scott@vtx-cpd.com
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I think that is a great approach Simon!
It really is all about communication… and respect. We all have to listen to each other and realise that we all have so much to learn from each other. I would be greatful to be told a better way to do it!
You are right about the reversal first if HR super low.
While I am on… massive congratulations to Gail on her place on the Masters in anaesthesia at Edinburgh University!
Scott 🙂
I would not get through the day without Google!
Differentials for causes of an absolute polycythemia:
1. Primary (neoplasia, genetic).
2. Secondary
(a) Appropriate (cardiac (right-to-left shunting patent ductus arteriosus, persistent truncus arteriosus, ventricular septal defect, atrial septal defect, tetralogy of Fallot), respiratory (pulmonary parenchymal disease, pulmonary vascular amyloidosis), environmental (high altitude, severe obesity)).
(b) Inappropriate (renal disease (pyelonephritis, local hypoxia), neoplasia (renal lymphoma, renal fibrosarcoma, renal cell carcinoma, nasal fibrosarcoma, Schwannoma), metabolic (hyperadrenocortisism and hyperthyroidism), iatrogenic (exogenous erythropoietin therapy)).
Primary absolute polycythemia is a neoplastic myeloproliferative disorder of the erythroid stem cells. The neoplastic stem cells produce red blood cells independant of erythropoetin. Secondary polycythemia can be either appropriate or inappropriate. Appropriate secondary polycythemia is due to systemic hypoxia causing an appropriate compensatory response increasing erythropoetin production resulting in an increase in red blood cells which increases oxygen carrying capacity of the blood. Inappropriate secondary polycythemia is the increase of erythropoetin in the absence of hypoxic stimuli. The main causes of inappropriate polycythemia have been reported to be neoplastic in origin, such as renal sarcoma.
Differentiating between primary and secondary polycythemia is difficult. It is possible to measure erythropoetin concentrations at a specialised laboratory. However, the clinical evaluation of these results is limited as there can be an overlap between erythropoetin concentration in clinically normal and polycythaemic patients. As such erythropoetin measurement, where available, is recommended to be used as an aid in confirming a diagnosis of secondary polycythemia.
Scott 🙂
You are totally right!
I ran the bloods again and they were totally normal!
This sample most likely had a blood clot in it!
I am just pleased I did repeat the sample and did not go ahead with the transfusion!
Scott 🙂
Hey.
Bloods were all fine. I think this is most likely to be a ‘gravel sign’. The gravel sign is seen radiographically as multiple, variously sized mineral fragments in the stomach or intestine, which build up as a result of poor gastric motility and/or emptying, and indicate a chronic stasis of food. It can be present in cases of both partial and complete obstruction. Heavier particles tend to settle in front of a partial obstruction, as fluid and less dense particles move beyond the obstruction.
The puppy was later reported to have possibly have eaten some cat litter which might help explain it!
Scott 🙂
Thanks so much for picking this discussion back up! 🙂
Initially the patient was placed in an oxygen chamber. Butorphanol 0.3mg/kg was administered, intramuscularly. After twenty minutes, the patient’s respiratory rate was still 50 breaths per minute and no change in respiratory effort was noted. The patient was removed from the oxygen chamber and flow-by oxygen therapy was administered. It was not possible to obtain an arterial blood sample. An intravenous catheter was placed into the right cephalic vein. A venous blood sample was obtained for a minimum database (PCV, total solids, glucose and blood urea nitrogen (BUN)), acid-base analysis, electrolytes and haematology. Manual PCV and total solids were 74g/l and 70g/l respectively. Both glucose and BUN were within the normal reference range. The patient was hyperkalaemic; 4.8mmol/L (2.9 – 4.2). Haematocrit was 72% (24-40) and cHgb was 24.4 g/dL (8.0-13.0). All other haematological and electrolyte results were within the normal reference range. Coagulation testing showed that partial prothrombin (PT) time was within the normal reference range, however activated partial thromboplastin time (aPPT) was mildly prolonged at 167.2s (94-125) (Table 2). A thoracic ‘point of care’ ultrasound examination was performed and was negative for free fluid. Subjectively the left atrium was dilated with an abnormal left atrial to aortic (LA:Ao) ratio, however further assessment of the heart was not possible due to the cat’s temperament. No free fluid was present on abdominal point of care ultrasound. SpO2 was 97% from pinna.
