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Issue #20 Welcome to the Veterinary Lifeline Partner Program newsletter, brought to you by the ASPCA Animal Poison Control Center. ContentsProcedural Change to Hotline Calls Procedural Change to Hotline CallsFallout from the pet food recall in March, as well as our normal seasonal increase in calls, has led to unprecedented high call volumes coming in to the ASPCA Animal Poison Control Center. Many of these are “information only” calls about the recall, in which animals are not affected. In order to help filter out calls that do not really need to go to APCC veterinary professionals, we have instituted a Help Desk staff to triage calls and send them to the appropriate staff. What this means to you is that when you call the APCC this summer, you will initially speak with a Help Desk operator, who will ask for basic information on the case, then transfer the case to the appropriate veterinary staff after assigning a case number and follow-up number. In times of high-call volume, this may mean a wait time between speaking with the Help Desk staff and speaking with a veterinary professional if all of our veterinary staff are engaged in calls. We appreciate your patience during these busy times and hope this new procedure will help us answer calls as quickly and efficiently as possible. What's New on the APCC Hotline?In March, a nationwide pet food recall was instituted due to reports of cats and dogs developing renal insufficiency subsequent to ingestion of a variety of brands of pet food manufactured by Menu Foods. Later tests would determine that the contaminants melamine and cyanuric acid were thought to be responsible for the crystalluria and renal damage that developed in animals ingesting contaminated foods. In response to the recall, the ASPCA has developed an online resource center to provide pet owners and veterinarians with up-to-date and accurate information. Included on the website are links to:
Did You Know?The ASPCA Animal Poison Control Center currently has 10 board-certified toxicologists (American Board of Toxicology and/or American Board of Veterinary Toxicology) on staff! And Did You Know?That in calendar year 2006 the ASPCA Animal Poison Control Center managed more than 116,500 cases! Summer Hazards
Low Toxicity: (may cause gastrointestinal upset, but unlikely to cause serious problems unless very large amounts are ingested)
Moderate toxicity: (may cause significant signs beyond mild gastrointestinal upset)
High toxicity: (potential for very serious or life-threatening signs)
Hot Links for the SeasonPoison prevention for pet owners: Refer clients to our website to read about proper use of flea products on their cat, poisonous plants to watch out for (find lists of toxic and non-toxic plants, and 10 most common poisonous plants), and tips for making their homes “poison proof” for their pets. For pesticide information, search Extoxnet at http://extoxnet.orst.edu/ghindex.html For information about fertilizers, visit http://apps.ecy.wa.gov/fertilizer/choice.asp For toxic plant information, visit the University of Illinois poisonous plant garden at http://apps.ecy.wa.gov/fertilizer/choice.asp Need to identify a plant? The USDA has a database that can help you and your clients identify plants in their pets’ environment. Practice Tips—How You Can Help Us to Help You Better!
Ask client if their pet is having life-threatening signs prior to getting off the phone with them. We often receive calls from pet owners who have been instructed to call us and get a case number prior to coming in to the clinic. While we are always happy to help these clients, occasionally their pets are already showing significant or life-threatening clinical signs. It may be more beneficial for you to call us while they are on their way, or call us once the patient has been stabilized. Ask client what their pet was exposed to, if their pet has prior health concerns, and if their pet is showing any signs before recommending they induce vomiting at home. Emesis is not recommended in cases of ingestion of caustic materials, petroleum products or products that may cause rapid, life-threatening signs. Patients with underlying problems like heart disease or seizure disorder may be at risk if emesis is induced. Inducing emesis in a patient that is already showing clinical signs is unlikely to be beneficial and may exacerbate their clinical signs or lead to other problems, such as aspiration. Instruct the client to bring the product container or pill vial in to your clinic when they bring the patient. This may allow for better identification of the product, and we will then be able to provide you with more detailed treatment recommendations. Please let your client know there may be a fee for the consultation. Human poison control centers receive government funding from tax dollars and therefore do not charge a fee. Your client may expect that an animal poison control center would be a free service as well. If the first time they hear about the fee is on our recording, they may be surprised or agitated. They may even hang up prior to speaking with someone here. This will delay the ultimate goal of obtaining immediate management information for their pet. Medication Update: IbuprofenIbuprofen is a widely used NSAID available as an over-the-counter medication in 50, 100, and 200 mg pills, as well as in liquid formulations. Prescription strength ibuprofen is available as 400, 600 and 800 mg sizes. Combination (cold and sinus) products are also available—many of these contain decongestants such as pseudoephedrine, which can cause significant CNS effects. The published therapeutic dose for ibuprofen in dogs is 5mg/kg, but it is not recommended for therapeutic use by APCC due to the risk of gastric ulcers and perforation. Generally, the target organs with ibuprofen toxicosis are the GI tract and the kidneys. Signs of toxicosis may occur within hours or may be delayed up to 2-3 days. With acute