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Renal, genitourinary and sexual health medicine
onset, male sex, urological symptoms, persistent haematuria, especially if aged more than 40years, unusual organisms
(such as Pseudomonas) and recurrence of infections.
A renal tract ultrasound scan should be performed for
UTI in children and men, if they have more than two episodes per year, fail to respond to treatment, pyelonephritis,
unusual organism or persistent haematuria. A CT scan can
also show evidence of structural abnormalities or features of
a pyelonephritis. In recurrent urinary infections, a dynamic
test such as micturating cystogram can show evidence or reflux, and a dimercaptosuccinic acid scan can be performed
to assess the patient for split renal function and scarring.
HINTS AND TIPS
Sterile pyuria is bacteruria with no growth. Causes
include:
• tuberculosis of the urinary tract
• partially treated UTI
• neoplasia
• urethritis (e.g. chlamydia, gonorrhoea)
Management
Treatment should be started after urine has been sent for culture and antibiotic sensitivity testing but, commonly, before
results are available. Broad-spectrum antibiotics may then be
changed if necessary according to the results. High fluid intake should be encouraged. More than 80% of lower urinary
tract infections respond to a short course of an antibiotic such
as trimethoprim, nitrofurantoin or amoxicillin. For complicated UTIs a 5–10-day course of therapy is indicated. Patients
with acute pyelonephritis usually require admission to hospital for treatment with intravenous fluids and antibiotics.
Patients with recurrent infections require a high fluid intake; frequent and complete voiding should be encouraged.
Long-term, low-dose prophylaxis using rotating antibiotics may be of benefit but the need for continued treatment
should be reassessed after 6months.
If infection is related to sexual intercourse, the patient
should void after intercourse and may benefit from a single
dose of an antibiotic.
– Nitrofurantoin is not effective in chronic kidney
disease of stage III or above; trimethoprim
impairs creatinine secretion and can cause
a rise in serum creatinine level despite not
worsening renal function.
RENAL CALCULI
Renal calculi (kidney stones) are common; they are more
common in men, with the initial presentation usually in the
third and fourth decade of life. Most common is calcium oxalate, followed by calcium phosphate. Struvite (also known as
‘triple phosphate’) is most commonly associated with Proteus
infection. These are all radio-opaque and can be seen on a
plain X-ray. Twenty percent of stones are radiolucent, including urate, cystine (only partially lucent) and xanthine.
Bladder calculi form 5% of all urinary tract stones; risks
for formation include foreign bodies (e.g. indwelling catheter, obstruction or infection).
General overview
The following four factors affect predisposition to forming
renal calculi:
• poor urinary drainage (i.e. urinary stasis)
• low urinary output (e.g. dehydration)
• high solute concentration (e.g. high oxalate
concentration, hypercalcaemia)
• urinary pH (acidic pH favours uric acid stone
formation, whereas alkali pH favours calcium oxalate
stone formation)
Clinical features
The classic presenting symptom of renal calculi is colicky severe loin to groin pain. The patient is unable to lie still. It is
often associated with nausea and vomiting. Frank haematuria may occur, but more commonly haematuria is not visible.
There may be renal angle tenderness, with pain referred to
the testes, although these should not be tender on palpation.
COMMON PITFALLS
– Do not treat asymptomatic bacteruria except in
pregnancy.
– You will not be able to clear bacteruria with the
presence of a catheter.
– It will be hard to clear infection if there is an
underlying renal calculus.
268
RED FLAG
Do not assume it is renal colic. Ensure a thorough
investigation to exclude an abdominal aortic
aneurysm (AAA), appendicitis or ectopic pregnancy.
If it is the first presentation of renal colic in an
individual older than 60years or an individual with
peripheral vascular disease, consider an AAA; it
can present with loin to groin pain.
