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The skin andits adnexae 95
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areas, hence the higher incidence on the legs of
females. They are rarely found in the pigmented skin
Caucasians, tending to be found in the non-
of nonpigmented skin on the sole of the foot or, less commonly, the palm (acral lentiginous melanoma). A
premalignant form, lentigo maligna, also exists.
Presentations
The two main presentations of malignant melanoma
are the superficial spreading type and the nodular
type.
Superficial spreading melanoma. The most com-
•
mon presentation of malignant melanoma is of a
previously dormant naevus starting to spread
superficially. The surface has patches of deep
pigmentation.
Nodular melanoma. The naevus is nodular and
•
deeply pigmented and may bleed or ulcerate.
Such a nodule may occur on a pigmented
background such as the lentigo maligna (see
below). It tends to invade deeply rather than
spread superficially and carries a poorer prognosis with earlier lymphatic involvement.
In addition to the common types of malignant melanoma above, less common forms include the
following:
Lentigo maligna. This is a brown pigmented patch
•
with an irregular outline and is usually found on
the cheeks of elderly patients, often called a
Hutchinson’s freckle.
over several years; malignant change is indicated
by darker, irregular pigmentation or nodule formation. Lentigo maligna has a small lifetime risk
of malignant transformation into a melanoma, so
complete excision should be considered.
Acral melanoma. These are so called because they
•
occur at the extremities, commonly on the palms
and soles of the feet. It is this type that also occurs
in dark- skinned races (Fitzpatrick skin types V and
VI). Subungual melanoma is a variant of acral
melanoma (see earlier in this chapter).
•
Mucosal melanoma. Malignant melanoma may be
found on the mucous membranes of the nose,
mouth, anus and intestine.
8
Sir Jonathan Hutchinson (1828–1913), Surgeon, e
London Hospital, London, UK. Described numerous
conditions and was the rst to perform a successful
operation for reduction of intussusception in a child.
8
The pale patch appears
• Choroidal melanoma. Melanomas may arise from
melanocytes in the pigment layer of the retina.
These are renowned for presenting many years
after enucleation with hepatic metastases; hence,
the aphorism ‘beware the patient with the large
liver and the glass eye’.
•
Amelanotic melanoma. Paradoxically, melanomas
are not always pigmented, but they remain dihydroxyphenylalanine (DOPA)-
positive.
Signs ofmalignant change
inapigmented lesion– ABCDE
• Asymmetry.
• Border is irregular.
• Colour– two or more colours of pigment.
• Diameter– >6mm.
•
Evolution– change in size, shape, colour, develop-
ment of a nodule.
Spread of pigment from the edge of the naevus.
•
• Itching or pain.
• Satellite pigmented nodules (late change).
•
Palpable regional lymph nodes or evidence of dis-
tant spread (often due to delayed presentation).
Pathology
Microscopically, pleomorphic cells are seen. These
spread through the layers of the epidermis and are
usually pigmented (occasionally the cells are
amelanotic).
Spread
As well as local growth and ulceration, malignant melanoma can spread by local and regional lymphatics,
which can produce cutaneous satellite or
in- transit
metastases by progressive proximal spread, and by
lymphatic transit to regional lymph nodes. There is
also a much smaller risk of haematogenous spread to
distant organs, for example, brain, lungs and liver.
Staging
The prognosis of malignant melanoma depends upon
its depth of invasion, according to its measured depth
(Breslow depth
management of melanoma are informed by the
tumour stage (Table 11.2) and national treatment
guidelines.
9
Alexander Breslow (1928–1980), Pathologist, George
Washington University Hospital, Washington, DC, USA.
9
). Multidisciplinary discussion and
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Table11.2 Ten- year survival according to
Breslow depth
year
10Tumour
thickness
(mm)
<0.8 No T1a 1A 98%
<0.8 Yes T1b 1A 96%
0.8–1.0 Either T1b 1A
>1.0–2.0 No T2a 1B 92%
>1.0–2.0 Yes T2b 2A 88%
>2.0–4.0 No T3a 2A
>2.0–4.0 Yes T3b 2B 81%
>4.0 No T4a 2B 83%
>4.0 Yes T4b 2C 75%
American Joint Committee on Cancer staging system (2017)
and melanoma specific survival for stage 1 and 2 melanomas
(i.e. those without nodal spread)
Ulcerated
or not T Stage
melanoma
specic
survival
Treatment ofpigmented lesions
The following is a general guide to the management of
pigmented lesions of the skin.
