2016 WINTER: Deicing Dangers | Cranberry Juice | Marijuana | Pancreatitis | Meet Dr. Forrest Cummings, Internal Medicine
The winter season is here with the cold, snow and ice. When snow is on the ground, municipalities apply commercially prepared snow and ice melting products. Home and business owners also apply similar chemicals to sidewalks, porches and driveways. Most ice melting compounds contain salt products that can damage vegetation and hard surfaces and are toxic to people and their pets. A national survey shows that 60% of American households use rock salt and salt-based ice melt products, but only about 38% are aware of the hazards. During the winter season, part of our job as veterinary professionals is to educate our clients on the risk these products may pose to their pets.
What are the risks of the ice melting products to pets? Many ice melting salt products contain sodium chloride. With exposure of the salt to water and low temperatures, an exothermic reaction occurs that causes melting with temperatures generated up to 175F. This reaction can burn the pet’s food pads and skin with contact and can burn the mouth and rest of the GI tract with ingestion. Dogs and cats can ingest the salt by licking snow or icy surfaces or by licking their paws after being outside and picking up the ice melting pellets between their toes.
Salt toxicity is also a risk with the salt-based ice melting products. Ingestion of salt can result in high blood sodium concentration leading to thirst, vomiting, lethargy, anorexia, renal damage and possible neurologic signs including seizures, coma and even death. It is difficult to know how much salt is a “toxic dose.” Even small amounts of pure salt can be dangerous to a pet, or even a child, if ingested.
A pet with clinical signs suspected of ingesting rock salt should be assessed by a veterinarian. Serum sodium level will be elevated and reestablishing normal fluid and electrolyte balance may be necessary with fluid support and in-hospital care with 24-hour observation. It is important if hypernatremia is documented that water replacement be managed carefully because rapid shifts in water and electrolytes from the CNS to the peripheral circulation can potentiate neurologic signs.
Are there alternative products that can be safely used?
Salt-based ice melting products are the least expensive. There are other, more expensive formulations that contain potassium chloride, magnesium chloride, calcium carbonate or calcium magnesium acetate. The potassium and magnesium salts are less toxic if ingested but can still burn the foot pads. The calcium-based products do not create an exothermic reaction but still can be drying to the skin surface with exposure.
What advice should the veterinary staff give their clients to protect their pets from deicing products?
There are steps that the pet owner can take to minimize risk for the pet:
- Monitor/modify your pet’s behavior to minimize the risk of salt exposure.
- Use waterproof pet boots during winter walks with dogs.
- Wash off the pet’s feet, abdomen and chest after being outside with exposure to deicing salts.
- Use sand, crushed cinder or cat litter to provide traction on icy pavement being aware that these products will not melt the snow or ice.
- Immediately remove slush and dissolved deicing product after the snow and ice have melted enough.
- Seek veterinary care if you suspect food pad or skin burning from salt exposure or that your pet has ingested a significant amount of a salt product.
If you or your staff have any questions about the many other winter hazards, please feel free to call our emergency service anytime.
A Cranberry a Day Keeps the UTI Away
Some believe that drinking cranberry juice to prevent urinary tract infections (UTIs) is just an old wives’ tale. However, laboratory studies in dogs and humans suggest otherwise. A proanthocyanidin extract produced from cranberries has been shown to impair the adherence of P-fimbria on E. coli bacteria to the surface epithelium of the urinary system. P-fimbria are the adhesive pili coating the surface of E. coli organisms. Colonization and multiplication of E. coli cannot occur without adherence of the bacteria to the uroepithelium.
In placebo controlled human clinical trials, supplementation with cranberry proanthocyanidins reduced the recurrence frequency of UTIs caused by E. coli. The effectiveness of the extract was dose-dependent. There are no reported clinical studies in dogs or cats, so it remains to be determined whether cranberry extract would similarly benefit our patients. The appropriate dose and frequency of extract administration has also not been determined.
