scott@vtx-cpd.com
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So this was actually Phosphofructokinase (PFK) deficiency!
This is the report from the genetic testing in the dog:
PFKD/ PFKD (Genetically Affected)
Interpretation:
The examined animal is homozygous for the causative mutation for PFKD in the PFKM-gene.
Trait of inheritance: autosomal-recessive
Scientific studies found correlation between the mutation and symptoms of the disease in the following breeds: American Cocker Spaniel, English Springer Spaniel, WhippetIn PFK deficiency, haemolytic crises are precipitated due to alkaemia-induced of red blood cells following excessive barking, panting, strenuous exercise and high temperatures. Therefore, the patient was kept calm, cool and rested. On subsequent testing the anaemia resolved but a reticulocytosis remained, indicating that there was ongoing increased red blood cell turnover but that the management regime allowed the dog to compensate.
So basically support care is required. I would not use immunosuppression in these cases.
Scott 🙂
Replying to Alison Lambert 18/03/2023 - 10:05
Hey Alison.
Thank you for your kind words! I am really pleased you enjoyed the course.
We really appreciate the support.
Scott 🙂
Replying to Gisela T. 11/03/2023 - 22:40
Hello Gisela.
I am so sorry for the delay in getting back to you. I am so glad you enjoyed the session and thank you for the brilliant questions:
This is a great question. Endoscopy is indeen the most definative way of diagnosing oesophagitis. It is a tricky diagnosis to make overall. I think it is reasonable to make this call in patients that are at high risk. We do have evidence that BOAS patients and some patients undergoing prolonged orthopaedic surgery can experience potentially significant gastro-oesophageal reflux (GOR). The use of omeprazole in these patients has also now been shown to help prevent the change in distal oesophageal pH that accompanies GOR, but this is probably as a result of the change in gastric pH that omeprazole mediates, not because omeprazole reduces the actual frequency of GOR. However, preventing acid damage to the distal oesophagus where there is a known risk is appropriate, so it is therefore rational to use omeprazole in some surgical patients where there is a risk of GOR, and especially in BOAS patients where GOR is a known risk.
Metoclopramide may indeed help in these cases. It may have a little effect on LOS tone, but probably not that much. The drug I am using more and more is cisapride. I think that is a good option for these cases.
2. Another PDSA vet! Love it! Which PDSA are you at?
One thing to consider is that the BOAS may be contributing to the GI signs. I realise this may not always be an option, but it might be worth looking at correcting airway in some cases:
https://onlinelibrary.wiley.com/doi/abs/10.1111/jsap.12914
I think regarless of airway issues/correction, some will also require treatment of their GI disease separately:
https://pubmed.ncbi.nlm.nih.gov/15971897/
Honestly I would consider feeding some of the severely effected ones from a height. Like the Bailey chairs we discussed in the lesson. The do not have ‘true megaoesophagus’ but will often have quite significant oesophageal diviations. Due to the possiblity of concurrent enteropathy, I would consider a hydrolysed diet in the severe ones. The best hydrolysed diet for growing dogs is Purina AH. My go-to in these cases would be cisiaptide, if that is not avaiable then I would use metoclopramide. How long to use this for is tricky to say. It depends on the severity of the signs, but in severe cases when all else is failing you can use long term.
I would try and avoid long term PPIs if possible and reserve if you can for cases that are at risk of reflux during GA. However, there are some severe cases that will need long term administration. I would try everything else first! I would also co-administer a probiotic. The key thing to remeber is that the omeprazole may reduce the oesophageal injury, but will increased the bacterail load in the regurgitated material and could make the aspiration events worse! It is so tricky… lesser of two evils and all that!
The other drug that can be helpful in some cases is steroids. This may deal with some of the residual/background inflammation in the airways and GI tract.
I hope that helps?
Scott 🙂
Hey Magda!
Honestly, such a joy to have you on the course! I am glad you enjoyed the first session. Thank you for your brilliant questions:
1. This is a great question. I think you raise a good point. In patients with megaoesophagus that are at high risk of regurgitation, it is much safer to protect the airway and do a full GA.
If you just need the radiograph and the risk is not too high, I would try butorphanol alone. This could then be ‘topped up’ with a little alfaxalone if needed.
Otherwise, If the plan is to do a full GA for other investigations I would pre-med normally (opioid and dexmedetomidine) and see if I could get the radiograph with just that.
2. This is another great question. I included a little extra in less than 3 to help cover this. There is a bit of a divided opinion on this! In any brachy dog with a history of regurgitation and GI signs, I would hive omeprazole and cisapride the day before surgery, the day of surgery, and the day after. I would also administer maropitant on the day of surgery and in an ideal world I would give them a probiotic to try and navigate the dysbiosis caused by the omeprazole.
Honestly, in brachycephalic that are ‘well’, I would probably use the same regimen. Many anesthetists would give at least one dose of omeprazole before any surgery in brachycephalic dogs. One study showed the benefit of giving it 4 hours before. There is a more recent study that suggests the benefit of omeprazole the night before and morning of GA.
