Basics
▸Acidosis is defined as pH < 7.35
▸Bicarbonate decreases in acidosis
▸Anion Gap = Na - [Cl + HCO3]
▸Ketones are anions - acetoacetate and beta-hydroxybutyrate
▸Acetone is produced as a byproduct --> sweet odor breath
▸Insulin deficiency is present in all types of ketoacidosis
Alcoholic Ketoacidosis
▸Occurs in chronic alcoholics or binge drinkers
▸Pathophysiology:
▸Decreased nutritional intake contributes to a low-insulin state which promotes ketogenesis.
▸Alcohol metabolism generates NADH which impairs conversion of lactate to pyruvate and impairs gluconeogenesis which then leads to ketogenesis
▸Volume depletion decreases kidney perfusion and excretion of ketoacids in the urine
Starvation ketosis
▸Fasting > 24 hours
▸Pathophysiology:
▸Once glycogen stores are depleted, the liver converts fatty acids to ketones
▸Typically starvation causes a lesser degree of ketosis than DKA and alcoholic ketoacidosis
Presentation
▸GI symptoms: abdominal pain, vomiting
▸Generally fluid down - tachycardia, hypotension, dry mucous membranes, poor skin turgor
▸Significant acidosis can cause altered mental status
▸Labs: Anion gap acidosis, elevated lactic acid, elevated beta-hydroxybutyrate, electrolyte abnormalities,
▸Hypo - or euglycemia typically
Management
▸Fluid resuscitation: isotonic fluids preferred
▸Glucose repletion: increases insulin production --> decreases ketogenesis
▸Repletion of electrolytes
▸K can decrease as more insulin is produced
▸Not recommended to give sodium bicarbonate, even in significant acidosis
▸Allow the patient to eat
References
▸LITFL - Ketoacidosis
▸CorePendium - Alcoholic Ketoacidosis, Acid-Base
▸“Ketone bodies: a review of physiology, pathophysiology and application of monitoring to diabetes” Laffel et al, 2000
Aneesa Ali, DO