Diabetic Man's Head Injury Leads to SIADH Under 40
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Case 23 A 58-year-old type II diabetic with
confusion and hyponatraemia
Mr Sanjay Singh is a 58-year-old type II diabetic. He is
admitted following a road trafļ¬c accident with a head injury
and fractured tibia and ļ¬bula. Glasgow Coma Score (GCS)
on admission was 15 and a CT head did not show any
obvious fracture, haematoma or contusion. His lower limb
fractures are ļ¬xed in plaster of Paris (POP) and he is
admitted for observation and analgesia.
Bloods on admission are shown below.
Na 135mmol/L, K 4.0mmol/L, Urea 7.3mmol/L, Creatinine
112Ī¼mol/L, Glc 6.8mmol/L
Hb 15.8g/dL, WBC 5.7 Ć 109
/L, Platelets 230 Ć 109
/L
He is seen on ward round the next day and a plan is made
to discharge him later in the day. Unfortunately, he becomes
increasingly confused during the afternoon. His temperature
is 38o
C, pulse 90bpm, BP 145/85mmHg and JVP is visible.
He has no peripheral oedema. O2 saturations are 93% on air
and there are some crackles at the right base. There are no
focal neurological signs. Repeat bloods are shown below
and Mr Singhās drug chart is shown in Figure 23.1.
Na 125mmol/L, K 3.8mmol/L, Urea 5.7mmol/L, Creatinine
108Ī¼mol/L, Glc 10.6mmol/L
Hb 15.5g/dL, WBC 6.2 Ć 109
/L, Platelets 353 Ć 109
/L
What is the most likely cause of
Mr Singhās hyponatraemia?
The causes of hyponatraemia are summarised in Box
23.1. Mr Singhās hyponatraemia is acute and he is not
obviously oedematous, ļ¬uid overloaded or dehydrated
(thus CCF, nephrosis, cirrhosis and diarrhoea are unlikely
to be the cause of his hyponatraemia). He is not on any
medications, particularly diuretics, which might directly
affect renal salt handling. We are not told anything about
Mr Singhās ļ¬uid replacement regimen, therefore if he has
been given an excess of 5% dextrose in the past 36 hours,
this may have caused hyponatraemia. However, given
all of the above exclusions, the most likely diagnosis is
the syndrome of inappropriate antidiuretic hormone
(SIADH).
Review of Mr Singhās ļ¬uid charts shows that he has had
free oral intake but no intravenous ļ¬uids.
What investigations would you
undertake to conļ¬rm the diagnosis
of syndrome of inappropriate
antidiuretic hormone?
Serum and urine osmolalities should be measured.
Plasma osmolality is usually kept within a tight range. In
SIADH there is dilute plasma with osmolalities of
<260mmol/kg and inappropriately concentrated urine
with urine osmolalities of >500mmol/kg. Urinary
sodium levels are usually >20mmol/L.
Mr Singhās urine osmolality is 549mosmol/kg and his serum
osmolality is 258 mosmol/kg, conļ¬rming the diagnosis of
SIADH.
What is the likely cause of syndrome of
inappropriate antidiuretic hormone in
Mr Singhās case?
Syndrome of inappropriate antidiuretic hormone can be
caused by many pathologies, as summarised in Box 23.2.
In this particular case, it is most likely to be due to head
injury. However, there may be other contributory fea-
tures. His examination ļ¬ndings suggest the possibility of
a right basal pneumonia (febrile, crackles at right base).
In addition, he has been given opiates for his pain and is
receiving chlorpropamide (see drug chart in Figure 23.1).
Where is antidiuretic hormone produced
and what are its actions?
Antidiuretic hormone (ADH, also known as vasopressin)
is produced in the hypothalamus, stored in vesicles in the
Nephrology: Clinical Cases Uncovered. By M. Clatworthy.
Published 2010 by Blackwell Publishing.
