Clinical Haematology Flashcards
(182 cards)
1
Q
Define erythropoiesis.
A
Production of erythrocytes.
2
Q
Where does erythropoiesis occur?
A
Bone marrow within the medullary cavity of larger bones of axial and appendicular skeleton. Can also occur at extramedullary sites at times of increased demand or if the bone marrow is failing.
3
Q
Outline the stages and time markers of erythropoiesis.
A
Pluripotent hematopoietic stem cell > proerythroblast > erythroblast > loses nucleus some organelles > reticulocyte = 5-7 days
Reticulocyte > loses remaining organelles > erythrocyte = 1-2 days
4
Q
How are RBC removed?
A
Senescent/end of life RBC removed in spleen or haemolyse
5
Q
What are the species differences in RBC lifespan in the circulation?
A
70 days in cats
110 days in dog
145 days in horse
160 days in cattle
6
Q
Which blood tube is used for haematology collection?
A
EDTA
7
Q
List the common artefacts that can interfere with haematology.
A
Clots
Platelet clumps
Macroplatelets
Cell (RBC, leukocyte) agglutination
Nucleated RBC – machine counts nucleated cells as white cells
Heinz bodies
Lipaemia
Delay in sample handling causing haemolysis and cell swelling
8
Q
When evaluating RBC, what are the limitations?
A
- Risk of artefact
- No automated machine can evaluate morphology
- MCH, MCV and MCHC are averages
- Some analyses also provide RBC distribution width and reticulocyte count/indices
9
Q
How is packed cell volume measured manually?
A
- Centrifuged whole anti-coagulated blood
- RBS read as a percentage of column
- Different to haematocrit
10
Q
What does evaluating PCV manually allow us to do?
A
- Buffy coat assessment – platelets and white cells
- Plasma colour evaluation – haemolysis, jaundice, lipaemia
- Plasma total proteins measurement using refractometer
11
Q
Name the 3 main parts of a blood smear?
A
Base or head
Monolayer
Feathered edge – where bigger cells and clumped cells often get dropped
12
Q
Compare dog and cat platelets.
A
Dog platelets are smaller than RBC, cats have bigger platelets, closer to RBC size.
13
Q
What is anisocytosis and what are the possible causes?
A
Variability in size. Due to macrocytosis, microcytosis, both these, polychromasia
14
Q
What does macrocytosis with polychromasia indicate?
A
Indicates RBC regeneration
15
Q
How is erythroid maturation shown?
A
Progressively smaller cells
16
Q
What does macrocytosis without polychromasia indicate?
A
FeLV
Familial macrocytosis
Common laboratory artefact - increased sodium, increased glucose, excess EDTA, storage
17
Q
What does microcytosis indicate?
A
Iron deficiency – with or without hypochromasia
18
Q
What is polychromasia and what can it be caused by?
A
- Variability in cell colour
- Due to increased presence of immature RBC, which are larger, bluer (polychromatophils)
- More notable in some species, like dogs
19
Q
Distinguish nucleated RBCs and Howell-Jolly bodies.
A
Retained nuclei = nRBC
Retained nuclear material = H-JB
20
Q
What does the presence of nucleated RBCs and Howell-Jolly bodies without regeneration indicate?
A
Lead poisoning
Splenic disease/removal
Bone marrow disease
Heat stroke
21
Q
What is the appearance of bird and reptile RBCs?
A
Have oval, large and nucleated RBC
22
Q
What is hypochromasia and when is it seen?
A
- RBC have less haemoglobin than normal
- Associated with iron deficiency anaemia and copper deficiency
- Often accompanied by poikilocytosis/abnormal RBC shape and microcytosis
23
Q
What are schistocytes?
A
RBC fragments
Evidence of shear injury
24
Q
What are some examples of shear injuries?
A
Vascular neoplasia – common in spleen or liver
Disseminated intravascular coagulopathy
Iron deficiency anaemia – cells are more fragile
Glomerulonephritis
Heartworm
Portosystemic shunts
25
What are acanthocytes?
RBC with large, blunt ended projections, seen in liver disease, lipid disorders and alongside shear injury.
26
What cells can also occur from shear injury?
