CARDIOVASCULAR DISORDERS

41 Managing lower limb arterial

insufficiency, the diabetic foot
and major amputations
CHRONIC LOWER LIMB ISCHAEMIA. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 496 THE DIABETIC FOOT. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 505
Intermittent claudication. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 496 Management of neuropathic foot complications . . . . . . . . . . . . . . . . . . . 506
Severe ischaemia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 497 LOWER LIMB AMPUTATION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 508
Managing lower limb ischaemia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 497 Level of amputation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 508
ACUTE LOWER LIMB ISCHAEMIA . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 502
Principles of managing the acutely ischaemic limb. . . . . . . . . . . . . . . . . 505

INTRODUCTION statins, optimal blood pressure treatment and diabetic control,

The specialty of peripheral vascular surgery has evolved over smoking cessation, exercise) is often more important than
the last 50 years, with increasing cooperation between sur- dealing with the leg problem.
geons and interventional radiologists, ultrasonographers and Chronic lower limb arterial insufficiency can be asympto-
vascular physicians. Peripheral atherosclerosis is well recog- matic or picked up on screening (e.g. for diabetic foot), or
nised as a marker for coronary and cerebrovascular atheroscle- cause mild to severe intermittent claudication or rest pain/
rosis (approximately 30% 5-year mortality in intermittent ulceration/distal gangrene.
claudication), and best medical therapy (antiplatelet agent,

CHRONIC LOWER LIMB ISCHAEMIA

risk of developing PAD, depending on gender. The presence
INTERMITTENT CLAUDICATION of coexisting risk factors increases the risk exponentially, par-
SYMPTOMS ticularly cigarette smoking. Polycythaemia is a rarer causative
factor. There is also some evidence of thrombotic risk factors
Intermittent claudication is the usual presentation of lower clustering in healthy male relatives of men with PAD.
limb peripheral arterial disease (PAD). It more often affects
men and is present in 5% of the male population over 65. PHYSICAL SIGNS OF INTERMITTENT CLAUDICATION
The patient experiences cramping pain in leg muscles on
Peripheral pulses are usually absent or reduced on the
walking which is relieved by rest. The calf is involved first
affected side but local examination is otherwise unremarka-
because the superficial femoral artery is the most commonly
ble. The dorsalis pedis, posterior tibial and popliteal pulses
affected with atherosclerosis. If arterial disease is also more
are almost invariably absent; the femoral pulse is weak or
proximal (i.e. iliac artery), the pain may ascend to the thigh
absent in about 30%. Trophic (nutritional) skin changes are
or the buttock if walking continues. The distance before onset
rarely present. General systematic examination should seek
of pain is often reproducible and is reduced by walking uphill.
other signs of atherosclerosis likely to bear on management
Symptom onset is usually insidious and often attributed to
and prognosis.
musculoskeletal causes. The patient seeks medical advice only
when symptoms have lasted a few months without improv- NATURAL HISTORY OF INTERMITTENT
ing. Risk factors for intermittent claudication are as for any
CLAUDICATION
atherosclerotic disease and patients often have ischaemic
heart disease (angina, previous MI, coronary artery bypass The fate of the leg
grafting) or cerebrovascular disease (previous stroke or tran- The clinical course of intermittent claudication is largely
sient ischaemic attack). Intermittent claudication is about benign. Three quarters of patients either stay the same or
twice as common in diabetic patients as in non-diabetics. improve their walking distance. Only 510% with claudica-
Nearly all have smoked cigarettes at some stage. The severity tion will need endovascular or surgical intervention by 5
of PAD increases with the number of cigarettes smoked, with years for worsening claudication or severe limb ischaemia.
heavy smokers having a four-fold risk of claudication. Non- Only 2% with claudication progress to needing major ampu-
smokers affected invariably have other risk factors; most are tation. Smoking increases the risk of reconstructive surgery or
hypertensive, with a two and a half to four-fold age-adjusted major amputation. Patients with diabetes have a higher risk
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 Managing lower limb arterial insufficiency, the diabetic foot and major amputations
of major amputation in part due to small and distal vessel
atherosclerosis.
The fate of the patient
Lower limb PAD is a marker of systemic atherosclerosis. The
severity of PAD (as estimated by ankle brachial pressure index
(ABPI) is associated with increasing coronary artery disease
and the overall mortality rate. Some 10% of claudicants have
a non-fatal cardiovascular event (myocardial infarction or
stroke) within 5 years and the 5-year mortality rate is 30%
with being cardiovascular. Smoking increases mortality
rates amongst claudicants by 1.53.0 times.
SEVERE ISCHAEMIA
