Volume 1, Issue 7 j November/December 2011 Feline Dermatophytosis: An Update on Diagnosis and Treatment Jeanne B. Budgin, DVM, DACVD Animal Specialty Center D ermatophytosis, or “ringworm,” is a superficial infection of the keratinized tissues including the claws, hair, and outer layer of the skin. The fungus that causes most infections in the cat is Microsporum canis (M .canis). It is an important zoonotic agent; approximately 60% of human household members are likely to develop lesions. Young, immunosuppressed, and previously unexposed animals are most susceptible; this implies a role of protective immunity in the disease. Clinical Signs The lesions in cats consist of the “classic” circular expanding alopecic lesions with or without inflammation, scale, crusts, and widespread patchy hair loss (fig 1). Miliary dermatitis, kerion reaction, onychomycosis, eosinophilic plaques, and an unapparent carrier state may also be observed. These clinical presentations are extremely variable and may closely mimic other common dermatoses including allergies. Persian and Himalayan breeds are more susceptible to infection. Diagnosis Wood’s lamp examinations frequently yield false positive and negative reactions and should not be relied upon for a definitive diagnosis. Approximately 30-50% of M. canis strains will fluoresce. Fungal culture is the diagnostic procedure of choice. Skin biopsy may also be helpful in reaching a definitive diagnosis, but is not usually necessary nor is it as sensitive as fungal culture. Dermatophyte test medium (DTM) is used most commonly for fungal culture. Dermatophytes produce a red color change simultaneously with observable colony growth, whereas non-pathogenic fungi begin to utilize the protein in the medium only after the carbohydrate source has been exhausted, resulting in a later color change. False positive DTM results occur if this late color change is incorrectly interpreted. Malassezia sp. may also produce an early color change with growth on DTM. Fungal culture may be performed by several different techniques. A hemostat may be used to pluck hairs along the advancing edge of active lesions, or hair that fluoresces on Wood’s lamp examination. If the cat has more generalized lesions, or a carrier state is suspected, a sterile toothbrush should be brushed through the entire coat to collect scale and hair. The tips of the bristles are then embedded in the media. Figure 1 : Classic lesions associated with M. canis infection: circular areas of alopecia, erythema, and peripheral crust. The fungal culture plates should be incubated for four weeks. And while specific conditions for incubation have been recommended in the past, Moriello et al. determined that colony growth and sporulation were not influenced by light and temperature. Under all experimental conditions, consistent sporulation was evident on all plates at five days. Growth may be delayed in patients who are already receiving treatment. Daily examination for white to off white, fluffy growth with a simultaneous color change is recommended. The importance of microscopic examination of the fungal hyphae cannot be over emphasized to prevent a false positive report. This is easily accomplished by grasping a piece of clear acetate tape Feline Dermatophytosis Figure 2 : Spindle or canoe shaped macroconidia of M. canis. with a hemostat and touching the sticky side of the tape to the culture growth. A drop of new methylene blue or lactol phenol cotton blue is placed on a slide and the tape is then stuck to the slide and examined at 40x. Spindle or canoe-shaped macroconidia, with thick walls, a terminal knob, and compartments with greater than 6 cells are consistent with M. canis (fig 2). Rational selection of therapy for dermatophytosis depends on several factors including the severity of the infection, the age of the patient, and the possible presence of underlying concurrent disease. Currently topical treatments for dermatophytosis are only recommended when combined with systemic therapy. The endpoint of treatment is at least two negative consecutive fungal cultures collected at bi-weekly intervals. A combination of oral therapy, clipping of the hair coat (especially for cats with long hair and/ or generalized infection), topical rinses (lime sulfur dips every 5-7 days), and environmental decontamination is necessary for effective treatment. Fungal cultures should be performed every 2-4 weeks until mycological cure, as clinical cure (the resolution of lesions) often occurs before mycological cure. Systemic antifungal therapy is the treatment of choice for dermatophytosis. Itraconazole, griseofulvin, fluconazole, and terbinafine are all effective systemic antifungal agents. Ketoconazole is considered contraindicated in cats due to the high incidence