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Chantal Simon et al.

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Book cover for Oxford Handbook of General Practice (4 edn) Oxford Handbook of General Practice (4 edn)
Chantal Simon et al.
Disclaimer
Oxford University Press makes no representation, express or implied, that the drug dosages in this book are correct. Readers must therefore always … More Oxford University Press makes no representation, express or implied, that the drug dosages in this book are correct. Readers must therefore always check the product information and clinical procedures with the most up to date published product information and data sheets provided by the manufacturers and the most recent codes of conduct and safety regulations. The authors and the publishers do not accept responsibility or legal liability for any errors in the text or for the misuse or misapplication of material in this work. Except where otherwise stated, drug dosages and recommendations are for the non-pregnant adult who is not breastfeeding.

Commonly ordered test to detect renal dysfunction. Rough guide to glomerular filtration rate (GFR) when corrected for age, gender, and weight—↓ in GFR is associated with ↑ in serum creatinine. Causes of an abnormal serum creatinine—see Table 14.1.

Table 14.1
Causes of an altered serum creatinine and urea
↑ creatinine (>150micromol/L) ↓ creatinine (<70micromol/L) ↑ urea (>6.7mmol/L) ↓ urea (<2.5mmol/L)

Renal disease/renal failure

Drugs (e.g. trimethoprim, probenecid, cimetidine, potassium-sparing diuretics)

Large muscle bulk

Muscle breakdown (e.g. muscular dystrophy)

Muscular dystrophy (late stage)

Myasthenia gravis

Renal failure

GI bleeding

High-protein diet

Drugs—high-dose steroids, tetracycline

Dehydration

Liver disease (↓ urea production)

Anabolic state

High ADH levels (high GFR)

Starvation or low-protein diet

Pregnancy

↑ creatinine (>150micromol/L) ↓ creatinine (<70micromol/L) ↑ urea (>6.7mmol/L) ↓ urea (<2.5mmol/L)

Renal disease/renal failure

Drugs (e.g. trimethoprim, probenecid, cimetidine, potassium-sparing diuretics)

Large muscle bulk

Muscle breakdown (e.g. muscular dystrophy)

Muscular dystrophy (late stage)

Myasthenia gravis

Renal failure

GI bleeding

High-protein diet

Drugs—high-dose steroids, tetracycline

Dehydration

Liver disease (↓ urea production)

Anabolic state

High ADH levels (high GFR)

Starvation or low-protein diet

Pregnancy

More sensitive measure than serum creatinine to assess renal function. Calculated from:

Serum creatinine

Age

Gender, and

Ethnicity—people of Afro-Caribbean origin tend to have ↑ muscle mass so their eGFR must be multiplied by 1.21

Changes in eGFR can be used to monitor changes in kidney function.

Normal eGFR is >90mL/min/1.73m2

eGFR 60–90mL/min/1.73m2 does not indicate CKD unless additional markers of damage are present—persistent microalbuminuria, persistent proteinuria, persistent microscopic haematuria, or structural abnormality, e.g. polycystic kidneys

eGFR <60mL/min/1.73m2 indicates CKD (graphic p. 440)

graphicRenal function ↓ with age (approximately 1mL/min/y >40y). Many elderly patients have a GFR <60mL/min which, because of ↓ muscle mass, may not be indicated by a ↑ serum creatinine. Measuring eGFR gives a better indication of renal function.

Commonly ordered test to detect renal dysfunction. While ↓ in GFR is associated with ↑ in serum urea, serum urea may also vary independently of the GFR. Causes of abnormal serum urea—see Table 14.1.

High serum potassium (>5mmol/L). Causes: See Table 14.2. Treat the cause.

Table 14.2
Causes of altered serum electrolytes
↑ potassium (>5mmol/L) ↓ potassium (<3.5mmol/L) ↑ sodium (>145mmol/L) ↓ sodium (<135mmol/L)

Renal failure

Drugs (e.g. ACE inhibitors, excess K+ therapy, K+ sparing diuretics)

Addison’s disease

Metabolic acidosis (DM)

Artefact (haemolysed sample)

Diuretics

Cushing’s syndrome/steroids

Vomiting and/or diarrhoea

Conn’s syndrome

Villous adenoma of the rectum

Purgative or liquorice abuse

Intestinal fistula

Renal tubular failure

Hypokalaemic periodic paralysis—intermittent weakness lasting <72h

Fluid loss without water replacement (e.g. diarrhoea, vomiting, burns)

Diabetes insipidus—suspect if large urine volume

Osmotic diuresis

Primary aldosteronism– suspect if ↑ BP, ↓ K+, alkalosis

Diuretic excess—especially thiazides

Renal failure or nephrotic syndrome

Diarrhoea/vomiting

Fistula

Rectal villous adenoma

Small bowel obstruction

CF (graphic p. 330)

Heat exposure

SIADH (graphic p. 371)

Water overload (e.g. polydipsia)

Severe hypothyroidism

Addison’s disease

Glucocorticoid deficiency

Cardiac failure

Cirrhosis

↑ potassium (>5mmol/L) ↓ potassium (<3.5mmol/L) ↑ sodium (>145mmol/L) ↓ sodium (<135mmol/L)

Renal failure

Drugs (e.g. ACE inhibitors, excess K+ therapy, K+ sparing diuretics)

Addison’s disease

Metabolic acidosis (DM)

Artefact (haemolysed sample)

Diuretics

Cushing’s syndrome/steroids

Vomiting and/or diarrhoea

Conn’s syndrome

Villous adenoma of the rectum

Purgative or liquorice abuse

Intestinal fistula

Renal tubular failure

Hypokalaemic periodic paralysis—intermittent weakness lasting <72h

Fluid loss without water replacement (e.g. diarrhoea, vomiting, burns)

Diabetes insipidus—suspect if large urine volume

Osmotic diuresis

Primary aldosteronism– suspect if ↑ BP, ↓ K+, alkalosis

Diuretic excess—especially thiazides

Renal failure or nephrotic syndrome

Diarrhoea/vomiting

Fistula

Rectal villous adenoma

Small bowel obstruction

CF (graphic p. 330)

Heat exposure

SIADH (graphic p. 371)

Water overload (e.g. polydipsia)

Severe hypothyroidism

Addison’s disease

Glucocorticoid deficiency

Cardiac failure

Cirrhosis

graphic Plasma potassium >6.5mmol/L needs urgent treatment.

Check it is not an artifact, e.g. due to haemolysis inside the bottle

Admit for investigation of cause and treatment

Tall tented T-waves; small P-wave; wide QRS complex becoming sinusoidal VF.

Low serum potassium (<3.5mmol/L). Presents with muscle weakness, hypotonia, cardiac arrhythmias, cramps, and tetany. Causes: see Table 14.2. If K+ >2.5mmol/L and no symptoms, give oral potassium supplement. graphic If the patient is taking a thiazide diuretic, hypokalaemia >3.0mmol/L rarely needs treating.

graphic Plasma potassium <2.5mmol/L needs urgent treatment—admit.

Small/inverted T-waves; prominent U-wave; prolonged P-R interval; depressed ST segment.

Low serum sodium (<135mmol/L). Rarely symptomatic in general practice. May present with signs of water excess— confusion, fits, ↑ BP, cardiac failure, oedema, anorexia, nausea, muscle weakness. Causes: see Table 14.2. Management: treat the cause. If unwell admit for investigation.

Excess serum sodium (>145mmol/L). Rare in general practice. Presentation: thirst, confusion, coma, fits, signs of dehydration—dry skin, ↓ skin turgor, postural hypotension, and oliguria if water deficient. Causes: see Table 14.2. Management: admit for investigation.

See Table 14.3. Renal disease may present with:

Haematuria (graphic p. 446) or proteinuria

UTI/pyelonephritis (graphic p. 448)

Outflow tract obstruction (graphic p. 454)

Nephrotic syndrome

Nephritic syndrome (graphic p. 439)

Renal failure (graphic p. 440)

Hypertension (graphic p. 248)

Table 14.3
Presentation of renal disease
GN Interstitial disease Vascular disease Outflow tract obstruction
AIN ATN CIN Small Large RVT

Nephrotic syndrome

++

0

0

0

(+)

0

+*

0

Nephritic syndrome

++

(+)

0

0

(+)

0

+

0

Acute kidney injury

+

+

++**

0

+

+

(+)

++

Chronic kidney disease

++

(+)

0

++

(+)

+

0

++

Pyelonephritis/UTI

0

0

0

0

0

0

+

+

Hypertension

(+)

(+)

0

(+)

(+)

(+)

0

+

GN: glomerulonephritis—graphic p. 442

CIN: chronic interstitial nephritis—graphic p. 442

ATN: acute tubular necrosis

RVT: renal vein thrombosis—graphic p. 443

AIN: acute interstitial nephritis—graphic p. 442

GN Interstitial disease Vascular disease Outflow tract obstruction
AIN ATN CIN Small Large RVT

Nephrotic syndrome

++

0

0

0

(+)

0

+*

0

Nephritic syndrome

++

(+)

0

0

(+)

0

+

0

Acute kidney injury

+

+

++**

0

+

+

(+)

++

Chronic kidney disease

++

(+)

0

++

(+)

+

0

++

Pyelonephritis/UTI

0

0

0

0

0

0

+

+

Hypertension

(+)

(+)

0

(+)

(+)

(+)

0

+

GN: glomerulonephritis—graphic p. 442

CIN: chronic interstitial nephritis—graphic p. 442

ATN: acute tubular necrosis

RVT: renal vein thrombosis—graphic p. 443

AIN: acute interstitial nephritis—graphic p. 442

*

Renal vein thrombosis is a complication not a cause of nephrotic syndrome.

**

Acute tubular necrosis is the most common cause of acute renal failure.

