A 2-year-old male Springer Spaniel presented with a 3-month history of intermittent, unilateral epistaxis and occasional cough that had not responded to previous treatments. Clinical examination revealed pale mucous membranes, tachycardia, and a small amount of blood in the right nostril. Diagnostic testing showed a regenerative mild anemia, mild thrombocytopenia, and strong positive results for Angiostrongylus vasorum on antigen testing and fecal examination. Fresh frozen plasma was administered and anthelmintic treatment was started. The epistaxis resolved within 24 hours and hematological parameters normalized over 2 weeks, confirming angiostrongylosis as the cause of the bleeding disorder and clinical signs

1. Signalment:
2-year-old, male-entire, Springer spaniel
Clinical history:
Presented with a three-month history of worsening, intermittent, unilateral (right-sided) epistaxis and
occasional cough. Concurrently, poor coat quality, particularly caudally.
They were up to date with vaccinations, given Advantix (imidacloprid / permethrin) intermittently, and
given a supermarket wormer intermittently. No history of travel outside of southern Wales.
No improvement following treatment with antimicrobials or non-steroidal anti-inflammatory
medication.
Recent blood analysis revealed a strongly regenerative mild anaemia (haematocrit 35%) and a mild
thrombocytopenia. Serum biochemistry was unremarkable.
QUESTION 1: What are your problems?
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Case example 2B
Physical examination:
Extremely bright and in good body condition. A small amount of clotted blood was visible at the entrance to the right nares.
Mucous membranes were pale pink and no petechiations were visible. Heart rate was increased (160/min) with slightly bounding pulses.
Rectal temperature was borderline increased (39.2°C).

2. QUESTION 1: What are your problems?
ANSWER:
• Major concerns
o 3-month history of intermittent, unilateral epistaxis that was progressive and had not responded to
antimicrobial / anti-inflammatory medication
• Minor concerns
o Strongly-regenerative mild anaemia
o Mild thrombocytopenia
o Pale mucous membranes
o Tachycardia on physical exam
o Occasional cough over the same time frame
o Poor coat
o Borderline hyperthermia
QUESTION 2: What are your differentials?
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3. QUESTION 2: What are your differentials?
ANSWER:
• Epistaxis
o Structural disorder – infection (fungal rhinitis / aspergillosis); neoplasia; inflammation (chronic rhinitis); dental
disease; others
o Haematological disorder – coagulopathy (angiostrongylosis; rodenticide toxicity; haemophilia)
o Vascular disorder – hypertension
Notes: The major concern is a 3-month history of intermittent, unilateral epistaxis that was progressive and had not
responded to antimicrobial / anti-inflammatory medication
• It is chronic – ruling out trauma; this also makes rodenticide toxicity less likely, as they would have to be repeatedly
ingesting it!
• Coagulopathy due to hyperviscosity (hyperglobulinaemia-related) has been ruled out with the unremarkable serum
biochemistry
• It is unilateral and progressive – making a localised structural problem more likely
• It did not respond to empirical treatment – but most of the differentials would not have responded to this treatment
anyway
• The discharge was purely blood making most inflammatory conditions less likely – but due to its destructive nature
fungal rhinitis can do this
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4. … continued… QUESTION 2: What are your differentials?
Whilst, we tend to focus on the major problems, considering the minor issues can sometimes raise the suspicions of differentials for the major
problem. It also highlights areas we might want to assess before proceeding to more invasive procedures.
• Strongly-regenerative mild anaemia
o Blood loss
o (very well compensated) immune-mediated haemolysis
• Mild thrombocytopenia
o Consumption – blood loss; disseminated intravascular coagulopathy
o Immune-mediated destruction
o Production issue
• Pale mucous membranes
o Anaemia – blood loss; red cell destruction
o Reduced peripheral perfusion – adrenaline response (stress); hypovolaemia (blood loss); reduced cardiac output
• Cough
o Post-nasal drip
o Disease somewhere else in the respiratory tract e.g. tracheobronchial (infectious; inflammatory), pulmonary (leading to fluid in the
airways e.g. angiostrongylosis)
• Poor coat
o Systemic disease – chronic inflammatory disease; poor nutrition; endocrinopathy
• Hyperthermia
o Physiological – stress of travel
o Pathological – systemic inflammation
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5. … continued… QUESTION 2: What are your differentials?
Notes: The strongly regenerative mild anaemia is likely related to chronic blood loss from the epistaxis. The regenerative response
rules out non-regenerative causes of anaemia and with immune-mediated haemolysis the anaemia is typically severe. But would you
expect an otherwise fit young dog to be pale and have tachycardia with an haematocrit of 35%?
Chronic haemorrhage is a potent stimulator of platelet production, as compared to following acute haemorrhage consumption of
platelets may reduce their numbers. Therefore, the presence of mild thrombocytopenia is suspicious, but could potentially be
explained by an acute on chronic episode. In immune-mediated conditions a lower value (often absolute thrombocytopenia) might be
expected. Spontaneous haemorrhage is not seen until platelets drop below 40-50 x109/L and, even then, large bleeds are not
expected but petechiation would.
