Endocrine Emergencies Answers 529(Kussmaul respirations)reflects respiratory compensation for metabolic
acidosis.Fruity breath odorin this patient is the result of acetoacetate acid
conversion to acetone, which is eliminated during respiration.
Administering antiemetics and analgesics (b and c)will temporarily
treat the symptoms without addressing the underlying problem. A basic
metabolic panel (d)is necessary to check for electrolyte abnormalities.
Abdominal radiographs (e)might be appropriate if you suspect abdominal
pathology. In this case, GI distress is a symptom of a metabolic disturbance.
481.The answer is c.(Tintinalli, p 1291.)Potassiumis the most impor-
tant electrolyte to follow in DKA therapy. Renal losses and vomiting in DKA
cause profound total body potassium deficit.The measured potassium
levels, however, are often falsely normal or elevatedbecause of acidosis
and total body fluid deficit. Acidemia causes extracellular shift of potassium
in exchange for hydrogen ions. With initiation of DKA therapy, potassium
levels will quickly fall to true levels causing significant hypokalemia,if not
closely monitored and replaced.
Although sodium and calcium levels (a, b, d, and e)should be moni-
tored, they are not affected as much as potassium. Hyperglycemia-related
osmotic diuresis leads to renal losses of sodium chloride in urine. The mea-
sured sodium level is artificially lowered further by the hyperglycemia. For
every 100 mg of glucose over 100 mg/dL, 1.6 mEq should be added to the
measured serum sodium level. In treating DKA, normal saline infusion
replaces lost sodium. Hypertonic saline should not be used for sodium
replacement in DKA. Osmotic diuresis also causes renal losses of calcium,
magnesium, and phosphorus. Initially their levels might be elevated owing
to hemoconcentration. These electrolytes should be monitored and restored
appropriately during treatment.
482.The answer is e.(Tintinalli, p 1312.)This patient presents in a
hyper-adrenergic state, altered mental status, and a large goiter,plac-
ing the diagnosis of thyroid stormon top of the differential. The patient is
likely to have undiagnosed hyperthyroidism. This is a clinical diagnosis
and has to be treated empirically and rapidly since mortality is high despite
treatment. The management of thyroid storm involves supportive care (air-
way protection, oxygenation, IV hydration) and specific therapy to treat
adrenergic symptoms and to decrease synthesis and release of thyroid hor-
mone.β-Adrenergic blockersare given to reverse adrenergic hyperactivity.
PTUblocks de novo synthesis of thyroid hormone. Iodineblocks release