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Abstract: SA-PO520

Detergent Pica Causing Alkalemia, Life-Threatening Hypokalemia, and Profound Hypochloremia

Session Information

Category: Fluid, Electrolytes, and Acid-Base Disorders

  • 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

  • Barakat, Munsef, Medical University of South Carolina, Charleston, South Carolina, United States
  • Achanti, Anand, Medical University of South Carolina, Charleston, South Carolina, United States
  • El Sheikh Mohammed, Waleed A., Medical University of South Carolina, Charleston, South Carolina, United States
Introduction

Metabolic alkalosis is characterized by elevated serum bicarbonate and result from either a net loss of acid via the renal or GI tracts or via accumulation of exogenous base. History may reveal unusual cause like detergent PICA. Renal handling of excess bicarbonate is limited by the low GFR, hypovolemia, hypokalemia and hypochloremia.

Case Description

32 years old lady presented with progressive lower limb weakness, nausea and one episode of vomiting without hematemesis. On further history she reported drinking detergent (Gain & Oxiclean).
Examination: BP125/70mmHg, HR 77bpm (no orthostatic changes), and normal oxygen saturation 96%.
Neurological exam showed mild weakness in proximal lower limbs muscle with normal reflexes.
Labs: BMP: K 1.3mmo/l, Cl 65mmol/l, HCO3- 49mmol/l, CPK 3042U/L.
Normal TSH, genetic testing was negative for Bartter, Gitelman and Liddle syndrome.
PH 7.71, PCO2 51mmHg, HCO3- 62mmol/l, ionized calcium 0.93mmol/l.
Urine study: Cl 87mmol/l, K 8.6mmol/l, Na 24 mmol/l and Cr 90mmol/l
ECG: prolonged QTc interval and low T- wave amplitude with U-wave.
Based on presentation, the likely diagnosis was metabolic alkalosis secondary to pica disorder with consumption of bicarbonate found in detergents which is exacerbated further by the hypokalemia and hypochloremia which limited the kidney ability to mitigate such high alkali load. Furthermore, her severe hypokalemia caused mild rhabdomyolysis as evident by the elevated creatine kinase level.
She was admitted to the ICU for telemetry monitoring, started IV chloride rich IV fluids, aggressive parenteral potassium replacement via central venous catheter, she required total of 560mEq of potassium chloride and another 360mEq of oral potassium chloride. 72 hours post admission alkalemia resolved with resolution of the hypokalemia and correction of hypochloremia.

Discussion

Approach to metabolic alkalosis should takes into consideration its different phases of development, the generation, maintenance, and recovery phase. Both hypochloremia and hypokalemia have an inhibitory effect on the pendrin exchanger in the B-intercalated cells as hypochloremia impair the bicarbonate secretion and hypokalemia will downregulate the pendrin expression.

In conclusion the correction of metabolic alkalosis require correction of concomitant hypokalemia, hypochloremia and volume resuscitation when clinically appropriate.