Anaemia Flashcards
(57 cards)
1
Q
What is anaemia?
A
- a decreased haematocrit (HCT/Hct)/ packed cell volume (PCV) or haemoglobin (Hb)
2
Q
What is haematocrit?
A
- A calculated value from the mean cell volume and red blood cell [RBC] count, and haemoglobin concentration, which are provided by automated analysers
- Hct can be affected by machine errors
- HCT = (MCV x RBC count) + 10
3
Q
What is PCV?
A
- A directly measured value measured as a percentage of packed red cells in blood volume
- PCV can be affected by how RBCs pack together
4
Q
Signs of anaemia
A
o Inadequateperfusion/oxygenation
– Pale mm
– Lethargy, exercise intolerance
o Compensatorymechanisms
– Tachypnoea, tachycardia
o Othersigns
– Poor pulse quality
– Haemic/Flow heart murmur
o Signs related to underlying pathology
o Splenomegaly, lymphadenopathy, pain, pica, icterus, melaena
5
Q
Where can you see apparent (non-pathological) anaemia?
A
- young animals
- anaesthesia
- over hydration
6
Q
Categorising Anaemia
A
- Severity
- RBC indices
- Regeneration?
- Other haematology clues
7
Q
Why is assessing severity of anaemia useful?
A
- Doesn’t necessarily relate to clinical condition (chronicity may do more so)
- Can be useful during diagnosis of cause, eg a severe anaemia would rarely be due to anaemia of chronic disease
8
Q
Grade of anaemia
A
None (reference interval):
- 41-58 (canine)
- 31-48 (feline)
Mild
- 30-40 (canine)
- 25-30 (feline)
Moderate
- 20-30 (canine)
- 15-25 (feline)
Severe
- <20 (canine)
- <15 (feline)
9
Q
RBC indices
A
Mean corpuscular volume (MCV):
- The average volume of the RBCs will change if large/small RBCs are present
Mean corpuscular haemoglobin concentration (MCHC):
- The amount of haemoglobin in RBCs will change dependent on absolute amount of Hb but also is affected
by cell volume
10
Q
Normocytic
A
- MCV within reference interval
11
Q
Microcytic
A
- small cells
- MCV below reference interval
12
Q
Hyperchromic
A
- more colour, darker in colour
- MCHC above ref interval
- usually a false increase (not a true in vivo finding), e.g. lipaemia can falsely increase the [haemoglobin] relative to HCT, therefore falsely increasing the MCHC
13
Q
Polychromatic
A
- many colours
- there’s variability of RBC colour
14
Q
Normochromic
A
- MCHC within ref interval
15
Q
Hypochromic
A
- lighter in colour
- less colour
- MCHC below ref interval
16
Q
Regeneration?
A
- i.e. are there cells that suggest the bone marrow is trying to correct the reduced RBC number?
- reticulocytes?
- Anisocytosis = variable size RBCs seen
17
Q
Non-specific RBC indicators common in regenerative anaemia
A
o Nucleated RBCs (nRBC)
o Basophilic stippling
o Howell-Jolly bodies.
o Heinz Bodies
18
Q
Cause of regenerative anaemia
A
- haemorrhage or haemolysis
19
Q
Causes of non-regenerative anaemia
A
- Decreased bone marrow production of RBCs
*Pre-regenerative anaemia. The bone marrow takes 3-5 days to respond to anaemia so acute conditions may initially appear non-regenerative.
*Chronic haemorrhage or haemolysis that was regenerative will eventually become non-regenerative.
20
Q
Other haematology clues of anaemia
A
Other weird RBCs?
What is the WBC count doing and what do they look like on a smear?
Thrombocytopaenia?
Cells you might see:
- acanthocytes (spur cells)
- echinocytes (burr cells)
- schistocytes
- spherocytes
21
Q
Acanthocytes - what do they look like? what can cause them?
A
- Irregular, blunt-tipped spicules;
- Liver disease (due to alterations in lipid metabolism);
- Fragmentation injury – clots/ DIC; fragile RBCs (eg iron deficiency)
22
Q
Echinocytes - what do they look like? what can cause them?
A
- Sharp or blunt projections, tend to be uniform and evenly-spaced.
- Artifact
- Drug exposure (eg frusemide, doxorubicin)
- Electrolyte disturbance (typically low IC K+)
- Renal disease, especially glomerulonephritis (unknown mechanism)
- Snake envenomation (form due to phospholipases in the venom)
23
Q
Schistocytes - what do they look like? what can cause them?
A
- RBC fragments
- Mechanical injury; often some level of vascular damage eg DIC, glomerulonephritis, vasculitis, PSS, vascular neoplasms (eg HSC)
24
Q
Spherocytes - what do they look like? what can cause them?
