CONTINUING EDUCATION I SMALL ANIMAL

Anaemia in dogs and cats (part 2)

In the second part of this article, RCVS recognised and European veterinary
specialist in small animal medicine, Polly Frowde MAVetMB DipECVIM MRCVS
examines the causes and management of regenerative anaemia
Regenerative anaemia is often acute in onset and causes
more marked clinical signs for a given drop in haematocrit
(Hct) compared to non-regenerative anaemia. However,
some forms of regenerative anaemia can be mild/insidious
(eg. low-grade haemolysis or gastrointestinal bleeding).
Confirmation of a regenerative response was discussed in
part 1. Regenerative anaemia is caused by either red blood
cell (RBC) destruction (haemolysis) or haemorrhage.

HAEMOLYSIS: IMMUNE-MEDIATED HAEMOLYTIC

ANAEMIA
Immune-mediated haemolytic anaemia (IMHA) is a common
cause of regenerative anaemia in dogs and can be primary
(idiopathic) or secondary to a variety of underlying diseases/
drug therapy. Definitive diagnosis requires fulfilment of the Figure 1: Spherocytes and reticulocytes. Photo: Roger Powell.
following criteria:
• Regenerative anaemia; jaundice, pigmenturia, hepatosplenomegaly and, less
• Evidence of haemolysis (eg. bilirubinaemia/bilirubinuria, commonly, petechiae, vomiting, diarrhoea, pica, pyrexia and
haemoglobinuria, spherocytosis); and lymphadenomegaly. The anaemia is usually regenerative
• Evidence of immune-mediated red blood cell (RBC) (macrocytic, hypochromic with polychromasia), although
destruction (eg. spherocytosis, in-saline agglutination, can be non-regenerative in peracute disease (ie. pre-
Coombs test positive, flow cytometry). regenerative) or non-regenerative IMHA (precursor
The pathogenesis involves a type II hypersensitivity destruction – discussed in part 1). Reticulocytosis can be
reaction targeting antibody-bound RBCs, leading to marked (more so than with haemorrhage, due to differences
direct complement-mediated haemolysis (intravascular in iron availability). Spherocytosis (see Figure 1) may be
haemolysis) or phagocytosis (extravascular haemolysis). difficult to appreciate (especially in cats) and can occasionally
Various mechanisms for auto-antibody formation have be seen in other types of anaemia, eg. pyruvate kinase
been proposed, eg. RBC damage-exposing antigens that (PK) deficiency. Auto-agglutination (which occurs with
have escaped immune tolerance; cross-reacting antibody intravascular or severe extravascular IMHA) confirms the
targeting foreign RBC-bound antigen (eg. mycoplasma); presence of anti-RBC Ab.
or non-specific lymphocyte activation during inflammation. Neutrophilia is common due to tissue hypoxia/necrosis
Anti-RBC IgG is more common than IgM but the latter is and cytokine induction – this can be dramatic with toxic
associated with intravascular haemolysis and greater disease changes/a left shift. Concurrent thrombocytopenia can
severity. occur due to co-existing ITP (‘Evans-like’ syndrome) or
Predisposed breeds include Cocker and Springer Spaniels, consumption, eg. thromboembolic disease, disseminated
Bichon Frise, Old English Sheepdogs, Poodles, Irish Setters intravascular coagulation ([DIC]; aPTT/PT and D-dimers can
and Dachshunds. Disease is more common in young, aid assessment). In cats, IMHA seems to be more insidious
middle-aged dogs and possibly neutered females (there and less inflammatory, with patients often only showing
may be minimal gender/neuter-status bias once breed/age clinical signs once anaemia is severe.
is taken into account). Secondary IMHA can be triggered Biochemistry can reveal hyperbilirubinaemia, especially with
by the following: infection (with specific pathogens or intravascular haemolysis or concurrent hepatic dysfunction/
any infectious focus, eg. abscess); neoplasia (especially hypoxia, however a healthy liver is very efficient at clearing
haematopoietic neoplasms); drug therapy; inflammation excess bilirubin so this may not be present. Hepatic hypoxia
or necrosis (especially in cats); or multi-systemic immune- secondary to anaemia is common, and liver enzymes
mediated disease eg. systemic lupus erythematosus (SLE). are therefore often mildly elevated. There may be other
Secondary IMHA is considered more common than consequences of inappetance/malaise and hypoxia,
primary disease in cats. An association with vaccination eg. azotaemia. Protein levels are usually normal (to help
remains controversial – many clinicians avoid repeating any differentiate from many forms of haemorrhage). Bilirubinuria
vaccinations given within one month of IMHA onset. can occur with intra or extravascular disease, whereas,
Clinical signs include: pallor, weakness, tachypnoea haemoglobinuria is an indicator of intravascular haemolysis
(hypoxia, pulmonary thromboembolism), anorexia, (and severe disease).

