Pediatric emergency medicine trisk 1879 1879
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focused assessment of the patient’s presenting problem. Understanding which specific
hormone deficits the presenting patient has will help guide further history, physical, and the
treatment.
Cortisol deficiency can present insidiously with fatigue, anorexia, vomiting, and failure to
thrive. Consider it specifically in patients with unexplained hypoglycemia and/or
hyponatremia. Of note, hyperkalemia and severe hyponatremia are seen in primary adrenal
insufficiency due to an absence of appropriate aldosterone synthesis—this is not related to
hypocortisolemia. Cortisol deficiency can also present more acutely, as in patients who have
fluid and pressor refractory hypotension (see Acute Adrenal Insufficiency section for more
information).
Patients with thyroid hormone deficiency due to hypopituitarism will often have general
complaints of fatigue, cold intolerance, constipation, weight gain, and hair thinning/loss.
Children often have delayed growth. Infants can have hypotonia, hypothermia, and significant
constipation (see Congenital Hypothyroidism section).
Patients with DI have extreme thirst and polydipsia as well as polyuria. Consider in patients
who have a history of polydipsia, however, appear volume depleted on examination (see
Diabetes Insipidus section).
Isolated growth hormone deficiency is most likely to present with poor linear growth,
although occasionally an infant or young child will present with hypoglycemia or with
microphallus (less than 2 cm, stretched length).
In the older child, no specific symptoms or signs indicate a lack of LH and FSH. An
association between a lack of these hormones and anosmia has been noted (Kallmann
syndrome). In the adolescent, a deficiency of LH and FSH may be evidenced as pubertal delay.
In the neonatal male, hypopituitarism may be accompanied not only by hypoglycemia, but also
by microphallus (less than 2 cm, stretched length). This condition illustrates the role of LH and
FSH in stimulating testicular function in utero.
No specific signs or symptoms have been associated with a deficiency of prolactin in
childhood. Significant liver dysfunction in the neonatal period may be associated with
congenital hypopituitarism. Hypopituitarism is seen with various midline structural anomalies,
including optic nerve hypoplasia, cleft palate, absence of the septum pellucidum, and spina
bifida. In the older child, intracranial mass lesions, particularly with craniopharyngioma and
other pituitary abnormalities, may cause hypopituitarism. The presence of visual field
abnormalities may aid in localizing the site of the lesion. A history of severe head trauma,
surgery for CNS tumors, or CNS irradiation should increase the suspicion of hypopituitarism.
Management/Diagnostic Testing
The child with hypopituitarism may require any or all the following therapies. Adequate
cortisol replacement is an absolute necessity in children with known or suspected secondary
adrenal insufficiency (ACTH deficiency) during a time of physiologic stress. Cortisol
replacement under stress conditions (e.g., trauma, fever, sepsis) should be the equivalent of 50
mg of hydrocortisone/m2/day (hydrocortisone IV infusion 12.5 mg/m2 every 6 hours;
hydrocortisone continuous IV infusion at 50 mg/m2/day; cortisone 50 mg/m2 intramuscularly
every 24 hours). A child with hypopituitarism presenting in extremis or with severe electrolyte
abnormalities should immediately receive an initial rescue dose of hydrocortisone of 50
