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SMALL ANIMAL > 4.3.4: Anaemia - diagnosis and management > Flashcards

4.3.4: Anaemia - diagnosis and management Flashcards

1
Q

Reticulocytes present in significant numbers on an anaemic dog’s blood smear are indicative of what process?
a) acute, severe haemorrhage
b) bone marrow disorder
c) regenerative anaemia
d) red blood cell fragmentation, destruction or damage
e) oxidative damage e.g. due to paracetamol toxicity

A

c) regenerative anaemia

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2
Q

What would be the an appropriate initial treatment protocol for a 3 y.o. cat who presents clinically stable with pyrexia 39.6C, PCV 18%, positive saline agglutination and smear as below?
a) blood transfusion with packed RBCs
b) immunosuppressive doses of glucocorticoids
c) doxycycline
d) N-acetylcysteine
e) Vitamin K injections

A

c) doxycycline
The parasite shown is Mycoplasma haemofelis

Glucocorticoids would not be appropriate in pyrexic animal - MUST rule out infection before giving these!

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3
Q

Which of the following sets of lab findings would be most consistent with an acutely bleeding splenic haemangiosarcoma?
a) PCV 25%, numerous schistocytes and acanthocytes
b) PCV 30%, polychromasia and many reticulocytes
c) PCV 5%, thrombocytopaenia and autoagglutination
d) PCV 15% with numerous spherocytes
e) PCV 12% with numerous Heinz bodies in the red blood cells

A

a) PCV 25%, numerous schistocytes and acanthocytes
* Suggests neoplasia

b) PCV 30%, polychromasia and many reticulocytes
* Suggests regenerative anaemia

c) PCV 5%, thrombocytopaenia and autoagglutination
* Suggests bleeding

d) PCV 15% with numerous spherocytes
* Suggests IMHA

e) PCV 12% with numerous Heinz bodies in the red blood cells
* Usually associated with toxic change

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4
Q

You are presented with a 5 y.o. Lab with anaemia, PCV 21%. You perform a smear, shown below. What do you suspect is the cause of anaemia in this dog?
a) Rodenticide toxicity
b) Thrombocytopaenia
c) Von Willebrand’s disease
d) IMHA
e) Babesia canis infection

A

d) IMHA

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5
Q

Emergency stabilisation of the anaemic animal

A
  • Oxygen supplementation
  • Temperature management
  • Fluid therapy e.g. IV fluids, blood transfusion as indicated
  • Analgesia in the event of trauma
  • Investigation of and specific therapy for root cause/ concurrent conditions e.g. PCV + blood smear, TFAST, rads, abdo US, biochem and haematology, infectious disease screen
  • Emergency surgery if warranted e.g. for bleeding haemangiosarcoma, splenic rupture, arterial bleeds
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6
Q

How should you deliver fluid replacement therapy in the acute patient?

A
  • Inadequate circulating volume will kill the patient first -> replacement of fluid volume with isotonic fluid is often more important than correction of oxygen carrying capacity
  • Fluid replacement should be carried out in a response-driven manner i.e. 5-10ml/kg at a time, assess cardiovascular parameters, and judge if repeat needed
  • Beyond the peracute phase, moderate to severe anaemia -> need to rectify oxygen-carrying capacity with blood products
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7
Q

What cardiovascular parameters can you assess to see if your patient needs more fluids?

A
  • Heart rate
  • Pulse quality
  • CRT
  • Blood pressure
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8
Q

Fresh whole blood

A
  • Collected and administered within 8 hrs
  • Contains all blood components including platelets and clotting factors
  • Generally used for acute blood loss/ active bleeding
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9
Q

Stored whole blood

A
  • Stored (<4C) and used >8hrs later
  • No platelets and less clotting factors (factors V, VIII and vWF are unstable and will be gone)
  • Generally used for acute blood loss/ bleeding
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10
Q

Packed RBCs (pRBCS)

A
  • RBCs in nutrient solution
  • No platelets or clotting factors
  • Stored for 1-2 months
  • Good for anaemic animals that have low tissue oxygenation
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11
Q

Fresh frozen plasma (FFP)

A
  • Collected, processed and stored within 24hrs
  • Can be stored ~1 yr
  • Contains all clotting factors
  • Good for use in coagulopathies
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12
Q

Frozen plasma (FP)

A
  • i.e. not fresh
  • Frozen >24hrs after collection OR is FFP stored for >1 yr
  • Will not store labile clotting factors
  • Good for use in coagulopathies that require non-labile clotting factors
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13
Q

True/false: platelets are available as a product in the UK.

