Tag: Diabetes Mellitus

Oh, CR*P! Using point-of-care C-reactive protein tests
Few companies now offer affordable point-of-care tests for canine C-reactive protein (CRP). As we did when we recently received our new box of CRP slides, you might soon be asking the question: what do we even do with this stuff?

Here’s what we’ve learnt…

CRP is one of the acute phase proteins produced by the liver in response to inflammation. Healthy patients have very low levels of CRP, but a systemic inflammatory condition will cause an increase in CRP within four to six hours. Conversely, increased levels will decrease rapidly on resolution of inflammation. This provides an almost real time measure of inflammation that is more responsive and reliable than the white blood cell response.

In other words, CRP can indicate the presence of inflammation before the patient’s white blood cell count gives any clues, or before it becomes pyrexic – and, unlike the white blood cell count, stress and steroids do not affect CRP levels.

Uses

So, how do we use it?
- I love it for early pickups of problems in those grey area cases: the dog seems okay on clinical examination, but something about it bothers me. A normal or mildly increased CRP test will make me sleep more easy, while a surprise high reading will prompt me to admit for full diagnostics, or at least get the patient in for a follow-up CRP the next day. Conversely, a localised problem – such as an abscess – combined with a normal CRP test might mean you can hold off on antibiotics and just recheck CRP in 24 hours.
- It’s great for monitoring response to treatment. If my plan is working then I’d expect CRP to show a significant decrease by day two or three. If it’s not dipping by then, I need to reassess my treatment plan. Do I need to change antibiotics? Scan it again? Maybe we need to consider surgery? It can also be a good prognosticator. Research has shown failure of CRP to decrease significantly (around a 3× decrease) by around day three is generally bad news for patients with inflammatory conditions such as pancreatitis and immune-mediated haemolytic anaemia.
- We are starting to play with it for post-surgical monitoring. Any surgery will cause inflammation with an increase in CRP levels, but in an uncomplicated postoperative period, you should expect levels to start decreasing by day three to five. A base line CRP 24 hours after surgery with a recheck on day three should pick up early signs of postoperative problems such as infection, and prompt investigation or intervention.
- A potentially nifty use for it that we haven’t yet had the opportunity to use is in differentiating inflammatory lamenesses (arthritis, infection, injury) from a neurological causes – that is, is it arthritis or a nerve problem?
Limitations
- Remember, it’s very sensitive, so will increase with almost any inflammation. A mild upper respiratory infection or a bad gingivitis will likely induce some changes, so it’s important not to over-interpret (keep in mind that the magnitude of the increase in CRP does generally correspond with the severity of the inflammatory response). A pancreatitis case where the CRP fails to drop does not always mean death is looming – you may have just missed the concurrent skin disease. Always interpret CRP values in concert with your clinical examination.
- Be aware that pregnancy and intense exercise can increase CRP values.
- Not all serious conditions have an inflammatory component. CRP will be unchanged in most veterinary cases of heart disease; in common hormonal disease, such as adrenal disease and uncomplicated diabetes; urinary obstructions; many localised cancers; epilepsy and many others. Don’t presume that just because CRP is normal, everything is fine.
- No similar test exists for cats.
Sit up and say…

My favourite way to explain how to use this test is by using its highly appropriate acronym – any unexpected increase should make you sit up and say: “Oh CR*P! What am I missing?”
April 10, 2024

Hyponatraemia, pt 2: causes

The causes of hyponatraemia can be divided into three major categories, based on serum osmolality. This is further divided based on the patient’s volume status (Table 1).

Most patients we see in clinic fall into the hypovolaemic category, except patients with diabetes mellitus.

Table 1. Causes of hyponatraemia based on osmolality and volume status (from Guillaumin and DiBartola, 2017).
Hypo-osmolar			Hyperosmolar	Normo-osmolar
Hypovolaemic	Normovolaemic	Hypervolaemic	Hyperosmolar	Normo-osmolar
Gastrointestinal fluid loss Third-space fluid losses Shock Hypoadrenocorticism (Addison’s disease) Renal insufficiency Excessive diuretic administration Salt-losing nephropathy Cerebral salt wasting syndrome	Syndrome of inappropriate antidiuretic hormone secretion (SIADH) Hypotonic fluid administration Hypothyroidism Glucocorticoid insufficiency Psychogenic polydipsia Reset osmostat (SIADH type B)	Congestive heart failure Acute or chronic renal failure Nephrotic syndrome Hepatic cirrhosis Accidental ingestion or injection of water (water intoxication)	Hyperglycaemia Mannitol Severe azotaemia	Hyperlipidaemia Hyperproteinaemia

Common causes

In dogs, the three most common causes of hyponatraemia are:

gastrointestinal (GI) fluid loss
third-space fluid loss
fluid shift from intracellular fluid to extracellular fluid (ECF) as a result of hyperglycaemia

In cats, the three most common causes of hyponatraemia are:

urologic diseases
GI fluid loss
third-space fluid losses

In most patients, more than one pathophysiologic factor is likely to be contributing to the hyponatraemia.

