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Management of hyperkalemia involves treatment of elevated serum potassium levels in patients in the neonatal intensive care unit (NICU), particularly those dependent on parenteral fluids.
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Initially, neonates should be in good fluid and electrolyte balance and thus have normal serum potassium concentrations. Exceptions can and do occur rarely but need to be recognized in a timely fashion.
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Maternal history suggestive of abnormal fluid and electrolyte status
Renal diseases with abnormal electrolytes
Diuretic therapy
Malnutrition or very abnormal diet
Oligohydramnios
Physical findings suggestive of abnormal electrolyte balance
Edema/anasarca
Ascites, abdominal/flank masses
Ambiguous genitalia
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Confirmatory/Baseline Tests
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The usual neonate, even the very premature patient, does not need serum electrolytes measured immediately after birth. Initially, a neonate’s electrolytes and creatinine should reflect the mother’s status. Patients with a history or physical findings like those mentioned in the discussion of clinical findings may need an electrolyte panel early in life. Note that in the face of normal placental and maternal renal function, a totally anephric neonate may have normal (ie, maternal) serum creatinine and potassium levels at birth.
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Serum electrolytes should be followed closely in all low birth weight (LBW) and sick patients in the NICU. Serum potassium levels in neonates tend to be somewhat higher than in older children and adults and not uncommonly will be in the range of 5 to 6 mEq/L. However, levels greater than 6.5 should be watched closely, and those greater than 7 are associated with poor outcomes.
Hyperkalemia results in specific recognizable changes in the electrocardiogram (ECG) in the following progression:
Tall, peaked T waves
Prolonged P-R interval
Widened QRS
Bradycardia with abnormal QRS axis
Ventricular fibrillation
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Differential Diagnosis/Diagnostic Algorithm
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Hyperkalemia in the neonate can be thought of in 4 categories:
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Nonoliguric hyperkalemia (NOHK) occurs in the first few days of life in very low birth weight infants in the presence of normal urine output. It is caused by the transfer of potassium from the very high intracellular concentration (∼150 mEq/L) to the relatively low concentration in extracellular fluids. Factors that contribute to this potassium flux include
Immaturity of the energy-dependant Na+-K+ ion pump, which may be worsened by perinatal hypoxia or hypoglycemia
Acidosis resulting in increased H+-K+ exchange across cellular membranes
Epidemiologic findings associated with NOHK, including
(1) Birth weight less than 1000 g
(2) Fetal distress
(3) Metabolic acidosis
(4) Hyperglycemia (caused by osmolality and low insulin)
(5) Polyuric renal failure
(6) No antenatal steroid treatment
Tissue breakdown (eg, hemolysis, necrosis) is a minor contributor1 to NOHK. Indeed, severe hemolytic disease of the newborn does not commonly result in life-threatening hyperkalemia. Rare situations exist in which tissue breakdown may result in hyperkalemia:
(1) Tumorlysis (eg, congenital leukemia)
(2) Rhabdomyolysis from trauma, commonly concomitant with ...