Examine both femoral arteries by palpating and then
auscultating them. A bruit may be heard if the artery
is narrowed. Next palpate the following pulses: popliteal
(behind the knee—see Fig. 6.5(a): if this is difficult to
feel when the patient is supine, try the method shown
in Fig. 6.5(b)), posterior tibial (under the medial
malleolus, see Fig. 6.6(a)) and dorsalis pedis (on the
forefoot, Fig. 6.6(b)) on both sides.2
Patients with exertional calf pain (intermittent
claudication) are likely to have disease of the peripheral
arteries. More severe disease can lead to pain even
at rest and to ischaemic changes in the legs and feet
(see Good signs guide 6.1). Look for atrophic skin
and loss of hair, colour changes of the feet (blue or
red) and ulcers at the lower end of the tibia.3 Venous
and diabetic ulcers can be distinguished from arterial
ulcers (see Figs 6.7–6.9).
Look for reduced capillary return (compress the
toenails—the return of the normal red colour is slow).4
In such cases, perform Buerger’sb test to help confirm
your diagnosis: elevate the legs to 45° (pallor is rapid
if there is a poor arterial supply), then place them
dependent at 90° over the edge of the bed (cyanosis
occurs if the arterial supply is impaired). Normally
there is no change in colour in either position.
The ankle–brachial index (ABI) is a measure of
arterial supply to the lower limbs; an abnormal index
indicates increased cardiovascular risk.5 The systolic
blood pressure in the dorsalis pedis or posterior
tibial artery is measured using a Doppler probe and
a blood pressure cuff over the calf.
DISEASE ChART:
LR = likelihood ratio.
SignLR+LR−
Sores or ulcers on feet5.90.98
Feet pale, red or blue2.30.80
Atrophic skin1.650.72
Absent hair1.60.71
One foot cooler5.90.92
Absent femoral pulse5.80.94
Absent dorsalis pedis or posterior tibial pulse3.70.37
Limb bruit present5.70.58
Capillary refill time >5 seconds1.90.84
Venous refill time >20 seconds3.60.83
ACUTE ARTERIAL OCCLUSION
Acute arterial occlusion of a major peripheral limb
artery results in a painful, pulseless, pale, ‘paralysed’
limb that is perishingly cold and has paraesthesias (the
six Ps). It can be the result of embolism, thrombosis
or injury. Peripheral arterial embolism usually
arises from thrombus in the heart, where it may be
secondary to:
1. atrial fibrillation
2. myocardial infarction
3. dilated cardiomyopathy, or
4. infective endocarditis.
CHAPTER 6 THE lImb ExAmINATION ANd PERIPHERAl vASCulAR dISEASE 115
FIGURE 6.8
Arterial ulcer.
This arterial ulcer has a regular margin and
‘punched out’ appearance. The surrounding
skin is cold. The peripheral pulses are absent.
(See List 6.4.)
(From McDonald FS, ed. Mayo Clinic images in internal medicine,
with permission. © Mayo Clinic Scientific Press and CRC Press.
Reproduced by permission of Taylor and Francis Group, LLC, a
division of Informa plc.)
FIGURE 6.9
diabetic (neuropathic) ulcer.
Neuropathic ulcers are painless and are
associated with reduced sensation in the
surrounding skin.
(From McDonald FS, ed. Mayo Clinic images in internal medicine,
with permission. © Mayo Clinic Scientific Press and CRC Press.
Reproduced by permission of Taylor and Francis Group, LLC, a
division of Informa plc.)
DEEP VENOUS
THROMBOSIS
Deep venous thrombosis (DVT) is a difficult clinical
diagnosis.7 The patient may complain of calf pain. On
examination, the clinician should look for swelling of
the calf and the thigh, and dilated superficial veins.
Feel then for increased warmth and squeeze the calf
(gently) to determine whether the area is tender.
Homans’
c sign (pain in the calf when the foot is sharply
dorsiflexed, i.e. pushed up) is of limited diagnostic value
and is theoretically dangerous because of the possibility
of dislodgement of loose thrombus.
The causes of thrombosis were described by
Virchowd in 1856 under three broad headings (the
famous Virchow’s triad):
1. changes in the vessel wall
2. changes in blood flow
3. changes in the constitution of the blood.
Deep venous thrombosis is usually caused by
prolonged immobilisation (particularly after lower
limb orthopaedic surgery), cardiac failure (stasis)
or trauma (vessel wall damage), but may also result
from neoplasm, sepsis, chronic inflammatory bowel
disease, disseminated intravascular coagulation,
the contraceptive pill, pregnancy and a number of
inherited defects of coagulation (the thrombophilias:
e.g. antithrombin III deficiency or the factor V Leiden
mutation).
VARICOSE VEINS
If a patient complains of ‘varicose veins’, ask him or
her to stand with the legs fully exposed.8 Inspect the
front of the whole leg for tortuous, dilated branches
of the long saphenous vein (below the femoral vein in
the groin to the medial side of the lower leg). Then
inspect the back of the calf for varicosities of the short
saphenous vein (from the back of the calf and lateral
malleolus to the popliteal fossa). Look to see whether
c John Homans (1877–1954), a professor of surgery at Harvard University,
Boston. He described his sign in 1941, originally in cases of thrombophlebitis.
