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Surgery > Vascular > Flashcards

Vascular Flashcards

1
Q

DDx for calf pain

A

PVD claudication
Musc: knee/ankle/hip pathology
Neuro: spinal stenosis
DVT
Cellulitis
Lymphodoedema
Baker’s cyst ruptured

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2
Q

What questions should you ask a patient with tissue loss?

A

What drew their attention to the ulcer?
Site
Duration
Persistence
Progression
Multiplicity
Other Sx

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3
Q

What is included in a lower limb examination

A

INSPECTION: anterior and lateral of LL, sole of foot, bw toes
- amputation
- ulcers
- erythema
- varicosities
- atrophy
- scars
- discolouration (e.g., venous staining)
- loss of hair

PALPATION
- temp: use dorsum of hand from hips to foot comparing L to R
- CR: use great toenail –> normal is within 3s
- venous filling: occlude dorsal venous arch of foot using 2 fingers then release distal finger and look for venous refilling –> absence suggests poor arterial supply to foot
- Pulse: femoral, popliteal (flex leg), posterior tibial, dorsalis pedis, and check for AAA

AUSCULTATION
- abdominal, renal, femoral bruits

SPECIAL TESTS
- Buerger’s test
- Measure ABI
- Test lower limb sensation
- Test for glucose in urine

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4
Q

How is a vascular exam performed?

A

UPPER LIMBS AND CHEST
- hands/fingers for ulceration, surgery, clubbing
- radial, brachial, carotid pulse
- bilateral BP
- auscultate for subclavian and carotid bruit
- examine face for facial droop and palate for Marfans
- chest: scars, heart sounds, breath sounds, rhythm

ABDOMEN
- scars
- pulsation
- bruits: aorta, renal, mesenterics, iliacs
- bowel sounds
- palpate for AA and fem-fem crossover grafts or axillo-femoral bypass grafts

GROIN
- scars, pulsation
- pulse, thrill, collection
- bruit

LOWER LIMBS
- symmetry, scars, ulcer, skin changes, colour, hair, veins (varicosities), structural defects (Charcot’s)
- check bw toes
- pulses, temp, CR
- sensation/power
- tenderness
- check venous disease by getting patient to stand and check distribution of long saphenous (medial) and short saphenous (posterior calf) veins

SPECIFIC TESTS
- Buerger’s Test
- ABI
- Toe pressures (requires specialised machine but same principle as ABI)

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5
Q

What is Buerger’s Test and how is it performed?

A

Test for critical limb ischemia

Patient is supine and foot is elevated to 45 degrees –> if the foot turns white and then ischaemic rubor returns with dependency the test indicates CLI and high risk of foot loss

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6
Q

What is the Ankle Brachial Index and why is it measured

A

The ratio of systolic ankle blood pressure to systolic brachial blood pressure

First line diagnostic test for nonacute PAD

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7
Q

How is ABI measured and what is a limitation

A

Take blood pressure on both arms and use the highest reading
Take blood pressure over ankle using BP cuff and doppler

Heavily calcified vessels e.g., DM/renal disease can give falsely high readings
Also limited by absent limbs, dressings, ulcers

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8
Q

What are normal and abnormal ABI values

A

Normal = 0.9 - 1.2
Mild PAD/claudication = 0.71 - 0.9
Moderate = 0.41 - 0.7
Severe < 0.4
Medial calcific sclerosis with incompressible vascular wall > 1.3

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9
Q

Compare neurogenic and vascular claudication

A
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10
Q

What are the non-modifiable and modifiable risk factors for PAD?

A

Non-modifiable
- Age: > 50year olds have increased risk if they have other vascular risk factors, or > 65yo with no other vascular risk factors
- FHx/genetics
- Male
- Known atherosclerosis at other sites

Modifiable
- HTN
- DM –> increased risk of ulcer and limb loss
- Smoking
- Dislipidaemia
- Obesity/metabolic syndrome
- CKD

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11
Q

What are the non-modifiable and modifiable risk factors for peripheral venous disease

A

NON-MODIFIABLE
Age
Female
FHx
Ligamentous laxity (e.g., hernia/flat feet)
Hereditary conditions/congenital abnormalities

MODIFIABLE
Prolonged standing
High BMI
Pregnancy/high oestrogen states
Smoking
Lower extremity trauma
Prior venous thrombosis (post-thrombotic syndrome)
Sedentary lifestyle

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12
Q

Discuss the pathophysiology of diabetic foot

A
  1. Macro- and microvascular disease –> reduced perfusion and integument breakdown, reduced wound healing and clearance of pathogens
  2. Peripheral sensory neuropathy (pain, pressure, temperature, proprioception, vibration) –> failure to notice repeated injuries and abnormal pressure loading –> tissue loss over bony prominences
  3. Peripheral motor neuropathy –> abnormal gait and paralysis of intrinsic muscles of foot –> abnormal biomechanics and structural abnormalities –> abnormal pressure loading and tissue loss
  4. Peripheral autonomic neuropathy –> dry skin, loss of sweat and secretions –> fissuring and sites for pathogen entry
  5. Gylcation of collagen and tendons e.g., Achilles and gastrocnemius glycosylation resulting in Ankle Equinus and impaired dorsiflexion and increased forefoot pressure –> structural deformity including Charcot arthropathy/rockerbottom foot (collapse of midfoot)
  6. Immunocompromise and increase risk of opportunistic ifnection
  7. High tissue glucose levels create a favourable environment for organisms
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13
Q