2. 160 Part 2: Cases
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SANJAY
MRC BEECH
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ASPIRIN
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ATORvASTATIN
CHLORPROPAMIDE
COPROXAMOL
22/10 ul
M
A30694
Surname
First names
Consultant
Date of birth Sex
Ward
Weight
Height
Date Drug/substance
Drug sensitivities
Regular prescriptions
Month and date
Tick times or enter other times
1. Drug (approved name)
2. Drug (approved name)
3. Drug (approved name)
4. Drug (approved name)
5. Drug (approved name)
6. Drug (approved name)
Dose Route Start date Stop date
Dose Route Start date Stop date
Dose Route Start date Stop date
Dose Route Start date Stop date
Pharm
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Bleep no.:
Signature:
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Pharm
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Pharm
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Dose Route Start date Stop date
Pharm
Signature:
Bleep no.:
Additional instructions
Additional instructions
Additional instructions
Additional instructions
Additional instructions
Dose Route Start date Stop date
Pharm
Signature:
Bleep no.:
Additional instructions
Doctor must enter this information on FRONT of case folder
Signature
Hospital No.
Prescription chart
Figure 23.1 Mr Singhās prescription chart.
4. 162 Part 2: Cases
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Why is important not to correct
hyponatraemia too quickly?
If plasma Na+ is corrected too quickly then central
pontine myelinolysis (CPM) can occur, where neurones
in the pontine region become demyelinated. This is
thought to be due to rapid ļ¬uid shifts out of the brain in
response to large increases in plasma sodium. Patients
rapidly develop para- or quadraparesis, dysphagia, dys-
arthria, diplopia and loss of consciousness. Diagnosis
is by clinical features and MRI (showing a high signal in
the pons).
Aim to correct plasma sodium by 5mmol/L/24h.
Maximum correction 8mmol/L/24h. Reports of CPM
have occurred where Na has risen by >10mmol/
L/24h.
Mr Singh is placed on a 1000mL ļ¬uid restriction over the
next 4 days. A chest X-ray conļ¬rms a likely right basal
Table 23.1 Causes of hypontraemia according to volume
status and urine Na excretion
Hypovolaemia Euvolaemia/
hypervolaemia
Urine Na+
>20mM Diuretics
Hypoadrenalism /
Addisonās
SIADH
Hypothyroidism
Chronic renal failure
Urine Na+
<20 mM Vomiting
Diarrhoea
LVF
Cirrhosis
Nephrotic syndrome
CASE REVIEW
A 58-year-old type II diabetic is admitted following an
accident. Over the next 36 hours he becomes confused.
Investigations show signiļ¬cant hyponatraemia (Na
125mmol/L), reduced serum osmolality and increased
urine osmolality in keeping with a diagnosis of SIADH.
This has probably been caused by the head injury sustained
during the accident. He is ļ¬uid restricted to 1L in 24 hours
and his sodium begins to rise. He improves rapidly and is
discharged 5 days later with a sodium of 136mmol/L.
KEY POINTS
ā¢ Mild hyponatraemia is common and usually asymptomatic.
If the sodium falls to around 120mmol/L then there is
often restlessness, irritability and confusion. Sodium levels
of <110mmol/L lead to progressive coma and seizures.
ā¢ Hyponatraemia occurs if there is too little sodium, too
much water or both.
ā¢ When assessing the cause of hyponatraemia, it is
important to establish the volume status of the patient.
ā¢ If the patient is hypovolaemic then hyponatraemia may be
caused by diuretics, hypoadrenalism, salt-wasting
nephropathy (see Table 23.1).
ā¢ If the patient is euvolaemic or ļ¬uid overloaded then
hyponatraemia may be due to SIADH, chronic renal
failure, LVF, cirrhosis or nephrotic syndrome (see
Table 23.1).
ā¢ In SIADH, typical ļ¬ndings are:
ä Na <125mmol/L
ä patient is normovolaemic
ä urinary Na >20mmol/L
ä plasma osmo <260mosmol/kg
ä urinary osmo >500mosmol/kg.
ā¢ Syndrome of inappropriate antidiuretic hormone may be
caused by intracranial pathology such as head injury or
infection, pulmonary pathologies including pneumonia,
malignancies and drugs (particularly chlorpropamide and
chlorpromazine).
ā¢ Treatment of SIADH is with ļ¬uid restriction. The aim
should be to bring the sodium up slowly in order to avoid
central pontine myelinolysis.
pneumonia and he is therefore commenced on appropriate
antibiotic therapy. His sodium rises from 125 to 129mmol/L
on day 1, to 132mmol/L on day 2 and to 136mmol/L by
day 3. He is ļ¬nally discharged on oral antibiotics on day 6.