Keratocytes and blister cells
27
What are echinocytes?
Crenated RBC. Common artefact. If real then usually seen alongside other shear injury related changes.
28
When are elliptical RBCs normal?
In camelids, and therefore not considered poikilocytes.
29
What are spherocytes?
Spherocytes and ghost cells are seen with certain types of anaemia. Spherocytes have the same volume and smaller surface area due to no central pallor. They are more challenging to recognise in cats.
30
What can occur upon RBC oxidative injury?
Heinz bodies
Mathaemoglobinaemia
Eccentrocytes
31
What are Heinz bodies?
Oxidation of Hb causes non-functional Hb. Pushed to edge of cell = Heinz body
Species susceptibility varies: cats > horses > dogs
32
What are the causes of RBC oxidative injury?
Toxicity - garlic, onion and baby food, zinc, paracetamol, naphthalene
Some diseases in cats - DM, lymphoma, hyperthyroidism
33
What are codocytes?
Codocytes (target cells) commonly seen with regenerative anaemia or hypochromasia.
34
What is LEMON representative on haematology?
L, E decrease, Mo, N increase
Decreased neutrophils on haematology. Decreased lymphocytes and eosinophils and increased monocytes and neutrophils as systemic response. So decreased neutrophils is not an appropriate response
35
Define anaemia.
Decreased red blood cell mass as determined by decreased concentration of erythrocytes in blood
35
Define erythrocytosis.
Increased concentration of erythrocytes in blood as measured by increased RBC, Hb, HCT, PCV).
36
How is anaemia identified in the kidney?
EPO production
37
Describe the clinical presentation of anaemia in increasing severity.
Subclinical > non-specific lethargy > exercise intolerance > overt collapse/tachypnoea > death
37
What is the acute clinical presentation of anaemia?
- Haemolytic
- PCV 18%
- Tachycardic
- Haemic murmur
- Tachypnoeic
- Weak
- Barely ambulatory
38
What is the chronic clinical presentation of anaemia?
Bone marrow disease, PCV 14%: exercise intolerant, lethargic at home, but walked into consult room interactive and looking for food, can lead to pica.
39
How is reticulocytosis a sign of regenerative anaemia?
Demand for increased RBC production, leading to premature release of RBC precursors, especially reticulocytes. Reticulocytosis = regeneration. Reticulocytes are larger than mature RBC.
40
What are reticulocyte aggregates?
Immature reticulocytes retain large amounts aggregates of RNA. Mature within 1-2 days in circulation
41
What is the appearance of reticulocyte aggregates?
Appear as polychromatophils when stained with routinely used Romanowsky stains. Without these stains they just look bigger and purple.
42
What is reticulocyte punctuate?
- Mature – retain only small punctuates of RNA
- Visualisation requires staining with intravital dyes
- Only present in cats, not dogs. May persist for a few weeks in circulation
43
What is the most objective measure of regeneration in dogs and cats?
Reticulocytes
44
When are retics seen in species?
Horses – retain retics in bone marrow not seen in circulation
Cattle/sheep – variable release of retics, often only seen with severe anaemia
45
What are the other morphological features of regeneration?
Polychromasia
Anisocytosis
Nucleated RBC
46
How are the morphological changes of regeneration reflected in RBC indices?
Cell size (MCV) – normocytic, macro (high MCV), micro (low MCV)
Cell haemoglobin/concentration (MCH/MCHC) – normochromic, hypo, hyper
47
How does hypochromic anaemia develop?
1. Erythropoiesis - RBCs become progressively smaller, Hb accumulates
2. Hb threshold, nucleus extruded = nRBC > reticulocyte
3. Low Hb = ongoing cell divisions, increased time to accumulate = microctic
4. Inadequate Hb = hypochromic RBC = iron deficiency = microcytic +/- hypochromic anaemia
48
What is the presence of regeneration indicative of?
Haemorrhage or haemolysis
49
Distinguish extra and intravascular haemolysis.
Extra – RBCs phagocytosed (primarily in the spleen) and components released
Intra – RBCs lyse in circulation due to membrane damage
50
What can be present in the event of haemolysis?
