Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_623_Библиотеки_им_академика_М_И_Перельмана
.pdf
Arterial disease 105
https://t.me/medicina_free
The annual risk of rupture for an aneurysm with a
maximum antero-
5.5cm is less than 1%, rising to 5% per annum for an
aneurysm of 6 cm diameter, which is the point at
which surgery is recommended for men. The threshold for women is slightly less, at 5.0 to 5.5 cm. The
threshold for aneurysm repair is also dictated by the
estimated operative mortality, which in a fit man is
considered to be less than 5%.
Patients may present with abdominal and/or back
pain but with no evidence of rupture on CT imaging.
These patients are of concern as the pain may represent impending rupture, and in the absence of other
causes of abdominal or back pain, urgent repair
should be considered.
posterior diameter of less than
Management
Patients with small asymptomatic aortic aneurysms
(defined as having a maximal diameter < 5.5cm) are
followed up by regular ultrasound scans to monitor
the rate of growth. Once the threshold diameter is
reached, or if the aneurysm becomes symptomatic
then treatment is advised. Size and anatomy are then
defined by CT angiograms. The options for intervention include:
•
open surgical repair;
• standard endovascular repair with an infrarenal
stent graft;
•
complex endovascular repair (either a fenestrated
or branched endovascular device);
continue with non- operative management.
•
The decisionof the natural history of the aneurysm and associated
risk of rupture, technical consideration and the fitness of the patient for surgery. Decisioncommonly undertaken in a multi- disciplinary setting
and needs to also involve the patient. The preoperative cardiorespiratory assessment will vary
between clinical settings, but if open surgical repair is
to be undertaken, then a thorough objective evaluation of the cardiac and respiratory system is required.
making process will involve assessment
making is
Operative management
(Figure12.2)
Open surgical repair
Open surgery involves replacement of the aneurysmal aorta with a synthetic graft, which is usually made
of Dacron. The aneurysm sac is opened, any lumbar
arteries oversewn, thrombus removed, and the graft
sewn into healthy artery proximal and distal to the
aneurysm. The operative mortality rate for such a
procedure is between 3% and 5%.
Standard endovascular aneurysm
repair (EVAR)
Suitability for an EVAR is determined by the anatomy of the aneurysm, iliac arteries and the infrarenal aortic neck. If suitable, the main body of the stent
graft is inserted through a femoral artery and the
stent positioned into place below the renal arteries.
The stent is then deployed under fluoroscopy with
the stent sealing against a normal infrarenal neck by
radial force. The stent graft requires continuation
into the iliac arteries (a bifurcated device) to allow
the stent to seal appropriately into normal iliac
arteries and prevent retrograde perfusion of the
aneurysmal sac.
Complex endovascular repair
Complex endovascular repair of juxta- renal and
supra- renal aneurysms is possible. The aim is still to
provide an appropriate seal of the stent graft in normal artery above and below the aneurysm to prevent
arterial flow into the aneurysmal sac. There is a subset of patients in whom standard EVAR is not possible as the proximal seal would be inadequate due to
a short infrarenal neck. In such circumstances, it is
possible to manufacture a customated specific to the patient’s anatomy, that has windows cut into the stent graft that align with the
position of the visceral vessels (e.g. the superior mesenteric artery and renal arteries) to facilitate stenting
of these vessels with covered stents from the aortic
graft. These are known as fenestrated or branched
devices.
made device, cre-
Complications ofsurgery
Complications associated with abdominal aortic
aneurysm surgery are similar for open and endovascular management but are more frequent in those
patients undergoing open surgery. The complications
include:
Haemorrhage.
•
Myocardial infarction and arrhythmia secondary
•
to coronary artery disease, which is common in
106 Arterial disease
https://t.me/medicina_free
Right renal artery Left renal artery
Abdominal
Aortic
Aneurysm
Common iliac artery
Open
repair
Dacron graft
sewn to the aorta
above and
below the
aneurysm sac
patients who develop aneurysms. Cross- clamping
the aorta during surgery and reperfusion of the
legs cause additional myocardial stress.
• Chest infection, in relation to smoking- related pulmonary disease, post- operative pain on inspiration and prolonged anaesthesia.
