Tag: Hypocalcaemia

  • Ionised hypocalcaemia, pt 4: controversies and prognostic indications

    Ionised hypocalcaemia, pt 4: controversies and prognostic indications

    Ionised hypocalcaemia (iHCa) is a well-known electrolyte abnormality in critical human patients, which is also beginning to be recognised in our critical feline and canine patients.

    The exact mechanism for the development of iHCa is still unknown – making prevention difficult, if at all possible. Controversy also exists as to whether treating iHCa is of any benefit, especially in non-clinical cases.

    Despite these issues, serum concentration is proving to be an accurate prognostic indicator for the morbidity and mortality rates of some of the more critical patients.

    Research

    Over the past 30 years, significant resources have been put into trying to demystify the pathophysiological causes of iHCa in critically ill people; however, the exact mechanisms are still to be determined.

    Some proposed mechanisms include:

    • abnormal parathyroid hormone secretion or function
    • abnormal vitamin D synthesis or function
    • hypomagnesaemia
    • calcium chelation
    • alkalaemia
    • calcium sequestration in tissue or cells
    • an increase in calcitonin precursors (procalcitonin)

    In a canine study where endotoxaemia was induced, it was found hypovitaminosis D was associated with iHCa (Holowaychuk et al, 2012).

    Veterinary studies

    The true incidence of iHCa in critically ill canine and feline patients is yet to come to a consensus, due to the limited veterinary studies.

    In one retrospective study, 90% of 55 cats with septic peritonitis was reported to have iHCa (Kellett-Gregory et al, 2010), while only 24% of septic dogs (n=58) was reported to have iHCa (Luschini et al, 2010).

    Regardless of the true incidence, the commonness of this change questions whether a need exists to treat iHCa, especially cases in the mild or non-clinical categories.

    No consensus

    At this stage, no consensus exists to either support or prohibit the treatment of hypocalcaemia in critically ill patients.

    Well-designed prospective studies are scarce in human literature and non-existent in the veterinary field; no evidence-based guidelines are available for treatment.

    Based on logic, arguments for the administration of calcium to critically ill patients include:

    • iHCa during hospitalisation is a negative predictor for morbidity and mortality of patients.
    • Hypocalcaemia can cause decreased myocardial contractility.
    • In hypotensive patients dependent on vasopressors or inotropic agents, the supplementation of calcium may be beneficial.

    Arguments against calcium supplementation include:

    • Calcium accumulation within cells predisposes to hypoxia and ischaemia-reperfusion injury.
    • Increased mortality in experimental models of sepsis when calcium is supplemented, on top of the lack of evidence to support this act.

    Prognostic use

    Serum calcium concentrations – or, rather, the trend of it in hospital – appears to be of valuable prognostic indicators.

    Kellett-Gregory et al (2010) found although no direct associations existed between the presence or severity of iHCa at the time of patient admission, a positive correlation existed between the lowest iCa post-hospitalisation, and the length of hospitalisation and duration of intensive care stay.

    Of the cats that had iHCa, those that failed to return to a normal ionised calcium (iCa) during hospitalisation had a significantly lower rate of survival to discharge. Interestingly, iHCa was not associated with the status of hypotension, coagulopathy or arrhythmias, so cannot be used to predict the occurrence of these.

    These findings were echoed by Luschini et al (2010), where low mean ionised calcium and lowest documented ionised calcium concentrations were found to be associated with a poor outcome. The severity and duration of iHCa appears to be important in determining prognosis in these patients.

    Conclusion

    Controversy exists regarding whether treatment of mild iHCa in critically ill patients is recommended; however, one thing we now know is serum iCa concentration is a reliable predictor of mortality and morbidity in canine and feline patients.

    References

  • Ionised hypocalcaemia, pt 3: acute treatment and management

    Ionised hypocalcaemia, pt 3: acute treatment and management

    Treatment of ionised hypocalcaemia (iHCa) is reserved for patients with supportive clinical signs, then divided into acute and chronic management.

    Since the most common cases of clinical hypocalcaemia in canine and feline patients are acute to peracute cases, this blog will focus on the acute treatment and management of hypocalcaemia.