Discuss the presentation of diabetic foot

A

Foot ulcer (arterial/neuropathic)
Foot pain
Loss of sensation (peripheral neuropathy with glove and stocking distribution) assessed with 10g monofilament
Foot deformity e.g., collapse of midfoot, hammer toe, hallux valgus
Absence of pedal pulses, reduced CR, cold extremities
Motor weakness/areflexia
Recurrent foot infections
Dry skin, loss of sweat, fissuring

Fever/chills/malaise/anorexia suggests severe infection
Foot erythema/oedema suggests cellulitis with or without deep soft tissue infection (abscess) - may not manifest with warmth and erythema in presence of severe ischaemia
Fluctuance suggests abscess
Cutaneous bullae, soft tissue gas, skin discolouration, foul odour suggests necrotising infection

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14
Q

What is Charcot foot?

A

A neuropathic osteoarthropathy resulting in progressive degeneration of a bone/joint from repetitive trauma, abnormal vascular flow, and inflammation. Typically precipitated by conditions that result in decreased sensation (e.g., peripheral neuropathies caused by diabetes, tabes dorsalis, spinal cord injury).

Manifestations include erythema, edema, warmth, and the formation of pressure ulcers near the affected area.

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15
Q

Investigations for diabetic foot

A

FBC, BGL, HbA1C, ESR, CRP (UECs if giving ABx)

XR foot (hypolucencies, cortical destruction/osteolysis, joint subluxation, gas in soft tissues, deformities)

Infection suspected: MC&S from soft-tissue/bone samples of wound or a deep swab
MRI foot for Dx OM (T1: hypo-intense areas of bone, T2: hyper-intense)

ABI to Ix PVD in pt with ulcer
Arterial duplex USS for PVD Dx
Angiography for PVD +/- revascularisation Tx
MR angiography if renal Fx okay provides strategy for revascularisation

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16
Q

Mx of diabetic foot?

A

MADADORE

  1. Manage blood glucose levels and comorbidities and involvement of multidisciplinary foot care team
  2. Assess foot
  3. Sharp debridement of slough, necrotic tissue, and surrounding callus of ulcer
    - if abscess/infected joint space/fasciitits/myonecrosis/necrotic bone perform surgical debridement/drainage
  4. Antibiotics
    - do not Tx non-infected ulcers with ABx
  5. Dress wound with a non-adherent dressing that maintains a clean moist environment
    - consider split-thickness skin grafting for patients with a large epithelial defect that has a tissue bed with healthy granulation
  6. Pressure offloading: podiatry review and offloading footwear
  7. Refer: multidisciplinary foot team should provide regular care and follow up (vascular RF optimisation, blood glucose targets etc.)
  8. Educate

Consider endovascular revascularisation or surgical bypass in PVD

Consider amputation in areas with irreversible gangrene, OM, deep tissue infection

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17
Q

What antibiotics are indicated for mild diabetic foot infection

A

Dicloxacillin/flucloxacillin 500mg PO 6hourly
MRSA risk: trimethoprim + sulfamethoxazole 160mg + 800mg PO 12 hourly

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18
Q

What antibiotics are indicated for moderate diabetic foot infection

A

Amoxicillin + clavulanic acid 1 + 0.2g IV 8hourly (if bone involved increase to 6hourly)

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19
Q

What antibiotics are indicated for severe diabetic foot infection

A

Piperacillin + tazobactam 4 + 0.5g IV 6 hourly
MRSA risk: vancomycin 25-30mg/lg as a loading dose

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20
Q

What is acute limb ischaemia

A

Sudden decrease in limb perfusion threatening limb viability

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21
Q

Aetiology of acute limb ischaemia

A

Embolus from arrythmia/AF, valvular disease e.g., RHD, MI
Cholesterol embolism (blue toe syndrome)
DVT embolus (paradoxical embolism with PFO)
Septic emboli from endocarditis
Popliteal aneurysm thromboses or embolises

Hypercoagulability -> thrombosis (e.g., malignancy, thrombophilia, vasculitis)
Stent or graft thrombosis
Thrombosis of existing atherosclerotic plaque
Aneurysmal thrombosis (popliteal = MC)

Trauma leading to transsection/dissection/thrombosis
- Posterior knee dislocation –> popliteal artery thrombosis
- Iatrogenic (arterial access site –> femoral artery thromosis)
Crush injury

Compartment syndrome (extrrinsic compression)

Vasoconstriction –.> shock, Raynaud, drugs e.g., norepinephrine

Aortic dissection

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22
Q

Risk factors for acute limb ischaemia

A

Existing atherosclerotic disease
CVD/previous MI/stroke etc.
HTN
DM
Obesity
Dyslipidaemia
Age
Smoking
Previous intermittent claudication or rest pain
Renal disease

