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Renal Disease; Fluid and Electrolyte Disorders
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
The normal plasma sodium concentration is 135–145 mmol/L. As sodium is the major extracellular electrolyte, hyponatraemia is usually associated with hypo-osmolality and hypernatraemia is usually associated with hyperosmolality. Both plasma hypo-osmolality and hyperosmolality can have adverse effects on cells, especially neural cells. In each case, the diagnosis and treatment depends on an assessment of body fluid volume.
Fluid and electrolyte disorders
Published in Philip E. Harris, Pierre-Marc G. Bouloux, Endocrinology in Clinical Practice, 2014
Ploutarchos Tzoulis, Pierre-Marc G. Bouloux
Hypernatremia has also effects on other physiological functions. Hyperosmolality disturbs insulin-mediated glucose use and potentially contributes to the development of hyperglycemia. Also, hypernatremia has a negative effect on left ventricular contractility.97
Water and sodium
Published in Martin Andrew Crook, Clinical Biochemistry & Metabolic Medicine, 2013
Large rises in the osmotic gradient across cell membranes may result in the movement of enough water from the intracellular compartment to dilute extracellular constituents. Consequently, if the change in osmolality has not been caused by sodium and its associated anions, a fall in plasma sodium concentration is appropriate to the state of osmolality. If, under such circumstances, the plasma sodium concentration is not low, this indicates hyperosmolality.
Is a hyperosmolar pump prime for cardiopulmonary bypass a risk factor for postoperative delirium? A double blinded randomised controlled trial
Published in Scandinavian Cardiovascular Journal, 2023
Helena Claesson Lingehall, Yngve Gustafson, Staffan Svenmarker, Micael Appelblad, Fredrik Davidsson, Fredrik Holmner, Alexander Wahba, Birgitta Olofsson
The hyperosmolar pump prime produced a lower net volume fluid balance, which is believed to protect against POD [2,21,22]. The inclusion of mannitol increased the urine output, which is one explanation for the more favourable fluid balance. The other is related to the osmotic effects generated by the combination of mannitol and sodium chloride. From a physiological viewpoint, this is explained by the shift of water from the interstitial and intracellular compartments into the plasma volume. As a result, it will lower the requirement of extra fluids during CPB to maintain a normal circulatory blood volume. This is indicated by the significantly lower haematocrit level measured during CPB. The negative consequences of using body water as plasma volume expander are the effects it might have on organ function, especially the brain. While commencing CPB, the volume of 1400 mL is introduced intra-arterially in close connection of the cerebral circulation over a time-period less than 3 min, with an osmolality threefold higher than normal. Of note is that hyperosmolality is seldom suspected to cause POD, but should be considered. In the worst scenario, it may lead to osmotic demyelination [23]. It may also shrink glia cells [24], especially if the blood–brain barrier is disrupted, which is common after cardiac surgery [25].
Optimization of potassium management in patients with chronic kidney disease and type 2 diabetes on finerenone
Published in Expert Review of Clinical Pharmacology, 2023
Alberto Ortiz, Roberto Alcázar Arroyo, Pedro Pablo Casado Escribano, Beatriz Fernández-Fernández, Francisco Martínez Debén, Juan Diego Mediavilla, Alfredo Michan-Doña, Maria Jose Soler, Jose Luis Gorriz
For decades, renin-angiotensin system (RAS) inhibitors such as angiotensin-converting enzyme inhibitors (ACEI) or angiotensin II receptor blockers (ARB), have been the standard treatment for CKD. In the last years, sodium/glucose cotransporter 2 (SGLT2) inhibitors, and more recently, the new mineralocorticoid receptor antagonist (MRA), finerenone, have shown to be effective in reducing the risk of renal progression, as well as cardiovascular complications in this population [4–10]. However, hyperkalemia, which is more common in patients with CKD, is not only a potential life-threatening condition, but also may limit the use of some of these drugs [11–13]. In addition, diabetes mellitus is an independent predictor of hyperkaliemia compared with the general population, as diabetic status generates hyporeninemic hypoaldosteronism, hyperosmolality and insulin deficiency on top of the development of CKD or the use of RAS inhibition [14]. As a result, focusing on reducing the risk of hyperkalemia should be a target to reduce complications and increase the use of protective CKD and cardiovascular drugs [12,13].
Nicotine intoxication by e-cigarette liquids: a study of case reports and pathophysiology
Published in Clinical Toxicology, 2020
Gerdinique C. Maessen, Anjali M. Wijnhoven, Rosalie L. Neijzen, Michelle C. Paulus, Dayna A. M. van Heel, Bart H. A. Bomers, Lucie E. Boersma, Burak Konya, Marcel A. G. van der Heyden
Exposure to highly concentrated substances in e-liquids through unwarranted use such as oral consumption, goes hand in hand with a substantial risk of severe toxicity [12]. Life-threatening nicotine intoxication in young children due to accidental ingestion of e-liquid has been reported [13]. Another concern is nicotine intoxication resulting from suicide attempts using e-liquids [14]. With the introduction of e-cigarettes, e-liquids containing highly concentrated nicotine have become widely available. However, the clinical consequences of nicotine intoxication through e-liquid ingestion remain unclear. Moreover, at present, there is no consensus on the lethal dose of nicotine since different values have been reported. For oral intake, 60 mg of nicotine is often suggested as the lethal dose in the literature; although, research has shown that adults survive dosages much higher than this (up to 500 mg) [15]. Furthermore, the implications of combined nicotine and PG/VG intake, the main constituents of e-liquids, are uncertain. The symptoms most frequently seen in nicotine intoxication are vomiting, agitation, pallor, hypertension, tachycardia and headache [16]. Symptoms of PG intoxication vary between hyperosmolality and lactic acidosis to haemolysis, renal failure and CNS depression [17]. VG related symptoms are usually headache, nausea, diuresis and hyperglycaemia, mostly due to dehydration [18,19].