Hematology Flashcards
What type of clinical presentation do animals with acute, severe hemorrhage show?
- SHOCK
- low BP, tachycardia, tachypnea
- pale MM & prolonged CT
- poor peripheral pulses & cool extremities
- trembling, weakness, depression
With acute blood loss, how long does it take for anemia to become clinically important?
12-24 hours
What clinical signs are associated with anemia?
- pale MM
- tachycardia/tachypnea
- weakness/exercise intolerance
- anorexia/depression
- physiological heart murmur
What is a good indicator of regeneration in the horse?
MCV > 60 fl
Common causes of hemorrhage in the horse
- uterine rupture (pregnant mares, late gestation)
- NSAID toxicity
- renal medullary necrosis
- GI bleeding
- exercise-induced pulmonary hemorrhage
- guttural pouch mycosis (internal carotid rupture)
- trauma (internal or external hemorrhage)
- coagulopathy
When do TP & PCV changes occur after an acute blood loss event?
- TP-4-6 hours after
*may not drop significantly if internal bleeding - PCV-12-18 hours after
What bloodwork findings are evidence of acute blood loss anemia?
regenerative anemia & hypoproteinemia without evidence of hemolysis
Appropriate diagnostic steps if hemorrhage suspected but not evident externally
- peritoneal or abdominocentesis
- thoracic or abdominal US
- rectal examination
- endoscopy
- fecal occult blood
- urinalysis
Hemorrhage is what kind of fluid loss?
isotonic
Why should acepromazine be avoided in horses with acute blood loss?
Don’t use in hypotensive animals because it reduces peripheral vasoconstrictive response
What is one potential reason to avoid colloids in a hemorrhage situation?
colloids can inhibit coagulation, so be careful using unless positive that bleeding is controlled
Fluid support for horse that suffered hemorrhage and is in shock
- Hypertonic fluids first (5% NaCl)
- follow with isotonic fluids (LRS)
When is a blood transfusion warranted in hemorrhage situations?
- PCV<15 if acute
- PCV<8-10 if chronic
- HR>90 een after circulatory support
- PCV decreases to <20% in 12 hours
Describe the ideal universal blood donor
- non-thoroughbred
- gelding
- Aa, Qa, and Ca-negative
What is the lifespan of transfused RBCs?
2-5 days
After treating an acute hemorrage, horses should rest until PCV is ______
>20%
What causes clinical signs seen with chronic hemorrhage?
poor oxygen delivery
What findings provide evidence of iron deficiency?
- non-regenerative anemia
- LOW serum iron concentration
- LOW serum transferrin saturation
- HIGH iron-binding capacity ‘
What is the pathophysiology of chronic hemorrhage?
- bone marrow suppression d/t underlying disease
- bone marrow failure
- iron deficiency anemia may be factor
What is the focus of treatment for chronic hemorrhage?
treat the underlying cause
What is the dominant clinical picture of chronic hemorrhage?
Anemia
- pale MM
- tachycardia/tachypnea
- weakness/exercise intolerance
- anorexia/depression
- physiological heart murmur
Differentials for chronic anemia
- chronic blood loss (iron deficiency)
- underlying disease (anemia of chronic disease or inflammation)
- EPO administration
- aplastic anemia
Oral iron should not be given to what age horses?
neonates (2-3 weeks)-Hepatotoxic
What findings are used to diagnose hemolytic diseases?
- anemia with normal plasma protein, hyperbilirubinemia, hemoglobinemia, and/or hemoglobinuria
- altered RBC morphology (spherocytes, eccentrocytes, Heinze bodies, etc.)
What are other rule-outs for hemolytic diseases?
- liver disease
- anorexia
What are some main differences between EV and IV hemolysis?
MCHC
- Normal w/ extravascular hemolysis
- High w/ intravascular hemolysis
Hemoglobinemia & hemoglobinuria-intravascular
Splenomegaly-extravascular
Infectious causes of hemolytic disease in horses
- Anaplasma phagocytophila
- EIA
- Babesiosis/Piroplasmosis
Possible immune-mediated causes for hemolytic disease
- Drugs (Penicillin)
- Infection (S. equi)
- Neoplasia
- Neonatal isoerythrolysis
Toxic causes of hemolytic diseases
- Red maple
- onions
- phenothiazine
- rattlesnake venom
What type of virus is EIA?
