Canine and Feline Digoxin Toxicity PDF

Canine and Feline, Seventh Edition 407 Digoxin Toxicity all patients with con...

Canine and Feline, Seventh Edition 407 Digoxin Toxicity all patients with concentrations >1.5 ng/mL have signs of toxicity; some with values in the normal range have signs of toxicity, especially ­ BASICS if hypokalemic. To minimize the risk of ­ FOLLOW-UP D toxicity, the author aims to achieve a digoxin Inform owner that reduction in appetite is OVERVIEW Not uncommon in patients treated with level between 0.5 and 1 ng/mL. an early indication of digoxin toxicity. digoxin due to digoxin’s narrow therapeutic Monitor renal function and electrolytes IMAGING frequently in patients receiving digoxin; lower index and prevalence of renal impairment in N/A elderly patients with cardiac disease. Becoming digoxin dose if renal disease develops. less common in clinical practice as use of DIAGNOSTIC PROCEDURES Monitor serum digoxin concentration digoxin has decreased in management of periodically. ECG heart failure. Monitor ECG periodically to assess for Conduction disturbances—atrioventricular arrhythmias or conduction disturbances that SIGNALMENT (AV) block, arrhythmias, and ST segment may suggest digoxin toxicity. Dog and cat. depression in some patients. Monitor bodyweight frequently; alter More common in geriatric patients. Digoxin can cause any arrhythmia. digoxin dosage accordingly; patients with SIGNS congestive heart failure often lose weight. Historical Findings Anorexia. Vomiting. ­ TREATMENT Diarrhea. Discontinue digoxin until signs of toxicity ­ MISCELLANEOUS Lethargy. resolve (24–72 hours); reevaluate need for the medication; if necessary, resume treatment at SEE ALSO Depression. Atrioventricular Block, Complete (Third a dosage based on the serum digoxin concen- Physical Examination Findings tration. Degree). Heart rate may range from severe bradycardia Maintain hydration and correct any Atrioventricular Block, First Degree. to severe tachycardia. electrolyte disturbance (especially hypoka- Atrioventricular Block, Second Degree— lemia) with parenteral fluid administration. Mobitz Type I. CAUSES & RISK FACTORS Atrioventricular Block, Second Degree— Renal disease—impairs digoxin elimination. Discontinue drugs that slow digoxin metabolism or elimination (e.g., quinidine, Mobitz Type II. Chronic pulmonary disease—results in verapamil, amiodarone). Ventricular Tachycardia. hypoxia and acid-base disturbances. Obesity—if dosage not calculated on lean Severe arrhythmias (ventricular tachycardia) ABBREVIATIONS bodyweight. and conduction disturbances—can be life- AV = atrioventricular. Drugs and conditions that alter digoxin threatening; require hospitalization for treatment and monitoring. ­Suggested Reading metabolism or elimination (e.g., quinidine Teerlink JR, Gersh BJ, Opie LH. Heart and hypothyroidism). failure. In: Opie LH, Gersh BJ, eds., Drugs Rapid IV digitalization. for the Heart, 8th ed. Philadelphia, PA: Overdosage or accidental ingestion of Elsevier Saunders, 2013, pp. 169–223. owner’s medication. ­ MEDICATIONS Author Francis W.K. Smith, Jr. Administration of diuretic leading to Consulting Editor Michael Aherne hypokalemia. DRUG(S) OF CHOICE Treat clinically important bradyarrhythmias with atropine or a temporary transvenous pacemaker. Treat clinically important ventricular ­ DIAGNOSIS arrhythmias with lidocaine or phenytoin; phenytoin also reverses high-degree AV block. DIFFERENTIAL DIAGNOSIS Digoxin-binding antibodies (e.g., Digibind®) Arrhythmias and conduction distur- rapidly drop digoxin concentration in critically bances—may reflect structural heart disease, ill animals; the use of these products is limited not digoxin toxicity. in veterinary practice by their exorbitant cost. Anorexia—common in animals with heart Thyroxin supplementation if hypothyroid- failure. ism confirmed. CBC/BIOCHEMISTRY/URINALYSIS CONTRAINDICATIONS/POSSIBLE Animals with hypokalemia, hypercalcemia, hypomagnesemia, and renal failure are INTERACTIONS Avoid or discontinue drugs that slow predisposed to toxicity. digoxin elimination or metabolism (e.g., OTHER LABORATORY TESTS quinidine, verapamil, and diltiazem). Consider checking thyroid status. Avoid drugs that could worsen conduction Obtain digoxin serum concentration 8–10 disturbances (e.g., beta blockers and calcium hours after an oral dose—therapeutic range is channel blockers). 0.5–1.5 ng/mL. A recent study in humans Class 1A antiarrhythmic drugs (e.g., quinidine found digoxin levels greater than 1 mg/ml and procainamide) may worsen AV block. were associated with increased mortality; not  408 Blackwell’s Five-Minute Veterinary Consult Diisocyanate Glues Elevated total proteins/prerenal azotemia— PREVENTION/AVOIDANCE may occur secondary to dehydration from Prevent exposure. vomiting. D ­ BASICS EXPECTED COURSE AND PROGNOSIS IMAGING With removal of FBO, prognosis is OVERVIEW Survey radiographs (4–24 hours post excellent. Diisocyanate glues include wood glue, exposure)—glue appears as a mottled gas and Without surgical removal, the FBO is not construction glue, and some “high-strength soft tissue opacity distending the stomach. expected to resolve on its own. or extra strength” glues. The appearance can resemble recent food Gorilla Glue is one popular brand name. ingestion (see Web Figure 1). There are non-Gorilla brand glue types that contain diisocyanate as the active ingredient and not all types of Gorilla Glue contain ­ MISCELLANEOUS diisocyanates. Confirm the actual product ASSOCIATED CONDITIONS with the owner, using the packaging if ­ TREATMENT Gastritis. necessary. Generally, not recommended due to risk Dermatitis. Typically, the owner finds a chewed bottle of esophageal or GI obstruction. Potential of glue or glue stuck on the animal. use immediately after a large ingestion. ABBREVIATIONS Gastric lavage is rarely of benefit as glue FBO = foreign body obstruction. Diisocyanate glue rapidly expands in the expands too rapidly. GDV = gastric dilatation-volvulus. moist environment of the stomach, causing Dilution with water or other fluids should GI = gastrointestinal. bloat and foreign body obstruction (FBO). The glue is not absorbed and does not cause be avoided as excess moisture allows further ­Suggested Reading systemic toxicity. Ingestions as small as 2 oz expansion of the glue. Horstman CL, Eubig PA, Cornell KK, et al. (56 g) can require surgical intervention to IV fluids as needed for dehydration. Gastric outflow obstruction after ingestion resolve obstruction. Wash exposed skin with warm soapy water, of wood glue in a dog. J Am Anim Hosp Glue is also adhesive and an irritant to the rub vegetable oil into the hair, or clip hair to Assoc 2003, 39:47–51. paws, oral cavity, and stomach lining. remove as much glue as possible. Glue can be Peterson KL. Glues and adhesives. In: Hovda Inhalation may cause irritation to the left adhered to the skin if nonirritating and LR, Brutlag A, Poppenga R, Peterson K, lungs. will fall off over time. eds., Blackwell’s Five Minute Veterinary Oxygen as needed for signs related to Consult: Small Animal Toxicology, 2nd ed. SIGNALMENT inhalation. Dogs and less commonly cats, birds, and Ames, IA: Wiley-Blackwell, 2016, pp. Surgical removal of