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PERIPHERAL VASCULAR DISEASE (ABDOMINAL AORTIC ANEURYSM (AAA) (EPIDEMIOLOGY…
PERIPHERAL VASCULAR DISEASE
PERIPHERAL ARTERIAL DISEASE
partial or complete obstruction of arterial blood supply to upper and/or lower limbs
majority of cases are secondary to long standing atherosclerosis (chronic limb ischaemia); however sudden deterioration may occur secondary to thrombosis or embolism (Acute limb ischaemia)
CHRONIC LIMB ISCHAEMIA
blood supply to limbs deteriorates with time as a consequence of progressive atherosclerotic disease, with symptoms initially on exertion but eventually at rest where it is termed critical limb ischaemia
EPIDEMIOLOGY
RF - MALE, AFRO-CARRIB, SMOKING, HYPERLIPIDAEMIA, HTN, FAM HX OF ATHEROSCLEROSIS
Critical limb ischaemia is seen in 1% of pts with PVD
incidence inc with age (1 in 10 pts over 69 have evidence of periph arterial disease)
AETIOLOGY - athersclerosis is main disease process underlying the development of chronic limb ischaemia - accelerated by presence of other CV RF
pathophysiology
mismatch between circ supply and metabolic/nutrient demands of the skin and skeletal muscles
in early stage of disease metabolic demands are not compromised and pt is asymptomatic and may be case if collateral vessels are well developed
CLINICAL FEATURES
KEY FEATURES
intermittent claudication and rest pain determined by the severity of atherosclerosis and presence of collateral vessels
ischaemia type pain (aching) on exertion eg walking that resolves promptly with cessation of activity and rest
location of pain depends on site of stenosis
buttock and thigh pain: aorta, iliac vessls
calf pain - femoral or popliteal vessels
ankle and foot pain - tibial or peroneal vessels
leriche syndrome - presence of erectile impotence, nilateral butttock claudication with reduced or absent femoral pulses and indicates involvement of the common or internal iliac artery
asymptomatic - 2/3rds of pts
CRITICAL LIMB ISCHAEMIA
presence of pain at rest, often accompanied by:
paraesthesia in the foot or toes
ulceration
necrosis and gangrene
symptoms are exacerbated by leg elevation and relieved with leg dependency - pain is typically worse at night relieved by hanging the foot off the bed
pts with diabetic neuropathy may exp little to no pain despite severe ischaemia
EXAMINATION FINDINGS
Absent or decreased periph pulses
bruits in aorta and groin
buerger's test - elevation of leg with pt supine elicits ischaemia and the leg goes pale (flow fails to overcome gravity). more severe = lower angle required
rubor on dependency - after elevation, hanging leg off bed causes change in colour from whit eto blue and eventually very dark red (reactive hyperaemia)
EXAM ESSENTIALS (SIGNS OF CHRONIC ISCHAEMIA)
smooth, shiny, cool skin
muscle atrophy
ulcers at sites of pressure and distal extremities
buerger's sign positive
hair loss
DDX
spinal stenosis - usually there is a hx of back pain, worse with lumbar spine flexion
arthritis (hips, knees) - usually occurs at rest and with activity and does not resolve quickly
IX
FIRST LINE
BLOOD TESTS
Renal function, lipids,glucose and anaemia assessed
US (ABPI)
RATIO BETWEEN SYST BP OF ANKLE AND BRACHIAL ARTERY
MORE THAN 1.4 = stiffened arteries (DM)
0.9-1.1 normal
0.75 - 0.9 CLAUDICATION
0.5-0.75 CLAUDICATION AT SHORT DISTANCES
<0.5 CRITICAL LIMB ISCHAEMIA
SECOND LINE
indicated if normal ABPI, diagnostic uncertainty or intervention is considered
DUPLEX ULTRASOUND ASSESSMENT
able to identify vascular lesions