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23
Q

Presentation of acute limb ischaemia

A

Sudden onset of severe limb pain, pallor and mottling, absent/diminished femoral/popliteal/dorsal pedalis pulses, cold temperature, numbness/paraesthesia, paralysis/weakness

Possibly on a background of chronic PVD Sx

ABI
- .9 – 1.2 = normal (> 1.4 suggests medial calcification e.g., HTN/DM/CKD -> use TBI)
- .5 - .9 = intermittent claudication
- .4 and below = critical limb ischaemia

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24
Q

Ix for acute limb ischaemia

A
  • FBC, UECs, coags
  • ABI and TBI
  • Duplex USS (localisation and degree of stenosis)
  • MR/CT angiography
  • DSA (digital subtraction angiography = type of catheter angiography) involves peripheral cannulation and contrast injection so reserved for immediately pre-intervention
  • Investigate possibility of embolus from heart (echo)
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25
Q

Mx of acute limb ischaemia

A

INITIAL
Transfer immediately to facility that can provide angiography and vascular surgery
Protect limb using cage and heel pad (do not elevate)
IV unfractionated heparin 80U/kg loading dose followed by 18U/kg/hr (adjust according to APTT)
Analgesia with paracetomol and opioid

Non-viable limb: tissue loss, nerve damage, sensory loss  amputation

Viable limb: no significant tissue loss, nerve damage or sensory loss -> urgent revascularisation
- Endovascular revascularisation –> percutaneous angioplasty with balloon dilation, stents, mechanical thrombus extraction, thrombo-aspiration, intra-arterial thrombolysis e.g., urokinase
- Surgical revascularisation –> thrombectomy and bypass
– Aortoiliac disease if stenosis > 10cm, chronic occlusion > 5cm, heavily calcified lesions, or lesions associated with AA
– Femoral artery disease if lesion > 10cm, heavily calcified lesion > 5cm, lesions involving ostium of SFA, lesions involving popliteal artery
– Common femoral endarterectomy

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26
Q

What is critical limb ischaemia

A

Limb threatening arterial occlusion characterised by the presence of any of: rest pain lasting 2+ weeks, non-healing ulcers, tissue loss (gangrene)

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27
Q

Presentation of critical limb ischaemia

A

Limb pain at rest, worse when supine and improves when pt is dependent

Gangrene: necrosis involving 1+ toes/other parts of foot

Non-healing wound/ulcer in lower extremities below level of knee (esp. if persists despite wound care)

Muscle atrophy of lower extremity (reduced circumference compared with contralateral extremity)

Pallor when leg is elevated and dependent rubor (Buerger’s test)

Loss of hair of dorsum of foot
Thickened toenails
Shiny/scaly skin due to loss of SC tissue

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28
Q

Management of critical limb ischaemia

A
  1. Referral to vascular surgeon and assessment for revascularisation
    - Vascular reconstruction e.g., bypass grafting, endarterectomy, endoluminal techniques
    - If revascularisation not possible due to extent/distal nature of disease –> primary amputation
  2. Analgesia - even opioids
  3. Protect limb with cage and heel pad but do not elevate
  4. Antiplatelets (aspirin/clopidrogel)
  5. Consider use of prostanoids (aloprostadil) in pts in whom arterial reconstruction is not possible
  6. Maintain high to normal systolic BP to assist blood perfusion. This may involve reducing the dose of a BP-lowering drug in patients with pre-existing elevated BP.
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29
Q

What is endovascular revascularisation for PVD

A

Endovascular techniques include: balloon dilation (angioplasty), stents, and atherectomy.

Endovascular revascularisation is recommended for aortoiliac disease with stenosis <10 cm and chronic occlusions that are <5 cm.

For femoropopliteal artery stenosis, endovascular therapy is recommended if there is a discrete stenosis <10 cm, or calcified stenosis <5 cm.

For infrapopliteal artery lesions, endovascular treatment has been limited to threatened limb loss only.

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30
Q

What is surgical revascularisation in PVD and who is it recommended for

A

Bypass surgery

Surgical revascularisation is recommended for aortoiliac disease if stenosis >10 cm, chronic occlusion >5 cm, heavily calcified lesions, or lesions associated with aortic aneurysm.

Surgical revascularisation is recommended for common femoral artery disease if lesion >10 cm, heavily calcified lesions >5 cm, lesions involving the ostium of superficial femoral artery, and lesions involving the popliteal artery.[2]

Common femoral endarterectomy is frequently performed for common femoral artery lesions. This surgery has a high patency rate but may be associated with significant complications.[71] This can be combined with other procedures or carried out as a stand-alone procedure.

