61 Arterial disorders

AMPUTATION General
ANEURYSM General
ARTERIAL STENOSIS AND OCCLUSION Cause and effect
ARTERIOVENOUS FISTULA
ARTERITIS AND VASOSPASTIC CONDITIONS Thromboangiit
Abdominal aortic aneurysm
Acrocyanosis
Acute limb ischaemia
Acute mesenteric ischaemia
Clinical features
Cystic myxomatous degeneration
Distal and transmetatarsal amputation
Embolic occlusion
FURTHER READING
Features of chronic arterial stenosis or occlusion
Femoral aneurysm
GANGRENE
Iliac aneurysm
Introduction
Investigation of arterial occlusive disease
Learning objectives
Major amputation
Management of arterial stenosis or occlusion
Miscellaneous
Operations for arterial stenosis or occlusion
Other forms of arteritis
Other forms of embolism
PERIPHERAL ANEURYSM Popliteal aneurysm
Raynaud’s disease
Raynaud’s syndrome
Separation of gangrene
Speciﬁc varieties of gangrene
Sympathectomy
Treatment of gangrene
disease

AMPUTATION General

Amputation should be considered when part of a limb is dead, deadly or a dead loss. A limb is dead when arterial occlusive disease is severe enough to cause infarction of macroscopic portions of tissue, i.e. gangrene. The occlusion may be in major vessels (atherosclerotic or embolic occlusions) or in small peripheral vessels (diabetes, Buerger’s disease, Raynaud’s disease, inadvertent intra-arterial injection). If the obstruction cannot be reversed and the symptoms are severe, amputation is required. Gabrielle Falloppio (Fallopius) , 1523–1563, Professor of Anatomy , Surgery and Botany , Padua, Italy . Friedrich Trendelenburg , 1844–1924, Professor of Surgery , successively at Rostock, Bonn and Leipzig, Germany . Leo Buerger , 1879–1943, Professor of Urologic Surgery , New Y ork Polyclinic Medical School, New Y ork, NY , USA, described thromboangiitis obliterans in 1908. Maurice Raynaud , 1834–1881, physician, Hôpital Lariboisière, Paris, France, described this condition in 1862. moist gangrene spreads to surrounding viable tissues. Cellulitis and severe toxaemia are the result. Amputation is required as a lifesa ving operation. Antibiotic cover should be broad and massive. Other life-threatening situations for which ampu - tation may be required include gas gangrene (as opposed to simple infection), neoplasm (such as osteogenic sarcoma) and arteriovenous ﬁstula. Filaria A limb may be deemed a dead loss in the following circum - stances: ﬁrst, when there is relentless severe rest pain without g angrene and reconstruction is not possible – amputation will improve quality of life; second, when a contracture or paralysis makes the limb impossible to use and renders it a hindrance; and third, when ther e is major unrecoverable traumatic damage. Summary box 61.3 Indications for amputation /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF - /uni25CF /uni25CF

Dead limb Gangrene Deadly limb Wet gangrene Spreading cellulitis Arteriovenous /f_i stula Other (e.g. malignancy) ‘Dead loss’ limb Severe rest pain with unreconstructable critical leg ischaemia Paralysis Other (e.g. contracture, trauma)

ANEURYSM General

Dilatations of localised segments of the arterial system are called aneurysms when there is a ≥ 50% increase in the diam - eter of the vessel; below 50% they are termed ectatic. They can either be true aneurysms, containing the three layers of the arterial wall (intima, media, adventitia) in the aneurysm sac, or false aneurysms, having a single layer of ﬁbrous tissue as the wall of the sac, e .g. aneurysm following trauma. Aneu - rysms can also be grouped according to their shape (fusiform, saccular) or their aetiology (atheromatous, traumatic, mycotic, etc.). The term mycotic is a misnomer because, although it indicates infection as the cause of the aneurysm, it is due to bacteria, not fungi. Aneurysms may occur in the aorta or in the iliac, femoral, popliteal, subclavian, axillary , carotid, cerebral, mesenteric, splenic and renal arteries and their branches. The majority are true fusiform atherosclerotic aneurysms.

Tibial tuberosity 10 cm 10 cm 2/3 1/3 = Incision (b) (c)

ARTERIAL STENOSIS AND OCCLUSION Cause and effect

Peripheral arterial stenosis or occlusion is predominantly caused by atherosclerosis and/or thromboembolic disease, but may also occur as a result of trauma. Stenosis or occlusion produces symptoms and signs that relate to the organ supplied by the artery: e.g. lower limb – claudication, rest pain and gangrene; brain – transient ischaemic attacks (TIAs) and stroke; myocardium – angina and myocardial infarction; intestine – abdominal pain and infarction ( 61.1 ). The severity of the symptoms relates to the size of the vessel occluded and whether the stenosis or occlusion occurs suddenly (acute) in a previously normal artery or gradually (chronic) with progressive narrowing of the artery over time. In chronic stenosis symptoms may be abated despite being a ﬀ ected by signiﬁcant steno-occlusive disease as a result of Claudication from the Latin ‘claudicare’ – to limp. The Roman emperor Claudius (10 /uni00A0 the development of a collateral circulation that provides an alternative, albeit less e ﬀ ective, route for blood to reach the target tissue/organ ( Figure 61.2 ). - Figure /b.sc/c.sc/e.sc to 54 /uni00A0 /c.sc/e.sc ) walked with a limp, which was possibly due to poliomyelitis.

The nature and presentation of aneurysmal disease, • including the abdominal aorta and popliteal artery The investigation and treatment options for aneurysmal • disease The arteritides and vasospastic disorders • CA Aorta SMA Figure 61.1 Antegrade aortogram via retrograde brachial artery access demonstrating superior mesenteric artery stenosis (arrow). CA, coeliac artery; SMA, superior mesenteric artery.

CFA PA PFA Figure 61.2 (a) Digital subtraction angiogram from the common fem oral artery (CFA) demonstrating a /f_l ush right super /f_i cial femoral artery occlusion (arrow). (b) Reconstitution of the popliteal artery (PA) at the adductor hiatus via collateral /f_l ow from the profunda femoris artery (PFA) via the geniculate arteries (arrows).

ARTERIOVENOUS FISTULA

Communication between an artery and a vein may be either a congenital malformation or the result of trauma. Arteriovenous ﬁstulae for haemodialysis access are also created surgically . All arteriovenous communications have a structural and a physiological e ﬀ ect. The structural e ﬀ ect of arterial blood ﬂow on the veins is characteristic; they become dilated, tortuous and thick walled (arterialised). The physiological e ﬀ ect, if the ﬁstula is large, is an increase in cardiac output that may lead to cardiac failure. A pulsatile swelling may be present if the lesion is superﬁ - cial. A thrill is detected on palpation and auscultation reveals a buzzing continuous bruit (‘machinery murmur’). Dilated veins may be seen and pressure on the artery proximal to the ﬁstula reduces the swelling and the thrill and bruit cease. Duplex scan and/or angiography conﬁrms the lesion that shows rapid venous ﬁlling. Treatment is often complex and usually involves embolisation. Excision surgery is sometimes used for severe deformity or recurrent haemorrhage; the assistance of a plastic surgeon is wise. Ligation of a ‘feeding’ artery usually fails and may preclude treatment by embolisation.

ARTERITIS AND VASOSPASTIC CONDITIONS Thromboangiit

ARTERITIS AND VASOSPASTIC CONDITIONS Thromboangiitis obliterans (Buerger’s disease)

This is characterised by occlusive disease of small and medium-sized limb arteries, thrombophlebitis of superﬁcial or deep veins and Raynaud’s syndrome; it usually occurs in young male smokers. Histologically , there are inﬂammatory changes in the walls of arteries and veins, leading to thrombo sis. Treatment is total abstinence from smoking, which arrests, but does not reverse, the disease. Established arterial occlusions are treated as for atheromatous disease, b ut amputations may eventually be required.

Abdominal aortic aneurysm

Abdominal aortic aneurysm is by far the most common type of large-vessel aneurysm and is found in 2% of the population at autopsy; 95% have associated atheromatous degeneration and 95% occur below the renal arteries. Most remain asymptomatic until rupture occurs; the risk of rupture increases with increasing size (diameter) of the aneurysm. Asymptomatic aneurysms are found incidentally on physical examination, radiography or ultrasonography investigation. A UK national screening programme for abdominal aortic aneurysm commenced in 2009 o ﬀ ering an ultrasonography scan to men in their 65th year. Symptomatic aneurysms may cause minor symptoms, such as back and abdominal discomfort, before sudden, severe back and/or abdominal pain develops from expansion and compression of surrounding structures, e.g. aortoenteric ﬁstula or ureteric obstruction. Asymptomatic abdominal aortic aneurysm An asymptomatic abdominal aortic aneurysm ( Figure 61.39 ) in an otherwise ﬁt patient should be considered for repair if >55 /uni00A0 mm in diameter, measured by ultrasonography in the anteroposterior plane. The annual incidence of rupture rises exponentially as the aneurysm size passes 55 /uni00A0 mm: ≤ 1% are in aneurysms that are <55 /uni00A0 mm in diameter, 5–10% are in those that are 55–60 /uni00A0 mm in diameter and ~25% are in those that are ≥ 70 /uni00A0 mm in diameter. Assuming that open elective surgery (transabdominal) carries a 5% mortality rate, the balance is in favour of elective operation once the maximum diameter is >55 /uni00A0 mm, provided there is no major comorbidity . Regular ultrasonography surveillance is indicated for asymptomatic aneurysms <55 /uni00A0 mm in diameter. Investigations Full blood count, electrolytes, liver function tests, coagulation tests and blood lipid estimation should be performed. Blood should be cross-matched a few days prior to surgery . Many

(a) (b) Figure 61.39 Ultrasonogram of an aortic aneurysm showing the large clot- /f_i lled sac with a small central lumen (transverse and longitudinal scans).

