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314 Vascular Surgery
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Fig. 35.1.
Fingertip ulcer in a patient with systemic sclerosis.
fingers (sclerodactyly) but elsewhere the skin was normal. She had digital pitting of
the right index and middle fingers. There were no other abnormal findings.
Question 2
What investigations would you perform?
A. Full blood count and erythrocyte sedimentation rate.
B. Angiography.
C. Testing for antinuclear antibody (ANA).
D. Testing for anticentromere antibody.
E. Nailfold capillaroscopy.
Full blood count and erythrocyte sedimentation rate (ESR) were normal. On
immunological testing she was strongly antinuclear antibody (ANA) positive (titre
1/1000) and she was anticentromere antibody positive. Chest X-ray showed no cervical rib. Hand X-rays were normal. Nailfold microscopy was abnormal, showing
widened, dilated loops with areas of avascularity (Fig. 35.2).
Question 3
What is the diagnosis?
A. Limited cutaneous systemic sclerosis (“CREST” syndrome).
B. Hyperviscosity state, for example secondary to malignancy.
C. Extrinsic vascular compression.
D. Atherosclerosis.
E. Buerger’s disease.
Raynaud’s Phenomenon 315
Fig. 35.2.
with areas of avascularity.
Typical appearances on nailfold microscopy in systemic sclerosis – several capillary loops are dilated,
Question 4
Which of the following are true of systemic sclerosis (also termed “scleroderma”):
A. Digital pitting is a characteristic feature.
B. Males are more commonly affected than females.
C. The two subtypes – limited cutaneous and diffuse cutaneous – are separated on
the basis of the extent of the skin involvement.
D. Raynaud’s phenomenon often precedes the diagnosis of limited cutaneous sys-
temic sclerosis by many years.
E. Anticentromere antibody is a risk factor for severe digital ischaemia requiring
amputation.
The diagnosis of limited cutaneous systemic sclerosis was explained to the
patient. She was told that her Raynaud’s phenomenon and her upper gastrointestinal symptoms were most likely related, and that some checks of her cardiorespiratory function would be arranged on a routine basis.
Question 5
How would you have treated her Raynaud’s phenomenon had you seen her
6 months previously, when there was no digital ulceration?
A. Avoidance of cold exposure.
B. Low dose prednisolone.
C. Stop smoking.
316 Vascular Surgery
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D. Nifedipine (sustained release).
E. Biofeedback.
The patient was prescribed nifedipine (sustained release) and a course of
flucloxacillin. When reviewed one week later, the fingertip had deteriorated and
some of the tissue had become necrotic, with surrounding erythema.
Question 6
What would you do now?
A. Admit to hospital for intravenous prostanoid therapy.
B. Intravenous antibiotics.
C. Debridement of the ulcer.
D. Cervical sympathectomy.
E. Anticoagulation.
The patient was admitted for intravenous antibiotic therapy, intravenous
prostanoid infusions, and a vascular opinion. The fingertip was debrided. The
patient was discharged home 6 days later, with instructions to dress warmly, avoid
cold exposure, and to seek medical advice early should any further ulcers develop.
Commentary
Raynaud’s phenomenon – episodic digital ischaemia usually in response to cold
exposure or stress – can be either primary (idiopathic) or secondary to a number of
different diseases/conditions, including connective tissue disease (most characteristically systemic sclerosis), external vascular compression (as with a cervical rib),
vibration exposure, hyperviscosity, drug treatment (for example beta-blockers,
ergotamine) and occupational chemical exposure. The terminology is confusing:
primary Raynaud’s phenomenon was previously termed “Raynaud’s disease”, and
secondary Raynaud’s phenomenon “Raynaud’s syndrome”. However, “primary
Raynaud’s phenomenon” and “secondary Raynaud’s phenomenon” are now the
preferred terms [1].
The pathophysiology of Raynaud’s phenomenon (either primary or secondary) is
poorly understood. Raynaud’s phenomenon can occur because of abnormalities in
vascular structure, vascular function, or the blood itself [2]. These are interdependent and may occur together, as in systemic sclerosis when structural vascular
problems inevitably impair vascular function, and platelet and white blood cell
activation, together with impaired fibrinolysis, are also thought to contribute to
pathophysiology. It is generally accepted that primary Raynaud’s phenomenon is
mainly vasospastic and does not progress to irreversible tissue damage. In contrast,
Raynaud’s phenomenon secondary to connective tissue disease such as systemic
sclerosis is associated with structural vascular abnormality, and patients often
develop ulceration, scarring, and even gangrene necessitating amputation.
