History A 79-year-old woman is brought to hospital by her daughter because of increasing confusion. This has developed over the last 3 weeks and prior to this her daughter says that she had normal cognitive function. She also complains of loss of her appetite, headache and muscle cramps. She had hypertension diagnosed 5 years ago and was on treatment with atenolol but this was stopped 2 months ago because she complained of cold hands and feet. Her medication was changed to bendroflumethiazide 2.5mg once a day and she has had no problems with these tablets. She lives on her own with her daughter nearby. She neither drinks alcohol nor smokes. She is on no other medication although she takes vitamins that she buys from the chemist.
Examination Her skin turgor is normal. Her pulse is 80/min regular, blood pressure 146/90mmHg, jugular venous pressure normal, heart sounds normal with no peripheral oedema. Respiratory and abdominal systems are normal. Her abbreviated mental test score is 6/10 with disorientation in time and place. There is no focal neurology. Funduscopy shows silver-wiring and arteriovenous nipping but no papilloedema.
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Normal Haemoglobin 12.2g/dL 11.7–15.7g/dL White cell count 6.2 109/L 3.5–11.0 109/L Platelets 172 109/L 150–440 109/L Sodium 113mmol/L 135–145mmol/L Potassium 3.3mmol/L 3.5–5.0mmol/L Urea 3.4mmol/L 2.5–6.7mmol/L Creatinine 64amol/L 70–120amol/L Glucose 5.0mmol/L 4.0–6.0mmol/L Albumin 36g/L 35–50g/L Urinary osmolality 318mosmol/kg 360–1200mosmol/kg Urinary sodium 55mmol/L 5–300mmol/L Urinalysis: no protein; no blood Chest X-ray: normal INVESTIGATIONS
Questions • What is the likely cause of this patient’s confusion? • How would you correct this problem?
History A 79-year-old woman is brought to hospital by her daughter because of increasing confusion. This has developed over the last 3 weeks and prior to this her daughter says that she had normal cognitive function. She also complains of loss of her appetite, headache and muscle cramps. She had hypertension diagnosed 5 years ago and was on treatment with atenolol but this was stopped 2 months ago because she complained of cold hands and feet. Her medication was changed to bendroflumethiazide 2.5mg once a day and she has had no problems with these tablets. She lives on her own with her daughter nearby. She neither drinks alcohol nor smokes. She is on no other medication although she takes vitamins that she buys from the chemist.
Examination Her skin turgor is normal. Her pulse is 80/min regular, blood pressure 146/90mmHg, jugular venous pressure normal, heart sounds normal with no peripheral oedema. Respiratory and abdominal systems are normal. Her abbreviated mental test score is 6/10 with disorientation in time and place. There is no focal neurology. Funduscopy shows silver-wiring and arteriovenous nipping but no papilloedema.
Normal Haemoglobin 12.2g/dL 11.7–15.7g/dL White cell count 6.2 109/L 3.5–11.0 109/L Platelets 172 109/L 150–440 109/L Sodium 113mmol/L 135–145mmol/L Potassium 3.3mmol/L 3.5–5.0mmol/L Urea 3.4mmol/L 2.5–6.7mmol/L Creatinine 64amol/L 70–120amol/L Glucose 5.0mmol/L 4.0–6.0mmol/L Albumin 36g/L 35–50g/L Urinary osmolality 318mosmol/kg 360–1200mosmol/kg Urinary sodium 55mmol/L 5–300mmol/L Urinalysis: no protein; no blood Chest X-ray: normal INVESTIGATIONS
Questions • What is the likely cause of this patient’s confusion? • How would you correct this problem?
ANSWER 79
This woman’s confusion is due to hyponatraemia. There are many causes of confusion in the elderly but the very low sodium level of 113mmol/L in this case is an adequate explanation. Her serum is profoundly hypo-osmolar. In her case, osmolality can be calculated from the following equation: 2 ([Na] [K]) [urea] [glucose]
241mosmol/kg (normal range: 278–305mosmol/kg). Hyponatraemia may be asymptomatic, but when it falls rapidly or reaches very low levels (below 120mosmol/kg) it can cause confusion, anorexia, cramps, fits and coma. Hyponatraemia is associated with hypovolaemia when there is excess loss of fluid and sodium (sweating, burns, diarrhoea and vomiting), or when there is renal loss of sodium and water (diuretic use, Addison’s disease). Hyponatraemia with hypervolaemia occurs when there is excess retention of water. Normally, the dilutional fall in plasma osmolality suppresses arginine vasopressin (AVP, antidiuretic hormone) secretion which allows excretion of excess water. In congestive cardiac failure and cirrhosis with ascites, baroreceptors register reduced perfusion causing AVP secretion, but in most other cases of hyponatraemia there is an inability to suppress AVP secretion normally. In rare cases of primary polydipsia, the huge water intake may overwhelm this mechanism, and in severe renal failure the kidneys cannot excrete a water load. The syndrome of inappropriate anti-diuretic hormone secretion (SIADH) occurs in relation to malignancy, neurological disorders or pneumonia. Circulating volume is usually normal. Normovolaemia with hyponatraemia also occurs after administration of too much intravenous hypotonic fluid and in hypothyroidism. The low plasma sodium, potassium and urea in this patient are consistent with water excess. Measurement of urinary sodium and osmolality is useful. In primary polydipsia the urine can be maximally diluted to 100mosmol/kg, whereas in states with excess AVP the urine osmolality is usually 320mosmol/kg while plasma osmolality is low. Urinary sodium is usually 25mmol/L in hypovolaemic states, but 40mmol/L in SIADH where patients are normovolaemic and the rate of sodium excretion depends on dietary intake and taking of diuretics. Diuretic-induced hyponatraemia tends to occur within a few weeks of starting treatment, and occurs mainly in elderly women often concurrently on non-steroidal antiinflammatory drugs (NSAIDs) which inhibit water excretion. The clinical and biochemical picture in this woman is consistent with diuretic-induced hyponatraemia.
• Low plasma osmolality with high urinary osmolality suggests excess ADH