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31
Q

What is an AAA

A

Abdominal Aortic Aneurysm
Permanent pathological dilation of aorta with a diameter of > 1.5x the expected AP diameter for that segment based on patient sex and body size
- MC threshold = 3cm or more

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32
Q

Where are most AAAs and why

A

Most are infrarenal (L2 and below)
AA lacks vasa vasorum –> more susceptible to ischaemia

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33
Q

What morphology can AAAs be

A

Saccular or fusiform

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34
Q

What are the risk factors for AAA

A
  • Most important = smoking (altered tissue metalloproteinases may diminish integrity of wall and impaired cell repair in vascular SMCs)
  • Age
  • Male
  • Hypertension
  • Hypercholesterolaemia
  • Genetic: EDS, Marfan
  • Infection (salmonella, e. coli, staph, syphilis)
  • trauma
  • Intimal atherosclerosis
  • Obliteration of collagen and elastin in media and adventitia
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35
Q

What is the histology of AAAs

A
  • Loss of collagen and elastin in media and adventitia
  • Loss of smooth muscle cells
  • Tapering of medial wall
  • Infiltration of LOs, MOs
  • Neovascularisation
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36
Q

What is the pathophysiology of AAAs

A

SMC loss from ischaemia (atherosclerotic thickening of intima increases oxygen diffusion distance + HTNive narrowing of vasa vasora) + MMPs produced by inflamm cells –> net proteolytic destruction of wall
4 mechanisms
1. Increased proteolytic degradation of aortic wall CT: increased activity of MMPs and proteases –> deterioration of structural matrix proteins e.g., elastin/collagen
2. Inflammation and immune responses: transmural MO and LO infiltration –> cytokine release and protease activation
3. Biomechanical wall stress: elastin levels and elastin-collagen ratio decrease progressively distal down aorta increasing risk of dilatation and rupture (plus increased MMP9 activity, disordered flow, and relative tissue hypoxia distally)
4. Genetics

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37
Q

What are the special types of AAA

A
  • Congenital: accelerated medial degeneration in Marfan syndrome and bicuspid aortic valves
  • Infectious: infection of aortic wall (mycotic aneurysm) MC secondary to salmonella or staphylococcus (+ syphilis)
  • Inflammatory: abnormal accumulation of MOs and cytokines –> perianeurysmal fibrosis, thickened walls and adhesions
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38
Q

What is the presentation of AAAs

A
  • MC asymptomatic
  • Pulsatile expansile mass on palpation
  • Expansion/rupture –> epigastric/lower abdominal/testicular/flank pain radiating to back, hypotension, tachycardia, abdominal distension, pallor, collapse/LOC, sudden death (pain can mimic renal colic or diverticulitis)
  • Vertebral body erosion –> back pain
  • Haematemesis secondary to aorto-duodenal fistula
  • Compression of surrounding structures by inflammatory aneurysm e.g., ureters, IVC, duodenum
  • Dusky discolouration of feet/toes secondary to emboli from aortic thrombus
  • Popliteal aneurysm
  • Obstruction of branch vessel –> downstream tissue ischaemic injury
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39
Q

What is the risk of AAA rupture according to size

A

< 4cm = 0 risk
4-5cm = 1% risk/year
5-6cm = 11% risk/year
>6cm 25% risk/year
Most expend 2-3mm/year but some expand rapidly

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40
Q

What Ix should be done for AAA

A
  • FBC, UEC, coags, G&CM if ruptured (ESR/CRP/blood cultures if concern RE inflammatory)
  • Aortic USS (screening and Dx)
  • CTA or MRA (Dx and operative planning)
41
Q

What is Mx for ruptured AAA

A

Supplemental O2
IV access (wide bore x 2)
- Blood: 1: 1 ratio of FFP and PRBCs
- Prophylactic Abx IF undergoing EVAR/open surgical repair to cover GP and GNs and prevent graft infection
- Analgesia: PCA, epidural, continuous infusion of LA into wound
Arterial catheter
Urinary catheter
VTE prophylaxis with intermittent pneumatic compression until risk of major bleeding subsided
–> once risk subsided (4-8 hours of surgery) start enoxaparin/heparin
Urgent EVAR/open surgical repair/end of life care

42
Q

Mx for symptomatic AAA unruptured

A

Symptomatic AAA or > 5cm in female or > 5.5cm in males or rapid growth > 1cm/yr  repair and CVS risk reduction (antihypertensives, statins, antiplatelets, exercise, diet, smoking cessation)

EVAR: fluoroscopic guidance (DSA) expandable stent placed intraluminally at site of aneurysm via iliac or femoral arteries
- Not suitable for EVAR: short angulated aneurysm neck, extreme tortuosity or calcification
Open: laparotomy and replacement of dilated portion of aorta with tube graft or Y-prosthesis

43
Q

Asymptomatic AAA Mx

A

Asymptomatic < 5.5cm  surveillance
- 3 – 4 cm 2 yearly USS
- 4 – 4.5cm yearly
- 4.5 – 5cm 6 monthly
- > 5cm 3 monthly

44
Q

Complications of AAA

A

AAA rupture 80-90% mortality (esp. intraperitoneal)
Distal embolisation
Dissection
Post-op
o Bowel ischaemia, AKI, SC ischaemia
o Aortoenteric fistula
o Graft infection
o Endoleak from EVAR (flow outside stent within aneurysm sac)
o Abdominal compartment syndrome
o Ileus
o Amputation secondary to lower limb ischaemia
o Pseudoaneurysm formation
Ureteric/duodenal (GOO)/SVC obstruction