Severe lower limb ischaemia most commonly presents without
claudication but sometimes manifests after a period of dete-
riorating claudication. In general, these patients are older and
less physically active than typical claudicants.
The first manifestations of severe ischaemia develop in the
foot and include:
l Intolerable rest pain initially at night, later becoming
continuous during the day
l Trophic skin changesatrophic shiny red skin of the leg;
ischaemic ulcers between toes, in foot pressure areas or
on the leg
l Patchy necrosis of the toes or skin of the foot
l Positive Buergers test
l Failure of trivial injuries to heal
l Extreme vulnerability of feet to pressure sores
If untreated, a very small proportion improve and lose their
pain, but most smoulder on with intolerable pain or progress
to necrosis. Once the deep tissues of the foot become necrotic,
local defences are overwhelmed and infection spreads widely
in vulnerable ischaemic tissue, especially in diabetics. This
causes wet gangrene and, ultimately, death from sepsis and
multi-organ dysfunction. This sequence rarely runs its course
since rest pain is so severe and signs of sepsis so obvious
that vascular reconstruction or amputation becomes
unavoidable.
Critical ischaemia
Critical ischaemia occurs when arterial insufficiency is so
severe that it threatens the viability of foot or leg. This is for-
mally defined by a European consensus document as follows:
persistently recurring rest pain requiring regular analgesia for
more than 2 weeks, or ulceration or gangrene affecting the
foot, plus an ankle systolic pressure of less than 50mmHg
(Note: in diabetics, absent ankle pulses on palpation replace
pressure as calcification may artificially elevate pressures).
MANAGING LOWER LIMB ISCHAEMIA
INVESTIGATION OF CHRONIC LOWER LIMB
ARTERIAL INSUFFICIENCY
How far to investigate a patient with symptomatic ischaemia
depends on the clinical picture (claudication vs. critical ischae-
mia) and, in claudication, whether it seriously impairs quality
of life. Note that patient-reported claudication distance is
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41
unreliable and alone, is not an indication for treatment. All
patients with critical limb ischaemia should be considered for
revascularisation.
The ankle brachial pressure index (ABPI)
All claudication patients should have resting ankle systolic
pressures measured in clinic to confirm the diagnosis, plus a
full blood count to exclude polycythaemia and thrombo-
cythaemia. Pressure is measured using a Doppler ultrasound
flow detector (see Fig. 5.9, p. 72). Normal pressure is slightly
above brachial systolic whilst patients with claudication
usually range between 50 and 120mmHg. Results are often
expressed as a ratio, the ankle brachial pressure index (ABPI),
with normal values from 0.9 to 1.2. Note that Doppler pres-
sures can be misleading; experience is needed in taking and
interpreting measurements, and radical treatment should not
be based on random pressure measurements. Values may be
spuriously elevated in patients with diabetes owing to calcifi-
cation in the arterial media which prevents cuff compression.
In non-classical exercise-induced leg pain or those with a good
history of claudication but normal resting ABPI, a treadmill
test with pre- and post-exercise pressure or ABPI helps the
diagnosis. A drop in ankle pressure after exercise gives an
indication of arterial disease severity and the recovery rate an
indication of collateral compensation.
Duplex ultrasonography
This combines greyscale ultrasound imaging (GSUS) and
colour Doppler blood flow estimation. GSUS allows estima-
tion of plaque narrowing and colour Doppler allows estima-
tion of flow velocities, which increase in areas of stenosis.
These methods provide a road map of atherosclerosis in the
arterial tree and are usually performed in a vascular laboratory
by specialist ultrasonographers. It is non-invasive and rarely
requires intravenous contrast media. There is substantial user
dependency in the results.
Arteriography (see Ch. 5)
Arteriography should be reserved for patients thought to
require angioplasty or reconstructive surgery. It maps the arte-
rial system (see Fig. 41.1), showing sites and severity of sten-
oses and occlusions, the quality of inflow (arteries feeding the
area of concern) and the runoff (arteries beyond the main
obstruction, see Fig. 41.2). Arteriography is sometimes used
wrongly by non-specialists to assess chronic arterial insuffi-
ciency but it cannot measure blood flow to the tissues or
dynamic circulatory responses to exercise; it helps only with
the mechanics of revascularisation. Traditional arteriography
is performed via direct arterial puncture but carries risks of
vessel trauma and high doses of contrast aggravating chronic
renal impairment. It is being replaced by less invasive CT and
MR angiography which use lower doses of intravenous con-
trast media.
APPROACH TO MANAGEMENT OF CHRONIC LOWER
LIMB ARTERIAL INSUFFICIENCY
Treatment options range from conservative or expectant treat-
ment for most, to reconstructive procedures for the few with
severe ischaemia. Treatments are summarised in Box 41.1.
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4 SYMPTOMS, DIAGNOSIS AND MANAGEMENT: CARDIOVASCULAR DISORDERS

