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The acute complications of diabetes mellitus
include diabetic ketoacidosis and hyperglycemic
hyperosmolar syndrome. Acute complications of
uncontrolled hyperglycemia with life-threatening
consequences can occur if not recognized and treated early.
Let's go to this case. A 10-year-old boy
is brought to the emergency department by his mother
due to frequent vomiting, abdominal pain, and
weakness. Over the last 5 days, he felt excessively
thirsty and has been urinating frequently.
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Family history is non-contributory.
His temperature is 37.1°C, his blood pressure is 80/55, and
his pulse rate 110 beats/minute. On physical exam,
he is non-responsive to verbal commands.
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He has sunken eyes, poor skin turgor,
and rapid deep respirations. His lab findings reveal a random
plasma glucose of 460 mg/dL. He has an undetectable
fasting C-peptide, his serum beta-hydroxybutyrate
is elevated, and his GAD antibodies are positive.
What is the most likely diagnosis? This is a
young boy with vomiting, abdominal pain, and
weakness that is progressive. He also manifested
with polydipsia and polyuria. Signs of
dehydration and tachypnea, that is shallow and rapid
respiration, are also present which makes us
suspect a respiratory alkalosis. He also has profound
hyperglycemia. The presence of undetectable
fasting C-peptide is an indication that he has no
endogenous insulin production. Also, the fact
that his serum ketones are elevated confirms the
presence of diabetic ketoacidosis. And finally,
the positive GAD antibodies imply that the etiology
of his type 1 diabetes is an immune-mediated process.
And confirming the diagnosis, this young
boy has presented in acute diabetic ketoacidosis.
DKA typically occurs in the setting of hyperglycemia
with relative or absolute insulin deficiency
and an increase in counter-regulatory hormones.
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Sufficient amount of insulin are not present
to suppress lipolysis and oxidation of free fatty
acids. This in turn leads to ketone body production
by the body and a subsequent metabolic acidosis.
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DKA occurs more frequently with type 1 diabetes,
although 10-30% of it can occur in patients
with type 2 diabetes. It may be the initial clinical
presentation in some patients with previously
undiagnosed type 1 or type 2 diabetes.
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This next case highlights an increasingly recognized form of diabetic ketoacidosis - euglycemic DKA.
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While our patient illustrates
the SGLT2 inhibitor variant,
it's crucial to understand that euglycemic DKA
can occur in several important clinical scenarios.
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Our patient, a 45-year-old woman, presented with nausea, vomiting, and poor oral intake
while continuing her empagliflozin.
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Her labs revealed the diagnostic challenge:
a near-normal glucose of 145 mg/dL despite significant
ketoacidosis,
with a pH of 7.21, anion gap of 22, and elevated beta-hydroxybutyrate of 5.8 mmol/L.
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But here's the broader perspective:
euglycemic DKA isn't limited to SGLT2 inhibitor use.
03:47
We see it in several other
important clinical scenarios:
pregnant women,
where metabolic demands are altered;
patients who've received insulin
just before presenting to the ED;
and in any patient with prolonged poor oral intake.
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The common thread is the
presence of ketoacidosis
without the classic severe hyperglycemia
we typically expect in DKA.
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The key teaching point is that we can't exclude DKA
based on glucose levels alone.
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Whether it's a pregnant patient
with nausea,
someone who took their insulin but couldn't eat,
or a patient on an SGLT2 inhibitor,
we need to maintain a high index of suspicion
when the clinical picture suggests ketoacidosis,
even if the glucose isn't markedly elevated.
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Management principles remain the same
across all these scenarios –
these patients need both insulin
to reverse the ketoacidosis
and glucose supplementation to prevent
hypoglycemia during treatment.
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The recognition of euglycemic DKA
in any of these settings can be lifesaving.
The lecture Diabetic Ketoacidosis with Cases by Michael Lazarus, MD is from the course Diabetes Mellitus. It contains the following chapters:
What is the significance of an undetectable c-peptide level in a patient?
By what mechanism are ketone bodies produced?
What is the most likely diagnosis in the case described below? A 10-year-old boy is brought to the emergency department by his mother because of frequent vomiting, abdominal pain, and weakness. Over the last 5 days, he felt excessively thirsty and has been urinating frequently. Family history is noncontributory. Physical examination results: Temperature is 37.1°C (98.7°F), blood pressure is 100/70 mm Hg, pulse is 110 beats/min. He is nonresponsive to verbal commands and has sunken eyes; poor skin turgor; and rapid, deep respirations. Laboratory test results: Random plasma glucose level of 460 mg/dL, undetectable fasting C-peptide, elevated serum beta-hydroxybutyrate level, and positive results for antiglutamic acid decarboxylase (GAD) antibodies
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