Vascular Flashcards
What is an ulcer? What are the three different types?
Abnormal breaks in the skin or mucous membranes
1) Venous ulcers
2) Arterial ulcers
3) Neuropathic ulcers
Describe the differences between the types of ulcers
Venous ulcer – shallow ulcers with a granulated base, often with other clinical features of venous insufficiency present
Neuropathic ulcers – painless ulcers over areas of abnormal pressure, often secondary to joint deformity in diabetics
Arterial ulcers – found at distal sites, often with well-defined borders & other evidence of arterial insufficiency
Describe the pathophysiology of venous ulcers
Valvular incompetence/venous outflow obstruction leads to impaired venous return
Resultant venous hypertension causes trapping of WBCs in capillaries & formation of fibrin cuff hinders oxygen transportation into the tissue
WBCs become activated, with release of inflammatory mediators -> tissue injury, poor healing & necrosis
List risk factors for venous ulcers
Increasing age
Pre-existing venous incompetence/history of VTE
Pregnancy
Obesity/physical inactivity
Severe leg injury/trauma
List clinical features of venous ulcers
Painful (particularly worse at the end of the day) & often found in the gaiter region of the legs
Associated symptoms of chronic venous disease: aching, itching, bursting sensation
Examination: varicose veins, ankle/leg oedema, features of venous insufficiency (varicose eczema/thrombophlebitis, haemosiderin skin staining)
List investigations for venous ulcers
Clinical diagnosis
Underlying venous insufficiency confirmed by Duplex ultrasound
Ankle brachial pressure index: assess for any arterial component to the ulcers
Swab cultures if suspecting an associated infection
Outline the management for venous ulcers
Conservative management – leg elevation & increased exercise
Lifestyle changes
Abx only with clinical evidence of wound infection
Mainstay – multicomponent compression bandaging changed once/twice every week (ABPI must be > 0.6 before bandaging)
Concurrent varicose veins – treated with endovenous techniques/open surgery
Describe an arterial ulcer
Ulcer caused by a reduction in arterial blood flow, leading to decreased perfusion of the tissues & subsequent poor healing
Form as small deep lesions with well-defined borders & necrotic base (commonly occur distally at sites of trauma and in pressure areas)
List risk factors for an arterial ulcer
Smoking
Diabetes mellitus
Hypertension
Hyperlipidaemia
Increasing age
Positive family history
Obesity
Physical inactivity
List clinical features of arterial ulcers
Preceding history of intermittent claudication/critical limb ischaemia
Ulcer may be painful & often develops over a long period of time, with little to no healing
Other signs: cold limbs, thickened nails, necrotic toes & hair loss
Examination – limbs will be cold & have reduced/absent pulses
(NOTE: in pure arterial ulcers, sensation is maintained)
List investigations for arterial ulcers
Ankle brachial pressure index measurement: quantify the extent of any peripheral arterial disease
Imaging: duplex ultrasound, CT angiography/magnetic resonance angiogram
Describe the management for arterial ulcers
Urgently referred for a vascular review:
1) Conservative: lifestyle changes
2) Medical: CVS risk factor modification (statin therapy, antiplatelet agent), optimisation of BP and glucose
3) Surgical: angioplasty/ bypass grafting
Describe a neuropathic ulcer
Occurs as a result of peripheral neuropathy
Loss of protective sensation -> repetitive stress & unnoticed injuries forming -> painless ulcers forming on the pressure points on the limb
List risk factors of neuropathic ulcers
Develop with any condition with peripheral neuropathy:
1) Diabetes mellitus
2) B12 deficiency
Foot deformity
Concurrent peripheral vascular disease
List clinical features of neuropathic ulcers
History of peripheral neuropathy/symptoms of peripheral vascular disease
Examination: neuropathic ulcers are variable in size and depth (punched out appearance)
List investigations for neuropathic ulcers
Blood glucose levels & serum B12 should be checked
Signs of infection: microbiology swab & any evidence of deep infection may warrant an x-ray
Important to assess the extent of peripheral neuropathy
Describe the management of neuropathic ulcers
Specialised diabetic foot clinics – managed by MDT
Diabetic control should be optimised
Improved diet & increased exercise should be encouraged
Regular chiropody to maintain good foot hygiene
What is Charcot’s foot?
Neuroarthropathy whereby a loss of joint sensation results in continual unnoticed trauma & deformity occurring -> predisposes people to neuropathic ulcer formation
Patients present with swelling, distortion, pain & loss of function
Requires a specialist review for consideration of off-loading abnormal weight & sometimes immobilisation of the affected joint in plaster
What is an abdominal aortic aneurysm?