patients now have an anaesthetic assessment and the need for cardiac and respiratory function tests is decided at this time. ECG and chest radiographs are essential; further assessment may include echocardiograph, cardiopulmonary exercise testing and spirometry . The morphology of the aneurysm is best assessed by computed tomography (CT) scan; this can be reconstructed on imaging software to create a three-dimensional model of the aneurysm ( Figures 61.40 and 61.41 ). Seventy-ﬁve per cent of aneurysms are suitab le for endovascular (minimally invasive) repair, usually via the femoral arteries in the groin. If occlusive disease that should be assessed by DUS initially . Further assessment with CT , MRA or digital subtraction angiography may be required and angioplasty may be appropriate. The aneurysm is often ﬁ lled with cir cumferential clot ( Figure 61.42a ) that produces a falsely narrowed appearance on DSA ( Figure 61.42b ); this method should not therefore be used to assess aneurysm size. Choice of operation: open or endovascular repair In recent years there has been much discussion regarding the optimal way to treat an abdominal aortic aneurysm with both open surgical repair and endovascular aneurysm repair (EV AR) having vocal advocates in the scientiﬁc literature. The National Institute for Health and Care Excellence (NICE) in the UK published guidelines in 2020 recommending open surgical repair unless contraindicated, reserving EV AR for high-risk patients or those with a hostile abdomen. This compares to the European Society for Vascular Surgery 2019 guidelines, which recommend EV AR as the ﬁrst-line treatment option with open surgical repair to be considered for patients with long life expectancy . Pragmatically , the clinician should be prepared to undertake what they and the patient (after a detailed conversation) agree to be the best option, taking into account the skillset and resource availability and often, unfortunately , the ﬁnancial constraints of the patient or healthcare system. Open aneurysm repair Under general anaesthesia, with the patient lying supine, a full-length midline or supraumbilical transverse incision is made. The small bowel is lifted to the patient’s right and the aorta identiﬁed. The posterior peritoneum overlying the aorta is opened and the upper limit of the aneurysm identiﬁed. The aorta immediately above the dilatation is exposed; this is generally just inferior to the left renal vein and renal arteries ( Figure 61.43 ). The common iliac arteries are then exposed and clamps applied above and below the lesion.

Figure 61.40 Computed tomography of the abdomen showing an infrarenal aortic aneurysm in the coronal plane (arrow). Blood /f_l owing through the thrombus-containing sac is enhanced with contrast agent and appears white. (a) (b) Figure 61.41 (a) Maximum intensity projection reconstruction of an aortic aneurysm from a spi

ral computed tomogram. (b) Three-dimensional reconstruction of an abdominal aortic aneurysm.

Many surgeons give systemic heparin (3000–5000 /uni00A0 U) before clamping. The aneurysm is opened longitudinally and back- bleeding from the lumbar and mesenteric vessels is controlled by sutures placed from within the sac. Upper and lower aortic necks are prepared to which an aortic prosthesis is then sutured end-to-end inside the sac with a monoﬁlament non-absorbable suture ( Figure 61.44 ). Clamps are released slowly to prevent sudden hypotension. If haemostasis is satisfactory at this point, the aneurysm sac is closed around the prosthesis to exclude both it and the suture lines from the bowel to reduce the risk of adherence and potential ﬁstula formation. The abdomen is then closed. Occasionally , when the iliac vessels are also involved with dilatation or severe atheroma, it is necessary to construct an aortobi-iliac or aortobifemoral bypass, rather than use a simple aortoaortic tube. Endovascular aneurysm repair EV AR is now established in clinical practice and has been shown to reduce mortality compared with open repair over the ﬁrst 6 years but there are concerns about long-term durability . Currently about 75% of infrarenal aneurysms are suitable for EV AR, depending on the morphology of the aneurysm as assessed by CT scan. Common causes of unsuitability include a short, ﬂared or angulated neck and di ﬃ cult iliac artery access because of narrowing or tortuosity . The usual technique is to expose both femoral arteries (under general or local anaesthetic), which allows access to the aorta. Then, under radiological control, guidewires and catheters are used to cross the aneurysm and an angiogram performed to mark the level of the renal arteries. The endovascular prosthesis (often termed a ‘stent graft’) is usually made up of three separate parts: a main body ( Figure 61.45a ) and two limbs that are enclosed in separate delivery catheter s ( Figure 61.45b ). Some types have only two pieces: a main body with an ipsilateral limb attached and a separate contralateral limb. The prosthesis is made from Dacron or PTFE with integral metallic stents for support. The delivery catheter is inserted into the aneurysm sac and the stent–graft deployed by withdrawal of the delivery system. Most systems now have hooks or barbs to anchor the prosthesis in the aortic wall, and some surgeons inﬂate a moulding balloon catheter in the stent–graft to ensure that the hooks and barbs are engaged and a good seal is obtained ( Figure 61.46 ). Although the top edge of the fabric of the stent–graft has to be deployed below the renal arteries (infrarenal ﬁxation), some systems have additional bare metal stents at the proximal end of the main body that lie across the renal arteries to give better support and ﬁxation (suprarenal ﬁxation). Blood ﬂows between the metal struts of the stent into the renal arteries. Success is dependent on a good seal between the stent–graft and the proximal and distal ‘landing zones’ in the aorta and iliac arteries. Failure to achieve a good seal results in an endoleak, which means that the aneurysm is not excluded from the circulation and may still expand and rupture. Patients who undergo EV AR require lifelong follow-up and surveillance with duplex ( Figure 61.47 ) or CT scans to detect endoleak, disconnection

(b) Figure 61.42 (a) Thrombus removed from an abdominal aortic aneurysm; this thrombus is the reason an angiogram may give a false impression of aneurysm diameter on digital subtraction angiography (b) . Figure 61.43 Operative appearance of a large, non-ruptured infrarenal abdominal aortic aneurysm.

Figure 61.44 (a) Aneurysm sac opened. Note that the posterior wall of the aorta immediately above and below the sac is not divided. A Dacron tube graft is laid in place within the sac ready for suture. (b) The graft is sutured in place and the vascular clamps removed. (a) (a) (b) (b) Figure 61.45 (a) Endovascular prosthesis main body; with separate limbs (b) . Figure 61.46 Infrarenal aortic aneurysm before (a) and after (b) endovascular aneurysm repair.

of the components and migration of the stent–graft, all of which predispose to late rupture ( Figure 61.48 ). Ruptured abdominal aortic aneurysm Abdominal aortic aneurysms can rupture anteriorly into the peritoneal cavity (20%) or posterolaterally into the retroperitoneal space (80%). Less than 50% of patients with rupture survive to reach hospital. Anterior rupture results in free bleeding into the peritoneal cavity; very few patients reach hospital alive. Posterior rupture on the other hand produces a retroperitoneal haematoma ( Figure 61.49 ). Often a brief period ensues when a combination of moderate hypotension and the resistance of the retroperitoneal tissues arrests further haemorrhage and may allow transport to hospital. The patient may remain conscious but in severe pain. If no operation is performed, death is virtually inevitable. Operative mortality is around 50% and the overall combined mortality (community and hospital) is around 80–90%. Ruptured abdominal aortic aneurysm is a surgical emergency; it should be suspected in a patient with the triad of severe abdominal and/or back pain, hypotension and a pulsatile abdominal mass. If there is doubt about the presence of an aneurysm an ultrasonog raphy scan may help but this cannot diagnose rupture. CT scanning should be used to establish the diagnosis and to conﬁrm a rupture and whether an EV AR is possible: EV AR should be considered as the ﬁrst-line option for all anatomically suitable ruptured aortic aneurysms. Good venous access is needed for infusion of saline or volume-expanding ﬂuids, but the systolic blood pressure should not be raised any more than is necessary to maintain

Figure 61.47 Duplex ultrasonography scan post endovascular aneurysm repair (EVAR), showing the aortic sac in cross-section and two limbs of EVAR (red ovals). There is a type II endoleak from the inferior mesenteric artery, with blood /f_l owing retrogradely into the aneurysm sac (arrow). Figure 61.48 A stent–graft retracted into the aneurysm sac, creating a type Ib endoleak. Figure 61.49 The retroperitoneal haematoma of a ruptured aortic aneurysm. The aortic pulsation is palpated through the haematoma at its upper limit and /f_i ngers are insinuated on each side of the aorta. With /f_i nger control, the upper clamp is positioned and closed on the aorta. The procedure is then as for a planned case. Here, the clamp is at the proximal end of the aneurysm; the haematoma has spread from the left paracolic gutter to encircle the aneurysm and the aortic bifurcation.

After CT scanning, the patient should be transferred immediately to an operating theatre where a urinary catheter and arterial line are usually inserted. If the patient appears stable, surgery may be delayed until cross-matched blood is available but surgery should commence immediately if haemodynamic instability develops. For open surgical repair the abdomen is usually prepared and draped with the patient awake, minimising potential delays in cross-clamping the aorta as general anaesthesia is often accompanied by haemodynamic deterioration. Endovascular repair can often be performed under local anaesthetic and, if indicated, an aortic occlusion balloon catheter can be inserted to gain control in a patient with signiﬁcant haemodynamic compromise. Always remember that the treatment of ruptured aneurysm is an operation, not monitoring and resuscitation. Summary box 61.5 Management of ruptured abdominal aortic aneurysm /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF Symptomatic abdominal aortic aneurysm These patients most commonly present with abdominal and/ or back pain but the aneurysm is not ruptured on CT scan. Pain may also occur in the thigh and groin because of nerve compression. Gastrointestinal, urinary and venous symptoms can also be caused by pressure from an abdominal aneurysm. About 3% of all aneurysms cause pain as a result of inﬂamma tion of the aneurysm itself ( Figure 61.50 ). Finally , a few cause symptoms from distal embolisation of intraluminal thrombus. An operation is usually indicated in patients who are otherwise reasonably ﬁt. Pain ma y be a warning sign of stretching of the aneurysm sac and imminent rupture; surgery should be performed as soon as possible (usually on the next available operating list). The operative mortality of symptomatic aneu rysms is usually higher than that for elective cases. Postoperative complications The most common complications after open repair are cardiac (ischaemia and infarction) and respiratory (atelectasis and lower lobe consolidation). A degree of colonic ischaemia because of a lack of a collateral blood supply occurs in about 10% of patients, but this usually resolves spontaneously . Acute kidney injury is an uncommon event after elective procedures but may complicate procedures undertaken for rupture. Acute kidney injury is more likely if there is preoperative renal impairment or considerable intraoperative blood loss. Neurological compli cations include sexual dysfunction and spinal cord ischaemia. An aortoduodenal ﬁstula is an uncommon but treatable complication of abdominal aortic replacement surgery . It should be suspected whenever haematemesis or melaena - occurs in the months or years after operation. Prosthetic graft infection is also uncommon; it may require explantation of the original graft and replacement with an autologous deep vein (superﬁcial femoral vein) graft or removal of the original graft with oversewing of the aortic stump and limb revascularisation by insertion of an axillobifemoral bypass. Both techniques are associated with signiﬁcant risk of perioperative morbidity and - mortality . Cardiac, respiratory , renal and neurological complications are less common after endovascular repair. However, there are complications that are unique to EV AR, suc h as endoleak ( Table 61.3 ), graft migration, metal strut fracture and graft limb occlusion. Lifelong surveillance with duplex or CT scans (together with plain abdominal radiographs for strut fracture) is required to detect endoleak and migration. High-pressure endoleaks may require repeat ballooning or a proximal cu ﬀ or distal limb extension to reseal the endograft. Migration may also require extension of the graft. Overall, 10–20% of patients with EV AR will require secondary interventions to - treat complications at some future date, although many of the interventions can be performed with a percutaneous approach via the femoral artery in the angiography suite.

