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Tag: Dogs

  • It’s time to hydrate: nutritious hydration solution hits veterinary wholesalers!

    It’s time to hydrate: nutritious hydration solution hits veterinary wholesalers!

    They’re not eating. They’re not drinking. And they’re turning their nose up at everything you offer. Add post-operative food aversions to a need to initiate voluntary fluid and food intake, and it can feel like an uphill battle of wills.

    What have you got that supports hydration, is easily digestible and is palatable enough to encourage eating and drinking in your hospitalised and at-home patients?

    Furr Boost has the answer…

    It started with the bladder

    Encouraging her poorly beagle Phoebe to drink is a battle Louise Toal faced after her vet diagnosed urinary issues. She just wasn’t interested in drinking. Luckily for Phoebe, Louise is a Food Technologist and began experimenting with protein shakes for dogs, to bolster hydration and combat inappetence. This is when Furr Boost was born.

    It’s more than a hydration drink; it supports healthy digestion, immunity, metabolism and anxiety… plus, it’s delicious.

    Furr Boost has taken the pet market by storm and even braved the Dragon’s Den dragons. Now, this highly palatable, nutritious hydration solution has hit your wholesalers for use in clinic!

    What is Furr Boost?

    In short, it’s a nutritional superfood smoothie for your canine and feline patients. Packed with 100% natural, functional ingredients and no fillers. It’s a low fat, but irresistible blend of meat, fruit and vegetables to use as a drink, food topper or boredom breaker.

    Low in purine, protein, sodium and phosphorous, it’s ideal for encouraging inappetent patients to eat and hydrate post-operatively, during hospitalisation, and at home.

    Hydration

    Water… but tasty! More than 75% moisture content to replenish lost fluid and nutrients.

    Healthy metabolism

    Contains low-fat protein sources plus a blend of oils to provide energy for metabolism and to support a normal recovery.

    Immunity

    Packed with ingredients to support a robust immune system.

    Digestion

    Pre-biotics and dietary soluble fibre aid normal digestion and maintain healthy gut motility.

    Anxiety

    B vitamins and water combat anxiety. Use frozen or on lick mats to distract anxious patients.

    Skin and coat

    Full of naturally occurring fatty acids and omega 3 and 6 for hydrated, healthy skin and a glossy coat.

    Furr Boost case study – meet Ozzy

    Meet Ozzy the Saluki who was diagnosed with canine meningitis on 24 June, weighing in at 16Kg and was stabilised by the wonderful medical team who treated him.

    Owner Jayne was very worried for her beloved pet and could see the visible signs of not only his weight loss after his ordeal, but also his mood.

    Jayne said: “When he came home he was so skinny, dehydrated and reluctant to engage with food and drink despite what I tried. Then I discovered Furr Boost and imagine my delight when he absolutely lapped it up with real enthusiasm. He absolutely loves it!

    “I was struggling to get him interested in eating anything to try and build him up while he was taking seven steroids a day. A Furr Boost a day has aided his progress I am sure. He is still on four steroids a day but his weight is now a healthier 22kg. Hoping for dose to reduce to two per day next week.

    “It’s been a long job and he is very flat with the medication, which hopefully will start to improve. I was just so grateful to find your drink when things were looking very grim for him.”

    While Furr Boost is mainly for hydration, the all-natural and human-grade ingredients are used to entice the dog to drink or eat if used as a topper. Our highly palatable formula is irresistible to even the fussiest of dogs and is packed with oils and nutraceuticals to get dogs back on their feet. Our drinks can be used in their pourable form or, for dogs who are not drinking, watered down by up to 50% to push fluids*.

    * We recommend dogs drink 50ml of fluid per body weight and in extreme cases fluid intake should always be monitored.

    Where does Furr Boost fit into your practice?

    Whether it’s in the kennels, in recovery, or to recommend to your clients, Furr Boost is a highly palatable, convenient source of hydration and nutrition. Give as a drink to replenish lost fluids and nutrients, or feed it to encourage voluntary enteral eating and drinking, and to support normal gut motility.

    If patients are food-averse, or the palatability of recommended diets is causing food refusal, add Furr Boost as a topper to soften kibble and entice their tongues back into action, with a range of lip-smackingly delicious flavours.

    Furr Boost is suitable for:

    • all dogs and cats over the age of eight weeks
    • pregnant and whelping bitches and queens
    • recovery
    • dogs requiring a low sodium, protein, phosphorous or purine diet
    • maintaining hydration
    • supporting weight management or low-fat diets
    • encouraging inappetent dogs
    • end-of-life support
    • distraction and enrichment, particularly for anxious or immobile patients

    Get your free sample at The London Vet Show

    Have you got a patient in mind that Furr Boost could support? Would you like to test it in your clinic?

