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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2826_Библиотеки_им_академика_М_И_Перельмана.pdf
Tumours of the Kidney and Genitourinary Tract 393
Management
Localized disease. Radical nephrectomy is the preferred treatment. Partial
nephrectomy is used if there is bilateral involvement or the contralateral
kidney functions poorly. Ablative techniques (cryoablation or radiofrequency
ablation) are used in patients with significant comorbid disease who would
not tolerate surgery.
Metastatic or locally advanced disease. Interleukin-2 and interferon
produce a remission in 20% of cases. Targeted therapies which block the
vascular endothelial growth factor (sunitinib, sorafenib, bevacizumab) or
mTOR (temsirolimus) pathway are used in patients who cannot tolerate or do
not respond to this treatment.
Prognosis
The 5-year survival rate is 60%–70% with tumours confined to the renal
parenchyma, but less than 5% in those with distant metastases.
Urothelial tumours
The calyces, renal pelvis, ureter, bladder and urethra are lined by transitional
cell epithelium. Bladder tumours are the most common form of transitional cell
malignancy. They occur most frequently after the age of 40 years and are four
times more common in males. Predisposing factors for bladder cancer include:
• Cigarette smoking
• Exposure to industrial chemicals, e.g. β-naphthylamine, benzidine
• Exposure to drugs, e.g. phenacetin, cyclophosphamide
• Chronic inflammation, e.g. schistosomiasis.
Clinical features
Patients with bladder cancer usually present with painless haematuria
(either visible or non-visible) or sometimes symptoms suggestive of a UTI
(frequency, urgency, dysuria) in the absence of bacteriuria. Pain is usually
due to locally advanced or metastatic disease but may sometimes occur from
clot retention. Transitional cell cancers of the kidney and ureters present with
haematuria and flank pain.
Investigations
Presentation is usually with haematuria. Any patient over the age of 40 years
with haematuria should be assumed to have a urothelial tumour until proven
otherwise (see Fig. 9.3).
Management
Pelvic and ureteric tumours are treated with nephroureterectomy. Treatment
of bladder tumours depends on the stage, but options include local diathermy
394 Renal disease
or cystoscopic resection, bladder resection, radiotherapy and local and systemic chemotherapy.
DISEASES OF THE PROSTATE GLAND
The common diseases of the prostate gland are benign enlargement, carcinoma and prostatitis. Prostate-specific antigen (PSA) is a glycoprotein that
is expressed by normal and neoplastic prostate tissue and secreted into
the bloodstream. Serum concentrations can be increased in any of these
conditions and also after perineal trauma and mechanical manipulation of
the prostate (cystoscopy, prostate biopsy or surgery). Serum PSA concentration >4.0 ng/mL is abnormal and can be due to benign disease or cancer.
However, prostate cancer is present in 50% of men with a serum PSA
>10 ng/mL.
Benign enlargement of the prostate gland
Benign prostatic hypertrophy (BPH) is common particularly after the age of 60
years. There is hyperplasia of both glandular and connective tissue elements
of the gland. The aetiology is not known.
Clinical features
Frequency of micturition, nocturia, delay in initiation of micturition and postvoid dribbling are common symptoms. Acute urinary retention or retention
with overflow incontinence also occurs. An enlarged smooth prostate may be
felt on rectal examination.
Investigations
Serum electrolytes and renal ultrasonography are performed to exclude renal
damage resulting from obstruction. Prostate cancer may present with similar
symptoms. Serum PSA may be elevated in benign disease but an elevated
value is usually an indication for specialist referral and prostate biopsy.
Management
Patients with mild symptoms are managed by ‘watchful waiting’. Selective
α1-adrenoceptor antagonists, such as tamsulosin, relax smooth muscle in the
bladder neck and prostate, producing an increase in urinary flow rate and an
improvement in obstructive symptoms. The 5α-reductase inhibitor finasteride blocks conversion of testosterone to dihydrotestosterone (the androgen
responsible for prostatic growth) and is an alternative to α-antagonists,
particularly in men with a significantly enlarged prostate. Patients with acute
urinary retention or retention with overflow require urethral catheterization or,
if this is not possible, suprapubic catheter drainage. Further management is
then with prostatectomy or a permanent catheter.
Testicular Tumour 395
Prostatic carcinoma
Prostatic adenocarcinoma is common, accounting for 7% of all cancers in
men. Malignant change within the prostate is increasingly common with
advancing age, being present in 80% of men aged 80 years and over. In most
cases these malignant foci remain dormant.