Cranberry juice extract would not be expected to replace treatment with antibiotics. The value in administering cranberry extract would be in preventing the recurrence of E. coli UTIs after successful treatment. Cranberry supplementation could be given concurrently with appropriate antibiotic therapy or immediately after antibiotic therapy has eradicated the infection. It is unknown whether cranberry extract has a similar inhibitory effect on other uropathogens such as Staphyloccus, Enterococcus and Proteus.
How about D-Mannose?
D-Mannose is a type of sugar. The P-fimbria of E. coli bacteria attach to the urinary tract surface by binding to D-Mannose receptors on the epithelial cells. Supplementation with D-Mannose provides alternative sites for the E. coli P-fimbria to bind, in effect competing with binding sites on the bladder surface. In one laboratory study, the addition of D-Mannose caused displacement of E. coli already bound to the epithelial surface, so D-Mannose may be helpful both for treating and preventing E. coli UTIs. Clinical studies, however, are lacking, so its efficacy in dogs and cats is purely anecdotal.
A Growing Toxicity
Marijuana is believed to be the most commonly used illicit drug in the United States. With its legalization for medical use in humans and its recent decriminalization in Colorado and Washington, the frequency with which pets are being exposed to marijuana or one of its derivatives is increasing.
The toxic chemical in marijuana is delta 9-tetrahydrocannabinol or THC. Dried leaves and flowers of the hemp plant Cannabis sativa contain 1-8% THC. Hashish, compressed resin produced from the flowering tops of the plants, contains 10% THC. Hash oil or butter, a concentrated form of hashish or marijuana in which the cannabinoids are extracted into the fat of oil or butter, can have a THC concentration exceeding 50%.
The most common means by which dogs and, uncommonly, cats are exposed to marijuana is by ingestion of home cooked or commercial products containing THC. THC is stored in the tissues of the brain, liver and kidneys. Being highly lipid soluble the chemical is also stored in fat deposits where it can remain for days. The majority of the THC is excreted via the biliary system and eliminated via the feces.
Signs of marijuana intoxication typically occur within 60 minutes of exposure and can last several days. The THC binds to cannabinoid receptors in the brain where it interacts with the neurotransmitters norepinephrine, dopamine, serotonin and gamma-aminobutyric acid inducing varying stimulatory and inhibitory signs involving the GI, cardiovascular and neurologic systems.
Signs of marijuana intoxication
- Depression or dysphoria
- Hyperstartle response
- Urine dribbling
Is it marijuana?
The challenge in diagnosing marijuana toxicity is getting the pet owner to confirm the pet’s potential exposure. Routine blood testing and imaging typically fail to demonstrate significant abnormalities. Furthermore, over-the-counter drug tests as well as laboratory tests for THC have not yet been proven effective in pets. Luckily the signs of THC toxicity, i.e. dysphoria, drowsiness, a hyperstartle response and especially urine dribbling are pretty recognizable.
What’s the best treatment?
Treatment after immediate exposure to marijuana could include induction of emesis and the administration of activated charcoal. Both would be contraindicated if the clinician feels the patient’s mental state predisposes the pet to the possibility of aspiration pneumonia. Interestingly, induction of emesis may not be effective as one of the marijuana’s medical uses is to inhibit nausea and vomiting in human cancer patients. The repeat administration of activated charcoal 6-8 hours after an initial administration should be considered to reduce GI absorption of the THC as it goes through eneterohepatic circulation.
Symptomatic supportive care should be individualized to the patient and would typically include IV fluids to ensure hydration and perfusion, external heating or cooling as indicated, and anti-anxiety therapy. More severely affected patients may require cardiovascular medications, oxygen supplementation or even ventilation. Intralipid therapy should be considered in more severely affected patients and those with prolonged duration of signs. Because THC is lipid soluble, it can be leached from the body with intralipid therapy. Close monitoring of these patients is important. Luckily THC has a high safety margin. To be lethal most dogs must be exposed to greater than 3 g/kg.
Could marijuana be beneficial for treating ill pets?