    Come along to stand F66 at the London Vet Show on 14-15 November 2024 to grab your free carton!

    Not going to be at the show?

    No worries, Furr Boost is now available via MWI Animal Health, Covetrus, and IVC Evidensia, or you can order directly at www.furrboost.com/veterinary where our team is also available to answer any questions.

  • Highlighting oesophageal foreign bodies on radiographs

    Highlighting oesophageal foreign bodies on radiographs

    before
    Lateral feline chest radiograph before contrast.

    QUICK TIP: Need to know if there is an oesophageal foreign body but can’t be certain on radiographs?

    We have all been in the scenario where we are unsure whether there is an oesophageal foreign body on the radiographs we have just taken.

    You might think of using a contrast medium to help, and the first that always comes to mind is barium. However, my personal first choice is a iodinated contrast medium – urografin, for example.

    Advantages

    Why? Their use is typically limited to myelograms or intravenous contrast studies but they can be given orally as well, for the assessment of oesophageal foreign bodies.

    after
    Lateral feline chest radiograph after contrast.

    The advantage of using this over barium is that if this dye is accidentally aspirated it does not cause pneumonia like barium can.

    How to

    Using iodinated contrast medium is simple:

    • Given orally non-diluted, Dogs: 5-10ml, Cats: 5ml – you can give more if necessary
    • Immediately repeat the radiographs
    • If there is anything in the oesophagus, it will be highlighted

    Tip of the Week author Gerardo Poli is the author of The MiniVet Guide to Companion Animal Medicine – now available in the UK.

  • Oh, CR*P! Using point-of-care C-reactive protein tests

    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?”

  • Managing thrombocytopenia in cats and dogs: part 2

    Managing thrombocytopenia in cats and dogs: part 2

    Last week we discussed the causes and diagnostic pathway for investigating immune-mediated thrombocytopenia. This week we will go through the management of this condition.

    Despite the fact red blood cells are not actually being destroyed, a severe anaemia can develop from blood loss due to coagulopathy – a common reason for why they present to emergency practices. The management of these patients is broken down into three main areas:

    • improving oxygen delivery
    • commencing immunosuppression
    • management of the underlying cause (if identified)

    Optimising oxygen delivery in the acute phase is going to keep them alive long enough for immunosuppression to work. This is achieved through IV fluids to help improve perfusion and blood transfusions to replace red blood cells. If fresh whole blood is available, it can assist in increasing platelet numbers, but generally it is not very effective.

    Platelet transfusions using platelet-rich plasma can be considered if it is available. Plasma transfusion is not effective at managing the coagulopathy as it is due to a loss of platelets, not a loss of coagulation factors.

    Immunosuppression

    Large areas of ecchymotic haemorrhage on the skin are a quite obvious sign of thrombocytopenia.
    Large areas of ecchymotic haemorrhage on the skin are a quite obvious sign of thrombocytopenia.

    Immunosuppression therapy is often commenced concurrently as the patient is being stabilised.

    The first choice is either dexamethasone 0.5mg/kg IV every 24 hours if the patient is not stable enough for oral medications; otherwise, once stable, start prednisolone at 2mg/kg by mouth per day divided every 12 hours.

    Other immunosuppressive agents include:

    • Azathioprine – 2mg/kg by mouth every 24 hours then 0.5mg/kg by mouth every other day. The main concerns are bone marrow suppression and hepatoxicity – also, it is very toxic in cats.
    • Ciclosporin – 5mg/kg to 10mg/kg by mouth divided twice a day; cats 5mg/kg by mouth every 24 hours.
    • Chlorambucil could also be used at a dose of 0.1mg/kg/day to 0.2mg/kg/day by mouth if the response to prednisolone is insufficient.

    Management

    Management of the underlying cause should be commenced if a cause is identified, but this is often not the case.

    Other management options include:

    • Vincristine can be trialled to increase platelet number as it stimulates the release of platelets from the bone marrow.
    • Gastroprotectants can be considered if gastrointestinal bleeding has occurred – these include proton pump inhibitors and sucralfate.
    • Strict confinement, potentially sedatives and minimal blood sampling are important to minimise injury that may result in further bleeding and blood loss.
    • Antithrombotic therapy is not part of standard management as, unlike immune-mediated haemolytic anaemias, thrombotic events rarely occur.

    When it comes to monitoring, platelet counts are performed daily until more than 40 × 109/L – this can take up to two weeks to occur.

    Once above this level, take weekly counts until the numbers have normalised. Once they have, taper immunosuppressive medications over four to six months, with 20% dose reduction every couple weeks, generally with the adjunctive immunosuppressants first and prednisolone last.

  • Managing thrombocytopenia in dogs and cats: part 1

    Managing thrombocytopenia in dogs and cats: part 1

    Thrombocytopenia is a condition characterised by a decrease in platelet numbers, which is often caused by increased destruction of platelets or a decrease in production.