Prophylactic/diagnostic excision biopsy
Any pigmented tumour on the hand, sole or genitalia, or
any that, in other situations, are subjected to trauma
should be considered for excision; these are the most
common among the small percentage of naevi to
undergo malignant change. Such lesions are sent for
histological examination and should always be removed
in their entirety with a 2mm measured margin.
Suspicious naevi
If the pigmented lesion shows any of the features
already listed that suggest that malignant change has
taken place, the naevus is first removed for urgent histological examination. If malignant melanoma is confirmed, a wide local excision of the area is then
performed, with a margin of clearance (1–2 cm), as
recommended at the multidisciplinary team discussion of the melanoma’s pathology.
Wide local excision andsentinel lymph node
biopsy formalignant melanoma
Wide local excision of the scar at the site of the primary melanoma can often be undertaken under local
anaesthetic and is the minimum treatment recommended to minimize risk of local recurrence.
Wide local excision is usually undertaken in conjunction with sentinel lymph node biopsy for stage
IB or greater stage, under a general anaesthetic.
Sentinel lymph node biopsy offers additional prognostic information and informs further followand management.
The primary lymphatic drainage of the tumour,
known as the sentinel node, is identified and excised
for histological examination. Identification of the sentinel node is by injection of patent blue dye around the
scar at the site of initial excision biopsy of the primary
melanoma, combined with preoperative lymphoscintigraphy to map the lymphatic drainage. If the sentinel
node is involved, this upstages the melanoma (see
American Joint Committee on Cancer, AJCC, Staging
Classification, Table11.2) and will inform the follow up regimen and need for referral to the melanoma
oncology team for consideration for adjuvant therapy.
Adjuvant therapy
Specific targeted and immunotherapy regimens are
now available for stage 3 and stage 4 melanoma, with
significant improvements in longthese patient groups. Their use is directed by melanoma oncologists as core members of the melanoma
multidisciplinary team.
term outcomes for
up
Prognosis
Prognosis depends on a large number of factors:
Breslow depth of the primary lesion, measured
•
vertically from the top of the granular layer to the
deepest point of tumour invasion. This is the most
important prognostic factor. Prognosis is good
when this depth is less than 1.0 mm. The deeper
the lesion, the greater the risk of lymph node
metastasis and the worse the 10(Table11.2).
• Ulceration of the lesion carries a poorer
prognosis.
• Type of lesion. A superficial spreading melanoma
has a better prognosis than a penetrating and
ulcerating lesion.
• The anatomical site. Tumours on the trunk and
scalp have a poorer prognosis.
• Lymph node metastases. They indicate poor prog-
nosis, more so if there are cutaneous deposits. The
presence of sentinel node involvement, or satellite
lesions, reduces 5- year survival to under 30%.
year survival
Tumours ofsweat glands
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andsebaceous glands
Benign and malignant tumours of these glandular
adnexae of the skin are rare.
The skin andits adnexae 97
Campbell de Morgan spots
Campbell de Morgan spots10 are generally found on
the trunk of middleare bright red aggregates of dilated capillaries, which
can be emptied by pressing on them with the tip of a
pencil. They are of no significance
aged and elderly subjects. They
Sebaceous adenoma
These are more in the nature of a hyperplasia of the
glands than true tumours. They occur as pink or
yellow papules on the nose, cheek and forehead.
Microscopically, they are merely overgrowths of sebaceous glands.
Adnexal- derived skin
cancers
Sebaceous carcinoma
Found rarely on the face and scalp in elderly subjects,
this is an uncommon but aggressive cancer, arising
from the epithelium of the sebaceous gland. They
may have a clinical appearance similar to a basal cell
carcinoma.
