Approach to the patient with hyponatraemia

Author(s):  
Ewout J. Hoorn ◽  
Robert Zietse

Hyponatraemia is the most common electrolyte disorder in hospitalized patients and is primarily a water balance disorder. Therefore, hyponatraemia is due to a relative excess of water in comparison with sodium in the extracellular fluid volume. Hyponatraemia is usually due to the release of vasopressin despite hypo-osmolality; this secretion is either ‘appropriate’ (i.e. due to a low intravascular volume) or ‘inappropriate’. The diagnostic approach to hyponatraemia relies on the assessment of the time of development, symptoms, and volume status, along with laboratory parameters such as urine sodium and urine osmolality. Complications are mainly neurological and usually depend on the rate of development and correction. If hyponatraemia develops acutely, treatment should be directed towards counteracting the water shift to or brain cells. Conversely, in more chronic cases of hyponatraemia, treatment should be directed at the underlying cause, while avoiding over-correction.

Author(s):  
Robert Zietse ◽  
Ewout Hoorn

Hypernatraemia is much less common than hyponatraemia, and its prevalence is higher in certain populations, including children, the elderly, and critically ill patients. A common feature is that patients affected have been unable to drink water to correct the disorder. Hyponatraemia and hypernatraemia are both primarily disorders of water balance. Hypernatraemia is caused by a relative deficit of total body water in comparison to total body sodium. Both disorders are often associated with disturbances in the hormone governing water balance, arginine vasopressin (antidiuretic hormone). Hypernatraemia may be due to an inability to secrete vasopressin or a resistance to its actions in the kidney. The diagnostic approach relies on the assessment of the time of development, symptoms, and volume status, along with laboratory parameters such as urine sodium and urine osmolality. If hypernatraemia develop acutely, treatment should be directed towards counteracting the water shift to or from brain cells. In more chronic cases, treatment should be directed to the underlying cause while avoiding overcorrection.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A560-A561
Author(s):  
Gonzalo Francisco Miranda ◽  
Karen Evelyn Ramos Rodríguez ◽  
Clinical Research

Abstract Hyponatremia is the most common electrolyte disorder, which can occur in outpatients and hospitalized patients, so both first-contact doctors and specialists must keep up-to-date on the prevention, recognition, diagnosis and management of this complication. A 68-year-old male patient presents to Dos de Mayo National Hospital Emergency Department. He was diagnosed as COVID-19 pneumonia and hospitalized for management of acute respiratory failure. The patient had neurological impairment associated with poor oral tolerance. Initial laboratory examinations were C-reactive protein in 363.5 mg/L, serum sodium of 128.42 mmol/L and urine sodium was 83 meq/L. Osmolality in plasma was 266.15 mOsm/Kg and urine osmolality was 420 mOsm/Kg. Thyroid function tests as well as cortisol levels were in normal range. Our patient was diagnosed as SIAD by hyponatremia, osmolality in plasma <275 mOsm / kg, urine osmolality > 100 mOsm / kg, urine sodium > 40 mEq / l, euvolemic state and exclusion of cortisol and thyroid hormone deficiency. Treatment of hyponatremia was initiated and rapidly elevate plasma sodium by 4 meq/l in the first 6 hours. There was clinical improvement. Blood sodium levels ranged from 115 to 135 mmol/L with bolus therapy of hypertonic solutions in 72 hours. Intravenous boluses of hypertonic saline should be administered to rapidly elevate plasma sodium by 4 to 6 mEq/L in the first 6 hours. The data shows that fluid bolus therapy is more effective in acutely elevating plasma sodium than traditional low-dose hypertonic saline infusion that may lead to avoidable deaths according to recent guidelines. In this case a strategy based with bolus therapy for reversal of hyponatremia was used effectively. A number of cases of COVID-19 pneumonia are associated with SIAD. The presence of SIAD could be a clue to diagnosing COVID-19. SIAD is a major complication of COVID-19 and could be the first and only manifestation. In cases of SIAD without a clear etiology we should suspect COVID-19 in a patient with respiratory distress in the current pandemic. Syndrome of inappropiate antidiuresis (SIAD) should be assessed in every patient with COVID-19 as their treatment and early identification decreases mortality. The association between COVID-19 pneumonia and SIAD should be further identified, requiring doctors to be aware of this condition. Additional studies are required to determine the incidence and pathogenesis of SIAD in patients with COVID-19.