• Acute kidney injury. In open surgery, this is related
to clamping the aorta adjacent to the renal artery
ostia and temporarily occluding them in open surgery. In endovascular surgery, this relates to the
use of large amounts of radio- opaque contrast
during stent grafting, and partial occlusion of the
renal artery ostia by the proximal position of
thestent. In both cases, hypotension exacerbates
the renal injury.
• Distal embolization of thrombus displaced from
the aortic sac or atheroma from arterial walls may
Endovascular
repair
Stent graft
secured to
the infrarenal
aorta above and
iliac arteries
below the
aneurysm sac
Figure12.2 Aortic repairs.
block small vessels in the foot and lower leg, causing acute ischaemia.
• Graft infection occurs in around 1% and may result
in an aorto- duodenal fistula.
• Endoleaks. There is a continued risk that the aneurysm sac may be reperfused with arterial blood, a
complication known as an endoleak (Figure12.3).
Patients with a type 1 or 3 endoleak need urgent
re- intervention to reduce the risk of rupture.
Patients with other leaks can be carefully monitored with intervention required when there is
associated sac enlargement. For this reason,
patients undergoing any form of endovascular
repair of an abdominal aortic aneurysm needtobe
enrolled into a lifelong surveillance programme,
usually with a combination of ultrasound and
plain abdominal X- ray.
Arterial disease 107
https://t.me/medicina_free
Type I
Proximal or distal
graft attachment
site leaks.
Figure12.3 Classication of endoleaks.
Type II Type III Type IV Type V
Retrograde flow into
the aneurysm sac from
aortic side-branches
such as the lumbar or
inferior mesenteric
arteries.
Caused by a defect in
the graft either due
to a fabric tear or
disconnection of
modular overlap.
Ruptured abdominal
aortic aneurysm
A patient with a ruptured aneurysm classically presents with severe back or abdominal pain, collapse and
hypotension. Sometimes, the pain may radiate to the
groin, mimicking renal colic. Occasionally, only groin
or iliac fossa pain may be the presenting symptom, or
the pain is confined to the epigastrium, leading to the
mistaken diagnosis of myocardial infarction.
Fifty percent of patients die from the initial rupture
and never reach hospital. Those patients who do
make it to hospital usually have a rupture contained
within the haematoma aided by the hypotension that
follows rupture. The diagnosis is suggested by an
ultrasound scan performed in the emergency department (a Focused Assessment with Sonography for
Trauma [FAST] scan). If the patient is awake and alert
and has a stable blood pressure (even if hypotensive),
then it is appropriate to undertake a CT angiogram to
(i) confirm the diagnosis and (ii) determine whether
the anatomy would be suitable for an EVAR. If the
anatomy is suitable and the patient continues to
Graft wall porosity. Increase in maximum
aneurysm diameter
with no identifiable
endoleaks.
remain stable then an EVAR, ideally performed under
local anaesthetic, is the most appropriate intervention. If the patient is unstable, then they need to proceed immediately for an open surgical repair.
Popliteal aneurysm
Popliteal aneurysms are the most common peripheral aneurysms. They are commonly associated with
other aneurysms and are frequently bilateral.
Clinical features
Popliteal aneurysms are generally asymptomatic.
When they do cause symptoms, this is usually due to
distal embolization of the thrombus from within the
aneurysm sac, leading to digital infarction or acute
thrombosis of the aneurysm itself. Rupture or symptoms due to compression are less common.
Examination confirms a prominent pulsation in the
popliteal fossa, often extending proximally. Distal
pulses should be sought for evidence of embolization.
108 Arterial disease
https://t.me/medicina_free
The popliteal arteries should be examined in any
patient with an abdominal aortic aneurysm.
Special investigations
• Duplex ultrasonography. Determines the size of
the aneurysm.
CT or MR angiography. Provides anatomical detail
•
of the aneurysm and the arterial tree distal to the
aneurysm.
Treatment
Symptomatic popliteal aneurysms
Acute limb ischaemia (see below) due to acute thrombosis of the aneurysm requires emergency treatment,
usually in the form of a bypass from the distal superficial femoral artery to the distal below knee popliteal
artery, with thrombectomy of the infra- popliteal
arteries. Even with this, the amputation risk is approximately 50%. For symptomatic aneurysms without
acute limb ischaemia, urgent treatment should be
performed usually with a bypass with ligation of the
aneurysm, but occasionally an endovascular procedure may be performed using a covered stent.
