Petechiae and ecchymoses are red to purple discolorations of the skin or mucosa and occur due to blood vessel disruption. Petechiae are generally <3 mm in diameter and form as a result of capillary bleeding. Ecchymoses are larger lesions caused by arteriolar and venular bleeding. Most cases of petechiation or ecchymoses tend to be multifactorial with multiple mechanisms contributing to their presence. 

Following are differential diagnoses for patients presented with petechiation and/or ecchymoses.

• Immune-mediated thrombocytopenia (ie, platelet destruction)
  • Primary or idiopathic (most common cause in dogs, rare in cats)
  • Secondary  
    • Infectious (eg, Angiostrongylus vasorum, Leishmania infantum, Anaplasma phagocytophilum [dog])
    • Inflammatory (eg, meningoencephalitis of unknown origin [cat], African bee envenomation [dog])
    • Neoplasia (eg, mast cell tumor, disseminated carcinoma, lymphoma, osteosarcoma [dog])
    • Drug-related (eg, gold salts [auranofin], carprofen, cephalosporins, chlorambucil, trimethoprim/sulfadiazine [dog])
• Platelet consumption
  • Disseminated intravascular coagulation
  • Vasculitis
  • Hepatic failure
  • Pancreatitis
• Myelosuppression
  • Myelodysplasia (eg, myelodysplastic syndrome with excess blasts [MDS-EB], myelofibrosis, myelophthisis [dog])
  • Drug-induced (eg, carbimazole, linezolid [cat], azathioprine, vincristine, chloramphenicol, cephalosporins, estrogen [dog])
  • Infection (eg, FeLV/FIV [cat], ehrlichiosis, parvovirus [dog]) 
  • Neoplasia (eg, lymphoma, lymphoid leukemia, histiocytic sarcoma)
• Sequestration (rare; although this mechanism is frequently considered as a cause for thrombocytopenia, it is unlikely to result in petechiae or ecchymoses) 
  • Hepatomegaly
  • Splenomegaly
  • Hypotension
  • Endotoxemia 
  • Hypothermia

• Inherited (rare in cats)
  • Glanzmann thrombasthenia (Great Pyrenees, otterhound, crossbreed dogs)
  • Canine thrombopathia (basset hound thrombopathia, spitz, Landseer Newfoundland)
  • Platelet P2Y12 receptor disorder (Greater Swiss mountain dog)
  • Leukocyte adhesion deficiency (LAD)-III (LAD-I variant; German shepherd dog)
  • Delta-storage pool deficiency (American cocker spaniel)
• Acquired
  • Infectious disease (eg, Ehrlichia canis, E platys [dog])
  • Snake envenomation (eg, copperhead, other pit vipers) 
  • Hepatic disease
  • Anticoagulant rodenticides
  • Uremia
  • Neoplasia (eg, essential thrombocythemia, acute megakaryocytic leukemia, chronic myeloid leukemia)
  • Disseminated intravascular coagulation 
  • Monoclonal gammopathies (eg, multiple myeloma, Ehrlichia canis) 
  • Platelet-inhibiting medications (aspirin, clopidogrel, heparin, dextran) 
  • Idiosyncratic drug reaction (carprofen, hydroxyethyl starch, omega fatty acids)

• Rarely causes petechiation 

• Vasculitis
  • Immune-mediated
    • Primary
    • Secondary to medication, infection, neoplasia
• Infectious (eg, Rickettsia rickettsii) 
  • Hyperadrenocorticism (dog)   

Following are the 5 most common ophthalmic sequelae of systemic hypertension in the author’s experience.

Decreased or altered vision, vision disturbance, and sudden blindness are emergencies. Patients with systemic hypertension may exhibit initial clinical signs of acute vision loss with varying degrees of mydriasis (Figures 1 and 2), negative or incomplete pupillary light reflexes, negative to varying degrees of light perception, and/or reduced ability to navigate a maze test or recognize humans.⁵ Systemic hypertension can cause visual disturbance or acute blindness from intraocular hemorrhage, subretinal edema, retinal detachment, or secondary glaucoma.^1,6,7

Differential diagnoses for changes in vision are old age, corneal disease, uveitis, cataracts, glaucoma, progressive retinal atrophy (dogs; less common in cats), retinal detachment, retinal edema, sudden acquired retinal degeneration (dogs), and optic nerve or intracranial disease.⁵ Common causes of vision loss in cats are uveitis, corneal disease, cataracts, glaucoma, retinal degeneration, retinal detachment, retinal edema, and optic nerve and intracranial disease. 

Retinal hemorrhage is a common sequela to hypertension.¹ Hemorrhages may be focal, multifocal, or large hemorrhagic subretinal areas (Figures 3 and 4). The mechanism is related to arteriolar vascular permeability changes.^8,9 Autoregulatory mechanisms cause initial vasoconstriction, followed by possible arteriole lumen occlusion and ischemic necrosis. Increased vascular permeability can affect the choroid and cause subretinal fluid and retinal detachment.^8,9

Retinal hemorrhages are also common with other conditions (eg, trauma, infectious disease, coagulopathy, neoplasia, diabetes, congenital disorders) that cause vasculitis, as well as hyperviscosity syndrome.⁸ In dogs, tick-borne diseases are infectious agents that can be associated with retinal hemorrhage.⁸

Differential diagnoses for retinal hemorrhage are coagulopathy, infectious disease, neoplasia, trauma, congenital disorders, and hyperviscosity syndrome secondary to multiple myeloma.

Hyphema is a classification of intraocular hemorrhage that refers to a collection of erythrocytes in the anterior chamber (Figures 5 and 6). Intraocular hemorrhage can develop with any systemic condition that affects the vasculature of intraocular structures and can occur in the anterior chamber, surface of the iris, vitreous cavity, retina, choroid, supra- or subchoroidal space, and around or on the optic disc. Blood accumulates in the anterior chamber or vitreous humor due to disruption of the iris or ciliary body vessels in response to sustained systemic hypertension. Altered permeability of the uveal vasculature (iris, ciliary body, choroid) may then lead to intraocular hemorrhage,^8,9 which may be visualized as a few strands of blood in the anterior chamber or on the iris surface, partial or complete hyphema in the anterior chamber, focal or large areas of vitreal hemorrhage, or retinal hemorrhage. Hemorrhage may be substantial and obscure large areas of the fundus, depending on chronicity and severity of systemic hypertension.

Differential diagnoses for intraocular hemorrhage are trauma, intraocular tumor, systemic neoplasia, coagulopathy, chronic glaucoma, chronic uveitis, and retinal detachment.¹⁰

Exudative or serous retinal detachment is common in patients with hypertension.¹¹ Clear to yellow fluid accumulation or blood in the subretinal space that may appear as the retina billowing toward the examiner is characteristic during ophthalmoscopy (Figures 7 and 8). Retinal detachment can also be secondary to vascular, inflammatory, and/or neoplastic diseases of the retina, choroid, and retinal pigmented epithelium.¹²

Leaking fluid can overwhelm the retinal pigmented epithelium pumping mechanism, causing fluid accumulation in the subretinal space and leading to retinal detachment and vision loss. Vision loss may be acute or gradual and partial or complete, depending on the degree of vitreal hemorrhage and retinal edema. Correction of the underlying cause may allow resorption of subretinal fluid; vision recovery is possible if the condition is treated before retinal ischemia occurs. Morphology of the retina and retinal pigmented epithelium interface may not recover, even after 6 months.¹³

Less likely differential diagnoses for retinal detachment are systemic infections (eg, fungal, bacterial [eg, ehrlichiosis, borreliosis], protozoal [eg, toxoplasmosis], viral [eg, FeLV, FIP, FIV]), neoplasia (eg, multiple myeloma, lymphoma), primary ocular conditions (eg, glaucoma), and immune-mediated conditions (eg, uveodermatologic syndrome, hyperviscosity syndrome secondary to multiple myeloma).