1993 ◽  
Vol 71 (5-6) ◽  
pp. 379-386 ◽  
Author(s):  
Guus H. M. Schoorlemmer ◽  
Mark D. Evered

Rats with bladder and venous cannulas were deprived of water from midnight (00:00) to 10:00. Water deprivation reduced food intake within 2 h, reducing the amount of water sequestered in the gut and the solute load to the tissues. There was little change in either urinary water loss or osmolality, but water-deprived rats excreted more Na+, K+, and Cl− than food-matched controls. The change in solute balance helped preserve osmolality and cell volume at the expense of extracellular fluid volume. When water was returned, rats quickly drank enough to restore the intracellular but not the extracellular fluid deficit. Plasma osmolality and sodium concentration fell below predeprivation values. Urine osmolality and excretion of Na+, K+, and Cl− fell rapidly after drinking. Drinking continued at a slower rate for at least 4 h, but urine flow also increased so water balance stabilized. The changes in intake and electrolyte excretion during water deprivation and rehydration illustrate the important role of changes in solute balance in fluid homeostasis.Key words: water deprivation, thirst, drinking, water balance, sodium balance.


BIOspektrum ◽  
2021 ◽  
Vol 27 (2) ◽  
pp. 165-167
Author(s):  
Sandrine Baltzer ◽  
Enno Klussmann

AbstractVasopressin-mediated water reabsorption from primary urine in the renal collecting duct is essential for regulating body water homeostasis and depends on the water channel aquaporin-2 (AQP2).Dysregulation of the process can cause water balance disorders. Here, we present cell-based high-throughput screenings to identify proteins and small molecules as tools to elucidate molecular mechanisms underlying the AQP2 control and as potential starting points for the development of water balance disorder drugs.


1987 ◽  
Vol 72 (3) ◽  
pp. 321-327 ◽  
Author(s):  
A. Louise Sugden ◽  
Barbara L. Bean ◽  
James A. Straw

1. These studies were designed to investigate the effects of high dietary K+ on electrolyte and water balance in young spontaneously hypertensive rats (SHR) and to relate these effects to changes in blood pressure. 2. The high K+ diet reduced blood pressure by approximately 10 mmHg during the development of hypertension. Blood pressure, however, plateaued at the same maximum level as control by age 13 weeks. 3. Rats fed the high K+ diet showed a significant increase in water intake and urine volume throughout the treatment period but no change in plasma volume or extracellular fluid volume occurred. 4. A slight natriuresis was also observed in rats on the high K+ diet, but this was not of sufficient magnitude to decrease total body Na+. 5. These results confirm previous findings that K+ causes a diuresis and a natriuresis, but demonstrate that the diuretic action of K+ cannot explain its antihypertensive properties in young SHR.


1989 ◽  
Vol 257 (3) ◽  
pp. F341-F346 ◽  
Author(s):  
E. Bartoli ◽  
A. Satta ◽  
F. Melis ◽  
M. A. Caria ◽  
W. Masala ◽  
...  

We tested the hypothesis that changes in extracellular fluid volume are reflected by pressure changes within structures of the inner ear and that through neural pathways, a control mechanism exerts an influence on antidiuretic hormone (ADH) release and Na excretion. The study was performed on 35 guinea pigs. In protocol 1, 13 animals were studied before and after decompression of the inner ear by bilateral fluid withdrawal in an experimental setting of sustained isotonic expansion that kept the osmoreceptor partially activated and the intrathoracic volume receptors suppressed. A group of six sham-operated animals served as control. In protocol 2, nine animals were studied before and after a unilateral rise in their inner ear pressure during slightly hypertonic low-rate infusions that kept the osmoreceptor and thoracic volume receptors stimulated. A group of seven sham-operated guinea pigs served as controls. Decompression of the inner ear was attended by a rise in plasma ADH from 11.9 +/- 2.4 to 29.1 +/- 6.9 pg/ml, in urine osmolality (Uosmol) from 470 +/- 48 to 712 +/- 46 mosmol/kg (P less than 0.001), and a fall in urine flow rate (V) from 184 +/- 47 to 71 +/- 11 microliters/min (P less than 0.01), whereas plasma Na (PNa) and osmolality (Posmol) did not change. During inner ear hypertension, plasma ADH fell from 25.6 +/- 3.9 to 18.4 +/- 3.1, Uosmol from 829 +/- 58 to 627 +/- 43 (P less than 0.001), and V rose from 51 +/- 11 to 130 +/- 23 (P less than 0.001), whereas glomerular filtration rate, PNa, and Posmol did not change.(ABSTRACT TRUNCATED AT 250 WORDS)


1997 ◽  
Vol 8 (4) ◽  
pp. 524-529
Author(s):  
M Gowrishankar ◽  
C B Chen ◽  
S Cheema-Dhadli ◽  
A Steele ◽  
M L Halperin