    Clinical signs

    The severity of clinical signs of iHCa is proportional to the magnitude, as well as the rate of decline in ionised calcium (iCa) concentration.

    The normal reference range for iCa is 1.2mmol/L to 1.5mmol/L in dogs and 1.1mmol/L to 1.4mmol/L in cats. Serum iCa concentrations in younger dogs and cats are, on average, 0.025mmol/L to  0.1mmol/L higher than adults.

    Mild iHCa (0.9mmol/L to 1.1mmol/L) – as seen in critically ill dogs and cats with diabetic ketoacidosis, acute pancreatitis, protein-losing enteropathies, sepsis, trauma, tumour lysis syndrome or urethral obstructions – often has no observable clinical signs.

    Moderately (0.8mmol/L to 0.9mmol/L) to severely (lower than 0.8mmol/L) affected animals – in the case of eclampsia and those with parathyroid disease – often display severe signs.

    Early signs of iHCa are often non-specific, and include:

    • anorexia
    • rubbing of the face
    • agitation
    • restlessness
    • hypersensitivity
    • stiff and stilted gait

    As the serum iCa concentration further decreases, patients often progress to:

    • paresthesia
    • tachypnoea
    • generalised muscle fasciculations
    • cramping
    • tetany
    • seizures

    In cats, the gastrointestinal system can also be affected, presenting as anorexia and vomiting.

    Treatment

    The need for treatment of hypocalcaemia is dependent on the presence of clinical signs, rather than a specific cut-off of serum concentration of iCa itself.

    Moderate to severe iHCa should always be treated. Mild hypocalcaemia, on the other hand, may not be necessary, especially if it is well tolerated. It should be remembered the threshold for development of clinical signs is variable, and treatment may benefit critical cases with an iCa concentration of less than 1.0mmol/L.

    Treatment is divided into the acute treatment phase and chronic management.

    In the tetanic phase, IV calcium is required – 10% calcium gluconate (equivalent to 9.3mg/ml) administered at 0.5ml/kg to 1.5ml/kg dosing to effect. This should be administered slowly with concurrent ECG monitoring. Infusion of calcium needs to be stopped if bradycardia develops or if shortening of the QT interval occurs.

    Some suggest calcium gluconate (diluted 1:1 with 0.9% sodium chloride) of half or the full IV dose can be given SC and repeated every six to eight hours until the patient is stable enough to receive oral supplementation. However, be aware calcium salts SC can cause severe necrosis or skin mineralisation.

    Calcium chloride should never be given SC, as it is a severe perivascular irritant.

    Correcting iCa

    Irrespective of the chronicity of the treatment, the rule of thumb is correction of calcium should not exceed 1.1mmol/L.

    Correction of iCa to normal or hypercalcaemic concentration should always be avoided, as this will result in the desensitisation of the parathyroid response, predisposing renal mineralisation and formation of urinary calculi.

    Some of the more common calcium supplementation medications – both parenteral and oral formulas – are detailed in Table 1. Supplementation of magnesium may also benefit some patients, as it is a common concurrent finding in critically ill patients with iHCa.

    Table 1. Common calcium supplementation medications
    Drug Calcium Content Dose Comment
    Parenteral calcium
    Calcium gluconate
    (10% solution)
    9.3mg/ml
    i) slow IV dosing to effect (0.5ml/kg to 1.5ml/kg); acute crisis, 50mg/kg to 150mg/kg over 20 to 30 minutes
    ii) 5mg/kg/hr to 15mg/kg/hr IV or 1,000mg/kg/day to 1,500mg/kg/day (or 42mg/kg/hr to 63mg/kg/hr)
    Stop if bradycardia or shortened QT interval occurs.
    Infusion to maintain normal Ca level
    SC calcium salts can cause severe skin necrosis/mineralisation.
    Calcium chloride
    (10% solution)
    27.2mg/ml 5mg/kg/hr to 15mg/kg/hr IV Do not give SC as severe perivascular irritant
    Oral calcium
    Calcium carbonate
    (many sizes)
    40% tablet 5mg/kg/day to 15mg/kg/day
    Calcium lactate
    (325mg, 650mg)
    13% tablet 25mg/kg/day to 50mg/kg/day
    Calcium chloride
    (powder)
    27.2% 25mg/kg/day to 50mg/kg/day May cause gastric irritation
    Calcium gluconate (many sizes) 10% 25mg/kg/day to 50mg/kg/day

