Managing hyponatraemia secondary to primary polydipsia: beware too rapid correction of hyponatraemia

Pericardial effusion has been identified as a rare cause of hyponatremia. In most patients, pericardiocentesis results in rapid correction. We describe a 67-year-old male who presented with pericardial effusion-associated hyponatremia secondary to cardiac resynchronization therapy-D placement that resolved following evacuation. In addition, we review the literature on pericardial effusion-associated hyponatremia.

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RAPID CORRECTION OF ACIDOSIS AND DEHYDRATION OF CHOLERA WITH ORAL ELECTROLYTE AND GLUCOSE SOLUTION

The Lancet ◽

10.1016/s0140-6736(70)91350-4 ◽

1970 ◽

Vol 296 (7672) ◽

pp. 549-550 ◽

Cited By ~ 17

Author(s):

RichardA. Cash ◽

JohnN. Forrest ◽

DavidR. Nalin ◽

Elias Abrutyn

Keyword(s):

Glucose Solution ◽

Rapid Correction

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Rapid correction of severe hyponatremia in the rat: histopathological changes in the brain

AJP Renal Physiology ◽

10.1152/ajprenal.1985.248.5.f711 ◽

1985 ◽

Vol 248 (5) ◽

pp. F711-F719 ◽

Cited By ~ 10

Author(s):

J. C. Ayus ◽

R. K. Krothapalli ◽

D. L. Armstrong

Keyword(s):

Serum Sodium ◽

Brain Lesions ◽

The Other ◽

Histopathological Changes ◽

Water Restriction ◽

Severe Hyponatremia ◽

Group Iii ◽

Group I ◽

The Brain ◽

Rapid Correction

The purpose of the present studies was to examine the effects of rapid correction of severe hyponatremia (serum sodium less than 120 meq/liter) either to mildly hyponatremic levels (serum sodium = 130 meq/liter) or to normonatremic levels (serum sodium = 150 meq/liter) on the brain histology of rats. In group I, 13% of the rats revealed brain lesions following correction to mildly hyponatremic levels by the administration of 855 mM NaCl. All the rats (100%) in group II had brain lesions following correction to normonatremic levels by 24 h of water restriction. Similarly, all the rats in group III showed brain lesions following correction to normonatremic levels by the administration of 855 mM NaCl. Severe hyponatremia by itself did not cause any brain lesions in another group. We conclude that rapid correction of severe hyponatremia to mildly hyponatremic levels by the administration of 855 mM NaCl does not cause significant brain lesions. On the other hand, rapid correction to normonatremic levels either by water restriction or by the administration of 855 mM NaCl results in significant brain lesions.

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Impairment of osmotically stimulated AVP release in patients with primary polydipsia

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1993.265.6.r1247 ◽

1993 ◽

Vol 265 (6) ◽

pp. R1247-R1252 ◽

Cited By ~ 1

Author(s):

A. M. Moses ◽

B. Clayton

Keyword(s):

Diabetes Insipidus ◽

Arginine Vasopressin ◽

Plasma Osmolality ◽

Normal Subjects ◽

Urine Concentration ◽

Published Data ◽

Posterior Pituitary ◽

Primary Polydipsia ◽

Number Of Factors

The secretion of arginine vasopressin (AVP) from the posterior pituitary is primarily and finely regulated by the osmolality of plasma. Even though a number of factors alter osmolality-induced release of AVP, there are no published data in humans that have addressed the role of chronic overhydration on this phenomenon. To address this problem we have identified eight patients with primary polydipsia using criteria not involving measurement of AVP, and have subjected them to standardized infusions of hypertonic saline. These patients had less AVP in both plasma and urine in relation to plasma osmolality than was found in normal subjects. In addition, their rate of rise of plasma and urine AVP was less than in normal subjects. Their osmotic threshold for AVP release may have been higher than normal. These data demonstrate that chronic overhydration in humans downregulates the release of AVP in response to hypertonicity. This phenomenon may explain the impairment of urine concentration in patients with primary polydipsia and emphasizes the basis of the difficulty that may occur clinically in differentiating between patients with primary polydipsia and partial central diabetes insipidus.

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Clinical characteristics and relationship between rate of sodium correction and outcomes in patients with primary polydipsia: retrospective observational analysis

Journal of the Japanese Society of Intensive Care Medicine ◽

10.3918/jsicm.28_119 ◽

2021 ◽

Vol 28 (2) ◽

pp. 119-120

Author(s):

Noriko Miyagawa ◽

Hajime Furukawa ◽

Masakazu Kobayashi ◽

Yoshitaro Yoshida ◽

Shigeki Kushimoto

Keyword(s):

Clinical Characteristics ◽

Observational Analysis ◽

Primary Polydipsia ◽

Sodium Correction

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Refractory Amiodarone-induced Thyrotoxicosis: The Surgical Option

World Journal of Endocrine Surgery ◽

10.5005/jp-journals-10002-1119 ◽

2013 ◽

Vol 5 (1) ◽

pp. 21-24 ◽

Cited By ~ 1

Author(s):

Avraham Ishay ◽

Julia Carmeli ◽

Ehud Rozner ◽

Rafael Luboshitzky

Keyword(s):

Total Thyroidectomy ◽

Treatment Planning ◽

Medical Therapy ◽

Cardiac Disease ◽

Amiodarone Therapy ◽

Standard Medical Therapy ◽

Surgical Option ◽

Rapid Correction ◽

Severe Cardiac Disease

ABSTRACT Amiodarone-induced thyrotoxicosis is often poorly tolerated owing to underlying cardiac disease, and frequently resistant to medical therapy. We describe a 48-year-old patient with severe cardiac disease who developed amiodarone-associated thyrotoxicosis, refractory to standard medical therapy. Due to the unremitting thyrotoxicosis, a total thyroidectomy was performed without complications resulting in rapid correction of the thyrotoxicosis and enabling resumption of amiodarone therapy. Despite the concerns inherent to severe cardiac disease, total thyroidectomy can be performed safely in patients with resistant amiodarone-induced thyrotoxicosis. We believe that surgery should be considered early in the treatment planning. How to cite this article Ishay A, Carmeli J, Rozner E, Luboshitzky R. Refractory Amiodarone-induced Thyrotoxicosis: The Surgical Option. World J Endoc Surg 2013;5(1):21-24.

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