Pediatric emergency medicine trisk 3070 3070
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The effects of digoxin are largely related to its inhibition of sodium–potassium
adenosine triphosphatase (ATPase), which is responsible for maintaining the
electrical potential of excitable tissues through transmembrane concentration of
electrolytes.
Clinical Considerations. There are two distinct phenotypes of toxicity: acute and
chronic. The patient with acute digoxin ingestion is typically a healthy toddler
who ingests a relative’s medication. The child with chronic digoxin poisoning,
however, has pre-existing heart disease and is likely to be taking other
medications that modulate the effects of digoxin poisoning (e.g., diuretics).
Therefore, it is the latter patient who is more likely to have severe toxic
manifestations.
Digoxin pharmacokinetics includes absorption within 2 to 4 hours, then rapid
redistribution, resulting in dramatic falls in serum concentration as tissue
concentrations increase. This principle has particular importance with the patient
of acute digoxin intoxication who may have an initial serum digoxin
concentration (SDC) in the highly toxic range that falls to the therapeutic range
within a matter of hours. After redistribution, digoxin elimination occurs
primarily through renal excretion of unchanged drug. Therefore, any condition
associated with decreased renal function may be associated with the insidious
development of intoxication.
The therapeutic SDC is less than 2 ng/mL. A concentration in the slightly
higher range often does not correlate with clinical manifestations and may be of
limited value. However, when SDC exceeds 4 ng/mL, some evidence of
intoxication usually appears. This toxicity is influenced by many host factors,
including patient age; underlying illness; and disturbances in serum potassium,
magnesium, and calcium.
With significant intoxication, the symptoms of digoxin poisoning include
nausea, vomiting, and visual disturbances. With more severe intoxication,
additional symptoms, including lethargy, disorientation, electrolyte disturbances,
and cardiac disturbances, appear. The hallmark of severe acute digoxin toxicity is
hyperkalemia, the result of profound inhibition of sodium–potassium ATPase
activity. The typical pattern of cardiac toxicity with digoxin overdose initially is
prolonged AV dissociation that appears as heart block that ranges from first to
third degree. These conduction disturbances can lead to the development of
ventricular or supraventricular escape rhythms. In patients with chronic digoxin
intoxication, these symptoms may be more striking than in those with acute,