Other rare adnexalinclude trichilemmal carcinoma, porocarcinoma,
eccrine carcinoma and apocrine carcinoma
derived skin malignancies
Vascular anomalies
Tumours of blood vessels usually lie in the dermis,
although the underlying muscles and soft tissues may
be involved. The abdominal viscera, central nervous
system and bone may also be the sites of these lesions.
Vascular anomalies can be classified into tumours
and malformations.
Vascular tumours
Vascular tumours are characterized by endothelial
cell hyperproliferation. They tend to be rapid growing. Most are not present at birth.
Spider naevus
Spider naevus is another example of a capillary haemangioma. Isolated ‘spiders’ are present in normal
people, but they are more common during pregnancy
and in chronic liver disease. They comprise a central
arteriole from which capillaries radiate. Pressure on
the central arteriole with a pinhead causes the lesion
to disappear while pressure is maintained.
Infantile haemangioma
(strawberry naevus)
This is the most common benign tumour in children,
appearing in the first weeks of life, usually on the head
and neck, and affecting girls more commonly than
boys. Preterm infants appear more susceptible, as do
those where the mother suffered pre- eclampsia.
Most strawberry naevi increase in size over a period
of 3months, and then slowly regress over a period of
years before disappearing spontaneously.
Cavernous haemangioma
These are made up of large blood spaces lined with
endothelium. They occur on the skin and lip and,
quite commonly, as multiple nodules in the liver.
They are usually present at birth and grow to keep
pace with normal body growth.
The lesions are blue, may be raised and may partly
empty on pressure. They may infiltrate the underlying
tissues and may be associated with unsightly overlying cutaneous thickening.
Treatment
This is often difficult. The condition may be disguised by the use of cosmetics, or thrombosis can be
encouraged by injection of sclerosing agents. Very
10
Campbell de Morgan (1811–1876), Surgeon, Middlesex
Hospital, London, UK.
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unsightly small lesions may be excised, and skin
grafted if required.
Glomus tumour
Glomus bodies are found in the subcutaneous tissues
of the limbs, particularly the fingers, toes and their
nail beds. They are convoluted arteriovenous anastomoses with a cellular wall comprising a thick layer of
cuboidal ‘glomus’ cells, which are modified plain
muscles; between these cells are abundant nerve
fibres. These structures are perhaps concerned with
cutaneous heat regulation. Glomus tumours are blue
or reddish, small, raised lesions, which occur in young
adults at the common sites of glomus bodies. Their
characteristic is exquisite tenderness, which makes
the slightest touch agonizing.
Treatment
Treatment is by excision of the lesion and subsequent
histological confirmation of the diagnosis.
Kaposi’s sarcoma
This tumour has a multicentric origin. It used to be
most common in the elderly in central Europe, particularly Ashkenazi Jews;
tumour in patients with acquired immune deficiency
syndrome (AIDS) and also occurs in immunosuppressed organ transplant recipients. DNA extracted
from Kaposi’s sarcoma
tain human herpes virus type 8 (HHV8), now known
as Kaposi sarcoma herpes virus (KSHV), indicating a
significant aetiological role for this virus. It presents as
a number of bluish red or dark blue nodules scattered
over the extremities of one or more of the limbs. The
nodules spread centrally along the limb, may ulcerate
and can metastasize to the liver and lungs. In the
aggressive form, which occurs in the immunosuppressed, visceral involvement occurs with bowel perforation, haemorrhage or intussusception.
Histologically, there are two components: blood
vessels and fibroblasts. The latter show the malignant
features, thus distinguishing this tumour from a
haemangiosarcoma.
11
Ashkenazi Jews: contrast Sephardic and Oriental Jews.
Migrated to Germany, Poland and Russia.
12
Moriz Kaposi (1837–1902), Professor of Dermatology,
Vienna, Austria.
11
now, it is a more common
12
tissue has been found to con-
Treatment involves control of HIV infection with
highly active antiretroviral treatment (HAART) or
reduction of immunosuppression in transplant recipients, together with local radiotherapy or cytotoxic
drugs.
