July / August 2022 | Volume 20 | Issue 5
Top 5 Ocular Consequences of Systemic Hypertension
Chronic Large Bowel Diarrhea in a Young Irish Setter
Systemic Hypertension in Dogs
Lethargy & Anxiety in a Dog
Seizures in a Young Portuguese Water Dog
Petechiation & Ecchymoses
Barry Hedgespeth, BVSc, North Carolina State University
Barry Hedgespeth
BVSc North Carolina State University
Barry Hedgespeth, BVSc, is a clinician investigator at North Carolina State University, where he recently completed a small animal internal medicine residency. He is now completing a PhD in immunology with a specific focus on mast cell biology and manipulation using splice-switching antisense oligonucleotides.
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)
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
Hepatic failure
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)
Splenomegaly
Endotoxemia
Thrombopathia
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)
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)
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
Vascular disorders
Immune-mediated
Secondary to medication, infection, neoplasia
Infectious (eg, Rickettsia rickettsii)
Hyperadrenocorticism (dog)
Have you ever seen hyperadrenocorticism cause petechiation or ecchymoses?
Thank you for responding.
Suggested Reading & Author Information
Bexfield NH, Villiers EJ, Herrtage ME. Immune-mediated haemolytic anaemia and thrombocytopaenia associated with Anaplasma phagocytophilum in a dog. J Small Anim Pract. 2005;46(11):543-548.
Blois S. Petechiae and ecchymoses. In: Ettinger SJ, Feldman EC, Côté E, eds. Textbook of Veterinary Internal Medicine. 8th ed. Saunders Elsevier; 2017:217-219.
Bloom JC, Blackmer SA, Bugelski PJ, Sowinski JM, Saunders LZ. Gold-induced immune thrombocytopenia in the dog. Vet Pathol. 1985;22(5):492-499.
Boudreaux MK, Catalfamo JL. Molecular and genetic basis for thrombasthenic thrombopathia in otterhounds. Am J Vet Res. 2001;62(11):1797-1804.
Boudreaux MK, Crager C, Dillon AR, Stanz K, Toivio-Kinnucan M. Identification of an intrinsic platelet function defect in Spitz dogs. J Vet Intern Med. 1994;8(2):93-98.
Boudreaux MK, Kvam K, Dillon AR, et al. Type I Glanzmann's thrombasthenia in a Great Pyrenees dog. Vet Pathol. 1996;33(5):503-511.
Callan MB, Bennett JS, Phillips DK, et al. Inherited platelet delta-storage pool disease in dogs causing severe bleeding: an animal model for a specific ADP deficiency. Thromb Haemost. 1995;74(3):949-953.
Cortese L, Sica M, Piantedosi D, Ruggiero G, Pero ME, Terrazzano G, Mastellone V, Ciaramella P. Secondary immune-mediated thrombocytopenia in dogs naturally infected by Leishmania infantum. Vet Rec. 2009;164(25):778-782.
Ellis J, Bell R, Barnes DC, Miller R. Prevalence and disease associations in feline thrombocytopenia: a retrospective case study of 194 cases. J Small Anim Pract. (2018);59(9):531-539.
Haysom LZ, Kennerly RM, Müller RD, Smith-Carr S, Chostopherson PW, Boudreaux MK. Identification and characterization of Glanzmann thrombasthenia in 2 closely related mixed-breed dogs. J Vet Intern Med. 2016;30(2):642-646.
Hedgespeth BA, Tefft KM, Kendall AR. Reversible myelosuppression suspected to be secondary to linezolid in a cat with infected subcutaneous ureteral bypass systems. J Fel Med Surg. 2020;6(2):2055116920967226.
Jo'neill E, Acke E, Tobin E, McCarthy G. Immune-mediated thrombocytopenia associated with angiostrongylus vasorum infection in a Jack Russell terrier. Ir Vet J. 2010;63(7):434-440.
Mellor PJ, Roulois AJA, Day MJ, Blacklaws BA, Knivett SJ, Herrtage ME. Neutrophilic dermatitis and immune-mediated haematological disorders in a dog: suspected adverse reaction to carprofen. J Small Anim Pract. 2006;46(5):237-242.
Nakamura R, Fenty RK, Bianco D. Presumptive immune-mediated thrombocytopenia secondary to massive Africanized bee envenomation in a dog. J Vet Emerg Crit Care. 2013;23(6):652-656.
Pritchard JC, Birkenheuer AJ, Hanel RM, Wood MW. Copperhead (Agkistrodon contortrix) envenomation of dogs: 52 cases (2004-2011). J Am Anim Hosp Assoc. 2014;50(5):338-344.
Shropshire S, Dow S, Lappin M. Detection and dynamics of anti-platelet antibodies in thrombocytopenic dogs with and without idiopathic immune thrombocytopenia. J Vet Intern Med. 2020;34(2):700-709.
Wallisch K, Trepanier LA. Incidence, timing, and risk factors of azathioprine hepatotoxicosis in dogs. J Vet Intern Med. 2015;29(2):513-518.
Weiss D, Aird B. Cytologic evaluation of primary and secondary myelodysplastic syndromes in the dog. Vet Clin Path. 2001;30(2):67-75.
Michael H. Brown, DVM, MS, DACVO, Veterinary Ophthalmology Services, Oradell Animal Hospital, Paramus, New Jersey
Michael H. Brown
DVM, MS, DACVO Veterinary Ophthalmology Services, Oradell Animal Hospital, Paramus, New Jersey
Michael H. Brown, DVM, MS, DACVO, is president and owner of Veterinary Ophthalmology Services and a consultant staff veterinary ophthalmologist at Oradell Animal Hospital, both in Paramus, New Jersey. Dr. Brown earned his DVM from Kansas State University, where he also completed a comparative ophthalmology residency and earned his MS. He completed a small animal internship at The Animal Medical Center in New York, New York. Dr. Brown has written numerous scientific papers and lectures nationwide. His interests include diseases of the cornea, corneal surgery, intraocular surgery, diseases of the retina, laboratory animal ophthalmology, ophthalmic photography, and the role of oxidative stress and nutrition on diseases of the eye.
FIGURE 1 Mydriasis and altered tapetal reflection secondary to serous retinal detachment in a cat
Hypertension is a common cause of vision changes and loss and increased risk for damage to the brain, kidneys, and heart.1-4 Ocular lesions are often an initial clinical sign (see Diagnosing & Treating Hypertension).
Following are the 5 most common ophthalmic sequelae of systemic hypertension in the author's experience.
Decreased Vision/Blindness
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
FIGURE 2 Fixed, dilated pupil (common secondary to systemic hypertension) and subsequent serous retinal detachment in a cat
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
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
FIGURE 3 Fresh, characteristic keel-boat–shaped preretinal hemorrhages (arrows) between the retina and vitreous humor secondary to systemic hypertension in a dog
FIGURE 4 Multifocal retinal hemorrhages of varying shapes in the tapetum secondary to systemic hypertension in a dog
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/Intraocular Hemorrhage
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.
FIGURE 5 Ventral anterior chamber hyphema secondary to hypertension in a dog
FIGURE 6 Progressing hyphema secondary to hypertension in a dog that obscures intraocular structures
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
FIGURE 7 Serous retinal detachment in a cat with hypertension. Characteristic billowing retina (arrow) due to subretinal fluid is visible.
