Oxford Handbook of Clinical Surgery (4 edn)
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Acute limb ischaemia 642
Chronic upper limb ischaemia 644
Chronic lower limb ischaemia 647
Intermittent claudication 648
Critical limb ischaemia 650
Aneurysms 652
Ruptured abdominal aortic aneurysm 654
Vascular developmental abnormalities 656
Carotid disease 658
The diabetic foot 660
Amputations 662
Vasospastic disorders 664
Varicose veins 666
Deep venous thrombosis 668
Thrombolysis 670
Complications in vascular surgery 672
Acute limb ischaemia
Definition
Any sudden decrease in limb perfusion that causes a \ potential threat to viability.
Prevalence
One in 6000 of the population.
Causes and features
Acute thrombosis in a vessel with pre-existing atherosclerosis (60% of cases)
Predisposing factors are: dehydration, hypotension, malignancy, polycythaemia, or inherited prothrombotic states.
Features suggestive of thrombosis are:
Previous history of intermittent claudication.
No obvious source of emboli (see below).
Reduced or absent pulses in the contralateral limb.
Emboli (30% of cases)
Eighty per cent have a cardiac cause (AF, MI, ventricular aneurysm).
Arterial aneurysms account for 10% of distal emboli and may be from the aorto-iliac, femoral, popliteal, or subclavian arteries.
Rarely, acute thrombosis in pre-existing atherosclerosis (see above) will embolize.
Commonest sites of impaction are the brachial, common femoral, popliteal, and aortic bifurcation (‘saddle embolus’).
Features suggestive of embolism are:
No previous history of claudication.
Presence of AF or recent MI.
Rare causes
Aortic dissection, trauma, iatrogenic injury, peripheral aneurysm (particularly popliteal), and intra-arterial drug use.
Symptoms and signs (any cause)
Six Ps:
Pain, pallor, pulselessness, paraesthesia, paralysis, perishingly cold.
Complications
Death (20%).
Limb loss (40%). Severe ischaemia leads to irreversible tissue damage within 6h.
Emergency management
Remember, patients will usually have coexisting coronary, cerebral, or renal disease.
Resuscitation
Give 100% O2.
Get IV access and consider crystalloid fluid up to 1000mL if dehydrated.
Take blood for FBC, U&E, troponin, clotting, glucose, group and save.
Request CXR and ECG (look for dysrhythmias).
Give opiate analgesia (5–10mg morphine IM).
Call for senior help.
Establish degree of urgency
Limb viability assessment. Involve senior help early.
Irreversible. Fixed mottling of skin, petechial haemorrhages in skin, woody hard muscles.
Immediate treatment needed. Muscles tender to palpation/swollen, loss of power, loss of sensation.
Prompt treatment after investigation. Pulseless, pale, cold, reduced capillary refill.
Treatment of all patients
Give heparin (5000IU unfractionated heparin IV bolus and start an infusion of 1000IU/h) if there are no contraindications (e.g. aortic dissection, multiple trauma, head injury).
Recheck APTT in 4–6h.
Aim for a target time of 2–2.5 x the normal range.
Definitive management
Depends on the severity of ischaemia (as above) and there are three broad categories.
Irreversible (non-salvageable limb). Amputation is inevitable and urgent (but not emergency).
Immediate treatment needed (to prevent the systemic complications of muscle necrosis—hyperkalaemia, acidosis, acute renal failure, and cardiac arrest). Consider amputation if ischaemic changes advanced and life-threatening. Surgery to revascularize limb and perform fasciotomies (to prevent or treat compartment syndrome).
Prompt treatment after investigation. Continue heparinization. Angiogram (stop heparin 4h before) or duplex/CT angio to determine cause/location of disease. Thrombolysis, angioplasty, arterial surgery, or combination. Limb may remain viable and functional after period of heparinization alone.
Principles of embolectomy
(see 
p. 746)
Chronic upper limb ischaemia
Key facts
Upper limb ischaemia occurs less frequently than in the lower limb.
Causes
Previous trauma or axillary irradiation, leading to arterial stenosis.
Atherosclerosis. As in the lower limb.
Buerger's disease. Affects small vessels of the hands and feet, principally in smokers, associated with Raynaud's phenomenon, mostly young men, but women may be affected, presents with digital gangrene/ischaemia and may present with acute limb ischaemia in young people.
Subclavian steal syndrome. Stenosis of subclavian artery proximal to vertebral artery origin; arm claudication causes reversed flow in the vertebral artery/diminished hindbrain perfusion (dizziness/syncope).
Takayasu's arteritis. Uncommon in Europe; major arch/upper limb vessels affected.
Thoracic outlet syndrome (see Fig. 18.1).
Term used to cover a spectrum of symptoms resulting from the compression of the neurovascular bundle (NVB) as it leaves the chest to enter the upper limb, in an area enclosed by the first rib, clavicle, and the scalenus anterior muscle.
Presents as a variable combination of neural, arterial, and venous symptoms exarcebated by elevation of the limb, with shoulder, arm, or head pain, and parasthesiae, weakness, or arm claudication. Ninety-five per cent are neurogenic and 5% are arterial or venous manifestations (arm engorgement, swelling with subclavian vein stenosis or thrombosis—Paget–Schroetter syndrome).
Structures involved in thoracic outlet syndrome.
Clinical features
Weakness, cramp or exercise-related pain, and digital ischaemia/gangrene.
Examine bilateral upper limb pulses, BP in both arms (elevated/at sides), wrist Doppler pressures.
Roos test. Arm abducted to 90°, hands up with elbows braced backward, chin elevated, hands serially clenched/opened for 1–2min, positive if pain or weakness in hand or forearm.
Adson's test. Pulse diminishes or absent on elevation/abduction of arm with head turned to contralateral side. Reliability improved by using in conjunction with arterial duplex.
Allen's test. Assesses integrity of the palmar arch and dominant vessel (radial or ulnar).
Tinel's test. For carpal tunnel syndrome.
Diagnosis and investigation
Cervical spine and thoracic outlet X-rays, wrist Doppler pressures.
CT/MRI to look for fibrous bands/ribs and stenoses/occlusions.
Arterial duplex or angiography to diagnose proximal arterial lesions.
Duplex or venography for subclavian vein stenosis or occlusion.
Treatment
Thoracic outlet syndrome
Mild neurogenic problem. Simple analgesia, physiotherapy, and advice on risk factors.
Surgery (supraclavicular or axillary approach) has good results for those with arterial or venous symptoms/complications.
