Pediatric emergency medicine trisk 1863 1863
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compensated for by a respiratory alkalosis (hyperventilation), with a resultant lowering of PCO
−
2 and plasma bicarbonate (HCO3 ).
Intracellular potassium is depleted because of transcellular shifts of this ion brought about
by the exchange of potassium with excess free hydrogen ions and extracellular dehydration.
Protein catabolism secondary to insulin deficiency causes a negative nitrogen balance and
results in additional efflux of potassium from cells. The potassium is then lost in the urine
during the osmotic diuresis. Volume depletion causes secondary hyperaldosteronism, which
further promotes urinary potassium excretion. Thus, total body depletion of potassium occurs,
although the plasma potassium concentration may not reflect the loss at the time of
presentation.
Clinical Considerations
Clinical Recognition
In cases of new-onset diabetes, the child usually has a history of polyuria and polydipsia for a
few days or weeks before the acute decompensation. Significant weight loss often occurs
despite a vigorous appetite. Vomiting is common once the child has ketoacidosis; these further
losses plus the inability to compensate for polyuria contribute to the hypovolemia.
In children known to have diabetes, the prodrome may be less than 24 hours and
precipitated by an intercurrent illness, inappropriate sick day management, or omission of
insulin doses.
Triage
On physical examination, particular attention should be paid to the degree of dehydration,
including skin turgor and dryness of mucous membranes. Urine output is not a reliable sign of
hydration status. In severe cases, the child may exhibit signs of compensated shock, including
a thready pulse and cold extremities, and rarely, as uncompensated shock with hypotension.
The smell of ketones on the breath and the presence of hyperpneic (Kussmaul) respirations
reflect the ketoacidosis. The patient’s consciousness level, which may range from full alertness
to deep coma, should be noted.
Initial Assessment/H&P
Patients may complain of nausea, vomiting, and abdominal pain, and the parents may have
noticed increasing listlessness. Less than 1% of children are in coma at the time of hospital
admission, although a higher percentage has an altered state of consciousness. The history and
physical examination usually suggest the diagnosis; however, particularly in the patient with
new-onset diabetes, presenting clinical features can be misdiagnosed, especially in the infant
or young child. For example, abdominal pain may be misinterpreted as appendicitis;
hyperpnea may be mistaken as a sign of pneumonia or asthma; and polyuria may be
incorrectly diagnosed as a urinary tract infection. Enuresis, polydipsia, and irritability are
sometimes wrongly categorized as behavioral problems. The child may have exquisite
abdominal tenderness with guarding and rigidity, which can mimic an acute abdomen. The
ears, throat, chest, and urine should be examined because infection is often a precipitating
factor. Careful attention should be paid to the skin examination because there have been
several case reports of fasciitis co-presenting with DKA. The presence of hyperpigmentation
