Vascular disease (arterial/venous insufficiencies, aortic diseases etc) Flashcards
Definition of acute arterial occlusion/insufficiency & how many hours within do you have to treat to avoid irreversible ischaemia & myonecrosis?
- acute occlusion/rupture of a peripheral artery
- urgent management required: treat within 6 h or irreversible ischemia and myonecrosis may result
- tends to be lower extremity > upper extremity; femoropopliteal > aortoiliac
What are the risk factors (congenital & acquired) for acute arterial occlusion/insufficiency?
Hypercoagulable state
Congenital:
- group 1: reduced anticoagulants (antithrombin, protein C, S)
- group 2: increased coagulants (factor V Leiden, prothrombin, factor VIII, hyperhomocysteinemia)
Acquired: • Immobility • Cancer • Pregnancy/OCP • Antiphospholipid antibody syndrome • Inflammatory disorders (e.g. IBD) • Myeloproliferative disorders (e.g. ET) • Nephrotic syndrome (acquired deficit in Protein C and S) • Disseminated Intracascular Coagulation (DIC) • Heparin-Induced Thrombocytopenia
Clinical Px of acute arterial occlusion/insufficiency
6 Ps
- Pain: absent in 20% of cases
- Pallor: within a few hours becomes mottled cyanosis
- Paresthesia: light touch lost first then sensory modalities
- Paralysis/Power loss: most important, heralds impending gangrene
- Polar/Poikilothermia (cold)
- Pulselessness: not reliable
Ix of acute arterial occlusion/insufficiency
- history and physical exam: depending on degree of ischemia may have to forego investigations and go straight to OR
- ABI (ankle-brachial index): extension of physical exam, easily performed at bedside
- ECG, troponin: rule out recent MI or arrythmia
- CBC: rule out leukocytosis, thrombocytosis or recent drop in platelets in patients receiving heparin
- PT/INR: patient antocoagulated/sub-therapeutic INR
- echo: identify wall motion abnormalities, intracardiac thrombus, valvular disease, aortic dissection (type A)
- CT angiogram: underlying athelosclerosis, aneurysm, aortic dissection
- conventional catheter based angiography: can be obtained in OR; prelude to thrombolytics
Cx of acute arterial occlusion/insufficiency
- compartment syndrome with prolonged ischemia; requires fasciotomy
- renal failure and multi-organ failure due to toxic metabolites from ischemic muscle
Rx of acute arterial occlusion/insufficiency
• immediate heparinization with 5000 IU bolus and continuous infusion to maintain PTT >60 s
• if absent power and sensation: emergent revascularization
• if present power and sensation: work-up (including angiogram)
• definitive treatment
embolus: embolectomy
thrombus: thrombectomy ± bypass graft ± endovascular therapy irreversible ischemia: primary amputation
• identify and treat underlying cause
• continue heparin post-op, start warfarin post-op day 1 x 3 mo depending on underlying etiology
Prognosis of acute arterial occlusion/insufficiency
- 12-15% mortality rate
* 5-40% morbidity rate (amputation)
What is the main cause of chronic arterial occlusion/insufficiency?
Ahterosclerosis (primarily lower extremities)
Risk factors for chronic arterial occlusion/insufficiency
- major: smoking, DM
* minor: HTN, hyperlipidemia, family history, obesity, sedentary lifestyle
Px of (2) main types of chronic arterial occlusion/insufficiency
- Claudication
- pain with exertion: usually in calves or any exercising muscle group
- relieved by short rest: 2 to 5 min, and no postural changes necessary
- reproducible: same distance to elicit pain, same location of pain, same amount of rest to relieve pain - Critical limb ischaemia
- includes rest pain, night pain, tissue loss (ulceration or gangrene)
- ankle pressure
Ix of chronic arterial occlusion/insufficiency
Non-invasive
- routine bloodwork, fasting metabolic profile
- ABI: take highest brachial and highest ankle [dorsalis pedis (DP) or posterior tibial (PT)] pressures for each side generally
- ABI
DDx of claudication (vascular, neurologic, MSK)
Vascular
• Atherosclerotic disease
• Vasculitis (e.g. Buerger’s disease, Takayasu’s arteritis)
• Diabetic neuropathy
• Venous disease (e.g. DVT, varicose veins)
• Popliteal entrapment syndrome (e.g. Baker’s cyst, tumour)
Neurologic
• Neurospinal disease (e.g. spinal stenosis)
• Reflex sympathetic dystrophy
MSK
• Osteoarthritis
• Rhematoid arthritis/connective tissue disease
• Remote trauma
Rx of chronic arterial occlusion/insufficiency
Conservative
- reduce RF (stop smoking, Rx HTN, HChol, DM)
- exercise program
- foot care
Pharm
- antiplatelet agents (clopidogrel)
- cilostazol (antiplatelet + vasodilator)
Surgical
- indications: severe life impairment, vocational impairment, critical ischaemia
- endovascular (stenting/angioplasty)
- endarterectomy
- bypass graft
- chemical sympathectomy: sympathetic plexus is destroyed with EtOH injection into nerve plexus to stimulate vasodilation
- amputation: if persistent serious infections/gangrene
Prognosis of chronic arterial occlusion/insufficiency
• claudication: conservative therapy: 60-80% improve, 20-30% stay the same, 5-10% deteriorate, 5% will require intervention within 5 yr,
What are signs of poor perfusion?