Urinary tract malignancies
3030
Management
Renal colic is a typical ‘end of the bed’ diagnosis. Diagnosis
is based on a suggestive history, examination and classically haematuria on urine dipstick testing. A noncontrast
CT scan of the kidneys, ureter and bladder is the firstline investigation. This will identify the site, size of the
stone and importantly if there is hydronephrosis, or an
alternative exchange disorder for diagnosis. The size of
the calculi will help guide management. Only one-third
of stones, greater than 5 mm in diameter and positioned
in the upper third of the ureter, will pass spontaneously,
most stones, typically those smaller than 4 mm, pass spontaneously however. Renal calculi that are unlikely to pass
spontaneously need to be urgently referred to a urologist,
as they may result in ureteric obstruction. It is important
to be aware that a kidney can be obstructed without the
presence of hydronephrosis on imaging. Immediate treatment is analgesia with NSAIDs (typically diclofenac, but
consider the renal function) and fluids. Surgical treatments
involve ureteroscopy or lithotripsy. To avoid future stones,
the patient should maintain a high urine output through
high fluid intake. Patients who form recurrent stones need
a metabolic study to guide directed treatment.
RED FLAGS
An infection in the context of obstruction (i.e.
pyonephrosis) is a medical emergency, and
needs urgent decompression with a nephrostomy
and intravenous antibiotics. The nephrostomy
is generally performed by an interventional
radiologist.
RED FLAGS
Renal calculi in patients with a single kidney or
underlying renal failure needs to be managed with
great caution.
URINARY TRACT MALIGNANCIES
Renal cell carcinoma
Renal cell carcinoma is the commonest renal tumour in
adults; it is twice as common in men. Most renal cell carcinomas are of the clear cell type, named after their distinctive clear cytoplasm on microscopy. The peak age of onset is
between 50 and 60years. Risk factors include smoking, obesity and genetic disease (e.g. von Hippel Lindau, polycystic
kidney disease). The classic triad is haematuria, loin pain
and a palpable mass, although this is rarely seen. Other
features may include pyrexia, weight loss, polycythaemia,
visible haematuria, bone pain with hypercalcaemia, and
left-sided varicocele associated with left renal vein obstruction. Spread is into adjacent structures (e.g. adrenal glands,
local lymph nodes), and it may extend into the renal vein
and into the inferior vena cava. Metastases are common,
with cannon ball lung metastases being a classic feature.
Other sites of metastases include bone.
Investigations include urinalysis, urinary cytology, ultrasound scan, CT scan of the kidneys, CXR (cannon ball
metastasis-associated feature), bone scan for metastases
and magnetic resonance imaging of the abdomen to assess
spread to the inferior vena cava.
Treatment is by radical nephrectomy if possible, although nephron-sparing surgery and laparoscopic procedures are becoming more common. Metastases may regress
after the primary tumour is removed. This can be enhanced
with immunotherapy (e.g. interferon alfa and interleukin-2
administration). Molecular therapy may be used additionally to this with advanced metastatic disease, and may
include sunitinib and pazopanib, both tyrosine kinase inhibitors. These are licensed in those fit enough to tolerate
interferon-based immunotherapies. Metastases are resected
if possible. Radiotherapy may be used for palliative therapy
for bone pain or for brain metastases. The overall 5-year
survival rate is approximately 60%, but it is greater if the
tumour is confined to the renal parenchyma and lower if
there are metastases or there is lymph node involvement.
CLINICAL NOTES
Tumours presenting with polycythaemia include
renal cell carcinoma, hepatoma and cerebellar
haemangioblastoma.
COMMUNICATION
Ask the patient to sieve the urine (or collect the
urine in a clear container) to try to collect a stone.
Analysis of the composition of the stone can guide
directed preventative strategies.
Transitional cell carcinoma
This occurs mainly in those older than 40years and most
commonly affects the bladder, although the ureter and renal pelvis are other sites. It is three times more common
in men than women. Predisposing factors include cigarette
269
Renal, genitourinary and sexual health medicine
smoking, exposure to industrial carcinogens (e.g. aniline
dyes), exposure to drugs (e.g. cyclophosphamide) and
chronic inflammation (e.g. schistosomiasis).
Patients usually present with painless haematuria, although pain may occur. There may be symptoms like UTI.
Investigations include urine cytology, cystourethroscopy
and abdominal CT scanning.
Treatment options include local resection with regular
follow-up cystoscopy, bacillus Calmette–Guérin (BCG)
intravesical immunotherapy, cystectomy, radiotherapy and
local or systemic chemotherapy.
Prostatic carcinoma
Prostatic carcinoma is the second most common malignancy in men; the incidence increases with age and it may
be very indolent. Patients are often asymptomatic but may
present with symptoms of ‘prostatism’, although this is more
seen in benign prostatic hypertrophy, where the urethral part
of the prostate is most affected. Symptoms may arise from
metastatic spread, classically to bone, presenting with back
pain. A hard irregular prostate may be palpable on rectal
examination.
