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The chest andlungs 135
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Clinical features
There is usually a history of the underlying cause. The
patient is febrile, toxic and may be anaemic. There are
signs of fluid in the chest on the affected side. In
chronic cases, finger clubbing may be present.
Special investigations
• Full blood count will reveal a leucocytosis.
Inflammatory markers are elevated.
Chest X- ray demonstrates an effusion, and there
•
may be evidence of the underlying lung disease.
CT scan will demonstrate the anatomy and magni-
•
tude of the problem.
•
Bronchoscopy is useful in determining the primary
pathology.
Aspiration of the chest confirms the diagnosis and
•
identifies the responsible bacteria. The infecting
organisms are usually Pneumococcus, Streptococcus
or Staphylococcus.
Treatment
An acute empyema may respond to drainage together
with antibiotic therapy, based on the sensitivity of the
responsible organism. Simple drainage with an adequately sized chest drain (ideally 28F or larger) may
suffice. If this fails, intrapleural fibrinolytic therapy
can be considered. If this fails, surgery should be considered. This is usually by VATS, but sometimes thoracotomy is needed.
After a few weeks, the cavity becomes thick walled
and open removal (decortication) is required. The
aim is to restore normal lung function.
Lung tumours
Classication
Benign
• Adenoma.
• Hamartoma.
• Haemangioma (rare).
Malignant
1 Primary:
a small- cell lung cancer (SCLC);
b non- small- cell lung cancer (NSCLC) includes
the histological subdivisions of:
squamous cell carcinoma;
•
•
adenocarcinoma;
large- cell carcinoma.
•
c
neuroendocrine (carcinoid) tumours.
2
Secondary:
carcinoma (especially breast, kidney);
a
b
sarcoma (especially bone);
melanoma.
c
Carcinoid tumours
These are a form of neuroendocrine carcinoma of
which there are four types, all of which share the same
neural crest origin:
typical carcinoid;
•
atypical carcinoid;
•
• large- cell neuroendocrine carcinoma;
•
small- cell carcinoma.
Each has particular histological features along a spectrum from benign to malignant.
Typical carcinoid tumours
Nine out of 10 carcinoid tumours are ‘typical carcinoids’, and tend to follow a very benign course with
metastases being rare and most other problems
being due to local effects. Carcinoids presenting in
central airways typically present with cough and
dyspnoea, but rarely haemoptysis. Sometimes, it is
thought to be latemon condition. Any late ‘asthma’ that has no
response to bronchodilators should be investigated.
If the airway becomes obstructed, secretions can
collect distally. These can then become infected
and cause pneumonia.
Investigations
• Chest X- ray is often normal.
•
CT scan usually reveals a mass, and evidence of
spread (enlarged lymph nodes, distal metastases).
• Biopsy, either at bronchoscopy if a large central
airway, or CT guided if peripheral.
• CT- positron emission tomography (CT- PET) scan
and brain imaging if curative resection is planned,
to exclude metastases.
onset asthma, which is a com-
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Treatment
A patient who has presented with distal infection due
to a proximal obstruction can have the lesion bronchoscopically debrided. The aim of this is to open the
airway, relieve obstruction and reduce sepsis prior to
definitive resection. Bronchoscopy can be repeated if
the patient is too frail to undergo surgery.
Surgery consists of local removal, ensuring complete clearance. In central airways, it can almost
always be done by lung- preserving techniques such
as sleeve resection. Only occasionally is lung resection, such as lobectomy, required.
Lung cancer
This is the second most common cancer affecting
men (after prostate) and in women is second only to
breast cancer. In the period 2016–2018, there were
49,000new cases per annum, with 35,000 deaths; the
predicted long- term (10- year) survival for patients
diagnosed in 2018 in England is just 10%. This is
improving due to more cases being treated as a consequence of increased awareness and earlier presentation. When lung cancer is diagnosed early, survival
is considerably improved with surgical resection.
The incidence of lung cancer in men has been falling since the late 1970s, reflecting a reduction in
smoking. This fall is yet to be seen in women, although
the rate of increase is slowing. Nine out of 10 cases
occur in people 60 years and older.
Aetiology
In the UK, the main aetiological factor is smoking.