Telangiectasia
Telangiectases, although not truly tumours, are
conveniently mentioned in this section. They are dilations of normal capillaries and are seen in a number
of circumstances, such as on the weatherfaces and legs of some people, who may complain of
their cosmetic appearance.
Hereditary haemorrhagic telangiectasia (HHT;
Osler–Weber–Rendu syndrome
autosomal dominant disease characterized by tiny
capillary angiomas of the skin, lips and mucous membranes; they may give rise to repeated nosebleeds and
gastrointestinal haemorrhage. The genetic abnormality is a mutation of either endoglin (HHT type 1) or
activin receptorOccult arteriovenous malformations are common,
such as within the liver and spleen.
like kinase (HHT type 2) genes.
13
) is an inherited
beaten
Vascular malformations
A variety of types of congenital capillary malformation may be found in the skin, usually at birth:
Salmon pink patch is a common blemish on the
•
head or neck of a newborn child and rapidly disappears spontaneously.
Port- wine stain, flush with the skin, usually on the
•
face, lips and buccal mucosa, produces an extensive area of dark red, blue or purple discolouration. It is present from birth and shows no
tendency to regress with age. Port- wine stains may
respond to cutaneous laser therapy, but the simplest treatment remains camouflage with
cosmetics.
Note that portsegmental distribution corresponding to the cutaneous branches of the trigeminal nerve and may be
13
Sir William Osler (1849–1919), Professor of Medicine,
successively at McGill University, Montreal, Canada; Johns
Hopkins University, Baltimore, MD, USA; and the University
of Oxford, Oxford, UK. Frederick Parkes Weber (1863–1962),
Physician, London, UK. Henri Rendu (1844–1902),
Physician, Hôpital Necker, Paris, France.
wine stains of the face may have a
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associated with angiomas of the cerebral piaarachnoid, which may manifest themselves by focal
epileptic attacks (the Sturge–Weber syndrome
14
).
Lymph vessel tumours
Lymphangiomas are congenital in origin and similar
to haemangiomas; they are lined by endothelium but
contain lymph. They are relatively uncommon, but
occur mainly on the lips, tongue and cheek, resulting
in macrocheilia or macroglossia.
Cystic hygroma
A form of lymphangioma, the aetiology of cystic
hygromas is thought to be a combination of a failure
of lymphatics to connect to the venous system, abnormal growth of embryonal lymphatics and sequestered lymphatic channels. Most occur in the neck,
usually the left side, and are thought to be related to
the embryonic precursor of the jugular part of the
thoracic duct. They consist of a multilocular cystic
mass, which is often present at birth or noticed in
early infancy. Characteristically, they are supremely
transilluminable. They may respond to injection of
sclerosant agents such as alcohol or doxycycline.
Surgical treatment consists of excision, but this is a
difficult procedure as the cysts ramify throughout the
structures of the neck.
(the vestibular schwannoma or acoustic neuroma;
Chapter 16). Tumours may arise within the spinal
canal, particularly from the dorsal nerve roots, resulting in an extramedullary, intrathecal, slow-
growing
spinal tumour (Chapter18). Part of this tumour may
protrude through the intervertebral foramen, producing a dumb-
bell tumour, which projects into either the
thoracic cavity or the abdominal cavity.
In the skin and subcutaneous tissues, there is a wide
range of presentations, from a solitary tumour arising
from a peripheral nerve to large tumour numbers
involving the whole of the body (von Recklinghausen’s
16
disease;
his name is also applied to the osteitis
fibrosa cystica of hyperparathyroidism– Chapter40).
Clinical features
The tumours may appear in childhood, and there is
often a family history. Three types of neurofibromatosis are recognized, and all are autosomal dominant.