45
Q

Carotid Artery Disease Risk Factors and Aetiology

A

Atherosclerosis

Risk factors: advanced age, tobacco use, arterial HTN, DM

46
Q

Where does carotid artery stenosis usually occur

A

Carotidartery stenosis typically occurs within2cmof common carotid arterybifurcation

47
Q

Symptoms of carotid artery stenosis

A
  • Many patients are asymptomatic
  • Symptomatic patients may present with TIAs, SX of ischaemia of common carotid artery territory e.g., ipsilateral amaurosis fugax, contralateralweakness,contralateralsensory deficits (ischaemic stroke)
  • Does not typically cause vertigo, lightheadedness, or syncope
48
Q

What is the difference bw symptomatic and asymptomatic carotid artery stenosis

A

Symptomatic carotid stenosis: Sx attributable to carotid stenosis within the past6 months

Asymptomatic carotid stenosis: no recent (< 6 months) Sx attributable to carotidarterystenosis → nonspecific Sx (dizziness, ataxia, impaired consciousness) not considered to bepathognomonicfor carotid stenosis

49
Q

Exam findings carotid artery stenosis

A

Carotid bruit: pathologic sound heard onauscultationover carotidarterythat is caused byturbulent blood flow (may be an incidental finding during a routinephysical Ex → Sn and Sp ofcarotid bruit for carotidarterystenosis are low)

Hollenhorst plaque on fundoscopy

50
Q

Describe Ix of carotid artery stenosis

A

Evaluate for and manage acute neurological symptoms (evaluate for stroke and TIA)

Noncontrast CT head or MRI brain is indicated for all patients with ischemic stroke or TIA

Perform carotidartery imaging in all patients withsymptomatic carotid stenosis
- Carotid duplexUS(CDUS) = first-line imaging modalityfor suspected symptomatic carotid stenosis
- Magnetic resonance angiography(MRA) orCT angiography(CTA) = confirmatory test ifCDUSfindings are suggestive of carotid stenosis
- Digital subtraction angiography (DSA)

51
Q

Classify carotid artery stenosis by severity

A
  • Clinically significant carotid stenosis: narrowing of the carotidartery≥ 50%
    • Moderate carotid stenosis: narrowing of the carotidartery by50%–69%
    • Severe carotid stenosis: narrowing of the carotidartery 70%–99%
52
Q

Describe use of CDUS in carotid artery disease

A

First-line imaging modalityfor suspected symptomatic carotid stenosis

  • Permits direct visualisation of vessel wall and flow measurement at site of the stenosis bycolour Doppler USS
  • Findings: focally increased velocity of blood flow(HGstenosis) or absence of blood flow (total occlusion), increased peaksystolic velocity, increased thickness of intima-media
53
Q

Describe use of MRA/CTA in carotid artery stenosis

A

Confirmatory test ifCDUSfindings are suggestive of carotid stenosis

  • Simultaneous evaluation of head and neck vessels in pts with ischaemic stroke (+ no iodinising radiation or exposure to iodinated IV contrast)
  • MRA has a tendency to overestimate degree of stenosis
  • CTAis suitable for patients withcontraindications for MRI (e.g., implanted devices, claustrophobia)
54
Q

Describe use of DSA in carotid artery stenosis

A
  • Commonly considered gold standard for evaluatingCAS → consider ifCDUSis inconclusive in patients who cannot undergoCTAor MRA or for preprocedural planning (i.e., before cartotid endarterctomy or carotid artery stenting)
  • Findings: Similar toCTAor MRA
  • NB. DSA is invasive with a higher risk of mortality andstroke than imaging modalities with comparable diagnostic accuracy(e.g.,CTA)
55
Q

Describe overview of management of carotid artery stenosis

A

Lifestyle modification and atherosclerotic plaque prevention → heart healthy diet (reduce saturated fat, cholesterol, sodium), exercise, smoking cessation, limit alcohol

Medical: longterm antiplatelet Tx, longterm high-intensity statin therapy, manage modifiable risk factors for atherosclerosis e.g., DM, HTN

Symptomatic: carotid revascularisation

Asymptomatic: consider revascularisation if stenosis severe and low risk of procedural morbdity and mortality

Periprocedural risk and patient life-expectancy, comorbidities, and preferences must also be considered RE revascularisation

56
Q

When should carotid revascularisation be formed

A

Ideally performed within14 daysof symptom onset

57
Q

What are CI to carotid revascularisation

A

Carotid stenosis< 50%, chronic complete carotid occlusion, severely disabling stroke

58
Q

What are the methods for carotid revascularisation

A

Carotid Endarterectomy CEA: usually considered first-line treatment for carotid stenosis
Carotid artery stenting:angioplastyandstentingof the carotid artery (via transfemoral or transcarotid approach)
Carotidarterybypass grafting: Uncommonly required; may be considered for recurrent or bilateralsevere carotid stenosis

59
Q

Carotid Endarterectomy CEA:

A

Carotid Endarterectomy CEA: usually considered first-line treatment for carotid stenosis

  • Surgical procedure in which inner lining of a carotidartery is removed, along with any associated atherosclerotic deposits
  • If the patient is not a good candidate forsurgeryor lesion characteristics preclude surgical treatment, carotid artery stenting may be preferred.
60
Q