Sites of atherosclerotic Box 41.1 Treatment options for chronic lower limb
occlusive disease
Numbers indicate ischaemia
Arterial anatomy prevalence from most
common (1) to least Mild to moderate claudication
common(7)
l No active treatment except advice to stop smoking, exercise
Abdominal aorta 7 Stenosis of the aorta regularly, take statin and aspirin, lose weight
l Balloon angioplasty

Disabling claudication
2 Common iliac l Balloon angioplasty
Common iliac stenosis/occlusion
l Reconstructive arterial surgery

Critical ischaemia
Internal iliac
l Intravenous drug therapies such as prostacyclin
6 External iliac/common
External iliac femoral disease l Lumbar sympathectomy (surgical or by phenol injection)
l Balloon angioplasty
INGUINAL 4 Stenosis at profunda
origin l Reconstructive arterial surgery
LIGAMENT
l Amputation (below, through or above knee)
Profunda femoris
1 Superficial femoral l Palliative care including appropriate analgesia
Superficial artery occlusion
femoral

Adductor hiatus

Popliteal

KNEE JOINT with the phosphodiesterase inhibitor cilostazol provides a

5 Popliteal
stenosis/occlusion
Popliteal
trifurcation
Anterior tibial
3 Patchy disease beyond
Posterior tibial trifurcation
Peroneal
Fig. 41.1 Typical patterns of lower limb arterial disease
Conservative management
In intermittent claudication, management starts with lifestyle
measures such as stopping smoking, attention to diet (reduced
fat, more fruit and vegetables, weight reduction) and system-
atic exercise. Cigarette smoking is a primary risk factor
in causing atherosclerosis and a secondary risk factor in
causing deterioration, as well as causing occlusions or sten-
oses of angioplasty or graft after reconstruction. Symptoms are
more likely to resolve (by collateral development) if the
patient stops smoking. Giving up is difficult as nicotine is
highly addictive but smoking cessation programmes can help
as well as pharmacological aids such as nicotine replacement
therapy, bupropion (Zyban) and varenicline (Champix).
All family members need to give up together to reinforce
the message.
Medical management is important, with blood pressure
control and regular anti-platelet agents (usually aspirin) and
a statin (even if cholesterol levels are normal). These measures
aim to reduce mortality by treating systemic atherosclerosis,
as well as encourage collateral vessels to develop. Treatment
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small increase in walking distance but does have significant
side-effects.
The degree of handicap in claudication is assessed clinically
by careful history-taking and perhaps by walking with the
patient. There is a marked trend towards conservative treat-
ment these days, now we know many patients recover func-
tion and this recovery is more durable than intervention. The
choice of active treatment depends on the handicap, the
patients willingness to give up smoking, the potential for
treating the pattern of atherosclerosis and the patients overall
preference. Severe and critical ischaemia are clear indications
for revascularisation (or amputation) since the symptoms
cannot be tolerated in the long term.
Mild to moderate claudication
Most patients are optimally treated with best medical
management and lifestyle advice. Symptoms often improve
spontaneously over 618 months, especially if the patient
stops smoking, exercises regularly and loses excess weight.
Simple advice to walk more slowly and use a walking stick
often greatly extends the claudication distance. Supervised
exercise programmes produce a sustained increase in walking
distance but need to continue for at least 3 months to show
benefitthere is often a problem with compliance. These
programmes are not yet offered in the NHS.
Disabling claudication
Disabling claudication usually requires treatment unless the
patient is too unfit even for angiography. Symptoms may
include severe exercise restriction in younger patients or mark-
edly worsening symptoms, especially if proximal arterial
obstruction is the cause (shown by absent femoral pulses),
which is often easily treated by angioplasty. Reconstructive
surgery is sometimes needed.
 Managing lower limb arterial insufficiency, the diabetic foot and major amputations
(a)
TECHNIQUES OF REVASCULARISATION FOR
CHRONIC ARTERIAL INSUFFICIENCY
Percutaneous transluminal angioplasty (PTA)
PTA involves cannulating an artery (usually the common
femoral but occasionally the brachial), introducing a guide-
wire into this remote artery and advancing it to lie across the
stenosis. A balloon catheter is passed over the wire and into
position (see Fig. 41.3) and the balloon inflated to a high
pressure (515 atmospheres), crushing the atheroma into the
arterial wall to relieve the obstruction. Success is very operator-
dependent and also depends upon the site, length and nature
of the diseased artery. PTA is most effective for isolated short
stenoses in iliac arteries. With increasing experience, longer
stenoses and occlusions in smaller vessels can be tackled,
avoiding the need for major surgery. The method is less suc-
cessful for distal calf arteries. Angioplasty often provides
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41
Fig. 41.2 Arteriograms comparing the
normal with typical patterns of arterial
obstruction affecting the lower limbs
(a) This magnetic resonance angiogram is
entirely normal, showing smooth, regular
arterial walls, all branches intact and three
normal infra-inguinal arteries below knee on
each side. (b) This composite subtraction
arteriogram was performed because the patient
suffered bilateral severe claudication. The aorta
is irregular and narrowed by atherosclerosis
from above the renal arteries to the bifurcation.
The common, internal and proximal external
iliacs are normal and smooth but the right
external iliac is occluded and the left stenosed.
Both profunda femoris arteries are occluded.
The superficial femoral arteries are both
diseased and occluded distally. On the left side,
collaterals are visible around the knee area.
The infrageniculate vessels are diseased on
both sides with stenoses and occlusions.
Reconstruction would have been extensive,
difficult and risky, and hence conservative
management alone was undertaken, in the
absence of rest pain or tissue loss
(b)
symptom improvement for a few years but disease progression
(and failure to modify lifestyle) is a limiting factor.
Arterial reconstructive surgery
Arterial reconstructive surgery began in the 1950s with open
removal of atheromatous plaques and thrombus from the
aorta and iliac arteries. This is known as thrombo-
endarterectomy, and is technically difficult, bloody and
time-consuming. It has been replaced by bypass grafting,
except for carotid endarterectomy, which remains the stand-
ard operation for stenosis and for isolated common femoral
artery occlusions.
Arterial bypass grafting was first developed during the
Korean War to treat arterial trauma, using homografts from
human cadavers. The initial results were excellent but grafts
eventually suffered from aneurysmal dilatation and rupture.
This led to the introduction of synthetic graft materials for
499
4 SYMPTOMS, DIAGNOSIS AND MANAGEMENT: CARDIOVASCULAR DISORDERS

G
B

BC

(a) (b)

(c)

(d)
Fig. 41.3 Percutaneous transluminal angioplasty
(a) Balloon angioplasty equipment. This catheter is used for balloon dilatation of arterial stenosis. First, an artery some distance from the stenosis (usually
the femoral) is punctured with a needle. A flexible guide-wire G is passed through the needle, along the artery and manipulated across the stenosis.
The catheter is then threaded over the guide-wire until the distal balloon B (which is designed to only be inflated to a predetermined diameter) lies
within the stenosis. The balloon is then inflated to high pressure using a special syringe attached to the balloon channel BC. Note the radio-opaque
markers at each end of the balloon to allow it to be sited radiographically. (b) Arteriogram showing a tight stenosis at the distal end of the left common
iliac artery (arrowed). (c) Catheter access proved impossible via the left femoral artery, so a guide-wire was passed from the right femoral, over the
bifurcation and across the stenosis. An angioplasty balloon catheter was then guided across the stenosis. As it was inflated the waist caused by the
arterial stenosis became clearly visible (arrowed). With further inflation to 4 atmospheres pressure, the waist disappeared. (d) Appearance of the arteries
post angioplasty. This procedure was completed in under an hour on a day-case basis under local anaesthesia and proved durable over several years