should be performed in the management of PAD
CT or MR angiography
digital subtraction angiography - previously gold standard but superseded by non-invasive imaging
MANAGEMENT
lifestyle changes
smoking cessation
exercise rehab (supervised exercise 3mths)
Mediterranean diet
symptomatic relief and claudication
cilostazol and naftidrofuryl indicated if still symptomatic after exercise rehab or unwilling to undergo angioplasty or bypass surgery
best medical treatment
bp control - target <140/90 or <130/80 in diabetic
diabetic control HbA1c <48mmol/mol (<6.5%)
lipid modification - diet, statins
antiplatelet therapy - aspirin is first line in order to reduce risk of stroke, MI and vasc death
ENDOVASC TREATMENT - ANGIOPLASTY AND STENTING
indicated in CLI and where there is failure of lifestyle and pharmacological interventions in improving symptoms
disadv are lower long-term patency and lack of evidence for long term benefit over exercise rehab and best medical treatment
VASC SURGERY
bypass surg most commonly performed
indicated in those severely limited by IC even after endovascular intervention
AMPUTATION
in 25% of LCI pts due to sig necrosis or paresis
PROGNOSIS
5YRS 50% of pts with intermittent claudication will improve 25% worsen 25% same
heart disease and stroke commonest cause of death in pts with PAD
ACUTE LIMB ISCHAEMIA
sudden reduction in arterial BF to a limb
AETIOLOGY
thrombosis in situ (60%)
thrombosis superimposed on an atherosclerotic plaque is termed acute on chronic limb ischaemia
may be due to occlusion of bypass graft
in normal arteries it may be seocndary to underlying disease eg THROMBOPHILIA and MYELOPROLIFERATIVE DISEASES and certain malignancies eg PANCREATIC, BREAST, LUNG CANCERS
ARTERIAL EMBOLI (30%)
AF (2/3rds)
mural thrombus (1/3rd)
other causes (10%)
arterial dissection
trauma
external compression (Eg entrapped popliteal artery)
if secondary to thrombosis
onset = progressive or acute-on-chronic (hours to days)
hx of claudicatiom
affected limb - leg, rarely arm
contralteral limb pulses - decreased or absent
affected sites - single
diagnosis - angiography
if secondary to embolus
contralateral limb pulses are present
upper limb can be affected
no claudication hx
sometimes multiple affected sites
onset - acute (minutes)
clinical diagnosis
REMEMBER 6Ps of acute limb ischaemia - PAIN, PALLOR, PERISHINGLY COLD, PARAESTHESIA, PULSELESS, PARALYSIS
EXAMINATION FNDINGS
signs of chronic ischaemia
buerger's angle <20 degrees
differences in BP between arms or legs
IX
do not delay definitive revascularisation for diagnostic tests
duplex assessment to identify the site of occlusive vascular lesion
MANAGEMENT
GENERAL MEASURES
resuscitation - ABC
warm room temperature - to prevent cutaneous vasoconstriction
position patient so feet are below chest level - to maximise limb perfusion by gravity
analgesia
involve the vascular multidisciplinary team
anticoagulation - all pts should receive heparin
clot removal
embolism - embolectomy
surgery if there is presence of motor/sensory deficit or if endovasc therapy is unfeasible
thrombosis - endovascular thrombolysis or emolectomy
revascularisation (thrombosis)
post operative reperfusion injury (And subsequent compartment syndrome) is avoided by maintaining hydration and close observation
once clot removed, underlying arterial lesion should be treated as for chronic limb ischaemia. also indicated if theres continued symptoms despite thrombolysis
amputation
for a non-viable limb or irreversible limb ischaemia