Variations of retinal edema, retinal vessel tortuosity, perivascular edema, and papilledema are possible in patients with hypertension.¹⁴ Vascular ischemic changes and changes to vascular permeability occur with hypertension. 

Vascular tortuosity refers to abnormal twists and turns (often at acute angles; different from the natural arborizing branching pattern of retinal vasculature) related to mechanical forces associated with hypertension that affect wall rigidity, blood pressure, blood flow, axial tension, and wall structural changes (Figure 9).¹⁵ Retinal edema may appear via indirect ophthalmoscopy as areas of the tapetum that are gray, are indistinct, have altered reflectivity, or have pale yellow or patchy irregularities compared with the surrounding tapetum (Figure 10).

Differential diagnoses for intraretinal edema and vessel tortuosity are fungal, bacterial, parasitic, and protozoal infections; immune-mediated and tick-borne diseases; toxicosis; trauma; algae; metabolic conditions; and neoplasia.

Systemic diagnostic evaluation should be performed to rule out renal disease, endocrine disorders, and cardiac disease. Hypertension may be undetected, as ocular lesions may not occur until blood pressure has been elevated for weeks or months. Blood pressure can increase with age,¹⁶ and patients at risk for hypertension (eg, cats >10 years of age, dogs with pre-existing risk factors) may benefit from routine indirect blood pressure measurement and funduscopic evaluation.

Edward, a 3.5-year-old, 75.2-lb (34.1-kg), intact male Irish setter was presented with recurrent large bowel diarrhea (Table) of 3 months’ duration during the winter months. He lived in a consistently subfreezing area. The diarrhea was initially managed by his owner (a clinician) and an internal medicine service. Three months after diarrhea was observed by his owner, Edward was presented to a nutrition service.

Episodes often started with vomiting, decreased interest in food, and mildly decreased energy, and then progressed to diarrhea with hematochezia, mucus, and tenesmus that continued even as initial clinical signs improved. The episodes only sometimes coincided with a change in routine; the 2 episodes prior to presentation developed precipitously after consuming a few pieces of buttered popcorn or a bite of buttered toast. Fluctuations in body weight were minor, with small decreases (<2%-5% body weight) during acute episodes that quickly returned to baseline when Edward was feeling well.

A trial of fenbendazole (50 mg/kg PO every 24 hours for 3 days; 2 doses repeated 2 months apart), 2 trials of metronidazole (11 mg/kg PO every 12 hours for 7 days; only one trial was completed, the second was stopped after a few days due to lack of response and apparent nausea with administration), and a trial of tylosin (12 mg/kg every 12 hours for 14 days) were completed without resolution or consistent improvement. Edward’s owner had also administered probiotic kaolin-pectin paste and probiotic capsules (per package directions). An elimination food trial using a dry, extruded, hydrolyzed soy protein diet fed for 4 weeks elicited no clinical response. 

Edward was up to date on routine preventive care and had no significant medical history other than mild separation anxiety. His owner characterized him as a high-energy dog.

Physical examination was unremarkable. Edward was bright, alert, and responsive, and vital signs were normal. BCS was 4/9, and muscle condition was normal. No masses or irregularities were palpated. Rectal examination revealed a smooth, normal-feeling prostate; no enlargement was appreciated by palpation.

Differential diagnoses for chronic large bowel diarrhea include infectious diseases (eg, parasites), chronic inflammatory enteropathy, food-responsive enteropathy, functional disorders (eg, stress colitis, idiopathic diarrhea), and neoplasia.^1-3

CBC, serum chemistry profile, and urinalysis were performed 3 weeks prior to presentation at the nutrition service; results were normal. Fecal flotation and Giardia spp and Cryptosporidium spp immunofluorescence assays were negative. ACTH stimulation test did not support a diagnosis of hypoadrenocorticism. Abdominal radiography and ultrasonography were unremarkable except for mild prostatic enlargement consistent with the patient’s intact status. PCR tests for Escherichia coli, Salmonella spp, Campylobacter spp, Cryptosporidium spp, Clostridium perfringens enterotoxin, Clostridium difficile toxins A and B, canine distemper virus, canine circovirus, enteric coronavirus, parvovirus, and Giardia spp were negative. Consultation with a veterinary nutritionist was pursued prior to intestinal and colonic biopsy. 

Chronic inflammatory enteropathy, food-responsive enteropathy, and chronic idiopathic large bowel diarrhea were the top differentials based on diagnostic results. The etiology of chronic idiopathic large bowel diarrhea is not completely understood, but some dogs appear to respond to a change in dietary fiber, whereas other dogs benefit from behavioral therapy or drugs for treatment of stress; some dogs require both. Need for concurrent administration of medications (eg, loperamide) for control of clinical signs is variable.

Studies of dogs with chronic diarrhea have shown that many conditions respond to simple therapeutic trials (eg, parasiticides, diet trials).^1,4-6 A variety of interventions and less-invasive diagnostics may therefore be beneficial prior to colonoscopy and other advanced diagnostics.⁷

A subset of dogs with chronic idiopathic large bowel diarrhea respond positively to some changes in dietary fiber, and fiber has the potential to more broadly support gut health. A fiber supplementation trial was therefore administered by adding unflavored psyllium husk (0.3 g/kg every 24 hours divided between meals, then slowly increased over a few weeks to slightly <1 g/kg every 24 hours) to Edward’s current hydrolyzed diet. Bowel movements were monitored, and his owner was instructed to return to the previous tolerated dose if adverse effects (eg, overly soft stool) occurred with the increasing dose. The dose was re-evaluated at follow-up appointments based on clinical signs. Treatment with psyllium fiber was deemed successful based on no recurrence of large bowel diarrhea. 

The published median effective dose for coarse psyllium husk is 1.33 g/kg every 24 hours⁵; however, a range (0.31-4.9 g/kg) has been effective.⁵ Patients with no change after receiving doses at the upper end of the published effective range (ie, 4.9 g/kg every 24 hours) are considered nonresponsive.⁵

Edward’s stool quality was consistently good (ie, formed, moist to semimoist, left little to no residue when picked up) while he was being fed the hydrolyzed soy protein diet with added psyllium; however, his willingness to consume the diet decreased. Water and baked, skinless, boneless chicken breast were added to his diet without apparent negative effect. Long-term continuation of feeding chicken breast could have unbalanced his diet if it exceeded 10% of total daily kilocalories in combination with the psyllium supplement, as treats and other foods may unbalance a diet when they exceed 10% of kilocalorie intake. 

Given Edward’s apparent tolerance for chicken, it is possible he did not need a hydrolyzed protein diet; however, there is not always perfect correlation between tolerated commercially processed ingredients and those prepared in the home. His owner continued to avoid butter as a possible trigger, but other dairy products were successfully reintroduced several weeks later without issue.  

After several weeks, no further episodes occurred. Based on Edward’s tolerance of a nonhydrolyzed, chicken-based diet and the need to feed at least 90% of total daily kilocalories from a complete and balanced food, he was transitioned to a therapeutic GI diet containing a prebiotic fiber blend with psyllium. His owner was instructed this was to be a long-term diet or an attempt should be made to transition back to the original diet.

The prognosis for most dogs with fiber-responsive large bowel diarrhea is good to excellent. Success in reducing or eliminating psyllium supplementation or using over-the-counter diets was only 20% to 50% in previous studies^3,4; however, these were referral cases, which may underrepresent success in the general population.

