Compare conditions

Put any two — or three — conditions side by side, adult or pediatric, to spot the look-alike differences fast, row by row.

Microangiopathic Hemolytic Anemia (MAHA)

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In one line

·MAHA is red blood cell destruction (hemolysis) caused by red blood cells being physically sheared apart as they squeeze through abnormal clots or damaged tiny blood vessels.

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Normal physiology

·Red blood cells (erythrocytes) are flexible disk-shaped cells that carry oxygen from the lungs to all body tissues. They flow smoothly through arteries, capillaries (the tiniest blood vessels), and veins without breaking. The inner lining of blood vessels (endothelium) is smooth and releases chemicals that prevent clots from forming. Red blood cells live about 120 days before being removed by the spleen.

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What goes wrong

·In MAHA, something damages the lining of small blood vessels or causes fibrin strands (tiny protein threads) to form clots inside them. When red blood cells try to squeeze through, the sharp edges slice them into pieces called schistocytes (fragmented red cells). The cells break open, spilling hemoglobin into the blood and causing anemia and organ damage.

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Hallmark signs

·Dark or tea-colored urine
·Pale skin and mucous membranes
·Fatigue and weakness
·Shortness of breath with mild activity
·Yellowing of skin or eyes (jaundice)
·Pinpoint bleeding spots (Petechiae) or purple bleeding blotches (purpura) (small red or purple spots on skin)
·Confusion or altered mental status
·Decreased urine output

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Red flags · escalate now

·Platelet count below 30,000/microL with confusion or neurologic changes suggests TTP requiring immediate plasma exchange
·Hemoglobin below 7 g/dL with chest pain or severe shortness of breath needs urgent transfusion
·Creatinine rising despite fluids with decreased urine output indicates acute kidney injury needing nephrology consultation
·New pinpoint bleeding spots (petechiae) or purple bleeding blotches (purpura) with any mucosal bleeding requires platelet count check and hematology evaluation within hours

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Workup

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Treatment

·Plasma exchange (plasmapheresis)
·Packed red blood cell transfusion
·Supportive care with IV fluids and electrolyte monitoring
·Delivery of fetus and placenta in pregnancy-related MAHA
·Blood pressure control to target <140/90 in malignant high blood pressure (hypertension)
·Avoidance of platelet transfusion in TTP unless life-threatening bleeding

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NCLEX trap

·In TTP, platelet transfusions can worsen microthrombi and are contraindicated unless life-threatening bleeding occurs. Focus on treating the underlying cause with plasmapheresis first.
·DIC shows prolonged PT/INR and low fibrinogen from consumption of clotting factors, while MAHA typically has normal coagulation studies. DIC can cause MAHA, but MAHA does not always mean DIC.
·Schistocytes confirm MAHA but treatment depends on the cause. TTP needs plasmapheresis, HUS needs supportive care, and malignant high blood pressure (hypertension) needs blood pressure control—not surgery.
·The anemia in MAHA is from red cell destruction (hemolysis), not iron deficiency. Iron levels are usually normal or high from released hemoglobin. Treating the underlying cause stops red blood cell destruction (hemolysis).
·Dark brown or cola-colored urine in MAHA comes from hemoglobinuria (free hemoglobin in urine from red cell destruction). Urinalysis shows blood on dipstick but few intact red cells under microscope.
·MAHA is diagnosed by peripheral smear showing schistocytes plus evidence of red blood cell destruction (hemolysis) (elevated LDH, low haptoglobin, elevated indirect bilirubin). Bone marrow biopsy is not needed and delays treatment.

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