© Springer International Publishing Switzerland 2017
Rebecca A. Fisher, Kamran Ahmed and Prokar Dasgupta (eds.)Introduction to Surgery for Studentshttps://doi.org/10.1007/978-3-319-43210-6_1818. Vascular Surgery
(1)
GKT School of Medical Education, King’s College London, Great Maze Pond, London, SE1 3QD, UK
(2)
Vascular Surgery, Guy’s and St. Thomas’ NHS Foundation Trust, Westminster Bridge Road, London, SE1 7EH, UK
Keywords
Vascular surgeryVascular anatomyVascular diseaseEndovascular abdominal aortic aneurysm repair (EVAR)Carotid endarterectomyCritical limb ischaemiaStudentIntroduction
Vascular surgery is a speciality in which diseases of the arteries, veins and lymphatic system are diagnosed and managed. It emerged from general surgery and has been considered a separate surgical speciality in the UK since 2013. Minimally invasive surgery now forms a large part of a vascular surgeon’s workload and endovascular approaches are often used during procedures.
This chapter outlines the core concepts of vascular surgery including: core clinical anatomy, commonly treated conditions and descriptions of five commonly performed procedures.
Clinical Anatomy
This section will summarise the anatomy relevant to this chapter. It is not intended to be comprehensive, and for more information, a dedicated anatomy textbook is recommended.
The Aorta
The aorta originates from the left ventricle of the heart and extends down into the abdomen where it bifurcates into the common iliac arteries at vertebral level L4.
It can be divided into the following sections:
The ascending aorta:
Gives rise to the right and left coronary arteries.
The aortic arch which has three major branches:
The brachiocephalic trunk (sometimes called the innominate artery), which divides into the right common carotid artery and the right subclavian artery.
The left common carotid artery.
The left subclavian artery.
The descending thoracic aorta:
Branches include the intercostal arteries.
The abdominal aorta:
Has multiple branches including the renal arteries which arise between L1 and L2.
The majority of abdominal aortic aneurysms (AAAs) originate below L1/L2 – the origin of the renal arteries – and above the bifurcation of the abdominal aorta. Although thoracic aortic aneurysms also occur, these are much less common and do not feature in exams as much as AAAs.
The Carotid Arteries
There are two common carotid arteries which provide the majority of the blood supply to the head and neck:
The right common carotid artery originates from the brachiocephalic trunk (a branch of the aortic arch).
The left common carotid artery originates directly from the aortic arch.
Both common carotid arteries divide to form internal and external carotid arteries at vertebral level C4.
The carotid arteries are contained in the carotid sheath and are positioned posterior to the sternocleidomastoid muscles in the neck. They are found in close proximity to three cranial nerves:
Cranial nerve IX i.e. the glossopharyngeal nerve
Cranial nerve X i.e. the vagus nerve
Cranial nerve XII i.e. the hypoglossal nerve
During carotid endarterectomy, these nerves are at risk of damage. Damage may cause:
Difficulty swallowing and an absent gag reflex (cranial nerve IX damage).
Hoarseness as a result of paralysed vocal cords (cranial nerve X damage).
Wasting of the ipsilateral side of the tongue (cranial nerve XII damage).
The Femoral Artery
The femoral artery is the main blood supply to the lower limb, and hence its occlusion can result in gangrene and the need for amputation if untreated. It is a continuation of the external iliac artery (a branch of the common iliac artery).
It passes into the lower limb under the inguinal ligament, midway between the anterior superior iliac spine (ASIS) and the pubic symphysis.
It descends through the thigh in the femoral sheath, lateral to the femoral vein and medial to the femoral nerve (the nerve is not in the sheath).
It gives off several branches, the largest being profunda femoris, which supplies most of the thigh via its circumflex and perforating branches.
It passes into the popliteal fossa through the adductor hiatus (an opening in the adductor magnus muscle), becoming the popliteal artery.
The Popliteal Artery
The popliteal artery, a continuation of the femoral artery, runs through the popliteal fossa, ending at the lower border of the popliteus muscle. It divides into the anterior and posterior tibial arteries to supply the leg.
