Fetch San Diego 2019 addendum proceedings
Table of Contents
Parasitology Dr. Michael Dryden All about fecal diagnostics: Classic and cutting edge ...... 1 Intestinal parasites of dogs and cats: A changing clinical perspective ...... 4 Itchy pets and systemic flea control ...... 8 The quagmire that is giardiasis ...... 13 Ticks on the West Coast – do we need to be concerned? ...... 16
Practice Management Dr. Jeff Werber and Brandon Werber Connected care and telemedicine: It’s not the future… it’s now! ...... 19
Soft Tissue Surgery Dr. Bronwyn Fullagar Gastric dilatation volvulus: It doesn’t have to make your stomach turn ...... 22 Gastrointestinal foreign bodies: Minimizing the risk of post-operative dehiscence ...... 27 Gastrointestinal surgery pearls: Tips and tricks you won’t find in the textbook ...... 31 Going with the flow: A practical guide to lower urinary tract obstruction ...... 35 Open wounds: We’ve got you covered! Demystifying the world of wound management ...... 39 What lies beneath: Managing thoracic trauma from the ER to the OR ...... 43 All About Fecal Diagnostics: Classic and Cutting Edge Michael W. Dryden DVM, MS, PhD, DACVM (parasitology) College of Veterinary Medicine, Kansas State University, Manhattan KS 66502
To ensure the health and well-being of pet dogs and cats, examination of feces for parasite eggs, oocysts, and cysts are an important part of the daily routine for most veterinary practices. Many different procedures and techniques are used, each with its own advantages and limitations. Direct fecal smears are useful for detecting motile protozoa, and sedimentation examinations are useful for recovering heavy (e.g., Physaloptera spp) or operculated (e.g., fluke) eggs that do not float well because of the hypertonic effects exerted by the flotation solution. The methods most frequently used to recover parasite eggs, oocysts, and cysts are flotation techniques that rely on the differences in the specific gravity (SG) of the egg(s), fecal debris, and flotation solution.
The SG of most parasite eggs is between 1.05 and 1.23.1 For parasite eggs to float, the SG of the flotation solution must be greater than that of the eggs. Ideally, all helminth eggs and protozoan cysts and oocysts would float and still maintain their morphologic integrity while fecal debris would sink in the chosen flotation solution. Flotation solutions are made by adding a measured amount of salt or sugar to a specific amount of water to produce a solution with the desired SG. Common flotation solutions include saturated sodium chloride (NaCl; SG 1.18), sugar (Sheather’s solution; SG 1.27 to 1.33), sodium nitrate (NaNO3; SG 1.18 to 1.2), magnesium sulfate (MgSO4; SG 1.2), and zinc sulfate (ZnSO4; SG 1.2). These solutions are effective, easy to make or commercially available, and relatively inexpensive.
Flotation procedures vary from the simple to the complex. The simplest procedure involves mixing a small amount of feces with flotation solution in a cylinder (shell vial or centrifuge tube) and adding solution until the cylinder is nearly full. The preparation is then allowed to stand until the eggs float to the top, and a sample from the top is removed to a microscope slide using a tool such as a wire loop, straw, needle hub, or glass rod. A refinement of this method involves filling the cylinder until a slight positive meniscus is formed and placing a glass coverslip over it. Again, the cylinder is allowed to stand until the eggs have had time to float to the top, and the coverslip is then removed to a microscope slide and examined. Several commercial apparatuses that use a screen to retain debris from floating to the top are variations of the simple shell vial technique.
A further refinement of the flotation technique involves centrifugation to spin down the debris and allow the eggs to float to the surface of the solution where they can be recovered. If a fixed-angle centrifuge head is used, the centrifuge tubes cannot be filled completely and thus should be removed from the centrifuge after spinning and placed vertically in a test tube rack. If a swing-head centrifuge is used, the tubes can be filled to a slight positive meniscus and covered with 18- or 22-mm2 coverslips before centrifuging. When tubes are spun with coverslips in place, care should be taken not to open the centrifuge before it stops spinning, or the coverslips can shift and ruin the preparation. Veterinary hospitals usually use one or more of these methods based on cost, ease of use, availability of hardware, or simply tradition.
The Ovassay method with 1.1-SG ZnSO4 solution readily floats, hookworm (A. caninum) eggs (SG 1.05591); however, ascarid (T. canis) eggs (SG 1.0900) may not be recovered and whipworm (T. vulpis) eggs (SG 1.1453) are virtually impossible to float with such a solution.2 This points out the necessity for using care in weighing the salts and measuring water when preparing flotation solutions and for assuring proper SG by testing the solution with an SG hydrometer. When the SG of the salt solution (ZnSO4) is raised to 1.2, T. vulpis, and T. canis eggs are recovered in the Ovassay but in fewer numbers than with a centrifugation method using either ZnSO4 or sugar. A centrifugation method will recover significantly higher fecal counts compared with the Ovassay method.
For A. caninum, a centrifugation method using 1.2-SG NaNO3 solution results in significantly higher fecal egg counts than the simple flotation method, which is allowed to stand for 5 or 10 minutes.2 A 15- or 20- minute simple flotation method recovers significantly similar fecal counts as compared with the centrifugation method. With low numbers of T. vulpis eggs the 5’ and 10’ simple floats can miss eggs in 2 out of 3 samples.
Over the past decade a number of studies have been conducted to evaluate and compare the performance of various fecal diagnostic techniques.2-9
1 From 2000 to 2004, students at KSU evaluated 206 fecal samples known to contain hookworm (A. caninum) eggs.2 When all hookworm data were combined, the direct smear technique failed to detect hookworm eggs 72.82% of the time. The Ovassay and centrifugation techniques yielded false-negative results 4.85% and 0.97% of the time, respectively, and recovered more than 50 eggs/slide 36.41% and 74.76% of the time, respectively.2
Students evaluated 171 fecal samples known to contain ascarid (T. canis or T. cati) eggs. When all ascarid data were combined, the direct smear technique failed to detect ascarid eggs 85.38% of the time. The Ovassay and centrifugation techniques yielded false-negative results 25.88% and 10.53% of the time, respectively, and recovered more than 50 eggs/slide 1.18% and 42.69% of the time, respectively.2
Students evaluated 203 fecal samples known to contain whipworm (T. vulpis) eggs. When all whipworm data was combined, the direct smear technique failed to detect whipworm eggs 92.61% of the time. The Ovassay and centrifugation techniques yielded false-negative results 32.02% and 4.93% of the time, respectively, and recovered more than 50 eggs/slide 2.96% and 23.65% of the time, respectively.2
Students also evaluated 53 fecal samples known to contain tapeworm (Taenia sp) oocysts and 26 samples known to contain coccidia (Isospora sp) oocysts. The direct smear technique failed to detect tapeworm eggs 96.15% of the time. The Ovassay and centrifugation techniques yielded false-negative results 76.92% and 11.54% of the time, respectively. When the two sets of coccidia data were combined, the direct smear technique failed to detect coccidia oocysts 94.34% of the time. The Ovassay and centrifugation techniques yielded false-negative results 50.94% and 5.66% of the time, respectively.2
Evaluations of centrifugation fecal techniques and IDEXX SNAP® Giardia fecal antigen test kits of puppy fecal samples by 2nd year veterinary students showed that almost half (56/116) of the fecal samples were recorded as positive for Giardia. The direct smear technique detected the fewest number of positives with students recording only 4 positive samples. This data may be artificially low since the fecals were collected several hours prior to laboratory and trophozoites may have been dead at time of examination. Students recorded that the SNAP® Giardia fecal antigen test identified 55 of 116 samples as Giardia positive and ZnSO4 centrifugation technique recorded 45 of 116 samples as positive.
At a wet lab conducted at the Central Veterinary Conference in 2005 twenty-seven (27) participants returned completed fecal data forms. When a centrifugation fecal flotation technique was compared to passive flotation technique the data demonstrated that centrifugation with either 1.18 sp. gr. ZNSO4 or 1.27 sp. gr. Sheather’s sugar solution routinely recovers more eggs and oocysts than the passive Ovassay technique. Not only did the centrifugation technique recover more eggs and oocysts in addition the participants recorded many more samples as positive with the centrifugation technique. Strikingly only once (T. canis – Ovassay - ZNSO4) did the Ovassay technique recover all parasites in all samples, while only once did the centrifugation technique fail to recover all parasites in all samples. In the group that used 1.18 sp. gr. ZNSO4 solution only 2 of 14 participants recovered Taenia sp. eggs. While in the group using 1.27 sp. gr. Sheather’s sugar solution all 13 participants recovered Taenia sp. eggs using.
Even though the participants knew the samples were positive for Giardia recovery and identification of Giardia sp. oocysts was problematic for the 27 participants regardless of technique. Only 6 of the 27 participants were able to recover and identify Giardia sp. oocysts from a known positive sample. One participant each using the Centrifugation with ZNSO4, Ovassay with ZNSO4 and Ovassay with Sugar was able to recover and identify Giardia sp. cysts. Three participants using the Centrifugation with Sugar were able to recover and identify Giardia sp. cysts. All 27 participants had a positive SNAP® Giardia fecal antigen test on the mixed sample.
As part of a weeklong clinical Parasitology training program, veterinarians participated in a wet-lab evaluating fecal examination techniques.9 Three classes were offered during 2010, 2011 and 2012, for a total of 9 classes that included 56 participants. Fecal samples were collected from dogs at the local animal shelter, verified as positive for various parasite diagnostic stages and mixed to form composite samples.
2 While species of parasites in fecal samples varied, all 9 classes evaluated samples that contained A. caninum, T. canis and T. vulpis eggs. Each participant conducted a direct smear, an Ovassay using a 1.18 sp. gr. ZnSO4 solution, a centrifugation procedure using 1.18 sp. gr. ZnSO4 solution and a centrifugation procedure using 1.24 sp. gr. sugar solution. Using the direct smear technique, participants recovered T. canis, T. vulpis and A. caninum eggs 30.4% (17/56), 26.8% (15/56) and 30.4% (17/56) of the time, respectively. The Ovassay recovered T. canis, T. vulpis and A. caninum eggs 57.1% (32/56), 41.1% (23/56) and 87.5% (49/56) of the time, respectively. The centrifugation procedure with ZnSO4 recovered T. canis, T. vulpis and A. caninum eggs 94.6% (53/56), 85.7% (48/56) and 100% (56/56) of the time, respectively. The centrifugation procedure with the sugar solution recovered T. canis, T. vulpis and A. caninum eggs 96.4% (54/56), 100% (56/56) and 100% (56/56) of the time, respectively. When the Ovassay technique was used, only 33.3%, 11.1% and 44.4% of the time did every participant recover T. canis, T. vulpis and A. caninum eggs, respectively. When the participants used the centrifugation procedure with sugar solution, every participant in every class recovered eggs of T. vulpis and A. caninum and 77.8% of the time every participant recovered eggs of T. canis.
Fecal Antigen Testing for intestinal nematodes.10,11 New method for detecting protein biomarkers secreted or excreted (ES) by nematodes in the intestinal lumen. Unique marker for ascarid, hookworm, whipworm and recently Echinococcus. These biomarkers are produced by the worms and not the eggs. It is also important to note that antigen is cleared once parasites are eliminated following treatment. Fecal antigen testing appears to be more accurate that standard fecal examinations, they detect prepatent infections and do not react when dogs are passing spurious eggs from coprophagy.
References
1) David ED, Lindquist WD: Determination of the specific gravity of certain helminth eggs using sucrose density gradient centrifugation. J Parasitol 68:916–919, 1982. 2) Dryden MW, Payne PA, Ridley R, Smith V. Comparison of common fecal flotation techniques for the recovery of parasite eggs and oocysts. Vet Therapeutics 6(1), 14 – 28, 2005. 3) Blagburn B. The elusive whipworm, Trichuris vulpis. NAVC Clinician’s Brief September(Suppl):2-4, 2008. 4) Dryden MW, Payne PA, Smith V. Accurate diagnosis of Giardia spp. and proper fecal examination procedures. Vet Therapeutics 7(1), 4 – 14, 2006. 5) Dryden MW, Payne PA, Ridley R, Smith V. Gastrointestinal Parasites: the practice guide to accurate diagnosis and treatment. Supplement to Compendium: Continuing Education for Veterinarians. 28 (8A): 3 -13, 2006. 6) Gates MC, Nolan TJ. Comparison of Passive Fecal Flotation Run by Veterinary Students to Zinc- Sulfate Centrifugation Flotation Run in a Diagnostic Parasitology Laboratory. J. Parasitol., 95(5):1213–1214, 2009. 7) O’Horo M, et al. A Comparison of Fecal Examination Techniques for the Recovery of Parasite Ova in Large Animals. Vet Tech July:442-443, 2007. 8) Zajac A, Johnson J, King S: Evaluation of the Importance of Centrifugation as a Component of Zinc Fecal Flotation Examinations. J Am An Hosp Assoc 38(3):221-224, 2002. 9) Dryden MW, Payne PA. Further evaluation of fecal examination techniques for the recovery of Toxocara canis, Trichuris vulpis and Ancylostoma caninum eggs. Am. Assoc. Vet. Parasitol. 57th Annual Meeting, 4-7 August 2012, San Diego, CA. P.74. 10) Elsemore D, Geng J, Flynn L, et al. Enzyme-linked immunosorbent assay for coproantigen detection of Trichuris vulpis in dogs. Journal of Veterinary Diagnostic Investigation 2014; March:1-8. 11) Elsemore DA, Geng J, Cote J, Hanna R, Lucio-Forster A, Bowman DD. Enzyme-linked immunosorbent assays for coproantigen detection of Ancylostoma caninum and Toxocara canis in dogs and Toxocara cati in cats. J Vet Diagn Invest. 2017 Sep;29(5):645-653
3 Intestinal parasites of dogs and cats: A changing perspective Michael W. Dryden DVM, MS, PhD, DACVM (parasitology) College of Veterinary Medicine, Kansas State University, Manhattan KS 66502
Preventive health care, including the prevention of common parasitic infections in cats and dogs, is an approach that is relatively easy to accomplish. Veterinarians and pet owners must realize that proper selection of parasiticides will not only prevent heartworms but also can prevent a variety of internal and external parasites. This approach has been advocated by the Companion Animal Parasite Council (CAPC; www.capcvet.org). CAPC recommends “year-round treatment with broad-spectrum heartworm anthelmintics that have activity against parasites with zoonotic potential.” The council also states: “Pet-owner awareness of heartworms and fleas can serve as the foundation for effective prevention and control of other parasites.” These recommendations should be adopted for both cats and dogs.
When beginning a parasite control program, it is important to find the foundation parasite from which the success of the program hinges. The foundation parasite may be the most common, the most pathogenic or of the most concern to the client. The foundation parasite is the one disease that you and your clients recognize must be included in your parasite control program. Therefore, the foundation parasite in dogs is often Heartworm, but in other areas other parasites such as ticks and the diseases they transmit may also resonate with pet owners. While cats are not as commonly afflicted with heartworms as dogs the increased awareness of the pathology and potentially deadly nature of heartworm disease in cats1,2 may allow D. immitis to rise to the forefront of concern with many clients. However, this author feels that fleas are often the foundation parasite for a parasite control program in cats.3 However, practitioners must use their knowledge and experience to choose the foundation parasite for cats and dogs in their area or even for an individual pet and client.
Next it is important to remember that while we might focus initially on prevention of a “foundation” parasite, we must stress to the pet owner that we are actually implementing a “broad spectrum” parasite prevention package. Explain that not only will we be preventing heartworm disease in dogs, but we will also potentially be controlling fleas, ticks, lice, certain mites, and several common intestinal nematodes. In addition, we will be reducing the chance that their dog could transmit a parasitic disease to them or other members of their family. Similarly, in cats, we might tell them we will try to ensure that their cat and home does not become flea infested, but we will also be preventing their cat from becoming infested with ear mites, face mange, lice, intestinal nematodes and potentially deadly heartworm.
The program often begins with broad-spectrum heartworm medications that also prevent several common intestinal parasite infestations. Because prevention of heartworm in cats and dogs using macrolides is well documented, this article will focus on the epidemiology and prevention of the other common parasites of cats and dogs that can be controlled using monthly heartworm medications.
Internal Parasites Many pet owners do not want to think their cat or dog, a member of their family, may have preyed on a mouse, bird or other animal. However, this natural predator–prey relationship is a common mode of transmission of many feline parasites, including Alaria spp., Ancylostoma tubaeforme, Cystoisospora spp. (Isospora) (, Physaloptera spp., Sarcocystis spp., Taenia taeniaeformis, Toxocara cati, Toxascaris leonina, and Toxoplasma gondii.3 Similarly many parasites of dogs can be acquired through predation, including Alaria spp., Cystoisospora spp.( Isospora), Physaloptera spp., Sarcocystis spp., Taenia spp., Toxocara canis, and Toxascaris leonina.4-5
Toxocara sp. Predation on infected paratenic hosts is commonly underestimated by veterinarians and likely completely unknown by most pet owners as a mode of Toxocara spp. transmission. Larvae commonly become encysted in the tissues of chickens, cockroaches, earthworms, and mice when they ingest infective larvated eggs in feces or contaminated soil. Similarly, children may also become infected with somatic tissue stages of T. cat or T. canis, which can cause visceral or ocular larva migrans. In addition, cats and dogs become infected after ingesting larvated eggs.
4 Three of the broad-spectrum heartworm medications currently approved for use in cats are effective in eliminating T. cati; oral milbemycin6, topically applied selamectin7 and the topically applied imidacloprid– moxidectin formulation8.
Several of the broad-spectrum heartworm medications that are currently approved for use in dogs are effective for the elimination of T. canis including the imidacloprid:moxidectin topical formulation,9 the oral ivermectin/pyrantel pamoate formulation,10 oral milbemycin oxime,11 and the oral milbemycin oxime/lufenuron formulation.12 In addition the oral ivermectin/pyrantel pamoate, the topical imidacloprid:moxidectin and the oral milbemycin formulations are also labeled for Toxascaris leonina.
Ancylostoma sp. In cats larvae may be ingested, penetrate the skin or rodents with encysted larvae may serve as paratenic hosts, but there is no evidence for either transmammary or transplacental transmission of A. tubaeforme in cats.13 All of the broad-spectrum heartworm medications approved for use in cats in the U.S. and Canada are effective in eliminating A. tubaeforme.9, 14,15 Similarly A. caninum which is an important parasitic disease in dogs and a potentially life threatening disease in puppies following transmammary transmission, can be effectively managed with several of the broad-spectrum heartworm medications including the imidacloprid:moxidectin topical formulation,16 the oral ivermectin/pyrantel pamoate formulation,17 oral milbemycin oxime,18 and the oral milbemycin oxime/lufenuron formulation.
It should be remembered that when these formulations are administered as approved, the dog or cat is essentially “dewormed” on a monthly basis. If a pet is frequently exposed to infective third-stage larvae of Ancylostoma spp, the worms can mature and deposit eggs between monthly applications, given that the prepatent period of Ancylostoma spp. can be as short as 2 to 3 weeks. However, monthly application should prevent development of hookworm disease. Uncinaria sp. a mildly pathogenic hookworm species can be controlled by the administration of broad-spectrum heartworm medications that contain milbemycin, moxidectin or pyrantel.
