It involves the cooling of the patients serum to 4°C to allow the absorption of anti-P autoantibodies to the red cells, followed by warming to 37°C to activate complement fixation and hemolysis. Indirect DL test with addition of ABO-compatible P antigen-positive blood can be performed in case the direct DL test is negative, since the complement in the original serum may be consumed and result in false negative.The hematopathological findings can reflect both the presence of intravascular hemolysis and the underlying immunological process. The complete blood count usually shows normocytic anemia. Reticulocytosis may be subtle in the acute phase. Peripheral blood smear may show corresponding polychromasia. Neutrophil erythrophagocytosis is suggestive of PCH, while the absence of red cell agglutination as in CAD or microspherocytosis in WAIHA should also be noted. Classification
AIHA can be classified as warm autoimmune hemolytic anemia  or cold autoimmune hemolytic anemia, which includes cold agglutinin disease and paroxysmal cold hemoglobinuria. These classifications are based on the characteristics of the autoantibodies involved in the pathogenesis of the disease. Each has a different underlying cause, management, and prognosis, making classification important when treating a patient with AIHA. Autoimmune hemolytic anemiaWarm-antibody typePrimary
Secondary  (lymphoproliferative disorders, autoimmune disorders): 259 Cold-antibody type (anemia)Primary cold agglutinin disease
Secondary cold agglutinin syndromeAssociated with malignant disease
Acute, transient, infection-associated  (acute cold antibody mediated AIHA complicating Mycoplasma pneumoniae or viral infections)
Chronic (lymphoproliferative disorders): 259 Paroxysmal cold hemoglobinuria: 259 Idiopathic
SecondaryAcute, transient (Infections other than syphilis): 259 
Chronic (syphilis): 259 Mixed cold- and warm-antibody typeIdiopathic
Secondary (lymphoproliferative disorders, autoimmune disorders)Drug-induced immune hemolytic anemia: 259 Autoimmune type
Drug absorption type
Neoantigen type

Management
Acute PCH is usually transient and self-limiting.
Triphalangeal thumb (TPT) is a congenital malformation where the thumb has three phalanges instead of two. The extra phalangeal bone can vary in size from that of a small pebble to a size comparable to the phalanges in non-thumb digits. The true incidence of the condition is unknown, but is estimated at 1:25,000 live births. In about two-thirds of the patients with triphalangeal thumbs, there is a hereditary component. Besides the three phalanges, there can also be other malformations. It was first described by Columbi in 1559. Signs and symptoms
The triphalangeal thumb has a different appearance than normal thumbs. The appearance can differ widely; the thumb can be a longer thumb, it can be deviated in the radio-ulnar plane (clinodactyly), or thumb strength can be diminished. In the case of a five fingered-hand it has a finger-like appearance, with the position in the plane of the four fingers, thenar muscle deficiency, and additional length. There is often a combination with radial polydactyly. Complications
Generally, triphalangeal thumbs are non-opposable. In contrast to most people with opposable thumbs, a person suffering from TPT cannot easily place his or her thumb opposite the other four digits of the same hand. The opposable thumbs ability to effortlessly utilize fingers in a "pinch" formation is critical in precision gripping. For the thumb to adequately grip, certain thumb criteria must be met (e.g. suitable position and length, stable joints and good thenar muscle strength).