In humans, marijuana and its derivatives have been shown or suggested to have many potential medical uses including
- Stimulating appetite and reducing nausea in cancer patients
- Treatment of glaucoma
- Increasing lung capacity
- Controlling epilepsy
- Reducing cancer spread
- Slowing the progression of Alzheimer’s disease
- Reducing the pain of multiple sclerosis
- Relieving arthritis discomfort
- Treating inflammatory bowel disease
Reports of marijuana’s effectiveness for treating ill pets are very limited and at best anecdotal. Marijuana is a Schedule I narcotic. Even if you live in a state where medical marijuana is sanctioned, as a veterinarian it remains illegal for you to prescribe or recommend it to treat a patient.
If you feel you may be dealing with a pet who has a potential toxicity or desire closer 24 hours or after-hours monitoring of your patient, please don’t hesitate to give us a call. Our emergency and critical care services have loads of experience dealing with all types of toxicities.
Pancreatitis in Dogs and Cats
Pancreatitis is a disease process that affects both dogs and cats; however, there are species differences seen in clinical presentation, possible etiologies, diagnostics and appropriate therapies. In both species, the conclusive diagnosis of pancreatitis can be difficult and management challenging. The goal of this article is to provide a comprehensive overview of pancreatic disease in dogs and cats with discussion, as appropriate, of the species differences.
Pancreatitis refers to infiltration of inflammatory cells into the exocrine pancreatic tissue. Acute and chronic forms are recognized with chronic disease characterized by persistence or relapse of clinical signs, persistent laboratory abnormalities, and development of histopathologic changes in the pancreas including fibrosis and atrophy. Depending on the study referenced, 6% to 10% of cats and dogs have histopathologic signs of pancreatitis at necropsy.
What causes pancreatitis?
The etiology in most cases of pancreatitis is not determined. The most common etiology suspected in dogs is dietary indiscretion, the classic “dog got into the garbage.” The correlation with dietary indiscretion is not usually seen in cats. Other risk factors in the canine include chronic hyperlipidemia, obesity, small breed size, and prior history of GI disease, diabetes mellitus, Cushing’s disease or hypothyroidism. Viral infections (FIP, herpesvirus, calicivirus), chronic hyperlipidemia, hypercalcemia, trauma (high rise syndrome), and prior history of diabetes mellitus and gastrointestinal (GI) or hepatic disease are considered risk factors for pancreatitis in the feline.
Certain drugs can also predispose to pancreatitis. In dogs, potassium bromide, phenobarbital, and certain chemotherapies have been implicated in the development of pancreatic disease. In cats, chemotherapeutics, certain antibiotics and organophosphates have been associated with pancreatitis.
What are the clinical signs of pancreatitis?
Most dogs present with an acute form of the disease. Middle-aged to older dogs (>5 years old) who are overweight are commonly presented to the veterinarian. There may be a higher breed risk for miniature schnauzers, Yorkshire terriers, silky terriers, and miniature poodles. Common clinical canine symptoms include lethargy, anorexia, hunched stance, vomiting (+/- blood), diarrhea (+/- blood), increased respiratory rate and painful abdomen. Physical examination findings are variable with some dogs showing only lethargy and mild abdominal discomfort. More severely affected dogs may be moribund, febrile or severely dehydrated with signs of shock.
Cats tend to present with a more chronic form of pancreatitis. Symptoms may seem acute to the owner, but cats commonly develop pancreatitis in association with other chronic diseases including inflammatory bowel disease and hepatitis. Middle-aged to older neutered domestic shorthaired breed cats are overrepresented. Clinical signs with cats tend to be more nonspecific including lethargy, anorexia and weight loss. Vomiting and diarrhea are less common in cats. Abdominal pain may not be easily identified on physical examination.
It is important to remember that other diseases can present with signs that mimic pancreatitis in both dogs and cats. Acute gastroenteritis, GI obstruction or torsion, pyelonephritis, GI neoplasia and even acute back pain can present with similar clinical symptoms.
What tests are appropriate to diagnose pancreatitis?
Definitive confirmation of pancreatitis in the individual pet may be difficult. No all-typical clinical signs are present in the individual pet. There is no one test that is pathognomonic for pancreatitis except pancreatic histopathology, a test not usually indicated or pursued in the average patient. Diagnosis is based on evaluating a combination of clinical, hematologic, biochemical and imaging findings in both cats and dogs.