Large bowel diarrhea develops when the colon’s capacity to resorb water or store feces decreases. Mucosal damage and inflammation can lead to hematochezia and mucus in the stool. Multiple disease processes can result in large bowel diarrhea, some of which can be challenging to definitively diagnose. Despite extensive testing, many diagnoses are based on response to treatment.⁴ Following an evidence-based treatment protocol may circumvent advanced diagnostics and increased costs.⁷ 

Large bowel diarrhea can respond to parasiticides, antibiotics, or diet changes. Trials of highly digestible GI diets or diets with novel or hydrolyzed protein can be given safely in many cases. Overall, many enteropathies are food responsive.^4,6,7 Younger dogs with large bowel diarrhea are likely to respond to diet change (eg, highly digestible diets, hydrolyzed diets, high-fiber diets) alone.⁴ Dogs that do not respond to highly digestible or novel-protein diets may benefit from a high-fiber diet or psyllium fiber supplementation. 

Fiber-responsive large bowel diarrhea is a subset of chronic idiopathic large bowel diarrhea (a diagnosis of exclusion) that may overlap with irritable bowel syndrome or other stress-related issues.^1-3,5,8 Chronic idiopathic large bowel diarrhea may account for 20% to 25% of referral cases,^1,5 but prevalence in the general population is less understood. Clinical signs may be potentiated by stress, certain dietary triggers, or other factors not currently understood, but specific signs are not predictive of response to fiber.

Dietary fiber is classified by structure, solubility, viscosity, fermentability, ability to adsorb substances, and effect on GI physiology. Viscosity and fermentability are especially pertinent to digestive health. Viscous gels slow gastric emptying, increase small intestine transit time, and slow absorption or reduce digestibility of some nutrients.^9,10 Fermentation by gut microflora has the potential to be highly beneficial but can be detrimental if excessive. 

Patients with chronic idiopathic large bowel diarrhea that respond well to fiber supplementation or a high-fiber diet generally have a positive prognosis. Fiber-responsive large bowel diarrhea can affect dogs of any age, weight, or breed, and clinical signs are commonly intermittent.^1,5 Despite primarily affecting the large bowel, reduced appetite, abdominal pain, slight weight loss, and frequent vomiting are possible. 

Success of psyllium or other fiber supplementation with a desirable insoluble:soluble fiber ratio and fermentability in cases of fiber-responsive large bowel diarrhea is likely multifactorial. Duration of treatment and ability to decrease or discontinue fiber supplementation in patients with fiber-responsive large bowel diarrhea is variable.^1,5 In one study, up to 50% of dogs appeared to tolerate a decrease or discontinuation of fiber supplementation after 2 to 3 months.³ Some patients benefit further from additional treatments (eg, behavioral therapy, probiotics, medical management).^1,5,8

Chronic allergic otitis externa requires both short- and long-term treatment plans. In short-term plans, any active infections and inflammation need to be resolved; dozens of commercial products are available for this purpose. In long-term plans, inflammation and infection must be prevented to avoid flares of disease; however, few commercial products are available in this capacity. Because of this, many clinicians make their own solutions by adding a steroid to a commercial ear-flush product; however, few data exist regarding the long-term stability of such solutions.

This study investigated the stability of dexamethasone (2 mg/mL) added to 4 different commercial ear flushes (ie, Tris-EDTA + ketoconazole, Tris-EDTA + ketoconazole + chlorhexidine gluconate, salicylic acid, and phytosphingosine) at different concentrations (0.1 mg/mL and 0.25 mg/mL). Solutions were stored in their original bottles and tested at room temperature (71.6°F [22°C]) and when refrigerated (39.2°F [4°C]). 

Stability was measured using mass spectrometry at 10 time points over 90 days. The solution was considered stable if the dexamethasone concentration remained >90% of the starting concentration. All solutions were stable at 90 days, except Tris-EDTA + ketoconazole with 0.25 mg/mL dexamethasone, which was only stable up to 14 days at the refrigerated temperature and up to 21 days at room temperature.

Key pearls to put into practice:

Veterinary dermatologists frequently use topical corticosteroids to manage allergic otitis externa; however, there is a scarcity of commercial therapeutic products that contain a corticosteroid without added antibiotics. Many over-the-counter products contain hydrocortisone, which, as a weak steroid, may not be adequate for severe cases of otitis. Clinicians can instead consider making their own steroid-containing ear flushes using injectable dexamethasone that can be applied regularly to the ears to prevent flares of allergic otitis. Frequency (eg, daily to weekly) varies based on severity of disease.

Prevention of otitis flares is important to limit chronic pathologic changes (eg, fibrosis, calcification) to the ear canal, as these severe changes result in the need for surgical ablation in order to resolve the chronic ear disease.

In this study, dexamethasone (2 mg/mL) was added to commercial ear products. Although a 4 mg/mL product is also available and may be stable when added to commercial flushes, further testing and peer-reviewed studies on long-term safety and efficacy are needed.

Efficacy studies of therapeutic cannabinoid use in dogs are available, but literature evaluating use in cats is lacking. 

This randomized, placebo-controlled, blinded study* aimed to determine the safety and tolerability of increasing doses of cannabidiol (CBD) and tetrahydrocannabinol (THC), alone and in combination, in healthy cats using a well-defined cannabis formulation. 

Twenty healthy adult cats were placed in 1 of 5 groups. Placebo groups received either sunflower (SF) or medium-chain triglyceride (MCT) oil. Cannabidiol groups received CBD in MCT oil, THC in MCT oil, or CBD/THC (1.5:1 ratio) in SF oil. Up to 11 escalating oral doses of each formulation were administered to fasted subjects with at least 3 days between doses. 

Cats were monitored for adverse effects, and vital signs were recorded at predetermined intervals. Blood samples for CBC and serum chemistry profile were collected at 24 hours and 7 days after the final dose was administered. Blood was also drawn for cannabinoid analysis immediately prior to and 1, 2, 3, 4, 6, and 24 hours (±15 minutes) following the ninth dose; 4 and 24 hours (±15 minutes) following the tenth and final (eleventh) doses; and 7 days following the final dose.

All adverse effects were mild and did not require intervention. Most common effects were GI (27.6%), respiratory (15.4%), neurologic (14.6%), and ocular (8.3%). Nonspecific signs affecting multiple body systems (29.9%) were also documented. 

In the placebo groups, most cases of vomiting and diarrhea occurred when MCT oil was given. 

Nonspecific signs (most commonly, lethargy and hypothermia) were more frequently noted in cats in the CBD/THC treatment group than in those receiving CBD or THC alone. On average, lethargy began more quickly (≈2.8 hours) and lasted for a shorter period (1.2 hours) in the CBD group than in the THC group (lethargy began after 4.2 hours and lasted 8 hours) or the CBD/THC group (lethargy began after 4.3 hours and lasted 5.7 hours). Ataxia was seen in all patients in the CBD/THC and THC groups. Cats in the CBD group did not demonstrate ataxia until the ninth and tenth doses. 

There were no clinically significant changes on CBC and serum chemistry profile in any treatment group. Levels of plasma cannabinoids and metabolites were higher after CBD/THC administration compared with CBD or THC alone, although the dose of each drug in the combination was less than the dose given alone. This suggests a pharmacokinetic interaction (eg, change in cannabinoid absorption, distribution, or elimination) between CBD and THC and warrants further investigation.

Key pearls to put into practice:

With the increased popularity of CBD and CBD/THC products for pets, it is important to be familiar with the adverse effects and potential benefits of these products, as well as variations in cannabis formulations and noncannabinoid components. The most common adverse effects include vomiting, lethargy, and ataxia. Other potential adverse effects that occur less frequently include hypersalivation, diarrhea, tachypnea, protrusion of the nictitating membrane, and vocalization.

According to the AVMA, state laws legalizing the use of cannabis in humans do not apply to animals.^1,2 State practice laws should be consulted prior to making medical recommendations. Hemp-derived cannabis products (including CBD) cannot be recommended or prescribed with the intent to prevent or treat a medical condition.³

CBD (≤30.5 mg/kg), THC (≤41.5 mg/kg), and CBD/THC (≤13 mg/kg and ≤8.4 mg/kg, respectively) were well tolerated in young, healthy male and female cats. SF oil appeared to be tolerated better than MCT oil as a carrier. 

