Dilution acidosis and contraction alkalosis: Review of a concept

Garella, Serafino; Chang, Bruce S.; Kahn, Sewell I.

doi:10.1038/ki.1975.114

Cited by 122 publications

(49 citation statements)

References 16 publications

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“…Another possibility is that dilution induces a diffusion of bicarbonate outside the cell (62) and that this is associated with an intracellular shift of OA. Another mechanism could be a modification of the anionic charges of albumin, which has been reported to be influenced by volemia: Decrease in the negative charge of albumin during volume expansion and increase during hypovolemia (63).…”

Section: Anion Gap and Bicarbonate In Siadhmentioning

confidence: 99%

Clinical Laboratory Evaluation of the Syndrome of Inappropriate Secretion of Antidiuretic Hormone

Decaux

Musch²

2008

Clinical Journal of the American Society of Nephrology

145

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Hyponatremia secondary to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is a frequent cause of hypotonicity. Although the differential diagnosis with other causes of hypotonicity such as salt depletion is sometimes challenging, some simple and readily available biologic parameters can be helpful in the diagnosis of SIADH. In SIADH, urea is typically low; this is less specific for elderly patients, for whom lower clearance of urea accounts for higher values. Low levels of uric acid are more often seen in SIADH (70%) compared with salt-depleted patients (40%). Typically, patients with SIADH will show a lower anion gap with nearly normal total CO 2 and serum potassium, this despite dilution. In patients with hyponatremia secondary to hypocorticism, total CO 2 is usually lower than in nonendocrine SIADH despite low urea and uric acid levels. Urine biology can also be helpful in diagnosis of SIADH because patients with SIADH have high urine sodium (Na; >30 mEq/L), and most of them will have a high fractional excretion of Na (>0.5% in 70% of cases), reflecting salt intake. Conversely, low urine Na in patients with SIADH and poor alimentation is not rare. Finally, measurement of urine osmolality is useful for the diagnosis of polydipsia and reset osmostat and could further help in the choice of therapeutic strategy because patients with low urine osmolality will benefit from water restriction or urea, whereas those with high urine osmolality (>600 mOsm/kg) would be good candidates for V 2 antagonist.

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Section: Anion Gap and Bicarbonate In Siadhmentioning

confidence: 99%

Clinical Laboratory Evaluation of the Syndrome of Inappropriate Secretion of Antidiuretic Hormone

Decaux

Musch²

2008

Clinical Journal of the American Society of Nephrology

145

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“…Doberer and colleagues conducted a number of in vitro physico-chemical laboratory experiments, predominantly diluting alkaline solutions with a more neutral solution under either closed (constant PCO 2) or open (variable PCO 2 ) conditions, and showed that a dilutional acidosis was associated with a reduced SID, but this was a reflection of the dilutional effect per se and did not mechanistically explain the acidosis. The predominant cause of dilutional acidosis in their laboratory experiments was dilution of the bicarbonate buffer capacity, with continued carbon dioxide generation [14]. Gattinoni used an in vitro model of fresh frozen plasma diluted with distilled water, 0.9% saline and Ringer's lactate, and confirmed Doberer's result that in a closed system, pH did not fall with dilution.…”

Section: Commentarymentioning

confidence: 81%

Dilutional acidosis or uncovered cellular metabolism?

Davenport

2009

Intensive Care Med

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“…In fact, this ratio in a pure high anion gap metabolic acidosis should be between 1 and 2, while values lower than 1:1 indicate mixed normal and high anion gap acidosis (15). It is possible, however, that the deterioration of metabolic acidosis observed during the treatment could at least in part be attributed to saline administration (16). In fact, it is known that the administration of HCO3 -free solutions may induce mild hyperchloremic metabolic acidosis by causing rapid volume expansion.…”

Section: Discussionmentioning

confidence: 99%

Metabolic Acidosis during Treatment of Mushroom Poisoning: A Diagnostic Pitfall

et al. 2012

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Metabolic acidosis is a frequently encountered acid-base disturbance in hospitalized patients that occasionally develops in the course of treatment with medications used in everyday clinical practice, including propylene glycol-containing drugs (lorazepam, diazepam, etomidate, pentobarbital). Disruption of enterohepatic circulation with activated charcoal is a common practice for several intoxications, including mushroom poisoning. Herein, we present a patient who was hospitalized due to mushroom intoxication and developed severe metabolic acidosis as a treatment side effect rather than from the mushroom poisoning. Τo the best of our knowledge, this is the first report on propylene glycol-containing activated charcoal-induced metabolic acidosis.

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Dilution acidosis and contraction alkalosis: Review of a concept

Cited by 122 publications

References 16 publications

Clinical Laboratory Evaluation of the Syndrome of Inappropriate Secretion of Antidiuretic Hormone

Clinical Laboratory Evaluation of the Syndrome of Inappropriate Secretion of Antidiuretic Hormone

Dilutional acidosis or uncovered cellular metabolism?

Metabolic Acidosis during Treatment of Mushroom Poisoning: A Diagnostic Pitfall

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