the expanded glue 95–100. small mammals. Young animals are more foreign body is almost always indicated in often affected. Author Tyne Hovda ingestions greater than 2 oz or with lesser Consulting Editor Lynn R. Hovda SIGNS amounts in smaller animals. Acknowledgment: The author and book Occur within 15 minutes to 24 hours after editors acknowledge the prior contribution of ingestion. Catherine A. Angle. Ingestion—consistent with FBO and may include gagging, retching, vomiting, anorexia, abdominal distension, abdominal pain; ­ MEDICATIONS  Client Education Handout hematemesis in prolonged or severe cases. DRUG(S) OF CHOICE available online Inhalation—coughing, sneezing, increased Antiemetic—maropitant citrate 1 mg/kg secretions within 4–8 hours. SC/IV q24h. Dermal—irritation, redness, rash. H2 blocker (for gastric inflammation or ulceration)—ranitidine 1–2 mg/kg PO/IM/ CAUSES & RISK FACTORS SC/IV q6–12h; famotidine 0.5–1.1 mg/kg Pets with access to diisocyanate glue products. PO q12h; pantoprazole 0.7–1 mg/kg IV over 15 minutes q24h. Sucralfate (for a gastric ulcer if present)— 0.5–1 g PO TID on an empty stomach. ­ DIAGNOSIS CONTRAINDICATIONS DIFFERENTIAL DIAGNOSIS Emetics—emesis should not be performed History of exposure and clinical signs unless done immediately after a witnessed generally facilitate diagnosis. ingestion. Expansion of the glue is rapid: late Presenting signs are consistent with gastric emesis stresses the stomach wall and could dilatation-volvulus (GDV), bloat, pancreatitis, damage the esophagus. inflammatory bowel disease, and other causes Do not dilute with water as exposure to of FBO. moisture leads to rapid expansion of the glue. Radiographs are highly suggestive of FBO (see Web Figure 1). CBC/BIOCHEMISTRY/URINALYSIS CBC—generally no significant changes. ­ FOLLOW-UP Electrolyte disturbances—consistent with PATIENT MONITORING gastrointestinal (GI) obstruction and Monitor in hospital until eating and drinking anorexia. normally. Recheck 10–14 days post surgery.  Canine and Feline, Seventh Edition 409 Discolored Tooth/Teeth with release into adjacent dentinal tubules; orthophosphate complex in the collagen discoloration goes from pink to purple matrix of enamel; occurs on multiple teeth; (pulpitis) to gray (pulpal necrosis) to black results in a yellow-brown discoloration. ­ BASICS (liquefactive necrosis). Long-term use of tetracyclines in mature D DEFINITION Amelogenesis imperfecta—developmental animals can involve secondary dentin Normal tooth color varies and depends on alteration in the structure of enamel affecting formation. the shade, translucency, and thickness of all teeth; chalky appearance with a pinkish Amalgam (as with extrinsic stains). enamel. Translucent enamel is bluish-white, hue; problem in the formation of the organic Iodine/essential oils. opaque enamel is gray-white. matrix, mineralization of the matrix, or the In endodontically treated teeth from the Extrinsic—from surface accumulation of maturation of the matrix. medicants penetrating the dentinal tubules. exogenous pigment. Dentinogenesis imperfecta—developmental Macrolide antibiotic (reported in humans)— Intrinsic—secondary to endogenous factors alteration in dentin formation; enamel results in vacuolar degeneration of the discoloring the underlying dentin. separates easily from the dentin, resulting in ameloblast and cystic change at maturation grayish discoloration. and hypocalcification, giving a white PATHOPHYSIOLOGY Infectious agents (systemic)—parvovirus, discolored lesion with horizontal stripes on Extrinsic Discoloration distemper virus, or any agent that causes a the enamel. Bacterial stains—chromogenic bacteria: sustained body temperature rise; affects the Bacterial “creeping” (leakage)—occurs green to black-brown to orange color, usually formation of enamel; a distinct line of around the margins of a restoration and 1 mm above the gingival margin on the tooth. resolution is visible on the teeth; affects all usually is blackish in color. Plaque related—a black-brown stain; teeth developing at the time of the insult; SYSTEMS AFFECTED usually secondary to the formation of ferric results in enamel hypoplasia or hypocalcifica- Gastrointestinal—oral cavity. sulfide from the interaction of bacterial ferric tion where the abnormal enamel can have sulfide and iron in the saliva. Plaque is usually black edges and the dentin is brownish. GENETICS white. Dental fluorosis—affects all teeth; excess Amelogenesis imperfecta and dentinogenesis Foods—charcoal biscuits and similar fluoride consumption affects the maturation imperfecta in humans are inherited conditions products penetrate the pits and fissures of the of enamel, resulting in pits (enamel hypo- that have many modes of inheritance. The enamel; food with abundant chlorophyll can plasia) with black edges; the enamel is a mode of inheritance in animals has not been produce a green discoloration. lusterless, opaque white, with yellow-brown studied. Gingival hemorrhage—green or black zones of discoloration. Congenital hypothyroidism. staining from the breakdown of hemoglobin Tooth erosion from constant vomiting Metabolic diseases. into green biliverdin. results in enamel pitting and darkened INCIDENCE/PREVALENCE Dental restorative materials—amalgam: staining. Discoloration of the teeth or a tooth is black-gray discoloration. Attrition—tooth-to-tooth wear results in extremely common in all animals. Medications—products containing iron or crown loss and reparative dentin formation Extrinsic staining is very common, iodine give a black discoloration; sulfides, (yellow-brown color). especially bacterial stains; others are less silver nitrate, or manganese: gray-to-yellow to Abrasion—tooth wear against another common. brown-to-black discoloration; copper or surface; chewing on tennis balls or from a Intrinsic staining is likewise very common, nickel: green discoloration; cadmium, yellow dermatologic condition. Reparative dentin especially internal and external resorption, to golden brown discoloration (e.g., 8% (yellow-brown color) forms. followed by localized red blood cell destruc- stannous fluoride combines with bacterial Aging—older animals’ dentition is more tion; the other causes are rare. sulfides, giving a black stain; chlorhexidine yellow and less translucent. gives a yellowish-brown discoloration). Malnutrition (generalized, vitamin D GEOGRAPHIC DISTRIBUTION Metals—wear from chewing on cages or deficiency, and vitamin A deficiency)—if Heavy metals from mining operations. food dishes. severe can result in demarcated opacities on Fluoridation forms areas of excessive From removed orthodontic brackets or the enamel. fluoride in the drinking water. bands. Otherwise none. Internal/External Resorption Crown fragments—less translucency due to SIGNALMENT Internal—follows pulpal injury (trauma) dehydration of fragment. causing vascular changes with increased Species Discolored restorations. oxygen tension and decreased pH, resulting Dogs and cats. Tooth wear with dentin exposure—tertiary in destruction (resorption) of the tooth from Mean Age and Range dentin, reparative dentin, secondary dentin. within the pulp from odontoclasts; tooth has The reported age range varies—when the A calculus-covered