Vascular 2 Flashcards
What is the Fontaine Classification?
Fontaine: Outlines the progression of chronic limb peripheral arterial disease 1 - asymptomatic 2 - intermittent claudication 3 - ischaemic rest pain 4 - ulceration/gangrene
What ABPI values suggest PAD?
> 1.2: may indicate calcified, stiff arteries. This may be seen with advanced age or PAD
1.0 - 1.2: normal
0.9 - 1.0: acceptable
< 0.9: likely PAD. Values < 0.5 indicate severe disease which should be referred urgently
What does ABPI >1.2 signify?
May be a false negative due to calcification giving abnormally stiff vessels
More common in diabetics
What are the causes of ABPI >1.2?
Atherosclerosis: by far the most common
Fibromuscular dysplasia: non-inflammatory artery wall thickening
Buerger’s disease (thromboangiitis obliterans): acute inflammation and thrombosis of lower limb arteries/veins, common in young, heavy smokers
What are the symptoms of intermittent claudication?
Ischaemic ‘cramping’ muscle pain on walking, relived by rest
Pain reproducible at a similar level - ‘claudication distance’
most commonly in the calf, suggesting femoral disease
Pain in the thigh/buttock suggests ileal disease, which will often be bilateral
Ask about penile function - ‘Leriche syndrome’
What are the signs of intermittent claudication?
Absent pulses Cold, pale legs Atrophic, hairless and shiny skin Buerger's angle: <20 degrees: look for reactive hyperaemia arterial ulcers
What is ischaemic rest pain indicative of?
Critical lower limb ischaemia
What is the presentation of ischaemic rest pain?
Classically occurs at night in the forefoot - due to the decreased effects of gravity and decreased BP
Pain wakes a patient from sleep
They can gain relief by swinging the leg over the side of the bed or walking on a cold floor
History of intermittent claudication and signs of arterial insufficiency in the leg
Why are arterial ulcers more likely to be formed if there is ischaemic rest pain?
More likely to form from minor injuries as healing is impaired and infection of these ulcers can lead to rapidly spreading gangrene (more common in those with co-morbid diabetes)
What investigations are done for intermittent claudication/ischaemic rest pain?
Bloods: FBC (rule out anaemia: HbA1c, lipids
ABPI is the most important initial investigation
Management depends on ABPI result and level of symptoms
What is the management if ABPI >0.6?
Progression from intermittent claudication to critical ischaemia is unlikely, so conservative measures are used
Progression more likely in diabetics, and those with a claudication distance <50m
More aggressive treatment may be considered in these patients
What are the conservative measures for peripheral arterial occlusive disease?
Lifestyle changes: stop smoking, exercise to the point of claudication to improve collaterals, weight loss
Raising the heel of shoes (decreased calf work)
Foot care to prevent minor trauma leading to ulceration etc
Optimisation of blood pressure (avoid beta-blockers) and diabetes
Started on anti platelet (clopidogrel and a statin (atorvastatin)
What is the management if ABPI <0.6?
Highly symptomatic - leading to a loss of function, or conservative measures ineffective PTA surgical reconstruction sympathectomy amputation
What is PTA?
Percutaneous transluminal angioplasty
Balloon inflated in narrowed segment, good for short stenosis
Endoluminal stents may be used to keep the segment patent
What surgical reconstruction procedures are used for peripheral arterial occlusive disease?
Bypass grafting may be required in more extensive disease if distal arteries are not diseased, with saphenous vein harvests common
What are the indications for amputation?
May relieve intractable pain, and prevent death from septicaemia
Level of amputation must be high enough to ensure healing but above knee amputation has worse rehabilitation than below knee
Gabapentin started pre-op may help phantom limb pain
What is the effect of diabetes on peripheral arterial disease?
Diabetics are at a greater risk of developing peripheral arterial disease and presentation can be different due to the presence of peripheral neuropathy, which has three main effects:
sensory neuropathy
autonomic neuropathy
motor neuropathy
How does sensory neuropathy affect peripheral arterial disease?
reduces protective reactions to minor injury and reduces awareness of symptoms of infections / ischaemia
How does autonomic neuropathy affect peripheral arterial disease?