Asymptomatic popliteal aneurysms
Size is still the key factor that determines whether an
asymptomatic popliteal aneurysm requires intervention. There is no definitive size threshold, but typically, a diameter of 2.5 to 3 cm is an indication for
surgery. The presence of significant intraluminal
thrombus, marked angulation or the occlusion of one
or more infraintervention. Open surgery or (covered) stent insertion may be considered when intervening on a popliteal aneurysm.
popliteal arteries may encourage earlier
Box 12.1 Risk factors foratherosclerotic
disease
•
Smoking
•
Hyperlipidaemia
•
Hypertension
•
Diabetes mellitus
•
Male sex
•
Increasing age
•
Family history
Curiously, the upper limb vessels are commonly
spared from atherosclerotic disease. Other conditions
that may cause arterial disease include diabetic
microangiopathy, thromboembolic disease, Buerger’s
disease, Raynaud’s phenomenon and the vasculitides, together with arterial injury from trauma, cold
or chemicals.
Risk factors for atherosclerosis
(Box12.1)
Many factors have been shown to contribute to atherosclerosis. While there is a familial tendency to the
disease, the most common aetiological factors are
smoking and diabetes followed by hyperlipidaemia/
hypercholesterolaemia and hypertension. It is a disease that predominantly affects men, although, with
increasing age, women become more susceptible.
Management of atherosclerotic disease involves
optimization of modifiable cardiovascular risk factors.
This includes smoking cessation, exercise and diet
advice; lipidhigh- dose statin therapy; and an antiplatelet agent. Coexistent diabetes mellitus and hypertension should be
sought and treated. A chest X- ray will pick up an asymptomatic bronchial carcinoma, a common finding in
patients with smoking- induced vascular disease.
lowering therapy, which will usually be
Assessing thepatient
witharterial disease
Arterial disease commonly causes impaired blood
supply to the legs. The most common cause of such
arterial disease is atherosclerosis. Given that atherosclerosis rarely localizes to the peripheries, involvement of other organs, particularly the heart, carotid
arteries and abdominal viscera, must be kept in mind.
Lower limb peripheral
arterial disease
Patients with lower limb atherosclerotic disease most
commonly present with intermittent claudication
5
Claudication, from the Latin claudere, to limp. e Roman
emperor Claudius (10 BC to 54 AD) was aicted with a limp
from childhood.
5
. If
Arterial disease 109
https://t.me/medicina_free
the degree of atherosclerosis is more extensive, then
patients may present with symptoms of critical limbthreatening ischaemia (gangrene / foot ulcer / rest
pain). Some patients may have peripheral arterial
disease yet display no symptoms– this is commonly
because they do not walk far enough to elicit
claudication-
type symptoms.
Intermittent claudication
Intermittent claudication manifests as a gripping,
tight, cramp- like pain in the muscles of the leg brought
on by exercise and relieved by rest. It most commonly
affects the calf but can affect the thigh and buttock.
Pain that is present on standing and that requires the
patient to sit down before it is relieved is more typical
of cauda equina compression (spinal claudication)
(Chapter18).
Calf claudication is usually due to atherosclerosis
within the superficial femoral artery, whereas buttock
claudication is due to a reduced blood flow down the
internal iliac arteries, owing to a lesion either there or
higher up in the common iliac artery or the aorta.
Bilateral buttock claudication is associated with
impotence, as both internal iliac arteries are compromized (Leriche’s syndrome
intermittent claudication of the buttock muscles, pale
cold legs and impotence).
The natural history of the limb in claudication is
relatively benign. In approximately 75% of patients,
the symptoms will remain static or improve over time
with no intervention. Patients with claudication have
a higher risk of heartwhen compared to patients without peripheral arterial disease.
6
: absent femoral pulses,
related complications or stroke
Rest pain
Rest pain occurs when the blood supply to the foot is
insufficient. Initially, the pain occurs at night after the
foot has been horizontal for a few hours in bed. The
patient gains relief by sleeping with the leg hanging
out of bed. As the disease progresses, the pain
becomes continuous throughout the day.
