HO Reuter: 4 September 2022. We have discussed white rhino anaesthesia, importance to get blood supply to hindlegs, etc. I know all this and never have lost a rhino directly from muscle trauma to hind legs. I recently lost a white rhino cow, that went down un-expectantly while walking her into the crate (2mg Etorphine, 10 mg Medetomidine, 20 mg Azaperone, 2500IU Hyalase. We really struggled to get her up again, but eventually got her into the crate and stood up well after full reversal with Atipamazole, Yohimbine and Trexonil. She was restless during transport at first, then lay down, some froth on her nostrils at arrival. She got out the crate ok, but soon afterwards had a heart attack, fell and suddenly lots of blood tinged froth from nose as she died. Massive lung oedema on PM and histopathology findings at Pathcare as follows: “COMMENT The salient findings from the histopathology include: diffusely contracted bronchioli (suggestive of bronchospasm); low protein oedema, alveolar emphysema, scattered eosinophils and marked acute necrosis of the heart (the latter is most likely hypoxic change). Although not a histopathological diagnosis, (and usually more peracute in nature) in the absence of overt necrotising/inflammatory change in any of the organs, these findings support the clinical observations (foam from the nostrils and severe lung oedema) which points to a hypersensitive /anaphylactic-type reaction. It is not possible from the microscopy to establish the nature of the allergen though. DIAGNOSIS Full body tissues: SUSPECTED ANAPHYLAXIS REFER TO COMMENTS Signed Out by DR SOPHETTE GERS . I have been very for the use of Hyalase when darting from chopper, but do wonder if this rhino had an allergic reaction to Hyalase? After this very traumatic incident, and once before struggling to get a rhino to walk on Medetomidine, I went back to my old regime of for adult rhino 5-6 mg Etorphine, 40mg Zoletil, 40 mg Azaperone, 10-15x opioid dose Butorphanol, etc. I did 31 rhino dehorning/ translocations with no hassles or complications on this regime last week, and 1 today. Another 4-5 year old rhino today seemed all good on 4mg Etorphine, 30mg Zoletil, 40 mg Azaperone, 60mg Butorphanol. He struggled to get up on rocky sloping terrain. We put him in lateral recumbency, messaged and pumped legs and topped up with another 20 mg butorphanol and 2 mg Diprenorphine. When he still struggled to get up we took off all ropes and blindfold and gave 150 mg Trexonil. He still struggled to get up, and we left him alone for1 hour. Still not up well after sun set. Is there any point to try any therapy tomorrow morning, e.g. anti-inflammatories, fluids, corticosteroids (he had 50 ml Kyroligo and 50 ml BCobolic) or is euthanasia the kindest? Probably so, I guess. Erik Verrynne: I had a similar reaction with similar histopathology of eosinophils in a 5 year old white rhino bull in 2006/7. I used 3.5mg Etorphine, 30 azaperone and hyalase. We thought it to be the hyalase. My case went into cardiac and respiratory arrest within 6 minutes of dart hit ( ground darting) and I could not reverse or revive it with anything. I still use hyalase because the incidence seems super rare and we do not know what triggers it. The young bull. If he is still down tomorrow, the prognosis is not good. My policy with cases like that. If I do not get them up within 20 -30 minutes of ample butorphanol, rolling and trying, I wake them up fully, give BCo and Dexa and let go. The longer they struggle, the higher the risk of extensive damage and not getting up, especially bulls seem to be more sensitive. But I have not tried Zoletil and we discussed it earlier this year. Sorry about that. It’s not nice when it happens. Rob Jackson: Conjecturing : Were they animals that had been darted before, could they develop antibodies to hyalase? Or any other drug? Could dirt/faecal matter carried through the skin trigger a reaction? Heather Nixon: 5 September 2022 Is it possible that the reaction is due to some of the drugs going directly into the blood stream? Erik Verrynne: Your down time is usually much faster if the etorphine is deposited iv. One would expect that the cocktail as a whole will be deposited into the blood. In my case down time was normal, and the animal had never been darted before HO Reuter: 6 September 2022 The rhino cow I lost with severe lung oedema / anaphylactic reaction had been darted a month before, but not with hyalase in the