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Questions depth of anesthesia and adequacy of ventilation in fish article

In the article “Surgical removal of an anal cyst caused by a protozoan parasite (Thelohanellus kitauei) from a koi (Cyprinus carpio)” by Sang Phil Shin et al,1 the authors state that “Anesthesia was maintained with tricaine methanesulfonate delivered onto the gill in a solution containing 100 mg/L administered at a rate of 100 μL/min.” Anesthesia was reportedly induced by immersing fish in water containing 200 mg of tricaine methanesulfonate/L for 5 minutes.

Although the article does not state the total duration of the surgical procedure, I question both the adequacy of anesthesia (ie, depth of anesthesia) and the adequacy of ventilation in this fish.

In anesthetized fish, flowing water over the gills serves two functions: one is to deliver the anesthetic, and the other is to provide ventilation.

The anesthetic induction procedure described in the report might have kept this fish anesthestized at an appropriate depth for the duration of the surgical procedure without additional anesthetic, but this would depend on the anesthetic depth induced by the induction procedure and the duration of the procedure. If the procedure was longer than a few minutes, the anesthetic depth would no longer have been adequate. However, the amount of anesthetic delivered at the reported water flow rate over the gills would also have been inadequate for maintenance of an appropriate depth of anesthesia.

In fish, ventilation is provided by the flow of water over the gills. The water flow rate is equivalent in function to ventilation of the lungs in mammals, and the flow rate for adequate ventilation is dependent on the size, species, and activity of the fish. The authors of this report said the fish weighed 38.9 g. The typical water flow rate over the gills is variously reported but is about 1 L/kg/min in many species of fish,2 and that is what I would have used. For the fish described in the report, given a body weight of 38.9 g and a desired flow rate of 1 L/kg/min (1 mL/g/min), the flow rate should have been 38.9 mL/min or 38,900 μL/min. Given the reported flow rate (100 μL/min), I believe the fish was severely underventilated. If the procedure was very short, the fish could have survived (as was the case). However, if the procedure was longer than a few minutes, I believe that the depth of anesthesia and the ventilation were inadequate.

Alan M. Klide, vmd

Professor of Veterinary Anesthesiology, Retired University of Pennsylvania Oxford, Pa

  • 1.

    Shin SPJee HHan JE, et al. Surgical removal of an anal cyst caused by a protozoan parasite (Thelohanellus kitauei) from a koi (Cyprinus carpio). J Am Vet Med Assoc 2011; 238: 784786.

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  • 2.

    de Salvo Souza RHSoncini RGlass ML, et al. Ventilation, gill perfusion and blood gases in dourado, Salminus maxillosus Valenciennes (Teleostei, Characidae), exposed to graded hypoxia. J Comp Physiol B 2001; 171: 483489.

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The authors respond:

Thank you for your thoughtful comments on our article.1 You expressed concerns regarding the depth of anesthesia and adequacy of ventilation for the fish described in our report, suggesting that the amount of anesthetic delivered at the reported water flow rate over the gills would have been insufficient to maintain an appropriate depth of anesthesia or adequate ventilation.

However, during surgery in fish, use of an artificial ventilation system is necessary only for procedures that last > 10 minutes and for all but the shortest out-of-water procedures.2 Our total surgery time was < 15 minutes, including time for induction of anesthesia. Thus, we did not need to maintain a deep plane of anesthesia for a prolonged period.

The 20,000 extant species of fishes vary greatly in regard to their tolerance of hypoxia. Species that rely extensively on aerobic metabolism for rapid and sustained swimming, such as salmon and tuna, are moderately to extremely sensitive to anoxia, whereas carp, eels, and hagfish can perform well at low oxygen concentrations,3 and carp, including koi, are tolerant of prolonged hypoxia as a result of metabolic suppression, tolerance of metabolite accumulation, free-radical defenses during reoxygenation, and gill remodeling.3,4 After surgery, our koi recovered well and we did not observe any clinical problems, including dyspnea.

Sang Phil Shin, dvm

Se Chang Park, dvm, PhD

Laboratory of Aquatic Animal Medicine Seoul National University Seoul, Republic of Korea

  • 1.

    Shin SPJee HHan JE, et al. Surgical removal of an anal cyst caused by a protozoan parasite (Thelohanellus hitauei) from a koi (Cyprinus carpio). J Am Vet Med Assoc 2011; 238: 784786.

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  • 2.

    Neiffer DLStamper MA. Fish sedation, analgesia, anesthesia, and euthanasia: considerations, methods, and types of drugs. ILAR J 2009; 50: 343360.

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  • 3.

    Bickler PEBuck LT. Hypoxia tolerance in reptiles, amphibians, and fishes: life with variable oxygen availability. Annu Rev Physiol 2007; 69: 145170.

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  • 4.

    Nilsson GE. Gill remodeling in fish—a new fashion or an ancient secret? J Exp Biol 2007; 210: 24032409.

Kudos on One Health Commission move

It was good news that the One Health Commission has found a permanent home at Iowa State University as reported in a recent JAVMA News story.1 Many times, a great concept slips into a short-lived existence once the initial publicity fades. We cannot let this happen with the one-health movement.