of side effects; 25% of patients may experience anorexia, fever, depression, vomiting, diarrhea, hepatopathy, and cholangiohepatitis. Itraconazole (Sporanox®, Janssen Pharmaceutica and generic) is not labeled for use in animals in the United States. However, it is considered the 2 Continued from page 1 treatment of choice for dermatophytosis in cats and is dosed at 5-10 mg/kg orally every 24 hours. Itraconazole is available as a 100 mg capsule and a 10 mg/ml solution; compounding the drug renders it less effective. Long tissue half-life and high levels in the skin, hair follicles, and glandular structures makes this drug amenable to “pulse” dosing regimens. Several dosing schedules are recommended including (1) daily dosing; (2) combined continuous/pulse therapy: daily dosing for 28 days, then on an alternate week regimen; and (3) cycle therapy: daily dosing for 15 days, followed by fungal cultures 10-15 days post treatment. The cycle is repeated until the cat is cured. Finally, treatment for two consecutive days per week is useful in preventing infection for long haired cats in contaminated environments, since relapse is common under these circumstances. Side effects of itraconazole include anorexia, depression, vomiting, weight loss, elevated ALT activity, jaundice, and hepatotoxicity. The drug should not be used in cats with pre-existing liver disease. Hepatic enzymes should also be monitored monthly during treatment. Griseofulvin (Fulvicin-U/F®, Schering-Plough) is available in two formulations: microsize dosed at 50 mg/kg orally every 24 hours or divided every 12 hours, and ultramicrosize dosed at 10-15 mg/kg orally every 24 hours or divided every 12 hours. Side effects include bone marrow suppression, increased liver enzyme activity, anorexia, vomiting, depression, ataxia, and pruritus. As a potent teratogen, griseofulvin must not be used in pregnant animals. Cats should also test negative for feline leukemia and feline immunodeficiency virus due to the potential for immunosuppressive side effects. Kittens may be more susceptible to side effects and should be monitored very closely. Fluconazole (Diflucan®, Roerig and generic) may be used effectively at a dose of 50 mg/cat orally every 24 hours or 5 mg/kg orally every 1224 hours. Fluconazole appears to be relatively safe with inappetence most commonly reported. Because it is primarily eliminated through renal excretion, doses or dosing intervals may need to be adjusted in patients with renal impairment. Terbinafine (Lamisil®, Novartis and generic) is the newest systemic agent and is available in a 250 mg size tablet. Based on pharmacologic data, a dose of 30 to 40 mg/kg orally every 24 hours is appropriate for therapy. At this dose, significantly higher concentrations are found in hair, therefore resulting in potential for pulse or cycle therapy similar to itraconazole. The drug appears to be well tolerated with gastrointestinal side effects most commonly reported. The clinical efficacy of lufenuron (Program®) has been disappointing, thus its use in the treatment of dermatophytosis is not recommended. Vaccination with a commercial vaccine, currently off the market, was also not recommended for prophylaxis or treatment, as sterile abscesses were observed at the injection site, and lesions often resolved but cats remained positive for disease, thus complicating treatment duration. Environmental decontamination must be emphasized in every case. Fungal spores are highly resistant and may survive in the environment for 18 months. Animals in the household may be asymptomatic carriers harboring spores on their coat without clinical signs. All animals should be tested and/or treated. All brushes, beds, leashes, collars, and other sources of infection should be thoroughly cleaned or discarded and replaced. Current recommendations for cleaning the environment include thoroughly vacuuming, cleansing, and disinfecting all surfaces, floors, and tolerant fabrics with a 10-20% bleach solution. Steam cleaning may also be beneficial, but professional steam cleaning should be utilized, as high water temperature is very important. In households with many animals or in breeding situations, infected animals and those that test positive on fungal culture should be isolated for the duration of treatment. Owners should be advised to avoid direct contact with the lesions or hair of the infected animal by wearing protective clothing and gloves. Hand washing should occur after every encounter. Confining the infected animal(s) to one room or to a cage/crate will help prevent spread of infection to other animals, people, and environments. Effective diagnosis, treatment, and client education is essential for the successful management of dermatophytosis. j References: Moriello KA. Treatment of dermatophytosis in dogs and cats: a review of published studies. Vet Dermatol 2004;15:99-107. Scott DW, Miller WH, Griffin CE. Small Animal Dermatology. 