Abstract: PUB144
Potassium Chloride Saves a Life: A Case of Severe Metabolic Alkalosis
Session Information
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- De, Srijisnu, Baylor College of Medicine Margaret M and Albert B Alkek Department of Medicine, Houston, Texas, United States
- Menjivar, Juan J., Baylor College of Medicine Margaret M and Albert B Alkek Department of Medicine, Houston, Texas, United States
- Kassem, Hania, Baylor College of Medicine Margaret M and Albert B Alkek Department of Medicine, Houston, Texas, United States
Introduction
Metabolic alkalosis is reported to be associated with a high rate of mortality in hospitalized and critically-ill patients. Diuretic use is a common etiology of metabolic alkalosis. However, other causes such as volume depletion and hypokalemia can also contribute to metabolic alkalosis as illustrated by this case.
Case Description
A 36-year-old female with a past medical history of HTN and bipolar disorder presented after a syncopal episode. She has been on long-term HCTZ for hypertension and reported a few syncopal episodes prior to presentation. She did not report vomiting or diarrhea but acknowledged food insecurity. Upon presentation, the patient had orthostatic hypotension and an otherwise unremarkable exam. She had a pH of 7.58, pCO2 53.6, bicarb 50, low urine Cl, Na, K and osm, and chemistry as per the table below. She was initially given Lactated Ringer’s in the emergency room.
Recent thiazide use, volume depletion, and very low solute intake were suspected to be the cause of the presenting symptoms, electrolyte disorders, and prerenal AKI.
The patient was given repetitive doses of IV KCl and then started on normal saline with improvement in her labs and symptoms. She was discharged off thiazides, on short term potassium chloride supplementation, and instructions on adequate solute intake.
Discussion
Volume depletion, low chloride delivery, and hypokalemia in this patient caused upregulation of the RAAS and increased ammoniagenesis contributing to both generation of new bicarbonate and maintenance of alkalosis via increased reabsorption of bicarbonate and increased hydrogen secretion. The patient responded well to correction of hypokalemia and volume resuscitation with IV KCl and NaCl, which decreased ammoniagenesis, restored chloride delivery to the macula densa, and suppressed the RAAS. We present this case hoping to shed light on the pathophysiological causes of metabolic alkalosis that guided our patient’s management and the importance of chloride-based solutions rather than balanced solutions for resuscitation in this setting.
| 0 hour | 24 hours | 48 hours | 72 hours | 96 hours | |
| Serum Chemistry | On Presentation | On aggressive KCl and initial LR bolus | On aggressive KCl only | KCl and started on IV NS | Maintenance KCl and IV NS |
| Sodium | 110 | 118 | 124 | 132 | 135 |
| Potassium | 2.0 | 2.9 | 3.9 | 4.3 | 4.5 |
| Bicarbonate | >45 | >45 | 38 | 38 | 34 |
| Chloride | 52 | 63 | 74 | 87 | 93 |
| Creatinine | 1.4 | 1.3 | 1.5 | 1.6 | 1.0 |