Trichuris vulpis T. vulpis is a pathogenic parasite of dogs that can produce mild to severe blooding diarrhea and chronic debilitation. This parasitic disease can be controlled by the monthly administration of broad-spectrum heartworm medications that contain milbemycin and the imidacloprid/moxidectin formulation also label claims against whipworms.
Tapeworms While Dipylidium and Taenia sp. generally not considered highly pathogenic in dogs and cats they can be extremely disturbing to pet owners. However, infections with Echinococcus spp. while not producing gastrointestinal disease in dogs or cat, their very presence and shedding of eggs is of major concern to public health. Hydatid disease is still one of the most lethal human parasitic infections. In areas where this is comm in wildlife such as coyotes and bobcats, it may be wise to consider regular administration of preventives containing praziquantel to dogs and cats.
Overview of Internal Parasite Prevention Several broad-spectrum heartworm medications are effective in controlling Toxocara spp. and Ancylostoma spp. but cats and dogs may become infected with a variety of internal parasites against which these formulations may not be effective. Therefore, fecal examinations utilizing a centrifugal procedure should be performed two to four times during the first year of the pet’s life and one to two times annually as an adult depending on the pet’s health and lifestyle factors (www.capcvet.org). In addition, for pet health and to minimize egg shedding kittens should be given biweekly anthelmintic treatments beginning at 3 weeks of age. When cats reach 8 or 9 weeks of age, they can be put on a monthly broad-spectrum heartworm medication. Puppies should be administered anthelmintic treatments at 2, 4, 6, 8, and 10 weeks post-partum. Then they can be placed on a monthly broad-spectrum heartworm medication.
Historically, many veterinarians and pet owners attempted to administer broad-spectrum heartworm medications seasonally. Although seasonal prevention of heartworm and other parasites may at seem appropriate in many regions of North America, it is actually difficult to accomplish.
5 Veterinarians must first attempt to estimate heartworm larvae development rates in mosquitoes so they can seasonally time the administration of heartworm preventives. Then they are faced with the difficulty if not impossibility of attempting to estimate the rate of flea development, tick questing patterns, mite and louse transmission, and development of infective roundworm eggs and hookworm larvae. Because of differences in the biologic requirements of each parasite, the specific transmission “seasons” vary among parasites. Changing climatic conditions from one year to the next can have marked effects on parasite “seasonality.”
Studies have not been published comparing the effectiveness of year-round versus seasonally timed prevention programs, but it is this author’s experience that determining when to start and stop seasonally timed applications of broad-spectrum parasite prevention programs is difficult. Considering the various and changing climatic epidemiologic factors and historic poor pet owner compliance it is understandable why the CAPC recommends year-round treatment with broad-spectrum heartworm medications (www.capcvet.org)
References
1. Browne LE, Carter TD, Levy JK, Snyder PS, Johnson CM. Pulmonary arterial disease in cats seropositive for Dirofilaria immitis but lacking adult heartworms in the heart and lungs. Am J Vet Res 66(9):1544- 9,2005. 2. Nelson CT, McCall JW, Rubin SB, Buzhardt LF, Dorion DW, Graham W, Longhofer SL, Guerrero J, Robertson-Plouch C, Paul A; Executive Board of the American Heartworm Society. 2005 Guidelines for the diagnosis, prevention and management of heartworm (Dirofilaria immitis) infection in cats. Vet Parasitol 133(2-3):267-75, 2005. 3. Dryden MW, Payne PA. Preventing parasites in cats. Vet Ther 6(3):260-7, 2005. 4. Soulsby EJL. Helmiths, Arthropods and Protozoa of Domestic Animals 7th edition. Lea and Febiger, Philadelphia 1982, pp809. 5. Bowman DD, Lynn RC, Eberhard ML. Georgis’ Parasitology for Veterinarians 8th Edition. Saunders, St. Louis MO. 2003.pp422. 6. Fukase T, In T, Chinone S, Akihama S, Itagaki H; Anthelmintic efficacy of milbemycin D against Toxocara cati and Ancylostoma tubaeforme in domestic cats. J Vet Med Sci 53(5):817-21, 1991. 7. McTier TL, Shanks DJ, Wren JA, Six RH, Bowman DD, McCall JW, Pengo G, Genchi C, Smothers CD, Rowan TG, Jernigan AD: Efficacy of selamectin against experimentally induced and naturally acquired infections of Toxocara cati and Ancylostoma tubaeforme in cats. Vet Parasitol 91(3-4):311-9, 2000. 8. Reinemeyer CR, Charles S: Evaluation of the efficacy of a combination of imidacloprid and moxidectin against immature Toxocara cati in cats. Parasitol Res 90 Suppl 3:S140-1, 2003. 9. Hellmann K, Knoppe T, Radeloff I, Heine J. The anthelmintic efficacy and the safety of a combination of imidacloprid and moxidectin spot-on in cats and dogs under field conditions in Europe. Parasitol Res 90 Suppl 3:S142-143, 2003. 10. Clark JN, Daurio CP, Plue RE, Wallace DH, Longhofer SL. Efficacy of ivermectin and pyrantel pamoate combined in a chewable formulation against heartworm, hookworm, and ascarid infections in dogs. Am J Vet Res 53(4):517-520, 1992. 11. Bowman DD, Parsons JC, Grieve RB, Hepler DI. Effects of milbemycin on adult Toxocara canis in dogs with experimentally induced infection. Am J Vet Res 49(11):1986-1989, 1988. 12. Schenker R, Cody R, Strehlau G, Alexander D, Junquera P. Comparative effects of milbemycin oxime- based and febantel-pyrantel embonate-based anthelmintic tablets on Toxocara canis egg shedding in naturally infected pups. Vet Parasitol 30;137(3-4):369-373, 2006. 13. Bowman DD, Barr SC, Hendrix CM, Lindsay DS: Gastro-intestinal Parasites of Cats (Last Updated: 24- Jan-2003). In Companion and Exotic Animal Parasitology, Bowman D.D. (Ed.). International Veterinary Information Service, Ithaca NY (www.ivis.org), 2003. 14. Humbert-Droz E, Buscher G, Cavalleri D, Junquera P: Efficacy of milbemycin oxime against fourth-stage larvae and adults of Ancylostoma tubaeforme in experimentally infected cats. Vet Rec 154(5):140-3, 2004. 15. Nolan TJ, Niamatali S, Bhopale V, Longhofer SL, Schad GA: Efficacy of a chewable formulation of ivermectin against a mixed infection of Ancylostoma braziliense and Ancylostoma tubaeforme in cats. Am J Vet Res 53(8):1411-3, 1992. 16. von Samson-Himmelstjerna G, Epe C, Schimmel A, Heine J. Larvicidal and persistent efficacy of an imidacloprid and moxidectin topical formulation against endoparasites in cats and dogs. Parasitol Res ;90 Suppl 3:S114-115, 2003.
6 17. Reinemeyer CR, Faulkner CT, Assadi-Rad AM, Burr JH, Patton S. Comparison of the efficacies of three heartworm preventives against experimentally induced infections with Ancylostoma caninum and Toxocara canis in pups. J Am Vet Med Assoc 206(11):1710-1715, 1995. 18. Bowman DD, Johnson RC, Hepler DI. Effects of milbemycin oxime on adult hookworms in dogs with naturally acquired infections. Am J Vet Res 51(3):487-490, 1990. 19. Dryden MW, Burkindine S, Lewis T, Houdeshell L, Rodriquez I, Hack R: Efficacy of selamectin in controlling natural flea infestations on pets and in private residences in comparison with imidacloprid and fipronil In proceedings of the Am Assoc of Vet Parasitol Ann Meeting. July 14 – 15, 2001 Boston MA. P34. 20. Arther RG, Bowmann DD, McCall JW, Hansen O, Young DR: Feline Advantage Heart (imidacloprid and moxidectin) topical solution as monthly treatment for prevention of heartworm infection (Dirofilaria immitis) and control of fleas (Ctenocephalides felis) on cats. Parasitol Res. 90 Suppl 3:S137-9, 2003. 21. Dryden M, Brown H, Buck S, Schwahn R, Sloan T, Summers S. Effective Long Term Protection Against Flea Infestations Vet. Med. June. 16 – 18, 1998. 22. Shanks DJ, Gautier P, McTier TL, Evans NA, Pengo G, Rowan TG. Efficacy of selamectin against biting lice on dogs and cats. Vet Rec 152(8):234-237, 2003. 23. Hanssen I, Mencke N, Asskildt H, Ewald-Hamm D, Dorn H. Field study on the insecticidal efficacy of Advantage against natural infestations of dogs with lice. Parasitol Res 85(4):347-348, 1999. 24. Six RH, Clemence RG, Thomas CA, Behan S, Boy MG, Watson P, Benchaoui HA, Clements PJ, Rowan TG, Jernigan AD. Efficacy and safety of selamectin against Sarcoptes scabiei on dogs and Otodectes cynotis on dogs and cats presented as veterinary patients. Vet Parasitol 91(3-4):291-309, 2000. 25. Itoh N, Muraoka N, Aoki M, Itagaki T: Treatment of Notoedres cati infestation in cats with selamectin. Vet Rec 154(13):409, 2004. 26. Fourie LJ, Heine J, Horak IG. The efficacy of an imidacloprid/moxidectin combination against naturally acquired Sarcoptes scabiei infestations on dogs. Aust Vet J 84(1-2):17-21, 2006.
7 Itchy pets and systemic flea control Michael W. Dryden DVM, MS, PhD, DACVM (parasitology) College of Veterinary Medicine, Kansas State University, Manhattan KS 66502
Fleas are a common and important external parasite of dogs and cats. The most common flea species infesting dogs and cats in North America and in many areas of the world is Ctenocephalides felis felis, the cat flea.1,2 Cat fleas are voracious blood feeders consuming up to 15 times their body weight in blood daily and female fleas use that blood to produce up to twice their bodyweight in eggs daily.1-3 So it does not take long before a flea infestation can get completely out of hand. These fleas can cause allergic skin disease (FAD), produce anemia through their blood feeding activities, transmit tapeworms and bacterial pathogens.1,2 It is therefore important for the health and well-being of our pets that we control these harmful parasites.
It must be understood that it often takes several weeks to eliminate a flea infestation. That is because all flea infestations of dogs and cats originated from a flea-infested environment and it takes time to eradicate the immature stages living in the carpet or outdoors. Once these fleas jump on a dog or cat they will feed, mate and female fleas will begin laying eggs within 24 hours.1-3 Then within a few days each female flea will be producing 40 – 50 eggs per day, with hundreds and potentially thousands of eggs being deposited into the home or yard.3 The in-home and potentially outdoor premises rapidly becomes infested with egg, larvae, pupae and emerging adult fleas, often referred to as the flea biomass.
Historically veterinarians and pet owner treated the premises directly through the application of insecticides and insect growth regulators into the carpet and yard.4 This was done in an attempt to kill emerging fleas and prevent development of eggs & larvae. Premises treatments were considered necessary to break the flea lifecycle. The primary reason that premises treatments were necessary was that prior to the mid-1990s topical products (dips, sprays, collars, powders etc..) had no substantial duration of residual activity.5 Premises treatments were difficult to conduct, time consuming, expensive, environmentally unfriendly and often ineffective.
However, with modern topical and systemic residual flea products, control of infestations in the premises is now achieved by preventing flea reproduction.6,7 Reproduction is halted either through the use of highly effective residual adulticides that kill most newly acquired fleas before they begin reproduction (killing fleas within 24 hours after jumping on treated pet) or through the use of insect growth regulators (or insecticides) with ovicidal activity to kill any eggs that might be produced.6,7 Simply if you cannot reproduce as a species you go extinct in the local premises.
When focusing on residual adulticides it is the residual speed of kill of a product that is of utmost importance.8 Residual speed of kill relates to how rapidly a product kills newly acquired fleas at some time point (days or weeks) after administration. If a product can kill newly acquired fleas fast enough it can prevent flea reproduction and markedly reduce the amount of salivary proteins injected by the fleas, thus minimizing or eliminate FAD symptoms.5,8
Although modern residual flea adulticides provide prolonged adulticidal activity, it has been determined that efficacy and speed of kill of most products will decrease over time following administration.5,9-12 As the residual efficacy decreases and fleas are not killed within 24 hours, female fleas can live long enough to produce eggs.5,9,10 Therefore, it is important to use a product that is effective enough to suppress reproduction between scheduled reapplications. Residual efficacy can also be affected by under-dosing by clients, bathing or swimming that can reduce insecticide levels of topical formulations, poor G.I. absorption with oral products and natural variability in susceptibility or outright resistance.13
Proper administration of effective residual flea products to all dogs and cats means no more fleas reproducing and no more eggs dropping into the environment. Therefore, within 2 to 7 days, eggs that were previously deposited have developed into larvae, within 1 to 2 weeks the larvae have now developed into pupae, and 1 to 4 weeks later those pupae are now adult fleas. As these fleas emerge and jump on treated pets they are hopefully being killed by the flea product. Therefore within 3 to 8 weeks or occasionally as long as 3 months, all the adult fleas and immature life stage biomass should be gone.6,7
8 How bad a flea infestation becomes and how rapidly a flea infestation is eliminated is not only affected by the product used, but also by environmental conditions. Relative humidity in the microenvironment is primary determining factor in flea populations. This is because flea larvae are weak link in the life-cycle chain and are very susceptible to heat and desiccation.1,2 In addition, the rate of flea development and therefore how rapidly the biomass is exhausted can be very temperature dependent.1,2 If a flea infestation continues beyond the expected 3 to 8 weeks (or longer), a commonly encountered problem is an untreated flea host in the home or maybe the product itself is not stopping reproduction.
Another issue that must be expected in a small number of homes is that the flea infestation may get worse before it gets better.7,14 These cases are referred to as “Red-line homes”. By definition a red-line home is a house were premises trap flea counts increase > 20% over day 0 trap counts within 1 to 4 weeks post- treatment.14 These surges in emerging fleas occurs because of a large preexisting biomass in the indoor premises. Such surges in emerging fleas and resulting increase in flea numbers on household pets can give the perception of product failure. Often extensive and frequent mechanical intervention (vacuuming, washing pet bedding and area and throw rugs, etc..) and even application of insecticides into the premises may be necessary in these cases.
Fluralaner, afoxolaner, lotilaner and sarolaner are recently introduced oral flea and tick adulticides in the isoxazoline class of drugs. These drugs work as GABA-Chloride antagonists causing over excitation of the insect and arachnid nervous system and rapid ectoparasite death.15-19 These compounds have demonstrated rapid and persistent efficacy against fleas and multiple species of ticks. In field studies evaluating dogs not managed with associated medications, afoxolaner, fluralaner, lotilaner and sarolaner not only managed flea infestations, but also managed clinical signs associated with FAD and pruritus.19-21
Following administration of these systemic isoxazolines, flea populations on pets are typically reduced by ≈99.0% within 7 days.19-21 Flea population reductions on treated then typically remain at or above 99% until populations are eliminated. Marked improvement was observed in FAD lesion scoring, Atopic Dermatitis lesions scoring (CADESI-4) and pruritus scores also occur following administration of these formulations.19-21
Spinosad first became available as an oral treatment for the control of flea infestations on dogs in late 2007. A multi-clinic, investigator-blinded study was undertaken in client-owned dogs to investigate and compare the flea control provided by 3 consecutive monthly treatments of oral spinosad (SPN) or fipronil/(s)—methoprene topical (FSM) spot-on.22 On day 0, geometric mean flea counts were 57.7 (range: 10-1,469) and 44.8 (10-717) for the SPN and FSM groups, respectively. On Day 90, 55 of 58 (95%) and 21 of 55 (38%) index dogs completing the study were flea-free in SPN and FSM groups, respectively; mean SPN pruritus scores declined to 0.92 (6.67 on day 0), and to 3.83 (6.33 on day 0) for FSM; geometric mean flea counts (% control) were 0.08 (99.9%) and 5.19 (88.4%), for SPN and FSM groups, respectively.
Flea allergy dermatitis or flea bite hypersensitivity is the most common dermatologic disease of domestic dogs. Cats are also afflicted with FAD, which is one of the major causes of feline miliary dermatitis. Historically, it has been said that one flea is all that is necessary to maintain the clinical signs of FAD and therefore total flea eradication is necessary. Newer adulticides such as fipronil, imidacloprid, metaflumizone, nitenpyram, selamectin, and spinosad have had a positive clinical effect on dogs and cats with FAD. However, data on flea biology and the effect of these products on flea feeding bring into question the once perceived dogma of the ‘one flea bite’.5 Adult cat fleas begin feeding almost immediately once they find a host, with many fleas feeding within minutes. In one study, 25–60% of fleas were blood fed within 5 min and in another study the volume of blood consumed by fleas was quantifiable within 5 min Feeding is so rapid that partially digested blood can be defaecated in as little as 2–6 min after fleas acquire a host. After rapid transit through the flea, the excreted blood dries within minutes into reddish black faecal pellets or long tubular coils (flea dirt). While initiation of feeding is rapid, daily blood consumption is voracious. Female cat fleas can consume up to ten times their body weight in blood the very first day. They are on the host and peak consumption occurs within a few days at 15 times their body weight (13.6 lL) daily. With such rapid and voracious blood feeding, is it reasonable to assume that residual insecticides can truly prevent flea biting and feeding?
9 A study was conducted at Kansas State University, Manhattan KS, USA to evaluate the residual activity of fipronil and imidacloprid on egg production and blood feeding. There were two objectives to these studies 1) to evaluate if these compounds will kill newly acquired fleas prior to them feeding and 2) to determine how long these compounds will prevent viable egg production after application. In the first experiment six cats were treated with either a fipronil spray (0.29% w/w) formulation, an imidacloprid spot-on (9.1% w/w) formulation at labeled rates or were left as untreated controls. Surprisingly when 100 Ctenocephalides felis were placed on cats 6 days after treatment with imidacloprid or fipronil, the percent of fleas that fed and consumed blood was 89 and 92%, respectively.5 While the adulticidal efficacy of the products was 100%, neither product killed fleas before the vast majority could bite, feed and consume at least some quantity of blood.
In another study conducted in Europe it was determined that the topical application of imidacloprid or fipronil to cats did not prevent fleas from biting and feeding. Unconfined fleas placed on cats treated with imidacloprid and fipronil had reductions in the percent of fleas blood feeding of 49.6 and 39.5%, respectively, on day seven; while reductions in percent of fleas feeding on day 28 was 0 and 3.4%, respectively. While topical applications of dichlorvos/fenitrothion or permethrin did reduce the percent of fleas feeding by greater than 80%, these compounds also did not completely prevent flea bites or feeding. The data on percent of fleas feeding on imidacloprid and fipronil treated cats in the European study differ from the data in the Kansas State University Study. This likely occurred due to the known reduced susceptibility of the KSU flea strain to imidacloprid and fipronil.