Plant awns and other foreign bodies are common causes of draining tracts in dogs and cats. Recommended treatment involves removing the foreign body, debriding infected tissue, and administering appropriate antibiotic therapy; however, foreign bodies can be challenging to find during surgery.

Preoperative radiography, ultrasonography, scintigraphy, CT, and MRI have been used to localize foreign bodies with varying success rates.^1-5 Reported sensitivity rates for each modality are inconsistent but are generally low for identifying foreign body location. Surgeons often must rely on removing abnormal tissue en bloc, anticipating the foreign body is in resected tissue.

Recent evidence suggests intraoperative ultrasonography increases successful retrieval of plant material from the iliopsoas muscle.6 Removing the foreign body (vs removing infected tissue en bloc) can eliminate the need for a more aggressive procedure.^7,8

This study sought to determine whether preoperative ultrasonography was more sensitive than either preoperative CT or MRI for locating a foreign body and whether surgical removal was more successful with intraoperative ultrasonography compared with relying on preoperative imaging alone.

Study results demonstrated that preoperative ultrasonography was more sensitive than CT or MRI for detecting migrating foreign bodies, and intraoperative ultrasonography resulted in higher success rates of foreign body removal. Overall resolution of clinical signs was 90.2%, with no difference between dogs that did and did not undergo intraoperative ultrasonography. A greater number of cases may be needed to determine whether intraoperative ultrasonography improves recovery.

Results indicated that ultrasonography is useful for localizing and removing migrating foreign bodies but depends on operator experience. A multimodal approach to imaging (combining CT or MRI with ultrasonography) may increase overall treatment success.

Key pearls to put into practice:

Foreign bodies are common causes of draining tracts in small animals. Localizing a foreign body before and during surgery can be challenging.

Ultrasonography performed by an experienced operator may be more sensitive than CT or MRI for localizing foreign bodies.

Intraoperative ultrasonography can increase localization rates and removal of foreign bodies, but additional studies are needed to determine whether intraoperative ultrasonography improves clinical resolution of signs.

Keratomalacia (ie, corneal melting) is a complex ocular surface disease that can rapidly lead to loss of vision or rupture of the eye. Brachycephalic dog breeds and dogs with dry eye are at higher risk for developing melting corneal ulcers.^1-3 This condition often begins with a superficial corneal wound that becomes infected, triggering a cascade of enzymatic destruction. Protease and collagenase enzymes produced by bacteria and local inflammatory cells can quickly digest the corneal tissue, leading to melting of the corneal stroma (Figure).¹ 

This retrospective study sought to identify the bacteria and antimicrobial susceptibility profile associated with melting corneal ulcers in dogs. Gram-negative Pseudomonas aeruginosa and gram-positive beta-hemolytic Streptococcus spp were the predominant cultured organisms from 110 melting corneal ulcers in 106 dogs. Bacterial susceptibility testing found these isolates to have different antibiotic sensitivity patterns. 

P aeruginosa showed sensitivity to gentamicin and fluoroquinolones. Beta-hemolytic Streptococcus spp were most sensitive to amoxicillin/clavulanate, cephalexin, and clindamycin, followed by doxycycline and chloramphenicol; some resistance to fluoroquinolones was noted. 

All bacterial isolates grouped together showed the highest sensitivity to fluoroquinolones. Results of a recent study showed similar bacterial isolates (eg, Staphylococcus pseudintermedius, beta-hemolytic Streptococcus spp, P aeruginosa) from canine corneal ulcers and minimal resistance to fluoroquinolones.3 

Medical management of melting ulcers is successful in 55% to 80% of patients that receive aggressive treatment, but referral for surgical management may be required in some dogs.^1,2,4 Geographic variation and initial antibiotic selection may influence the corneal bacterial population. Prompt diagnosis and an intensive treatment plan can help provide a successful outcome in patients with melting ulcers.

Key pearls to put into practice:

Corneal cytology combined with culture and susceptibility testing is recommended in all patients with deep or melting ulcers. In-clinic cytology can help direct initial antibiotic therapy.

Multimodal topical antibiotic therapy with a combination of both gram-positive and gram-negative activity may help improve the spectrum of antimicrobial coverage. Potential combinations include tobramycin/cefazolin, gentamicin/chloramphenicol, and ciprofloxacin/cefazolin. Alternatively, monotherapy with a second-generation fluoroquinolone may be sufficient in many cases pending culture and susceptibility testing.

Anticollagenase therapy (eg, topical serum or plasma) and oral doxycycline may help slow progression of keratomalacia.

Frequent, rigorous (eg, every 2 hours during waking hours and every 4 hours overnight) topical medication application is important to manage melting ulcers. Daily or frequent recheck examinations can help determine whether surgical stabilization is necessary. Referral to a veterinary ophthalmologist early in the course of disease may improve the long-term outcome.

Feline eosinophilic keratoconjunctivitis is a common disorder of the cornea and conjunctiva characterized by inflammation and plaque formation with eosinophils. The etiopathogenesis is unknown, but an immune-mediated component has been proposed.¹ Cytology of raised corneal lesions or plaques is critical for diagnosis, and the presence of one eosinophil can confirm diagnosis. 

This study sought to correlate clinical and cytologic findings in cats with eosinophilic keratoconjunctivitis. Corneal cytology slides from 18 eyes (15 cats) were retrospectively examined and compared with clinical images of the patient. Slides and clinical images were scored with a standardized system. Cell types (including eosinophils, mast cells, neutrophils, globule leukocytes, small lymphocytes, and plasma cells) were recorded and compared with degree of conjunctival inflammation and discharge, corneal inflammation, and fluorescein uptake. 

Larger conjunctival discharge scores were correlated with higher cytologic scores for eosinophils and neutrophils; higher neutrophil scores were associated with increased corneal opacity area scores. A wide variation in cell type combinations was also seen on cytology. 

Future studies should investigate potential disease subtypes of eosinophilic keratoconjunctivitis and the ability to correlate cytologic changes with medication choices or clinical prognosis.

Key pearls to put into practice:

Diversity of cell types found on cytology in cats with eosinophilic keratoconjunctivitis suggests there may be several subtypes of this disorder that are currently categorized as one group. This may account for differences in clinical course and treatment response.

Number of eosinophils found on cytology does not correlate with overall severity of clinical disease. Only a few eosinophils or mast cells may be noted despite substantial clinical disease.

Globule leukocytes may be present on cytology, but this has not been previously reported, and the clinical significance is unknown.

The etiology of canine idiopathic pulmonary fibrosis (ie, a chronic, progressive, interstitial fibrosing lung disease) is unclear; however, development of disease is thought to have a genetic component because West Highland white terriers are primarily affected. Gastroesophageal reflux and reflux aspiration may also play a role in development. This study evaluated protein expression in bronchoalveolar lavage fluid obtained from West Highland white terriers with and without canine idiopathic pulmonary fibrosis and sought to identify protein markers suggestive of reflux aspiration. The methods used allowed discrimination between dogs with and without canine idiopathic pulmonary fibrosis, but no clear evidence for GI aspiration was found.

Dietary management is a key therapeutic component in dogs diagnosed with protein-losing enteropathy (PLE)¹; many dogs with PLE have hyporexia or anorexia.² Guidelines for select enteropathies in humans suggest that feeding tubes (eg, nasogastric tubes) may be considered in cases in which oral enteral nutrition is not tolerated.³

This retrospective study evaluated whether assisted enteral nutrition (via nasogastric, esophagostomy, gastrostomy, or jejunostomy feeding tubes) improved outcome in dogs diagnosed with inflammatory PLE. Criteria for enrollment included serum albumin <2.8 g/dL, >3-week history of GI signs, exclusion of extra-intestinal disease (eg, protein-losing nephropathy, hepatic disease, hypoadrenocorticism, exocrine pancreatic insufficiency, pancreatitis), and histopathologic confirmation of inflammatory GI disease. 