6th ed. Philadelphia: WB Saunders Co.; 2001. Moriello KA, Verbrugge MJ, Kesting RA. Effects of temperature variations and light exposure on the time to growth of dermatophytes using six different fungal culture media inoculated with laboratory strains and samples obtained from infected cats. J Feline Med Surg 2010;12(12):988-990. Full Circle Forum Attacked by a Snake: A Case Report Danna M. Torre, DVM, DACVECC VCA Shoreline Veterinary Referral & Emergency Center “G riffin,” a 10-year-old castrated male Brussels Griffon, presented to VCA Shoreline Veterinary Emergency and Referral Center as a referral from Dr. James St. Clair at Meriden Animal Hospital. Two days prior to being transferred to VCA Shoreline, Griffin had been bitten by a venomous snake, which his owners suspected was a Copperhead, as they had seen Copperheads on their property. Griffin had been treated with intravenous steroids, antibiotics, pain medications, and fluids, however he had become progressively more anemic and was transferred to VCA Shoreline for more intensive treatment. On presentation, Griffin was quiet but alert and responsive. His heart rate and temperature were within normal limits, however he was panting excessively and had pale mucous membranes. He was hypotensive with a systolic blood pressure of 70 mmHg. Griffin had several bite wounds generalized over his body. His right front leg was swollen and he had necrotic bite wounds in the axilla and antebrachium (medial aspect). Two puncture wounds were noted on the ventral thorax with a small area (about 1 cm in diameter) of necrotic black skin adjacent to wounds. Initial diagnostic evaluation included a venous critical care and blood gas analysis, a coagulation panel, and a CBC/mini chemistry panel (performed by the referring hospital that morning). The critical care panel showed a hyponatremia (135.4 mmol/L, reference range 142 -150 mmol/L), a mild hypokalemia (3.75 mmol/L, reference range 3.80-4.90 mmol/L), a mild hyperlactatemia (3.5 mmol/L, reference range 0.3-1 mmol/L), and mild azotemia with a BUN of 40 mg/dL (reference range 7-28 mg/dL) and a creatinine of 1.7 mg/ dL (reference range 0.5-1.3 mg/dL). The CBC showed anemia and thrombocytopenia (HCT 18%, platelets 48,000). The mini chemistry panel from that morning showed hypoproteinemia (4.7 g/dL), hyperglycemia (158 mg/dL), an increased BUN (45 mg/dL), and an increased alkaline phosphatase (174 U/L, reference range 20-150 U/L). The prothrombin time (PT) was normal at 17 seconds (reference range 12-17 sec). The activated partial thromboplastin time (PTT) was out of range (reference range 71-102 sec). Griffin was admitted to the hospital. November/December 2011 An intravenous catheter was placed for the administration of medications/fluids. He was started on broad spectrum antibiotic coverage (ampicillin and enrofloxacin). Hydromorphine was given intravenously for pain management every 4 hours. A wet to dry bandage was placed on the right front leg. Our goal was to have the bite wounds declare themselves in order to determine how much of the skin was going to need to be debrided. He was given a single unit of packed red blood cells over 4 hours. He was also given a single unit of fresh frozen plasma over 2 hours. Crystalloid therapy was instituted to maintain Griffin’s fluid requirements after the blood transfusions were complete. By day 2 of Griffin’s hospitalization, his coagulation profile had normalized (PT 14 sec, PTT 113 sec). His PCV/TS was 27%/4.3 g/ dL. A fentanyl patch was placed for continued pain management. Hetastarch was started to minimize his crystalloid fluid requirement and, given his low protein levels and suspected decreased oncotic pressure, to help with oncotic pressure. The remainder of the treatments remained unchanged throughout the duration of hospitalization. The wet to dry bandage was replaced, as debridement was not deemed necessary yet. Later in the day, Griffin started to eat for the technical staff. and a nonadherent bandage was placed over the medial aspect of the antebrachium. On day 5 of hospitalization, Griffin’s vital signs were stable, his PCV/TS was holding (31-33%/5.4 g/dL), and he was eating intermittently on his own. The wet to dry and nonadherent bandages were replaced and no further debridement was necessary at that time. The decision was made to discharge Griffin with frequent follow up examinations. He was discharged on Clavamox, Baytril, and tramadol. Over the next month, Griffin had frequent recheck examinations. He had two additional surgeries to debride necrotic tissue over his ventral thorax and right axilla. He continued to get stronger