    Next time…

    The next blog will look at the pathophysiology behind iHCa among critically ill animals. It will also look at the controversy regarding treatment of non-clinical iHCa cases and the prognostic indications of iCa concentrations.

  • Ionised hypocalcaemia, pt 2: eclampsia

    Ionised hypocalcaemia, pt 2: eclampsia

    As discussed in part one of this blog series, a myriad of disease processes can lead to ionised hypocalcaemia (iHCa).

    Despite this, only hypocalcaemia caused by eclampsia and hypoparathyroidism (primary or iatrogenic – post-surgical parathyroidectomy) are severe enough to demand immediate parenteral calcium administration.

    Hypoparathyroidism is quite rare, so this blog will not explore the detailed pathophysiology behind this syndrome. However, it is worthwhile mentioning – aside from primary hypoparathyroidism – no other disease state requires long-term calcium supplementation.

    Eclampsia, on the other hand, is the most common cause of clinical hypocalcaemia in dogs and cats. Multiple factors can predispose animals to the development of this phenomenon, so understanding the pathophysiology behind this potentially fatal disease will not only help with future diagnosis and treatment, but also help prevent this issue.

    Periparturient occurrence

    Eclampsia – also known as puerperal tetany or periparturient hypocalcaemia – occurs in the periparturient period anywhere from the final few weeks of gestation to four weeks postpartum, with the latter being the more common time frame of manifestation.

    The serum concentration of ionised calcium (iCa) is often less than 0.9mmol/L in bitches or less than 0.8mmol/L in queens. It presents as muscle fasciculation and tetany, but not usually in seizure since most patients maintain consciousness. Exceptions occur when these patients are left untreated – these patients may develop refractory seizures, cerebral oedema and death.

    The increased muscle activity generates a lot of heat and uses a significant amount of glucose; therefore, hyperthermia and hypoglycaemia are common sequelae in patients with delayed presentations.

    Reduced iCa

    Eclampsia occurs as a result of reduced iCa in the extracellular compartment. In lactation-associated hypocalcaemia, it is the result of the body’s inability to maintain serum iCa through increased osteolytic activity and gastrointestinal calcium absorption, and reduced renal calcium excretion to compensate for the loss of calcium through milk production.

    Other factors often predispose animals to developing eclampsia. These can include poor periparturient nutrition, excessive calcium supplementation and large litter size.

    Excessive calcium supplementation in the prenatal period causes parathyroid gland atrophy, preventing parathyroid hormone release – resulting in reduced gastrointestinal calcium absorption and osteoclastic activity, and increased kidney calcium loss.

    Clinical signs

    Clinical signs can progress rapidly and become fatal if left untreated.

    In the early phases, non-specific signs can present as:

    • facial pruritus
    • hyperaesthesia
    • panting
    • tremors
    • muscle fasciculations
    • paresis
    • ataxia

    Within a few hours, these clinical signs rapidly progress to rigidity, and tonic and clonic spasms with opisthotonos. By this stage, animals will develop severe tachycardia, tachypnoea and hyperthermia. Without treatment, a high mortality rate exists.

    kitten
    “Early supplementation of puppies and kittens with commercial milk formula will significantly reduce the lactation demand on the dam.” Image © Dobroslav / Adobe Stock

    Patients presenting with eclampsia require immediate medical intervention, as well as concurrent supportive therapy. The acute management of clinical iHCa is the same, regardless of the cause, and will be discussed in detail in part three.

    Supportive therapies required to manage and prevent a patient relapsing in eclampsia often include active cooling and glucose supplementation. In cases that seizure, anti-seizure medications – such as diazepam and barbiturates – and mannitol for cerebral oedema may be required.

