Metabolic Alkalosis Secondary to Baking Soda Treatment of a Diaper Rash

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820 PEDIATRICS Vol. 67 No. 6 June 1981

Metabolic

Alkalosis

Secondary

to Baking

Soda

Treatment

of a Diaper

Rash

Jose Gonzalez, MD, and Ronald J. Hogg, MD

From the Department of Pediatrics, The University of Texas Health Science Center at Dallas, Dallas

ABSTRACT. A 4-month-old infant was seen with

hypo-kalemic 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 bak-ing soda applications. This case report provides a re-minder of the significant side effects that may result from the excessive use of a seemingly harmless household substance. Pediatrics 67:820-822, 1981; metabolic alka-losis, baking soda, diaper rash.

In infants most cases of metabolic alkalosis are generated by increased gastric losses of hydrochlo-ric acid.’ Other cases are usually associated with deficient intake2 or excessive output35 of chloride ions. Metabolic alkalosis resulting from excessive intake of bicarbonate is distinctly unusual because under normal circumstances the kidneys are able to excrete the excess load. This case report concerns a patient who developed hypokalemic metabolic alkalosis secondary to transcutaneous sodium bi-carbonate absorption from topically applied baking soda.

CASE REPORT

The patient was seen at the age of 4 months with a

severe diaper rash that had been present for more than

a week. During that time his mother had treated the rash

by applying liberal amounts of sodium bicarbonate (USP

baking soda, Arm & Hammer) and petroleum jelly (Vase-line) at every diaper change. The infant had had no

Received for publication June 30, 1980; accepted Oct 15, 1980. Reprint requests to (R.J.H.) Department of Pediatrics, Univer-sity of Texas Health Science Center at Dallas, 5323 Harry Hines Blvd. Dallas, TX 75235.

medical problems prior to this presentation. There was no history of vomiting, polyuria, pulmonary problems, or abnormal stools. His dietary intake had consisted of 32 oz/day of Similac 20, and he had not received

Neo-Mull-Soy at any time. On physical examination, the patient

showed no clinical evidence of volume depletion. His

height (59 cm) was between the third and tenth percen-tiles, and his weight (4.8 kg) was less than the third percentile. A diffuse erythematous rash with large areas of denuded skin extended over his lower abdomen, pen-neum, buttocks, medial thighs, scrotum, and penis. His systolic blood pressure was 90 mm Hg, heart rate was 120 beats per minute, and respiratory rate was 34/mm. Initial laboratory studies revealed hypokalemic metabolic alka-losis and mild hypernatremia, as shown in the Figure. Other pertinent laboratory data not shown in the Figure included: serum creatimne level, 0.5 mg/100 ml, chloride level, 92 mEq/liter; and hemoglobin level, 10 gm/100 ml.

Urine specific gravity was 1.003, and urine chemistry values on the morning following admission were: sodium, 24 mEq/liter; chloride, <10 mEq/liter, potassium, <10 mEq/liter; and creatinine, 8.5 mg/100 ml. From these data, the following fractional excretion rates were calcu-lated: sodium, 1%; chloride, <0.7%; and potassium, <18.4%.

Following admission, the patient was treated with ap-plications of Burow’s solution and zinc oxide to the de-nuded areas. Fluid therapy consisted of only Pedialyte and Isomil with intravenous fluids and medications being withheld. With this therapy, the patient progressed well clinically, and his laboratory studies showed rapid reso-lution of the metabolic alkalosis as shown in the Figure. This restoration of electrolyte balance occurred in the absence of weight gain. After 1 1 days his acid-base status was normal and he was discharged from the hospital with the only specific therapy being discontinuation of bicar-bonate of soda use. His weight at discharge was 250 gm greater than on admission (an increase of 4%).

Follow-up examination of the patient two weeks after discharge revealed no abnormalities. Since that time the infant has shown no recurrence of metabolic alkalosis. As shown, laboratory studies were normal four months later when the patient was again returned to the hospital with the history of a diaper rash. On this occasion, there were no areas of denuded skin and only zinc oxide had been

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ARTICLES 821 SERUM 145L \____________

‘50r SODIUM

____________

(mEq/L)

135L

SERUM POTASSIUM (mEq/L) SERUM BICARBONATE (mEq/L) 7.6 VENOUS pH 7.4 9 URINE pH 5 ‘.o- -

.---I 2 3 4

HOSPITAL DAYS

5 I

(4 MONTHS

,t LATER

Figure. Serial changes in blood and urine chemistries in patient J.B.

applied to the rash. The result of a sweat chloride test at that time was 13 mEq/liter. The rash resolved quickly

following treatment with nystatin (Mycostatin) powder following which the infant has continued to do well.

DISCUSSION

Although direct evidence linking the two is ab-sent, we would hypothesize that the hypokalemic metabolic alkalosis seen in this infant resulted from excessive sodium bicarbonate absorption from the baking soda that was applied to his diaper rash.

