Hemolytic Anemia Explained by Dr. Kishore Mangal

Estimated reading time: 3 minutes

Hemolytic anemia happens when red blood cells are destroyed faster than the body can replace them. It is often seen in ICU patients, but it can occur in many other situations. Knowing what causes it, how it presents, and how to manage it is important, both in exams and in clinical practice.

Causes You Should Know

Hemolytic anaemia can arise due to several factors:

• Autoimmune conditions: Warm or cold autoimmune hemolytic anaemia.
  
• Medications: Drugs like 5-FU, methyl dopa, quinine, dicloquinac, penicillins (especially piperacillin), and cephalosporins.
  
• Infections: Malaria, viral hepatitis, Epstein-Barr virus, or septic shock.
  
• Transfusion reactions: Sometimes anemia appears after a blood transfusion.
  
• Medical devices: Patients on ECMO, Impella, or other extracorporeal devices can develop hemolysis.
  
• Underlying conditions: SLE, L-syndrome, G6PD deficiency.
  
• Toxins and bone marrow suppression: Certain chemicals or marrow problems can trigger it.

Exam tip: A patient’s history often gives the clue. Look for recent blood transfusions, new drugs, fever, or travel history.

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Clinical Signs to Watch

Physical examination and history are very helpful:

• Jaundice: Most patients show unconjugated hyperbilirubinemia.
  
• Urine color: Dark urine suggests conjugated bilirubin. Pale urine usually indicates unconjugated bilirubin.
  
• Extravascular hemolysis signs: You may notice splenomegaly.
  
• Vascular complications: Seen in conditions like sickle cell anemia.

History points to consider:

• G6PD deficiency: Triggers include surgery, infection, or certain oxidant drugs.
  
• Weight loss or night sweats: Could indicate hematological malignancy.
  
• Joint pain: May suggest autoimmune disease such as SLE.

Lab Clues

Certain lab tests can help confirm hemolysis:

• Peripheral blood smear:
  
  • Schistocytes indicate microangiopathic hemolytic anemia (like TTP, HUS, or DIC).
    
  • Microspherocytes are typical of autoimmune hemolytic anemia.
    
  • Sickled cells appear in sickle cell disease.
    
  • Bite cells suggest G6PD deficiency.
    
  • Target cells and basophilic stippling indicate thalassemia or alcohol abuse.
    
  • Ringed sideroblasts can be seen in congenital disorders or myelodysplastic syndromes.
    
• Other lab markers:
  
  • Reticulocyte count is usually high—showing active marrow response.
    
  • LDH is often elevated.
    
  • Haptoglobin is low in hemolysis.
    
  • Direct Coombs test helps differentiate warm vs. cold hemolytic anemia.

Warm vs. Cold Hemolysis

• Warm hemolysis: IgG antibodies attack RBCs at body temperature. Causes include idiopathic autoimmune anemia, infections, certain drugs, lymphoproliferative disorders, and SLE.
  
• Cold hemolysis: IgM antibodies act at cooler temperatures. Often post-infectious, like EBV or influenza, or paroxysmal cold hemoglobinuria.

Management

Treatment depends on type and severity:

• Acute hemolysis: Plasmapheresis may be necessary in emergencies.
  
• Warm hemolysis: Steroids are first-line. Refractory cases may need splenectomy or immunosuppressants. Rituximab is also useful. IVIG has a limited but occasional benefit.
  
• Cold hemolysis: Avoid cold exposure. Severe cases may require plasmapheresis. Rituximab can help if the problem persists.

Intravascular vs. Extravascular Hemolysis

• Intravascular: RBCs are destroyed in circulation. Labs show free hemoglobin in plasma or urine, very low haptoglobin, high LDH, and abnormal RBC shapes.
  
• Extravascular: RBCs are destroyed in the liver and spleen. Less free hemoglobin is released, LDH is mildly elevated, and blood smears may show fewer abnormalities.

Takeaway

Hemolytic anemia has many faces, from autoimmune causes to infections, drugs, and genetic conditions. Careful history, thorough examination, and targeted lab tests are key. Knowing the differences between warm and cold hemolysis, as well as intravascular vs. extravascular destruction, guides treatment and improves patient outcomes.