Excision of the first rib/band will improve symptoms in over 90%.
Careful evaluation is needed prior to surgery for pure neurological symptoms, e.g. nerve conduction studies.
Cervical sympathectomy in upper limb disease
Indications
Palmar hyperhidrosis (less effective and infrequently used for axillary).
Buerger's disease/small vessel disease with digital ischaemia.
Approach
Aim is to de-innervate the second and third thoracic ganglia.
Approach is almost universally thoracoscopic and open approaches have been largely abandoned.
Complications
Horner's syndrome.
Pneumothorax.
Haemorrhage.
Compensatory truncal hyperhidrosis.
Frey's syndrome (gustatory sweating).
Axillary hyperhidrosis
Treatment of choice is now subcutaneous botulinum toxin A injections to the axillary sweat glands, repeated as necessary, often 6-monthly.
Several structures can compress the neurovascular structures.
Cervical rib. Articulates with C7.
Scaleneus anterior. Aberrant anatomy or scarring/swelling from trauma.
Costoclavicular ligament.
Chronic lower limb ischaemia
Atherosclerosis is a generalized disease and has a predilection for the coronary, cerebral, and peripheral circulations (see p. 152).
In the lower limb, it may affect the aorto-iliac, femoral or popliteal, and calf vessel levels singly or in combinations (see Fig. 18.2).
Single-level disease usually results in intermittent claudication (IC) and two-level disease in critical limb ischaemia (CLI).
The arterial supply to the leg. Reproduced with permission from Longmore, M. et al. (2007). Oxford Handbook of Clinical Medicine, 7th edn. Oxford University Press, Oxford.
I. Asymptomatic.
II. Intermittent claudication.
III. Rest pain.
IV. Ulcers/gangrene.
Grades III and IV = critical limb ischaemia.
Intermittent claudication
Key facts
Affects 4% of people over 55y, mostly men.
One-third of patients improve, one-third remain stable, and one-third deteriorate.
Four per cent require an intervention and 2% result in amputation.
Risk factors and association. See Table 18.1.
| Risk factors | Associations |
|---|---|
Hypertension | Obesity |
Hyperipidaemia | Diet |
Diabetes mellitus | Sedentary lifestyle |
Tobacco smoking | Gender |
Positive family history | Occupation |
| Risk factors | Associations |
|---|---|
Hypertension | Obesity |
Hyperipidaemia | Diet |
Diabetes mellitus | Sedentary lifestyle |
Tobacco smoking | Gender |
Positive family history | Occupation |
Clinical features
Muscular pain on exercise of the affected limb, worsened with increasing level of exercise, relieved by rest; most commonly, calf.
Differential diagnosis.
Spinal stenosis. Neurogenic pain caused by drop in distal cauda equina blood flow due to exercise, leading to neurogenic pain.
Osteoarthritis, especially hip joint.
Nerve root entrapment, e.g. sciatica.
Popliteal artery entrapment (rare). Due to compression of popliteal artery over medial head of gastrocnemius during exercise. Distal pulses reduced/absent on plantar flexion alone. Treated by surgical release after MRI defines anatomy.
Diagnosis and investigation
Diagnosis is mostly clinical and not based on imaging.
Post-exercise fall in ankle–brachial pressure index (ABPI) can be diagnostic.
Measure BP, serum glucose, cholesterol, FBC.
Imaging only if treatment by intervention planned. Angiography (usually digital subtraction (DSA), may be CT angiogram, or magnetic resonance angiogram (MRA).
Abdominal ultrasound if aneurysm disease suspected.
Treatment
Risk factor modification
Forty per cent of peripheral vascular disease (PVD) patients have significant coronary or cerebral arterial disease; the mainstay of treatment is aggressive risk factor modification. Stop smoking, oral statin treatment, increased exercise, control of BP and serum glucose, antiplatelet therapy.
Endovascular treatment
Angioplasty ± stent. Excellent results in the aorto-iliac segment (>90% success) and good results in the superficial femoral segment (90% success and 60–80% patency at 2y).
Usually performed under LA percutaneously as a day case.
Rarely performed for claudication in the popliteal and tibial segments due to high risk of occlusion.
Most useful in short stenoses/occlusions.
Surgery
Used for short distance claudication, severe lifestyle limitation, and failure/unsuitability of endovascular treatment in the aorto-iliac segments.
Procedures available are:
Aortobifemoral graft. 5y patency of >90%, but carries 5–8% mortality and a risk of impotence. Used for younger patients.
Femorofemoral cross-over bypass graft. Used for isolated unilateral iliac disease; 90% 1y patency.
Common femoral endarterectomy. Used for isolated common femoral disease; good results and a low complication rate.
Femoro-above knee popliteal bypass. 80% 2y patency with vein or prosthetic graft.
Femoro-below knee popliteal bypass. 70% 2y patency with vein graft.
Femoro-distal (below knee) bypass. 5y patency <35%; usually reserved only for critical ischaemia.
Most commonly used for long stenoses/occlusions and combined with endovascular treatment.
Critical limb ischaemia
Key facts
Often progresses to limb loss or progressive tissue loss if it remains untreated.
High risk condition, often occuring in high risk patients with multiple comorbidities.
Clinical features
European consensus statement defines critical ischaemia if there is:
Rest pain for >2 weeks not relieved by simple analgesia; or
Doppler ankle pressure <50mmHg (toe pressures <30mmHg if diabetic).
Tissue necrosis (i.e the presence of gangrene or ulceration).
Rest pain typically worsens at night and during elevation of the limb and is relieved by hanging the limb dependent.
Arterial ulceration cannot reliably be distinguished from other causes.
Diagnosis and investigation
Diagnosis is clinical. Investigation should aim to:
Identify and treat risk factors. Treat BP, stop smoking, optimize diabetes control, reduce cholesterol (statins by choice), use antiplatelet agent (aspirin/clopidogrel by choice).
Identify location and severity of all arterial stenoses involved. May include:
Colour duplex Doppler ultrasound. Zero risk, non-interventional, best for proximal vessels (iliac, common femoral).
Angiography (usually DSA). Interventional, carries risk of arterial injury and renal toxicity of contrast, good for popliteal and distal vessel assessment.
MRA. Low risk.
CT angiography. Low risk (radiation and contrast).
Treatment
All efforts should be made to revascularize if possible (providing the general condition of the patient allows it).
General principle is to deal with most proximal disease first and progress to distal disease only if critical ischaemia still present.
Medical care
Nursing care.
Analgesia. Opiates (e.g. Oramorph®, MST Continus®).