Passive smoking; air pollution with diesel, petrol and
other volatile hydrocarbon fumes; asbestos exposure;
and exposure to radioactive gases such as radon in
uranium mines are also predisposing factors. The
incidence is higher in urban than in rural populations. There is also a familial element to lung cancer,
with a 50% increase in risk if a first- degree relative has
it. Although this could be due to similar environmental risks such as smoking, there are also genetic factors. Particular genotypes are associated with worse
outcomes and also greater or lesser response to
molecular therapy.
Carcinoma of the lung has a poor prognosis, and
the gravity of this condition should be impressed on
all patients who are smokers. The decision whether or
not to continue smoking depends on the patient, but
there is no doubt that the advice should be to stop
smoking. There is an increased incidence of lung cancer even in patients who smoke only a few cigarettes a
day, and this danger is greatly increased in patients
smoking more than 20 cigarettes a day for a number
of years.
Pathology
There are two main types of lung cancer, small-cell
and non-small-cell lung cancer.
Macroscopic appearance
About half the tumours arise in the main bronchi
(particularly squamous carcinoma), and 75% are visible at bronchoscopy. The growth may arise peripherally (particularly adenocarcinoma), and some appear
to be multifocal.
The bronchial wall is narrowed and ulcerated.
Surrounding lung tissue is invaded by a pale mass of
tumour, which may undergo necrosis, haemorrhage
or abscess formation. The lung segments distal to
the occlusion may show collapse, bronchiectasis or
abscess formation.
Microscopic appearance
1 SCLC (15%) (in the past called ‘oat’ cell). The
tumour comprises small cells with little cytoplasm. It has neuroendocrine properties and can
produce molecules giving rise to paraneoplastic
syndromes. It has a poor prognosis, has generally
spread by the time of diagnosis, and is best treated
by chemotherapy and sometimes radiotherapy.
It behaves very differently to typical carcinoid
tumours.
NSCLC (85%).
2
a Squamous cell carcinoma. Usually occurring in
the main bronchi, it is mostly poorly differentiated and arises in an area of squamous metaplasia of bronchial epithelium.
b Adenocarcinoma. This has glandular features
and can be multifocal. It is the most common
NSCLC.
c Large- cell carcinoma. Large cells containing
abundant cytoplasm and without evidence of
squamous or glandular differentiation; this is
also a rapidly growing cancer.
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Spread
• Local: to pleura, left recurrent laryngeal nerve
(hoarse voice), phrenic nerve, pericardium,
oesophagus (bronchopathetic chain (Horner’s syndrome
plexus (Pancoast’s tumour
Lymphatic: to mediastinal and cervical nodes.
•
oesophageal fistula), sym-
1
2
at lung apex).
) and brachial
Compression of the superior vena cava by massive
mediastinal node involvement produces gross
oedema and cyanosis of the face and upper limbs
(superior vena cava syndrome).
•
Blood: to bone, brain, liver and adrenals.
• Transpleural: pleural seedlings and effusion.
Clinical features
Carcinoma of the lung often presents late. Early cases
are more commonly found at the time of investigation
for other problems or by screening. Clinical presentation may be with one or more of the following:
•
Local features, namely cough, dyspnoea, haemop-
tysis or lung infection. Chest pain suggests spread
to pleural surface or a pleural effusion.
Secondaries (metastases), especially likely to occur
•
in the brain, adrenal, liver and bones; thus, the
patient may present with evidence of a space
occupying lesion within the skull, pathological
fracture, jaundice and hepatomegaly, or adrenocortical failure. Skin lesions may also occur and
are readily biopsied.
•
Paraneoplastic syndromes due to the remote
effects of a hormone or cell product produced by
the tumour. Smalladrenocorticotrophic hormone (ACTH), while
squamous carcinomas may produce parathormone (PTH) and present with hypercalcaemia.
•
General effects of neoplasm: loss of weight,
anaemia, cachexia and endocrine disturbances.
Patients may also present with bizarre
neuropathies and myopathies.
Unfortunately, by the time lung cancer is diagnosed,
most cases are incurable. About half the patients will
be found to have inoperable tumours when they have
had no symptoms at all, with a lesion discovered on
1
Johann Horner (1831–1886), Professor of Ophthalmology,
Zurich, Switzerland.
