ANEMIA

FOAL DISORDERS

Anemia is a common finding in neonatal foals. The normal ranges of hematologic parameters
must be considered when determining the significance of any anemia. The PCV at birth is 40% to
52% but decreases to 32% to 46% after colostrum and milk intake by 24 hours of age. PCV, red blood
cell (RBC) count, and the hemoglobin (Hb) concentration are similar to adult values at 24 hours of
age, before decreasing over the first 2 weeks of postnatal life to values that are in the lower level of
the normal adult ranges. These relatively low levels are sustained for several months. The mean
corpuscular volume (MCV) decreases over the first 4 months of life, leading to microcytosis and
anisocytosis. The MCV increases after weaning. Foals typically have reduced serum ferritin
concentrations and increased total iron binding capacity when compared with adults. Serum fer- ritin
increases significantly on day 1 and is attributed to ingestion of colostral iron, before reducing. Data
support relative iron deficiency as a cause of common foal anemia, but supplementation with iron
does not improve RBC indices. Supplementation of normafoals with a specific iron preparation,
ferrous fumarate, resulted in acute hepatic failure and death. There are reports of absolute iron
deficiency anemia in foals, including stabled Dutch Warmblood foals fed cut grass. Findings include a
low PCV, low serum iron and ferritin concentration, and normal to increased total iron binding
capacity. Improvement is seen in those foals with orairon supplementation.
Clinical Signs
Clinical signs of anemia are related to the magnitude and timing of the underlying disease
process. Rapidly developing hemolytic anemias, such as NI, produce signs of weakness, lethargy and
somnolence, mucous membrane pallor and icterus, tachycardia, and possible mild fever. Intravascular
hemolysis will typically cause brown-red discoloration of urine. Cardiac murmur is accentuatedFoals
with hemoabdomen or internal umbilical remnant hemorrhage are often colicky. Hemorrhage at the
apex of the bladder can produce stranguria. Bleeding into the respiratory cavity can produce
clinicasigns of respiratory distress, and blood loss into the GI tract wilcause melena. Lameness will be
seen in foals with spontaneous hemarthrosis.
Causes
Hemolysis is most commonly seen after consumption of colostra antibodies that are directed
against foal erythrocytes. The syndrome is known as NI and is discussed in detail in Chapter 53. Less
common causes of hemolysis include non-NI immune-mediated hemolysis, intracellular RBC
parasites, rapid administration of hypotonic or hypertonic solutions such as dimethyl sulfoxide, or
equine infectious anemia. RBC hemolysis can be caused by bacterial toxins, most commonly
associated with clostridial infections.
Blood loss occurs commonly with separation of the umbilicacord. Hemorrhage most
commonly occurs externally but can occur internally into the umbilical remnants, the urinary bladder,
or the peritoneal cavity. Most external cord hemorrhage is a small volume and rarely impacts
hematologic parameters. Trauma can cause both internal and external blood loss. Rupture of the
spleen often leads to uncontrolled internal blood loss, potentially requiring splenectomy.
Hemoperitoneum can also occur as a result of rupture of juvenile granulosa cell tumors in foals. Rib
shaft fractures can cause hemorrhage into the pleural cavity; on rare occasions fatal hemorrhage can
occur if a major vessel or myocardium is lacerated.
Blood loss can occur as a result of problems in homeostasis. Affected foals may have
spontaneous hemorrhage into joints, muscle or subcutaneous tissues, or the GI tract. Disseminated
intravascular coagulation (DIC) is an acquired homeostatic problem resulting from severe sepsis.
Adult horses with DIC tend to present with signs associated with failure of fibrinolysis, such as
widespread thrombosis. In contrast, septic foals often present with spontaneous or traumainduced
hemorrhage. Inherited disorders are discussed elsewhere in this text but include intrinsic platelet
disorders, such as Glanzmann thrombasthenia, in which the glycoprotein complex IIb-IIIa Is reduced
or absent on the surface of platelets, and extrinsic disorders, including type 2 Von Willebrand disease.
Decreased erythrocyte production is associated with absolute or relative iron deficiency and
chronic inflammatory diseases. Anemia of chronic disease (ACD) is a complex disorder that involves
altered iron metabolism, bone marrow depression, and reduced production or action of erythropoietin.
Increased levels of hepcidin, released in response to inflammation, may be pivotal in the development
oanemia by decreasing iron absorption and iron recycling. Classically ACD Is reflected by low serum
iron, normal or decreased totairon-binding capacity, and increased serum ferritin concentration.
A syndrome of bone marrow aplasia or hypoplasia was reported in three foals born to mares
that were under therapy for equine pro-tozoal myeloencephalitis. Therapy included sulfonamides,
pyrimethamine, folic acid, and vitamin E.
Determination of the nature of the anemia may allow specific treatment. The treatment of NI
is discussed in Chapter 53. Druginduced or autoimmune anemias may be treated with corticosteroids
(0.05 To 0.1 mg/kg dexamethasone bid IM Or IV). Blood Transfusion following crossmatch may be
indicated when anemia develops rapidly or PCV drops below 12%. Associated conditions such as
metabolic acidosis and hypoglycemia should be corrected. ACD requires correction of the primary
disease condition.
 ANEMIA
RUMINANT DISORDERS