crown ranges in color pinkish hue. condition affects the developing enamel or from dark yellow to dark brown. External—many factors possible: trauma, dentin it can be first noted after tooth Intrinsic Discoloration orthodontic treatment, excessive occlusal eruption (6 months of age). Hyperbilirubinemia—affects all teeth; forces, periodontal disease (and treatment), during dentin formation bilirubin accumulates tumors, periapical inflammation, and Predominant Sex in the dentin from excess red blood cell unknown factors; resorption can start None breakdown; extent of discoloration depends anywhere along the periodontal ligament and SIGNS on the length of hyperbilirubinemia (lines of can extend to the pulp and into the crown resolution occur once the condition has been causing a pinkish discoloration; osteoclasts Historical Findings resolved); green discoloration. and odontoclasts resorb the tooth structure. Owner reports a variation in color of a tooth Localized red blood cell destruction, one or teeth. Medications and Discoloration tooth or focal area—usually follows a Physical Examination Findings Tetracycline—during enamel formation, it traumatic injury to the tooth; discoloration Abnormal coloration of tooth or teeth. binds to calcium, forming a calcium from hemoglobin breakdown within the pulp Pitted enamel with staining.  410 Blackwell’s Five-Minute Veterinary Consult Discolored Tooth/Teeth (continued) Fractured tooth. Appropriate preoperative diagnostics when Rings or lines of discoloration around tooth indicated prior to procedure. or teeth. D Wear on crowns of the dentition or in PATHOLOGIC FINDINGS ­ MEDICATIONS See Pathophysiology. selected areas as in behavioral causes (cage DRUG(S) OF CHOICE biters—distal aspect of the canines is N/A affected). Erosion of enamel. CAUSES & RISK FACTORS ­ TREATMENT Extrinsic discoloration—bacterial stains APPROPRIATE HEALTH CARE ­ FOLLOW-UP from plaque and calculus; foods; gingival Extrinsic stain removal—mainly cosmetic. hemorrhage; dental restorative materials, Intrinsic stain treatment—functional and PREVENTION/AVOIDANCE medications (chlorhexidine, 8% stannous pain relieving. See Pathophysiology. fluoride), metal. Good oral care at home will help prevent NURSING CARE the reoccurrence of certain specific stains. Intrinsic discoloration—internal (trauma); Extrinsic stain—remove inciting cause. external tooth resorption; localized red blood Intrinsic stain—soft food; remove chew POSSIBLE COMPLICATIONS cell destruction in the tooth (trauma); toys. See Client Education. systemic infections; medications (tetracy- ACTIVITY EXPECTED COURSE AND PROGNOSIS cline); fluorosis; hyperbilirubinemia; Curtail or treat specific behavioral abnormali- Vary dependent upon the etiology, but can amelogenesis imperfecta; dentinogenesis ties (cage biting). range from mere aesthetics to significant pain. imperfecta. DIET N/A CLIENT EDUCATION ­ DIAGNOSIS To prevent it in future animals or litters if ­ MISCELLANEOUS preventable (medication use). ASSOCIATED CONDITIONS DIFFERENTIAL DIAGNOSIS Intrinsic causes—irregular enamel surfaces are Enamel hypoplasia/hypocalcification Calculus on the teeth. more likely to accumulate plaque and calculus, Juvenile purpura. Normal tooth aging—increased translucence. leading to subsequent periodontal disease. AGE-RELATED FACTORS Food debris lodged in the spaces between Abnormally formed teeth or teeth that have All ages affected, depends on the cause. the teeth (diastema). localized red blood cell destruction are more prone to fracture or development of tooth ZOONOTIC POTENTIAL CBC/BIOCHEMISTRY/URINALYSIS abscessation. None. Anemia—blood-related disorders. Some causes are painful (tooth resorption). PREGNANCY/FERTILITY/BREEDING Bilirubin—increased with liver diseases. Tetracycline administration during SURGICAL CONSIDERATIONS OTHER LABORATORY TESTS Extrinsic stain (cosmetic)—internal and/or pregnancy may result in permanent tooth T3/T4—low in congenital hypothyroidism. external bleaching; veneers or crowns. discoloration in offspring. Specific metabolic enzyme decrease or Polishing the affected teeth with 3% See Genetics. absence—tyrosinemia. hydrogen peroxide in pumice will help SYNONYMS IMAGING remove external stain. Also good home care Chlorhexidine staining. Dental radiography is extremely useful in with plaque control will minimize Extrinsic staining. identifying internal or external resorption, redevelopment of some stains (plaque/ Intrinsic staining. restorative materials, or bacterial stain from calculus/bacteria stain). Tetracycline staining. coronal percolation. Intrinsic stain (functional and pain ­Suggested Reading relief )—possible endodontic treatment DIAGNOSTIC PROCEDURES Hale FA. Localized intrinsic staining of teeth (internal resorption and localized red blood If many teeth are affected, one tooth can be due to pulpitis and pulp necrosis in dogs. cell destruction). extracted and sent for histologic evaluation J Vet Dent, 2001, 18(1):14–20. Restorative procedures such as crowns or (see below). Lobprise HB, Dodd JR. Wiggs’ Veterinary veneers to protect both tooth and pulp. Transillumination with a strong fiberoptic Dentistry Principles and Practice. Hoboken, Extraction of affected teeth may be light may help distinguish between vital and NJ: Wiley-Blackwell, 2019. required, especially with external resorption. necrotic pulp. Author Kristin M. Bannon Consulting Editor Heidi B. Lobprise  Canine and Feline, Seventh Edition 411 Discospondylitis Physical Examination Findings Urine cultures—indicated; positive in about Focal or multifocal areas of spinal pain in 30% of patients. >80% of patients. Organisms other than Staphylococcus ­ BASICS Any disc space may be affected; lumbo­sacral spp.—may not be the cause. D DEFINITION space is most commonly involved. Serologic testing for Brucella canis— A bacterial, fungal, and rarely algal infection Paresis or paralysis, especially in chronic, indicated as this presents zoonotic potential. of the intervertebral end plates, discs, and untreated cases. IMAGING adjacent vertebral bodies. Fever in ~30% of patients. Spinal radiography—usually reveals lysis of Lameness. PATHOPHYSIOLOGY vertebral end plates adjacent to the affected Hematogenous spread of bacterial or fungal CAUSES disc, collapse of the disc space, and varying organisms—most common cause. Bacterial—Staphylococcus pseudintermedius degrees of sclerosis of the end plates and Seeding secondary to migrating foreign is most common. Others include Streptococcus, ventral spur formation; may not see lesions body (grass awn) is also reported. Brucella canis, and Escherichia coli, but until 3–4 weeks after infection (therefore Neurologic dysfunction—may occur; virtually any bacteria can be causative. normal radiographs do not rule out). usually the result of spinal cord compression Fungal—Aspergillus, Paecilomyces, Myelography—indicated with substantial caused by proliferation of bone and fibrous Scedosporium apiospermum, and Coccidioides neurologic deficits; determine location and tissue; less commonly owing to luxation or immitis. degree of spinal cord compression, especially pathologic fracture of the spine, epidural Grass awn migration is often associated if considering