2
Henry Pancoast (1875–1939), Professor of Radiology,
University of Pennsylvania, Philadelphia, PA, USA.
cell carcinomas often produce
routine chest X-
ray. Any middle- aged or elderly
person presenting with a respiratory infection or
cough that has continued for more than 2 weeks
should have a chest Xand nothing shows on the chest X-
ray, and if the symptoms persist
ray, a CT scan
should be considered.
On examination, special attention should be paid
to evidence of stridor or hoarseness of the voice due
to recurrent laryngeal nerve involvement by the cancer. There may be clubbing of the fingers in addition
to nicotine staining. The heart may be invaded, resulting in atrial fibrillation or a pericardial effusion. There
may be enlarged lymph nodes, especially at the root
of the neck, and signs in the chest of consolidation,
fluid or collapse.
Special investigations
Investigation aims to confirm the presence of a cancer, and to identify its stage (spread) and histological
type.
Chest X- ray may show an opacity in the lung and
•
enlargement of the hilar lymph nodes. The
differential diagnosis of a mediastinal mass on
radiological examination of the chest is listed in
Box14.1. There may be a raised hemidiaphragm
due to paralysis secondary to involvement of the
Box 14.1 Abnormal opacity inthe
mediastinum
•
Retrosternal thyroid
•
Aneurysm of the thoracic aorta
•
Thymic tumour and cysts
•
Lung cancer with a mediastinal mass
•
Heart enlargement: cardiac failure, valve
incompetence, pericardial effusion, left–right
shunts and cardiomyopathies
•
Enlarged lymph nodes: sarcoid, Hodgkin’s
disease, other lymphoma, leukaemia and
secondary deposits
•
Oesophageal enlargement: tumour, hiatus hernia
and mega- oesophagus in achalasia of the cardia
•
Paravertebral abscess, particularly due to
tuberculosis
•
Scoliosis
•
Dumb- bell tumour of neurofibroma
•
Dermoid cyst or teratoma
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phrenic nerve. Abnormalities on chest X- ray
should prompt a CT scan.
Contrast- enhanced CT scan of the neck, chest and
•
upper abdomen, including the whole chest, liver,
adrenal glands and neck to base of skull, including
the vocal cords, to assess the primary lung lesion
and seek evidence of metastatic spread.
• PET- CT scan is an invaluable means of both con-
firming likely malignancy in peripheral lesions and
identifying mediastinal spread. In conjunction
with CT, it also permits diagnosis of, for instance,
adrenal adenomas mimicking metastases.
• Bronchoscopy and biopsy. Bronchoscopy may
reveal an ulcerating or exuberant growth, and
involved lymph nodes may widen the carina.
Brushings and washings may be taken for cytology
in addition to biopsy of a visible tumour.
•
Percutaneous needle biopsy of a peripherally
placed lesion under imaging guidance.
Endobronchial/endo- oesophageal ultrasound guided
•
biopsy. Mediastinal lymph nodes can be sampled.
Mediastinal spread is usually a contraindication to
primary surgery.
• Mediastinoscopy, performed through a small
suprasternal incision, may be indicated to remove
lymph nodes from the region of the carina for histological examination to aid in staging. VATS may
also be helpful.
• Pulmonary function tests to determine lung
reserve and, hence, the capacity to withstand surgery. Chronic obstructive pulmonary disease is
common in this patient group. Patients with a
forced expiratory volume in 1 second (FEV
can usually tolerate pneumonectomy (removal of
the whole lung); those with an FEV
ally tolerate lobectomy (removal of one lobe of the
lung). This should be coupled with a test of alveolar function (gas transfer), and in surgical candidates, a prediction of remaining function with a
perfusion scan. Patients with impaired fitness
must be carefully assessed to determine if surgery
is appropriate.
) >2.0L
1
>1L can usu-
1
Treatment
Surgery
Patient treatment will be determined in an MDT
meeting. Surgery is undertaken in a subset of
patients with sufficient respiratory reserve who
have disease localized to one lobe or lung (T1, T2
tumours, and sometimes T3 and rarely T4) but with
only intrathy. Mediastinal (N2) or more distal lymph node
involvement is a marker of poorer prognosis, so
generally such patients do not undergo resection.
