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Surgical Management of Canine Hip Dysplasia-Part IIOperations: Two Viable Options-Modern technology and an old standby method are analyzed as CHD treatmentsBy John C. Cargill, M.A., M.B.A., M.S. and Susan Thorpe-Vargas, M.S. This is the eighth and final article in a series on canine hip dysplasia. What follows is written from the perspective that the readers of the series are serious and conscientious breeders who are the guardians of the genetic pools that constitute their breeds. While this series of articles will not replace a stack of veterinary and medical texts, it is a relatively in depth look at the whole problem of canine hip dysplasia. Furthermore, the series is designed to be retained as a reference. When you finish reading this series, you will have a sufficient background to make rational breeding choices and will be able to discuss the subject from an informed basis with your veterinarian. You may not like what you read, but you will be more competent to deal with the problem. Conclusions from Part 1: Genetics is the foremost causative factor of canine hip dysplasia. Without the genes necessary to transmit this degenerative disease, there is no disease. Hip dysplasia is not something a dog gets; it is either genetically dysplastic or it is not. An affected animal can exhibit a wide range of phenotypes, all the way from normal to severely dysplastic and functionally crippled. Hip dysplasia is genetically inherited. Conclusions from Part II: While environmental effects, to include nutrition and exercise, may play a part in mitigating or delaying the onset of clinical signs and symptoms, hip dysplasia remains a genetically transmitted disease. Only by rigorous genetic selection will the incidence rate be reduced. In the meantime, it makes sense to have lean puppies and to avoid breeding animals from litters that showed signs of hip dysplasia. It is probable that even normal exercise levels may increase the phenotypic expression of CHD of a genetically predisposed dog. Stay away from calcium supplementation of any kind; all it can do is hurt. There is no conclusive evidence that vitamin C can prevent hip dysplasia, but there is some evidence that vitamin C may be useful in reducing pain and inflammation in the dysplastic dog. Fortunately, large doses of vitamin C are readily excreted, but it is still possible to cause inward side effects with megadoses. Conclusions from Part III: Canine hip dysplasia can be difficult to diagnose, as a number of other orthopedic, neurological, autoimmune and metabolic problems may mimic it. Controversy surrounds the question of positioning for hip X-rays and what part joint laxity plays in hip dysplasia. Hip dysplasia may be more common in large and giant breeds and is one of the most overdiagnosed and misdiagnosed conditions. Conclusions from Part IV: Sadly, no breed registry in the United States requires genetic screening of parents as a prerequisite for litter registration or even offers a "fitness for breeding" certification. The current registries for hip dysplasia (and other genetically transmitted problems) cover so little of the American Kennel Club-registered dog population that their impact so far has been minimal. The tools we need are there. Joint responsibility for failing to use the tools at hand lies with the AKC, United Kennel Club, parent clubs and individual breeders. Conclusions from Part V: The two major methods of diagnosing canine hip dysplasia available to the fancy in the United States are that followed by the orthopedic Foundation for Animals and PennHIP. Both are diagnostic; however, the hip-extended protocol followed by OEA may produce false-negative results. The protocol followed by PennHIP has a prognostic capacity through the use of statistics and a carefully guarded data base that allows a prediction to be made with respect to the probability of phenotypic expression of canine hip dysplasia. No one has a clear quantification of the gray area between obviously clear and obviously dysplastic hips. Conclusions from Part VI: For many animals, canine hip dysplasia is a manageable condition, and they can lead relatively normal and active lives given that caution is exercised. Every dog is different in its response to pain and the treatment protocol needs to be tailored specifically to the particular animal. Only aspirin and phenylbutazone ("bute") are FDA-approved drugs for use in dogs, but they are not without serious side effects. Corticosteroids are dangerous and may require experimenting to find proper dosage levels and intervals. Favorable results have been reported from chiropractic, physical, drug and nutritional therapy. Conclusions from Part VII: Surgery is a viable option given the suitability of the candidate animal, the financial resources available, the expected activity level, longevity and the use and value of the animal. Choice of intervention, whether medical or surgical, and activity level depend upon the disease process. Problems with certain procedures may be associated with improper patient selection relative to the stage of the disease. To be fair, patient compliance, i.e., owner post-operative management, may also be a significant factor.
Surgery is indicated when:
In this final article we will explore two surgical options not previously discussed. The first is an old standby that has relieved the pain and suffering of many a dysplastic dog over the years. It is radical and invasive surgery, but under the right circumstances has produced very acceptable results. The second is modern technology in a modular form that produces exceptional, though expensive, results. The beauty of this approach is that through careful selection of components, fit to the animal's skeleton can be optimized.