It was initially suspected that the patient’s haemoconcentration was due to severe dehydration. As such, a fluid therapy plan was implemented. A 15ml/kg intravenous fluid bolus of Hartmann’s solution (Vetivex 11; Dechra) was administered over 15 minutes, after which intravenous fluid therapy (IVFT) was continued at a rate of 4ml/kg/hr for eight hours . Seven hours post presentation the patients PCV was 67%, and IVFT was continued at a reduced rate of 2ml/kg/hr thereafter. After twenty-four hours of fluid therapy the patient’s PCV was 65%. The patient was quiet, alert and responsive; however, the breathing had become more laboured despite continued oxygen therapy, and her respiratory rate was consistently between 60-70 breaths per minute .
The PCV and haematocrit are elevated, indicating that the patient is polycythemic; PCV>55%. It is important to distinguish between a relative polycythemia and an absolute polycythemia. Relative polycythemia is the loss of plasma water without the loss of red blood cells. It is caused by fluid imbalances causing reduced plasma fluid volume, such as dehydration, reduce fluid intake, redistribution of vascular blood, cutaneous losses or splenic contraction (in the dog). Absolute polycythemia occurs when red blood cell number increases and is classed as either primary or secondary. Despite fluid therapy, although slightly improved, the patient’s PCV was still significantly increased and as such this case is termed an absolute polycythemia.
What would be the differentials for an absoute polycythemia in this patient? Or is that an unfair question for a saturday night?!?!?
Scott 🙂
Yes! I had all the question marks too!!!
So… there is definately something abnormal in the stomach. The DV really allows us to see that it is definatley still in there. So… I did decide to scope this dog. There was lots of thick mucus in stomach with likley food material in it. Definately nothing obstructive and nothing I could remove with the scope.
I took a radiograph post endoscopy and the same opacity was there… what might be the other reason for this radiographic abnormaity?
Scott 🙂
Thanks for the update!
I do think some dogs just do this after castrayion, it would be good to hear others experience.
Do you think you will do further investigations? If not, it may be good to consider tranexamic acid before future surgery?
Scott 🙂
My relpy…
“Hope the wee guy is doing better.
This could definitely be one of this situations where this could be something or nothing. I have definitely seen dogs that have bleeding and bruising like this post castration and there is no real explanation for this.
In order to fully assess primary coagulation I would make sure to run a platelet count (manual) and consider a BMBT. A BMBT would be an easy way to asses for a thrombocytopathia. Can be tricky though in a conscious dog!
If PT and aPTT are normal then you could also consider D-dimers and fibrinogen.
The way to really assess coagulation in the best way would be to do TEG! That may give you the ultimate peace of mind!”
What do you all think?
Scott x
Sooo…
This is a very interesting point… I love this trick. When I first graduaed I remeber my mentor saying to me that I should mix 0.5ml of ketamine and 0.5ml of diazepam in a 1ml syringe and give to effect!… and I never looked back! Does work really well.
Scott 🙂
This is really interesting Simon!
I think Andy’s question about intralipid is a really good one… I might indeed be a consideration in these cases.
Why have the human medics moved away from gastric lavage? Is there evidence to support worse outcomes? I wonder if the outcomes are worse in these cases because they have the more severe toxins to begin with?
It is always a worry inducing emesis in the cases that are neurological or likely to become neurological. If they are obviously neurological on presentation when I would not induce emesis. If they are clinically normal on presentation I often will.
Scott 🙂
Andy…
I think this actually raises a really good point. Is an epidural something a nurse can do?!
I dont know the answer?!
Anyone?
Scott 🙂
Sure.
Do you worry about toxicity?
Scott 🙂
Totally agree Sybil. More data needed… is that not the story of veterinary medicine!
I think paracetamol is a great option for many of the cases you mention. Much less of the potential negative GI effects you also touch on. Paracetamol might also be an option for pregnant and lactating bitches. As far as I am aware paracetamol is one of the only drugs pregnant humans are allowed to take?! Others in the group will have more experience of that than me!
Scott 🙂
Such great discussion!
Has this really all come down to a question of basic maths?!
Scott 🙂
And one more…
There is never such a thing as a silly question!
Scott 🙂
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