Von Recklinghausen’s disease is type 1neurofibroma-
17
tosis
and results from a mutation in the
neurofibromin gene. The cutaneous lesions are soft
and often pedunculated. They are usually painless,
although pressure may produce pain along the line of
the nerve, particularly when larger nerve trunks are
involved. The tumour is mobile from side to side but
not longitudinally, in the line of the nerve to which it
is attached. There may be associated cafépatches of pigmentation. In some cases, there are
disfiguring masses of neurofibromatous tissue over
which the thickened skin hangs in ugly folds.
au- lait
Nerve tumours
Tumours of the peripheral nerves arise from the neurilemmal sheath of Schwann,
lemmoma, neurofibroma or schwannoma. They push
the fibres of the nerve to one side or actually grow
within the substance of the nerve. The tumours may
be solitary or multiple and may involve any peripheral
nerve in the body. Of the cranial nerves, the eighth is
most commonly involved, often as a solitary tumour
14
William Allen Sturge (1850–1919), Physician, Royal Free
Hospital, London, UK, and Frederick Parkes Weber (1863–
1962), Dermatologist, Mount Vernon Hospital, London, UK,
with a lifelong interest in rare diseases.
15
eodor Schwann (1810–1882), Professor of Anatomy,
Louvain and then Liège, Belgium.
15
hence the terms neuri-
Treatment
Where the neurofibromas are solitary or few in number, removal can be performed, either by enucleation,
if the nerve fibres are pushed to one side, or by resection with suture of the divided nerve. Incomplete
removal must not be performed, as sarcomatous
change may follow. Where the whole body is covered
16
Friederich Daniel von Recklinghausen (1833–1910),
Professor of Pathology, successively at Königsberg,
Germany; Würzburg, Germany; and Strasbourg, France.
17
Type II neurobromatosis (mutation in neurobromin
2 gene) is characterised by eighth nerve tumours,
meningiomas and schwannomas of the dorsal roots of the
spinal cord; type III neurobromatosis has features of both
type I and type II, with café- au- lait spots, cutaneous lesions
and intracranial neurobromas and meningiomas.
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by these lesions, some cosmetic improvement can be
affected by excising the more noticeable lesions from
the face and hands.
Neurofibrosarcomas are uncommon. They may
arise de novo or as malignant change in a neurofibroma. Clinical features are pain, rapid growth, and
peripheral anaesthesia or paralysis. Treatment is by
wide excision.
Fatty tumours
Lipoma
Lipomas are the most common benign tumours. They
usually occur in adults, and the sex distribution is
equal. Lipomas may arise in any connective tissue but
especially in the subcutaneous fat, particularly
around the shoulder and over the trunk. They do not
occur in the palm, sole of the foot or scalp, because in
these areas the fat is contained within dense fibrous
septa. Occasionally, lipomas appear in large numbers
subcutaneously and are tender (adiposis dolorosa or
Dercum’s disease,
with obesity), and it is sometimes quite difficult to differentiate them from neurofibromas. Elsewhere, it is
useful to remember that ‘lipomas occur beneath everything’; thus, in addition to being subcutaneous,
they may be subfascial, subperiosteal, subperitoneal,
submucosal or subpleural.
18
Francis Xavier Dercum (1856–1931), Professor of Clinical
Neurology, Jeerson Medical College, Philadelphia, PA,
USA.
18
a familial condition associated
Where diagnostic doubt exists, ultrasound may
confirm the diagnosis and it may be further characterized by an MRI scan. Any rapidly growing, painful soft tissue tumour raises the concern of a soft
tissue sarcoma and warrants urgent referral for multidisciplinary clinical and radiological assessment
to exclude sarcoma.
Treatment
Treatment consists of excision if the lipoma is symptomatic or diagnostic doubt exists. If there is clinical
concern regarding a soft tissue sarcoma, rapid referral
to a specialist sarcoma centre is mandated.
Liposarcoma
A rare tumour, which probably arises as an unusual
event in a pre- existing benign lipoma. The retroperitoneal site is most common, but it also commonly
occurs around the thigh and should be suspected if
the tumour is very large, firmer than usual, vascular
or rapidly growing.
Additional resources
Case 10: Lumps on the scalp
Case 11: A lump on the wrist
Case 12: Recurrent abscesses over the sacrum
Case 13: A septic great toe
Case 14: A skin tumour
Case 15: Two men with facial ulceration
Case 16: A pigmented spot on the face
Case 17: A pigmented skin lesion that has got bigger
Case 18: A lump on the chest wall
Arterial disease
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Patrick Coughlin
Learning objectives
✓ To know the types of arterial trauma and their management.