Gangrene
The presence of gangrene indicates a severe degree of
vascular impairment. Typically, it occurs in the toes
or at pressure areas on the foot, particularly the heel
or on the plantar aspect of the ball of the hallux.
Gangrene results from infection of ischaemic tissues.
Minimal trauma, such as a nick of the skin while cutting the toenails or an abrasion from a tight shoe, enables ingress of bacteria into the infarcted tissues; the
combination of these two factors results in clinical
gangrene.
Diabetic foot ulceration
Diabetic foot ulceration can be primarily neuropathic
or neuropoorly controlled diabetes, can affect the sensory,
motor and/or the autonomic nervous system. This
causes limited sensation to the foot; abnormal shape
of the foot, leading to a change in pressure areas; and
reduced sweating, leading to dry skin and cracking,
all of which predispose to ulceration. Patients with
diabetes are also prone to atherosclerosis and small
vessel disease. The atherosclerosis has a tendency to
affect the infra- popliteal arteries, which makes revascularization more challenging and less successful.
ischaemic in nature. Neuropathy, caused by
Critical limb- threatening
ischaemia
Critical limb- threatening ischaemia may be defined
as rest pain, ulceration or gangrene associated with
absent pedal pulses. An ankle brachial pressure index
(ABPI) of less than 0.5 also signifies critical ischaemia.
Without revascularization, the natural history of a
critically ischaemic leg is progression to major lower
limb amputation. The five- year mortality in this group
of patients is 50%.
6
René Leriche (1879–1955), Professor of Surgery
successively at Lyon, Strasbourg and Paris.
Examination
Careful clinical examination will usually provide a
very clear indication of the severity and nature of the
ischaemic disease.
•
Heart rhythm. The presence of atrial fibrillation or
other cardiac arrhythmias should be noted, particularly if there is a history of acute limb ischaemia (see below).
• Inspection of limbs. Inspection of the legs may
reveal marked skin pallor, an absence of hairs,
ulcers (usually lateral malleolus and often in the
interdigital clefts) and gangrene, all being evidence of impaired circulation.
110 Arterial disease
https://t.me/medicina_free
• Venous guttering. The veins of the foot and leg in a
patient with diminished arterial supply are often
very inconspicuous compared with normal veins.
Indeed, the veins may be so empty that they
appear as shallow grooves or gutters, especially in
the elevated limb.
•
Buerger’s test
the horizontal and keeping them there for a couple of minutes. A poor arterial supply is shown by
rapid pallor. The legs are then allowed to hang
dependent over the examination couch. The feet
reperfuse with a dusky crimson colour in contrast
to a normally perfused foot, which has no colour
change. In severe cases, the foot may remain pale
and some time may pass before the reactive hyperaemia appears.
Capillary return. The speed of return of capillary
•
circulation after the blanching produced by pressure on the nails is a very useful gauge of the
peripheral circulation.
• Skin temperature. Skin temperature can be readily
assessed by palpation, which is especially sensitive when the dorsum of the hand is used. A difference between the temperatures of one part of the
leg and another or between the two legs can be
readily ascertained. A clearly marked change of
temperature may reveal the site of blockage of a
main artery.
• Peripheral pulses. The peripheral pulses throughout the body should be examined. Whereas normal pulsation can be appreciated easily, palpation
of weak pulsation requires practice, care and,
above all, time. The presence of a weak pulse that
is palpated is of considerable significance diagnostically and can be important prognostically, as
even a weak pulse means the vessel is patent.
Careful recording of the peripheral pulses will
often clearly delineate a blockage in the arterial
system. For instance, the presence of a good femoral pulse and absence of pulses distal to the femoral suggest a superficial femoral arterial block.
Ischaemia of the digits in the presence of all
pulses, including the radial and ulnar pulses, is a
typical finding in Raynaud’s phenomenon or small
vessel disease.
Aneurysmal arteries. The abdomen should be
•
examined for any evidence of abnormal aortic
7
Leo Buerger (1879–1943), born in Vienna, Surgeon and
Urologist in various hospitals in NewYork and Los Angeles.
Also described thromboangiitis obliterans in 1908.
7
involves raising the legs to 45° above
pulsation suggestive of an aneurysm; the popliteal
and femoral arteries should also be examined
with this in mind.