A lack of sweating leads to development of dry, fissured skin allowing entry of bacteria
How does motor neuropathy affect peripheral arterial disease?
Wasting of the small muscles of the foot - leading to loss of the arches and development of abnormal pressure areas in the feet
What is the difference between peripheral neuropathy and ischaemic rest pain?
Stabbing pains in feet
red and warm feet - STRONG pulses
Unlikely to be relieved by swing foot over bed/walking on a cold floor
How are diabetics with peripheral arterial disease likely to present
Can be severely ischaemic, but painleess
More likely to present with ulceration, due to the combination of sensory, autonomic and motor neuropathy combined with poor arterial supply to heal ulcers
This can rapidly progress to gangrene
What is gangrene?
Dead tissue, normally colonised by bacteria
Wet gangrene: infected with proliferating organisms
Dry gangrene: colonised, but organisms are not proliferating
Presents in the toes first, progressing proximally to line where there is adequate oxygenation
What is the appearance of gangrene?
Blue-purple in colour, with progressive blacking of tissues and numbness
What is the presentation of gangrene in diabetics?
In diabetics, usually presents earlier - affecting smaller areas e.g. a single toe, or ischaemic area of the heel
This is due to the more extensive atherosclerotic changes of smaller vessels seen in diabetes
Which area is most usually affected by intermittent claudication?
Calf - as it is the femoral Artery that most commonly becomes atheromatous
Why does intermittent claudication occur?
At rest, the oxygen requirement of muscles is met by the collateral system of the profonda femoris (deep femoral artery that joins the popliteal artery just below the knee)
Exercise produces a demand that cannot be met and the calf muscles become ischaemic
By resting, the collateral system can once again supply enough blood for the pain to be relieved
What are the ddx of intermittent claudication?
Spinal stenosis
venous claudication
What is the cause of spinal stenosis?
Spinal osteophyte formation
symptoms are due to lumbar nerve roots / cauda equina compression
What are the features of spinal stenosis?
features similar to intermittent claudication, but pain is relieved by sitting down or flexing the spine rather than standing still
Symptoms vary day to day
associated with numbness/tingling and pulses will be present
Diagnosis confirmed with MRI
What is the cause of venous claudication?
Obstruction of the venous outflow of the leg (ileofemoral occlusion)
Pain comes on gradually from the moment walking starts
Pain affects the whole leg, and is bursting in nature
leg elevation can relieve the pain
There are signs of venous disease and often a history of DVT
What are the other causes of leg pain?
intermittent claudication spinal stenosis venous claudication musculoskeletal (OA/RA) peripheral neuropaty popliteal artery entrapment - young patients with normal pulses
What proportion of leg ulcers are venous?
85%
many also have an arterial element
what is the cause of venous leg ulcers?
occur due to venous hypertension and oedema causing subcutaneous hypoxia
an episode of minor trauma then precedes development of an ulcer as the skin is poorly nourished and cannot heal
Secondary infections common
What is the cause of an arterial ulcer?
10% ulcers are entirely the consequence of arterial disease
occur after an episode of minor trauma, with inadequate healing due to poor arterial supply
Arterial vs venous ulcer: history
arterial: IC, IHD, HTN, DM
venous: DVT, varicosities, obesity
Arterial vs venous ulcer: pain
arterial: very painful
venous: rare
Arterial vs venous ulcer: site
arterial: lateral malleolus, also toes/heels
venonus: medial malleolus and gaiter area
Arterial vs venous ulcer: progression
arterial: rapidly increasing but painful so present small
venous: slowly increasing but can become very large
Arterial vs venous ulcer: oedema
arterial: uncommon
venous: common
Arterial vs venous ulcer: skin appearance
arterial: shiny, hairless, atrophic nails
cool and pale
venous: signs of venous insufficiency, red and warm
Arterial vs venous ulcer: ulcer appearance
arterial: small and punched out
venous: shallow with a flat margin
How do diabetic ulcers occur?
occur due to the three neuropathy processes described above, which are compounded by arterial disease and infection
Usually occur on the foot with a classic unbalanced looking foot with ulcers on the pressure area
How are ulcer causes initially investigated?
Consider diabetes / vasculitic causes
Perform ABPI / Duplex USS (can show arterial and venous disease
What are the conservative measures for ulcers?