Another study conducted at KSU using dogs evaluated the ability of a 65% permethrin spot-on, a 13.8% fenthion spot-on and an 8% Chlorpyriphos collar to reduce blood feeding by fleas.5 At two weeks post-treatment evaluation of the blood fed status of fleas revealed that an average of 66.7% of fleas from permethrin treated dogs had fed. Fleas from chlorpyrifos collared dogs and fenthion treated dogs averaged 53.0 and 37% blood fed status, respectively. In this study the percent of fleas feeding on organophosphate and pyrethroid treated dogs was considerably higher than in the study conducted in Europe. It was later determined that the flea strain used in the KSU study was tolerant/resistant to certain organophosphates and pyrethroids.
Additional research has now been conducted to quantify the amount of blood consumed by fleas on insecticide treated cats.23 In this study fleas were confined for 24 hours in confinement feeding chambers attached to treated cats once a week for four 4 weeks. Confinement feeding chambers were used so that fleas and their feces could be collected for quantification and analysis. Cats were treated on day 0 with fipronil, imidacloprid, selamectin at label rates or were left untreated. In addition, another group of cats was administered nitenpyram one hour prior to each weekly infestations. After each 24-hour infestation fleas and feces were removed, microcell removed and the quantity of blood consumed and excreted was determined spectrophotometrically using the Drabkin’s Reagent Method. Fleas placed on imidacloprid and fipronil-treated cats seven days post-treatment had reductions in blood consumption of 90.78 and 69.77%, respectively. Whereas, at 14 days post-treatment fleas on fipronil-treated cats had no statistically significant reduction in blood consumption as compared to fleas on untreated controls while fleas on imidacloprid-treated cats consumed 55.73% less blood as fleas on controls. Then by three weeks post-treatment fleas on imidacloprid- treated cats had no statistically significant reduction in blood consumption as compared to fleas on untreated controls. Of particular interest was that fleas placed on cats treated orally with nitenpyram never consumed more than 1.63% (98.37% reduction) as much blood as fleas placed on control cats. Topically applied, but transdermally absorbed selamectin also had a pronounced effect upon blood consumption of fleas. Even on day 28 post-treatment there was an 88.9% reduction in blood consumption as compared to fleas on untreated controls.
As stated previously compounds such as fipronil, imidacloprid, metaflumizone, and selamectin and spinosad have had a major impact on reducing the occurrence of FAD. However, the data from the qualitative and quantitative studies demonstrates that these compounds do not stop flea bites nor completely stop flea feeding. Therefore, it appears their role in managing FAD is likely related to a decrease in prolonged flea feeding and thereby the amount of salivary protein delivered to the pet and in the long-term reducing flea numbers.
10 It is this author’s opinion that FAD is related to the degree of hypersensitivity of an individual animal, the numbers of fleas feeding and amount of antigen injected. This certainly brings into question the old dogma of a single flea bite eliciting an FAD reaction, at least in the majority of clinically afflicted animals. If a single flea bite was responsible, it appears no flea product would provide much relief, at least not until the flea population was eradicated. Also of importance to note is that regardless rather as to whether an insecticide works topically or systemically may be irrelevant in the management of fleas or FAD, since in the one study the systemically active compounds had a pronounced effect on blood feeding.5
References:
1. Rust M, Dryden M. The biology, ecology and management of the cat flea. Ann Rev Entomol 1997; 42:451- 473. 2. Blagburn BL, Dryden MW. Biology, treatment and control of flea and tick infestations. Vet Clin N Am 2009; 39(6):1173-1200. 3. Dryden M: Host association, on-host longevity and egg production of Ctenocephalides felis. Vet Parasitol 1989; 34:117–122. 4. Dryden M, Bennett G, Neal J. Concepts of Flea Control. Comp An Pract 1989; 19(4-5):11-22. 5. Dryden MW. Flea and tick control in the 21st century, challenges and opportunities. Vet Dermatol 2009; 20: 435–440. 6. Chin A, Lunn P, Dryden M. Persistent flea infestations in dogs and cats controlled with monthly topical applications of fipronil and methoprene. Aust Vet Pract 2005; 35(3):89-96. 7. Dryden MW. How you and your clients can win the flea control battle. Vet. Med. Supplement 2009; March: 17-26. 8. Dryden, MW. Spotlight on Research: How residual speed of kill affects flea control in dogs and cats. Vet Med 2014; 109(7): 1-4. 9. Dryden M, Payne P, Smith V. Efficacy of Selamectin and Fipronil/(S)-Methoprene Spot-on Formulations Applied to Cats against the Adult Cat Flea, Ctenocephalides felis, Flea Eggs and Adult Flea Emergence. Vet Therapeutics 2007; 8(4):255-262. 10. Blagburn BL, Young DR, Moran C, et al. Effects of orally administered spinosad (Comfortis) in dogs on adult and immature stages of the cat flea (Ctenocephalides felis). Vet Parasitol 2010; 168:312–317. 11. Dryden MW, Payne PA, Smith V, et al. Efficacy of indoxacarb applied to cats against the adult cat flea, Ctenocephalides felis, flea eggs and adult flea emergence. Parasites & Vectors 2013; 6:126. 12. Beugnet F, Doyle V, Murray M, et al. Comparative efficacy on dogs of a single topical treatment with the pioneer fipronil/(S)-methoprene and an oral treatment with spinosad against Ctenocephalides felis. Parasite 2011; 18(4):325-31. 13. Coles TB, Dryden MW. A review of insecticide/acaricide resistance in fleas and ticks infesting dogs and cats. Parasites & Vectors 2014, 7:8 (6 January 2014) 14. Dryden M, Carithers D, McBride A, et al. A comparison of flea control measurement methods for tracking flea populations in highly infested private residences in Tampa FL, following topical treatment of pets with FRONTLINE® Plus (fipronil/(S)-methoprene). Intern J Appl Res Vet Med 2011; 9:356-367. 15. Gassel M, Wolf C, Noack S, et al. The novel isoxazoline ectoparasiticide fluralaner: Selective inhibition of arthropod Y-aminobutyric acid- and L-glutamate-gated chloride channels and insecticidal/acaricidal activity. Insect Biochem Molec Biol 2014; 45:111-124. 16. Hartline EJ, Gould BR, Waddell ME, et al. Discovery and mode of action of afoxolaner, a new isoxazoline parasiticide for dogs. Vet Parasit 2014; 201:179-189 17. Breitschwerdt E, Little S, Rugg D Sarolaner-a novel isoxazoline-addresses the need for enhanced flea and tick control. Vet Parasitol 2016; 222:1-2. 18. Dryden MW, Smith V, Bennett T, et al. Efficacy of fluralaner flavored chews (Bravecto ®) administered to dogs against the adult cat flea, Ctenocephalides felis felis, and egg production. Parasites & Vectors 2015; 8:364. 19. Dryden MW. Canfield MS, Herrin BH, Bocon C, Bress TS, Hickert A, Kollasch TM, Phan L, Rumschlag AJ, Ryan WG, Sampeck B, Smith N, Smith V, Warcholek SA In-home assessment of flea control and dermatologic lesions in dogs provided by lotilaner (Credelio®) and spinosad (Comfortis®) in west central Florida. Vet. Parasitol: X 1 (2019) 100009 20. Dryden MW, Canfield MS, Kalosy K, et al. Evaluation of fluralaner and afoxolaner treatments to control flea populations, reduce pruritus and minimize dermatologic lesions in naturally infested dogs in private residences in west central Florida USA. Parasites & Vectors 2016; 9:365.
11 21. Dryden MW, Canfield MS, Niedfeldt E. et al. Evaluation of sarolaner and spinosad oral treatments to eliminate fleas, reduce dermatologic lesions and minimize pruritus in naturally infested dogs in West Central FL. USA. Parasites & Vectors 2017; 10:389. 22. Dryden MW, Ryan WG, Bell M, et al. Assessment of owner-administered monthly treatments with oral spinosad or topical spot-on fipronil/(S)-methoprene in controlling fleas and associated pruritus in dogs. Vet. Parasitol. 2013; 191:340– 346. 23. McCoy C, Broce, AB, Dryden MW. Flea blood feeding patterns in cats treated with oral nitenpyram and the topical insecticides imidacloprid, fipronil and selamectin. Vet. Parasitol 2008; 156(3-4):293-301.
12 The quagmire that is giardiasis Michael W Dryden DVM, MS, PhD, DACVM (parasitology) Department of Diagnostic Medicine/Pathobiology Kanas State University, Manhattan KS
Several morphologically distinct Giardia species are recognized. However, Giardia isolated from humans and other mammals are morphologically identical and therefore the taxonomic status and zoonotic potential are not clear. The species name of the organism that infects most mammals has undergone several changes, but currently G. intestinalis and G. duodenalis are most commonly used. Giardia infections are very common in dogs in the U.S. Nationwide 4% of 1.3 million dogs positive for giardia with rates in some areas as high as 12.6%.1 Regionally prevalence can even be higher. The prevalence of Giardia sp. in Phoenix shelter dogs was 40.4% and in pet dogs was 11.4%.2 The various genotypes of Giardia sp. are now termed genetic assemblages. Four genetic loci are used in these studies: ITS1-5.8 S-ITS2 ( ITS), glutamate dehydrogenase (gdh), triosephosphate isomerase ( tpi), and beta-giardin ( bg). Interestingly these genetic loci do not always result in agreement of genetic assemblage classification. Numerous studies published worldwide have attempted to evaluate the zoonotic potential of Giardia isolates from dogs and cats. Results of these studies differ and are occasionally controversial.3,4 Humans are often infected with assemblages AI & AII, but these may also rarely be found in dogs, cats & livestock. There are also assemblages AIII & AIV that appear to almost exclusively non-human and are found in beavers, guinea pigs and some other animals including dogs. Then there are the B assemblages with BIII & BIV being found in humans and interesting chinchillas. Whereas assemblages BI & BII are typically found in chinchillas, beavers, rats, muskrat, rabbit, livestock and rarely dogs, coyotes, cats, & rarely humans. Then are dog exclusive assemblages C & D and Cat exclusive assemblage F. Yes, very complicated. But generally, in North America, finding dog or cat assemblages in humans is rare. It is clearly worth noting that the CDC published a report of human giardia outbreaks from 1971 – 2011. During that 40-year period not a single outbreak was every attributed to a dog or cat. In fact, only three animal associated outbreaks, a rabbit, cattle and a pet-reptile (species not given). Given the current data the Companion Animal Parasite Council (https://capcvet.org/guidelines/giardia/) currently states on its website, “Human infection from a dog or cat source has not been conclusively demonstrated in North America. Canine strains of G. duodenalis are not known to be infective to immunocompetent human hosts. However, people with increased susceptibility to infection due to underlying disease should consider limiting their exposure to Giardia-infected pets.” The CDC (https://www.cdc.gov/parasites/giardia/infection-sources.html) is stating “The risk of humans acquiring Giardia infection from dogs or cats is small. The exact type of Giardia that infects humans is usually not the same type that infects dogs and cats.”. Finally, the Center for Food Safety and Public Health (http://www.cfsph.iastate.edu/Factsheets/pdfs/giardiasis.pdf) position is “Several recent reviews conclude that zoonotic transmission from domesticated animals is possible but unproven, and likely to be of minor importance compared to person-to-person transmission. However additional well-designed epidemiological studies that use genetic tools are needed before the extent of zoonotic giardiasis can be fully evaluated.” The lifecycle of Giardia can seem rather simple, but is actually fairly complex.6 It has a trophozoite (9- 21 x 5-15µm) stage (motile, teardrop or pear shaped, flagella, with one side shaped into a sucking disc for attachment to epithelium). Trophozoite contains two nuclei each with a large endosome. Trophozoites are bilaterally symmetrical and dorsoventrally flattened. As trophozoites travel down the gastrointestinal tract with the ingesta and it is in the lower jejunum that the complex process of encystation begins. The presence of bile salts and a decrease in cholesterol signal the trophozoites to initiate the encystation process. The trophozoites’ endoplasmic reticulum produces the building blocks which form the outer cyst wall. The material is packaged into encystation vesicles. The vesicles transport the material to the cell surface where it is released. After the cell wall components are released the vesicle can reseal and may be endocytosed by the parasite or remain empty.
13 The completed cyst wall consists of a thick fibrillar outer cover and two inner cell membranes adjacent to the plasma membrane of the parasite. D-galactosamine polymer, cyst wall protein 1, cyst wall protein 2, and cyst wall protein 3 have been identified as structural components of the cyst wall. The membrane components are deposited first at the lateral flange area. This causes cell rounding and a depression in the central ventral region of the parasite. Flagella are modified and are internalized by the elongating ventral membrane. The caudal flagella remain external until the last steps of encystation, and then they are retracted into a vacuole within the cysts. These flagella can be observed to be beating within the cyst. This cyst wall is what makes the cysts environmentally resistant. As cyst wall production is occurring, the trophozoite partially divides. Trophozoites undergo nuclear replication but not cytokinesis. These nuclei are genetically separate from each other. Daughter cells inherit one copy of each nucleus. The nuclei can be asymmetrical in their karyotypes and DNA content. It has been proposed that there is at least one copy of each chromosome in each nucleus. To what extent they are different has yet to be discovered. When the encystation process is completed, the cyst (8-12 x 7 - 10µm) contains four nuclei, two bi-lobed adhesive disks and doubled flagella which are encapsulated by the cyst wall. Further division of the mitotically arrested trophozoite will occur during excystation. The newly formed cysts are passed into the environment with the feces. Ingestion of cysts by a new host starts the life cycle over again. The prepatent period, the time from ingestion of cysts to shedding cysts in the feces has been shown to be 5 – 16 days. Cysts may survive for weeks in water or moist environment. Pathology is likely multifactorial. Mechanical interference due to massive numbers of trophozoites blanketing intestinal epithelium and thus blocking absorption. Damage of the brush border of epithelial cells resulting in a deficiency of several disaccharidases especially lactase. Toxins produced by the parasite seem to interfere with enzyme activity at level of villus. Excessive mucous secretion due to irritation by parasites. Clinical signs in dogs and cats are highly variable, from no clinical signs to severe diarrhea. Animals less than 1 year of age most susceptible. Most prominent sign is diarrhea, stool is soft, greasy and mucoid. Weight loss is not uncommon. Some animals may pass large number of cysts and still have formed feces. Dry skin and poor hair coat due to deficiency of fat and soluble vitamins absorption. Growth retardation in young animals secondary to malabsorption can also occur. Infected animals may also have flatulence. Most adult dogs and cats that are shedding oocysts are asymptomatic, even if an adult dog or cat has diarrhea and has Giardia, it is likely that Giardia is not the cause of the clinical disease.6 Giardia promotes only superficial epithelial disruption, impaired intake of water, electrolytes, nutrients and is a non-invasive organism, therefore diarrhea should not contain blood, unless other pathogens are present and causing invasion and/or erosion of epithelium. If a dog or cat has bloody diarrhea and is Giardia positive, look for the true cause of the tissue damage. Giardia may be incidental or an opportunist and not the primarily problem.
Diagnosis: • Use ZnSO4 flotation for cysts (Centrifugation) - Cysts shrivel within minutes to hours - Want sp. gr. 1.18 & Use Lugol’s iodine to stain cyst - Most sugar and salt solutions distort cysts • Fecal ELISA - Canine fecal ELISA (Idexx Giardia snap test - detects Giardia cyst wall antigen) • Wet mounts (direct smear) of a fresh sample is the only way trophozoites can be observed – however, the diagnostic sensitivity of a direct smear is considered poor. In one study sensitivity of the fecal smear in dogs was only 31.8% of the Giardia Snap test.7 • Excretion of Giardia sp. cysts is intermittent, so check more than one stool6 o Well conducted fecal flotation exam using zinc sulfate or Giardia Snap test are only positive approximately 80% of the time in known positive puppies. o If fecal exams or Snap tests conducted on 3 consecutive days on these puppies then approximately 95% chance of finding cysts or cyst antigen. • Detection of cyst wall antigen in chronically infected asymptomatic adult dogs can be problematic.
14 • May be one of the most commonly over-diagnosed, under-diagnosed and misdiagnosed parasitic diseases. ❖ Treatment There are current approved treatments for dogs and cats in the U.S. for giardiasis. The most common current therapy for dogs is orally administered fenbendazole at 50mg/kg SID for 3 to 5 days. Alternatively, Drontal Plus (Praziquantel, Pyrantel pamoate, Febantel) can be administered orally at standard label dose for intestinal nematodes SID for 3 to 5 days.6 Metronidazole has also been historically used administered orally at 25 mg/kg BID x 5 – 10 days. It is not uncommon to administer fenbendazole and metronidazole simulateneously. Metronidazole is effective against anaerobic infections, has antinflammatory properties, and is effective for diarrhea associated with colitis. Therefore, metronidazole often firms up loose stools regardless of the cause of the diarrhea. Studies have also conclusively demonstrated that animals shedding giardia cysts must also be bathed during the treatment regimen and especially on the last day of treatment. This is done to remove infective cysts from hair and skin. If animals are not bathed to remove cysts from hair coat, reinfection and reshedding of oocysts within 1 to 3 weeks is common if not assured.6
References:
1.Little SE, Johnson EM, Lewis D, et al. Prevalence of intestinal parasites in pet dogs in the United States. Vet Parasitol 2009;166:144–152. 2. O'Neal, P. R.; Wong, V. M.; Noah, D. L Survey of intestinal parasitism in dogs in the Phoenix metropolitan area. JAVMA 25:539-545 3.Ballweber LR, Xiao L, Bowman DD, Kahn G, Cama VA. Giardiasis in dogs and cats: update on epidemiology and public health significance. Trends Parasitol. 2010 Apr;26(4):180-189. 4.Scorza AV, Ballweber LR, Tangtrongsup S, Panuska C, Lappin MR. Comparisons of mammalian Giardia duodenalis assemblages based on the β-giardin, glutamate dehydrogenase and triose phosphate isomerase genes.Vet Parasitol. 2012 May 8. 5. Adam EA et al. Giardiasis outbreaks in the United States, 1971–2011. Epidemiol Infect 144(13): 2790- 2801, 2016. 6.Payne PA, Artzer M. The biology and control of Giardia spp and Tritrichomonas foetus. Vet Clin North Am Small Anim Pract. 2009 Nov;39(6):993-1007. 7. Olson ME, Leonard NJ, Strout J. Prevalence and diagnosis of Giardia infection in dogs and cats using a fecal antigen test and fecal smear. Can Vet J. 2010 Jun;51(6):640-2
15 Ticks on the west coast – Do we need to be concerned? Michael W. Dryden DVM, MS, PhD, DACVM (parasitology) College of Veterinary Medicine, Kansas State University, Manhattan KS 66502
Controlling tick infestations in dogs and cats is important not only because ticks are nuisance parasites, but also because they are vectors of numerous bacterial and protozoal diseases. Tick control is, therefore, a major component of disease prevention and should begin with an understanding of tick ecology in your practice’s region.1 You need to know the various aspects of tick biology and control so that you can educate staff members and clients. The three most important aspects to convey are the changing geographic distribution of ticks, our inability to control ticks’ wildlife hosts, and the differences between flea and tick control. These factors likely cause most of the real and perceived tick-control product failures.