and gain weight. His laboratory values continued to improve. After two months, he was reevaluated and was found to have made a full clinical recovery. Case Discussion North American venomous snakes are divided into two major taxonomic groups. The first is the Crotalidae, or pit vipers, which contains the rattlesnakes (genera Crotalus and Sistrurus) and moccasins (genus Agkistrodon), the latter genus containing the Copperhead (Agkistrodon contortix) and the Cottonmouth. The second major group On day 3 of hospitalization, Griffin’s PCV fell to 19% (TS 4.4 g/dL) and he appeared clinical for his anemia. A re-check coagulation was normal (PT 13 sec, PTT 92 sec). After crossmatching, he was given a second packed red blood cell transfusion. His recheck PCV/TS was 36%/4.8 g/dL. Griffin ate for his owner after the transfusion was complete. On day 4 of hospitalization, Griffin was placed under general anesthesia to assess his wounds. The wound on his thorax was still declaring itself so it was left alone. About 40% of the medial surface of the right antebrachium was deemed nonviable tissue. The skin was debrided until bleeding was noted. The subdermal muscle layer/fascia was healthy viable tissue. The skin was closed in a simple interrupted pattern. The skin in the right axilla had questionable viability, and the decision was made to continue to assess the region daily. A wet to dry bandage was placed in the right axilla Griffin and his family pictured with Dr. Holahan and Dr. Torre. Continued on page 4 3 Attacked by a Snake of venomous North American snakes contains representatives of the family Elapidae, the eastern (Micrurus fulvius) and western (Micruroides euryxanthus) coral snakes. This review will focus on the first group, the Crotalidae. Although each type of snake venom has its own level of virulence, the clinical sequelae of bites are similar. The Pathogenesis of Venom Crotalid venom consists of 90% water, numerous enzymes, and peptides. Hyaluronidase and collagenase aid in spreading venom through interstitial spaces, proteases can lead to coagulopathies and necrosis, and phospholipases cause cytotoxic effects that lead to both endothelial cell damage and resultant inflammation. Crotalid venom increases the permeability of capillary cell membranes, which allows the venom to spread within the prey.1 Polypeptides cause capillary endothelial cell damage, which leads to endothelial cell swelling and rupture. The resultant gaps in the microvasculature allow third spacing of plasma and erythrocytes, leading to both edema and ecchymosis.2 This process occurs in any capillary exposed to venom, including skeletal muscle, kidneys, myocardium, and endothelium. The cardiovascular effects manifest as hypotension secondary to an increase in vascular permeability causing third spacing of fluid out of the intravascular space. Hypotension can also occur secondary to fluid losses from vomiting and hemorrhage. Skeletal muscle can become necrotic due to a myotoxin within the venom that causes increases in intracellular calcium leading to activation of damaging enzymes. Acute renal failure is occasionally reported and the pathogenesis includes hypotension, circulatory collapse, intravascular hemolysis with resultant hemoglobinuria, myoglobinuria, direct toxic effects to the kidney and thromboembolic events. The hematological effects of venom can be classified into four categories: procoagulants, anticoagulants, fibrinolytic enzymes, and thrombocytopenia. Although all areas of the coagulation cascade appear to be targeted, the net effect of venom on hemostasis is an anticoagulative state. Diagnosis The diagnosis of envenomation is often based on the owner’s observation as well as clinical signs. Toxicity depends upon several variables including the volume of venom injected, the depth of the bite, and the size of the victim. If there has been little or no envenomation, clinical signs will consist of minor swelling. With moderate to severe envenomation, immediate and progressive pain is noted.3 Clinical signs usually develop within 10 to 30 minutes. Ecchymosis, 4 Continued from page 3 with resultant tissue necrosis at the site of injury, is a common clinical finding. Common signs include lethargy, weakness, hypotension, arrhythmias, ataxia, bleeding, vomiting, diarrhea, respiratory distress, and shock. 