Lifestyle changes in ?arterial disease
avoid prolonged standing in suspected venous disease, tightly control DM
What is the management if ?venous disease and ABPI >0.8?
4-layer compression bandaging is the gold standard initial treatment
Leg elevation important to help decrease the venous hypertension
Once healed, long term compression stockings advised
If duple shows superficial disease only - treatment of varicose veins may resolve the venous outflow issues, to allow ulcer healing
What is the manamgent if ABPI <0.8?
Refer to GP for CV risk modification
Refer to vascular surgery for investigation of arterial disease
What is the management for mixed arterial/venous ulcers?
Arterial problem should be surgically corrected, and then compression can occur
Arterial ulcers are signs of critical limb ischaemia and thus are treated surgically if the patient is fit
Only swab if there is signs of infection
Biopsy if the ulcer looks atypical!
What are the sx of chronic small bowel ischaemia?
Severe post-prandial colic: (gut claudication)
PR bleeding
Weight loss
Malabsorption
How is small bowel ischaemia visualised?
Angiography - treated with angioplasty
What are the sx of large bowel ischaemia?
Presents with ischaemic colitis Left sided abdominal pain Bloody diarrhoea Pyrexia, tachycardia leucocytosis
Can progress to gangrenous colitis with peritonitis an shock
What are the investigations for large bowel ischaemia?
Barium enema /AXR: thumb printing
MR angiography: diagnostic
What is the management of large bowel ischaemia?
Conservative: most recover with fluids and antibiotics
Percutaneous transluminal angioplasty and stenting for severe cases
What are the causes of renal artery stenosis?
80% due to atherosclerosis
10% due to fibromuscular dysplasia
What is the presentation of renal artery stenosis?
Resistant HTN
Worsening renal function after ACEis (if bilateral)
Sudden onset pulmonary oedema (with normal LV function)
renal bruits on examination
How is renal artery stenosis diagnosed?
Renal USS: small affected kidney, Doppler showing disturbance in renal flow
CT/MR angiography can then confirm diagnosis
Renal angiography gold standard
What is the treatment of renal artery stenosis?
Medical: ACEi with statins and anti-platelets
Contraindicated in bilateral disase
surgical management: angioplasty and stenting
thought to be equally effective as medical management
What are the causes of acute arterial occlusion?
Embolus (40%)
Thrombus (40%)
Trauma (including during angioplasty
What is Virchow’s triad?
What is the meaning?
thrombus is Predisposed to by Virchow’s triad:
Endothelial dysfunction: trauma, inflammation or atheroma
Changes in blood flow: stasis or slow blood flow
Changes in blood coagulability: inflammatory response / congenital causes
What is embolic occlusion?
Occlusion of a vessel by a mass of material transported in the blood stream, most commonly fragments of thrombus (thromboemboli)
Where might thromboemboli arise from?
Left atrium in AF
left ventricle post MI
heart valves in endocarditis
mural thrombi from an AAA
What are the clinical features of the acutely ischaemic limb?
Six Ps: Pulseless Pallor Painful Perishingly cold Paralysis Paraesthesia
(final two indicate a threatened limb, as well as pain on passive movement or squeezing the calf)
What are the indications of a ‘non viable limb’
Fixed staining (colour changes that are non-blanching of the leftest) and rigid muscles
What is the maximum time to re-establish flow in an acutely ischaemic limb?
6 Hours
What is the management of the acutely ischaemic limb?
A-E
IV heparin as soon as the diagnosis is made, to prevent propagation of the clot
Assessment of the limb - If block seems to be resolving, collateral circulation may negate the need for surgery/thrombolysis may be used
Urgent CT angiogram - can help differentiate between thrombotic/embolic causes
Embolus management - open embolectomy
interval investigation to the underlying cause
thrombosis management - thrombolysis to restore patency
interval angioplasty to treat underling disease
How is an open embolectomy performed?
Using a Fogarty catheter
local thrombolysis if the clot has propagated beyond the original embolus
What is the management if the leg is not thought to be viable?
AMPUTATION
What are the important things to observe for post-operatively?