500
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 Managing lower limb arterial insufficiency, the diabetic foot and major amputations
Aorto-bifemoral
bypass grafting
1 l Complications of generalised arteriopathy: acute myocardial
1 Proximal anastomosis
end of graft to side of
aorta (occasionally aorta
transsected and end-to-
end anastomosis
performed)
2 Distal anastomosis
end of graft to side of
common femoral and
profunda femoris junction,
opening the profunda
orifice to minimise future
stenosis
2 2
Fig. 41.4 Aorto-bifemoral bypass for aorto-iliac disease using a
trouser or Y graft
A Dacron bifurcation graft or prosthesis is used to bypass the aorto-iliac
segment when it is occluded or stenosed, or to replace it when aorta and
iliacs are aneurysmal. In the latter case, the distal anastomoses are to the
iliac arteries not the femorals so as to maintain pelvic perfusion.
large arteries, now available in a variety of shapes, sizes and
types of cloth. Knitted polyester (Dacron) is the most popular
and is the standard material for aorto-iliac obstruction. Many
grafts are now sealed with gelatin or other proteins to mini-
mise porosity. For smaller arteries, autogenous long saphen-
ous vein from the leg is the best conduit, provided it is large
enough (usually >3mm in diameter) and not damaged by
thrombosis. Vein is also inherently resistant to infection, a
useful attribute when treating infected lower limb wounds
and ulcers.
Recognition that conservative management of claudication
is often as good as intervention, and the availability and
success of angioplasty, has meant that surgical reconstruction
is now sparingly used and is largely reserved for severely
ischaemic limbs, or when angioplasty is unsuitable or
unsuccessful.
The most common procedures are synthetic trouser graft-
ing for aorto-iliac (supra-inguinal) disease and femoro-
popliteal grafting using saphenous vein, for infra-inguinal
disease (see Figs 41.4 and 41.5). However, a range of other
bypasses and endarterectomy techniques sometimes have to
be employed to cope with non-standard disease.
Aorto-iliac disease
The usual surgical procedure is a Dacron trouser or Y graft
(see Fig. 41.4), anastomosed to the side of the aorta below the
renal arteries and to both common femorals below the
inguinal ligament (aorto-bifemoral graft). This is a major
operation, needing a laparotomy to access and cross-clamp
the aorta and carries a mortality risk of about 5%. In patients
with critical ischaemia but poor physiological reserve, legs can
be revascularised using extra-anatomic synthetic grafts with
a lower operative risk. Examples include a cross-over graft to
supply blood from one femoral artery to the other or an
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41
Box 41.2 Complications of arterial surgery
ischaemia, cerebrovascular accidents, renal failure, intestinal
ischaemiaearly or late
l Haemorrhage: arterial or venousearly
l Thrombosis of reconstructed vessels or graft leading to
profound distal ischaemia (usually a technical fault)early
l Embolism into limb vessels or renal vessels (particularly
aneurysm surgery)early
l Graft infectionearly or late
l False aneurysm formationlate
l Progressive atherosclerotic lower limb ischaemialate
axillo-bifemoral graft, supplying blood from one axillary
artery to both femorals, tunnelling the graft subcutaneously
along the lateral chest and abdominal wall.
Femoro-popliteal disease
The superficial femoral artery is the most commonly obstructed
peripheral artery. If PTA is unsuitable, femoro-popliteal
bypass grafting is employed using an autogenous vein graft.
The long (great) saphenous vein (LSV) is dissected from groin
to knee, its tributaries ligated and then reversed proximal to
distal so the valves do not obstruct flow. An end-to-side anas-
tomosis is performed at each end. If the LSV is unsuitable (i.e.
diseased, small diameter or previously removed for CABG),
the LSV from the other leg or veins from the arm can be used.
An alternative technique leaves the vein in situ and destroys
the valves with a valvulotome. As the vein tapers from
proximal to distal, this allows bypasses to tibial, dorsalis
pedis artery or smaller foot arteries for distal disease. These
infrapopliteal or femoro-distal grafts are used only
for severe ischaemia because of the higher risk of graft
occlusion.
Synthetic materials (e.g. PTFE or Dacron) are much less
satisfactory; these have lower long-term patency, particularly
when crossing the knee joint, and are more prone to
infection.
Complications of arterial surgery
These are summarised in Box 41.2.
OTHER THERAPIES FOR ARTERIAL INSUFFICIENCY
Intravenous and intra-arterial drug therapies
Drug therapy has no substantial effect in relieving claudica-
tion or severe ischaemia but recent research has examined
gene therapy and local stimulation of angiogenesis (new
blood vessel formation) in patients with critical limb ischae-
mia. However, the results are currently not yet robust enough
to employ clinically.
Sympathectomy
Blood flow in the skin (but not muscle) is controlled by the
sympathetic nervous system. Thus, early rest pain affecting the
501
4 SYMPTOMS, DIAGNOSIS AND MANAGEMENT: CARDIOVASCULAR DISORDERS

1 Femoral arteries exposed in groin

and dissected to control all
branches

2 Popliteal artery exposed either

above knee AK or below knee BK
according to level of atherosclerotic
obstruction
AK

3 Long (great) saphenous vein

exposed over length required and
all tributaries ligated

4 For more usual reversed graft,

BK saphenous vein is removed after
ligating proximal and distal stumps.
It is then reversed so that the
valves do not obstruct flow.
Proximal end is anastomosed to
side of common femoral artery
and distal end to side of popliteal
artery

For in situ grafts (most commonly

used where distal anastomosis
must be to one of the tibial
arteries), saphenous vein is not
removed but valves are destroyed
by passing a valvulotome through
it. Ends are anastomosed as
(a) above

Fig. 41.5 Techniques of arterial bypass for femoro-popliteal grafting

(a) Technique of femoro-popliteal grafting. (b) Composite arteriogram showing patent femoro-popliteal bypass
after operation (b)

skin may sometimes be relieved by sympathetic blockade even
if the overall arterial supply is inadequate. It is not beneficial
in claudication.
Sympathectomy can be performed by excision of part
of the lumbar sympathetic chain or, more commonly, by
translumbar injection of 6% aqueous phenol. Chemical
sympathectomy is performed under local anaesthesia with
radiographic control. Only about 15% of patients obtain suf-
ficient relief to avoid reconstructive operation or amputation
and there is no way of selecting those likely to benefit; sym-
pathectomy is certain to fail in the presence of tissue loss
(gangrene) and is most likely to succeed in early rest pain. It
may also help heal ulcers where moderate ischaemia coexists
with chronic venous insufficiency.