- Haemoglobinaemia > haemoglobinuria
- Bilirubinaemia > clinical jaundice above 40 and bilirubinuria
- Ghost cells
- Spherocytes, autoaggulination,
51
List some possible differentials for haemolysis.
- Primary immune-mediated haemolytic anaemia
- Infectious agents
- Oxidative damage - toxins, systemic disease
- Hypophosphataemia
- Neonatal isoerythrolysis
- Transfusion reactions
- Microangiopathic disease
- Hereditary RBC enzymopathies
52
Distinguish the aetiology of primary and secondary immune mediated haemolytic anaemia.
Primary – autoimmune
Secondary to molecular mimicry, haptenisation - neoplastic, inflammatory/infectious disease, penicillin, cephalosporins, trimethoprim-suplphonamides, intra/extracellular paraites
53
What does Coombs' testing evaluate?
Presence of antibody and/or complement on RBC surface
54
When is Coombs' testing clinically pointless?
If autoagglutination present = will be positive, may be positive in cases without haemolytic anaemia
55
Distinguish internal and external haemorrhages.
Internal in body cavities due to haemothorax or haemoabdomen
External, either seen visibly from body surface or hidden from external surfaces - GI, genitourinary or respiratory tract.
56
What are some examples of secondary causes of body cavity haemorrhages?
Secondary haemostatic disorder, such as coagulopathy
- Acquired – rodenticide intoxication, angiostrongylosis, liver disease
- Congenital – haemophilia
57
What are some examples of primary causes of body cavity haemorrhages?
Traumatic
Non-traumatic: abdominal/splenic > hepatic, adrenal, renal. Thoracic is less common but could be thymic involution or neoplasia
58
How can external haemorrhages be idnetified?
Haematemesis/haematochezia/melaena so through rectal examination
Occult – regenerative anaemia > iron deficiency > poorly/non-regenerative microcytic/hypochromic) . GI blood loss is the most common cause of iron deficiency anaemia
Increased urea, thrombocytosis, occasional spherocytes
59
Describe iron deficiency anaemia in terms of serum iron, total iron binding capacity, % transferrin saturatoin, and bone marrow stoes.
- Low
- Normal/high
- Low
- Low
60
Describe anaemia of chronic disease in terms of serum iron, total iron binding capacity, % transferrin saturatoin, and bone marrow stoes.
- Low
- Low
- High
- High
61
Why might a urinary tract external haemorrhage occur?
Macroscopic pigmenturia or primary pathology - urinary tract tumours, idiopathic renal haematuria
62
Why might a respiratory tract external haemorrhage occur?
- Angiostrongylus vasorum
- Rodenticide intoxication
- Primary pathology
- Thrombocytopenia
- Reproductive tract – rare post-partum complication
63
What is the appearance of a non-regenerative anaemic blood smear?
Smear exam will be normocytic, normochromic, red cell indices will be normal
64
What consideration must be taken with pre-regenerative anaemias?
Takes 3-5 days to mount to regenerative response, repeat haematology in 3-5 days if not sure
65
Which anaemia is associated with FeLV infection?
Macrocytic non-regenerative anaemia
66
What are the possible extra-bone marrow diseases that could cause non-regenerative anaemia?
- Chronic GI blood loss - microcytic +/- hypochromic
- Chronic disease - kidney, endocrinopathies, inflammatory, neoplasia
- Oestrogen producing tumour
- Chemotherapeutic drugs
67
What are the possible primary bone marrow diseases that could cause non-regenerative anaemia?
- Infiltrative disease - leukaemia, multiple myeloma
- Infectious disease - FeLV, parvo
- Non-regenertaive IMHA - primary/autoimmune or secondary
- Myelofibrosis
68
What is the normal PCV range for most breeds of cats and dogs?
35-55% in dogs
25-48% in cats
69
Distinguish relative from absolute erythrocytosis.
- Relative is haemoconcentration and absolute is increased RBC mass
- Relative should not push PCV above 65% dog/60% cats.
- Relative typically has concurrent increase in total proteins (except acute haemorrhagic diarrhoea syndrome)
70
When can a mild absolute erythrocytosis/polycythaemia be normal?
- Certain breeds
- Following splenic contraction in dogs (fear)
- Systemic diseases – hyperadrenocorticism and hyperthyroidism
71
What is the clinical presentation of erythrocytosis?