Femoral Head and Neck Excision (Ostectomy)Surgical options for the treatment of canine hip dysplasia have, for the most part, been adaptations of human orthopedic procedures. In 1943, a Lancet article (British medical journal) described a surgery done in 1929 to relieve the pain caused by a tubercular hip joint in a human. This was possibly one of the first complete excisions of the femoral head and neck seen-- at least it was the first example we have been able to find in the literature. Since its inception, this procedure has been modified and used extensively by veterinary surgeons. Often considered an alternative to total hip replacement, the femoral head ostectomy is sometimes the only affordable surgical option available to many dog owners. While there is significant potential for long-term complications, femoral head ostectomy should be carefully considered within its narrow recommended parameters. A prolonged recovery, muscle atrophy and "bed sore"- type ulcers are frequent problems associated with this procedure. Best results are achieved and fewer complications are encountered when the dog weighs less than 50 pounds. Some clinicians feel that the procedure is most effective for dogs less than 35 pounds.For dogs weighing more than 50 pounds, the femoral head ostectomy has been modified to include a muscle "sling" to support and cushion the femoral shaft. The sling is formed from the biceps femoris muscle (biceps muscle of the thigh). Two other options include using a part of the gluteal muscle (buttocks muscle) to pad the area between the excised femoral shaft and the pelvis, or using the joint capsule itself to accomplish this. These "pads" are sewn into place to fix their position. Over time, the muscle pad is transformed to a fibrous mass that is better able to absorb the impact of the forces exerted by the femor. Nothing will replace the near-frictionless and hydrostatic dampening of the cartilage of the original joint when it was in good condition, but if forces are limited, the muscle pad has been shown to serve well in this function in many cases. Once the femoral head and neck have been removed, the surgeon takes the joint through a complete range of motion. This ensures that there are no obstructions to normal articulation. The muscle pad is sewn into place so it will attach securely to the acetabulum. The clinician also checks for crepitus, which is a dry, crackly sound. Ovary crepitus may indicate that not enough of the femoral neck was removed or that bony fragments are still at the excision site. Both conditions would cause loss of function and pain after surgery. It is much better to reduce the problem at the time of surgery than to have to go back into the joint a second time. As mentioned before, femoral head excision tends to be more effective and fewer complications are encountered when the dog weighs less than 50 pounds. A study published in 1988 evaluated the use and efficacy of the biceps femoris muscle sling. Sixteen dogs with normal hips were given the biceps femoris muscle sling surgery and six normal dogs were given the conventional excision of the femoral head and neck. While both control and treatment animals had similar post-surgical limb functions, there was marked edema and swelling of the affected limb in half of the dogs with slings and not in the control dogs. Four of the sling dogs developed post-operative infection and all of the treatment animals had elevated temperatures after the procedure. Their results indicated that the added risk of infection and complications was not justified and that further clinical trials needed to be run before the efficacy of this adjunct treatment could be established. For those considering this type of surgery, it should be noted that this is a strictly end-stage salvage procedure. Only those animals demonstrating severe bony changes in the coxofemoral joint and clinical signs of pain should be considered for this procedure. Also, excisions without adding a prosthesis shortens the leg, which affects the gait, and the biceps sling can cause a slight adduction (drawing in toward the center line) of the affected limb during exercise. On the positive side, this procedure has worked well over the years and is still the standby short of total hip replacement.
