[1][2][3] Early acute hemolytic transfusion reactions are typically characterized by fever, which may be accompanied by rigors (chills).
More severe cases may be characterized by shortness of breath, low blood pressure, hemoglobinuria, and may progress to shock and disseminated intravascular coagulation.
[4] The most common cause of acute hemolytic transfusion reaction is ABO incompatibility, which is typically due to human error that results in a recipient receiving the incorrect blood product.
Isohemagglutinins also activate the complement cascade via C3a and C5a, which then promote inflammatory cytokine release from white blood cells.
[6] These inflammatory cytokines include IL-1, IL-6, IL-8, and TNF-alpha, which cause increased capillary permeability and vasodilation leading to symptoms of low blood pressure, fever, chest pain, nausea, vomiting, and wheezing.
[4][6] The diagnosis of AHTR is made with microscopic examination of the recipient's blood and a direct antiglobulin test (direct Coombs test) which detects IgG antibodies or complement bound to red blood cells and is usually diagnostic of acute hemolytic transfusion reactions.
[6] Furosemide is the diuretic of choice in treatment of AHTR with decreased urine output, because it increases the amount of blood that reaches the renal cortex.