Kerry Doolin

Hi Scott,

I get asked this a lot by my OOH vets when managing patients exposed to renal toxins. The evidence to support IVF therapy in exposure NOT AKI is based around maintaining normal renal perfusion and as such GFR. It is reasonable to provide IVF therapy for a short period to maintain this normal renal perfusion. Remember that we may have reasons for reduced intake from vomiting as a presenting complaint, vomiting and reduced intake when we induce emesis and then some sedation from the emetic drugs. So there is a small period of time where preload/volume may be low and the patient a little dehydrated. That along with ensuring perfusion to at risk nephrons is why we do this. The evidence is not specifically from renal toxin exposure. The duration is very unclear years ago we recommended 2-3 days, now I tend to suggest 24h if a renal toxic dose ingestion.

Regarding AKI – the same rates – as long as perfusion is maintained I tend to match UOP as these cases can be oliguric or anuric then polyuric in the recovery phase so we need to monitor that with indwelling urinary catheters and closed collection systems. These cases are at high risk of fluid and electrolyte imbalances so we need to be careful and monitor closely.

This is my general plan!

Hi Scott,

I really like this concept as a viable way to manage the financially constrained cases of pneumothorax. Did you know the early cases of this used Talc powder! I have seen blood patch pleurodesis used this was a few times when I worked in Manchester – both of the two cases were successful.

Really interesting paper!

Hello everyone!

Thank you Scott for a lovely welcome. I am so happy to be teaching everyone about toxicities again. Managing a toxicity can be so rewarding – especially if you have the right tools to get you started. so I hope you are stocked up on your charcoal and intralipid and apomorphine.

Make sure you upload any questions you have here in the forum.

Happy learning!

Hi Sybil,
This sounds like a really sick dog. Those sound like very extensive wounds. Any chance on top of the infection you had some MODS with hepatic dysfunction – that would also make your glucose very hard to control. Managing the hypoglycaemic patient can be hard or even impossible when the underlying cause is not controlled – so despite best efforts it can be fruitless unfortunately.

When you have a severely or refractory more so hypoglycaemic patient, running dextrose over 5-10% can be required. Just remember that if you need solutions over 7.5% of dextrose, you need a central line to be placed to prevent injuries and issues related to the high osmolality of the solution.

Replying to Ornella R. 28/02/2023 - 13:57

Hi Ornella,

That is a really great question – I am so glad to read about good antimicrobial stewardship. Short answer is I am very conservative with antibiotics. When I am concerned a patient has aspirated (from GI signs such as vomiting or regurgitation), I check to see if there is fever r changed SPO2 (this can often be normal). Though I do the following:
– check CRP
– ideally perform thoracic radiographs too but CRP alone can save money

There is some good evidence for using CRP to guide antibiotic use antibiotic use is aspiration pneumonia vs pneumonitis:
1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9151469/pdf/JVIM-36-1082.pdf
2. There is another good one in JVECC somewhere.

Hi Ornella,

This is an interesting phenomena. However, very important as it means we have ti be very cautious with blood transfusions in cats. There are multiple factors involved:
– the reduced O2-carrying capacity of blood in anaemia –> tissue hypoxia –> normal compensatory mechanisms initiated to manage this.

Two things occur and both lead to reduced afterload:
1. Peripheral vasodilation due to low haemoglobin
2. Reduced systemic vascular resistance due to reduced blood viscosity

When afterload is reduced there will be an appropriate increase in stroke volume and cardiac output AS COMPENSATION. This progresses in chronic anaemia (common in cats). So when the patient is transfused, the body takes time to reduced this increased cardiac output. Additionally in chronic anaemia, there can be remodelling of the left ventricle leading to thickening as a result of this compensation. So unless haemorrhage, the patient needs red cells not volume.

Complicated but hopefully makes sense!

Cheers,

Kerry.

Hi Ornella,

These are some great questions.

Let’s start with sepsis. The antibiotics we choose in sepsis are going to be mostly like how we choose antibiotics for other infections. These are the factors I consider each time I choose an antibiotic:
1. What is the source? So for example, if I am treating septic peritonitis due to a ruptured GI tract or aspiration pneumonia, then my pathogens will likely be enteric such as E. coli or Enterococcus for example. So here I would start with a beta lactam perhaps such as potentiated amoxicillin.
2. Is the patient sick enough in sepsis here to make me want to cover all 4 quadrants very strictly? So if we come back to this septic peritonitis case, I may consider adding a fluoroquinolone. If we have gone down this route it is imperative to obtain cultures so that we can de-escalate ASAP (meaning try to stop one of these drugs if not needed). I always try to start with less antibiotics if possible. Consider that we are often achieving source control with surgery in septic peritonitis whereas with aspiration pneumonia the drugs are doing all the work.
3. Get samples for culture. Hospitalised patients, especially if already on antibiotics before or in ICU have a lot of resistance. We see this commonly in fluoroquinolones and other commonly used drugs.

Now anaphylaxis…..
Pulmonary oedema is not a common feature in anaphylaxis which itself is not common – so we are lucky for that. The big question is what exactly was occurring as you could have had multiple causes:
– non-cardiogenic pulmonary oedema due to histamine release (most commonly what is going on), leading to leaking of the pulmonary endothelium and epithelium causing all this exudation.
– this can progress to ARDS in humans (really hard to diagnose in our patients)
– often can see periods of upper airway obstruction too which can worsen all this.
So treatment is two pronged:
1. treat the anaphylaxis –> a lot of your treatment is very much what I would have done:
– maintain blood pressure with fluid therapy judiciously due to that leakage and rapidly get on a vasopressor. I would reach for norepinephrine or epinephrine as a CRI. Current guidelines recommend either – but take cause as epinephrine has been reported in humans to lead to flash oedema which is what you have already. If you dont have these drugs – dopamine would be my third line.
– antihistamines are appropriate.
– i do use steroids but know they take time to take effect and are not much use in the emergency.
2. treat the hypoxaemia –> with intubated and mechanical ventilation. There is so much fluid in the lung the compliance is terrible so no matter ho hard to do IPPV, they need good positive pressure ventilation on a machine.

Lastly pneumothorax…..
The way to define this in on a DV survey radiograph, tension pneumothorax has mediastinal shift, the reason this is so critical is the vascular structures are compromised reducing venous return which reduces cardiac output. Though – defining this clinically is not so relevant – if the patient is compromised with respiratory distress or hypotension, drain the chest (ideally under little or no sedation). I will see if I can remember the case I saw when I was working with Neus at Glasgow – she might be able to track down the CT images – they were ver interesting.

Hope this helps!

I do love TXA acid myself – it is great to have a relatively new treatment to manage some of our haemorrhaging patients. I also wanted to mention the use of TXA as a mouthwash. There is mixed reports of its effectiveness; but the most recent evidence shows an oral solution of 4.8% TXA is as effective as systemic TXA (which can cause emesis).