Clinical features
In developed countries, many patients now present as a result of screening for
prostate cancer by measurement of serum PSA, although this is not widely recommended (see later). Presentation is also with symptoms of bladder outflow
obstruction identical to those of BPH. Occasionally, presenting symptoms are
due to metastases, particularly to bone. In some cases, malignancy is unsuspected until histological investigation is carried out on the resected specimen
after prostatectomy. Rectal examination may reveal a hard irregular gland.
Investigation
The diagnosis is made using transrectal ultrasound of the prostate, elevated
serum PSA and transrectal prostate biopsy. If metastases are present, serum
PSA is usually markedly elevated (>16 ng/mL). Endorectal coil MRI is used to
locally stage the tumour.
Management
Microscopic tumour is sometimes managed by watchful waiting. Treatment of
disease confined to the gland is radical prostatectomy or radiotherapy, both
resulting in 80%–90% 5-year survival. The treatment of metastatic disease
depends on removing the androgenic drive to the tumour. This is achieved
by bilateral orchidectomy, synthetic luteinizing hormone-releasing hormone
analogues (e.g. goserelin), or antiandrogens (e.g. cyproterone acetate).
Screening
Screening for prostate cancer by annual measurement of serum PSA and
digital rectal examination reduces the mortality from prostate cancer but the
benefit is small and there is the potential for overdiagnosis and treatmentrelated complications. Most major medical organizations worldwide do not
recommend screening for prostate cancer.
TESTICULAR TUMOUR
Testicular cancer is the most common cancer in young men. More than 96%
of testicular tumours arise from germ cells. There are two main types: seminomas and teratomas. The aetiology is unknown and the risk of malignant
change is greater in undescended testes.
396 Renal disease
Clinical features
Typically, the man or his partner finds a painless lump in the testicle.
Presentation may also be with metastases in the lungs, causing cough and
dyspnoea, or para-aortic lymph nodes, causing back pain.
Investigations
• Ultrasound scanning will help to differentiate between masses in the
body of the testes and other intrascrotal swellings.
• Serum concentrations of the tumour markers α-fetoprotein (AFP) and/
or the β-subunit of human chorionic gonadotrophin (β-hCG) are elevated
in most men with teratomas. They are used to help make the diagnosis,
to assess response to treatment and in following up patients. β-hCG is
elevated in a minority of men with seminomas. AFP is not elevated in
men with pure seminomas.
• Tumour staging is assessed by chest X-ray and CT scanning of the chest,
abdomen and pelvis.
Treatment
Orchidectomy is performed to permit histological evaluation of the primary
tumour and to provide local tumour control. Seminomas with metastases
below the diaphragm only are treated by radiotherapy. More widespread
tumours are treated with chemotherapy. Teratomas with metastases are also
treated with chemotherapy. Sperm banking should be offered prior to therapy
to men who wish to preserve fertility.
URINARY INCONTINENCE
Normal bladder physiology
As the bladder fills with urine, two factors act to ensure continence until it
is next emptied:
• Intravesical pressure remains low as a result of stretching of the bladder
contract involuntarily.
• The sphincter mechanisms of the bladder neck and urethral muscles.
At the onset of voiding, the sphincters relax (mediated by decreased
sympathetic activity) and the detrusor muscle contracts (mediated by increased
parasympathetic activity). Overall control and coordination of micturition is by
higher brain centres, which include the cerebral cortex and the pons.
Stress incontinence
Stress incontinence occurs as a result of sphincter weakness, which may be
iatrogenic in men (post-prostatectomy) or the result of childbirth in women.
Urinary Incontinence 397
There is a small leak of urine when intra-abdominal pressure rises, e.g. with
coughing, laughing or standing up. In young women, pelvic floor exercises
may help. In post-menopausal women the contributing factor of urethral
atrophy may be helped by oestrogen creams.
Urge incontinence
In urge incontinence there is a strong desire to void and the patient may be
unable to hold his or her urine. The usual cause is detrusor instability, which
occurs most often in women, and the aetiology is not known. Mild cases
may respond to bladder retraining (gradually increasing the time interval
between voids). More severe cases are treated with anticholinergic agents,
e.g. oxybutynin, which decrease detrusor excitability. Less commonly, urge
incontinence is caused by bladder hypersensitivity from local pathology (e.g.
UTI, bladder stones, tumours) and treatment is then of the underlying cause.
Overflow incontinence
Overflow incontinence is most often seen in men with prostatic hypertrophy
causing outflow obstruction. There is leakage of small amounts of urine,
and on abdominal examination the distended bladder is felt rising out of the
pelvis. If the obstruction is not relieved with urethral or suprapubic catheterization, renal damage will develop.