Most ticks that infest dogs in North America are considered three-host ticks; each successive stage (larva, nymph, and adult) feeds on separate hosts after molting. The adult female feeds on a host until engorged, drops off, deposits an egg mass typically numbering in the thousands in the environment, and dies.
The most common tick species that infest dogs in Western N.A are, Dermacentor andersoni, D. occidentalis, D. variabilis, Ixodes pacificus, and Rhipicephalus sanguineus. The one-host tick, Otobius megnini, may also be recovered from dogs. Dermacentor spp. and I. pacificus can also infest cats, but not as frequently as dogs.
The most common tick species that infest dogs in Eastern N.A are Amblyomma americanum, Amblyomma maculatum, Dermacentor variabilis, Ixodes scapularis, and Rhipicephalus sanguineus. A. americanum, Dermacentor species and I. scapularis can also infest cats, but not as frequently as dogs.
Historically, Dermacentor species were some of the most common ticks infesting dogs. In the typical life cycle of Dermacentor variabilis (American dog tick), the larvae feed on small mammals, such as rats and mice. Nymphs feed on dogs, rabbits, raccoons, opossums, and other small- to medium-sized mammals. The adult ticks feed on dogs, horses, cattle, and other large mammals—including people. In the western U.S. D. variabilis populations occur along the Pacific West Coast. A closely related species, Dermacentor occidentalis (Pacific Coast Tick) is a three-host tick which commonly feeds on rodents, especially squirrels, as subadults, and on cattle, horses, deer, and humans as adults. This is one of the most widely distributed ticks in California. It is found throughout the state except for the very dry regions of the central valley and the southeastern desert region. It has also been collected in Oregon and Baja, Mexico.
The third Dermacentor species that infests dogs in the western U.S. is Dermacentor andersoni (Rocky Mountain wood tick). It is a three-host tick which as a subadult primarily feeds on small rodents; as adults they focus on large mammals, especially deer, humans, canids, and livestock. This tick is well known as a vector of the Rocky Mountain spotted fever rickettsia in the northwestern U.S. and Canada, the Colorado tick fever virus, and the bacteria which causes tularemia (hunter's disease). It is also commonly responsible for tick paralysis in humans, livestock, and wild mammals
Rhipicephalus sanguineus (brown dog tick) is a three-host tick that prefers to feed on dogs. This species is of considerable concern because it can inhabit kennels and human dwellings. Kennel or home infestations distress pet owners and are extremely difficult to eradicate. This tick often crawls up walls and hides in false ceilings. The species is intolerant of cold and persists in temperate regions. Rhipicephalus sanguineus can transmit Ehrlichia canis (canine monocytic ehrlichiosis) and Babesia canis (canine babesiosis).
Amblyomma americanum (lone star tick) is increasing in importance across much of the Southern, Midwestern, and Eastern states. Once primarily considered a Southern-dwelling tick, its geographic range appears to have expanded. Several environmental and host factors may have contributed to its increased geographic distribution and abundance. A. americanum prefers woodland habitats with dense underbrush. Therefore, urban and rural reforestation efforts have increased this tick’s suitable habitat. In addition to infesting a wide range of mammalian and avian hosts, A. americanum has expanded its geographic range with the help of two of its wildlife hosts. The white-tailed deer is considered the preeminent A. americanum host because all three life stages feed successfully on white-tailed deer.
16 The ticks generally fall off into wooded habitats after engorgement.5 The growing numbers and increased geographic range of white-tailed deer have had a major effect on A. americanum populations. The second host, the wild turkey, utilizes similar habitats and is an excellent host for larval and nymphal A. americanum. As wild turkey populations have increased across much of North America, they have helped to reintroduced and increased A. americanum populations. Numerous animals can serve as larval and nymphal hosts for this species, including rodents, rabbits, dogs, cats, fox, coyotes, deer, people, and a variety of birds. Adult ticks feed on hosts, such as deer, cattle, horses, sheep, dogs, cats, and people. A. americanum is also a vector of Ehrlichia chaffeensis (human monocytic ehrlichiosis), E. ewingii, and Borrelia lonestari (Southern tick-associated rash illness). It has also been implicated in the transmission of tularemia. While not as common, A. maculatum (Gulf Coast tick) can infest dogs and carries Hepatozoon americanum, the etiologic agent of American canine hepatozoonosis. This disease’s transmission is unique because infection occurs when dogs ingest the ticks.
Another tick species with well-documented geographic expansion is I. scapularis (blacklegged tick, also referred to as the deer tick, or Lyme disease tick). This species is found throughout the Midwest and Eastern United States. Like A. americanum, I. scapularis distribution is linked to white-tailed deer abundance and distribution. While adult females feed primarily on white-tailed deer, they will also parasitize dogs, raccoons, and other wildlife. Larvae feed on a variety of small mammals, including mice, squirrels, voles, shrews, and raccoons. Nymphs feed on mice, squirrels, chipmunks, raccoons, opossums, shrews, cats, and people. Ixodes scapularis is the primary vector of Anaplasma phagocytophilum (formerly Ehrlichia phagocytophila or human granulocytic ehrlichiosis agent) and Borrelia burgdorferi (Lyme disease) in the Central and Eastern United States. Transmission of B. burgdorferi by I. scapularis in the southeastern United States differs from the pattern described above. In the southeastern part of the country, Ixodes affinis and Ixodes minor, which rarely bite humans, maintain B. burgdorferi in their natural enzootic cycles in the cotton mouse, hispid cotton rat, and eastern wood rat. I. affinis and I. minor have substantially higher B. burgdorferi infection rates than do I. scapularsi8
The transmission cycle of B. burgdorferi in the western United States is markedly different than in the eastern U.S. The western black-legged tick, I pacificus, is the tick vector to humans and dogs, but it is not directly involved in the maintenance cycle.
In a field efficacy trial conducted in Kansas U.S.A, an imidacloprid (8.8% w/w)-permethrin (44.0% w/w) formulation was evaluated on dogs against naturally occurring populations of Amblyomma americanum. When dogs were walked in a naturally tick infested environment the 48-hour post-exposure efficacy of imidacloprid-permethrin formulation was 93.5%, 98.9%, 94.6%, 94.1% and 96.6% on days 3, 7, 14, 21 and 28 respectively, post-treatment.
Variation in product efficacy occurs. In two studies conducted at K-State, different results were found when evaluating the efficacy of acaricides against Dermacentor variabilis infestations in dogs from two different regions of the USA. In the first study, the efficacy of imidacloprid–permethrin and fipronil–(s)- methoprene formulations were evaluated against a D. variabilis isolate from California. The 48-h post- infestation efficacy on day 30 post-treatment was 92.0% and 83.2%, respectively, for the imidacloprid– permethrin and fipronil–(s)-methoprene formulations. In the second study, the 48-h post-infestation efficacy on day 30 for the imidacloprid–permethrin and fipronil–(s)-methoprene formulations against a D. variabilis isolate from Oklahoma was17.5% and 75.7% respectively.
Recently a new class of insecticide/acaracide has provided the first orally administered approach to tick control. Afoxolaner, fluralaner, lotilaner and sarolaner are members of the isoxazoline class and work by inhibiting insect GABA and Glutamate-gated chloride channels leading to hyper-excitation and death of insects and arachnids. These compounds are potent broad-spectrum insecticides/acaracides and exhibit striking efficacy through their rapid neurotoxic effect on ticks and thorough systemic coverage.
While product efficacy is often excellent in most studies, significant variation in efficacy can occur and 100% control is rarely achieved. Therefore, it can be expected that under natural conditions in areas where dogs are being frequently exposed to ticks, pet owners will see ticks on treated dogs. We might also expect that efficacy in real world situations might be lower due to such factors as bathing and swimming, differences between dog breeds and haircoat types and frequency and correctness of product application.
17 Since 100% tick kill is rarely achievable, perceived efficacy of acaracides may be directly related to the numbers of ticks to which dogs are exposed. If a dog is treated with one of these highly efficacious acaracides and encounters just a few ticks it is likely all those ticks will be killed. However, if tick exposure is considerably larger, we can expect a few ticks to be observed on these dogs and pet owners may perceive a lack of efficacy. Therefore, in areas where tick populations are increasing the perception may be that the products are not as effective as they once were.
Pet owners often view tick infestations of their pets differently than flea infestations. Whether this is due to concerns about tick transmitted diseases or simply a phobia, the presence of a couple of ticks on the pet often elicits a more pronounced negative reaction than the presence of a couple of fleas. A 95% effective flea product may provide great client satisfaction while a similarly effective tick product may be perceived as a failure. Therefore, it is not uncommon that label recommended application of a product does not appear to control the problem. This may be real or perceived, based upon pet owner expectations of product performance. Given pet owner concerns, a need to reduce tick borne disease and lack of 100% efficacy; occasionally additional control measures are needed. If additional control measures are deemed necessary, pet owners need to be educated as to why additional control measures are necessary and notations made in the pets record before extra label uses are conducted.
One of the most common practical attempted solutions to this problem in dogs is to increase the frequency of application. Here increased residual efficacy is the expected outcome, since you are increasing the residual acaracides levels with the shorter application intervals. Additionally, with many 3-host ticks destruction of tick habitat can reduce exposure pressure. Areas that serve as refuge for ticks and wild mammals such as grass, weeds, and brush piles, between runs and along buildings, can be eliminated or treated with an approved acaricide.
In some situations, especially in tropical and subtropical regions and in climate-controlled kennels brown dog ticks may infest buildings with ticks crawling up walls, curtains and throughout the home or kennel.14-15 In these situations acaracides may need to be sprayed indoors into cracks and crevices, behind and under furniture or cages and along walls and the ceiling. Following application, make sure the acaricide is dry before you allow animals or humans back into the premises to minimize toxicity problems. Finally, restricting pet access from tick-infested environments may be necessary.
It is apparent that the range and local density of certain tick species has increased in many areas. Whatever the factors it must be recognized that tick infestation pressure may be much higher and associated tick transmitted diseases may be more prevalent in some locations today than in the past. The increase in tick populations means that pets are encountering ticks more frequently, are exposed to more ticks per encounter and clients may be seeing more ticks on their pets than in the past. Since tick products do not kill or repel all ticks instantly, clients may get the false impression that the products are not performing as well as in the past. These situations necessitate that veterinarians set client expectations, before clients set their own unrealistic expectations of control.
Suggested References
1. Dryden MW, Payne PA. Biology and control of ticks infesting dogs and cats in North America. Vet Ther 5:139-154, 2004. 2. Blagburn BL, Dryden MW. Biology, treatment and control of flea and tick infestations. Vet. Clin. N. Am. 39(6):1173-1200, 2009. 3. D.P. Furman and E.C. Loomis. 1984. The Ticks of California. University of California Publications, Bulletin of the California Insect Survey, Vol. 25. University of California Press, California. 4. Childs JE, Paddock CD. The ascendancy of Amblyomma americanum as a vector of pathogens affecting humans in the United States. Annu Rev Entomol 2003;48:307-337. 5. Brown RN, Lane RS: Lyme disease in California: a novel enzootic transmission cycle of Borrelia burgdorferi. Science 256: 1439-1442, 1992.
18 Connected care and telemedicine: It’s not the future… it’s now! Jeff Werber, DVM and Brandon Werber
Part I The Problems:
1. Technology and innovation quickly reshapes industries one by one. One of the latest industries to have a technological facelift is human medicine. A few years ago, telemedicine became a hot topic, making its way into the human space with a couple startups wanting to make care more accessible and more efficient. However, it was being leveraged solely by what we call the “early adopters.” Now, just a few years later, 90% of medical practices are either already offering or currently building a telemedicine platform. It’s become the rule, not the exception. Now, we’re now seeing the beginnings of the very same trend in veterinary medicine. The opportunity, however, may be even larger in the pet space than it is in the human space. Why? The core demographic for telemedicine is a millennial. Millennials now represent the largest, fastest growing, and highest spending segment of pet owners, while in the human space, 80% of healthcare costs come from people over 60 (not the primary demographic for telemedicine). This gives the veterinary industry the ideal opportunity to pave the way for the next revolution. • With so much adoption of telemedicine in the human space, millennials across the board have grown to expect that access to care be available 24/7. • While these expectations are being met with their human doctors, they are falling short with their veterinary counterparts. • So much so that the veterinarian is beginning to get phased out of the conversation. • How do we know? The data says it all, as 70-80% of millennial pet parents say that they go online and to social media for veterinary advice and information before even ATTEMPTING to talk to a veterinarian. • That means that they would rather get bad advice right away than to wait to get good professional advice from a veterinarian. • Is it a cost savings thing? Actually, no. In fact, ~40% of millennial pet parents say that when it comes to the health of their pets, money is of NO consequence. • How long before veterinarians become little more than a last resort for specialty and surgery only? • It’s time we leverage technology to get back to the forefront of the conversation and cement our place in the next 100+ years of veterinary medicine.
With telemedicine, veterinarians have the opportunity to connect with their clients more effectively and efficiently than ever before. Veterinarians can (finally) monetize their time while prioritizing a healthy work/life balance all while boosting client retention, client visits, client lifetime value, and of course, clinic revenue.
2. The Basics - Telemedicine vs. Telehealth: Telemedicine is what doctors practice when they’re connecting with their own clients in the presence of a valid VCPR (Veterinarian-Client-Patient-Relationship). Telemedicine implies that a VCPR exists and without one, doctors can practice varieties of what’s known as telehealth, teleadvice, and teletriage. Here, no “medicine” is being practiced, but rather high level guidance and advice.
3. The VCPR: The Veterinarian-Client-Patient-Relationship (in most states) can only be established after an in-person, hands-on examination of the patient along with access to medical records. Be sure to check with your state(s) where you practice, to understand what constitutes a VCPR and what the regulations are around what you can do without one. Having a VCPR means you may practice telemedicine, where you can do 3 main things - Treat, Diagnose, and Prescribe. We often talk about what you can’t do without a VCPR that we ignore the discussion of what we CAN do without one. In nearly every state, veterinarians without a VCPR can still leverage their license to practice telehealth. While they cannot prescribe, treat, or diagnose, they can still provide general medical advice, triage, guidance, support, and education. And, in a huge amount of situations, particularly after-hours, that’s really all that’s needed.
19 4. Driving client visits and revenue: The average pet parent only comes to see their veterinarian an average of 1.6 times a year (even less so for cat owners). An even scarier statistic is that the average amount of face-to-face time clients spend with their veterinarians each year is just 16 minutes! That’s hardly enough frequency and time to build real lasting relationships with most clients, and certainly not enough to reach peak levels of client lifetime value. If veterinarians could even drive ONE more average visit a year, that would be an increase of 62.5%! And if you were to LOSE 1 visit a year, that would really hurt. By leveraging telemedicine, we have the opportunity to increase the ability for clients to almost effortlessly connect with their veterinarian (or a vet) instead of going online. Why is that so important? Because if we can increase the amount of touchpoints between clients and their veterinarians, then we can hopefully convert some of those connections into in-person visits. Especially after-hours where vets are not accessible, it becomes absolutely critical that clients can access trusted vet care to help triage a situation before rushing to an emergency. We all know that the vast majority of emergency visits are typically not emergencies at all, and are things that could have and should have waited until the next day to see their primary vet. But, because there is such poor access to care at 11pm, for example, that the emergency becomes the only option. Don’t forfeit that case or revenue. Better access to care means more visits and more revenue for you and your practice, period.
5. Monetizing your time: Historically, veterinarians give a lot of their time to clients via phone and/or text without any compensation. Will your lawyer do that? Your accountant? What about your cardiologist? Many of us like to believe that we’re accessible via phone and text around the clock, and that that’s a good thing – but it’s not a good thing if it’s not done in the right way, as those messages usually lead to a client NOT coming in, and then we don’t even charge for those messages! And they usually don’t make their way into the medical records either. As a profession we need to stop giving our time away for free, and if we’re going to be accessible, to do it in the right way. That means doing it in a way that we can monetize, track, and consolidate, while sharing the data into our medical records. In fact, as mentioned previously, when it comes to the care of their pets, the average pet owner actually prioritizes access to care at the very top of the list of things they care about, not cost savings. 70%+ of pet owners have even said that they’d be happy to do a consult virtually.
6. Increasing client retention and lifetime value: Roughly 34% of pet owners have said that they’d be willing to switch veterinarians from one that didn’t offer virtual care to one that did. Clients are savvy and they’re going to go (or stay) with facilities that offer levels of care that they expect. Veterinarians should adopt these new platforms and trends to both keep their existing clients and to create new ones from those vets who don’t adopt these tools for the future.
7. A big change in our “emergency clinics!” Many of our emergency hospitals are now usually associated with specialty hospitals, whereas the emergency clinics of old were often funded by local veterinarians. Back then, their focus was triage and essential emergency care only, to get the patient through the night so it can be transferred back to THEIR veterinarian in the morning. Now, as parts of specialty groups, they essentially take a case over, often performing tests and providing treatments that are not of an emergent nature, which could be done by the primary veterinarian the next morning. Additionally, care provided by emergency hospitals is more expensive than that provided by most primary hospitals
8. Provides veterinarians an opportunity to increase their income stream: Young veterinarians are graduating schools with an average debt of $275,000, and their average starting salaries are often less than $70,000. To make their loan payments, many need to find ways to supplement their incomes, both on the clock and off. Telemedicine is an excellent way to supplement a veterinarian’s income.
Part II What You Can Do:
What are we fighting? What are many veterinarians afraid of? Many veterinarians think if this “telemedicine thing” as something totally new and perhaps even scary. The fact is that while the term “telemedicine” is beginning to popularize and become commonly discussed as if it were something new, it is by definition something that all of us have been utilizing since the day we started practicing! Every time you speak to a client on the phone, talk via text, or e-mail about their pet, you are utilizing “Telemedicine!”
20 There is no legal or regulatory distinction whatsoever between a phone call, email, or text, and a proper telemedicine platform we’re discussing here. So, instead of ignoring or resisting what’s already happening, and will continue to happen over the next several years, WE as a profession, need to be the ones to be in front of it and actually take control in molding HOW we use these new technologies and how we integrate them into our workflows. There’s nothing to be afraid of if we embrace the future by shaping it ourselves. So, by now you may (and should) be considering implementing telemedicine into your practice. Here’s a good place to start...
Start with the basics. Find a telemedicine platform that fits into your practice based on how you want to leverage it. Think about how you’d like to implement telemedicine and what problems you’d be looking for it to solve. There are many platforms available to you and some of them are quite good, but they certainly vary in what they do. They each have their own limitations and strengths. While some are great for after- hours care, others allow for real-time connected care during the day as well, enabling veterinarians to do virtual follow-ups, post-ops, re-checks, etc., and one platform actually does both.
To learn more about these truly exciting innovations in veterinary technology, reach out to me at [email protected]
21 Gastric dilatation volvulus: It doesn’t have to make your stomach turn Bronwyn Fullagar, BVSc, MS, DACVS-SA
Whether you perform surgery yourself or refer your patient to a specialty veterinary facility, aggressive stabilization can make all the difference.