decompressive surgery; spinal abscess, or extension of infection to the with mixed infections, especially Actinomyces; cord compression caused by discospondylitis meninges and spinal cord. tends to affect the L2–L4 disc spaces and typically displays an extradural pattern. vertebrae. CT or MRI—more sensitive than radio­- SYSTEMS AFFECTED Other causes—surgery, bite wounds. graphy; indicated when radiographs are Musculoskeletal—infection and RISK FACTORS normal or inconclusive. inflammation of the spine. Nervous—compression and/or infection of Urinary tract infection; reproductive tract DIAGNOSTIC PROCEDURES the spinal cord. infection. CSF analysis—occasionally indicated to Periodontal disease. rule out meningomyelitis; usually normal or GENETICS Bacterial endocarditis. reveals mildly high protein. No definite predisposition identified. Pyoderma. Bone scintigraphy—occasionally useful for An inherited immunodeficiency has been Immunodeficiency. detecting early lesions; helps clarify if detected in a few cases. Recent steroid administration. radiographic changes are infectious or INCIDENCE/PREVALENCE Intact male status. degenerative (spondylosis deformans). Approximately 0.1–0.8% of dog hospital Fluoroscopically guided fine-needle admissions. aspiration of the disc—valuable for obtaining GEOGRAPHIC DISTRIBUTION tissue for culture when blood and urine cultures are negative and there is no improve- More common in the southeastern United ­ DIAGNOSIS ment with empiric antibiotic therapy. States. DIFFERENTIAL DIAGNOSIS Grass awn migration and coccidiomycosis— PATHOLOGIC FINDINGS Intervertebral disc protrusion—may cause more common in certain regions. Gross—loss of normal disc space; bony similar clinical signs; differentiated on the SIGNALMENT proliferation of adjacent vertebrae. basis of radiography and myelography. Microscopic—fibrosing pyogranulomatous Species Vertebral fracture or luxation—detected on destruction of the disc and vertebral bodies. Dog; rare in cat. radiographs. Vertebral neoplasia—usually does not affect Breed Predilections adjacent vertebral end plates. Large and giant breeds, especially German Spondylosis deformans—rarely causes shepherd and Great Dane. clinical signs; has similar radiographic ­ TREATMENT Mean Age and Range features, including sclerosis, ventral spur APPROPRIATE HEALTH CARE Mean age—4–5 years. formation, and collapse of the disc space; Outpatient—mild pain managed with Range—5 months–12 years. rarely causes lysis of the vertebral end plates. medication. Focal meningomyelitis—often identified by Predominant Sex Inpatient—severe pain or progressive cerebrospinal fluid (CSF) analysis. neurologic deficits require intensive care and Males outnumber females by ~2 : 1. CBC/BIOCHEMISTRY/URINALYSIS monitoring. SIGNS Hemogram—often normal; may see Historical Findings NURSING CARE leukocytosis. Nonambulatory patients—keep on clean, dry, Onset usually relatively acute; however, Urinalysis—may reveal pyuria and/or some patients may have mild signs for well-padded surface to prevent decubital bacteriuria with concurrent urinary tract ulceration. several months before presenting for infections. examination. ACTIVITY OTHER LABORATORY TESTS Restricted Pain—difficulty rising, reluctance to jump, Aerobic, anaerobic, and fungal blood and stilted gait are most common signs. CLIENT EDUCATION cultures identify the causative organism in Ataxia or paresis. Explain that observation of response to about 35% of cases; obtain if available. Weight loss and anorexia. treatment is very important in determining Sensitivity testing—indicated if cultures are Lameness. the need for further diagnostic or therapeutic positive. procedures.  412 Blackwell’s Five-Minute Veterinary Consult Discospondylitis (continued) Instruct the client to immediately contact ALTERNATIVE DRUG(S) ZOONOTIC POTENTIAL the veterinarian if clinical signs progress or Initial therapy—cephradine (dogs: 20 mg/kg Brucella canis—human infection uncommon recur or if neurologic deficits develop. PO q8h); amoxicillin trihydrate/clavulanate but may occur. D potassium (dogs: 13.75–22 mg/kg PO q12h). SURGICAL CONSIDERATIONS PREGNANCY/FERTILITY/BREEDING Curettage of a single affected disc space— Refractory patients—clindamycin (dogs N/A occasionally necessary for patients that are and cats: 10 mg/kg PO q12h), enrofloxacin (dogs: 10 mg/kg PO q24h; cats: 5 mg/kg PO SYNONYMS refractory to antibiotic therapy. Diskitis. Goals—remove infected tissue; obtain q24h), orbifloxacin (dogs and cats: 2.5– 7.5 mg/kg PO q24h). Intervertebral disc infection. tissue for culture and histologic evaluation. Intradiskal osteomyelitis. Decompression of the spinal cord by Vertebral osteomyelitis. hemilaminectomy or dorsal laminectomy— indicated for substantial neurologic deficits SEE ALSO and spinal cord compression evident on MRI ­ FOLLOW-UP Brucellosis or myelography when there is no improve- ABBREVIATIONS PATIENT MONITORING ment with antibiotic therapy; also perform CSF = cerebrospinal fluid. Reevaluate after 5 days of therapy. curettage of the infected disc space; it may be NSAID = nonsteroidal anti-inflammatory No improvement in pain, fever, or necessary to perform surgical stabilization if drug. appetite—reassess therapy; consider a more than one articular facet is removed from a disc site. different antibiotic, percutaneous ­Suggested Reading aspiration of the affected disc space, Ameel L, Martlè V, Gielen I, et al. or surgery. Discospondylitis in the dog: a retrospective Improvement—evaluate clinically and study of 18 cases. Vlaams Diergeneeskundig radiographically every 4 weeks. Tijdschrift 2009, 78(5):347–353. ­ MEDICATIONS PREVENTION/AVOIDANCE Bagley RS. Diskospondylitis. Fundam Clin DRUG(S) OF CHOICE Early identification of predisposing causes Neuro 2005, 172–173(283–285):346. and prompt diagnosis and treatment—help Braund KG, Sharp NJH. Discospondylitis. In: Antibiotics Vite C, ed., Braund’s Clinical Neurology in Selection based on results of blood cultures reduce progression of clinical symptoms and neurologic deterioration. Small Animals: Localisation, Diagnosis and and serology or end plate aspirate culture and Treatment. Ithaca, NY: IVIS, 2003. https:// sensitivity. POSSIBLE COMPLICATIONS www.ivis.org/library/braunds-clinical- Negative culture and serology—assume Spinal cord compression owing to neurology-small-animals-localization- causative organism is Staphylococcus spp.; treat proliferative bony and fibrous tissue. diagnosis-and-treatment/degenerative with a cephalosporin (e.g., cephalexin 22 mg/kg Vertebral fracture or luxation. Burkert BA, Kerwin SC, Hosgood GL, et al. PO q8h) for 8–12 weeks. Meningitis or meningomyelitis. Signalment and clinical features of Acutely progressive signs or substantial Epidural abscess. diskospondylitis in dogs: 513 cases neurologic deficits—initially treated with EXPECTED COURSE (1980–2001). J Am Vet Med Assoc 2005, parenteral antibiotics (e.g., cefazolin; dogs 227(2):268–275. and cats: 22 mg/kg IV q8h). AND PROGNOSIS Recurrence is common if antibiotic therapy Fischer A, Mahaffey MB, Oliver JE. Brucellosis—treated with tetracycline (dogs: Fluoroscopically guided percutaneous disk 15 mg/kg PO q8h) and streptomycin (dogs: is stopped prematurely (before 8–12 weeks of treatment). aspiration in 10 dogs with diskospondylitis. 