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Royd is confused
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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.
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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.
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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.
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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
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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)
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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
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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
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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
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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
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