Just before closing time, a large-breed dog arrives at your clinic with a history of non-productive retching, lethargy and a progressively distending abdomen. You know gastric dilatation-volvulus (GDV) is likely, but where do you begin? Should you refer the patient straight away? Will you need to perform surgery yourself?
If this scenario makes your palms sweat and your adrenals squeeze, fear not. GDV is a true medical and surgical emergency, but with a logical diagnostic and treatment approach and a focus on thorough preoperative stabilization, a good outcome can be achieved in the majority of cases. Even if you intend to refer the case to a specialist or emergency facility, the early stabilization procedures you perform can make a big difference to your patient’s success, and your clients will appreciate your help in their decision-making process as they grapple with a very stressful situation.
Triage: What is the patient’s status? Patients that present with a history suggestive of GDV should be brought immediately to the treatment area and assessed as soon as possible by a veterinarian. In the meantime, the owners should be asked to sign a consent form authorizing initial stabilization procedures and diagnostics. Remember that although middle- aged, large and giant breed, deep-chested dogs are the poster children of GDV, dogs of any breed between 10 months and 14 years of age—and even cats—may be affected.
Patients with GDV are often hypersalivating with a painful abdomen, and a tympanic quality can be auscultated on abdominal percussion. Patients may present in a critical condition with an unstable cardiovascular status. Heart rate, respiratory rate, temperature, blood pressure and pulse quality should be evaluated immediately.
Stabilization: Improve perfusion and tissue oxygenation The first priority in treating patients with suspected GDV is to stabilize their cardiovascular status. The sooner you treat shock and restore oxygen delivery to the tissues, the less likely it is that the patient will require resection of necrotic gastric wall and the better the overall prognosis. Although it can be tempting to perform radiographs immediately, this step should be postponed until after initial resuscitation.
Use initial physical exam findings to guide your stabilization efforts and be aware that patients may present in varying degrees of shock. Those presented earlier in the disease process will have signs consistent with hyperdynamic, hypovolemic shock due to their blood volume being restricted to the caudal half of their body by the enlarged stomach compressing the caudal vena cava. These dogs will be tachycardic and tachypneic, with normal femoral pulses, pale mucous membranes and a slow capillary refill time.
As the syndrome progresses, dogs will develop injected mucous membranes and weak femoral pulses— signs of endotoxemic shock. Eventually, patients will decompensate to a point where they are hypotensive and bradycardic with white mucous membranes; at this stage they often present laterally recumbent.
Fluid resuscitation is the most important component of GDV patient stabilization. Place two venous catheters in the cranial half of the body (cephalic or jugular veins can be used). Select the largest size catheters possible to allow rapid delivery of fluids. Provide crystalloid fluid therapy (e.g. lactated Ringer’s solution, Plasmalyte or 0.9% sodium chloride) initially at a dose of 40-90 ml/kg over the first 30 to 60 minutes. As a rule of thumb, a large breed (30-kg) dog will require 1.5 to 3 L crystalloids, while a giant breed (60-kg) dog will require 2.5 to 5.5 L. Alternatively, you can use colloid fluids (e.g. hydroxyethyl starch) at a dose of 10-20 ml/kg combined with crystalloids at 10-40 ml/kg. Titrate fluids to effect until you note improvements in heart rate, respiratory rate, mucous membrane color and refill, and blood pressure.
Patients with GDV can be painful, so administration of opioid analgesia is helpful. Pure mu agonists (fentanyl, methadone, hydromorphone) are preferred over agonist-antagonists (buprenorphine) or partial agonists (butorphanol), as these can interfere with the effects of pure mu agonists administered perioperatively. Nonsteroidal anti-inflammatory drugs (NSAIDs) are always contraindicated in cases of GDV.
22 Gastric decompression is an important part of stabilization as it relieves pressure on the caudal vena cava, thus allowing blood to flow from the caudal half of the body back to the heart (improved preload). It also helps to improve gastric perfusion and patient comfort. Decompression can be performed either via orogastric intubation or trocharization. Although orogastric intubation is more effective in decompressing the stomach, it can be challenging in awake patients and is generally reserved for those that are sedated or recumbent. Take care to protect the airway; intubation may be required to avoid aspiration pneumonia. Premeasure a large- bore, smooth tube to the last rib and lubricate it. Note that often the tube cannot be passed past the lower esophageal sphincter due to the torsion, and care must be taken not to force the tube as esophageal perforation is possible.
If orogastric intubation is not possible or not safe, you can perform trocharization over the region of greatest gastric tympany, usually over the right lateral abdomen caudal to the last rib. Clip and aseptically prepare the skin, insert a 14- to 18-ga over-the-needle catheter, and remove the stylette. You may need to repeat trocharization if surgery is delayed as the stomach will continue to fill with gas.
An electrocardiogram should be performed on GDV patients prior to surgery. Up to 70% of dogs with GDV develop cardiac arrhythmias,1 which are frequently ventricular in origin. Arrhythmias may occur up to 72 hours postoperatively. Patients with ventricular tachycardia, R on T complexes, multiform ventricular premature complexes, or clinical hypotension related to their arrhythmia should be treated with lidocaine (2 mg/kg slow intravenous bolus, then constant rate infusion [CRI] of 25-80 μg/kg/min).
Diagnostics: GDV, GD or something else? A right lateral abdominal radiograph is the view of choice to diagnose GDV and is important to differentiate dogs with gastric dilatation from those with true dilatation and volvulus. In the latter, a soft tissue band will be present between the distended pylorus and the fundus—the so-called “double bubble” or “Popeye arm.” Dogs with gastric dilatation without volvulus will have a distended stomach without the soft tissue fold between the two regions.
The radiograph should also be evaluated for free peritoneal gas, which may indicate gastric perforation, a poor prognostic indicator. Note that patients that received gastric trocharization prior to radiographs may develop some scant free peritoneal gas in the absence of perforation. Thoracic radiographs may be indicated for patients in which aspiration pneumonia is suspected or for elderly patients in which GDV may be secondary to neoplastic causes.
Initial bloodwork should include packed cell volume and total solids, blood glucose and venous blood gas with electrolytes if available. In patients that will undergo surgery, complete blood count and serum biochemistry are indicated to assess platelet number, leukogram, liver and kidney function, and albumin levels. Coagulation testing (PT and aPTT) can help to identify patients that are coagulopathic or trending towards disseminated intravascular coagulation (DIC) preoperatively.
Decision-making: “Should I pursue surgery for my dog?” Ultimately, patients with GDV require surgery after medical stabilization. The decision to proceed with surgery can be difficult for owners, and family veterinarians play an important role when they’re able to provide accurate information about the pet’s prognosis to help with the process. Historically, GDV was thought to carry a poor prognosis, but the most recent studies report improved rates of survival of 73% to 90%.2,3,4
The variable most consistently associated with a poor prognosis is gastric necrosis,1,2,3,4,5 but unfortunately there is no way of definitively determining whether gastric necrosis is present until surgery is performed. However, several prognostic factors have been identified that can offer insight into whether your patient is likely to have a successful outcome.
In general, dogs that present with clinical signs of less than six hours’ duration and those that “walk in” to the clinic do better than those that present laterally recumbent. Dogs that present with sepsis, gastric perforation or DIC have a worse prognosis.1,2,4,5 In one study, dogs with an increased amount of time between presentation and surgery had a decreased mortality rate, which speaks to the importance of aggressive preoperative stabilization.3
23 Blood lactate has been evaluated in several studies as an indicator of gastric necrosis. Normal canine lactate is <2.5 mmol/L, and increased lactate indicates poor tissue perfusion. If a blood lactate meter is available, measuring trends in lactate (rather than absolute values) can reflect the success of your stabilization efforts. A change (decrease) in lactate of greater than 42.5% after fluid resuscitation was associated with a survival rate of 100% in one study.6
Surgery: Derotate, assess viability, pexy Once you’ve made the decision to pursue surgery, the next consideration is whether to refer the case to a specialty or 24-hour facility or perform surgery at your own clinic. There are a number of factors that affect this decision, but referral is strongly recommended in all cases where gastric necrosis is suspected. Gastrectomy greatly increases the technical difficulty of the surgery, surgical stapling equipment available in specialty practices improves the efficiency and safety of the procedure, and postoperative care is significantly more intensive in patients that have undergone gastrectomy. Of course, it’s not possible to know for sure preoperatively that a gastrectomy will be required, but using the prognostic indicators above can give a reasonable idea of which cases will be more complicated.
Anesthesia for GDV patients should prioritize maintaining blood pressure and tissue oxygenation and avoiding arrhythmogenic agents. Therefore, alpha-2 agonists (dexmedetomidine, medetomidine), acepromazine and ketamine should be avoided. If possible, patients should remain in lateral recumbency for as long as possible during preparation for surgery to avoid additional pressure on the caudal vena cava, and preoxygenation is beneficial.
A common protocol is premedication with a benzodiazepine (e.g. midazolam or diazepam) and an opioid (e.g. hydromorphone or fentanyl), induction with propofol or alfaxalone, rapid intubation and endotracheal tube cuff inflation, and maintenance with isoflurane and oxygen. A fentanyl CRI of 5-10 μg/kg/h can be helpful to reduce the minimum alveolar concentration of isoflurane required. A lidocaine CRI can be administered concurrently with fentanyl—this has the dual effect of treating cardiac arrhythmias and providing analgesia.
Perioperative antibiotics are indicated in all cases of GDV, and a first-generation cephalosporin (e.g. cefazolin) or ampicillin-sublactam is appropriate. Administer the first dose at anesthetic induction and then every 90 minutes intraoperatively.
Be sure to clip a wide area—the caudal half of the thorax and the entire abdomen to the pubis should be prepared aseptically. The surgeon stands to the patient’s right side. Perform a ventral midline celiotomy from the xyphoid to the fourth mammary glands or prepuce. Be prepared to encounter a hemoabdomen, as avulsion of the short gastric arteries from the greater curvature of the stomach has often occurred. In most cases, hemorrhage is self-limiting or can be addressed after gastric derotation. In patients with GDV, the greater omentum will be draped over the stomach upon entering the abdomen. Occasionally the stomach has derotated itself, in which case you will encounter the ventral surface of the stomach and spleen first, without omentum covering them.
In most cases, the stomach has rotated 180 to 270 degrees. To derotate the stomach, it may be necessary to first decompress it, which can be performed either by having an assistant pass an orogastric tube or by trocharizing the stomach with a needle intraoperatively. Then use your right hand to reach the pylorus, which is usually located dorsal to the esophagus on the patient’s left side. With your left hand, form a fist and push the distended fundus (malpositioned on the dog’s right side) dorsally while you pull the pylorus ventrally and to the right. The spleen will usually derotate with the stomach.
After derotation, perform complete exploration of the abdomen. Residual hemorrhage from the short gastric arteries may need to be controlled with ligatures. Palpate the stomach carefully for a gastric foreign body— gastrotomy is required in this case. Assess the color of the spleen—splenic engorgement is expected and the spleen should return to a dark purple color following derotation. If the spleen is black in color or thrombosis of the splenic artery has occurred (or both), a splenectomy is indicated.
Next, assess the gastric wall. This is a subjective assessment; accuracy improves with surgeon experience. When gastric wall color, thickness, peristalsis and bleeding on incision are evaluated in combination, accuracy of assessment is about 85%.7 The most common region affected by ischemic injury is the fundus along the greater curvature. Be sure to evaluate the stomach all the way to the lower esophageal sphincter.
24 If the gastric wall remains black without improvement following reperfusion, if the serosal surface is pale greenish or grey, if there is absence of the normal mucosal “slip” or the wall is very thin, or if the serosal surface does not bleed when a partial thickness incision is made, partial gastrectomy is required. Gastrectomy can be performed by either a cut-and-sew technique with an inverting suture pattern, the use of surgical stapling equipment, or invagination of the ischemic gastric wall. The procedure is well described elsewhere.8
If you have performed a gastrectomy, lavage the abdomen with warm sterile saline and suction it, then exchange gloves and instruments for a sterile set. The next step is gastropexy. Incisional gastropexy is technically simple and highly effective, with reported rates of GDV recurrence almost 0%.9 Gastropexy takes place between the pylorus and the patient’s right abdominal wall, so it’s easiest if the surgeon moves to stand on the patient’s left side. The pexy site on the stomach is located 2 to 3 cm oral to the pylorus, on the ventral surface, between the greater and lesser curvatures. The pexy site on the body wall is located in the right transverse abdominis, caudal to the last rib, parallel to the skin incision and approximately one-third of the distance from ventral to dorsal. In some larger dogs it may be necessary to place the pexy slightly more cranial, over the last ribs, but take care not to pass the insertion of the diaphragm on rib 11 to avoid an inadvertent thoracotomy!
It is helpful to have an assistant stand on the patient’s right side, grasp the right abdominal wall along the linea alba with towel clamps and elevate it toward the ceiling for better visualization. A description of one way to perform the procedure is below:
1. Place two partial-thickness (seromuscular layer only) stay sutures of 2-0 PDS 4 to 5 cm apart at either end of the proposed pexy site on the stomach (leave about 3 cm between the pexy site and the pylorus). Knot the stay sutures to the stomach and leave the needles attached, with a long suture tag. 2. Make a partial-thickness (seromuscular) incision in the gastric wall between stay sutures using a new No. 15 scalpel blade. The submucosa can be visualized, but do not enter the gastric lumen. 3. Suture each 2-0 PDS stay suture to the right transverse abdominis at the site of proposed pexy. Leave the needles attached to the sutures. 4. Make a full-thickness incision in the transverse abdominis between the stay sutures. 5. Suture each seromuscular layer of gastric wall to the cut edge of the transverse abdominis, using a simple continuous appositional pattern (2-0 PDS). Suture the dorsal edge first.
Postoperative care: Continue support and resuscitation; monitor for complications Patients will require 24-hour care postoperatively, so transfer to a referral facility may be necessary. Continue fluid resuscitation and address electrolyte imbalances. Continue analgesia with pure mu agonists until the patient is able to tolerate oral analgesia. NSAIDs are contraindicated. You can continue to provide a lidocaine CRI to provide analgesia as well as to treat cardiac arrhythmias. Continuous ECG is helpful to screen for ventricular arrhythmias, which may persist for 48 to 72 hours postoperatively. Discontinue antibiotics within 24 hours of surgery unless gastric necrosis was present.
Patients can be fed within 12 to 24 hours of surgery, either via nasogastric (NG) feeding tube or orally. Small meals of a bland or gastrointestinal diet are ideal. Prokinetic therapy (e.g. metoclopramide or cisapride) and intermittent suctioning of the NG tube may be necessary in cases of ileus, and an antiemetic (e.g. maropitant) is helpful to prevent vomiting secondary to ischemic gastritis. H2 antagonists (e.g. famotidine) or proton pump inhibitors (e.g. omeprazole, pantoprazole) can be administered to treat gastric ulceration.
Major complications of surgery following GDV include peritonitis, sepsis and DIC.8 Peritonitis is most often due to ongoing gastric necrosis that was not adequately assessed initially and repeat surgery is required.
Prophylactic gastropexy: Prevention is better than cure! Did you know that Great Danes have a 42% of developing GDV in their lifetime?10 Other large and giant breeds have a lifetime risk of 4% to 37%.11 Prophylactic gastropexy in predisposed dogs reduces their mortality rate by 29 times,3 and incidence of GDV after incisional gastropexy is nearly 0%.12
Gastropexy can be performed at the time of spay or neuter and is recommended once dogs are close to adult size. Pexy can be performed either via a traditional “open” approach (as described above) or via laparoscopy or laparoscopic-assisted techniques. Minimally invasive approaches result in less postoperative pain and a faster return to normal activity than open approaches and are equally as effective.12,13 25 Next time you meet a puppy of a predisposed breed or are performing abdominal surgery for another reason on a large or giant breed dog, consider recommending prophylactic gastropexy—it may just save a life.
Approach your next case with confidence GDV is a true medical and surgical emergency, but most patients can do well with aggressive early stabilization and prompt surgical care. Taking the time to stabilize your patient prior to surgery will greatly improve postoperative outcomes, whether you plan to perform surgery yourself or transfer the patient to a referral facility. Palpating as many normal stomachs as possible and performing gastropexy in a prophylactic setting first will improve your technical expertise and confidence if and when you are required to perform surgery on a clinical GDV case.
Client education plays a major role in both the prevention of GDV through prophylactic gastropexy and rapid identification of the condition, which allows for timely veterinary care. Treating patients with GDV can be challenging, so don’t hesitate to seek advice from your local emergency or specialist veterinary facility.
References 1. Brourman J, Schertel E, Allen D, et al: Factors associated with perioperative mortality in dogs with surgically managed gastric dilatation-volvulus: 137 cases (1988-1993). J Am Vet Med Assoc 1996;208:1855. 2. Beck JJ, Staatz AJ, Pelsue DH, et al: Risk factors associated with short-term outcome and development of perioperative complications in dogs undergoing surgery because of gastric dilatation-volvulus: 166 cases (1992-2003). J Am Vet Med Assoc 2006;229:1934. 3. Mackenzie G, Barnhart M, Kennedy S, et al: A retrospective study of factors influencing survival following surgery for gastric dilatation-volvulus syndrome in 306 dogs. J Am Anim Hosp Assoc 2010;46:97. 4. Zacher LA, Berg J, Shaw SP, et al: Association between outcome and changes in plasma lactate concentration during presurgical treatment in dogs with gastric dilatation-volvulus: 64 cases (2002-2008). J Am Vet Med Assoc 2010;236:892. 5. Brockman DJ, Washabau RJ, KJ Drobatz: Canine gastric dilatation-volvulus syndrome in a veterinary critical care unit-295 cases (1986-1992). J Am Vet Med Assoc 1995;207:460. 6. Beer KAS, Syring RS, Drobatz KJ: Evaluation of plasma lactate concentration and base excess at the time of hospital admission as predictors of gastric necrosis and outcome and correlation between those variables in dogs with gastric dilatation-volvulus: 78 cases (2004-2009). J Am Vet Med Assoc 2013;242:54. 7. Matthiesen D: The gastric dilatation-volvulus complex: medical and surgical considerations. J Am Anim Hosp Assoc 1983;19:925. 8. Tobias KM and Johnston SA, ed. Veterinary Surgery: Small Animal. 2nd ed. St Louis: Elsevier, 2018. 9. Benitez ME, Schmiedt CW, Radlinsky MA, et al: Efficacy of incisional gastropexy for prevention of GDV in dogs. J Am Anim Hosp Assoc 2013;49:185. 10. Glickman LT, Glickman NW, Schellenberg DB, et al: Incidence of and breed-related risk factors for gastric dilatation-volvulus in dogs. J Am Vet Med Assoc 2000;216:40. 11. Ward MP, Patronek GJ, Glickman LT: Benefits of prophylactic gastropexy for dogs at risk of gastric dilatation-volvulus. Prev Vet Med 2003;60:319. 12. Przywara JF, Abel SB, Peacock JT, et al: Occurrence and recurrence of gastric dilatation with or without volvulus after incisional gastropexy. Can Vet J 2014;55:981-984. 13. Rawlings CA, Mahaffey MB, Bement S, et al: Prospective evaluation of laparoscopic-assisted gastropexy in dogs susceptible to gastric dilatation. J Am Vet Med Assoc 2002;221:1576.