- Increased RBC mass leading to increased viscosity
- Hyperaemic/darker mucous membranes with/without cyanosis
- Blood sludges due to spontaneous thrombosis
- Local hypoxia > tachycardia, tachypnoea, lethargy, exercise intolerance, syncope
- Epistaxis
72
What are some potential causes of EPO dependent absolute erythocytosis?
Appropriate/systemic hypoxia - altitude, right-left cardiac shunt, chronic upper airway obstruction, severe pulmonary disease
Inappropriate - paraneoplastic EPO produtcion due to a renal carcinoma
73
How are white blood cells assessed in a lab?
Haematology analysers
Morphology and total WBC count and differential estimation
74
What are neutrophil pools?
Bone marrow > circulating and marginating blood > tissue
Blood samples only harvest from the circulating pool
75
What is the half life of neutrophils in the circulation and in tissue?
Short - 6-12 hours
A few days, accumulate at sites of inflammation, may be reduced in disease states
76
What is neutrophilia?
Increased circulating neutrophils
77
What causes neutrophilia?
- Increased production independent of demand – neoplastic proliferation, rare
- Redistribution – stress/steroid response, hyperadrenocorticism
- Increased persistence in circulation – stress/steroid response
- Increased production due to increased demand – infection, sterile inflammation (IMHA or pancreatitis), neoplasia, tissue necrosis
78
What is neutrophil left shift?
Increased demand causes release of immature neutrophils. Bands/immature and segmental/mature neutrophils
79
Distinguish regenerative and degenerative neutrophil left shift.
Regenerative – left shift with neutrophilia
Degenerative – left shift with normal or reduced neutrophil count
80
When does toxic change in neutrophils occur?
Due to neutrophil production under overwhelming demand, causing reduced maturation and enhanced neutrophil turnover.
81
What changes in the bone marrow occur to cause toxic change in neutrophils?
- Cytoplasmic basophilia – retained residual cytoplasmic RNA (becomes bluer)
- Döhle bodies – ribosomes clump together, indicating rapid production in bone marrow
- Cytoplasmic vacuolation – white dots
- Toxic granulation – persistence of primary granules, splatter pattern in cells
- Giant neutrophils
- Ring nuclei
82
What is neutropenia?
Decreased circulating neutrophils
83
What causes neutropenia?
- Destruction – immune mediated
- Anomaly – breed associated/individual
- Artefact – sampling error, agglutination
- Overwhelming demand – severe inflammatory process, with/without left shift
- Decreased production in bone marrow disease
84
What can cause decreased production of neutrophils at the bone marrow/due to bone marrow disease?
- Infectious – FeLV, parvovirus, leishmania, ehrlichiosis
- Toxins or drugs – oestrogens, chemotherapeutics, bracken fern poisoning, chloramphenicol
- Myelophthisis
- Hypoadrenocorticism
- Cyclic neutropenia
85
What is monocytopenia?
Decreased circulating monocytes, not clinically significant
86
What is monocytosis?
Increased circulating monocytes
87
What causes monocytosis?
- Redistribution – stress/steroids response, hyperadrenocorticism
- Increased production independent of demand
- Increased demand – chronic inflammatory diseases processes, acute inflammation
88
What are eosinophils and their effect on tissues?
Granules that contain highly irritant/pro-inflammatory substances, causing local secondary tissue damage. Parasite and allergic response
89
What is eosinophilia?
Increased circulating eosinophils
90
What causes eosinophilia?
- Redistribution – lack of glucocorticoids
- Increased production independent of demand – hypereosinophilic syndromes, paraneoplastic syndromes, neoplastic proliferation
- Increased demand - parasites, hypersensitivity, inflammation of mast cell rich tissue
91
What is the significance of eosinopenia?
Common finding as part of stress leukogram, otherwise of little clinical significance.
92
What can accompany eosinophil changes?
Basopenia, not of clinical significance
93
What is lymphocytosis?
Increased lymphocyte count
94
What causes lymphocytosis?