Sometimes, such patients will undergo induction
treatment with chemotherapy and in selected cases
radiotherapy to downstage the tumour before surgery. There is emerging evidence that molecular
therapies can also downstage cancers, rendering
them suitable for surgery.
The aim of surgery is complete resection of the
tumour and the related local lymph nodes, together
with extensive sampling of other ipsilateral
mediastinal node stations. For many patients, this
will require lobectomy with a mortality risk of
1–2%. Pneumonectomy is now performed relatively
rarely – it is a major physiological insult, with a
mortality risk of at least 4%.
When lung cancer is diagnosed early, survival is
considerably improved with surgical resection. A
patient with Stage 1NSCLC (less than 4cm, no nodal
spread) that has been completely resected by lobectomy has at least a 60% five- year survival and in some
groups even better. There is increasing interest in
lesser lung resections (subticularly with smaller peripheral lesions. The outcomes of these resections appear similar to radical
radiotherapy.
The majority of lung cancer resections in some
countries, including the UK, are now performed by
minimally invasive VATS, as long as appropriate
oncological principles of surgical margin, gentle tissue handling and complete node clearance are
adhered to. For patients with small tumours and limited reserve, segmental resections, following anatomi-
cal borders, give good long-
pulmonary or hilar (N1) lymphadenopa-
lobar resections), par-
term results.
Radiotherapy
Radiotherapy can be used with curative or palliative
intent. In all such cases, there is careful assessment of
the case by an oncologist who will determine a treatment plan. Radiotherapy may give useful palliation
for inoperable cases. Although it may not prolong life,
it may stop distressing haemoptysis, relieve the pain
from bone secondaries and produce dramatic
improvement in a patient with acute superior vena
cava obstruction. It may also give some relief from the
irritating cough and dyspnoea resulting from early
bronchial obstruction.
Chemotherapy
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Cyclical cytotoxic therapy combined with radiotherapy is the treatment of choice for smallChemotherapy is also used in the adjuvant setting
surgery) if high- risk features are identified. This
(postincludes the presence of lymph node involvement.
Sometimes, chemotherapy is used pre‘downstage’ tumours, with the aim of increasing the
chance of successful surgery.
cell tumours.
operatively to
Targeted chemotherapy
Cancer specimens undergo sequencing to search for
genetic mutations, usually involving pathways causing increased cell proliferation. These mutations are
targets susceptible to particular inhibitors:
•
Epidermal growth factor receptor (EGFR) muta-
tions, targeted by gefitinib and afatinib, for
example.
•
Anaplastic lymphoma kinase (ALK), a tyrosine
kinase. Mutation present in 5% of NSCLC, and is
blocked by crizotinib and ceritinib, for example.
•
ROS1, a tyrosine kinase similar to ALK.
• K- RAS gene, targeted by sotorasib.
The chest andlungs 139
Secondary tumours
The lung is second only to the liver as the site of metastases, which may be from carcinoma (especially breast,
kidney and colorectal), sarcoma (especially bone) or
melanoma. Spread may be as a result of either vascular
deposits or lymphatic permeation from involved
mediastinal nodes– lymphangitis carcinomatosa.
Pulmonary metastases are so common that it
should be routine practice to image the chest by CT
scan in every case of malignant disease to aid staging
the primary cancer.
A low volume of metastatic disease to the chest may
be treated by surgical excision, radiotherapy or radiofrequency ablation.
Additional resources
Case 19: A patient with a chest drain
Case 20: A fatal lung disease
15
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15
Venous disorders ofthe
lower limb
Manj Gohel
Learning objectives
✓ To understand the normal anatomy and physiology of the venous
system.
✓ To know the causes and treatment of supercial and deep venous
insuciency of the lower limb.
Normal venous function
The venous system of the legs returns deoxygenated
blood from the peripheries to the right heart via a
network of lowFlow in the correct direction is maintained by a series
of unidirectional valves in the peripheral veins, and
flow is driven by muscle pumps, predominantly in
the calf but also in the feet. As the calf and foot muscles contract, the deep veins within them are compressed and emptied, the blood passing upwards,
directed towards the heart by the nonAs the muscles relax, blood flows in from the superficial system via perforators, as well as from more distal segments of the vein, only to be forced upwards
again by the next contraction of the calf muscles,
which thus act as a pump.
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
resistance superficial and deep veins.
return valves.