Normally detected with urine dipstick. If +ve, then repeat with another sample to exclude spurious results, and send sample for M,C&S to exclude UTI. Treat the cause where necessary. Causes:

UTI

Vaginal mucus

DM

↑ BP

Glomerulonephritis

Pyrexia

Pregnancy (and PET)

Postural proteinuria—2–5% adolescents; rare >30y

Haemolytic uraemic syndrome

CCF

SLE

Myeloma

Drugs, e.g. gold, penicillamine

Amyloid

Albuminuria in the range 30–200 mg/L. Not detectable with standard urine dipsticks. Special sticks are available for routine screening of high-risk groups, e.g. diabetics. Causes:

DM Microalbuminuria precedes frank proteinuria—graphic p. 356

Arteriopathy Microalbuminuria may be present in patients with CCF or ↑ BP. Presence of microalbuminuria predicts ↑ risk of MI, CVA, CCF, and cardiovascular and all-cause mortality

Other chronic illness Malignancy, COPD

Acute illness Inflammatory bowel disease, MI, acute pancreatitis, trauma, burns, meningitis

graphic p. 446

graphic p. 342

Proteinuria, hypoalbuminaemia, and oedema. Often associated with ↑ cholesterol. Causes:

Minimal change GN (90% children, 30% adults)

Membranous GN

Focal segmental glomerulosclerosis

Membrano-proliferative GN

DM

Amyloid

Neoplasia

Endocarditis

PAN

SLE

Sickle cell disease

Malaria

Drugs (penicillamine, gold)

Swelling of eyelids and face; ascites, peripheral oedema; urine froth due to protein. Nephrotic crisis: unwell with oedema, anorexia, vomiting, pleural effusions, and muscle wasting.

Urine—total protein:creatinine ratio (TPCR) >200mg/mmol; microscopy for red cells, casts; Blood—U&E, creatinine, eGFR, albumin (<25g/L), cholesterol, FBC, ESR.

Refer all suspected cases of nephrotic syndrome to a renal physician. Complications include:

Thromboembolism

Hypercholesterolaemia

Infection—especially pneumococcal; if persistent nephrotic syndrome, offer vaccination

Hypovolaemia and renal failure

Loss of specific proteins, e.g. transferrin (causes hypochromic anaemia, which is iron-resistant)

Central feature is blood and protein in the urine from glomerular inflammation.

Causes Glomerulonephritis (may occur after throat, ear, or skin infection with group A β-haemolytic streptococci), vasculitis.

Features Oliguria, haematuria and proteinuria, fluid retention, ↑ BP, uraemia, and ↑ creatinine

Management Refer suspected cases immediately to renal medicine

Risks Hypertensive encephalopathy, pulmonary oedema, acute kidney injury

Prognosis Excellent in children; in adults some proteinuria/urine sediment may persist. CKD is rare

Deposition of Ca2+ in the kidneys. X-ray— calcification. May cause symptoms of UTI or renal stones. Causes:

Medullary (95%). Hyperparathyroidism, distal renal tubular acidosis, medullary sponge kidney, idiopathic calciuria, papillary necrosis, oxalosis

Cortical Serious renal disease or chronic GN

graphic p. 448

graphic p. 248

Distressing desire to pass something per urethra that will not pass, e.g. stone.

UK National Kidney Federation graphic 0845 601 02 09 graphic  www.kidney.org.uk

Urine output <400mL/24h. Causes: dehydration, cardiac failure, ureteric obstruction, renal failure.

Also known as acute renal failure (ARF). ↓ renal function over hours/days ± oliguria/anuria. Refer immediately if acute ↑ in urea/creatinine or ↓ in eGFR (to <60mL/min/1.73m2 if normal in last 3mo, or ↓ of >15% over 5d). Causes: acute tubular necrosis (80%—due to acute circulatory compromise); renal tract obstruction (5%); GN.

Also known as chronic renal failure (CRF). Slow ↓ renal function over months/years. Causes:

DM

↑ BP

SLE

↑ Ca2+

Urinary tract obstruction

Chronic pyelonephritis

Polycystic kidneys

Glomerulonephritis

Renovascular disease

Interstitial nephritis

Amyloid

Myeloma

PAN

History FH (polycystic kidneys); UTI; drugs (especially analgesics)

Symptoms Often no symptoms. Nausea, anorexia, lethargy, itch, nocturia, impotence. Later: oedema, dyspnoea, chest pain (from pericarditis), vomiting, confusion, fits, hiccups, neuropathy, coma

Signs Pallor, ‘lemon tinge’ to skin, pulmonary/peripheral oedema, pericarditis, pleural effusions, metabolic flap, ↑ BP, retinopathy

Urine M, C&S, microalbuminuria, albumin:creatinine ratio (ACR) or TPCR, RBCs, glucose

Blood U&E, creatinine, eGFR, glucose, Ca2+, PO4   urate, protein, FBC, ESR, serum electrophoresis.

Renal tract USS If progressive or advanced (stage 4/5) disease, refractory ↑ BP, haematuria, or palpable bladder/lower urinary tract signs

—see Table 14.4

Treat reversible causes. Stop/avoid nephrotoxic drugs (e.g. NSAIDs). Consider ↓ dose of other drugs as excretion/metabolism may be impaired. graphic Metformin should be stopped if eGFR <30 mL/min/1.73m2

Monitor Cr/eGFR and dipstick urine (see Table 14.4). If proteinuria, send urine for M,C&S. If no infection but proteinuria persists, test TPCR or ACR in early morning urine. If TPCR >100mg/mmol or ACR >70mg/mmol, refer

Manage CVD risk. Monitor/treat ↑ cholesterol and ↑ BP (target 130/80—ACE/ARB is first-line). Treat DM. Smoking cessation

Monitor and treat anaemia and renal bone disease

Table 14.4
Classification of chronic kidney disease
Stage GFR mL/min Description Prevalence % Complications Testing frequency

1

>90

Kidney damage with normal or ↑ GFR

3.3

↑ BP

Yearly

2

60–89

Kidney damage with mild ↓ GFR

3

↑ BP

Yearly

3A

45–59

Moderate ↓ GFR

4.3

↑ BP, Ca2+ and PO4   changes, renal anaemia, LVF

6mo

3B

30–44

4

15–29

Severe ↓ GFR

0.2

As above + ↑ K+

3–6mo

5

<15

Established renal failure

0.2

As above + salt/ water retention

6wk

Stage GFR mL/min Description Prevalence % Complications Testing frequency

1

>90

Kidney damage with normal or ↑ GFR

3.3

↑ BP

Yearly

2

60–89

Kidney damage with mild ↓ GFR

3

↑ BP

Yearly

3A

45–59

Moderate ↓ GFR

4.3

↑ BP, Ca2+ and PO4   changes, renal anaemia, LVF

6mo

3B

30–44

4

15–29

Severe ↓ GFR

0.2

As above + ↑ K+

3–6mo

5

<15

Established renal failure

0.2

As above + salt/ water retention

6wk

graphic If sudden ↓ in renal function (↓ eGFR of >15% between tests or >5mL/min/1.73m2 in <1y or >10mL/min/1.73m2 in <5y) suspect infection, dehydration, uncontrolled ↑ BP, metabolic disturbance (e.g. ↑ Ca2+), obstruction, nephrotoxins (e.g. drugs). If unable to find cause or treatment does not ↑ renal function, refer.

To a renal physician if:

Stage 4/5 CKD

Significant proteinuria (TPCR >100mg/mmol or ACR >70mg/mmol)

Sudden ↓ in eGFR (>15%) and UTI excluded

Persistent microscopic haematuria and <50y (to urologist if >50y)

Functional consequences of CKD, i.e. anaemia (<11g/dL), bone disease, or refractory hypertension (>140/90 on 4 agents)

80 new patients/million population/y. Irreversible. Dialysis starts when GFR is 10–15% normal. Dialysis is needed lifelong unless a kidney transplant becomes available. Refer back to the renal unit managing the patient if you have any problems.

Blood flows opposite dialysis fluid and substances are cleared along a concentration gradient across a semi-permeable membrane. Problems: pulmonary oedema; infection (HIV, hepatitis, bacteria); U&E imbalance; BP ↓ or ↑; problems with vascular access; dialysis arthropathy (especially shoulders and wrists); aluminium toxicity; time.

A permanent catheter is inserted into the peritoneum via a subcutaneous tunnel. ~2L dialysis fluid is introduced and kept in the peritoneum. This is changed for fresh fluid up to 5x/d at home. Does not tie the patient to a dialysis machine. Problems: peritonitis; catheter blockage (refer as an emergency); weight ↑; poor DM control; pleural effusion; leakage.

2° anaemia due to ↓ kidney erythropoietin production is universal amongst people with ESRD. Exclude other causes. Recombinant erythropoietin is given if Hb <10.5g/dL (75%).

Transplanted kidneys are usually sited in an iliac fossa. 5y graft survival is ~88% for adults. Closer genetic matches have better survival rates. Problems:

Rejection

Persistent ↑ BP and ↑ cholesterol

Atherosclerosis (5x ↑ risk MI death)

Renal artery stenosis at 3–9mo post-op

Obstruction at ureteric anastmosis

Ciclosporin-induced nephropathy

Infection 2° to immunosuppression

Malignancy from immunosuppressants

NICE CKD (2008) graphic  www.nice.org.uk

Important cause of renal failure. Associated with inflammatory cell infiltration of the renal interstitium/tubules. Causes:

Acute interstitial nephritis Idiosyncratic reaction to drugs (penicillin, NSAIDs, furosemide) or infection (Staphylo- or Streptococcus)

Chronic interstitial nephritis Idiopathic (most), drugs, sickle-cell disease, analgesic nephropathy.

Presents with AKI/CKD, raised temperature, arthralgia, eosinophilia. Patients with AKI have good prognosis. Those with CKD have gradual deterioration over time.

graphic p. 356

Caused by prolonged heavy use of analgesics (including NSAIDs). Presents with an interstitial nephritis-like picture. Associated with ↑ incidence of UTI. Carcinoma of the renal pelvis is a rare complication. Investigate promptly if the patient develops haematuria.

