gap acidosis
TRANSCRIPT
Interesting Case Conference
THE CASE
• 70 y/o CF admitted to the ICU for ataxia and change of mental status. Was found to be in high anion gap metabolic acidosis with AG 25 and HCO3 10 and a Ph of 7.25.
• Workup was negative for any cause of HAGMA.• Pt was given NaHCO3 and experienced rapid
resolution of her symptoms with spontaneous closure of the AG in 24h.
• Relevant PMH include gastric bypass surgery
THE CASE
• Exam was unremarkable
THE ANION GAP
THE ANION GAP
• Low anion gap– relatively rare– the most common causes of a low anion gap is
a low albumin level • which constitutes ~80% of the unmeasured anions
– increase in the number of cations • organic paraproteins • inorganic bromide, lithium, Iodine or polymyxin B
can lead to low anion gap values.
KETOACIDOSIS
KETOACIDOSIS
KETOACIDOSIS
KETOACIDOSIS
KETOACIDOSIS
LACTIC ACIDOSIS
LACTIC ACIDOSIS
Increased lactate production
• A. Increased pyruvate production– 1. Enzymatic defects in glycogenolysis or
gluconeogenesis (as with type 1 glycogen storage disease)
– 2. Respiratory alkalosis, including salicylate intoxication
– 3. Pheochromocytoma
Increased lactate production
• B. Impaired pyruvate utilization– 1. Decreased activity of pyruvate
dehydrogenase or pyruvate carboxylase • a. Congenital
• b. Possibly a role in diabetes mellitus, Reye's syndrome
Increased lactate production
• C. Altered redox state favoring pyruvate conversion to lactate– 1. Enhanced metabolic rate
• a. Grand mal seizure• b. Severe exercise• c. Hypothermic shivering• d. Severe asthma
– 2. Decreased oxygen delivery• a. Shock• b. Cardiac arrest• c. Acute pulmonary edema• d. Carbon monoxide poisoning• e. Severe hypoxemia (PO2 <25 to 30 mmHg)• f. Pheochromocytoma
Increased lactate production
• C. Altered redox state favoring pyruvate conversion to lactate – 3. Reduced oxygen utilization
• a. Cyanide intoxication
• b. Drug-induced mitochondrial dysfunction due to zidovudine or stavudine
• D. D-Lactic acidosis
Primary decrease in lactate utilization
• A. Hypoperfusion and marked acidemia
• B. Alcoholism
• C. Liver disease
Mechanism uncertain
• A. Malignancy
• B. Diabetes mellitus, including metformin in the absence of tissue hypoxia
• C. Acquired immune deficiency syndrome
• D. Hypoglycemia
• E. Idiopathic
UREMIA
TOXINS
TOXINS
Toxins
Isopropanol is primarily metabolized via alcohol dehydrogenase to acetone
TOXINS
TOXINS
Clinical course in acute ethylene glycol intoxication
30 minutes to 12 hours Central nervous system
Inebriationeuphoria ataxiaslurred speechdrowsinessirritation restlessness
disorientation Gastrointestinal
Nausea and vomiting Metabolic
Elevated osmolal gap
Clinical course in acute ethylene glycol intoxication
12 to 24 hours Cardiovascular
Mild hypertension, tachycardia, and shock Pulmonary
Tachypneaadult respiratory distress syndromepulmonary edemapneumonitis
Metabolic Metabolic acidosis with elevated anion gap decreased osmolal gappossible tetany from hypocalcemia, and hyperventilation
• 24 to 72 hours – Renal
• Flank pain
• costovertebral angle tenderness
• oliguric renal failure, hyperkalemia, and hypocalcemia
– Metabolic • May have normal anion and osmolal gaps
TOXINS
TOXINS
TOXINS
TOXINS
Conclusion
• D Lactic Acid is under diagnosed.
• Usually reversible
• Avoid large Carbohydrate Loads