Neurological causes
These are usually apparent from the history and examination, which reveal
accompanying neurological deficits. Brainstem damage, e.g. trauma, may
lead to incoordination of detrusor muscle activity and sphincter relaxation, so
that the two contract together during voiding. This results in a high-pressure
system with the risk of obstructive uropathy. The aim of treatment is to
reduce outflow pressure, either with α-adrenergic blockers or by sphincterotomy. Autonomic neuropathy, e.g. in diabetic individuals, decreases
detrusor excitability and results in a distended atonic bladder with a large
residual urine which is liable to infection. Permanent catheterization may
be necessary.
In elderly people, incontinence may be the result of a combination of
factors: diuretic treatment, dementia and difficulty in getting to the toilet
because of immobility.
Cardiovascular
10
COMMON PRESENTING SYMPTOMS
OFHEARTDISEASE
The common symptoms of heart disease are chest pain, breathlessness, palpitations, syncope, fatigue and peripheral oedema, but none are specific for
cardiovascular disease. The severity of anginal pain, dyspnoea, palpitations or
fatigue may be classified according to the New York Heart Association (NYHA)
grading of ‘cardiac status’ (Table 10.1).
Chest pain
Chest pain or discomfort is a common presenting symptom of cardiovascular
disease and must be differentiated from non-cardiac causes. The site of
pain, its character, radiation and associated symptoms will often point to the
cause (Table 10.2).
Dyspnoea
Causes are discussed on page 507. Left heart failure is the most common
cardiac cause of exertional dyspnoea and may also cause orthopnoea and
paroxysmal nocturnal dyspnoea.
Palpitations
Palpitations are an awareness of the heartbeat. The normal heartbeat is
sensed when the patient is anxious, excited, exercising or lying on the left
side. In other circumstances it usually indicates a cardiac arrhythmia, commonly ectopic beats or a paroxysmal tachycardia (p. 411).
disease
Syncope
This is a temporary impairment of consciousness due to inadequate cerebral
blood flow. There are many causes and the most common is a simple faint
or vasovagal attack (Table 17.3; page 693). The cardiac causes of syncope
are the result of either very fast (e.g. ventricular tachycardia) or very slow
heart rates (e.g. complete heart block) which are unable to maintain an
adequate cardiac output. Attacks occur suddenly and without warning. They
last only 1 or 2 minutes, with complete recovery in seconds (unlike epilepsy,
Common Presenting Symptoms ofHeartDisease 399
Table 10.1 The New York Heart Association grading of ‘cardiac
status’ (modified)
Grade 1 Uncompromised (no breathlessness)
Grade 2 Slightly compromised (on severe exertion)
Grade 3 Moderately compromised (on mild exertion)
Grade 4 Severely compromised (breathless at rest)
Table 10.2 Common causes of chest pain
Central
Angina pectoris Crushing pain on exercise, relieved by rest. May radiate
ACS Similar in character to angina but more severe, occurs
Pericarditis Sharp pain aggravated by movement, respiration and
Aortic dissection Severe tearing chest pain radiating through to the back
Massive PE With dyspnoea, tachycardia and hypotension
Musculoskeletal Tender to palpate over affected area
GORD May be exacerbated by bending or lying down (at
Lateral/peripheral
Pulmonary infarct
Pneumonia
Pneumothorax
Musculoskeletal Sharp, well-localized pain with a tender area on
Lung carcinoma Constant dull pain
Herpes zoster Burning unilateral pain corresponding to a dermatome
ACS, acute coronary syndrome; GORD, gastro-oesophageal reflux disease;
PE, pulmonary embolus.
to jaw or arms
at rest, lasts longer
changes in posture
night). Pain may radiate into the neck
Pleuritic pain, i.e. sharp, well-localized, aggravated by
inspiration, coughing and movement
}
palpation
that appears 2 to 3 days before the typical rash
where complete recovery may be delayed for some hours). Obstruction to
ventricular outflow also causes syncope (e.g. aortic stenosis, hypertrophic
cardiomyopathy), which typically occurs on exercise when the requirements
for increased cardiac output cannot be met. Postural (orthostatic) hypotension is a drop in systolic blood pressure (BP) of 20 mmHg or more on standing
from a sitting or lying position.
400 Cardiovascular disease
Other symptoms
Tiredness and lethargy occur with heart failure and result from poor perfusion of brain and skeletal muscle, poor sleep, side effects of medication,
particularly β-blockers, and electrolyte imbalance due to diuretic therapy.
Heart failure also causes salt and water retention, leading to oedema, which
in ambulant patients is most prominent over the ankles. In severe cases it
may involve the genitalia and thighs.