3 Patients that present with suspected or known envenomation should have complete bloodwork and a urinalysis and coagulation profile performed. Throughout the duration of hospitalization, a patient’s electrolytes, renal parameters, hematocrit, platelet count, protein level, and coagulation status should be continuously monitored. Typical bloodwork abnormalities include echinocytosis, spherocytosis, thrombocytopenia, anemia, leukocytosis, and prolonged clotting times.4 Echinocytosis are erythrocytes with uniform, regularly spaced membrane projections.Echinocyte formation is thought to be caused directly by the venom itself, is dose dependent, and is self-limiting with changes resolving within 48 hours. Common chemistry profile abnormalities include azotemia, hypoalbuminemia, hypoproteinemia, and elevated levels of creatinine kinase, alkaline phosphatase, alanine transaminase, g-glutamyl transferase, and aspartate transaminase.4 First Aid Treatment Although safe and rapid transport to a veterinary emergency center is recommended, owners can institute some initial first aid treatment en route. First they should be instructed to slow the spread of venom. This can be performed by limiting the patient’s activity level or immobilizing the bitten area. If signs of envenomation occur, a constricting band applied tightly enough to impede lymph flow can be applied. Lymphatic outflow is the main dissemination route for envenomation.2 In addition, the owner should monitor their pet very closely on the way to the veterinary hospital. The owner can be very helpful to the veterinarian in providing an assessment of the initial clinical course of the bite. In-Hospital Treatment The treatment for snakebite envenomation is multi-faceted and depends upon the individual patient’s clinical presentation, laboratory abnormalities, and wound care requirements. Initial emergency treatment should consist of stabilization of the cardiovascular and respiratory systems. At least two large bore intravenous catheters (or a multiple lumen central catheter if the patient is not coagulopathic) should be established for the administration of either crystalloids, or a combination of crystalloids and colloids, and intravenous medications. Clinical parameters, such as mucous membrane color, capillary refill time, pulse quality, blood pressure, urine output, and improvement in the degree of lactic acidosis, can all be used as a guide to gauge appropriate fluid therapy. If respiratory compromise is observed, initial treatment with oxygen via a facemask or nasal cannula is recommended. Thoracic radiographs and arterial blood gas analysis are indicated if respiratory compromise continues despite supportive measures as acute lung injury (ALI) or adult respiratory distress syndrome (ARDS) are known sequelae of envenomation. Although anemia and coagulation abnormalities are common, the use of blood products for envenomation is controversial. Coagulopathy associated with envenomation is consumptive and unresponsive to either heparin or blood products while unneutralized venom is circulating.1 Providing coagulation factors and blood products adds substrate for unneutralized venom, which leads to potential thromboembolic events.1 Current recommendations emphasize neutralization of venom with antivenin.1 In the current case, the decision was made to give Griffin blood products as we did not feel there was circulating venom to neutralize and he was clinical for his anemia and coagulopathy. Antivenin administration is recommended for cases in which there is worsening local injury, clinically significant coagulopathy, or systemic signs (i.e. hypotension).1 Antivenin should ideally be administered within the first 4 hours after envenomation.1 The benefits of antivenin decrease if administration is delayed, but antivenin can still have clinically positive effects for up to 24 hours after envenomation.1 When administered early, antivenin binds to the venom itself, subsequently neutralizing it, reversing some clinical manifestations of envenomation, and preventing further progression. Local tissue necrosis, unfortunately, cannot be stopped by antivenin administration.1 There are two commercially available antivenins for animals in the United States. Antivenin (Crotalidae) Polyvalent (ACP; Fort Dodge Animal Health) and Crotalidae Polyvalent Immune Fab (ovine; CroFab, FabAV, Protherics, Nashville, TN). The use of the ACP antivenin is considered more favorable due to less clinical side effects and its reasonable price. Acutely, the area of the snakebite should be clipped of fur and cleaned using aseptic scrub and kept dry. The circumference of the swelling should be measured and recorded every 15 minutes to help determine progression and requirements for antivenin administration.1 If the wound progresses and local necrosis occurs, the affected area should be treated like an open wound until a healthy granulation bed forms. Surgical debridement may Full Circle Forum be needed for necrotic tissue after several days.1 renal compromise due to their side effects. Additional treatment should consist of broad spectrum antibiotic therapy as numerous pathogenic bacteria have been isolated from the mouths of crotalid species.4 