Anatomy ofthe venous
drainage ofthe lower limb
To understand venous disease in the leg, it is essential
to understand the functional anatomy of the venous
system. The venous system consists of a complex network of superficial veins, deep veins and perforating
veins (Figure15.1). Most of the venous flow is in the
deep veins (around 90%), but both superficial and
deep veins can cause disease.
The deep venous system
The deep veins of the leg usually accompany (and
share the name of) the main arteries of the lower limb
and are located deep to the fascia that envelops the
muscular compartments. Crural veins in the calf
(anterior tibial, posterior tibial and peroneal veins)
drain into the popliteal vein behind the knee, which
ascends as the femoral vein, becoming the common
femoral vein in the groin and then the external iliac
vein above the inguinal ligament. From there, blood
flows up the common iliac vein, via the inferior vena
cava, to the right atrium.
Deep
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fascia
malleolus
Valve at sapheno-
femoral junction
Great
saphenous
vein
Mid-thigh
perforator
Femoral vein
Small
saphenous
vein
Ankle
perforatorsLateral
Venous disorders ofthe lower limb 141
veins (particularly the anterior accessory saphenous
vein, in the territory of the great saphenous vein).
These veins are located superficial to the deep fascia
and drain the skin and superficial tissues.
Perforating veins
In addition to the saphenofemoral and saphenopopliteal junctions, there are numerous additional
communications between superficial and deep
veins. These are called perforating veins, or ‘perforators’, as they typically pierce the fascia to reach the
deep veins. Although the anatomy of perforators is
notoriously variable, there is typically a midperforator (called the Hunterian perforator on
account of its relationship to Hunter’s canal
several calf perforators located on the medial aspect
of the tibia from the ankle to the knee.
thigh
1
), and
Aetiology ofvenous
disease
The aetiology of venous disease may be classified as
follows:
• Congenital;
• Primary, the most common;
• Secondary (post- thrombotic);
• Idiopathic, where no venous cause for disease is
identified.
Figure15.1 The venous system of the leg. Note that
there are two main supercial veins, the great saphenous
and small saphenous veins, each of which drains into the
deep veins, at the saphenofemoral and saphenopopliteal
junctions, respectively, but also via several perforating veins.
The supercial venous system
This comprises the medially placed great (long)
saphenous vein, draining from the dorsum of the foot
to the saphenofemoral junction in the groin, and the
small (short) saphenous vein, which drains the lateral
aspect of the lower limb into the popliteal vein behind
the knee. There may also be accessory saphenous
Primary venous disease
The underlying cause of venous disease is chronic
venous hypertension. Persistent high pressure in the
venous system of the leg can result in symptoms, clinical
manifestations and complications of venous disease. A
common cause of venous hypertension is damage or
failure of the vein valves in superficial or deep veins,
which can result in blood flow away from the heart,
termed ‘reflux’ or ‘incompetence’ (Figure 15.2). The
causes of valve incompetence are poorly understood,
but there are likely to be genetic and acquired factors.
When trying to understand the development of varicose veins, some scientists favour the ‘descending’
theory, where superficial vein valve failure starts at the
junctions and progresses down the leg. Alternatively,
1
John Hunter (1728–1793), Surgeon, St George’s Hospital,
London, UK.
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Increased
pressure
Competent
the ‘ascending’ theory suggests that varicose veins start
distally and progress up the leg, and this is supported
by the observation that varicose veins often exist with a
competent saphenous junction. The development of
varicose veins is likely to be multifactorial.
It was previously thought that superficial vein reflux
causes only varicose veins, whereas venous skin
changes and ulceration were caused by deep venous
disease. Our understanding of venous pathophysiology has evolved, and it is now widely accepted that
superficial venous reflux alone can (and often does)
result in oedema, venous skin changes and ulceration. While the precise pathophysiological mechanisms linking venous hypertension and skin damage
are debated, high capillary hydrostatic pressure
results in diffusion of fluid, red cells and white cells
into the soft tissues, resulting in chronic inflammation
and skin changes.
incompetence
Incompetent
Congenital venous disease
Dilated veins may be seen as part of a number of
inherited syndromes, such as Klippel–Trenaunay syn-
2
drome
. The syndrome involves three elements: multiple congenital venous malformations producing
varicose veins, hypertrophy of bones and soft tissues
and extensive cutaneous haemangiomas. It usually
affects the lower limbs.