Raynaud’s Phenomenon 317
The vascular surgeon is likely to encounter patients with Raynaud’s phenomenon
for two main reasons:
1. Diagnosis. Why does this patient have episodic digital ischaemia?
2. Treatment of a critically ischaemic digit, or of severe Raynaud’s phenomenon
unresponsive to medical therapy.
The onset of primary Raynaud’s phenomenon is most commonly in the teens or
twenties: onset in later years should always raise the suspicion of an underlying
cause. Women are more commonly affected. For Raynaud’s phenomenon to be
primary, there should be no clinical features of underlying connective tissue disease
or other disease/disorder (including absence of digital pitting or sclerodactyly),
there should be no digital ulceration or gangrene, the ESR should be normal, testing
for ANA negative (titre <1/100) and the nailfold capillaries should be normal [1].
[Q1: C, D] In the absence of any worrying features in the history and examination, the
usual investigation screen therefore comprises a full blood count and ESR, testing
for ANA, nailfold capillaroscopy and, if there is any question of a cervical rib, a
chest or thoracic outlet X-ray. Anaemia and/or a high ESR may indicate an underlying connective tissue disease or other illness. However, a normal haemoglobin level
and ESR (as in our patient) do not exclude a diagnosis of systemic sclerosis, in
which the vascular abnormalities are primarily non-inflammatory [3]. In primary
Raynaud’s phenomenon, the nailfold capillaries should be fairly regular “hair-pin”
loops as opposed to the abnormal dilated loops, with areas of loop drop-out, that
are characteristic of systemic sclerosis [4].
Other investigations are indicated by the history and examination. For example,
if there is sclerodactyly (scleroderma of the fingers) and/or digital pitting (Fig. 35.3),
which are both characteristic of systemic sclerosis, then anticentromere antibodies
and antibodies to topoisomerase (anti-Scl-70 antibodies) should be looked for.
These antibodies are highly specific for systemic sclerosis [5]. If there is any
Fig. 35.3.
Digital pitting in a patient with systemic sclerosis.
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question of a proximal vascular obstruction (absent peripheral pulses) then angiography should be considered, but in the majority of patients with systemic sclerosis
and digital ischaemia this is not necessary. [Q2: A, C, D, E]
Systemic sclerosis, similarly to primary Raynaud’s phenomenon, is more
common in women than in men. There are two main subtypes of systemic sclerosis
– limited and diffuse cutaneous – defined on the basis of the extent of the skin
involvement. In patients with limited cutaneous disease (previously termed CREST
– calcinosis, Raynaud’s, oesophageal dysmotility, sclerodactyly, telangiectases),
only the skin of the extremities and face is thickened, whereas in those with diffuse
cutaneous disease there is proximal skin thickening, involving proximal limbs
and/or trunk [6]. The patient described has clinical features typical of limited cutaneous disease: Raynaud’s phenomenon preceding the diagnosis of systemic sclerosis by a number of years, sclerodactyly, digital pitting, and upper gastrointestinal
problems. [Q3: A] Patients with limited cutaneous disease typically have more severe
digital vascular disease than patients with diffuse cutaneous disease, and anticentromere antibody is predictive of severe digital ischaemia [7]. [Q4: A, C, D, E]
Treatment of Raynaud’s phenomenon is initially conservative – keeping warm,
avoiding cold exposure, and refraining from smoking (smoking is a risk factor for
severity of digital ischaemia in patients with systemic sclerosis [8]). If these measures do not suffice, then a vasodilator is prescribed, usually a calcium channel
blocker [9, 10]. There is no role for steroid therapy in most patients with systemic
sclerosis (and steroids are relatively contraindicated in patients with diffuse cutaneous disease). Biofeedback has gained considerable attention but was not found to
be effective in a randomised trial of primary Raynaud’s phenomenon [11]. [Q5: A, C,
D] If a patient has very severe digital ischaemia, with or without digital ulceration,
then the patient should be admitted for intravenous prostanoids [12] and, if there is
any question of infection, then intravenous antibiotics are also indicated.