Dilation of the abdominal aorta greater than 3cm
List risk factors of AAA
Atherosclerosis
Trauma
Infection
Connective tissue disease
Inflammatory disease (Takayasu’s aortitis)
Smoking, hypertension, hyperlipidaemia, family history, male gender & increasing age
List clinical features of an AAA
Many are asymptomatic/ simply detected on incidental finding or screening
Can present with: abdominal pain, back/loin pain, distal embolisation
Examination – pulsatile mass can be felt in the abdomen (above the umbilical level)
Describe the screening programme for AAA
Abdominal US for all men in their 65th year
Most men with a detected AAA will spend 3 to 5 years in surveillance prior to reaching the threshold for elective AAA repair
Describe the medical management of an AAA
AAA < 5.5 cm, can be monitored via duplex USS
- 3 to 4.4cm = yearly USS
- 4.5 to 5.4cm = 3 monthly USS
CVS risk factors should be reduced as appropriate: smoking cessation, improve BP control, commence statin and aspirin therapy & weight loss/increased exercise
Describe the surgical management of an AAA
Should be considered for:
- AAA > 5.5cm
- AAA expanding at >1cm/year
- Symptomatic AAA
Main treatment options are open repair/endovascular repair:
1) Open repair: midline laparotomy/long transverse incision, exposing the aorta & clamping the aortic proximally & iliac arteries distally, before segment is removed & replaced with a prosthetic graft
2) Endovascular repair: introducing a graft via femoral arteries & fixing the stent across the aneurysm
List complications of an AAA
AAA rupture
Retroperitoneal leak
Embolisation
Aortoduodenal fistula
Describe the clinical features of a ruptured AAA
Abdominal pain
Back pain
Syncope
Vomiting
Examination: haemodynamically compromised with a pulsatile abdominal mass & tenderness
Classic triad (50% of patients) – flank/back pain, hypotension & a pulsatile abdominal mass
Describe the management of a ruptured AAA
Immediate high flow O2, IV access & urgent bloods taken with crossmatch
Any shock should be treated very carefully (aim to keep the BP < 100mmHg)
Patient should be transferred to local vascular unit:
- Unstable – require immediate transfer to theatre for open surgical repair
- Stable – require a CT angiogram to determine whether the aneurysm is suitable for endovascular repair
What are varicose veins?
Tortuous dilated segments of vein associated with valvular incompetence
Arise from incompetent valves -> results in venous hypertension & dilatation of the superficial venous system
List causes of varicose veins
Primary – idiopathic
Secondary – DVT, pelvic masses or arteriovenous malformations
List risk factors of varicose veins
Prolonged standing
Obesity
Pregnancy
Family history
Describe the clinical features of varicose veins
Typically present initially with cosmetic issues – unsightly visible veins/discolouration of the skin
Aching/itching
Skin changes, ulceration, thrombophlebitis or bleeding
Examination – varicosities will be present in the course of the great and/or short saphenous veins, clinical features of venous insufficiency (ulceration, varicose eczema, haemosiderin deposition)
List investigations for varicose veins
Gold standard – duplex ultrasound
- Assess valve incompetence at the great/short saphenous veins & any perforators
Describe the non-invasive treatments for varicose veins
Patient education – avoid risk factors
Compression stockings if interventional treatment is not appropriate (need to be worn for the rest of the patients life)
Any venous ulceration – four-layer bandaging
Describe surgical treatment for varicose veins
Should be referred if they meet the following NICE criteria:
- Symptomatic primary or recurrent varicose veins
- Lower-limb skin changes
- Superficial vein thrombosis
- Venous leg ulcer
Treatment options include: vein ligation, stripping & avulsion, foam sclerotherapy & thermal ablation
List complications of untreated varicose veins
Worsen over time
Typical complications seen post-operatively include haemorrhage, thrombophlebitis, DVT, disease recurrence & nerve damage
What is aortic dissection?
Tear in the intimal layer of the aortic wall, causing blood to flow between & splitting apart the tunica intima and media
Aortic dissections from the initial intimal tear can progress distally, proximally/in both directions from the point of origin
List the two classification systems for aortic dissection
Stanford
DeBakey
List risk factors for aortic dissection
Hypertension
Atherosclerotic disease
Male gender
Connective tissue disorders
Bicuspid aortic valve
Describe the clinical features of aortic dissection
Tearing chest pain, classically radiating through to the back
Tachycardia, hypotension, new aortic regurgitation murmur or signs of end-organ hypoperfusion
List differential diagnoses of aortic dissection
Myocardial infarction
Pulmonary embolism
Pericarditis
MSK back pain
List investigations for aortic dissection
Baseline blood tests, ECG
Imaging: CT angiogram, transoesophageal ECHO
Describe the management of aortic dissections
Urgent initial assessment – start high flow oxygen & gain IV access, fluid resus should be done cautiously
Type A dissections – managed surgically in the first instance
Any uncomplicated type B dissections – usually be managed medically
All patients need lifelong antihypertensive therapy & surveillance imaging
List complications of aortic dissections
Aortic rupture
Aortic regurgitation
Myocardial ischaemia
Cardiac tamponade
Stroke or paraplegia
Define acute limb ischaemia
Sudden decrease in limb perfusion that threatens the viability of the limb