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ADDITIONAL LABORATORY TESTS

Coombs (direct antiglobulin test) is indicated if there is
insufficient evidence for immune-mediated RBC destruction,
(eg. in-saline auto-agglutination is negative). Recent
studies have challenged previous concerns regarding false
negative results with prior immunosuppressive therapy or
transfusions,1 however, false-positive results can occur, eg.
with neoplasia infection. Flow cytometry is sensitive/specific
at identifying anti-RBC antibody, but expense/availability
limits its clinical use in IMHA. Osmotic fragility tests are
occasionally used, but are also affected by hereditary RBC
disorders.
As soon as IMHA is suspected, the search should begin for
possible underlying triggers.

INFECTIOUS DISEASE SCREENING

Tick-borne disease testing should be indicated post-travel to
Figure 2: Zinc-gastric foreign body causing haemolytic
mainland Europe, eg. for babesia, ehrlichia and leishmania,
anaemia in a dog. Photo: Dr Nat Whitley.
depending on geographical exposure. An endemic profile
for non-travelled dogs should also be considered, especially poor perfusion. Rates of 1-2x maintenance are unlikely to
if tick exposure is likely. In the UK, this could include borrelia, dilute the PCV dramatically. Oxygen is not indicated unless
bartonella, anaplasma +/- ehrlichia and babesia, however, there is concurrent respiratory compromise (eg. pulmonary
a recent review of tick-borne diseases specific to Ireland thromboembolism [PTE], aspiration pneumonia) since
showed only evidence for borrelia in cats/dogs.2 It might still hypoxia is due to reduced oxygen content (RBC count),
be worthwhile screening for possible emerging diseases, rather than oxygen saturation (often already maximal).
especially if the patient is responding poorly to standard
therapy. Feline immunodeficiency virus (FIV)/feline leukaemia IMMUNOSUPPRESSIVE THERAPY
virus (FeLV) and mycoplasma screening should be performed Immunosuppressives are indicated in all 1° and some 2°
in cats. Since many pathogens are theoretically capable IMHA, however 2° IMHA may resolve with treatment of the
of triggering 2° IMHA, appropriate screening should be underlying disease alone (and immunosuppression may be
performed if clinical features raise suspicion for a specific detrimental, eg. infectious focus).
infection.
STEROIDS
DIAGNOSTIC IMAGING Steroids are the first drug of choice (unless contraindicated)
Thoracic radiographs and abdominal radiographs/ and there is insufficient data to compare their efficacy with
ultrasound are an essential part of the screening process any alternative agent monotherapy. Therapeutic actions
for potential secondary causes, (eg. inflammatory focus, include inhibition of RBC phagocytosis, giving them a
neoplasia), but also help rule out some non-immune rapid speed of onset (unlike certain cytotoxics that only
mediated causes of haemolysis, eg. zinc foreign body (see inhibit lymphocytes/antibody production). Prednisolone
Figure 2). Imaging should be performed before starting 1mg/kg bid is used initially in dogs (<2mg/kg bid in cats);
immunosuppressive treatment in case further sampling is there is no additional benefit to using higher doses, only a
required prior to steroids, or steroids are contraindicated/ greater incidence of side effects. Alternatively, parenteral
treatment needs to focus on the underlying disease. dexamethasone 0.2mg/kg sid can be given if anorexia or
vomiting prevents oral therapy, but switch to oral as soon as
TREATMENT possible.
Regardless of whether IMHA is primary or secondary (or even There is no evidence that co-administration of additional
confirmed), the first treatment decision is whether a blood immunosuppressives improves outcome, however, most
transfusion is indicated. This depends on clinical signs more would agree that they are indicated in IMHA refractory to
than lab values – the rate of decline in red cell mass will steroids alone (eg. after one week), or when ‘steroid-sparing’
influence the patient’s ability to compensate. Tachycardia, is necessary (ie. severe side effects). Steroids unfortunately
weakness, and decreased mentation attributable to anaemia contribute to the risk of thrombosis.
are definite indications; commonly adopted PCV thresholds
are <15-20% for acute IMHA (dogs) or <10-15% for chronic/ AZATHIOPRINE
NR-IMHA (or acute IMHA in cats), but clinical parameters Azathioprine is a purine synthesis inhibitor (inhibits
should be the main guide. Fluid therapy is indicated in lymphocytes), used in dogs only. Adverse effects include
most cases (unless eating, well hydrated, no azotaemia myelosuppression, hepatotoxicity and pancreatitis, making
and no suspicion of thromboembolic disease) since regular monitoring (haematology and biochemistry)
dehydration is common and exacerbates tissue hypoxia/ essential, since myelosuppression and hepatotoxicity are