The purpose of this report is to determine the mechanisms that lead to hyponatremia when isotonic saline was the only fluid infused into rats given antidiuretic hormone (ADH), and what might minimize the degree of this hyponatremia. Normal rats were deprived of food and water for the 24-hr study period. They received an infusion of isotonic saline to expand their extracellular fluid (ECF) volume with and without exogenous ADH administration (N = 8 in each of the four groups). Similar studies were also carried out in 32 rats fed a low electrolyte diet for 72 hr before the experiment. An additional control group was fed the low electrolyte diet supplemented with sodium (Na), potassium (K), and chloride (Cl). Hyponatremia developed over 24 hr in rats fed their usual diet if treated with ADH and isotonic saline (fall, 13 +/- 2 mM, P < 0.01). The hyponatremia was caused by negative balance for Na + K salts. Hyponatremia did not develop after the saline + ADH treatment if rats were pretreated for 3 days with a low electrolyte diet. Two factors were required to develop this hyponatremia--generation of electrolyte-free water as a result of the excretion of a large quantity of Na + K salts at a high concentration in the urine, and prevention of the excretion of this electrolyte-free water by ADH. Increasing the avidity for Na reabsorption by the kidney prevented this type of hyponatremia from developing.


2019 ◽  
Author(s):  
Danilea M. Carmona Matos ◽  
Herbert Chen

Hypernatremia is an electrolyte disorder most prevalent in the elderly and the critically ill, with over 60% of cases developing over the course of an inpatient stay. Characterized by elevated serum sodium concentrations, this disorder is manifested either by pure-water loss without replacement, or excessive sodium intake without appropriate water balance. Left untreated it may lead to seizures and coma. General treatment in the case of severe hypernatremia is infusion of isotonic saline followed by pure-water after the patient is stabilized. Further treatment of the underlying cause may involve diuretics, thiazides, and a variety of other medications in conjunction with dietary and lifestyle modifications. This review offers an overview of various disorders of water balance: diabetes insipidus, nephrotic syndrome, cirrhosis, idiopathic edema, and volume depletion, as well as their clinical presentations, lab tests, and management. This review contains 1 figure, 1 table, and 25 references. Key words: Hypernatremia, Edematous States , Diabetes insipidus, Volume Depletion, Cirrhosis, Diuretics


1991 ◽  
Vol 261 (6) ◽  
pp. R1381-R1387
Author(s):  
M. G. Ross ◽  
D. J. Sherman ◽  
M. G. Ervin ◽  
L. Day

During oral rehydration of adult mammals, oropharyngeal stimulation, the act of swallowing, and/or gastric factors contribute to a rapid decrease in plasma arginine vasopressin (AVP) that precedes plasma osmolality changes. To determine whether similar mechanisms are present in the developing fetus, six chronically prepared ovine fetuses were rehydrated with intraruminal (IR) distilled water infusions (1 ml.kg-1.min-1 for 60 min) after 43 +/- 3 h of maternal water deprivation. In response to maternal dehydration, significant increases were noted in maternal and fetal mean plasma osmolalities, sodium and AVP concentrations, and fetal urine osmolality. As estimated by hematocrit, fetal intravascular volume decreased by 11%. Fetal rehydration via IR distilled water infusion evoked a significant decrease in fetal plasma osmolality but no change in urine osmolality. Unexpectedly, fetal arterial blood pressure increased and arterial PO2 decreased while fetal hematocrit indicated a further 7% decrease in intravascular volume after the IR infusion. There was a nonsignificant trend toward increased fetal glomerular filtration rate, urine volume, and plasma AVP concentrations. Identical IR water infusions to five euhydrated fetuses resulted in significant decreases in fetal plasma osmolality and increases in glomerular filtration rate, urine flow, and osmolar excretion. The euhydrated fetuses also exhibited significant increases in mean arterial blood pressure and hematocrit and decreased fetal arterial PO2. These results indicate that IR water does not suppress AVP secretion in the dehydrated ovine fetus. Rather, both euhydrated and dehydrated fetuses exhibit an idiosyncratic vasoconstrictive response to IR water.


2009 ◽  
Vol 22 (2) ◽  
pp. 212-215
Author(s):  
I Mahmood ◽  
MK Rahman ◽  
MMR Khan ◽  
MA Haque ◽  
MMH Chowdhury ◽  
...  

Hyponatraemia is a common electrolyte disorder in central nervous system (CNS) disease and is often attributed to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). By contrast, there are patients with intracranial disease who develop hyponatraemia with similar characteristics, but differ in that there is clinical evidence of a contracted extracellular fluid (ECF) volume. This form of hyponatraemia is caused by excessive renal Na excretion, resulting from a centrally mediated process, and is termed cerebral salt wasting (CSW). Hyponatraemia, if acute that is developed within hours or days may cause confusion, coma restlessness or seizures. 72 patients with ischemic stroke admitted at RMCH were selected for this prospective cohort study. Among the subjects 34 (47.22%) cases were found to have hyponatraemia. The number was quite large and screening patients with stroke for electrolytes may be extremely helpful to reduce mortality and morbidity.TAJ 2009; 22(1): 212-215


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