It has five genicular branches, which anastomose with branches of the lateral femoral circumflex artery (from the profunda femoris) and the anterior tibial to supply the knee joint. If the femoral artery must be ligated due to the presence of an aneurysm, this anastomosis ensures that blood will still reach the leg. A femoropopliteal bypass operation is used to ensure limb survival in the case of a popliteal aneurysm.
The Great Saphenous Vein
The great saphenous vein is the longest vein in the body. It originates from the dorsal venous arch of the foot and passes in front of the medial malleolus of the ankle, running medially up the leg and anteriorly up the thigh before passing through the saphenous opening of the fascia lata to join the femoral vein.
The great saphenous vein is the most common vein to be used by vascular surgeons as a conduit in bypass operations.
Core Conditions
Vascular surgeons commonly manage peripheral vascular disease, aneurysms, carotid artery disease and varicose veins. These conditions may have a chronic course (e.g. varicose veins) or they may present as vascular emergencies (e.g. ruptured abdominal aortic aneurysms). Vascular repairs are usually carried out using either an open or endovascular approach.
Peripheral Vascular Disease
Peripheral vascular disease (PVD) is obstruction of the peripheral arterial blood flow. This definition therefore excludes the intracranial and coronary arteries. In some patients PVD may be mild with only asymptomatic plaques present. Others may suffer from moderate disease and present with intermittent claudication (IC). Finally, severe disease is likely to present as critical limb ischaemia (CLI), which may result in amputation. Both the presence and severity of PVD is determined by the ankle-brachial pressure index (ABPI). In health the ABPI is greater than 1 mmHg.
The main risk factors for PVD include:
Smoking
Hypertension
Hyperlipidaemia
Diabetes Mellitus
A family history of PVD
Considering mild disease is mainly asymptomatic the majority of patients present with IC as a result of moderate lower limb ischaemia. The ABPI is typically 0.5–0.9 mmHg. Patients complain of muscular pain in the calf, although pain may also be felt in the thigh and buttocks. Pain is provoked by exercise, most commonly at a ‘claudication distance’ and relieved by rest. Symptoms often follow a cyclical pattern in which they progress then resolve as ischaemia promotes the development of collateral vessels. PVD can be managed conservatively by risk factor reduction strategies, including smoking cessation and supervised exercise programmes. If conservative measures fail vasoactive drugs can be used. Some patients ultimately require surgical treatment.
Severe Limb Ischaemia
Severe limb ischaemia (SLI) is the end stage of PVD. It presents with severe pain at rest which awakens the patient from sleep and requires opiate analgesics. Patients must have symptoms for more than 2 weeks and may also present with ulceration and/or gangrene. SLI encompasses both subcritical limb ischaemia (SCLI) and CLI. Patients with SCLI have an ABPI of greater than 0.5 mmHg with rest pain only. CLI is defined by an ABPI of less than 0.5 mmHg with the clinical features described above. While CLI is usually due to a single-segment of plaque, SCLI is due to plaques at multiple levels within the vascular tree. SCLI can lead to amputation if untreated. Management includes surgical repair by bypass graft or angioplasty.
Bypass Grafts
A huge variety of bypass grafts are carried out as part of vascular surgical procedures. They provide a better blood supply to a tissue, redirecting blood around a narrowed or blocked blood vessel. Considering the nomenclature of the grafts, the first part of the graft name originates from the artery the graft comes from, and the second part comes from the artery the graft is sewn on to. Examples include femoro-popliteal and axillo-femoral grafts.
Aneurysms
An aneurysm is a localised, abnormal, dilatation of a blood vessel (Gr. aneurusma; widening).
Types of Aneurysm
True aneurysms:
Involve all three layers of the vessel wall (the tunica intima, tunica media and tunica adventitia).
Have a diameter that is greater than 150 % of the original vessel diameter.
Usually develop as a result of atherosclerosis.