The vascular surgeon is likely to be called to see a patient with severe Raynaud’s
(often in the context of systemic sclerosis) because of either non-healing ulceration
or because of very severe (sometimes critical) ischaemia. The reduced blood supply
Fig. 35.4
. Digital pulp calcinosis in a patient with systemic sclerosis – there is a risk that this deposit will
ulcerate.
Raynaud’s Phenomenon 319
impairs ulcer healing. Debridement often aids healing. However, a proportion of
patients come to amputation. Some patients have calcinosis at the site of the ulceration, and so this may be a complicating factor (Fig. 35.4). Severe ischaemia often
coexists with ulceration. Cervical sympathectomy is no longer advocated for upper
limb Raynaud’s phenomenon. Recently digital sympathectomy has attracted interest for the treatment of severe digital ischaemia in patients with systemic sclerosis
[10, 13]. Digital sympathectomy is unlikely to be indicated at this stage in our
patient, unless things do not settle with intravenous prostanoids, antibiotics and
debridement. At present there is no evidence base for anticoagulation in patients
with systemic sclerosis and digital ischaemia and/or ulceration although the possibility of an underlying coagulopathy, for example antiphospholipid syndrome,
should always considered in patients presenting with digital ischaemia. [Q6: A, B, C]
Finally, although the vascular abnormalities in systemic sclerosis are predominantly microvascular, an increased prevalence of large vessel disease in patients
with systemic sclerosis has recently been reported [14]. Thus the possibility of a
proximal obstruction should always be considered in patients with systemic sclerosis presenting with an ischaemic digit.
References
1. LeRoy EC, Medsger TA. Raynaud’s phenomenon: a proposal for classification. Clin Exp Rheumatol
1992;10: 485–8.
2. Herrick AL. Pathogenesis of Raynaud’s phenomenon. Rheumatology (in press).
3. Campbell PM, LeRoy EC. Pathogenesis of systemic sclerosis: a vascular hypothesis. Semin Arthritis
Rheum 1975;4:351–68.
4. Maricq HR, LeRoy EC. Patterns of finger capillary abnormalities in connective tissue disease by
“wide-field” microscopy. Arthritis Rheum 1973:16:619–28.
5. Harvey GR, McHugh NJ. Serologic abnormalities in systemic sclerosis. Curr Op Rheumatol
1999;11:495–502.
6. LeRoy EC, Black C, Fleischmajer R, et al. Scleroderma (systemic sclerosis): classification, subsets and
pathogenesis. J Rheumatol 1988;15:202–5.
7. Wigley FM, Wise RA, Miller R, Needleman BW, Spence RJ. Anticentromere antibody as a predictor
of digital ischemic loss in patients with systemic sclerosis. Arthritis Rheum 1992;35:688–93.
8. Harrison BJ, Silman AJ, Hider SL, Herrick AL. Cigarette smoking: a significant risk factor for digital
vascular diseases in patients with systemic sclerosis. Arthritis Rheum 2002:46:3312–16.
9. Thompson AE, Shea B, Welch V, Fenlon D, Pope JE. Calcium-channel blockers for Raynaud’s phenomenon in systemic sclerosis. Arthritis Rheum 2001;44:1841–7.
10. Herrick AL. Treatment of Raynaud’s phenomenon – update, new insights and developments. Curr
Rheumatol Rep 2003:5:168–74.
11. Raynaud’s Treatment Study Investigators: Comparison of sustained-release nifedipine and temperature biofeedback for treatment of primary Raynaud phenomenon. Results from a randomized clinical trial with 1-year follow-up. Arch Intern Med 2000;160:1101–8.
12. Wigley FM, Wise RA, Seibold JR, et al. Intravenous iloprost infusion in patients with Raynaud phenomenon secondary to systemic sclerosis. A multicenter, placebo-controlled, double-blind study.
Ann Intern Med 1994;120:199–206.
13. Tomaino MM, Goitz RJ, Medsger TA. Surgery for ischemic pain and Raynaud’s phenomenon in scleroderma: a description of treatment protocol and evaluation of results. Microsurgery 2001;21:75–9.
14. Ho M, Veale D, Eastmond C, Nuki G, Belch J. Macrovascular disease and systemic sclerosis. Ann
Rheum Dis 2000;59:39–43.