Anemia in the neonate should be interpreted in the context of the realization that normal
hematologic values of the neonate may vary from those of the adult. In calves the incidence of anemia
(hemoglobin < 10 g/dL) is quite high, ranging from 15% to 30% in many herds, and is normocytic,
normochromic, and poikilocytic. Anemia is reported to be a result of iron deficiency. Potential causes
are reduced amounts of iron in milk, poor placental transfer of iron, or decreased intestinal absorption.
Anemic calves with poikilocytosis have similar levels of serum iron, total iron binding capacity, and
marrow iron and plasma copper levels compared with normal calves. Anemic calves do not appear to
have an increased incidence of disease or decreased growth rates. An overall higher plane of nutrition
versus iron supplementation alone produces higher PCVs and hemoglobin levels. Calves less than 6
weeks of age have three types of hemoglobin in various amounts: adult, 28%; fetal, 40%; and
neonatal, 25%. The poikilocytosis may be a function of erythrocyte membrane defects or maturation
transitions.
In addition to frank blood loss from an injury, diseases causing anemia in the neonate include
neonatal isoerythrolysis (NI), non-NI immune-mediated hemolytic anemia, blood loss caused by
gastric ulcer, anemia resulting from bone marrow necrosis, and anemia of chronic disease associated
with localized infections. Hemolytic disease of newborn calves is uncommon but has occurred after
vaccination of pregnant cows against anaplasmosis or babesiosis. The presence of red cell antigens in
the vaccine causes the production of antierythrocyte antibody, primarily against the A and F systems.
Cows mated to bulls carrying these red cell antigens may have hemolytic Disease develop in their A-
And F-positive Calves after ingestion of colostrum-containing alloantibodies.
Hemolytic disease processes produce signs of weakness, pale or jaundiced mucous
membranes, fever, and depression. Blood loss produces weakness and pale mucous membranes.
Intestinal parasitism does not normally lead to anemia during the neonatal period. Intravascular
hemolysis may produce hemoglobinuria and hemoglobinemia. Icterus develops when the ability of the
liver to conjugate bilirubin is exceeded. Mainly, indirect bilirubin is elevated. Anisocytosis is
observed in responsive anemias. Nonspecific stimulation of bone marrow may produce a
leukocytosis. Anemia has also been reported in calves infected with BVDV as a result of bone
marrow necrosis.
Determination of the nature of the anemia may allow specific treatment. Blood transfusion
may be indicated when anemia develops rapidly or PCV Drops below 14%. Associated Conditions
such as metabolic acidosis and hypoglycemia should be corrected. Anemia of chronic disease
requires correction of the primary disease condition.