hair loss, hypertrophic nails, atrophic muscle, skin ulcerations and infections, slow capillary refill, prolonged pallor with elevation and rubor on dependency (Buerger’s test), venous troughing (collapse of superficial veins of foot)
Range of ankle-brachial indices
> 1.2: Suspect wall calcification (most common in diabetics)
0.95: Normal/no ischemia
0.50 – 0.8: Claudication range
Describe acute traumatic ulcers
failure of lesions to heal, usually due to compromised blood supply and unstable scar
usually over bony prominence ± edema ± pigmentation changes ± pain
Rx of acute traumatic ulcers
- debridement of ulcer and compromised tissue,
- left to heal via secondary intention with dressings,
- may need reconstruction with local or distant flap in select cases,
- vascular status of limb must be assessed clinically and via vascular studies (i.e. sonographically)
What are the major (3) types of non-traumatic chronic ulcers?
- Venous (70% of vascular ulcers)
- Arterial
- Diabetic
Describe venous ulcers
- Cause: valvular incompetence, venous HTN
- Hx of dependent edema, trauma
- medial malleolus common
- yellow exudates, granulation tissue
- IRREGULAR margin
- superficial depth
- venous stasis, discolouration (brown) surrounding skin!!
- normal distal pulses
- moderately painful, more painful with leg dependency, no rest pain
- Rx: leg elevation & rest, moist dressings
Describe arterial ulcers
- secondary to small/large vessel disease
- arteriosclerosis, claudication common
- slow progression
- distal locations common
- pale/white, necrotic base
- “punched out” appearance
- thin SHINY dry skin, hairless, cool
- decreased distal pulses
- Buerger’s sign
- extremely painful, decreased with dependency (hanging legs off the end of bed)
- Rx: rest, no elevation
Describe diabetic ulcers
- due to peripheral neuropathy (decreased sensation ) & atherosclerosis (decreased regional blood flow)
- diabetes mellitus, peripheral neuropathy Hx
- Pressure point distribution affected
- necrotic base appearance
- irregular OR punched out or deep appearance
- Superficial/deep
- thin dry skin, hyperkeratotic border
- hypersensitive/ ischemic surrounding skin
- decrased pulses likely
- ABI inaccurately high due to calcifications
- PAINLESS
- no claudication or rest pain
- paraesthesia, anaesthesia
- Rx: control DM, careful wound care, foot care, orthotics, early intervention for infections
What % of pts with symptomatic proximal DVT develop PE?
50% often within days to weeks of the event
Risk factors for VTE
THROMBOSIS
- Trauma, travel
- Hypercoagulable, HRT
- Recreational drugs (IVDU)
- Old (age >60)
- Malignancy
- Birth control pill
- Obesity, obstetrics
- Surgery, smoking
- Immobilization
- Sickness (CHF, MI, nephrotic
syndrome, vasculitis)
• Virchow’s triad
- alterations in blood flow (venous stasis e.g. flights)
- injury to endothelium (e.g. recent surgery)
- hypercoagulable state (including pregnancy, use of OCP, malignancy)
• clinical risk factors
Px of DVT
calf pain, leg swelling/ erythema/edema, palpable cord on exam; can be asymptomatic
Px of PE
dyspnea, pleuritic chest pain, hemoptysis, tachypnea, cyanosis, hypoxia, fever
Ix of DVT/PE
- ECG and CXR are useful to look for other causes (e.g. ACS, pneumonia)
- D-dimer is only useful if it is negative in low risk patients (highly sensitive)
- ultrasound has high sensitivity and specificity for proximal clot but only 73% sensitivity for DVT below the knee (may need to repeat in 1 wk)
- CT angiography has high sensitivity and specificity for PE, may also suggest other etiology
- V/Q scan useful when CT angio not available, or patient unable to tolerate IV contrast (e.g. renal failure, allergy)
Rx of DVT/PE
• LMWH unless patient also has renal failure (bridging warfarin)
- dalteparin 200 IU/kg SC q24h or enoxaparin 1.5 mg/kg SC q24h
• warfarin started at same time as LMWH (5 mg PO OD initially)
• LMWH discontinued when INR has been therapeutic (2-3) for 2 consecutive days.