Early diagnosis (abdominal/back pain, pulsatile mass, shock) Immediate resuscitation (oxygen, intravenous replacement therapy, central line) Maintain systolic pressure, but not >100 /uni00A0 mmHg Urinary catheter Cross-match blood Rapid transfer to the operating room Figure 61.50 An in /f_l ammatory abdominal aortic aneurysm. Note the white ‘icing’ effect. Such lesions can be technically dif /f_i cult to manage.

endovascular aneurysm repair. Type of endoleak De /f_i nition Type I Persistent /f_i lling of the aneurysm sac owing to an ineffective seal at the proximal (Ia) or distal (Ib) end of the stent–graft Type II Persistent /f_i lling of the aneurysm sac owing to retrograde /f_l ow of blood from aortic collaterals, e.g. IMA, lumbar arteries Type III Persistent /f_i lling of the aneurysm sac owing to structural failure of the stent–graft as a result of component disconnection (IIIa) or stent fabric tear (IIIb) Type IV Persistent /f_i lling of the aneurysm sac owing to stent–graft fabric porosity Type V (endotension) Persistent /f_i lling of the aneurysm sac without evidence of types I–IV endoleak IMA, inferior mesenteric artery.

Acrocyanosis

Acrocyanosis may be confused with Raynaud’s disease but it is painless and not episodic. It tends to a ﬀ ect young women and the mottled cyanosis of the ﬁngers and/or toes may be accompanied by paraesthesia and chilblains.

Acute limb ischaemia

ALI is an emergency that requires rapid, accurate clinical assessment and emergency surgical treatment. ALI typically - occurs as a result of embolic arterial occlusion or trauma, but less common causes, including thrombosed popliteal artery aneurysm and popliteal artery entrapment, should be kept in mind during patient assessment. Clinicians reviewing a patient with sudden onset leg pain should have a high index of suspicion for ALI as an incorrect diagnosis can be catastrophic for the patient; ischaemia beyond 6 hours is usually irreversible and results in limb loss. Clinical features Patients presenting with ALI secondary to embolism typically give no history of prior claudication and complain of the sudden development of severe pain or numbness of the limb. Bedside clinical assessment should be aimed at (i) conﬁrming the diagnosis of ALI, (ii) assessing the severity of the limb ischaemia, and (iii) identifying the underlying cause, including an embolic source. The skin is initially cold and pale, but as time progresses it slowly becomes mottled; ﬁrst, non-ﬁxed (blanching to pressure) and then ﬁxed (non-blanching), indicating skin death. Neu - rological function deteriorates with time, prog ressing from paraesthesia to eventual complete loss of sensory and motor function, causing an insensate and paralysed limb (a poor prog - nostic sign). Muscle groups are weakened and painful; manual compression of a ﬀ ected muscle groups may cause pain owing to ischaemia-induced injury – rhabdomyolysis.

Figure 61.31 Aortic bifurcation thrombosis: claudication is worse but there is no dramatic event owing to the network of collaterals formed as a result of the insidious nature of the stenosis; acute on chronic disease.

Pulses are absent distally but the femoral pulse may be palpable, even thrusting, as distal occlusion results in forceful expansion of the artery with each pressure wave despite the lack of ﬂow . Insonation of the pedal vessels with a hand-held Doppler may elicit faint monophasic signals or no signals at all. Assessment of ﬂow in the limb veins, including the GSV and popliteal vein, can be useful as concurrent venous thrombosis is a very poor prognostic indicator. Following thorough clinical examination, the limb should be classiﬁed according to the Rutherford categories of ALI: class I, viable; class IIa, marginally threatened; class IIb, immediately threatened; and class III, irrever sible. The management options and urgency of treatment depend on the appropriate categorisation of the limb ( Table 61.2 ). Investigations should be undertaken as clinically indicated and may include: /uni25CF ECG to assess for myocardial infarction and/or atrial ﬁbrillation; /uni25CF creatinine kinase to assess for rhabdomyolysis; /uni25CF renal function as rhabdomyolysis may lead to myoglobin uria and acute kidney injury; /uni25CF imaging assessment of the a ﬀ ected limb’s arterial tree, e.g. DUS or CTA, if readily available and not likely to unnec essarily delay emergency treatment when indicated, e.g. Rutherford class IIb A similar picture will occur in the arm with a brachial embolus. Treatment Because of the ensuing stasis, a thrombus can extend distally and proximally to the embolus. The immediate administration of 5000 /uni00A0 U of heparin intravenously can reduce this extension and maintain patency of the surrounding (particularly the distal) vessels until the embolus can be treated. The relief of pain is essential because it is severe and constant. Embolectomy and thrombolysis are the treatments available for patients with limb emboli. Embolectomy Local or general anaesthesia may be used. The artery (usually the femoral), bulging with clot, is exposed and held in silastic vessel loops. Through a transverse incision the clot Robert Rutherford , 1931–2013, Professor of Surgery , Colorado, USA. Thomas J Fogarty , b. 1934, surgeon, University of Oregon Medical School, Portland, OR, USA. begins to extrude and is removed, together with the embolus ( Figure 61.32 ), with the help of a Fogarty balloon catheter. The catheter, with its balloon tip, is introduced both proximally and distally until it is deemed to have passed the limit of the clot. The balloon is inﬂated and the catheter withdrawn slowly , together with any obstructing material ( Figure 61.33 ). The procedure is repeated until bleeding occurs. An angiogram (a) (b ) - -

Grade Category Sensory loss Motor de /f_i cit Doppler signals Prognosis I Viable None IIA Marginally threatened None or minimal None (toes) IIB Immediately threatened More than toes Mild/moderate Inaudible Audible Salvageable with immediate III Irreversible Profound or Paralysed Inaudible Inaudible Limb irreversibly damaged, major insensate Arterial Venous None Audible Audible No immediate threat Inaudible Audible Salvageable if promptly treated revascularisation tissue loss, amputation Figure 61.32 Embolic material removed from the common femoral artery, along with a long distal extension thrombus. Figure 61.33 (a) A Fogarty catheter is inserted through an arteriotomy in the common femoral artery and fed distally down the super /f_i cial femoral artery and through the embolus. (b) The balloon is in /f_l ated and the catheter withdrawn, removing the embolus; the deep femoral and iliac arteries are similarly treated.

may be performed in the operating theatre at the end of the procedure to ensure that ﬂow to the distal leg has been restored. Postoperatively , heparin therapy is continued until long-term anticoagulation with warfarin is established to reduce the chance of further embolism. Thrombolysis If ischaemia is not so severe that immediate operation is essen tial, it may be possible to treat either embolus or thrombosis by intra-arterial thrombolysis ( Figure 61.34 ). At arteriography of the ischaemic limb (usually via the CFA) a narrow catheter is passed into the occluded vessel and left embedded within the clot. Tissue plasminogen activator is infused thr ough the catheter and regular arteriograms are carried out to check on the extent of lysis, which, in successful cases, is achieved within 24 hours. The method should be abandoned if there is no progression of dissolution of clot with time. There are several contraindications to thrombolysis, the most important of which are recent stroke, bleeding diathesis and pregnancy , and results in those over 80 years old are poor. Compartment syndrome In limbs that have been subject to sudden ischaemia followed by revascularisation, oedema is likely . Muscles swell within conﬁned fascial compartments and this can itself be a cause of tissue ischaemia, with both local muscle necrosis and nerve damage due to pressure and systemic e ﬀ ects such as renal failure secondary to the liberation of muscle breakdown products. The classical clinical picture is that of severe pain out of proportion with clinical ﬁndings that worsens with time despite appropriate analgesia. The patient often complains of numbness/paraesthesia in the distribution of nerv es running within the compartment (non-myelinated type C sensory ﬁbres are most sensitive to hypoxia). Examination of the limb reveals a tense compartment with passive ﬂexion and extension of - muscles causing pain. The presence of palpable pulses does not rule out compartment syndrome. The treatment is urgent compartment fasciotomy to release the compression. The usual site for fasciotomy is the calf (espe - cially the anterior tibial compartment), but compartment syn - drome may occasionally a ﬀ ect the thigh, arm and foot. Liberal concomitant usage of calf with/without thigh fasciotomies following r evascularisation of a prolonged ischaemic limb is advisable ( Figure 61.35 ).

Figure 61.34 Angiogram of an occluded popliteal artery before thrombolysis (a) , during successful lysis (b) and after completion of lysis (c) . (b) Figure 61.35 (a) Foot and calf fasciotomies; (b) thigh fasciotomy: the medial compartment rarely requires decompression

Acute mesenteric ischaemia

Acute mesenteric occlusion may be either thrombotic (follow - ing atheromatous narrowing) or embolic. Embolic occlusion results in sudden, severe abdominal pain, with bowel emptying (vomiting and diarrhoea) and a source of emboli present (usually cardiac). Unfortunately , the diagnosis is often only made at y with widespread infarction of the small and large laparotom bowel present; in this situation it is often fatal. Occasionally , the degree of bowel infarction is more limited; resection of the dead bowel and embolectomy of the superior mesenteric ity rate in these patients. A ‘second look’ laparotomy 24 hours later to check the viability of the bowel may be indicated.