Although alkalosis resulting from excess transcu-taneous passage of bicarbonate has not been de-scribed previously, it is difficult to reconcile the clinical and laboratory findings with any other mechanism. Certainly, there was no evidence of (1) excess gastric losses of hydrochloric acid (no vom-iting, well hydrated clinically, and relatively high fractional excretion of sodium); (2) deficient duo-ride intake (no history of use of Neo-Mull-Soy), (3) excess oral or parenteral intake of alkali, (4) excess renal retention of bicarbonate (urinary pH 9; serum creatinine level, 0.5 mg/100 ml), or (5) previous

hypercapneic state.

However, it is well established that metabolic alkalosis secondary to excess bicarbonate loads is a

rare entity in the presence of normal renal function.6 When the effects of prolonged administration of

massive doses of sodium bicarbonate (up to 140 gm) have been studied in adults,7 considerable increases

in plasma pH and bicarbonate have been noted in some cases although adverse symptoms were de-scribed as “few and trivial.” In the present case, we

postulate that the metabolic alkalosis resulted from excess sodium bicarbonate absorption in the pres-ence of immature renal function such that the load of bicarbonate exceeded the renal capacity for bi-carbonate excretion. An approximation of the load/ capacity ratio has been estimated as follows.

Baking soda (sodium bicarbonate) contains 41.8 mEq of sodium (0.952 gui) and 41.8 mEq of bicar-bonate per teaspoon (manufacturer’s data). If we assume, in our patient, an average application of 2

teaspoons per diaper change (a conservative amount according to the history) and an approxi-mate number of applications per day of 10, this would represent an exogenous load of 836 mEq of bicarbonate per 24 hours. We can estimate the

glomerular filtration rate (GFR) by using the

for-mula:8 GFR (ml/min/1.73 sq m) = 0.55

x

(body

length [cm]/serum creatinine [mg/100 mi]). Thus,

in our patient, who had a body surface area of 0.4 sq m: GFR = 0.55

x

(60/0.5) = 66 ml/min/1.73 sq

m. From this, we can determine that the absolute

GFR = (66 x 0.4)/1.73 = 15 ml/min. Thus, the

amount of bicarbonate ifitered in 24 hours is: (15

x 37

x

60 x 24)/bOO = 799.2 mEq.

The approximate load of bicarbonate applied to the denuded skin, and the maximal renal bicarbon-ate excretory capacity (assuming no bicarbonate reabsorption) may thus be estimated by these

rather simplistic calculations. There would not, of course, have been complete absorption of sodium bicarbonate from the skin, and thus the amount that reached body fluids would have been consid-erably less. However, it is also reasonable to expect that some of the sodium bicarbonate in the glomer-ular filtrate was reabsorbed and, hence, the amount of bicarbonate excreted was less than the amount

filtered. Thus, both of the figures represent

over-estimates of

the factors that governed the

bicarbon-ate balance in this child. The calculation does, however, give some indication of the tremendous load of bicarbonate that resulted from the

indis-criminate

use of

this readily available household

item. From anecdotal experience, it seems that bak-ing soda is a common remedy for a multitude of conditions, not the least of which is the local appli-cation for skin rashes, especially those in the diaper area. As our patient’s case history shows, baking soda with its high content of sodium bicarbonate may be harmful when used excessively. It is appar-ent from this case that transcutaneous absorption of alkali across a damaged integument needs to be considered as a rare additional cause of metabolic alkalosis in infants.

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822 METABOLIC ALKALOSIS

REFERENCES

1. Winters RW: Metabolic alkalosis of pyloric stenosis, in Win-ters RW (ed): The Body Fluids in Pediatrics. Boston, Little, Brown and Co, 1973

2. Roy 5, Arant BS: Alkalosis from chloride deficient Neo-Mull-Soy. N Engi J Med 301:615, 1979

3. Lock JE, Lynch RE, Mauer SM: Metabolic alkalosis in children with congestive heart failure. J Pediatr 87:938, 1975

4. Black JA, Harris F, Lenton EA, et al: Alkalosis in burns in children. Br Med J 4:387, 1971

5. Beckerman RC, Taussig LM: Hypoelectrolytemia and met-abolic alkalosis in infants with cystic fibrosis. Pediatrics 63:

580, 1979

6. Seldin DW, Rector FC: The generation and maintenance of metabolic alkalosis. Kidney

mt

1:306, 1972

7. Van Goidsenhoven GM-T, Gray OV, Price AV, et al: The effect of prolonged administration of sodium bicarbonate in man. Clin Sci 13:383, 1954

8. Schwartz GJ, Haycock GB, Edelmann CM, et al: A simple estimate of glomerular ifitration rate in children derived from body length and plasma creatinine. Pediatrics 58:259, 1976.

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Submitted by S. C. Copps, MD

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1981;67;820

Pediatrics

Jose Gonzalez and Ronald J. Hogg