Investigation includes prostate-specific antigen (PSA),
transrectal ultrasound examination and prostatic biopsy
(the Gleeson score is used to assess tumour grade), which
shows an adenocarcinoma, or prostatic magnetic resonance imaging. Evidence of local invasion, nodal spread
and metastases should also be sought (used to stage tumour
spread).
Treatment of local disease may be observation alone,
transurethral resection of the prostate, radical prostatectomy or radiotherapy. Radical prostatectomy can lead to incontinence and impotence. Testosterone is a growth factor
for prostate cancer and therefore prostate cancer responds
well to antagonizing the effect of testosterone. This can be
achieved with orchidectomy, luteinizing hormone-releasing
hormone analogues (e.g. goserelin) and antiandrogens (e.g.
cyproterone acetate).
Prognosis, even with metastases, may be excellent if the
tumour responds to hormonal treatment.
PSA is very useful as a tumour marker to allow the response to therapy to be assessed when prostate disease is
present. However, how to screen patients for prostate cancer
and how to follow up abnormal PSA test results is a cause
of much debate for urologists and public health authorities.
Currently, it does not meet the criteria for a national screening
programme.
RED FLAGS
With an elderly man with back pain and
hypercalcaemia, check the prostate-specific
antigen level and send a myeloma screen.
Testicular cancer
Testicular cancer is the most common malignancy to affect
males in their second to fourth decade. Typical presentation
is a painless testicular mass. Risk factors include maldescended testicle, infant hernia, family history of infertility
and previous testicular malignancy. Ninety-five percent are
derived from the germ cells, 50% of these are seminomas
and 50% are nonseminomas. Nonseminomas include teratomas and yolk sac tumours. The rarer tumours include
Leydig and Sertoli tumours. Patients tend to present with
a painless lump in their testes. Investigations include ultrasound scan and histological assessment either from biopsy
or after orchidectomy. All patients must have a CT scan to
rule out metastases. Alpha-fetoprotein (level typically raised
in yolk sac tumours) and β-human chorionic gonadotropin
are tumour markers (level raised in teratomas and seminomas) which are particularly helpful in monitoring response
to treatment.
Ninety percent of patients achieve complete remission
with treatment; even metastatic disease is potentially curable. Younger patients may suffer from the long-term toxicity of treatment. Treatment is with orchidectomy; before this,
patients should be offered sperm storage and the option of a
testicular prosthesis. Seminomas are extremely sensitive to
radiotherapy and have the best prognosis. Nonseminatous
germ cell tumours respond well to combination chemotherapy with bleomycin, cisplatin and etoposide.
COMMUNICATION
Tell all your male patients to examine themselves
for lumps in their testes.
MISCELLANEOUS CONDITIONS
CLINICAL NOTES
Prostate-specific antigen level will increase after
catheterization, with urinary infections and even
after rectal examination.
270
Adult polycystic kidney disease
This is an autosomal dominantly inherited disease; the
genes, PKD2 and PKD1, lie on chromosomes 4 and 16 respectively. Patients are usually ages between 30 and 50years.
There is not always a family history, and the disease can
present de novo. Cysts develop in the kidney parenchyma,
Miscellaneous conditions
3030
Table30.8 Criteria for diagnosing polycystic kidney
disease on ultrasonography
Age (years) Family history No family history
<30 Two cysts
bilaterally (or
unilaterally)
30–60 Four cysts
bilaterally
>60 Eight cysts
bilaterally
From Kumar, A., Hamid, S., Bali, S.K., Akhter, M. and Hamid, S.,
2012. A Prospective Study on Clinical Profile of Autosomal
Dominant Polycystic Kidney Disease (ADPKD) in Jammu for a
Period of 1 Year. Open Journal of Nephrology, 2(04), p. 123.
Five cysts
bilaterally
Five cysts
bilaterally
Eight cysts
bilaterally
the number and size increase with age and they can lead
to progressive renal failure. Approximately 40% of patients
also have cysts in the liver. Haematuria, infection and painful kidneys are common presenting features. The disease
tends to affect families similarly (e.g. age of onset and age of
reaching ESRF). There is an association with subarachnoid
haemorrhage, and this tendency runs in families.