26 Gastrointestinal foreign bodies: Minimizing the risk of post-operative dehiscence Bronwyn Fullagar BVSc, MS, DACVS-SA
Objectives • To discuss healing of the small intestine and factors leading to failure of intestinal healing (dehiscence) • To focus on specific techniques to maximize successful intestinal healing, including: o Pre-operative stabilization and anesthesia considerations o Surgical technique o Post-operative care and monitoring
Introduction Gastrointestinal foreign bodies can be some of the most rewarding surgical emergency cases. However, a simple procedure can quickly turn into a life-threatening situation if inadequate intestinal healing results in septic peritonitis. Failure of intestinal healing can occur due to a number of patient and surgeon factors, and understanding these factors is fundamental in the prevention of dehiscence. Intestinal wound healing differs from other parts of the body in significant ways, so as a surgeon it is important to take steps pre-operatively to maximize intestinal perfusion, intra-operatively to respect the delicate intestinal tissues and post-operatively to support patients until their appetite and intestinal motility has normalized. Case selection is key when learning gastrointestinal surgery, as the technical difficulty of cases can vary from simple to very complex. This lecture aims to provide some important principles in gastrointestinal surgery so that you can approach your next case with confidence.
Healing of the gastrointestinal tract The phases of gastrointestinal healing are the same as other tissues: inflammation, proliferation and maturation (figure 1). However, several important differences exist between intestinal healing and skin healing. When gastrointestinal wounds heal, there is a lag phase, which occurs during the first 3-5 days post operatively. During this phase of healing in the GI tract, there is both collagen synthesis and collagen lysis, due to collagenase activity. This results in a 64% decrease in GI wound strength in the first 48 hours after surgery. Success of the intestinal repair therefore depends on the ability of the remaining collagen to hold suture. This is why gentle tissue handling and maintenance of GI perfusion are so critical, as low oxygen saturation and tissue trauma can impair collagen synthesis and lead to an overall failure of repair.
Additionally, there are several other important differences between GI and skin healing: a) Increased bacterial numbers, both aerobic an anaerobic in GI tract. b) Constant vascular perfusion of skin compared to GI, can rapidly fluctuate with changes in cardiac output (e.g. shock hypoperfusion of GI). c) Increased wound shear stress in GI due to constant peristalsis and intestinal motility. The stomach heals faster, regains more of its original strength following surgery and is generally more ‘forgiving’ than the small intestine – dehiscence of gastrotomy incisions is very rare in otherwise healthy patients. Novice surgeons should start by practicing gastrotomy techniques and gradually progress to simple enterotomies before attempting linear foreign body surgeries or intestinal resection-anastomosis.
Incidence and prognosis of dehiscence following intestinal surgery The reported incidence of dehiscence of small intestinal incisions is 7-16%. Cats may be less likely than dogs to develop peritonitis following intestinal surgery (Ralphs et al, JAVMA 2003). Septic peritonitis resulting from enterotomy or anastomosis leakage is a surgical emergency and carries a guarded prognosis, with a reported mortality of approximately 50% (range 5-85%). Intensive postoperative care is required for these patients to treat systemic inflammatory response syndrome (SIRS) at a cost of ~$10,000 in most referral hospitals.
What factors contribute to intestinal dehiscence? Several studies have evaluated risk factors for patients undergoing intestinal surgery. Some of the most consistently reported are: • Hypoalbuminaemia ≤ 25 g/L (Ralphs et al, JAVMA 2003; Grimes et al, JAVMA 2011) • Intra-operative hypotension: MAP <60mmHg (Grimes et al, JAVMA 2011) o Hypovolaemic shock decreased vascular perfusion to GI o If cardiac output is adequate, hematocrit levels up to 15% below normal do not impair gastrointestinal wound healing.
27 • Multiple GI incisions in a single surgery; linear GI foreign body (Schwartz et al, Vet Surg 2018) • Pre-operative septic peritonitis: 38% dehiscence for dogs with pre-operative peritonitis, 6% dehiscence for dogs without pre-operative peritonitis (Grimes et al, JAVMA 2011).
Detection of pre-operative septic peritonitis Given the detrimental effect of preoperative septic peritonitis on intestinal wound healing, it is vital that patients be evaluated for gastrointestinal perforation prior to surgery (see list below). Bear in mind that very dehydrated patients may not have abdominal effusion initially, but that it may become apparent after fluid resuscitation. Patients with septic peritonitis present some of the most challenging surgical and post-operative patients and referral to a 24-hour facility with specialist care is strongly recommended. • Paracentesis: 1-3cm caudal to umbilicus or U/S guided • Cytology: toxic and degenerate neutrophils +/- intracellular bacteria, foreign material • Blood-to-fluid glucose difference > 1.1mmol/L • Blood-to-fluid lactate difference below -2.0mmol/L
How can intestinal dehiscence be prevented? It is important to consider both local and systemic factors when performing gastrointestinal surgery. Local factors include meticulous preservation of blood supply to intestine, through gentle tissue handling. Wounds should be closed without tension and with a full-thickness, appositional suture pattern that incorporates the submucosa, the holding layer of the small intestine. Systemic factors include maintain adequate cardiac output (aim for MAP 90mmHg) and optimal oxygen saturation levels at the wound edges. Pre-operative fluid resuscitation, close monitoring of blood pressure under anesthesia, adequate analgesia and maintaining patient body temperature will all aid in maintaining perfusion of the intestinal wound edges. Early enteral nutrition within 12 hours of surgery, through either oral feeding (if tolerated) or placement of a feeding tube provides enterocytes with energy and protein for repair. This is particularly important in hypoproteinemic patients.
Pre-operative stabilization goals • Rehydrate, improve volume status o Crystalloid bolus 10-20ml/kg IV over 20min, repeat until HR, BP normalize o +/- colloid 5-10ml/kg IV bolus • Analgesia o Methadone 0.3-0.5mg/kg IV, fentanyl CRI 3-5mcg/kg/h IV • Prevent vomiting/aspiration antiemetics o Maropitant 1mg/kg IV q 24h • Protect oesophagus, stomach antacids o Pantoprazole 1mg/kg IV q 12h
Antibiotic prophylaxis • Gram positive and gram negative bacteria • First generation cephalosporins (Cefazolin) or Ampicillin-sublactam (Unasyn) • 1st dose: at induction, then q90min intra-operatively • Discontinue within 24h of surgery • •Extended use of antibiotics does not prevent infections and increases the incidence of resistant bacteria.
Surgical tips for success The lecture will cover specific techniques for gastrotomy, enterotomy and intestinal resection-anastomosis. Intestinal surgery requires the surgeon to be a perfectionist and it is well documented that experienced surgeons have a lower complication rate than novices, so mindful practice is important. Useful methods include practicing intestinal suturing on cadaver tissues – if small animal cadavers are not available then pig or sheep intestine can also be used. Practice gentle tissue handling, particularly avoiding grasping the intestinal edges with forceps, as this can lead to increased inflammation and disruption of intestinal blood flow, which in turn contributes to poor wound healing. Use the forceps to ‘spread’ the edges of an open hollow viscus, rather than grasping them. Start with gastrotomy surgery and gradually progress to enterotomies where clinical signs are acute and resection-anastomosis is unlikely to be necessary.
28 Since linear foreign bodies are more likely to have extensive intestinal damage that may require resection, patients with suspected linear obstructions should be treated by a more experienced surgeon.
When closing enterotomy incisions, use 4-0 monofilament absorbable material (polydioxanone [PDS] is ideal). A simple interrupted, full thickness appositional pattern is most consistent for novice surgeons and care should be taken to incorporate the submucosa into each bite and to avoid eversion of the mucosa wherever possible. The affected section of bowel should be isolated from the rest of the abdomen with moistened laparotomy sponges and contaminated gloves and instruments should be replaced with separate, sterile gloves and instruments when the enterotomy is complete.
Assessment of intestinal viability Determining whether an intestinal resection-anastomosis is necessary in cases that have not yet perforated can be challenging. Decision making during intestinal surgery can be subjective and improves with surgical experience. Factors that can be used to assess whether intestine is viable enough to heal include: • Colour o Pink, bright red usually ok o Dark red, purple questionable o Black, grey, white resect • Intestinal wall thickness o Thick – usually ok, indicates edema o Thin – usually indicates loss of layering, impending perforation • Peristalsis o Improvement in peristalsis more likely to be viable • Perforation o Carefully evaluate mesenteric border of intestine, this is the most likely site of perforation
Post-operative care Post operatively, patient body temperature is maintained through active warming. Opioid analgesia (pure mu agonists) are provided either intermittently or via continuous infusion until the patient is able to take oral medications. NSAIDs should always be avoided following gastrointestinal surgery. Crystalloid fluid support is provided to continue to correct dehydration, correct electrolyte imbalances, provide maintenance and manage ongoing losses (GI secretions, vomiting, diarrhea). Antiemetic medication (e.g. maropitant) is helpful to reduce stress on suture lines caused by vomiting and to improve appetite. Except in cases of pre-operative septic peritonitis, antibiotics are discontinued within 24 hours of surgery. Enteral feeding is provided within 12 hours post operatively and a nasogastric feeding tube can be useful to suction gastric residuals and prevent nausea, as well as to feed a liquid diet. Post-operative monitoring should include PCV/TP, USG and bodyweight daily, electrolytes if derangements were present pre-operatively, gastric residuals if a nasogastric tube was placed and abdominal FAST scan to monitor peritoneal effusion if available. A more detailed discussion of post-operative care and complications is covered in the next lecture.
References
• Adams RJ, Doyle RS, Bray JP, et al.: Closed suction drainage for treatment of septic peritonitis of confirmed gastrointestinal origin in 20 dogs. Vet Surg. 43 (7):843-851 2014.
• Allen DA, Smeak DD, Schertel ER: Prevalence of small intestinal dehiscence and associated clinical factors: a retrospective study of 121 dogs. J Am Anim Hosp Assoc. 28(1):70-76 1992.
• Grimes J, Schmiedt C, Milovancev M, et al.: Efficacy of serosal patching in dogs with septic peritonitis. J Am Anim Hosp Assoc. 49 (4):246-249 2013.
• Grimes JA, Schmiedt CW, Cornell KK, et al.: Identification of risk factors for septic peritonitis and failure to survive following gastrointestinal surgery in dogs. J Am Vet Med Assoc. 238 (4):486-494 2011.
• Hansen, Monnet EL: Evaluation of serosal patch supplementation of surgical anastomoses in intestinal segments from canine cadavers. Am J Vet Res. 74 (8):1138- 1141 2013.
29 • Mouat EE, Davis GJ, Drobatz KJ, et al.: Evaluation of data from 35 dogs pertaining to dehiscence following intestinal resection and anastomosis. J Am Anim Hosp Assoc. 50(4):254-263 2014.
• Ralphs SC, Jessen CR, Lipowitz AJ: Risk factors for leakage following intestinal anastomosis in dogs and cats: 115 cases (1991-2000). J Am Vet Med Assoc. 223 (1):73-77 2003.
• Tobias KM and Johnston SA: Veterinary Surgery: Small Animal, Second Edition. St Louis, Missouri: Elsevier. 2018
• Weisman DL, Smeak DD, Birchard SJ, et al.: Comparison of a continuous suture pattern with a simple interrupted pattern for enteric closure in dogs and cats: 83 cases (1991- 1997). J Am Vet Med Assoc. 214 (10):1507-1510 1999.
• Wylie KB, Hosgood G: Mortality and morbidity of small and large intestinal surgery in dogs and cats: 74 cases (1980-1992). J Am Anim Hosp Assoc. 30 (5):469-474 1994.
30 Gastrointestinal surgery pearls: Tips and tricks you won’t find in the textbook Bronwyn Fullagar BVSc, MS, DACVS-SA
Objectives: • To maximize available pre-operative imaging of vomiting patients for early detection of GI foreign bodies • To share some useful surgical techniques o Approach to linear foreign bodies in dogs and cats o Gaining good visualization of all parts of the GI tract (covered in lecture) o Managing luminal disparity (covered in lecture) • To discuss complications of GI surgery and how to manage them
Maximizing pre-operative imaging • Radiographs of the vomiting patient o Take three views: right lateral, left lateral, VD o LEFT lateral shows “what’s LEFT” in the stomach o Helpful for gastric and linear FBs o Gas in pylorus (on right side) will rise o Radiographs equivocal and no signs of sepsis? Repeat in 8-12 hours, treat symptomatically, consider abdominal ultrasound. • Detecting linear foreign bodies o 50% of dogs with linear FB have no evidence of SI dilation (Sharma, 2010) o Comma-shaped (“paisley-shaped”) or “interrupted” gas pattern o +/- gastric foreign body on LEFT lateral (dogs) o Intestinal plication, loss of serosal detail o Note that normal fat cats will have intestinal ‘bunching’ due to intra-abdominal fat, with intestines located on right side of abdomen on VD. Use plication, gas pattern, ultrasound to differentiate. o Ultrasound is usually diagnostic • Detecting pre-operative intestinal perforation using imaging o Loss of serosal detail o Free peritoneal gas - cranial to liver, not associated with GIT ▪ Serosal and luminal margins of small intestine visible ▪ Horizontal beam radiograph will highlight peritoneal gas dorsally. o Free fluid on FAST scan o Cytology: septic suppurative inflammation
Surgical approach to canine linear foreign bodies The same general surgical principles apply to linear foreign bodies as were discussed in the previous lecture for enterotomy. Exploration of the abdomen in cases of intestinal plication should be very gentle and is often cursory until the linear foreign body has been removed, to reduce the risk of intestinal tearing along the mesenteric border. In dogs, 67-83% of linear foreign bodies are anchored at the pylorus and most extend to the jejunum. Note that 40% of dogs with linear FB will have septic peritonitis at the time of surgery, so the surgeon should be experienced and prepared to perform intestinal resection-anastomosis in these cases. If you do not feel comfortable with intestinal R&A, referral to a more experienced or specialist surgeon is recommended.
The first step in removing linear foreign bodies is to ‘release’ the anchor point of the foreign body via gastrotomy. The foreign material should be removed from the stomach without excessive traction on the linear portion in the small intestine. The material is cut, the gastrotomy incision is closed and the foreign material is then gently ‘milked’ down the duodenum and jejunum to remove plications. Ideally, all of the foreign material is removed through a single, jejunal enterotomy, aboral to the affected bowel. However, in cases where additional damage to the intestine is likely (foreign material very abrasive), multiple enterotomies may be performed, but this may increase the likelihood of post-operative dehiscence. Most canine linear foreign bodies that do not have intestinal perforation can be removed in a single gastrotomy and a single enterotomy. In cases of intestinal perforation or where a resection-anastomosis is deemed necessary due to questionable intestinal viability, the foreign body can be milked into the section of bowel to be resected and then removed en bloc.
31
Surgical approach to feline linear foreign bodies The principles of surgery for feline linear foreign bodies are similar to those in canine patients. However, several important differences exist. Cats are more likely to ingest string, whereas dog foreign bodies tend to be thicker fabric or toy material. 50-63% of feline linear FB are anchored around the base of the tongue so a thorough oral examination should be performed in every cat with gastrointestinal clinical signs. Conservative management of cats with string foreign bodies is only appropriate in cases with no clinical signs (i.e. string is an incidental finding) and is reported to have been successful in 47% non-clinical cases. 33% of cats with linear foreign bodies have intestinal perforation at the time of diagnosis.
Once the anchor point of the foreign body has been determined, it should be released to relieve the plicated bowel. However, unlike the thick fabric ingested by dogs, string can be difficult to palpate in the intestine and can be embedded in the intestinal wall at the mesenteric border. Therefore, it is usually helpful to make a small, mesenteric enterotomy midway along the plicated region of bowel and to grasp the string with a mosquito hemostat, prior to release of the plications. Then, the string can either be cut from under the cat’s tongue, or if the material is anchored at the pylorus, a gastrotomy can be performed as for dogs. The string can then be gently milked down the duodenum while very gentle traction is placed with the hemostat. Cats are more likely than dogs to require more than one enterotomy to remove all of the foreign material, to avoid the string tearing through the mesenteric border of the intestine.
Selected complications of gastrointestinal surgery
1. Septic peritonitis This is the most serious complication of intestinal surgery and is a surgical emergency. Prompt detection of leakage from an enterotomy or anastomosis site is crucial to give patients the best chance of a successful outcome. Despite repeat surgery and critical care, the reported mortality of septic peritonitis following intestinal surgery is ~50%. If septic peritonitis is diagnosed, referral to a specialist facility for repeat surgery and post-operative care is strongly recommended.
Dehiscence of intestinal incisions usually occurs in the first 3-5 days after surgery. This corresponds to the ‘lag phase’ of intestinal healing (see previous lecture). Dehiscence in the immediate post-operative period is uncommon except in cases of surgeon error. Clinical signs include inappetence or anorexia (particularly in a patient who was previously eating), vomiting and abdominal pain. Pyrexia and a palpable abdominal fluid wave may also be present. Bloodwork may show band neutrophilia. Repeated abdominal FAST scans are helpful in quantifying peritoneal effusion in the post- operative period – a mild amount of peritoneal fluid is expected post operatively in patients without preoperative peritonitis, but this should decrease each day. Radiographs are not useful, as free peritoneal gas may be present in any patient who has undergone abdominal surgery for up to 2 weeks post operatively.
Definitive diagnosis of septic peritonitis requires abdominocentesis and cytologic evaluation of peritoneal fluid. Obtain fluid directly from abdomen and make direct and centrifuged smears, then stain with Diff Quick. Evaluate microscopically for large numbers degenerate neutrophils, intracellular (or large numbers of extracellular) bacteria or plant/food/foreign material. Submit fluid for bacterial culture. Note that blood-to-fluid glucose and lactate differentials are not reliable for detecting septic peritonitis post operatively. If sepsis is confirmed, broad spectrum IV antibiotics should be started immediately, and the patient should be transferred directly to a referral facility, if possible. A detailed discussion of surgery and post-operative care for septic peritonitis is beyond the scope of this lecture. If clients decline repeat surgery, euthanasia is the only reasonable alternative – medical management is not appropriate.
2. Ileus Ileus is a common complication of gastrointestinal surgery, particularly following linear foreign body removal or intestinal resection-anastomosis. Clinical signs of anorexia, nausea and regurgitation begin within 24 hours of surgery. Laparotomy, intestinal manipulation, long operative time and extensive resection all contribute to sympathetic overactivation, which reduces normal gastrointestinal motility. The syndrome is exacerbated by anesthesia, opioid use, sepsis and electrolyte derangements.