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often picked up on blood tests prior to causing clinical signs.

Maximal efficacy may take less than weeks. The starting dose
(2mg/kg sid) is given for a maximum of six weeks before
dropping to 2mg/kg eod to reduce the risk of side effects.

CICLOSPORIN
Ciclosporin inhibits T-cell activity, macrophage function
and antibody production, theoretically giving it a faster
mechanism of action than azathioprine. The most common
side effects are transient vomiting and diarrhoea – often
managed with symptomatic treatment or temporary dose
reduction. The standard immunosuppressive dose is 5mg/
kg bid (NB higher than licensed atopy dose). Commercial
pharmacodynamic testing (available via Mississippi State Figure 3: Spontaneous echocontrast within the left ventricle
of a dog with primary IMHA: a hypercoagulable disease.
University) is more reliable for guiding efficacy/dose
adjustments than monitoring serum levels. Ciclosporin can management,4 however this remains controversial and
also be pro-thrombotic.3 larger studies are needed to assess safety and outcome.
Proposed candidates are those with significant extravascular
CYCLOPHOSPHAMIDE haemolysis, stable enough for anaesthesia and preferably
Cyclophosphamide has largely fallen out of favour – not yet on cytotoxic drugs.
studies have failed to show convincing efficacy, sometimes
suggesting a poorer prognosis with its use. As an alkylating LIPOSOMAL CLODRONATE
agent, its main action is to reduce antibody production Liposoma clodronat holds possible future potential (studies
(ie. delayed efficacy), and side effects are common underway) – the bisphosphonate may inhibit splenic
(myelosuppression, haemorrhagic cystitis, gastroenteritis). phagocytosis.