FIGURE 8 Characteristic subretinal edema and billowing of the retina (arrows) associated with systemic hypertension in a cat
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).
Intraretinal Edema/Vessel Tortuosity
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).
FIGURE 9 Tortuous course of retinal vasculature due to hypertension in a dog
FIGURE 10 Retinal folding, hemorrhages, and multifocal areas of blurred and indistinct areas in the tapetum of a cat with hypertension
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.
DIAGNOSING & TREATING HYPERTENSION
Normal systolic blood pressure via Doppler ultrasonography is 131 to 154 mm Hg in dogs and 115 to 162 mm Hg in cats.6
Clinician experience, patient anxiety, and patient familiarity with the environment can affect blood pressure readings. Patients should thus be given 5 to 10 minutes in a quiet area to acclimate to the environment before blood pressure is measured.
Veterinary oscillometric devices with specially designed cuffs should be used. Circumference of the patient's limb should be measured to determine appropriate cuff size; cuff width should be 40% of the limb circumference in dogs and 30% of the limb circumference in cats. The cuff should be placed at the base of the tail, on a pelvic limb above the tarsus, or on a thoracic limb above the carpus. Hair should be clipped at the transducer location. Using ultrasonic gel, the transducer should be placed distally over the coccygeal artery at the base of the tail, the anterior tibial artery, or the ulnar artery on the palmar side of the distal aspect of the limb. Approximately 5 to 7 consecutive, consistent measurements should be obtained.14 Measurements with extreme variation should be discarded.
Environmental factors (eg, stress), disease processes (eg, secondary hypertension), and idiopathic factors can affect blood pressure. Kidney disease, hyperadrenocorticism, diabetes mellitus, obesity, primary hyperaldosteronism, and pheochromocytoma are associated with hypertension.14 CBC, serum chemistry profile, urinalysis, and abdominal ultrasonography are warranted in affected patients. Cardiac diagnostic investigation may be necessary to verify normal cardiac function. Complete eye examination should be performed, including Schirmer tear test, tonometry, fluorescein stain, and indirect ophthalmoscopy.17-22
Treatment is needed in patients with systolic blood pressure consistently >160 mm Hg via the Doppler oscillometric method. Patients with clinical signs of hypertension, a single measurement >160 mm Hg, and concurrent retinopathy lesions, encephalopathy, or chronic kidney disease also warrant treatment.14 Systolic blood pressure of 160 to 179 mm Hg is associated with moderate risk for damage to the kidneys, heart, brain, and eyes.14 Blood pressure >180 mm Hg indicates high risk for organ damage. Factors that can affect blood pressure and concurrent systemic disease should be considered when choosing a treatment protocol.
Effective early treatment of hypertension can resolve ocular clinical signs and result in vision recovery.4,23,24 Lack of treatment for ≥3 weeks generally results in a less favorable prognosis for recovery.24
Hypertension can be situational, secondary, or idiopathic. Once situational factors are ruled out, possible underlying disease or pharmacologic agents (eg, glucocorticoids, mineralocorticoids, erythropoiesis stimulants, phenylpropanolamine, phenylephrine, toceranib, sodium chloride) associated with secondary hypertension should be identified. Treatment for secondary hypertension should begin before the underlying condition is stabilized.
Once-daily treatment with antihypertensive medication is generally preferred, with the goal of gradual, consistent decrease in blood pressure to <140 mm Hg over several weeks.14 Rapid decrease in blood pressure should be avoided. If the first medication is not effective, the dose should be increased or consideration given to adding a second therapeutic agent. Therapy should be gradually adjusted if blood pressure remains between 140 and 160 mm Hg. Blood pressure <120 mm Hg may be associated with lethargy, tachycardia, syncope, and/or weakness, and treatment should be adjusted. Dietary salt restriction is generally not associated with a decrease in blood pressure.25,26
Hypertension in dogs is typically not an emergency. Angiotensin-converting enzyme inhibitors (eg, benazepril, enalapril, telmisartan) or calcium channel blockers (eg, amlodipine) are recommended. Amlodipine besylate is the first-choice treatment for cats with hypertension.27-29
Systemic Hypertension Medication Guidelines14
Dogs: 0.5 mg/kg every 12 to 24 hours
Cats: 0.5 mg/kg every 12 hours
Dogs: 0.1-0.25 mg/kg every 24 hours
Cats: 0.625-1.25 mg per cat every 24 hours
Telmisartan30
Dogs: 1-2 mg/kg every 24 hours
Cat: 1-2 mg/kg every 24 hours
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.
Leblanc NL, Stepien RL, Bentley E. Ocular lesions associated with systemic hypertension in dogs: 65 cases (2005-2007). J Am Vet Med Assoc. 2011;238(7):915-921.
Littman MP, Robertson JL, Bovée KC. Spontaneous systemic hypertension in dogs: five cases (1981-1983). J Am Vet Med Assoc. 1988;193(4):486-494.
Littman MP. Spontaneous systemic hypertension in 24 cats. J Vet Intern Med. 1994;8(2):79-86.
Maggio F, DeFrancesco TC, Atkins CE, Pizzirani S, Gilger BC, Davidson MG. Ocular lesions associated with systemic hypertension in cats: 69 cases (1985-1998). J Am Vet Med Assoc. 2000;217(5):695-702.
Martin CL. Evaluation of patients with decreased vision or blindness. Clin Tech Small Anim Pract. 2001;16(1):62-70.
Dixon-Jimenez A, Rapoport G, Brown SA. Systemic hypertension in dogs & cats. Today's Veterinary Practice. 2011;1(2):20-26.
Sessums K, Mariani C. Intracranial meningioma in dogs and cats: a comparative review. Compend Contin Educ Vet. 2009;31(7):330-339.
Cullen CL, Webb AA. Ocular manifestations of systemic diseases. In: Gelatt KN, ed. Veterinary Ophthalmology. 4th ed. Wiley-Blackwell; 2007:1477-1481.
Keyes JE, Goldblatt H. Experimental hypertension IV. Clinical and pathologic studies of the eyes: a preliminary report. Arch Ophthamol. 1937;17(6):1040-1054.
Telle MR, Betbeze C. Hyphema: considerations in the small animal patient. Top Companion Anim Med. 2015;30(3):97-106.
Roels E, Merveille AC, Moyse E, Gomart S, Clercx C, Mc Entee K. Diagnostic value of the pulmonary vein-to-right pulmonary artery ratio in dogs with pulmonary hypertension of precapillary origin. J Vet Cardiol. 2019;24:85-94.
Anand R, Tasman WS. Nonrhegmatogenous retinal detachment. In: Ryan SJ, Wilkinson CP, eds. Retina. Vol 3. 3rd ed. Mosby; 2001:2076-2099.
Anderson DH, Guérin CJ, Erickson PA, Stern WH, Fisher SK. Morphological recovery in the reattached retina. Invest Ophthalmol Vis Sci. 1986;27(2):168-183.
Acierno MJ, Brown S, Coleman AE, et al. ACVIM consensus statement: guidelines for the identification, evaluation, and management of systemic hypertension in dogs and cats. J Vet Intern Med. 2018;32(6):1803-1822.
Han HC. Twisted blood vessels: symptoms, etiology and biomechanical mechanisms. J Vasc Res. 2012;49(3):185-197.