- Age appropriate in young animals
- Adrenaline-stimulated release
- Mobilisation – hypoadrenocorticism
- Due to increased demand – antigenic stimulation, post vaccination
- Independent of demand – chronic lymphocytic leukaemia, acute lymphoblastic leukaemia, lymphoma (stage V)
95
What are the 2 ancillary diagnostic methods when suspicious of neoplasia driven lymphocytosis?
PARR (PCR for Antigen Receptor Rearrangement) – evaluates for clonality by amplification of cellular DNA. Can differentiate B-cell from T-cell
Flow cytometry – evaluates for presence of specific cellular markers. May facilitate differentiation between neoplastic and inflammatory
96
What is lymphopenia?
Decreased lymphocyte count
97
What causes lymphopenia?
- Redistribution – steroid stress-associated
- Decreased production – viral infection or immunodeficiency
- Loss of lymphocytes – via chylous effusions (drained, not returned to circulation), lymphangiectasia (lost in faeces)
98
When are abnormal white blood cell counts normal?
- Age-related – lymphocytosis is age appropriate in young animals
- Breed-related – greyhounds/sighthounds have a lower reference range for neutrophils
- Stress/steroid-related
99
What is the leukocyte pattern for physiological leukocytosis?
- Increased total WBC
- Increased segmental neutrophils
- Increased lymphocytes
- Variable monocytes
- No change in band neutrophils and eosinophils
100
What is the leukocyte pattern for steroid/stress?
- Increased total WBC, segmental neutrophils and monocytes
- Mild increase/no change in band neutrophils
- Decreased lymphocytes
101
What is the leukocyte pattern for acute inflammation?
- Increased total WBC, band neutrophils, segmental neutrophils
- Decreased lymphocytes
- Variable monocytes and eosinophils
102
What is the leukocyte pattern for chronic inflammation?
- Increased total WBC and segmental neutrophils
- Variable band neutrophils, lymphocytes, monocytes and eosinophils
103
What are the species differences in neutrophils?
Dominant cell type in healthy cats, dogs, horses, camelids
104
What are the species differences in lymphocytes?
Dominant cell type in healthy cattle, rodents
105
What are the WBC species differences in rabbits?
Heterophils - neutrophils morphology in rabbits
106
What are the WBC species differences in reptiles and amphibians?
Additional WBC type, leading to azurophils
107
What are the haematological considerations of bird, reptiles, fish and amphibian blood analysis?
- Oval RBC are nucleated
- Platelet equivalent (= thrombocyte) is nucleated, can look like a lymphocyte
- Counting cannot be performed by analysers as cannot differentiate RBC and thrombocytes from WBC
108
What is haemostasis?
The process of preventing haemorrhage.
109
Give a brief overview of the process of haemostasis.
1. Endothelial damage exposes subendothelial matrix, which is thrombogenic. Exposure of von Willebrand factor/vWF.
2. Platelet adhesion via vWF to the subendothelial matrix/vessel wall.
3. Platelet activation
4. Release mediators
5. Additional platelet recruitment
6. Platelet aggregation
7. Primary platelet plug
8. Phosphatidylserine exposed, the surface on which coagulation factors assemble in secondary haemostasis.
9. Formation of fibrin in secondary haemostasis via coagulation cascade.
10. Platelet is stabilised by fibrin/factor 1a.
11. Fibrinolysis in tertiary haemostasis. Produces bradykinin, inducing tissue plasminogen activator release.
12. tPA catalyses the breakdown of plasminogen to plasmin
13. Plasmin produces fibrin(ogen) degradation products/FDPs and lyses cross-linked fibrin, yielding D-dimers
110
What do primary haemostatic disorder typically present as?
- Petechial or ecchymotic haemorrhages
- Mucosal bleeds – gingival margins/oral cavity, nasal, pulmonary (rare), gastrointestinal, urinary
111
What are the 3 possible causes of primary haemostatic disorders?
Platelet disorders
von Willebrand disease
Vasculopathies
112
How do you check that thrombocytopenia is true?
Clean sample, no clots, no clumps
113
What are the 2 types of thrombocytopenia?
Immune-mediated thrombocytopenia – usually absolute
Consumptive level thrombocytopenia – due to chronic disseminated intravascular coagulation
114
Distinguish spontaneous and induced haemorrhage with thrombocytopenia alone.