MYCOPHENOLATE MOFETIL ADJUNCTIVE TREATMENT

Mycophenolate mofetil is a purine synthesis inhibitor with Antacids are not essential in most cases – reserve for cases
fewer side effects than azathioprine (IV preparation available with additional ulcerogenic risk factors (eg. vomiting,
as well as oral and gastrointestinal [GI] side effects are gastritis) or perhaps with concurrent thrombocytopenia
common). (when GI haemorrhage could be catastrophic).
Anti-thrombotic therapy is recommended during acute
LEFLUNOMIDE haemolysis (when the risk of thromboembolic disease is
Leflunomide is a pyrimidine synthesis inhibitor (inhibits high (see Figure 3). Options include heparins and platelet
B and T cells). Side effects are rare (myelosuppression, inhibitors, but optimal protocols/dose rates remain
hepatotoxicity), but periodic monitoring is recommended. controversial.
Clopidogrel has been proven more effective than aspirin in
CHLORAMBUCIL cats with thromboembolic disease (18.75mg/cat po sid).5
Chlorambucil is the most popular adjunctive agent used Although we don’t have the same evidence for Clopidogrel
in feline IMHA. Side effects include anorexia, nausea in dogs (2-4mg/kg po sid), it is at least not ulcerogenic,
and (uncommonly) myelosuppression. Ciclosporin, whereas latest recommendations for optimum aspirin dosing
mycophenolate or leflunomide could also be considered in (1-2mg/kg sid) seem less confident of being risk-free with
cats. regards to increasing the risk of ulceration during concurrent
There is insufficient evidence to recommend one second steroid therapy. Heparins can be given by injection; low
agent over another. Selection is often based on personal molecular weight heparins (LMWHs) eg. Dalteparin (150iu/
preference, relative risk of side effects, perceived speed of kgscq eight hours) may be safer than unfractionated heparin,
action, availability for parenteral administration, cost and but drug monitoring is inconvenient (via ‘anti-Xa activity’).
patient size or convenient dosing. Oral direct factor-Xa inhibitors (eg. rivaroxaban) have
recently become available/affordable and may provide a
ALTERNATIVE THERAPIES more practical option for outpatients, although monitoring is
HUMAN INTRAVENOUS GAMMA GLOBULIN still advised.6
This inhibits macrophage Fc receptors. Current evidence for
efficacy is limited (improved haematological parameters but MONITORING/TAPERING
no clear survival benefit) but studies are ongoing. PCV/TP is monitored daily until >20% (dogs) or >15% (cats),
at which point patients can usually be discharged. A full
SPLENECTOMY haematology profile is then performed weekly until Hct near
Splenectomy is occasionally performed as a salvage normal (eg. >30%). Gradual drug tapering can then start with
option for idiopathic IMHA cases refractory to medical ongoing monitoring (reduced to repeat for two weeks) to

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ensure no relapse. Total treatment duration is usually at least and latent infection can recrudesce during times of stress/
three months. If on combination therapy, taper one drug at concurrent illness (eg. infection, trauma). Jaundice is
a time, starting with the drug perceived to be causing more uncommon, but other clinical signs of haemolytic anaemia
side effects (usually steroids). Prednisolone is tapered by 25- may be accompanied by cyclic fever.
33% every 10-14 days until on a maintenance dose (0.5mg/ Although infection can sometimes be diagnosed on a fresh
kg eod for four weeks). Any second agent is continued blood smear, PCR is more sensitive.
unchanged until on the maintenance steroid dose, then However, a positive result does not guarantee that
either this or the steroids stopped, with all therapy ceasing mycoplasma is the current cause of anaemia (subclinical
another two to four weeks later. Azathioprine is an exception carriers exist) – although always warrants treating in an
– as discussed previously. anaemic cat.9 Doxcycline (10mg/kg sid) is the treatment of
Regardless of drugs used, prolonged immunosuppression choice and usually resolves disease, although may not clear
can predispose to opportunistic infection. In people, infection (chances are increased with prolonged therapy less
there is an increased risk of neoplasia with chronic than eight weeks).
immunosuppression – probably related to the degree of Secondary IMHA is sometimes suspected, but often resolves
immunosuppression rather than any particular drug. with antibiotics alone – steroids are best reserved for cases
with refractory signs of IMHA despite antibiotics.
PROGNOSIS
Reported mortality rates have ranged between 20- OXIDATIVE DAMAGE
70% (probably nearer to 30% with current standards of Common causes of oxidative RBC damage include: onion,
care), with the first two weeks carrying the highest risk of garlic, propylene glycol, zinc, copper, cyanide, napthalene
death. Thromboembolic disease (especially pulmonary (mothballs), paracetamol and occasionally, (in cats), diabetes
thromboembolism) is a significant contributor. IMHA relapse mellitus, hyperthyroidism, lymphoma, lipidosis.
can occur both during and after treatment but is most Oxidative damage (OD) can manifest as
common in the first few weeks and usually necessitates a methaemoglobinaemia and/or oxidative haemolytic
return to initial immunosuppressive doses. anaemia.
Any potential trigger factors should be avoided (eg. Haemoglobin is oxidised from Fe2+ to Fe3+ forming
medications +/- vaccinations). Negative prognostic factors methaemoglobin, which cannot bind oxygen. OD also
include hyperbilirubinaemia, concurrent thrombocytopenia, causes haemoglobin aggregation/direct RBC membrane
prolonged clotting times, intravascular haemolysis or a left damage, forming Heinz bodies (see Figure 4) and
shift.7,8 eccentrocytes. This makes RBCs more fragile, resulting in
predominantly extravascular/splenic destruction.
HAEMOLYSIS: NON-IMMUNE-MEDIATED Altered RBC conformation occasionally triggers 2° IMHA.
INFECTION Clinical signs of methaemoglobinaemia include cyanosis/
BABESIA muddy membranes, lethargy, dyspnoea.
Babesia canis is transmitted by the tick species Dermacentor Heinz body/eccentrocyte induced haemolysis presents
(present in much of Europe, spreading north) and similarly to IMHA but usually without immune-mediated
Rhipicephalus (Mediterranean). There are also reports of features, ie. agglutination, spherocytes.
direct transmission (eg. blood transfusions +/- fighting dogs). Most in-house analysers of oxygen saturation/content
Immunosuppressed dogs (including splenectomised) cannot detect reductions due to methaemoglobinaemia
are more susceptible to infection. Babesia causes direct – external analysis is required. Paracetamol poisoning
haemolysis of infected RBCs (and may also trigger 2’ IMHA)
+/- thrombocytopenia.
Diagnosis can be confirmed on a direct smear (more
sensitive if collected from a peripheral, eg. ear vein); or with
PCR (PCR/RLB). Anti-protozoal drugs, eg. imidocarb are
the main treatment (+/- blood transfusions), with alternative
drugs (atovaquone + azithromycin) being necessary for some
smaller species, (eg. gibsoni) due to imidocarb resistance.
Immunosuppression is generally advised against for
European babesia species (or only used with great care if
no response to initial therapy). Tick repellents are the main
means of prevention.