Sansom J, Rogers K, Wood JLN. Blood pressure assessment in healthy cats and cats with hypertensive retinopathy. Am J Vet Res. 2004;65(2):245-252.
Williamson JA, Leone S. Noninvasive arterial blood pressure monitoring. In: Burkitt Creedon JM, Davis H, eds. Advanced Monitoring and Procedures for Small Animal Emergency and Critical Care. Wiley-Blackwell; 2012:134-144.
Kittleson MD, Olivier NB. Measurement of systemic arterial blood pressure. Vet Clin Small Anim Pract. 1983;13(2):321-336.
Haskins S. Monitoring anesthetized patients. In: Grimm KA, Lamont LA, Tranquilli WJ, Greene SA, Robertson SA, eds. Veterinary Anesthesia and Analgesia: The Fifth Edition of Lumb and Jones. Wiley-Blackwell; 2015:86-113.
Alexander B, Cannesson M, Quill T. Blood pressure monitoring. In: Ehrenwerth J, Eisenkraft J, Berry J, eds. Anesthesia Equipment Principles and Application. 2nd ed. Saunders; 2013:273-282.
Monteiro ER, Campagnol D, Bajotto GC, Simões CR, Rassele AC. Effects of 8 hemodynamic conditions on direct blood pressure values obtained simultaneously from the carotid, femoral and dorsal pedal arteries in dogs. J Vet Cardiol. 2013;15(4):263-270.
McMurphy RM, Stoll MR, McCubrey R. Accuracy of an oscillometric blood pressure monitor during phenylephrine-induced hypertension in dogs. Am J Vet Res. 2006;67(9):1541-1545.
Komáromy AM, Andrew SE, Denis HM, Brooks DE, Gelatt KN. Hypertensive retinopathy and choroidopathy in a cat. Vet Ophthalmol. 2004;7(1):3-9.
Young WM, Zheng C, Davidson MG, Westermeyer HD. Visual outcome in cats with hypertensive chorioretinopathy. Vet Ophthalmol. 2019;22(2):161-167.
Greco DS, Lees GE, Dzendzel G, Carter AB. Effects of dietary sodium intake on blood pressure measurements in partially nephrectomized dogs. Am J Vet Res. 1994;55(1):160-165.
Buranakarl C, Mathur S, Brown SA. Effects of dietary sodium chloride intake on renal function and blood pressure in cats with normal and reduced renal function. Am J Vet Res. 2004;65(5):620-627.
Elliott J, Barber PJ, Syme HM, Rawlings JM, Markwell PJ. Feline hypertension: clinical findings and response to antihypertensive treatment in 30 cases. J Small Anim Pract. 2001;42(3):122-129.
Jepson RE, Brodbelt D, Vallance C, Syme HM, Elliott J. Evaluation of predictors of the development of azotemia in cats. J Vet Intern Med. 2009;23(4):806-813.
Henik RA, Snyder PS, Volk LM. Treatment of systemic hypertension in cats with amlodipine besylate. J Am Anim Hosp Assoc. 1997;33(3):226-234.
Desmet L, van der Meer J. Antihypertensive treatment with telmisartan in a cat with amlodipine-induced gingival hyperplasia. JFMS Open Rep. 2017;3(2):2055116917745236.
Tammy J. Owens, DVM, MS, DACVN, University of Saskatchewan, Saskatoon, Saskatchewan, Canada
Tammy J. Owens
DVM, MS, DACVN University of Saskatchewan, Saskatoon, Saskatchewan, Canada
Tammy J. Owens, DVM, MS, DACVN, is an assistant professor and runs a clinical nutrition service for the Veterinary Medical Centre at University of Saskatchewan in Saskatoon, Saskatchewan, Canada. She earned her DVM from The Ohio State University, completed a rotating internship in small animal medicine and surgery at Mississippi State University, and completed a residency in small animal clinical nutrition and earned her MS in nutritional biology at University of California, Davis. Her research interests are clinical use of dietary fiber, nutritional content of whole-prey diets, and enteroendocrine signaling in response to diet.
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.
CLINICAL SIGNS OF SMALL VS LARGE BOWEL DIARRHEA
Clinical Sign
Small Bowel
Large Bowel
Constipation or tenesmus Rare Common
Frequency Normal or increased (2-3× per day) Increased (>3× per day)
Urgency Not common Common
Volume Increased Decreased
Mucus Rare Common
Hematochezia Not common Common
Weight loss Common Not common
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.
PRESUMPTIVE CHRONIC IDIOPATHIC LARGE BOWEL DIARRHEA SUBSET: FIBER-RESPONSIVE LARGE BOWEL DIARRHEA
Treatment & Management
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
A fiber trial should be used in patients with large bowel diarrhea that are stable and unresponsive to other initial interventions.
Psyllium fiber has a unique combination of attributes (see Properties of Psyllium Fiber) and has been beneficial in treatment of multiple diseases in several species.
The estimated median effective dosage of coarse psyllium fiber is 1.33 g/kg (range, 0.31-4.9 g/kg) every 24 hours5 and should be titrated to effect. The author typically starts at the lower end of the range for large bowel diarrhea (dividing the dose over daily meals) and increases the dose slowly as needed. Higher doses may be needed in some patients.
The effective dose may change depending on base diet, types and amounts of fiber already present, variabilities in individual patient gut microbiome, and other factors. For example, although total dietary fiber concentrations may be known for some pet foods, the amounts of individual fiber types and their total physiologic effects on the gut are typically unknown. Providing a diet that contains a special fiber blend and adding supplemental fiber is often based on trial and error and titration to effect.
A large subset of dogs with chronic idiopathic large bowel diarrhea responds to fiber.1,3,5 Further diagnostics or additional treatment (eg, behavioral therapy, antispasmodic medications) may be needed. Inflammatory bowel disease may need to be ruled out in patients that do not respond to routine interventions (eg, fenbendazole, metronidazole, tylosin, fiber).
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 studies3,4; however, these were referral cases, which may underrepresent success in the general population.
PROPERTIES OF PSYLLIUM FIBER
Psyllium, which is derived from seeds of Plantago spp plants, provides predominantly soluble dietary fiber that can increase digesta viscosity or form mucilaginous gels in water at sufficient concentration.11 Psyllium is less rapidly fermented in the colon compared with other soluble dietary fiber, which benefits the distal colon by allowing fermentation to occur there.
Psyllium increases concentrations of short-chain fatty acids, particularly n-butyrate, after fermentation by gut microflora. Short-chain fatty acids are beneficial in restoring microbial balance8 and acidifying colonic contents. N-butyrate is preferentially oxidized by colonocytes, increasing colonocyte proliferation, mucosal weight, brush border enzymes, and mucin secretion. Intestinal function is enhanced by increased absorption of water and electrolytes, improvement of the mucosal barrier and immune function, and inhibition of pathogenic bacteria.10,11
Psyllium also promotes peristalsis, cleansing, and viscosity or softening; slows transit time; and binds certain toxins.11 Psyllium has demonstrated success in patients with chronic idiopathic large bowel diarrhea and possesses unique attributes as a single fiber source in the author's experience.
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 idiopathic large bowel diarrhea is a diagnosis of exclusion, but the index of suspicion may be increased in some cases (eg, history of stressful events or possible anxiety-related behavior, absence of major abnormalities on physical examination or initial diagnostics, absence of significant or progressive weight loss, minimal or inconsistent response to standard empiric therapies).