Every patient should receive a physical examination and a minimum database including complete blood count (CBC), serum chemistries, urinalysis, pancreatic specific enzymes, abdominal radiographs and/or abdominal ultrasound.
CBC in dogs may show an inflammatory or infectious leukogram. Mild increase in packed cell volume can be seen associated with dehydration. Thrombocytopenia can be seen in dogs with associated coagulopathy or inflammatory destruction of platelets. In cats, the CBC more commonly will show a mild nonregenerative anemia. Neutrophilia without a left shift and lymphocytosis can also be seen in cats associated with more chronic inflammatory disease.
Serum chemistry abnormalities in dogs include azotemia (prerenal and renal); increased liver enzymes (ALP, ALT, GGT, AST); increased bilirubin; increased lipids; hyperglycemia; decreased serum proteins and calcium; and possible sodium, potassium, and chloride changes associated with metabolic acidosis. In cats, increased liver enzymes (ALP, ALT, GGT); increased bilirubin, cholesterol, and glucose; and decreased potassium, calcium, and albumin are the most common biochemical abnormalities seen. Azotemia may or may not be present in feline patients.
Urinalysis, in both dogs and cats, helps characterize azotemia as renal or prerenal. Urinalysis helps assess for the possibility of primary or associated pyelonephritis. Proteinuria can be seen in dogs with associated pancreatic enzyme damage or antibody complex deposition affecting glomerular tissue.
Pancreatic specific enzymes: Classically, elevations in serum amylase and lipase have been used, in cats and dogs, to help diagnose pancreatitis, but they are not specific indicators of pancreatic inflammation. Elevated amylase or lipase can be indicative of pathology in the pet, but it may be associated with gastrointestinal, hepatic, renal or pancreatic disease. If other clinical parameters and laboratory results are consistent with pancreatitis, increases in these enzymes may support that diagnosis. These enzymes usually remain part of most basic chemistry panels.
Trypsin-like immunoreactivity (TLI) is also used clinically to assess the pancreas. Serum TLI is produced only by the pancreatic tissue and is elevated early in dogs and cats with pancreatitis, but the level diminishes rapidly after initial elevation, within 3 days in dogs and within 48 hours in cats. TLI is cleared by glomerular filtration, so it can be increased with renal disease. In both dogs and cats, a clearly increased serum TLI without azotemia is consistent with a diagnosis of pancreatitis, but the diagnosis cannot be ruled out if the TLI is normal.
Pancreatic lipase immunoreactivity (PLI) assays are considered the most sensitive and specific tests used to help diagnose pancreatitis in dogs and cats. The immunoassays are used to quantify lipase exclusively of pancreatic origin. The molecular structure of PLI is different in each species, and species-specific assays are used in the laboratory (canine PLI and feline PLI; abbreviated cPLI and fPLI). There is a wide reported sensitivity range for cPLI assays (21% to 78%) and fPL assays (58% to 100%). This variation reflects differences between study design, population of animals used in each study and severity of disease. The sensitivity of PLI assays may be decreased in more chronic or mild disease because enzyme leakage from the pancreas is diminished. Because the PLI enzyme is specific to the pancreas, the specificity of these assays is high, canine 81% to 100% and feline 67% to 100%. Abnormal species-specific pancreatic lipase results may be consistent with a diagnosis of pancreatitis in the cat or dog, but the results must be interpreted with all other clinical data. Pancreatic inflammation may be primary disease or may be secondary to other systemic illness (acute gastroenteritis, pyelonephritis, cholangiohepatitis or neoplasia).
The originally developed assay for PLI is still available at many labs along with other newer immunoassays that show similar clinical performance. These include the quantitative Spec cPL® for dogs and Spec fPL® for cats. SNAP cPL® and SNAP fPL® are available as rapid in-clinic semi-quantitative immunoassays that are most useful to help rule out pancreatitis in the patient. A normal result for these rapid assays makes pancreatitis less likely. It is important to remember to interpret the results with all other clinical factors considered.