Examination may reveal large irregular palpable kidneys,
and the patient is often hypertensive. Mitral valve prolapse,
diverticular disease and hernias may also be associated features. Diagnosis is based on ultrasound scan showing multiple cysts. There are diagnostic criteria for this, as cysts can
be a normal finding, and are more common with ageing
(Table 30.8). A family history or genetic testing will help
confirm the diagnosis. Management includes tight blood
pressure control and avoidance of dehydration and nephrotoxins. Renal function declines progressively over time with
cyst growth. Tolvaptan, a competitive vasopressin receptor antagonist, has now been licensed by NICE to slow the
progression of cyst development and renal insufficiency in
those with rapidly progressive disease. (National Institute for
Health and Care Excellence (2015). Tolvaptan for treating autosomal dominant polycystic kidney disease. Technology appraisal guidance 358) (see Clinical Notes box). Patients with
polycystic kidney disease tend to be excellent candidates for
renal transplantation, occasionally with the polycystic kidney
needing to be removed to make space for the transplant.
CLINICAL NOTES
First-degree relatives should be offered screening.
There is now a treatment to prevent renal cyst
growth: tolvaptan. This is an aquaretic which can
delay progression of end-stage renal failure. It is
licensed for only a few groups of patients with
stage II or stage III chronic kidney disease and
rapidly progressing disease.
Hepatorenal syndrome
Hepatorenal syndrome (HRS) is defined as renal failure in
patients with severe liver disease. The underlying problem is
with the liver. It is a diagnosis of exclusion: exclude sepsis,
hypovolaemia, nephrotoxic drugs and glomerulonephritis. In
HRS the problem is of renal perfusion, with liver failure leading to splanchnic vasodilatation and subsequent activation of
the sympathetic nervous system and the renin– angiotensin–
aldosterone system, resulting in intrarenal arteriolar vasoconstriction. Expect the results of urine analysis to be bland
(i.e. no blood or protein). There are two types:
• HRS 1: rapidly progressive renal failure often in
tandem with acute liver failure, alcoholic hepatitis or
decompensation of chronic disease.
• HRS 2: renal failure is more slowly progressive, often
over months.
HRS occurs in about 20% of patients with cirrhosis in the
presence of ascites. Treatment is mainly supportive. You
should have a high clinical suspicion for infection, which
often presents atypically, and treat it aggressively when
recognized. Renal function recovers if the liver recovers,
including after liver transplantation. Splanchnic vasoconstrictors are used, including terlipressin in combination
with albumin. Octreotide or noradrenaline may also be
used to improve renal haemodynamics. Prognosis is poor.
Thrombotic microangiopathies
‘Thrombotic microangiopathies’ encompasses haemolytic
uraemic syndrome (HUS) and thrombotic thrombocytopenic purpura, which form a spectrum of disorders. They
are diseases attributed to disordered complement activation, leading to endothelial damage. HUS is characterized
by microangiopathic haemolytic anaemia, renal failure
and thrombocytopenia. Thrombotic thrombocytopenic
purpura rarely results in renal failure; classically it is associated with very low platelet count and has associated
neurological features. Diagnosis is from blood test showing ADAMTS13 deficiency. It requires urgent plasma
exchange.
HUS is often associated with AKI. It can be divided into
typical and atypical forms. Typical HUS is associated with
diarrhoea; it is often triggered by Escherichia coli O157:H7.
Test stool for Shiga toxin to support the diagnosis. Treatment
is supportive, and dialysis may be required. Generally, most
patients recover normal renal function. Atypical HUS is
a diagnosis of exclusion. It is associated with underlying
complement mutations. Renal biopsy shows a thrombotic
microangiopathy. If the clinical picture is suggestive of atypical HUS and there is no ADAMST13 deficiency, then it can
be treated with eculizumab. This is a monoclonal antibody
and a terminal complement inhibitor. It is very effective but
extremely expensive, needs to be taken indefinitely and can
increase the risk of encapsulated bacterial infections (e.g.
meningococcal sepsis).
271
Renal, genitourinary and sexual health medicine
RED FLAG
If there are low platelet levels, acute kidney
injury and diarrhoea, think of haemolytic uraemic
syndrome. Look for evidence of haemolysis
by sending a blood film (to look for red cell
fragments). If haemolysis is present, the levels of
reticulocytes and LDH will be raised and the levels
of haptoglobins will be low.