•
Auscultation of vessels. In all areas where pulses
are felt, auscultation should be performed. Partial
blockage of arteries very often causes bruits,
which are usually systolic in timing; they may even
be felt as thrills. Arteriovenous communications
will produce continuous bruits with systolic
accentuation (machinery murmur) and pulsating
dilated veins.
•
Ankle brachial pressure index. The ABPI should be
measured in each leg as part of the routine examination. A Doppler probe is held over the brachial
artery and a blood pressure cuff inflated to occlude
the blood flow. As the blood pressure cuff is
deflated, a Doppler signal reappears and a systolic
pressure can be recorded. Similar pressure readings are taken from the dorsalis pedis and posterior tibial arteries with a cuff just above the ankle.
The ABPI is the ratio of pressure at the foot pulse to
that at the brachial artery. A value between 0.9 and
1.1 is normal and values less than 0.5indicate significant (‘critical’) ischaemia. Heavily calcified
vessels, as are common in patients with diabetes,
may be incompressible and give false normal or
high readings.
Exercise test. If it is difficult to obtain a clear history
•
of the diagnosis of peripheral arterial disease in
the context of exertional leg pain and a normal
resting ABPI (common if spinal claudication is
considered), then an exercise test is useful to perform. The patient should be exercised (corridor
walking / treadmill test / heelwith pre- and post- exercise ABPI measurements.
A significant reduction in post- exercise ABPI indicates ischaemia.
to- toe- tip exercise)
Management
Intermittent claudication (Box12.2)
Conservative treatment
If patients stop smoking and continue exercise or, better still, are enrolled into a programme of supervised
exercise, over one- third will extend their claudication
distance owing to the development of collateral vessels that bypass the blockage. Only one- third will
deteriorate. In addition to cessation of smoking, the
other risk factors for the development of arterial disease should be treated: diabetes should be sought
Arterial disease 111
https://t.me/medicina_free
Box 12.2 Treatment ofclaudication
Conservative
•
Stop smoking
•
Exercise to increase the collateral circulation
•
Learn to live within a claudication distance,
involving a change in lifestyle and perhaps
employment
•
Foot care, to prevent minor trauma which may
lead to gangrene
•
Treat co- existing conditions such as diabetes,
hypertension and hyperlipidaemia
Interventional
•
Angioplasty
•
Endoluminal stenting
•
Bypass surgery, but only if severely handicapped
by symptoms
and treated aggressively, and all patients should be
treated with intense lipid-
lowering and antiplatelet
therapy.
Interventional treatment
If claudication is a significant handicap to the patient
and impacts their day-
to- day quality of life, the possibility of reconstructive surgery or angiographic
intervention may be considered, taking into account
the natural history of the leg in patients with claudication alongside the short-
and long- term risk of inter-
vention (Figure12.4).
Critical limb- threatening
ischaemia.
Without revascularization, the leg will not be salvaged, and this will lead to either major lower limb
amputation or palliation.
Superficial
femoral
artery
Deep
femoral
artery
Tortuous
dilated
collateral
channel
Popliteal
artery
(a) (b)
Figure12.4 Tracings of arteriograms.
(a) An example of a good ‘run- off’
from the occluded supercial femoral
artery, with a patent popliteal artery;
this is suitable for reconstructive
surgery. (b)The main arterial tree is
obliterated, and reconstruction cannot
be carried out.
112 Arterial disease
https://t.me/medicina_free
• Angioplasty involves inflating a balloon within the
vessel to open up a stenosis or occlusion to allow
more blood to pass through. This is most successful with concentric stenoses or occlusions in the
iliac system, and is less successful with longer
occlusions over 10cm, particularly in the distal
femoral and popliteal arteries. An endovascular
stent may be used to maintain patency.
Angioplasty carries the risk of distal embolization
and vessel perforation, and is prone to restenosis.
Bypass surgery. Bypass surgery is reserved primarily
•
for critical limb- threatening ischaemia. Successful
surgical reconstruction demands four things:
– Inflow. A good arterial supply up to the area of
blockage is necessary to ensure that enough
blood can be carried distally via the conduit to
the ischaemic area.
– Outflow (run- off). There should be good ves-
sels below the area of disease onto which a
conduit can be anastomosed. If there is
nowhere for the blood to go, the conduit will
occlude.
