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Tag: Panleukopenia

  • 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.

  • 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 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.
  • Blood transfusions, pt 2: what do I give?

    Blood transfusions, pt 2: what do I give?

    To make the most of a precious resource, donated blood is often separated into two components: red blood cells (packed red cells) and plasma (fresh frozen plasma, most commonly).

    Haematocrit tube
    Haematocrit tube from a patient with immune mediated haemolytic anaemia and a slide demonstrating autoagglutination.

    This not only extends the life span of plasma component, but it also means you can pick and administer which component you need the most as not all anaemic patients need the same product.

    Which product?

    Here are three different examples of patients with different blood product requirements:

    Immune mediated haemolytic anaemia

    This a prime example of a patient that can have an anaemia with transfusion triggers, but are rarely coagulopathic. The key component required here is packed red cells.

    Internal bleed

    This is a grey zone – an anaemia with transfusion triggers can occur, but not always a coagulopathy. A coagulopathy may develop later if the bleed continues. So, packed red cells can be used initially, and the plasma administered after, if required.

    Rodenticide intoxication

    typing kit
    Commercial feline blood typing kit.

    These patients will often need both red blood cells and plasma. So, whole blood – either fresh or stored – can be used, or a unit of packed red cells combined with a unit of fresh frozen plasma.

    Blood typing and crossmatching

    Before administration of the product there is one critical step. Blood typing is important – not only for cats, but also dogs – as it helps rule out blood type incompatibilities and can significantly reduce the risk of an acute transfusion reaction. Easy-to-use commercial blood typing kits (pictured) are available.

    Just because you blood typed doesn’t mean there is no value in crossmatching. Other factors or uncommon red blood types, such as DAL (dogs) and Mik (cats) can cause acute reactions.

    Both these tests do not 100% rule out the possibility of an acute reaction, so, whenever a blood product is being administered, the patient needs to be monitored closely.

    Next week, we cover how much to give.

  • Pancreatitis, pt 2: treatment and prognosis

    Pancreatitis, pt 2: treatment and prognosis

    Last week we covered diagnosing pancreatitis and the challenges associated with doing so. This week we look at management.

    The treatment of pancreatitis largely involves supportive care and monitoring for potential complications. Here, we recap the fundamentals.

    IV fluids

    IV fluids are critical in the acute phase to restore perfusion to core organs and correct hydration deficits. Once achieved, the goal is then to cover maintenance requirements and ongoing losses.

    Hypoproteinemia can develop due to a combination of haemodilution, increased losses in to inflammatory exudates or into gastrointestinal tract, and decreased production due to reduced intake.

    Colloidal therapy or plasma can be considered, but enteral nutrition is more effective and has numerous other benefits.

    Pain relief

    Pain relief largely involves the use of opioids.

    Pure opioid agonists, such as methadone, fentanyl constant rate infusions (CRIs) or fentanyl patches, are most commonly seen in dogs. In cats, partial agonists, such as buprenorphine, are favoured as the condition is generally less painful compared to dogs.

    NSAIDs should be avoided due to concerns of poor perfusion, concurrent kidney and gastrointestinal involvement.

    Antiemetic therapy

    Metoclopromide CRI and maropitant are the mainstays. Antacids, such as esomeprozole, are included to help reduce the risk of gastric ulceration from stress.

    Early enteral nutrition

    Numerous studies have demonstrated the benefit of early enteral nutrition and patients should be encouraged to eat a low-fat diet as soon as possible. Enteral nutrition has been shown to be more beneficial than withholding food as it reduces recovery times and helps maintain enterocyte health.

    If there has been a protracted period of anorexia then a nasogastric or nasoesophageal tube should be placed. A nasoesophageal tube has the added benefit of allowing excessive gastric secretions to be suctioned, as well as for feeding. Due the chronic nature of the disease in cats, oesophagostomy tubes are often placed so that nutritional support can be delivery for prolonged periods of time.