ACUTE LOWER LIMB ISCHAEMIA

PATHOPHYSIOLOGY distal arteries are not usually atherosclerotic, collateral net-
The lower (or upper) limb can become acutely ischaemic from works have not developed and ischaemia is all the more
embolism or thrombosis. severe. Most large emboli originate in the heart, as a result of
atrial fibrillation or mitral stenosis or both (left atrial throm-
Embolism bus), or of myocardial infarction (mural thrombus). Emboli
A large embolus impacting in a major distributing artery usually impact at branching points where the lumen abruptly
causes the distal blood supply to cease abruptly; since the narrows. Common sites are the aortic bifurcation (saddle
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 Managing lower limb arterial insufficiency, the diabetic foot and major amputations 41
Fig. 41.6 Embolic occlusion of popliteal arteries

CASE HISTORY
(b)

(a) Angiogram showing the thigh and upper leg arteries in a woman of 70 who
presented with rest pain for 48 hours and necrosis of the dorsum of her foot and
black toe tips for 24 hours. The left popliteal is occluded with a sharp cut-off
typical of embolism. The patient was in atrial fibrillation and the likely source of
the embolus was the left atrium. She underwent a successful embolectomy, but
because of the delay, a below-knee fasciotomy was performed to prevent
compartment syndrome. (b) The foot ulcer 3 weeks after revascularisation. The
(a) ulcer gradually healed completely

embolus), the common femoral bifurcation and the popliteal is often less severe because collaterals have developed to
trifurcation. Aortic or popliteal aneurysms can be a source of maintain distal circulation. This may allow time for less urgent
embolism if thrombus accumulated in the sac travels distally investigation and management.
(see Figs 41.6 and 41.7).

Thrombosis CLINICAL FEATURES OF ACUTE LOWER LIMB

Thrombotic causes include thrombosis of a popliteal aneu-
rysm and acute occlusion of a previous bypass graft or angi-
oplasty site. Occasionally, widespread thrombosis occurs in
normal arteries causing acute ischaemia. This can be a com-
plication of blood disorders including polycythaemia vera,
thrombocythaemia or leukaemias, in nephrotic syndrome or
in hyperosmolar hyperglycaemic states in diabetics.
Acute thrombotic occlusion causes catastrophic results
when it occurs in critical sites, namely the popliteal artery
(with few useful collaterals), the external iliac/common
femoral arterial trunk (the axial blood supply of the limb) or
the profunda femoris (if the superficial femoral artery is
already occluded).
If an essential distributing artery narrowed by atheroscle-
rosis becomes obstructed by secondary thrombosis or by
rupture of an atherosclerotic plaque (acute-on-chronic occlu-
sion) acute ischaemia may develop. The clinical presentation
ISCHAEMIA (Box 41.3)
The condition usually presents as a sudden onset of pain,
coldness and pallor, extending from the foot for a variable
distance up the leg. If the blood supply is completely cut off,
nerve ischaemia causes loss of sensation and then muscle
paralysis after an hour or two (the six Pssee Ch. 40, p. 489).
Acute severe arterial occlusion must be recognised quickly as
limb viability is in immediate danger and urgent steps are
needed to revascularise it. Unfortunately, this urgency is not
always appreciated by the patient, nursing staff or inexperi-
enced doctors. Even with successful revascularisation, ischae-
mic changes may already be irreversible and with late
intervention, there is a serious risk of muscle necrosis and
permanent nerve injury from reperfusion injury and/or com-
partment syndrome (see Ch. 17, p. 235).
Later, tissue ischaemia becomes obvious when the affected
area becomes mottled, dusky blue and discoloured. If the

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4 SYMPTOMS, DIAGNOSIS AND MANAGEMENT: CARDIOVASCULAR DISORDERS

CFA

PFA

SFA

(c)

(a)
(b)
Fig. 41.7 Femoral artery embolectomy
(a) Surgical exposure of the femoral artery bifurcation, usually performed under local infiltration anaesthesia (but with full monitoring). The common
femoral artery CFA, the profunda femoris PFA and the superficial femoral artery SFA are dissected cleanly and silicone slings placed around each artery.
A transverse arteriotomy is made just proximal to the bifurcation (position arrowed). (b) A Fogarty balloon catheter is passed distally, the balloon is gently
inflated and the catheter withdrawn to extract embolic and thrombotic material. This is performed in stages until the catheter can be passed to ankle
level and back-bleeding occurs. (c) Embolic material removed at operation from the superficial femoral artery and beyond using a Fogarty catheter. Note
the paler embolic material (arrowed) and the darker thrombus propagated beyond it

Box 41.3 Clinical features of acute severe lower limb ischaemia

Risk factors predisposing to embolism or thrombosis l Sudden and persistent coldness, usually in one periphery
l Recent chest pain or other evidence of myocardial infarction l Sudden numbness or paraesthesia, usually in one periphery
l History of rheumatic heart disease Signs of acute lower limb ischaemia
l History or finding of atrial fibrillation
l Pallor or blueness of the periphery; in late cases, the fixed
l Previous arterial embolism
pigmentation of necrosis or skin blistering
l History of intermittent claudication or other symptoms of
l Unexpected coldness of the peripheral part of one or (less
peripheral arterial disease (thrombosis)
commonly) both legs
l Polycythaemia vera (prone to intravascular thrombosis)
l Absent lower limb pulses (particularly if known to have been
l Popliteal aneurysm in contralateral limb (possible thrombosis
present before)
or embolism in affected limb)
l Poor peripheral capillary return after pressure blanching
l Aortic aneurysm (possible source of embolism)
l Progressive paralysis and foot drop (late sign)
Symptoms suggesting acute lower limb ischaemia l Ankle pulses undetectable by Doppler or very low ankle
l Sudden onset of continuous pain, usually in one periphery. systolic pressure
Note: may be painless in diabetic neuropathy