Clinical features

The majority of arterial aneurysms are asymptomatic at the time of identiﬁcation and are often identiﬁed during routine health checks or investigations for other pathologies. Aneurysms measuring twice the size of the corresponding normal vessel are at increased risk of becoming symptomatic. The symptoms relate to the vessel a ﬀ ected and the tissues it supplies and occur as a result of compression of surrounding structures, thrombosis, rupture or the release of emboli. Many aneurysms of clinical signiﬁcance can be palpated and, typically , an expansile pulsation is felt. Transmitted pulsation through a mass lesion, cyst or abscess lying adjacent to a large artery may be mistaken for aneurysmal pulsation. Before incising a swelling believed to be an abscess it is essential to make sure that it does not pulsate. Finally , a tortuous (and often

(e) (f) Figure 61.37 (a) Schematic representation of operative markings for a long posterior /f_l ap below-knee amputation. (b) Lateral view of opera

tive markings. (c) Anterior view of operative markings. (d) Lateral view following removal of the leg. (e) Anterior view following removal of the leg. (f) Wound closure with a suction drain and local anaesthetic infusion ‘stump’ catheter.

Summary box 61.4 Classiﬁcation of aneurysms /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF ectatic) artery , usually the innominate or carotid, may seem like an aneurysm to the inexperienced clinician.

Figure 61.38 In /f_l atable arti /f_i cial limb. Wall Aetiology True (three layers: intima, Atheromatous media, adventitia) Mycotic (bacterial rather than fungal) False (single layer of /f_i brous tissue) Collagen disease Traumatic Morphology Fusiform Saccular

Cystic myxomatous degeneration

This is typiﬁed by an accumulation of clear jelly (like a synovial ganglion) in the outer layers of a main artery , especially the popliteal artery . The lesion may narrow the vessel, causing claudication. Duplex scan is the investigation of choice. Decompression, by removal of the myxomatous material, may be successful but in some cases excision of the diseased artery with interposition vein graft repair is required.

Distal and transmetatarsal amputation

In patients with small-vessel disease, typically caused by DM, gangrene of the toes may occur with relatively good blood supply to the surrounding tissues. In such circumstances local amputation of the digits can result in healing. However, if the metatarsophalangeal joint region is involved, a ray excision is required, taking part of the corresponding metatarsal bone and cutting tendons back. Most surgeons leave the wound open. Early mobility aids drainage, provided that cellulitis is not present. For less extensive gangrene, if amputation is taken through a joint, healing is improved by removing the cartilage from the joint surface. A transmetatarsal amputation may be required when several toes are a ﬀ ected but the proximal circulation is adequate. The wound may be closed with a viable long plantar ﬂap or left open ( Figure 61.36 ).

Figure 61.36 Transmetatarsal amputation for diabetic gangrene of the toes.

Embolic occlusion

An embolus is an object that has become lodged in a vessel and causes obstruction, having been carried in the bloodstream from another site. It is often a thrombus that has become detached from the heart or a more proximal vessel. Sources include the left atrium in atrial ﬁbrillation; a left ventricular mural thrombus following myocardial infarction; vegetations on heart valves in infective endocarditis; and thrombi in aneu rysms and on atherosclerotic plaques. Emboli may lodge in any organ and cause ischaemic symptoms. /uni25CF Arm and leg – pain, pallor, paraesthesia, paralysis and pulselessness (the ﬁve Ps of acute limb ischaemia [ALI]) (see Acute limb ischaemia ) ( Figure 61.29 ). Acute arterial occlusion due to an embolus di ﬀ ers from occlusion due to thrombosis on pre-existing atheroma; in the latter ( Figures 61.30 and 61.31 ). It is essential to di ﬀ erentiate between the two as they require di ﬀ erent management. - /uni25CF Brain – the middle cerebral artery (or its branches) is most commonly a ﬀ ected, resulting in TIA or stroke. /uni25CF Retina – amaurosis fugax is ﬂeeting blindness caused by a minute thrombus emanating from an atheromatous plaque in the carotid artery passing into the central retinal artery . Lasting obstruction causes permanent blindness. /uni25CF Mesenteric vessels – possible gangrene and perfora - tion of the corresponding loop of intestine.

Embolus Pain Paralysis Pallor Pulseless Figure 61.29 The symptoms and signs of embolism (four Ps). The /f_i fth feature, anaesthesia, is often stated to be paraesthesia (the /f_i fth P), but, in truth, complete loss of sensation in the toes and feet is characteristic. Figure 61.30 Aortic bifurcation embolus. The source of the embolus is a recent myocardial infarct or atrial /f_i brillation. This causes severe, dramatic symptoms.

Features of chronic arterial stenosis or occlusion

Features of chronic arterial stenosis or occlusion in the leg

Intermittent claudication Intermittent claudication occurs as a result of anaerobic muscle metabolism and is classically described as debilitating cramp-like pain felt in the muscles that is: /uni25CF brought on by walking; /uni25CF not present on taking the ﬁrst step (unlike osteoarthritis); /uni25CF relieved by rest in both the standing and sitting positions, usually within 5 minutes (unlike nerve compression from a lumbar intervertebral disc prolapse or osteoarthritis of the spine or spinal stenosis, which are typically relieved only when resting in the sitting position for longer than 5 /uni00A0 minutes). The distance that a patient is able to walk without stopping varies (claudication distance) only slightly from day to day . It René Leriche , 1879–1955, Professor of Surgery , Strasbourg, France, described this syndrome. is decreased, ﬁrst, by increasing the work demands and hence oxygen requirements of the muscles a ﬀ ected, e.g. walking up hill, increasing the speed of walking and/or carrying heavy weights, and, second, by general health conditions that reduce the oxygen delivery capacity of the arterial system, e.g. anae - mia or cardiorespiratory disease. The muscle group a ﬀ ected by claudication is classically one anatomical level below the level of arterial disease and is usually felt in the posterior calf as the superﬁcial femoral artery is the most commonly a ﬀ ected artery (70% of cases). Aortoiliac disease (30% of cases) may cause thigh or buttock claudication; Leriche’ s syndrome is buttock claudication com - bined with sexual impotence, which is secondary to arterial insu ﬃ ciency ( Figure 61.3 ). Rest pain As disease progression occurs the claudication distance decreases and perfusion to the leg may be so severely

CIA CIA

Figure 61.3 Aortoiliac bifurcation disease with an occluded right com

mon iliac artery (CIA) and critically stenosed left CIA. Collateralisation has occurred via the lumbar arteries (black arrow) and the inferior mesenteric artery (white arrow).

compromised that anaerobic respiration occurs even at rest, typically a ﬀ ecting the foot and/or calf. The pain is exacer bated by lying down or elevation of the foot because of the loss of gravitational e ﬀ ects on the perfusion pressure in the foot. The patient characteristically describes pain that is worse at night and may be lessened by hanging the foot out of or by sleeping in a chair (e ﬀ ects of gravity restored). Even the pressure of bedclothes on the foot may exacerbate the pain. Ulceration and gangrene Ulceration occurs with severe arterial insu ﬃ ciency and may present as painful erosions between the toes or as shallow , especially around the malleoli. The blackened mummiﬁed tissues of frank gangrene are unmistakable ( Figure 61.4 ), and superadded infection often makes the gangrene wet. P atients with ischaemic rest pain with or without ulceration/gangrene (tissue loss) are termed to have chronic limb-threatening isch - aemia (CLTI). These patients should be considered to have an imminently threatened leg and require urgent vascular assessment/revascularisation to prevent major amputation. Colour, temperature, sensation and movement Unlike an acutely ischaemic foot that is often cold, white, paralysed and insensate, a chronically ischaemic limb tends to equilibrate with the temperature of its surroundings and may feel quite warm under the bedclothes. Chronic ischaemia does not produce paralysis and sensation is usually intact. Patients with CLTI who have been waiting for a consultation with their leg in dependence may have a red swollen foot that may be mistaken for cellulitis by the unwary clinician. However, elevation of the limb reveals the severity of the ischaemia with venous guttering and foot pallor that changes to a red/ purple colour when the limb is allowed to hang down again (dependent rubor or the sunset foot sign) ( Figure 61.5 ). The capillary reﬁll time may be elicited by pressing the skin of the - heel or toe pulp, causing blanching (press for 5 seconds), and then releasing to allow colour to return; normally this takes 2–3 seconds but may be prolonged to 10 seconds in severe ischaemia. bed Arterial pulses It is standard practice to examine the femoral, popliteal, posterior tibial and dorsalis pedis arteries together with the abdomen for an aortic aneurysm, which may coexist with lower limb occlusive disease. Diminution of a femoral and/

Figure 61.4 Chronic limb-threatening ischaemia with dry gangrene. (a) Figure 61.5 Colour changes with elevation (a) and dependency (b) (b) .

with its opposite number; however, pedal pulses are either clinically palpable or absent. Popliteal pulses may be di ﬃ cult to appreciate; a popliteal artery aneurysm should be suspected if the popliteal pulse is prominent with concomitant loss of the natural concavity of the popliteal fossa. Pulsation distal to an arterial occlusion is usually absent, although the presence of a highly developed collateral circulation may allow distal pulses to be palpable – this is most likely to occur with an iliac stenosis. In this case, exercise (walking until claudication develops) usually causes the pulse to disappear as vasodilation occurs below the obstruction, thereby reducing the pulse pres sure. An arterial bruit, heard on auscultation over the pulse, indicates turbulent ﬂow and suggests a stenosis. However, it is an unreliable clinical sign as tight stenoses often do not have bruits. A continuous ‘machiner y’ murmur over an artery usually indicates an arteriovenous ﬁstula. Summary box 61.1 Features of chronic lower limb arterial stenosis or occlusion /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF Relationship of clinical ﬁndings to the site of disease In most cases the anatomical level of arterial stenosis can be determined from accurate assessment of the symptoms and signs ( Table 61.1 ). Limb-threatening ischaemia is predominantly caused by multilevel disease, e.g. iliac and femoropopliteal disease.