    Antibiotics

    Antibiotics are generally not indicated in canine pancreatitis unless markers of sepsis or if a septic exudate are found (this is an indication for exploratory surgery). In which case, triple antibiotic therapy consisting most commonly of amoxicillin, enrofloxacin and metronidazole are indicated.

    It has been reported 35% of feline pancreatitis patients have bacterial infections; therefore, antibiotics are often included in the treatment of feline pancreatitis.

    Exploratory laparotomy

    This is indicated when the following has occurred:

    • Extra-hepatic biliary obstruction that does not resolve with medical management.
    • Septic abdomen (as mentioned above).
    • Pancreatic abscessation.

    Prognosis

    The prognosis for pancreatitis is variable and dependent on the severity of the disease.

    In mild to moderate canine pancreatitis (which is the most common), the prognosis is generally good as they will normally respond well to supportive therapy and resolution of clinical signs occurs within several days of initiating treatment. However, with severe acute, necrotising pancreatitis, the prognosis is guarded as it can progress into systemic inflammatory response syndrome, disseminated intravascular coagulation and multiple organ failure – which has a high mortality rate.

    The prognosis of acute feline pancreatitis is generally guarded due to the chronic nature of the disease and the propensity to involve multiple organ systems.

  • Pancreatitis, pt 1: diagnosis

    Pancreatitis, pt 1: diagnosis

    Pancreatitis is one of the most common exocrine conditions seen in small animal practice. It is caused by premature activation of enzymes (zymogens) within the pancreas leading to autodigestion, and can result in severe morbidity with the potential to lead to mortality.

    To this day, the diagnosis of pancreatitis remains a challenge – especially in feline patients – and relies on the use of a combination of history, signalment, clinical signs and diagnostic findings.

    Presenting signs

    In dogs, overweight middle aged to older (more than five years old) are at higher risk. Miniature schnauzers, Yorkshire terriers and silky terriers are some breeds identified as higher risk. Approximately 90% present with anorexia and vomiting, 50% with abdominal pain and 30% with diarrhoea.

    In cats, no common age range exists, although domestic shorthair and longhair cats are the most commonly affected. They present more commonly with anorexia and lethargy; 30% presenting with vomiting and 25% with abdominal pain.

    Diagnostic changes

    Pancreatitis-Image---Pancreatitis
    Cases can be confirmed with ultrasound.

    A summary of the commonly seen diagnostic changes are included below, many of which due to the nature of the disease are non-specific:

    • Hyperlipaemia and an inflammatory leukogram can be present, but are both non-specific.
    • Hyperlipasaemia and hyperamylasaemia are commonly seen, but the sensitivity and specificity of both are only about 50%.
    • Elevation in alkaline phosphatase and bilirubin can indicate pancreatic bile obstruction. Other changes may be present and can indicate wider organ system involvement – azotemia, for example.
    • Canine pancreatic specific lipase immunoreactivity (cPLI) has a high sensitivity, but poor specificity – approximately 50%. This means, if real pancreatitis is present, it will show positive; but a positive result will only actually be real pancreatitis 50% of the time. A negative result, however, can be interpreted as “highly unlikely for pancreatitis to be present”. A positive cPLI should be confirmed with ultrasound, which is the gold standard for canine pancreatitis.
    • Feline pancreatic lipase immunoreactivity (fPLI) has been reported to have a sensitivity of 67% and specificity at 91%. This means, 90% of the time, a positive indicates real pancreatitis – but these figures vary between studies. To make things even more difficult, cats with pancreatitis can have normal fPLI/spec fPL and normal ultrasonographic findings.
    • Common changes on ultrasound with acute pancreatitis include free abdominal fluid (generally a non-septic exudate) and hypoechoic pancreas surrounded by hyperechoic peripancreatic fat. As mentioned above, feline pancreatitis often has no visible changes.
    • Radiography may show reduced serosal detail around the pancreatic regions – again, this is not specific or sensitive, but is helpful at ruling out other differentials, such as foreign bodies.