Having a home at a major university is a step in the right direction, as it gives the commission a secure platform to promote its message. With health-care costs increasing, it behooves all of us in the health-care professions to maximize the one-health concept through collaborative efforts. The results of these research and teaching efforts can then be applied in both community and clinical settings.

We need to support the commission, as Dr. Roger Mahr, CEO, points out, by aiding and promoting the value of a one-health approach.

William F. McCulloch, dvm, mph

Beaverton, Ore

1.

One Health Commission moves to ISU. J Am Vet Med Assoc 2011; 238: 835.

Another perspective on the horse welfare issue

Having read the recent letter to the editor by Drs. Dodman and Winand1 regarding horse slaughter, I wanted to share my own perspective. According to our oath, veterinarians have an obligation to, among other things, conserve animal resources and relieve animal suffering. In my experience, there is clear evidence that horses have suffered more since slaughter has been outlawed in the United States. Thus, I believe that for veterinarians to work to deny owners the opportunity to send their horses to slaughter is not consistent with our oath.

In the county where I live, it costs at least $200 to have a horse euthanized and the carcass buried. In contrast, before the slaughter ban, the minimum price for a horse at the local sale barn was typically $400. Thus, prior to the slaughter ban, selling one horse meant that you could afford to feed 10 other horses for a month. In contrast, since the slaughter ban, euthanizing one horse means that you can't afford to feed five other horses for a month. These are the decisions horse owners in my county are forced to make every day, and the result is that more horses suffer. Once you dispatch as many starving horses as I have, you'll know what animal suffering really looks like.

Daniel Eisenhour, dvm

Canadian Valley Animal Clinic El Reno, Okla

1.

Dodman NHWinand NJ. Debate continues on horse welfare issue (lett). J Am Vet Med Assoc 2011; 238: 839840.

Treatment options for portosystemic shunts

I read with interest the “What Is the Evidence?” article1 in the April 1, 2011, issue of JAVMA. I realize the primary intent of the article was to address current best evidence as it applies to the medical management of portosystemic shunts (PSSs). As stated, complete or partial occlusion of a PSS is considered the treatment of choice. It is generally accepted that medical management will ameliorate clinical signs and improve quality of life; however, a normal life expectancy is not achieved. In one study,2 surgical correction of PSSs in dogs greater than one year of age was associated with a greater incidence of postoperative seizures and death.

The patient of this report was a six-month-old Labrador Retriever with a large intrahepatic PSS and several additional smaller anomalous vessels accompanying it. Although I do agree that interventional intravascular occlusion would not have been possible, I am not convinced a grave surgical prognosis was completely accurate. Attenuating or occluding the branch of the portal vein that supplies the shunting vessel is a useful but sometimes forgotten option.3,4 The portal segment giving rise to the PSS was identified in this patient from the mesenteric angiogram. The lack of vessel branching to the balance of the hepatic parenchyma was most likely due to hypoperfusion and not hypoplasia of the portal vasculature. Surgical exploration with isolation of the portal vein branches to the various liver lobes is not difficult to accomplish. Intraoperative portal vein catheterization can be done directly or through a mesenteric vein. This catheter can then be used to measure portal vein pressure and to perform portography. Temporary occlusion of the various portal vein branches while measuring the pressure in the main portal vein will isolate the branch supplying the shunt vessel. Additionally, intraoperative portography during occlusion of the portal branch supplying the PSS will assist in evaluating the balance of the intrahepatic portal circulation. Partial, complete, or gradual attenuation of the portal vein branch giving rise to the shunt can then be undertaken. Hepatic arterial supply provides adequate blood flow to the liver lobe, and occluding the portal branch to that lobe has no adverse consequences on liver function. This technique can be performed with moderate risk and can achieve an excellent clinical outcome. In the dog of this report, the close association of the smaller aberrant vessels with the single large anomalous shunt vessel suggests the same origin from a single intrahepatic portal vein branch. Attenuation or occlusion of this branch would have decreased or eliminated blood flow through all the anomalous vasculature.

I am not sure whether the owners of this dog declined to pursue surgical intervention because the risks were stated to be so great or if costs or other considerations were the determining factor. Also, I do not know whether the technique discussed above was offered and also declined.

The article is an excellent review regarding medical management of PSSs. For many owners, the costs involved or the risks associated with surgery may preclude definitive treatment. As the authors have shown, medical management can ameliorate clinical signs and provide a good quality of life, the length of which is still to be determined.

David L. Pendray, dvm

Advanced Veterinary Care Center Cody, Wyo

  • 1.

    Owens SLParnell NK. What is the evidence? J Am Vet Med Assoc 2011; 238: 859861.

  • 2.

    Mehl MLKyles AEHardie EM, et al. Evaluation of ameroid ring constrictors for treatment for single extrahepatic portosystemic shunts in dogs: 168 cases (1995–2001) J Am Vet Med Assoc 2005; 226: 20202030.

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  • 3.

    Breznock EMBerger BPendray D, et al. Surgical manipulation of intrahepatic portocaval shunts in dogs. J Am Vet Med Assoc 1983; 182: 798805.

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  • 4.

    Tobias KM. Portosystemic shunts and other hepatic vascular anomalies. In: Slatter D, ed. Textbook of small animal surgery. 3rd ed. Philadephia: WB Saunders Co, 2003; 740747.

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