Poster Presentation The Annual Scientific Meeting of the Endocrine Society of Australia and the Society for Reproductive Biology 2014

An unusual case of hyponatraemia (#275)

Nadia Patel 1 , Anders Taylor 2 3 , Andrew Nicol 4 , Christine Rowland 5
  1. Diabetes and Endocrinology, Princess Alexandra Hospital, Brisbane, QLD, Australia
  2. Cardiology, Greenslopes Private Hospital, Brisbane, QLD, Australia
  3. Senior Lecturer , University of Queensland, Brisbane, QLD, Australia
  4. Haematology, Greenslopes Private Hospital, Brisbane, QLD, Australia
  5. Diabetes and Endocrinology, Greenslopes Private Hospital, Brisbane, QLD, Australia

Hyponatraemia is a commonly encountered electrolyte disturbance which has a variety of causes. We describe the case of an 80 year old gentleman with a history of multiple myeloma who developed hyponatraemia during an admission with congestive cardiac failure and a respiratory tract infection. His serum sodium fell from 131mmol/L to 126mmol/L within 2 days and continued to drop progressively.

Paired biochemistry, once the serum sodium fell to 117mmol/L, revealed a serum osmolality of 265mmol/kg with urine osmolality 402mmol/kg and urinary sodium <20mmol/L.  Cortisol and thyroid hormone levels were normal.  Given what appeared to be a mixed picture, he was managed with free water restriction plus salt tablets, which was unsuccessful.  A chest x-ray revealed globular cardiomegaly and echocardiography confirmed the presence of a large pericardial effusion with increased filling pressures but no overt tamponade.  

Pericardiocentesis resulted in a rise in serum sodium from 119mmol/L to 124mmol/L within 3 hours of evacuating 800mL of pericardial fluid. Continuing improvement in the serum sodium, associated with a significant diuresis, was noted over subsequent days with normalisation of serum sodium in the absence of any additional interventions.

Cardiac tamponade is a recognised cause of hyponatraemia but has been reported infrequently in the literature with only 5 published case reports between 1983 and 2012. The underlying mechanisms for this phenomenon remain unclear but are postulated to involve both antidiuretic hormone (ADH) and atrial natriuretic peptide (ANP), along with the renin-aldosterone system. These responses appear to be the result of the effects of the pericardial effusion on cardiac output and effective circulating volume, plus effects on atrial transmural pressures and wall tension.

This case will be presented along with a discussion of the available literature and the proposed hormonal mechanisms involved in the development of hyponatraemia secondary to pericardial effusions and cardiac tamponade.

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