3.4 mg/kg IM q24h) or enrofloxacin (dogs: J Vet Intern Med 1997, 11:284–287. 10 mg/kg PO q24h). Some patients require prolonged therapy (1 year or more). Johnson RG, Prata RG. Intradiskal osteomy- One study suggested that antibiosis be elitis: a conservative approach. JAAHA continued until radiographic signs were Prognosis—depends on causative organism and degree of spinal cord damage. 1983, 19:743–750. resolved (range of 40–80 weeks). The roll of Kerwin SC, Lewis DD, Hribernik TN, et al. imaging in definitively determining length of Mild or no neurologic dysfunction (dogs)—usually respond within 5 days of Diskospondylitis associated with Brucella treatment has not been proven, however. canis infection in dogs: 14 cases (1989– starting antibiotic therapy. Analgesics Substantial paresis or paralysis (dogs)— 1991). J Am Vet Med Assoc 1992, Signs of severe pain—treated with an prognosis guarded; may note gradual 201:1253–1257. analgesic (e.g., oxymorphone; dogs: 0.05– resolution of neurologic dysfunction after Kornegay JN. Diskospondylitis. In: Kirk RW, ed., 0.2 mg/kg IV/IM/SC q4–6h). several weeks of therapy; treatment Current Veterinary Therapy IX. Philadelphia, Taper dosage after 3–5 days to gauge warranted. PA: Saunders, 1986, pp. 810–814. effectiveness of antibiotic therapy. Brucella canis—signs usually resolve with Ruoff CM, Kerwin SC, Taylor AR. therapy; infection may not be eradicated; Diagnostic imaging of discospondylitis. Vet CONTRAINDICATIONS recurrence common. Clin North Am Small Anim Pract 2018, Glucocorticoids 48:85–94. PRECAUTIONS Thomas WB. Diskospondylitis and other Use nonsteroidal anti-inflammatory drugs vertebral infections. Vet Clin North Am (NSAIDs) and other analgesics cautiously— Small Anim Pract 2000, 30:169–182. may cause temporary resolution of clinical ­ MISCELLANEOUS Author Mathieu M. Glassman signs even when infection is progressing; ASSOCIATED CONDITIONS Consulting Editor Mathieu M. Glassman when used, discontinue after 3–5 days to See Risk Factors. assess efficacy of antibiotic therapy. AGE-RELATED FACTORS  Client Education Handout POSSIBLE INTERACTIONS N/A available online None  Canine and Feline, Seventh Edition 413 Disseminated Intravascular Coagulation INCIDENCE/PREVALENCE Suspect DIC any time thrombocytopenia Associated with severe systemic inflammatory and prolonged clotting tests are seen disease. together. ­ BASICS Patients showing predisposing conditions D SIGNALMENT DEFINITION should have laboratory monitoring every An acquired complex hemostatic defect Species 24–48 hours. A sudden drop in platelet count arising from a variety of inciting causes that Dogs and cats; diagnosed more in dogs. and a 20–30% prolongation in APTT is leads to intravascular activation of coagula- Breed Predilections suspicious for non-overt DIC. This is a tion and consumption of clotting factors. It None critical stage for intervention to prevent results in widespread formation of micro- progression to overt DIC. Mean Age and Range Hepatic insufficiency may mimic DIC. thrombi with clinical manifestations of Depends on the primary disease. Decreased production of clotting factors is thrombosis and/or hemorrhage. Non-overt disseminated intravascular coagulation (DIC) Predominant Sex common. Decreased clearance of normal is the early, compensated form of DIC that None fibrin(ogen)olytic by-products may increase features consumption of coagulation factors SIGNS FDP values. Mild idiopathic thrombocyto­ and generation of microthrombi without clear Vary with the primary disease and with penia may also be seen. Spontaneous bleeding clinical signs. Overt (decompensated) DIC DIC-associated organ dysfunction. is uncommon unless DIC is present. refers to the classic phenotype associated with Petechiae. CBC/BIOCHEMISTRY/URINALYSIS hemorrhage, thrombosis, and organ failure. Bleeding from venipuncture sites, mucosa, Inflammatory leukogram, often with a PATHOPHYSIOLOGY or into body cavities. stress component. DIC represents a complication of a variety Bleeding is infrequent in cats, possibly Mild to moderate thrombocytopenia of primary conditions. It begins with a leading to underdiagnosis. (40–100 × 103/μL); less reliable in cats. hypercoagulable state that leads to production Anemia is possible. Red blood cell (RBC) CAUSES or embolization of microthrombi in small Gastric dilatation-volvulus. fragmentation is a supportive finding. vessels. Biochemical changes reflect affected organs; Heart failure. The primary conditions act through Heartworm disease. acute kidney injury may result in increased exposure/production of tissue factor Heat stroke. isosthenuria, oligo-anuria, or the (TF) that activates the extrinsic coagulation Hemolysis, especially immune mediated. identification of casts in urine sediment. pathway. Hemorrhagic gastroenteritis. OTHER LABORATORY TESTS TF is normally restricted from intravascular Infectious diseases, systemic (especially Prolonged clotting tests (PT, APTT); exposure. Increased TF exposure occurs endotoxemia). APTT is prolonged first, PT becomes through widespread endothelial injury and/or Inflammation, severe—regardless of prolonged with transition to overt DIC. inflammation. underlying cause. Hypofibrinogenemia, although Inflammation activates endothelial cells, Liver disease, severe. inflammatory increase may mask platelets, and monocytes leading to membrane Malignancies, especially hemangiosarcoma, consumption. expression of TF. Inflammatory cytokines also mammary carcinoma, and pulmonary Increased FDPs and D-dimers. D-dimers induce vesiculation of these membranes, adenocarcinoma in dogs and lymphoma in cats. are very sensitive and specific. DIC is unlikely releasing large quantities of microparticles Pancreatitis. if D-dimers are low/negative. Neither test is into circulation that are enriched with both Protein-losing nephropathy. specific enough alone to diagnose DIC. TF and phosphatidylserine (PS) and facilitate Shock, hypoxia, acidosis. Decreased AT; may be a positive acute initiation of coagulation. Some neoplastic Thrombocytopenia, especially immune- phase reactant in cats, masking consum- cells constitutively produce membrane TF mediated. ption. and also release microparticles. Transfusion incompatibility. Thromboelastography may provide Microparticles provide a suitable membrane Trauma. evidence of hypocoagulability or fibrinolysis. surface for amplifying intrinsic and common Envenomation. pathway coagulation, potentially leading to DIAGNOSTIC PROCEDURES uncontrolled production of thrombin that RISK FACTORS Diagnostic procedures should be focused on overwhelms endogenous coagulation inhibitors. Vary with cause. identifying the inciting cause of inflamma- Fibrin clots generated by thrombin can cause tion, and may include imaging, tissue biopsy, vascular occlusion and lead to organ or surgery as dictated by clinical signs. dysfunction. PATHOLOGIC FINDINGS Widespread microthrombus formation ­ DIAGNOSIS Usually related to the primary disease or consumes coagulation factors and platelets DIC-affected organs. while initiating fibrinolysis. By-products of DIFFERENTIAL DIAGNOSIS Petechiae common. Key differentials—immune-mediated fibrinolysis (fibrin degradation products [FDPs]) have anticoagulant properties and thrombocytopenia, anticoagulant toxicity, inhibit platelet function. Hemorrhage at a coagulation factor deficiency, paraproteinemia. Highly variable diagnostic pattern includes variety of sites can follow. Uncontrolled progression leads to thrombocytopenia, prolonged clotting times ­ TREATMENT widespread tissue hypoxia, multiorgan (prothrombin time [PT], activated partial APPROPRIATE HEALTH CARE dysfunction, and death. thromboplastin time [APTT]), decreased Requires intensive inpatient treatment. fibrinogen, decreased antithrombin (AT), and Aggressive treatment of the primary disease SYSTEMS AFFECTED increased products of fibrinolysis (FDPs, Multisystemic syndrome. is essential (e.g., antimicrobials for sepsis). D-dimers).  