– The conduit. Ideally, the saphenous vein,
reversed or used in situ with valve destruction,
should be used. If this is unavailable, then arm
vein or an inert prosthetic material such as
polytetrafluoroethylene (PTFE) may be used
for the conduit. The conduit will take blood
from the proximal to the distal segment of the
artery beyond the blockage. In grafts that start
and finish above the knee, there is little to
choose between PTFE and vein in terms of
term patency, but a graft that crosses the
longknee is much more likely to remain patent if it
issaphenous vein rather than PTFE. Infection
is less likely with autologous vein.
– The patient. Critical ischaemia is often the first
sign of the endinevitably results in death. Surgery for critical
ischaemia has a high mortality, reflecting this
general deterioration.
Technical complications of surgery include intimal
dissection, distal embolization and graft thrombosis,
which worsen the initial situation.
Lumbar sympathectomy. Palliation may be
•
achieved by lumbar sympathectomy, which
increases the blood supply to the skin and which
can be performed percutaneously. The small
increase in blood supply may make some clinical
difference and is a relatively low- risk procedure.
stage vascular disease that
• Amputation. Pain that is not controlled and ulceration or gangrene that is associated with lifethreatening infection are indications for major
lower limb amputation (defined as an aboveamputation). The general principle is to achieve a
viable stump that heals primarily, and a secondary
goal is to make the stump as distal as possible to
facilitate rehabilitation on a prosthesis.
ankle
Acute limb ischaemia
(Box12.3)
Acute limb ischaemia is the sudden onset of pain in
the leg / foot due to an abrupt deterioration in the circulation of the foot. It classically presents with the six
Ps – pain, pallor, paraesthesia, paralysis, pulselessness and perishingly cold. The signs of paralysis and
paraesthesia are important to determine as the presence of these are suggested of a threatened limb, and
such patients require immediate revascularization.
The two main causes are (i) an embolus or (ii) in
situ thrombosis due to atherosclerotic plaque rupture. Differentiating between the two is important as
the management will differ. Other causes of acute
limb ischaemia, which need to be borne in mind
when assessing a patient, are a thrombosed popliteal
aneurysm, aortic dissection and trauma.
Embolism
An embolus is abnormal undissolved material carried
in the bloodstream from one part of the vascular system to impact in a distant part. While the embolus
may comprise air, fat or tumour (including atrial myxoma), it is most commonly thrombus that becomes
Box 12.3 Acute limb ischaemia
•
Pain
•
Pallor
•
Pulselessness
•
Paraesthesia
•
Paralysis
•
Perishingly cold
Aortic valve
https://t.me/medicina_free
disease with
vegetation
Atrial septal
defect with
paradoxical
embolus
from DVT
Mitral valve disease
with vegetation
Arterial disease 113
Atrial fibrillation
or enlarged left
atrium with
thrombus
Aortic aneurysm
Mural infarct
or left ventricular
aneurysm with
thrombus
Figure12.5 Source of
peripheral emboli. DVT, deep
vein thrombosis.
dislodged from its source, usually the heart or major
vessels (Figure12.5).
Emboli tend to lodge at the bifurcation of vessels;
their danger will depend upon the anatomical situation. Blockage of arteries of the central nervous system (CNS), retina and small intestine will produce
dramatic effects. Emboli in the renal arteries will produce haematuria and pain in the loin. Emboli in the
splenic artery will produce pain under the left costal
margin. Large emboli straddling the aortic bifurcation (a saddle embolus) may cause bilateral signs.
Patients with an embolic cause of acute limb
ischaemia will not have a previous history of claudication and are likely to have a normal set of palpable
lower limb pulses on the contralateral leg. They will
possibly have an evident source of the embolus:
•
Atrial fibrillation is by far the most common cause
of arterial emboli. Atrial fibrillation is most commonly due to myocardial ischaemia, but historically was due to rheumatic heart disease.
A mural thrombus, typically forming following a
•
myocardial infarction, may also dislodge and embolize. This typically occurs around 10days after infarct.
•
Aortic dissection is an uncommon differential
diagnosis, when ischaemia may progress down
the body, often with spontaneous recovery corresponding to the intimal flap dissecting away from
the true lumen (Chapter13).