Reperfusion injury
Compartment syndrome
What is a reperfusion injury?
inflammation and oxidative damage when blood flow is restored to a tissue after a long period of anoxia
Can lead to oedema and comportment syndrome
Embolus vs thrombosis onset?
embolus - sudden onset, very severe symptoms due to lack of collaterals
Thrombosis - insidious onset, less severe symptoms as advanced collateral
Embolus vs thrombosis source?
embolus: normally identifiable, e.g. AF/AAA
thrombosis: no obvious course
Embolus vs thrombosis pulses?
Embolus: previously normal, normal contralateral pulses
thrombosis: long-standing decreased pulses bilaterally
Embolus vs thrombosis history
embolus: no history of arterial disease
thrombosis: previous history of IC, stroke, MI etc
What investigations are used in suspected arterial bleeds?
Angiography or contrast CT
What is the management of transection?
Haemorrhage can normally be arrested by applying pressure to gauze swabs
If there is significant ischaemia, vascular grafting/repair may be needed
If the main artery and vein have been severed, the vein will always be repaired first to allow venous drainage before repairing the artery
What is an arterio-venous fistula?
acquired communication between an artery and vein
What are the causes of an AVF?
penetrating trauma: most common
erosion of aneurysm into a neighbouring vein
iatrogenic: patients on haemodialysis
Describe how a AVF occurs
there Is shunting from the high pressure arterial side to the Low pressure venous side
increased flow leads to dilation, thickening and tortuosity of the vein ( ‘arterialisation’ ) and the turbulent flow gives a palpable thrill
What is the effect of an AVF on peripheral venous and arterial pressures?
Peripheral venous pressures are increased, leading to swelling, varicosities and sometimes venous ulceration in the limb
Peripheral arterial resistance decreases, thus the heart responds by increasing stroke volume, eventually leading to left ventricular dilation and heart failure
What might patients with AVF (non iatrogenic) complain of?
limb heaviness, aggravated with dependency and relieved by elecation
Pain also common
What examination findings will there be if pt has an AVF?
Oedema and prominent veins with an audible murmur or palpable thrill (can be pulsatile)
rarely - signs of CCF if the communication is very large
Blood gas will show higher oxygen sats distal to the AVF and also there will be consumptive coagulopathies due to the changes in blood flow activating the clotting cascade
Duplex USS / Contrast CT can confirm
What is the management of AVF?
surgery / interventional measures
What is Raynaud’s phenomenon?
General term describing episodic digital vasospasm in the absence of an identifiable associated disorder
What is Raynaud’s syndrome?
Raynaud’s phenomenon occurring secondary to another condition
What are the secondary cause of Raynaud’s syndrome?
Connective tissue disorders: systemic sclerosis, mixed connective tissue disease, SLE, Sjogren’s syndrome, polyarteritis nods
Macrovascular disease: atherosclerosis, thoracic outlet syndrome, Buerger’s disease
Occupational trauma: vibration white finger, repeated extreme cold or chemical exposure
Drugs: beta blockers, cytotoxic drugs
Others: malignancy, AVF
How does Raynaud’s phenomenon occur?
Cold exposure or emotional stress
What are the three phases of Raynaud’s phenomenon?
Pallor: due to digital artery spasm
Cyanosis: due to accumulation of deoxygenated blood
Rubor: erythema due to reactive hyperaemia
As the fingers return to normal, there may be numbness, a burning sensation and severe pain
Attacks are usually <45 mins in duration but can last for hours with very severe cases involving tissue infarction and loss of digits
What are the features suggesting a secondary cause of Raynaud’s?
Dilated nail fold capillary loops (seen with an ophthalmoscope)
Presentation in early childhood, or over the age of 30
Asymmetrical distribution
Male sex
What baseline investigations should be done for raynauds?
FBC: polycythaemia, malignancy U+Es: renal impairment / dehydration Coagulation: hepatic dysfunction Glucose: DM TFTs ANA/RF/APA: autoimmune screen if suspecting secondary cause
What is the management of Raynaud’s?
Keep extremities warm (heated gloves etc)
Stop smoking and stop exacerbating drugs e.g. B-blocker/OCP
Medical: nifedipine
losartan/prazosin/fluoxetine first line
Sympathectomy may help those with severe disease but may be short lived
