R030

Hyponatraemia: Be(er) Aware

R Ratnasabapathy, H Tetlow, S Qureshi, S Stevens, R Smail, S Siddiqui, K Ahmed, E Hui. West Middlesex Hospital.

Abstract:

A 57 year old male was found confused by a friend at home.  He had no significant past medical history and was not on any regular medication. His plasma sodium on admission was 98 mmol/L (NR 136mmol – 146mmol). He had normal potassium of 4.1 mmol/L (3.5-5.1mmol/L) and renal function. On examination, his mini mental score was 4/10. He was clinically hypovolaemic. He also had deranged liver function test with impaired synthetic function: platelet 88x10e9/L (150-400x10e9/L), albumin 19g/L (35-52g/L), INR 1.7 and macrocytosis. On further questioning, he had a history of alcohol abuse and had an alcohol intake of 10 units per day for 20 years.His serum osmolality was low at 221mosm/kg (275-295mosm/kg) with a low urine osmolality of  81mosom/kg (50-1200mosm/kg). Urinary Na was 7mmol/24h (40-200mmol/24h). His random cortisol was 779nmol/L (83-607nmol/L) which made acute hypoadrenal crisis unlikely. He also had normal thyroid function (TSH 1.35, free T4 = 13pM) and normal lipid profile (triglycerides 0.57), which excluded pseudohyponatraemia secondary to hypertriglyceridaemia. Immunoglobulin levels were normal and 24-hour urinary protein was 2.08g/24h. Chest X-ray revealed a left hilar opacity, but further CT chest showed emphysematous bullae with no focal pulmonary masses.He was initially treated with slow intravenous fluids and Demeclocycline, which was initially commenced for syndrome of inappropriate ADH, was discontinued following the osmolality findings. His sodium gradually increased to 131mmol/L in five days with fluid restriction of 1.5L although he did not fully abide to it. His confusion resolved gradually with concomitant alcohol withdrawal treatment.

Hyponatraemia is commonly found in chronic alcoholic patients. Common causes include hypovolaemia, and pseudohyponatraemia due to hypertriglyceridaemia. This case is likely due to the syndrome of ‘beer potomania’. It is believed that in beer potomania, chronic consumption of beer which is a hypotonic alcoholic solution, combined with protein malnutrition, lead to profound hyponatraemia. Collateral history confirmed that this gentleman consumed large volumes of beer exclusively, and had a poor dietary intake. The kidneys respond appropriately to this high water and low solute state by maximally diluting the urine. Even with maximal ADH suppression a mandatory solute loss of 50-100mOsm/kg of urine exists. Additionally, binge drinkers can only typically produce up to 2.5 litres of urine per day. Hence some of the total volume consumed is not excreted, resulting in hyponatraemia. The risk of central pontine myelinolysis is high and slow correction of hyponatraemia of less than 10 mmol/L in the first 24 hours is recommended. Since the hyponatraemia in this condition is multifactorial, there is no definite consensus on treatment. Careful correction with intravenous 0.9% normal saline has been recommended in patients with seizure or reduced GCS. Fluid restriction has been suggested for milder asymptomatic cases.