving factors, uni/bilateral, associated symptoms (incontinence, haemorrhage)
- Tx options:
* Radiological/endovascular Tx: Angiplasty and stenting
* Surgical Tx: Bypass
- Tx options:
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Chronic mesenteric vascular occlusive disease (may be thought of as ‘intestinal angina)
- Presentation: Severe, colicky, post-prandial abdominal pain (gut claudication); weight loss (due to pain); upper abdominal bruit; PR bleeding; malabsorption; N&V
- Investigation: CT angiogram, contrast-enhanced MR angriography, ?AXR
- Ddx: Bowel obstruction, diverticulitis, IBS, IBD
- Treatment: Endovascular approach - angioplasty and stent insertion. Treatment should be considered due to the ongoing risk of acute infarction
- LOOK UP - acute mesenteric ischaemia (small bowel), ischaemic colitis (large bowel, specifically watershed areas e.g. splenic flexures)
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Renal artery stenosis - 90% due to atherosclerotic disease, 10% due to fibromuscular dysplasia
- Clinical presentation: Hypertension, reduced renal function (eGFR, elevated urea/creatinine/potassium, oedema), flash pulmonary oedema
- Investigation: Duplex US ,CT angiogram, renal US, bloods (serum creatinine, serum potassium, urinalysis and sediment evaluation2, aldosterone-to-renin ratio1)
- Management:
- Medical: 1st line and includes antihypertensive therapy and lifestyle modification, statin and antiplatelet may also be considered.
- Surgical: 2nd line is stent insertion and continutation of medical therapy
- Surgical cure: Phaechromocytoma, Radiological cure:
1: Aldosterone:Renin ratio is used to exclude primary aldosteronism (Conn’s syndrome) as a cause of hypertension
2: RAS is not associated with proteinuria or abnormalities in urinary sediment
ACUTE ARTERIAL OCCLUSIVE DISEASE
- Causes, symptoms, signs and initial management of acute arterial occlusion
- Differentiate acute arterial and venous occlusion
- Differentiate embolic from thrombotic occlusion
- Contrast the indications for surgical and medical treatment of acute arterial occlusion
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Acute limb ischaemia: Sudden onset loss of arterial supply to the limb
- Causes:
- Embolic: AF, MI, pericarditis, malignancy, hyoercoagulability (pregnancy, COCP)
- Thromboembolic (vessel atherosclerosis/damage, exposure to endothelium leads to platelet activation and adhesion, with subsequent occlusion of the vessel)
- Trauma - including compartment syndrome
- Symptoms: Severe pain, loss of function/movement, loss of sensation
- Signs: Cold, pale, absent pulses, ABPI < 0.4, reduced ankle and toe pressures (0.6, 0.2)
- Initial management:
- Seek vascular input
- Analgesia
- IV unfractioned heparin - acts to ensure collateral supply remains patent. Unfractioned heparin is advantageous as it may be reversed prior to surgery.
- Causes:
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Arterial occlusion symptoms: Pain (disporportionate to visible pathology), pallor, pulselessness, paraesthesia, paralysis, perishingly cold
- Venous occlusion symptoms: Pain, swelling, rubor
- Embolic describes occlusion of the vessel by a thrombus/fat/amniotic fluid from a distal site. Thrombotic occlusion describes occlusion by a thrombus that has formed at the site, such as following atheroma plaque rupture and subsequent platelet adhesion to exposed endothelium.
- Treatment is dependent upon the cause, viability of the limb/severity of ischaemia, location/extent of the thrombus and pt factors e.g. age, comorbidities, good graft/input/output
- Medical treatment: Thrombolysis (fibrinolytic drug given by regional catheter infusion)
- Endovascular: Embolectomy for embolic causes; angioplasty and stent insertion for thrombotic causes
- Surgical: Bypass: amputation (if the limb is mottled, non-blanching with hard woody muscles)
AMPUTATION:
- List types of lower limb amputation and contrast rehabilitation potential
- List the indications for amputation and selection of amputation site
- Outline rehabilitation for above and below knee amputation
- Toe; ray (toe and metatarsal); tarsometatarsal; mid-tarsal (between talus and calcaneus); ankle disarticulation (through the ankle joint); below knee; through knee; above knee
- tarsometatarsal; mid-tarsal and ankle disarticulation tend to be performed in children to preserve leg length and keep the epiphyseal plate intact
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Indications for amputation: Non-viable limb (gangrenous, grossly ischaemic, malignancy, infection, secondary to trauma) or non-functional.
3.
VASOSPASTIC DISORDERS:
- List underlying diseases or disorders associated with vasospastic changes in the extremities
- Specify the clinical characteristics of Raynaud’s disease
- List clinical features and investigations that may distinguish primary from secondary Raynaud’s disease
- List laboratory investigations used to assess vasospastic disorders
- Medical and surgical approaches for vasospastic disease
- Describe anatomical mechanisms responsible for producing thoracic outlet compression syndromes and list investigations. Describe surgical principles for correction
- Autoimmune/CT conditions (SLE, scleroderma, RA, polymyositis, mixed connective tissue disease); occupational (vibrating tools); obstructive (thoracic outlet obstruction, Buerger’s disease, atheroma); haematological (thrombocytosis, polycythaemia ribra vera); beta-blockers; hypothyroidism
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Raynaud’s disease: A vasospastic disorder which sees excessive constriction of peripheral (arterial) vessels, such as in response to cold.