414 Blackwell’s Five-Minute Veterinary Consult Disseminated Intravascular Coagulation (continued) NURSING CARE Inhibitors of fibrinolysis should not be used. SYNONYMS Maintain tissue perfusion and oxygenation The use of antiplatelet medications in Consumptive coagulopathy. using fluids, transfusions, and oxygen therapy. thrombocytopenic patients is not indicated. Disseminated intravascular coagulopathy. D Restore depleted factors by blood/plasma Corticosteroids impair function of SEE ALSO transfusions. Use fresh frozen plasma mononuclear phagocytes and do not have a Coagulation Factor Deficiency. (10–20 mL/kg) to correct bleeding due to clear indication for DIC unless important for Thrombocytopenia. factor deficiency. therapy of the underlying disease (e.g., lymphoma). ABBREVIATIONS ACTIVITY APTT = activated partial thromboplastin Limited by disease severity. PRECAUTIONS time. Heparin may cause hemorrhage, and DIET AT = antithrombin. Maintain nutritional support as appropriate therapy should be monitored. DIC = disseminated intravascular Volume overload may occur in cases with for the clinical condition of the patient. coagulation. renal or pulmonary compromise. FDP = fibrin degradation product. CLIENT EDUCATION Inform the owner that the condition is POSSIBLE INTERACTIONS PS = phosphatidylserine. life-threatening with a guarded to poor None PT = prothrombin time. prognosis. RBC = red blood cell. TF = tissue factor. SURGICAL CONSIDERATIONS Related to primary disease. Plasma or whole ­Suggested Reading blood transfusion to restore clotting factors is ­ FOLLOW-UP Dunn ME. Acquired coagulopathies. In: a presurgical consideration. Surgery may be Ettinger SJ, Feldman EC, eds. Textbook of PATIENT MONITORING contraindicated with uncontrolled bleeding. Veterinary Internal Medicine: Diseases of Clinical improvement and the arrest of the Dog and Cat, 7th ed. St. Louis, MO: bleeding are key positive findings. Saunders, 2010, pp. 797–801. Daily lab testing (e.g., coagulation tests, O’Brien M. The reciprocal relationship fibrinogen, platelet counts) is warranted in severe between inflammation and coagulation. ­ MEDICATIONS cases to identify positive or negative trends. Less Top Companion Anim Med 2012, frequent testing may suffice in milder cases. DRUG(S) OF CHOICE 27:46–52. Coagulation times and fibrinogen often There is no specific pharmacologic therapy Ralph AG, Brainard MB. Update on normalize more rapidly than FDPs and for DIC per se. disseminated intravascular coagulation: platelet counts. Heparin may be used in patients that have when to consider it, when to expect it, overt thrombosis or in those at high risk of PREVENTION/AVOIDANCE when to treat it. Top Companion Anim thrombosis with normal coagulation times. Early detection of non-overt DIC can allow Med 2012, 27:65–72. Unfractionated heparin is preferred to low therapy before disease progresses to overt DIC. Stokol T. Laboratory diagnosis of dissemi- molecular weight heparin in human patients POSSIBLE COMPLICATIONS nated intravascular coagulation in dogs and with DIC. Aside from the primary disease, affected cats: the past, the present, and the future. Heparin binds to and potentiates the action organs may have permanent dysfunction or Vet Clin North Am Small Anim Pract 2012, of AT. Plasma or blood transfusions may be marginal reserve capacity. 42:189–202. needed to replenish AT for heparin to be an Author John A. Christian EXPECTED COURSE AND PROGNOSIS Consulting Editor Melinda S. Camus effective anticoagulant. For overt DIC, mortality rates for dogs range Starting doses for unfractionated heparin from 50% to 77%. For cats, rates may be >90%. are 150–200 U/kg SC q8h. It may also be  Client Education Handout given as a CRI starting at 20–30 U/kg/h IV available online (i.e., same total daily dosage). Therapy should be monitored using serial measurements of APTT or anti-Xa activity. ­ MISCELLANEOUS CONTRAINDICATIONS PREGNANCY/FERTILITY/BREEDING Heparin therapy should be avoided in Unlike in humans, obstetric complications are patients with coagulopathy. not a common cause in dogs and cats.  Canine and Feline, Seventh Edition 415 Drowning (Near Drowning) hemoconcentration and increases in sodium, 10–20 mg/kg IV q24h in the dog, 5 mg/kg chloride, and urine specific gravity. IV q24h in the cat) for aspiration pneumonia. Beta-2 agonists may help animals with ­ BASICS OTHER LABORATORY TESTS suspected bronchospasm. Pentoxifylline D Arterial blood gas reveals hypoxemia (partial OVERVIEW pressure of oxygen [PaO2] 50 mmHg), and acid-base CONTRAINDICATIONS/POSSIBLE immersion in liquid; near drowning defined as derangements. INTERACTIONS water submersion followed by survival for at IMAGING Corticosteroid therapy not indicated; use least 24 hours; recent changes in terminology Radiographic changes may not be detectable could be detrimental in animals with aspiration prefer the use of “death, morbidity or no for 24–48 hours. Focal or diffuse alveolar pneumonia. Use of enrofloxacin in young morbidity following a drowning episode.” pattern due to aspiration pneumonia or animals may result in cartilage erosion. Following submersion, elevations in CO2 levels in the bloodstream stimulate respiration, noncardiogenic pulmonary edema. Mixed and subsequent aspiration of water occurs. patterns may be present, ± radiopaque material Fresh water aspiration dilutes pulmonary filling the airways (“sand bronchogram”). surfactant, leading to alveolar collapse ± Foreign body inhalation may produce ­ FOLLOW-UP infectious pneumonia; hypertonic seawater segmental atelectasis. Progression of pulmonary injury to acute respiratory distress PATIENT MONITORING aspiration leads to diffusion of interstitial water Continuous monitoring of heart rate and into alveoli; large volumes of water are not syndrome (ARDS) is possible and may appear as bilateral, diffuse, symmetric alveolar infiltrates. rhythm, respiratory rate, mucous membrane typically aspirated, but any amount results in color and capillary refill time, urine output, ventilation–perfusion mismatch, hypoxemia, DIAGNOSTIC PROCEDURES arterial blood pressure, rectal temperature, and and metabolic acidosis. Submersion time, Endotracheal or transtracheal wash with neurologic status. Arterial blood gas, CBC, temperature of water, and type of water (fresh cytologic evaluation and culture with biochemical profile, coagulation profile, and vs. salt vs. chemical water) significantly