2
Maurice Klippel (1858–1942), Neurologist, Salpêtrière
Hospital, Paris, France. Paul Trenaunay (b.1875), Neurologist.
Valvular
Figure15.2 Normal veins and
incompetent varicose veins. Note that
the vein dilates under pressure and the
valve becomes incompetent.
Secondary (post- thrombotic)
venous disease
Previous deep vein thrombosis may result in chronic
changes and damage to the vein, resulting in venous
hypertension. There are several contributing factors:
• Deep vein reflux, secondary to valvular damage
and inability to maintain the one- way flow after
thrombosis.
•
Scarring of deep veins, remodelling the vein wall.
• Venous obstruction may cause additional pressure
on competent vein valves (in deep and superficial
veins), causing further valve failure and compounding the clinical picture. There is a tendency
for the condition to get worse as further valves are
involved.
Tortuous, dilated veins may also be seen in patients
with deep vein obstruction. These are important collateral veins providing an alternative route for venous
return to the heart and should not be confused with
varicose veins.
Clinical presentation
Patients with venous disease may seek help for a wide
variety of reasons, including symptoms, complications or cosmetic concerns (or any combination of
these). Typical symptoms include aching, throbbing
or heaviness/tiredness in the legs as well as swelling
of the ankles, particularly after long periods of
Venous disorders ofthe lower limb 143
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standing. Patients with superficial or deep venous
disorders may present with a range of overlapping
symptoms and clinical signs. The CEAP classifica-
3
tion
is the most widely accepted.
Thread veins / reticular veins
Also referred to as ‘spider veins’, or telangectasia,
these are very small, superficial veins that can cause
cosmetic concern. Treatment is not usually offered in
public healthcare systems.
Leg swelling andskin changes
Peripheral oedema is a common manifestation of
chronic venous disease, as the increased hydrostatic
forces (Starling’s forces
4
) result in increased volumes
of interstitial fluid that the lymphatic system is unable
to drain. Oedema may only affect the ankle after prolonged standing, but constant and extensive swelling
may also be seen.
Often occurring on the medial lower calf (the medial
gaiter area), there are several skin manifestations that
are associated with venous disease, including:
Haemosiderinosis and pigmentation: extravasation
•
of red blood cells, which become deposited as haemosiderin in the skin and subcutaneous tissues.
Venous eczema / stasis dermatitis: a common early
•
skin complaint, characterized by dry, itchy and
scaly skin.
•
Lipodermatosclerosis: thickening and fibrosis of the
skin and soft tissues, resulting in the ‘inverted cham-
pagne bottle’ appearance, which occurs due to chronic
inflammation secondary to venous hypertension.
Venous ulceration
A chronic leg ulcer is defined as a defect in the skin of
the lower leg, remaining unhealed for more than
4 weeks. Chronic venous hypertension accounts for
the vast majority of chronic leg ulcers and is recognized as an enormous cause of patient distress and
health service resource use worldwide. Ulcers are
usually superficial, can be very painful, and may start
with minor trauma or without any obvious precipitant. Ulceration is considered the most extreme
3
Clinical, Etiological, Anatomical and Pathophysiological
(CEAP) classication of venous disorders.
4
Sir Ernest Starling (1866–1927), Professor of Physiology,
University College, London, UK.
presentation in the spectrum of venous disorders and
patients usually have other signs of venous disease
such as skin changes, varicose veins or oedema.
Venous ulcers either have an edge, which is ragged,
or where the ulcer is healing, the margins will be
shelving with a faint blue rim of advancing ep ithelium.
Previous scarring appears as a white rim around the
ulcer, known as atrophie blanche. Rarely, a squamous
carcinoma can develop in the edge of a longulcer (Marjolin’s ulcer
5
). Approximately 90% of all
standing
ulcers of the legs are venous in origin, but other, rarer,
causes should always be considered (Box15.1).
Other complications ofvaricose
veins
In addition to the clinical presentations described
above, patients may also present with specific complications of varicose veins.
1
Bleeding. Prominent, superficial dilated veins may
bleed profusely if knocked. The high venous
pressure in the incompetent vein can result in
Box 15.1 Differential diagnosis ofleg ulcers
•
Chronic venous ulcer due to venous
hypertension.
