Osmolar gap hyponatremia in critically ill patients: Evidence for the sick cell syndrome?

Guglielminotti, Jean; Pernet, Pascal; Maury, Éric; Alzieu, Marc; Vaubourdolle, Michel; Guidet, Bertrand; Offenstadt, G.

doi:10.1097/00003246-200205000-00016

Cited by 38 publications

(27 citation statements)

References 19 publications

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“…A previous study showed that there was no association among contrast agents, plasma osmolarity and osmolar gap 30 minutes after the performance of a contrastenhanced computed tomography; however, that study only enrolled 14 children. In contrast, increased plasma osmolar gap plus hyponatremia may reflect organ dysfunction in critically ill patients (Guglielminotti et al 2002). However, there is no study on the diagnostic usefulness of plasma osmolar gap for the early detection of CIAKI.…”

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Increased Plasma Osmolar Gap Is Predictive of Contrast-Induced Acute Kidney Injury

Kim

Sung

Kang

et al. 2012

Tohoku J. Exp. Med.

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Contrast-induced acute kidney injury (CIAKI) is a common complication after percutaneous coronary artery intervention (PCI). It is urgent to find a novel, easily measurable and accurate predictor for the early detection of CIAKI. Hyperosmolarity and large amounts of contrast media are risk factors for CIAKI. However, there is no study on plasma osmolar gap as a predictor of CIAKI. We enrolled 89 patients undergoing elective PCI and tested changes of serum sodium, osmolar gap, and renal function at 0, 6, 12 and 24 hours. Plasma osmolar gap was calculated using the following formula: measured plasma osmolarity -[2(Na) + serum urea nitrogen/2.8 + glucose/18]. CIAKI was defined as follows: increase in serum creatinine of ≥ 50%, increase in serum creatinine of ≥ 0.3 mg/dL, or decrease in estimated glomerular filtration rate of ≥ 25% within 24 hours after PCI. The incidence of CIAKI was 13.5% (12/89 patients). The CIAKI group had higher plasma osmolar gaps 6 hours after PCI. The adjusted hazard ratio of the plasma osmolar gap from hour 6 (1-mOsm/L increments) to the development of CIAKI was 1.12 (95% confidence interval [CI], 1.01-1.26; P = 0.041). Sensitivity and specificity of 7 mOsm/L or higher plasma osmolar gap at hour 6 were 70.0% and 76.6%, respectively (area under the ROC curve = 0.77 [95% CI, 0.65-0.89]). Increased plasma osmolar gap may precede the development of CIAKI in patients undergoing PCI. In conclusion, plasma osmolar gap may be a useful predictor for the development of CIAKI.

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confidence: 99%

Increased Plasma Osmolar Gap Is Predictive of Contrast-Induced Acute Kidney Injury

Kim

Sung

Kang

et al. 2012

Tohoku J. Exp. Med.

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“…The determination of osmolar gap -difference between measured and calculated osmolality, normal <10 mOsm/kg -helps with the interpretation and suggests which solutions should be utilized in the treatment 6 . Hypertonic hyponatremia is typically observed during hyperglycemia or after mannitol use and is also known as translocational hyponatremia.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…High levels of plasma proteins and lipids increase the nonaqueous, non-Na + fraction of plasma while overall H 2 0 stays stable. That interferes in the laboratorial evaluation characterizing a pseudohyponatremia 1,2,4,6,7 .The hypotonic hyponatremia deserves special attention and should be stratified according to volemic status as hypervolemic, hypovolemic or euvolemic. The hypervolemic hypotonic hyponatremia associated with water retention is often observed in congestive heart failure, renal failure, nephrotic syndrome, hepatic cirrhosis or pregnancy.…”

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Excessive water ingestion and repeated seizures: the domino effect

Santos-Soares¹,

Bacellar

Póvoas

et al. 2008

Arq. Neuro-Psiquiatr.