INVESTIGATIONS IN CARDIAC DISEASE
The chest X-ray
A chest X-ray is usually taken in the postero-anterior (PA) direction at
maximum inspiration (p. 495). A PA chest film can aid the identification of
cardiomegaly, pericardial effusions, dissection or dilatation of the aorta,
and calcification of the pericardium or heart valves. A cardiothoracic ratio
(p. 496) of greater than 50% on a PA film is abnormal and usually indicates
cardiac dilatation or pericardial effusion. Examination of the lung fields may
show signs of left ventricular failure (Fig. 10.1), valvular heart disease (e.g.
markedly enlarged left atrium in mitral valve disease) or pulmonary oligaemia
(reduction of vascular markings) associated with pulmonary embolic disease.
THE ELECTROCARDIOGRAM
The electrocardiogram (ECG) is a recording from the body surface of the electrical
activity of the heart. Each cardiac cell generates an action potential as it becomes
depolarized and then repolarized during a normal cycle. Normally, depolarization
of cardiac cells proceeds in an orderly fashion beginning in the sinus node (lying in
the junction between superior vena cava and right atrium) and spreading sequentially through the atria, atrioventricular (AV) node (lying beneath the right atrial
endocardium within the lower interatrial septum), and the His bundle in the interventricular septum, which divides into right and left bundle branches (Fig. 10.2).
The right and left bundle branches continue down the right and left side of the
interventricular septum and supply the Purkinje network which spreads through
the subendocardial surface of the right ventricle and left ventricle, respectively.
The main left bundle divides into an anterior superior division (the anterior
hemi-bundle) and a posterior inferior division (the posterior hemi-bundle).
The standard ECG has 12 leads:
• Chest leads, V1–V6, look at the heart in a horizontal plane (Fig. 10.3).
• Limb leads look at the heart in a vertical plane (Fig. 10.4). Limb leads are
unipolar (AVR, AVL and AVF) or bipolar (I, II, III).
The ECG machine is arranged so that when a depolarization wave spreads
towards a lead the needle moves upwards on the trace (i.e. a positive deflection),
and when it spreads away from the lead the needle moves downwards.
The Electrocardiogram 401
Fig. 10.1 Chest X-ray in acute left ventricular failure. This chest X-ray demon-
strates cardiomegaly, hilar haziness, Kerley B lines, upper lobe venous blood
engorgement and fluid in the right horizontal fissure. Hilar haziness and Kerley B
lines (thin linear horizontal pulmonary opacities at the base of the lung periphery)
indicate interstitial pulmonary oedema.
ECG waveform and definitions (Fig. 10.5)
Heart rate. At normal paper speed (usually 25 mm/s) each ‘big square’
measures 5 mm wide and is equivalent to 0.2 s. The heart rate (if the rhythm
is regular) is calculated by counting the number of big squares between two
consecutive R waves and dividing into 300.
The P wave is the first deflection and is caused by atrial depolarization.
When abnormal, it may be:
• Broad and notched (>0.12 s, i.e. three small squares) in left atrial
enlargement (‘P mitrale’, e.g. mitral stenosis)
• Tall and peaked (>2.5 mm) in right atrial enlargement (‘P pulmonale’, e.g.
pulmonary hypertension)
402 Cardiovascular disease
Sinoatrial node
His bundle
Atrioventricular
Fig. 10.2 The conducting system of the heart. In normal circumstances
only the specialized conducting tissues of the heart undergo spontaneous
depolarization (automaticity), which initiates an action potential. The sinoatrial
(SA) node discharges more rapidly than the other cells and is the normal
pacemaker of the heart. The impulse generated by the SA node spreads first
through the atria, producing atrial systole, and then through the atrioventricular
node to the His-Purkinje system, producing ventricular systole.
• Replaced by flutter or fibrillation waves (p. 419–421)
• Absent in sinoatrial block (p. 412).
• A negative (downward) deflection preceding an R wave is called a Q
• A deflection upwards is called an R wave whether or not it is preceded
• A negative deflection following an R wave is termed an S wave.
right (see Fig. 10.2). Subsequently, the main free walls of the ventricles are
depolarized. Thus in the right ventricular leads (V1 and V2) the first deflection
is upwards (R wave) as the septal depolarization wave spreads towards
those leads. The second deflection is downwards (S wave) as the bigger left
ventricle (in which depolarization is spreading away) outweighs the effect
of the right ventricle (see Fig. 10.3). The opposite pattern is seen in the left
ventricular leads (V5 and V6), with an initial downwards deflection (small Q
wave reflecting septal depolarization) followed by a large R wave caused by
left ventricular depolarization.
node
Left posterior
bundle
Right bundle
Purkinje
fibres
The QRS complex represents ventricular activation or depolarization:
wave. Normal Q waves are small and narrow; deep (>2 mm), wide
(>1 mm) Q waves (except in AVR and V1) indicate myocardial infarction
(MI) (p. 444).
by a Q wave.
Ventricular depolarization starts in the septum and spreads from left to