Types and presentation—see Table 14.5. Refer all suspected cases urgently to a renal physician. Terminology:

Focal Some glomeruli affected

Diffuse All glomeruli affected

Segmental Part of each glomerulus affected

Global All of each glomerulus affected

Table 14.5
Types of glomerulonephritis
Type Features

Minimal change

Most common in children. Presents with nephrotic syndrome

Membranous

30% adult nephrotic syndrome. Underlying malignancy in 10% of adults. 1 in 3 enter remission, 1 in 3 are proteinuric, 1 in 3 progress to ESRD

Focal segmental glomerulosclerosis

Proteinuria or nephrotic syndrome. May be associated with heroin abuse. >50% progress to CKD

Membrano-proliferative

50% present as nephrotic syndrome. Associations—endocarditis, C3 nephritic factor (autoantibody), hepatitis C, measles

Proliferative

Presents with nephritic syndrome. Classically seen 2wk after Strep. infection. Prognosis is excellent

IgA disease (Berger’s disease)

Causes recurrent haematuria in young men. A similar histological picture is seen in Henoch–Schönlein purpura (graphic p. 526). 30% progress to ESRD

Rapidly progressive/crescentic

Presents with haematuria, oliguria, ↑ BP, acute renal failure. Vigorous treatment may preserve renal function. Causes: anti-glomerular basement membrane disease (Goodpasture’s disease), Wegener’s granulomatosis, Henoch–Schönlein purpura

Type Features

Minimal change

Most common in children. Presents with nephrotic syndrome

Membranous

30% adult nephrotic syndrome. Underlying malignancy in 10% of adults. 1 in 3 enter remission, 1 in 3 are proteinuric, 1 in 3 progress to ESRD

Focal segmental glomerulosclerosis

Proteinuria or nephrotic syndrome. May be associated with heroin abuse. >50% progress to CKD

Membrano-proliferative

50% present as nephrotic syndrome. Associations—endocarditis, C3 nephritic factor (autoantibody), hepatitis C, measles

Proliferative

Presents with nephritic syndrome. Classically seen 2wk after Strep. infection. Prognosis is excellent

IgA disease (Berger’s disease)

Causes recurrent haematuria in young men. A similar histological picture is seen in Henoch–Schönlein purpura (graphic p. 526). 30% progress to ESRD

Rapidly progressive/crescentic

Presents with haematuria, oliguria, ↑ BP, acute renal failure. Vigorous treatment may preserve renal function. Causes: anti-glomerular basement membrane disease (Goodpasture’s disease), Wegener’s granulomatosis, Henoch–Schönlein purpura

Presents as CKD or one of its complications. Probably arises from UTIs, vesico-ureteric reflux and consequent renal scarring in childhood (graphic p. 878). Refer to a renal physician.

graphicHaemolytic uraemic syndrome

Most common cause of AKI in children. Usually follows gastroenteritis. Due to E. coli toxin. Have a high index of suspicion in any child with bloody diarrhoea. Occasionally occurs without diarrhoea. Other features:

Dehydration

Oliguria (though may be polyuria)

Proteinuria/haematuria

Haematological features—anaemia, thrombocytopenia ± purpura

CNS symptoms—irritability, drowziness, ataxia, coma

↑ BP (associated with non-diarrhoeal disease)

Management

Admit for specialist care—often including dialysis. If associated with diarrhoeal illness, >80% make full recovery. Mortality is 1.8%. Poor prognostic indicators are age >5y at onset and dialysis for >2wk. Disease in the absence of diarrhoea has poorer prognosis.

Autosomal dominant disease (1:1,000). Cysts develop in the kidney causing gradual ↓ in renal function. Common cause of CKD. Presents with haematuria, UTI, abdominal mass (30% have cysts in the liver/pancreas too), lumbar/abdominal pain, and/or ↑ BP. May be associated with mitral valve prolapse and SAH/berry aneurysms. USS shows large kidneys with multiple cysts. Refer to a renal physician if CKD 3–5. Treat infections and ↑ BP. Check family members (though cysts may not be seen <30y). 45% progress to ESRD by 60y.

Developmental abnormality of the medullary pyramids of the kidney, characterized by dilatation of the renal collecting tubules. ♂ > ♀. There may be a family history. Most are asymptomatic and the condition is an incidental finding. If symptomatic, presents with UTIs, renal stones, haematuria. Refer if symptomatic. Usually prognosis is very good and most require no treatment.

Causes: nephrotic syndrome (15–20% develop RVT); membranous GN (30%); acute dehydration. Presentation varies from no symptoms to severe pain and loin tenderness. Suspect in at-risk individuals if unexplained loss of renal function and RBCs in urine. Refer to a renal physician for further investigation.

Causes: atheroma, fibromuscular hyperplasia (in the young). Presents with ↑ BP (may be severe or drug-resistant); vascular disease elsewhere; abdominal bruit; ↑ Cr, ↓ eGFR, and proteinuria. If bilateral or extensive, renal failure may be precipitated by dehydration, ↓ BP, or drugs (ACE/ARB initiation; NSAIDs). Refer to a renal physician (if diagnosis is unsure) or vascular surgeon (if diagnosis is known).

X-linked or autosomal inherited disease. Congenital sensorineural deafness, haematuria, proteinuria, and renal failure. Associated with lens abnormalities, platelet dysfunction, and ↑ BP. Causes ESRD by third decade in ♂; ♀ rarely develop ESRD. Renal failure does not recur after transplantation. A.C. Alport (1880–1959)—South African physician.

UK National Kidney federation graphic 0845 601 02 09 graphic  www.kidney.org.uk

12% of ♂ and 3% of ♀ will develop a renal stone at some point; peak age 20–50y. Symptoms are not dependent on size of the stone.

Family history—↑ risk x3. Specific conditions: X-linked nephrolithiasis, cystinuria, hyperoxaluria

Anatomically abnormal kidneys, e.g. horseshoe kidney, medullary sponge kidney

Metabolic disease, e.g. gout, hypercalcaemia/hypercalciuria, cystinuria, renal tubular acidosis or other acidosis (ileostomy, adenomatous polyp), oxaluria, aminoaciduria

Dehydration

Immobilization

Chronic UTI

Acetazolamide, allopurinol, aspirin, steroids, indinavir, nelfinavir, loop diuretics, probenecid, quinolones, sulfonamides, theophylline, thiazides, triamterene, antacids, calcium/vitamin D supplements, high-dose vitamin C.

Usually presents with pain ± nausea/vomiting. Location and type of pain gives clues about the site of the stone:

Loin pain—kidney stone

Renal colic—ureteric stone

Strangury—bladder stone

Interruption of flow—urethral stone

Symptoms Severe pain with waves of ↑ severity. Usually starts abruptly as flank pain which then radiates around the abdomen to the groin as stone progresses down the ureter. May be referred to testis/tip of penis in men or labia majora in women

Signs Patient is obviously in pain—usually unable to sit still and keeps shifting position to try to get comfortable (in contrast to peritonitis where patients tend to keep still). May be pale and sweaty. May be mild tenderness on deep abdominal palpation or loin tenderness, though often minimal signs. If fever suspect infection

UTI, haematuria, retention, renal failure (rare).

Pyelonephritis; ruptured AAA; cholecystitis; pancreatitis; appendicitis; diverticulitis; obstruction; strangulated hernia; testicular torsion; pethidine addiction.

Dipstick urine if possible. Absence of RBCs does not exclude renal colic but consider alternative diagnosis.

Stones usually pass spontaneously. Give pain relief (diclofenac 75mg IM/100mg PR) ± antiemetic. Consider admission to hospital if:

Fever

Oliguria

Poor intake of fluid

Pregnant

Lives alone

Uncertain diagnosis

Analgesia ineffective /short-lived

Symptoms >24h

Encourage ↑ fluid intake; sieve urine for stones. Monitor/review pain relief and for complications.

Can wait until the next working day and include:

Blood U&E, creatinine, eGFR, Ca2+, PO4  3–, alkaline phosphatase, uric acid, albumin

Urine M,C&S; RBCs. Consider checking ‘spot’ test for urine cystine, and TPCR, Ca2+, PO4  3–, uric acid, and sodium excretion

Radiology X-ray of kidneys, ureters, and bladder—90% of renal stones are radio-opaque—only urate and xanthine stones are radio-transluscent; renal tract USS

50% recur in 5–7y. Give general advice on prevention of stones (see Table 14.6). If investigations show any loss of renal function, renal obstruction, or remaining stones—refer to urology. Dependent on composition of stones, give dietary advice/refer to dietician (see Table 14.6).

Table 14.6
Prevention of renal stones
Type of stone Preventative measures

All types

↑ fluid intake (>2–2.5L/24h), especially in hot weather; ↓ weight if obese; ↓ animal protein and ↑ fruit/vegetables in diet; ↓ salt intake

Calcium oxalate

Urinary alkalinization with potassium citrate; avoid chocolate, tea, rhubarb and spinach, nuts, beans, beetroot; ↓ citrus fruits; bendroflumethiazide 2.5mg od may help if hypercalciuria; hyperoxaluria is treated with pyridoxine

Calcium phosphate

Low Ca2+ diet; avoid vitamin D supplements. Bendroflumethiazide 2.5mg od may help if hypercalciuria

Staghorn/triple phosphate (calcium, magnesium, and ammonium)

Associated with UTI due to Proteus species and urinary stasis, e.g. due to anatomical abnormality. Treat UTI with antibiotics

Urate

Avoid beer as has uricosuric effect; allopurinol; urinary alkalinization with potassium citrate (pH >6.5)

Cystine

Urinary alkalinization with potassium citrate

Type of stone Preventative measures

All types

↑ fluid intake (>2–2.5L/24h), especially in hot weather; ↓ weight if obese; ↓ animal protein and ↑ fruit/vegetables in diet; ↓ salt intake

Calcium oxalate

Urinary alkalinization with potassium citrate; avoid chocolate, tea, rhubarb and spinach, nuts, beans, beetroot; ↓ citrus fruits; bendroflumethiazide 2.5mg od may help if hypercalciuria; hyperoxaluria is treated with pyridoxine

Calcium phosphate

Low Ca2+ diet; avoid vitamin D supplements. Bendroflumethiazide 2.5mg od may help if hypercalciuria

Staghorn/triple phosphate (calcium, magnesium, and ammonium)

Associated with UTI due to Proteus species and urinary stasis, e.g. due to anatomical abnormality. Treat UTI with antibiotics

Urate

Avoid beer as has uricosuric effect; allopurinol; urinary alkalinization with potassium citrate (pH >6.5)

Cystine

Urinary alkalinization with potassium citrate

May be 1° (autosomal recessive condition) or 2° to gut resection/malabsorption or dietary excess of spinach or vitamin C. Take specialist advice on management. There are two types of 1° hyperoxaluria:

Type 1 hyperoxaluria Calcium oxalate stones are widely distributed throughout the body. Presents as renal stones and nephrocalcinosis in children. 80% have chronic renal failure in <20y.

Type 2 hyperoxaluria More benign but less common—nephrocalcinosis but no chronic renal failure.

Most common aminoaciduria. Usually presents with stones at age 10–30y. Urine: cystine ↑, ornithine ↑, arginine ↑, lysine ↑. Take specialist advice on management.

graphic p. 366

graphic Hypercalciuria may occur without hypercalcaemia and is found in ~ 80% of patients with calcium oxalate stones.

Blood in the urine. Causes—see Table 14.7.

May be frank (visible) or microscopic (up to 20% population).