affect sensitivity indicated if animal is stable. ECG acid-base status checked as needed. development of organ damage. monitoring. Cervical radiographs, CT or MRI of brain, and brainstem auditory evoked PREVENTION/AVOIDANCE SIGNALMENT Close monitoring of animals (especially Dogs and cats. Approximately half of animals response (BAER) assessment in select cases. young and old/debilitated animals) near involved in immersion accidents are 104 °F (>40 °C) almost always important. Fevers >106 °F (>41.1 °C) may lead to granulomatous diseases, portosystemic Temperatures >107 °F (>41.7 °C) usually not cerebral edema, bone marrow depression, shunting, thrombophlebitis, infarctions, fever, more likely to be primary hyperthermia. arrhythmia, electrolyte disorders, multiorgan pansteatitis, panosteitis panniculitis, damage, DIC. CBC/BIOCHEMISTRY/URINALYSIS hypertrophic osteodystrophy, blunt trauma, Historical Findings cyclic neutropenia, intracranial lesions, CBC and blood smear—leukopenia or Clinical history (e.g., contact with pulmonary thromboembolism. leukocytosis, left shift, monocytosis, infectious agents, lifestyle, travel, recent lymphocytosis, thrombocytopenia or Drugs and Toxins thrombocytosis, spherocytes, organisms. vaccination, drug administration, insect bites, Tetracycline, sulfonamide, penicillins, Biochemistry profile and urinalysis vary previous illness, allergies) and physical nitrofurantoin, amphotericin B, barbiturates, with organ system involved. examination (including retinal examination) iodine, atropine, cimetidine, salicylates, may help identify underlying disease OTHER LABORATORY TESTS antihistamines, procainamide, heavy metals. condition. If infectious disease suspected, attempt to Fever patterns (e.g., sustained, intermittent) FUO—Dogs culture an organism—urine culture, blood rarely helpful. Infection (28%)—discospondylitis, fungal cultures (i.e., three anaerobic/aerobic cultures, infections, endocarditis, abscesses, bacteremia, taken 20 min apart; try to use as much Physical Examination Findings septic arthritis, septic meningitis, pyothorax, volume as possible to increase diagnostic yield; Hyperthermia. pulmonary foreign body/abscess, stump use special blood culture bottles), fungal and Lethargy. pyometra, pneumonia, osteomyelitis, cerebrospinal fluid cultures, synovial and Inappetence. peritonitis, prostatitis, pancreatitis, prostatic fluid, biopsy specimens. Tachycardia.  Canine and Feline, Seventh Edition 527 (continued) Fever FeLV and FIV test, Snap 4DX test, NURSING CARE Glucocorticoids serologic tests or PCR for Toxoplasma, Fluid administration (IV) often lowers body Do not use unless infectious causes have Borrelia, Mycoplasma, Bartonella, Anaplasma, temperature. been ruled out. Ehrlichia, Rickettsia, FIP, systemic mycoses. Topical cooling if fever is severe (convection May mask clinical signs, may lead to Fecal examination. cooling with fans, evaporative cooling with immunosuppression, and not recommended Tracheal wash or bronchoalveolar lavage. alcohol on foot pads, axilla, and groin). for use as antipyretics; administration of If immune disorders suspected—cytologic Only use antipyretic treatment when fever corticosteroids to cats with intractable FUO after ruling out infectious diseases may F examination of synovial fluid; Coombs’ test, is prolonged and life-threatening (>106 °F, rheumatoid factor, antinuclear antibodies. >41.1 °C) and topical cooling is unsuccessful. promote favorable response. Pancreatic lipase immunoreactivity. Impaired patients (e.g., with heart failure, Primarily indicated for fever associated with T4 in cats. seizures, or respiratory disease) require immune-mediated disease and certain steroid- IMAGING antipyretic treatment earlier. Antipyretic responsive tumors (e.g., lymphoma). treatment may preclude elucidation of cause, PRECAUTIONS Radiography delay correct treatment, and complicate Abdominal radiographs—tumors and Side effects of antipyretics include emesis, patient monitoring (e.g., reduction of fever is diarrhea, gastrointestinal ulceration, renal effusion. important indication of response to Thoracic radiographs—pneumonia, damage, hemolysis, hepatotoxicity. treatment). neoplasia, pyothorax. POSSIBLE INTERACTIONS Survey skeletal radiographs—bone tumors, DIET Combination of nonsteroidal anti- multiple myeloma, osteomyelitis, discospondylitis, Febrile patients in hypercatabolic state require inflammatory drugs and steroids raises risk of panosteitis, hypertrophic osteopathy, high caloric intake. gastrointestinal hemorrhage. hypertrophic osteodystrophy. CLIENT EDUCATION Dental/skull radiographs—tooth root abscess, Work-up of patients with FUO often sinus infections, foreign bodies, neoplasia. extensive, expensive, and invasive, and may Contrast radiography (e.g., gastrointestinal not result in definitive diagnosis. and excretory urography). ­ FOLLOW-UP SURGICAL CONSIDERATIONS PATIENT MONITORING Ultrasonography Surgery may be necessary in some animals Body temperature at least q12h. Abdominal (plus directed aspirate or (e.g., pyometra, peritonitis, pyothorax, liver If cause of fever not found, repeat history biopsy)—abdominal neoplasia, abscess or abscess, neoplasms). and physical exam along with screening other site of infection (e.g., pyelonephritis, laboratory tests. pancreatitis, pyometra). If fever develops or worsens during Echocardiography if endocarditis suspected. hospitalization, consider nosocomial infection Nuclear Imaging ­ MEDICATIONS or superinfection. Radionuclide scanning procedures to DRUG(S) OF CHOICE EXPECTED COURSE AND PROGNOSIS evaluate for bone tumors, osteomyelitis, Do not use broad-spectrum (i.e., “shotgun”) Vary with cause; in some patients (more pulmonary embolism. treatment in place of thorough diagnostic commonly cats), underlying cause cannot be CT, MRI, or positron emission tomography workup unless patient’s status is critical and determined. scan if indicated. deteriorating rapidly. DIAGNOSTIC PROCEDURES Antibiotics Arthrocentesis (culture and cytology). Based on results of bacterial culture or Bone marrow aspirate and biopsy if malignancy or myelodysplasia suspected. serology. ­ MISCELLANEOUS In emergency situations, combination Lymph node, skin, or muscle biopsy if ASSOCIATED CONDITIONS antibiotic therapy can be started after culture clinically indicated. Young animals—infectious disease more specimens obtained (e.g., cephalothin 20 mg/ Fine-needle aspirate or biopsy of any mass common; prognosis better. kg IV q6–8h; combined with enrofloxacin or abnormal organ. Old animals—neoplasia and intra-abdominal 10 mg/kg IV q24h). Additional antimicrobials Central spinal fluid tap if neurologic signs. infection more common; signs tend to be more depend on main clinical suspicion based on Endoscopy and biopsy if gastrointestinal nonspecific; prognosis often guarded. preliminary laboratory and clinical evidence. signs. SYNONYMS Do not give antibiotics longer than 1–2 Exploratory laparotomy—last resort if all Pyrexia weeks if ineffective. other diagnostic tests fail to determine cause and patient not improving. Antipyretics SEE ALSO Aspirin—dogs: 10 mg/kg PO q12h; cats: Heat Stroke and Hyperthermia. 