The step-by-step guide to understanding your patient's blood results
Stop me if you’ve ever felt like this…
You’re in the lab, running bloods and you can see a ton of red and blue on your printout.
So you let the vet know… and that’s the end of the discussion.
But do you want to know more about how to actually interpret these results? So that you’re understanding more of what they mean for your patient, and so that you’re not just dictating them to the vet then doing what they ask you to do?
Having even just a basic understanding of what our blood results tells us is so important for us as nurses and technicians.
Why? Well, it gives us some autonomy in our nursing!
When we understand what these results mean, we start to identify things to watch out for, deterioration to be prepared for, and tweaks we need to make to our nursing care. This means more nursing (and less just administering treatments).
And, most importantly - more use of our skills, and with that, more job satisfaction.
In this post, I’m going to talk you through a patient, and their blood results. I’ll break down:
What these parameters tell us
How this guided the veterinary surgeon’s diagnosis and further tests, and
How we used this information as nurses to change the patient’s care.
Meet your patient…
Our lovely case example is a 7-year old female spaniel, who presented with ascites.
She had no other significant medical history prior to presentation. She had been eating normally and had been bright and happy. She had normal activity and energy levels, and had not had any vomiting, diarrhoea, pain, or any other abnormal signs before her presentation.
On our physical examination, the only abnormality noted was marked ascites.
So firstly, we think about the common causes of ascites. These include:
Cardiac disease (e.g. right-sided heart failure)
Decreases in colloidal oncotic pressure (e.g. due to hypoalbuminaemia)
Portal hypertension (increased pressure in the circulation between the GI tract and liver, e.g. due to ligation of a portosystemic shunt)
Our patient doesn’t show signs of cardiac disease and has no murmur on auscultation, and has no pre-existing hepatic or post-hepatic disease that we know of.
The next step to narrow down the list of causes and allow the veterinary surgeon to reach a diagnosis is to perform diagnostics. These include full bloods and imaging.
Let’s look at our results…
So we pull a biochemistry and see the following results:
Total protein: 30.7 g/l LOW (Reference Range 50.0 - 72.0)
Total globulin 20.8 g/l (Reference Range 19.0 - 46.0)
Albumin 9.9 g/l LOW (Reference Range 26.0 - 40.0)
Calcium 2.01 mmol/l LOW (Reference Range 2.20 - 3.00)
Phosphate 1.99 mmol/l HIGH (Reference Range 0.60 - 1.80)
Urea 18.8 mmol/l HIGH (Reference Range 1.7 - 7.4)
Creatinine 96 umol/l (Reference Range 20-124)
Sodium 141 mmol/l (Reference Range 139 - 154)
Potassium 4.40 mmol/l (Reference Range 3.60 - 5.60)
Chloride 111 mmol/l (Reference Range 102 - 122)
The remaining results, including the liver parameters, glucose, cholesterol and triglycerides, were within normal limits.
What do you think of these results?
Our patient has severe hypoalbuminaemia causing a low total protein. We know only albumin levels are affected, since our other plasma proteins (globulins) are within normal limits. As albumin is the most abundant plasma protein, the hypoalbuminaemia also causes the total protein levels to be low.
So our patient has low colloidal oncotic pressure, causing their ascites.
Albumin levels can be low due to:
Loss (usually as a result of damage to the kidneys or the gastrointestinal tract)
Reduced intake (e.g. prolonged malnutrition/anorexia)
The elevated urea and phosphate levels alongside the hypoalbuminaemia increase the suspicion of a renal cause. This is a condition known as protein-losing nephropathy (PLN).
To investigate this further, a urinalysis is requested. This reveals severe proteinuria - the protein:creatinine ratio is 13 (normal is up to 0.5!)
Why does this happen?
When blood enters the glomerulus, the capillary bed in the renal nephrons where blood is filtered, proteins are usually retained.
They stay in the bloodstream since they are too large to pass through the glomerular wall and into the urine.
In protein-losing nephropathy, the glomerulus becomes 'leaky' due to diseases that target this part of the nephron. The plasma proteins (of which albumin is the most abundant) then pass through the leaky nephrons and into the urine.
Let’s talk about albumin in a bit more detail….
One of the main functions of albumin is maintaining colloidal oncotic pressure or COP. This basically means the large protein molecules can 'hold' water in the plasma, maintaining plasma volume.
When albumin levels significantly drop, so does COP. This means the fluid begins to leak out of the vessels and into 'third spaces' such as the abdominal cavity (causing ascites) or the pleural space (causing pleural effusion).
What about our renal parameters?
The two main parameters we look at when it comes to renal function are urea and creatinine. Both are waste products eliminated from the kidneys.