Complete/even partial occlusion of the arterial supply to a limb
Describe the aetiology of acute limb ischaemia
1) Embolisation – thrombus from a proximal source travels distally to occlude the artery
2) Thrombosis in situ
3) Trauma, including compartment syndrome
List the signs and symptoms of acute limb ischaemia
Pain
Pallor
Pulselessness
Paraesthesia
Perishingly cold
Paralysis
List investigations for acute limb ischaemia
Routine bloods – serum lactate, a thrombophilia screen & a group and save along with an ECG
Bedside Doppler ultrasound scan, followed by potential CT angiography
If limb is considered salvageable, a CT arteriogram can provide more information regarding the anatomical location of the occlusion & can help decide the operative approach
Describe the initial and conservative management for acute limb ischaemia
Initial management – surgical emergency: start patient on high-flow oxygen & ensure adequate IV access
Conservative management – prolonged course of heparin
Describe the surgical management of acute limb ischaemia
If cause is embolic:
- Embolectomy via a Forgarty catheter
- Local intra-arterial thrombolysis
- Bypass surgery
If cause is thrombotic:
- Local intra-arterial thrombolysis
- Angioplasty
- Bypass surgery
Irreversible limb ischaemia – urgent amputation/taking a palliative approach
Describe the long term management of acute limb ischaemia
Reduction of the CVS mortality risk – promoting regular exercise, smoking cessation & weight loss
Most cases should be started on an anti-platelet agent
Cases resulting in amputation will require OT, PT with long term rehab plan
List complications of acute limb ischaemia
Reperfusion injury
Compartment syndrome
Release of substances from damaged muscle cells – hyperkalaemia, acidosis & significant AKI
Describe chronic limb ischaemia
Form of peripheral arterial disease that results in a symptomatic reduced blood supply to the limbs
Typically caused by atherosclerosis, rarely vasculitis & commonly affect the lower limbs
List risk factors for chronic limb ischaemia
Smoking
Diabetes mellitus
Hypertension
Hyperlipidaemia
Increasing age
A strong family history
Obesity
Physical inactivity
Describe the clinical features of chronic limb ischaemia
Fontaine classification:
- Stage I: asymptomatic
- Stage II: intermittent claudication
- Stage III: ischaemic rest pain
- Stage IV: ulceration or gangrene, or both
Examination: affected limbs will be colder, may be evidence of arterial ulcers, patients will typically have reduced/absent peripheral pulses
What is critical limb threatening ischaemia?
Advanced form of chronic limb ischaemia
Defined in three ways:
1) Ischaemic rest pain > 2 weeks duration
2) Presence of ischaemic lesions/gangrene
3) ABPI less than 0.5
Examination: limbs may be pale and cold with week or absent pulses, limb hair loss, skin changes & thickened nails
List investigations of chronic limb ischaemia
Ankle-brachial pressure index
Doppler ultrasound
CT angiography/MR angiography
CVS risk assessment
Describe the medical management for chronic limb ischaemia
CVS risk factor modification: lifestyle advice, statin therapy, anti-platelet therapy, optimise diabetes control
Local supervised exercise programme
Describe the surgical management of chronic limb ischaemia
Surgical intervention can be offered in suitable patients
- Risk factor modification has been discussed
- Supervised exercise has failed to improve symptoms
Any patients with critical limb ischaemia should be urgently referred for surgical intervention
Two main surgical options:
-angioplasty with/without stenting
-bypass grafting, typically used for diffuse disease/in younger patients
List complications of chronic limb ischaemia
Sepsis
Acute-on-chronic ischaemia
Amputation
Reduced mobility & quality of life
What is deep venous insufficiency?
Chronic disease that can result in significant morbidity
Commonly caused by either DVT or valvular insufficiency, and together with varicose veins
Occurs as a result of the failure of the venous system – valvular reflux, venous hypertension and obstruction
List causes of deep venous insufficiency
Primary – underlying defect to the vein wall/valvular component (includes congenital defects & connective tissue disorders)
Secondary – defects occur secondary to damage (post-thrombotic disease, post-phlebitic disease, venous outflow obstruction & trauma)
List risk factors of DVI
Increasing age
Female gender
Pregnancy
Previous DVT or phlebitis
Obesity
Smoking
Describe the clinical features of deep venous insufficiency
Chronically swollen lower limbs – aching, pruritic & painful
May report venous claudication
Examination: varicose eczema, thrombophlebitis, haemosiderin skin staining, lipodermatosclerosis or atrophie blanche
Varying degree of dependent pedal oedema & may also have venous ulcers
List investigations for DVI
Doppler ultrasound scan, allowing the assessment for the extent of venous reflux
Routine blood tests
Documentation of foot pulses & ABPI
Describe the management of DVI
Early treatment may reduce long-term complications
Conservative management – compression stockings & suitable analgesic control
Surgical management is less successful (some evidence that patients who had deteriorating symptoms had a mild clinical improvement)
Describe the complications of DVI
Swelling, recurrent cellulitis, chronic pain and ulceration
More serious but less common complications – DVT, secondary lymphoedema & varicose veins
Marjolin ulcer – rare type of cutaneous SCC developing at the site of severe/recurrent inflammation
