POTASSIUM CHLORIDE 0.22% IN DEXTROSE 5% AND SODIUM CHLORIDE 0.11% IN PLASTIC CONTAINER
Clinical safety rating: safe
No significant drug interactions Can cause hypernatremia and fluid overload.
Potassium chloride replenishes potassium stores. Dextrose provides caloric support via glucose metabolism. Sodium chloride maintains osmotic balance and fluid volume.
| Metabolism | Potassium primarily excreted renally; negligible metabolism. Dextrose metabolized via glycolysis. Sodium chloride not metabolized. |
| Excretion | Potassium is primarily excreted renally (about 90%) with the remainder eliminated via feces. In this formulation, the dextrose and sodium chloride are also excreted renally, with dextrose being fully reabsorbed when normoglycemic. Excretion data for potassium: renal ~90%, fecal ~10%. |
| Half-life | Potassium does not have a defined terminal half-life in the traditional sense, as it is tightly regulated. The elimination half-life of potassium ions from the plasma is approximately 1-1.5 hours for acute distribution, but the overall body turnover is much slower. In clinical context, after IV infusion, plasma concentration declines rapidly due to cellular uptake and renal excretion. |
| Protein binding | Potassium is minimally protein-bound (<2%). Dextrose and sodium chloride are not protein-bound. |
| Volume of Distribution | Potassium: Vd is approximately 0.5-0.7 L/kg total body water, but for potassium ions, the apparent Vd is about 10 L (0.14 L/kg) in the extracellular space, with slow distribution into intracellular space (total body potassium ~3500 mEq). Clinical meaning: The small extracellular Vd means rapid changes in serum potassium with small amounts given IV. |
| Bioavailability | Intravenous: 100% bioavailability. |
| Onset of Action | Intravenous: Onset of effect on serum potassium is immediate upon infusion, with measurable changes within minutes. Full effect on correcting hypokalemia may take 1-2 hours depending on infusion rate. |
| Duration of Action | Intravenous: Duration of effect on serum potassium is short-lived after infusion ceases, lasting approximately 2-4 hours due to rapid redistribution and renal excretion. Continuous infusion is often required for sustained correction. |
Intravenous infusion only; typical adult dose is 1 L at a rate of 100-200 mL/hour, delivering 0.22% KCl (2.2 g KCl = 29.9 mEq K+), 5% dextrose, and 0.11% NaCl (1.1 g NaCl = 18.8 mEq Na+, 18.8 mEq Cl-). Dose depends on potassium deficit and renal function.
| Dosage form | INJECTABLE |
| Renal impairment | Contraindicated in anuria or severe renal impairment (GFR <30 mL/min, not on dialysis) due to risk of hyperkalemia. For GFR 30-50 mL/min: reduce potassium content or use lower concentration potassium solutions; monitor serum potassium closely. For GFR >50 mL/min: standard dosing with monitoring. |
| Liver impairment | No specific Child-Pugh based dose adjustments for this solution; however, hepatic impairment may increase risk of hyperkalemia due to reduced aldosterone clearance. Use with caution and monitor serum potassium in decompensated cirrhosis (Child-Pugh C). |
| Pediatric use | Weight-based dosing: 0.2-0.5 mEq/kg/hour of potassium (max 1 mEq/kg/hour) via IV infusion. For this solution (0.22% KCl = 0.297 mEq K+/mL), typical rate is 0.67-1.68 mL/kg/hour. Dextrose and sodium content should be considered in fluid and electrolyte management. |
| Geriatric use | Elderly patients may have reduced renal function; start at lower infusion rates (e.g., 50-100 mL/hour) and titrate based on serum potassium, renal function, and volume status. Monitor for hyperkalemia, volume overload, and hyperglycemia due to dextrose. |
| 1st trimester | Consult provider |
| 2nd trimester | Consult provider |
| 3rd trimester | Consult provider |
Clinical note
No significant drug interactions Can cause hypernatremia and fluid overload.
| FDA category | Animal |
| Breastfeeding | Potassium, dextrose, and sodium chloride are normal constituents of breast milk. No adverse effects on breastfed infants are expected at therapeutic doses. M/P ratio not applicable as these are endogenous substances; no dose adjustment required. |
| Teratogenic Risk | Potassium chloride, dextrose, and sodium chloride are physiological electrolytes and nutrients. At therapeutic doses, there is no evidence of teratogenic risk in any trimester. Excess potassium or sodium may cause maternal electrolyte disturbances affecting fetal homeostasis, but standard concentrations are safe. |
■ FDA Black Box Warning
Concentrated potassium solutions must be diluted before administration to avoid fatal hyperkalemia. Do not administer undiluted.
| Common Effects | fluid replacement |
| Serious Effects |
Hyperkalemia, severe renal failure (unless dialysis), hypernatremia, hyperglycemia, anuria, severe metabolic acidosis, Addison's disease, severe dehydration, concurrent use of potassium-sparing diuretics or ACE inhibitors without monitoring.
| Precautions | Monitor serum potassium, glucose, and electrolytes. Risk of hyperkalemia, especially in renal impairment. Avoid in patients with hyperkalemia or severe metabolic acidosis. Use caution in heart failure or edema due to sodium load. May cause hyperglycemia in diabetic patients. |
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| Fetal Monitoring | Monitor serum potassium, sodium, glucose, and renal function periodically. Assess for signs of fluid overload or electrolyte imbalance during prolonged infusion. Fetal monitoring not routinely required unless maternal complications arise. |
| Fertility Effects | No known effects on fertility at therapeutic doses. Electrolyte disturbances may impact reproductive function but are not expected with appropriate use. |