What are the advantages of carotid artery endarterectomy

A

Lower peri-procedural stroke rate than carotid artery stenting esp. in pts > 70yo

61
Q

What are the disadvantages of carotid artery endarterectomy

A

Higher risk of periprocedural MIthanstenting, potentially difficult in patients with prior neckirradiationand/orsurgery, potential complications include cranial nerve palsy

62
Q

What are the advantages of carotid artery stenting

A

Alternative tosurgery in pts with poor surgical access or increased risk of peri-operative complications e.g., pts with active cardiac or pulmonary disease,contralateralcarotidartery occlusion,contralaterallaryngeal nerve palsy, previous neck radiation, recurrent stenosis after priorCEA

63
Q

What are the disadvantages of carotid artery stenting

A

Higher risk of periproceduralstroke thanCEA

64
Q

What are the complications of carotid artery stenosis

A

Stroke due tothromboticocclusion of carotidartery or embolic occlusion of cerebralarteries (annual risk is 0.5–1% in pts withasymptomatic carotid stenosis > 50%,)
MI
False aneurysms due to weakening of the vessel wall

65
Q

Complications of carotid revascularisation

A

Complications of endarterectomy:
- Intraoperativehaemorrhageand postoperativehaematoma → may be large enough to compress neighbouring structures (e.g., trachea after carotid endarterectomy)
- Injury to adjacent structures e.g., injury to facial nerves (peripheral facial palsy), RLN (hoarseness of voice),hypoglossal nerve (tongue deviation toipsilateralside), Horners syndrome in carotid endarterectomy; injury to bowel in aortic endartectomy etc.
- During/aftercarotid endarterectomy: stroke, HTN, and hypotension due to baroreceptor stimulation
Wound infection

66
Q

What are varicose veins

A

Dilated, elongated, tortuous veins superficial/subcutaneous veins(diameter> 3 mm) produced by prolonged, increased intraluminal pressure with vessel dilation and incompetence of venous valves

67
Q

Where do varicose veins MCly occur

A

Superficial veins of upper and lower legs commonly involved because venous pressures in these sites can be markedly elevated by prolonged dependent pressure

68
Q

What is venous insuffiency

A

Disturbance in venous outflow; may be congenital (e.g., congenital absence of valves) or acquired (e.g., valvular injury secondary to deep vein thrombosis) and when chronic is characterised by advanced changes to skin and veins including oedema, skin changes, and venous ulceration

69
Q

What is the pathophysiology of venous insuffiency and venous ulceration

A

Sustained venous HTN in superficial veins due to incompetent valves in deep or perforating veins or due to previous DVT –> increased oressure causes extravasation of fibrinogen through capillary walls –> perivascular fibrin deposition –> poor oxygenation of surrounding skin

70
Q

What is the pathophysiology of varicose veins

A

Varicose veins: elevated venous pressure (as per risk factors) →incompetenceof venous valves(superficial ordeep veins)→reflux of blood intosuperficial veinsand back intoextremity→further elevation of venous pressure →formation of varicose veins

71
Q

What are examination signs of chronic venous disease

A

Varicose veins
Corona phlebectatica (malleolar flare or ankle flare) = fan-shaped pattern of small intradermal veins on ankle or foot = early physical sign of advanced venous disease
Ankle oedema
Reddish-brown discoloration affecting the ankle and lower leg from extravasation of blood and deposition of haemosiderin in tissues due to long-standing venous HTN
Lipodermatosclerosis = fibrosing pannicilutitis of SC tissue/localised chronic inflammatory and fibrotic condition affecting the skin and subcutaneous tissues of the lower leg, especially in the supramalleolar region
- severe lipodermatosclerosis can kead to contracture of the Achilles tendon
Atrophie blanche: scarring white atrophic skin surrounded by telangiectasia
- Venous ulcers
- Venous stasis dermatitis (dry scaly skin)

72
Q

What are symptoms of chronic venous disease

A

Leg fatigue/aching/heavy legs: worsening toward end of day and with prolonged standing, improving with elevation

Leg cramps: associated with venous stasis and eczema

Pruritis and burning (associated with venous stasis eczema)

73
Q

Dx of venous disease

A

Varicose veins and chronic venous insufficiency are diagnosed based on Hx and Ex. Imaging only used when clinical Dxof CVI cannot be established and/orconservative managementhas failed.

