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G6PD Deficiency

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In one line

·G6PD deficiency means red blood cells cannot protect themselves from oxidative stress, so they suddenly burst when exposed to certain triggers like fava beans, infections, or specific medications.

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Normal physiology

·Red blood cells live about 120 days and constantly face oxidative stress (damage from unstable oxygen molecules). G6PD (glucose-6-phosphate dehydrogenase) is an enzyme inside red blood cells that powers a protective pathway. This enzyme helps make NADPH (a molecule that carries energy), which keeps glutathione (a powerful antioxidant) in its active form. Active glutathione neutralizes hydrogen peroxide and other oxidants, preventing damage to the cell membrane and hemoglobin.

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What goes wrong

·People with G6PD deficiency inherit a gene that makes a weak or low-functioning version of the G6PD enzyme. When the red blood cell faces extra oxidative stress from infections, certain drugs, or foods like fava beans, the small amount of G6PD cannot keep up with demand. Without enough protective glutathione, hydrogen peroxide and other oxidants damage hemoglobin and the cell membrane, causing the red blood cells to burst open suddenly.

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Hallmark signs

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Red flags · escalate now

·Dark tea-colored urine with decreased urine output suggests acute kidney injury from hemoglobin precipitation requiring immediate IV hydration
·Chest pain, severe shortness of breath, confusion, or altered mental status indicates life-threatening anemia needing urgent transfusion
·Hemoglobin below 7 g/dL with ongoing red blood cell destruction (hemolysis) requires hospital admission and transfusion consideration
·Recent exposure to triggering medications (sulfa drugs, antimalarials, aspirin, nitrofurantoin) or fava beans with symptoms starting within 24-72 hours

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Workup

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Treatment

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NCLEX trap

·Aspirin is an oxidizing drug that triggers red blood cell destruction (hemolysis) in G6PD deficiency. Use acetaminophen instead for fever or pain control.
·Increase IV fluids during destroying red blood cells (hemolytic) crisis to maintain high urine output. This protects the kidneys from free hemoglobin damage and prevents acute kidney injury.
·G6PD enzyme levels can be falsely normal during acute red blood cell destruction (hemolysis) because young red blood cells (reticulocytes) have higher enzyme levels. Test 2 to 3 months after the crisis resolves for accurate results.
·Females can have G6PD deficiency if they inherit the gene on both X chromosomes (homozygous) or have unfavorable X-inactivation (lyonization) as carriers. Always consider it in symptomatic females.
·Stop the oxidizing medication immediately and switch to a non-oxidizing alternative. Continuing any dose of the trigger will cause ongoing red blood cell destruction.
·Red blood cell destruction (Hemolysis) usually stops within days after removing the trigger. Hemoglobin stabilizes and then rises as the bone marrow produces new red blood cells. Ongoing drops suggest continued oxidative stress or another problem.

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