    Thrombocytopenia can manifest in many ways – the signs can be subtle and easily missed, such as small petechiae on gums, or quite obvious signs, such as large areas of ecchymotic haemorrhage on the skin.

    Ecchymotic haemorrhages are often attributed to disorders of secondary haemostasis, such as rodenticide intoxication, but it can also occur with thrombocytopenia depending on the severity and chronicity.

    Other common clinical signs include:

    • epistaxis
    • blood in stools, urine or vomit
    • pale mucus membranes
    • lethargy
    • weakness

    Therefore, the first step to managing a patient with a severe thrombocytopenic episode that has resulted in significant blood loss is to manage shock, if present, with IV fluids, then administer a red blood cell transfusion.

    Patient handling

    Careful patient handling is critical as these patients can bleed easily, leading to blown veins, large bruises that contribute to the development of anaemia and significant patient discomfort. Beyond initial patient stabilisation, the next step is to determine the underlying cause.

    Diagnosing thrombocytopenia is relatively straightforward with the demonstration of low platelet counts. Generally, bleeding does not occur until the platelet count drop below 40,000 thousands per cubic milliliter (k/uL). This can be determined by either a haematology machine or manually via blood smear analysis.

    When assessing blood smears, the general rule is one platelet per high-powered field on the monolayer is equal to 15,000k/uL. With either method, you must assess for platelet clumping on a blood smear as this can artefactually drop platelet numbers, leading to a false diagnosis.

    Causes

    PCR
    The thrombocytopenic diagnostic pathway includes assays such as PCR. Image © science photo / Adobe Stock

    The diagnostic pathway should not stop there. It needs to continue to determine the underlying cause.

    The most common cause of thrombocytopenia is immune-mediated destruction. This can be either a primary (diagnosis of exclusion) or secondary cause (such as Rickettsia infection, and drugs such as sulphonamides, toxins and neoplasia). Other less common causes include:

    • splenomegaly, which can lead to platelet sequestration
    • disseminated intravascular coagulation and acute blood loss, leading to platelet consumption
    • bone marrow disease, which results in reduced platelet production

    Signalment and history will refine such a diagnosis, as certain breeds are more prone to developing thrombocytopenia than others – for example, grey collies due to a defect in haematopoietic stem cells, and whippets and greyhounds, which traditionally have a lower platelet count than other breeds.

    The generally diagnostic pathway continues to include haematology and biochemistry, thoracic radiographs, abdominal ultrasound and depending regional prevalence testing for infectious organisms with PCR and ELISA assays.

    Next week I will cover the management principles of the thrombocytopenic patient.

  • Using lactate measurements in general practice

    Using lactate measurements in general practice

    Several easy and affordable ways exist to measure lactate in general practice, which means the clinical applications of monitoring lactate is no longer the reserve of specialist and emergency centres.

    But why and how should you be using it in general practice?

    What is lactate again?

    When oxygen is not effectively delivered to cells throughout the body – which, in our patients, will mostly be due to hypoperfusion (for example, hypovolaemia, vasodilatory shock and cardiac disease) – cells will switch from aerobic to anaerobic metabolism to stay alive.

    Think of anaerobic metabolism as the fuel-powered generator that kicks in during a power cut – it’s not as good, but it’ll keep the lights on for a while. However, unless the power comes back on, the generator will eventually also fail and plunge you into darkness.

    Lactate is the end product of this process of anaerobic metabolism. To be clear, lactate is not the bad guy – in fact, it plays an important role in keeping the cells going until they have access to sufficient oxygen again. It’s simply the bearer of bad news.

    Why should I care?

    Anaerobic metabolism – similar to a fuel generator being used during a power cut. Image © bildlove / Adobe Stock
    Anaerobic metabolism – similar to a fuel generator being used during a power cut. Image © bildlove / Adobe Stock

    Because lactate is the harbinger of doom; it’s the leading horseman of the apocalypse…

    When lactate is high, you should stop whatever else you are doing and pay attention to the patient in question – this patient is probably surviving on anaerobic metabolism. It is critically ill and possibly heading for a long walk in the great park in the sky…

    How should I use it?

    It is valuable in any patient with any serious illness or injury. Things that should make you consider checking lactate would be:

    • slow capillary refill time
    • any mucous membrane colour other than a nice, healthy pink
    • increased heart rate
    • weak or bounding pulses
    • significant dehydration
    • depressed mentation
    • history of major trauma
    • major infections
    • significant blood loss
    • any disease that has the potential to progress into a life-threatening condition

    …basically, any animal sick enough to make you worry about it possibly dying.

    Run it with your initial diagnostics to get a baseline level, and run it within 10 minutes of taking the sample.

