1/7. Overcorrection of hyponatremia: where do we go wrong?Predicted sodium concentrations [Na( )] based on traditional calculations for the correction of hyponatremia often do not match treated [Na( )], for various reasons. In many situations, hyponatremia is corrected at unexpectedly rapid rates. The authors present an analysis of two cases of overly rapid correction of hyponatremia despite apparently appropriate management based on initial evaluations. The mistakes involved are discussed and simple calculations demonstrated to prove that the overcorrections did not occur at random. Overcorrection in one case involved miscommunications between the emergency room and admitting physicians regarding the amount of saline and potassium already administered to the patient. Unexpected hypoosmotic polyuria was responsible for overcorrection in the other case. Overcorrection of hyponatremia may be preventable in many cases. In general, overcorrection of hyponatremia is caused by either "too much salt (Na( ) K( )) gained" or "too much water lost." Recognizing common pitfalls will enable physicians to avoid overcorrection and its attendant risk of fatal osmotic demyelinating syndrome (ODS).- - - - - - - - - - ranking = 1keywords = physician (Clic here for more details about this article) |
2/7. The hyponatraemic hypertensive syndrome in a 2-year-old child with behavioural symptoms.In this case report we present a 2-year-old girl with the classical signs of the hyponatraemic hypertensive syndrome. She initially presented with a history of behavioural abnormalities and hyponatraemia (126 mmol/l) and her blood pressure was as high as 220/160 mmHg. After admission, somnolence developed. Intravenous anti-hypertensive therapy was started immediately. The hyponatraemia was treated with i.v. sodium supplementation. The cause of this syndrome proved to be fibromuscular dysplasia of the left renal artery. Finally, a left nephrectomy was performed. With this therapy, blood pressure and serum sodium normalised and the girl promptly regained normal consciousness and behaviour. CONCLUSION: Behavioural abnormalities in the history of a child without any other neurological symptoms might be one of the first signs of hypertensive encephalopathy. In combination with hyponatraemia, these symptoms should alert the physician to consider the hyponatraemic hypertensive syndrome.- - - - - - - - - - ranking = 0.5keywords = physician (Clic here for more details about this article) |
3/7. Diagnostic approach to a patient with hyponatraemia: traditional versus physiology-based options.The usual diagnostic approach to a patient with hyponatraemia is based on the clinical assessment of the extracellular fluid (ECF) volume, and laboratory parameters such as plasma osmolality, urine osmolality and/or urine sodium concentration. Several clinical diagnostic algorithms (CDA) applying these diagnostic parameters are available to the clinician. However, the accuracy and utility of these CDAs has never been tested. Therefore, we performed a survey in which 46 physicians were asked to apply all existing, unique CDAs for hyponatraemia to four selected cases of hyponatraemia. The results of this survey showed that, on average, the CDAs enabled only 10% of physicians to reach a correct diagnosis. Several weaknesses were identified in the CDAs, including a failure to consider acute hyponatraemia, the belief that a modest degree of ECF contraction can be detected by physical examination supported by routine laboratory data, and a tendency to diagnose the syndrome of inappropriate secretion of antidiuretic hormone prior to excluding other causes of hyponatraemia. We conclude that the typical architecture of CDAs for hyponatraemia represents a hierarchical order of isolated clinical and/or laboratory parameters, and that they do not take into account the pathophysiological context, the mechanism by which hyponatraemia developed and the clinical dangers of hyponatraemia. These restrictions are important for physicians confronted with hyponatraemic patients and may require them to choose different approaches. We therefore conclude this review with the presentation of a more physiology-based approach to hyponatraemia, which seeks to overcome some of the limitations of the existing CDAs.- - - - - - - - - - ranking = 1.5keywords = physician (Clic here for more details about this article) |
4/7. Inappropriate antidiuretic hormone complicating histiocytic lymphoma.The syndrome of inappropriate antidiuretic hormone (IADH) often causes the hyponatremia that may be seen in patients with malignant disorders. Most physicians correctly associate IADH with small cell carcinoma of the lung. We describe two patients in whom IADH was caused by histiocytic lymphoma. One patient was thought to have small cell carcinoma of the lung on the basis of marrow infiltration and the IADH. When the proper diagnosis was made and therapy instituted, both patients responded, with rapid resolution of their disease and the IADH. The identification of the neoplasm that produces the IADH is important, since histiocytic lymphoma may mimic small cell carcinoma of the lung, yet may be very responsive with newer treatment regimens.- - - - - - - - - - ranking = 0.5keywords = physician (Clic here for more details about this article) |
5/7. Thiazide-induced hyponatremia.We have described a case of severe acute hyponatremia developing in a patient who had been taking thiazides for the previous eight months without having any electrolyte abnormalities. The onset of the electrolyte disturbance coincided with a physician-recommended hydration regimen, which we believe unmasked a drug-related impairment of water excretion. Withdrawal of thiazide therapy promptly resulted in water diuresis and rapid correction of the hyponatremia.- - - - - - - - - - ranking = 0.5keywords = physician (Clic here for more details about this article) |
6/7. Acute hyponatremia in ultra-endurance athletes.The case of a 57-year-old male athlete who developed acute hyponatremia during participation in a 100 mile ultra-marathon is discussed. The initial presentation was one of rapid neurological deterioration and transient cardiovascular instability. Current theories on how hyponatremia develops in athletes are discussed. Treatment modalities, such as the use of hypertonic saline and the management of increased intracranial pressure, are addressed. With increasing interest in ultra-endurance events, the incidence of acute hyponatremia may increase. It is important that emergency physicians recognize this phenomenon and be familiar with the principles of acute intervention.- - - - - - - - - - ranking = 0.5keywords = physician (Clic here for more details about this article) |
7/7. The treatment of severe hyponatremia.Severe hyponatremia may be chronic (days) or acute (hours), symptomatic or asymptomatic. Severe chronic symptomatic hyponatremia (serum sodium concentration < 110 to 115 mM/liter) occurs most commonly in the syndrome of inappropriate antidiuretic hormone secretion (SIADH). The treatment of this hyponatremia is a challenge to practicing physicians, in part because an overly rapid correction of hyponatremia may cause brain damage. The latter sometimes takes the form of central pontine myelinolysis (CPM). On the basis of available clinical and experimental literature, the rate of correction of this symptomatic hyponatremia should be no more than 0.5 mM per liter per hour, and the initial treatment should be halted once a mildly hyponatremic range of the serum sodium concentration has been reached (approximately 125 to 130 mM/liter). In contrast, severe chronic asymptomatic hyponatremia may be treated sufficiently by a fluid restriction. On the other hand, severe symptomatic acute hyponatremia should be treated promptly and rapidly, using hypertonic saline, to initially reach a mildly hyponatremic level.- - - - - - - - - - ranking = 0.5keywords = physician (Clic here for more details about this article) |