The administration of pain medication is an essential part of treatment. Opioids, as intermittent injections or as a continuous rate infusion, should be instituted as early as possible in the course of treatment. The use of nonsteroidal anti-inflammatory drugs are contraindicated in hypotensive patients with Prognosis The mortality rate of envenomation in dogs has reportedly been as low as 3.7% with treatment.4 Snakes bites have a variable prognosis, with the more important parameters being time from envenomation to presentation, the number of bites (as well as the areas bitten) and the degree of hematologic abnormalities. Aggressive therapy with intravenous fluids, antibiotics, pain medications, and antivenin (when appropriate) should be considered. It is not uncommon to have extensive necrotic wounds from snake bites which will require surgical attention. j References: Gold B, Dart R, Barish R. Bites of venomous snakes. N Engl J Med 347(5): 347-356, 2002. 2 Walter FG, Bilden EF, Gilby RL. Envenomations. Crit Care Clin 15(2): 353-386, ix, 1999. 3 Hudelson S, Hudelson P. Pathophysiology of snake envenomation and evaluation of treatments, part 1. Compend Contin Educ Pract Vet 17(7):889-897, 1995. 4 Hudelson S, Hudelson P. Pathophysiology of snake envenomation and evaluation of treatments, part II. Compend Contin Educ Pract Vet 17(8):10351041, 1995. 1 The Use of Ultrasound for Diagnosis of a Gastric Foreign Body Joseph D. Stefanacci, VMD, DACVR VCA Veterinary Referral & Emergency Center “B ailey,” a 10 year old, spayed female Puli, presented to Dr. Christian Benyei at Schulhof Animal Hospital in Westport, CT, with a clinical history of difficulty walking, weakness, ataxia, chronic anemia, and (most recently) a significantly decreased appetite bordering on complete anorexia. Bailey had been medicated since April of the same year with a tapering dose of prednisone for a previous bout of nonspecific ‘back pain.’ The patient had been seen Figure 1 Figure 2 November/December 2011 at that time by Dr. Heather Galano, VCA Shoreline’s neurologist, but despite a thorough workup (including MRI), no definitive cause was found and empirical treatment with prednisone was successful in resolving clinical symptoms. Upon current examination Bailey’s neurological status was determined to be within normal limits so Bailey was referred to Dr. Larry Berkwitt, internal medicine specialist for VCA Shoreline, for anemia and inappetence. Dr. Berkwitt determined that the anemia was likely related to chronic corticosteroid therapy but was unable to find a cause for the anorexia. Bailey was then referred to me for an abdominal ultrasound examination. During Bailey’s abdominal ultrasound examination I noted that the wall of the stomach was symmetrically, abnormally thickened (fig 1). The wall layers were intact but the outer rim of the wall was diffusely hypoechoic (dark). Also, within the lumen of the fundus there was a solid appearing, hyperechoic curvilinear ‘band’ beyond Figure 3 which an intense shadow was noted. This structure moved independently within the gastric lumen, and was not attached to any portion of the gastric wall. It continued to cast a dark shadow regardless of the angle of insonation (the direction of the ultrasound beam). Gastric motility was decreased. No other abdominal abnormalities were noted. My differential diagnoses for this abnormal ultrasonographic finding included: intraluminal gastric foreign body, inspissated food ball, Figure 4 Figure 5 5 Ultrasound for Diagnosis of a Gastric Foreign Body and atypical gastric wall mass, i.e. a neoplasm, granuloma, or large polyp. The patient was then returned to VCA Shoreline in Shelton, CT, for endoscopy. During endoscopy a large trichobezoar (hairball) was discovered in the fundic lumen (fig 5). The large size of this foreign object made removal via endoscopy impossible; a decision to take Bailey into surgery for an exploratory laparotomy and gastrotomy was then made. At surgery a single gastrotomy incision was made over the fundus and the hairball and other debris was removed (fig 3). Bailey recovered uneventfully from this surgery and is currently doing well at home. His appetite returned almost immediately following and he continues to eat well to this day. Gastric foreign bodies are often easily recognized in animals on survey abdominal radiographs, CT examination (fig 2) and with abdominal ultrasound evaluation. Survey radiographs of a patient with a suspected gastric foreign body, however, can look normal depending on the amount of gas and fluid present within the gastric lumen and the type and size of the foreign body present. Case Discussion Ultrasound examination of the gastrointestinal tract is a safe and noninvasive imaging modality that can provide important diagnostic