Circulating volume

Hypovolaemic patients – those with, for example, GI losses, hypoadrenocorticism, renal losses and haemorrhagic shock – have a reduced effective circulating volume. ECF contraction triggers antidiuretic hormone (ADH) secretion, which leads to increases in free water absorption and thirst, and results in dilution of the serum sodium concentration. Aldosterone secretion is reduced in hypoadrenocorticism, so an overall reduction in sodium reabsorption compounds the problem.

Hypervolaemic patients are those with an increased fluid retention state, such as:

congestive heart failure (pulmonary oedema)
advanced hepatic failure (ascites, third-space fluid)
renal failure
free water ingestion

Congestive heart failure patients have a reduced cardiac output and, therefore, a decreased effective circulating volume, despite the presence of the extra fluid status. Renin-angiotensin activation leads to release of ADH and aldosterone, resulting in sodium and free water reabsorption, and increased thirst. Both lead to an excess of free water retention.

Advanced hepatic (cirrhosis) or renal failure (nephrotic syndrome) both result in hypoalbuminaemia, leading to fluid shifting into the interstitial space and third space, reducing effective circulating volumes. This leads to activation of ADH to increase free water reabsorption, to restore the circulating volume in the face of existing hypervolaemia and hyponatraemia.

Diabetic patients

Moderate to severe hyperglycaemic diabetic patients can be either hyperosmolar or normo-osmolar, depending on the serum blood glucose concentration. Hyponatraemia occurs when water shifts from the intracellular fluid to the ECF down the osmotic gradient, diluting the serum sodium content.

Despite this osmotic shift, not all diabetic patients develop hyponatraemia. Glucosuria also causes also causes a renal osmotic shift, sometimes resulting in urine water loss in excess to sodium. This offsets the hyponatraemia – in some cases, hypernatraemia results.

Treatment

Treatment of hyponatraemia hinges on how quickly it developed and the volume status of the patient. The rule of thumb is to correct hyponatraemia slowly – not exceeding 0.5meq/L/hr – especially in chronic cases, or cases where the duration of hyponatraemia is unknown. Keeping to this rate is paramount until serum sodium concentration reaches 130meq/L.

In acute patients with severe clinical signs, such as seizures, some clinicians may choose to use a higher rate of 1meq/L/hr to 2meq/L/hr until clinical signs resolved.

It should be emphasised, once again, this rate should never be used in chronic patients, patients with an unknown duration of hyponatraemia, or where frequent serum sodium concentration cannot be monitored. The rapid correction of hyponatraemia can lead to osmotic demyelination syndrome (myelinolysis).

Its effect will not be apparent until three or four days after therapy, and can result in neurological abnormalities such as:

weakness
ataxia
dysphagia
paresis
coma

For that reason, frequent electrolyte measurements are required, starting hourly then once a suitable rate of increase has been established and less frequently thereafter.

Part 3 will look at how to correct patients with hyponatraemia.

Reference

Guillaumin J and DiBartola SP (2017). A quick reference on hyponatremia, Veterinary Clinics of North America: Small Animal Practice 47(2): 213-217.

April 3, 2023

Lipaemia – the bane of biochemistry
Last week we covered haemolysed samples – this week we’re looking at lipaemic samples.

Lipaemic samples are caused by an excess of lipoproteins in the blood, creating a milky/turbid appearance that interferes with multiple biochemical tests and can even cause haemolysis of red blood cells.

A severely lipaemic sample (red arrow). IMAGE: eClinPath.com (CC BY-NC-SA 4.0).

Lipaemia can follow recent ingestion of a meal – especially one high in fat. Although not pathognomonic for any diseases, its presence can help increase the suspicion of certain diseases, including:
- pancreatitis
- diabetes mellitus
- hypothyroidism
- hyperadrenocorticism
- primary hyperlipidaemia (in some specific breeds, such as the miniature schnauzer)
It warrants further investigation in patients that have been ill and inappetent.

Irksome interpretations

Lipaemia can dramatically impact laboratory testing and is often troublesome in critically ill patients, making interpretation of biochemistry particularly difficult, if not impossible.

Lipaemia can affect different analysers in different ways, most commonly causing:
- Falsely increased calcium, phosphorus, bilirubin, glucose and total protein (via refractometer) and some liver parameters such as alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, haemoglobin concentration, and mean corpuscular haemoglobin concentration.
- Falsely decreased sodium, potassium, chloride, albumin and bicarbonate.
Tube tips

Assessment of a centrifuged haematocrit tube before running a biochemistry panel can help reduce wasted biochemistry consumables.