Test of choice:duplex USS → presence ofvenous reflux confirms diagnosis of CVI, examine patency ofdeep vein, examine sufficiency of superficial and perforating veins

MR or CT venography(MRV or CTV) → better Sn and Sp, typically used in complicated cases, whenduplex USSis inconclusive → visualises venous anatomy and depicts venous reflux and/or obstruction

CT abdomen and pelvis: Used to rule out extrinsic compression as a cause for iliac vein compression

Venous plethysmography: noninvasive measurement of velocity of venous recovery (while exercising) via infrared light (emptyveinsresult in lightenedskin)
- IDs reflux and obstruction

74
Q

Conservative Mx for venous insufficiency

A
  • compression stockings
  • frequent elevation of legs, physio, manual lymphatic drainage
  • avoid long periods of standing and sitting (with bent legs) and heat
  • emmolients for venous stasis dermatitis
75
Q

Mx of varicose veins

A

Ablation (goal = endothelial destruction in dilatedveinsand formation of afibroticcord)

  • Chemical ablation: USS-guided foam sclerotherapy = injection of toxic substance → fibrosis
  • Endovenous thermal ablation(laser and radiofrequency) = 1at line
  • Opensurgery with partial or complete removal of vein only forveins that are not accessible by interventional techniques (more pain and increased convalescent time)
76
Q

Complications of varicose veins

A
  • Venous ulcers
  • Vein haemorrhage → superficial veinsareprone to haemorrhage and may be treated withsclerotherapyor ligation after haemorrhage has been controlled by leg elevation and application of pressure to bleeding site to prevent recurrent bleeding
  • Superficial thrombophlebitis → often occurs in varicose veinsand is an inflammationthat presents with redness, swelling and tenderness of vein; usually resolves on own but may require ligation or stripping to prevent recurrence and/orDVT
  • DVT
77
Q

What are the causes of leg ulcers

A
78
Q

What is a venous ulcer

A

An ulceration of the skin caused by sustained venous HTN in superficial veins due to chronic venous insufficiency/incompetent valves in dee or perforating veins and lack of drainage of blood (pools) or to previous DVT

79
Q

What is the pathophysiology of venous ulcers

A

increased pressure → extravasation of fibrinogen through capillary walls → perivascular fibrin deposition → poor oxygenation of the surrounding skin

80
Q

What is the epidemiology of venous ulcers

A

older pts (> 70yo)

81
Q

What is the site of venous uclers

A

medial gaiter region (triangle above ankles)

82
Q

What are the clinical features of venous ulcers

A

Clinical: painful, chronic and recurrent

Associated Sx: oedema of lower legs, venous eczema, brown pigmentation from haemosiderin, varicose veins, lipodermatosclerosis (fibrosing panniculitis of SC tissue; combination of induration, reddish brown pigmentation and inflammation), scarring white atrophy with telangiectasia (atrophie blanche).

Base: red, inflamed with some granulation and exudative tissue (blood supply is sufficient for inflammation)

Edges: diffuse; regular or irregular; slope edges with sign of slow healing

Depth: shallow

83
Q

What is the Tx for venous ulcers

A
  • High-compression bandaging (e.g. four-layer bandaging) and leg elevation to try to decrease venous HTN (doppler studies should always be done before to exclude arterial disease)
  • Debride any firm eschar or slough to provide a clean wound be
  • Ulcer dressings used to keep ulcer moist and free of slough and exudates
  • Diuretics are sometimes helpful to reduce the oedema.
  • Antibiotics are necessary only for overt bacterial infection
  • Analgesia
  • Split-thickness skin grafting is used in resistant cases.
  • Support stockings (individually fitted) should be worn lifelong after healing as this lessens recurrenc
  • Moisturise skin using a simple emollient. For very dry skin, consider using ointments.
  • Managevenous eczema
  • Encourage regular walking, leg elevation, and avoidance of standing for long periods
  • If the ulcer fails to heal, considerpentoxifylline
84
Q

What is an arterial ulcer

A

An ulceration caused by decreased arterial blood flow (e.g., due to PVD)

85
Q

Where do arterial ulcers occur

A

pressure points of foot, or higher up on leg

86
Q

What are the clinical features of arterial ulcers

A

Clinical: painful

Base: cyanotic, pale, no granulation, necrotic tissue (blood supply is not sufficient for inflammation)

Edges: irregular, punched out, no signs of healing

Depth: deep

Surrounding tissue: dry, cold, pale, shiny skin, collapsed veins, prolonged capillary refill, time, absent pulses, lack of hair, arterial bruits, signs of PVD

Possible Hx of claudication, HTN, angina or smoking → doppler USS confirms arterial disease

87
Q

What is the Tx for arterial ulcers

A
  • Keep ulcer clean and covered, adequate analgesia
    • If the wound is dry keep dry paint with betadine and apply padded dry dressing
    • If the wound is wet use an appropriatetopical antimicrobial dressing
  • Request vascular surgery review forrevascularisation/vascular reconstruction if appropriate → shunting (e.g., femoral popliteal bypass) can be performed for revascularisation in PVD
  • Compression bandaging must not be used
  • Prevent pressure damage. Ensure bony prominences have pressure redistributed with pressure-relieving equipment.
88
Q

What is a neuropathic ucler

A

An ulceration/open sore caused by impaired sensation of progressive damage/repeated trauma

89
Q

Where do neuropathic ulcers occur

A

pressure points (sole, heel, bony prominences, metatarsal heads)

90
Q

What are the clinical features of neuropathic ulcers

A

Clinical: not painful

Base: red, inflamed with necrotic or doughy tissue (blood supply is sufficient for inflammation)

Edges: punched out

Depth: deep

Surrounding tissue: foot deformities, warm and dry, shiny skin, decreased sensation

