P. 93

E. Rudloff1
1Lakeshore Veterinary Specialists, Emergency and Critical Care, Glendale, USA
Elke Rudloff, DVM, DACVECC
Lakeshore Veterinary Specialists, Glendale, WI USA
Hemolytic anemia can result from infection, toxin/drug exposure, hypophosphatemia, hereditary de ciencies, and immune-mediated processes. Immune-mediated hemolytic anemia (IMHA) is a type-II immune reaction to red blood cell (RBC) surface antigen that activates the compliment cascade, antibody-dependent cytotoxicity, and/or facilitated phagocytosis by the spleen and
liver. Destruction of the RBC by the spleen and liver is IgG-mediated, and termed extravascular hemolysis. Destruction of RBC within the vascular space is IgM- mediated and termed intravascular hemolysis. IMHA often occurs in conjunction with a thrombocytopenia.
The underlying cause of the immune activation is not usually identi ed; however, it has been associated with secondary causes such as infection, neoplasia, drugs, vaccines, incompatible transfusions, and neonatal isoerythrolysis, or primary (auto-immune) causes. IMHA is diagnosed more commonly in dogs than cats, and cats more commonly have secondary IMHA.
Signi cant anemia results in decreased oxygenation of the tissues and organ dysfunction and acute clinical signs related to hypoxemia, including weakness, pale mucous membrane color, prolonged capillary re ll, increased heart rate, bounding pulses, increased breathing rate or effort and fever. Hemolysis may
also result in jaundice and orange/red colored urine. Occasionally vomiting is described, and might represent gastrointestinal hypoxemia. If a thrombocytopenia accompanies hemolysis, petechia/ecchymosis, hematemesis and/or blood in the stool may also be seen.
Supplemental oxygen should be administered, a peripheral IV catheter placed and blood collected for an emergency laboratory database (packed cell volume (PCV), total protein (TPr), serum color, electrolyte
panel, venous blood gas and lactate level). A hemolytic syndrome is suspected if there exists an anemia with a normal TS, and yellow (icteric) or pink-red (hemolysed) serum color. It is essential that a hemolytic anemia without an immune-mediated cause be ruled-out
before making a diagnosis of IMHA and instituting immunosuppressive treatment.
Additional laboratory analysis that supports an IMHA diagnosis includes evaluation of a blood smear (red blood cell destruction and regeneration, spherocytes (dog), or ghost cells (cat)) and a saline agglutination test. Macro- and micro-agglutination requires a saline-agglutination microscopic exam. Cells may stick together without an immune-mediated process, and cause the appearance of false macro-agglutination. A drop of blood directly from phlebotomy is mixed with one drop of saline, and the sample examined microscopically. Rouleaux is the con guration where RBC stick together appearing like
a ‘stack of coins’ but disperse when mixed with saline. True microagglutination occurs when the RBCs cluster together like grapes that do not disperse when mixed with saline.
Blood samples are submitted for a complete blood count, reticulocyte count, serum biochemical pro le, tick-related and other infectious screening (e.g. feline- leukemia virus, feline coronavirus, haemoplasmosis), and thyroid panel. Thoracic radiographs and abdominal ultrasound are used to evaluate for neoplastic lesions, or other systemic diseases that may be stimulating the immune system.
Reticulocytosis may or may not be present depending on when RBC destruction was activated. Outside of
the ER setting a positive direct antiglobulin test (DAT; Coomb’s test), differentiating Coomb’s test, or RBC surface associated immunoglobulin test may help support a diagnosis when auto-agglutination is not easily identi ed, but these tests do not differentiate primary from secondary IMHA, and they can produce positive results from non-IMHA related causes (e.g. corticosteroid use). Additional diagnostic evidence for IMHA includes erythrophagocytosis on splenic or bone-marrow samples.
Successful treatment of severe cases may require
3-5 days of hospitalization before the overactive immune system is suf ciently suppressed after starting immunosuppressive medication. The patient may bene t from  uid replacement, transfusion, anticoagulation,
and nutritional support. Prior to making the decision to treat, the client must be made aware of the need for chronic medication (up to or greater than 6 months), their potential side effects, and follow up care.
In most cases, intravenous  uid therapy is indicated to replace preexisting or ongoing  uid losses and to promote rheology. Judicious  uid support is provided if the patient is anemic but euvolemic. Packed red blood cell transfusion may be necessary if clinical signs of severe anemia exist, including tachypnea, tachycardia, weakness, etc. The
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