Medical records of 57 dogs were reviewed, and assisted enteral feeding was found to be significantly associated with a positive outcome in dogs that required both diet and immunosuppression management. Insufficient data were available to determine the effects of assisted enteral nutrition in dogs managed with diet alone. A positive outcome was defined as survival ≥6 months or death unrelated to PLE. 

Many dogs that did not receive assisted-enteral feeding (47%) were hyporexic or anorexic. Previous experimental studies have shown that anorexia may lead to impaired intestinal immune function and a higher risk for bacterial translocation.^4,5 

Assisted enteral feeding was associated with a 14% complication rate, but this may have been underestimated due to lack of follow-up. The overall median survival time for dogs with PLE was 360 days (range, 0-3,766 days). Median survival time for dogs with assisted enteral nutrition was longer than for those without assisted enteral nutrition (559 vs 282 days). Prospective studies are needed to fully determine the effects of assisted enteral nutrition on dogs with inflammatory PLE.

Key pearls to put into practice:

Assisted enteral nutrition via a feeding tube may improve the outcome in dogs with inflammatory PLE. Pet owners should understand potential adverse effects associated with feeding tubes and their placement.

Almost 50% of the dogs in this study that did not receive assisted enteral nutrition were hyporexic or anorexic. Hyporexia or anorexia in patients with PLE may have adverse physiologic effects.

Dogs with PLE can have prolonged survival times with appropriate management.

Dexmedetomidine is commonly used as a sedative or premedication for isoflurane anesthesia in dogs. Vagally mediated, dose-dependent, hemodynamic adverse effects (eg, bradycardia, atrioventricular [AV] block) are often profound. Lidocaine IV has been shown to increase heart rate in dogs when vagal tone is high.¹

This randomized crossover study was designed to evaluate the effects of lidocaine 2% as both an IV bolus and a CRI on heart rate and AV block after IV administration of dexmedetomidine. Six healthy, 18-month-old beagles were randomly assigned to one of 3 treatment groups; 2 groups included conscious (ie, SED1, SED2) dogs, and the third group was anesthetized with isoflurane (ie, ISO). Dexmedetomidine (10 µg/kg IV) was administered to all groups. 

Treatment in the SED1 and ISO groups included a lidocaine 2% bolus (2 mg/kg IV) 30 minutes after dexmedetomidine administration, followed 20 minutes later by a second bolus  and a 30-minute lidocaine 2% CRI (50 µg/kg/minute in the SED1 group and 100 µg/kg/minute in the ISO group). 

Treatment in the SED2 group included a lidocaine 2% bolus and a 50 µg/kg/minute lidocaine 2% CRI given 5 minutes after dexmedetomidine administration. 

All dogs in the SED1 and SED2 groups became bradycardic, and AV block was seen in 5 out of 6 dogs from each group 5 minutes after dexmedetomidine administration. One dog in the ISO group experienced AV block 5 minutes after dexmedetomidine administration. Lidocaine 2% increased heart rate significantly in all dogs; AV block persisted after 30 minutes in one dog in each of the SED1 and SED2 groups. Values for all cardiopulmonary variables improved after administration of lidocaine 2%.

Systemic vascular resistance index and mean arterial blood pressure were elevated after administration of dexmedetomidine. Lidocaine 2% decreased both parameters to clinically suitable levels. The authors noted that this response was unexpected, and the cause is unknown. 

Based on these results, lidocaine 2% to increase heart rate in dogs with bradycardia due to dexmedetomidine IV may be more desirable than an anticholinergic or reversal with atipamezole. Sedative and analgesic effects of dexmedetomidine are not affected by lidocaine 2%. 

This was a small study in healthy dogs; results may not apply to those with underlying disease.

Key pearls to put into practice:

In healthy dogs, negative hemodynamic responses (ie, bradycardia, AV block, hypertension) after dexmedetomidine IV is administered for sedation or premedication for isoflurane anesthesia are significantly decreased by lidocaine 2% (2 mg/kg IV).

In dogs that receive dexmedetomidine IV, lidocaine 2% (2 mg/kg IV bolus and/or 50-100 µg/kg/minute CRI) may improve hemodynamics more effectively than an anticholinergic or reversal with atipamezole.^2-4

The sedative and analgesic effects of dexmedetomidine are maintained in dogs when lidocaine 2% is used to improve cardiovascular variables.

Although time to efficacy of allergen-specific immunotherapy for treatment of canine atopic dermatitis is expected to be slower than with other treatments (eg, antiallergic drugs, biologics), time to clinical efficacy of allergen-specific immunotherapy is unclear. This study reviewed data on 194 dogs from 12 publications to obtain information on efficacy rate and time to efficacy of subcutaneous immunotherapy for treatment of atopic dermatitis. Efficacy was defined as a ≥50% reduction in pruritus and/or skin lesions. Efficacy rate ranged from 65% to 100%, and time to efficacy ranged from 3 to 9 months. Novel allergen-specific immunotherapy regimens resulted in similar to higher efficacy rates and shorter time to efficacy than aqueous and alum-precipitated–based subcutaneous immunotherapy formulations. Because time to efficacy for current aqueous and alum-precipitated regimens is variable, the authors recommend that atopic dogs receiving this type of subcutaneous immunotherapy undergo progress evaluations at least every 3 months.

• Cobalamin (vitamin B₁₂) is critical to the function of many metabolic processes. Therefore, deficiencies in cobalamin can occur for many reasons and lead to a variety of clinical signs.
• Cobalamin deficiency can lead to poor outcomes in dogs and cats with chronic enteropathy and/or exocrine pancreatic insufficiency, and patients with cobalamin deficiency often will not respond to management of the underlying disorder unless or until cobalamin is supplemented.
• Oral cobalamin supplementation has traditionally been suggested not to be as effective as parenteral supplementation; however, recent studies show that oral supplementation is as effective as parenteral administration.
• COBALEQUIN® is an oral cobalamin supplement with the added benefit of containing 5-methyltetrahydrofolate (5-MFT), a naturally occurring form of folate that is well absorbed at varying pH levels and has minimal interactions with other drugs or supplements. COBALEQUIN® is a chewable tablet specifically formulated to provide stable cobalamin for dogs and cats.

Cobalamin deficiency in small animals can result from various causes,^2,3 such as chronic GI disease, hereditary defects (reported in Chinese shar-peis and isolated families of giant schnauzers, border collies, and beagles), short-bowel syndrome, small intestinal dysbiosis, and exocrine pancreatic insufficiency.⁴ Plant foods contain little to no cobalamin; therefore, feeding a vegan diet can potentially lead to cobalamin deficiency.² Older cats are also more susceptible to cobalamin deficiency, regardless of other physical or hereditary factors.⁵ Small intestinal dysbiosis can be associated with cobalamin deficiency, although this association is not specific or sensitive.

Most dogs and cats with cobalamin deficiency show clinical signs of GI disease, such as anorexia, vomiting, and/or diarrhea, which could be a cause or effect of cobalamin deficiency. Other clinical signs include failure to thrive and both central and peripheral neuropathies.³ Laboratory findings such as nonregenerative anemia, leukopenia, hypoglycemia, and hyperammonemia have been associated with cobalamin deficiency.³ In a 2005 case study, a border collie with selective cobalamin deficiency was presented with hyperammonemic encephalopathy that fully responded to cobalamin supplementation.⁶ In another case report, an 8-year-old female cat was presented with neurologic signs and found to have hyperammonemia. Treatment with cobalamin resulted in resolution of the neurologic signs within 8 weeks.⁷

Although cobalamin deficiency is defined as a lack of cobalamin on a cellular level, there are no direct means of assessing cobalamin status on a cellular level. When cobalamin is lacking on a cellular level, metabolism changes and methylmalonic acid accumulates; thus, serum methylmalonic acid concentration can be used as a surrogate marker of cellular cobalamin status.^8,9 However, measurement of this metabolite is technically involved and time-consuming and is only available on a limited basis (see Suggested Reading). Because of this, measurement of serum cobalamin concentration has traditionally been used to help assess cobalamin status, although some patients with cobalamin deficiency do not have severely decreased serum cobalamin concentrations on a cellular level. Therefore, supplementation is recommended for patients with a low or low-normal serum cobalamin concentration (<400 ng/L).