36. Aortofemoral Graft Infection
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Christopher P. Gibbons
A 66-year-old man, an ex-smoker with hypertension and hypercholesterolaemia,
had undergone a Dacron bifurcated aortic graft and bilateral ureteric stents for
an inflammatory aortic aneurysm with ureteric obstruction at another hospital
4 years previously. The left limb of the graft had been anastomosed to the
common femoral artery and the right limb to the common iliac bifurcation.
Postoperatively he had suffered a mild groin wound infection, which had healed
with antibiotics. At follow-up he complained of left calf and thigh claudication.
On examination, he appeared generally well with a midline abdominal scar and a
left vertical groin scar. He had good right femoral pulse but an absent left
femoral pulse.
Question 1
What should be the first investigation?
A. Intra-arterial digital subtraction angiography.
B. Duplex ultrasound scan of the aortic graft.
99
C.
Technetium-labelled leucocyte scan.
D. CT angiography of the graft.
E. Erythrocyte sedimentation rate.
A duplex scan showed an occluded left limb of the aortic graft with patent
common femoral arteries. There was no evidence of any stenosis of the left common
femoral artery but a perigraft fluid collection was noted around the intra-abdominal
portion of the graft.
323
324 Vascular Surgery
Fig. 36.1.
CT scan of aortic graft showing fluid and a gas bubble around the graft.
Question 2
What further investigations should be performed?
A. CT scan of the graft.
B. Digital subtraction angiography.
C.99Technetium-labelled leucocyte scan.
D. Erythrocyte sedimentation rate.
E. Aspiration of the collection.
A CT scan confirmed the presence of fluid and gas around the intra-abdominal
portion of the graft and the occlusion of the left limb, indicating graft infection (Fig.
36.1). Digital subtraction angiography (Fig 36.2) confirmed the occluded left limb of
the aortic graft and showed a stenosis at the origin of the right graft limb, presumably as a result of external compression. Aspiration of the perigraft collection would
have allowed preoperative bacterial culture but was considered to be too difficult to
perform safely.
Question 3
Having confirmed the presence of infection what is the best option for management?
A. Prolonged antibiotic therapy.
B. Drainage of the perigraft pus under anaesthesia.
C. Insertion of gentamicin beads.
Aortofemoral Graft Infection 325
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Fig. 36.2.
Intra-arterial digital subtraction angiography (DSA) of the aortoiliac region.
D. Excision of the graft.
E. Excision of the graft with in situ replacement with an antibiotic bonded graft.
F. Graft excision and extra-anatomical prosthetic bypass.
G. Graft replacement with autologous vein.
H. Graft replacement with an aortic allograft.
In situ replacement with autologous vein was chosen because of the reduced risk
of persistent infection.
Question 4
Which autologous veins may be used for aortoiliac or aortofemoral graft replacement?
A. Long saphenous vein.
B. Cephalic vein.
C. Femoropopliteal vein.
D. Iliac vein.
Femoropopliteal vein was used as it is ideally suited to supra-inguinal graft
replacement as it is relatively thick-walled, is of adequate diameter and has
sufficient length.
326 Vascular Surgery
Question 5
What further preoperative investigations should be performed?
A. Plain abdominal X-ray.
B. Bone scan.
C. MRI scan of the abdomen.
D. Duplex scan of the femoral veins.
E. Repeat abdominal ultrasound scan.
A duplex scan of the femoral veins confirmed that they were patent and of adequate calibre. The patient was operated on electively on the next available operating
list.
Question 6
What other preoperative preparations should be undertaken?
A. Routine full blood count.
B. Urea and electrolyte estimation.
C. Chest X-ray and electrocardiogram (ECG).
D. Compression stockings.
E. Subcutaneous heparin.
F. Combination antibiotic therapy.
Routine blood investigations, chest X-ray and ECG were all performed, and in
view of the magnitude of the procedure, echocardiogram and lung function tests
were also ordered. They were all satisfactory. Because the bacteriology of the infection was not known preoperatively in this patient, intravenous combination
antibacterial therapy with teicoplanin, ciprofloxacin, co-amoxiclav and metronidazole was given immediately before surgery.
Question 7
How should the operation be performed?
A. Laparotomy, excision of the aortic graft, harvesting of the femoral veins and
graft replacement.
B. Harvesting of femoral veins followed by laparotomy, excision of the infected
graft and replacement with femoral vein.
C. Laparotomy and exposure of the infected graft, then femoral vein harvest fol-
lowed by graft replacement.
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