Intermittent claudication Arterial pulsation diminished or absent Rest pain Slow capillary re /f_i lling Ulceration Arterial bruit Gangrene Dependent rubor or sunset foot

Femoral aneurysm

True aneurysm of the femoral artery is uncommon. Complications occur in less than 3% so conservative treatment is generally indicated, but it is important to look for aneurysms elsewhere as over half are associated with abdominal or popliteal aneurysms. Large aneurysms should be repaired. False aneurysm of the femoral artery occurs in 2% of patients after arterial surgery at this site. Local repair may involve reanastomosis of the bypass in the groin under suitable antibiotic cover. However, if infection is the cause, the treatment may involve excision of the infected graft and insertion of a further bypass routed around the infected area. In the latter case, the failure rate is high, and limb loss may be unavoidable. For false aneurysms caused by femoral artery puncture measuring ≤ 3 /uni00A0 cm, thrombin injection under ultrasonography guidance may be successful and avoids surgery . False aneurysms measuring >3 /uni00A0 cm usually require open surgical repair with suturing of the puncture site. -

GANGRENE

Gangrene refers to the death of macroscopic portions of tissue, which turns black because of the breakdown of haemoglobin and the formation of iron sulphide. It usually a ﬀ ects the most distal part of a limb because of arterial obstruction (from thrombosis, embolus or arteritis). Dry gangrene occurs when the tissues are desiccated by gradual slowing of the blood - stream; it is typically the result of atheromatous occlusion of arteries. Wet gangrene occurs when superadded infection and putrefaction are present. Crepitus may be palpated as a result of infection b y gas-forming organisms, commonly in diabetic foot problems, and should be considered a surgical emergency with urgent tissue debridement or amputation required.

Iliac aneurysm

This usually occurs in conjunction with aortic aneurysm and only rarely on its own. When occurring in isolation it is di ﬃ cult to diagnose clinically so about half present already ruptured. Open surgery usually involves an inlay graft but some iliac aneurysms may be suitable for endovascular repair.

Introduction

CH A P TER INTRODUCTION

Arterial disorders represent the most common cause of morbidity and early death in western societies. Much of this is as a result of atheromatous plaque build-up causing steno ses (atherosclerosis) within the arteries that supply the heart muscle (coronary thrombosis and myocardial infarction) and brain (stroke) and the peripheral arterial system. This chapter addr esses diseases that are typically the domain of the vascular surgeon, namely those a ï¬€ ecting the peripheral arterial system: vascular disease that alters the normal structure and function of the aorta, its visceral branches and the arteries of the lower extremity .

Investigation of arterial occlusive disease

Most patients with symptomatic lower limb ischaemia pres ent with mild symptomatology and do not require invasive treatment, such as angioplasty or surgical reconstruction, and the decision of whether or not to intervene can often be made without recourse to special investigations. When further investig ation is indicated the purpose is to conﬁrm the presence and severity of peripheral arterial disease (PAD), identify the anatomical location of disease and assess the suitability of the patient for intervention. General investigation Patients with arterial disease tend to be elderly and athero sclerosis is often a multisystem disease process; the presence of arterial disease in the leg is suggestive of disease in other arterial Christian Johann Doppler , 1803–1856, Professor of Experimental Physics, Vienna, Austria, enunciated the ‘Doppler principle’ in 1842. - trees, including the coronary (50%) and cerebral (25–50%) trees. Many patients have other age-related diseases, such as chronic obstructive pulmonary disease and malignancy , that may impact on both their symptoms and suitability for inter - vention. Blood tests to exclude anaemia, diabetes, renal disease and lipid abnormalities should include a full blood count, blood glucose, lipid proﬁle and serum urea and electrolytes. High blood viscosity (polycythaemia and thrombocythaemia) may be caused by smoking, but may also be associa ted with cancer; renal impairment (raised serum creatinine and low estimated glomerular ﬁltration rate) may be caused by drugs and may be exacerbated by intravenous contrast agents used during angiography . An electrocardiogram (ECG) may show coronary isch - aemia, left ventricular hypertrophy or a cardiac dysrhythmia, although a normal ECG does not exclude these conditions. More information may be gained by an echocardiogram or exercise testing . Arterial blood gases and a pulmonary function test may be appropriate in patients with severe lung disease. Doppler ultrasound blood ﬂow detection - A hand-held Doppler ultrasound probe is very useful in the assessment of steno-occlusive arterial disease ( Figures 61.6 and 61.7 ). A continuous-wave ultrasound signal is transmitted from the probe at an artery and a receiver within the probe itself picks up the reﬂected beam. The change in frequency in the reﬂected beam compared with that of the transmitted beam is due to the Doppler shift, which results from the reﬂec - tion of the beam by moving blood cells. The frequency change may be converted into an audio signal that is typically pulsatile. Doppler ultrasound equipment can be used in conjunction - with a sphygmomanometer to assess systolic pressure in small vessels. This is possible even when the arterial pulse cannot be palpa ted. Both the pressure and signal quality are important;

disease. Aortoiliac obstruction Claudication in the buttocks, thighs and calves Femoral and distal pulses absent in both limbs Bruit over the aortoiliac region Impotence (Leriche) Iliac obstruction Unilateral claudication in the thigh and calf and sometimes the buttock Bruit over the iliac region Unilateral absence of femoral and distal pulses Femoropopliteal Unilateral claudication in the calf obstruction Femoral pulse palpable with absent unilateral distal pulses Distal obstruction Femoral and popliteal pulses palpable Ankle pulses absent Claudication in the calf and foot

a normal artery has a triphasic signal whereas a diseased artery may have a biphasic or monophasic signal depending on the extent of disease. However, although the presence of a Doppler signal indicates moving blood, it does not necessarily indicate that the blood ﬂow is su ﬃ cient to maintain limb viability and prevent limb loss. Quantitative assessment can be carried out at the bedside by performing an ankle–brachial pressure index (ABI), which is the ratio of the systolic pressure at the ankle to that in the ipsilateral arm. T he highest pressure in the dorsalis pedis, posterior tibial or peroneal artery serves as the numerator, with the highest brachial systolic pressure being the denominator. The normal resting ABI is 0.9–1.4; values below 0.9 indicate a haemodynamically signiﬁcant arterial lesion; a value less than 0.4 suggests CLTI. Values are merely a guide and normal values may be present with intermittent claudication. Retesting after exercise to the onset of pain can be useful; a drop in the resting ABI of >20% after exercise is indicative of ﬂow-limiting arterial disease. Artiﬁcially high ABI readings (>1.4) can be caused by media sclerosis and calciﬁcation of the arterial wall, causing vessel incompressibility and a falsely elevated ABI; this pattern of disease typically occurs in patients with diabetes mellitus (DM). Toe (digital) arteries are rarely a ﬀ ected by sclerosis and a toe–brachial pressure index (TBI) in combination with ABI is advocated as a more reliable diagnostic tool for the detection of signiﬁcant large-vessel steno-occlusive disease in patients with DM. A TBI less than 0.6 suggests a signiﬁcant arterial lesion that may have been overlooked if ABI was used in isolation ( Figure 61.8 ). However, there are limitations to the usage of TBI in the DM population: one in six patients with DM presenting with CLTI will have gangrene or will have undergone an amputation of the hallux. Duplex Doppler ultrasound This major non-invasive technique uses B-mode ultrasound to provide an image of vessels ( Figures 61.9 and 61.10 ). The image is created because of the varying ability of di ﬀ erent tissues to reﬂect the ultrasound beam. A second ultrasound beam is then used to insonate the imaged vessel and the Doppler shift obtained is analysed by a computer. Most scanners now have colour coding, which allows detailed visualisation of blood ﬂow , turbulence, etc. Di ﬀ erent colours indicate changes in direction and velocity of ﬂow with areas of high ﬂow usually indicating a stenosis. In experienced hands, duplex Doppler ultrasound (DUS) is as accurate as angiography and has the advantages of cost-e ﬀ ectiveness and safety . However, there are limitations: the aortoiliac segment can be di ﬃ cult to visualise because of

Figure 61.6 A simple hand-held Doppler ultrasound probe. Figure 61.7 A hand-held Doppler probe and sphygmomanometer used to determine systolic pressure in the dorsalis pedis artery, as part of assessing the ankle–brachial pressure index. Figure 61.8 Toe pressures being performed from the hallux. An abso

lute pressure from the hallux of <50 mmHg indicates severe ischaemia that is likely to prevent healing of ulceration.

bowel gas or obesity; vessels that are heavily calciﬁed may limit the ability of DUS to accurately assess the severity of steno- occlusive disease; the overall accuracy of DUS is determined by operator experience. When DUS inadequately visualises or quantiﬁes the level of disease within an arterial segment an alternative imaging modality , e.g. digital subtraction percutaneous angiography (DSA) or computed tomography angiography (CTA), may be undertaken to delineate the anatomy and extent of disease. Digital subtraction percutaneous angiography DSA involves injection of a radio-opaque dye into the arterial tree. Access to the vessel, typically the common femoral artery (CFA), is achieved using the Seldinger technique and is usually done percutaneously ( Figures 61.11 and 61.12 ). The images obtained are digitalised by computer and the extraneous back ground (bone, soft tissues, etc.) is removed to provide clearer images. The beneﬁts of DSA are that it provides dynamic Sven Ivar Seldinger , 1921–1998, radiologist, Karolinska Institutet, Stockholm, Sweden, introduced percutaneous arterial catheterisation in 1956. tive endovascular intervention w hen indicated. However, it is associated with potential complications, including bleeding, haematoma, false aneurysm formation, thrombosis, arterial dissection, distal embolisa tion, renal dysfunction and allergic reaction, which may occur in up to 5% of procedures. Further - more, it is relatively expensive compared with other investiga - tion modalities and its usage should be limited to patients in whom a concomitant intervention is predicted. Computed tomography angiography and magnetic resonance angiography The use of CTA as a minimally invasive alternative to DSA has increased as availability has improved. When used as an adjunct to DSA, CTA is beneﬁcial where DUS is not possible (intrathoracic arteries) or produces poor images (aortoiliac segment). With increased ease of access, better image quality and modern three-dimensional image reconstruction software, CTA has become an invaluable tool when planning revascu - larisation procedures, enabling the surgeon to visualise and measure diseased arterial segments prior to intervention. The major concern with CTA, in addition to the exposure to ionising radiation, is the use of iodinated contrast. A substantial proportion of patients presenting with PAD have concomitant renal d ysfunction, which may be acutely exacerbated by iodinated contrast, causing contrast-induced nephropathy . -

Figure 61.9 Duplex Doppler ultrasound scan being performed of the right carotid bifurcation. Figure 61.10 Normal duplex Doppler ultrasound of the carotid vessels in the neck. CCA, common carotid artery; ECA, external carotid artery; ICA, internal carotid artery; STA, superior thyroid artery. Figure 61.11 A Seldinger needle and guidewire for introducing an arterial catheter.