- White → blue → red
- Pain
- Symptoms associated with cold temperatures, stress
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Investigations for secondary Raynaud’s disease:
- Clinical features of 2° disease: Dilated nail fold capillary loops, presentation in early childhood or > 30, asymmetrical distribution and male gender
- Antinuclear antibody: SLE
- Low Hb and WCC in secondary anaemia
- ESR: Elevated in 2° disease
- Urinalysis: RBC and/or protein in secondary RP such as in SLE or vasculitis with active glomerulonephritis
- TFTs
- Medication Hx
- Secondary causes include CT disorders (systemic sclerosis, mixed CT disorders, SLE, Sjogren’s syndrome, polyarteritis nodosa); macrovascular disease (atherosclerosis, thoracic outlet obstruction, Buerger’s disease); occupational trauma; medications (beta blockers, cytotoxic drugs); malignany and AF
- FBC: Polycythaemia, malignancy
- U&Es: Renal impairment
- Coagulation: Hepatic dysfunction
- Glucose: DM
- TFTs
- ANA/RF/APA: Autoimmune screen
- Medical approach:
- Lifestyle changes: Smoking cessation; keep extemities warm (e.g. gloves) and cease exacerbating medications e.g. B-blockers
- Nifedipine (provides vasodilation)
- Surgical approach:
- Sympathetectomy
- Medical approach:
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Thoracic outlet syndrome: Compression of neurovascular structures (brachial plexus, subclavian artery, subclavian vein) between the 1st rib and the clavicle. A key ddx of cervical myelopathy (upper limb ‘clumsiness’ and reduced dexterity, may have sensory impairment).
- Abnormalities of the 1st rib
- Cervical rib
- Long transverse cervical process
- Bands within the thoracic outlet
- Previous clavicular fracture with abnormal bony healing
- Excess muscle development
Presentation:
- Neurological deficits in T1 distribution: Wasting of small muscles of the hand, paraesthesia of the inner forearm and hand
- Arterial symptoms: Claudication if working with hands above the head, post-stenotic aneurysm
- BP lower in affected arm and may vary with posture
Investigations
- Ateriography
- Plain CXR may confirm cervical rib or first rib abnormality
Surgical principles for correction:
- Supraclavicular or transaxillary approach
- Excision of the 1st or cervical rib. Any restrictive bands can be released too
VASCULAR TRAUMA
- In a pt with recent trauma, outline the physical findings and diagnostic plan for suspected arterial injury. Include indications for radiological investigation in the extremities
- Differentiate the pathophysiology, findings and treatment in common types of arterial injury
1.
Features of Hx: *symptoms of ischaemia (including of neuronal tissue)*
- Paraesthesia
- Pain
- Paralysis
Features of examination:
- LOOK: Visible pallor; visible blood loss, visible haematoma1
- FEEL: Cold to touch; reduced/absent peripheral pulses; thrill and pulsatile mass (with murmur/bruit) suggests AV fistula formation
- MOVE: Loss of active movement; pain continues on passive movement
- VITALS: Symptoms of shock
- API (arterial pressure index): Similar principle to ABPI. The cuff is placed distal to the site of injury and the systolic pressure determined. Systolic pressure of injured extremity/brachial systolic pressure.
Indications for radiological investigation (Duplex, CTA)
- ABPI < 0.9
- ‘Hard signs’ of arterial injury present: Absent pulses, signs of haematoma, bruit/thrill/active haemorrhage, signs of limb ischaemia/compartment syndrome (6 Ps)
2.
Types of arterial injury:
- Intimal injuries(flaps, disruptions, subintimal/intramural haematomas)
- Complete wall defects (pseudoaneurysm, haemorrhage)
- Complete transection
- AV fistulas
- Spasm
1: Haematoma suggests clotting has been initiated. A pulsatile or expanding haematoma is a ‘hard sign’ in arterial injury. (?rupture)
VENOUS DISEASE
- Outline normal venous physiology and describe the roles of superficial/deep/perforating veins and venous valves
- Recognise varicose veins. Describe their anatomical distribution and potential complications
- Describe the use of different investigations in diagnosing venous disease
- Outline the management of a venous ulcer
- Outline the management of varicose veins, including indications for surgery
- Describe the treatments available for pts with venous disease
- Superficial veins: Venous drainage of the skin and superficial tissues. Vessels include the great and short saphenous veins. Pathology = simple varicose veins
- Deep veins: Drain the muscular compartment. Accompany the major arteries of the lower limb. Pathology = deep venous insufficiency
- Perforating veins: Provide communication between the deep and superficial venous system. Allow drainage of superficial into deep for venous return to the heart
- Venous valves: Prevent backflow within venous vessels
- Appearance: Engorged ‘blue-ish’ vessels, tortuous appearance
- Anatomical distribution: Venous disease within the superficial veins in simple varicose veins.