Spontaneous haemorrhage when platelets <30x10^9/L
Induced haemorrhage when platelets <50x10^9/L
115
If there is bleeding and the platelet count is above 50x10^9/L, what must be done?
Need to look for another cause of bleeding – vasculitis, thrombocytopathia, secondary haemostatic disorder
116
What causes primary immune mediated thrombocytopenia?
Autoimmune
117
What are the causes of secondary immune mediated thrombocytopenia?
- Infectious causes – leptospirosis, FeLV, Ehrlichia, Anaplasma, Babesia, leishmaniasis, FIP
- Systemic inflammatory or neoplastic disease
- Secondary to drug/toxin exposure
118
What is consumptive level thrombocytopenia secondary to?
- Angiostrongylus vasorum
- Leptospirosis, Leishmania, Dirofilaria, Ehrlichia, Anaplasma, Babesia, FeLV
- Systemic inflammatory or neoplastic disease, especially splenic haemoangiosarcoma
119
When can decreased production of platelets occur?
Bone marrow disease (expect neutropenia first)
Secondary to infection, chemotherapeutic agents and idiosyncratic drug reactions
120
How are platelets sequestered and lost?
Sequestration in the spleen
Loss – post-major haemorrhage
121
What are 2 examples of primary haemostatic disorders without thrombocytopenia?
Thrombocytopathia – Angiostrongylus is an increasingly important cause
von Willebrand Disease:
122
What are the tests of secondary coagulation and when would each be used?
Isolated prolonged PT = extrinsic pathway problem
Isolated prolonged aPTT = intrinsic pathway problem
Prolonged PT and aPTT = common pathway or multiple factor/pathway problem
123
What are some extrinsic pathway problems of secondary coagulation?
- Congenital Factor VII deficiency
- Early combined deficiency
124
What are some intrinsic pathway problems of secondary coagulation?
- Congenital (isolated) factor VIII, IX, XI or XII deficiency. Includes haemophilia A and B
- Liver failure
- Angiostrongylus vasorum infection
- Disseminated intravascular coagulation
125
What are some common pathway problems of secondary coagulation?
- Vitamin K inactivation/deficiency, rodenticide intoxication, severe cholestasis/fat malabsorption
- Liver failure
- Angiostrongylus vasorum infection
- Disseminated intravascular coagulation
126
What is disseminated intravascular coagulolation?
A global loss of the equilibrium between coagulation activation and inhibition. Usually secondary to severe systemic disease
127
What is the evidence of DIC?
Prolonged aPTT with/without PT, thrombocytopenia (consumptive), increased D-dimers, evidence of shear injury
128
What are the differential diagnoses of thrombocytosis?
- Rebound post-haemorrhage
- Secondary to systemic inflammatory or neoplastic disease
- Bone marrow neoplasia or paraneoplastic production of thrombopoietin
129
An EDTA blood sample taken for pre-anaesthetic assessment from a healthy animal has been left on the windowsill in direct sunlight on a hot day in summer for 6 hours. What change is likely to occur in the sample?
Haemolysis
130
What is mean corpuscular haemoglobin concentration equal to?
MCHC = Hb/Haematocrit
131
Prolonged storage of an EDTA blood sample at high temperatures will cause haemolysis. How could you tell if the sample was haemolysed?
Increased MCHC (mean corpuscular haemoglobin concentration) reported on results from haematology analyser, as analyser will measure erythrocytes and free haemoglobin in the plasma due to haemolysis because MCHC = Hb/Haematocrit. A pink/red tinge to the plasma is also seen as the free haemoglobin from the lysed cells stains the plasma.
132
What haematological changes would you expect to see in each of the following parameters of an EDTA sample which was analysed 3 days after collection?
HCT increase due to swelling of RBCs over time resulting in artificially increased RBC volume and so increased haematocrit. MCV increase, as RBCs will swell which will increase their volume. MCHC will decrease as MCHC = Hb/HCT and HCT = RBC x MCV and HCT has increased, so MCHC will decrease.
133
What electrolyte is commonly observed in haemolysed samples?
