Hyponatraemia was initially thought to be at least partly due to low solute intake and excessive fluid intake. The patient's diet contained a daily solute intake of approximately 200 mOsmol/24 h (normal is approximately 750 mOsmol/24 h) and he drank approximately 6 litres of dilute alcohol and other fluid per day. As maximally dilute urine has an osmolarity of around 50 mOsmol/litre, the patient's maximum possible daily free water clearance was approximately 200/50 = 4 litre. The remaining free water excess of approximately 2 litre/day could have led to significant hyponatraemia—a pattern recognised in both primary polydipsia and excessive beer drinking. However, the patient had a surprisingly high urine osmolality and was oedematous; neither of these findings would have been expected in polydipsic hyponatraemia.
Hypothalamic osmoreceptors detect plasma osmolality and regulate ADH secretion by the posterior pituitary. Dilute plasma would, under normal circumstances, inhibit ADH secretion, increasing free water clearance by the kidney leading to restoration of normal osmolality.
Atrial and carotid baroreceptors detect intravascular volume status. Significant circulating volume depletion causes these receptors to override hypothalamic osmoreceptors and stimulate release of ADH. The net effect is to protect the circulation against further volume loss.
True volume depletion may occur with conditions such as gastrointestinal fluid losses, burns or haemorrhage. Apparent volume depletion can occur in states of overall volume overload, such as congestive cardiac failure and cirrhosis.
Cardiac tamponade is associated with antidiuresis via release of ADH.1
Though the mechanism is poorly understood, decreased effective circulating volume due to the effect of tamponade on cardiac chamber filling and diastolic compliance may lead to stimulation of atrial and carotid baroreceptors.2
There are a variety of other mechanisms responsible for control of ADH secretion3
that may also be involved. An elevation of ADH might not only have contributed to the hyponatraemia, but also the relatively high urine osmolality. Further impairment of urine dilution may have been caused by other ADH-independent mechanisms in the presence of a habitually high fluid intake.4
Cardiac tamponade is also associated with antinatriuresis partly via activation of the sympathetic nervous system and partly via activation of renin-angiotensin-aldosterone (due to combined renal and extrarenal effects of decreased cardiac output). There is evidence that in tamponade, although atrial pressure rises, there is no increased release of atrial natriuretic peptide (ANP) as atrial stretch rather than atrial pressure is thought to be more important in stimulating ANP release.2,5
A study of 10 patients with pericardial tamponade found that the level of ANP increased approximately fivefold after pericardial fluid was evacuated with a corresponding rise in urine output. These findings correspond to the patient's initially low urine sodium and rapid diuresis following pericardiocentesis.
Antidiuresis and antinatriuresis usually balance in cardiac tamponade resulting in normal serum sodium. The patient's excessive fluid intake may have caused these responses to become imbalanced.
Two case reports in the English literature associate hyponatraemia with cardiac tamponade caused by a slowly accumulating haemorrhagic effusion due to warfarin toxicity6
and adenocarcinoma of the lung.7
One case report published in 2007 by Shafique et al4
described a patient strikingly similar to our patient. Their patient was 59 y, previously healthy, who, as an electrician, habitually drank 1–2 gallons of water daily. He presented with a 2-week history of productive cough and fever. Examination revealed paradox of 15 mm Hg and peripheral oedema. Sodium on presentation was 104 mmol/litre. Urine sodium and urine osmolality showed a similar pattern to our patient: 5 mmol/litre (low) and 641 mOsm/kg (high), respectively. ECHO demonstrated large pericardial effusion with evidence of tamponade. Following pericardiocentesis, there was a similar rapid diuresis but with a much faster correction of serum sodium (from 105 to 123 mmol/litre within 18 h). Chest x-ray and CT showed evidence of right-sided consolidation. Despite extensive analysis of pericardial fluid, no cause was found for the accumulation of the effusion. Both their patient and our patient had idiopathic pericardial effusions, which might have related to infection at another site or another systemic disorder.
In conclusion, we report an unusual case of hyponatraemia, associated with chronic excess fluid intake and tamponade secondary to an idiopathic pericardial effusion. Why an imbalance between antinatriuresis and antidiuresis develops in some rare cases of tamponade is unclear—it is possible that excessive fluid intake in the context of tamponade might predispose to the development of hyponatraemia. The true incidence of hyponatraemia associated with cardiac tamponade is unknown.
- In patients with hyponatraemia and dilute urine, consider water intoxication.
- Hyponatraemia with a high urine osmolality suggests water intoxication is not the cause or not the only cause.
- Cardiac tamponade is usually associated with normal serum sodium.
- The combination of chronic excessive fluid intake with cardiac tamponade may lead in some cases to hyponatraemia with high urine osmolality.