Pediatric emergency medicine trisk 2863 2863
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significant potassium content, and potassium salt infusions. Given
improvements in blood bank procedure, hyperkalemia is less common with
transfusion of red cells. Endogenous sources of potassium may result from
tissue damage, including burns, trauma, rhabdomyolysis, hemolysis, tumor
lysis, and gastrointestinal bleeding with enteral reabsorption. Clinical
scenarios associated with extracellular shift include metabolic acidosis,
hyperosmolarity, insulin deficiency, and the use of β-adrenergic receptor
antagonists. Reduced renal excretion of potassium may occur in acute or
chronic renal insufficiency, hypovolemia, mineralocorticoid deficiency,
inherited or acquired renal tubulopathy, and due to the use of certain
medications ( Table 100.8 ).
Evaluation begins with a thorough history with specific inquiries
regarding injuries, muscle pain, history of renal disease, and medications
taken. Serum potassium should be repeated to rule out pseudohyperkalemia,
which results from a hemolyzed specimen due to difficulties in obtaining
the specimen. Serum sodium, chloride, calcium, phosphorus, bicarbonate
levels, and measures of renal function should also be obtained. Serum
creatinine kinase (CK) should be submitted if there is suspicion for
rhabdomyolysis. A complete blood count (CBC) should be obtained if there
is possibility of hemolysis. Urine electrolytes and osmolality should be
obtained. An ECG should be obtained to monitor for cardiac effect.
Clinical manifestations. The clinical features associated with
hyperkalemia are a consequence of altered cellular transmembrane
potassium gradient, which reduces the resting membrane potential. Initially
this increases membrane excitability, which is followed by a sustained
reduction in excitability. Unless the rise is rapid, symptoms or signs
generally do not become apparent until the serum potassium concentration
exceeds 7 mEq/L. Clinical features predominantly involve cardiac
conduction and neuromuscular disturbance. Cardiac dysrhythmias are the
most serious consequence, and toxicity is exacerbated by a rapid rise in
potassium concentration, acidosis, hyponatremia, and hypocalcemia. Early
ECG changes include narrow, peaked T waves with shortened QT interval,
which is followed by progressive lengthening of the PR interval and
widening of the QRS complex. There may be loss of P-wave amplitude and
eventual “sine wave” pattern when the QRS merges with the T wave. This
is typically followed by ventricular fibrillation or standstill. Neuromuscular