Hyperkalaemia as intracellular potassium is released into the serum. Some species and breeds have high potassium RBCs – horses, camelids, pigs, primates, Akitas, other Asian dog breeds, Holstein cattle.
134
What are the causes of regenerative anaemia?
External haemorrhage
Haemolysis
Internal haemorrhage
Pyruvate kinase deficiency
RBC damage
135
How is a severe inflammatory response evidenced?
Presence of band/immature neutrophils at high numbers indicates that there is a marked demand for WBC
136
What are the possible causes of a stress leukogram?
Stress due to any chronic illness
Hyperadrenocorticism
Treatment of animals with glucocorticoids
137
How is acute haemorrhage managed?
- Local pressure, adhesives, bandages and tourniquets
- Abdominal wraps
- Hypovolaemia more critical than anaemia in acute blood loss – IVFT
- Blood transfusion to be considered if RBC loss is significant
138
In the management of acute haemorrhage, should oxygen be supplemented?
Of limited benefit as RBCs may have reached saturation. Methods of supplementing oxygen can be stressful so oxygen demand would increase. So priority is to reduce oxygen demand to the tissues in anaemic patients (and chronically haemorrhaging patients).
139
How should chronic haemorrhages be managed?
- Blood transfusion
- Treat the underlying cause and/or symptomatically
- It can lead to iron deficiency anaemias. Measure this and require oral or injectable supplementation
140
How should haemolysis immune mediated haemolytic anaemia be treated?
- Corticosteroids orally
- No evidence for routine gastroprotectant use
- Adjunctive therapy sometimes required
- Antithrombotic treatment
141
What should be monitored with haemolysis IMHA?
Myelosuppression
Hepatotoxicity
Secondary infections
142
How is Heinz body-associated haemolysis managed?
Remove underlying cause, with/without pRBC, O2, IVFT
143
How is hypophosphataemia-associated haemolysis managed?
Potassium phosphate CRI, treat underlying cause
144
How is blood transfusion haemolysis or neonatal isoerythrolysis managed in cats?
Stop transfusion, remove kittens for 1st 24 hours of life
145
How does the management of anaemia of inflammatory/chronic disease differ to iron deficiency anaemia?
Inflammatory/chronic disease – common, iron (Fe) limited erythropoiesis but body Fe stores normal. Treat underlying cause
Iron deficiency – chronic blood loss or insufficient iron in diet, can give iron. May require blood transfusion if severe
146
What general supportive care is needed for management of immune mediated thrombocytopenia?
- Small veins for blood samples only and avoid IM and SC injections
- Padded cage rest
- Oral medications
- Blood transfusion may be required if anaemic
147
What immunosuppressive treatment may be needed for immune mediated haemolytic anaemia/thrombocytopenia?
Vincristine increases numbers of platelets in the peripheral circulation
148
How is von Willebrand's disease managed?
- Normal numbers but with abnormal function
- Buccal mucosal bleeding time
- Cryoprecipitate treatment
- Desmopressin increases vWF for around 4 hours
149
How does secondary haemostasis due to rodenticide toxicity present haemoatologically?
Vitamin K if PTT increased or haemorrhage with/without plasma if actively haemorrhaging. In dogs, takes 48 hours for clotting times to increase as body uses up all clotting factors first until liver cannot produce more.
150
What is peripheral blood evaluation in horses?
Assess quantity of erythrocytes in circulation: RBC count, Hb, PCV. In the first few weeks of life, RBC count, Hb, PCV decrease rapidly.
151
What is Hb concentration in normal horses?
Hb concentration is a 1/3 PCV and increases with intravascular haemolysis
152
What are the erythrocyte morphologies in horses?
Anisocytosis
Acanthocytes
Rouleaux formation
153
What is anemia of chronic disease?
Not that there is insufficient iron but cannot process iron being eating
154
What is erythrocytosis or polycythaemia?
Increased blood viscosity – normal up to a point
155
What are the clinical signs of erythrocytosis/polycythaemia?
Tissue hypoxia
Thrombosis
Haemorrhage
Weakness
Lethargy
Exercise intolerance
156
What is relative erythrocytosis in horses?