Total Hip Replacement/ Total Hip ArthroplastyThe first human total hip replacement was performed in 1891 using an ivory ball-and-socket joint that was attached to the bone with nickel-plated screws. After this pioneering effort, replacement of just the femoral head or the acetabulum (unipolar) was the accepted practice until the 1950's. Later, the bipolar procedure (replacing both the femoral head and the acetabulum) was adopted as the preferred way to achieve long-term success. Better results were obtained, too, after the advent of polymethylmethacrylate (PMMA, or bone cement, which was approved by the FDA in 1967. Not only was the prosthesis stabilized by the cement, but its use was effective in preventing bone resporption where metal contacted bone. Orthopedic surgery has never been the same since.In 1953, the first unipolar arthroplasty performed on a canine was described by R.E. Brown. His procedure replaced just the femoral head with a stainless-steel prosthesis. It was not until 1957, though, that H.A. Gorman did the first total bipolar hip replacements on 53 military working dogs. Much of the work done today is based on Gorman's truly pioneering efforts. Besides the secondary osteoarthritis associated with canine hip dysplasia, total hip replacement is indicated for failed femoral neck and head excisions, irreparable femoral head and neck fractures, non-reducible chronic hip luxations, avascular necrosis of the femoral head and repair of a failed total hip arthroplasty. Major surgical failure lead directly to a requirement for total hip replacement. In a nutshell, when all else has failed, especially surgical procedures, total hip replacement may be the solution to restoring function and a pain-free quality of life. The ideal candidate must have obtained adult growth, usually between 9 to 12 months of age, and must have obtained at least 30 pounds lean weight (no fat little dogs need apply). Other contraindications include infection anywhere in the body, anemia, neurological disease and concurrent orthopedic problems. A dog with arthritic hips and pain-free normal function is not a candidate for total hip replacement. The most recent innovation developed for this type of surgery is the use of modular components in a sort of "mix and match" attempt to optimize the fit of the prosthesis. In June 1990, a canine modular hip prosthesis and instrument system was introduced at Ohio State University and marketed under the name of BioMedtrix. This system has the obvious advantage of being able to customize the fit of the various prosthesis components to better match the dog's original skeletal conformation. Thus femoral neck lengthening can be accomplished through choosing a particular femoral head and a particular femoral shaft. Note from Figure 1 that there is a set of prosthetic hip components for virtually any dog; specifically there are five-stem sizes, four standard and one nonstandard, acetabular cup sizes and three neck lengths\ offsets. Figure 2 shows an example of the prosthetic acetabulum, femoral head and neck. Figure 3 shows a "junk" hip on a 1 and a half year old Labrador Retriever. Figure 4 shows the same animal eight years and one month post-surgery. This ought to dispel doubts as to the length of benefit to be derived from total hip replacement. Look at the X-rays for a while. This is a good result, and it shows what can be expected from the technology. Although expensive (our quick, non-statistical survey revealed $1,300 to $1,600 per hip was common), replacement of the arthritic hip with the appropriately sized mix of prosthesis components allows early if not immediate post-operative use of the limb. Most dogs are able to resume their normal level of activity within two months after surgery. Where there is clear indication that conditions will only worsen with time, a total hip replacement may make social and economic sense consistent with the age, purpose and value of the animal and the financial condition of the owner. We found that though results are not guaranteed, they tend to be consistently good to excellent, as supported by reports in the medical literature. Complication due to infection is the most common occurrence associated with hip replacement and is directly related to the number of surgeries and the duration of the procedure. In dogs, blood-borne infections have been reported at 22 to 28 weeks after surgery. Infection rates in the 1970s ranged from 7.7 to 11 percent. More recently, infection rates of 1.5 to 3 percent have been reported. Another complication that occurs with this surgery is a condition called "cement disease" or aseptic loosening. A fibrous membrane normally develops between the bone and the cement. With cement disease, however, a synovial like membrane containing particulate debris develops that produces large amounts of bone resorbing factors such as prostaglandin E2, collagenase, interleukin-1 and tumor necrosis factor. Newer techniques using a cement gun to introduce PMMA under pressure have decreased the incidence rate of cement disease. Mixing gentamyacin and the cephalosporins in the cement has also reduced the rates of infection. Another complication due to the use of cement is sciatic neuropraxia (the inability of the nerve to conduct impulses). Nerve contact with PMMA during its exothermic or heat-generating reaction has been implicated. How well does a total hip replacement work? Very well, indeed. Olmstead, Hohn and Turner (1983) did follow-ups on 221 total hip replacements done between 1976 and 1981. After a four-week convalescent period, 216 cases (91.2 percent) had satisfactory function. A follow-up study of 174 THRs was done with 95.2 percent of the cases being restored to satisfactory function. We conclude that the total hip replacement, in suitable candidates, provides exceptional results. Olmstead boasts, as well he should, that one of his THRs won an international field trial. Total hip replacement restores function and relieves pain. Be aware that surgery cannot undo generations of genetic makeup, or prevent that which is predisposed. Total