Endovascular treatments
Angioplasty 9 stent proximal disease (aorto-iliac, common femoral, superficial femoral). Less successful in popliteal disease and distal disease.
Surgery
Femoro-distal (e.g. to popliteal, tibioperoneal trunk, or anterior or posterior tibial arteries).
Aorto-iliac bypass (‘anatomical’) or axillo-femoral or femoro-femoral (‘extra-anatomical’) bypass.
Amputation.
Usually below knee or above knee in smoking-related atherosclerosis.
Distal amputations (toe, forefoot, ankle) may be appropriate in diabetic disease.
There is little evidence of benefit from treatment with prostacyclin or sympathectomy (surgical or chemical).
Aneurysms
Key facts
An aneurysm is an abnormal localized dilatation of a blood vessel.
It may be associated with structural abnormalities of collagen and elastin in the vessel wall.
Prevalence of abdominal aortic aneurysm, 4% of men aged 65, increasing with age.
♂:♀, 9:1.
Associated with hypertension, tobacco smoking, and family history (all associated with atherosclerosis).
Pathological features
Types
True aneurysms. Contain all three layers of artery wall. May be fusiform (symmetrical dilatation) or saccular. Underlying cause is usually atherosclerosis-related, but may be associated with infective causes (‘mycotic aneurysm’), Marfan's and Ehlers–Danlos syndromes (collagen and elastin abnormalities).
False aneurysms. Do not contain all three layers of vessel wall and often only lined by surrounding connective tissue or adventitia. Usually secondary to penetrating trauma, including iatrogenic injury (e.g. femoral cannulation, surgery).
Sites
Thoracic, abdominal, and peripheral (iliac, femoral, popliteal, visceral, carotid or subclavian), cerebral ‘berry’ aneurysms.
Clinical features
Thoraco-abdominal
Crawford classification types I–IV (dependent on involvement of descending thoracic/abdominal aorta); managed in specialist centres.
Often asymptomatic.
Different clinical features to thoracic aortic dissection (acute chest pain (angina/MI), back pain, acute aortic regurgitation, or cardiac failure).
Diagnosed by widened mediastinum on CXR or on CT/MRI.
Rupture has high mortality and rare without prior symptoms.
Elective surgery has up to 20% mortality and risk of paraplegia; 10% require dialysis after surgery.
Endovascular stenting is a potential future treatment of choice due to high surgical risks.
Abdominal aortic
Ninety-five per cent start below the origin of the renal arteries (‘infrarenal’).
Fifteen per cent extend down to involve the origins of the common iliac arteries.
Associated with other peripheral aneurysm (e.g. popliteal).
Five to ten per cent are ‘inflammatory’ (have gross connective tissue changes around the aortic wall in the retroperitoneum).
Most are asymptomatic; 40% are detected incidentally (clinical examination, ultrasound, AXR, IVU).
A national ultrasound screening programme exists.
Six-monthly scans for surveillance if size 4–5.4cm (1% per year risk of rupture).
Mycotic aneurysms are rare, but have a high rupture rate.
Risk of rupture and mortality increases with increasing aneurysm diameter.
Surgical intervention is indicated for:
AP diameter >5.5cm in fit individuals.
Rapid increase in diameter on serial surveillance scans, e.g. >0.5cm in 6 months.
Peripheral aneurysms
Iliac. Two per cent of patients >70y. Mostly common iliac and asymptomatic. Rarely palpable and rupture may be missed as acute abdomen or renal colic.
Femoral. Mostly asymptomatic pulsatile groin swelling or pain. May present with lower limb ischaemia.
Popliteal. Many asymptomatic and over half are bilateral. May present with acute limb ischaemia. Aneurysm thrombosis is associated with high risk of limb loss. Prophylactic bypass probably best for symptomatic, embolizing aneurysms.
Carotid. Rare and may be bilateral. May present with neurological or pressure symptoms. May present simply as a pulsatile neck swelling. Rarely presents with rupture. Diagnosis with duplex scan.
Visceral. Account for 1% of all aneurysms. Generally small and asymptomatic until rupture. Splenic artery most common followed by hepatic and renal arteries.
Treatment of abdominal aortic aneurysm (AAA)
Aim is to prevent death as 80% of patients with ruptured AAA will die.
Elective surgery
Open repair by inlay synthetic graft. May be ‘straight’ if aneurysm confined to aorta or ‘bifurcated/trouser’ if there are common iliac aneurysms as well; 3–7% operative mortality.
Laparoscopic repair may offer earlier return to normal function and reduced hospital stay.
Endovascular repairs
Endovascular aneurysm repair (EVAR) with a stent graft. Percutaneous insertion of covered stent to exclude the aneurysmal segment from arterial pressure.
Advantages. Percutaneous technique, reduced early mortality.
Disadvantages. High early re-intervention rate, requires lifelong surveillance, no long-term survival benefits over open repair shown to date.
Ruptured abdominal aortic aneurysm
Causes and features
Associated with hypertension (especially uncontrolled), smoking, family history, and atherosclerosis.
Rare in patients aged <55.
Risk of rupture relates to maximum AP diameter.
Less than 0.5% per year, <4.0cm diameter.
One per cent per year, 4–5.5cm.
Over 3% per year, >5.5cm.
Patients with a ‘contained leak’ with initial haemodynamic stability proceed rapidly to rupture.
Less than 50% of patients with a ruptured AAA reach hospital alive and the overall mortality of the condition may be as high as 75–95%.
Outcome is best in the hands of an experienced vascular team (vascular surgeon, vascular anaesthetist, theatre nursing team, two assistants, and ITU) and a rapid transfer from the emergency department to theatre.
Symptoms
Severe/sudden onset epigastric and/or back/loin pain.
History of sudden ‘collapse’, often with transient hypotension.
May have history of AAA under surveillance.
Signs
Cardinal signs are unexplained rapid onset hypotension, pain, and sweating.
A pulsatile abdominal mass is not always easy to feel (due to pain and abdominal wall rigidity).
Emergency management
Resuscitation
If the diagnosis is seriously considered, call for senior surgical assistance immediately. Transfer to theatre may be required even as resuscitation continues.
‘Permissive hypotension’. Do not ‘chase’ a ‘normal’ systolic BP to reduce the risk of worsening the rupture.
If the patient is critically hypotensive, consider calling a peri-arrest cardiac emergency.
IV access via two large bore cannulae, catheterize, cross-match blood (10U), order FFP and platelets.
High flow O2 via non-rebreathing mask.
