PCV - Canine
TP - Canine
TP - Feline
Large mean corpuscular volume (MCV) - average erythrocyte is larger than standard size
Small mean corpuscular volume (MCV) - average erythrocyte is smaller than reference size
Mean corpuscular volume is WNL
Erythrocytes vary obviously in size.
Mean Cell Hemoglobin Concentration (MCHC) is lower than normal
Mean Cell Hemoglobin Concentration (MCHC) is WNL
individual cell hemoglobin concentration varies obviously between erythrocytes.
Macrocytosis with concurrent hypochromia
Occurs during regeneration.
May be normal in poodles.
Microcytosis with concurrent hypochromia
Seen during iron deficiency, portosystemic shunts (PSS), and normal in some Akitas
Anemia - defined
A disease state defined by decreased erythrocyte number and/or decreased hemoglobin
Clinical signs of Acute Blood Loss
Causes hypovolemia but NOT anemia
PCV/TP will be initially normal; both will lower as volume increases and dilutes RBC and serum protein levels.
After 3-4 days, RBC numbers start to increase with anisocytosis, polychromasia
Clinical signs of Chronic Blood Loss
May not see any clinical signs, even with low PCV, as body compensates with erythropoietin release. When CS are seen, they include pale mm, lethargy, weakness, and compensatory tachypnea and tachycardia.
Usually very regenerative, with anisocytosis, polychromasia, reticulocytosis, nucleated RBCs
If concurrent iron deficiency, may also lead to non-regenerative anemia
Hormone necessary for erythropoesis (RBC formation).
Released by kidney at site of renal tubules.
Affects RBC formation, also involved in production of 2,3-disphosphoglyceric which promotes oxygenation of tissues with greatest demand by changing affinity of oxygen to hemoglobin
Treating blood loss
Ideally, pinpoint and treat underlying cause.
If hypovolemia, replace blood loss/volume. May also be indicated with chronic blood loss.
If iron deficiency, ferrous sulphate indicated for longer term --> C/I if infection is present!
DDx Hemolytic anemia
- Heinz body anemia
- Copper toxicity
- Severe hyperphosphatemia
- Mycoplasma hemofelis (FIA)
- Only RBCs affects --> normal volume, protein concentration, and leukocyte concentration.
- Initially appears non-regenerative, until marrow responds after 3-5 days
- May cause jaundice,hemoglobinuria, hemoglobinemia
Pathological basis of jaundice following hemolytic anemia
Hemoglobin from RBC lysis is metabolized by liver and excreted into the bile, which may overwhelm the liver and lead to jaundice.
- Binds hemoglobin from intravascular hemolysis
- Once reserve become overwhelmed, Hg remains in blood and is excreted in urine, resulting in the hemoglobinemia and hemoglobinuria seen with hemolytic anemia
- Does not cause Hg to enter circuation, so jaundice is only seen during a crisis
Heinz body anemia
- RBC anti-oxidant system is overwhelmed
- Results in oxidative damage to the RBC globin and sbsequent damage to the RBC membrane
Commonly after toxicities --> paracetamol/acetaminophen, onions, zinc, propylene glycol
- Appear as single, rounded protrusions of the RBC membrane, or pale and non-staining regions that are non-central
Immune-mediated hemolytic anemia
- #1 cause of canine hemolysis
- Possible concurrent thrombocytopena (Evan's syndrome)
- Dx: via slide agglutination, spherocytosis, and a positive coombs test
- Tx: underlying cause (if known), transfusion prn or oxyglobin, immunosuppressive drugs (prednisolone, cyclosporin, azithioprine, vincristine for thrombocytopenia)
- Causes include drugs, toxicity, immune-related, parasites, post-vax, but most are idiopathic
irregularly contracted RBCs, are smaller and w/o normal center