This is particularly pertinent to the patient with diabetes, in whom one also needs to be mindful of the interactions between contrast and certain pharmacotherapies, e.g. metformin, as their periprocedural usage may cause dangerous metabolic injury . Magnetic resonance angiography (MRA) is a non-invasive test that avoids the need for ionising radiation and iodinated contrast, thereby having advantages over DSA and CTA. It is becoming more widely utilised, particularly as the propor tion of patients with diabetes increases; this patient population typically has calciﬁed crural vessel disease, which is di ﬃ cult to assess using DUS or CTA. MRA has the ability to separate out contrast from ves sel wall calciﬁcation and has become the preferred imaging modality in many institutions. MRA has a number of limitations and may be contra indicated in patients with claustrophobia or certain metallic implants, e.g. pacemakers. The majority of peripheral arterial stents are now compatible with MRA, although the image quality will often be downgraded, making interpretation of ﬂow di ﬃ cult. MRA uses gadolinium as a contrast agent and patients with renal dysfunction are at risk of gadolinium- induced nephrogenic systemic ﬁbrosis ( Figure 61.13 ).

Figure 61.12 Digital subtraction angiogram of the femoral artery complex performed through a sheath (arrow) positioned percutaneously in the common femoral artery (CFA) using the Seldinger technique. PFA, profunda femoris artery; SFA, super /f_i cial femoral artery.

Learning objectives

To understand: The nature and associated features of occlusive peripheral • arterial disease The investigation and treatment options for occlusive • peripheral arterial disease The principles of management of the severely ischaemic • limb

Major amputation

Choice of operation The major choice is between an above- and below-knee operation. A below-knee amputation preserves the knee joint and gives the best chance of walking again with a prosthesis ( Figure 61.37 ). However, an above-knee amputation is more likely to heal and may be appropriate if the patient has no prospect of walking again. If the femoral pulse is absent, the amputation should be above the knee. Unfortunately , the presence of a femoral pulse does not guarantee healing of a below-knee amputation and sometimes a failed below-knee amputation may require revision to an above-knee procedure. For above- or below-knee amputations with a good stump shape, it is possible to hold a prosthesis in place simply by suc tion, without any cumbersome and unsightly straps. The stump should be of su ﬃ cient length to give the required leverage, i.e. not less than 8 /uni00A0 cm below the knee (preferably 10–12 /uni00A0 cm) and not less than 20 /uni00A0 cm above the knee. Thr ough-knee or knee disarticulation has regained popularity as an alternative to above-knee amputation if soft-tissue viability permits. This amputation preserves the full length of the femur and patella and pr ovides a long mechanical lever that is controlled by stronger muscles as the line of muscle transection is distal and occurs through fascial tissue as opposed to thick muscular bellies, as is the case with an above-knee amputation. The bulbous nature of the amputation end, initially thought a hindrance for subsequent suspending prosthetic that is less likely to rotate than an above- knee amputation pr osthetic. For patients unlikely to mobilise with a prosthetic, e.g. elderly patients or patients with bilateral amputations, the increased length of the stump provides better counterweight to the torso, enabling better core stability . Postoperative care of an amputee Opiate pain relief should be given regularly . Care of the good limb must not be forgotten – a pressure ulcer on the remaining foot will delay mobilisation despite satisfactory healing of the stump. Exercise and mobilisation are of the greatest impor - tance. After surgery , ﬂexion deformity must be prevented and exercises started to build up muscle power and coordination. Mobility is progressively increased with walking between bars and the use of an inﬂa table artiﬁcial limb, which allows weight bearing to be started before a pylon or temporary artiﬁcial limb is ready ( Figure 61.38 ). Early assessment of the home is part of the programme; this allows time for minor alterations, such as the addition of stair rails, movement of furniture to give support near doors and provision of clearance in conﬁned passages. Complications Early complications include haemorrhage, which requires return to the operating room for haemostasis; haematoma, which requires evacuation; and infection, usually in associ - ation with a haematoma. Any abscess must be drained and appropriate antibiotics given. Gas gangrene can occur in a mid-thigh stump from faecal contamination. Wound dehis - cence and gangrene of the ﬂaps are caused by ischaemia; a higher amputa tion may be necessary . Amputees are at risk of deep vein thrombosis and pulmonary embolism in the early postoperative period and prophylaxis with subcutaneous heparin is essential. Later complications include pain resulting from unresolved infection (sinus, osteitis, sequestrum), a bone spur, a scar adher - ent to bone and an amputation neuroma. Patients frequently remark that they can feel the amputated limb (phantom limb) and sometimes remark tha t it is painful (phantom pain). The sur geon’s attitude should be one of ﬁrm reassurance that this sensation will almost certainly disappear with time; gabapentin or amitriptyline may help. Other late complications include ulceration of the stump because of pressure e ﬀ ects of the pros - thesis or increased ischaemia. -

Management of arterial stenosis or occlusion

General Only one-quarter of patients presenting with intermittent claudication will experience symptomatic deterioration during their lifetime and the overall risk of progression to CLTI and amputation is small, with <5% of patients requiring amputa tion over a 5-year period. Patients with an ABI of <0.50 are twice as likely to deteriorate as patients with an ABI of >0.50, and a deteriorating ABI is predictive of future limb loss. For patients with rest pain or tissue necrosis, intervention is usually required to prevent major amputation. Claudication is often a marker of silent coronary arterial disease whose extent correlates with the ABI: a decrease of 0.1 in ABI below 0.9 is associated with a 10% increase in the rela - tive risk of a major cardiovascular e vent. Similarly , one-quarter - of patients with claudication have signiﬁcant atherosclerotic disease a ﬀ ecting their carotid and renal arterial systems. It is thus not surprising tha t the risk of having a major cardiovascu - lar event per year in patients with claudication is >5%, and that - 50% of claudicants will die within 10 years from myocardial infarction or stroke. The common modiﬁable risk factors for PAD mirror those f or coronary artery disease: smoking, DM, - hypertension and hyperlipidaemia. Therefore, the two main aims when treating claudication are (i) prevention of major cardiovascular morbidity through risk factor modiﬁcation and (ii) symptom relief/improvement. Non-surgical management For many patients with claudication a structured exercise programme of at least 2 hours of exercise per week for 3 months in combination with smoking cessation will lead to sustained improvement in claudication distance and a reduc - tion in cardiovascular risk. DM increases the risk and severity of claudication proportional to the duration of a ﬄ iction. Strict control in combination with weight loss in obese patients is vital to reduce cardiovascular risk and prevent symptom deterioration. Drugs - Medication may be required for diseases associated with arterial disorders, such as hypertension and diabetes; some

Figure 61.13 Magnetic resonance angiogram showing a tight stenosis at the midpoint of the left common iliac artery.

claudication. Raised blood lipids require active drug treat ment, but even when the lipid proﬁle is normal a statin (3-hydroxy-3-methylglutaryl coenzyme A [HMG-CoA] reductase inhibitor) should be prescribed as it may stabilise atherosclerotic plaques and protect against cardiac death inde pendently of baseline serum lipid levels. An antiplatelet agent is also necessary: global guidelines recommend 75 /uni00A0 mg per day of clopidogrel or 75 /uni00A0 mg per day of aspirin as an alternative. Other agents, such as vasodilators, are unlikely to provide either signiﬁcant or sustained beneﬁt. Drugs are now available to help with smoking cessation. Transluminal angioplasty and stenting Arterial occlusive disease may be treated by inserting a balloon catheter into an artery and inﬂating it within a stenosed or occluded segment ( Figures 61.14 and 61.15 ). This technique is suitable for patients with claudication, rest pain or tissue - - necrosis ( Figures 61.16 and 61.17 ). Following percutaneous femoral artery puncture under local anaesthetic a guidewire is inserted and negotiated through the stenosis or occlusion under ﬂuoroscopic control. A balloon catheter is positioned within the lesion over the guidewire and inﬂated at high pressure for approximately 30 seconds. Satisfactory dilatation of the lesion is conﬁrmed by performing an angiogram. Percutaneous transluminal angioplasty (PTA) has proved very successful in dilating the iliac and femoropopliteal segments; the results below the knee are less successful but improving. Long occlusions may be treated by the technique of subintimal angioplasty , in which the guidewire crosses the lesion in the subintimal space (in the arterial wall) and a new lumen is created by inﬂation of the balloon. Complications occur in about 5% of cases and include failure, haematoma, bleeding, thrombosis and distal embolisation; these may impact on the surgeon’s ability to perform a subsequent open surgical revascularisation procedure. If the vessel fails to stay adequately dilated (often caused by elastic recoil of the artery), it may be possible to hold the lumen open using a metallic stent ( Figures 61.18 and 61.19 ). This may be introduced on a balloon catheter and expanded

Figure 61.14 Balloon catheter for percutaneous transluminal angio plasty. (a) (b) Figure 61.15 (a) Catheter balloon de /f_l ated; (b) balloon in /f_l ated. Figure 61.16 (a) Digital subtraction angiogram (DSA) demonstrat

ing multiple stenoses within the super /f_i cial femoral artery (SFA). /uni00A0 (b) Balloon angioplasty of the SFA. (c) Postangioplasty DSA of the SFA demonstrating improvement in the previously stenotic regions. This technique can be carried out under local anaesthesia using the Seldinger technique of percutaneous arterial puncture. It is therefore especially useful in the treatment of patients who are medically un /f_i t for major bypass surgery.

by balloon inﬂation. Alternatively , a self-expanding (typically nitinol) stent may be used; this is contained inside a plastic sheath and deployed by withdrawal of the sheath.