Give modest doses of analgesia (morphine 5–10mg).
Alert anaesthetist, theatres, ITU.
Witnessed verbal consent for surgery may be the only practical way and is acceptable here.
Establish a diagnosis
If patient stable and diagnosis uncertain, request contrast CT.
If going to CT, ensure blood is sent for cross-match and IV access has been established before going.
Early management
Ruptures fall into three groups:
Considered not a candidate for surgery. For analgesia and palliative care. Mortality approximates to 100%. The decision is based on age, physiological status, comorbidities, expressed patient preference, family wishes.
Free rupture with collapse and critical condition. All candidates for surgery require emergency transfer to theatre.
Contained leak. May be stable after initial presentation, but likely to progress to free or complicated rupture unless urgently surgically treated.
Principles of surgery for rupture
Go straight to the operating table, not anaesthetic room.
If unstable, muscle relaxation/anaesthesia is not started until patient is prepared/draped and surgical team ready to go.
If haemodynamically stable, central line and arterial line sited while waiting for blood to arrive and surgical team in theatre.
Give antibiotic prophylaxis.
Proximal neck is controlled rapidly with aortic cross-clamping. Full fluid expansion with blood can now safely begin.
Distal outflow of aneurysm is controlled.
The sac is opened and lumbar vessels and inferior mesenteric artery are oversewn to control back bleeding.
Dacron/Gore-Tex® graft is sewn to proximal neck and tested.
Distal anastomosis performed next and tested.
Sequential reperfusion is undertaken accompanied with volume expansion to minimize post-declamping shock. Ideally the systolic BP should be maintained over 85mmHg.
Blood products at this stage may be required to correct coagulopathy (e.g. platelets and FFP).
The sac is closed over the graft to reduce the risk of aortoenteric fistula.
Post-operative care
Transfer to ITU.
Normalize core temperature.
Correct clotting and maintain Hb >10g/dL.
Adequate analgesia and accurate fluid balance.
Attention to cardiac/renal/pulmonary dysfunction.
Complications
Death (overall up to 50% of operated cases).
MI.
Renal failure.
Lower limb embolism.
Gut ischaemia/infarction.
Abdominal compartment syndrome.
Vascular developmental abnormalities
Key facts
Classified broadly into two principal groups.
Vascular tumours (e.g. haemangiomas)
All congenital or idiopathic.
Mostly sporadic, but may rarely be part of a familial syndrome (e.g. von Hippel–Lindau).
Pulmonary haemangiomas, commonly seen in hereditary haemorrhagic telangiectasia, are linked to a deficiency in endoglin (endothelial growth factor).
Vascular malformations
Vascular malformations are histologically categorized as capillary, venous, lymphatic, arteriovenous malformations (AVM), or mixed-in type, depending on the predominant vessel type affected and subdivided into low or high flow (AVMs) varieties.
AVMs have three main causes.
Congenital. Origin/cause unknown.
Traumatic. May follow relatively minor trauma.
Iatrogenic. Following a variety of surgical/interventional procedures.
Clinical features
Congenital AVMs are usually evident at birth and the superficial lesion may only represent a part of the overall abnormality.
Symptoms are dependent on the size, site, and type of vessel affected, and whether the AVMs are high or low flow.
Low flow
May result in considerable cosmetic deformity if large (e.g. Klippel–Trenaunay—port wine stain + ipsilateral hypertrophy, usually limb).
Pain may be a feature due to spontaneous thrombosis of some/all of the venous elements.
Typically, the symptoms are worse after exercise when blood flow is maximized.
High flow
These are largely asymptomatic, but there may be a detectable venous hum or bruit.
They may result in local hyperhidrosis, heat, ulceration, or present with profuse bleeding.
May lead to high output cardiac failure if large and untreated.
Diagnosis and investigation
Colour duplex. Diagnoses lesion, can estimate flow rate, and is useful for follow-up monitoring.
MRI has replaced CT as the best imaging modality and gives both the extent and related anatomy for complex lesions.
Angiography is reserved for high flow lesions when suitability for embolization or surgery is being assessed.
Treatment
Largely conservative.
Congenital AVMs frequently reduce in size with growth of the child and treatment is rarely easy with recurrence common.
Adult AVMs only require treatment for complications or occasionally cosmesis.
Interventional radiology
Percutaneous or intravascular embolization using wire coils or sclerosant under radiological guidance.
Risks include:
Those of percutaneous puncture (infection, false aneurysm formation, inadvertent embolization of adjacent vessels).
Tissue necrosis after successful lesion embolization.
Post-embolization syndrome may occur with pain at the site of embolization, accompanied by malaise, fever and leucocytosis, hyperkalaemia. This usually settles with symptomatic treatment in 24–48h. Due to tissue necrosis and cytokine release.
Surgery
Small lesions may be excised completely.
Obliteration of small superficial venous malformations can be undertaken by direct puncture and injecting a sclerosant such as STD (sodium tetradecyl sulphate).
Open surgery is mostly confined to high flow lesions after preoperative embolization.
Carotid disease
Key facts
A cerebrovascular accident (CVA) or ‘stroke’ is ‘a rapidly developing neurological deficit lasting >24h’.
A transient ischaemic attack (TIA) is ‘an acute episode of focal (cerebral or visual) neurological deficit which resolves within 24h’.
CVA is the third most common cause of death in UK after coronary heart disease and cancer.
Incidence—stroke 200 per 100 000, TIA 35 per 100 000.
Approximately 150 000 CVAs occur in the UK per year and approximately 15% of these are due to atherosclerotic disease of the carotid arteries.
Pathological features
CVA or TIA arises from disease at the origin of the internal carotid artery (ICA) and may be due to platelet or atheromatous embolization from the surface of the plaque (usually after an acute rupture or opening of the plaque surface).
Clinical features
Several clinical variants of a classic CVA are recognized.
Stroke in evolution. Progressive neurological deficit occurring over hours/days.
Completed stroke. The stable end result of an acute stroke lasting over 24h.
Crescendo TIA. Rapidly recurring TIA with increasing frequency, suggesting an unstable plaque with ongoing platelet aggregation and small emboli.
Carotid bruits are detectable in over 10% of patients aged >60, poor correlation with the degree of stenosis/risk of CVA, and may not arise from the ICA.
Patients with a significant stenosis may have no audible bruit.
Neurological features
Depend on the territory supplied by the vessel affected by the embolism, the degree of collateral circulation to that territory, and the size/resolution of the embolism.