    What do I do about my results?

    Normal range

    What do my results mean?

    < 2.5  ?

    3-4 ? ?

    4-6  ? ?

    > 6  ? ?

    (levels in mmol/L)

    If it’s within the normal range then check regularly – ideally until your patient is well on its way to a full recovery.

    Lactate levels may start increasing in response to hypoperfusion before the patient starts showing overt signs of deterioration – the fuel in the generator hasn’t run out yet – which makes it a very useful monitoring tool to detect problems early on.

    We find a six to eight-hourly check in very sick patients will pick up deterioration fast enough to give you time to react, while a twice-a-day check in more stable animals will suffice.

    Elevated

    If it is increased at any point, you need to focus immediately on trying to reduce it.

    This usually means starting with fluid boluses for shock. Recheck lactate one hour after initiating the appropriate therapy. Your goal is for the lactate value to be reduced by approximately 50% within one to three hours (ideally one hour) of initiating therapy. If it’s coming down nicely then keep checking every two to three hours.

    You want it to be back to normal within 24 hours (48 hours max).

    Nothing working?

    If it has not decreased as expected – or, especially, if it increases despite treatment – it means things are going seriously wrong. At this stage you need to:

    • Devote all your attention on trying to find and correct the underlying cause while you adjust your emergency therapy to address hypoperfusion.
    • Speak to the owners.
    • If you do not have the time, facilities or experience to deal with shock cases, you need to consider referring the patient to a specialist centre urgently for stabilisation, if this is an option available to you.

    Remember…

    Intense exercise, muscle tremors and seizures are associated with anaerobic muscle activity and can, therefore, cause significant increases in lactate levels (the cause of the “deep burn” when you’re dying in that CrossFit class). This can also occur when a patient resists when you are taking blood, or starts trembling in fear the moment it walks into the clinic, which can cause misleading lactate results.

    Puppies can have a higher “normal” level of plasma lactate up to seven months of age.

    Anaemia does not generally cause hyperlactataemia unless it is very severe, but by this stage you shouldn’t need lactate to tell you the patient is in serious trouble.

    Having said that, normal lactate levels that suddenly start climbing in a hospitalised “stable” anaemic patient could be the push you need towards giving that blood transfusion.

  • 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

  • Rat bait’s sneaky trick: bleeding into the dorsal tracheal membrane

    Rat bait’s sneaky trick: bleeding into the dorsal tracheal membrane

    Most of us are familiar with anticoagulant rodenticide toxicosis and the range of clinical signs it can present with, but there is one potentially fatal manifestation of coagulation pathology that is perhaps not as widely known…

    Dogs with severe clotting problems will occasionally bleed into the dorsal tracheal membrane. This causes collapse of the thoracic trachea and can lead to severe respiratory distress.

    Presenting signs

    These cases can present with none of the other signs of bleeding normally associated with coagulopathies, so rat bait poisoning may not come to mind as a differential diagnosis if you are not aware of this syndrome.

    The typical case will present as an otherwise healthy dog that develops acute respiratory problems. Early signs can be as mild as a persistent cough, but it can quickly escalate into a life-threatening respiratory crisis.

    Severe cases will have an obvious stridor on both inspiration and expiration, cyanotic mucous membranes, and patients may be very distressed.

    It will look very much like:

    • a dog that is choking from a tracheal foreign body
    • an old dog with tracheal collapse
    • the end stages of laryngeal paralysis – except the stridor will come from much lower in the respiratory tract than it does in laryngeal paralysis

    So, what do you do?

    On initial presentation you would approach it as any respiratory distress case: oxygen, oxygen, oxygen, calm and stress-free handling, and light sedation (butorphanol, for example).

    bleeding_dorsal-tracheal-membrane

    Once it is safe to do so, you should take chest rads to look for what you’ll probably suspect is a tracheal foreign body, and you’ll get an image like the one above (although it may not be this severe). Then you’ll remember this article, have an “aha!” moment and run a clotting profile (but if it’s as bad as this case, you’ll obviously first save the animal’s life by passing an ET tube).

    Once a clotting problem is confirmed you’ll need to stop the bleeding with standard therapy for anticoagulant rodenticide toxicity: plasma and vitamin K.

    Severe cases

    In a severe case you may need to keep the dog intubated for several hours, until the clotting times have normalised, before cautiously attempting to extubate.

    If the patient is unable to stay well oxygenated without an ET tube (mucous membrane colour, pulse oximetry, blood gas), consider placing a long oxygen catheter past the narrowing – either via a tracheostomy or a nasal O2 catheter.

    If these cases are quickly recognised for what they are, and an open airway can be maintained, the prognosis should be good. These are potentially very satisfying cases with great potential for you to be a total hero.

  • 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.