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Emboli
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Arterial disease 115
Ipsilateral
hemisphere
Ipsilateral
eye
External
Internal
carotid
artery
stenosed
Figure12.6 Consequences and treatment of carotid artery stenosis.
Clinical features
• Amaurosis fugax. The patient commonly complains of a loss of vision like a curtain coming
down across their visual field. The blindness is
unilateral, ipsilateral to the diseased carotid
artery, and usually lasts a few minutes.
•
Cerebrovascular accidents (stroke). Emboli in the
carotid territory of the cerebral circulation of the
ipsilateral hemisphere will result in symptoms
affecting the contralateral side of the body, commonly loss of use of the arm. If the dominant
hemisphere is involved, speech may be affected.
• Transient ischaemic attack. By definition, these
mimic strokes, but last less than 24 hours.
Examination may reveal a bruit over the affected side
(although very tight stenoses are often silent) and
carotid
artery
Common
carotid
artery
evidence of vascular disease elsewhere. During an
attack, unilateral weakness affecting the arm or leg,
dysphasia, and retinal emboli and infarction may
benoted.
Differential diagnosis
Other causes of focal neurological deficits include
hypoglycaemia, focal epilepsy, migraine, intracerebral neoplasm, and emboli secondary to cardiac
arrhythmias and valve disease.
Special investigations
• Duplex ultrasonography. By measuring flow
patterns, it is possible to quantify the degree of stenosis of a vessel because the blood velocity
Contralateral
eye
Diseased
intima
removed
Patch
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increases as it crosses a stenosis in order to maintain the same flow rate. This gives an accurate
invasive assessment of the degree of stenosis
nonand is useful to screen for the disease.
MR/CT angiography can also give good images of
•
the carotid vessels and allows good visualization
of the vertebral system to assess the complete cerebral perfusion. It is less accurate in the measurement of the degree of stenosis.
• CT of the brain is indicated in any patient with a
stroke or if any doubt over symptoms exists, since
intracranial tumours may mimic carotid artery
disease, and may co-
•
MR of the brain. A diffusion- weighted MRI scan
will provide evidence of infarction.
ECG/echocardiography. This may be necessary to
•
exclude a cardiac cause of cerebral symptoms.
exist.
Treatment
Patients who have had a recent TIA, amaurosis fugax
or stroke with full recovery in the presence of a significant internal carotid stenosis are at high risk of a subsequent stroke in the months following. The definition
of a significant stenosis varies depending on the measurement parameters used (Figure12.7). If the North
American Symptomatic Carotid Endarterectomy Trial
(NASCET) measurement is used, then a significant
stenosis is defined as greater than 50%, and for the
European Carotid Surgery Trial (ECST) measurement,
it is greater than 70%, emphasizing the importance of
understanding how a stenosis was defined. These
patients benefit from carotid endarterectomy to
remove the diseased intima and recarotid flow. All patients should be started on antiplatelet therapy and a statin upon diagnosis, and this
should be continued indefinitely as prophylaxis
against further events. Surgery should ideally be
undertaken within 2weeks of symptoms. Patients with
asymptomatic stenoses may also benefit from surgery,
but here the risk/benefit ratio is not as favourable.
Carotid endarterectomy is performed as prophylaxis against future stroke. The diseased intima is
removed. A shunt may be used during the surgery to
preserve blood flow to the brain.
establish normal
Complications ofcarotid
endarterectomy
• Disabling stroke. Up to 3% of patients will suffer a
stroke.
Death, usually as a consequence of stroke, in up
•
to 2%.
•
Haemorrhage. Bleeding is common, as the
patients are on antiplatelet therapy. Occasionally,
operative haemorrhage requires wound
postre- exploration.
• Hypoglossal neuropraxia. The hypoglossal nerve
crosses the upper part of the incision and may be
damaged during surgery, resulting in a hypoglossal palsy, manifested by protrusion of the tongue
to the ipsilateral side.
•
Reperfusion syndrome. The sudden increase in
blood flow to the brain may result in cerebral
oedema and fitting or haemorrhage. Good postoperative blood pressure control is, therefore, vital.