- May be a primary (due to valvular incompetence) or secondary condition, with superificial varicosity occuring secondary to deep venous imcompetence ( the latter being caused by previous DVT or raised systemic venous pressure, e.g. compression by malignancy)
- Potential complications:
- Chronic venous insufficiency
- Rupture
- Ulceration, lipodermatosclerosis and haemosiderin deposition *all associated with chronic venous insufficiency*
- Hand-help doppler: Can identify reflux at the junctions where the deep and superficial venous systems meet
- Duplex ultrasonography: Doppler in combination with US
- Venography: Fluroscopy is used to image venous return
- Swab taken for MC&S if there are signs of infection
- Bandaging and compression therapy *must be ABPI prior to application*
- ?Pentoxifylline to aid ulcer healing (vasoactive - improving peripheral blood flow)
- Below knee graduated compression stockings to prevent reoccurence *must be ABPI prior to application
- Conservative management: Elevation when at rest, avoid prolonged periods of standing, regular exercise and weight loss
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Medical management:
- Graduated compression stockings *check ABPI prior to application (> 0.8)
- Endothermal ablation - causes thrombosis of the vein
- Sclerotherapy - USS guided foam sclerotherapy and 2/52 compression
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Surgical management:
- Great saphenous vein is disconnected from the femoral vein (a.k.a. stripped) and perforators are ligated
- Indications include symptomatic superficial vein insufficiency with failure or less invasive interventions, deep vein insufficiency (ulcers/lipoderm./haemosid.)
- SEE ABOVE - endothermal ablation, sclerotherapy, surgery, compression
LYMPHATIC DISORDERS
- Define lymphoedema
- Differentiate primary from secondary lymphoedema, explain the pathophysiology and treatment
- Chronic, progressive swelling of tissue with protein-rich fluid (accumulation of interstitial fluid) as a consequence of distruption to the lymphatic system. Resulting in non-pitting oedema.
- Pitting oedema: Occurs due to increased hydrostatic pressure/permability in capillaries, leading to osmotic driven movement of fluid into the tissues. Causes include fluid retention (CCF (2º to activation of RAAS), calcium channel blockers), protein deficiency, hydrostatic and increased capillary permeability.
Primary lymphoedema:
- Congenital abnormality e.g. deficiency of lymphatic vessels (Milroy’s disease)
Secondary lymphoedema: Due to obstruction of the lymphatic vessels.
- Filaria infection a.k.a. elephantitis (thread-like worms)
- Repeated cellulitis
- Malignancy
- Post-operative
Treatment
- 1st line: Skin care - moisturising and regular bathing PLUS compression bandaging, elevation, exercise and weight control
- Manual lymph drainage (massage)
- Long term abx for recurrent cellulitis
DIAGNOSTIC RADIOLOGY IN VASCULAR DISORDERS
- Describe the indications for magnetic resonance angiography (MRA), Duplex ultrasounds, CT angiography and invasive investigations (fluroscopy via catheter insertion) of the venous and arterial system.
- List the common insertion sites for arterial catheter studies
- Discuss risks and complications of angiographic studies
- Transluminal angioplasty
- List the indications for pulmonary arteriography
- MRA: Evaluation of the arterial system. Thoracic, abdominal and limb disease
- CTA: Evaluation of the arterial system. More for carotid and cerebral disease
- Duplex USS: Gives anatomical and physiological information non-invasively, using doppler and US
- Angiography: Used when invasive procedures are planned. Uses contrast injected by a series of catheters. Fluoroscopy is then used to visualise the arterial system. E.g. PPCI
- Femoral artery, brachial artery
- Contrast reaction
- Haematoma/pseudoaneurysm/AVF formation
- Arterial occlusion
- Transluminal angioplasty: Insertion of a balloon-tipped catheter, which is then inserted to leave a stent in situ
- Suspected PE
- PDA
- Aortic dissection
SKILLS IN VASCULAR MEDICINE AND SURGERY
- Measure blood pressure using a correct cuff size and interpretation of the Korotkov sounds.
- Discuss a diagnosis of hypertension with a patient in lay terms.
- Interpret an ECG.
- Test a urine sample for blood and protein using a standard test strip
- Demonstrate the site for palpation of all peripheral pulses and determine whether they are present or absent
- Given a patient with ischaemic rest pain in a foot, demonstrate the physical findings, including dependent rubor, pallor on elevation and delayed capillary refill.
- Measure the ankle-brachial pressure index and interpret the results.
- Demonstrate the use of unidirectional Hand Held Doppler to: auscultate the pedal arteries; Measure the systolic blood pressure in the arm and ankle ; Demonstrate reflux at the sapheno-femoral junction
- Describe the technique used to puncture the femoral artery for a blood sample including the necessary equipment and potential complications.