scott@vtx-cpd.com
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Me again!
We also have a whole webinar on plasma products if you are interested:
Scott 🙂
Hopefully that helps!
Let me know if you have any other questions.
Scott 🙂
Q: Thank you for sharing! Just a quick question… would you use in HGE case? I can see it might be useful in hypoalbuminaemic GI patients, but what about ones with normal albumin? Do you think plasma would be a good shout?
In hypoalbuminaemic GI patients. How low is too low for albumin? Would you use albumin below a certain value, or just when you start to see third spacing?
Hope that makes sense?
A: The glycocalyx is so interesting isn’t it!
So… yes I would use them in dogs with severe haemorrhagic diarrhoea/gastroenteritis a lot. I think I may be biased to the ones we see, so I am talking about the ones that come unwell with signs of hypovolaemic shock and severe dehydration/haemoconcentration. These ones typically come with high PCV and “normal” TS so for example 65%/60g/L, in these ones I know that if hypovolaemic I will need to fluid resuscitate so may end up needing 5-20mL/kg over a few boluses and then I will need high rates of IVFT to account for on going losses, rehydration and maintenance and when you calculate this sometimes is as high as 6-8mL/kg/h. There is two sides to this and one is that we know that actually the use of crystalloids itself will damage the glycocalyx and you will gave shedding and then this will lead to increased vascular permeability etc. and the second side to this is that when my PCV is normalised when the patient is rehydrated, say comes from 65 to 45%, I know my solids will ave tanked and probably be from 60 to 30-40g/L and at this stage this becomes a problem also with on going increased permeability, increased oncotic pressure etc. So that is why I tend to come in early with plasma to prevent this from happening, and when plasma is used as is a colloid… you can also allow yourself to use lower fluid rates so in the same example if you calculated you may need 6-8mL/kg/h if you combine plasma and crystalloids you may get away with 4-5mL/kg/h instead.
For the hypoalbuminaemic GI patients… I don’t think there is a number really. So if I think PLE that I have treated alongside medicine; these patients are different as stable so unless I had to fluid resuscitate or need IVFT I would not consider it, even if their albumin is really low. Now for a PLE patient who isn’t great and is now third spacing and say it has abdominal effusion, and that is increasing the abdominal pressure which is compromising the gut blood supply and they are not doing great. I tend to remove abdominal fluid really slowly over a few hours, then replace with plasma – and the times we have done this they tend to have really low alb on low teens.
Not sure this answers the question, and really this is more “what I do” rather than tons of evidence based so would also like to hear how you approach these guys, and see if Kerry agrees or does something different!
Hello Victoria.
I hope you are well. We chatted about this over on the ECC corse. I will pop that conversation here:
Q: If I understood correctly, you do plasma transfusions in septic patients as plasma helps repairing the glicocalix?
A: Great question about glycocalyx, gotta love it!! Yes I think you understood this correctly.
I replied to this before but never posted it so hope for better luck this time! Will also wait and see what Kerry replies but I can share the two reasons why I may use plasma in septic patients 🙂The first one would be as a fluid therapy of choice as “crystalloid sparring”. So typically the septic patients that have septic peritonitis and are having large fluid losses through high protein abdominal exudates will have hypoproteinaemia and decreased COP. Normally they do require large volume of fluid to resuscitate them so I would use plasma to provide some oncotic support, allow me to use smaller volume of fluids and not use as much crystalloids that I know would damage the glycocalyx further, and would worsen the TP/alb/COP and potentially cause interstitial oedema and other issues.
The second one is the glycocalyx.
So as you know the glycocalyx is a thick negatively charged carbohydrate rich layer that coats the vascular endothelium. Under physiological conditions, positively charged soluble components like plasma proteins and water are trapped in the glycocalyx forming an extended endothelial surface layer.The glycocalyx has a lot of functions specifically it is a barrier between blood and vessel wall, it maintains blood fluidity by modulating interactions with endothelium with blood cells and proteins and regulates cell adhesion and vascular permeability. Also creates a high intravascular colloid osmotic gradient and acts as a mechano-transducer (so it is super clever and when it senses shear stress and will then induce as a response endothelial release of nitric oxide to counteract this).
Shedding of the endothelial glycocalyx components has been proven to happen in response to ischaemia and hypoxia, secondary to ROS, inflammation and sepsis as well as trauma (specifically haemorrhagic shock).
Animal model studies have shown that resuscitation with plasma partially restores it whilst crystalloids such as lactated ringers do not, and neither do synthetic colloids like hydroxyethyl starch.
We think this is due to the albumin in the plasma that preserves the endothelial integrity as provision of albumin will attenuate glycocalyx shedding and reduce interstitial oedema in other animal models. It may also be because albumin can attenuate neutrophil adhesion to endothelium, and it has other anti-inflammatory properties. There may be other components in the plasma, howeverm that also help protect or restore the glycocalyx in plasma…. lots of studies still on-going! I reckon that glycocalyx resuscitation is something we will be useing in the not so distant future :)!If you want some papers on this I would suggest:
Rahbar MH, del Junco DJ, Huang H, Ning J, Fox EE, Zhang X, et al. A latent class model for defining severe hemorrhage: experience from the PROMMTT study. J Trauma Acute Care Surg (2013) 75(1 Suppl 1):S82–8Holcomb JB, del Junco DJ, Fox EE, Wade CE, Cohen MJ, Schreiber MA, et al. The prospective, observational, multicenter, major trauma transfusion (PROMMTT) study: comparative effectiveness of a time-varying treatment with competing risks. JAMA Surg (2013) 148(2):127–36
Pati S, Matijevic N, Doursout MF, Ko T, Cao Y, Deng X, et al. Protective effects of fresh frozen plasma on vascular endothelial permeability, coagulation, and resuscitation after hemorrhagic shock are time dependent and diminish between days 0 and 5 after thaw. J Trauma (2010) 69(Suppl 1):S55–63
Schott U, Solomon C, Fries D, Bentzer P. The endothelial glycocalyx and its disruption, protection and regeneration: a narrative review. Scand J Trauma Resusc Emerg Med (2016)
Hello Alice!