information for animals with GI disease. Despite the potential limitations imposed by intraluminal gas, which can result in lesionmasking artifacts, this imaging procedure can still be performed prior to any other diagnostic test by employing minimal patient preparation, i.e. overnight fasting. Also, ultrasound imaging can follow screening survey radiography to help confirm a diagnosis when a suspicion of GI pathology exists. Gastric distention, excessive small bowel dilatation, intraluminal abnormalities (such as foreign bodies or masses), bowel wall thickness and GI motility can all be assessed using ultrasound. Based on any or all of these abnormal findings, the decision as to which diagnostic direction to then take, i.e. endoscopy, exploratory laparotomy, guided sampling procedures (aspiration, biopsy), can be made with confidence. Also, any suspicious findings can be re-evaluated during additional examinations. Because of its usefulness in evaluating the GI tract, ultrasound has generally replaced the gastrointestinal contrast study. However, if choosing to perform a contrast study, the ultrasound examination should be done prior to giving barium because this contrast medium will effectively stop transmission of the sound beam. When performing an ultrasound examination of the GI tract, it is important to slowly and methodically evaluate the entire system from stomach to colon. The walls of the stomach and intestines have a distinctive 5-layer Continued from page 5 appearance of alternating echogenicities (fig 4). The innermost layer visible with ultrasound is the mucosal-luminal interface, which is hyperechoic (bright). This is followed from the inside out by a hypoechoic (dark) mucosa, a hyperechoic (bright) submucosa, a hypoechoic muscularis and a hyperechoic serosa-subserosa. The thicknesses of the different parts of the GI tract vary from 3-5 mm in the stomach, 2.5-3.5 mm in the small bowel, and 1-2 mm in the colon. A bezoar, by definition, is a hard, indigestible, mass of material such as hair, vegetable fibers or seeds and skins of fruits; trichobezoars are a mass of hair, i.e. excessive grooming. When in the stomach, the size and density of these structures can make passage through the pylorus into the duodenum impossible, often causing chronic patient nausea and anorexia and abdominal discomfort. Also, the size and shape of the foreign body may require an invasive procedure such as gastrotomy to remove it. The density of this material and its often large size (by the time it is usually diagnosed), a trichobezoar presents a strongly attenuating surface to the ultrasound beam. The beam is completely absorbed and reflected by this highly acoustic interface giving the described appearance of a classic, or pathognomonic, hyperechoic curvilinear ‘band’ with a strong acoustic shadow deep to this band (see fig 1). j Osteoma on the Forelimb of a Cat Kate Margalit, DVM, DACVS Fifth Avenue Veterinary Specialists “G ordo” is a six-year-old male neutered domestic shorthair that was referred to the surgery service at Fifth Avenue Veterinary Specialists by Dr. Eric Dougherty of The Cat Practice in New York City. Gordo initially presented for right carpal swelling and right thoracic limb lameness that his owner first observed three days prior to examination. On presentation, Gordo was bright and alert. Physical examination revealed a grade 1 lameness of the right thoracic limb. There was a firm, affixed 3 x 3 cm mass on the cranial aspect of the distal radial and carpal region. 6 The mass was nonpainful on palpation, but there was mildly decreased range of motion of the right carpus. Gordo had a body condition score of 8/9. The remainder of the physical examination was unremarkable. Bloodwork performed by Dr. Dougherty just prior to referral revealed: mild thrombocytopenia with evidence of platelet clumping at 132 103/μL (reference range 200-500 103/μL), mild basophilia at 166 109/L (reference range 0-150 109/L), mild hyperalbuminemia at 4.1 g/dL (reference range 2.5-3.9 g/dL), and mild hypertriglyceridemia at 204 mg/dL (reference Dr. Dougherty of The Cat Practice, NYC Full Circle Forum occur more frequently in horses and cattle. There are rare reports of osteomas in cats in the veterinary literature. The largest case series reports 7 cats with osteomas in the oral and maxillofacial regions.1 Two distinct patterns of osteoma were characterized on CT scan: compact (or cortical) and cancellous. Compact osteoma was well marginated and smooth, while cancellous osteoma was more irregular and expansile with some destruction of adjacent bone. Due to the small sample size of this study, no conclusion can be drawn as to the significance of this distinction. Figure 1 Figure 2 range 25-160 mg/dL). The remainder of his complete