✓ To know the causes of arterial aneurysms, their manifestation and
treatment.
✓ To have knowledge of occlusive arterial disease (including
thromboembolic disease), its risk factors, manifestations and treatment
options.
Arterial trauma
Traumatic arterial injuries are due to either closed
(blunt) trauma or open (penetrating) trauma.
Closed injuries
The artery is injured by extraneous compression such
as a crush injury, fractures of adjacent bones with displacement of the artery (e.g. supracondylar fracture of
the humerus in children) or joint dislocation.
Penetrating injuries
Penetrating arterial injuries may result from gunshot
wounds, stabbing, penetration by bone spicules in
fractures or iatrogenic injury.
Types ofarterial injury
• Mural contusion with secondary spasm.
• Intimal tear. This injury is usually a result of distraction, in which the artery is stretched and the
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
Full- thickness tear. All layers of the artery are
•
Consequences ofinjury
• Haemorrhage. This may be concealed or overt.
• Thrombosis. Immediate or delayed.
• Arteriovenous fistula formation.
• False (pseudo- ) aneurysm formation (see later in
• Arterial dissection.
• Compartment syndrome. Ischaemic muscle swells,
1
Richard von Volkmann (1830–1889), Professor of Surgery,
Halle, Germany.
12
intimal layer tears, while the surrounding adventitia remains intact. The intima then buckles and
causes a localized stenosis, which may or may not
result in thrombosis or dissection.
divided, and this may be partial or complete. Partial
tears bleed copiously, while complete division of
the artery often results in contraction and spasm of
the divided vessel with surprisingly little blood loss.
this chapter).
and if the muscle is contained by a fibrous fascial
compartment, such as in the forearm or in the
lower leg, the swelling further exacerbates the
ischaemia as the compartment pressure increases.
Volkmann’s
is a result of compartment syndrome.
1
ischaemic contracture (Chapter19)
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Clinical features
The features of arterial injury may be those of acute
ischaemia, haemorrhage or often both. Acute ischaemia is characterized by:
•
pain (in the limb supplied, starting distally and
progressing proximally);
pallor;
•
•
pulselessness;
•
paraesthesia;
•
paralysis;
• coldness.
Haemorrhage may be overt (bright red blood) or concealed (e.g. closed limb fractures). Symptoms are
those of rapidly developing hypovolaemic shock
(cold, clamminess, tachycardia, hypotension, loss of
consciousness, oliguria progressing to anuria).
Treatment
Closed injuries
• Treat causative factors. If the cause of ischaemia is
a tight plaster cast, remove or split the cast. If it is
due to a supracondylar humeral fracture, the
peripheral pulses should return when the fracture
is reduced; if the radial pulse does not return rapidly, surgical exploration is indicated.
•
Angiography. A computed tomography (CT) angio-
gram will reveal whether ischaemia is due to spasm,
intimal tear or arterial disruption. Intraangiography may need to be performed in a radiology suite or intraoperatively. Partial tears in large
vessels may be amenable to intravascular stenting.
• Operative exploration. If a limb fails to reperfuse
after a fracture or dislocation is reduced, and angiography is unhelpful or shows a tear or block,
exploration is mandatory. Either the affected vessel is repaired directly, or a segment of saphenous
vein is interposed to replace the damaged area.
• Fasciotomy. Muscle ischaemia leads to swelling
and compartment syndrome. The fascial compartments should be opened by splitting the deep
fascia widely to relieve compartment pressure.
arterial
ischaemic; therefore, prompt management is
needed to deal with the arterial injury.
Resuscitation. Replace blood loss.
•
•
Exploration. Small vessels that are part of a large
collateral supply may be sacrificed and ligated
above the site of injury. Partial tears may be
directly sutured or closed with a vein patch; complete division often requires interposition of
reversed saphenous vein. The use of prosthetic
material after trauma is avoided if possible, owing
to the risk of contamination and graft infection.