The pale mucous membranes and tachycardia could be due to progression of the anaemia, hypovolaemia or another cause of
adrenaline release. Blood loss via another route was not reported, but cannot be ruled out.
The occasional cough could be i) as a result of nasal disease (post-nasal drip), ii) the same disease process as in nose now in the lungs
(infection; inflammation – eosinophilic broncho-pneumopathy; neoplasia), iii) something unrelated.
The poor coat could be a reflection of systemic disease leading to metabolic compromise, or be a ‘red herring’.
The hyperthermia could reflect a systemic inflammatory response or the stress of travel.
QUESTION 3: What do you want to do next?
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6. QUESTION 3: What do you want to do next?
ANSWER
• Haematology (repeat) – check for progression of the anaemia (e.g. severity; degree of regenerative response);
check platelets
• Clotting screen – check for coagulopathy (before making any further holes in the patient!)
• Angiostrongylus vasorum serology – check for angiostrongylosis (can cause bleeding disorder in the absence of
detectable changes on haematology / clotting screen)
• Faecal analysis – check for angiostrongylosis (sensitivity of the AngioDetectTM is not 100%)
• Diagnostic imaging – CT head and thorax
• Endoscopy – rhinoscopy with biopsy; bronchoscopy with bronchoalveolar lavage
Estimate to get an answer (i.e. does not include treatment) £4000 (£3000-3500 if do not perform CT of thorax or
bronchoscopy/BAL). As serum biochemistry was recently performed, and was unremarkable, it was not repeated.
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7. Investigation
Blood analysis was performed, whilst an IV catheter was placed
and blood pressure measured.
Blood analysis
Haematology and clotting screen
Infectious disease screening
Lateral flow for Angiostrongylus vasorum
antigen in serum (AngioDetectTM) was
strongly positive
Faecal analysis
Angiostrongylus spp. larvae were noted on
faecal examination
Additional tests
Blood pressure was acceptable.
An episode of marked epistaxis started
shortly after presentation.
QUESTION 4: What do you think is
going on? What do you want to do
next (i.e. have these results changed
your investigation plan)?
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8. QUESTION 4: What do you think is going on? What do you want to do next (i.e. have these results changed your
investigation plan)?
ANSWER:
Conclusions, Treatment & Outcome
Preliminary conclusions
• Severe coagulopathy—most likely consumptive (cf. inherited clotting factor deficiency, as haemophilia should only affect
the PTT pathway, unless a combination)
• Mild anaemia, but evidence of regenerative response (a reticulocyte count would be required to confirm this). No
evidence of spherocytes to suggest an immune-mediated haemolytic process
• A moderate-severe thrombocytopenia—most likely consumptive (cf. immune-mediated, as these are usually extreme).
Insufficient to cause haemorrhage in its own right
• Mild mature neutrophilia and monocytosis—consistent with chronic inflammation (non-specific)
• Angiostrongylus vasorum infection
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9. Most likely scenario
Angiostrongylus vasorum infection  chronic DIC (consumptive thrombocytopenia ; coagulopathy )  haemorrhage (epistaxis ;
regenerative anaemia )
Angiostrongylosis could also account for the cough—either as a result of post-nasal drip or due to primary pulmonary disease
But
Could not rule out: structural nasal disease; concurrent pulmonary disease; rodenticide toxicity
Plus, the degree of anaemia does not account for the tachycardia
Initial treatment
• Fresh frozen plasma—two units were administered (based upon size) immediately; then, as clotting screen was still abnormal and
epistaxis persisted, a subsequent third unit
• Vitamin K
• Advocate (imidacloprid / moxidectin)
• Fenbendazole (50mg/kg orally once daily) for 10 days
As they were actively bleeding a plasma transfusion was indicated and the calculated initial treatment volume was given; however, as
clinical signs persisted (likely due to ongoing losses and consumption) this was continued ‘to effect’ (i.e. normalisation of clotting times).
Although transfusion of packed red cells had been considered, it was not deemed necessary as his heart rate improved following this colloid
support. Ultimately, the haematocrit then dropped to 23%.
Were only whole blood available for transfusion this could have been considered, but a greater number of units may have been required.
The vitamin K would have been necessary if the coagulopathy is rodenticide related (in addition to the plasma); however, even if the
coagulopathy was not rodenticide related it is not going to be harmful and could be of benefit.
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10. Outcome
Rectal temperature normalised during hospitalisation, and was subsequently ignored. The heart rate normalised
during hospitalisation / following plasma transfusion. The tachycardia could then have been situational or due to
blood-loss hypovolaemia. The epistaxis stopped 24 hours after starting the plasma transfusions. No further
investigation was performed at that time.
The haematocrit and clotting times normalised over the following two weeks. It was therefore assumed that both had
solely been due to the angiostrongylosis. Further investigation was deferred, pending recurrence of clinical signs—
which did not happen. Both the epistaxis and the cough were therefore attributed to angiostrongylosis. With time his
coat quality improved. Monthly Advocate was continued for him (and all other dogs in the household).