A 65 year old male with oxygen dependent COPD, alcohol abuse and CHF presented to the ER with asymptomatic hypotension. On the day in question, he consumed approximately 2‐3 tablespoons of baking soda for his chronic severe GERD as well as his regular dose of Lasix. During transportation to ER he received NS bolus of 250 ml.
On arrival to ER he was afebrile with BP 116/60 and Pulse 92/min. EKG showed QTc = 542ms.
His initial labs were:Na+: 127meq/L, K+: 4.2meq/L that dropped to 2.7meq/L in 4 hours, Cl‐: 82mmol/L, CO2: 36mmol/L, Cr‐: 1.3mg/dl with normal CBC. His CXR showed mild nonspecific airspace disease. His initial ABGs were pH: 7.9, pCO2: 16.9, pO2: 32 and HCO3: 33.1
Upon presenting to the hospital his constellation of symptoms and acute change in pH was most consistent with severe metabolic alkalosis compounded by respiratory alkalosis. His acid deficit was calculated at about 360 mEq. Given the severity of the alkalemia, he was started on 0.1 N HCl gtt with close monitoring of pH and K+. Within 13 hrs, his pH improved to 7.45.
The sequence of his ABG correction is as follows:
|17:16 pm||18:08 pm||22:40 pm||00:26 am||02:41 am||04:22 am||06:27 am|
His pC02 also returned to the baseline. Clinically, he improved and HCl was d/c’d in favor of Diamox for final adjustment in his HCO3 and aggressive potassium replacement was continued. He was transferred to a telemetry bed until his potassium was sufficiently replaced, at which point he was discharged with optimal medical alterations.
It was in 1946 when the relationship between serum HCO3 and its renal excretion; thanks to Pitts et al who infused themselves with HCO3 to define it’s renal curve. In the later years HCO3 reabsorbtion, its relation with blood pressure change, effective blood volume, GFR and filtered load of HCO3 was defined. Since then, with the invention of micropuncture and microperfusion techniques, we have come to know various factors that can affect HCO3 metabolism like pH, urine and blood flow rate, various hormones/electrolytes and acid base status.
Metabolic alkalosis is one of the most important acid base disturbances as it accounts for more than half the acid base disorders in ICU. It’s associated with increase in the morbidity and mortality by various mechanisms like cardiac arrhythmias, altered consciousness, seizures, decreased Hb‐oxygen dissociation, tetany, uremia and respiratory depression.
Metabolic Alkalosis is devisable in 2 phases (Laski et al), a generation phase (excess alkali intake, gastric alkalosis, Diuretics, RTA, Cl‐ losing diarrhea or Licorice ingestion), and a maintenance phase (changes in volume, renal acid loss 2o to aldosterone secretion or potassium depletion). A maintenance mechanism is necessary in order to sustain a metabolic alkalosis.
Treatment is addressed in a similar fashion as the causative mechanism, i.e. to treat the etiology. Important approaches are volume expansion, electrolyte repletion and HCO3 diuresis using acetazolamide. Hemodialysis or Hydrochloric acid therapy is rarely needed to correct refractory or acute life‐threatening metabolic alkalosis.
Baking Soda along with diuretics can induce lifethreatening metabolic alkalosis especially in a patient with underlying acid base disorder sometimes requiring hydrochloric acid therapy. It’s physician’s duty to caution patients about the use of these medication.
To cite this abstract:Bajwa M, Buddhdev A, Young A, Hayner C. Hydrochloric Acid Therapy Can Be Life Saver in Baking Soda Induced Life Threatening Acute Onset Metabolic Alkalosis. Abstract published at Hospital Medicine 2014, March 24-27, Las Vegas, Nev. Abstract 336. Journal of Hospital Medicine. 2014; 9 (suppl 2). https://www.shmabstracts.com/abstract/hydrochloric-acid-therapy-can-be-life-saver-in-baking-soda-induced-life-threatening-acute-onset-metabolic-alkalosis/. Accessed March 28, 2020.