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Despite variations in sodium and water concentrations, our body relies on several mechanisms to maintain the plasmatic osmolality within the normal range of 275-290 mOsm/L 1 . Hyponatremia is defined as a reduction in plasma sodium concentration below 136 mmol/L 2 . It occurs in 12% of the hospitalized patients and in 30% of the patients in the intensive care unit (ICU) 3 . Hyponatremia installed progressively usually causes no symptoms. If installed acutely, severe symptoms such as vomiting, progressive somnolence and confusion, coma and seizures often occur 2,4 . Hyponatremia related to the ingestion of free water is uncommon in healthy subjects that are neither athlete nor have psychiatric disorders [2][3][4][5] . Thus, after approval of the Hospital Ethics Committee and signed informed consent obtained from a patient representative.We report a case of hyponatremia associated with fast ingestion of large amounts of potable water causing severe neurological impairment. CaSeA 34-year-old male, previously healthy, was admitted in ICU of the Hospital da Cidade (Salvador BA, Brazil). The patient was transferred from the emergency department with a history of ingestion of 40 glasses of potable water, equivalent to approximately 8 liters, during a period of a few hours. The patient was playing domino and the players bet that one who loses a game should drink a full glass of water. The unlucky patient lost one game after the other and started to become sleepy, culminating with a generalized tonic-clonic seizure. Taken to the hospital, he developed new episode of seizure, lingered, requiring intubation and mechanical ventilation. The admission tests revealed plasma sodium of 123 mmol/L and mild cerebral edema at CT scan. The diagnosis of hypovolemic hyposmolar hyponatremia with low urinary osmolality ("the marathon runner's hyponatremia") was made based on plasmatic osmolality (262 mmol/L), urinary osmolality, urinary sodium (undetectable) and the volemic status was estimated by pre-load pressures. Since the installation of hyponatremia was rapid with severe symptoms, 3% saline solution was started with infusion rate of 0.5 mL/kg/h. Plasma sodium was measured hourly, aiming for an elevation of sodium level by 0.5 mEq/L/hour. After discontinuing sedation he gradually recovered, being disconnected from mechanical ventilation in the third day of hospitalization. He was discharged from ICU after five days without any neurological deficit. diSCuSSionThe initial approach to hyponatremia requires determination of plasmatic osmolality , in order to classify the hyponatremia in hypertonic, isotonic or hypotonic. The determination of osmolar gap -difference between measured and calculated osmolality, normal <10 mOsm/kg -helps with the interpretation and suggests which solutions should be utilized in the treatment 6 . Hypertonic hyponatremia is typically observed during hyperglycemia or after mannitol use and is also known as translocational hyponatremia. Isotonic hyponatremia is diagnosed in settings of severe hypertriglyceri...

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“…33,41 The concept of ''sick cell syndrome'' may be an underrecognized mechanism of hyponatremia in critically ill and postoperative patients. [42][43][44][45] Sick cell syndrome is believed to be caused by dysfunctional cell membrane integrity and increased permeability associated with cellular Na ? /K ?…”

Section: Iso-osmolar Hyponatremiamentioning

confidence: 99%

Les troubles de l’équilibre hydrosodé chez les patients hospitalisés

Bagshaw

Townsend

McDermid

2008

Can J Anesth/J Can Anesth

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Purpose To review and discuss the epidemiology, contributing factors, and approach to clinical management of disorders of sodium and water balance in hospitalized patients. Source An electronic search of the MEDLINE, Embase, and Cochrane Central Register of Controlled Trials databases and a search of the bibliographies of all relevant studies and review articles for recent reports on hyponatremia and hypernatremia with a focus on critically ill patients. Principal findings Disorders of sodium and water balance are exceedingly common in hospitalized patients, particularly those with critical illness and are often iatrogenic. These disorders are broadly categorized as hypo-osmolar or hyper-osmolar, depending on the balance (i.e., excess or deficit) of total body water relative to total body sodium content and are classically recognized as either hyponatremia or hypernatremia. These disorders may represent a surrogate for increased neurohormonal activation, organ dysfunction, worsening severity of illness, or progression of underlying chronic disease. Hyponatremic disorders may be caused by appropriately elevated (volume depletion) or inappropriately elevated (SIADH) arginine vasopressin levels, appropriately suppressed arginine vasopressin levels (kidney dysfunction), or alterations in plasma osmolality (drugs or body cavity irrigation with hypotonic solutions). Hypernatremia is most commonly due to unreplaced hypotonic water depletion (impaired mental status and/or access to free water), but it may also be caused by transient water shift into cells (from convulsive seizures) and iatrogenic sodium loading (from salt intake or administration of hypertonic solutions). Conclusion In hospitalized patients, hyponatremia and hypernatremia are often iatrogenic and may contribute to serious morbidity and increased risk of death. These disorders require timely recognition and can often be reversed with appropriate intervention and treatment of underlying predisposing factors.

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Osmolar gap hyponatremia in critically ill patients: Evidence for the sick cell syndrome?

Cited by 38 publications

References 19 publications

Increased Plasma Osmolar Gap Is Predictive of Contrast-Induced Acute Kidney Injury

Increased Plasma Osmolar Gap Is Predictive of Contrast-Induced Acute Kidney Injury

Excessive water ingestion and repeated seizures: the domino effect

Les troubles de l’équilibre hydrosodé chez les patients hospitalisés

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