    Summary

    In summary, canine pancreatitis is less of a diagnostic challenge compared to its feline counterpart. There is no single test that can accurately confirm the presence of feline pancreatitis, apart from in biopsies via exploratory laparotomy – which are understandably invasive and costly.

    Next week, we will cover the fundaments of managing pancreatitis patients.

  • Feline aortic thromboembolism

    Feline aortic thromboembolism

    If a cat comes in unable to walk, consider the three Ps:

    • pain
    • paralysis
    • pulselessness

    gerardo_paws
    Figure 1. Colour change in the paws of a cat.

    Feline aortic thromboembolism (FATE) should be on top of your differentials.

    Figure 1 demonstrates the colour change in the paws of an affected cat outlining blood flow: the pink pad is the unaffected cat’s front paw, while the pale pad is on the affected hind limb that will be cold to the touch.

    Cardiological problems

    Often FATE is a secondary condition in cats with heart disease.

    The heart forms clots in the distal aorta that occlude flow to the femoral arteries. With the femoral arteries being the main arteries providing blood flow to the hind limbs, symptoms become apparent.

    Symptoms can include:

    • sudden hind limb paralysis
    • cold hind limbs
    • vocalising
    • pain
  • Temporary catheters in obstructed FLUTDs: buying time with a blocked cat

    Temporary catheters in obstructed FLUTDs: buying time with a blocked cat

    Obstructive feline lower urinary tract disease (FLUTD) is a common presentation in both general practice and emergency settings.

    Every clinician has his or her own approach to treating and managing a cat with obstructive FLUTD signs. Working in an emergency setting, once I have confirmed an obstructed bladder via palpation, I focus on trying to relieve the obstruction as quickly as possible.

    The first step is obtaining consent from the client to administer pain relief (an opioid IV or IM), place an IV catheter, collect blood for biochemistry, electrolyte and blood gas analysis, and temporarily relieve the obstruction.

    At our hospital, we achieve temporary relief of the obstruction generally within 15 minutes of patient arrival.

    Process

    blocked cat
    Obstructive feline lower urinary tract disease is a common presentation in general practice.

    We do this in three steps:

    1. Assess the tip of the penis, occasionally a crystal/mucus plug is all that is blocking the penis.
    2. If this is not the case, I pass a pre-lubricated 22g IV catheter tip (without the stylet) into the penis with a 10ml syringe, containing 0.9% NaCl, connected for hydropropulsion. In the vast majority of cases, this helps to dislodge the urethral blockage enough to enable some urine to pass (urination suggests active urination by the cat).
    3. Once urine is flowing, I pass a 12cm or 14cm rigid catheter, tape it to the tail and leave it in place to allow constant drainage.

    If the 22g IV catheter does not relieve the obstruction, I would use a rigid catheter and progressively advance it up the urethra while hydropropulsing with the saline the entire time. Once unblocked, then I will tape it to the tail as aforementioned.

    Quick Tip: Once you have the catheter in the tip of the penis, pull the prepuce straight out to straighten the penis and thus the penile urethra. Otherwise, the bend in the penile urethra may hinder the passage of the catheter.

    Benefits

    The benefits I see of placing a temporary urinary catheter include:

    • immediate relief to the patient and reduces their stress levels
    • provides a sample for urinalysis
    • allows you time to run through the diagnostic and treatment plan in more detail with clients
    • buys you time to stabilise the patient for their anaesthetic later to place a closed system indwelling urinary catheter and then bladder lavage

    Quite often, your patient would present unwell enough that you should have no issues (resistance to) passing this temporary urinary catheter, provided you have given pain relief on presentation.

    In fractious patients, I usually forgo the temporary catheter and focus on stabilising the patient. The aim is to have them stable as soon as possible for sedation or a general anaesthesia to place a longer indwelling urinary catheter.