hip replacement is not prophalaxis to the problem; it is but a band-aid to the underlying genetic problems. Conclusions: Femoral head and neck ostectomy and total hip arthroplasty are two of the major surgical options available to the owner of a dysplastic animal. If economically feasible, the THA/THR option is the more viable in terms of predictable outcome in larger animals. In smaller animals, favorable results have been reported with the femoral head and neck ostectomy, though obviously, somewhat less than total function is restored. With the advent of the use of PMMA and adjunct of antibiotic therapy, infection and "cement disease" rates have dropped remarkably during the past decade to the extent that they should be viewed as manageable concerns. There is no substitute for genetic screening and refraining from breeding, no matter how attractive a particular breeding might be unless there is a clear indication that the parents, their siblings and get are free of hip dysplasia. To that end, we support the concept of open registries and place the blame for much of the genetic disease we find in the fancy today squarely on the shoulders of the various registries that have the power to make a difference. Until the time that the genetic disease aspect is recognized and successfully handled, there will a continued necessity for the surgical option. We, the authors, wish to thank those professionals and caring veterinarians and researchers who have provided much of the information, without which this series would have been impossible. They not only gave generously of their time, but even shared unpublished manuscripts and unpublished manuscripts and unpublished insights to the various procedures. The result has been a survey of the recent literature with comments extracted from those at the very forefront of technology. Controversy has raged throughout the research process as the many professional opinions struggle for primacy. We have attempted to present not only the mainstream but also the fringe where there was adequate documentation of beneficial results. Special acknowledgment goes to Doctors of Veterinary Medicine Marvin Olmstead, Gail Smith, Barclay Slocum, William Inman, Daniel Richardson and Terry Braden, all of whom we found to be genuinely concerned with the welfare of their animal charges. They are truly pioneers in the treatment of canine hip dysplasia. Special thanks go to Doctors of Veterinary Medicine Rachel St. Vincent and Veronika Kiklevich of the Washington State Veterinary School. For more information about PennHIP contact International Canine Genetics Inc., 271 Great Valley Parkway, Malvery, Pa. 19355; (800) 248-8099. Special dedication goes to author Susan Thorpe-Vargas' dog-- call name "Smash," or if we're being more formal, Belaya Sobaka's simply Smashing-- a Samoyed who touched our hearts as we wrote this series. Last, but not least, we thank the readers who steered us in the right directions to those important researchers mentioned above and sincerely appreciate how DOG WORLD Editor Donna Marcel and her staff went out on a limb to approve and schedule this long series of eight articles.
References
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Poisoned!by John Cargill, MA, MBA, MS and Susan Thorpe-Vargas, M.S, Ph.D.Here’s the deal! Regardless of what others, including your vet, may have told you, in many poisoning situations, there is no time to lose. Your dog staggers towards you, collapses at your feet. What now? Is there time to call the vet? In many cases, no. This is the topic and focus of this article. In short, if you are not ready to concede to a dead dog, you must become Johnny on the Spot. As author Cargill relates from his Vietnam days, How are you going to act? The dog owner facing a poisoning situation has but few precious moments in which to collect himself/herself and to determine what to do. This is the time for immediate action, time to get something done. Question: What if you lack the tools and supplies with which to begin treatment? Answer: Dead dog. This is a hard way to start an article to be read by dog lovers, but the reality is this: If you are not prepared to treat poisoning resulting from ingesting a toxic substance, you lose. Not only do you lose, but your dog dies. Acute poisoning requires accurate assessment. The threat is not only related to the potency of the poison, but also to the quantity consumed, the duration of exposure, and to the presence of other active ingredients, such as adjuvant and solvents. The difference between immediate appropriate action and delayed response is the difference between life and death. To this end, the authors advocate that a significant effort be made to be prepared for what might happen, given the environment in which you keep your animals. Being prepared means not only having antidotes and treatment materials on hand, but it means being familiar with the signs and symptoms of poisoning, and knowing what risks are in your dog's environment. The first step in treating poisoning is prior knowledge. You have to be able to recognize that there has been a poisoning. Symptoms vary significantly from animal to animal, from substance to substance and with the amount ingested. You must be accurate in your differential diagnosis. To treat based on the wrong diagnosis is to increase the probability of death. The second step in treating poisoning is prior knowledge. You have to know the poisons that are in your dog’s environment. So many potential poisons are readily available, it is truly amazing more dogs are not poisoned. The third step in treating poisoning is prior knowledge. You must know the immediate actions required, which can include artificial respiration/resuscitation. If you are picking up on a trend here, it is intentional. Because there may be little time in which to reflect on or to research the subject, or to find a veterinarian because of time of day, or distance from a veterinary facility, etc., the owner who is not equipped with the knowledge of the symptoms, the effects of various