Endocrine Emergencies
Answers
475.The answer is d.(Rosen, pp 1750-1754.)The mainstay of treatment for
DKAisaggressive fluid resuscitationandinsulintherapy. The patient
should receive 2 L of normal saline within 2 hours of presentation followed by
4 to 6 L over the next 8 to 12 hours depending on the patient’s fluid status. In
DKA, the average adult has a water deficit of 5 to 10 L. After fluid administra-
tion, regular insulin is administered usually first as a 10-U bolus intravenously
and then at a rate of 0.1 U/kg/h. Insulin must be administered for ketosis and
acidosis to resolve.
(a)Intramuscular and subcutaneous insulin administration is avoided in
DKA as absorption may be erratic secondary to volume depletion and poor per-
fusion.(b)Currently, no study shows a benefit of using bicarbonate in DKA.
Bicarbonate administration can cause worsening hypokalemia, paradoxical
central nervous system (CNS) acidosis, impaired oxyhemoglobin dissociation,
hypertonicity, and sodium over load. (c)Metoprolol, a β-blocker, is not indi-
cated in DKA. The tachycardia in DKA is secondary to volume depletion and
acidosis. Correcting the underlying cause will treat the tachycardia. (e)Potas-
sium replacement may be necessary later in therapy because of an overall loss of
potassium, but should not be included in the initial fluid boluses. Rapid admin-
istration of potassium has potential to precipitate fatal dysrhythmias.
476.The answer is d.(Rosen, pp 1770-1774.)Thyroid stormis a medical
emergencythat will lead to death if not treated in time. The manifestations
of thyroid storm include temperature greater than 100°F, tachycardia out of
proportion to fever, widened pulse pressure, and dysfunction of the CNS
(eg, confusion,agitation), cardiovascular system (eg, high-output congestive
heart failure, atrial fibrillation), or gastrointestinal (GI) system (eg, diarrhea,
abdominal pain). Thyroid storm is a clinical diagnosissince no confirma-
tory tests are immediately available. The most important factor in reducing
mortality is blocking peripheral adrenergic hyperactivity with propranolol,
aβ-blocker. PTUis used to inhibit new hormone synthesis in the thyroid
and has a small effect on inhibiting peripheral conversion of T 4 to T 3 .Iodine
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