gap acidosis

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