poisons, and what treatment regimen goes with what poison, stands a very good chance of losing the dog. Remember, also, that not all poisonings are accidental. One excellent way to think of poisoning in dogs is to relate it to poisoning in human children. Whatever poisons are available for a child to ingest, are also available to poison a dog. Children and dogs tend to be attracted to many of the same things. For example, a dog walking through antifreeze might lick its paws afterwards, much as a child might put its fingers in its mouth after playing with an attractive looking puddle of green stuff on the driveway. Potential dangers in the child’s environment tend to be the same as in the puppy’s environment. According to the Agency for Toxic Substances and Disease Registry of U.S. Department of Health and Human Services,the element lead is first on the prioritized list of 275 toxic substances. (1) The poisoning of greatest concern for children is lead poisoning. That poisoning is also one of the great concerns for puppies who may chew surfaces painted with lead based paint. Since 1978 Federal regulations control use of lead in paint and other products; however, there are enough old products in your dog’s environment to constitute a very real hazard. Morgan, et al, looked at lead poisoning in 347 companion animals.(2) Ramsey, et al, concluded that succimer (meso- 2,3-dimercaptosuccinic acid) administered orally for 10 days, effectively reduced blood lead concentrations and eliminated clinical signs of lead poisoning.(3) Berny, et al, concluded that paint was the most common source of lead poisoning in dogs (537 cases) in Europe and North America 1985-1989.(4) One of the more common sources of lead is in copper water pipes with lead solder joints. In 1988, Congress banned using pipe with more than 8% lead and the use of solder with more than 0.2% lead. Note that carbon, sand and cartridge water filters do not remove lead. Only a reverse osmosis system removes lead. It is commonly believed that significant amounts of lead are present in soil and in various sources of dust that have accumulated from years of vehicle emissions from leaded gasoline. Over time, as lifestyles change, the types of toxic substances available to companion dogs have increased significantly. Lead is not the only hazard. Household cleaners are notoriously toxic. Just think Tidy Bowl® does to your dog just what it does to that which you want it to remove from the toilet bowl. Similar effects may be expected with Draino® and other drain cleaners. For most households, the area under the kitchen sink, with its cleaners, polishes and dishwasher soaps, is a chemical warfare zone waiting to happen. Likewise, the garage with its paint removers, carburetor cleaners, antifreeze, bird repellents, insecticides, rodenticides, snail bait, herbicides, fertilizers and concrete driveway cleaners, is a dangerous place, indeed, for the inquisitive puppy. Figure 1. lists easily accessible ingestible poisons and their sources. As if this were not enough, many common household and garden plants are extremely toxic. It is a wonder that more dogs and children are not poisoned. The opportunity is there. The best way to treat poisoning is to prevent access to toxic substances. While this sounds good at first, it is not always possible to do, as will become quickly evident when scanning the Figure 2. list of toxic plants. Even the landscape timbers edging the flower beds tend to be toxic, having been preserved to prevent termite infestation and wood rot. The mole holes may be poisoned with strychnine, out of reach of your dog. The mole, however, may die above ground and be scavenged by the dog. Strychnine, whether or not in a mole, is strychnine nonetheless. The medicine cabinet is another major repository of doggie-killing substances. Over the counter analgesics/NSAIDS are responsible for many poisonings, and are not safe for dogs, except in very narrowly defined amounts. The following are presented to make the point that commonly available over-the-counter drugs often given to dogs by their owners are potentially dangerous at some level of ingestion. The Georgia Animal Poison Information Center over a 19 month period, 1989-1990 documented 240 cases of NSAID toxicosis through administration by owners or accidental consumption of improperly safeguarded drugs.(5) The most common cases were ibuprofen, acetaminophen, aspirin and indomethacin. Aspirin (salicylic acid) Toxic doses disrupt the acid/base balance and may result in metabolic acidosis (low blood pH) or compensated respiratory alkalosis (high blood pH). Symptoms include restlessness, hyperventilation, deafness, tachycardia (rapid pulse), nausea, vomiting, hyperthermia (high temperature), dehydration, pulmonary edema (abnormally large amounts of fluid in intercellular tissue spaces), acute renal (kidney) failure, hypokalaemia (less alkaline than normal), hypoglycaemia (abnormally low blood glucose levels), hypothrombinaemia (deficiency of thrombin in blood—leads to abnormal bleeding). Stupor and coma are indications of severe poisoning. Pepto- Bismol®, commonly used to combat upset stomach and diarrhea, also contains salicylates (aspirin), and must be evaluated for use with all of its active ingredients in mind. NSAIDS are non-steroidal anti-inflammatory drugs with narrow safety ranges. Acute poisoning may produce symptoms of nausea, vomiting, epigastric pain, deafness, dizziness, and oliguria (diminished urine output relative to fluids intake). Apnea (cessation of breathing) and near coma, hepatic (liver) and renal (kidney) failure are possible. Mefenamic acid preparations (Ponstel®) are prescription NSAIDS used to treat moderate pain and dysmenorrhea and may cause convulsions in overdose quantities. Note: acetaminophen is found in many over-the-counter products with antihistamines and decongestants (Co-Tylenol®, Nyquil®, etc.). With the advent of widespread drug abuse, it is not uncommon to find dogs getting into the stash with the result that dogs, too, overdose. Opiates remain the ultimate drug of choice