MYCOPLASMA HAEMOFELIS
Mycoplasma is transmitted between cats via indirect (fleas
are implicated) and direct mechanisms (eg. fighting and
blood transfusions).
Disease predominantly involves extravascular haemolysis, Figure 4: Heinz Bodies due to oxidative RBC damage in a cat.
Photo: Roger Powell.

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manifests as methaemoglobinaemia within hours, and to 2° complications). PK deficiency in cats (documented

haemolytic anaemia within days (+/- hepatic necrosis) – cats in several pedigree breeds) tends to cause milder (often
are particularly susceptible to haematologic toxicity. asymptomatic) anaemia and may improve with splenectomy
Treatment is supportive (blood transfusions, antioxidants if treatment is indicated.
eg. SAMe +/- methylene blue or vitamin C for
methaemoglobinaemia), with some toxins warranting MICROANGIOPATHIC ANAEMIA
specific management, eg. N-acetylcysteine (paracetamol), Seen with mechanical RBC trauma, eg. due to DIC, splenic
foreign body removal (zinc). disease (including torsion), vascular neoplasms, vasculitis,
heartworm and typically accompanied by signs of RBC shear
HYPOPHOSPHATAEMIA injury, eg. schistocytes.
Significant hypophosphataemia (<0.8mmol/l) can cause
haemolysis via increased RBC fragility and susceptibility ENVENOMATION
to Heinz bodies. It is most commonly seen with re- Direct haemolysis can result from certain venom toxins, most
feeding syndrome, treatment of DKA or excessive use of commonly those produced by exotic snake/spider species.
phosphate binders. Signs of anaemia may be accompanied There have been occasional reports of haemolytic anaemia
by muscle weakness. Supplementation needs to be in dogs after bee stings, usually with a 2° immune-mediated
carefully titrated with close electrolyte monitoring to avoid component and spherocytosis.
hyperphosphataemia or hypocalcaemia.
HAEMOPHAGOCYTIC SYNDROME
HEREDITARY HAEMOLYTIC ANAEMIAS This benign proliferative disorder of macrophages causes
Inherited membrane defects are more common in cats, eg. bone marrow invasion (+/- liver, spleen) and phagocytosis
osmotic fragility – reported in Abyssinian, Somali, Siamese of haematopoietic cells, causing at least two cytopenias.
and even Domestic Short Hair cats.10 Disease is often Disease can primary (rare), or occurs secondary to immune-
associated with hyperglobulinaemia and splenomegaly mediated disease, infection or neoplasia (especially
and diagnosis is confirmed by osmotic fragility testing. histiocytic disease). The prognosis is poor unless there is
Transient improvement may be seen with steroids, however treatable underlying disease, eg. infection.
splenectomy seems to achieve better long-term disease
control (but not cure). Hereditary spherocytosis has been
documented in Golden Retrievers and appears to be
associated with osmotic fragility. Stomatocytosis is seen in
Alaskan Malamutes, Miniature Schnauzers and can cause
mild, regenerative anaemia.

