Hyponatremia is a common electrolyte disturbance associated with considerable morbidity and mortality [9]. Hyponatremia causes nonspecific symptoms and may be overlooked easily. Nonetheless, it might reflect the severity of underlying diseases [9, 10].
In our study, 65 % of patients were presented with hyponatremia and cardiac tamponade. We considered cardiac tamponade to be one but not the only factors to determine the sodium level in these patients. Undeniable, there still existed some confounding factors in our study. Congestive heart failure, hypothyroidism, acute kidney injury and malignancies are all possible causes for hyponatremia [9]. We could not exclude all these because of small case numbers; besides, they were very common clinical problems in the cardiac tamponade patients. We inferred that tamponade is a possible etiology of hyponatremia because the pericardial drainage recovered the hyponatremia soon and effectively without additional management. Furthermore, we did not check their antidiuretic hormone (ADH) level, or record their daily urine output, osmolality or monitor their intra-cardiac pressure because of high cost and ineffectiveness.
About one third of our patients with hyponatremia had underlying malignancy. In addition, comparing the diagnosis of pericardial effusion, malignancy-related tamponade showed higher rates of hyponatremia than those without malignancy. The severity of hyponatremia and the increase of sodium level after pericardial drainage in the malignancy group were also higher than the non-malignancy group. Malignancy seemed to be a predictor for the development of hyponatremia. The mechanism was unknown but possibly related with tumor secreting factors such as ADH and atrial natriuretic peptide [11–13]. To clarify this, we need a further large clinical trial.
Cardiac chambers compression, especially for ventricles, is a strong indication for pericardial drainage [7]. There was strong positive correlation between hyponatremia and cardiac chambers compression. In contrast to some elective situations that patients underwent pericardial drainage because of acute symptoms and worsening conditions, patients with cardiac compression had higher incidence and severity of hyponatremia. After pericardial drainage, they also had prominent sodium level increase. Therefore, we considered cardiac chambers compression is also a predictor of the development of hyponatremia.
Hyponatremia developing in the setting of cardiac tamponade was rarely reported [1–5]. Mouallem et al. reported a patient with lung cancer complicated with malignant pericardial effusion [4]. Rehan et al. reported an idiopathic pericarditis with large amount of pericardial effusion leading to symptomatic pericardial tamponade [2]. Peter et al. presented a 29-year-old paraplegic man who was being treated with warfarin [3]. Hyponatremia rapidly resolved after pericardiocentesis. These patients’ laboratory data before pericardiocentesis showed high urine osmolality and high urine sodium waste. Removal of pericardial fluid by means of pericardiocentesis resulted in rapid improvement in cardiac output and hemodynamic status. In response to these changes, urine output increased promptly with excretion of large volume of dilute urine and rapid correction of hyponatremia. The authors commented 2 possible hypotheses to explain the relationship of hyponatremia and cardiac tamponade. First, the increased pressure in the compressed cardiac chambers may reactivate the ADH release [5, 6, 13]. The ADH would keep free water retention and cause hyponatremia. Second, the decreased cardiac output may contribute to impairment of urine diluting ability and make the free water clearance much less.
In our study, we did not collect the urine and serum osmolality, urine sodium and the urine amount after pericardiocentesis. It is warranted that further prospective study to investigate the relationship of urine and serum osmolality in patients with cardiac tamponade.
Furthermore, we did not collect the N-terminal pro-B-type natriuretic peptide (NT-proBNP) level. Kim et al. reported that NT-proBNP level may be a useful marker of disease severity in patients suffering from pericardial effusion [14]. In our study there was only few of our patients that NT-proBNP level was checked and the data was insufficient to be analyzed.
We calculated the ESC Cardiac Tamponade score of all 48 patients. There was no differences of the average score of overall and between the higher and lower sodium level. According to the algorithm, any patient with score ?6 or with compromised hemodynamic status needed to receive emergent pericardial drainage. There was no evidence that hyponatremia was related with high ESC Cardiac Tamponade score [8].
Study limitation
Hyponatremia can have multifactorial causes. In practice, we cannot workup all possible causes for those patients who need emergent pericardiocentesis, therefore lack of the complete data of pericardial drainage of some of our patients may interfere our analysis. The conclusion we made in this article was inferred from the indirect evidence. A larger and well-designed trial should be conducted.
The chamber compression was defined as the right ventricle was compressed that had detected via echocardiography. Thirty-three of 48 patients met the definition and the other 15 patients did not have compression sign of right ventricle but still received pericardial fluid drainage due to unstable hemodynamics clinically. The relation between compression of right ventricle and hyponatremia was seen in our study but still need further larger and well-designed trial to be conducted.
Furthermore, due to retrospective collection of data, there was no any documentation of intrapericardial pressures before and after pericardial drainage, nor the measurement of left ventricular end-diastolic pressure or pericardial cavity pressure before and after pericardial drainage. There was no data of intrapericardial C-reactive protein or other inflammation markers due to the same reason above.