for abusers, however cocaine and barbiturates and steroids are also commonly abused. Respiratory depression is the most important toxic effect of the opiod analgesics, and death is common from respiratory arrest. Symptoms include drowsiness (on the nod), coma, shallow respiration or apnea, miosis (excessive contraction of the pupils), hypotension (lowered blood pressure) and hypothermia (low body temperature). This article contains a number of charts and tables. It is not practical to memorize them; therefore, we suggest that you save this article and keep it handy in your dog medicine cabinet for reference in case of poisoning. Probably the easiest way to think of poisons is by category. This organization makes it possible to treat a class of poisons with relative confidence, even when the identity of the exact poison is unknown. Figure 1. Lists the categories we have found helpful. Please note that common classification schemes are ordered by symptom, by treatment, or by mechanism of poisoning. For the dog owner, who rarely treats for poisoning, diagnosis by category of poison is probably the most important information that can be given to the attending veterinarian. We recommend that you keep a copy of Michelle Bamberger, D.V.M.’s book Help1 The Quick Guide to First Aid for Your Dog, Howell Book House, NY, and the revised and expanded Dog Owner’s Home Veterinary Handbook, by D.G. Carlson and J.M. Griffin, put out by the same publisher. Books are nice, but if you really need help and you are unsure of the situation, the telephone number for the National Animal Poison Control Center run by the American Society for Prevention of Cruelty to Animals, is the number to call. This non-profit database is maintained by Dr. Louise M. Cote and her husband Dr. W. M. Buck. There is a $30 fee for a consultation. It is worth every penny, as these two veterinarians are the premier consulting toxicology veterinarians, and have thousands of successful interventions under their belts. Their number is 1-800-548-2423/1-900-680- 000 and a direct line to Dr. Cote is (217) 333-2053. Being prepared also means that you must have certain supplies on hand. The absolute minimum is: Syrup of Ipecac, 3% hydrogen peroxide, activated charcoal and vegetable or mineral oil. Some breeders also keep Valium® on hand to reduce convulsions, or to take themselves, we are not sure which. Author Cargill routinely keeps a blood volume expander and IV kit to treat for shock. If you are comfortable with starting an IV, nothing beats extra blood volume in preventing shock or dehydration. If a dog is on a farm where concentrated agricultural pesticides are mixed, it might be worthwhile to keep atropine and 2-PAM in case of organophosphate poisoning. Crop dusters regularly stock atropine auto-injectors (like those used by military when under chemical threat) and 2-PAM in case of accidents. Organophosphates do not have to be ingested. They work quite nicely on contact. The lethality of modern toxins is such that the niceties of having a veterinarian administer all treatment is overcome by events and a lack of time in which to respond.
When a dog has been poisoned, it will often present with drooling,
vomiting, fatigue or
weakness and convulsions. While many things will make a dog drool, vomit,
be tired or
have convulsions, this combination in an otherwise healthy animal, not
known to have
central nervous system problems from trauma, high fever or distemper,
etc., is
immediately suggestive of poisoning. Following is a listing of
categories of poisons and
their associated treatments. The immediate first aid generally breaks out
into two
protocols:
It is extremely important to get these two protocols correct. For poisoning with acids, alkalis, petroleum distillates and stinging nettles, DO NOT INDUCE VOMITING. These substances can cause great damage coming out, especially if aspirated. In both protocols, treatment for shock and other supportive therapy such as CPR, IV fluids, oxygen, etc., may be required. In any case, standard first aid procedures of checking the airway, breathing and circulation should be part of the initial evaluation. Note: Some poisons have antidotes, others have none. The sooner the poison is removed or absorbed or moved through the system, the less its effects will be. Gastric emptying is not controversial, but Pond, et al, in a prospective randomized controlled trial of 876 humans, aged 13-82, presenting with overdoses occurring within twelve hours prior to presentation, concluded that there was no apparent benefit of gastric emptying in drug overdose patients.(6) They recommend that gastric emptying be omitted in adults with acute oral overdose, to include those presenting shortly after ingestion and exhibiting severe signs and symptoms. On the other hand, Teshima, et al, determined that induced vomiting could recover 42-65% of acetaminophen ingested.(7) The American College of Emergency Physicians (ACEP) recommends keeping Ipecac syrup for inducing vomiting and activated charcoal for gastric lavage.(8) Similarly, Bamberger in Help! The Quick Guide to First Aid for Your Dog, recommends the use of 3% hydrogen peroxide, 1-2 teaspoons by mouth every 15 minutes until vomiting occurs; or syrup of ipecac, 2-3 teaspoons by mouth, given once. For dogs with cast iron stomachs that do not respond to hydrogen peroxide, ipecac or soapy water, your vet may try Apomorphine. After vomiting, follow with activated charcoal mixed with water to a slurry consistency (1 teaspoon for dogs <25 lbs., 2 teaspoons for dogs >25 lbs.)(9) A quick survey of medical and veterinary texts yielded generally the same recommendation as Bamberger. With the above caveat having been made, we will address the various categories of poisons and their related treatment protocols. Common examples are given following the category name. Please note that it is impossible to provide a comprehensive list of products in each category, and some products contain more than one active ingredient. For example, there are many aspirin combinations, and many narcotic combinations.