SEXUALLY TRANSMITTED DISEASES
Sexually transmitted infections (STIs) are often asymptomatic and can lead to long-standing problems with fertility,
chronic abdominal pain and multiple organ disorders.
Infected individuals with an STI may be coinfected with
other STIs. Take the opportunity to screen patients for
these. These diseases are best managed in a sexual health
clinic, where a full screen for other STIs, repeated testing
and partner notification can be performed. HIV infection is
discussed in Chapter37.
Chlamydia
Chlamydia trachomatis is a gram-negative bacterium that
infects human columnar and transitional epithelium. It is
the most common STI in the United Kingdom, with 75%
of infections in individuals younger than 25 years. It is
the most common preventable cause of infertility. It is asymptomatic in about 50% of men and 70% women. Most
cases are detected through screening or investigation of
other genitourinary infection. Symptoms include vaginal
discharge, dysuria, intermenstrual bleeding and dyspareunia. In men the most common symptom is urethritis with
dysuria, or testicular pain. Diagnosis is by vulvovaginal
swab in women and first-catch urine in men (this can also
be used in women but is less sensitive). Treatment is with
doxycycline for 7days or a single dose of azithromycin. If
left untreated, it can lead to pelvic inflammatory disease
(PID), ectopic pregnancy, infertility in women and epididymitis and epididymo-orchitis in men.
HINTS AND TIPS
Remember to give antibiotic treatment to the
index case, screen the patient for other sexually
transmitted infections and notify the patient’s
partner(s). This is best done by a sexual health
clinic.
COMMUNICATION
The patient should be advised to abstain from sex
(even if the patient is using barrier contraception)
whilst receiving treatment.
CLINICAL NOTES
Reiter syndrome, a triad of urethritis, arthritis and
conjunctivitis, can be triggered by chlamydia.
Gonorrhoea
This is caused by Neisseria gonorrhoeae, a gram-negative
diplococcus. It infects mucous membranes of the urethra,
endocervix, rectum, pharynx and conjunctiva. Symptoms
will be local to the infected mucous membrane site, and the
condition is diagnosed through swabs of the infected site.
Gonorrhoea is increasing in prevalence, particularly in men
who have sex with men, with the incidence of drug- resistant
strains rising. Coinfection with other STIs is common.
Ninety-five percent of men will have symptoms, compared
with only 50% of women. Symptoms are related to the site of
infection, and may include penile/vaginal discharge, dysuria
and anal bleeding/pruritus. Examination findings are generally normal but may reveal discharge, contact bleeding of the
endocervix or epididymal tenderness. Diagnosis involves a
nucleic acid amplification test of endocervix/urethral, pharyngeal and rectal swabs or urine culture (the latter being
less sensitive). The organism will then be cultured to detect
the strain and antibiotic sensitivities. Treatment is with ceftriaxone intramuscularly, and a single dose of azithromycin.
Complications of gonorrhoea include urethral strictures in
men, which can lead to bladder outflow obstruction and pelvic inflammatory disease, and infertility in women.
The general principles of partner notification and
screening for other STIs applies.
Syphilis
Syphilis is caused by Treponema pallidum, and can be ac-
quired or congenital. It is divided into stages. In the first
stage, primary syphilis, there is local infection (e.g. a
small painless papule which forms an ulcer, the chancre).
Secondary syphilis develops in 25% of untreated primary
infections, and is associated with generalized infection.
Symptoms of secondary syphilis classically include a generalized polymorphic rash affecting the palms, soles and
face, with generalized lymphadenopathy. The papules of
the rash enlarge into condylomata lata (pink-grey discs)
272
Further reading
3030
and then disappear. There is then a latent phase, during
which infectious relapses can occur. During these phases,
although patients are asymptomatic, serological testing will
confirm syphilis. Tertiary syphilis can then develop and
cause cardiovascular syphilis (aortitis and ascending aortic
aneurysm and aortic regurgitation), neurosyphilis (tabes
dorsalis and dementia) and gummatous syphilis (fibrous
nodules affecting bone and skin). The incidence of syphilis is increasing rapidly, particularly amongst men who
have sex with men. Testing includes treponemal enzyme
immunoassay, which can detect IgM in early disease. The
Venereal Disease Reference Laboratory (VDRL) test can be
used as an indication for the stage of syphilis, with false negatives occurring in secondary disease. Treat primary disease
HINTS AND TIPS
Jarisch–Herxheimer reaction is an acute febrile
illness that occurs after the patient commences
antibiotic treatment. It is thought to be caused by
endotoxin-like products being released during the
death of the Treponema.
with high-dose penicillin (benzathine penicillin intramuscularly); this is given as a single dose in primary disease and
for up to 14days in neurosyphilis.
