Pediatric Hyperkalemia Follow-up
- Author: Michael J Verive, MD; Chief Editor: Timothy E Corden, MD more...
Further Inpatient Care
Hyperkalemia, by itself, is not a disease and is generally the result of diseases such as congenital adrenal hyperplasia, acute renal failure, rhabdomyolysis, or tumor lysis syndrome.
Following emergent management and stabilization of hyperkalemia, the patient should be hospitalized, and further workup should be initiated to determine the inciting cause and to prevent recurrence.
Further Outpatient Care
Continuing care relates to the basic disease process that led to the hyperkalemia.
In patients with salt-wasting congenital adrenal hyperplasia, corticosteroid and mineralocorticoid supplementation are necessary.
Continued renal replacement therapy may be needed for patients with acute renal failure.
Patients with chronic mineralocorticoid deficiency require mineralocorticoid supplementation (eg, fludrocortisone).
Transfer
Patients with acute life-threatening hyperkalemia should receive care in a pediatric or neonatal ICU capable of providing emergent hemodialysis.
Any child who develops hyperkalemia as a result of renal failure should be referred to a pediatric nephrologist for continuing care.
Complications
If untreated, severe hyperkalemia can result in cardiac arrhythmia or death.
Treatment of pseudohyperkalemia may result in hypokalemia; thus, treatment of non–life-threatening hyperkalemia should be deferred pending verification of hyperkalemia.
Failure to determine and treat the underlying disease process causing hyperkalemia can predispose patients to recurrent, life-threatening hyperkalemia.
Prognosis
Prognosis depends on the etiology.
Patient Education
Teach patients to recognize the symptoms of hyperkalemia, such as palpitations, dizziness, and weakness.
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| Factor | Effect on Plasma K+ | Mechanism |
| Aldosterone | Decrease | Increases sodium resorption, and increases K+ excretion |
| Insulin | Decrease | Stimulates K+ entry into cells by increasing sodium efflux (energy-dependent process) |
| Beta-adrenergic agents | Decrease | Increases skeletal muscle uptake of K+ |
| Alpha-adrenergic agents | Increase | Impairs cellular K+ uptake |
| Acidosis (decreased pH) | Increase | Impairs cellular K+ uptake |
| Alkalosis (increased pH) | Decrease | Enhances cellular K+ uptake |
| Cell damage | Increase | Intracellular K+ release |
| Succinylcholine | Increase | Cell membrane depolarization |