A

False.
Not currently available in the UK.

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14
Q

How is Mycoplasma haemofelis transmitted?

A

Mycoplasma haemofelis: worldwide, blood-borne pathogen that affects RBCs.
* Transmission is by fleas and ticks, and vertically
* Disease process is waxing and waning
* Carrier states exist and may be very critical to transmission and life cycle

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15
Q

Clinical signs of Mycoplasma haemofelis

A

May be asymptomatic, or may be severely anaemic, jaundiced animals
* Young animals/ immunosuppressed animals are more prone to severe disease
* Pyrexia
* Lethargy
* Anorexia
* Weight loss
* Pale mm
* Jaundice

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16
Q

Diagnosis of Mycoplasma haemofelis

A
  • Blood smear: Romanowski stain or acridine orange
  • PCR is more sensitive
  • Sample when sick and before beginning treatment to minimise chance of false -ves (possible due to carrier state/waxing and waning disease process)
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17
Q

Treatment of Mycoplasma haemofelis

A
  • First line: doxycycline 10mg/kg SID for 2-8 weeks
  • Second line: enrofloxacin 5mg/kg
  • Use repeat PCR to assess carrier state
  • We aim to achieve clinical cure rather than remission; consider multi-cat household/ cattery implications
  • Supportive treatment: blood transfusion may be necessary in severe cases
18
Q

Side effects of doxycyline in cats

A

Oesophageal stricture

19
Q

Side effects of enrofloxacin in cats

A
  • Retinal degeneration and blindness
20
Q
A

Mycoplasma haemofelis

21
Q

What is Babesia canis and how is it transmitted?

A
  • = intracellular protozoan
  • Transmission by ticks
  • Epidemiology: widely spread across world, endemic in much of Europe, seen in sporadic cases in UK esp dogs from Europe
  • Non-travelled UK dogs have contracted disease via Dermacentor reticulatus ticks
22
Q

What is the incubation period of Babesia and what type of haemolysis does it result in?

A
  • Incubation period: 10-21 days
  • Results in intravascular and extravascular haemolysis
23
Q

Clinical signs of Babesia

A
  • Typical of haemolytic anaemias: pallor, icterus, cardiovascular signs, haemoglobinuria
  • Some cases have concurrent thrombocytopaenia - mechanism not fully understood
  • Pyrexia
  • Weakness
  • Inappetence
24
Q

Diagnosis of Babesia

A
  • Micoscopy very useful but may give false -ves
  • PCR/ real-time PCR = much more sensitive
  • Can sometimes be suspected by travel history + haemoglobinuria + IMHA (often + elevated liver enzymes + hyperbilirubinaemia)
25
Q

Treatment of Babesia

A
  • Doxycycline
  • Supportive treatment: transfusion, liver support
  • Should should clinical improvement in 1-2 days
  • Treatment may result in remission rather than cure
26
Q

True/false: glucocorticoids are an acceptable first line treatment for the acute patient presenting with IMHA.

A

False!!!
You must rule out an infectious cause before proceeding with immunosuppressive doses of glucocorticoids.

27
Q

Control of Babesia

A
  • Parasite control in affected areas is critical -> control of ticks
  • It takes at least 24hrs for transmission of Babesia organisms so vigilant tick-checking is also valuable
  • A vaccine is available but not licensed in the UK and only partially effective
28
Q
A

Babesia

29
Q

How can oxidative damage affect RBCs?