Imaging: In both cats and dogs, abdominal radiographs may show loss of serosal detail with increased opacity in the right cranial abdominal quadrant. Outflow tract duodenum may be displaced ventrally and laterally and may be dilated with plication of the serosal margin. The transverse colon may be displaced caudally. In more chronic pancreatitis, punctate calcification in the area of the pancreas may be seen associated with calcium deposition in saponified peripancreatic fat.
Abdominal ultrasound, along with species specific PLI, is one of the best tools to help in the diagnosis of acute pancreatitis in the dog and cat. The sensitivity of ultrasound is affected by the skill of the person using this tool. Ultrasound findings may include enlarged pancreas with hypoechoic tissue and dilation of the pancreatic duct. Cavitary lesions (abscess, cyst and pseudocyst) may be seen associated with the pancreatic tissue. Other findings may include dilated hypomotile duodenum, biliary tract dilation in the liver, and peripancreatic or diffuse peritoneal fluid. There is a higher sensitivity reported for ultrasound diagnosis of pancreatitis in dogs (90%) compared to cats (35% to 70%). This may reflect the more chronic nature of the disease in cats with fewer acute tissue changes seen at the time of clinical presentation. It is important to remember that other diseases can have identical ultrasound appearance to pancreatitis. Differential diagnoses to consider with ultrasound evaluation include pancreatic neoplasia, pancreatic edema associated with hypoproteinemia or portal hypertension, and enlargement of peripancreatic structures.
What therapies are appropriate to manage pancreatitis in dogs and cats?
Medical treatment for acute pancreatitis in dogs and cats is aimed at restoring adequate tissue perfusion, limiting bacterial translocation and inhibiting the inflammatory process. No studies have evaluated the treatment modalities in dogs or cats with naturally occurring pancreatitis. Initial medical management is often started before a diagnosis of pancreatitis is obtained. Dehydration and hypovolemia are treated with intravenous fluids with electrolyte, calcium and acid base management as indicated by the minimum data base results. Colloids may be indicated in the presence of hypoproteinemia or shock. Insulin therapy may be needed if concurrent diabetes mellitus is present. In cats, stress hyperglycemia may need to be differentiated from diabetes.
Antiemetics (chlorpromazine, metoclopramide, ondansetron or maropitant) and antacids (famotidine, omeprazole) are given for vomiting. Prophylactic antibiotics are indicated in patients with shock, fever, leukocytosis or other evidence of infection or breakdown of the GI barrier such as severe diarrhea with blood.
Analgesia is important in both cats and dogs even if clinical signs of pain are not apparent. Buprenorphine, oxymorphone and/or fentanyl therapy can be used in both species. Nonsteroidal analgesics can be considered but are present risks of GI ulceration, renal failure and hepatotoxicity especially in patients with severe disease, dehydration or shock.
Many dogs with acute pancreatitis respond to fluid therapy and withholding food and water for 48 hours along with GI supportive management. More aggressive therapy is indicated for dogs that do not respond to minimum supportive care. When a coagulopathy or hypoproteinemia are present, or the patient is clinically deteriorating, fresh frozen plasma may be beneficial to treat the coagulation disorder or hypoproteinemia, and to restore a more normal protease-antiprotease balance. Heparin may be useful in treatment of coagulopathies and improving microcirculation to the pancreas. Cats frequently have combination disease with pancreatitis associated with chronic liver and GI disease. Treatment plans may need to be modified to include simultaneous treatment of liver (Denamarin®, ursodiol) and inflammatory bowel disease (metronidazole, cobalamin and steroids).
Nutritional management is important in the recovery from pancreatitis in both dogs and cats. In dogs, it has been traditional to withhold food and water for several days with the concern that feeding would continue to induce production of pancreatic enzymes that would make the pancreatitis worse. Withholding food actually leads to gastrointestinal ileus and villous atrophy. Significant catabolic deficits, increased susceptibility to GI bacterial translocation, and decreased immune function occur with protein deficits created by fasting. Withholding food from cats with pancreatitis has not been a traditional recommendation but many cats present with prolonged anorexia and may not offer to eat on their own. Enteral feeding has advantages over parenteral feeding including stabilization of the GI barrier, improvement in GI motility, decreasing the need for antibiotic therapy, and possibly decreasing hospitalization time.
