Warm antibody autoimmune hemolytic anemia (WAIHA) is the most common form of autoimmune haemolytic anemia. About half of the cases are of unknown cause, with the other half attributable to a predisposing condition or medications being taken. Contrary to cold autoimmune hemolytic anemia (e.g., cold agglutinin disease and paroxysmal cold hemoglobinuria) which happens in cold temperature (28–31 °C), WAIHA happens at body temperature. Causes
AIHA may be:

Idiopathic, that is, without any known cause
Secondary to another disease, such as an antecedent upper respiratory tract infection, systemic lupus erythematosus or a malignancy, such as chronic lymphocytic leukemia (CLL)

Medications
Several medications have been associated with the development of warm AIHA. These medications include quinidine, nonsteroidal anti-inflammatory drugs (NSAIDs),  alpha methyldopa, and antibiotics such as penicillins, cephalosporins (such as ceftriaxone and cefotetan), and ciprofloxacin. Pathophysiology
The most common antibody isotype involved in warm antibody AIHA is IgG, though sometimes IgA is found. The IgG antibodies attach to a red blood cell, leaving their FC portion exposed with maximal reactivity at 37 °C (versus cold antibody induced hemolytic anemia whose antibodies only bind red blood cells at low body temperatures, typically 28-31 °C). The FC region is recognized and grabbed onto by FC receptors found on monocytes and macrophages in the spleen. These cells will pick off portions of the red cell membrane, almost as if they are taking a bite. The loss of membrane causes the red blood cells to become spherocytes.
Major aortopulmonary collateral arteries (or MAPCAs) are arteries that develop to supply blood to the lungs when native pulmonary circulation is underdeveloped. Instead of coming from the pulmonary trunk, supply develops from the aorta and other systemic arteries. Pathogenesis and anatomy
Major aortopulmonary collateral arteries (MAPCAs) develop early in embryonic life but regress as the normal pulmonary arteries (vessels that will supply deoxygenated blood to the lungs) develop. In certain heart conditions the pulmonary arteries do not develop. The collaterals continue to grow, and can become the main supply of blood to the lungs. Though it is usually associated with congenital heart diseases with decreased pulmonary blood flow like tetralogy of Fallot or pulmonary atresia it may be seen sometimes in isolation i.e. not associated with any congenital heart disease in that case it is termed as isolated aortopulmonary collateral artery. In these cases it may be one of the cause of congestive cardiac failure in neonates.Pulmonary arteries come from the right side of the heart, and usually carry deoxygenated blood from the body. These collateral arteries carry blood which has already been oxygenated by the lungs, so are of little use in helping the body to get oxygen. Associated conditions
Pulmonary atresia with ventricular septal defect (or Tetralogy of Fallot with pulmonary atresia) will result in the development of systemic collaterals. Implications of a systemic collateral supply
Major aortopulmonary collateral arteries come from the systemic circulation, because of this they will often have higher pressure than normal found in the lungs, leading to pulmonary hypertension.