ingestion of 25-50 mg/kg, GI irritation or ulceration is possible. Although the published lethal dose is approximately 600 mg/kg, dogs ingesting dosages greater than 120 mg/kg are at risk for acute renal failure. Dosages exceeding 400mg/kg may also cause severe CNS signs including ataxia, seizures and coma. These dosages are guidelines for healthy dogs, as geriatric or juvenile dogs may be at increased risk for toxicosis at lower dosages. Cats, in general, are more sensitive to NSAIDS. Generally, healthy adult cats are thought to be about twice as sensitive as dogs to ibuprofen. Ferrets are also sometimes exposed to ibuprofen, and even just one pill can be lethal. Recent ingestion of ibuprofen may be managed by emesis induction and activated charcoal administration. Induction of emesis is contraindicated in animals showing significant clinical signs, animals with other health issues (e.g. cardiac disease, seizure disorder), and if more than 2 hours has elapsed since ingestion. Depending on the amount if ibuprofen ingestion, multiple doses of activated charcoal may be recommended, as enterohepatic recirculation occurs with many NSAIDS, including ibuprofen. Gastrointestinal protectants (sucralfate, an H2 blocker, and misoprostol) are normally recommended for 7-10 days. For ingestions where renal injury is possible, fluid diuresis should be instituted and maintained for at least 48 hours. Baseline serum chemistries and monitoring renal values daily for at least 48 hours are also routinely recommended if the patient is at risk for ARF. Case StudyComatose dog presents to emergency clinic : A 4 year old, 17 pound, spayed female Jack Russell Terrier named Isabella (“Izzy”) was presented to your emergency clinic comatose. Physical exam findings were pale mucous membranes, hypothermia (97 degrees F), bradycardia (HR 60 bpm), and normal systolic blood pressure. Pupils were normal in diameter and unresponsive to light. Owner also reported that there had been vomiting and marked diuresis earlier in the day, prior to Izzy collapsing. Fluids were started, the patient was intubated, and blood and urine samples were obtained. Question 1: Metabolic, traumatic and toxic differential diagnosis for coma were considered due to the abrupt onset of the clinical signs in an apparently healthy dog. Without a full history, what are some possible differentials? Answer: trauma, hypoadrenocortism, hypoglycemia, poisoning (e.g. alcohol, marijuana, ethylene glycol, barbiturates, ivermectin), acute intracranial hemorrhage (e.g. anticoagulant rodenticide intoxication), ischemia, inflammatory or infectious brain disease, post-ictal coma. A history was obtained from the owner. There was no known exposure to any of the above poisons mentioned. Dog was with the family in the back yard swimming all day in a treated in-ground swimming pool. The CBC was unremarkable. Urine specific gravity was 1.008. Coagulation profile was normal. There were a number of serum biochemical profile abnormalities: glucose 51, sodium 120, potassium 2.9, chloride 99, total protein 2.9. Radiographs were negative for pulmonary edema. Question 2: What is the patient’s illness most likely due to based on the diagnostic findings and physical exam? a. Drowning b. Pool chemical poisoning c. Addison’s disease d. Water intoxication e. Trauma Answer: d. Water intoxication Discussion:
Water loading results in dilution of serum sodium. Since sodium is the major determinant of plasma osmolality, dilutional hyponatremia results in hypo-osmolality. Decreased plasma osmolality produces an osmotic gradient which favors the intracellular movement of water in the brain, causing swelling. Signs resulting from cerebral edema may include ataxia, obtundation, seizures, and coma, and may be referred to as hyponatremic encephalopathy. Pulmonary edema may also occur. Question 3: Now that we have our diagnosis, what fluid therapy should be instituted as part of the treatment in this case? a. None. Restrict water for 24 hours, with close monitoring b. 3% NaCl. Bolus initially, and then 2X maintenance until serum sodium reaches a normal level c. Increase sodium levels at a rate of 0.5 mEq/L/h until sodium levels reach 125. d. None of the above. Answer: c. Increase sodium levels at a rate of 0.5 mEq/L/h until sodium levels reach 125 Severe, symptomatic hyponatremia of acute onset (<24 48 hours duration) can cause seizures and cerebral edema, requiring prompt and aggressive treatment. However, it is important to realize that raising the serum sodium concentration too rapidly can result in CNS damage (myelinolysis). In a dog with a sodium level of 125mEq/L or over, it is safest just to fluid-restrict with close monitoring. In dogs that are symptomatic, and have a serum level of <125mEq/L, use sufficient normal saline to raise serum sodium by approximately 5%, at a rate of 0.5 mEq/L/h, to improve the cerebral edema without risking myelinolysis. After that point, fluid-restrict with careful monitoring. These simple calculations may provide a guideline to assure that treatment is adequate, but not too aggressive. This 7.7 kg patient has a serum sodium of 120mEq/L (your lab normal is 155 mEq/L). A 5% increase in serum sodium would require adding 6 mEq/L (120 X 5% = 6). In this patient, this would be 28 mEq of sodium (0.6 X 7.7kg X 6mEq/L). Note that 0.6 refers to volume of distribution. If normal saline is used, this would require an infusion of 182 ml (28mEq/154 mEq/L X 1000 ml/L) in this patient. 6mEq/L / 0.5 mEq/L/h = 12 hours………so give 182 ml over 12 hours. Question 4: After fluid requirements are determined, what other monitoring parameters are important in a water intoxication case? Answer: Sodium, q 1-2 hours Blood glucose; dextrose prn for hypoglycemia Potassium; potassium supplementation if < 2.5 mEq/L PCV and TP Urine output (normal is 1-2ml/kg/hour) CNS monitoring CV monitoring: HR, rhythm, BP Body temperature Monitor for pulmonary edema Hotline Humor
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