Plant PoisonsPoisonous plants are common, and are within easy access for most dogs. It is virtually impossible to eliminate poisonous plants from most dogs’ environments. A complete list of poisonous plants is beyond the scope of this article. Treatment generally involves inducing vomiting, giving activated charcoal slurry, with CPR and supportive treatment as necessary.Plant poisoning mechanisms are extremely varied, but can be broken down into the twelve basic categories listed in Figure 3. As with the previously listed non-plant toxins, treatment varies somewhat by category. Most adult dogs leave toxic plants alone, but this cannot be said of puppies before their brains have caught up with their mobility and ability to mouth, chew and swallow. Example: What puppy can resist mouthing mushrooms? Both authors have caught their puppies playing with mushrooms of various varieties. Fortunately, they never played with Amanita phalloides (death cap), A. verna (fool’s mushroom), A. virosa (death angel), or A. bisporiger (smaller death angel). Amanita sp. are abundantly available in the United States, especially in the Mid- Atlantic down to Florida and west to Texas. Expect them between October and December. There are no approved antidotes. However, the human literature does list recoveries after liver transplants! The preceding was to set the stage for other really poisonous plants like oleander and dumb cane and jimson weed and choke cherry. Figure 2. shows asterisks by exceptionally poisonous plants. Note that many of the poisonous plants are ornamentals common in the United States. Next time you trim back the English ivy, English holly, the Oleander bush, the laurel bush, or trim the privet hedge, do not leave the trimmings on the grass to be mulched up next time you mow the lawn with a mulching lawnmower. Your dog may just drop a sticky bone on a mulched pile of trimmings and go off to chew his bone later. It is not just puppies that are at risk from poisoning; adults dogs may not set out to intentionally chew or ingest a poisonous plant, but they can come by the poisons quite innocently (as in the example) or by grooming themselves.
Figure 3. One of ways the liver helps to rid the body of toxins is to chemically alter them so as to make them more water-soluble; at this point the poison can be excreted by the kidneys and to some extent the skin and lungs. But sometimes, these breakdown products, or metabolites, can actually be more dangerous in their chemically activated forms. Ethelene glycol (a major component of anti-freeze) is a good example of this. The various metabolites formed when the liver breaks down this substance will sequentially attack the central nervous system, lower the pH of the blood to fatal levels and damage the kidneys. Detoxification by the liver is carried out by three principal enzyme systems. Enzymes are proteins that catalyze chemical reactions; i.e., they increase the rate of these reactions. The first system is called Phase I. At this point in the detox cascade, chemical modification is handled by a series of mixed-function oxidase enzymes. One of the major routes is a two-step pathway involving the enzymes of the liver (cytochromes P450) and an enzyme associated with the high-density lipoprotein (HDL, or good cholesterol particle). The second enzyme is called paraoxonase or PON1. In humans, an amino acid substitution at position 192 of this protein results in the existence of two different forms of this enzyme in the serum, one with the amino acid arginine at this position and a second with the amino acid glutamine at this position. Thus, people and animals are genetically capable of breaking down poisons at different rates. One form is better for some insecticides, while the second is better for other insecticides. In addition to the activity differences observed with the two different genetic types, individuals can have varying levels of the protein in their blood. The combined effect of different levels of enzyme and its form, can cause up to a 100-fold difference in the clearance rates for a given insecticide. Much research is being carried out by Dr. Clement Furlong and coworkers at the University of Washington.14 In addition to examining the molecular basis of differential sensitivity to insecticides, they also are working on developing treatment procedures for organophosphate poisoning in humans and animals. Drs. Furlong, Lucio Costa and graduate student Wan-Fen Li have shown injected PON1 provides protection against organophosphate poisoning either pre- or postexposure. They are working on procedures for producing large quantities of recombinant enzyme. One other comment should be made regarding exposure of young animals (or humans) to organophosphate compounds processed through the P450/PON1 pathway. Newborns have very low levels of PON1 and are correspondingly much more sensitive to these compounds, so extreme caution should be taken to avoid such exposure. Those metabolites not excreted by the kidneys are processed by the Phase II system enzymes. These are fat-soluble toxins preferentially stored in the fat cells. Phase III enzymes have a similar function. However, if there is a lack of Phase II enzymes, the "activated" metabolites produced by the Phase I enzymes build up in the bloodstream and wreak havoc on the liver and kidneys. If the level of Phase I enzymes is high and the amount of Phase II enzymes is low, there is great danger of a toxic detox reaction, because the intermediate metabolites are processed too slowly. Nutritional support favors the sequential elimination of toxins and can prevent or ameliorate the damage done to the liver and kidneys. What follows are specific recommendations for the canine only. Cats have unique metabolic and dietary needs that cannot be addressed here.
