title: Osmolar gap hyponatremia in critically ill patients: evidence for the sick cell syndrome?
abstract: OBJECTIVE
  Accumulation of nondiffusible solutes in plasma leads to redistribution hyponatremia with an increased osmolar gap (i.e., the difference between measured and calculated osmolality). In critically ill patients, intracellular solutes may leak out of the cell because of an increased membrane permeability and may lead to redistribution hyponatremia with increased osmolar gap, a concept called the "sick cell syndrome." The aims of this prospective study were to determine whether an increased osmolar gap related to endogenous solutes accumulation was present in intensive care patients with true hyponatremia and to identify the solutes accounting for this increased osmolar gap.
  
  
  METHODS
  A 14-bed medical intensive care unit in an 821-bed university hospital.
  
  
  METHODS
  A 20-wk prospective observational study.
  
  
  METHODS
  Fifty-five consecutive patients with a measured plasma sodium concentration <or=130 mmol/L (mean +/- sd, 126 +/- 6 mmol/L) were automatically identified by the Biochemistry Department. Patients were excluded in the case of reduced plasma water content resulting from hyperlipidemia or hyperproteinemia, in the case of hyperglycemia, or if exogenous compounds known to increase the osmolar gap were present.
  
  
  METHODS
  Plasma osmolar gap was calculated.
  
  
  RESULTS
  Plasma osmolar gap was considered significant if >10 mosm/kg. Total plasma amino acid concentration also was measured. Organ dysfunctions were assessed with the Sequential Organ Failure Assessment. Thirty of the 55 patients (54%) had an osmolar gap >10 mosm/kg (17.2 +/- 7.1 mosm/kg). Sequential Organ Failure Assessment score was significantly higher in the osmolar gap patients (6.4 +/- 3.2 vs. 4.5 +/- 2.0; p =.015). No difference of amino acids concentration was observed between osmolar gap and non-osmolar gap patients, and no correlation was observed between osmolar gap and amino acid concentration. Accumulation of ketone bodies and lactic acid was also unlikely. During correction of hyponatremia in osmolar gap patients, a significant decrease of plasma osmolar gap was observed and a statistically significant inverse relationship was demonstrated between osmolar gap decrease and plasma sodium concentration increase.
  
  
  CONCLUSIONS
  Hyponatremia with increased osmolar gap related to endogenous solutes accumulation is observed frequently in hyponatremic intensive care patients, especially in patients with the most severe organ dysfunctions. The nature of the endogenous solutes accounting for the increased osmolar gap remains to be determined. Simultaneous correction of sodium and osmolar gap suggests a causal link between increased osmolar gap and hyponatremia and may support the concept of sick cell syndrome.
authors: Service de Réanimation Médicale, Hôpital Saint-Antoine, Assistance Publique-Hôpitaux de Paris, Paris, France.
authors: Jean
authors: J
authors: Guglielminotti
authors: Pascal
authors: P
authors: Pernet
authors: Eric
authors: E
authors: Maury
authors: Marc
authors: M
authors: Alzieu
authors: Michel
authors: M
authors: Vaubourdolle
authors: Bertrand
authors: B
authors: Guidet
authors: Georges
authors: G
authors: Offenstadt
mesh_terms: D000596:Amino Acids / Q000097:blood; D016638:Critical Illness; D005260:Female; D006801:Humans; D007010:Hyponatremia / Q000378:metabolism*; D007657:Ketone Bodies / Q000097:blood; D019344:Lactic Acid / Q000097:blood; D008297:Male; D008875:Middle Aged; D009102:Multiple Organ Failure / Q000378:metabolism; D009994:Osmolar Concentration; D011446:Prospective Studies; D012964:Sodium / Q000097:blood; D013577:Syndrome; D014883:Water-Electrolyte Imbalance
chemical_list: D000596:Amino Acids; D007657:Ketone Bodies; D019344:Lactic Acid; D012964:Sodium