Hope that helps!
Scott x
Hey Ornella.
I am glad you enjoyed the session. Great questions!
1- Hey. This is a great question. A one off episode of self resolving haematemesis – I would probably not give omeprazole to this case. Intermittent chronic episodes of haematemesis – I probably would start omeprazole in this case while investigating. Blood in the vomit is suggestive of GI ulceration, but this is not the only cause.
GI heamorrhage in dogs and cats can be the result of a primary insult to the GI tract or may be secondary to a systemic disease process. It may originate in the oesophagus, stomach, small intestine, or large intestine. As such, a number of pathologic processes have been associated with GI haemorrhage. In general, these can be divided into three broad categories: diseases causing ulcers, diseases causing coagulopathies, and diseases associated with vascular anomalies. Some diseases are difficult to classify into one of the above categories, and animals may have single or multiple predisposing causes. Diseases associated with GI ulceration and/or GI hemorrhage are extensive. This recent paper is helpful regatding causes:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8692196/
The study concludes:
“Results
In the final multivariable model, the following factors were associated with GUE: Nonsteroidal anti‐inflammatory drug (NSAID) administration (odds ratio [OR], 6.3; 95% confidence interval [CI], 2.3‐17.4; P = .0004), glucocorticoid administration (OR, 3.0; 95% CI, 1.5‐5.9; P = .001), gastrointestinal neoplasia (OR, 13.5; 95% CI, 1.7‐108.0; P = .01) and gastrointestinal mechanical disease (foreign bodies, gastric dilatation, and volvulus; OR, 4.8; 95% CI, 1.2‐19.7; P = .03). Additionally, working dog breeds were predisposed to GUE compared to mixed breed dogs (OR, 2.8; 95% CI, 1.1‐7.4; P = .04). Insufficient clinical data was available to either support or refute a role of other putative risk factors evaluated.Conclusion and Clinical Importance
Administration of NSAID or glucocorticoid and gastrointestinal neoplasia or mechanical disease were associated with GUE in dogs. The potential predisposition of working breed dogs for GUE requires further investigation.”2. This is an interesting case… really sad too! I would agree with your conclusing, probably compromise to GI perfusion and a degree of necrosis. If material is not moving from the stomach, I would pass the feeding tube all the way into the stomach and siphon off the fluid every 4-6 hours and then replace it with some liquid food. This works well in parvovirus puppies. You would expect the ileus to respond within a couple of days with the metoclopramide and cisapride. If neither of these was working I would also consider erythromycin. I would make sure to correct all electrolyte imbalances as this can worsen the ileus. I would also be careful will opioid use and minimise this as much as possible, obviously not compromising the cat’s analgesia.
I hope that helps.
Scott 🙂
I ahve popped the radiograph here:
Scott 🙂
Hey lesley.
These are really tricky and often very sad cases! The following paper is probably most helpful:
https://journals.sagepub.com/doi/full/10.1177/1098612X19895053
The goal of this study was to assess long-term outcome and prognostic factors in cats with sacrocaudal luxation. Seventy cats were evaluated retrospectively; 60 had absent tail tone and 53 had absent tail-base sensation. Anal tone was absent in 20 cats and decreased in an additional 13 cats. Inability to urinate voluntarily was noted in 53 cats; inability to defecate voluntarily was observed in 29 cats. Twenty-one of the cats with an inability to defecate voluntarily were constipated, whereas 8 were fecally incontinent.
Of the 61 cats for which urinary outcomes were available, 90% regained voluntary urinary function; 87% of those regained it in <30 days. Cats with a flaccid incontinent urinary bladder had a significantly worse prognosis, with only 50% regaining urinary control at a median of 33 days. With regard to fecal continence, 25% of those incontinent at presentation remained so, and 68.4% of those experiencing constipation at the time of injury continued to experience it at the time of follow-up. Age, sex, tail-base sensation, anal tone, perineal sensation, fecal continence, degree of vertebral displacement, and tail amputation did not affect outcome. Despite nerve dysfunction commonly being noted at the time of injury, most cats regained function with time. Because early tail amputation did not affect outcome, the authors did not recommend this as a treatment for cats with sacrocaudal luxation.
In reality:
1. Cats with sacrocaudal luxation should undergo a thorough neurologic examination, including careful evaluation of bladder and anal tone.
2. Overall, cats with sacrocaudal luxation have a good prognosis for return to function; urinary incontinence with a flaccid bladder may be associated with a worse prognosis.
3. Based on the high percentage of cats that returned to function in this study, aggressive decisions about euthanasia or tail amputation should not be made until at least 6 weeks postinjury.
I suppose it is easy to say wait 6 weeks... but in reality, that might not be an option for all patients/owners!
What medication do you have the cat on?