91
Q

What is the epidemiology of neuropathic ulcers

A

Epidemiology: MC in DM pts with peripheral neuropathy (also leprosy in some countries)

92
Q

What is the Tx for neuropathic ulcers

A

Treatment: keep clean, remove pressure/trauma from affected area, DM pts should pay particular attention to foot care and correctly fitting shoes with help of a specialist podiatrist

NB. Secondary infection of foot ulcers may lead to cellulitis, acute or chronic osteomyelitis, and/or septicaemia (additional risk factor = immune suppression in DM)

93
Q

What are general Tx principles for ulcers

A

Treatment: wound dressings, IV antibiotics if risk of infection, debridement/amputation of necrosed tissue

  • Shunting (e.g., femoral popliteal bypass) can be performed for revascularisation in PVD
  • If suspected malignant ulcer, consider biopsy with surgical excision.
94
Q

What are DDx for PVD

A

Spinal canal claudication (pulses present), osteoarthritis hip/knee (knee pain often at rest), peripheral neuropathy (associated with numbness and tingling), popliteal artery entrapment (YAs with normal pulses), venous claudication (bursting pain on walking with previous Hx of a DVT), fibromuscular dysplasia, Buerger’s disease (young males, heavy smokers)

95
Q

What is the Fontaine classification for PVD

A
  • Stage I: Asymptomatic
  • II: Intermittent claudication → exertional discomfort/cramp-like pain MC in calf, relieved by rest and consistent/reproduced by same level of exercise (usually worse up hill)
    • Pain, cramps, or paraesthesia distal to arterial occlusion (site depends on level and extent of arterial disease)
      • Femoropopliteal disease (MC; superficial femoral artery commonly occluded in Hunters canal) → calf claudication
      • Aorto-iliac disease (Leriche syndrome; occlusion at level of aortic bifurcation or occlusion of iliac arteries) may experience bilateral pain in buttock, hip, or thigh and may notice erectile dysfunction, and absent/diminished femoral pusles
      • Tibiofibular disease: typically causes footclaudication
    • Worsens on exertion as arterial occlusion reduces O2 supply to muscles and during exercise, oxygen demand increases, but cannot be met because of reducedperfusion → increased ischaemia and pain
    • Reproducible on asking the patient to walk same distance at which Sx typically occur
    • Completely relieved by restor lowering affected limbs → relief achieved when O2 demand of specific muscle groups is reduced by rest or if blood flow to muscles increases, which is achieved by lowering the affected limb
  • III: Rest pain/nocturnal pain → severe, unremitting aching pain often in distal in foot which stops pt from sleeping (occurs as disease progresses and indicates severeischaemia)
    • Partially relieved by dangling foot over edge of bed/standing on a cold floor and exacerbated by movement or pressure
    • Typically occurs first in the toes and forefoot and worsens with reclining (e.g., while sleeping)
  • IV: Tissue loss/ulceration and necrosis/gangrene of tissue (severe PVD/critical lower limb ischaemia)
    • Ulcer = area of discontinuity of surface epithelium
    • Gangrene = dead tissue
96
Q

What is the pathophysiology and risk factors for PAD

A

Atherosclerosis in aorta and peripheral arteries → insufficient tissueperfusion→PAD where atherosclerotic plaquesreduce arterial lumen → arterial insufficiencydistal occlusion (revise atherosclerosis with mindmap)

Often coexists withCAD, stroke, AFand renal disease

Common risk factors: smoking, DM, hypercholesterolaemia, HTN

Premature atherosclerosis in pts <45yo may be associated with thrombophilia and hyperhomocysteinaemia

97
Q

Clinical features of Peripheral Arterial Disease

A

Most patients with PAD are asymptomatic and diagnosis is based on risk factors.

Intermittent claudication: exertional discomfort/cramp-like pain MC in calf, relieved by rest and consistent/reproduced by same level of exercise (usually worse up hill)

Thigh/buttock claudication indicative of narrowing of the deep femoral artery or aorto-iliac level disease.

Diminished or absent pulses

Erectile dysfunction may be an early sign of PAD/may be a symptom of aorto-iliac atherosclerotic disease

98
Q

Dx of PAD

A

ABI </= .9

Consider:
TBI (used when ABI test is not reliable due to non-compressible vessels)
Segmental pressure examination: Plethysmographic cuffs sequentially placed along the limb at various levels measuring arterial pressure - able to determine the location and magnitude of stenosis: gradient of >20 mmHg between adjacent segments suggests PAD
Duplex USS
MRA/CTA
DSA/catheter angiography

99
Q

Mx of PAD/intermittent claudication

A

Conservative and medical
- graduated walking exercise program
- foot care/podiatry
- CV risk modification: smoking cessation, statins, consideration of ACEIs, aspirin 100-150mg PO daily/clopidrogel 75mg PO daily
- cilostazol or pentoxifylline (oxpentifylline) may be used for a short period to improve exercise tolerance while a patient with intermittent claudication is beginning a walking program

Invasive
- percutaneous transluminal angioplasty or bypass grafting for the treatment of limb-threatening ischaemic events or disabling symptoms

Surgery (17 decks)

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