- Splenic contraction – excitement/stress, recovers after a few hours
- Loss plasma volume without change in RBC numbers – dehydration, endotoxic shock
157
What is primary absolute erythrocytosis?
Rare myeloproliferative disorder
158
What is secondary absolute erythrocytosis?
Secondary, appropriate – response to tissue hypoxia, such as cardiac anomalies
Secondary, inappropriate – increased erythropoietin release without hypoxia, usually neoplasia
159
How does duration and blood loss severity affect clinical signs in equine anaemia?
- Can lose up to 1/3 (10-12l) blood volume
- Severe clinical signs at PCV 12-20%
160
What are the clinical signs of anaemia in horses?
Hypovolaemic shock - tachycardia, pale mucous membranes, weakness, oliguria
Acute haemorrhage – initially RBC parameters normal, hypoproteinaemia
161
How is haemorrhage treated in horses?
- Identify and stop source of bleeding
- Tranexamic/aminocaproic acid – unlikely to have in car
- Isotonic fluids or colloids
- Blood – care
- Oxyglobin – cost
- Not hypertonic saline – makes them bleed more
162
What does haemolysis in regenerative anaemia lead to in horses?
- Haemoglobinaemia – increased MCHC
- Haemoglobinuria
- Nephrotoxic
- Can lead to renal failure
163
How is IMHA diagnosed in horses?
- Decreased RBC count
- Spherocytosis
- Increased MCV
- Anisocytosis
- Increased total and indirect bilirubin
- Haemoglobinuria if intravascular haemolysis
- Autoagglutination – not rouleaux formation
- Coombs’ test
164
How is IMHA in horses treated?
- Identify underlying cause
- Discontinue previously administered drug
- Treat underlying disease
- If severe, blood transfusion
- If haemoglobinuria, IV fluids as risk nephropathy
- Corticosteroids
165
What are the clinical signs of equine infectious anaemia virus?
Fever
Lethargy
Anorexia
Thrombocytopaenia
166
What are the clinical signs of chronic infection of equine infectious anaemia virus?
Recurrent fever
Weight loss
Ventral oedema
Anaemia
Seropositive
167
What are the clinical signs of haematopoietic neoplasia in horses?
Depression
Weight loss
Fever
Oedema
Petechial haemorrhage
Anaemia
168
How is haematopoietic neoplasia diagnosed in horses?
Peripheral blood smear
Bone marrow aspirate
169
What are the clinical signs of lymphoid neoplasia in horses?
Weight loss
Fever
Ventral oedema
Paraneoplastic syndromes
170
How is equine lymphoid neoplasia diagnosed?
- Demonstration of neoplastic lymphocytes in affected tissue and biopsy mass
- Rectal biopsy
- Abdominoparacentesis
- Laparoscopy
- Laparotomy
171
What are the clinical signs of equine thrombocytopenia?
Abnormal primary haemostasis
Epistaxis
Petechial haemorrhage
172
In equine thrombocytopenia, what is increased and decreased platelet destruction indicative of?
Decreased platelet production – bone marrow suppression
Increased platelet destruction – immune-mediated thrombocytopaenia, equine infectious anaemia
173
What are the clinical signs of equine haemostatic disorders?
- Abnormalities of primary haemostasis
- Abnormalities of secondary haemostasis
- Spontaneous or excessive haemorrhage in response to surgery or trauma
174
How is equine haemostais diagnosed?
- Whole blood clotting time
- Platelet count (smear)
- Buccal mucosal bleeding
175
Which method of measuring clotting times is more reliable in horses?
APTT – measure of activity of factors XII, XI, X, IX, VIII and V, prothrombin, fibrinogen, more reliable than PTT
176
Name 3 conditions that increase the risk of thrombophlebitis in horses?
Sepsis
Endotoxaemia
DIC
177
What are the risks of thrombophlebitis in horses?
Bilateral thrombophlebitis
Endocarditis
178
How are blood transfusions done in emergency equine patients?
- No time to cross match
- Usually fine even to have multiple transfusions for the first 3-4 days
- Chances of an adverse reaction increase when either donors or recipients are mares that have been bred previously
179
How much blood is usually safe to remove from horses?
5-10 L
180
What is a major sign of how a horse is coping with acute blood loss?
Heart rate