PROGNOSIS
poor long term outcomes becasue pts usually have comorbid CV diseases. risk of limb loss depends on severity of ischaemia and time before revascularisation
CLINICAL FEATURES
ACUTE
no tissue loss
no tissue loss
pale and motting
no change in colour on dependency
sudden pain
young and old pts
CHRONIC
often loss of tissue
rubor on dependency
red
usually older pts
gradual inc of pain severity
PERIPHERAL VENOUS DISEASE
VARICOSE VEINS
irreversibly torturous and dilated superficial veins - CAN GO ON TO DEVELOP Chronic Venous Insufficiency, Recurrence is high
EPIDEMIOLOGY
IN 1/3 OF POP
females more likely to present
inc with age
AETIOLOGY
primary varicose veins (95%)
unknwon cause
some indviduals have inherently weak vein walls, which may predispose them to develop varicose veins
congenital valve absence (very rare)
there is a strong familial component
secondary varicose veins
obstruction to venous flow
intravasc - DVT
extravasc - trauma or compression from eg an ovarian tumour, cirrhotic liver, fetus and May-Thurner syndrome (left iliac vein compressed by right iliac artery)
valvular damage - DVT
RF
PROLONGED STANDING AND SITTING
FAM HX
OBESITY
OCP
PREG
TRAUMA
PATHOPHYSIOLOGY
if the valve becomes leaky, there is retrograde flow and blood remains in the superficial veins
this causes venous HTN of the superficial venous system, manifesting as toruturous and dilated sup. veins = varicose veins
these veins have a one way valve that allows blood to flow from the superficial veins to the deep veins of the leg
Perforator veins connect the superficial and deep veins of the leg
CLINICAL FEATURES
KEY FEATURES
itching, discomfort and heaviness in the legs
other features: pain, oedema, night cramps, restless legs
Cosmetic concerns
symptoms may be exacerbated by prolonged standing, pregnancy, menstruation, HRT, hormonal contraceptives
EXAMINATION FINDINGS
SIGNS OF CHRONIC VENOUS INSUFFICIENCY
ulcers (usually above the medial malleolus)
atrophie blanche (white skin surrounding a healing ulcer)
telangiectasia
lipodermatosclerosis (hard skin from fibrosis of subcut fat)
Eczema
haemosiderin staining
tourniquet test - apply tourniquet to thigh with leg up and ask pt to stand - absence of varicosity below tourniquet indicates the level of reflux is occurring above the compression. if not, the tourniquet is applied at gradually lower levels of leg above important perforators until varicosity disappears
EXAM ESSENTIALS
PRESS - if empty and refills = varicose
phlebitis = tender to touch
thrombosis = hard to touch
DDX
cellulitis
superficial phlebitis
benign telangiectasia
DVT
IX
first line
duplex USS - combines doppler with conventional US techniques - TO CONFIRM DIAGNOSIS, USED FOR PLANNING MANAGEMENT
MANAGEMENT
if secondary - treat underlying cause
lifestyle modification
doesn't reverse varicose may prevent progression
weight loss
regular exercise
avoid exacerbating factors (prolonged standing)
compression stockings
interventional treatment [contraindicated in preg]
offered to all pts
1st line - RADIOFREQUENCY ABLATION or ENDOVENOUS LASER TREATMENT (endothermal ablation)
2nd line - USS- guided foam sclerotherapy
3rd line - surgery
ABDOMINAL AORTIC ANEURYSM (AAA)
definition - aortic aneurysm is the pathological focal dilatation of the aorta predisposing to its rupture. both the thoracic and abdo aorta can be affected, but the latter more commonly so
true aneurysm is when there is full thickness dilatation of the blood vessel, usually more than 50% of its normal diameter.