Investigate all cases of haematuria further

Check MSU for M,C&S, and blood for U&E, creatinine, and eGFR. Free Hb and myoglobin make urine test sticks +ve in absence of red cells

Urine discoloration can result from beetroot ingestion, porphyria, or rifampicin

If cause is identified (e.g. sample taken when menstruating, UTI)—repeat the check for blood in urine once treated/resolved

Refer if no cause is found. Rapid access one-stop clinics are now operated in most areas

Table 14.7
Causes of haematuria

Kidney

Stones

Tumour

Infection

Glomerulonephritis

Ureter

Stones

Tumour (rare)

Bladder

UTI

Stones

Tumour

Chronic inflammation

Prostate

Prostatitis

Tumour

Urethral inflammation

Kidney

Stones

Tumour

Infection

Glomerulonephritis

Ureter

Stones

Tumour (rare)

Bladder

UTI

Stones

Tumour

Chronic inflammation

Prostate

Prostatitis

Tumour

Urethral inflammation

Presence of white cells in the urine in the absence of UTI. Causes:

Inadequately treated UTI

Appendicitis

Calculi

Prostatitis

Bladder tumour

Renal TB

Papillary necrosis

UTI with failure to culture organism

Interstitial nephritis or cystitis

Polycystic kidney

Chemical cystitis, e.g. due to radiotherapy

Initially repeat with clean-catch MSU. If finding persists refer to urology.

Management of haematuriaN
Urgent referral

Patients:

Of any age with painless macroscopic haematuria

Aged ≥40y with recurrent/persistent UTI associated with haematuria

Aged ≥50y with unexplained microscopic haematuria

With an abdominal mass identified clinically or on imaging that is thought to arise from the urinary tract

Non-urgent referral

Patients <50y with microscopic haematuria. If proteinuria, ↑ serum creatinine, or ↓ eGFR, refer to a renal physician. Otherwise refer to urology.

graphic In male patients with symptoms suggestive of UTI and macroscopic haematuria, diagnose and treat the infection before considering referral. If infection is not confirmed, refer urgently.

graphic p. 906

Incidence: 10,540 cases/y in the UK; ♂:♀ ≈5:2. Transitional cell carcinoma (TCC) is most common in the UK—squamous cell carcinoma (SCC) is most common worldwide. Risk factors:

Smoking (50% male cases are attributable to smoking)

Aromatic amine exposure (textile or rubber industries)

Schistosomiasis (SCC)

Stasis of urine

Chronic UTI

Haematuria—painless or painful. Less commonly:

Recurrent UTI

Frequency

Loin pain

Pelvic pain

Bladder outflow obstruction

MSU—excludes UTI and detects sterile pyuria and/or microscopic haematuria.

Refer urgently to urology to be seen in <2wk. Treatment depends on stage at diagnosis—see Table 14.8.

Table 14.8
Stage of bladder cancer, treatment, and prognosis
Stage Description and treatment Prognosis

T1 (80%)

Disease confined to mucosa/submucosa. Treated with transurethral resection of the tumour (TURBT) ± single intravesical chemotherapy treatment. Follow-up is with regular cystoscopy

Very good—most die from other causes

T2

Invasion into connective tissue surrounding the bladder. Treatment is with TURBT ± radiotherapy. Follow-up as for T1

60% survive 5y

T3

Invasion through the muscle into the fat layer. Radical cystectomy and/or radiotherapy

40–50% 5y survival

T4

Spread beyond the bladder. TURBT for local symptoms. Palliative radiotherapy ± chemotherapy. Palliative care

20–30% 5y survival—less if para-aortic nodes are involved

Stage Description and treatment Prognosis

T1 (80%)

Disease confined to mucosa/submucosa. Treated with transurethral resection of the tumour (TURBT) ± single intravesical chemotherapy treatment. Follow-up is with regular cystoscopy

Very good—most die from other causes

T2

Invasion into connective tissue surrounding the bladder. Treatment is with TURBT ± radiotherapy. Follow-up as for T1

60% survive 5y

T3

Invasion through the muscle into the fat layer. Radical cystectomy and/or radiotherapy

40–50% 5y survival

T4

Spread beyond the bladder. TURBT for local symptoms. Palliative radiotherapy ± chemotherapy. Palliative care

20–30% 5y survival—less if para-aortic nodes are involved

Clear cell adenocarcinoma of renal tubular epithelium. Incidence: 9,300 cases/y in the UK. Typical age: 50y. ♂:♀ ≈1.5:1. Spread can be local or haematogenous (bone, liver, lung—causes cannon ball metastases seen on CXR).

Haematuria

Loin pain

Abdominal mass

Anaemia

Left varicocele

Occasionally night sweats

Urine: RBCs. Blood:↑ PCV (2%), anaemia, hypercalcaemia. Radiology: USS, CXR.

Refer to urology urgently to be seen in <2wk. Treatment includes surgery where possible ± chemotherapy, radiotherapy, and/or biological therapy. Overall 50% 5y survival.

NICE Referral guidelines for suspected cancer (2005) graphic  www.nice.org.uk

Cancer Research UK graphic 0808 800 4040 graphic  www.cancerhelp.org.uk

Macmillan Cancer Support graphic 0808 808 0000 graphic  www.macmillan.org.uk

Urinary tract infection (UTI) is one of the most common conditions seen in general practice, accounting for up to 6% of consultations (one case/average surgery). ♀ > ♂. 20% of women at any time have asymptomatic bacteriuria and 20–40% of women will have a UTI in their lifetime.

E. coli (>70%), Proteus spp., Pseudomonas spp., streptococci, staphylococci.

Prior infection

DM

Stones

Pregnancy

Dehydration

GU instrumentation

Catheterization

↓ oestrogen (menopause)

Sexual intercourse

Diaphragm use

GU malformation

Urinary stasis (e.g. obstruction)

Delayed micturition (e.g. on long journeys)

Cystitis Frequency, dysuria, urgency, strangury, low abdominal pain, incontinence of urine, acute retention of urine, cloudy or offensive urine, and/or haematuria

Pyelonephritis Loin pain, fever, rigors, malaise, vomiting, and/or haematuria

Painful micturition resulting from urethral or bladder inflammation. Causes: UTI, urethral syndrome, inflammation (e.g. interstitial cystitis, radiation-induced cystitis), intravesical lesion (tumour, stone), atrophy (menopause).

Passage of urine more often than usual. Causes:

UTI

Urethral syndrome

Detrusor instability

Inflammation (e.g. interstitial cystitis)

Fibrosis (e.g. post-radiotherapy)

Atrophy (menopause)

Neurogenic bladder (e.g. MS)

External pressure (e.g. pregnancy, fibroids)

Bladder tumour or stone

Enlarged prostate

Drugs (e.g. diuretics)

DM

Excessive fluid intake

Habit

If uncomplicated UTI in an otherwise healthy woman, test urine with a leucocyte and nitrite dipstick. If +ve, treat for UTI. Reasons to send MSU for M,C&S:

Unresolved infection after antibiotics

Recurrent UTI

Uncatheterized man with UTI

Catheterized man or woman with symptomatic UTI

Child—graphic p. 878

Pregnant woman—graphic p. 812

Suspected pyelonephritis

Haematuria—microscopic or macroscopic; always investigate further (graphic p. 446)

graphic For women with severe or 3 or more symptoms of cystitis, start treatment without urine dipstick. Take MSUs prior to starting antibiotics—send to the laboratory fresh. Consider chlamydia infection in young men or women with symptoms of UTI.

Consider further investigation with blood tests (U&E, Cr, eGFR, and/or PSA if >40y and ♂) and/or radiology (e.g. renal tract USS, KUB) if:

UTI in a man

UTI in a child (graphic p. 879)

Recurrent UTI in a woman

Pyelonephritis

Unclear diagnosis (e.g. persisting symptoms but negative MSU)

Unusual infecting organism

Sterile pyuria (graphic p. 446)

graphic p. 453

graphic p. 812

graphic p. 878

↑ fluid intake (>3L/24h). Alkalinize urine (e.g. potassium citrate solution) to ease symptoms

Prescribe oral antibiotics, e.g. trimethoprim 200mg bd (80% organisms are sensitive). Use a 3d course for women with uncomplicated UTI, a 7d course for men, patients with GU malformations or immunosuppression, relapse (same organism) or recurrent UTI (different organism). Use a 7d course of a quinolone (e.g. ciprofloxacin 500mg bd) for patents with pyelonephritis

Refer to urology if any abnormalities are detected on further investigation or unable to resolve symptoms. Admission is rarely needed

Reinfection after successful treatment of infection (90%) or relapse after inadequate treatment.

General advice Advise patients to urinate frequently; ↑ fluid intake; double void (i.e. go again after 5–10min) and void after intercourse. graphic Efficacy of cranberry juice is controversial

Prophylactic antibiotics Consider prescribing either post-coitally (e.g. nitrofurantoin 50mg stat) or continuously (trimethoprim 100mg nocte or nitrofurantoin 50mg nocte)

Men with BPH Finasteride or dutasteride and/or doxazosin ↓ incidence of UTI

HRT Topical oestrogen ↓ recurrent UTI in women of all agesR

Vaccines Results of large-scale trials are awaited

graphic p. 456

graphic p. 442

Symptoms of cystitis with −ve MSU. Unknown cause. Associated with cold, stress, nylon underwear, CHC, and intercourse. Advise fluids ++ and to wear cotton underwear. Consider changing/stopping CHC or trying topical oestrogen if post-menopausal. Tetracyclines (e.g doxycycline 100mg bd for 14d) or azithromycin (500mg od for 6d)R are helpful in some. If not settling, refer to urology. Urethral dilatation/massage may be helpful.

Predominantly middle-aged women. Can cause fibrosis of the bladder wall. Main symptoms—frequency, urgency, and pelvic/suprapubic pain especially when the bladder is full. Often misdiagnosed as recurrent UTI. MSU—no bacteriuria. Refer to urologist for confirmation. There is no satisfactory treatment, though antispasmodics, amitriptyline, and bladder stretching under GA may help some patients.

Involuntary loss of urine which is objectively demonstrable and a social or hygienic problem. 1 in 3 with incontinence consult at outset, 1 in 3 consult later, 1 in 3 suffer in silence. Opportunistic questioning can identify sufferers.

Frequency of complaint

Volume passed

Degree of incapacity

Whether occurs with standing/coughing/sneezing

Urgency/dysuria/frequency of micturition

Past obstetric and medical history

Medication

Mobility and accessibility of toilets

Abdominal including DRE—enlarged bladder, masses, loaded colon, faecal impaction, anal tone

Pelvic—prolapse, atrophy, neurological deficit, retention of urine, and pelvic masses

Intake/output diary (at least 3d, including working and leisure days)—evaluates problem and benchmark for progress—record drinks and passage of urine; urine—RBCs, MC&S; consider blood for U&E, eGFR, FBC, FBG/HbA1c if renal impairment/DM is suspected.