ECA
A
C
CCA
ICA
B
NASCET:
ECST:
B–A
B
C–A
C
× 100
× 100
Figure12.7 Different measurement
techniques for determining
the degree of carotid stenosis.
ECST: European Carotid
Surgery Trial; NASCET: North
American Symptomatic Carotid
Endarterectomy Trial.
Arterial disease 117
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• Restenosis. The vessel may restenose at the site of
the arteriotomy. To reduce this risk, a patch is usually used, made from saphenous vein or prosthetic
material such as PTFE or Dacron.
Raynaud’s disease and
Raynaud’s phenomenon
Raynaud’s disease is a vasospastic condition that
affects the digital arteries within the hands and occasionally the feet.
Aetiology
This may be primary Raynaud’s disease, almost invariably in women, or Raynaud’s phenomenon, secondary to some other aetiology, particularly connective
tissue disorders such as systemic sclerosis (scleroderma) and polyarteritis nodosa, the other symptoms
of which it may precede by several years. It may occur
in patients with cryoglobulinaemia, or it can result
from working with vibrating tools. It is important to
exclude other causes of cold, cyanosed hands, for
instance, pressure on the subclavian artery from a
cervical rib (sometimes complicated by multiple
emboli arising from the damaged artery wall at the
site of rib pressure), or blockage of a main artery in
the upper limb due to atherosclerosis or Buerger’s
disease.
Clinical features
The syndrome occurs as a result of intermittent spasm
of the small arteries and arterioles of the hands (and
feet). Spasm is usually precipitated by cold exposure.
During spasm, the hands go white. As the vasospasm
resolves, the pallor changes to cyanosis and then
crimson red as reperfusion and hyperaemia occur,
the process commonly taking 30–45min.
Treatment
Conservative
The management should initially be conservative.
Patients should be urged to keep their hands and feet
9
Maurice Raynaud (1834–1881), Physician, Paris. Described
the condition in his doctoral dissertation.
9
warm, to wear gloves and fur- lined boots in the winter, and to make sure that the house, especially the
bed, is warm at night. They should also avoid immersion of the limbs in cold water. Smoking must be
stopped. Treatment with vasodilator drugs is usually
tried, but the results are often disappointing.
Surgery
Sympathectomy almost invariably produces a
dramatic improvement in the symptoms, but unfortunately may not be longRarely, Raynaud’s phenomenon or disease leads to
actual necrosis of tissues and gangrene of the digits. If
this occurs, local amputation may be necessary, but,
as the circulation of the proximal part of the hand is
usually satisfactory, major amputations are seldom
required.
lasting in the upper limbs.
Buerger’s disease
Buerger’s disease (thromboangiitis obliterans) is a
rather poorly defined entity, usually affecting men
(90%), the salient features of which are similar to atherosclerosis, but the age incidence is much younger
and the association with heavy smoking is almost
invariable. Peripheral vessels tend to be affected earlier in Buerger’s disease, and it is characterized by
inflammation of smalland veins, in contrast to atherosclerosis, although the
symptoms of distal claudication and ischaemic ulceration of the toes are similar. It tends to affect the hands
and fingers more commonly than atheroma. An autoimmune association has been proposed. Smoking
cessation reduces but does not halt progression.
and medium- sized arteries
Cold injury
Frostbite may result from prolonged exposure to cold
and is caused by a combination of ice crystal formation
in the tissues, capillary sludging and thrombosis within
small vessels of the exposed extremities. Treatment
comprises gentle warming, anticoagulation with heparin to prevent further thrombosis and antibiotics to
inhibit infection of necrotic tissues. Local amputation
to remove necrotic digits is performed once clear
demarcation develops. Raynaud’s phenomenon may
be experienced as a late complication.