diameter >3cm is considered to be aneurysmal
EPIDEMIOLOGY
3-8% >50s
INC INCIDENCE
MALES 5X MORE COMMONLY AFFECTED
THE MAJORITY ARE INFRA-RENAL AORTA
CLINICALLY SIGNIFICANT WHEN LARGE >5.5cm
AETIOLOGY
TRAUMA/INFECTION(MYOCOTIC ANEURYSM), INFLAMMATION (TAKAYATSU'S ARTERITIS) & CONNECTIVE TISSUE DISORDERS (MARFAN'S SYNDROME)
UNKNOWN, MULTIFACTORIAL
RD: age >60, male, smoking, emphysema, HTN, hyperlipidaemia, atherosclerosis, fam hx(20%)
PATHOPHYSIOLOGY
in aneurysmal development there is - transmural inflammatory cell infiltration with subsequent chronic inflammation of the aortic wall
elastin and collagen degradation secondary to proteinases, consequently compromising the resilience and tensile strength of the aortic wall
aneurysmal degeneration of the aortic wall
the net product is a thin aortic wall prone to expansion and eventually rupture
CLINICAL FEATURES
KEY FEATURES
asymptomatic - the majority of AAAs are small <4cm and asymptomatic. most are picked up incidentally or on abdo USS screening
symptomatic but unruptured (5-22%) - insidious onset of vague abdominal, back or flank discomfort. having symptoms correlates with larger aneurysms and a greater risk of rupture
EXAMINATION FINDINGS - unreliable diagnostic tool
mild tenderness on abdo palpation
complete vascular exam - distal embolisation and ischaemia and other aneurysms (eg popliteal artery aneurysm)
pulsatile abdo mass (if >5.5cm or thin body habitus)
if ruptured there is often tachycardia, hypotension, pulsatile abdo mass and significant ecchymosis (flank and umbilical bruising)
IX
DIAGNOSIS BY AORTA BEING 1.5 TIMES ITS NORMAL DIAMETER
SECOND LINE - CT
FIRST LINE - abdo US
IMMEDIATE INTRA ABDOMINAL EXPLORATION/INTERVENTION SHOULD NOT BE DELAYED FOR IMAGING IF SUSPECTED RUPTURE (back pain, hypotension, delayed pulsatile abdo mass)
MANAGEMENT
CONSERVATIVE
surveillance if <5.5cm
smoking cessation most sig non surg intervention
treat CV RF - HTN, hyperlipidaemia and diabetes
moderate exercise reduces progression
SURVEILLANCE - 4.5-5.4 = 6monthly
3.5-4.4 = 12monthly
3-3.4 = 3yearly
SURGERY
indicated if there is
asymptomatic large AAA (>5.5) elective
symptomatic (unruptured) AAA - semi urgent
ruptured AAA - emergency
OPTIONS:
EVAR = endovascular aneurysm repair (preferred option) [stent graft via femoral artery]. inc risk of need for secondary intervention. post op surveillance with CTA recommended. long term outcomes are comparable with open surgery. complication = leaking, limb thrombosis, graft migration and infection
open surgery = aneurysm sac sewn together and a tube/graft anastomoses the proximal and distal aorta. COMPLICATIONS - early = cardiac, pulmonary, renal or colonic ischaemia. later = para-anastomotic aneurysm, graft infection, graft eteric fistula or erosion and graft occlusion
COMPLICATIONS
RUPTURE PRESENTS WITH TRIAD
expansile, pulsatile abdo mass
hypotension
abdo, back or flank pain
SCREENING
ONE TIME US SCREENING RECOMMENDED IN ALL MEN AT OR OLDER THAN 65 YRS (55 IF THERE IS A FAMILY HX OF AAA). ONE-TIME SCREENING IN WOMEN IS RECOMMENDED IF AT OR OLDER THAN 65 YRS AND A FAM HX OF AAA OR HX OF SMOKING
PROGNOSIS - rupture has 85% mortality rate
VASCULITIDES
Immunological response to specific antigens found on blood vessel walls. inflammatory cells infiltrate the vessel wall, with the potential for leaking, bleeding and downstream ischaemia and necrosis.