    Prevention

    Even before getting to the stage where an animal requires treatment, all effort must be taken to prevent a dam from developing hypocalcaemia. This can be easily achieved by improving the calcium content of the food during the perinatal period, as well as reducing the milk demand by early weaning kittens or puppies. This is likely particularly helpful for those with a history of eclampsia or with large litters.

    From the second half of gestation, it is recommended a commercial formulation of puppy/kitten food (1% to 1.8% calcium and 0.8% to 1.6% phosphorus) is to be fed to the dam without any additional minerals or vitamin supplementation.

    Postpartum calcium is similar to the second half of gestation, requiring a diet containing at least 1.4% calcium with a 1:1 ratio with phosphorus (most balanced growth formula for puppies and kittens).

    Less demand

    Early supplementation of puppies and kittens with commercial milk formula will significantly reduce the lactation demand on the dam. Together with this, starting at aged three to four weeks, solids can be introduced at this time. These techniques will be particularly helpful to those with a history of previous eclampsia or those with large litter sizes.

    Aside from the parenteral calcium supplementation required, other supportive therapy – such as active cooling, IV fluid therapy and glucose supplementation – may be required.

    Long term, the dam’s nutritional content of calcium must be optimal from the second half of gestation. All additional calcium or other vitamins and mineral supplementations should not occur prior to parturition.

    In the postpartum dam with a history of eclampsia or that is at risk, changing to a nutritionally balanced commercial food aim for growing puppies and kittens is ideal. Early weaning – or abrupt weaning if hypocalcaemia is severe – may be required in severe cases or those with a high risk of relapse/development.

  • Ionised hypocalcaemia, pt 1: introduction

    Ionised hypocalcaemia, pt 1: introduction

    Low ionised calcium (iCa) is a widely recognised electrolyte disturbance in critically ill human patients who have undergone surgery, are septic, have pancreatitis, or have sustained severe trauma or burns.

    Similar changes occur in our critical canine and feline patients, though less well documented.

    Calcium plays a vital role in a myriad of physiological processes in the body, so any deviation from the very narrowly controlled range is associated with severe repercussions.

    Low iCa has many causes; however, this three-part blog will only focus on the more common and peracute to acute causes. It will also discuss the treatment of low iCa and the controversy behind treatment of iCa in critically ill patients.

    Forms

    Calcium in the serum or plasma exists in three forms:

    • ionised or free calcium
    • protein-bound calcium
    • complexed or chelated calcium (bound to phosphate, bicarbonate, sulfate, citrate and lactate)

    iCa is the biologically active fraction of calcium and is not to be confused with total calcium (tCa). A lack of concordance exists between the two. Adjustment formulas are inaccurate, even with the correction of the tCa to serum total protein or albumin concentration, and should not be used to predict iCa.

    The normal reference range for iCa in dogs is 1.2mmol/L to 1.5mmol/L; in cats, it is 1.1mmol/L to 1.4mmol/L.

    Function

    An example of low ionised calcium.
    An example of low ionised calcium.

    Calcium is essential in maintaining normal physiological processes in the body. iCa regulates:

    • vascular tone
    • myocardial contraction
    • homeostasis

    In addition, it is needed for:

    • enzymatic reactions
    • nerve conductions
    • neuromuscular transmission
    • muscle contraction
    • hormone release
    • bone formation
    • resorption

    In critical patients, particularly those with severe trauma or sepsis, vascular tone and coagulation is particularly important. For this reason, iCa is tightly kept in a narrow range and regulated by the interactive feedback loop that involves iCa, phosphorous, parathyroid hormone, calcitriol and calcitonin.

    Diseases and causes

    Diseases commonly associated with low iCa in dogs and cats include:

    • acute kidney failure
    • acute pancreatitis
    • diabetic ketoacidosis
    • eclampsia
    • ethylene glycol intoxication
    • protein-losing enteropathies
    • sepsis
    • trauma
    • urethral obstruction
    • parathyroid diseases
    • tumour lysis syndrome

    Situations altering the fraction of extracellular calcium seen on a regular basis include:

    • acid-base disturbances
    • lactic acidosis
    • protein loss or gain
    • increased free fatty acids

    Iatrogenic causes include:

    • citrate (anticoagulant) administration during blood transfusions
    • phosphate
    • bicarbonate
    • sulfate administration

    Low iCa can also develop during cardiopulmonary resuscitation, quickly declining with increased duration.

