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Autoimmune Hemolytic Anemia

This document summarizes several types of autoimmune hemolytic anemia, including warm and cold types. It discusses characteristics, common causes, treatments using steroids or other immunotherapies. It also briefly covers other conditions like drug-induced hemolytic anemia, paroxysmal cold hemoglobinuria, extravascular vs intravascular hemolysis, and G6PD deficiency. Additional sections summarize brain abscesses in children, idiopathic intracranial hypertension, and make comparisons between MIS-C and Kawasaki disease.

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Samuel Wibowo
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70 views

Autoimmune Hemolytic Anemia

This document summarizes several types of autoimmune hemolytic anemia, including warm and cold types. It discusses characteristics, common causes, treatments using steroids or other immunotherapies. It also briefly covers other conditions like drug-induced hemolytic anemia, paroxysmal cold hemoglobinuria, extravascular vs intravascular hemolysis, and G6PD deficiency. Additional sections summarize brain abscesses in children, idiopathic intracranial hypertension, and make comparisons between MIS-C and Kawasaki disease.

Uploaded by

Samuel Wibowo
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
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1.

Autoimmune Hemolytic Anemia


Various other immune hemolytic anemia are autoimmune

Warm type (IgG class)


( primary idiopathic, or secondary to lymphoproliferative disorders, CTD, Non lymphoid
neoplasm, CID, immunodeficiency disorder)

Cold type (IgM class)


Primary cold agglutinin disease, secondary ( lymphoproliferative disorder, Mycoplasma, EBG,
Paroxysmal cold hemoglobinuria or primary idiopathic viral syndrome or congenital or tertiary
syphilis

Drug induced
Hapten/drug absportion ( penicillin, quinine, quinidine, methyldopa). Cephalosphorin are the
most common cause of drug induced immune hemolytic anemia.

Warm AIHA
May occur in 2 general clinical patterns, acute transient lasting 3-6 months and occurring in
children age 2-12 for 70-80 % . Spleen is usually enlarged, consistence response to
glucocorticoid, low mortality rate, full recovery are characteristics of acute form . Chronic form
is common in children > 12 years old. Hemolysis continue for months or years.

In many cases, Hb < 6, spherocytosis, polychromasia, nucleated RBC are present. In some cases,
low reticulocyte are found in early episode, leukocytosis is common. Concomitant immune
thrombocytopenic purpura are found in Evans syndrome. ( secondary to chronic disease SLE,
immunodeficiency syndrome)

Predisone 2mkd is started, in some severe cases, doses up to 6mkd may be required.Coombs
test may be positive even after Hb return to normal. Discontinue prednisone once Coombs test
is negative. If despite glucocorticoid therapy there is severe anemia, IVig or rituximab may be
started.

Cold AIHA
Required complement for hemolytic activity. Noted rouleaux formation. Less common in
children, acute self limited episode. Steroids less effective, avoid exposure to cold.

PCH
D-L hemolysin

Extravascular vs intravascular hemolysis


Urine Hb hemosiderin is present in urine, dec haptoglobin

Intravascular hemolysis is due to HUS or TTP or Kasabach Merrit syndrome . Acquired TTP
( ADAM TS 13) HUS( E coli, pneumococcal) or DIC.
G6PD in crisis
Heinz bodies are seen within 3-4 days of illness because of rapid clearance from blood,
polychromacia ( incrased reticulocyte) , Haptoglobin saturated. Enzyme activity < 10 % of
normal .

Brain Abscess
Etiology: meningitis, otitis media, mastoiditis, sinusitis, orbital cellulitis, dental infection) ,
penetrating head injuries, immunodeficiency

Occur in both hemisphere in children. 80 % in frontal parietal, and tempora lobes. 18 %, multiple
brain abscess are present. Frontal ( sinusitis, orbital ) , temporal ( otitis media, mastoiditis).
Early signs are low grade fever, headache, lethargy./ Focal neurologc signs develop. Cerebellar
( nystagmus, ataxia, dysmetria). If abscess ruptures, shock and death occur in 27- 85 % of cases.
Antibiotics: cephalosporin and metronidazole, with vancomycin, typically 6 weeks. Abscess < 2.5
cm or multiple can be treated with antibiotics alone without drainage.

Idiopathic Intracranial Hypertension


Diagnosed by opening pressure by age ,not have identifiable cause. A large proportion of
children will have secondary IH ,
IH with no obstructive lesion ( venous obstruction ,metabolic disorders, prolong steroids,
hypervitaminosis A, malnourished, severe vitamin A, refereeding syndrome, Addison, obesity,
menarche, contraceptive, infection n drugs ( nalidixic acid, doxy, mino, tetra, nitro, isotretinoin,
obstruction by CVT)

Rare under 10 yr, female sec , likely obese. Transient visual obscuration, diplopia, papiedema is
most consistent sign, but may be confused with optic neuritis and optic nerve head drusen. MR
venography to exclude venous thromvosis . Renal , liver ,thyroid, aotumimmune, hematologic,
inflammatory . Acetazolamide 10-30 mkd is effective , or some recommend topiramate or
furosemide. OCT is necesseray to followup papilledema.

MISC vs Kawasaki
MISC ( fever with abd pain or/ rash) dd( toxic shock syndrome, sepsis, abd abscess)
Develop 2-6 weeks after SARS CoV- 2 (
MISC lab workups

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