LARGE VESSEL VASCULITIS
TAKAYASU'S ARTERITIS
chronic large vessel vasculitis of the aorta and its primary branches. most commonly affects women (ASIAN) between ages 10-40
also known as the pulseless disease
corticosteroids are the mainstay of treatment
GIANT CELL ARTERITIS (temporal arteritis)
often present with jaw and limb claudication (upper>lower), scalp tenderness, worsening headaches and symptoms of polymyalgia rheumatica (aching and stiffness in the neck, shoulder and pelvic girdle)
visual loss is the most feared complication of GCA and is secondary to anterior ischaemic optic neuritis
chronic, granulomatous vasculitis that affects medium to large arteries. commonly affect women >50y/o
a raised ESR IN CONJUNCTION WITH typical symptoms prompt immediate corticosteroid therapy
temporal artery biopsy can confirm
relapse common
MEDIUM VESSEL VASCULITIS
POLYARTERITIS NODOSA
a necrotising vasculitis
systemic condition - may present with renal, muscular, GI, cutaneous and neurological symptoms. unlike wegener's, it spares the lungs.
most are idiopathic in origin, but may be secondary to hep B or C
diagnose via hx and exam and lab = raised ESR, neg ANCA and radiology - biopsy may be required to confirm diagnosis
treatment with oral corticosteroids is indicated for mild disease with addition of cyclophsophamide in moderate or severe cases
KAWASAKI DISEASE
in children
systemic with mucocutaneous involvement leading to: bilateral non-purulent conjunctivitis, cervical lymphadenopathy, erythema of oral mucosa with a strawberry tongue, swelling of fingers and a rash in context of prolonged pyrexia (>5 days)
disease usually self limiting - potential complications: coronary artery aneurysm, MI, HF
ECHO recommended to screen for cardiac complications
treat with IV Ig and aspirin
SMALL VESSEL VASCULITIS
WEGENER'S GRANULOMATOSIS (granulomatosis with polyangiitis)
systemic vasculitis seen in adults of either sex
causes granulomatous inflam of the kidney (crescentic glomerulonephritis) and upper and lower airways
pts may present with constitutional symptoms, nasal symptoms (crusting, sinusitis), saddle nose deformity (bone destruction), resp symptoms (cough, haemoptysis) and haematuria. the skin and nervous system may also be affected
PR3 ANCA positive
biopsy is diagnostic
treat with pulsed cyclophosphamide with azathioprine maintenance. steroids also given
MICROSCOPIC POLYANGIITIS (MPA)
systemic vasculitis affecting
MPO-ANCA
characterised by lack of granulomatous changes on biopsy when compared to Wegener's
similar features to wegener's
CHURG-STRAUSS SYNDROME (eosinophilic granulomatosis with polyangiitis)
systemic assoc with asthma
4 out of 6 criteria = diagnosis likely: ASTHMA, PARANASAL SINUSITIS, PULM INFILTRATES, PERPH BLOOD EOSINOPHILIA (>10%), BIOPSY CONFIRMED VASCULITIS & MONONEURITIS MULTIPLEX OR POLYNEUROPATHY
heart, skin, kidneys, GI tract may also be affected
40-70% p-ANCA positive
treat with high dose corticosteroids
MISCELLANEOUS
buerger's disease (thromboangiitis obliterans)
assoc closely with heavy smoking, low socio-economic status and male gender
classically presents with claudication of hands and feet, eventually occurring at rest. discoloration (raynaud's phenomenon) may occur - symptoms typically exacerbated by cold and stress. common sequelae are ulcerations and gangrene of the digits
inflam and thrombosis of small and medium sized vessels of upper and lower limbs
most important intervention is smoking cessation. other therapies such as CCB are ineffective. surgery may be required
Raynaud's phenomenon
often triggered by cold exposure
commonly women in 20s/30s
usually in the fingers and toes, but can affect the ears and nose as well
1 in 10 have underlying cause = SLE, scleroderma, RA
vaspospasm and subsequent vasodilatation of periph small arteries, causing extremities to go pale, cyanosed and then red (White-blue-red)
manage - smoking cessation most important, keep estremities warm, regular exercise limit stress. if insufficient = NIFEDIPINE given as prophylaxis