Metabolic Alkalosis Secondary to Baking Soda Treatment of a Diaper Rash

PEDIATRICS ◽  
1981 ◽  
Vol 67 (6) ◽  
pp. 820-822
Author(s):  
Jose Gonzalez ◽  
Ronald J. Hogg

A 4-month-old infant was seen with hypokalemic metabolic alkalosis that was associated with prior application of liberal amounts of sodium bicarbonate (baking soda) to a diaper rash. After exclusion of other etiologies of the infant's acid-base disturbance, a complete resolution occurred following discontinuation of the baking soda applications. This case report provides a reminder of the significant side effects that may result from the excessive use of a seemingly harmless household substance.

PEDIATRICS ◽  
1979 ◽  
Vol 63 (4) ◽  
pp. 580-583
Author(s):  
Robert C. Beckerman ◽  
Lynn M. Taussig

The records of all children in the Tucson area diagnosed as having cystic fibrosis (CF) before the age of 12 months were reviewed to ascertain the prevalence of metabolic alkalosis as a major presenting manifestation of CF. Five of eleven infants (46%) in whom CF had been diagnosed between 1 and 12 months of age initially were seen with hypokalemia, hypochloremia, and metabolic alkalosis unassociated with marked dehydration, hyperpyrexia, or major pulmonary and/or gastrointestinal symptoms. Two infants had repeated episodes of metabolic alkalosis; for one of these infants, both episodes of metabolic alkalosis occurred before the diagnosis of CF. It is postulated that chronic loss of sweat electrolytes together with mild gastrointestinal or respiratory illness may predispose the infant with cystic fibrosis to a severe electrolyte and acid-base disturbance. The lack of shock and hyperpvrexia together with the apparent chronicity of electrolyte losses differentiates metabolic alkalosis from the heat prostration syndrome, a more acute complication of cystic fibrosis. Quantitative sweat testing should be part of the evaluation of any infant with unexplained metabolic alkalosis. Serum electrolytes should be assessed regularly in infants with cystic fibrosis during hot weather months.


1990 ◽  
Vol 152 (1) ◽  
pp. 549-571 ◽  
Author(s):  
GREG G. GOSS ◽  
CHRIS M. WOOD

Adult rainbow trout fitted with arterial and bladder catheters were chronically infused with either bicarbonate (as NaHCO3) or NaCl for 19 h at approximately 410 μequiv kg−1h−1. NaHCO3 infusion produced a pure exogenous metabolic alkalosis of approximately 0.35 pH units accompanied by a decrease in plasma [Cl−] but no change in plasma [Na+]. Alkalosis stimulated Cl− influx and inhibited Na+ influx (measured at 10–16 h infusion), resulting in a negative Na+ balance, a positive Cl− balance and a large net basic equivalent excretion (=acidic equivalent uptake) across the gills. The latter was approximately equal to the rate of HCO3− loading. The kidney accounted for approximately 13% of the acid-base compensation. Kinetic analysis revealed that reductions in JinNa were accomplished by increases in KmNa (463 μequiv l−1; NaHCO3-infused vs 276 μequiv l−1; NaCl-infused) and large decreases in JmaxNa (262 μequiv kg−1 h−1vs 689 μequiv kg−1 h−1) while stimulation of JmaxCl was accomplished by large increases in JmaxCl only (674 μequiv kg−1 h−1vs 360 μequiv kg−1 h−1). Thus, Jmax can be increased or decreased in response to acid-base disturbance, but Km can only be increased; the Na+ and Cl− carriers operate close to maximum affinity under control conditions. Basic equivalent excretion was described by a virtually identical kinetic curve to that of the Cl− uptake. NaHCO3 infusion also induced a differential diffusive efflux of Na+ over Cl− which could account for up to 35% of the acid-base compensation during alkalosis.


1976 ◽  
Vol 64 (3) ◽  
pp. 711-725
Author(s):  
J. N. Cameron

1. Techniques for the measurement of unidirectional flux rates in fish which require no anaesthesia or surgery are described. 2. Resting values for Cl- uptake at 10 and 17 degrees C were 8–03 +/− 1–11 and 13–52 +/− 0–95 mu-equiv. 200 g-1 h-1 (+/− S.E.), respectively; and for Na+ the rates were 15–49 +/− 0–40 and 26–30 +/− 0–36, respectively. 3. Hypercapnic acidosis caused an increase in Na+ uptake, presumably through Na+/H+ (or NH+4) exchange. It is suggested that this is a compensation mechanism leading to the increase in blood buffering observed in response to hypercapnia. 4. Alkalosis was observed following acute temperature increase and was accompanied by an increase in the rate of Cl-/HCO-3 exchange and also by an increase in Na+/H+ exchange. 5. The role of these branchial ion exchange mechanisms in overall acidbase regulation is discussed.


1980 ◽  
Vol 84 (1) ◽  
pp. 273-287
Author(s):  
D. G. McDonald ◽  
R. G. Boutilier ◽  
D. P. Toews

Strenuous exercise results in a marked blood acid-base disturbance which is accompanied by large increases in ventilation rate, heart rate and mean arterial blood pressure. Recovery to normal resting values follows an exponential time course with a half-time of approximately 2 h for all parameters except Pa, CO2 and ventilation rate. The latter return to normal by 30 min following the exercise period. Analysis reveals that there is initially a large discrepancy between the quantity of metabolic acids buffered in the blood and the blood lactate levels. The significance of this finding is discussed. Significant changes in the concentrations of chloride, bicarbonate and lactate, in both plasma and erythrocytes, accompany the blood acid-base disturbance. Chloride and bicarbonate appear to be passively distributed between the two compartments according to a Gibbs-Donnan equilibrium whereas lactate only slowly permeates the erythrocyte.


1979 ◽  
Vol 79 (1) ◽  
pp. 47-58
Author(s):  
D. G. McDONALD ◽  
B. R. McMAHON ◽  
C. M. WOOD

Enforced activity causes a marked depression of haemofymph pH in Cancer magister. Both lactate concentration and PCOCO2 of the haemolymph are elevated immediately following exercise but resting PCOCO2 is restored within 30 min whereas resting lactate levels are not restored for at least 8 h. The haemolymph acid-base disturbance is caused largely by elevated haemolymph lactate levels but a Davenport analysis based on measurements of pH and total CO2 reveals a marked discrepancy between the amount of metabolic acid buffered by the haemolymph and the lactate anion concentration. This appears due to a more rapid release of lactate from the tissues than H+ ions produced with lactate.


2019 ◽  
Vol 86 (3) ◽  
pp. 187-197
Author(s):  
Samuel P. Wiles ◽  
Matthew Kiczek ◽  
Gregory W. Rutecki

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