If the sample is lipaemic in the haematocrit tube then maybe try some of the following tips.
- If blood tests are planned in advance, try fasting the patient beforehand for 12 to 24 hours.
- Repeat sampling a couple of hours later may yield a less lipaemic sample.
- Collecting and centrifuging a larger amount of blood (3ml to 5ml, for example) can sometimes yield enough clear sample between the lipid layer and red blood cells.
- Refrigeration of the sample can help the separation.
- Extract lipids using polar solvents, such as polyethylene glycol.
- Centrifugation at higher than normal speeds (if possible) can also assist in clearing the layer.
February 28, 2022
Fluid therapy part 4: ongoing losses
This month, we will look at the final part of a fluid therapy plan – accounting for ongoing losses. This can be challenging, but some general rules can be helpful.

Regular assessment is essential to track patients’ responses.

First, let’s recap the four parts of a fluid therapy plan:
1. Perfusion deficit
2. Hydration deficit
3. Maintenance requirements
4. Ongoing losses
When considering ongoing losses, try to not forget about patients with pre-existing polyuric diseases; chronic renal failure is a prime example. Patients with dehydrated chronic renal failure are unlikely to suddenly regain concentrating ability. Polyuria should be considered as an ongoing loss.

Other conditions that may result in additional urinary fluid losses include post-obstructive diuresis, diabetes mellitus, hyperadrenocorticism and hyperthyroidsim.

How much to add?

This is the tricky part. I often add an additional half to one maintenance and frequently reassess clinical parameters, or if a urinary catheter is placed matching ins and outs.

Gastrointestinal tract losses can be collected and weighed; 1g of vomitus or diarrhoea can be roughly equivalent to 1ml of water.

Fluid removed from drains placed in cavities or wounds should also be measured and accounted for.

Remember the key point is regular assessment of the patient’s hydration status, from repeat clinical exams, to track their response. Don’t forget regular retesting of electrolytes – for example, every 12 to 24 hours for patients on IV fluids and not eating.
January 24, 2022
RCVS council election manifesto: Thomas Lonsdale

THOMAS LONSDALE

BVetMed, MRCVS

PO Box 6096, Windsor Delivery Centre, NSW 2756, Australia.

T +61 2 4577 7061

M +61 437 2928 00

E tom@rawmeatybones.com

PROPOSERS: Roger Meacock, Andrew Stephens

1980s – woke from vet-school induced stupor to realisation junk pet-food industry relies on bogus science and negligent vet “profession”.

1991 – Blew whistle on junk pet food cult.

1993 – Preventive dentistry PGCVS.

1994 – Feeding versus nutrition, Aust Vet Practice.

1994 – Cybernetic hypothesis, J Vet Dent (postulates ecological theory of health and disease as extension of Gaia Hypothesis).

1994-7 – Junk pet food cult brought four disciplinary actions before New South Wales vet board.

1995 – Periodontal disease and leucopaenia, JSAP.

2001 – Raw Meaty Bones: Promote Health published.

2004 – Nominated for ACVSc award.

2014 – Most supportive vet award; FOI research: junk pet food grease in seven Australian vet schools.

2015 – Science death experiment.

Manifesto

Pompous, arrogant, mouthing incantations, the vet high priests worship at the altar of bogus science. Founded on fallacy, they oversee the junk food poisoning of pets, betrayal of consumers and brainwashing of vet students.

They must be stopped.

Morgan Spurlock embarked on a risky experiment. For 30 days he ate junk food at every meal. He gained 11kg, his liver turned to fat, cholesterol shot up and he doubled his risk of heart failure. Fortunately for Spurlock, he escaped addiction to junk food, followed his doctor’s orders and stopped the experiment.

The medical profession tells us carbohydrate-laden junk food injures health; that periodontal inflammation and obesity are precursors of systemic disease and early death. By contrast, the junk pet food industry controls the veterinary agenda. Vet schools deliver industry-funded propaganda on diabetes, periodontal disease and obesity – while simultaneously ensuring pious mumbo-jumbo obscures the despicable, lamentable truth.

Vet “experts” jet about the world spruiking the latest concoctions; extolling the alleged benefits of elaborate treatments instead of declaring that junk food contaminates all aspects of vet science, teaching and practice. According to them, natural food, as determined by evolution, is dangerous while their paymaster’s industrial junk represents the pinnacle of excellence.

For 20 consecutive RCVS elections, I’ve called for our “self-regulating” profession to act with integrity and honour. Alas, the high priests refuse even to consider. Time, then, for the courts to decide. I recommend legal proceedings against the RCVS, junk food companies, veterinary schools and individuals in respect to animal cruelty, breach of contract, theft and fraud.

Please vote in support; instruct your lawyers and brief the media. Pets, pet owners and the wider community need our help. Thank you.

March 24, 2016