Aneurysm
An aneurysm is an abnormal permanent dilation of
an artery or part of an artery, or the wall of the heart.
An arterial aneurysm is defined as having a diameter
1.5 times that of the normal arterial diameter. A true
aneurysm is an aneurysm that incorporates all three
layers of the arterial wall (intima, media and adventitia), whereas a false aneurysm (or pseudoaneurysm)
is bounded only by the adventitial layer of the arterial
wall and the surrounding tissue. False aneurysms are
commonly caused by trauma, including iatrogenic
trauma, and infection.
Aneurysm types (Figure12.1)
Saccular aneurysms
A saccular aneurysm is a focal bulge of one side of the
artery joined to the main arterial lumen by a narrow
neck. Mycotic aneurysms are often of this sort, in
which infection causes a local weakness of the wall,
resulting in aneurysmal dilation. Saccular aneurysms
may also develop from penetrating aortic ulcers,
which are areas of irregularity of the aortic wall
caused by plaque formation in atherosclerosis.
Fusiform aneurysm
A fusiform aneurysm is a more generalized dilation of
the artery. This is the most common type of aneurysm
to affect the abdominal aorta.
Open injuries
• Direct compression. Primary measures to staunch
haemorrhage should include direct pressure. The
use of a proximal tourniquet, properly applied,
can limit blood loss but will render the limb
False (pseudo- ) aneurysm
Blood leaks out of an artery and is contained by the
adventitia and surrounding connective tissue lined
with thrombus. The resultant blood collection communicates with the artery so it is pulsatile and
(a) True
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Arterial disease 103
Saccular Fusiform
(b) False
expansile. It will either thrombose spontaneously or
enlarge and rupture.
(c) Dissecting
Aneurysm complicating arterial
dissection
A dissection occurs where blood forces a passage
through a break in the intima of a vessel, creating a
separate ‘false’ channel between the layers of the
arterial wall. This false channel creates a weakness in
the arterial wall, which may predispose to rupture in
the acute period or aneurysm formation more
chronically.
Aetiology
Degenerative
Atheromatous degeneration of the vessel wall is the
most common cause of a true aneurysm and is predominantly seen in older men with a smoking history.
Traumatic
Penetration or weakening of the arterial wall by a
penetrating wound such as a bullet or knife, or iatrogenic injury during catheterization for angiography
and angioplasty, may cause a pseudoaneurysm. If
there has been concomitant injury of a neighbouring
vein, this may lead to an arteriovenous fistula.
Inammatory
Inflammatory aneurysms commonly affect the
abdominal aorta and differ from the more common
atherosclerotic aneurysms, in that there is an immune
Figure12.1 (a–c) Types of aneurysms.
response to components in the aortic wall, resulting
in a dense inflammatory response. Evidence suggests
this inflammation may be mediated through an IgG4
pathway. Patients are typically younger than those
with atherosclerotic aneurysms and tend to be symptomatic with back or abdominal pain. Investigation
reveals a raised erythrocyte sedimentation rate (ESR)
reactive protein (CRP). Imaging usually reveals
and Ca rind of inflammatory tissue surrounding the aortic
wall, which characteristically extends laterally into
the retroperitoneum as retroperitoneal fibrosis when
it may encase the ureters, causing bilateral hydronephrosis. The inflammatory component may subside
with corticosteroid or other immunosuppressive
treatment.
Mycotic
Mycotic aneurysms were historically seen in the thoracic aorta of patients with tertiary syphilis. They are
now equally seen involving the abdominal aorta, typically as a consequence of salmonellosis, direct seeding from discitis or originating from infective
endocarditis. Patients with immunodeficiency,
whether resulting from immunosuppression for
organ transplantation, chemotherapy or human
immunodeficiency virus (HIV) infection, are prone to
mycotic aneurysms from unusual bacteria and fungi.