Can be fusiform or saccular:
Fusiform aneurysms involve the entire circumference of the artery – often referred to as spindle shaped aneurysms.
Saccular aneurysms involve only part of the circumference of the artery – often referred to as saclike aneurysms.
False/pseudo aneurysms:
Result from a breach in the vessel allowing blood to leak through. The blood is contained by the adventitia. The haematoma surrounding the artery mimics an aneurysm.
A common complication of arterial catheterisation (e.g. coronary angiogram).
Can also be caused by trauma and infection.
Can be identified on ultrasound by a yin-yang sign (due to turbulent flow).
Aortic Aneurysms
AAAs are the most common type of aortic aneurysm. The most common site is the infrarenal aorta.
The suprarenal aorta and thoracic aorta can also be affected.
The ascending aorta is usually spared.
Aortic aneurysms are usually asymptomatic until they rupture.
Clinical features of rupture include:
Shock: hypotension, cyanosis, mottling, tachycardia and confusion
Sudden onset pain at the site of rupture
A pulsatile abdominal mass
Rupture of an aortic aneurysm has a high mortality rate.
Surgical repair can be attempted using both open and endovascular techniques.
AAAs with a diameter >5.5 cm have a risk of rupture of over 3 % per year. Until an AAA has reached 5.5 cm the risks of surgery outweigh the risk of rupture. A diameter of 5.5 cm is therefore an indication for surgical repair. Elective, asymptomatic AAA repair has a 30-day mortality of 5–8 %. Emergency, symptomatic AAA repair has a 30-day mortality of 10–20 % and a rupture repair has a mortality of 50 %.
At present, there is a UK National Screening programme which utilises ultrasound to identify AAAs in all men aged 65 years and over. If the scan reveals an AAA <3 cm in diameter, no further follow up is required. An AAA 3–4.4 cm requires follow up in 1 year and a diameter of 4.5–5.4 cm requires follow up every 3 months. Vascular surgery referral is required in those patients with an AAA diameter of 5.5 cm or greater.
Carotid Artery Disease
Stenosis of the carotid arteries in the neck is caused by atherosclerosis and plaque formation. The plaque(s) may be stable and asymptomatic or be the source of embolization. As the embolus travels into the intracranial vasculature it may cause temporary ischaemia resulting in a transient ischemic attack (TIA) or manifest as a thromboembolic stroke resulting in permanent damage. Carotid artery disease may present as a carotid bruit (‘swooshing’ noise) on auscultation. Colour flow duplex ultrasound is the diagnostic modality of choice.
The main risk factors for carotid artery disease include:
Smoking
Diabetes Mellitus
Hypertension
Hyperlipidaemia
If there is a greater than 50 % stenosis of the internal carotid artery on investigation which has resulted in a TIA or stroke, the first line treatment is urgent carotid endarterectomy. This is only indicated within 14 days of the event. The North American Symptomatic Carotid Endarterectomy Trial (NASCET) has reported that carotid endarterectomy provides significant benefit in patients with severe symptomatic stenosis [1]. If the stenosis in the internal carotid artery is found incidentally and is asymptomatic, the evidence for surgery is less clear. The asymptomatic carotid surgery trial (ACST) found that while the procedure reduces stroke risk in asymptomatic patients younger than 75 years, benefit to patients depends on a variety of factors including life expectancy and future surgical risk [2]. Current management options in asymptomatic disease also include medical alternatives.
Varicose Veins
There are both superficial and deep venous systems in the lower limb. They are connected to each other by perforating veins and at the sapheno-femoral and sapheno-popliteal junctions. Venous blood is returned to the heart via the iliac veins and inferior vena cava.
When the calf muscles in the legs contract blood is pumped towards the heart as venous blood drains from superficial to deep veins. When the calf muscles relax the ‘one-way’ valves in the veins close. This closure prevents backflow of venous blood into the superficial venous system.
Valve incompetency will allow blood to flow into the superficial veins, converting them into a high-pressure system and producing the enlarged, tortuous appearance of varicose veins.