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Additional resources
Case 21: A pulsating abdominal mass
Case 22: Abdominal bruising
Case 23: A painful calf
Case 24: Black toes
Case 25: A useful instrument in vascular surgery
Case 26: A young woman with cold blue hands
The heart and
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thoracicaorta
David P. Jenkins
Learning objective
✓ To know the principal surgical conditions of the heart and thoracic
aorta, and how they are treated.
temperature. The tolerance to ischaemia can be
Introduction
There are several unique features of cardiac surgery
compared with other operations. The heart is continually beating to support life and, therefore, is a moving target; hence the use of cardiopulmonary bypass
during surgery and the routine need for intensive care
support following surgery.
Cardiopulmonary bypass
Background
If the circulation is temporarily stopped at normal
body temperature, organs suffer ischaemic damage
owing to lack of oxygen, the extent varying according
to the metabolic demand of the organ. The brain is
the most sensitive tissue in this respect and is liable to
irreversible changes after 4minutes of ischaemia. The
spinal cord is next, followed by heart muscle, which
will tolerate about 10minutes of ischaemia at normal
increased slightly by lowering the metabolic rate by
hypothermia.
bypass in the 1950s, surgery on the heart was limited
to procedures that could be performed rapidly on a
beating heart, such as mitral valvotomy to relieve
mitral stenosis, where a finger is passed blindly
through the left atrial appendage and through the
stenotic mitral valve. Another alternative was to cool
the whole patient, when periods of up to 10minutes
of absent circulation permitted very simple procedures to be performed relatively safely, such as closure of an atrial septal defect (ASD).
bypass, it is now possible to operate on the heart for
prolonged periods while the bypass machine is used
to take over the function of the heart and lungs, and
perfuse the body. Cardiopulmonary bypass has transformed the safety and reliability of cardiac surgery
and led to the development of the specialty. The
majority of heart operations performed today utilize
cardiopulmonary bypass.
13
Prior to the development of cardiopulmonary
Following the development of cardiopulmonary
Ellis and Calne’s Lecture Notes in General Surgery, Fourteenth Edition.
Edited by Christopher Watson and Justin Davies.
© 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd.
Companion website: www.wiley.com/go/Watson/GeneralSurgery14
Technique
The heart is approached with a median sternotomy
incision and the pericardium opened with an inverted
‘T’ incision. After full heparinization, cannulae are
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Oxygenated 'arterial' blood
Deoxygenated venous blood
Cannula in inferior and
superior venae cavae
secured by an external tape
Aortic cannula
sutured in
Pump
Figure13.1 Cardiopulmonary bypass.
inserted into the venae cavae via the right atrium to
syphon off the venous return from the systemic circulation. The blood is then pumped through an oxygenator, filter and a heat exchanger before returning to
the systemic circulation via a cannula in the ascending aorta or occasionally a peripheral artery (femoral
or axillary) (Figure13.1). This form of bypass will perfuse the whole body with oxygenated blood at an
adequate pressure while diverting it from the heart
and lungs. The heart may now be stopped and the
myocardium protected by ‘cardioplegic’ solution
containing potassium to produce rapid cardiac arrest
in diastole. The cardioplegia can be delivered antegrade into the aortic root or directly to the coronary
ostia, or retrograde via the coronary sinus. With the
aorta crossbloodless field with access to all chambers.
clamped, the heart may be opened in a
Cardiac intensive care
The nature of cardiac surgery means that patients
are rarely woken and extubated immediately following surgery. They are usually managed in intensive
Gas in
Gas out
Water in
Water out
care for the first night, with sedation and ventilation
continued until they are warm and haemodynamically stable without excessive bleeding. Standard
monitoring includes arterial and central venous
lines, a urinary catheter, ventilator parameters and
electrocardiograph.
Oxygenator
Heat exchanger to control
body temperature
Complications of cardiopulmonary
bypass andcardiac surgery
ingeneral
• Emboli. Air entrapped during formation of the
bypass circuit or entering during bypass, or thrombus forming in the bypass circuit, or atheroma from
the aorta may embolize occasionally into the cerebral and peripheral circulation with catastrophic
results, such as stroke and limb ischaemia.