He later became disenchanted with the sign and is reputed to have asked
why if a sign were to be named after him it couldn’t be a useful one.
d Rudolph Virchow (1821–1902), a brilliant German pathologist, regarded
as the founder of modern pathology, professor of pathological anatomy
in Berlin. He provided the first description of leukaemia. He died aged
81 after fracturing his femur jumping from a moving tram.the leg is inflamed, swollen or pigmented (subcutaneous
haemosiderin deposition secondary to venous stasis).
Palpate the veins. Hard leg veins suggest thrombosis,
whereas tenderness indicates thrombophlebitis. Perform
the cough impulse test. Put the fingers over the long
saphenous vein opening in the groin, medial to the
femoral vein. (Do not forget the anatomy—femoral
vein [medial], artery [your landmark], nerve [lateral].)
Ask the patient to cough: a fluid thrill is felt if the
saphenofemoral valve is incompetent.
The following supplementary tests are occasionally
helpful (and surgeons like to quiz students on them
in examinations):
• Trendelenburge test: with the patient lying down,
the leg is elevated. Firm pressure is placed on the
saphenous opening in the groin, and the patient
is instructed to stand. The sign is positive if the
veins stay empty until the groin pressure is
released (incompetence at the saphenofemoral
valve). If the veins fill despite groin pressure, the
incompetent valves are in the thigh or calf, and
Perthes’f test is performed.
• Perthes’ test: repeat the Trendelenburg test, but
when the patient stands, allow some blood to be
released and then get him or her to stand up and
down on the toes a few times. The veins will
become less tense if the perforating calf veins are
patent and have competent valves (the muscle
pump is functioning).
If the pattern of affected veins is unusual (e.g. pubic
varices), try to exclude secondary varicose veins. These
may be due to an intrapelvic neoplasm that has
obstructed deep venous return. Rectal and pelvic
examinations should then be performed.
CHRONIC VENOUS DISEASE
Chronic venous stasis is a common cause of leg oedema.
It is a result of increased pressure in the venous system.
There may be a history of previous deep venous
thrombosis or of varicose veins. These are associated
with incompetence of the valves of the perforating
e Friedrich Trendelenburg (1844–1924), a professor of surgery in Leipzig.
f
Georg Clemens Perthes (1869–1927), a German surgeon and professor
of surgery at Tübingen. He was the first to use radiotherapy for the
treatment of cancer (in 1903).
veins, which connect the deep and superficial veins
of the legs. This can lead to dilation of the upper part
of the long saphenous veins and make their valves
incompetent. Failure of the muscle pump mechanism
that directs blood up the veins can have similar effects. It
is common in elderly inactive patients. Chronic venous
stasis leads to oedema and a rise in tissue pressure,
which causes thinning of skin and subcutaneous tissue.
Skin ulceration and necrosis may occur.
Typically ulcers occur above the medial malleoli.
Eventual healing often has inadequate circulation and
skin will often break down again. The indurated skin
is often stained a purple black colour; this is a result
of staining with haemosiderin from red blood cells
that have been extravasated into the tissues. Chronic
venous eczema may complicate the condition. The legs
appear more swollen and erythematous (Fig. 6.10).
This is often misdiagnosed as cellulitis (skin infection),
but cellulitis is never bilateral.
This chronic oedema is described as brawny. It will
pit only slowly and unwillingly on compression. Signs
of right heart failure (raised JVP and pulsatile liver,
ascites) are absent.
CAUSES OF LEG ULCERS:
1. Venous stasis ulcer—most common
(see Fig. 6.7)
Site: around malleoli
Character: irregular margin, granulation tissue
in the floor. Surrounding tissue inflammation
and oedema
Associated pigmentation, stasis eczema
2. Ischaemic ulcer (see Fig. 6.8)
○ Large-artery disease (atherosclerosis,
thromboangiitis obliterans): usually lateral
side of leg (pulses absent)
○ Small-vessel disease (e.g. leucocytoclastic
vasculitis): palpable purpura
Site: over pressure areas, lateral malleolus,
dorsum and margins of the feet and toes
Character: smooth, rounded, ‘punched out’ pale
base that does not bleed
3. Malignant ulcer, e.g. basal cell carcinoma
(pearly translucent edge), squamous cell
carcinoma (hard everted edge), melanoma,
lymphoma, Kaposi’s sarcoma
4. Infection, e.g. Staphylococcus aureus, syphilitic
gumma, tuberculosis, atypical Mycobacterium,
fungal
5. Neuropathic (painless penetrating ulcer on sole
of foot: peripheral neuropathy, e.g. diabetes
mellitus, tabes [tertiary syphilis], leprosy) (see
Fig. 6.9)
6. Underlying systemic disease
○ Diabetes mellitus: vascular disease,
neuropathy or necrobiosis lipoidica (front of
leg)
○ Pyoderma gangrenosum
○ Rheumatoid arthritis
○ Lymphoma
○ Haemolytic anaemia (small ulcers over
malleoli), e.g. sickle cell anaemia