Urea is a byproduct of protein breakdown, and whilst increases are seen with renal dysfunction, it can also be affected by other things such as fluid balance, GI haemorrhage and liver function.
Creatinine is a more specific marker of renal function and increases when about 75% of the nephrons have been lost.
And how do we explain the calcium and phosphate changes?
The kidneys are responsible for excreting phosphate from the bloodstream. When they can't function properly, phosphate levels can increase - this is why we restrict phosphate levels in CKD patients.
Calcium and phosphate are inversely related - so when one goes up, the other can decrease. This means we commonly see changes to these minerals when patients have renal dysfunction!
What does all this mean for our nursing?
There are a few important nursing considerations in PLN patients. These include:
Monitoring fluid balance
As we can see with this patient, fluid shifting is common when colloidal oncotic pressure decreases. This means we can see complications like ascites, pleural effusion, and oedema.
Pleural effusion has a direct impact on ventilation. As it accumulates, it will reduce the ‘space’ available for the lungs to expand in, meaning our patients become less efficient at taking in oxygen and eliminating carbon dioxide. This can cause respiratory distress, hypoxaemia and hypercapnia.
Ascites and peripheral oedema can be uncomfortable for our patients. Peripheral oedema can also make things like placing IV catheters and collecting blood samples challenging.
We need to keep an eye out for any changes in our patient’s status due to their fluid accumulation, for example:
Respiratory changes
Discomfort
Mobility issues due to peripheral oedema/limb swelling
Monitoring our patient’s vitals
Changes to vital signs are common in PLN patients. This can be due to:
Lower plasma volumes due to reduced COP, causing hypovolaemia
Respiratory impact of pleural effusions
Thromboembolic disease (more on this in a second!)
Hypertension associated with renal disease (this is very common in PLN patients!)
Discomfort
We want to keep a close eye on those vitals, especially making sure we’re checking blood pressure regularly throughout hospitalisation.
[box] I usually check BP once every 6 hours in a PLN patient, more often if needed.
Monitoring for signs of thromboembolic disease
Patients with PLN lose a protein called antithrombin III in their urine, alongside albumin. This protein is responsible for regulating coagulation - it basically helps stop clots from forming.
When antithrombin is lost, our patients enter a hypercoagulable state - meaning they are prone to forming thrombi.
If these thrombi end up in a limb, we’ll see a lack of circulation to that area, resulting in pain, swelling, and non-function of the affected limb.
If they end up in the pulmonary circulation, blood cannot flow through the affected vessels to and from the lung. This causes severe respiratory distress and hypoxaemia and can be fatal.
How is PLN treated and monitored?
Our patient’s PLN is managed with:
Immunosuppressive drugs such as steroids or ciclosporin
ACE inhibitors to decrease proteinuria and delay the onset of renal failure
Antihypertensives to reduce blood pressure
+/- Diuretics such as spironolactone, to minimise oedema
Anti-thrombotics to minimise the risk of thrombus formation.
In terms of ongoing monitoring, we’ll see our patient back regularly for repeat blood and urine sampling. In particular, we’ll be checking:
Albumin/total protein levels, to ensure these are increasing
BUN and creatinine levels, to monitor renal function
Phosphate and calcium levels, due to the impact renal disease has on these parameters
Electrolytes, due to the impact renal disease has on these parameters
Urine analysis to check concentrating ability, protein:creatinine ratio, and sediment examination alongside urine chemistry analysis.
Alongside the blood and urine samples, we’ll also repeat blood pressure measurement to monitor our patient for hypertension. This can easily be performed by the nursing team, who can also collect the blood samples and work with the client to obtain a free-catch urine sample.
This means we don’t just use our nursing skills when the patient is hospitalised - we get to keep doing this at their revisits, too!
So that’s just one example of how we can use our blood results, alongside our clinician history and examination findings, to plan and deliver our nursing care!
Want to do this in your own hospital? Don’t be afraid to ask your vets how they interpret their results! And if you want to learn more about this, I have an exciting announcement for you…
The medical nursing academy is now officially open for enrollment!
That’s right, my signature CPD program, a community-meets-CPD-meets-coaching program, is now live! And if you sign up by Wednesday evening (at the time this blog post goes live) there’s still time to catch the Biochemistry 101 workshop LIVE with the rest of the academy members!
For more information and to join us, visit www.medicalnursingacademy.com! I can’t wait to see you there!
References
Langston, C. E. 2008. Protein Losing Nephropathy. DVM360, available from: https://www.dvm360.com/view/protein-losing-nephropathy-proceedings
Merrill, L. 2012. Small Animal Internal Medicine for Veterinary Technicians and Nurses. Iowa: Wiley-Blackwell, p. 301.