32 Treatment of ileus is focused on treating medical underlying causes (sepsis, electrolyte abnormalities) and stimulating normal gastrointestinal motility. Enteral feeding should be started within 12 hours of surgery at ¼ resting energy requirement (RER), either as a continuous infusion (e.g. Clinicare) or in bolus feedings q4-6h. I place a nasogastric feeding tube intra-operatively in all cases of R&A and most linear foreign bodies – it can easily be removed if the patient begins eating and they are very useful for suctioning gastric residuals which improves patient comfort. Prokinetic medications are also helpful and I usually start these immediately post operatively. Some useful prokinetics are: • Metoclopramide CRI 1-2mg/kg/d • Cisapride 0.1mg/kg PO q 8h • Erythromycin 0.5-1mg/kg IV q 8h Analgesia should be adjusted to the lowest possible dose of opioids that allows patient comfort while maximizing normal GI motility. Pure mu agonists (especially fentanyl, hydromorphone) cause more ileus than methadone or buprenorphine so it can be helpful to transition patients with ileus to less potent opioids.
3. Short bowel syndrome The normal length of canine and feline small intestines is five times the length of the patient’s trunk. Short bowel syndrome (SBS) is a condition of malabsorption and malnutrition that occurs following resection of 50- 85% of the small intestinal length. When performing a resection-anastomosis, it is therefore important to remove all abnormal intestine, but not to be overzealous with resection of viable bowel. Clinical signs include persistent, watery diarrhea and weight loss. Thorough and frank client communication is crucial in cases where a large small intestinal resection is required. Management of SBS can be lifelong and involves frequent feeding (6-8x per day) of a highly digestible diet. Adaptation of the small intestinal may occur but usually takes weeks to months. The prognosis for patients with SBS is worse if the small intestinal resection is more distal (ileal resection) and/or if the ileocecal valve is resected.
Conclusions In summary, to maximize your success with gastrointestinal surgery, case selection is key. Set yourself up for positive patient outcomes by starting with simpler cases (gastrotomy, single enterotomy) in systemically well patients with an acute onset of clinical signs. Referral is recommended for patients who are systemically ill, have linear foreign bodies, protracted clinical signs or septic peritonitis, especially if you are not experienced with intestinal resection-anastomosis and comfortable assessing intestinal viability. Practicing gentle tissue handling and intestinal suturing on cadaveric tissues will greatly improve your surgical confidence and efficiency and patient outcomes. A surgical assistant is invaluable, particularly in cases of resection anastomosis and for novice surgeons. Pre-emptively treating ileus post operatively will shorten your patients’ hospital stays and speed their recoveries. With careful case selection, deliberate practice, good mentorship and critical evaluation of outcomes, surgery for gastrointestinal foreign bodies can be some of the most rewarding cases in practice.
References
• Allen DA, Smeak DD, Schertel ER: Prevalence of small intestinal dehiscence and associated clinical factors: a retrospective study of 121 dogs. J Am Anim Hosp Assoc. 28(1):70-76 1992.
• Grimes JA, Schmiedt CW, Cornell KK, et al.: Identification of risk factors for septic peritonitis and failure to survive following gastrointestinal surgery in dogs. J Am Vet Med Assoc. 238 (4):486-494 2011.
• Hayes G. Gastrointestinal foreign bodies in dogs and cats: a retrospective study of 208 cases. J Small Anim Pract. 50: 576-583 2009.
• Hobday MM, Pachtinger GE, Drobatz KJ, Syring RS: Linear versus non-linear gastrointestinal foreign bodies in 499 dogs: clinical presentation, management and short-term outcome. J Small Anim Pract. 55: 560–565 2014.
• Mouat EE, Davis GJ, Drobatz KJ, et al.: Evaluation of data from 35 dogs pertaining to dehiscence following intestinal resection and anastomosis. J Am Anim Hosp Assoc. 50(4):254-263 2014.
33 • Ralphs SC, Jessen CR, Lipowitz AJ: Risk factors for leakage following intestinal anastomosis in dogs and cats: 115 cases (1991-2000). J Am Vet Med Assoc. 223 (1):73-77 2003.
• Sharma A, Thompson MS, Scrivani PV, Dykes NL, Yeager AE, Freer SR, Erb HN. Comparison of radiography and ultrasonography for diagnosing small-intestinal mechanical obstruction in vomiting dogs. Vet Rad US. 52:3, 248–255 2011.
• Tobias KM and Johnston SA: Veterinary Surgery: Small Animal, Second Edition. St Louis, Missouri: Elsevier. 2018.
• Weisman DL, Smeak DD, Birchard SJ, et al.: Comparison of a continuous suture pattern with a simple interrupted pattern for enteric closure in dogs and cats: 83 cases (1991- 1997). J Am Vet Med Assoc. 214 (10):1507-1510 1999.
• Wylie KB, Hosgood G: Mortality and morbidity of small and large intestinal surgery in dogs and cats: 74 cases (1980-1992). J Am Anim Hosp Assoc. 30 (5):469-474 1994.
34 Going with the flow: A practical guide to canine lower urinary tract obstruction Bronwyn Fullagar BVSc, MS, DACVS-SA
Objectives 1. To review the pathogenesis of urethral obstruction in dogs 2. To provide a practical framework for emergency and surgical management of patients with urethral obstruction 3. To discuss less invasive techniques for management of canine obstructive urolithiasis
Introduction Lower urinary tract (LUT) obstruction in dogs and cats is a common medical emergency. Obstruction of the urethra can be either benign, due to urolithiasis, or malignant, due to neoplasia (usually transitional cell carcinoma). Treatment of a patient with urethral obstruction involves identifying and correcting life-threatening azotemia, electrolyte and acid-base abnormalities, identifying the cause of obstruction, restoration of a patent urethra and in many cases, surgical removal of urolith(s). Successful treatment of LUT obstruction requires a comprehensive understanding of the pathophysiology of obstruction, the regional anatomy and the treatment options, which may be non- surgical (cystoscopic basket retrieval, laser lithotripsy) or surgical. Surgical procedures involve open surgery (cystotomy), minimally invasive surgery (percutaneous cystolithotomy – PCCL) or salvage procedures (scrotal urethrostomy).
Diagnosis of urethral obstruction A history of stranguria, dysuria or hematuria usually precedes LUT obstruction. Signalment and history may help to differentiate between benign and malignant obstruction – transitional cell carcinoma usually has a more insidious onset of signs and is common in older, female dogs, particularly Scottish terriers, Shetland sheepdogs and beagles, although any sex or breed may be affected. Patients with urethral obstruction who present with an unstable cardiovascular status should be stabilized immediately (see below). In stable patients, diagnostic imaging should be performed to determine the nature and location of obstruction. Plain radiographs can identify uroliths >1mm diameter and two lateral views should be taken: one with the pelvic limbs extended to highlight the bladder and one with the legs pulled forward to show the pelvic and penile urethra. Collimation should include the perineal region. Plain radiographs have a 25-27% incidence of false negative findings for urate, cysteine and calcium phosphate uroliths. Pneumocystography or double-contrast urethrocystography should be considered in patients with suspected urolithiasis and equivocal plain radiographic findings. Ultrasound can also be used to diagnose urolithiasis and false negatives occur in 3.4-6.5% of cases (equivalent to pneumocystography or double-contrast cystography). Ultrasound may also detect evidence of a bladder or trigonal mass. In some cases, urethroscopy or cystoscopy is required to detect neoplasia of the pelvic urethra or trigone region.
Emergency treatment of patients with urethral obstruction Urethral obstruction is a medical, rather than a surgical emergency. Initial physical examination and diagnostics should focus on diagnosing and treating cardiac arrhythmias, correcting electrolyte and acid-base disturbances and rehydration without inducing fluid overload. Initial diagnostics should include PCV/TP, BG, serum electrolytes, acid-base status, BUN and creatinine. An ECG should be evaluated for spiked T waves, short QT interval, wide QRS, or absence of P waves due to hyperkalemia.
• Emergency treatment of hyperkalaemia o Calcium gluconate (10%) 0.5 to 1 mL/kg IV over 10 to 20 minutes. Does not alter serum K+, cardioprotective. Onset within minutes, duration 1h. Monitor ECG for bradycardia. o Dextrose: 0.5 to 1g/kg IV, with or without exogenous insulin 0.5 to 1 IU/kg (IV or IM). Drives K+ intracellularly, lowers serum K+. Onset 1 h, duration several hours. Monitor BG. o Sodium bicarbonate: 0.5 to 2mEq/kg IV over 15 min. Drives K+ into cells in exchange for H+ ions. Monitor acid-base status.
35 Cystocentesis can be performed to decompress the bladder of obstructed patients to allow for correction of azotemia and electrolyte derangements. There is a low risk of bladder rupture if cystocentesis is performed by an experienced person in a relaxed, sedated, well restrained patient. Urine should be saved for urinalysis and culture. IV fluid diuresis can then be initiated with potassium deficient fluids (e.g. 0.9% NaCl).
Re-establishing urethral patency Once obstruction due to urolithiasis has been diagnosed and the location of the obstructive urolith(s) has been identified, urohydropulsion should be attempted to move obstructive uroliths back into the bladder. In male dogs, uroliths are commonly lodged at the base of the os penis and in female dogs obstruction may occur just proximal to the urethral papilla. A digital rectal exam can identify uroliths in the pelvic urethra. Urohydropulsion is strongly preferred over urethrotomy, which has a high complication rate and is ineffective in dislodging uroliths from the proximal (pelvic) or distal (within the os penis) urethra. Additionally, urethrotomy makes future attempts at urohydropulsion much more difficult.
Urohydropulsion in dogs requires very heavy sedation and epidural or general anesthesia (ideally). Attempting the procedure in an awake or inadequately sedated patient often is unsuccessful and is more likely to result in patient pain and complications such as bladder rupture or urethral tear. General anesthesia is only be performed once patients are cardiovascularly stable. Performing the procedure in the radiology suite allows for easy assessment of stone location.
Canine urohydropulsion step-by-step:
1) Premedicate and induce general anesthesia. 2) Perform epidural – ideal to relax skeletal muscle of urethra and prevent spasm. 3) Perform cystocentesis to empty bladder. 4) Take lateral abdominal radiograph to check location of stone(s). 5) Clip and aseptically prepare prepuce (or vulva in female dogs). 6) Non-sterile gloved assistant palpates urethra per rectum and places ventral pressure on urethra to occlude it. 7) Veterinarian places sterile, lubricated red rubber catheter into distal urethra and advances as far as obstruction, then digitally occludes penis around catheter. 8) While the assistant occludes the pelvic urethra, the veterinarian slowly injects saline into red rubber catheter and holds pressure on syringe – this dilates the urethra around the uroliths. 9) On count of ‘three’, assistant will release occlusion of pelvic urethra while veterinarian maintains occlusion of distal penile urethra and puts firm pressure on syringe to force saline through urethra into bladder and move uroliths. 10) Repeat radiographs and attempt to pass red rubber catheter into bladder to check success of procedure. 11) Multiple attempts may be necessary – remember to check bladder size and drain after each attempt via catheter or cystocentesis to prevent iatrogenic bladder rupture. 12) Once stones have moved into bladder, place indwelling (Foley) urinary catheter to prevent re- obstruction and allow further stabilization, or proceed directly to surgery for cystotomy or PCCL.
Surgical treatment of urethral obstruction:
A detailed description of the cystotomy procedure will be provided in the lecture. Key points include: • Ensure that the prepuce or vulva is included in the surgical field to allow normograde and retrograde passage of a catheter intra-operatively. • Exteriorize the bladder and isolate from the abdomen with moistened laparotomy sponges to prevent urine contamination of the abdomen. Cystotomy performed on ventral bladder surface. • Use stay sutures at the bladder apex and bladder walls after entering the bladder to allow visualization of the lumen. • Obtain sample of bladder mucosa for culture +/- histopathology. • Close using 3-0 or 4-0 monofilament, rapidly absorbable suture (e.g. Monocryl/poliglecaprone 25) in a simple interrupted or simple continuous single layer, full thickness, appositional pattern.
36 • Leak test bladder and place additional sutures or inverting pattern if concern for urine leakage. • Repeat radiographs (+/- positive or double contrast cystography) to ensure complete stone removal. Incomplete stone removal is reported in 20% dogs after cystotomy (Grant, 2010).
Patients should be maintained on IV fluid diruesis for 12-24h post operatively to encourage residual blood clots to be flushed from bladder. Broad spectrum antibiotics (cefazolin or amoxicillin-clavulanic acid) are continued for 7 days while awaiting culture results, since 76% dogs with cystic calculi have a urinary tract infection. An indwelling urinary catheter is usually not necessary, except in cases with pre- operative bladder rupture, severe urethral inflammation or urethral tear. Uroabdomen occurs in <1.5% of patients following cystotomy but minor complications (hematuria, stranguria) occur in 37-50% of cystotomies and are generally self-limiting (Thieman-Mankin, 2012).
Alternative methods for cystolith removal:
1. Lithotripsy • Using laser energy or shockwaves to crush or fragment uroliths – laser is safest and most efficient for LUT uroliths. • Holmium:yttrium-aluminium-garnet (Ho:YAG) laser used for canine cystic or urethral calculi. • Urolith fragments removed endoscopically via basket or via voiding hydropulsion. • Complications/failure of procedure due to small urethral diameter, bladder rupture, undetected residual uroliths. • Female dogs (larger diameter urethra) and/or dogs with low urethroliths make best candidates. • Small male dogs with multiple uroliths are not usually good candidates. • Reported to be as effective as cystotomy in removing canine uroliths but lithotripsy takes average of 20-25min longer to perform (Bevan, 2009). Equivalent cost, similar short-term complications for both procedures.
2. Percutaneous cystolithotomy (PCCL) • Alternative option for small patients and male patients with larger numbers of small uroliths. • Miniature laparotomy and cystotomy incision, then laparoscope or cystoscope passed into bladder. • Retrograde flushing via urethral catheter, uroliths removed via suction or basket retrieval through instrument channel of cystoscope. • Advantages over surgical cystotomy: decreased requirement for post-operative analgesia, allows magnified evaluation of bladder mucosa and uroliths. • Disadvantages over surgical cystotomy: longer operative time, more expensive. (Arulpragasam, 2012)
3. Voiding hydropulsion • NOT appropriate for patients with urethral obstruction • Useful for especially female patients with recurrent uroliths that are detected early (1-2mm diameter). • General anesthesia, bladder filled with saline via catheter, patient positioned vertically and even manual pressure applied to bladder to express uroliths through urethra. • Radiographs taken after procedure to ensure complete removal. • Urine culture and stone analysis performed as for cystotomy.
References: • Arulpragasam SP, Case JB, Ellison GW: Evaluation of costs and time required for laparoscopic-assisted versus open cystotomy for urinary cytolith removal in dogs: 43 cases (2009-2012). J Am Vet Med Assoc. 243:703-708 2012. • Bevan JM, Lulich JP, Albasan H, et al.: Comparison of laser lithotripsy and cystotomy for the management of dogs with urolithiasis. J Am Vet Med Assoc. 234:1286-1294 2009. • Grant DC, Harper T, Were SR: Frequency of incomplete urolith removal, complications, and diagnostic imaging following cystotomy for removal of uroliths from the lower urinary tract in dogs: 128 cases (1994-2006). J Am Vet Med Assoc.236:763-766 2010.
37 • Runge JJ, Berent AC, Mayhew PD, et al.: Transvesicular percutaneous cystolithotomyfor the retrieval of cystic and urethral calculi in dogs and cats: 27 cases (2006-2008). J Am Vet Med Assoc. 239:344-349 2011. • Thieman-Mankin KM, Ellison GW, Jeyapaul CJ, et al.: Comparison of short-term complication rates between dogs and cats undergoing appositional single-layer or inverting double-layer cystotomy closure: 144 cases (1993-2010). J Am Vet Med Assoc.240:65-68 2012. • Tobias KM and Johnston SA: Veterinary Surgery: Small Animal, Second Edition. St Louis, Missouri: Elsevier. 2018.
38 Open wounds: We’ve got you covered! Demystifying the world of wound management Bronwyn Fullagar BVSc, MS, DACVS-SA
Objectives: • To review normal wound healing and how it differs between surgical wounds and open/chronic/contaminated/infected wounds • To provide an algorithm for the management of open wounds in practice • To review open wound management techniques and products available • To discuss methods of wound closure and timing of closure
Introduction Open wounds are common in both general and specialty practice. They can be very rewarding cases and do not often require a large amount of expensive equipment, so can be effectively treated in a primary care setting. However, treatment can often take time, patience, money and owner commitment to achieve a successful outcome. As veterinarians (and surgeons in particular), we have a tendency to want to ‘fix’ things. The key with open wounds, particularly contaminated or chronic ones, is to resist the temptation to close the wound straight away and instead prepare the client (and yourself) for the long haul. Achieving a healthy, non-infected granulation bed is the holy grail of open wound management – it provides a microbially resistant, vascular substrate, after which various methods of wound closure can be considered. Although open wound management can be expensive and time consuming, it is less expensive and time consuming than complications (dehiscence, infection) that arise when a wound that is closed too early.
Primary closure Primary closure is indicated for surgically created wounds (or clean lacerations, e.g. cut on glass) that are clean or clean-contaminated. The ‘golden period’, 3-6 hours after creation of the wound, applies only to clean wounds and refers to the time taken for bacterial colonization of the wound from the environment. Contaminated wounds, or wounds with extensive tissue trauma (e.g. bite wounds, crushing/shearing injuries) are not good candidates for primary closure, even if they are treated immediately. If there is any doubt at all that the wound may be contaminated, if there is damage to the vascular supply of the wound edges, or if debridement is necessary, a wound should be left open for at least 24 hours, bandaged in a sterile fashion with a moist primary layer and reassessed. If the wound appears healthy and non-infected the following day, with no ongoing necrosis and healthy wound edges, the wound can be closed at that time (delayed primary closure), or open wound management can be continued. There is no detriment in the long term to leaving most wounds open a little longer to ensure the wound environment is healthy prior to closure. More complications occur in practice due to closing wounds too early than from failure to close a wound soon enough! The remainder of the lecture will focus on open wounds that are not suitable for primary closure at initial presentation.
Approach to an open wound case:
1. Triage. Goals: stabilize patient, reduce microbial burden, prevent contamination o Assess and stabilize cardiovascular status first o Provide IV fluids, analgesics o Perform initial diagnostics: thoracic radiographs, FAST scan, point of care bloodwork o Brief orthopedic/neurologic exam prior to sedation, pay attention to neurovascular supply of wounded region o Wear gloves – protect wound from nosocomial infection o Copious irrigation of wound with tap water or sterile isotonic solution o Cover wound with antibacterial contact layer, temporary sterile dressing o Continue with remainder of patient work-up (e.g. long bone radiographs, complete bloodwork)
2. Definitive wound care. Goals: decontaminate, debride necrotic tissue, provide moist wound environment, antimicrobial treatment o Sedate or anesthetize patient o Protect wound (fill with sterile lubricant), clip wide region around wound o Prepare surrounding skin for aseptic surgery (avoid chlorhexidine in wound but on surrounding skin is fine)
39 o Irrigate wound with balanced warm electrolyte solution o Perform deep tissue culture and sensitivity. Culture the wound after it has been clipped, cleaned and lavaged.
