Ketoacidosis Flashcards

1
Q

What is the primary cause of Alcoholic Ketoacidosis (AKA)?

A

AKA occurs due to chronic alcohol use and starvation, leading to depleted glycogen stores and increased ketone production.

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2
Q

What are the characteristic lab findings in Alcoholic Ketoacidosis?

A
  • Increased anion gap metabolic acidosis (due to ketoacid accumulation)
  • Increased osmolal gap
  • Ketosis with low to normal glucose levels (~<250 mg/dL)
  • No significant hyperglycemia, differentiating it from diabetic ketoacidosis (DKA)
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3
Q

How is Alcoholic Ketoacidosis managed?

A
  • IV fluids with dextrose (D5 normal saline or D5 half-normal saline)
  • Thiamine before glucose to prevent Wernicke encephalopathy
  • Electrolyte repletion (K+, Mg2+, PO4)
  • No need for insulin (unlike DKA)
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4
Q

How does Diabetic Ketoacidosis (DKA) differ from Alcoholic Ketoacidosis?

A
  • DKA has profound hyperglycemia (>250-300 mg/dL), while AKA has normal to slightly elevated glucose.
  • DKA is due to insulin deficiency, while AKA results from alcohol-induced glycogen depletion and starvation ketosis.
  • DKA requires insulin therapy; AKA does not.
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5
Q

How does starvation ketosis present?

A
  • Prolonged fasting (>2-3 days) leads to mild ketosis and normal glucose levels.
  • Ketosis is mild to moderate, and bicarbonate is usually >18 mEq/L.
  • No significant acidemia.
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6
Q

What are the characteristic lab findings of Diabetic Ketoacidosis (DKA)?

A
  • Glucose >250 mg/dL
  • Ketosis (β-hydroxybutyrate)
  • Anion gap metabolic acidosis (low bicarbonate)
  • High serum osmolality
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7
Q

What is the difference between Hyperosmolar Hyperglycemic State (HHS) and DKA?

A
  • HHS has severe hyperglycemia (>600 mg/dL) but no significant ketoacidosis.
  • More common in Type 2 Diabetes, with profound dehydration and altered mental status.
  • Treated with aggressive IV fluids and insulin.
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8
Q

What is Euglycemic Ketoacidosis, and what causes it?

A
  • Ketoacidosis with normal glucose levels
  • Causes:
    1) SGLT-2 inhibitors (e.g., canagliflozin, empagliflozin)
    2) Prolonged fasting with diabetes
    3) Pregnancy-related metabolic shifts
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9
Q

How does lactic acidosis differ from ketoacidosis?

A
  • Lactic acidosis is due to anaerobic metabolism and tissue hypoxia (shock, sepsis, metformin toxicity).
  • No significant ketone production.
  • High anion gap metabolic acidosis.
  • Elevated lactate (>4 mmol/L).
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10
Q

What is the preferred treatment for Diabetic Ketoacidosis (DKA)?

A
  • IV fluids (normal saline initially, then D5 once glucose <250 mg/dL)
  • IV insulin drip
  • Electrolyte repletion (potassium)
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11
Q

What is the key management step to avoid Wernicke encephalopathy in Alcoholic Ketoacidosis?

A

Always administer thiamine BEFORE giving glucose to prevent acute Wernicke encephalopathy.

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12
Q

Which conditions present with an increased anion gap metabolic acidosis?

A

1) Alcoholic Ketoacidosis (AKA)
2) Diabetic Ketoacidosis (DKA)
3) Lactic acidosis (shock, metformin toxicity, hypoxia)
4) Salicylate toxicity (early respiratory alkalosis, later metabolic acidosis)
5) Methanol/Ethylene glycol poisoning (toxicity, increased osmolal gap)

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13
Q

A 21-year-old woman presents to the emergency department because of two days of abdominal pain, nausea, malaise, and increased thirst. Symptoms were initially intermittent at onset but are now constant. The patient has no significant past medical history and does not currently take any medications. Temperature is 37.6 °C (99.7 °F), pulse is 120/min, respiratory rate is 20/min, and blood pressure is 110/66 mm Hg. On physical examination, the patient appears uncomfortable. Mucous membranes are dry, and there is decreased skin turgor. There is mild, diffuse abdominal tenderness to palpation without rebound or guarding. Laboratory results are shown below. The patient is given one liter of 0.9% saline. Which of the following is the most appropriate next step in management?
A) Oral sodium bicarbonate
B) Oral sodium polystyrene sulfonate
C) 0.45% saline infusion
D) Insulin infusion
E) Subcutaneous insulin

A

Patients with acute metabolic acidosis require an ABCDE assessment and usually IV fluid resuscitation. Diabetic ketoacidosis can be life- threatening, and patients require an insulin infusion to stop the ketosis, which is driving the acidosis, in addition to appropriate fluid resuscitation. This patient with abdominal pain, nausea, and polydipsia presents with an elevated anion gap metabolic acidosis with severe hyperglycemia and ketosis. Together, these findings indicate diabetic ketoacidosis, and the most appropriate treatment is an insulin infusion and IV fluid hydration (0.9% saline in this case). Metabolic acidosis refers to an increase in hydrogen ions and a decrease in bicarbonate concentration in the blood due to a metabolic cause. Metabolic acidosis can be classified as non- (or normal) anion gap or elevated (or high) anion gap. The anion gap is calculated by subtracting the concentrations of serum chloride and bicarbonate from serum sodium (AG = Na - CI - HCО3). Patients presenting acutely with metabolic acidosis can be extremely ill. They are often tachypneic as the body tries to compensate by inducing a relative respiratory alkalosis. An ABCDE assessment is crucial at the time of presentation. Intravenous fluid resuscitation is indicated for most patients presenting with acute metabolic acidosis. Once stabilized, the underlying issues causing metabolic acidosis should be addressed to prevent decompensation. Severe, untreated metabolic acidosis can lead to cardiac arrest. Life-threatening causes of metabolic acidosis include toxic ingestion (e.g., ethylene glycol, methanol, isoniazid, salicylates), septic shock with resultant lactic acidosis, severe acute kidney injury, and diabetic ketoacidosis (DKA). Patients with DKA are typically volume-depleted, requiring aggressive
IV fluid resuscitation. Insulin infusion is crucial for stopping the production of ketones and the resultant acidosis. Once the patient’s anion gap is closed, they can be transitioned to subcutaneous insulin for continued management of hyperglycemia.

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