Amaurosis fugax. Transient monocular visual loss (described as a curtain coming down across the eye), lasting for a few seconds or minutes—central retinal artery (occlusion can lead to permanent blindness).
Internal capsular stroke. Dense hemiplegia, usually including the face—striate branches of the middle cerebral artery.
Hemianopia. Loss of vision in one half of the visual field.
Prognosis of patients with TIA
Eighty per cent of TIAs are in the carotid territory. The risk of stroke following a TIA is around 18% in the first year, 10% in the first 90 days, and 4% in the first 24h.
Diagnosis and investigation
Colour duplex scan. All patients with TIA/CVA within last 6 months.
MRA or CT angiography (CTA). Used when duplex is inconclusive or difficult due to calcified vessels.
Treatment
Medical management
Best medical therapy is an antiplatelet agent (e.g. aspirin, dipyridamole), smoking cessation, optimization of BP and diabetes control, and a statin (e.g. simvastatin 40mg daily) for cholesterol lowering, irrespective of baseline cholesterol.
Acute thrombolysis in CT-proven ischaemia indicated in specialized units if detected early.
Surgery
Carotid endarterectomy (CEA)
Offered to patients with symptomatic >70% stenosis of the ICA or >50% stenosis if recent TIA/CVA and high ABCD2 risk score (age, BP, clinical, duration, diabetes).
Urgent CEA within 2 weeks now considered for all patients presenting of acute TIA/CVA.
ECST (Europe) and NASCET (North America) trials demonstrated ↓ CVA in the first year following CEA from 18% with best medical therapy to 3–5% with surgery and best medical therapy. No significant benefit to symptomatic patients with <70% stenoses.
ACST (UK) and ACAS (North American) trials have shown some benefit of CEA to asymptomatic patients with >70% stenosis, but the numbers needed to prevent one stroke are 22 patients treated.
Technical details.
Increasingly undertaken under local (LA) block.
Incision anterior to sternomastoid.
Carotid vessels controlled after dissection.
IV heparin prior to trial clamp (if patient awake).
Cerebral circulation protected in 10% of awake patients with a shunt (Pruitt/Javed) (without an intact circle of Willis, there is not enough collateral blood flow from the contralateral carotid).
Shunt in GA patients, depending on surgeon preference and cerebral monitoring (stump pressure of 50mmHg or transcranial Doppler monitoring of middle cerebral artery blood flow).
Patch closure of the arteriotomy common. Eversion endarterectomy technique may avoid the need for a patch.
Post-operatively, close monitoring of BP and neurological state.
Complications.
Death or major disabling stroke, 1–2%.
Minor stroke with recovery, 3–6%.
MI.
Wound haematoma.
Damage to hypoglossal nerve (weak tongue, moves to side of damaged nerve), glossopharyngeal nerve (difficulty swallowing), facial numbness.
The diabetic foot
Key facts
Foot ulceration is the commonest endpoint of diabetic vascular complications. Diabetics are 15 times more likely to undergo major lower limb amputation than non-diabetics.
Causes and features
Key features of the diabetic foot are:
Ulceration.
Infection.
Sensory neuropathy.
Failure to heal trivial injuries.
Ulceration
Risk factors for ulceration include:
Previous ulceration.
Neuropathy (stocking distribution loss and ‘Charcot's joints’).
Peripheral arterial disease (more commonly affects the below-knee calf vessels (trifurcation) which are frequently highly calcified, giving rise to falsely elevated ABPI readings or incompressible vessels).
Altered foot shape.
Callus, indicating high foot pressures.
Visual impairment.
Living alone.
Renal impairment.
Secondary to either large vessel or small vessel arterial occlusive disease or neuropathy or a combination of both.
Forty-five per cent of diabetic foot ulceration are purely neuropathic in origin, 10% are purely ischaemic, 45% are of mixed neuro-ischaemic origin.
Diagnosis and investigation
Pure neuropathic ulceration
Warm foot with palpable pulses.
Evidence of sensory loss, leading to unrecognized repeated local trauma.
Normal or high duplex flows.
Ischaemic/neuro-ischaemic ulceration
Foot may be cool.
Absent pulses.
Ulcers commonly on toes, heel, or metatarsal head.
Secondary infection may be present with minimal pus and mild surrounding cellulitis.
ABPIs may be misleadingly high.
Duplex ultrasound assessment.
Angiography for suspected critical ischaemia.
Treatment
Prophylactic management
Best undertaken in a specialist diabetes foot clinic with multidisciplinary input.
Regular foot inspection for evidence of pressure/ulceration.
Always use appropriate wide-fitting footwear.
Attention to nail care with regular chiropody.
Chiropodist debridement of pressure sites/callus.
Keep away from heat and do not walk barefoot.
Established ischaemic ulceration
Treat local or systemic infection.
Broad-spectrum antibiotics (local guidelines).
Debride obviously dead tissue, including digital amputation.
Drain collections of pus.
Take plain X-ray for signs of underlying osteomyelitis.
Consider revascularization if appropriate.
Angioplasty.
Femoro-distal bypass grafts.
Consider amputation for failed medical or surgical treatment.
Often possible to do limited distal amputations (e.g. transmetatarsal).
May be progressive if disease spreads.
The diabetic surgical patient
Renal disease requires close monitoring of hydration, BP, and renal function.
Metformin needs to be stopped for 48h before angiography to avoid lactic acidosis.
Insulin-dependent diabetics starved for any reason require a sliding scale.
Avoid pressure sores if immobile for any long period with foam leg troughs, heel elevation, and prompt attention to any skin breaks.
Amputations
Key facts
Ninety per cent for arterial disease, 10% for trauma, and rarely for venous ulceration, tumour, or deformity.
Amputation may be a very beneficial treatment for pain, to restore mobility or occasionally, to save a life in trauma or acute limb ischaemia.
Amputation for arterial disease carries a significant mortality and a major morbidity.
The surgical aim is to achieve a healthy stump for a suitable prosthesis and successful rehabilitation.
Amputees are at the centre of a large team, including surgeons, nurses, physiotherapists, prosthetists, occupational therapists, pain team, counsellors, and the family.
Causes and features
‘Dangerous’: life-saving.
Spreading gangrene, e.g. necrotizing fasciitis, gas gangrene.
Extensive tissue necrosis following burns or trauma.
Uncontrolled sepsis (diabetic foot) with systemic infection.
Primary malignant limb tumours not suitable for local excision.
‘Dead’: vascular events.
Critical limb ischaemia with unreconstructable disease.
Extensive tissue necrosis.
