the patient can accurately locate the position of the impacted foreign
body.
(a, b, and c)These are all areas of food impaction. The cricopharyn-
geus is the most common site of impaction in children less than 4 years old.
The pyloric sphincter (e)is not considered part of the esophagus; rather it
helps regulate food passage from the stomach to the duodenum. This can be
an area of obstruction as well, as in the case of pyloric stenosis, but is likely
to present with characteristic “projectile” vomiting in childhood.
77.The answer is d.(O’Brien, 2007.)The patient’s presentation is consis-
tent with alcoholic ketoacidosis (AKA).This is an acute metabolic acidosis
that typically occurs in people who (1) chronically abuse alcohol and have
arecent history of binge drinking,(2) have had little or no recent food
intake,and (3) have had persistent vomiting. AKA is characterized by elevated
serum ketone levels and a high anion gap (↑AG = Na −[HCO3 + Cl] > 12).
A concomitant metabolic alkalosis is common, secondary to vomiting and
volume depletion. AKA is the result of (1) starvation with glycogen deple-
tion and counterregulatory hormone production; (2) a raised NADH/NAD+
ratio (related to the metabolism of ethanol); and (3) volume depletion,
resulting in ketogenesis. The typical symptoms and physical findings relate
to volume depletion and chronic alcohol abuse and include nausea, vomit-
ing, abdominal pain, and/or hematemesis. The fruity odor of ketones may
be present on the patient’s breath. The patient’s mental status may be
impaired. Also associated with the presentation are dyspnea, tremulousness,
and dizziness. Rarely do patients present with muscle pain, fever, diarrhea,
syncope, seizure, or melena. In AKA, the β-hydroxybutyrate (β-OH)/
acetyl acetate (AcAc) formation ratio is 5:1. The nitroprusside reaction (Acetest)
may be negative or only weakly positive for serum ketones because nitroprus-
side reacts with AcAc, but not with β-OH. Therefore, ketosis may be more
severe than would be inferred from a nitroprusside reaction alone.
Once the diagnosis of alcoholic ketoacidosis is established, the mainstay
of treatment is (b) hydration with 5% dextrose in normal saline (D 5 NS
or^1 / 2 NS).With initial therapy, ketone formation shifts toward the produc-
tion of AcAc so that measured ketone levels rise, although β-OH levels
decrease. Carbohydrate and fluid replacement reverse the pathophysiologic
derangements that lead to AKA by increasing serum insulin levels and sup-
pressing the release of glucagon and other counterregulatory hormones.
Dextrose stimulates the oxidation of NADH and aids in normalizing the
NADH/NAD+ ratio.
106 Emergency Medicine