Diuretics, antihistamines, anxiolytics, α-blockers, sedatives and hypnotics, anticholinergic drugs, TCAs.

graphic 30% have a mixed pattern. Treat according to dominant symptom. Try general measures before referring to urology/gynaecology or for further investigations (see Table 14.9).

Table 14.9
Referral for incontinence problems

Specialist continence advisor/DN

Advice on aids or appliances

Advice on primary care management

Patient support

Urodynamic studies

If type of incontinence is uncertain

Atypical features of incontinence

After unsuccessful surgery

If a neurological problem is suspected

Gynaecology or urology opinion

GP management has failed

Severe symptoms and/or pain

Recurrent UTI

Concomitant gynaecological problems (e.g. prolapse)

Concomitant urological problems (e.g. chronic retention, prostate abnormality on rectal examination)

Failed incontinence surgery

Pelvic radiotherapy

Vesico-vaginal fistula

Haematuria graphic p. 446

Specialist continence advisor/DN

Advice on aids or appliances

Advice on primary care management

Patient support

Urodynamic studies

If type of incontinence is uncertain

Atypical features of incontinence

After unsuccessful surgery

If a neurological problem is suspected

Gynaecology or urology opinion

GP management has failed

Severe symptoms and/or pain

Recurrent UTI

Concomitant gynaecological problems (e.g. prolapse)

Concomitant urological problems (e.g. chronic retention, prostate abnormality on rectal examination)

Failed incontinence surgery

Pelvic radiotherapy

Vesico-vaginal fistula

Haematuria graphic p. 446

Manipulate fluid intake: amount, type (avoid tea, coffee, alcohol), timing

Promote weight ↓

Alter medication, e.g. timing of diuretics

Treat UTI and chronic respiratory conditions

Avoid constipation

Consider HRT (topical or systemic) for oestrogen deficiency

Consider scheduled voiding if cognitive deficit

graphic p. 452

graphic p. 914

Symptoms Small losses of urine without warning throughout the day related to coughing/exercise

Causes Prostatectomy; childbirth; deterioration of pelvic floor muscles/nerves

Treatment Pelvic floor exercises (graphic p. 841) continued >3mo help 60% (taught by physiotherapists/continence advisors; leaflets available)—may be assisted by vaginal cones and/or electrical stimulation. Mechanical devices (e.g. Contrelle Activguard®, FemSoft®) may help.

Detrusor instability or hyperreflexia cause the bladder to contract unintentionally

Symptoms Frequency, overwhelming desire to void (often precipitated by stressful event), large loss, nocturia

Causes Idiopathic, neurological problems (stroke, MS, DM, spinal cord injury, dementia, PD), local irritation (bladder stones, bladder cancer, infection), obstruction (BPH), surgery (TURP)

Treatment Bladder training—resist the urge to pass urine for ↑ periods. Start with an achievable interval based on diary evidence and ↑ slowly—continue for >6wk. If bladder training is ineffective, try oxybutinin first-lineN (alternatives: darifenacin, solifenacin, tolteridone, trospium). Spontaneously remits/relapses, so reassess every 3–4mo

Constant dribbling loss day and night. Causes: BPH, prostate cancer, urethral stricture, faecal impaction, neurological (LMN lesions), side effect of medication. Treatment is aimed at relieving the obstruction (graphic p. 454).

Communication between bladder and the outside—normally through the vagina. Results in constant dribbling loss day and night. Refer to gynaecology/urology. Causes: congenital, malignancy, complication of surgery.

No urological problem. Caused by other factors, e.g. inaccessible toilets/immobility, behavioural problems, cognitive deficit. Treat the cause.

European Association of Urology Guidelines on urinary incontinence (2012) graphic  www.uroweb.org

NICE Urinary incontinence (2006) graphic  www.nice.org.uk

Bladder and Bowel Foundation graphic 0845 345 0165 graphic  www.bladderandbowelfoundation.org

Many different types. DNs or continence advisors are best aware of those available via the NHS locally. They are not available on FP10 and supplied by local NHS Trusts on a ‘daily allowance’ basis. This varies across the country.

Absorb 1–4L of urine. Good laundry facilities are needed. If left wet can cause skin breakdown. Available via NHS Trusts.

Can be prescribed on NHS prescription. Approved appliances are listed in part IXB of the UK Drug Tariff. Used for men who have intractable incontinence and who are highly physically dependent, do not have urine retention and do not require an internal catheter. Assessment and fitting by a DN or continence adviser is essential.

Used in association with a drainage bag. Sheaths may be non-adhesive, self-adhesive or attached with adhesive strips. Adhesive sheaths can last several days but daily changing is recommended. Replace non-adhesive sheaths 2–3x/d (some are reusable).

Include ↑ susceptibility to UTI, sores on penis, and skin irritation due to the adhesive.

Can be prescribed on NHS prescription. Approved appliances are listed in part IXA of the UK Drug Tariff.

Only use catheters in patients who have:

Urinary retention or neurogenic bladder dysfunction

Severe pressure sores

Inoperable obstructions that prevent the bladder emptying

Terminal illness

Housebound without adequate carer support

Only long-term Foley catheters are suitable for use in primary care. They last 3–12wk.

Unless specified a 12 or 14Ch catheter is supplied. Use the smallest diameter of catheter that drains urine effectively. Catheters >16Ch are more likely to cause bypassing of urine around the catheter and urethral strictures.

Men require longer catheters than women. Specify ‘male’ or ‘female’ on the prescription.

10mL balloons are supplied unless specified otherwise. Pre-filled catheters contain sterile water which inflates the retaining balloon with water. They are more expensive but quicker to insert and there are no costs for syringes or sterile water.

graphic p. 455

Usually attached to a leg bag, although catheter valves are also available allowing the patient to use his/her bladder as a urine reservoir. The valve must be released every 3–4h to drain out the urine.

Leakage Check no constipation, check catheter not blocked, try smaller gauge catheter

Infection 90% develop bacteriuria <4wk after insertion. Always confirm suspected UTI with MSU—only treat if symptomatic or Proteus species grown. May prove difficult to eliminate. No good evidence bladder instillations help

Encrustation (50%) Deposition of minerals and other materials from the urine onto the catheter. Worse if there is infection with Proteus species. May cause catheter blockage or pain changing the catheter. Check pH of urine regularly in patients with problems. Citric acid patency solutions may help if pH >7.4, or a daily dose of vitamin C

Inflammation Results from physical presence of a catheter in the urethra. Exacerbated by encrustation and infection. There is no easy solution—try a different brand catheter (e.g. hydrogel catheter rather than silicone)

Blockage Change catheter. The interval of routine changes should be altered if there is regular blockage towards the end of the life of a catheter

Patient inserts a catheter into his/her bladder 4–5x/d to drain urine. ↓ problems of infection and blockage. Useful for neurological bladder dysfunction. Types:

Reusable silver or stainless steel

Reusable PVC—washed and reused for 1wk. Usually supply 5/mo

Single use—need 125–150/mo. Expensive. Only use on consultant advice

Can be prescribed on NHS prescription. Approved appliances are listed in part IXB of the UK Drug Tariff.

Leg bags Drainable bags last 5–7d. Usually 500/750mL. Larger capacity bags are too heavy for mobile patients. A variety of attachment systems are available on prescription. Long tubes are needed to wear a bag on the calf

Night drainage bags Connect to night bag attachment of day bags Single use, disposable non-draining bags are recommended. Bag hangers are not available on NHS prescription

graphic p. 915

NHSBSA Electronic drug tariff graphic  www.nhsbsa.nhs.uk/prescriptions

Bladder and Bowel Foundation graphic 0845 345 0165 graphic  www.bladderandbowelfoundation.org

(See Figure 14.1) Obstruction may be unilateral (kidney, pelvi-ureteric junction, or ureter) or bilateral (bladder, urethra, prostate). Unilateral obstruction may present late if the other kidney remains functioning. Suspect if loin ache worsened by drinking. Confirm with USS and refer to urology. Obstructing lesions may be in the lumen (e.g. stones) in the wall (e.g. tumours) or impinging from outside (e.g. retroperitoneal fibrosis).

 Causes of urinary tract obstruction
Figure 14.1

Causes of urinary tract obstruction

Sudden inability to pass urine → lower abdominal discomfort with inability to keep still. Differentiate from AKI. ♂ > ♀. Risk factors: age >70y; symptoms of prostatism/poor urinary stream.

Prostatic obstruction (82%); constipation; alcohol; drugs (anticholinergics, diuretics); UTI; operation (e.g. hernia repair). Rarer causes: urethral stricture; clot retention; spinal cord compression; bladder stone.

Abdomen—palpable bladder; DRE—enlarged ± irregular prostate; perineal sensation to exclude neurological cause.

MSU to exclude infection. Blood for U&E, Cr, and eGFR. Only investigate if catheterizing in the community.

Catheterize (record initial volume drained) or refer to urology for catheterization—local policies vary. Treat infection. Refer to DN for instruction on management of the catheter. Refer to urology for further assessment and treatment.

Insidious onset. Causes: benign prostatic hypertrophy; pelvic malignancy; CNS disease. May present as:

Nocturnal enuresis

Overflow incontinence

Acute on chronic retention

Lower abdominal mass

UTI

Renal failure

As for acute retention. Bladder is enlarged (may contain >1.5L) but usually non-tender.

Refer to urology for further assessment and treatment. Refer urgently or acutely if pain, UTI or renal failure (eGFR <60mL/min/1.73m2). Do not catheterize in the community.

Ureters become embedded in dense fibrous plaques in the retroperitoneal space. Associations:

Drugs, e.g. methysergide

Carcinoma

Crohn’s disease

Connective tissue disease

Raynaud’s syndrome

Fibrotic diseases (e.g. alveolitis)

Typically middle-aged men presenting with fever, malaise, sweating, leg oedema, ↑ BP, palpable mass, and/or acute/chronic renal failure. Refer for specialist care. Options include steroids and nephrostomies.

Congenital abnormality. Kidneys are fused in the midline to form a horseshoe-shaped mass. The kidney may function normally or may present with obstructive nephropathy or UTIs.

Passing a urethral catheter

graphic Technique learned through supervised experience. Only attempt alone if you are competent to do so.

