This is acute hemolytic transfusion reaction, a type II hypersensitivity where pre-formed IgM antibodies bind to incompatible ABO antigens on donor RBCs, which causes intravascular hemolysis. Rh incompatibility, like colonelred_ said, comes more into play with Rh-compatibility of pregnancy and it is due to IgG antibodies, which more often cause extravascular hemolysis since splenic macrophages have those Fc-gamma-R receptors to bind whatever IgG has caught. Extravascular doesn't cause that hypotension, fever, flank pain associated with hemoglobinuria since the macrophages hold on to the degraded RBCs and convert it to biliverdin, which can safely be excreted by the liver.

To conclude: 1) ABO: IgM -> Complement -> Intravascular 2) Rh: IgG -> Splenic Macrophage -> Extravascular

FA 2017 states that extravascular hemolysis has jaundice where ABO incompatibility would not.

Acute hemolytic transfusion reaction

Type II hypersensitivity reaction

Typically causes intravascular hemolysis (ABO blood group incompatibility)

During transfusion or within 24 hr (due to preformed antibodies)

Fever, hypotension, tachypnea, tachycardia, flank pain, hemoglobinuria (intravascular), jaundice (extravascular)

Donor RBC with A and/ or B group antigens react with Host anti-A, anti-B IgG, IgM.

Blood transfusion reactions:

• type I / Allergic Anaphylactic R- fever, urticaria, pruritus, wheeze, hypotension (2-3min) [Ig A defc]

• type 2/ Ac. Hemolytic R- fever, hypotension,tachycardia, tachypnea, flank pain, Hburia, jaundice. (Within 1 hr)

• Febrile non hemolytic R- Fever,chills, headache, but no Hburia or jaundice (1-6hr)

• TRALI- Resp.distress, noncardio plum edema. (6hr)