6 mg/kg PO q48h. ABBREVIATIONS Deracoxib—dogs: 1–2 mg/kg/day. DIC = disseminated intravascular coagulation. Carprofen—dogs: 2 mg/kg q12h. FeLV = feline leukemia virus. ­ TREATMENT Meloxicam—0.1 mg/kg/day. FIP = feline infectious peritonitis. APPROPRIATE HEALTH CARE Dipyrone—dogs: 25 mg/kg IV. FIV = feline immunodeficiency virus. Goals of treatment—reset thermoregulatory Flunixin meglumine—dogs: 0.25 mg/kg FUO = fever of unknown origin. set point to lower level; remove underlying SC once (give IV fluids). Authors Maria Vianna and Jörg Bucheler cause. Consulting Editor Michael Aherne  528 Blackwell’s Five-Minute Veterinary Consult Fiber-Responsive Large Bowel Diarrhea CAUSES & RISK FACTORS 2–4 weeks and then the original diet can be Unknown; stress or abnormal personality slowly introduced. Some dogs develop traits may play a role in some. diarrhea again, others can be maintained on ­ BASICS Clinical response to dietary soluble fiber their original diet. OVERVIEW supplementation suggests abnormal colonic Hypoallergenic diet trial for 2–3 weeks; no A form of chronic idiopathic large bowel motility and/or dysbiosis. Dysbiosis is defined improvement in stool quality. During the F diarrhea that occurs in dogs and usually as a microbial imbalance within the gastro­ food trial the dog must not receive any other responds favorably to dietary soluble fiber intestinal tract. Soluble dietary fiber is a nutrients, including flavored heartworm supplementation. prebiotic, fermented by colonic bacteria preventatives, vitamins, or any other At the author’s institution, chronic resulting in altered composition or activity of supplements. For this diet trial the author idiopathic large bowel diarrhea is diagnosed bacteria. Prebiotics are not digested by recommends using a hydrolyzed diet. The in approximately 25% of dogs referred for mammalian digestive enzymes and “feed” hydrolyzed protein in these diets is hypo­ evaluation of chronic large bowel diarrhea. colonic bacteria, potentially correcting allergenic. If the dog’s stool becomes normal Exclusion diagnosis that requires dysbiosis. Soluble fibers also adsorb water, during this diet trial a diagnosis of dietary eliminating known causes of chronic large improving stool quality. Fermentation of hypersensitivity or inflammatory bowel bowel diarrhea and clinical response to soluble fiber by colonic bacteria produces disease can be made. These hydrolyzed diets dietary fiber supplementation. volatile fatty acids, which are energy source are also highly digestible, low in fiber, and No pathophysiologic studies have been for colonic epithelial cells. restricted in fat. Some clinicians skip the performed. highly digestible diet trial and go directly to Only 3 reports in dogs comprising 83 cases. the hydrolyzed diet trial. Without performing May overlap with a stress-associated poorly a highly digestible diet trial first, response to defined syndrome that has been called irritable the hydrolyzed diet trial could also be due to ­ DIAGNOSIS digestibility, fat, and fiber content and not bowel syndrome, also referred to as nervous colitis, spastic colon, or mucus colitis. Some DIFFERENTIAL DIAGNOSIS due to dietary hypersensitivity. Many dogs dogs with irritable bowel syndrome respond to Dietary indiscretion. that respond to a hypoallergenic food trial can dietary fiber supplementation, while others Highly digestible diet-responsive diarrhea. be slowly switched back to their original diet require stress alleviation, antispasmodic Hypoallergenic diet-responsive diarrhea. after 12–14 weeks. medications, and/or anti-anxiety drugs. Whipworms. Colonoscopy; usually within normal Clostridium perfringens–associated diarrhea. limits or only mild nonspecific findings SIGNALMENT Lymphocytic plasmacytic colitis. such as slight increases in mucosal Dogs of all ages (0.5–14 years); median 6 Eosinophilic colitis. granularity or friability. years. Miscellaneous types of colitis. Many breeds, including mixed breeds; PATHOLOGIC FINDINGS Irritable bowel syndrome. common breeds include German shepherd Histopathologic evaluation of colonic Colonic neoplasia (adenocarcinoma, dog, miniature schnauzer, cocker spaniel, and biopsy samples; within normal limits. lymphoma, and adenoma are most common). miniature or toy poodle. Multiple biopsy samples should be Cecal inversion. evaluated from throughout the colon from SIGNS CBC/BIOCHEMISTRY/URINALYSIS the cecum to the rectum. Usually at least 5–6 Chronic diarrhea (soft to liquid) with classic No consistent or specific abnormalities, locations are sampled. large bowel characteristics; tenesmus, excess although can recognize peripheral eosinophilia fecal mucus, hematochezia, increased frequency occasionally in dogs with colonic whipworms, (median 3.5 times/day), and urgency. eosinophilic colitis, and food allergy. Diarrhea usually episodic alternating with periods of normal stool; diarrhea may OTHER LABORATORY TESTS ­ TREATMENT be continuous in approximately 25% of Multiple fecal flotations by zinc sulfate; Health care can be provided on an dogs. negative for whipworms and other parasites. outpatient basis and consists of dietary fiber Less common signs include occasional IMAGING supplementation. vomiting, decreased appetite during episodes Abdominal radiographs within normal Activity level does not have to be modified. of diarrhea, abdominal pain, and anal limits. A highly digestible “GI” diet should pruritus. Abdominal ultrasound within normal initially be supplemented with 1–3 tbsp daily Weight loss rare. limits. of psyllium hydrophobic mucilloid Stress factors or abnormal personality (Metamucil 10.2 g psyllium/tbsp). traits in approximately 35% of dogs; DIAGNOSTIC PROCEDURES Psyllium is a soluble fiber that adsorbs Clostridium perfringens enterotoxin fecal water, improving fecal consistency, and acts as household visitation, travel, moving, construction, instillation of an invisible ELISA; negative. a prebiotic promoting bacterial fermentation Therapeutic deworming for whipworms and production of volatile fatty acids, which fence; recent adoption or considered nervous, high-strung, sensitive, or (fenbendazole 50 mg/kg PO q24h for 5 are an energy source for colonic epithelial aggressive; or possess noise phobia, anxiety, days); no improvement. cells. Psyllium comes from the seeds or husks Highly digestible diet trial for 2–3 weeks; of the plant ispaghul and consists of or depressive disorders. Physical examination reveals no significant no improvement in stool quality. During the approximately 90% soluble fiber. Psyllium findings related to gastrointestinal tract. food trial the dog must not receive any other has been shown to be an effective treatment Digital rectal examination is usually nutrients. These diets are highly digestible, in some children with chronic nonspecific normal. Feces may be normal due to episodic low in fiber, and restricted in fat. If the dog’s diarrhea and in other people with several nature of the disease. Loose stool may be stool becomes normal during this diet trial, diarrheal disorders. present and it may contain hematochezia (red no further diagnostic tests are indicated. The Median dose is 2 tbsp/day, or 0.13 tbsp/kg/ blood) or excess mucus. highly digestible diet can be fed for another day, or 1.3 g psyllium/kg/day.