AUTSOMAL RECESSIVE ENZYME DEFECTS

Phosphofructokinase deficiency causes RBCs to become
fragile in an alkaline environment (via reduced ATP/2-3,
DPG). Haemolysis is therefore most commonly seen with
alkalaemia (eg. respiratory alkalosis due to hyperventilation
during barking/exercise) and may be accompanied by a
myopathy (muscle weakness/cramps due to PFK deficiency in
muscle). Affected breeds include Springer Spaniels, Cockers.
The anaemia is often mild but regenerative (PCV may even
be normal, but with a reticulocytosis maintaining it so) and
accompanied by haemoglobinuria, hyperbilirubinaemia and
elevated creatine kinase (CK). Genetic testing is available
for certain breeds and a more convenient diagnostic tool
than trying to arrange specific enzyme testing. Management
focuses on avoiding triggers, eg. heat, exercise. Prognosis is
good.
Pyruvate kinase deficiency causes more severe disease –
moderate to severe regenerative anaemia and eventually
myelofibrosis/osteosclerosis and liver disease due to chronic
erythropoietic stimulation and iron absorption. Affected
breeds include Basenjis, Beagles, Dachshunds, Miniature
Poodles, Springer Spaniels and West Highland White Terrier
(WHWTs) – genetic testing available in some breeds; specific
enzyme testing required in others). There is no specific
treatment and prognosis is guarded (survival <5 years due

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HAEMORRHAGE drive for regeneration). Specialist advice/referral should be