• long term anticoagulation
- if reversible risk factor: 3-6 mo of warfarin
- idiopathic VTE: may need longer term warfarin (5 yr or more)
Define superficial venous thrombosis
erythema, induration, and tenderness along the superficial vein; usually spontaneous but can
follow venous cannulation
Causes of superficial venous thrombosis
- infectious: suppurative phlebitis (complication of IV cannulation; associated with fever/chills)
- trauma
- inflammatory: varicose veins, migratory superficial thrombophlebitis, Buerger’s disease, SLE
- hematologic: polycythemia, thrombocytosis
- neoplastic: occult malignancy (especially pancreatic)
- idiopathic
Px of superficial venous thrombosis
- pain
- cord like swelling
- areas of induration, erythema, tenderness
- most commonly in greater saphenous vein
Ix of superficial venous thrombosis
non-invasive tests (e.g. Doppler) to exclude associated DVT
Rx of superficial venous thrombosis
Conservative
- moist heat, compression bandages
- mild analgesics
- anti inflammatory & anti-platelet, LMWH, ambulation
Surgical
- indication: failure of conservative measures (>2wk)
- Rx suppurative thrombophlebitis with broad spectrum IV antibiotics & excision
Cx of superficial venous thrombosis
- simultaneous DVT (
Define chronic venous insufficiency
venous insufficiency and skin damage
Causes of chronic venous insufficiency
• calf muscle pump dysfunction and valvular incompetence (valvular reflux) due to phlebitis,
varicosities, or DVT
• venous obstruction
• AV fistulas, venous malformations
Px of chronic venous insufficiency
- pain (most common), ankle and calf edema – relieved by foot elevation
- pruritus, brownish hyperpigmentation (hemosiderin deposits)
- stasis dermatitis, subcutaneous fibrosis if chronic (lipodermatosclerosis)
- ulceration: shallow, above medial malleolus, weeping (wet), painless, irregular outline
- signs of DVT/varicose veins/thrombophlebitis
Ix of chronic venous insufficiency
- ambulatory venous pressure measurement (gold standard)
- Doppler U/S (most commonly used)
- photoplethysmography
Rx of chronic venous insufficiency
Conservative
- elastic compression stockings, leg elevation, avoid prolonged sitting/standing
- ulcers: zinc-oxide wraps, split-thickness skin grafts, ABx, debridement
Surgical
- surgical ligation of perforators in region of ulcer
What is phlebitis?
inflammation of the walls of a vein
Define lymphedema
obstruction of lymphatic drainage resulting in edema with high protein content
Causes of lymphedema
Primary
- Milroy’s syndrome (congenital hereditary lymphedema)
Secondary
- infection: filariasis (#1 cause worldwide), postop
- malignant infiltration: axillary, groin or intrapelvic
- radiation/surgery (axillary, groin lymph node removal): #1 cause in N. America
Px of lymphedema
- classically non-pitting edema
* impaired limb mobility, discomfort/pain, psychological distress
Rx of lymphedema
• avoid limb injury (can precipitate or worsen lymphedema)
• skin hygiene (moisturiser, topical Rx of fungal infections)
• external support intensive: compression bandages
maintenance: lymphedema sleeve
• exercise (w/ use of compression bandage)
• massage and manual lymph drainage therapy
Prognosis of lymphedema
- if left untreated becomes resistant to treatment due to subcutaneous fibrosis
- cellulitis causes rapid increase in swelling: can lead to sepsis and death
What is thrombophlebitis?
inflammation of the wall of a vein with associated thrombosis, often occurring in the legs during pregnancy
What is Trousseau’s sign?