    • Part two will go into more depth regarding the most common causes of low iCa that require acute treatment, the treatment involved, controversies surrounding treatment of non-clinical low iCa, and prognostic indications.
  • Seizures, part 2: the differentials

    Seizures, part 2: the differentials

    In part one of this series we discussed the important questions to ask when taking a history from owners of dogs and cats that are having seizures. In this part, we look at the differential diagnoses for these cases.

    There are many ways to classify the different causes of seizures, but the simplest is as follows:

    • Structural – where intracranial pathology is causing the seizures.
    • Reactive – where an extracranial issue is causing a seizure response in a normal brain.
    • Idiopathic – a diagnosis of exclusion where we are unable to identify a reason for the disturbances in brain activity.

    Structural

    Intracranial differential diagnoses include:

    • inflammatory processes (meningoencephalitis), such as steroid responsive meningitis-arteritis
    • viral diseases (for example, distemper)
    • metabolic storage diseases
    • neoplasia
    • vascular accidents involving clots or bleeds
    • hydrocephalus
    • trauma

    Reactive

    Extracranial differentials include:

    • hepatic encephalopathy due to hepatic failure or a portosystemic shunt
    • various toxicities, such as lead, chocolate, caffeine, ethylene glycol, parasiticides and slug/snail bait
    • metabolic issues, such as hypoglycaemia, hypocalcaemia and thiamine deficiency

    Idiopathic

    If diagnostic investigations (including advanced imagery, such as MRI) are unable to identify an underlying cause of recurrent seizures, this is referred to as idiopathic epilepsy.

    To break down this list of differentials into a more relevant and concise list is to consider the most common differentials according to signalment.

    In dogs less than a year old:

    • portosystemic shunts
    • inflammatory conditions of the brain
    • distemper
    • hydrocephalus or storage disease
    • toxicity

    In dogs one to five years old:

    • idiopathic epilepsy
    • inflammatory
    • toxicity
    • cerebral neoplasia

    In dogs of five years or older:

    • cerebral neoplasia
    • inflammatory
    • toxicity
    • idiopathic epilepsy
    • metabolic disease
    • vascular issues

    In cats:

    • toxoplasmosis
    • FIP, FeLV and FIV
    • audiogenic reflex seizures (older cats)
    • neoplasia
    • trauma
    • toxins
  • Blood gas analysis, pt 2: acid-base disturbances

    Blood gas analysis, pt 2: acid-base disturbances

    Acid-base disturbances are common in critical patients. These changes must be identified, as even minor deviations from the normal range can lead to significant abnormal body functions.

    Acidaemia and alkalaemia

    Acidaemia, which occurs when blood pH falls below 7.35, will lead to:

    • impedance of cardiac output
    • reduced cardiac contractility
    • a blunted response to catecholamine manifesting as hypotension
    • antagonism to insulin
    • a compensatory hyperkalaemia (extracellular movement of potassium in exchange for hydrogen ions [H+])

    Alkalaemia – blood pH above 7.45 – although less critical compared to acidosis, will result in:

    • muscle spasm
    • stuporous mentation
    • hypocalcaemia
    • hypokalaemia (intracellular movement of potassium in exchange for H+)

    As well as the aforementioned altered functions, H+ is essential for the normal function of enzymes and maintenance of normal cell structures. This is why the body maintains a very narrow pH range and uses multiple buffering mechanisms to achieve this.

    Buffering systems

    The two main buffering systems are the kidneys and lungs.

    Kidneys adjust the pH via the excretion of H+ and the uptake of bicarbonate (HCO3-), which is the primary extracellular buffer and has a linear relationship with pH.

