What to Do When the Lab Is Closed--Interpreting Biochemistry and a Few Haematology Results
World Small Animal Veterinary Association World Congress Proceedings, 2008
Sandra Forsyth, BVSc, DACVA
Institute of Veterinary, Animal and Biomedical Sciences, Massey University
Palmerston North, New Zealand

Many practices today have access to bench top analysers and so it is possible to obtain the same amount of raw data that you receive from a commercial laboratory--what is missing is interpretation of the results. Interpretation of biochemistry results is a vast subject and so with that in mind we will only cover 'urgent' results i.e., those parameters that are commonly required in the emergency patient when immediate results are a priority.

Microhaematocrit Tube

If you are in situation where you don't have access to multiple analytes it is still possible to obtain sufficient information to make some important decisions about patient management.

A centrifuge will allow you to obtain a PCV which may raise the suspicion of dehydration or hypovolaemia (elevated PCV) or confirm the presence of anaemia in a patient that presents with pallor. Further information about the type of anaemia present cannot be determined without looking a blood smear (which will be covered in the next session). Before snapping the microhaematocrit tube to determine total solids (TS), look at the colour of the plasma above the red blood cells. Icterus may be determined by a yellow colour to the plasma and in conjunction with PCV, possible differentials can be considered. It may be seen in haemolytic anaemia, decreased bilirubin uptake by hepatocytes (reduced functional mass) or decreased excretion (hepatic and post-hepatic cholestasis). Red plasma above the RBCs may be due to haemolysis and once again in the presence of anaemia could suggest extravascular haemolysis. However, over-vigorous collection of blood and deposition into a vacutainer may cause post collection haemolysis, although this rarely results in a low PCV. Cloudy plasma suggests lipaemia and it may occasionally be pink in colour (looking like strawberry milk) because RBC fragility is increased in lipemic blood and so intravascular haemolysis may be seen.

The buffy coat layer is usually a white layer about 1 mm thick that sits above the RBCs and it is difficult to detect a leukocytosis unless it is profound. Leukopenia cannot be detected by looking at the buffy coat layer.

The final parameter that can be determined from a microhaematocrit tube is total solids with the use of a refractometer. TS may be elevated in the presence of dehydration or hypovolaemia (the latter depending upon the cause) and occasionally hyperglobulinaemia. A low TS may be due to decreased protein production or accelerated protein loss (through the gastrointestinal tract or kidneys, or rarely from massive skin exudation). It is useful to obtain albumin and globulin concentrations when TS is elevated to see which component(s) is causing the change.


Lists of causes for anaemia can be obtained from clinical pathology and small animal medicine texts. A factor to remember in the animal that has had substantial acute blood loss is that PCV and TS do not fall immediately but take about 24 hours to reach a nadir. Consequently they are not a reliable indicator of total lost volume immediately after injury. However, they remain an excellent means for monitoring a patient that has bled and aid in determining when a transfusion (or colloid administration) may be needed. Examination of a blood smear is necessary to determine whether an anaemia is regenerative or non-regenerative and we will cover that in the next session.

Quality Control

I will make a brief comment on quality control which is an important aspect of using and maintaining in-practice analysis. You have to feel confident that your equipment is giving you reliable results and this can only be achieved by undertaking some means of quality control. There are two ways of achieving this. The first is to purchase control solutions with a known quantity of the analyte(s) to be assessed and pass the solution through your analyser to determine how closely they match the results from the manufacturer. The second method is to divide patient blood into two aliquots and send one to a commercial laboratory to compare the results with those from your analyser. It should be remembered that when using the second technique, results are unlikely to be identical because the methodology is expected to be different. Ideally, quality control should be carried out daily but this is often impractical in veterinary clinics but at least weekly should be considered. Although results are not identical to those obtained by the commercial laboratory, over a period of time it should be possible to be assured that results from your analyser do not deviate markedly or randomly from those obtained from the laboratory.


Diabetes mellitus (DM) is common and the effects of both hyper- and hypoglycaemia can be profound if not life threatening. Consequently, blood, plasma or serum glucose concentrations are frequently assessed in practice. There are many and varied methods for obtaining this result, with just as much variation in reliability of the equipment used.