blood count and chemistry panel was unremarkable. FeLV and FIV retroviral testing was negative. radius and carpus. The mass was elevated from its attachment of the distal radius and proximal aspect of the joint capsule with a Freer elevator. An osteotome and mallet were utilized to smooth the cranial surface of the distal radial cortex. Histopathology was submitted and reconfirmed the initial diagnosis of osteoma. A soft padded bandage was placed on the right thoracic limb. Orthogonal right carpal radiographs were completed under sedation at The Cat Practice (figs 1, 2). Surrounding the distal radius, a large, smoothly margined mineralized mass was detected. The mass protruded distally and was seen slightly overlaying the radiocarpal joint, however the carpal bones did not appear to be involved. No evidence of bone lysis was visible. Three view thoracic radiographs were completed at the time of consultation at FAVS prior to anesthesia and were unremarkable. Incisional biopsy of the right carpal mass was completed. The outer surface of the mass appeared to have a smooth contour. A biopsy was obtained with use of a Jamshidi biopsy instrument and curette. Histopathology revealed branching and interconnecting osseous trabeculae that formed spaces containing fibrous tissue. Lacunae were irregularly clustered. Cells in lacunae and intertrabecular spaces had small nuclei with condensed chromatin and a low mitotic index. There were no significant inflammatory cell infiltrates. The mass was diagnosed as an osteoma. One week after the incisional biopsy was completed, the owners elected a more definitive surgery. An excisional biopsy was performed by making a cranial approach over the distal right November/December 2011 Gordo recovered uneventfully from his surgery and was discharged with sublingual buprenorphine. Two weeks post-operatively, Gordo’s sutures and bandage were removed. Gordo had subtle lameness and appeared more comfortable at home. Two months post-operatively, a follow up phone call was completed. The owner had not noted any recurrence of the carpal mass and he was ambulating normally at home. Case Discussion Differential diagnoses for an osseous mass involving the distal radius or carpal joint include: osteochondroma (either solitary or as part of multiple cartilaginous exostoses), synovial osteochondroma, osteoma, chondroma, chondrosarcoma, osteosarcoma, or metastatic neoplasia. An osteoma is a benign bone tumor that is generally slow growing. Some believe that an osteoma is not a true neoplasm, but a developmental anomaly that occurs secondary to trauma or infection. It can occur in all domestic species, but tends to The mandible was the most common location. Of the three biopsy samples that were cultured, only one grew E. cloacae; however this was believed to be a contaminant rather than a true infection. Only one cat underwent a debulking surgery of the mass and was reported to do well one year after surgery. Mandibulectomy or maxillectomy were pursued in three cats. Overall, the cats that underwent surgical intervention had follow up at 1 to 9 years after diagnosis and had a good quality of life and no signs of recurrence.1 There is one case report of extraskeletal osteoma in the cat.2 The mass was within the subcutaneous tissue adjacent, but not attached to the olecranon. The mass was easily excised and no recurrence was noted 3.5 months post-operatively. In Gordo’s case, give the benign nature of the mass, an amputation was mentioned, but not recommended. CT scan would have been a helpful imaging to modality to characterize the extent of the mass and bony involvement. At this time, Gordo is doing well with no observable lameness or recurrence two months post-operatively. While an osteoma is considered benign, early intervention is still recommended. Debulking surgery as opposed to aggressive resection can be a viable option to address osteomas. While there is no evidence in the literature that malignant transformation occurs, recurrence is possible. j References: Fiani N, Arzi B, Johnson EG, Murphy B, Verstraete FJ. Osteoma of the oral and maxillofacial regions in cats: 7 cases (1999-2009). J Am Vet Med Assoc 2011;238(11):1470-1475. 2 Jabara AG, Paton JS. Extraskeletal osteoma in a cat. Aust Vet J 1984;61(12):405-407 1 7 Upcoming Events November 15, 2011 — Fifth Avenue Veterinary Specialists will host an evening of CE at the Union Square Ballroom in NYC from 7:00 PM - 10:00 PM. Our featured speakers will be Lisa Mahlum, DVM, DACVECC, presenting a critical care lecture, and Mary Buelow, DVM (practice limited to dentistry), presenting “Recognition of Oral Pathology.” Please contact Monica Dunn at (212) 924-3311 or monica. [email protected] with any questions. 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