Several assays for measuring serum cobalamin concentrations have been developed and validated for human use. However, all assays must also be analytically validated for use in dogs and cats before they can be used to measure serum cobalamin concentration in these species. In addition, reference intervals are not transferrable between laboratories, and each laboratory should establish its specific reference interval. Thus, veterinarians should inquire whether the assay offered has been validated in the target species and whether a laboratory-specific reference interval has been determined.

Hypocobalaminemia has been suggested to be a negative risk factor for a poor outcome in dogs and cats with chronic enteropathy. Similarly, hypocobalaminemia is a negative risk factor for a poor outcome in dogs with exocrine pancreatic insufficiency (EPI), with a median survival time for dogs with EPI and hypocobalaminemia being 3.7 years and 7.4 years for those not hypocobalaminemic.¹⁰ More importantly, patients with cobalamin deficiency often do not respond to management of the underlying disorder unless or until cobalamin is being supplemented.

The most common form of cobalamin used for supplementation is cyanocobalamin. However, hydroxocobalamin or methylcobalamin may also be used in patients, although these are typically more challenging to obtain and can be more expensive. Traditionally, it has been suggested that oral cobalamin supplementation may not be effective, as absorption of orally administered cobalamin is complex and inhibited by cobalamin deficiency; however, European studies have suggested that high doses of cobalamin can successfully be used for oral supplementation in humans.^11,12 Recent data have shown that oral cobalamin supplementation is as effective as parenteral administration.⁴ Dosing schedules for oral supplementation are empiric, with daily supplementation administered for 3 months and recommendations for cobalamin concentrations to be re-evaluated 3 to 4 weeks after discontinuation.¹³

COBALEQUIN® is an oral cobalamin supplement with the added benefits of containing 5-methyltetrahydrofolate (5-MFT), the metabolically active form of folate. COBALEQUIN® is a chewable tablet specifically formulated to provide stable, palatable cobalamin for dogs and cats.

In a retrospective study, 51 client-owned dogs with low-normal or decreased serum cobalamin concentrations received oral cyanocobalamin (250-1000 μg once daily) for a variable period. On follow-up, serum cobalamin concentrations had increased in all dogs.⁴ Similarly, in a retrospective study of client-owned cats with hypocobalaminemia and clinical signs of GI disease, 25 cats with initial serum cobalamin concentrations <250 pmol/L (338.8 ng/L) were administered daily oral cobalamin tablets.¹⁴ After 27 to 94 days, all cats had serum cobalamin concentrations above the upper limit of the reference interval. In another study, 18 dogs diagnosed with EPI were administered oral cyanocobalamin.¹⁵ After 19 to 199 days of oral supplementation, all dogs showed normal or even supranormal concentrations (lowest serum cobalamin concentration after supplementation, 794 ng/L) after a median follow-up period of 41 days.¹⁵

More recently, there have been 2 prospective studies related to oral cobalamin supplementation In one prospective study of 49 hypocobalaminemic dogs randomly assigned to receive either oral or parenteral cobalamin supplementation, all 49 dogs showed normocobalaminemia after supplementation at the 90-day follow-up. There was no difference between the parenteral or oral route of cobalamin administration.¹³ In another prospective study, 46 hypocobalaminemic dogs (due to either chronic enteropathy or EPI) were randomly assigned to receive either oral or subcutaneous cobalamin supplementation, with both groups showing a significant increase in serum cobalamin concentrations and a significant decrease in serum methylmalonic acid concentrations at ≈80 to 90 days after initiation of supplementation.¹⁶

Hypocobalaminemia can have adverse clinical effects in both dogs and cats, and it is essential to recognize that there are a variety of causes of cobalamin deficiency. GI disease should be recognized as a cause and effect of cobalamin deficiency, and testing and supplementation should be initiated when indicated. Fortunately, oral cobalamin supplementation can provide serum levels comparable to parenteral supplementation for many, if not most, patients. Both retrospective and prospective studies have shown that the efficacy of oral cobalamin supplementation is similar to parenteral supplementation, regardless of the underlying etiology of either chronic enteropathy or EPI.

Preventing hospital-acquired infection is important for reducing morbidity in veterinary patients. Multimodal disinfection with chemical detergents is often used to clean gross material. Chemical disinfection can also reduce microbial counts; however, some microbes persist, and novel disinfection strategies may be beneficial.

This study evaluated use of a novel ultraviolet-C (UV-C) light in the operating room to reduce bacterial burden. Four surgical environments (ie, equine referral hospital, small animal referral hospital, academic research hospital, necropsy suite) were included. Microbial counts were evaluated before and after use of the UV-C light; overall mean microbial count was reduced by 94% after a single 45-minute treatment and 99% after a second treatment.

The authors concluded that reducing the environmental bacterial bioburden may decrease the number of surgical site infections.

UV-C light source is an expensive robot designed for human medicine. Other technologies, however, are under development and may help reduce the cost, making this treatment more feasible for smaller practices.

Key pearls to put into practice:

Detergents and chemical disinfecting agents cannot ensure a sterile environment. Routine microbial testing of common contact surfaces can help monitor for possible persistent environmental contamination.

A UV-C light may mitigate the environmental bacterial bioburden without contributing to antimicrobial resistance.

UV-C light systems can be cost prohibitive, but technology innovations may reduce the expense of these systems. The cost:benefit ratio of reducing surgical site infections and investing in such equipment should be evaluated.

According to this study, ≈1.2% of emergency veterinary visits are for mild allergic reactions. Type I hypersensitivity reactions occur when immunoglobulin E antibodies on the surface of mast cells and basophils (formed during initial exposure to an allergen) crosslink and trigger degranulation after re-exposure to the allergen. Exposure can occur via direct contact with or ingestion, inhalation, or injection of an allergen. Mast cell and basophil degranulation releases histamine, leukotrienes, and prostaglandins. Histamine activates H₁ receptors on the endothelium, vascular smooth muscle, hepatocytes, and lymphocytes. 

Clinical signs of a mild allergic reaction include urticaria, angioedema, and pruritus. Anaphylaxis is a systemic type I hypersensitivity reaction that can progress to anaphylactic shock, which involves multiorgan dysfunction with cardiovascular collapse. In humans, only 1% of allergic reactions are classified as anaphylactic.¹ 

Glucocorticoids block inflammation generated by the arachidonic acid cascade; steroids require 4 to 6 hours to downregulate this late-phase response and turn off proinflammatory gene transcription. Diphenhydramine is a rapidly acting H₁-histamine–receptor blocker that minimizes the effects of histamine on target organs.

This study retrospectively compared outcomes in dogs with mild allergic reactions that were given an initial treatment of diphenhydramine alone versus diphenhydramine and a glucocorticoid. A control group in which no treatment was given was not included. 

All 880 dogs in the study received diphenhydramine IM; dogs that were given glucocorticoids (n = 581) also received variable doses of dexamethasone sodium phosphate IV (range, 0.02-2 mg/kg; median, 0.19 mg/kg). Most dogs (72%) had a clinical response after initial treatment. Adding a glucocorticoid to the treatment regimen for a mild allergic reaction did not improve the response rate to initial therapy, need for additional care after discharge, or persistence of signs at follow-up.

