Ask the laboratory expert: Haematology results in equine practice
Dr Stacey Newton, Lead Clinical Pathologist at NationWide Labs, answers vets’ questions on haematology results in equine practice.
Pathology Focus
Lead Clinical Pathologist at NationWide Laboratories,Dr Stacey Newton answersvets’ questions on haematology results in equine practice.
Have you ever wanted to know what the most common equine bloodwork anomalies with Fasciola hepatica infestation are? How you can check for regenerative anaemia in horses? Or perhaps bloodwork has come back with an interesting anomaly that you just can’t place. Queries like these crop up all the time and there are always moments where we wish we could “ask the expert”.
In short, yes – any infectious disease process can result in a secondary immune-mediated haemolytic anaemia (IMHA).
The clinical signs of equine infectious anaemia (EIA) are very variable and can be categorised as acute, chronic or subclinical in presentation. The acute form may present with pyrexia, depression, increased heart rate (HR) and respiratory rate (RR), haemorrhaging, bloody diarrhoea, ataxia, weight loss and jaundice. On the other hand, clinical signs of chronic EIA include recurring pyrexia, depression, anaemia, weight loss and weakness with normal periods. If the horse presents with severe unexplained anaemia, you should isolate it and test for EIA.
Any infectious disease process can result in a secondary immune-mediated haemolytic anaemia.
There are several parameters that may be important in indicating prognosis in colic. However, the underlying cause of the colic should be considered as some causes will obviously have a much poorer prognosis than others; also, horses with surgical compared to medical colic will likely have a poorer prognosis.
A recent publication in Veterinary Clinical Pathology looked at some parameters and survival times for colic in a group of 17 horses (Nikvand et al., 2019). Though testing a relatively small group of animals, the study concluded that a combination of prolonged prothrombin time (PT), increased D-dimer and low fibrinogen could indicate that an individual is less likely to survive. Also, very high levels of renal and liver parameters would also have a poorer prognosis. This does appear to suggest these horses likely had disseminated intravascular coagulation (DIC).
Lactate is also a sign of inadequate tissue oxygenation and high levels may indicate a poor prognosis; however, this is a point-of-care or in-house test as it is too labile to send to an external lab. I would also say that cases with persistent high serum amyloid A (SAA), globulins (acute phase proteins) and low albumin may hold a poorer prognosis.
The underlying cause of the colic should be considered as some causes will obviously have a much poorer prognosis than others
Polychromasia is not seen in horses because their red blood cells (RBCs) are not released from the bone marrow until they are more mature than in other species. At this stage they will also have lost their RNA which gives the blue tinge to polychromatic cells with normal haematoxylin and eosin (H&E) stains. The RBCs are, however, larger in size and thus the mean corpuscular volume (MCV) is greater. This can be of use in some cases to suggest regeneration, depending on the time of sampling in relation to the incidence of haemorrhage or haemolysis. If increased, which in normal circumstances is not physically possible, mean corpuscular haemoglobin concentration (MCHC) suggests intravascular haemolysis, indicating that there is free haemoglobin as well as that measured in the RBCs.
Acute phase proteins include globulins, fibrinogen, SAA, iron and albumin. As well as D-dimers, platelets, PT and activated partial thromboplastin time (APTT), fibrinogen can also be used as a marker of DIC in horses, as it is low in many cases of DIC. Iron (Fe) is reduced with inflammation but can also be used as a marker of Fe deficiency anaemia alongside a reduced MCV (microcytic). It may also decrease with haemolysis and chronic anaemia, so is not specific on its own. Albumin is a negative acute phase protein and when significantly decreased, suggests other causes such as protein loss, eg protein losing enteropathy, protein losing nephropathy and, though rare, hepatic insufficiency.
I think in this case, blood tests can be helpful, and they may be helpful if there are obvious changes present. It is important to take a full history, signalment and duration of clinical signs (whether there is pyrexia or any colic signs, for example). Bear in mind that if several tests are done, you are more likely to have one or more come back abnormal, and it may not be significant depending on the test and value. Remember reference ranges only cover about 95 percent of the “normal” population.
Different laboratories usually establish reference ranges from the population of patients that they receive samples from, which will vary between labs, regions and countries.
An increased packed cell volume (PCV)/haematocrit (HCT) with normal total protein (TP) may be seen with splenic contraction. This is a relative increase in relation to water, but TP does not increase. An absolute increase in RBC mass, which is usually stimulated by erythropoietin, can be secondary or primary. Primary erythrocytosis (or polycythaemia vera) is uncommon and is a diagnosis of exclusion. Secondary causes, however, may include those that affect the oxygenation of RBCs such as respiratory or cardiac disease.
In most cases, this cannot be differentiated on haemograms. Therefore, correlation with other tests for underlying viral diseases is advised if appropriate, as determined by the clinical signs. Primary bacterial causes of respiratory disease, for instance, are uncommon compared to viral causes. So, if there is a primary viral cause with a secondary bacterial component, one may find that there is lymphocytosis and neutrophilia. If the bacterial infection becomes severe with a coexisting viral disease also present, we may then see a marked neutropenia with lymphocytosis with or without monocytosis. It may be more likely that thrombocytosis is seen with more severe bacterial infections.
I would say that most cases do not show a neutrophil count of greater than 15 x 109/l, and it is usually less than this. No left shift is seen.
Yes, though with repeated or serial haemograms if there is no clinical evidence of a haemorrhage (which is usually regenerative unless chronic). It can take three to five days for the bone marrow to respond to a single episode of haemorrhage or an uncomplicated regenerative haemolytic episode.
The response to anaemia is more sluggish in horses in comparison to other species: it can take one to two months following severe haemolysis or two to three months following severe haemorrhage for a horse’s HCT/PCV to return to normal.
First determine if there is an anaemia with PCV/HCT, RBCs and haemoglobin, then look at RBC parameters and morphology. Increased MCV may indicate regeneration but if absent, does not exclude regeneration (depending on the time frame of sampling and when the incident occurred). An increased MCHC may indicate intravascular haemolysis.
You may also see Howell–Jolly bodies, anisocytosis and occasionally reticulocytes although these are not commonly seen. Spherocytes may be seen but they are difficult to identify due to normal equine erythrocytes having no obvious central pallor. Other significant findings may include:
Heinz bodies – might indicate oxidative damage and haemolysis, usually regenerative
Schistocytes – can suggest underlying cause of haemolysis
Parasites in or on RBCs and/or white blood cells (WBCs) – causes of haemolysis
You might also take sequential samples to see if the MCV or RBC mass increases, while bone marrow aspirate can be taken for cytology and biopsy for histology.
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