‘Damn nuisance’: neuropathic or deformed. Failed, complicated orthopedic surgery with severely impaired gait.
Level
The level is chosen according to:
Lowest level where tissue is viable for healing.
Include as many working major joints as possible to improve function.
Ideally sited between large joints to allow prosthesis fitting.
Above knee. Most will heal, but only young and fit achieve walking with a prosthesis.
Through knee. Fewer heal and some achieve walking.
Below knee. About two-thirds heal and more achieve walking than with above-knee amputations.
Types
Hip disarticulation. Rarely needed, but indicated for trauma or tissue necrosis above high thigh.
Above knee amputation (AKA). Bone transected at junction of upper two-thirds and lower third of femur (12–15cm above knee joint), common in end-stage vascular disease.
Gritti–Stokes (supracondylar AKA). Increasingly popular for bilateral amputees as creates a long stump; especially good for wheelchair-dependent patients.
Through-knee amputation (TKA). Produces a wide stump, which is difficult for prosthesis fit.
Below-knee amputation (BKA). Weight bearing on patellar tendon with good prosthetic fit; good knee function essential.
Skew flap is arguably best technique as it produces a better stump for prosthetic fitting.
Alternative is a posterior flap, which is bulkier and leads to longer time to mobilization.
The tibia is transected 8–10cm distal to the tibial tuberosity and the fibula 2cm more proximally.
Post-operative mobilization is early and temporary limb aids can be used when the wound is sound.
Symes (ankle). Few indications for this in vascular patients and best avoided other than in trauma or diabetics. Prosthetic fitting is difficult and a good BKA is better for walking.
Transmetatarsal. Useful in diabetics or when several toes are gangrenous.
Ray. Used when digital gangrene extends to forefoot, especially useful for diabetics when infection tracks up tendon sheath.
Digital. Usually only for diabetic disease or local trauma.
Treatment
Preoperative care
Restore Hb levels and correct fluid and electrolyte balance.
Ensure good diabetes control.
Cross-match 2U of blood.
Adequate analgesia (epidural may reduce phantom pain).
ECG and CXR.
Optimize cardiac function.
Prophylactic antibiotics to include gentamicin.
Counselling if available.
Post-operative care
Pain control with epidural 9 PCA.
Regular physiotherapy to prevent muscle atrophy or contractures as well as upper limb exercises.
Early rehabilitation on temporary limb aid.
Own wheelchair to aid early mobilization.
Complications
Infection.
Non-healing of stump.
Progression of underlying disease and higher level amputation.
Phantom limb pain. Due to hypersensitivity in divided nerves, can be helped with gabapentin, amitryptyline, or carbamazepine.
Failed mobilization. Early regular analgesia and physiotherapy are important.
Perioperative cardiovascular events in arteriopathic patient.
Vasospastic disorders
Key facts
Many systemic disorders have vasospasm as part of their presentation.
Causes
Rheumatological disease
Often associated with autoimmune disease.
Systemic sclerosis.
Systemic lupus erythematosus (SLE).
Rheumatoid arthritis.
Sjögren's syndrome.
Dermatomyositis.
Polymyositis.
Neurological disease
Reflex sympathetic dystrophy.
Post-traumatic vasospasm.
Vibration white finger (due to exposure to handheld vibrating tools in miners, fitters, builders, platers).
Drug induced
α-agonist treatment (ergotamine).
Idiopathic
Raynaud's disease.
♂:♀, 9:1.
Affects 20–30% of young women, with a possible familial predisposition.
Possibly due to deficiency of a potent vasodilator (a calcitonin gene-related peptide) in the digital nerves, allowing action of unopposed cold stress-induced release of the vasoconstrictor, endothelin.
Features
Vasospasm of any cause results in ‘Raynaud's phenomenon’.
Intermittent attacks.
Initiated with pallor (‘white’). Due to local tissue oligaemia.
Proceeding to cyanosis (‘blue’). Due to venous stasis and deoxygenation.
Followed by rubor (‘red’). Due to reactive hyperaemia as blood flow is restored.
Diagnosis and investigations
Stop all vasoactive treatment 24h prior to assessment.
After local cooling to 15°C, finger Doppler pressures change (fall >30mmHg significant).
Screen. FBC, U&E, urinalysis, thyroid function tests, plasma viscosity, rheumatoid factor, autoantibody screen.
Treatment
Medical
Avoidance of precipitating factors (e.g. outdoor work, smoking).
Electrically heated gloves/socks.
Drug therapy used if symptoms are severe enough to interfere with work/lifestyle.
Calcium channel blockers (e.g. nifedipine 10mg/day increasing to 20mg/day tds) may help, but side effects (headache) may limit use.
Iloprost® (prostacyclin) infusion. Weight-related doses given IV over 48–72h, as tolerated by side effects, for severe pain or impending/actual tissue loss.
Surgical
Sympathectomy. Reserved for patients with failure to respond to medical therapy or secondary complications (e.g. digital ulceration).
Lumbar. Open/laparoscopic/chemical for foot symptoms; effects are mostly short-lived.
Cervical. Mostly now thoracoscopic technique; effects are poor response rate and high relapse rate.
Varicose veins
Key facts
The venous system of the leg comprises of three groups.
Superficial. Long (great) and short (lesser) saphenous systems and tributaries.
Deep. Between the muscle compartments of the legs following the major arteries.
Perforators. Connecting the superficial and deep systems.
Blood passes from the superficial to deep systems via perforators in the calf, and also at the saphenofemoral junction (SFJ), saphenopopliteal junction (SPJ), and mid-thigh perforators (MTP) which contain one-way valves.
Varicose veins are tortuous and dilated segments of veins, associated with valvular incompetence.
Affect 35% of the population.
Males and females almost equal prevalence.
Causes and features
Classification
Thread veins. Intradermal dilated veins, also called ‘flare’, ‘starburst’, or ‘broken’ veins.
Reticular veins. Subdermal 1–2mm diameter veins.
Truncal veins. The long or short saphenous systems.
Varicose veins. Usually arising from the truncal veins.
Venous malformations. For example, congenital (Klippel–Trenaunay syndrome).
Causes
Congenital.
Primary idiopathic (the majority).
Acquired.
Pelvic masses (e.g. pregnancy, uterine fibroids, ovarian mass, pelvic tumour).
Pelvic venous abnormalities (e.g. after pelvic surgery or irradiation, previous iliofemoral DVT).
Clinical features
Symptoms. Pain, aching, itching, heaviness, swelling, oedema, worse at end of day/hot weather/premenstruation, cosmetic concerns.