dart. Both times she was treated with Duplocillin for a superficial gun shot wound. Leith Meyer : These are horrible cases that you have had to experience and I commend you for sharing these as I’m sure everyone is learning from them. I suspect that this cow didn’t die from an anaphylactic reaction but rather from what is described as chronic capture myopathy and a delayed per-acute capture myopathy syndrome. Basically animals are compromised from a previous capture and then the exertion, stress and hypoxia of a follow up capture pushes them over the edge and generally acute heart failure occurs. Erik Verrynne: How do you explain the high eosinophils? We saw the same in my case in a young bull, never been darted before, and very relaxed during darting from the ground. Leith Meyer: I’m not an expert on this, and it would be good to hear the opinion’s from Johan Steyl or other pathologists. However, awhile ago I looked into this quite closely and even in humans the diagnosis of anaphylaxis is extremely difficult and eosinophils in the lungs are not pathognomonic for anaphylaxis. I’m not sure why their numbers may be high, but there are probably other reasons in addition to a parasitic cause. There may even be a haemodynamic cause related to heart failure? Erik Verrynne: If not related to anaphylaxis, then I agree with you there may be another mechanism involved. It will interesting to hear from the pathologists how often they encounter lung eosinophils in capture related mortalities. Johan Marais: Just a thought here. We recently lost a horse in the recovery box after a 20 min procedure. Upon recovery, there was a short period where his neck was badly bent, and could not breathe, then got corrected. He died within 10 minutes (although it can take 24h) with lots of froth and bright red blood from the nose. The pathogenesis of this condition is thought to be related to changes in venous return and an influx of fluid into the alveoli as a result of excessive negative pressures within the thorax. Rare condition, but I think possible if your rhino, while in the crate down, did not breathe properly for a short period of time. HO Reuter : Thanks to all for your comments. Unfortunately we often have to re-dart animals within a months or so of previous capture, increasing the risk of chronic capture myopathy. Would there be such a massive pulmonary oedema from acute heart failure? This rhino once up in the crate was standing nicely without pushing, but as I had given full reversal, the driver did notice her being restless and moving a lot in the crate. At some stage she may have pushed, occluded nostrils, which rhino sometimes do, and if noticed I always prod them to move back. I have never had them develop lung oedema and die before. But Johan’s thought might be a possibility?? How to prevent this again in future translocations? Johan Steyl: As previously shared, I have had a couple of cases of similar presentation with one of the common components in the epidemiology being the use of hyalase in the capture cocktail. The finding of pulmonary eosinophilia is not the only change but its also accompanied by increased numbers of mast cells which is what led us to think of anaphylaxis rather than the other possible causes of eosinophilia eg. pulmonary parasitosis. As with all allergies, one can argue that it is so rare that the benefit of using hyalase far outweighs the risk. That is for you to decide. Many vets will use it for a life time and never experience this adverse effect. Leith's suggestion is valid but will not explain the pulmonary eosinophilia and mastocytosis. If sampling of the heart was good, one would expect some evidence of previous significant insults visible histologically as interstitial scarring. Apart from previous strenuous capture event/s (chronic/peracute-delayed syndrome, the latter can be due to various other causes eg non-lethal cardiotoxicosis micromineral deficiencies and probably others. In all the "allergic cases" the myocardium did not show significant predisposing injury apart from acute /terminal degeneration which can be attributed to terminal hypoxia, vasogenic shock and hyperadrenalism aro anaphylaxis. Bottom line is that this type of reaction is clearly not common and all the above mentioned issues will clinically manifest identically. Good sampling for histopathology will provide some insight but may not always tick enough boxes to have 100% confidence in pathomechanism.