Chapter Summary
• In an individual with an acute kidney injury (AKI), always perform a urine dipstick test. If
protein is present in the absence of infection, quantify this loss with a spot albumin-to
creatinine ratio or protein-to-creatinine ratio measurement. If there is blood and protein
on the urine dipstick and an AKI, ask yourself whether there is a rapidly progressive
glomerulonephritis.
• AKI is largely predictable and avoidable. Take care to identify groups at higher risk of AKI.
Individuals with AKI have longer hospital stays and greater risk of death.
• Chronic kidney disease is divided into five stages. The rate of progression is determined
largely by the heaviness of proteinuria and hypertension. Ensure tight control of blood
pressure.
• Indications for emergency haemodialysis include resistant hyperkalaemia, pulmonary
oedema, uraemic pericarditis and severe acidosis.
• Renal obstruction and sepsis, a pyonephrosis, is an emergency and needs prompt
antibiotic treatment and decompression.
• Patients with a sexually transmitted infection need to be screened for other coexisting
sexually transmitted infections. This is best performed in a sexual health clinic, where
partner notification can be conducted.
FURTHER READING
Chadban, S.J., Atkins, R.C., 2005. Glomerulonephritis. Lancet 365,
1797–1806.
Gines, P., Guevara, M., Arroyo, V., Rodes, J., 2003. Hepatorenal
syndrome. Lancet 362, 1819–1827.
Jones, T., 2012. Crash Course: Renal and Urinary Systems, 4th ed.
Mosby, Edinburgh.
Lameire, N., van Biesen, W., Vanholder, R., 2008. Acute kidney in-
jury. Lancet 372, 1863–1865.
Renal Association. Clinical practice guidelines. Available online at:
https://renal.org/guidelines/Guidelines.aspx.
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Fluid balance and electrolyte
disturbances
Understanding fluid balance and electrolyte disturbance will
be essential in your medical career. You will need to appreciate it from the first day as a Foundation Programme doctor
when checking blood test results and prescribing fluids.
It is worth taking time to appreciate the following concepts. In a 70-kg man, the total fluid volume is 42 L (i.e.
60% of the body weight). The intracellular fluid volume is
28 L, or two-thirds of the total body fluid, and the extracellular fluid volume is 14 L, or one-third of the total body
fluid. The intravascular component is 3 L. The average total
fluid intake in 24 hours is 2500 mL (1500 mL drunk, 800 mL
in food and 200 mL via the metabolism of food), and output
usually matches this via urine, insensible loss and stool.
Sodium ingestion is approximately 2 mmol/kg in 24
hours and potassium ingestion is approximately 1 mmol/kg
in 24 hours.
Understanding the aforementioned requirements will
help you in prescribing fluids in a sensible and appropriate manner. Generally speaking, fluids can be divided into
crystalloids (e.g. ‘normal’ saline or Hartmann solution) and
colloids (e.g. albumin); see Table31.1.
SODIUM AND WATER BALANCE
Fluid balance is achieved in the body by ensuring that the
amount of water consumed in food and drink (and generated by metabolism) equals the amount of water excreted.
The consumption side is regulated by behavioural mechanisms, including thirst and salt cravings. Approximately 1 L
is lost each day through insensible losses, and the kidneys
can regulate the remaining excretion of water. This can
31
be achieved through the action of antidiuretic hormone
(ADH; also known as ‘vasopressin’) on the distal collecting
duct controlling water reabsorption (see Chapter15).
In addition to regulation of total volume, the osmolality
of bodily fluids is also tightly regulated. Regulation of osmolality is achieved by balancing the intake and excretion of
sodium with that of water. Fluid status and sodium level are
interdependent. Sodium balance can be controlled through
the action of the renin–angiotensin system. Disorders of sodium homeostasis are common.