A
  • Oxidation of haem iron to form methaemoglobin
  • Oxidation of haemoglobin to form Heinz bodies
30
Q

Examples of substances that may cause oxidative damage to RBCs

A
  • Heavy metals e.g. zinc, copper
  • Alliums e.g. onions, leeks, garlic
  • Rape, kale, cabbages
  • Drugs e.g. paracetamol (acetaminophen)
31
Q

Clinical signs of paracetamol toxicosis and toxic dose for different species

A
  • Cats - highly susceptible - toxic dose 10-40mg/kg - NEVER GIVE PARACETAMOL TO CATS
  • Dogs - more tolerant - toxic dose >100mg/kg
  • Clinical signs: methaemoglobinaemia, associated anaemia, liver damage may be extensive
32
Q

Treatment of oxidative damage

A
  • Immediate removal of oxidative agent: emesis, gastric lavage if <4hrs since ingestion, charcoal, supportive care e.g. IVFT
  • Antioxidants e.g. SAMe in feline paracetamol toxicity, N-acetylcystiene
  • Other supportive care: oxygen therapy, blood transfusion if required, FFP or whole blood to manage coagulopathy arising from hepatic necrosis, vitamin K1 in acute hepatic necrosis etc.
33
Q

Condition? Treatment?

A

Iron deficiency anaemia
* Long term treatment with supplemental iron to “restock” the bone marrow
* Address the cause of the chronic blood loss that led to this

34
Q
A

Ehrlichia (a.k.a. anaplasmosis)
* Group of rickettsial bacteria most commonly transmitted by Rhiphicephalus ticks
* Live inside monocytes and macrophages
* Widespread across world
* UK cases are sporadic and due to dogs who have travelled through S. Europe

35
Q

Clinical signs of Ehrlichia

A
  • Grumbling thrombocytopaenia
  • Hyperglobulinaemia
  • Vague depression, fever, weight loss, poor appetite
  • Enlarged LNs
  • Epistaxis, petechiae, ecchymoses
    If animals are diagnosed and treated in the acute phase, they will often recover. If not, can progress to a chronic infection state.
36
Q

Diagnosis of Ehrlichia

A
  • Direct microscopy may show classic lesions - morulae within macrophages
  • Antibody detection is useful in chronc cases, not acute
  • Antigen PCR from blood, splenic aspirate = more sensitive
  • 4DX (infectious disease screen) is readily avaulable and tests for Ehrlichia canis and ewingii, Dirofilaria immitis and Lyme disease
  • Always check for co-infection with Babesia spp as this is not uncommon
37
Q

Treatment and prevention of Ehrlichia

A
  • Doxycyline is cheap and effective; long term treatment protocol may be required for complete resolution
  • If there is a significant immune-mediated component then corticosteroids may be considered
  • Chronic monocytic ehrlichia (chronic form) carries a poorer prognosis, particularly once the bone marrow fails
  • Prevention = tick control
38
Q

True/false: both Cushing’s and hypothyroidism can result in anaemia of chronic disease.

A

True
The mechanism is uncertain.
Anaemia of chronic disease is often mild and non-regenerative.

39
Q

How does anaemia develop associated with Chronic Kidney Disease?

A
  • Anaemia associated with CKD is not uncommon
  • Develops due to reduced EPO production
  • Important to also check for simultaneous sources of blood loss e.g. GI ulcers due to uraemia
40
Q

What is the most common causes of oestrogen-induced bone marrow suppression and which species is this seen in?

A
  • Most commonly seen in ferrets with persistent oestrus
  • Ferrets are induced ovulators and unless mated/ stimulated to ovulate, oestrus will continue
  • Oestrus lasting over 1 month -> associated with hyperoestrogenism
  • High levels of oestrogen depress the bone marrow and cause hypoplasia of all cell lines
  • We may see this condition in dogs and cats e.g. use of oestrogen injection for misalliance in bitches, or presence of oestrogen-secreting tumours

SMALL ANIMAL (90 decks)

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