RecoveryThe road to recovery after a major poisoning episode may be long and uphill. Nutritional support is considered by many to be effective. First reduce the workload of the liver and the kidney. A bland diet of cooked white rice is recommended for several days. Do not feed any proteins or fats because these are processed by the liver and kidneys. To counteract the effects of the Phase I metabolites, some veterinarians suggest giving antioxidant vitamins and minerals. These include Ester-C or calcium ascorbate, vitamin E, selenium, beta carotene, bioflavonoids, selenium, copper, zinc and manganese, Coenzyme Q10, thiols (from garlic) and superoxide dismutase. Support for the Phase II enzymes: Do not fast the animal. Substances used by Phase II enzymes include sulfhydryl donors (N-acetylcysteine, cysteine, cystine, methionine and glutathione), sulfates (good sources are glutathione and cystine), pantothenic acid (B5), glycine, taurine, glutamine, arginine, ornithine, selenium and riboflavin. (Many of these nutritional supplements are available in Ultra Clear Plus available from Metagenics and similar manufacturers.)16 These substances can be used to speed up Phase II reactions. Glutathione levels are lowered with stress, so stress reduction especially is important when detoxing. After reviewing the symptoms, the treatment and follow-on veterinary and dietary care necessary to recover from poisoning, we think you will agree with our conclusion:
Conclusion:Prevention is better than cure. Potential for serious poisoning is everywhere. Anything you would do to poison proof your house, yard, garden, garage, etc., is worth doing for your dogs. Unfortunately, it is not feasible to remove all potential toxins from the environment. Therefore, being prepared includes knowing what toxins are in the environment, where they are located, and what to do in a poisoning situation. We suggest that dog owners conduct a survey of their animal’s environment. Write down the potential toxins to include the active ingredients in each product, and keep that survey with a copy of this article and one or both of the books mentioned immediately available for reference.
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ASPCA National Animal Poison Control Center
1-900-680-0000 $20 for 5 minutes and $2.95/minute thereafter What is the ASPCA National Animal Poison Control Center (ASPCA/NAPCC)? This 24-hour emergency service is the first only national animal-oriented poison information center in the United States. Since 1978, it has provided advice to animal owners and conferred with veterinarians about poisoning exposures. The Center's telephones are answered by licensed veterinarians and board-certified veterinary toxicologists. What makes the ASPCA/NAPCC different from other poison control centers? The Center is staffed by veterinary health professionals who are familiar with different species' response to poisons and treatment protocols. At their fingertips, they have a wide range of information specific to animal poisoning, including an extensive collection of individual cases - more than 250,000 - involving pesticide, drug, plant, metal and other exposures in companion, wild and food producing animals. This specialized information lets the experienced ASPCA National Animal Poison Control Center staff make specific, accurate recommendations for your animals, as opposed to the generalized poison information available from human poison control centers. What is the cost of this service? Depending on which option is chosen, the charge is $20 for the first 5 minutes, then $2.95/minute thereafter when using the 900 number, or $30 per case (Visa, MasterCard, Discover, or American Express ONLY) when using the 800 or 888 number. With the 800 or 888 access ONLY, the Center will make as many follow-up calls as necessary. Through the ASPCA/NAPCC Animal Product Safety Service, various veterinary medicine and chemical product manufacturers list a toll-free 800 telephone number on their products and help to underwrite cases involving those products. What is the ASPCA/NAPCC's Animal Product Safety Service? The ASPCA National Animal Poison Control Center offers manufacturers of veterinary, agricultural and chemical products an extensive animal product safety program. The program provides a toll-free telephone number which can be printed on product labels and literature, assisting owners and veterinarians with questions or suspected poisonings. The program also offers management of case records, compilation of quarterly case reports and consultations with the manufacturer's professional staff to improve product safety. Additional services are available to tailor an animal product safety program to meet each manufacturer's needs. What should be done if an animal has been poisoned?
Immediately call the ASPCA/NAPCC. Be ready to provide:
For flyers or more information about the Center's various services, please contact:
ASPCA National Animal Poison Control Center or
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