π©Έ Hemolysis β What It Is, Why It Happens, and How to Spot It
Hemolysis is the premature destruction of red blood cells (RBCs). Free hemoglobin is released, which can circulate, bind haptoglobin, get filtered into urine, or be processed to indirect bilirubin β jaundice and pigment gallstones.
π Two main pathways
Intravascular hemolysis β RBCs rupture in the bloodstream
Clues: β haptoglobin, β LDH, hemoglobinuria/hemosiderinuria, schistocytes
Extravascular hemolysis β RBCs destroyed by macrophages (spleen/liver)
Clues: Spherocytes, splenomegaly, β indirect bilirubin, jaundice
π§ͺ High-yield lab patterns (table)
Feature | Intravascular | Extravascular |
---|---|---|
Haptoglobin | Low | Normal / slightly low |
LDH | High | High |
Bilirubin | ↑ Indirect (mild–mod) | ↑ Indirect (often higher) |
Urine findings | Hemoglobinuria, hemosiderinuria | Usually absent |
Peripheral smear | Schistocytes | Spherocytes, bite cells (G6PD) |
𧬠Common causes to recognize
Immune
Warm AIHA (IgG): SLE, CLL, methyldopa; + direct Coombs.
Cold agglutinin (IgM): Mycoplasma, EBV; acrocyanosis.
Hereditary membrane/enzyme
Hereditary spherocytosis (spectrin/ankyrin; β MCHC; splenomegaly).
G6PD deficiency (oxidative stress: sulfa drugs, fava beans, primaquine β Heinz bodies/bite cells).
Sickle cell disease (vaso-occlusion + hemolysis).
Mechanical/microangiopathic
TTP/HUS, DIC, malignant HTN, prosthetic valves β schistocytes.
Complement
Paroxysmal nocturnal hemoglobinuria (PNH): CD55/59 deficiency; dark morning urine, thrombosis.
Infectious/toxic
Malaria, clostridial sepsis, snake venom; severe burns.
π― MCAT focus points
Distinguish intravascular vs extravascular patterns from labs.
Direct vs indirect Coombs in immune hemolysis.
Associate buzzwords: bite cells/Heinz (G6PD), spherocytes (HS), schistocytes (MAHA), and low haptoglobin (intravascular).
π©Ί NCLEX nursing pearls
Transfusion reaction: fever, flank pain, hypotension, chest tightness β STOP transfusion, keep IV open with normal saline, notify provider/blood bank, send tubing + blood, collect urine/Coombs labs, monitor urine output and vital signs.
Manage complications: hyperkalemia, AKI, jaundice; patient teaching about dark cola-colored urine.
π§© Rapid practice (answers below)
Dark morning urine, pancytopenia, thrombosis. Likely dx?
Child with jaundice, splenomegaly, βMCHC, spherocytes. Best definitive treatment?
Febrile patient with schistocytes, thrombocytopenia, neuro signs. Diagnosis to prioritize?
Keys: 1) PNH. 2) Splenectomy (after vaccines). 3) TTP (ADAMTS13 deficiency)βstart plasma exchange urgently.
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