Evidence-based protocols (eg, parasiticides, antibiotics, diet trials) prior to advanced diagnostics may avoid unnecessary diagnostics and reduce cost in patients with chronic diarrhea.
A highly digestible GI diet or elimination diet trials can be safely given prior to definitive diagnosis. If signs persist, transitioning to a high-fiber diet or supplementing with psyllium fiber may result in a positive response.
Patients with chronic large bowel diarrhea that respond to diet change with fiber supplementation have a good to excellent prognosis.
Titrating the fiber dose to effect is important. Administering a dose that is too low may prevent a positive response.
Long-term diet therapy and/or fiber supplementation may be needed.
Cave N. Nutritional management of gastrointestinal diseases. In: Fascetti AJ, Delaney SJ, eds. Applied Veterinary Clinical Nutrition. Wiley-Blackwell; 2012:175-219.
Lecoindre P, Gaschen FP. Chronic idiopathic large bowel diarrhea in the dog. Vet Clin North Am Small Anim Pract. 2011;41(2):447-456.
Leib MS. Chronic colitis in dogs. In: Bonagura JD, Kirk RW, eds. Current Veterinary Therapy XIII. W.B. Saunders; 1999:643-648.
Tilley LP, Smith FWK Jr. Fiber-responsive large bowel diarrhea. In: Tilley LP, Smith FWK Jr, Sleeper MM, Brainard BM, eds. Blackwell's Five-Minute Veterinary Consult: Canine and Feline. 7th ed. Wiley-Blackwell; 2021:528-529.
Leib MS. Treatment of chronic idiopathic large-bowel diarrhea in dogs with a highly digestible diet and soluble fiber: a retrospective review of 37 cases. J Vet Intern Med. 2000;14(1):27-32.
Volkmann M, Steiner JM, Fosgate GT, Zentek J, Hartmann S, Kohn B. Chronic diarrhea in dogs: retrospective study in 136 cases. J Vet Intern Med. 2017;31(4):1043-1055.
Bryan CE, Cade JC, Mackin AJ, Sullivant AM. Evaluation of a structured individualised protocol as a potential cost-effective diagnostic and therapeutic approach to chronic diarrhoea in the dog. Vet Med Sci. 2019;5(2):210-221.
Rossi G, Cerquetella M, Gavazza A, et al. Rapid resolution of large bowel diarrhea after the administration of a combination of a high-fiber diet and a probiotic mixture in 30 dogs. Vet Sci. 2020;7(1):21.
Ashraf W, Lof J, Jin G, Quigley EM. Comparative effects of intraduodenal psyllium and senna on canine small bowel motility. Aliment Pharmacol Ther. 1994;8(3):329-336.
Bednar GE, Patil AR, Murray SM, Grieshop CM, Merchen NR, Fahey GC Jr. Starch and fiber fractions in selected food and feed ingredients affect their small intestinal digestibility and fermentability and their large bowel fermentability in vitro in a canine model. J Nutr. 2001;131(2):276-286.
Singh B. Psyllium as therapeutic and drug delivery agent. Int J Pharm. 2007;334(1-2):1-14.
Stability of Dexamethasone When Added to Commercial Ear Cleaners
William Oldenhoff, DVM, DACVD, ACCESS Specialty Animal Hospital, San Fernando Valley, California
William Oldenhoff
DVM, DACVD ACCESS Specialty Animal Hospital, San Fernando Valley, California
William Oldenhoff, DVM, DACVD, is the staff dermatologist at ACCESS Specialty Animal Hospital in San Fernando Valley, California. Dr. Oldenhoff earned his DVM from University of Wisconsin–Madison, where he also completed a dermatology internship and residency. He has lectured worldwide, published numerous peer-reviewed articles, and contributed to several book chapters. His clinical interests are in recurrent pyoderma, Malassezia spp dermatitis, and allergy.
Emery CB, Outerbridge CA, Knych HK, Lam ATH, Gomez-Vazquez JP, White SD. Preliminary study of the stability of dexamethasone when added to commercial veterinary ear cleaners over a 90 day period. Vet Dermatol. 2021;32(2):168-e39.
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.
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.
CBD & THC Use in Cats
Lisa Sams Ebner, DVM, MS, DACVAA, CVA, Lincoln Memorial University, Harrogate, Tennessee
Lisa Sams Ebner
DVM, MS, DACVAA, CVA Lincoln Memorial University, Harrogate, Tennessee
Lisa Sams Ebner, DVM, MS, DACVAA, CVA, is an associate professor of anesthesiology at Lincoln Memorial University. She earned her DVM from University of Georgia and completed a residency in anesthesia at The Ohio State University. Her research interests include pharmacokinetics of anesthetic drugs, medical student education, acupuncture, and the relationship of wellness in the human-animal bond.
Kulpa JE, Paulionis LJ, Eglit GMI, Vaughn DM. Safety and tolerability of escalating cannabinoid doses in healthy cats. J Feline Med Surg. 2021;23(12):1162-1175.
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.
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.
*This study was funded by Canopy Animal Health.
American Veterinary Medical Association. Cannabis use and pets. AVMA website. Accessed October 6, 2021. https://www.avma.org/resources-tools/animal-health-and-welfare/cannabis-use-and-pets
American Veterinary Medical Association. Cannabis in veterinary medicine. AVMA website. August 2020. Accessed October 6, 2021. https://www.avma.org/sites/default/files/2021-03/APH-CannabisResources-Report-20201207.pdf
Hazzah T, Andre C, Richter G, McGrath S. Cannabis in veterinary medicine: a critical review. J Am Hol Vet Med Assoc. 2020;61:17-41.
Imaging Techniques to Detect Migrating Foreign Bodies
Sara A. Colopy, DVM, PhD, DACVS, University of Wisconsin–Madison
Sara A. Colopy
DVM, PhD, DACVS University of Wisconsin–Madison
Blondel M, Sonet J, Cachon T, Ségard-Weisse E, Ferrand FX, Carozzo C. Comparison of imaging techniques to detect migrating foreign bodies. Relevance of preoperative and intraoperative ultrasonography for diagnosis and surgical removal. Vet Surg. 2021;50(4):833-842.
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.
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.
Frendin J, Funkquist B, Hansson K, Lönnemark M, Carlsten J. Diagnostic imaging of foreign body reactions in dogs with diffuse back pain. J Small Anim Pract. 1999;40(6):278-285.
Schultz RM, Zwingenberger A. Radiographic, computed tomographic, and ultrasonographic findings with migrating intrathoracic grass awns in dogs and cats. Vet Radiol Ultrasound. 2008;49(3):249-255.
Armbrust LJ, Biller DS, Radlinsky MG, Hoskinson JJ. Ultrasonographic diagnosis of foreign bodies associated with chronic draining tracts and abscesses in dogs. Vet Radiol Ultrasound. 2003;44(1):66-70.
Jones JC, Ober CP. Computed tomographic diagnosis of nongastrointestinal foreign bodies in dogs. J Am Anim Hosp Assoc. 2007;43(2):99-111.
Bouabdallah R, Moissonnier P, Delisle F, et al. Use of preoperative computed tomography for surgical treatment of recurrent draining tracts. J Small Anim Pract. 2014;55(2):89-94.