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 Managing lower limb arterial insufficiency, the diabetic foot and major amputations
mottling still blanches, then the limb may still be saved but
worsening ischaemia leads to fixed mottling and skin blistering;
this is now irreversible and limb loss inevitable. These changes
always involve the foot and may extend proximally (though
rarely above the knee). At this stage, the upper limit of necrosis
is usually well demarcated from proximal viable tissue.
PRINCIPLES OF MANAGING THE ACUTELY
ISCHAEMIC LIMB
Management should be carefully planned at the outset. The
window of opportunity before necrosis is short and delay or
procrastination increases morbidity or mortality. Treatment is
best carried out by cooperation between vascular surgical and
radiological specialists so the full range of appropriate and
timely treatment can be offered. As a first step, the patient
should be anticoagulated with a bolus dose of 5000U of
intravenous heparin to prevent propagation of thrombus
proximal and distal to the occlusion. If the diagnosis is later
confirmed as embolism, oral anticoagulation is usually con-
tinued after surgery.
THROMBOSIS OR EMBOLISM?
Distinguishing clinically between thrombosis and embolism
is unreliable, although the history may provide clues. Evi-
dence of mitral stenosis, an arrhythmia or recent myocardial
infarction suggests embolism, whereas a history of claudica-
tion or a prothrombotic blood disorder points to thrombosis.
Examining the affected limb may not help distinguish but the
other limb provides evidence of the state of peripheral arter-
ies. If it is well perfused with good pulses and normal ankle
pressure, then embolism is more likely. If there is arterial
disease then in situ thrombosis is more likely; the severity of
ischaemia may also be less profound. The popliteal fossa must
always be palpated to exclude a thrombosed popliteal aneu-
rysm. A large saddle embolus lodging at the aortic bifurcation
often presents with severe ischaemia of both limbs extending
into the proximal leg and thigh. This can be fatal, partly from
THE DIABETIC FOOT
The evolving epidemic of diabetes means that managing
diabetic foot problems will become an increasing part
of the surgical workload. Treatment should be delivered
by a multidisciplinary diabetic team (vascular surgeon,
diabetologist, podiatrist, orthopaedic surgeon and
orthotist).
PATHOPHYSIOLOGY OF THE DIABETIC FOOT
Diabetic patients are prone to serious ulceration and infection
of the feet. The underlying disorder is neuropathy, obliterative
atherosclerosis or both together. Type 2 diabetic patients are
at greater risk than type 1, but remember there is no such
thing as mild diabetes. All diabetic patients should be
screened for potential complications of diabetes.
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41
the severity of ischaemia but also from intense reperfusion
injury once limbs have been revascularised.
If clinical signs are strongly in favour of embolism, imme-
diate surgical embolectomy can be undertaken with on-table
arteriography if necessary. If there is doubt, urgent duplex
scanning or angiography (usually CT angiography out of
hours) is available, a definitive diagnosis can be rapidly deter-
mined and the best intervention delivered. This may be radio-
logical rather than surgical.
In acute ischaemia, the speed of treatment is the key to
success. Any patient with sensory loss affecting more than just
the toes, especially with evidence of muscle weakness, requires
immediate treatment with embolectomy, thrombectomy or
bypass graft (see Fig. 41.4, 41.5, p. 502). In limbs that have
been profoundly ischaemic, fasciotomies at the time are often
required to prevent compartment syndrome. Thrombolysis is
now rarely undertaken, except for unblocking a thrombosed
bypass graft in a patient whose foot is predicted to remain
viable for at least 12 hours.
EMBOLECTOMY
Embolectomy is often performed under local anaesthesia but
the patient and theatre should be prepared for GA just in case;
full monitoring should be applied. The patient has usually
been anticoagulated with heparin. A groin incision exposes
the femoral artery bifurcation, the vessels are all temporarily
clamped and an incision (arteriotomy) made in the common
femoral artery (Fig. 41.7) which may reveal the obstructing
clot. A Fogarty balloon catheter is then passed gently into
each main vessel in turn, proximally and distally for 10cm or
so, the balloon is inflated gently and the catheter drawn back
to sweep out any obstructing clot. This is repeated 10cm
further each time until the distal limit is reached. The opera-
tion is successful if clot is retrieved and blood flows back
(back-bleeding) from each vessel as it is unclamped. If the
embolectomy catheter will not pass easily, this usually indi-
cates acute-on-chronic thrombosis. Immediate arteriography
and surgical treatment are required as delay carries a high rate
of limb loss and death.
Several factors may contribute to diabetic foot problems:
l Neuropathy. Microangiopathy probably causes
peripheral neuropathies affecting motor, sensory and
autonomic nerves. Affected motor nerves supply the
small muscles of the foot and the consequent
unmodified traction of the calf muscles distorts the
morphology and weight-bearing characteristics of the
foot. Sensory neuropathy lessens pain sensation and
hence awareness of potential injury from ill-fitting
footwear and foreign bodies in shoes. Damaged