3. Judicious debridement. Goals: remove foreign material, contaminated, devitalized or necrotic tissue o Aseptic technique (sterile skin preparation, sterile instruments, cap, mask and sterile gloves) o Be conservative, remove only tissue that is certainly non-viable, allow questionable tissue time to ‘declare itself’ o Explore wound, including subcutaneous pockets o Layered debridement - superficial to deep o Non-surgical debridement (e.g. wet-to-dry bandage)
4. Moist wound management. Facilitate debridement, promote granulation tissue formation, epithelialization o Moisture at wound surface facilitates autolytic debridement through cytokine-rich exudate o Maintains cells, cytokines, growth factors at wound surface o Current standard of care o Topical antimicrobials +/- systemic broad-spectrum antibiotics (1st generation cephalosporin or amoxicillin-clavulanic acid) o Primary layer – non-adherent surface +/- topical antimicrobials (Table 1) o Secondary layer – draws exudate away from wound surface (e.g. sterile 4x4 or sterile laparotomy sponges) o Cover with soft padded bandage or tie-over bandage o Bandage should be changed every 24 hours initially, then the frequency of bandage changes can be decreased as the amount of wound exudate lessens. Once a healthy granulation bed is present, it is often beneficial to leave dressings on for a week at a time, so as not to disrupt epithelialization.
Table 1: Examples of useful primary layers for open wound management
Level of wound Primary layer Antibacterial component exudate Petroleum (+/- chlorhexidine) Dry impregnated gauze None/chlorhexidine/topical (granulation Non-adherent dressing antibiotic tissue) + topical antibiotic ointment Calcium alginate or Mildly exudative Leptospermum honey hydrocolloid Silver, leptospermum Heavily exudative Alginate or foam honey
Second intention healing vs. secondary closure Once a healthy granulation bed is present, there are a number of methods by which final epithelialization may occur. For smaller wounds in low-motion areas, moist wound management can be continued, and the wound can be allowed to gradually contract and epithelialize via second intention healing. Advantages are that surgery is not required and therefore this can often be simplest and most cost-effective method of closure. Disadvantages are that the process can be time-consuming, new epithelium is fragile and easily damaged and contraction of the scar tissue may impede function.
Alternatively, once a healthy granulation bed has been established, surrounding skin can be mobilized free of the granulation bed and closed over the top (secondary closure). This surgery should occur in the operating room using aseptic technique as for clean surgery. The skin edges are sharply dissected from the granulation tissue and carefully undermined. Minimal debridement of the skin edges is necessary and it is not necessary to remove the granulation tissue as it contains important growth factors and cytokines that can assist in healing. A closed suction drain (e.g. Jackson-Pratt drain) should be placed at the time of surgery for larger wounds to treat dead space and prevent seroma formation.
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If there is excessive tension on the wound edges at this stage, then tension-relieving reconstructive techniques, local subdermal plexus flaps, axial pattern flaps or free skin grafts can also be performed at this time.
Negative pressure wound therapy (NPWT) Negative pressure wound therapy, sometimes referred to as vacuum assisted closure, or ‘the VAC’, is an alternative to traditional bandaging as a method of open wound management. Following initial lavage, culture and debridement of devitalized tissue, coarse open cell polyurethane foam is cut to size and placed in the wound bed. The skin edges are secured to the foam and an impermeable adhesive plastic dressing is placed to create an airtight seal. Although a wall suction unit can be used to perform NPWT, a specialized suction unit is preferred as a specific pressure can be achieved. Suction is applied continuously at -125mmHg. The unit removes exudate from the wound and the application of negative pressure improves wound perfusion, reduces edema, stimulates granulation tissue formation and may decrease bacterial colonization. This results in more rapid formation of healthy granulation tissue and means fewer bandage changes are required. NPWT can be used on wounds in most locations but is ideal for large wounds and those in locations that are difficult to bandage. Although the setup costs are higher than conventional bandages, final costs can be comparable for large wounds where large daily bandages under sedation would be required.
Chronic wounds Most wounds will progress through the following phases of wound healing: 1. Inflammation o Day 0-3 o Removal of diseased tissue by phagocytosis o Predominant cells are neutrophils and monocytes, coagulation cascade creates fibrin seal 2. Proliferation o Day 4-12 o Repair of wounded tissue, fibroblasts create collagen o Restoration of blood flow, extracellular matrix, epithelium 3. Maturation (remodeling) o Collagen synthesis complete 4-5 weeks o Collagen maturation 12-18 months o Return of proportion of pre-wound strength
Chronic wounds do not progress past the proliferation phase and usually present as a region of poorly formed granulation tissue. A checklist approach (table 2) is helpful when presented with a chronic wound, to ensure that both local and systemic factors have been addressed. This helps to identify why the wound is not healing, so that a patient-specific diagnostic and treatment plan can be generated.
Table 2: Factors that may hinder normal wound healing
Factor Treatment/management Excess motion Splint or external skeletal fixator, patient confinement Tension Tension relieving techniques, revise closure with flap or graft Pressure Adjust bandaging, make ‘doughnuts’ over pressure points Fluid accumulation Absorbent bandages, debride eschar, NPWT, active suction drain Necrotic tissue Serial debridement, remove eschar Ischaemia Correct systemic hypotension, correct anemia, check for thromboembolism Infection Culture and sensitivity, treat with appropriate topical and systemic ABs
41 Neoplasia Biopsy, previous chemotherapy or radiation therapy Underlying osteomyelitis, Radiographs, debride sequestrum, forage sequestrum or exposed bone exposed bone Immunocompromise Treat/manage underlying endocrinopathy, discontinue iatrogenic steroids, correct malnutrition, hypoalbuminemia (also consider FIV, effects of chemotherapy)
Take home messages: o Prepare yourself and your clients for the long haul o If in doubt, treat with moist open wound management o Optimize wound environment - use checklist for chronic wounds o Debride sparingly, allow tissue to ‘declare itself’ o Prevent nosocomial infection, culture all wounds, use rational antibiotic therapy based on sensitivity results o Goal is viable, non-infected tissue or healthy granulation tissue o Take photos along the way – it helps you and the clients to see progress!
References • Demaria M, Stanley BJ, Hauptman JG, et al.: Effects of negative pressure wound therapy on healing of open wounds in dogs. Vet Surg. 40:658 2011. • Jull AB, Walker N, Deshpande S. Honey as a topical treatment for wounds. (Jull AB, ed.). Chichester, UK: John Wiley & Sons, Ltd; 2013. • Pitt KA, Stanley BJ: Negative pressure wound therapy: experience in 45 dogs. Vet Surg. 43:380 2014. • Tobias KM and Johnston SA: Veterinary Surgery: Small Animal, Second Edition. St Louis, Missouri: Elsevier. 2018.
42 What lies beneath: Managing thoracic trauma from the ER to the OR Bronwyn Fullagar BVSc, MS, DACVS-SA
Objectives: 1. To discuss the mechanisms and sequellae of penetrating thoracic injuries in dogs and cats 2. To review a practical guide to triage and stabilization of patients with thoracic trauma 3. To discuss diagnostic imaging of patients with thoracic trauma 4. To develop a framework for decision making regarding surgery in patients with penetrating thoracic trauma
Introduction Thoracic trauma is a common emergency presentation in dogs and cats and may present as either blunt force trauma (e.g. hit by car, fall from height) or penetrating thoracic trauma (e.g. animal bite wounds, penetrating foreign bodies). This lecture will focus specifically on penetrating thoracic injuries, with an emphasis on decision making regarding surgery in these patients.
Sequellae of penetrating thoracic trauma include muscle trauma, rib or sternum fractures, flail chest, traumatic body wall hernias, diaphragmatic hernia, pneumothorax, hemothorax, pulmonary contusions and lung laceration. Patients frequently present with an unstable cardiovascular status. Not all penetrating thoracic injuries warrant surgical exploration and cardiovascular stabilization followed by diagnostic imaging are required prior to making a decision to proceed to emergency thoracotomy. In retrospective studies of dogs and cats who underwent surgery for thoracic trauma, the perioperative mortality rate was 14.6% for dogs and 13% for cats (Lux, 2018). A recent retrospective study of cats who suffered thoracic dog bite wounds found an overall mortality rate of 27% (Frykfors von Hekkel, 2019).
Patient assessment and stabilization Patients with penetrating thoracic injuries should be taken to the treatment area for immediate triage and evaluation. Supplemental oxygen is administered by mask if respiratory distress is present and an IV catheter should be placed. Minimum database bloodwork (PCV/TP, blood glucose, venous blood gas (i-STAT) and BUN) can be collected from the catheter and SPO2 should be monitored. Initial physical examination focuses on the cardiovascular system, lungs and brain. IV fluids are administered to treat hypovolemic shock and restore blood pressure, but should be used judiciously in patients with pulmonary contusions.
Opioid analgesia is preferred but hydromorphone and morphine can exacerbate panting and so are ideally avoided in favor of fentanyl or methadone. Bupivacaine intercostal nerve blocks can also be performed in cases of rib fractures for additional analgesia. A more detailed physical examination can then be performed, with careful palpation of the ribs and intercostal musculature and evaluation of the orthopedic and neurologic status of the patient. Evaluation of the abdomen via abdominal-focused assessment with sonography (A- FAST) is also indicated. Lacerations over the thorax should be noted as even small puncture wounds can cover large thoracic wall defects and significant intrathoracic trauma. Chest wounds that obviously allow environmental air to enter the thorax should be immediately clipped, cleaned and a sterile airtight dressing placed. Intravenous, broad-spectrum antibiotic therapy should be initiated.
Pneumothorax is common in small animals with penetrating thoracic injuries, and was present in 50-61% of cats and 24% of dogs who presented with dog bite injuries (Cabon, 2015; Frykfors von Hekkel, 2019), and in 46% of dogs and 37% of cats who underwent surgery for thoracic trauma (Lux, 2018). In patients in severe respiratory distress, immediate thoracocentesis may be indicated prior to diagnostic imaging to treat pneumothorax and improve ventilation. Thoracocentesis for pneumothorax is best performed dorsally, with the patient in sternal recumbency. In some cases, intubation and mechanical ventilation may be necessary to provide oxygenation while further assessment is carried out. If pneumothorax is recurrent or continuous after external thoracic injuries have been sealed, one or bilateral thoracic drainage catheters should be placed. Soft flexible Mila chest tubes work well for this purpose and are easily placed in the ER. Intermittent or continuous thoracic suction can then be applied, until either pneumothorax spontaneously resolves or until the patient is stable enough to undergo surgery (see below).
43 Thoracic radiographs are taken once patient stability permits, taking care, particularly in cats, not to further stress the patient to the point of respiratory collapse. Radiographs are evaluated for pulmonary contusions, pneumothorax, pleural effusion, rib fractures, diaphragmatic hernia, subcutaneous emphysema and fractures of the surrounding vertebrae and long bones. Thoracic-focused assessment with sonography (T-FAST) is also useful in the diagnosis of pneumothorax and pleural effusion. A full description of the technique has been described by Lisciandro et al (2008). Although T-FAST is a reliable method to detect pleural effusion, there are conflicting results regarding its accuracy in detecting pneumothorax. One study found T-FAST had an accuracy of 90% (Lisciandro, 2008), while another study found T-FAST to be unreliable in detecting pneumothorax when compared to thoracic computed tomography (Walters, 2018). Initial wound management should be efficient and involve clipping and cleaning skin surrounding thoracic wounds, removal of debris and contaminated material and gentle lavage with warm, sterile, isotonic solution. A sterile bandage should be placed and cling film or adhesive plastic drapes are useful to achieve an airtight seal. Further wound exploration and debridement can occur once the patient is more stable and a decision has been made as to whether exploratory thoracotomy is necessary (see below).
Decision making in emergency thoracic surgery 1. Indications for thoracic surgery following penetrating trauma In human medicine, emergency department thoracotomy (EDT) refers to open thoracotomy in the emergency room and is recommended only in patients with penetrating thoracic injuries who present pulseless but with signs of life. The survival rate reported in the human literature for EDT is 11.7% (Seamon, 2015). In veterinary patients, EDT is not practiced and the decision to proceed to surgery is made following initial patient assessment and stabilization (see above). • Several studies have suggested indications for surgery in small animal patients after thoracic trauma (Scheepens, 2006; Cabon, 2015; Frykfors von Hekkel, 2019; Peterson, 2015). In some cases, surgery is clearly indicated, such as in patients with impalement injuries, severe ongoing hemorrhage, large full-thickness thoracic wall defects, severe intrathoracic hemorrhage, diaphragmatic hernia or if cardiovascular stability cannot be achieved (e.g. continuous pneumothorax). In other patients, particularly those with thoracic puncture wounds +/- flail chest following thoracic bite wounds, decision making is more challenging. Although there is no consensus, general guidelines for the need for thoracotomy include rib fractures, flail chest, pulmonary contusions, pneumothorax, or greater than three thoracic radiographic lesions (Scheepens, 2006; Cabon, 2015; Frykfors von Hekkel, 2019). Unlike penetrating abdominal bite wounds, there is less concern for pyothorax following penetrating thoracic trauma and bite wounds can be successfully managed without surgery in some cases. However, in the author’s experience, patients with thoracic bite wounds who fulfill the above criteria generally have extensive damage to intercostal musculature +/- intrathoracic structures that benefit from surgical intervention.
If a decision is made that exploratory thoracotomy is necessary, referral to a specialist centre is strongly recommended. General anesthesia with mechanical ventilation is necessary, surgery must occur within a clean operating room and the surgeon must be comfortable with thoracic anatomy and experienced in procedures such as lung lobectomy and diaphragmatic herniorrhaphy. In a retrospective study of dogs who underwent thoracic surgery following trauma, 11% had diaphragmatic hernia, 26% required partial or complete lung lobectomy and 50% had muscle defects that required reconstruction (Lux, 2018). Flail segments of the thoracic wall can be stabilized to an external brace or to adjacent ribs, or can be treated conservatively with muscular and skin reconstruction and analgesia via bupivacaine intercostal nerve blocks. Fractured ribs rarely require surgical fixation and can be sutured to adjacent ribs to provide some stability and improve comfort. Indwelling thoracic drainage catheter(s) are placed post operatively to remove residual pleural fluid and air and to monitor cytology. Subcutaneous, closed suction drain(s) may also be necessary if extensive dead space is present.
If thoracotomy is not deemed necessary but partial thickness penetrating wounds are present, these are treated with general principles of open wound management once the patient is cardiovascularly stable. The surgeon should be prepared that skin wounds are ‘the tip of the iceberg’ and often overly much larger thoracic wall defects and extensive muscle damage. In some cases, there may be no externally visible puncture wound but extensive subcutaneous damage to the thoracic wall.
General anesthesia and intubation with positive pressure ventilation are therefore indicated for exploration of all but the most superficial skin wounds, given the risk of pneumothorax during wound exploration.
44 Extensive exploration of thoracic wounds outside of the OR should generally be avoided due to the high likelihood of entering the thoracic cavity. More superficial wounds are lavaged, gently explored, debrided and moist wound management applied along with a cross-my-heart thoracic dressing. Once wounds are free of infection, they can be closed or left open to heal via second intention.
2. Timing of surgery following penetrating thoracic trauma Patients who have sustained penetrating thoracic trauma frequently present in shock and are at risk for systemic inflammatory response syndrome (SIRS) – 55% of canine and 57% of feline patients requiring thoracotomy fulfilled SIRS criteria pre-operatively in retrospective studies (Lux, 2018). General anesthesia and surgery are therefore high risk and clinicians must be aware that surgery in the early post-traumatic period may worsen the inflammatory cascade, resulting in multiple organ failure and death – the ‘second hit phenomenon’ (Peterson, 2015). Timing is therefore a balancing act between not operating too soon and creating a ‘second hit’, while at the same time not increasing morbidity and expense by delaying surgery. Current recommendations are therefore to perform surgery as soon as a patient is cardiovascularly stable, or immediately if cardiovascular stability is not possible without surgical intervention.
Take-home messages • Patients with penetrating thoracic injuries present challenging emergency cases. • The presence of a penetrating thoracic wound, rib fracture(s) or flail chest are not necessarily indications for surgery. • Initial assessment and stabilization and diagnostics to evaluate the extent of intra-thoracic injury are performed prior to definitive management of thoracic puncture wounds. • Results of diagnostic imaging and patients’ response to stabilization measures will dictate whether thoracic surgical exploration is indicated. • If thoracotomy is deemed necessary, referral to a specialty centre is recommended if possible, as soon as the patient is hemodynamically stable. • Some penetrating thoracic injuries can be managed successfully conservatively, without surgery. • Extensive exploration of thoracic wounds outside of the OR should be avoided, and even patients with seemingly superficial thoracic puncture wounds should be intubated and positive pressure ventilation provided for wound exploration.
References: • Cabon Q, Deroy C, Ferrand F-X, et al: Thoracic bite trauma in dogs and cats: a retrospective study of 65 cases. Vet Comp Orthop Traumatol. 28:448-454 2015. • Frykfors von Hekkel AK, Halfacree ZJ: Thoracic dog bite wounds in cats: a retrospective study of 22 cases (2005-2015). J Feline Med Surg. 1-7 2019. • Lisciandro GR, Lagutchik MS, Mann KA, et al.: Evaluation of a thoracic-focused assessment with sonography for trauma (TFAST) protocol to detect pneumothorax and concurrent thoracic injury in 145 traumatized dogs. J Vet Emerg Crit Care. 18:258 2008. • Lux CN, Culp WTN, Mellema MS, et al: Factors associated with survival to hospital discharge for cats treated surgically for thoracic trauma. J Am Vet Med Assoc. 253:598-605 2018. • Lux CN, Culp WTN, Mellema MS, et al: Perioperative mortality rate and risk factors for death in dogs undergoing surgery for treatment of thoracic trauma: 157 cases (1990–2014). J Am Vet Med Assoc. 252:1097-1107 2018. • Peterson NW, Buote NJ, Barr JW: The impact of surgical timing and intervention on outcome in traumatized dogs and cats. J Veter Emer Crit Care. 25:63–75 2015. • Scheepens EFT, Peeters ME, E’Plattenier HF, et al.: Thoracic bite trauma in dogs: A comparison of clinical and radiological parameters with surgical results. J Small Anim Pract. 47:721 2006. • Seamon MJ, Haut ER, Van Arendonk K, et al: An evidence-based approach to patient selection for emergency department thoracotomy: A practice management guideline from the Eastern Association for the Surgery of Trauma. J Trauma Acute Care Surg. 79:159–173 2015. • Tobias KM and Johnston SA: Veterinary Surgery: Small Animal, Second Edition. St Louis, Missouri: Elsevier. 2018. • Walters AM, O’Brien MA, Selmic LE, et al. Evaluation of the agreement between focused assessment with sonography for trauma (AFAST/TFAST) and computed tomography in dogs and cats with recent trauma. J Vet Emer Crit Care. 28:429-435 2018.
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