HYPONATRAEMIA
This is a very common disorder, and the development of
hyponatraemia is a poor prognostic marker. In hospital it
is usually the result of neurohumoral changes in acute illness and the type, volume and route of fluid administered.
Consider what intravenous fluids to prescribe carefully. To
evaluate hyponatraemia, these questions should be answered:
• How low is the sodium level and how quickly has it
fallen?
• What is the patient's volume status?
• What is the urine osmolality?
• What is the urinary sodium value?
For example, in hypovolaemia secondary to dehydration
or diarrhoea, the kidneys retain salt and water, resulting
in low urinary sodium level (<20 mmol/L. Diuretics or
mineralocorticoid (principally aldosterone) deficiency
will cause hypovolaemia with a high urinary sodium level
(>20 mmol/L). With this information, the diagnostic algorithm shown in Fig.31.1 can be followed.
Table31.1 Composition of common intravenous fluids
Fluid type Use
Normal saline
(0.9% NaCl)
Hartmann solution Crystalloid
Dextrose, 5% Maintenance 0 0 0 0 50
Human serum
albumin, 5%
The daily requirements for a 70-kg man are approximately 140 mmol sodium and 70 mmol potassium.
Crystalloid
Maintenance and
resuscitation fluid
Maintenance and
resuscitation fluid
Colloid 130 130 0 0 0
Sodium
(mmol/L)
154 154 0 0 0
131 111 5 29 0
Chloride
(mmol/L)
Potassium
(mmol/L)
Lactate
(mmol/L) Glucose (g/L)
275
Fluid balance and electrolyte disturbances
Hyponatraemia
Yes
Urinary sodium
Yes
• Diuretics
• Renal failure
• Osmolar diuresis
(e.g. ↑glucose)
• Addison disease
Fig.31.1 Algorithm for investigation of hyponatraemia. SIADH, Syndrome of inappropriate secretion of antidiuretic hormone.
> 20 mmol/L
No
• Diarrhoea/
vomiting
• Villous adenoma
of rectum
• Small bowel
obstruction
• Burns
• Heat exposure
The symptoms depend on the chronicity of the hyponatraemia as well as the actual sodium level. The more
chronic the hyponatraemia, the better tolerated it is. In
general, a mild hyponatraemia may be asymptomatic but
may give symptoms of fatigue and confusion. As this becomes severer, the patient is likely to get more confused and
drowsy. In acute or severe hyponatraemia (i.e. sodium level
<115 mmol/L), seizures can occur.
Investigations
When you are investigating the patient with hyponatraemia,
firstly perform a fluid assessment by examining the patient
(see Chapter 15). Pay attention to the serum potassium,
glucose and lipid levels. A spot urinary sodium is the most
useful preliminary investigation. Send a urine sample to
biochemistry to check for this. Serum and urine osmolalities should also be measured, take a sample of blood and
urine at approximately the same time and send the samples
to biochemistry. Check thyroid function test results and a
random cortisol level. If the serum cortisol level is low, this
suggests Addison disease. To confirm this, perform a short
(tetracosactide) test (see Chapter32).
Dehydration?
No
Yes
• Nephrotic
syndrome
• Cardiac failure
• Cirrhosis
• Renal failure
Table31.2 Some causes of syndrome of inappropriate
antidiuretic hormone secretion
Groups Examples
Central nervous
system
Pulmonary Neoplasms
Malignancies Small cell lung cancer
Drugs Antidepressants–SSRIs
SSRI, Selective serotonin reuptake inhibitor.
Oedema
Yes
• SIADH
Stroke
Subarachnoid haemorrhage
Head trauma
Brain tumour, meningitis
Tuberculosis
Pneumonia
Pancreatic
Lymphoma
Neuroleptics
Chlorpropamide
Carbamazepine
Proton pump inhibitors (e.g. omeprazole)
No
Urine osmolality
> 500 mOsmol/kg
• Water excess
• Hypothyroidism
• Glucocorticoid
deficiency
No
COMMON PITFALLS
Look carefully at the medications. Diuretics,
especially thiazides, can cause a profound
hyponatraemia through their mechanism of
action. Other drugs can cause a syndrome of
inappropriate secretion of antidiuretic hormone
(see Table31.2).