Once vomiting is controlled, enteral feeding by mouth, placement of an esophagostomy tube, or nasogastric tube in both species is recommended. Parenteral nutrition or placement of a jejunostomy tube are options to consider if the patient cannot tolerate oral feedings. Low fat highly digestible protein diets are indicated for dogs with pancreatitis. In cats, there is no evidence that low fat diets prevent or treat pancreatitis. Hypoallergenic diets may be indicated in both species if pancreatitis is suspected associated with underlying inflammatory bowel disease. Oral pancreatic supplementation can be considered and may be helpful by inhibiting pancreatic enzyme secretion. Addition of appetite stimulants (mirtazapine or cyproheptadine), probiotic supplements, parenteral cobalamin, liver support supplements, or parenteral cobalamin therapy may be indicated in the individual dog or cat patient.
What is the prognosis for pets with pancreatitis?
The prognosis for dogs and cats with pancreatitis is related to the severity of their disease and response to initial therapy. The prognosis for dogs with mild acute pancreatitis is good. Severe or recurrent pancreatitis or dogs with pancreatic abscesses or necrotizing pancreatitis is associated with a more guarded prognosis. Cats usually have a favorable prognosis when presented with chronic pancreatitis. In both species, prognosis is poorer with evidence of multisystem disease (liver disease, renal disease, coagulopathy, diabetes mellitus and peritonitis). Owners need to be aware that recurrence of pancreatitis in both cats and dogs is common after the initial presentation and long-term diet, medication and supplement therapy is often necessary once the pet has been sent home. Death may result for both dogs and cats with pancreatitis if significant complications develop despite supportive therapy. Some owners may need to make decisions for humane euthanasia if cost-prohibitive therapies such as surgery or extended hospitalization are needed or if the patient declines despite supportive care.
We would like to thank our colleague from BluePearl in Illinois, Susan Yohn, DVM, MS, DABVP-Canine/Feline, DACVIM, for allowing us to use this article for Companion.
Relford R, Williams DA, Steimer JM, et al. Diagnosing and treating pancreatitis: A roundtable discussion; IDEXX Laboratories; 2006.
Armstrong PJ. Canine pancreatitis: Diagnosis and management. Western Veterinary Conference 2011.
Simpson KW. An update on pancreatitis in dogs and cats. Western Veterinary Conference 2012.
Xenoulis P. Laboratory diagnosis of pancreatitis in dogs and cats. ACVIM Conference 2013.
Armstrong PJ and Crain S. Feline acute pancreatitis. Today’s Veterinary Practice Jan/Feb 2015: 22-32.
Meet Dr. Forrest Cummings…
Internal Medicine Service
How do you go about helping ease the concerns of an upset client?
For many clients, their visit to the specialty hospital can be overwhelming. Clients make the decision to go based on recommendations by their primary care veterinarian, and I want to act as an extension of that existing relationship, not as a separate entity. If clients know that I am in constant communication with their primary care veterinarian, it makes them feel more comfortable in making decisions because they know that we are working together for the good of the patient.
What keeps you interested in cases day-after-day?
I believe it is the variety of cases that I could see on any given day. I never get bored with the cases because what appears straightforward is usually the furthest thing from it. It challenges me to never stop learning and wanting to teach others.
Tell us about a case that touched your heart and taught you something meaningful about yourself and your practice.
During my first month as an intern, a heatstroke dog came in on emergency. Despite the fact that we did everything medically for the dog, she had to be euthanized due to fatal complications. At that time, it was my most challenging case as a doctor and my first euthanasia. Although I was upset that I lost a patient, it was more upsetting that the owners lost a close member of their family. I learned that as veterinarians we need to be empathetic to others in difficult times and not just a doctor.