Prepare the equipment needed

Sterile rubber gloves, plastic sheet to prevent spills, paper sheet to provide sterile field, cleansing materials—cotton swabs, cleansing fluid

Local anaesthetic/lubricating gel e.g. 1% lidocaine + 0.25% chlorhexidine

Catheter—usually 12Ch or 14Ch; ensure the catheter is a long catheter if catheterizing a man (graphic p. 452); and if the catheter is not pre-filled—sterile syringe + 10mL of sterile water

Kidney dish/other receptacle to catch the urine before connecting the drainage bag; drainage tube and bag

Inserting the catheter

Ensure the patient is comfortable; protect against spills with a plastic sheet; cover area with a sterile paper sheet

Ensure strict aseptic technique. Cleanse the penis/vulva and squeeze lubricant/local anaesthetic gel into the urethra—allow to work

Gently but firmly, push the catheter into the urethra. Ensure the end of the catheter is over the receptacle. When the catheter enters the bladder, urine flows into the receptacle. Inflate the balloon with sterile water (if needed) once the catheter is inside the bladder. Connect the catheter to the collecting tube and bag

If male, pull the foreskin over the glans again to prevent paraphimosis

graphic If you are unable to pass a catheter, refer to urology.

10–30% of men in their early 70s have symptomatic benign prostatic hypertrophy (BPH). There is no relation between size of the prostate and symptoms. Assessment—see Table 14.10.

Table 14.10
Assessment of BPH
Assessment Comments

History

General well-being

Obstructive symptoms

Irritative symptoms

Haematuria

Pain

Polyuria and polydipsia

Neurological symptoms

Past history of urological instrumentation or STIs

Frequency-volume chart

Assess pattern and type of fluid consumption (e.g. alcohol/caffeine at night ↑ nocturia)

Symptom score (IPSS— graphic p. 458)

Objectively grade symptoms, giving measure of severity. IPSS scores:

0–7 mild

8–19 moderate

20–35 severe

A general quality of life measurement can be used to assess impact of symptoms

Abdominal examination

Look for distended bladder, palpable kidneys. Examine external genitalia

Digital rectal examination

Anal tone, size, shape, and consistency of prostate (normal prostate—size of a chestnut with smooth, rubbery consistency)

Serum urea, creatinine, and eGFR

Renal function assessment

MSU

Dipstick for blood and glucose. M,C&S

Ultrasound measurement of post-micturition residual  *

Maximum voiding flow rate  *

<15mL/s for voided volume >100mL is abnormal

Serum PSA

High values can indicate prostate cancer (graphic p. 459)

Assessment Comments

History

General well-being

Obstructive symptoms

Irritative symptoms

Haematuria

Pain

Polyuria and polydipsia

Neurological symptoms

Past history of urological instrumentation or STIs

Frequency-volume chart

Assess pattern and type of fluid consumption (e.g. alcohol/caffeine at night ↑ nocturia)

Symptom score (IPSS— graphic p. 458)

Objectively grade symptoms, giving measure of severity. IPSS scores:

0–7 mild

8–19 moderate

20–35 severe

A general quality of life measurement can be used to assess impact of symptoms

Abdominal examination

Look for distended bladder, palpable kidneys. Examine external genitalia

Digital rectal examination

Anal tone, size, shape, and consistency of prostate (normal prostate—size of a chestnut with smooth, rubbery consistency)

Serum urea, creatinine, and eGFR

Renal function assessment

MSU

Dipstick for blood and glucose. M,C&S

Ultrasound measurement of post-micturition residual  *

Maximum voiding flow rate  *

<15mL/s for voided volume >100mL is abnormal

Serum PSA

High values can indicate prostate cancer (graphic p. 459)

*

May be available through open-access prostate assessment clinics

Obstructive ↓ and intermittent urinary stream, double micturition, hesitancy, terminal dribbling, feeling of incomplete emptying, and straining to void. Differential diagnosis: prostatic enlargement, strictures, tumours, urethral valves, bladder neck contracture

Irritative (due to detrusor muscle hypertrophy)—Urinary frequency, urgency, dysuria, and nocturia. Differential diagnosis: enlarged prostate, UTI, polydipsia, detrusor instability, hypercalcaemia, uraemia

10% at presentation:

Recurrent UTI

Bladder stones

Haematuria

Chronic retention—graphic p. 454

Overflow incontinence—graphic p. 451

Obstructive nephropathy

Acute retention of urine (± prior obstructive symptoms)—graphic p. 454

Symptoms can improve spontaneously but overall progress slowly. 1–2%/y develop urinary retention. Options:

Patients with mild to moderate symptoms at presentation, with no complications of BPH and who are not severely troubled by their symptoms. Self-help includes: ↓ evening fluid intake, ↓ caffeine intake, bladder retraining, and prevention of constipation.

Those with mild/moderate symptoms who are troubled by their symptoms. Consider:

α-adrenoceptor antagonists, e.g. prazosin, doxazosin—watch for postural hypotension. ↓ symptomatic worsening

5α-reductase inhibitors, e.g. finasteride—best for patients with bulky prostates; takes up to 6mo to work. ↓ risk of urinary retention

Combination therapy— α-adrenoceptor agonist and 5 α-reductase inhibitor ↓ progression by 66% more than either agent alone

graphic Serenoa repens (saw palmetto) has no benefit over placeboC.

E = Emergency admission; U = Urgent; S = Soon; R = Routine.

Complicated BPH (e.g. acute retention)—E/U

↑ PSA (graphic p. 459)—U

Severe symptoms—S

Nodular/firm prostate on DRE—U

Failure to respond to drug therapy after 3–12mo (α-blocker) or 6–12mo (5α-reductase inhibitor)—R

Consider in men presenting with suspected UTI. Other features: fever; arthralgia/myalgia; low back, perineal, penile ± rectal pain. DRE reveals swollen, tender prostate. If suspected, check MSU and treat with 4wk course of oral antibiotic which penetrates prostatic tissue, e.g. ciprofloxacin 500mg bd, ofloxacin 200mg bd. Refer for specialist advice if not settling. Complications include: acute retention of urine, chronic bacterial prostatitis, and prostate abscess.

2–14% lifetime prevalence. Cause is unknown. Presents with >3mo history of:

Urological pain—lower abdomen, pelvis/perineum, penis (especially tip ± on ejaculation), testicles, rectum, low back ±

Irritative/obstructive symptoms and/or ejaculatory disturbance

Diagnosis is based on history with exclusion of other causes. Suitable investigations include DRE, MSU, urine cytology, STI screen (graphic p. 739), PSA ± urodynamic studies. Treatment is difficult—provide information and support; try α-blockers (e.g. doxazosin 4mg od for 6mo). Spontaneous improvement/remission often occurs.

Table 14.11
The International Prostate Symptom Score
Not at all Less than 1 time in 5 Less than half the time About half the time More than half the time Almost always Your score

Over the past month, how often have you had a sensation of not emptying your bladder completely after you finish urinating?

0

1

2

3

4

5

Over the past month, how often have you had to urinate again <2h after you finished urinating?

0

1

2

3

4

5

Over the past month, how often have you stopped and started several times when you urinated?

0

1

2

3

4

5

Over the past month, how often have you found it difficult to postpone urinating?

0

1

2

3

4

5

Over the past month, how often have you had a weak urinary stream?

0

1

2

3

4

5

Over the past month, how often have you had to push or strain to begin urinating?

0

1

2

3

4

5

Over the past month, typically from the time you went to bed to the time you got up in the morning, how many times did you get up to urinate?

0

1

2

3

4

5+

Total IPSS score

Not at all Less than 1 time in 5 Less than half the time About half the time More than half the time Almost always Your score

Over the past month, how often have you had a sensation of not emptying your bladder completely after you finish urinating?

0

1

2

3

4

5

Over the past month, how often have you had to urinate again <2h after you finished urinating?

0

1

2

3

4

5

Over the past month, how often have you stopped and started several times when you urinated?

0

1

2

3

4

5

Over the past month, how often have you found it difficult to postpone urinating?

0

1

2

3

4

5

Over the past month, how often have you had a weak urinary stream?

0

1

2

3

4

5

Over the past month, how often have you had to push or strain to begin urinating?

0

1

2

3

4

5

Over the past month, typically from the time you went to bed to the time you got up in the morning, how many times did you get up to urinate?

0

1

2

3

4

5+

Total IPSS score

Delighted Pleased Mostly satisfied Equally satisfied/dissatisfied Mostly dissatisfied Unhappy Terrible

If you were to live the rest of your life with your urinary condition the way it is now, how would you feel about it?

0

1

2

3

4

5

6

Delighted Pleased Mostly satisfied Equally satisfied/dissatisfied Mostly dissatisfied Unhappy Terrible

If you were to live the rest of your life with your urinary condition the way it is now, how would you feel about it?

0

1

2

3

4

5

6

0–7 = mildly symptomatic

8–19 = moderately symptomatic

20–35 = severely symptomatic

The International Prostate Symptom Score is reproduced with permission from the American Urological Association.

Prostatitis Foundation graphic  www.prostatitis.org

BASHH Management of prostatitis (2008) graphic  www.bashh.org.uk

Cochrane Tacklind J, MacDonald R, Rutks I, et al. (

2012
)
Serenoa repens for benign prostatic hyperplasia.
 
Cochrane Database of Systematic Reviews
, Issue 12. Art. No.: CD001423. DOI: 10.1002/14651858.CD001423.pub3.

Prostate-specific antigen (PSA) testing

There is no prostate screening programme in the UK but men can request a PSA test. The government has introduced a PSA Informed Choice Programme. Warn patients about the poor specificity of the test, before performing the test and provide information about the pros and cons of testing.

In addition, PSA is routinely measured in men with urological symptoms. Abnormal PSA is a common reason for referral to a urologist. Its sensitivity and specificity are poor.

Pros and cons of PSA testing
Benefits of PSA testing Downside of PSA testing

It may provide reassurance if the test result is normal

It may find cancer before symptoms develop and at an early stage when treatments could be beneficial

If treatment is successful, the consequences of more advanced cancer are avoided

It can miss cancer and provide false reassurance

It may lead to unnecessary anxiety and medical tests when no cancer is present

It might detect slow-growing cancer that may never cause any symptoms or shortened lifespan

The main treatments of prostate cancer have significant side effects, and there is no certainty that treatment will be successful

Benefits of PSA testing Downside of PSA testing

It may provide reassurance if the test result is normal

It may find cancer before symptoms develop and at an early stage when treatments could be beneficial

If treatment is successful, the consequences of more advanced cancer are avoided

It can miss cancer and provide false reassurance

It may lead to unnecessary anxiety and medical tests when no cancer is present

It might detect slow-growing cancer that may never cause any symptoms or shortened lifespan

The main treatments of prostate cancer have significant side effects, and there is no certainty that treatment will be successful

Reasons for increased PSA

Prostate cancer

Benign prostatic hypertrophy

Acute or chronic prostatitis

Physical exercise

Acute urinary retention

Prostate instrumentation (includes prostate biopsy and urinary catheterization)

Old age

graphic PSA may be normal when early prostate cancer is present.