Birettoni F, Caivano D, Rishniw M, et al. Preoperative and intraoperative ultrasound aids removal of migrating plant material causing iliopsoas myositis via ventral midline laparotomy: a study of 22 dogs. Acta Vet Scand. 2017;59(1):12.
Della Santa D, Mannucci T, Busoni G, Citi S. Sublumbar grass awns in two cats: ultrasonographic features and ultrasound-guided retrieval. JFMS Open Rep. 2019;5(2):2055116919885677.
Moretti G, Birettoni F, Caivano D, et al. Mini-invasive approach for removal of iliopsoas migrating grass awns with an atraumatic wound retractor. J Small Anim Pract. 2021;62(2):150-155
Caivano D, Birettoni F, Rishniw D. Ultrasonographic findings and outcomes of dogs with suspected migrating intrathoracic grass awns: 43 cases (2010-2013). J Am Vet Med Assoc. 2016;248(4):413-421.
Gibson EA, Balsa IM, Mayhew PD, et al. Utility of bronchoscopy combined with surgery in the treatment and outcomes of dogs with intrathoracic disease secondary to plant awn migration. Vet Surg. 2019;48(7):1309-1317.
Managing Melting Ulcers in Dogs
Georgina M. Newbold, DVM, DACVO, The Ohio State University
Georgina M. Newbold
DVM, DACVO The Ohio State University
Georgina M. Newbold, DVM, DACVO, is a clinical faculty member at The Ohio State University. She earned her DVM from University of California, Davis, and completed her comparative ophthalmology residency training at University of Tennessee. Dr. Newbold's areas of interest are cataracts and surgery of the lens, corneal disease, and feline ophthalmology.
Tsvetanova A, Powell RM, Tsvetanov KA, Smith KM, Gould DJ. Melting corneal ulcers (keratomalacia) in dogs: a 5-year clinical and microbiological study (2014-2018). Vet Ophthalmol. 2021;24(3):265-278.
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.
FIGURE Infected melting corneal ulcer in a wirehaired dachshund
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.
Whitley RD, Hamor RE. Diseases and surgery of the canine cornea and sclera. In: Gelatt KN, ed. Veterinary Ophthalmology. 6th ed. Wiley-Blackwell; 2021:1082-1172.
Guyonnet A, Desquilbet L, Faure J, Bourguet A, Donzel E, Chahory S. Outcome of medical therapy for keratomalacia in dogs. J Small Anim Pract. 2020;61(4):253-258.
McKeever JM, Ward DA, Hendrix DVH. Comparison of antimicrobial resistance patterns in dogs with bacterial keratitis presented to a veterinary teaching hospital over two multi-year time periods (1993-2003 and 2013-2019) in the southeastern United States. Vet Ophthalmol. 2021;24(6):653-658.
Cytology & Clinical Signs of Eosinophilic Keratoconjunctivitis in Cats
Kathern E. Myrna, DVM, MS, DACVO, University of Georgia
Kathern E. Myrna
DVM, MS, DACVO University of Georgia
Kathern E. Myrna, DVM, MS, DACVO, is a professor and ophthalmologist at University of Georgia. She earned her DVM from the Virginia-Maryland College of Veterinary Medicine and her MS from University of Wisconsin-Madison, where she also completed a residency. Dr. Myrna has received multiple teaching awards, including the Zoetis Distinguished Veterinary Teacher Award.
Lucyshyn DR, Vernau W, Maggs DJ, Murphy CJ, Leonard BC. Correlations between clinical signs and corneal cytology in feline eosinophilic keratoconjunctivitis. Vet Ophthalmol. 2021;24(6):620-626.
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.
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.
Prasse KW, Winston SM. Cytology and histopathology of feline eosinophilic keratitis. Vet Comp Ophthalmol. 1996;6(2):74-81.
Dean E, Meunier V. Feline eosinophilic keratoconjunctivitis: a retrospective study of 45 cases (56 eyes). J Feline Med Surg. 2013;15(8):661-666.
Speiss AK, Sapienza JS, Mayordomo A. Treatment of proliferative feline eosinophilic keratitis with topical 1.5% cyclosporine: 35 cases. Vet Ophthalmol. 2009;12(2):132-137.
Research Note: Role of GI Aspiration in West Highland White Terriers with Canine Idiopathic Pulmonary Fibrosis
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.
Maher RE, Mӓӓttӓ M, Beynon RJ, Laurila HP, McNamara PS, Rajamӓki MM. Quantitative proteomic analysis of bronchoalveolar lavage fluid in West Highland white terriers with canine idiopathic pulmonary fibrosis. BMC Vet Res. 2022;18(1):121. doi:10.1186/s12917-022-03202-x
Assisted Enteral Feeding in Dogs with Protein-Losing Enteropathy
Harry Cridge, MVB, MS, DACVIM (SAIM), MRCVS, Michigan State University
Harry Cridge
MVB, MS, DACVIM (SAIM), MRCVS Michigan State University
Harry Cridge, MVB, MS, MRCVS, DACVIM (SAIM), is an assistant professor of small animal internal medicine at Michigan State University. He earned his veterinary medical degree from University College Dublin in Ireland. Dr. Cridge also completed a small animal rotating internship, earned his MS, and completed an internal medicine residency at Mississippi State University. His clinical and research interests are in exocrine pancreatic disease, gastroenterology, and infectious disease.
Economu E, Chang Y, Priestnall SL, Kathrani A. The effect of assisted enteral feeding on treatment outcome in dogs with inflammatory protein-losing enteropathy. J Vet Intern Med. 2021;35:1297-1305.
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.
FIGURE Radiograph of a dog with an esophageal feeding tube placed in the distal third of the esophagus
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.
Craven MD, Washabau RJ. Comparative pathophysiology and management of protein-losing enteropathy. J Vet Intern Med. 2019;33(2):383-402.
Kathrani A, Sánchez-Vizcaíno F, Hall EJ. Association of chronic enteropathy activity index, blood urea concentration, and risk of death in dogs with protein-losing enteropathy. J Vet Intern Med. 2019;33(2):536-543.
Ruemmele FM, Veres G, Kolho KL, et al. Consensus guidelines of ECCO/ESPGHAN on the medical management of pediatric Crohn's disease. J Crohn's Colitis. 2014;8:1179-1207.
Hernandez G, Velasco N, Wainstein C, et al. Gut mucosal atrophy after a short enteral fasting period in critically ill patients. J Crit Care. 1999;14(2):73-77.
Deitch EA, Winterton J, Li M, et al. The gut as a portal of entry for bacteremia. Role of protein malnutrition. Ann Surg. 1987;205(6):681-692.
Treatment of Dexmedetomidine-Induced Bradycardia in Dogs
Julie Ann Smith, DVM, DACVAA, MedVet Medical and Cancer Center for Pets, Metairie, Louisiana
Julie Ann Smith
DVM, DACVAA MedVet Medical and Cancer Center for Pets, Metairie, Louisiana
Julie Ann Smith, DVM, DACVAA, is a staff anesthesiologist and department representative for MedVet Medical and Cancer Center for Pets in Metairie, Louisiana, as well as an owner and consultant for Veterinary Anesthesia and Analgesia Consulting. Dr. Smith earned her DVM from Texas A&M University. She also completed a small animal internship and anesthesiology residency at University of Missouri–Columbia and an anesthesiology residency at The Ohio State University.