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Treatment depends on the cause. If the patient is dehydrated, then volume replacement with normal saline is required. If the patient is hypervolaemic, treat the underlying
cause (e.g. cardiac, liver or renal failure). This tends to involve strict fluid restriction. In the case of a syndrome of
inappropriate secretion of ADH (SIADH), stop the use
of any possible causative medications and restrict the patient’s fluid intake. Start with 1-L restriction, and if this is
not effective, then decrease the amount allowed to 750 mL
then 500 mL. If this is still not effective, then tolvaptan (an
aquaretic) or demeclocycline (an ADH receptor blocker
Hypernatraemia
3131
which causes a partial diabetes insipidus) can be used. Take
great caution that sodium level does not rise too rapidly
with these therapies. Acute symptomatic hyponatraemia is
a medical emergency. Treatment involves carefully raising
the sodium level: the more chronic the hyponatraemia, the
slower the correction should be. In the case of a sodium
level below 115 mmol/L or severe symptoms, the patient
should be admitted to a critical care environment, and the
sodium level should be corrected only very slowly, not faster
than 1 mmol/L per hour, and not more than 10 mmol/L in
the first 24 hours as central pontine myelinolysis, osmotically induced demyelination, can ensue.
SIADH is characterized by hyponatraemia, (serum sodium level <135 mmol/L), low plasma osmolality with an inappropriately high urine osmolality (>100 mOsmol/kg) and
high urinary sodium level (>30 mmol/L). SIADH is a diagnosis of exclusion and can be diagnosed only if the patient is
euvolaemic and cardiac, adrenal, thyroid and renal dysfunction have all been excluded. Causes are shown in Table31.2.
COMMON PITFALLS
Watch your intravenous fluid prescription. If you
use 5% dextrose too frequently, you will induce
hyponatraemia.
HINTS AND TIPS
Is this true hyponatraemia? False low sodium
readings can occur in the presence of
hyperglycaemia and hypercholesterolaemia.
Table31.3 Causes of hypernatraemia
Total body sodium
Low total body sodium
level
Normal total body sodium
level
High total body sodium
level
Causes
Extrarenal: e.g. sweating,
diarrhoea
Renal: osmotic diuresis
Diabetes insipidus
Steroid excess: e.g.
Cushing disease, Conn
syndrome
Iatrogenic: e.g. hypertonic
sodium infusions
Self-induced: e.g. ingestion
of sodium chloride tablets
insipidus); see Table31.3. Excess saline replacement is a com-
mon iatrogenic cause due to inappropriate fluid prescribing.
Symptoms of hypernatraemia include central nervous system
dysfunction, including lethargy, weakness, confusion and
even seizures. In the case of diabetes insipidus, the patient will
have polydipsia and polyuria (see Chapter15). Investigations
include checking renal function, electrolyte levels, bone profile (pay attention to calcium) and plasma glucose level. Take
serum and urine samples at approximately the same time and
measure the osmolality of the serum and urine (paired osmolalities). In Diabetes Insipidus you would expect to find a
high serum osmolality and low urine osmolality. Treatment
is directed at the underlying cause. Review medications and
stop the use of any diuretics or laxatives and give appropriate fluid replacement. The sodium level should be reduced
no faster than 1 mmol/L per hour to avoid rapid fluid shifts
and cerebral oedema. Giving fluid replacement by the enteral
route if possible is best. If intravenous treatment is used, adjust the fluid prescription in relation to the serum sodium
level and monitor this level regularly.
RED FLAG
Patients with serum sodium levels below
120 mmol/L are best managed in a critical care
environment. Care needs to be taken to establish
the underlying cause and to carefully increase the
sodium level at a slow rate. The rate of correction is
dependent of the chronicity of the hyponatraemia.
Acute causes of hyponatraemia are likely to give
more symptoms and can be corrected faster.
HYPERNATRAEMIA
Hypernatraemia is defined as serum sodium level above
145mmol/L. It can occur with dehydration (e.g. with thirst
impairment in patients who have dementia and diabetes
CLINICAL NOTES
Try to establish how chronic the hypernatraemia
is. The more long-standing it is, the slower the
correction needs to be.
ETHICS
Patients with end-stage dementia often have
hypernatraemia caused by impairment of thirst.
There is often a debate whether these patients
should be given intravenous fluid replacement. This
needs careful consideration with the patient’s next
of kin and the multidisciplinary team.
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