Haemorrhage postoperatively, which may result in
•
cardiac tamponade and require re- exploration in
up to 3%. Although heparinization is reversed
after cardiopulmonary bypass is finished, the
bypass circuit activates the clotting cascade and
consumes platelets, thus increasing the risk of
haemorrhage.
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• Infection. Patients are at risk of all the potential
complications of any surgical procedure, including wound infections (in up to 3%) and chest
infections.
Low cardiac output. This is the result of right or left
•
heart failure postwith inotropic support.
Multi- organ failure. This results if heart failure
•
persists despite optimal management or if sepsis
develops during prolonged intensive care.
Although renal failure can be managed with haemofiltration, liver and gut failure are often fatal.
• Death. There are sophisticated risk stratification
tools available to estimate risk of death (e.g.
EuroSCORE
tine cardiac surgery is in the order of 1–3%.
surgery. It is usually managed
1
). The average risk of death for rou-
Valvular disease
Valve repair andreplacement
With the advent of cardiopulmonary bypass, it has
become possible to remove diseased valves and
replace them with artificial ones– mechanical, bioprosthetic or occasionally human allograft valves. In
mitral valve regurgitation, repair is now usually
undertaken in preference to replacement. In aortic
valve regurgitation, valve repair may also be possible.
For aortic valves, a minimal access option is also
available to replace the valve with percutaneous
access via peripheral arteries – transcatheter aortic
valve insertion (TAVI). Similar procedures are under
development for the mitral valve, but the access and
anatomy is more complex.
Mechanical valves
Many examples exist, the most common in use
today are bileaflet valves, where the valve comprises
two semi- circular tilting leaflets made of pyrocarbon set in a sewing ring. Prosthetic valves may
become obstructed by thrombus owing to turbulent
flow across the non- biological valve leaflets; recipients must, therefore, be anticoagulated with
warfarin indefinitely.
1
e EUROpean System for Cardiac Operative Risk
Estimation (http://www.euroscore.org).
Bioprosthetic valves
These are made from bovine pericardium or from pig
heart valves. The valve is suspended on a prosthetic
ring to allow it to be sewn in place. The bioprostheses
are treated with glutaraldehyde and usually sewn
onto a plastic frame. Once implanted, the recipient
does not require anticoagulation, although antiplatelet therapy is recommended. The valves do not cause
any immune reaction and are not rejected. The lifetime of such valves is generally shorter than prosthetic valves, but the avoidance of anticoagulation
makes them the preferred choice in the elderly.
Current guidelines recommend bioprostheses in the
aortic position from 55 years and in the mitral position from 70 years.
Complications ofvalve
replacement
• Valve thrombosis can cause embolus formation,
especially if not on anticoagulation.
•
Mechanical structural failure with embolism of
valve fragments, or outflow obstruction or massive
valve incompetence. This has become very rare
with modern mechanical valves.
• Haemorrhage, especially when anticoagulated.
• Paraprosthetic leaks, where blood leaks between
the artificial valve ring and the heart tissue, and
can cause haemolysis.
•
Infection of the valve, a situation akin to infective
endocarditis of a native valve.
Aortic stenosis
Stenosis of the aortic valve is increasingly common in
the elderly population. It may be as a result of:
•
Aortic sclerosis: degenerative calcification of a
standard three-
• Calcification of congenitally bicuspid valves; 1%
of the population have only two aortic valve
leaflets owing to fusion of two adjacent valve
cusps, and in these patients, stenosis can develop
earlier in life.
No matter what the cause, the aortic valve, when
stenosed, is usually grossly distorted and calcified
and unsuitable for valve repair; replacement is the
treatment of choice. Once calcification occurs, progression of the stenosis is inevitable. Aortic stenosis
leaflet valve.
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from rheumatic fever is now rare in the West, and usually coincides with mitral valve disease.
Clinical features
The three presenting symptoms of aortic stenosis are
angina, dyspnoea on exertion and syncope (occasionally
sudden death). Examination reveals a slow rising pulse
and an ejection systolic murmur. Electrocardiogram
(ECG) may show left ventricular hypertrophy and the
echocardiogram is diagnostic. Computed tomography
(CT) may show valve calcification and posttion of the aorta. Once the gradient across the valve
exceeds 60 mmHg, or the patient is symptomatic, surgery is advised.
stenotic dila-
Treatment
Valve replacement on cardiopulmonary bypass
remains the gold standard. Coincidental coronary
artery disease may be treated at the same time.