Aortopathies
Aortopathies are a group of genetic conditions that
are characterized by aneurysmal disease of the
aorta. Such diseases can be syndromic, familial or
sporadic, with common disorders being Marfan
104 Arterial disease
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syndrome2, Loeys- Dietz syndrome3 and EhlersDanlos syndrome (vascular type, formerly called
4
type 4)
. Such patients commonly develop arterial
complications at a young age.
Clinical features oftrue aneurysms
The clinical features of an aneurysm depend on its
location. It may present with symptoms due to local
complications of the aneurysm or due to a more distal
complication whose source is the aneurysm.
Rupture. The likelihood of rupture increases as the
•
diameter of the artery increases relative to its normal size.
Thrombosis. Thrombus naturally lines the wall of
the aneurysm. This may progress to cause complete occlusion of the artery with resultant distal
ischaemia.
• Embolism. Lining thrombus may detach and
embolize to distal circulation, either as small
emboli, resulting in digital ischaemia, or as a large
mass of thrombus threatening the entire limb.
• Pressure. Adjacent structures may be eroded or
displaced. Hence, backache and sciatica are common in patients with large abdominal aortic aneurysms, and occlusion of the femoral vein is
common with large femoral aneurysms.
Fistula. An aneurysm may rupture into an adja-
•
cent vessel or viscus, causing a fistula, such as an
aorto-
caval fistula.
When examining an artery, an aneurysm will be felt
as a dilation along the course of the artery. The aneurysm itself is both pulsatile and expansile. In smaller
peripheral aneurysms, direct compression may
empty the aneurysm sac or diminish its size, and
pressure on the artery proximal to the aneurysm may
reduce its pulsation. If the feeding vessel has a narrow
2
Antoine Marfan (1858–1942), Agrégé of Paediatrics,
University of Paris. Marfan syndrome is due to mutation in
the brillin- 1 gene
3
Bart L Loeys (contemporary), Professor of Cardiogenomics,
University of Antwerp, was a student of Harry (Hal) DietzIII
(b1958), Professor of Genetic Medicine, Johns Hopkins
University, Baltimore, MD, USA, when a mutation in the
TGFBR2 gene was identied as the cause of this Marfan- like
syndrome.
4
Edvard Ehlers (1863–1937), Dermatologist, Frederiks
Hospital, Copenhagen. Henri- Alexandre Danlos (1844–
1912), Dermatologist and chef de service, Hôpital Tenon,
Paris. e cause of the vascular type is a mutation in the
COL3A1 gene coding for type III collagen.
orifice, there may be a thrill and bruit, and if there
is an arteriovenous communication, a machinery
murmur is audible.
Aneurysms are most commonly an incidental finding in a patient undergoing imaging for something
else or as a result of an aortic aneurysm screening
protocol.
Special investigations
• Abdominal X- ray. This may show calcification in
the wall of the aneurysm.
Computed tomography (CT), magnetic resonance
•
(MR) and ultrasound scanning may delineate the
size and extent of an aneurysm, and its relationship to other structures, for example, the mesenteric and renal vessels in an abdominal aortic
aneurysm. A CT scan will confirm if the aneurysm
has ruptured.
Treatment
The treatment of an arterial aneurysm depends on its
nature (true or false), location, size and symptoms. In
asymptomatic patients with nonintervention is dictated by the size of the aneurysm
since the risk of rupture increases with increasing size.
Since elective aneurysm repair is done prophylactically to prevent rupture, the patient’s concurrent
health and the ease of treatment of the aneurysm need
to be balanced against the benefit of the intervention.
False aneurysms and mycotic aneurysms are more
prone to rupture and require more urgent attention
often irrespective of size.
mycotic aneurysms,
Abdominal aortic
aneurysm
Aneurysmal dilation of the abdominal aorta is a common finding in older men with a significant smoking
history and in those with a positive family history.
Around 10% will have a coincidental popliteal aneurysm. The speed at which an aneurysm grows is
dependent on the size of the aorta, with a smaller
aneurysm having a slower growth rate; on average, an
aneurysm grows at 2 to 3 mm per year, size being
measured in terms of the maximum antero- posterior
diameter. The larger an aneurysm gets, the more
likely it is to rupture.
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