Although anaemia due to blood loss is often easily considered in challenging cases.
diagnosed, some forms of haemorrhage may be more
occult. Gastrointestinal bleeding is not always accompanied REFERENCES
by elevated urea or overt melaena (faecal occult blood 1. Caviezel LL, Raj K, Giger U. Comparison of 4 direct
tests can be useful). Chronic haematuria can sometimes Coombs' test methods with polyclonal antiglobulins in
cause significant anaemia (eg. idiopathic renal haematuria). anemic and nonanemic dogs for in-clinic or laboratory
Spontaneous thymic haemorrhage occasionally occurs in use. J Vet Intern Med 2014; 28(2): 583-591
young dogs, causing acute anaemia/hypovolaemia as well 2. Zintl A, Moutailler S, Stuart P et al. Ticks and tick-borne
as respiratory signs. Retroperitoneal or deep intramuscular diseases in Ireland. Ir Vet J 2017; 70: 4
haemorrhage can escape initial examination/survey imaging. 3. Thomason J, Lunsford K, Stokes J et al. The effects of
As with haemolysis, the regenerative response may lag cyclosporine on platelet function and cyclooxygenase
behind acute haemorrhage, ie. the anaemia can be ‘pre- expression in normal dogs. J Vet Intern Med 2012; 26(6):
regenerative’. The true extent of anaemia may only be 1389-1401
apparent once intra and extravascular fluids have re- 4. Horgan JE, Roberts BK, Schermerhorn T. Splenectomy
equilibriated (do not be falsely reassured by a normal or as an adjunctive treatment for dogs with immune-
even elevated PCV (splenic contraction) in the face of acute mediated hemolytic anemia: ten cases (2003-2006). J Vet
haemorrhage, especially if cardiovascular parameters Emerg Crit Care 2009; 19(3): 254-261
suggest hypovolaemia). Hypoproteinaemia is supportive of 5. Hogan DF, Fox PR, Jacob K et al. Secondary prevention
blood loss but not always present (eg. internal bleeding). of cardiogenic arterial thromboembolism in the cat: The
Chronic occult haemorrhage may progress to iron deficiency double-blind, randomized, positive-controlled feline
and eventually poor regeneration. arterial thromboembolism; clopidogrel vs. aspirin trial
Haemorrhage into body cavities can be diagnosed via (FAT CAT). J Vet Cardiol 2015; 17: Suppl 1: S306-S317
centesis (if safe to do so/clotting function normal) and fluid 6. Yang VK, Cunningham SM, Rush JE et al. The use
PCV/TP analysis – the PCV is less than or equal to that of a of rivaroxaban for the treatment of thrombotic
venous blood sample with acute haemorrhage, but may be complications in four dogs. J Vet Emerg Crit Care 2016;
greater with chronic haemorrhage (due to re-absorption of 26(5): 729-736
plasma), or accidental splenic aspiration (in which case the 7. Piek CJ, Junius G, Dekker A et al. Idiopathic immune-
sample will clot). Haemophagocytosis also points towards mediated hemolytic anemia: treatment outcome and
chronicity in haemorrhagic effusions. prognostic factors in 149 dogs. J Vet Intern Med 2008;
Decisions about blood transfusions are based on estimations 22(2): 366-373
of blood volume lost (if known); failure to improve after 8. Weinkle TK, Center SA, Randolph JF et al. Evaluation
appropriate shock management with crystalloids/colloids; or of prognostic factors, survival rates, and treatment
follow-up PCV/TP monitoring. Most clinicians consider any protocols for immune-mediated hemolytic anemia in
acute, hypovolaemic drop in Hct to <20-25% in dogs, <15- dogs: 151 cases (1993–2002). J Am Vet Med Assoc 2005;
20% in cats as an indication to transfuse. 226(11): 1869-1880
9. Ishak AM, Radecki S, Lappin MR. Prevalence of
CONCLUSION Mycoplasma haemofelis, 'Candidatus Mycoplasma
We have approached anaemia in a systematic, logical way, haemominutum', Bartonella species, Ehrlichia species,
however some cases will not fit neatly into a particular and Anaplasma phagocytophilum DNA in the blood of
category and can pose a diagnostic challenge. For example, cats with anemia. J Feline Med Surg 2007; 9(1): 1-7
immune-mediated disease that apparently targets peripheral 10. Tritschler C, Mizukami K, Raj K, Giger U. Increased
and marrow cells simultaneously; or poorly regenerative erythrocytic osmotic fragility in anemic domestic
‘acute’ anaemia requiring urgent transfusion therapy shorthair and purebred cats. J Feline Med Surg 2016;
before allowing an opportunity to reassess reticulocyte 18(6): 462-470
response (following which there may not be the same

READER QUESTIONS AND ANSWERS

TRUE OR FALSE?
1. PYRUVATE KINASE DEFICIENCY CARRIES A GOOD PROGNOSIS IN BOTH DOGS AND CATS.
2. A POSITIVE MYCOPLASMA PCR RESULT IN AN ANAEMIC CAT CONFIRMS THIS AS THE CAUSE OF THE ANAEMIA.
3. FLUID THERAPY (EG. MAINTENANCE RATE CRYSTALLOIDS) IS FREQUENTLY INDICATED IN CASES OF IMHA, UNLIKE OXYGEN
THERAPY.
4. THROMBOEMBOLIC DISEASE IS ONE OF THE MAIN CONTRIBUTORS TO MORTALITY IN CANINE IMHA.
5. UREA ELEVATION IS A VERY SENSITIVE MARKER OF
1.FALSE 2. FALSE 3. TRUE 4. TRUE 5. FALSE
GASTROINTESTINAL HAEMORRHAGE.

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