Complications. Eczema, phlebitis, lipodermatosclerosis, ulceration, or bleeding.
Diagnosis and investigations
General history and examination. Oedema, eczema, ulcers (usually medial calf), lipodermatosclerosis, atrophie blanche, healed ulceration.
Visible standing. Cough impulse, thrill, or saphenovarix at SFJ.
Tap test. Tap downwards over vein from SFJ, impulse should be felt lower down if valves are incompetent (outdated and unhelpful).
Trendelenberg test. For competence of SFJ, MTP, and SPJ (rarely used now Doppler/duplex available).
With the patient supine, elevate the leg, empty veins, apply tourniquet high in the thigh, and ask patient to stand.
Look for venous filling and then release the tourniquet, observing filling of the veins.
If controlled by the tourniquet and then rapidly fill on release, the incompetent valve is above the level of the tourniquet, i.e SFJ.
Then repeat twice with tourniquet just above knee and below knee to test the MTP and SPJ, respectively.
Handheld Doppler (HHD). Listen over SFJ and SPJ and apply calf compression with other hand and listen for reflux lasting 1–2s. Most accurate outpatient method of diagnosis and localization of primary venous reflux disease.
Colour duplex. Gold standard investigation in defining anatomy and incompetence. Can be used for all or selectively for recurrent varicose veins, suspected short saphenous vein reflux, known or suspected previous DVT, mismatch between clinical examination and HHD.
Treatment options
Medical
Microsclerotherapy, laser sclerotherapy for thread and reticular veins.
Foam sclerotherapy for truncal and varicose veins.
Compression stockings.
Surgical
Local ‘stab’ avulsions. Deals with varicosities.
Saphenofemoral or saphenopopliteal disconnection.
Long saphenous vein stripping (effectively avulses all incompetent thigh perforators). Not usually done below the knee due to risk of saphenous nerve injury.
Endovenous laser therapy (EVLT).
Radiofrequency ablation (endoluminal heating).
Subfascial endoscopic perforator ligation (SEPL). For calf perforators.
Indications for treatment
Cosmetic.
For symptoms.
To prevent complications.
To reduce risk of recurrent complications.
Complications of surgery
Bruising (virtually universal).
Recurrence (50% cases at 10y).
Haemorrhage (minor or, rarely, major from damaged femoral vein).
Wound infection (commonest in groin).
Saphenous or sural nerve damage with paraesthesia (20% numbness, 1% dysaesthesia).
Damage to major arteries, e.g. femoral (rare).
Deep venous thrombosis
Causes and features
Occurs due to abnormalities of the vein wall, blood flow, or constituents of blood (Virchow's triad).
May be due to vein compression or stasis (immobility, trauma, mass, surgery, paralysis, long distance travel, including airline travel).
May be due to inherited hypercoagulability (factor V Leiden, protein C, protein S, or antithrombin insufficiency).
May be due to acquired hypercoagulability (surgery, malignancy, polycythaemia, smoking, hormone replacement therapy, oral contraceptive pill (OCP), dehydration).
Severity may vary from isolated asymptomatic tibial/calf thrombosis to severe iliofemoral segment thrombosis with phlegmasia caerulea dolens (venous gangrene).
Clinical features
Clinical manifestations may be absent.
Local features of venous engorgement and stasis.
Limb swelling.
Pain.
Erythema and warmth to the touch.
Mild fever and tachycardia result from release of inflammatory mediators.
Homan's sign. Calf pain on dorsiflexion of the foot is very unreliable and should NOT be performed.
Complications.
PE.
Venous gangrene (phlegmasia caerulea dolens).
Diagnosis and investigations
Aim to confirm presence and extent of thrombosis (to decide on necessity and type of treatment, risk of embolization).
Ascending venography. Rarely used now.
Duplex scan. Investigation of choice; visualizes anatomy, gives extent of thrombosis, and relies on flow of blood and compressibility of vein. Operator-dependent and has lower sensitivity for calf DVT.
VQ scan. If suspicion of PE.
CT pulmonary angiography (CTPA). Most sensitive and specific investigation for suspected PE.
Treatment
Effective prophylaxis is better than treatment (see p. 72).
Conservative measures. Elevation and good hydration.
Uncomplicated DVT. Low molecular weight heparin (LMWH), initially in hospital, may be as an outpatient via a dedicated DVT clinic. Subsequent treatment is with oral anticoagulation with warfarin for 3–6 months.
Complicated DVT. Initially with IV unfractionated heparin (UFH) or LMWH whilst converting to oral anticoagulation with warfarin.
Thrombolysis or surgical thrombectomy are reserved for severe thrombosis with venous gangrene.
Vena caval filter. Percutaneously inserted via jugular or femoral vein into infrarenal IVC to catch thromboemboli and prevent PE.
Used for patients with recurrent PE despite treatment, at risk of major central PE and anticoagulation contraindicated, requiring urgent or major surgery (so cannot be anticoagulated), major DVT with concomitant CNS injury or major fractures.
Risks include air embolism, arrhythmias, pneumo/haemothorax, IVC obstruction, renal vein thrombosis, retained, misplaced, migrating, eroding, embolizing or broken catheters/sheaths, complications of insertion (e.g. bleeding).
Chronic venous insufficiency
Severe forms are often secondary to extensive or recurrent lower limb DVT (post-phlebitic limb).
Clinical features
Leg/ankle oedema.
Varicose/eczema, pigmentation, lipodermatosclerosis.
Venous ulceration (medial more common than lateral).
Venous claudication (rare).
Assessment
Many (80%) venous disease alone, others mixed with arterial disease.
History of proven/suspected DVT is common.
Ulcers present in many patients and 70% are recurrent.
Investigations
Handheld Doppler pressures (e.g. arterial disease ABPI <0.85).
Venous duplex to detect DVT or deep venous incompetence and to look for superficial venous disease.
Treatment
Elevation, bed rest, and elevation of foot of bed.
Four layer bandaging (Charing Cross) if ulceration present and ABPI >0.85. Up to 75% ulcer healing at 12 weeks.
Graduated compression hosiery (when ulcers healed).
Class I. Ankle pressure <25mmHg, prophylaxis.
Class II. Ankle pressure 25–35mmHg, marked varicose veins and chronic venous insufficiency.
Class III. Ankle pressure 35–45mmHg, chronic venous insufficiency.
Class IV. Ankle pressure 45–60mmHg, lymphoedema.
Surgery
Skin grafts (split skin and pinch skin grafts).