Retrovirus
How is EIA transmitted?
hematophagous arthropods or contaminated instruments
What is the mechanism of anemia with EIA?
likely from BM suppresion AND hemolysis
Typical lab findings with EIA
- PCV 10-20%
- normal TP (to possibly marginally high)
- possible thrombocytopenia
- hyperbilirubinemia
Acute EIA clinical signs
- icterus
- depression
- fever
- edema
- petechia
Chronic EIA clinical signs
- intermittent fever
- icterus
- weight loss
- lethargy
- pale MM
*episodic
What is the vector for Anaplasma phagocytophila?
Ixodes spp.
What cells does A. phagocytophila infect?
neutrophils
Anemia due to A. phagocytophila is probably by what mechanism?
immune-mediated
What pathologies result from A. phagocytophila?
- systemic inflammation
- reduced granulocyte & platelet production/increased clearance
- vasculitis
What clinical signs are seen first with A. phagocytophila infection?
fever & depression
A. phagocytophila causes what clinical signs?
- fever (104-105) & depression first
- after 2-3 days:
- icterus
- petechia
- edema
- ataxia
- reluctance to move
Lab findings associated with A. phagocytophila
- anemia
- thrombocytopenia
- neutropenia with left shift
- hyperbilirubinemia
Treatment for A. phagocytophila
- Oxytetracycline IV SID slowly for 7 days
- Doxycycline PO BID for 2 weeks
- Supportive care
- Anti-inflammatory (flunixin meglumine IV 3 d)
A. phagocytophila diagnostic tests
- neutrophil inclusions on peripheral blood smear (during first few days of disease then become harder to find)
- serology (not helpful acutely)
- PCR-buffy coat-very sensitive
What type of hemolysis is most common with IMHA?
extravascular
Pathophysiology of IMHA
- immune-complex mediated RBC destruction
- direct (IV) or phagocyte-mediated(EV)
- tissue hypoxia
- organ dysfunction
- systemic inflammation/shock
Clinical signs of IMHA
- fever
- icterus
- lethargy
- tachycardia & tachypnea if anemia severe
- pale MM
- splenomegaly
- may also develop thrombocytopenia or DIC
- rarely hemoglbinemia or hemoglobinuria-if IV
IMHA diagnostics
- autoagglutination maybe evident (dilute whole blood in saline)
- Coombs-direct or indirect
- higher red cell fragility than normal
- flow cytomoetery for RBC bound IgG
What are some therapies for IMHA?
Dexamethasone
Prednisolone
Cyclophosphamide (if refractory)
Plasmapheresis (if refractory)
What is the purpose of using diuretics as part of treatment for IMHA?
help reduce the nephrotoxicity from pigmenturia-especially important with methemoglobin
Major components of Red Maple pathophysiology
- oxidative damage to hemoglobin causing methemoglobinemia
- oxidative damage to RBC membranes -> hemolysis
- systemic inflammation
Clinical signs of red maple toxicity
- icterus
- weakness, ataxia
- yellow-brown membranes
- brown urine
- brown serum
- tachypnea/tachycardia
- colic (especially prone; painful colic)
- oliguria or anuria
- DIC/acute death
Treatment for Red Maple toxicity
- remove source-activated charcoal via NGT
- fluids for circulatory support & diuresis
- blood transfusions-based on clinical signs since PCV/Hb may be inaccurate
- diuretics (furosemide)
- dopamine CRI if remain oliguric
- anti-oxidants-Vitamin C (?) - can’t hurt, not sure if works
What drugs should be avoided in animals with Red Maple toxicity?
corticosteroids
Causes of relative polycythemia
- hemoconcentration
- dehydration, endotoxemia
- splenic contraction
- excitement, shock
- drug-induced
Clinical signs of polycythemia
- bright red, congested membrane color-relative
- muddy red membrane color-absolute
- CS of dehydration/endotoxemia if cause
- tissue hypoxia signs if absolute
- thrombosis if absolute
What organism is sometimes a cause of thrombophlebitis?
Staphylococcus aureus
Treatment plan for thrombophlebitis
- early aggressive treatment of underlying disease
- aspirin for thrombosis
- antibiotics if septic
- drainage if infected