Tisotti T, Valverde A, Hopkins A, O'Sullivan ML, Hanna B, Arroyo L. Use of intravenous lidocaine to treat dexmedetomidine-induced bradycardia in sedated and anesthetized dogs. Vet Anaesth Analg. 2021;48(2):174-186.
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.
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.
Lieberman NA, Harris RS, Katz RI, Lipschutz HM, Dolgin M, Fisher VJ. The effects of lidocaine on the electrical and mechanical activity of the heart. Am J Cardiol. 1968;22(3):375-380.
Congdon JM, Marquez M, Niyom S, Boscan P. Evaluation of the sedative and cardiovascular effects of intramuscular administration of dexmedetomidine with and without concurrent atropine administration in dogs. J Am Vet Med Assoc. 2011;239(1):81-89.
Granholm M, McKusick BC, Westerholm FC, Aspegrén JC. Evaluation of the clinical efficacy and safety of intramuscular and intravenous doses of dexmedetomidine and medetomidine in dogs and their reversal with atipamezole. Vet Rec. 2007;160(26):891-897.
Lemke KA, Tranquilli WJ, Thurmon JC, Benson GJ, Olson WA. Hemodynamic effects of atropine and glycopyrrolate in isoflurane-xylazine anesthetized dogs. Vet Surg. 1993;22(2):163-169.
Research Note: Time to Efficacy of Allergen-Specific Immunotherapy in Dogs with Atopic Dermatitis
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.
Tham HL, Olivry T. Determination of the efficacy rate and time-to-efficacy of subcutaneous immunotherapy in dogs with atopic dermatitis. Vet Dermatol. 2022;33(2):155-e44. doi:10.1111/vde.13048
Management of Cobalamin Deficiency in Dogs & Cats: Oral Supplementation
Jörg M. Steiner, MedVet, DrMedVet, PhD, DACVIM, DECVIM-CA, AGAF, Texas A&M University
Jörg M. Steiner
MedVet, DrMedVet, PhD, DACVIM, DECVIM-CA, AGAF Texas A&M University
Jörg M. Steiner, MedVet, DrMedVet, PhD, DACVIM & DECVIM (Companion Animal), AGAF, is professor of small animal internal medicine and director of the gastrointestinal laboratory at Texas A&M University. Dr. Steiner frequently lectures on small animal gastroenterology and is involved in a number of research projects. He graduated from veterinary school in Munich, Germany. After completing an internship at University of Pennsylvania and residency at Purdue University, he achieved board certification with the American and European Colleges of Veterinary Internal Medicine. In 2000, Dr. Steiner received his PhD from Texas A&M.
|Sponsored
Sponsored by an Unrestricted Educational Grant from Nutramax Laboratories Veterinary Sciences, Inc.
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 (vitamin B12) is essential to multiple metabolic processes,1 including energy production, DNA and RNA synthesis, reproduction, protein synthesis, and the homeostasis of sulfur-containing amino acids. Cobalamin is absorbed from the ileum through a complex mechanism involving multiple cobalamin carrier proteins.
Causes of Cobalamin Deficiency
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.
Clinical Signs of Cobalamin Deficiency
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
Diagnosing Cobalamin Deficiency
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).
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.
Cobalamin Supplementation
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.
Recent data have shown that oral cobalamin supplementation is as effective as parenteral administration.
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.
References & Suggested Reading
Grützner N, Cranford SM, Norby B, Suchodolski JS, Steiner JM. Evaluation of serum cobalamin concentrations in dogs of 164 dog breeds (2006- 2010). J Vet Diagn Invest. 2012;24(6):1105-1114.
Kather S, Grützner N, Kook PH, Dengler F, Heilmann RM. Review of cobalamin status and disorders of cobalamin metabolism in dogs. J Vet Intern Med. 2020;34(1):13-28.
Hanisch F, Toresson L, Spillmann T. Cobalaminmangel bei Hund und Katze [Cobalamin deficiency in dogs and cats]. Tierarztl Prax Ausg K Kleintiere Heimtiere. 2018;46(5):309-314.
Toresson L, Steiner JM, Suchodolski JS, Spillmann T. Oral cobalamin supplementation in dogs with chronic enteropathies and hypocobalaminemia. J Vet Intern Med. 2016;30(1):101- 107.
Hill SA, Cave NJ, Forsyth S. Effect of age, sex and body weight on the serum concentrations of cobalamin and folate in cats consuming a consistent diet. J Feline Med Surg. 2018;20(2):135-141.
Battersby IA, Giger U, Hall EJ. Hyperammonaemic encephalopathy secondary to selective cobalamin deficiency in a juvenile border collie. J Small Anim Pract. 2005;46(7):339-344.
Simpson K, Battersby I, Lowrie M. Suspected acquired hypocobalaminaemic encephalopathy in a cat: resolution of encephalopathic signs and MRI lesions subsequent to cobalamin supplementation. J Feline Med Surg. 2012;14(5):350-355.
Berghoff N, Parnell NK, Hill SL, Suchodolski JS, Steiner JM. Serum cobalamin and methylmalonic acid concentrations in dogs with chronic gastrointestinal disease. Am J Vet Res. 2013;74(1):84-89.
Worhunsky P, Toulza O, Rishniw M, et al. The relationship of serum cobalamin to methylmalonic acid concentrations and clinical variables in cats. J Vet Intern Med. 2013;27(5):1056-1063.
Batchelor DJ, Noble PJ, Taylor RH, Cripps PJ, German AJ. Prognostic factors in canine exocrine pancreatic insufficiency: prolonged survival is likely if clinical remission is achieved. J Vet Intern Med. 2007;21(1):54-60.
Castelli MC, Friedman K, Sherry J, et al. Comparing the efficacy and tolerability of a new daily oral vitamin B12 formulation and intermittent intramuscular vitamin B12 in normalizing low cobalamin levels: a randomized, open-label, parallel-group study. Clin Ther. 2011;33(3):358-371.e2.
Kuzminski AM, Del Giacco EJ, Allen RH, Stabler SP, Lindenbaum J. Effective treatment of cobalamin deficiency with oral cobalamin. Blood. 1998;92(4):1191-1198.
Toresson L, Steiner JM, Razdan P, et al. Comparison of efficacy of oral and parenteral cobalamin supplementation in normalising low cobalamin concentrations in dogs: a randomised controlled study. Vet J. 2018;232:27-32.
Toresson L, Steiner JM, Olmedal G, Larsen M, Suchodolski JS, Spillmann T. Oral cobalamin supplementation in cats with hypocobalaminaemia: a retrospective study. J Feline Med Surg. 2017;19(12):1302-1306.
Toresson L, Steiner JM, Spodsberg E, et al. Effects of oral cobalamin supplementation on serum cobalamin concentrations in dogs with exocrine pancreatic insufficiency: a pilot study. Vet J. 2021;269:105619.
Chang C, Suchodolski J, Lindbury J, et al. Comparison of oral versus injectable cobalamin supplementation in dogs with hypocobalaminemia caused by chronic enteropathy or exocrine pancreatic insufficiency. 2022 (under review).