Migratory superficial thrombophlebitis
as often a sign of underlying malignancy
Define aortic dissection
tear in aortic intima allowing blood to dissect into the media;
acute 2 wk (mortality levels up to 75-80%)
Causes of aortic dissection
• most common: HTN -> degenerative/cystic changes -> damage to aortic media
• other: connective tissue disease (e.g. Marfan’s, Ehlers-Danlos), cystic medial necrosis,
atherosclerosis, congenital conditions (e.g. coarctation of aorta, bicuspid aortic valves, patent ductus arteriosus), infection (e.g. syphilis), trauma, arteritis (e.g. Takayasu’s)
Epidemiology of aortic dissection
Peak incidence 50-65 yr old; 20-40 yr old with connective tissue diseases
- incidence of 5.2 in 1 000 000
- male:female = 3.2:1
- small increased incidence in African-Canadians (related to higher incidence of HTN)
- lowest incidence in Asians
Px of aortic dissection
- Sudden onset, TEARING pain that radiates to the BACK
on a background of:
- HTN
- asymmetric BP & pulses b/w arms
- ischaemic syndromes due to occlusion of aortic branches
- rupture into pleura (dyspnoea, hemoptysis) or peritoneum (hypotension, shock) or pericardium (cardiac tamponade)
- syncope
- new diastolic murmur (20-30%)
Ix of aortic dissection
• CXR
- pleural cap (pleural effusion in lung apices)
- widened mediastinum
- left pleural effusion with extravasation of blood
• CT (gold standard), aortography, MRA: 100% sensitive and specific
• bloodwork: lactate (r/o ischemic gut), amylase (r/o pancreatitis), troponin (r/o MI) •TEE: can visualize aortic valve and thoracic aorta but not abdominal aorta
• ECG: LVH ± ischemic changes, pericarditis, heart block
Rx of aortic dissection
Pharm
- beta blockers to lower BP & contractility
- non dihydropyridine Ca2+ channel blocker if C/I to beta blockers
- target sBP of 110mmHg and HR of
Cx of aortic dissection
- Post op: renal faliure, intestinal ischemia, stroke, paraplegia, persistent leg ischaemia
- 2/3 of pts die of op or post op Cx
W/ treatment: 60% 5 year survival, 40% 10 year survival
Describe type A & B of aortic dissection. Which is worse?
Type A: proximal. Involves the ascending aorta and/or aortic arch, and possibly the descending aorta
Type B: distal. Involves the descending aorta or the arch (distal to the left subclavian artery), without involvement of the ascending aorta
Type A is worse due to possible continuous tear of coronary arteries at/beyond the proximal aortic root
Define an aneurysm
localized dilatation of an artery having a diameter at least 1.5 times that of the expected normal diameter
Compare true aneurysm to false aneurysm
- true aneurysm: involving ALL vessel wall layers (intima, media, adventitia)
- false aneurysm (also known as psuedo-aneurysm): disruption of the aortic wall or the anastomotic site between vessel and graft with containment of blood by a fibrous capsule made of surrounding tissue
What can happen to aneurysms?
aneurysms can rupture, thrombose, embolize, erode, and fistulize
Causes of aortic aneurysm
- degenerative (atherosclerotic)
- traumatic
- mycotic (Salmonella, Staphylococcus, usually suprarenal aneurysms)
- connective tissue disorder (Marfan syndrome, Ehlers-Danlos syndrome)
- vasculitis
- infectious (syphilis, fungal)
- ascending thoracic aneurysms are associated with bicuspid aortic valve
Risk factors for aortic aneurysm
smoking, HTN, age >70, family history
Who is in the high risk group of aortic aneurysm?
• incidence 4.7 to 31.9 per 100 000 for AAA and 5.9 per 100 000 for TAA
• high risk groups - 65 yr and older - male:female = 3.8:1 - PVD, CAD, CVD - family history of AAA
Px of aortic aneurysm
due to acute expansion or disruption of wall
- syncope
- pain (chest, abdo, flank, back)
- HYPOtension
- palpable pulsatile mass above umbilicus, pulsatile abdo mass in 2 directions (expansile)
- airway/esophageal obstruction
- hoarseness (left recurrent laryngeal nerve paralysis)
- hemoptysis, hematemesis
- distal pulse may be intact
75% asymptomatic
What is the classic triad of ruptured AAA
- Pain
- Hypotension
- Pulsatile abdo mass
Ix of aortic aneurysm
- bloodwork: CBC, electrolytes, urea, creatinine, PTT, INR, type and cross
- abdominal U/S (100% sensitive, up to ± 0.6 cm accuracy in size determination)
- CT (accurate visualization, size determination)
- MRI (accurate visualization, limited access)
- aortogram (only for EVAR)
- Doppler/duplex (r/o vascular tree aneurysms elsewhere, e.g. popliteal)
Rx of aortic aneurysm
Conservative
- reduce CV RF
- exercise
- watchful waiting. US every 6 months for 3 years
Surgical
- if risk of rupture > = risk of surgery (>5.5cm)
- elective AAA repair mortality 2.5%
- Open surgery with graft replacement
- Endovascular aneurysm repair (EVAR): decreased morbidity, mortality, procedure time, recovery time
Rx of ruptured AAA
• ABCs • No imaging (hemodynamically unstable) • Straight to OR (confirm diagnosis by laparotomy) • Crossmatch 10 units packed RBCs