Scott
Replying to Natalie Dicks 16/03/2023 - 19:11
Hello Natalie.
I really hope you enjoyed the course!
Please let me know if you have any other questions.
Scott 🙂
Replying to Ornella R. 10/03/2023 - 12:56
HAHAHAHA!
I know! It really is quite grim.
I was taken back by how many cases they collected!!!!
Scott 🙂
Replying to Magda Upton 13/03/2023 - 14:39
Magda!
What a joy to have you here! Thank you so much for all of the support!
I really appreciate it! I really hope you enjoy the course.
Scott 🙂
Replying to gemma.ives@protexin.com 13/03/2023 - 14:36
Gemma!
Lovely to see you here! Thank you so much for all of the support!
I hope you enjoy the course!
Scott 🙂
Replying to Rachel F. 14/03/2023 - 17:28
Thanks for the update.
Would be good to get an update with progress. I am alwats surprised by these cases, often insulin requirement does not reduce that much.
Thank you again for all of your support.
Scott 🙂
Replying to Rachel A. 14/03/2023 - 14:34
Hey Rachel.
Great questions. I think we are right to be concerned about the over prescription of PPI’s and the effect on the microbiome. I think there is probably a place for their use with brachycephalic patients however.
We do have evidence that BOAS patients and some patients undergoing prolonged orthopaedic surgery can experience potentially significant gastro-oesophageal reflux (GOR). The use of omeprazole in these patients has also now been shown to help prevent the change in distal oesophageal pH that accompanies GOR, but this is probably as a result of the change in gastric pH that omeprazole mediates, not because omeprazole reduces the actual frequency of GOR. However, preventing acid damage to the distal oesophagus where there is a known risk is appropriate, so it is therefore rational to use omeprazole in some surgical patients where there is a risk of GOR, and especially in BOAS patients where GOR is a known risk.
These are some useful references:
Panti, A. et al. (2009). The effect of omeprazole on oesophageal pH in dogs during anaesthesia. J. Small Anim. Pract. 50, 540–544
Kaye, B. M., Rutherford, L., Perridge, D. J. & Ter Haar, G. (2018). Relationship between brachycephalic airway syndrome and gastrointestinal signs in three breeds of dog. J. Small Anim. Pract. 59, 670–673
Shaver, S. L. et al. (2017). Evaluation of gastroesophageal reflux in anesthetized dogs with brachycephalic syndrome. J. Am. Anim. Hosp. Assoc. 53, 24–31
In short, I would consider using pre GA using this protocol:
https://pubmed.ncbi.nlm.nih.gov/33769569/
Hope that helps.
Scott 🙂
Replying to Ornella R. 10/03/2023 - 13:13
Hey Ornella.
Sorry for the delay in getting back to you!
I would only use omeprazole in NSAID toxicity when there are signs of ulceration (melena or haematemesis) or there are prolonged GI signs. In actutre cases where we induce emesis and support, I would not routeninely use.
The antioxidants is interesting. This come from human medicine:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1884640/
“The role of antioxidants, especially vitamins C and E, in the prevention of NSAID-induced gastric injury is relatively little studied, and large outcome studies are missing. Both vitamins C and E seem to play a role in the preservation of gastric mucosal integrity; vitamin C is actively secreted into the gastric lumen of healthy subjects, and its concentrations are decreased in patients with gastroduodenal diseases such as peptic ulcer disease, gastric malignancy, or H. pylori-associated gastritis. The underlying molecular mechanisms, however, are not fully understood.
We were recently able to show that the gastroprotective effects of vitamin C as observed in humans might – at least in part – be mediated by haeme-oxygenase-1 (HO-1). HO-1 is a ubiquitous and crucial tissue-protective enzyme with vasodilative, anti-inflammatory and antioxidant properties. In the stomach HO-1 might counteract the two major mechanisms of NSAID-induced gastric injury: disturbance of gastric microcirculation and free radical release. The mechanisms of HO-1 induction seem to be cell-type specific; a nonstressful induction was recently postulated as a therapeutic target. We identified vitamin C as a potential nonstressful inducer of HO-1 in the stomach. However, to date there are only very limited data about this enzyme in the stomach. Guo et al. showed that healing of gastric ulcers in rats is paralleled by an upregulation of HO-1. Further studies are needed to examine the role of HO-1 in the stomach in vivo. Our recent findings, however, are in favour of the supplementation of vitamin C in order to prevent NSAID gastropathy – showing an impact beyond its sole antioxidant properties.”
As far as I am aware, there is no evidence for this in our patients.
Interesting though!
Scott 🙂
Replying to Samanta A. 14/03/2023 - 16:06
Hey Samanta.
This is a great question! I hope you enjoyed the recording.
I think this depends a bit on the cat and how tricky tableting is!
If can tablet them, then I go for at least 4 weeks, then taper and stop, but if had recurrent episodes have ad some on for months.
What is your experience?
Scott 🙂
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