•
Ischaemic ulcer due to impaired arterial blood
supply; the peripheral pulses must always be
examined and ankle- brachial pressure indexes
checked.
•
Mixed ulcers, with ischaemic and venous
contributions.
•
Neuropathic ulcer, particularly common in
diabetics where they are often compounded by
ischaemia due to diabetic microangiopathy.
•
Malignant ulcer, a basal cell carcinoma, or a
squamous carcinoma (possibly arising in a
pre- existing chronic venous ulcer) or an ulcerated
malignant melanoma.
•
Ulcer complicating systemic disease, for
example, acholuric jaundice, ulcerative colitis and
rheumatoid arthritis.
•
Repetitive self- inflicted injury (factitious
ulceration).
5
Jean Nicholas Marjolin (1780–1850), Surgeon, Hôpital
Sainte- Eugènie, Paris, France
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life- threatening haemorrhage, particularly in
elderly or frail patients who may be unable to
apply pressure and elevate the leg.
2
Superficial vein thrombosis (SVT). Formally
referred to as ‘thrombophlebitis’ or ‘phlebitis’, SVT
is a common clinical condition presenting as a
hard, red, painful and engorged superficial vein.
Virtually, all cases occur in patients with preexisting varicose veins. Up to a quarter of patients
presenting with SVT also have a covein thrombosis, indicating that there is likely to
be a prothrombotic tendency in these patients.
existent deep
Assessment ofthe patient
withvenous disease
History
A detailed history should include information about
the presenting symptoms (including the severity and
impact on the patient’s quality of life). Patients should
be specifically asked about the presence of skin discolouration or eczema and the current or past presence of leg ulcers. Other points to note are a history of
deep vein thrombosis, or a history suggestive of
thrombosis such as swelling and pain postoperatively, during pregnancy or after a long period of
immobilization. Risk factors for venous thromboembolism (such as obesity, use of oestrogenmedication or thrombophilia) are important to ascertain, as this may direct the thromboprophylaxis plan
after any intervention. Previous venous interventions
should also be recorded as redo procedures are likely
to be associated with greater risks.
Clinical examination
A patient with venous disease should be examined
while standing, and the presence/extent of varicose
veins should be carefully recorded. Photographic
documentation may be of value. Examination of the
legs should include inspection of the medial gaiter
area for evidence of venous skin changes (eczema,
haemosiderosis, lipodermatosclerosis and/or ulceration). The presence of scars should be noted. The
arterial status of the leg (presence of peripheral
pulses) should also be recorded.
A saphena varix, a prominent dilation of the great
saphenous vein at the saphenofemoral junction, may
containing
be present. It gives a characteristic thrill to the examining fingers when the patient coughs, quite different
from a femoral hernia. It disappears when the patient
lies flat.
A handheld Doppler assessment can help identify
venous incompetence in large or small saphenous
veins but has also become largely obsolete due to the
widespread availability of colour duplex ultrasound
scanning
Special investigations
The aim of any venous investigations is to identify
potentially treatable superficial or deep venous
disease:
Duplex scan
•
which is non- invasive, painless and can accurately
map the superficial and deep veins in the leg to
diagnose both valvular and perforator incompetence and deep venous occlusion. Guidelines suggest it should be performed before any venous
intervention.
Ankle- brachial pressure index, using a handheld
•
Doppler, to assess the arterial supply to the leg in
cases of ulceration and thus determine the appropriateness of compression therapy.
• Cross- sectional imaging (CT or MR) may be
needed to assess proximal deep veins in the abdomen and pelvis.
•
Venography and intravascular ultrasound may
also be required to assess venous anatomy in
some circumstances.
6
: The ‘gold- standard’ investigation,
Treatment ofvenous
disease
The main principle of management for patients with
venous disease is to reduce venous hypertension,
ideally by treating the underlying cause, in order to
improve quality of life. Where it is not feasible or
desirable to try and address the underlying superficial or deep venous problem, there are several
general measures that may be used. Bed rest and leg
6
Duplex is a combination of grey- scale ultrasound looking
at physical structures and colour Doppler looking at ow
in vessels. Doppler is named after Christian Doppler
(1803–1853), an Austrian Physicist.
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