    An increase in HCO3– concentration will result in a pH increase and vice versa. This mechanism can take hours or days from the time a shift in the pH is detected.

    The main respiratory buffer is CO2 – an acid. CO2 has an inverse relationship with pH, so an increase is equivalent to a lower pH level and vice versa. The effect of respiratory adjustments is immediate. This occurs by altering the respiratory rate to adjust CO2 levels.

    The first step towards interpretation of acid-base disturbances is identifying whether an alkalaemia or acidaemia is present. The next blog will discuss determining what is causing it – identifying the primary disorder and the compensatory mechanism employed to balance it out.

  • How the vet degree has shaped my plate

    How the vet degree has shaped my plate

    Before coming to university, I never really gave much thought to the life or journey of my food before it ended up on my plate; I wasn’t well informed on the topics of air miles, methane production or abattoir welfare standards.

    If you had asked me if I wanted to make sure the foods I ate were ethically sourced, had a low carbon footprint, or had once lived a healthy and happy life, I would have said “of course” – all of these things mattered to me on a subliminal level, but I don’t think I really grasped how any of these concepts were within my control.

    Welfare

    Animal welfare makes up such a large part of the veterinary course from the very first year, so it’s no wonder so many students are vegetarian or vegan by the time they graduate. I must admit that my Easter Sunday lunch was a little hard to swallow after my first-year lambing placement… and one week on a pig farm certainly had me seeing my Christmas pigs in blankets in a whole new light.

    The vet course provides a window into the side of meat production the public will never access – and may not even want to.

    In an ideal world (where every animal has a full and healthy life devoid of stress, discomfort or suffering before it is killed), I would have no qualms about eating meat, but the sad truth is that’s just economically and logistically unviable – at least for now.

    But welfare isn’t as cut and dried as people might think. Take cows, for example: if you picture a happy cow, it’s probably roaming around in a field, right? Well, frustratingly, fields have many disadvantages – offering parasites, botulism and rogue pieces of metal, while providing no protection from the elements, nor a means for the farmer to moderate their food intake to ward off laminitis, hypocalcaemia and a bunch of other welfare issues.

    “One week on a pig farm certainly had me seeing my Christmas pigs in blankets in a whole new light.” Image © HQUALITY / Adobe Stock

    The environment

    Along with owning a pair of flared jeans, or developing calves of steel thanks to the endless hills, you didn’t go to the University of Bristol unless you’ve developed a complex over your carbon footprint.

    One of the simplest ways to be more environmentally friendly is to eat less meat, but many studies are showing that a global move to veganism/vegetarianism is not the answer for our ever-growing population. A lot of land just isn’t suitable for crops, and rice farming already makes up more than 10% of global methane production.

    Again, if we were looking for an ideal scenario, it would be to eat less meat, sourced locally and sustainably, and to value it enough to pay a price that would allow farmers to invest in greener technologies.

    Student budgets

    Working on farms at all levels of the course gives vet students an appreciation for how much farmers care about their animals, and how hard they work to balance that priority with sustaining a business. Even if you’re sceptical about the meat industry, there is always the option to do research into the farms and butchers that are close to you.

    Frustratingly, making good choices from both a welfare and environmental perspective can be much pricier than the alternatives, and this has been one of my own drivers for decreasing my meat consumption during my uni career. Despite this, I still try very hard to make informed choices, and when I do buy meat I aim to prioritise quality over quantity wherever possible.

    In very small, but meaningful ways, change is shaped by the decisions and purchases we all make, and understanding the steps that brought the ingredients from the farm to your plate fosters a respect and appreciation for what you are eating, beyond just its taste.

  • Should you employ a new grad?

    Should you employ a new grad?

    This weekend, I helped out with a talk at SPVS-VMG Congress on employing new graduates.

    It gave delegates – vets, VNs, employers and new grads themselves – the opportunity to reflect on how wildly different each new grad’s experience can be, and appreciate the challenges employers face when hiring new grads.

    The fact those in attendance had chosen to come to a talk on ensuring practice is right for new grads suggested most of our audience were forward-thinking employers who wanted to provide their new grads with a good start to their career.