Performing a PSA test

Digital rectal examination may cause a transient ↑ in PSA levels (graphic), so do the PSA test before doing a digital rectal examination. If that is not possible, delay the test for 1wk after the examination. Exclude urinary infection before PSA testing. Do NOT do a PSA test if the man has:

A proven UTI—treat the UTI and postpone the PSA test for ≥1mo

Ejaculated within 48h

Exercised vigorously in the previous 48h

Had a prostate biopsy <6wk ago

PSA cut-offs that should prompt referral
Age (y) Refer to urology if PSA (ng/mL)

50–59

≥3.0

60–69

≥4.0

≥70

>5.0

Age (y) Refer to urology if PSA (ng/mL)

50–59

≥3.0

60–69

≥4.0

≥70

>5.0

graphic Finasteride and dutasteride ↓ PSA by ~50%.

Prostate cancer is the sixth most common cancer worldwide. It is the second most common cancer affecting men and 10,720 men/y die from the disease in the UK. 1 in 6 men have clinical prostate cancer in their lifetime and the incidence is rising.

Can be divided into:

Clinically localized disease—cancer thought, after clinical examination, to be confined to the prostate gland

Locally advanced disease—cancer that has spread outside the capsule of the prostate gland but has not yet spread to other organs

Cancer that has spread outside the prostate gland to local, regional, or systemic LNs, seminal vesicles, or other body organs (e.g. bone, liver, brain).

Age Uncommon <50y; 85% are diagnosed aged >65y

Genetic ↑ incidence if first-degree relative affected

Racial Incidence varies according to location in the world and ethnic group. Highest rates are in men of black ethnic group in the USA—lowest in Chinese men

Dietary Links are proposed between prostate cancer, low intake of fruit (particularly tomatoes) and high intake of fat, meat, and Ca2+

A large-scale trial of screening for prostate cancer is underway in the UK. Problems with screening:

Incidental post-mortem evidence of prostate cancer is high (~75% men >75y); very few become clinically evident, so many more men would be found with prostate cancer by screening than would die or have symptoms from it

Natural history of prostate cancer is not understood—there is no means to detect which ‘early’ cancers become more widespread

Inadequate screening tests

It is not clear if early treatment enhances life expectancy

Peak incidence of morbidity and mortality is in old age (75–79y), so potential years of life saved by screening are small

Prostate-specific antigen (PSA)  graphic p. 459

Digital rectal examination (DRE) Operator-dependent, fails to detect early prostate cancers, and lacks specificity. Annual screening in the USA and Germany has not ↓ mortality

Transrectal ultrasound (TRUS) Too expensive

The most effective screening regime involves rectal examination and PSA testing followed by TRUS for suspicious lesionsS. Optimal screening interval is unknown but serial screening does ↑ detection.

Symptomless. Usually detected following an incidental finding of ↑ PSA. Hard nodule sometimes felt in prostate on DRE.

Prostatism

Urinary retention

Haematuria

Lower extremity oedema

On rectal examination, the prostate is hard and non-tender and sulci lose definition

Malaise

Weight loss

Bone pain

Pathological fractures

Spinal cord compression

Ureteric obstruction may cause renal failure

Signs depend on site of metastases

A digital rectal examination and PSA test (after counselling) are recommended for patients with any of the following unexplained symptoms:

Erectile dysfunction

Haematuria

Lower back pain

Bone pain

Inflammatory or obstructive lower urinary tract symptoms

Weight loss, especially in the elderly

graphic Exclude UTI before PSA testing and postpone digital rectal examination until after the PSA test is done.

Urgent referralN

Rectal examination—hard, irregular prostate typical of prostate cancer. PSA result should accompany the referral

Rectal examination—normal prostate, but rising/raised age-specific PSA ± lower urinary tract symptoms*

Symptoms and high PSA levels

Asymptomatic men with borderline, age-specific PSA results repeat PSA after 1–3mo. If the PSA level is rising, refer the patient urgently

graphic Referral is not needed if the prostate is simply enlarged and the PSA is in the age-specific reference range.

NICE  graphic  www.nice.org.uk

Prostate cancer: diagnosis and treatment (2008)

Cancer research UK  graphic  www.cancerresearchuk.org

National screening  graphic  www.cancerscreening.nhs.uk

Cancer Research UK graphic 0808 800 4040 graphic  www.cancerhelp.org.uk

Macmillan Cancer Support graphic 0808 808 0000 graphic  www.macmillan.org.uk

Prostate Cancer Charity graphic 0800 074 8383 graphic  www.prostatecancer.org.uk

Prostate Cancer Support Association graphic 0845 601 0766 graphic  www.prostatecancersupport.co.uk

Treatment is controversial. There are two arguments:

Benefits of treatment are outweighed by risks

or

Aggressive treatment before spread is the only way to ensure cure

Benefits of treatment are outweighed by risks

or

Aggressive treatment before spread is the only way to ensure cure

>50% of men >50y who die from other causes are found post-mortem to have prostate cancer—prostate cancer kills only a small minority of men who have it. The personal and economic cost of treating men whose cancer would never have caused them any problems must be considered.

Watchful waiting or active surveillance Monitor with PSA and regular rectal examination. ↑ in PSA or size of nodule triggers active treatment. At 10y follow-up <10% with moderately well-differentiated cancer will have died from their cancer. Progression rates are higher in patients with poorly differentiated cancer. Some men find the uncertainty of waiting difficult to cope with

Radical prostatectomy Has potential for cure, but in the age group most affected by prostate cancer mortality is 1.4%. Other common complications: impotence (50%), incontinence (25%)

Radiotherapy May not be effective—persistent cancer is found in 30% on biopsy. Brachytherapy (radioactive treatment in implanted seeds or wires) has proven efficacy in early prostate cancer

Hormone treatment No convincing evidence that this gives survival benefit in early disease

Others Minimally invasive treatments, e.g. cryotherapy and microwave therapy, are as yet unproven

30% 5y survival. Hormone manipulation is the mainstay of treatment and gives 80% ↓ in bone pain, PSA, or both, and a lower incidence of serious complications (e.g. spinal cord compression) if treatment starts at the time of diagnosis. Options:

(e.g. goserelin) sc injection every 4–12wk (depending on the preparation used). Testosterone levels ↓ to levels of castrated men in <2mo. Side effects: impotence, hot flushes, gynaecomastia, local bruising, and infection around injection site. When starting LHRH analogues, LH level initially ↑ which can cause increased tumour activity or ‘flare’. Counteracted by prescription of anti-androgens (e.g. flutamide) for a few days before administration of the first dose of LHRH and concurrently for 3wk. Response in most patients lasts for 12–18mo.

(e.g. cyproterone actetate, flutamide, bicalutamide). Do not suppress androgen production completely. Used to prevent side effects due to testosterone flare during initiation of LHRH analogues, as monotherapy (e.g. bicalutamide 150mg od) and in combination with LHRH analogues to produce maximum androgen blockade.

↓ testosterone secretion permanently without the need for medication. However, rarely used.

In addition to hormone therapy, local radiotherapy and corticosteroids are used for bone pain. Radioactive strontium ↓ the number of new sites of bone pain developed. Mean survival <5y.

No agreed treatment. Involve the multidisciplinary team-including urology, oncology, and palliative care. Dexamethasone 0.5mg daily or docetaxel may be helpful.

See Table 14.12.

Table 14.12
Factors affecting prognosis of prostate cancer
Stage Tumour Lymph nodes involved? Metastases?

T1

Inpalpable

N0

No

M0

No spread outside the pelvis

T2

Tumour completely within the prostate gland

N1

1 +ve LN <2cm diameter

M1

Spread outside the pelvis

T3

Tumour has breached the capsule of the prostate

N2

>1 +ve LN or 1 LN of 2–5cm diameter

T4

Spread within the pelvis, e.g. to bladder or bowel

N3

Any +ve LN >5cm diameter

Stage Tumour Lymph nodes involved? Metastases?

T1

Inpalpable

N0

No

M0

No spread outside the pelvis

T2

Tumour completely within the prostate gland

N1

1 +ve LN <2cm diameter

M1

Spread outside the pelvis

T3

Tumour has breached the capsule of the prostate

N2

>1 +ve LN or 1 LN of 2–5cm diameter

T4

Spread within the pelvis, e.g. to bladder or bowel

N3

Any +ve LN >5cm diameter

Gleason score

Histological grade. Cells are graded 1–5 the less differentiated they are. The two areas of the biopsy with the highest grade cells are added together. Low-grade tumours likely to grow slowly have low scores (2–4); high-grade tumours have high scores (7–10).

Age

Older patients with low-grade tumours are likely to die from something other than their prostate cancer.

PSA

PSA >40: high chance of nodal or metastatic spread

PSA >100: metastatic spread is very likely

Prognosis

5y survival rates for tumour stage:

1 or 2—tumour confined within the prostate (65–98%)

3—tumour has breached the capsule of the prostate (60%)

4—spread to LNs, within the pelvis or elsewhere (20–30%)

NICE Prostate cancer: diagnosis and treatment (2008) graphic  www.nice.org.uk

graphicPosterior urethral valves

Folds of mucosa inhibit or block passage of urine causing urethral, bladder, ureter, and renal pelvis dilatation.

Presentation

Usually detected on antenatal USS. Can present in neonates with urinary retention or dribbling urine + distended bladder, UTI or uraemia, or later in childhood with recurrent UTI or incontinence.

Investigation and management

MCUG confirms diagnosis. In all cases refer to urology for surgical disruption of the valves.

Hypospadias

1 in 400 male births. The urethral meatus opens on the ventral side of the penis. There is often hooding of the foreskin and ventral flexion of the penis. Refer to urology. Treated with corrective surgery, ideally preschool.

Non-retractile foreskin

Usually noted by parents. May be history of recurrent balanitis. Examination: foreskin adherent.

Management

Age <4y—do nothing unless recurrent balanitis. If >4y and/or recurrent balanitis, consider treatment with topical steroids (e.g. betamethasone 0.1% od) for 3–4mo. If ineffective, refer to paediatric surgery for circumcision.