Key pearls to put into practice:

Diphenhydramine (2 mg/kg IM once)² can treat uncomplicated allergic reactions.

Oral diphenhydramine (2 mg/kg PO every 8 hours for 2-3 days) can be administered to prevent recurrence of clinical signs in patients with possible persistent antigen exposure.

Corticosteroids are not needed during initial treatment, as they do not improve outcomes and may be associated with adverse effects (eg, GI upset, increased risk for infection).³

Cats with periuria (ie, urinary elimination outside the litter box) are less likely to be adopted or are likely to be returned shortly after adoption; thus, shelters have historically either refused intake of and/or elected euthanasia for these cats without further intervention.

In this study, investigators surmised there would be no differences in outcomes or length of shelter stay between periuric and nonperiuric cats in the authors’ shelter population.

Outcome data of 294 cats with known periuria were collected over a 6-year period and included length of shelter stay, adoption and return rates, and euthanasia rates. Average length of stay over the study period differed significantly between periuric and nonperiuric cats (52.6 and 31.6 days, respectively); however, year-by-year analysis showed no significant differences for the latter 4 years of the study. Although cats with periuria had slightly higher return rates (23.1% vs 15.4%), <50% were returned specifically because of periuria.

Intervention strategies were implemented for cats with periuria. Each cat reported or observed to have elimination problems was medically evaluated and given a litter box preference trial, including box and substrate options. Cats were only available for adoption once they were reliably using a litter box for 5 consecutive days. The shelter offered full transparency regarding medical and behavioral histories, as well as education and follow-up opportunities. Results suggest that in the absence of physical disease, cats often develop periuria as a result of environmental influences. Furthermore, these cats may return to normal, desirable elimination patterns when placed in an alternate environment (likely one more catered to their behavioral needs and elimination preferences).

Key pearls to put into practice:

A history of inappropriate elimination does not deter most potential cat adopters; this is important to consider when making intake and euthanasia decisions.

Behavioral periuria has a high likelihood of resolution when the environment is changed to better suit the cat’s needs.

Establishing litter and litter box preferences at the beginning of a cat’s shelter stay and providing education and support for adopters may be key to successful adoption of cats with periuria.

This short case series described use of printed electroceutical dressings for treatment of nonhealing, infected chronic wounds. Bacteria use electrostatic interactions for surface adhesion¹; electroceuticals generate electric fields from open circuit potentials to help disinfect wounds but have no current flow. Conversely, the printed electroceutical dressings in this study used direct current with a battery pack as a source of electrical potential. Direct current has inhibitory effects against gram-positive and gram-negative bacteria.^2-4 Wound size decreased by ≈4.2 times in a dog treated with a printed electroceutical dressing for 10 days and by ≈2.5 times in a cat after 17 days of treatment. Culture of wound punch biopsies were negative. Wounds were clinically healed by 67 days in the dog and 47 days in the cat; no further treatment was necessary.

Elimination diet trial and food challenge testing are the gold standard for diagnosing cutaneous adverse food reaction (CAFR), but many pet owners are reluctant to perform the 8-week food challenge.

This study included 46 dogs with CAFRs and characterized owner-observed adverse reactions to food challenge after elimination diet trial. A 4-week trial using a single-source protein (ie, horse meat, salmon) diet resulted in significant clinical improvement in pruritus scores. All dogs exhibited pruritus during food challenge: 23.9% within 3 to 6 hours and 60.9% within 12 hours. Only one dog developed clinical signs as late as 10 days after food challenge. Dogs were given prednisolone (1 mg/kg every 12 hours for 5 days) when pruritus was observed and returned to the elimination diet.

The most common sites of pruritus after food challenge were the limbs (56.5%) and face (26.1%). Time to recurrence of clinical signs may have been influenced by transit time in the GI tract. Orally administered antigens require a mean time of 3 hours to reach the blood.¹ No other clinical signs associated with CAFR were observed, and none of the dogs exhibited severe clinical signs (eg, anaphylaxis, respiratory signs) after food challenge.

Key pearls to put into practice:

All dogs in the study showed significant clinical improvement after 4 weeks of an elimination diet, but the small sample size may not be representative of the general population. Performing a diet trial for ≥8 weeks is recommended.

Dogs were given prednisolone (1 mg/kg every 12 hours) when clinical signs appeared after food challenge; a favorable response was observed. Many dogs with CAFR do not respond to a lower dose of prednisolone (1 mg/kg every 24 hours), possibly due to type III or type IV hypersensitivity. Twice-daily administration should be considered.

Clinical signs other than pruritus are not likely to occur with food challenges. Owners may be more likely to perform food challenge if they understand the risk is minimal and prednisolone is administered once pruritus is observed.

Bentley is fed a commercial diet. Vaccinations are current, but his owner reports administration of flea, tick, and heartworm preventives is inconsistent and often forgotten for 1 to 2 months at a time. 

Bentley has no travel history, lives in Florida, and is an active dog that swims in the family pool and goes on nightly walks. Two nights prior to presentation, he resisted going on his regular walk. On the next night, he was again reluctant to go on a walk and woke his owners up several times by whining and pacing. He was taken outside multiple times during the night and urinated normally each time.

On physical examination, Bentley’s temperature is 99.7°F (37.6°C). Respiratory rate is 36 breaths per minute at rest, heart rate is 180 bpm, and capillary refill time is 3.5 seconds. BCS is 8/10. 

It is difficult to auscultate the heart because of Bentley’s constant panting, but no murmurs or arrhythmias are identified. Lung sounds are normal over all lung fields. Pulses are weak and synchronous with the heartbeat. There is a palpable fluid wave in the abdomen and a positive hepatojugular reflux. All extremities feel warm to the touch. The remainder of the physical examination is normal. 

There is no evidence of trauma, and Bentley gets up a couple of times to reposition himself in the examination room. He does not seem anxious but appears uncomfortable when lying down, similar to the behavior that prompted presentation to the clinic.

Focused cage-side ultrasonography was performed on the abdomen and thorax. A large amount of both free abdominal fluid and pericardial effusion was identified. There was also evidence of cardiac tamponade. 

A peripheral catheter was placed for fluid, and possible lidocaine, administration. Pericardiocentesis was performed, and 450 mL of serosanguineous fluid was removed. Fluid packed cell volume was 11% and total solids was 2.3 mg/dL compared with peripheral blood packed cell volume of 43% and total solids of 8.2 mg/dL. Bentley did well during pericardiocentesis but remained uncomfortable. 

Abdominocentesis was then performed, and 3.1 L of serosanguineous fluid was removed. Bentley was visibly more comfortable afterward and slept the rest of the day while being monitored for increases in heart rate or unusual behavior. His heart rate was 40 to 60 bpm while he was asleep and 100 to 120 bpm when he was awake. 

Bentley was hospitalized for 24 hours, and a recheck thoracic-focused assessment with sonography for trauma was performed to ensure there was no further fluid accumulation. He was discharged the next day, and a full cardiac evaluation was scheduled for the 2-week recheck. 

At the recheck, there was recurrent pericardial effusion without evidence of tamponade; no masses were visualized. Repeat pericardiocentesis was performed at that time and 2 months later, at which time a pericardiectomy was also performed to prevent further episodes of tamponade. Histopathologic evaluation of the pericardium showed changes consistent with chronic inflammation and mesothelial proliferation.

Poncho, a 3-month-old intact male Portuguese water dog, was presented for lethargy, anorexia, and onset of seizures. He was purchased from a breeder and received one distemper/hepatitis/parvovirus/parainfluenza vaccination at a wellness examination 3 weeks prior. 

Lethargy and hyporexia were present 4 days prior to presentation. Trembling and mouth chattering began 2 days prior to presentation and progressed to fly-biting activity and, eventually, generalized seizures (duration, 1-2 minutes), including 2 seizures the night before and 3 seizures the day of presentation. It is unknown if there were additional seizures overnight.