Figure 61.17 Before (a) and after (b) balloon dilatation of a severely stenosed left renal artery in a 20-year-old woman with uncontrollable hypertension. The patient’s blood pressure fell to normal after the procedure. The stenosis was probably due to /f_i bromuscular hyperplasia, but no tissue was available for histological diagnosis. (a) (b) Figure 61.18 (a) A balloon catheter carrying a stent; (b) the expanded stent.

Miscellaneous

Other types of gangrene commonly encountered include bedsores and frostbite. Bedsores are gangrene caused by local pressure ( Figure 61.27 ), whereas frostbite is caused by exposure to cold ( Figure 61.28 ). Both are preventable with adequate protective measures.

Figure 61.28 (a) Frostbite of the foot. Note the clear demarcation. (b) Frostbite of the middle /f_i nger in the same patient. The index /f_i nger was lost 2 years before, also from frostbite.

Sudden occlusion of an artery is usually caused by an embolus. It may also happen when thrombosis occurs on an atheroscle rotic plaque, although the outcome is usually less dramatic because collaterals are likely to have developed in chronic arterial stenosis.

Operations for arterial stenosis or occlusion

Site of disease and type of operation Surgical operations are usually reserved for patients with severe symptoms (CLTI or lifestyle-limiting claudication) where angioplasty has failed or is not possible. Aortoiliac occlusion Justin H Miller , 1924–1994, vascular surgeon, Royal Adelaide Hospital, Adelaide, Australia. responds well to aortobifemoral bypass ( Figure 61.20a ) using a Dacron graft ( Figure 61.21a ), although the operation carries a perioperative mortality and systemic morbidity (stroke, cardio - respiratory failur e , renal injury) rate of about 5% and 15%, respectively . In unﬁt patients, an axillobifemoral bypass is an alternative, although patency rates are less. If only one iliac system is occluded, an iliofemoral or femorofemoral crosso ver graft may be performed. Superﬁcial femoral artery disease can be treated by femoro - popliteal bypass ( Figure 61.20b ); long-term graft patency is determined by the quality of inﬂow and outﬂow , graft length w the knee) and (whether the distal anastomosis is above or belo the conduit used for the bypass. Autologous great saphenous vein (GSV) gives the best results and can be used reversed or in situ after valve disruption. If the GSV is not available from either leg, the lesser saphenous or arm veins may be used. If no vein is available, a prosthetic polytetraﬂuoroethylene (PTFE) graft may be employed ( Figure 61.21b ), although patency rates are less; many surgeons construct the lower anastomosis using a small collar of vein (Miller cu ﬀ or St Mary’s boot) between the PTFE and the recipient artery , which may improve patency . Isolated CFA or profunda disease can be treated with endarterectomy and patch (vein or prosthetic) or a short bypass in the groin. Frequently , in patients with CLTI, particularly those with diabetes, the occlusion extends beyond the popliteal artery into the tibial (crural) vessels. Limb salvage can be attempted with a

Figure 61.19 (a) Occlusion of the popliteal artery extending into the tibioperoneal trunk. intraluminal positioning beyond the occlusion. (c) Balloon angioplasty. the lumen and balloon moulded. (f) Completion angiogram. (a) Figure 61.20 (a) Atherosclerotic narrowing of the aortic bifurcation. Aortobifemoral graft to bypass the stenosis. artery stenosis providing poor collateral circulation. A femoropopliteal graft is used to bypass the occluded area into good ‘run-off’ below. (b) A lesion crossed with a catheter angiogram con /f_i rming (d) Angiogram demonstrating vessel recoil. (e) Stents inserted to maintain (b) (b) Long super /f_i cial femoral

femorodistal bypass, with success even more dependent on the state of the run-o ﬀ vessel and the quality of the vein conduit (minimum diameter 3 /uni00A0 mm). The risk of early graft failure with limb loss is high (approximately 30% at 30 days) and these long bypasses are only appropriate for limb salvage. Technical details For aortobifemoral bypass, the aorta should be approached through a midline abdominal incision; a transverse abdominal incision divides the inferior epigastric vessels (important collateral vessels in patients with an occluded aorta) and should be avoided. The common femoral arteries and their branches are exposed through vertical groin incisions; an oblique or transverse groin incision may be preferred for patients with obesity . The small bowel is retracted to the right and the posterior peritoneum opened. Retroperitoneal tunnels are made from the aorta to the groins. Heparin (5000 /uni00A0 U) is given intravenously and the vessels clamped. A vertical incision is made in the anterior aspect of the aorta, to which an obliquely cut, bifurcated Dacron graft is sutured end-to-side with a non-absorbable suture (polypropylene). The graft limbs are then fed down to the groins, where they are anastomosed end-to-side to the common femoral arteries or, if there is evidence of profunda stenosis, to an arteriotomy running from the common femoral vessel down into the profunda. The posterior peritoneum is closed over the Dacron graft to prevent adhesion of the graft to the bowel, and the abdomen and groin wounds are closed. For femoropopliteal bypass the popliteal artery above or below the knee is exposed through a medial incision. The CFA is exposed at groin level. The GSV may be used in two di ﬀ erent ways. First, it may be excised, its tributaries tied and the vein used in a reversed fashion so the valves do not obstruct the ﬂow of blood. Alternatively , it may be left in place ( in situ ) and the valves disrupted with a valvulotome. The graft is sutured to the femoral artery proximally and to the popliteal artery distally . Femorodistal bypass involves fashioning the distal anastomosis to a tibial vessel. If no suitable vein is available, prosthetic material (usually PTFE) may be used, with or without a small vein collar (Miller cu ﬀ or St Mary’s boot) at its distal end ( Figure 61.22 ). A femorofemoral crossover graft involves tunnelling a prosthetic graft subcutaneously above the pubis between the groins. An axillofemoral graft is tunnelled subcutaneously between the axillary arter y proximally to reach one or both of the femoral arteries; the patency rates of an axillobifemoral bypass are better than those for an axillo(uni)femoral bypass. Results of operation The long-term results of aortoiliac reconstructive surgery are good and are usually marred only by progressive infrainguinal disease; 90% remain patent at 5 years post surgery . Femoro - popliteal surgery is less successful. Immediate postoperative success for vein bypass exceeds 90% but the 5-year patency is around 60%. PTFE bypass yields poorer results than vein bypass, with 5-year success rates of less than 50%. Although the results of femorodistal bypass are even less satisfactory , such surgery can ensure limb salvage in patients who are generally debilitated and whose expected lifespan is limited; long-term patency is less important.

(b) ® Figure 61.21 (a) A Dacron bifurcation graft; (b) a polytetra /f_l uoroeth ylene graft.

Figure 61.22 (a) Completion angiogram of a femoropopliteal bypass graft (with a Miller cuff). (b) Completion angiogram of a femorodistal bypass graft in situ.

Other forms of arteritis

Arteritis occurs in association with many connective tissue disorders, e.g. rheumatoid arthritis, systemic lupus erythema tosus and polyarteritis nodosa. Temporal arteritis is a disease in which localised inﬁltration with inﬂammatory and giant cells leads to arterial occlusion, ischaemic headache and tender, palpable, pulseless (throm bosed) arteries in the scalp. Irreversible b lindness occurs if the ophthalmic artery becomes occluded. The surgeon may be required to perform a temporal artery biopsy , but this should not delay immediate steroid therapy to arr est and reverse the process before the ophthalmic artery is involved. Takayasu’s disease is an arteritis that obstructs major arteries, particularly the large vessels coming o ﬀ the aortic arch. It usually pursues a relentless course.

Other forms of embolism

Infective emboli of bacteria or an infected clot may cause mycotic aneurysms, septicaemia or infected infarcts. Parasitic emboli, caused by the ova of T aenia echinococcus and sanguinis hominis , may occur in some countries. Tumour cells (e.g. hypernephroma and cardiac myxoma) are rare causes of emboli. Fat embolism may follow major bony fractures. However, it usually causes venous emboli that trav el to the lungs and cause acute respiratory distress syndrome. Air embolism Air may be accidentally injected into the venous circulation or sucked into an open vein during head and neck surgery or a cut throat. It may also occur following Fallopian tube insu ﬄ ation or illegal abortion. If a large volume of air reaches the right side of the heart it may form an airlock within the pulmonary artery and cause acute right heart failure. The treatment of air embolism is to put the patient in a head-down (Trendelenburg) position to encourage the air to enter the veins in the lower part of the body . The patient should also be placed on the left side to help the air to ﬂoat to the ventricular apex, away from the ostium of the pulmonary artery . In extreme cases air may be aspirated from the heart through a needle introduced below the left costal margin. Therapeutic embolisation This is used to arrest haemorrhage from the gastrointestinal, urinary , gynaecological and respiratory tracts, to treat arterio venous malformations by blocking their arterial supply and to control the growth of unresectable tumours. Arterial embolisation requires accurate selective catheterisation using the Seldinger technique . A variety of materials may be used, including Gelfoam sponge, plastic microspheres, balloons, ethyl alcohol, quick-setting plastics and metal coils.