Percutaneous aortic valve replacement (TAVI), via
the femoral artery, may be an alternative for some
patients who are frail or the elderly and have relative
contraindications to open surgery. This TAVI
approach can also be placed into existing failing bioprostheses– the ‘valve-
in- valve’ procedure.
Mitral regurgitation
This is now the most common lesion of the mitral
valve. It is commonly due to myxomatous degeneration, typically of the posterior leaflet, but often affecting both valve leaflets. In severe form, with thickening
and prolapse of both leaflets, it is termed Barlow’s
2
disease.
Pathology
In degenerative disease, there is elongation of both
leaflets but particularly of the chordae tendinae,
which may proceed to rupture. The result is a prolapse
of the leaflet into the left atrium during systole, with
regurgitation of blood through the non- co- apting
leaflets. This is followed by ventricular enlargement
as a response to the volume load, and by annular
2
John Bereton Barlow (1924–2008), Professor of Cardiology,
Johannesburg, South Africa.
dilation. Later in the disease progression, there is left
atrial enlargement and eventually loss of electrical
ordination and the onset of atrial fibrillation. In
cosome cases of ‘functional’ regurgitation, the regurgitation is due to dilatation and impairment of the left
ventricle.
Clinical features
The patient may be asymptomatic for many years,
with just a regurgitant murmur noted, until shortness
of breath or atrial fibrillation occurs. The former may
be of sudden onset, usually indicating a ruptured
chord and abrupt increase of regurgitation into a still
small left atrium. At a late stage, there may be secondary pulmonary hypertension and right heart failure.
Physical examination reveals an irregular pulse, a
pansystolic murmur and perhaps lateral displacement of the apex beat.
Treatment
Symptomatic patients with severe regurgitation and
preserved left ventricular function should have
surgery. The regurgitant volume can be followed by
surveillance echocardiography in the asymptomatic,
as can the left ventricular size. Once the former
reaches the classification ‘severe’, or if the left ventricle starts to enlarge, surgery is indicated.
For most patients, treatment can be valve repair;
this option preserves the native valve, avoiding the
need for replacement. It also optimizes left
function, because the whole mitral valve apparatus–
leaflet, chordae and papillary muscles – forms an
integral part of the left ventricle.
The repair is performed on cardiopulmonary
bypass, usually through a sternotomy. There is also a
minimal access surgical approach, via a small right
anterior thoracotomy and using telescopic vision and
specially adapted instruments. The tricuspid valve
may need to be repaired at the same time.
ventricular
Mitral stenosis
With the great decline of rheumatic fever, mitral stenosis has almost disappeared in the West, but is still
common in many parts of the world. At an early stage,
when the leaflets are fused but mobile, the valve can
be split open. This can be the conventional mitral
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valvotomy, historically done with a finger, or increasingly with a balloon placed under radiological
control.
When the valve is calcified, sophisticated repair
techniques can be used, but are less successful than
in the degenerative, regurgitant valves. Sometimes,
valve replacement is required, using the same sort of
valve options as discussed for the aortic valve.
Ischaemic heart disease
Angina, due to myocardial ischaemia, is caused by
atherosclerosis in the coronary arteries and may be
alleviated by increasing the arterial blood supply.
Two treatment options exist: endoluminal intervention with balloon angioplasty and stenting, and
surgical revascularization with coronary artery
bypass grafts (CABGs).
Aetiology
The risk factors for coronary artery disease are those
for atheroma in general (Box 12.1). In particular,
raised serum cholesterol, hypertension and cigarette
smoking, each double the risk of coronary artery disease. The presence of all three increases the risk
eightfold.
Special investigations
• Exercise ECG shows whether there is myocardial
ischaemia on exercise.