autonomic nerves disrupt vascular control and cause
loss of sweating. Ulceration and infection in
neuropathic feet are often painless and hence are often
neglected by the patient
505
4 SYMPTOMS, DIAGNOSIS AND MANAGEMENT: CARDIOVASCULAR DISORDERS
l Arteriovenous communications. These open beneath the
skin, perhaps diverting nutrient flow away from it.
Damaged tissue thus heals poorly and is vulnerable to
infection, even if the injury or pressure damage is minor.
This may also explain why an ischaemic diabetic foot can
be warm and pink
l Arterioles. In a few cases, these become narrowed and
restrict capillary perfusion
l Impaired intermediary tissue metabolism
and a glucose-rich tissue environment. Both
of these favour bacterial growth and spreading
infection
l Obliterative atherosclerosis. Diabetics have a markedly
increased predisposition to arterial insufficiency.
Although 15% of the general population have diabetes,
25% of patients with lower limb ischaemia have diabetes.
Atherosclerotic disease in diabetic patients follows the
usual pattern (although often more distal) but tends to
develop at a younger age
Identifying the causes of diabetic foot problems
Most diabetic foot problems can be identified as primarily
neuropathic or primarily atherosclerotic but some have ele-
ments of both. The term neuro-ischaemic foot is sometimes
used but is not clinically precise. Typically, the neuropathic
foot is painless, red and warm with strong pulses, whereas the
atherosclerotic foot without neuropathy is pale, painful, cold
and pulseless. However, when both occur together, the dia-
betic trap is that the limb can be seriously ischaemic yet
painless, warm and pink. If the foot is neuropathic and pulse-
less, only arteriography or duplex scanning will properly
demonstrate the arterial insufficiency.
Patients most at risk of neuropathic foot complications are
elderly, poorly controlled, maturity-onset (type 2) diabetics
and younger patients with longstanding type 1 diabetes. Simi-
larly, patients with diabetic renal or retinal complications
have an increased risk of foot problems. Recognising the at-
risk foot, i.e. the neuropathic foot, before trouble strikes is
fundamental, as virtually all neuropathic foot complications
can be prevented with proper education, regular inspection
and chiropody (podiatry) (Box 41.4).
Management of atherosclerotic ischaemia is similar in dia-
betic and non-diabetic patients. For mixed disease, the arterial
insufficiency must nearly always be treated first if there is to
be any hope of healing.
Clinical presentations of diabetic foot complications
Foot complications of diabetic neuropathy present in four
main ways (see Fig. 41.8):
l Painless, deeply penetrating ulcers. These usually
develop in pressure areas caused by distortion of foot
morphology, often beneath the first or fifth metatarsal
head. The infecting organism is usually Staphylococcus
aureus. Infection and necrosis spread through the plantar
spaces and along tendon sheaths. Infection and local
venous thrombosis appear to be the predominant factors
causing tissue destruction
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Box 41.4 The problem of the diabetic foot
l Diabetic gangrene is not heaven-sent but earth-born
(Joslin 1934)
l There is no such thing as mild diabetes; all diabetics are
potentially at risk
l Four out of five patients with diabetic foot problems have
type 2 diabetes
l Foot problems are responsible for 47% of days spent in
hospital by diabetics
l Diabetic foot problems are responsible for 12% of all
hospital admissions in (internal) medicine
l In diabetics with new foot ulcers, 90% have peripheral
neuropathy (compared with 20% in a diabetic control
group), whereas only 14% have peripheral arterial disease
compared with 10% in controls (Miami 19834)
l Patients with diabetic foot problems are incapacitated for
an average of 16 weeks
l Diabetic foot problems are largely preventable
l Care and prevention of diabetic foot problems require
specialist surveillance and management by a dedicated
team; foot ulceration in diabetics represents a failure of
medical management
l Chronic ulceration of pressure points and sites of
minor injury. Skin perfusion is otherwise adequate
l Extensive spreading skin necrosis originating in an ulcer
and caused by superficial or deep infection. This develops
very rapidly and spreads proximally, threatening limb
and life
l Painless necrosis of individual toes. These first turn
blue, then later become black and mummified, and may
eventually be shed spontaneously. This usually occurs in
mixed neuropathy and atherosclerosis and the
management hinges on whether local amputations will
heal or whether arterial reconstruction is needed
MANAGEMENT OF NEUROPATHIC FOOT
COMPLICATIONS
CONTROL OF INFECTION
After excluding ischaemia, control of infection is the first
priority in managing the diabetic foot. Minor foot lesions
must always be taken seriously and treated early with oral
antibiotics (including cover for anaerobes) and frequent
local cleansing and dressing.
If there is any sign of spreading infection or systemic
involvement (i.e. pyrexia, tachycardia or loss of diabetic
control), the patient should be admitted to hospital for inten-
sive treatment including parenteral antibiotics, elevation, exci-
sion of necrotic tissue and attention to blood glucose control.
Pus in superficial or deep tissues is a medical emergency and
 Managing lower limb arterial insufficiency, the diabetic foot and major amputations 41
Fig. 41.8 Foot complications of diabetes