PERIPHERAL ANEURYSM Popliteal aneurysm

Popliteal artery aneurysm accounts for 70% of all peripheral aneurysms classically diagnosed in men in their seventh decade of life; 50% are bilateral. Examination of the abdominal aorta is indicated if a popliteal aneurysm is found because one-third are accompanied by aortic dilatation. Popliteal aneurysms present as a swelling behind the knee or with symptoms caused by complications, such as severe ischaemia following throm bosis or distal ischaemia as a result of emboli. The diagnosis is usually conﬁrmed with DUS but assessment of the distal vessels (with CT , MRA or DSA) is important prior to repair if the foot pulses are diminished or absent. An asymptomatic aneurysm greater than 20 /uni00A0 mm in diameter should be considered for elective r epair to prevent future complications. Some surgeons would also o ﬀ er elective repair for smaller diameters if the sac contains thrombus because of a perceived increased risk of distal embolisation. All symptomatic popliteal aneurysms, including those in which single crural vessel embolisation has occurred, should be considered for repair. Two techniques for surgical repair may be used: exclusion bypass and inlay repair. An exclusion bypass involves a medial approach to the above- and below-knee popliteal arteries, ligation of the aneurysm and restoration of ﬂow to the foot with a bypass graft using saphenous vein. Many surgeons favour this approach because the anatomy is similar to that for a femoropopliteal bypass and therefore familiar. An inlay graft repair is performed through a posterior approach and has the beneﬁts of allowing free ligation of feeding geniculate branches as well as aneurysmectomy in patients with neurovascular compression. However, the posterior approach limits exposure of the superﬁcial femoral and crural arteries and should only be used when the popliteal aneurysm is conﬁned to the popliteal fossa. In the acute situation, the presentation is usually with aneurysms very rarely rupture. Aneurysm thrombosis tends to occur following a period of chronic embolisation to the run- o ﬀ vessels. As successive run-o ﬀ vessels occlude over time the outﬂow to the popliteal artery diminishes, resulting in reduced ﬂow rates in the aneurysm sac and eventual thrombosis. In such cases surgery is often unsuccessful because the outﬂow for the graft reconstruction is chronically diseased. Attempts to re-establish a patent run-o ﬀ vessel with embolectomy and intra-arterial thrombolysis may be successful, but the limb loss rate is high (50%).

Raynaud’s disease

This idiopathic condition usually occurs in young women and a ﬀ ects the hands more than the feet. There is abnormal sensi tivity in the arteriolar response to cold. These vessels constrict and the digits (usually the ﬁngers) turn white and become incapable of ﬁne movements. The capillaries then dilate and Mikito Takayasu , 1860–1938, Japanese ophthalmologist, described this disease in 1908. digits becoming swollen and dusky . As the attack passes o ﬀ , the arterioles relax, oxygenated blood returns into the dilated capillaries and the digits become red. Thus, the condition is recognised by the characteristic sequence of blanching, dusky cyanosis and red engorgement, often accompanied by pain. Superﬁcial necrosis is very uncommon. This condition must be distinguished from Raynaud’s syndrome, which has similar features (see Raynaud’s syndrome ). Treatment of Raynaud’s disease consists of protection from cold and avoidance of pulp and nail bed infection. Calcium antagonists, such as nifedipine, may also have a role to play and electrically heated gloves can be useful in winter. Sympathectomy has been used in the past but it is either ine ﬀ ective or its e ﬀ ects are short-lived.

Raynaud’s syndrome

Raynaud’s syndrome is the peripheral arterial manifestation of a collagen disease such as systemic lupus erythematosus or - rheumatoid arthritis. The clinical features are as for Raynaud’s disease but they may be much more aggressive. Raynaud’s syndrome may also follow the use of vibrating tools. In this context it is a recognised industrial disease and is known as ‘vibration white ﬁnger’. Treatment is directed primarily at the underlying con - dition, although the conservative measures outlined above are often helpful. The syndrome when secondary to collagen disease leads frequently to necrosis of digits and multiple - amputa tions. Sympathectomy yields disappointing results and is not recommended. Nifedipine, steroids and vasospastic antagonists may all have a role in treatment. Patients with vibration white ﬁnger should avoid vibrating tools. -

Separation of gangrene

A zone of demarcation between the truly viable and the dead or dying tissue will eventually appear. Separation is achieved by the development of a layer of granulation tissue, which forms between the dead and the living parts. In dry gangrene, if the blood supply of the proximal tissues is adequate, the ﬁnal line of demarcation appears in a matter of days and separation occurs neatly and with the minimum of infection. If bone is involved, complete separation takes longer than when soft tissues alone are a ﬀ ected, and the stump tends to be conical as the bone has a better blood supply than its coverings. In moist gangrene the infection and suppuration extend into the neighbouring living tissue, causing the ﬁnal line of demarcation to be more proximal than in dry gangrene. If the arterial supply to the proximal living tissue is poor, the line of ﬁnal demarcation is very slow to form or does not develop at all. Unless the arterial supply can be improved, the gangrene will spr ead to adjacent tissues or will suddenly appear as ‘skip’ areas further up the limb. These skip lesions may occur on the other side of the foot, on the heel, on the dorsum of the foot or even in the calf. Infection may also cause gangrene to spread proximally into areas of extensive inﬂammation. Local amputation in the presence of poor circulation will fail and gangrene will reappear in the wound or skin edges.

Figure 61.24 This patient presented with an ischaemic right hand. (a) A chest radiograph demonstrated a right cervical rib (black arrow). (b) A computed tomography angiogram showed stenosis of the subclavian artery (SCA) with poststenotic dila

tation (lined with thrombus) (white arrow) caused by the cervical rib. The patient had been embolising from the SCA into the hand. The patient was successfully treated with cervical rib resection, repair of the SCA and distal thromboembo

lectomy. Figure 61.25 The superior mesenteric artery lesion shown in 61.1 . It was successfully treated with angioplasty and primary stent insertion.

Speciﬁc varieties of gangrene

Diabetic gangrene Diabetic gangrene is usually caused by a combination of three factors: ischaemia secondary to macrovascular disease and microvascular dysfunction; peripheral sensorimotor neuropathy (PSN), which leads to trophic skin changes; and immunosuppression caused by an excess of sugar in the tissues, which predisposes to infection ( Figure 61.26 ). Macrovascular

Figure Figure 61.26 Diabetic gangrene.

with relative sparing of the pedal vessels, whereas increased microcirculatory shunting causes microvascular dysfunction. The PSN is usually sensory in the early phase – classically in a stocking distribution – and renders the patients at high risk of soft-tissue injury and its subsequent neglect. The PSN may extend to the joints of the foot and ankle, resulting in loss of nociceptive and proprioceptive protective reﬂexes and a repeated cycle of joint injury and bony destruction. Motor involvement causes an imbalance between ﬂexors and extensor muscle groups of the foot, promoting altered foot biomechanics and abnormal pressure loading, which result in thick callosities developing on the sole of the foot. Ischaemia and PSN act synergistically to increase the risk of diabetic foot ulceration and reduce its subsequent healing potential. Superadded infection due to poor wound care can spread rapidly and proximally in subfascial planes, leading to fulminant foot sepsis, gangrene and death. T reatment depends on the degree of arterial involvement, which should be investigated and treated rapidly with angio - plasty or surgery . The gangrene is trea ted by drainage of pus, liberal debridement of dead tissue and antibiotics. Unfortu - nately , a number of patients present with life-threatening sys - temic upset and should be considered for primary amputation.

(b) Figure 61.27 Bedsores typically appear over areas exposed to pres sure, such as the sacrum and (as in this case) the heel. They can quickly deteriorate from an area of discoloration (a) to gross ulceration extending to the calcaneum (b) . (a) (b)

Sympathectomy

Endoscopic transthoracic sympathectomy is now reserved as a minimally invasive treatment of palmar and axillary hyperhidrosis. Open cervical sympathectomy was used in the past as a treatment of vasospastic disorders but was usually unsuccessful. Lumbar sympathectomy was used to treat lower limb ischaemia in the past but has also become obsolete.

Treatment of gangrene

How much of a limb or digit can be salvaged depends on the blood supply proximal to the gangrene. Poor circulation should be improved by surgical revascularisation, enabling a more conservative debridement or distal amputation. However, major limb amputation may be required in the presence of life-threatening sepsis, when the blood supply cannot be improved or in patients whose limb is non-functional because of contractures, stroke, etc.

disease

The principles of arterial surgery outlined above can be applied at other arterial sites. Carotid stenosis (at the carotid bifurcation in the neck) may cause TIAs. These short-lived mini-strokes are often recurrent and cause unilateral motor or sensory loss in the arm, leg or face, transient blindness (amaurosis fugax) or speech impairment (dysphasia). They are caused by distal embolisation of platelet thrombi that form on the atheroma tous plaque into the cerebral circulation. They are a warning of impending major stroke. Patients should be assessed with a duplex scan. If a tight stenosis (>50%) is detected, carotid endarterectomy should be o ﬀ ered ( Figure 61.23 ). This involv es clamping the vessels, an arteriotomy in the common carotid artery continued up into the internal carotid artery through the diseased segment, removal of the occlusive disease (endarterectomy) and closure of the arteriotomy , often with a patch. Many surgeons also use a temporary shunt to maintain cerebral blood ﬂow while the carotid system is clamped. Subclavian artery stenosis may cause claudication in the arm or digital ischaemia from distal embolisation. It may be treated by angioplasty or surgical bypass. Sometimes subclavian Indications for carotid endarterectomy in symptomatic patients /uni25CF /uni25CF /uni25CF /uni25CF - /uni25CF /uni25CF artery lesions are associated with neck pathology , such as a cervical rib, which should be removed during arterial repair ( Figure 61.24 ). Subclavian steal syndrome may occur if the ﬁrst part of the subclavian artery is occluded. Arm exercise causes syncope because of reversed ﬂow in the vertebral artery , leading to cerebral ischaemia. It can be treated by angioplasty or surgery and is rare. Mesenteric artery occlusive disease may cause pain after eating (intestinal angina) and weight loss. In general, two of the three enteric vessels (coeliac axis, superior mesenteric artery , inferior mesenteric artery) must be occluded to produce symp - toms and other intestinal disorder s must be excluded before treatment with PTA, endarterectomy or bypass ( Figure 61.25 ). Renal artery stenosis may cause hypertension and eventual renal failure . Although it is possible to improve renal blood ﬂow with PTA or surgery , the mainstays of trea tment are drugs to control hypertension, diabetes, etc.

Figure 61.23 Carotid stenosis. A unilateral localised stenosis suitable for operation. CC, common carotid; EC, external carotid; IC, internal carotid. 50% or greater carotid stenosis and: Ipsilateral amaurosis fugax or monocular blindness Contralateral facial paralysis or paraesthesia Arm/leg paralysis or paraesthesia Hemianopia Dysphasia (if dominant hemisphere) Sensory or visual inattention/neglect