1. Royd is confused

2. 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.

3. Investigations Serum: – Sodium = 114 mmol/L (135-145 mmol/L) Potassium = 3.6 mmol/L (3.5-5.0 mmol/L) Bicarbonate = 22 mmol/L (25-33 mmol/L) Urea = 2.5 mmol/L (3.0-8.5 mmol/L) Random Glucose = 4.0 mmol/L (3.0-7.7 mmol/L) Total protein = 48 g/L (60-82 g/L) Osmolality = 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.

4. 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 – posterior and peripheral portions of the diaphragmatic pleura are supplied by the lower 6 intercostal nerves Neck/shoulder referred pain – 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.

5. 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

6. What are some of the causes of hyponatraemia and how might you differentiate between these causes? Volume StatusExamples Hypovolaemic (sodium deficit with a relatively smaller water deficit) 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)

7. What is the most likely cause of Royd's hyponatraemia? What are some of the causes of this condition? YES Is urinary Na >20mmol/L HYPONATRAEMIA Is the patient dehydrated? Is the patient oedematous? 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 NO Is the urine osmolality > 500mosmol/kg? NO Water overload Severe hypothyroidism Glucocorticoid insufficiency NO SIADH YES Nephrotic syndrome Cardiac failure Liver cirrhosis (hyponatraemia may precede oedema) Renal failure 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) YES

8. 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

9. 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

10. 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