Myocardial perfusion imaging. In patients unfit for
•
treadmill exercise, myocardial stress can be
induced pharmacologically using dobutamine or
adenosine while imaging perfusion with magnetic
resonance or methoxyisobutylisonitrile (MIBI).
• Stress echocardiography is an alternative to myo-
cardial perfusion imaging. The contraction of different segments of the left ventricle is studied
before and during pharmacologically induced
stress.
•
CT coronary angiogram. Modern high- resolution
scans, with software algorithms and appropriate
gating for heartbeat, can provide excellent definition of coronary anatomy and plaque disease, and
is useful to exclude significant disease.
• Coronary angiography is performed in patients
with ischaemic responses to exercise to determine
treatment options. It is important for accurate
anatomical diagnosis and may be combined with
endoluminal therapy.
Treatment
• Angioplasty. Isolated stenoses in proximal vessels
are most appropriate for percutaneous coronary
intervention (PCI) to reduce the symptoms of
angina, with endoluminal stenting having an
advantage over balloons alone to prolong patency.
• Surgical revascularization remains the procedure
of choice for total occlusions or stenoses in multiple
vessels and offers both symptomatic and prognostic benefits. It remains the guidelinetreatment for more complex coronary anatomy,
especially tripleimpaired left ventricular function and diabetes.
This involves anastomosing an internal mammary
(internal thoracic) artery to the diseased coronary
artery distal to the blockage (usually the left to the
left anterior descending coronary artery). For multiple grafts, autogenous reversed saphenous vein or
radial artery can also be used as aortocoronary
bypass conduits (Figure 13.2). Most CABG
operations are performed on cardiopulmonary
bypass, but surgery can be performed with the
heart beating using special stabilizers and intracoronary shunts.
As with all arterial surgery for atherosclerosis, there
is a tendency for recurrent disease with the passage of
time. This may require repeat surgery or may be amenable to endoluminal procedures. Secondary prophylaxis with drug therapy, including statins, βand angiotensin- converting enzyme (ACE) inhibitors
reduces the risk of further events, and antiplatelet
therapy should be continued for life.
vessel disease and in patients with
recommended
blockers
Surgery forthe complications
ofmyocardial infarction
1 Acute ventriculoseptal defect. When the infarcted
ventricular muscle is part of the septum and
undergoes necrosis, septal rupture may occur.
This occurs 1–2weeks after myocardial infarction
in 0.5% of patients and requires urgent repair,
which may be achieved surgically or via an endovascular approach. Mortality is high.
2 Ventricular aneurysm. If the infarcted ventricular
wall is apical, it may necrose and rupture, leading
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Ascending aorta
Saphenous
vein graft
Right
coronary
artery
Obstruction
Pulmonary artery
Left
internal
thoracic
artery
Anterior interventricular
coronary artery
Figure13.2 A saphenous vein graft from the aorta to the right coronary artery and a direct left internal mammary
(thoracic) artery graft to the anterior interventricular coronary artery (also known as the left anterior descending [LAD]
artery).
to rapid death by tamponade. Alternatively, it may
heal with fibrosis, and subsequently a ventricular
aneurysm may form. This may require excision if
paradoxical movement or thrombus becomes
symptomatic.
3 Mitral regurgitation. If the infarct involves a papil-
lary muscle and it ruptures, then acute mitral
regurgitation requires mitral valve replacement.
Heart transplantation
In patients with end- stage heart failure secondary to
ischaemic heart disease, severe valve disease or
dilated cardiomyopathy, heart transplantation is an
option. Potential recipients require careful assessment and extensive comorbidity is often a contraindication. Donor matching is mainly based on blood
group and size matching. The implant procedure is
performed with anastomosis of the left atrial cuff,
aorta, pulmonary artery, and finally inferior and
superior venae cavae.
Thoracic aortic disease
As with other organs, disease of the thoracic aorta can
be divided into congenital and acquired:
Congenital
• Persistent ductus arteriosus
• Coarctation of the aorta
Acquired
• Thoracic aortic aneurysm
• Thoracic aortic dissection
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