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1 PERIPHERAL VASCULAR DISEASE

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