    The others

    However, and sadly, not all employers have that at the top of their priority list. I would like to think such employers – who, as a result, are maybe not treating their new grads well – aren’t doing it maliciously, but rather just don’t have the time to teach and mentor properly, but also don’t have a choice but to take on new grads, given the employment crisis the profession faces.

    However, that is still no excuse. I should also mention, of course, the minority of employers that will hire a new grad simply for cheap labour – meaning there is little to no interest in them at all. If you cannot provide adequate support for a new grad, don’t employ one – it isn’t fair on anyone.

    My generation

    Clock
    Lazy? Or valuing non-work time? Image © Free Photos / Pixabay

    Many of the challenges of employing a new graduate stem from the difference in attitudes between different generations. The new grads moving through the system now are of the “millennial” generation often stereotyped as lazy, entitled and needy.

    Being a millennial myself, I inherently disagree with these generalisations – they just need looking at differently:

    • We are not lazy, we just don’t want to work horrendous hours. We are more than happy to work strange shifts (evenings/nights), but that doesn’t mean working the traditional expectation of five long days, a full weekend on call and a further five days.
    • We are not entitled, we just cannot justify the negatives of the profession long-term. The “love of veterinary medicine“ is very idyllic, but just isn’t sustainable in the real world. We could work less hours, be paid more, take holidays when we want and be paid reasonable sick pay in many other sectors, so why wouldn’t we? It’s not about the money, here – it’s about the injustice.
    • We are not needy, we just crave feedback. How do we know we’re doing okay unless you tell us? How do we know how to improve if you don’t guide us?

    Wake-up call

    Some vets of the older generations still have the attitude of “we had to go through it, so you have to get on with it too” – as though the horror of being left to your own devices, being unable to contact anyone in the middle of the night when you are out of your depth, and the sleep deprivation of internships are just a “rite of passage” of being a new grad. It may be news to these bosses, but the new grads of today just won’t put up with that crap.

    “The definition of insanity is doing the same thing over and over again, but expecting a different result” is a quotation often attributed to Einstein. Whether he ever actually said it is questionable, but it has applications in many walks of life. When these old-style partners still expect their new grads to be on call for 17 nights in a row, is it any wonder there is an employment crisis?

    If you want to attract any staff, not just new grads, you’ve got to adapt to the present. Veterinary is changing and the modern new grad doesn’t want – and won’t settle – for the same things they did 50 years ago.

    Let’s talk

    Two vets with a horse
    Support… it’s all we need. Image © 135pixels / Adobe Stock

    So, what do new grads want? Well, how long is a piece of string? The simple fact is: we are all different. The key to having a successful working relationship with a new grad is communication and flexibility.

    The one thing all new grads want is support, but what that support actually looks like can vary wildly. For example, sometimes the new grad themselves will underestimate or overestimate how much support they need, which is why it is important for the learning process to be continual, with frequent check-ins.

    It’s all very well saying I’ll only need second on-call backup for two months, but if, after that time, I still haven’t done a caesarean or calving, how can I be expected to be able to handle it alone?

    Of course, this works both ways – new grads need to be upfront and honest about what kind of support they think they need, and practices likewise need to be honest about what they can provide.

    If either party are overselling themselves to secure a job/vet, the arrangement will not work out long-term and both of you will be on the hunt again much quicker than you would like.

    What we can do

    So, why should you bother employing a new grad if you have to put lots of extra effort and time into it compared with employing an experienced vet? We new grads have a lot to offer:

    1. We are tech-savvy (usually much more than our older counterparts).
    2. We have lots of new ideas and experiences from a variety of placements in different practices.
    3. We have up-to-date knowledge since we are fresh out of universities undertaking research into the newest techniques and treatments.
    4. We are enthusiastic – despite refusing to put up with the poor working environments of the past, we are yet to become cynical about the veterinary profession.

    What we lack is experience – and that is what we ask of you. Sure, the harsh truth may be that you don’t really have a choice in the employment climate as it stands, but if you get it right – and your new grad stays with you for years to come – it will be a true investment.