Texas A&M University Gastrointestinal Laboratory. https://www.vetmed.cvm.tamu/gilab
Ultraviolet-C Light in the Veterinary Operating Theater
Jacob Rubin, DVM, DACVS-SA, Maine Veterinary Medical Center, Scarborough, Maine
Jacob Rubin
DVM, DACVS-SA Maine Veterinary Medical Center, Scarborough, Maine
Browne KL, Crowley JD, Tan CJ, O'Sullivan CB, Walsh WR. Effect of ultraviolet-C light on the environmental bacterial bioburden in various veterinary facilities. Am J Vet Res. 2021;82(7):582-588.
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.
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.
Dai T, Vrahas MS, Murray CK, Hamblin MR. Ultraviolet C irradiation: an alternative antimicrobial approach to localized infections? Expert Rev Anti Infect Ther. 2012;10(2):185-195.
Lualdi M, Cavalleri A, Bianco A, et al. Ultraviolet C lamps for disinfection of surfaces potentially contaminated with SARS-CoV-2 in critical hospital settings: examples of their use and some practical advice. BMC Infect Dis. 2021;21(1):594.
Treatment of Allergic Reactions in Dogs: Are Glucocorticoids Necessary?
Amanda Cavanagh, DVM, DACVECC, Colorado State University
Amanda Cavanagh
DVM, DACVECC Colorado State University
Amanda Cavanagh, DVM, DACVECC, is clinical faculty instructor of Small Animal Emergency and Critical Care at Colorado State University College of Veterinary Medicine. She received her DVM from Auburn University and acquired ACVECC board certification after completing a residency at North Carolina State University. Dr. Cavanagh has a special interest in traumatology, extracorporeal therapies, and fluid resuscitation.
Helgeson ME, Pigott AM, Kierski KR. Retrospective review of diphenhydramine versus diphenhydramine plus glucocorticoid for treatment of uncomplicated allergic reaction in dogs. J Vet Emerg Crit Care (San Antonio). 2021;31(3):380-386.
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.
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
Sheikh A, Shehata YA, Brown SG, Simons FER. Adrenaline (epinephrine) for the treatment of anaphylaxis with and without shock. Cochrane Database Syst Rev. 2008;2008(4):CD006312.
Plumb DC. Diphenhydramine. Plumb's Veterinary Drugs. Updated September 2020. Accessed September 2021. https://app.plumbs.com/drug-monograph/tDYQtMqVRGPROD
Levine JM, Levine GJ, Boozer L, et al. Adverse effects and outcome associated with dexamethasone administration in dogs with acute thoracolumbar intervertebral disk herniation: 161 cases (2000-2006). J Am Vet Med Assoc. 2008;232(3):411-417.
Adoptability of Cats with Periuria
Meghan E. Herron, DVM, DACVB, Gigi's Shelter for Dogs, Canal Winchester, Ohio
Meghan E. Herron
DVM, DACVB Gigi's Shelter for Dogs, Canal Winchester, Ohio
Liu S, Sung W, Welsh S, Berger JM. A six-year retrospective study of outcomes of surrendered cats (Felis catus) with periuria in a no-kill shelter. J Vet Behav. 2021;42:75-80.
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).
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.
Carney HC, Sadek TP, Curtis TM, et al. AAFP and ISFM guidelines for diagnosing and solving house-soiling behavior in cats. J Feline Med Surg. 2014;16(7):579-598.
Herron ME. Advances in understanding and treatment of feline inappropriate elimination. Top Companion Anim Med. 2010;25(4):195-202.
McGowan RTS, Ellis JJ, Bensky MK, Martin F. The ins and outs of the litter box: a detailed ethogram of cat elimination behavior in two contrasting environments. Appl Anim Behav Sci. 2017;194:67-78.
Research Note: Electroceutical Dressing for Infected Chronic Wounds in Cats & Dogs
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.
Source & References
Heald R, Salyer S, Ham K, Wilgus TA, Subramaniam VV, Prakash S. Electroceutical treatment of infected chronic wounds in a dog and a cat. Vet Surg. 2022;51(3):520-527. doi:10.1111/vsu.13758
van Loosdrecht MC, Lyklema J, Norde W, Zehnder AJ. Bacterial adhesion: a physiochemical approach. Microb Ecol. 1989;17(1):1-15. doi:10.1007/BF02025589
Renedo OD, Alonso-Lomillo MA, Martínez MJA. Recent developments in the field of screen-printed electrodes and their related applications. Talanta. 2007;73(2):202-219. doi:10.1016/j.talanta.2007.03.050
Kambouris ME, Markogiannakis A, Arabatzis M, Manoussopoulos Y, Kantzanou M, Velegraki A. Wireless electrostimulation: a new approach in combating infection? Future Microbiol. 2017;12:255-265. doi:10.2217/fmb-2017-0157
Sandvik EL, McLeod BR, Parker AE, Stewart PS. Direct electric current treatment under physiologic saline conditions kills Staphylococcus epidermidis biofilms via electrolytic generation of hypochlorous acid. PLoS One. 2013;8(2):e55118. doi:10.1371/journal.pone.0055118
Food Challenge to Diagnose Cutaneous Adverse Reaction in Dogs
Robert Kennis, DVM, DACVD, MS, Auburn University
Robert Kennis
DVM, DACVD, MS Auburn University
Robert Kennis, DVM, DACVD, MS, is a professor at Auburn University. He earned his DVM from and completed a residency at Michigan State University. Dr. Kennis earned his MS in veterinary immunology from Texas A&M University. He is past president of the American Academy of Veterinary Dermatology and has presented numerous continuing education seminars at the state, national, and international levels. Dr. Kennis has received the Pfizer Distinguished Teacher award at both Auburn University and Texas A&M University and the Texas A&M Association of Former Students' Distinguished Achievement award. His research interests include food allergy, endocrine alopecia, and feline bacterial infections.
Shimakura H, Kawano K. Results of food challenge in dogs with cutaneous adverse reactions. Vet Dermatol. 2021;32(3):293-e80.
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.
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.
Mizuta H, Kawazoe Y, Haga K, Ogawa K, Yokobe T. [Determination of small intestinal transit time in beagle dogs using salicylazosulfapyridine]. Yakugaku Zasshi. 1989;109(10):760-765.
Mark J. Acierno, DVM, MBA, DACVIM, Midwestern University
Mark J. Acierno
DVM, MBA, DACVIM Midwestern University
Mark J. Acierno, DVM, MBA, DACVIM, is a professor at Midwestern University. Dr. Acierno earned his DVM from Mississippi State University. He also completed an internship in small animal medicine and surgery and an internal medicine residency at Cummings School of Veterinary Medicine at Tufts University. His research and clinical interests include hypertension, kidney disease, and renal replacement therapies.
SIGNS OF TARGET ORGAN DAMAGE
SBP is categorized based on the risk for TOD, examples include:
Eye: tortuous vessels, retinal hemorrhage/edema, retinal detachment
Heart: left ventricular free wall hypertrophy (eg, systolic murmur, gallop murmur, arrhythmia); signs of heart disease possible
Kidney: progression of kidney disease; may be exacerbated by proteinuria
Brain: altered mentation, seizure, coma, death
CATEGORIES OF BLOOD PRESSURE BASED ON RISK FOR TARGET ORGAN DAMAGE
Risk for TOD
<140 mm Hg Minimal Normotensive
140-159 mm Hg Low Prehypertensive*
160-179 mm Hg Moderate Hypertensive
≥180 mm Hg High Severely hypertensive
*Prehypertensive patients are likely to become hypertensive.