Results from diverse glucose analysers may vary for multiple reasons but one of the more common and simple reasons is that the practice analyser may assess glucose in whole blood (common when using glucometers) and commercial laboratories assess glucose in plasma (in fluo-oxalate tubes). It can be anticipated that blood glucose concentration will be less than plasma glucose concentration because of the 'diluting' effect of the red blood cells. Consequently the reference range provided by your commercial laboratory should not be used as the reference range for the glucometer in your practice. The following formula can be used to extrapolate from whole blood to plasma:

[glucose]whole blood = [glucose]plasma x [1.0 - (0.0024 x PCV (%)]

There is also a difference between venous and capillary blood glucose concentrations with little difference (<0.5 mmol/l) in fasted samples, but this can rise to 2-3 mmol/l in post-prandial patients.

Samples collected into plasma or serum tubes should be analysed as soon as possible and certainly within an hour of collection, or serum should be harvested within that time. This is because glycolysis continues within the cells and so blood glucose concentrations decrease with time.


This is commonly seen in stressed animals and it cannot be automatically assumed that the patient is a diabetic. Stressed cats may show plasma glucose elevations up to 19 mmol/l which is sufficiently high to cause glucosuria. Dogs, however, rarely exceed 11 mmol/l when stressed and stress glucosuria does not occur. Higher concentrations of glucose are usually consistent with diabetes mellitus.


This may result in seizures when cerebral glucose delivery is reduced. The most common cause for apparent hypoglycaemia is in-vitro glycolysis by blood cells and possibly bacteria. Pathological causes include insulin over-dosage; insulinoma in which neoplastic β-cells of the pancreas secrete large quantities of insulin; hepatic insufficiency wherein there are too few hepatocytes to maintain normal glucose concentrations in the presence of fasting; profound starvation; decreased gluconeogenesis in neonatal and juvenile toy/miniature dogs; other neoplasms and sepsis.

Urea and Creatinine

Azotaemia, denoted by an elevation in serum urea and creatinine concentrations, is often assessed in practice to determine how effectively the kidneys are functioning. An elevation in urea and creatinine is commonly associated with dehydration or hypovolaemia when renal perfusion is inadequate to remove nitrogenous waste. Under these conditions azotaemia is rarely very high and 2-2.5x elevations in urea and/or creatinine are usual. Higher concentrations often indicate some degree of renal compromise. Renal failure may be accompanied by dehydration, and prolonged hypovolaemia may induce renal hypoxia and a decrease in function so it is not uncommon to see both a renal and pre-renal component to azotaemia. The major benchmark for differentiating pre-renal from renal causes for azotaemia is urine specific gravity. If azotaemia is due to pre-renal causes (i.e., related to decreased glomerular filtration rate) then urine SG should be > 1.030 (dog); > 1.035 (cat). If the urine SG is less than these values then it is due to either intrinsic renal disease or to pre-renal azotaemia combined with impaired concentrating ability due to extra-renal disease (e.g., hypercalcaemia, loop diuretics, prolonged hyponatraemia, liver disease). It is important that the urine sample for SG is taken at the same time as the blood is sampled. Intervening fluid administration (parenteral or oral) may result in misinterpretation of the azotaemia.

An increase in urea without a concurrent increase in creatinine may occur with increased intestinal protein (post-prandial, gastrointestinal haemorrhage), dehydration or hypovolaemia.

Other parameters that may be elevated in cats and dogs with renal failure include phosphate, potassium and when severe amylase and lipase.


Abnormalities in potassium concentration may be life threatening so it is useful to be able to measure this electrolyte. Many bed-side blood gas analysers have the ability to measure electrolytes and results can be obtained rapidly with only a small quantity of blood. Decreased excretion of potassium (renal failure, urinary tract obstruction or rupture, hypoadrenocorticism) is most commonly associated with hyperkalaemia and can produce marked increases. Occasionally, patients with severe diabetic ketoacidosis can present with hyperkalaemia and iatrogenic elevations in the electrolyte may be produced. There are also a number of less common conditions that produce hyperkalaemia.

Uncommonly, elevated serum potassium is artificial and is due to leakage of potassium from the RBCs in vitro.

Hypokalaemia is rarely life threatening but it can prolong muscle weakness and ileus in ill patients. Excessive loss (vomiting, diarrhoea) combined with decreased intake is the most cause for this electrolyte abnormality.


There are a number of parameters that can be assessed readily in the practice situation that can aid in diagnosis and monitoring of the critical patient and it is worth having some knowledge in these areas when managing these patients.

Speaker Information
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Sandra Forsyth, BVSc, DACVA
Institute of Veterinary, Animal and Biomedical Sciences
Massey University
Palmerston North, New Zealand

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