Phimosis

Foreskin obstructs urine flow. Common in small children. Time usually obviates the need for circumcision. Treat as for non-retractile foreskin if recurrent balanitis.

Hard lumps in the shaft of the penis. Unknown cause. 4% ♂ >40y. 1 in 3 have pain/bending of the penis when erect. Associated with erectile dysfunction (graphic p. 776). 5% have Dupuytren’s contracture. F.G. de la Peyronie (1678–1747)—French surgeon.

Reassurance usually suffices. No proven medical treatments. Refer to urology for surgery if pain or severe bending on erection so that intercourse is not possible.

Foreskin is retracted then (because of oedema) unable to be replaced. Commonly occurs in catheterized patients when the catheter is changed.

Try to replace foreskin using ice packs (↓ swelling) and lubrication (e.g. KY jelly). If unable to replace the foreskin, admit for surgery.

Acute inflammation of glans and foreskin. Common organisms—staphylococci, streptococci, coliforms, candida. Can occur at any age. Most common in young boys when associated with non-retractile foreskin/phimosis. In elderly patients consider DM.

Oral antibiotics (e.g. flucloxacillin) or topical antifungals (e.g. clotrimazole). If recurrent or secondary to phimosis consider referral for circumcision.

Chronic fibrosing condition of the foreskin which may become adherent to the glans. Treatment is with topical steroid creams, e.g betamethasone 0.1%. Consider referral for circumcision.

Torn frenulum—seen after poorly lubricated intercourse or if caught in a zip. No treatment required. If recurrent, consider referral for circumcision.

graphic p. 776

Persistent painful erection not related to sexual desire.

Medication for erectile dysfunction, idiopathic, leukaemia, sickle cell disease, or pelvic tumour.

Ask the patient to climb stairs (arterial ‘steal’ phenomenon), apply ice packs. If unsuccessful refer to A&E for aspiration of corpora. Rarely surgery is needed.

Pre-malignant condition of glans. Moist velvety-looking patches. Refer to urology. Treatment is surgical.

Squamous cell carcinoma (95%) or malignant melanoma. Usually elderly men. Rare in the UK.

Refer urgently patients with symptoms or signs of penile cancer. These include:

Progressive ulceration in the glans, prepuce, or skin of the penile shaft

Mass in the glans, prepuce, or skin of the penile shaft

graphic Lumps within the corpora cavernosa can indicate Peyronie’s disease, which does not require urgent referral.

Associated with urethritis, e.g. due to chlamydia or gonorrhoea. Refer to GUM clinic.

BASHH Management of balanitis (2008) graphic  www.bashh.org.uk

NICE Referral guidelines for suspected cancer (2005) graphic  www.nice.org.uk

Treat the cause:

Epididymo-orchitis

Torsion of the testis

Trauma and haematoma formation

Varicocele

Testicular tumour (rarely painful)

Torsion of the testis

Peak age 15–30y. Presents with sudden onset of severe scrotal pain. May be associated with right iliac fossa pain, nausea, and vomiting. Examination: tender, hard testis riding higher than contralateral testis. Admit urgently to surgical/urology team.

Small embryological remnant at the upper pole of the testis. Presents similarly to torsion of the testis. Refer as an emergency to exclude torsion of the testis.

Inflammation of the testis and epididymis due to infection. May occur at any age. The most common viral cause is mumps. The most common bacterial causes are chlamydia or gonococci (<35y) and coliforms (>35y). Chronic infection with TB or syphilis is rare.

Acute onset pain in testis; swelling and tenderness of testis/epididymis; fever ± rigors; may be urethritis, dysuria, and/or ↑ frequency.

May be difficult to distinguish from torsion of the testis. If in doubt, admit for urology/surgical opinion. Otherwise investigate and treat for the underlying cause.

See Figure 14.2.

 Diagnosis of testicular lumps
Figure 14.2

Diagnosis of testicular lumps

Collection of fluid in the tunica vaginalis. Occurs at any age.

hydrocele—no predisposing cause in scrotum

hydrocele—reaction to pathology in testis or covering (infection, tumour, torsion). In adults presenting with hydrocele always consider impalpable tumour beneath

Swelling in the scrotum. The examiner should be able to get above the swelling. Smooth surface, transilluminates; testis is within the swelling and not palpable separately.

Investigation is not required in children; refer adults for USS if testis is not palpable. Options for adults:

Conservative management—reassurance; small hydroceles

Tapping—may be suitable for large hydroceles where surgery is inappropriate; 2° infection and recurrence are common

Surgery—refer to urologist

graphicHydroceles in children are usually congenital. May be unilateral or bilateral. Most resolve spontaneously in the first year of life. Refer to urology if persists >1y.

Arises in part of the processus vaginalis in the spermatic cord above the testis. Rounded lump which slips up and down the inguinal canal. No action needed.

Referral guidelinesN

Refer urgently patients with a swelling or mass in the body of the testis

Consider an urgent ultrasound in men with a scrotal mass that does not transilluminate and/or when the body of the testis cannot be distinguished

NICE Referral guidelines for suspected cancer (2005) graphic  www.nice.org.uk

BASHH Management of epididymo-orchitis (2010) graphic  www.bashh.org.uk

Damage to the testis (e.g. due to a direct blow, vasectomy) can result in the testis rupturing and the tunica vaginalis filling with blood. Refer as an emergency for urological assessment.

Collection of varicose veins in the pampiniform plexus of the cord and scrotum. Can be 2° to obstruction of the testicular veins in the abdomen. L > R. Associated with infertility (thought due to ↑ temperature of testis). Presents with a dull ache in the testis especially at the end of the day or after exercise. Usually visible when the patient is standing. No treatment is needed—reassure. Occasionally surgery or radiological embolization may help if symptoms are severe.

Common and often multiple. Found in middle-aged/elderly men. Usually presents when the patient finds a painless lump.

Examination Smooth-walled cyst in epididymis (palpable above and behind testis), often bilateral

Investigation If unsure of diagnosis refer for USS

Management Reassurance. Refer to urology if painful

Cyst containing sperm. Typically situated in the head of the epididymis—more rarely in the spermatic cord. Clinically presents in the same way as epididymal cyst. Management is the same.

graphic p. 749

Rare (<2% tumours). Sertoli cell adenomas; Leydig cell adenomas. Produce sex hormones and cause feminization/masculinization respectively. Refer.

Most common malignancy in men age 20–34y. Devastating disease as sufferers tend to be young and fit and do not expect to be ill. Screening is not effective. Education to ensure men check their testes for lumps regularly and present early is preferable.

Undescended testes—bilateral undescended testis → 10x ↑ risk; past history of testicular cancer—4% risk second cancer.

Painless lump in testis; occasionally testicular pain or hydrocele; may present with metastases—back pain/dyspnoea.

Testicular lumps are tumours until proven otherwise. Refer for urgent urological opinion. USS can help diagnosis but do not delay referral. Definitive diagnosis is only made at biopsy. Specialist treatment depends on tumour type and extent (see Table 14.13). Sperm banking is routinely offered in case of ↓ fertility due to treatment.

Table 14.13
Types and features of testicular cancer
Seminoma (60%) Teratoma

Typical age

30–40y

<30y

Tumour markers

None

β-HCG

αFP

LDH—correlates with volume of metastatic disease

Nature of tumour

Solid

Solid/cystic components

40% occur within seminomas Mixed tumours are treated like teratomas

Growth speed

Slow-growing

Fast-growing—can ↑ x2 in size in days

Stage of presentation

90% stage 1 (tumour confined to testis)

60% stage 1 (tumour confined to testis)

Treatment

Treated with inguinal orchidectomy + radiotherapy

Relapses are treated with chemotherapy

More advanced disease is treated with radio- or chemotherapy

Treatment of stage 1 disease is with inguinal orchidectomy and surveillance of tumour markers. 25% relapse in <18mo

Treatment of relapses and metastatic disease is with chemotherapy

Survival

98% 5y survival for stage 1 disease. Overall >85% 5y survival

Prognosis depends on stage and degree of differentiation

Seminoma (60%) Teratoma

Typical age

30–40y

<30y

Tumour markers

None

β-HCG

αFP

LDH—correlates with volume of metastatic disease

Nature of tumour

Solid

Solid/cystic components

40% occur within seminomas Mixed tumours are treated like teratomas

Growth speed

Slow-growing

Fast-growing—can ↑ x2 in size in days

Stage of presentation

90% stage 1 (tumour confined to testis)

60% stage 1 (tumour confined to testis)

Treatment

Treated with inguinal orchidectomy + radiotherapy

Relapses are treated with chemotherapy

More advanced disease is treated with radio- or chemotherapy

Treatment of stage 1 disease is with inguinal orchidectomy and surveillance of tumour markers. 25% relapse in <18mo

Treatment of relapses and metastatic disease is with chemotherapy

Survival

98% 5y survival for stage 1 disease. Overall >85% 5y survival

Prognosis depends on stage and degree of differentiation

graphic Children conceived of men treated for testicular cancer are not at ↑ risk of congenital abnormality.

If the scrotum has never contained a testis, it is hypoplastic. If the scrotum has contained a testis in the past, it is normally developed but empty.

Undescended or retractile testis; surgical removal, e.g. for torsion, trauma, or tumour; testicular atrophy (e.g. due to mumps or trauma); ambiguous genitalia; testicular agenesis—diagnosis of exclusion.

SCC or melanoma. Uncommon <50y. Painless lump/ulcer of the scrotal skin ± enlarged inguinal LNs. If suspected, refer urgently to urology or dermatology.

Necrotizing fasciitis of the scrotal skin and/or penis. Patients are usually elderly and often have a hydrocele. Starts as a black spot and spreads rapidly. Early diagnosis is critical to survival so, if suspected admit as an acute urological emergency. Treatment is with surgical debridement and IV antibiotics.

graphicUndescended testis

Affects 2–3% of ♂ neonates—but most descend during the first year. Refer those that do not for surgical descent/fixation to avoid ↑ risk of malignancy and later infertility.

Retractile testis

Usually young boys with active cremasteric reflex. No treatment needed.

Examination

Scrotum is usually well developed. Try to find the testis, and milk it down into scrotum. May be found anywhere from the scrotum to the internal inguinal ring. If not found or you are unable to bring the testis down into the scrotum assume it is undescended.

Cancer Research UK graphic 0808 800 4040 graphic  www.cancerhelp.org.uk

Macmillan Cancer Support graphic 0808 808 0000 graphic  www.macmillan.org.uk

Notes
*

Consider discussion with specialist and patient ± carer before referral for very elderly patients/those compromised by other co-morbidities.

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