- Definition
- Pathophysiology
- Systems Affected
- Genetics
- Incidence/Prevalence
- Geographic Distribution
- Signalment
- Signs
- Causes
- Risk Factors
BASICS
Decreased erythrocyte count or hemoglobin content as a consequence of a decrease in PCV, RBC count, or Hb concentration.
- Anemia results from 1 or more of the following:
- Blood loss (internal or external hemorrhage)
- Increased RBC destruction (intravascular or extravascular hemolysis)
- Decreased or ineffective RBC production
- Characterization of anemia (regenerative vs. nonregenerative) is best done by examining bone marrow aspirates. Serial monitoring of PCV and plasma TP concentration may be useful
- Evaluation of immature RBCs and RBC indices in peripheral blood is unrewarding in horses, even during intense erythropoiesis
- The circulating RBC mass varies due to the effects of breed, age, activity, and splenic contraction, which can increase the RBCs by ~50%
- Nonregenerative anemia occurs when the rate of erythropoiesis is insufficient to replace aged RBCs, and develops slowly due to the long lifespan of equine RBCs (≈ 150 days)
- Mechanisms associated with nonregenerative anemia include:
- Diseases interfering with erythropoiesis (↓ erythrocyte life span or ↓ erythropoietin responsiveness)
- Deficiency or alterations in substances necessary for RBC production
- Diseases that damage or displace bone marrow elements and affect RBC precursors and/or all marrow precursors
Decreased circulating RBC mass, decreased oxygen-carrying capacity, and reduced blood viscosity are the main consequences of anemia, but severity is dependent on the magnitude and rate of development of anemia.
See Anemia, Heinz body.
Clinical signs relate to the compensatory mechanisms activated in response to anemia as well as the primary disease process (often more prominent).
- Dependent upon primary disease process
- Most common presenting complaints are exercise intolerance, signs of depression, and inappetence
- Horses with chronic anemia may be subclinical, but exercise may induce exaggerated tachycardia, weakness, and reduced performance
- In acute or severe cases, tachycardia, tachypnea, and low-grade holosystolic heart murmur are present at rest
- Pale mucous membranes
- Other signs depend on the primary disease process and may include:
- Icterus, fever, and pigmenturia (hemolysis)
- Weight loss, polyuria, and polydipsia (chronic renal failure)
- Weight loss, fever, and lethargy (chronic infectious, inflammatory, neoplastic, or immune-mediated processes)
External hemorrhage, epistaxis, hemothorax, hematuria, hemoperitoneum, GI hemorrhage, or coagulopathy.
- Immune-mediated disease (secondary immune-mediated anemia, autoimmune hemolytic anemia or NI)
- Infectious diseases (piroplasmosis, anaplasmosis, and EIA)
- Oxidant induced (red maple, phenothiazines, and wild onions)
- Iatrogenic (hypotonic or hypertonic IV solutions)
- Other toxicities (IV DMSO, heavy metal toxicosis, bacterial toxins, snake bite)
- Miscellaneous (endstage hepatic disease, hemolytic uremic syndrome, hemangiosarcoma, and disseminated intravascular coagulation)
- Anemia of chronic disease associated with infectious, inflammatory, neoplastic, or endocrine disorders
- Iron deficiency due to chronic hemorrhage or nutritional deficiency
- Bone marrow failure (myelophthisis, myeloproliferative disease, bone marrow toxins, radiation, immune mediated)
- Miscellaneous (chronic renal disease, chronic hepatic disease, or recent hemorrhage/hemolysis)
- Dependent on risk factors for the primary disease process
- Age (e.g. neoplasia, middle uterine artery rupture) and sex (e.g. idiopathic urethral hemorrhage in geldings)
- Any infectious or inflammatory disease
- Foals consuming incompatible colostrum are at risk for NI
- Inadequate preventative anthelmintic use or long-term high-dose NSAID administration
- Geographic location for exposure to infectious agents or toxic plants
DIAGNOSIS
TREATMENT
MEDICATIONS
FOLLOW-UP
MISCELLANEOUS