CASE HISTORY
(a)

(b)

(c)
(a) Chronic penetrating ulcers in a 60-year-old man with maturity-onset diabetes. He had no evidence of major vessel disease but had signs of
neuropathy. The deep ulcer beneath the head of the first metatarsal is characteristically surrounded with a thick keratin margin, and the ulcer on the
medial side of the foot has an exposed tendon in its base. (b) This patient has a combination of neuropathy and arterial insufficiency. This foot was
painless despite spreading necrosis and a collection of pus in the sole of the foot. He underwent femoro-popliteal bypass and local excision of dead
tissue and healing was eventually complete. (c) This man of 34 presented with a neglected infection in his foot. He had severe neuropathy but no
arterial disease. The entire dorsum of his foot was necrotic and he had to undergo a primary below-knee amputation. This complication would have
been entirely avoidable had he sought and received treatment earlier

requires immediate drainage. This is difficult to diagnose with a success rate of around 80%, or surgical excision. There
clinically and foot imaging with MRI is required. Specialist is no current consensus on optimal treatment but prolonged
management of blood sugar is often required as it is often antibiotics can increase the risk of C. difficile and emergence
grossly elevated. of multi-drug-resistant organisms.

REMOVAL OF NECROTIC TISSUE PREVENTION OF THE DIABETIC FOOT

Surgery may involve anything from simple desloughing of
an ulcer to major amputation (see Fig. 41.9). If performed
correctly, these result in complete and rapid healing. If good
foot care is available, amputation of more than single toes is
rarely required. Before debridement, arterial inflow must be
assessed and the foot revascularised if necessary before deb-
ridement or digital amputation to maximise the chances of
wound healing.
Osteomyelitis occurs in up to 20% with a diabetes-related
foot ulcer. Diagnosis is clinically if an ulcer can be probed
down to bone or else radiologically (plain X-ray or MRI).
Treatment consists of long-term antibiotics (often parenteral),
All clinicians dealing with diabetics should place the highest
priority on prevention. All patients should be screened for
peripheral neuropathy and those at risk given detailed advice
on self-care and high-quality chiropody or podiatry. Foot
ulceration occurs in about 15% of patients with diabetes and
precedes 84% of all diabetes-related lower leg amputations;
it can be prevented. Careful attention should be given to
footwear to correct abnormal pressure patterns. Special insoles
or special shoes may need to be made by an orthotist or surgi-
cal fitter. Careful follow-up and regular monitoring by a dia-
betic specialist nurse or clinic can successfully anticipate and
prevent dire trouble.

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4 SYMPTOMS, DIAGNOSIS AND MANAGEMENT: CARDIOVASCULAR DISORDERS

1 Excision of all necrotic tissue 2 Digit amputation using racquet-
from ulcer, which is left to shaped incision; toe is
granulate removed with both phalangeal
bones and cartilage is nibbled
from metatarsal (shaded)
(a)
3 Filleting of digit and metatarsal 4 Transmetatarsal amputation
if infection has spread more
deeply. A cake-slice is taken
out of the foot and the wound
left unsutured to heal by
granulation (see (b))

(b) (c)
Fig. 41.9 Operations on the diabetic foot (a) Types of local amputation. (b) This patient had a neuropathic ulcer and necrotic toes but no arterial
disease. The second and third metatarsals have been excised, together with all the necrotic tissue, in a cake slice procedure. The wound was left open to
heal by secondary intention, eventually giving a remarkably good functional result. (c) This elderly man suffered from a combination of neuropathy and
obliterative atherosclerosis. He was blind as a result of diabetic retinopathy. The right leg was eventually amputated below knee because of spreading
infection, but the left was saved by angioplasty of stenoses in the iliac and superficial femoral arteries, together with local surgery to remove necrotic
tissue. Note the typical clawed foot and distorted sole of motor neuropathy. Note also that the great toe has already been amputated. The heel has not
yet been debrided

LOWER LIMB AMPUTATION

Strenuous efforts should be made to preserve ischaemic limbs
by reconstructive surgery or interventional radiology. This is
because the functional results of successful revascularisation
are far better than even the best major amputation. Mobility
with artificial limbs is disappointing, especially in the elderly
or infirm. However, amputation cannot be avoided in patients
where revascularisation is technically impossible (particularly
in diffuse distal arterial disease), or if there is substantial tissue
necrosis and a functionally useless foot, or deep spreading
infection.
LEVEL OF AMPUTATION
Two principles guide the level of amputation (see Fig. 41.10):
l The amputation must be made through healthy
tissue. If not, there is a high risk of wound breakdown
and chronic ulceration, requiring further amputation
at a higher level. When amputation is for
(uncorrected) peripheral ischaemia, it is almost always
necessary to amputate at mid-tibial level or above to
ensure healing

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 Managing lower limb arterial insufficiency, the diabetic foot and major amputations 41
(a)

Ideal stump
lengths

2225 cm
below greater
trochanter Above knee
equal anterior and
posterior skin flaps
(b)

Below knee
long posterior
muscle flap
1012 cm below (Burgess type
tibial tuberosity or skew flap type)

Symes (heel flap)

malleoli cut level with
inferior surface of tibia

Mid-tarsal amputation

(c) (d) (e)

Fig. 41.10 Lower limb amputations

(a) Sites of election for lower limb amputations. (b) Above-knee stump in a diabetic patient. Unfortunately the original above-knee wound broke down
and necrotic muscle had to be excised. The wound was left open and had nearly healed by secondary intention two months later. (c) A well-healed
below-knee stump at 6 weeks. The operation used a long posterior muscle flap and equal length skew skin flaps. (d) The same patient fitted with a
modular below-knee prosthesis retained by a close-fitting socket and a small strap above the knee. Note the urinary catheter. (e) Breakdown of below-
knee stump because of inadequate arterial blood supply

l The choice of amputation level must take into account
the fitting of a prosthetic limb. For this purpose, the
mid-tibia (below-knee) and lower femoral levels (above-
knee) are preferred. If the knee joint can be saved, the
functional success of a prosthesis is much better. With
improved prostheses, through-knee amputation is
possible but healing rates are poor; most surgeons
and prosthetists prefer above-knee to through-knee
amputation as it has a better healing rate and easier
prosthetics
The traditional guillotine amputation of the battlefield
simply sliced off the limb, leaving the wound to heal by sec-
ondary intention. This reduced the risk of fatal gas gangrene
or tetanus but the outcome for fitting a prosthetic limb was
poor. There have been huge developments in amputation
techniques in recent decades, particularly in the use of myo-
plastic flaps. For below-knee amputations, a long posterior
flap of muscle and skin is wrapped forward over the ampu-
tated bone and sutured in place. This results in more reliable
healing and a suitably shaped and cushioned stump. A varia-
tion, the Robinson skew flap, uses a long posterior muscle
flap but equal skin flaps. The healing rate is no better but the
stump is better shaped for earlier prosthetic fitting. With these
techniques and in experienced hands, 70% or more of below-
knee amputations for ischaemia will eventually heal even
without revascularisation, preserving the knee joint and allow-
ing reasonable walking. Modern below-knee prostheses are
modular in construction and weight is borne mainly on the
patellar tendon.
For above-knee amputations, myoplastic flaps are used in
which the bony amputation level is proximal to the muscle/
skin amputation level. This allows the muscles to be sutured
over the exposed bone end. Short anterior and posterior skin
flaps are then closed over the muscle.

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