Really pleased you are enjoying the course!
I will tackle these brilliant question at the live Q&A tonight if that is OK?
Scott 🙂
Hello everyone!
This was a great session where Yvonne and I played endocrinology bingo!
Hope you enjoy watching it back!
Scott 🙂
Replying to Helen S. 29/05/2023 - 18:44
Hello Crina!
Thank you so much for joing the course. I am so pleased you have joined us.
Really pleased you enjoyed the first session.
Scott 🙂
Replying to Christina G. 23/05/2023 - 19:44
Christina!
Lovely to see you here. I hope you are safe and well.
Thank you so much for joining the course. I really hope you enjoy it.
Let me know if you have any questions.
Scott 🙂
Replying to Hayley O. 23/05/2023 - 21:06
Hey!
Yes, that is the dose I would go for.
Scott 🙂
Replying to Inga McDermott 24/05/2023 - 09:29
Great to see you here Inga!
I am so pleased you have found the course useful.
I am also pleased you will be making the most of the notebook!
Scott 🙂
Replying to Kathryn B. 19/04/2023 - 19:46
Here are some results!
Let me know your thoughts!
Scott 🙂
Replying to Liz Bode 22/04/2023 - 20:14
Thanks for your thoughts Liz,
The history revealed no toxin or drug exposure that would cause episodic weakness, PUPD or cataract formation. The theophylline was started after all of these clinical signs had developed. Likewise, the dietary history was complete, balanced and calorie appropriate for the dog’s needs. The age of onset of the clinical signs would make a congenital problem less likely. Neither the cataracts of heart murmurs had been noted at the annual vaccination check one year previously. None of the physical examination findings were consistent with pain or a neuromuscular disorder. Systolic blood pressure was documented within the normal range making hypotension a more unlikely cause for the episodic weakness.
For all investigations to be carried out the dog was hospitalised for just over 48 hours. Due to the detection of the heart murmurs and the possibility of the episodic weakness being due to cardiac disease an echocardiogram (looking for structural heart disease) (results below) and ECG (results below) were carried out. No abnormalities were detected with standard ECG. Despite early, mild degenerative changes, no significant structural heart disease was detected. The mitral regurgitation explained the murmur auscultated. It was clear at this stage that there were potential significant co-morbidities, and therefore it was decided to investigate and stabilise underlying diseases before further investigating the possibility of an arrhythmia.
Haematology, biochemistry, blood gas analysis and urinalysis (results below) were analysed to identify underlying metabolic, electrolyte, acid-base disorder or indicators of another systemic disease.
Would love to hear your thoughts on these!
Scott 🙂
Replying to Kathryn B. 19/04/2023 - 19:46
Hello everyone.
Here are my thoughts regarding the problem list and differential diagnosis:
1. Episodic Weakness:
• Primary heart disease (e.g. left-sided heart failure or arrhythmia)
• Electrolyte disorder (e.g. hypokalaemia and hypocalcaemia)
• Endocrinopathies (e.g. diabetes mellitus (DM), hyperadrenocorticism (HAC), hypoadrenocorticism or pheochromocytoma)
• Acid-base disorders (e.g. acidosis or alkalosis associated with pulmonary disease)
• Anaemia
• Inflammatory conditions
• Immune medicated disease (e.g. immune mediated polyarthropathy)
• Neuromuscular disorder
• Pain
• Nutritional derangements (e.g. insufficient calories)
• Hypotension
• Toxins or drugs (e.g. anticonvulsants or antihistamines)2. Heart Murmur
• Mitral insufficiency (e.g. endocardiosis)
• Tricuspid insufficiency (e.g. chronic degenerative valve disease)
• Aortic stenosis
• Pulmonic stenosis
• Ventricular septal defect
• Atrial septal defect
• Physiologic murmurs (e.g. anaemia or fever)3. PUPD:
• Renal disease (e.g. chronic renal failure or pyelonephritis)
• Electrolyte disorder (e.g. hypercalaemia or hypokalaemia)
• Endocrinopathies (e.g. diabetes mellitus (DM) or hyperadrenocorticism (HAC))
• Hepatobiliary disease
• Diet (e.g. increased salt intake)
• Miscellaneous (e.g. polycythemia, psychogenic or renal glycosuria)
• Toxins or drugs (e.g. corticosteroids or diuretics)4. Cataracts:
• Metabolic (e.g. diabetes mellitus or hypocalcaemia)
• Secondary to other ocular disease (e.g. glaucoma, generalised progressive retinal atrophy or retinal dysplasia)
• Senile cataracts
• Trauma
• Toxic or dietary
• Inherited
• CongenitalI would love to hear Liz’s comments on my heart disease DDX… nervously waits!
Scott 🙂
Replying to Hayley O. 19/05/2023 - 19:16
Hello!
Hope you are well and enjoying the course.
I will pop the dosing chart here. Let me know if you have any other questions.
Excited you will be using Vivomixx… let me know how you get on with it!
Scott 🙂
Replying to Magda Upton 20/05/2023 - 11:45
I would agree!
All the B12… reassuring to know we are doing no harm with it!
Scott 🙂
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