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Anemia, Hemolytic 59

Anemia, Hemolytic Client Education
Sheet
VetBooks.ir Diseases and Disorders

• Signalment, known risk factors may provide
BASIC INFORMATION
clues (e.g., neonatal kitten from breed with ○ Depletion of erythrocyte adenosine tri-
phosphate (ATP), diphosphoglycerate
Definition high prevalence of B blood type, young (DPG), and reduced glutathione;
Decrease in red blood cell (RBC) mass due to English Springer spaniel with hemolytic crisis decreased RBC deformability, increased
destruction or shortened life span of RBCs. after exercise, cat with history of acetamino- osmotic fragility, and susceptibility to
Immune-mediated hemolytic anemia (IMHA) phen administration) oxidative injury
is the most common cause and is discussed as • Signs related to concurrent disease (e.g., • Hereditary erythrocyte defects:
a separate topic (p. 60). diabetic ketoacidosis in animal with hemo- ○ PK deficiency: glycolytic enzyme defi-
lysis from hypophosphatemia) ciency, causing decreased ATP, leading to
Epidemiology osmotic fragility. Anemia typically not
SPECIES, AGE, SEX PHYSICAL EXAM FINDINGS manifested until early adulthood.
Any dog or cat • Pallor, weakness, lethargy, tachycardia, ○ PFK deficiency: glycolytic enzyme defi-
• Neonatal isoerythrolysis: neonatal kittens tachypnea ciency, causing decreased 2,3-DPG; results
• Inherited RBC defects: 6 months to 3 years • Icterus in increased intracellular pH and RBC
of age, dogs > cats • Hepatosplenomegaly fragility in alkaline conditions such as
• Caval syndrome: dogs • Fever and lymphadenopathy are less common hyperventilation during exercise
• Toxins: cats more susceptible, but dogs more • Murmur: systolic, soft (grade II/VI or less), ○ Feline porphyria: deficiency of uropor-
likely exposed left-sided phyrinogen III cosynthetase; decreased
• Cyanosis if methemoglobinemia is present production of hemoglobin
GENETICS, BREED PREDISPOSITION • Feline neonatal isoerythrolysis (p. 686): type
• Inherited RBC defects: Etiology and Pathophysiology B queens with anti-A alloantibodies in
○ Phosphofructokinase (PFK) deficiency: See Causes of Hemolysis (p. 1198). colostrum destroy RBCs in kittens with type
English springer spaniels, rarely cocker • Immune-mediated anemia (p. 60) A blood.
spaniels • Intoxication: • Miscellaneous causes: incompatible blood
○ Pyruvate kinase (PK) deficiency: basenjis, ○ Most but not all toxins that cause transfusion, hemolytic uremic syndrome,
beagles, West Highland white terriers, hemolysis do so by oxidative damage to hypotonic fluid administration, others
Cairn terriers, miniature poodles, toy RBCs. (p. 1198)
Eskimos, dachshunds, Chihuahuas, pugs; ○ Oxidant damage causes Heinz body
Abyssinian, Somali, Bengal, Maine coon, formation or methemoglobinemia, with DIAGNOSIS
and other pure-breed cats decreased RBC life span and decreased
○ Feline porphyria (rare): Siamese, domestic delivery of oxygen to tissues, respectively. Diagnostic Overview
short hairs ○ Heinz bodies make RBCs prone to Hemolytic anemia is suspected in a patient
• Infectious: intravascular lysis or phagocytosis. Heinz with anemia, no evidence of blood loss, and
○ Babesiosis: greyhounds and pit bulls bodies are considered an absolute marker typically, evidence of RBC regeneration. Signal-
overrepresented of oxidative RBC injury in dogs, less so ment, history, and physical examination can
• Histiocytic neoplasia: Bernese mountain in cats (present in 10%-50% of healthy provide direction for diagnostic testing, but
dogs, flat-coated retrievers, golden retrievers, cats). RBC morphology abnormalities are often key
rottweilers ○ Methemoglobinemia, suspected with to determining cause of hemolysis.
cyanosis or brown-colored blood, does not
RISK FACTORS affect RBC life span or induce hemolysis; Differential Diagnosis
Oxidative damage (cats at increased risk); it decreases the oxygen-carrying capacity • Blood-loss anemia (p. 57); bleeding may be
ectoparasites or endoparasites; hypophospha- of RBCs. overt or occult.
temia ○ Oxidant RBC injury can cause Heinz • Anemia due to decreased RBC production.
bodies, methemoglobinemia, or both; May be RBC specific (e.g., chronic kidney
GEOGRAPHY AND SEASONALITY Heinz bodies are more routinely identified disease, pure red cell aplasia) or may be
Cytauxzoonosis: Southeast, Midwest, and first (blood smear). part of pancytopenia (e.g., bone marrow
mid-Atlantic United States, South America • Infectious organisms: can infect RBCs disorders)
directly and cause hemolysis or can trigger
Clinical Presentation secondary RBC destruction. See Hemotropic Initial Database
DISEASE FORMS/SUBTYPES Mycoplasmosis (p. 438), Babesiosis (p. 105), • CBC/blood smear:
• Intravascular: direct RBC lysis within vas- and Cytauxzoonosis (p. 235). ○ Decreased hematocrit, RBC count, and
culature results in hemoglobinemia/-uria and • Microangiopathic: hemangiosarcoma, dis- hemoglobin
icterus. seminated intravascular coagulopathy (DIC), ○ Evidence of regeneration:
• Extravascular: RBCs are phagocytosed hepatic/splenic disease, heartworm disease ■ Absolute reticulocytes > 60,000/microL
by the mononuclear phagocytic system, (i.e., caudal caval syndrome), vasculitis ■ Macrocytosis, hypochromasia
resulting in splenomegaly, hepatomegaly, ○ Fragmentation of RBCs by abnormal ■ Regeneration may not be evident for
and bilirubinemia/-uria. vascular structures or narrowing of vessels 3-5 days (until bone marrow responds)
• Intravascular and extravascular hemolysis can • Hypophosphatemia: complication of keto- ○ Morphology: anisocytosis, polychromasia,
occur simultaneously. acidotic diabetes mellitus, hepatic lipidosis, Heinz bodies, schistocytes (microangiopa-
refeeding syndrome, phosphate-binding thy), parasites. If spherocytes are present,
HISTORY, CHIEF COMPLAINT antacids (p. 1241) suspect IMHA.
• Anorexia, weakness, exercise intolerance, ○ Usually with serum phosphorus < 1.5 mg/ • Serum biochemistry panel and urinalysis:
collapse/syncope dL (<0.48 mmol/L) hyperbilirubinemia/-uria if severe acute

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