Ulcer bed clearance of slough/infection (physical, chemical, larval—maggots, vacuum debridement).
Surgery for superficial venous disease only (as for varicose veins surgery).
Role in mixed superficial and deep venous disease is controversial.
May need arterial revascularization.
Thrombolysis
Key facts
Introduced over 30y ago.
Use diminishing over last 5y due to up to 5% risk of major haemorrhage or stroke.
Usually administered as a low dose intra-arterial infusion or as an adjunct to surgery intraoperatively.
Agents
Urokinase. Expensive, rarely used in UK other than for dialysis catheters.
Streptokinase. Cheap, but has systemic effects and 27min half-life. Has side effects of anaphylaxis, fever, and antibody resistance, limiting repeated use. Widely used for treatment of MI.
Recombinant tissue plasminogen activator (tPA). Powerful clot affinity, lower systemic effects and bleeding complications, and half-life <6min.
Indications
Treatment of acute limb ischaemia with viable limb due to in situ thrombosis or embolism not suitable for surgery or extensive distal (calf) thrombosis.
Treatment of acute surgical graft complications, e.g. prosthetic graft occlusion <2 weeks duration.
Treatment of residual thromboembolic disease during reconstructive surgery (intraoperatively).
Thrombosed popliteal artery aneurysm (allows clearance of distal calf vessels).
Venous thrombosis (axillary/femoral) may be treatable by venous or arterial lysis, but need to balance risk of haemorrhage and stroke.
Regimen
Administered via arterial catheter and simultaneous heparin via catheter sheath.
Regular clinical assessment and coagulation checks are needed with clear protocols. Half-hourly temperature, pulse rate, and BP as well as foot observations.
Regular review with repeat angiography.
Increased complication rate after 24–36h of infusion.
Contraindications
Increased risk of bleeding (haemorrhagic disorders, current peptic ulcer, recent haemorrhagic stroke, recent major surgery, or multiple puncture sites).
Evidence of muscle necrosis as may result in reperfusion syndrome and multi-organ failure.
Urgent cases because threatened limb viability if lysis takes too long to work.
Complications
Minor. Allergic, catheter problems (leak, occlusion), bruising, 15% risk of minor haemorrhage.
Major. Five per cent risk of major haemorrhage or stroke.
Complications in vascular surgery
Complications may occur in the perioperative, early, or late post-operative periods. In general, vascular patients are older and have increased cardiac, cerebral, pulmonary, and renal comorbidities. This is due to the associated risk factors of hypertension, diabetes mellitus, hypercholesterolaemia, and smoking.
General
Cardiac
(see p. 106)
Atherosclerosis is a systemic disease with a predilection for the cerebral, coronary, peripheral arterial, and renal circulations.
Forty per cent of patients with PVD have at least two other circulations affected.
Twenty per cent of patients undergoing non-cardiac vascular surgery have evidence of silent myocardial ischaemia.
Seventy per cent of the mortality associated with aortic surgery is attributable to perioperative cardiac dysfunction.
Pulmonary
(see p. 108)
Worsened by pre-existing pulmonary disease, smoking, and obesity.
Ensure adequate analgesia with PCA or epidural and good physiotherapy and early mobilization.
Haemorrhage
(see p. 102)
Perioperative. Bleeding from uncontrolled blood vessels.
Post-operative. May be due to breakdown of vascular anastomoses. Recognized by acute hypotension, shock, abdominal swelling, and pain. Return to the operating theatre.
Renal failure
Many vascular patients have pre-existing renal impairment due to renovascular disease, drug treatments, or surgery.
Acute perioperative risks include dehydration, use of IV contrast, use of NSAIDs, or nephrotoxic antibiotics.
Infection
Wound infections reduced by prophylactic antibiotics.
MRSA easy to prevent (hand hygiene), but difficult and expensive to treat.
Clostridium difficile enteritis (hand washing prevents) associated with antibiotic mis/overuse in inpatients.
Specific
Post-declamp shock (reperfusion syndrome)
Ischaemic extremities during surgery reperfused into circulation.
Features of acute haemodynamic instability due to release of toxins (potassium, myoglobin).
Prevented by controlled gradual reperfusion with fluid resuscitation and vasopressor treatment to maintain a good perfusion pressure to the coronary, cerebral, and renal circulations.
Mannitol often used as a free radical scavenger.
Trash foot
Embolization of debris to the skin of feet or buttocks after aorto-iliac surgery.
Avoided by careful surgical technique and distal vessel clamping first.
Swollen limb
Most are due to reperfusion injury of previously ischaemic limbs.
Consider investigations for DVT.
Lymphocoele
Occurs mostly after groin surgery.
Presents as a fluctuant, non-tender swelling.
Most will settle spontaneously, although larger collections may be aspirated under STRICT aseptic conditions.
Rarely require further surgery to oversew the lymphatics.
Gut ischaemia
May follow aortic surgery (ischaemic colitis); 2.5% after ruptured AAA surgery and <1% of elective aortic aneurysm surgery due to loss of gut blood supply.
May present as vague abdominal pain or bloodstained diarrhoea.
Sigmoidoscopy usually confirms the diagnosis.
If there is no evidence of peritonitis, then fluids to rehydrate and close observation are required.
If there is evidence of peritonitis, then an urgent laparotomy is needed with resection of the ischaemic bowel.
Impaired sexual function
Due to damage to the peri-aortic or hypogastric plexus and underlying vascular disease of the blood supply to the pelvis.
Late complications
Graft occlusion
Early failure (<30 days). Technical cause; recognized by acute deterioration in symptoms or acute limb ischaemia.
Late failure. Usually due to intimal hyperplasia, continued smoking, or disease progression; recognized by progressively worsening symptoms, falling ABPI, or duplex scanning showing graft stenosis.
False aneurysm
Usually secondary to infection or occasionally, fatigue of graft material (long-term). Further surgery is usually required.
Graft infection
Mostly gut bacteria or coagulase-negative staphylococci; MRSA an increasing problem.
Can be minimized by prophylactic antibiotics, meticulous technique, and infection control policies on vascular wards.
Once infected, the graft usually has to be removed and alternative reconstruction required.
Recognized by signs of low grade or chronic sepsis (↑ CRP, ↓ Hb, fever).
Aortoenteric fistula
Rare, usually fatal if not treated.
Usually follows aortic grafting. Can be years later.
Presents with small, often overlooked, GI bleeds or anaemia.
Diagnosis difficult. CT can be helpful; often all other causes of bleeding are negative.
Treatment by open surgery or endovascular exclusion and antibiotics.