HOW TO MINIMIZE RISK FOR SITUATIONAL HYPERTENSION
Place pet owner and patient in a quiet area away from other patients.
Allow patient to acclimate to new environment before measuring BP.
Measure BP before performing examination or obtaining vital signs.
Ensure owner is present unless their presence is disruptive.
ACEI = angiotensin-converting enzyme inhibitor, AKI = acute kidney injury, ARB = angiotensin receptor blocker, BP = blood pressure, CKD = chronic kidney disease, RAAS = renin-angiotensin-aldosterone system, SBP = systolic blood pressure, TOD = target organ damage
Amara Estrada, DVM, DACVIM (Cardiology), University of Florida
Amara Estrada
DVM, DACVIM (Cardiology) University of Florida
Amara H. Estrada, DVM, DACVIM (Cardiology), is a professor of cardiology and the associate chair for instruction in the department of small animal clinical sciences at University of Florida, where she also earned her DVM. Dr. Estrada completed a cardiology residency at Cornell University. She frequently speaks at continuing education meetings nationally and internationally. Her research interests include inherited cardiomyopathies and interprofessional education.
Bentley, an 8-year-old, 57-lb (26-kg) neutered male crossbreed dog, is presented for lethargy, panting, and anxious behavior of 2-days' duration. His owner reports he was previously healthy.
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.
John Macri, DVM, Angell Animal Medical Center, Boston, Massachusetts
Jennifer Michaels, DVM, DACVIM (Neurology), Angell Animal Medical Center, Boston, Massachusetts
John Macri
DVM Angell Animal Medical Center, Boston, Massachusetts
John Macri, DVM, is a rotating intern at Angell Animal Medical Center in Boston, Massachusetts. Dr. Macri earned his DVM from St. George's University and completed a clinical year at North Carolina State University, where he is working to complete a neurology and neurosurgery residency.
Jennifer Michaels
DVM, DACVIM (Neurology) Angell Animal Medical Center, Boston, Massachusetts
Jennifer Michaels, DVM, DACVIM (Neurology), is a staff veterinary neurologist at Angell Animal Medical Center in Boston, Massachusetts. Dr. Michaels earned her DVM with honors at Texas A&M University. She completed a small animal rotating internship and a residency in neurology and neurosurgery at University of Tennessee. Her areas of interest include neuro-oncology and neurosurgery.
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
FIGURE 1 Brain MRI of Poncho, on which a hyperintense, intra-axial lesion in the right thalamus can be seen on T2-weighted (A, arrow) and fluid-attenuated inversion recovery (B, arrow) axial images. The lesion is hypointense on the T1-weighted axial image (C, arrow). Findings suggest high fluid content common with inflammatory lesions. Postcontrast T1-weighted axial image following administration of gadolinium IV showed no contrast (D, arrow).
CANINE DISTEMPER VIRUS ENCEPHALITIS WITH SUSPECTED PNEUMONIA OR BRONCHITIS
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.
Vaccination is the primary method of CDV infection prevention and should be administered to puppies at 8 weeks of age, with boosters given at 12 weeks, 16 weeks, and 1 year.
Hospitalization may be needed for appropriate supportive care (eg, IV fluids, antiemetics, monitoring).
Parenteral nutrition should be provided for anorexic patients or those unable to eat due to neurologic signs, especially young patients.
Antibiotics should be considered to treat or prevent secondary infection if respiratory disease is suspected or confirmed.
Antiepileptic and hyperosmotic medications for seizure control should be administered as needed.
Short-term anti-inflammatory corticosteroids can be helpful but are controversial.
Despite aggressive antiepileptic and supportive treatment, Poncho continued to have breakthrough seizures and was humanely euthanized. Postmortem evaluation was declined.
Clinical Signs
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
Video Myoclonus in a dog with CDV infection
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
Figure 2 Cytoplasmic inclusion body (arrow) in a neutrophil on a blood smear. Cytoplasmic inclusion bodies in peripheral blood are transient and rare, occur only during the acute phase of CDV infection, and are a pathognomonic finding. Romanowsky-type stain, 1000× magnification
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.
CDV encephalitis should be a differential diagnosis for pediatric dogs with seizures, regardless of vaccination status.
Because transmission can occur through any bodily fluid, patients suspected to have CDV infection should be immediately isolated, and the environment should be disinfected.
Clinical signs vary, but neurologic (eg, myoclonus, ataxia, seizures) and systemic (most commonly, respiratory and GI) signs are common.
Diagnosing CDV infection can be challenging. A minimum database, thoracic radiography, PCR, antibody titers (interpreted with caution), MRI, and CSF analysis can be considered. Diagnosis can be suspected based on patient history and clinical suspicion alone.
Treatment focuses on supportive care and seizure control.
Prognosis is variable but declines considerably in patients with seizures or other neurologic signs that are difficult to control.
Prevention via vaccination reduces disease prevalence.
Green CE, Vandevelde M. Canine distemper. In: Greene CE, ed. Infectious Diseases of the Dog and Cat. 4th ed. Elsevier; 2012:25-42.
Martella V, Elia G, Buonavoglia C. Canine distemper virus. Vet Clin North Am Small Anim Pract. 2008;38(4):787-797, vii-viii.
Vandevelde M, Zurbriggen A, Steck A, Bichsel P. Studies on the intrathecal humoral immune response in canine distemper encephalitis. J Neuroimmunol. 1986;11(1):41-51.
Tipold A, Vandevelde M, Jaggy A. Neurological manifestations of canine distemper virus infection. J Small Anim Pract. 1992;33(10):466-470.
Amude AM, Alfieri AA, Alfieri AF. Clinicopathological findings in dogs with distemper encephalomyelitis presented without characteristic signs of the disease. Res Vet Sci. 2007;82(3):416-422.
Koutinas AF, Polizopoulou ZS, Baumgaertner W, Lekkas S, Kontos V. Relation of clinical signs to pathological changes in 19 cases of canine distemper encephalomyelitis. J Comp Pathol. 2002;126(1):47-56.
Newbury S. Canine distemper virus. In: Miller L, Janeczko S, Hurley K, eds. Infectious Disease Management in Animal Shelters. John Wiley & Sons; 2021:256-273.
Krakowka S, Higgins RJ, Koestner A. Canine distemper virus: review of structural and functional modulations in lymphoid tissues. Am J Vet Res. 1980;41(2):284-292.
Headley SA, Graça DL. Canine distemper: epidemiological findings of 250 cases. Braz J Vet Res Anim Sci. 2000;37(2):136-140.
Bathen-Noethen A, Stein VM, Puff C, Baumgaertner W, Tipold A. Magnetic resonance imaging findings in acute canine distemper virus infection. J Small Anim Pract. 2008;49(9):460-467.
Bergman RL, Coates JR. Seizures in young dogs and cats: management. Compend Cont Educ Pract Vet. 2005;27(7):539-550.
Bollo E, Zurbriggen A, Vandevelde M, Fankhauser R. Canine distemper virus clearance in chronic inflammatory demyelination. Acta Neuropathol. 1986;72(1):69-73.
Schubert T, Clemmons R, Miles S, Draper W. The use of botulinum toxin for the treatment of generalized myoclonus in a dog. J Am Anim Hosp Assoc. 2013;49(2):122-127.