A
- Sphere shaped, no central pallor, smaller and more dense than a normal RBC
- Normal-ish volume (MCV is normal)
- Moderate to severe spherocytosis → IMHA
- Low-moderate numbers → can be other things
25
What are the main causes of anaemia?
o RBC loss
o RBC destruction
o Reduced RBC production by the bone marrow
26
Causes of RBC loss
haemorrhage due to trauma or coagulopathy:
* Internally eg GIT, parasites, pulmonary, abdominal cavity, etc
* Externally eg wounds, epistaxis
27
Causes of RBC destruction
Haemolysis
* Lots of causes
* eg Toxicity, infection, immune-mediated, mechanical damage
28
Causes of reduced RBC production by the bone marrow
* Genetic, immune-mediated, infectious chronic disease/inflammation,
nutritional deficiencies (iron-deficiency anaemia), myelodysplasia
29
Acute and severe causes of blood loss/ haemorrhage
- traumatic wounds
- blunt force (intracavitary bleeding)
- D+/V+ (haemorrhagic diarrhoea, haematemesis)
- epistaxis
- DIC
30
Mild and chronic causes of blood loss / haemorrhage
- melaena
- chronic or multiple small
wounds
- GI or blood-borne parasitism
31
Is all blood loss non-regenerative to start with?
- yes
32
Is an immediate drop in PCV seen with blood loss?
- no
- but acute and severe haemorrhage will be quicker
33
What may result if blood loss is very prolonged?
- iron deficiency
34
What is a common cause of haemolysis seen in clinical practice?
- IMHA
35
Causes of haemolysis
- IMHA
- Reaction to normal self antigen (Ag):
* Primary immune system dysfunction and loss of tolerance
* Antigen exposed due to cell damage
* Similarity between self Ag and foreign Ag (eg infectious agent or drug)
- Reaction to infectious agents bound to cell surface
- Reaction to non-biologic Ag bound to cell surface (eg drug, toxin)
36
CS of haemolysis
o Pyrexia, pallor/jaundice, CV abnormalities
37
Clinpath of haemolysis
o Spherocytes, leucocytosis, thrombocytopaenia, RBC parasites
38
Haemolysis diagnosis
- autoagglutination
- Coombes test (more sensitive)
39
Causes of non-regenerative anaemia
Intra-marrow – a problem within the bone marrow:
* Infection
* Chronic damage
* Neoplasia
* Lack of raw materials (iron deficiency)
Extra-marrow
* CKD, excessive oestrogen
* Some types of FeLV
40
Most common form of non-regenerative anaemia in small animal clinical practice? How do the cells appear?
- anaemia of inflammation (aka anaemia of chronic disease)
- associated with functional iron deficiency
- anaemia of inflammation is
usually normocytic and normochromic
41
When does absolute (true) iron deficiency occur? Why type of anaemia is it? How do the cells appear?
- most commonly because of chronic haemorrhage, and thus loss of iron-rich haemoglobin
- can be regenerative or nonregenerative
- classically microcytic hypochromic
42
Other disease processes associated with non-regenerative anaemia
o Chronic Renal Failure
- erythropoeitin production is reduced in advanced renal disease
o Neoplasia
- haemorrhage, haemolysis, and decreased or ineffective erythropoiesis
o Endocrinopathies
- Hypothyroidism, diabetes mellitus, hypoadrenocorticism
o Myelodysplastic syndrome
- Erythropoiesis is ineffective
o Liver Disease
– anaemia of inflammation, abnormal nutrient metabolism, or defective iron handling
- PSS dogs are often microcytic, even if they are not anaemic
o Infection of Erythropoietic Cells
- FeLV: can infect hematopoietic precursors → direct suppression of early-stage erythropoietic cells, anaemia of
inflammation, and immune-mediated haemolysis
o Toxic Insult to the Bone Marrow
– eg chemotherapy
o Space-Occupying Disease in the Bone Marrow
- Eg fibrosis and neoplasia
o Other nutritional deficiencies
- such as copper deficiency, folate deficiency, or cobalamin deficiency
43
Why are there more severe signs in acute anaemia vs chronic anaemia (of the same PCV)? What are these signs?
o Compensatory mechanisms in chronic disease compared to a sudden loss of
circulating volume/o2 carrying capacity in acute disease
o Hypovolaemia, trauma, pain, pyrexia
o Acute anaemia more likely to have CV signs
44
Signs of severe anaemia
- CV signs
- lethargy/weakness
45
How do we treat anaemia?