On presentation, Poncho was actively experiencing a seizure. Levetiracetam (60 mg/kg IV once) was administered. Physical examination shortly after spontaneous cessation of the seizure revealed hyperthermia (104.6°F [40.3°C]), mildly increased lung sounds bilaterally, and a moist cough. Pulse was 148 bpm, and respiratory rate was 56 breaths per minute. Neurologic examination showed dull mentation, bilaterally absent menace response, ambulatory tetraparesis with pelvic limb proprioceptive ataxia, and postural reaction deficits in all limbs. The remainder of the physical examination was unremarkable.

Differential diagnoses for seizures included infectious meningoencephalitis (eg, canine distemper virus [CDV] infection, neosporosis, toxoplasmosis, tick-borne disease [eg, Rocky Mountain spotted fever, ehrlichiosis], fungal infection [less likely]), noninfectious meningoencephalitis (eg, meningoencephalitis of unknown etiology), congenital anomalies (eg, hydrocephalus, porencephaly), hepatic encephalopathy secondary to portosystemic shunt, and toxin exposure.

CBC results showed a mild neutropenia (2,900/µL; normal, 3,300-10,100/µL), lymphopenia (500/µL; normal, 1,000-3,900/µL), and normocytic, hypochromic, nonregenerative anemia (hematocrit, 34.7%; normal, 41.7%-58.1%). Serum chemistry profile, urinalysis, and paired serum bile acid test results were unremarkable; thoracic radiographs appeared normal.

CDV real-time reverse transcription-PCR (RT-PCR) and serology (virus neutralization) results were positive (48; normal, <8). Although other infectious disease testing (eg, neospora and toxoplasma titers, tick-borne disease titers or PCR) could have been considered, CDV testing was the initial focus because of Poncho’s signalment, clinical history, concurrent neurologic and respiratory signs, and CBC findings. 

Pending CDV results, brain MRI and CSF analysis were performed to evaluate for other structural causes of seizures. Brain MRI showed multifocal, asymmetric, intra-axial lesions in the left cerebrum and brainstem (Figure 1). Most likely differential diagnoses included infectious encephalopathies (eg, CDV infection) or meningoencephalitis of unknown etiology. CSF analysis was normal, and CSF distemper titer was negative (<1:4). Results likely reflected the acute stage of CDV encephalitis, during which CNS lesions are primarily characterized by direct viral replication and cellular injury leading to noninflammatory demyelinating lesions.^1-3

Treatment primarily focused on seizure control and supportive care. Levetiracetam (60 mg/kg IV once) was administered as initial treatment for cluster seizures. Active cooling with wet towels and fans was performed and lactated Ringer’s solution (120 mL/kg/day CRI) was administered until the patient’s temperature was <103°F (39.4°C).

Poncho was hospitalized, and levetiracetam (30 mg/kg PO every 8 hours) and lactated Ringer’s solution (120 mL/kg/day CRI) were continued. Phenobarbital (4 mg/kg IV once, then 3 mg/kg IV every 12 hours) was initiated due to continued breakthrough seizure activity, and broad-spectrum, empiric treatment for infectious and inflammatory conditions (dexamethasone sodium phosphate, 0.13 mg/kg IV every 12 hours; ampicillin/sulbactam, 50 mg/kg IV every 6 hours; clindamycin, 12.5 mg/kg IV every 12 hours) was administered, pending diagnostic test results.

Despite aggressive antiepileptic and supportive treatment, Poncho continued to have breakthrough seizures and was humanely euthanized. Postmortem evaluation was declined.

CDV encephalitis should be a differential diagnosis for young dogs presented with neurologic signs, especially with additional systemic signs, including fever, GI signs, respiratory signs, hyperkeratosis, and conjunctivitis.^1,4 CDV infection should be considered even in vaccinated patients; ≤30% of CDV cases occur in previously vaccinated dogs.⁴ 

Neurologic manifestations of CDV infection typically begin 1 to 3 weeks after systemic illness but can occur concurrently.¹ Most neurologic signs are possible because of multifocal distribution of CDV in the CNS, but common signs include seizures, cerebellar and vestibular signs, ataxia, paresis, and blindness.^1,4 Myoclonus (ie, sudden, repeated, involuntary contraction of a single small muscle or multiple large muscle groups; Video) is a classic sign of CDV infection and has been reported in <50% to 70% of dogs with CDV encephalitis.^4-6

Transmission can occur via body secretions but is most commonly spread by direct contact between dogs or by respiratory aerosols. Young dogs with respiratory or neurologic signs should be isolated in separate rooms or kennels. Personal protective equipment should be worn when handling these patients. CDV is a relatively labile virus that can be killed by most common disinfectants. Although CDV only survives hours to days (depending on the external environment), areas where other dogs can be exposed should be thoroughly disinfected, especially in shelter settings.^1,7

Antemortem diagnosis can be challenging and is often based on clinical suspicion alone.¹ Lymphopenia, often present due to the ability of CDV to cause immunosuppression, can help raise the index of suspicion.^1,8 Identifying intracytoplasmic inclusion bodies in RBCs and WBCs on a blood smear is pathognomonic (Figure 2). Inclusion bodies are only present in the acute phase of infection; thus, their absence does not rule out CDV infection.^1,6,9 

Thoracic radiographs may show an interstitial to alveolar lung pattern suggestive of bronchopneumonia.¹ MRI often shows multifocal, intra-axial lesions supportive but nonspecific for CDV encephalitis, as they can be consistent with other infectious or inflammatory diseases.^1,6,10 

CSF can be normal or show a mononuclear or lymphocytic pleocytosis and/or elevated protein.^1,6,10 Serologic examination has limited use because of high titers resulting from prior vaccination or previous subclinical or clinical infection.⁵ Real-time RT-PCR is the most sensitive and specific antemortem diagnostic test, but false-positive results are possible in patients that recently received a modified-live virus vaccine.^1,2 Quantitative RT-PCR may be better in these patients because the result can be used to distinguish between vaccine interference and wild-type infection.¹ 

Quantitative RT-PCR may have been preferable to confirm CDV infection in this case because the patient had been recently vaccinated; however, the positive real-time RT-PCR result was considered diagnostic based on supportive patient history, as well as clinical and other diagnostic findings.

There is no sufficient antiviral medication protocol to treat CDV infection. Treatment should therefore focus on supportive care, which can include IV fluids and antiemetics, parenteral nutrition, antiepileptics, hyperosmotic agents (eg, hypertonic saline, mannitol), and medications for systemic disease (eg, antibiotics for secondary pneumonia, GI supportive medications), as indicated. 

Seizure management in pediatric patients is generally similar to adult patients. Initial emergency stabilization can be achieved with a benzodiazepine bolus (with possible escalation to benzodiazepine CRI), ketamine bolus and/or CRI, or propofol CRI in refractory cases. Maintenance medications for pediatric use have not been well studied, but pediatric and adult seizures can usually be treated with the same anticonvulsant medications.¹¹ Drug disposition can be different in young patients compared with adults, requiring dosage alterations; adult dosages can be administered by 3 months of age.¹¹

Hyperosmotic agents can help reduce elevated intracranial pressure caused by inflammation and provide neuroprotective effects in patients with cluster seizures or status epilepticus; they could have been considered for this case, but the seizure stopped and the patient stabilized before they were administered.

Anti-inflammatory doses of corticosteroids can be administered to decrease inflammation and brain edema; however, use is controversial because inflammation has been associated with viral clearance.¹² Long-term signs (eg, myoclonus, for which there is no established, consistently effective treatment) are possible in patients that survive the acute phase of disease.¹ One case report used botulinum toxin to inhibit myoclonus.¹³

Preventive vaccination to decrease risk for infection is preferred for CDV management. Prognosis is variable. Severe seizures or other neurologic signs that cannot be managed result in poor to grave prognosis.