• Paradoxical emboli are also uncommon. In
patients with a patent foramen ovale or other septal defect, a clot originating in the veins may pass
up towards the chest. In addition to impacting in
the pulmonary arterial tree, the clot may pass
across the septal defect and lodge in the arterial
system. This is particularly likely after a pulmonary embolus, as the resultant raised pulmonary
artery pressure results in increased shunting
across a septal defect if present.
An atrial myxoma is rare, but may present with
•
distal embolization of adherent clot or tumour
fragments.
Treatment
Limb ischaemia following an embolic event is usually profound due to the lack of development of
collaterals.
1
Anticoagulation. As soon as the diagnosis is made,
the patient should be systemically heparinized, to
prevent propagation of clot from the site of
blockage.
2 Surgical embolectomy. The approach to the
involved vessel will depend on physical findings
indicating the level of the block. The operative
treatment is relatively simple: the vessel is
exposed, opened and the clot removed. A special
114 Arterial disease
https://t.me/medicina_free
balloon catheter (designed by Thomas Fogarty8
when he was a medical student) is passed into the
vessel with the balloon collapsed. The balloon is
then inflated and pulled back, the clot being
expelled by the balloon via the arteriotomy. Poor
results will be due to propagation of clot beyond
the embolus, particularly down the branches of
the popliteal artery, and a popliteal embolectomy
may also be required. Emboli in the upper limb
vessels usually produce less disability than those
in the lower limb, as a collateral circulation in the
upper limb is better. Surgery is, therefore, indicated less often.
3 Fasciotomy. Patients requiring an emergency
embolectomy commonly also require calf fasciotomy due to the high risk of compartment syndrome following reperfusion.
In situ thrombosis
Patients with in situ thrombosis associated with an
atherosclerotic plaque rupture usually have less profound ischaemia due to the prior development of a
collateral circulation that will still maintain some perfusion to the affected leg. They commonly give a history of claudication, will have atherosclerotic disease
in other arterial beds and will likely have evidence of
arterial disease in the contralateral leg evidenced by
poorly palpable lower limb pulses. Revascularization
in such patients is more complex.
Coronary occlusive
disease
Angina pectoris is the coronary circulation’s equivalent of intermittent claudication, with pain on exertion as oxygen demand exceeds supply, and rest pain
being analogous to unstable angina with resultant
infarction if the coronary circulation is not revascularized by either thrombolysis or bypass surgery.
Mesenteric occlusive
disease
Mesenteric angina occurs when the blood supply to
the gut is impaired and classically is precipitated by
eating. Patients present with central abdominal pain
after meals, a history of marked weight loss and fear of
eating because of pain. Loose motions or blood in the
stool may be present. Typically, two of the three mesenteric vessels (coeliac trunk, superior and inferior
mesenteric arteries) will be chronically diseased
before symptoms of mesenteric ischaemia manifest.
Diagnosis is usually late, and other causes of abdominal pain will need to be excluded.
Acute mesenteric arterial occlusion, usually secondary to embolus, results in bowel infarction
(Chapter29).
Atherosclerotic occlusive
arterial disease
Patients with lower limb arterial disease will commonly have atherosclerotic disease in other arterial
beds. Occlusive disease results in ischaemia of the
end organ or tissue that is supplied, and may manifest
as exercise induced ischaemia progressing to rest
pain, or acute ischaemia due to embolism or in situ
thrombosis.
8
omas Fogarty (b. 1934), medical student, Cincinnati,
later surgeon, Stanford University Medical Center,
California, and winery owner.
Carotid artery disease
(Figure12.6)
In the cerebral circulation, the most common symptoms are of transient ischaemic attack (TIA) or stroke.
Atheroma usually affects the bifurcation of the carotid
artery extending into the internal and external carotid
arteries. Atheromatous plaques may ulcerate and
thrombus forms on their surface. If this thrombus
breaks off, it forms an embolus comprising platelet
clumps or atheromatous debris. This may impact in
the ipsilateral retinal artery, producing ipsilateral
blindness, or the cerebral arteries of the ipsilateral
hemisphere, producing contralateral paralysis. This is
a medical emergency as patients with a significant
stroke may benefit from early thrombolysis to improve
cerebral perfusion.
Соседние файлы в папке Библиотека им академика М.И. Перельмана