Royd is confused
• Royd, 72 y.o. male
• Admitted to hospital in acute confusional state
• No history is available
– nicotine stains on his fingers indicate that he was/
is a heavy smoker.
– found to have digital clubbing
– also present are signs of a right-sided pleural
effusion
– neither dehydrated nor oedematous.
Investigations
• Serum:
– Sodium =
Potassium =
Bicarbonate =
Urea =
Random Glucose =
Total protein =
Osmolality =
114 mmol/L (135-145 mmol/L)
3.6 mmol/L (3.5-5.0 mmol/L)
22 mmol/L (25-33 mmol/L)
2.5 mmol/L (3.0-8.5 mmol/L)
4.0 mmol/L (3.0-7.7 mmol/L)
48 g/L (60-82 g/L)
236 mmol/L (282-295 mmol/ kg)
• Urine:
– Sodium = 50 mmol/L
– Osmolality = 350 mmol/ kg
• CXR: Right-sided pleural effusion and a mass in the lower
right zone with an appearance typical of carcinoma.
What are the clinical signs and X-ray
features of a pleural effusion?
Some pleural effusions are asymptomatic and are discovered incidentally during physical examination or
on chest x-ray.
• Many cause:
–
–
–
dyspnoea
pleuritic chest pain (inflammation of parietal pleura – felt over inflamed site)
or both.
•
Lower chest wall/abdominal pain
•
Neck/shoulder referred pain
–
–
•
posterior and peripheral portions of the diaphragmatic pleura are supplied by the lower 6 intercostal nerves
Irritation of the central portion of the diaphragmatic pleura, innervated by the phrenic nerves
Physical examination
–
–
absent tactile fremitus, dullness to percussion
decreased breath sounds on the side of the effusion.
•
–
These findings can also be caused by pleural thickening.
For large-volume effusions
•
•
respiration is usually rapid and shallow.
pleural friction rub is the classic physical sign (although infrequent)
–
–
The friction rub varies from a few intermittent sounds that may simulate crackles to a fully developed harsh grating,
creaking, or leathery sound synchronous with respiration, heard during inspiration and expiration.
Pericardial rub is best heard over the left border of the sternum in the 3rd and 4th intercostal spaces, is characteristically a
to-and-fro sound synchronous with the heartbeat, and is not influenced significantly by respiration. Sensitivity and specificity
of the physical examination for detecting effusion are probably low.
What are some of the signs and
symptoms of hyponatraemia?
• Often asymptomatic
• May be associated with symptoms of cerebral dysfunction such as:
–
–
–
–
–
–
–
Anorexia
Nausea
Vomiting
Confusion
Lethargy
Seizure
Coma
• The degree of cerebral symptomatology depends more on the rate
of development of the electrolyte abnormality than on its severity.
– Eg. rapid hyponatraemia causes more rapid cerebral cell swelling and
ischaemia than gradually occurring hyponatraemia, in which there is
time to reduce intracellular osmolality
What are some of the causes of hyponatraemia and how might
you differentiate between these causes?
Volume Status
Hypovolaemic (sodium deficit with a relatively
smaller water deficit)
Examples
Renal Na losses
Diuretic therapy (especially thiazides)
Adrenocortical failure
Gastrointestinal Na losses
Vomiting
Diarrhoea
Euvolaemic (water retention alone)
Primary polydipsia
Excessive electrolyte-free water infusion
SIADH
Hypothyroidism
Hypervolaemic (sodium retention with
relatively greater water retention)
Congestive cardiac failure
Cirrhosis
Nephrotic syndrome
Chronic renal failure (during free water intake)
What is the most likely cause of Royd's
hyponatraemia? What are some of the causes of this
condition?
HYPONATRAEMIA
Is the patient
dehydrated?
NO
YES
Is urinary Na >20mmol/L
YES
Na and H20 are not lost
via kidneys:
•Addison’s disease
•Renal failure, eg.
diuretic phase of renal
failure; nephrocalcinosis
or medullary cystic
disease
•Diuretic excess
•Osmolar diuresis
(glucose;urea)
NO
Na and H20 are lost
other than via the
kidneys;
•Diarrhoea
•Vomiting
•Fistulae
•Burns
•Rectal villous adenoma
•Small bowel
obstruction
•Trauma
•Cystic fibrosis
•Heat exposure
Is the patient oedematous?
YES
•Nephrotic syndrome
•Cardiac failure
•Liver cirrhosis
(hyponatraemia may
precede oedema)
•Renal failure
NO
Is the urine osmolality > 500mosmol/kg?
YES
•SIADH
NO
•Water overload
•Severe hypothyroidism
•Glucocorticoid insufficiency
Diagnosis of SIADH
• Low plasma sodium concentration (typically < 130 mmol/l)
• Low plasma osmolality (< 270 mmol/kg)
• Urine osmolality not minimally low
–
–
–
–
–
> 150 mmol/kg [davidsons] or
>200mmol/kg [sydney pathology]
>100mosmol/kg [Australian tg]
>500mosmol/kg [Oxford handbook]
???
• Urine sodium concentration not minimally low (> 30 mmol/l)
• Low-normal plasma urea, creatinine, uric acid
• Exclusion of other causes of hyponatraemia
Causes of SIADH
• Tumours, especially small-cell lung cancer
• (Royd’s smoking history, clubbed fingers [apparently more common in NSLC than SLC
though] & pleural effusion make this most likely in his case)
• CNS disorders: stroke, trauma, infection, psychosis
• Pulmonary disorders: pneumonia, tuberculosis
• Drugs
–
–
–
–
–
–
Anticonvulsants, e.g. carbamazepine
Psychotropics, e.g. haloperidol
Antidepressants, e.g. amitriptyline, fluoxetine
Cytotoxics, e.g. cyclophosphamide, vincristine
Hypoglycaemics, e.g. chlorpropamide
Opiates, e.g. morphine
• Sustained pain, stress, nausea, e.g. post-operative state, acute porphyria
• Idiopathic
How should a case of hyponatraemia
due to SIADH be managed?
• Treat the cause of SIADH
• Restrict fluid
• Consider salt + loop diuretic if severe (eg those with seizures,
mental status changes or extremely low sodium levels)
– In these patients it is important to weigh up the risk of aggressive
treatment against that of inducing CMP (cerebral pontine myelinolysis)
• Other treatments (second line):
– Demeclocycline is used rarely (acts by inducing a nephrogenic diabetes
insipidus)
– Vasopressin receptor antagonists (‘vaptans’) are an emerging class of
drug used in SIADH and hyponatraemia