1.Triage and emergency treatment, investigation and stabilisation
2. Fluid therapy, blood product transfusion if needed
3. Treat (or limit the symptoms of) the specific disease
-- Haemorrhage
-- Haemolysis
-- Infectious diseases
-- Oxidative damage
-- Bone marrow (intra- and extra- marrow)
46
Emergency stabilisation
o Oxygen supplementation
o Temperature management
o Fluid therapy
o Analgesia
o Treat cause/concurrent conditions
* Confirm and characterise anaemia – PCV/TP and blood smear
* TFAST, radiographs, AUS
* Full biochemistry and haematology,
* Infectious disease screening eg 4DX (Ehrlichia, Anaplasma, HW, Babesia), or PCR. Blood smear.
o Emergency surgery may be warranted for eg bleeding haemangiosarcoma, splenic rupture, arterial bleeds
47
Blood products
- Whole blood
- pRBCs
- FFP/FP
- (platelets)
48
Haemorrhage - what to do?
* Diagnose (and if possible treat) coagulopathy
* Physically stop the bleeding if you are able to (external sources)
* Address internal causes, for example:
- GI diseases causing melaena, haemorrhagic D+ or haematemesis
-- Eg GI protectants, tumour resection, antibiosis
- Genitourinary disease causing urinary or reproductive losses – eg surgery for bladder neoplasia, treat UTi/ uroliths, trauma following parturition.
- Intracavitary bleeding
-- Address coagulopathy
-- Address neoplasia, eg surgery on splenic haemangiosarcoma
* Transfuse if necessary
49
Treating haemolysis
Use of immunosuppressive therapy
* Ensure no untreated infectious cause
* Glucocorticoids are 1st line for IMHA
Adjunct agents may be required if response is not favourable:
o Azathioprine
o Mycophenolate Mofetil o Ciclosporin
o Leflunomide
* Transfuse if necessary (may need multiple)
* Consider antithrombotic treatment
50
Infectious disease causing anaemia (via haemolysis) - Babesia: What is it? CS? Tx?
* Intracellular protozoon; transmitted by ticks; worldwide spread but not endemic here (yet)
* IV and EV haemolysis → pallor, jaundice,
* pyrexia, haemoglobinuria, CV compromise; weakness, inappetence
* Microscopy (false –ves) vs PCR
* Treatment:
- Imidocarb (unlicensed), Azythromycin, Doxycycline are all effective
- Supportive treatment including transfusion, liver support
- Should show clinical improvement in 1-2 days; treatment may result remission rather than a cure
Important note: the IMHA is secondary to an infectious cause, so DO NOT give steroids.
Parasite control in affected areas.
It takes at least 24 hours for transmission of Babesia organisms and so vigilant tick- checking is also valuable
A vaccine is available, though it is not licensed in the UK and in only partially effective
51
Causes of oxidative damage
o Heavy metals (Zinc, copper)
-- more common in farm animals, especially as sheep are most susceptible
o Alliums - onions, leeks, garlic
-- Japanese dog breeds and cats particularly
susceptible; Eating >0.5% of body weight
o Rape, kale and cabbages
o Drugs, main one in small animals is paracetamol (aka acetaminophen)
52
Clinpath of oxidative damage
- Oxidation of haem iron to form methaemoglobin
- Oxidation of haemoglobin to form Heinz bodies
53
Paracetamol toxicity - who is most affected? CS?
o Cats are especially susceptible; Dogs are more tolerant
o Clinical signs include methaemoglobinaemia and associated anaemia. Liver damage can also be extensive.
54
Paracetamol toxicity - tx/decontamination
* N-acetylcysteine (dogs and cats)
* Methionine - Use if acetylcysteine is not available
* Ascorbic Acid (cats): Reduces methaemoglobin to
haemoglobin – however
* Supportive care: Oxygen therapy; IVFT Blood
transfusion: Fresh frozen plasma or whole blood to manage coagulopathy resulting from hepatic necrosis; Vitamin K1 in acute hepatic necrosis; Antibiotic therapy in acute hepatic necrosis
55
Infectious disease causing anaemia (via haemolysis) - Ehrlichia: What is it? CS?
Rickettsial bacteria transmitted by ticks; inside macrophages and monocytes.
* Grumbling thrombocytopaenia
* hyperglobulinaemia
* Vague depression, fever, weight loss, poor appetite
* Enlargedlymphnodes
* Epistaxis, petechiae, ecchymoses
Acute phase → often recover but otherwise can progress to a chronic infection state
56
Chronic monocytic ehrlich (CME)
* Profound thrombocytopaenia
* Failure of bone marrow – non regenerative anaemia, other cytopaenias
* Emaciation
* Swelling of hindlegs and scrotum – PLN
* Thrombocytopaenia - >uveitis, neuro signs
* Hyperglobulinaemia - >glomerulonephritis
57
Ehrlichia tx
- Doxycycline or imidocarb (unlicensed) are both cheap and very effective
