R
Rabies
BASIC INFORMATION 
DEFINITION
Fatal polioencephalitis of warm-blooded animals and humans caused by a Lyssavirus sp. and generally transmitted by the bite of an infected mammal
EPIDEMIOLOGY
SPECIES, AGE, SEX: Warm-blooded animals of all ages are susceptible:
• In the United States, cats are the domestic species most frequently reported rabid, with −200−300 cases/year.
• In the United States, the most important species-adapted strains are in the fox, raccoon, skunk, and bat.
• Salivary gland infections occur in vampire bats without producing clinical signs in the bats, resulting in prolonged viremia. Insectivorous bats may also be infected.
CLINICAL PRESENTATION
• Paralytic (dumb) form (majority of canine cases, minority of feline cases): o Characterized by lethargy, difficulty swallowing, ptyalism, voice or bark change, dropped jaw, and lower motor neuron paralysis, often first in the wounded limb
ETIOLOGY AND PATHOPHYSIOLOGY
• Virus replicates in local tissues, where it enters neuromuscular junctions and neurotendinous spindles.
• Spreads by intraaxonal flow through peripheral nerves to the spinal cord and brain. Replicates within the CNS and then moves outward through peripheral, sensory, motor, and cranial nerves.
• Large amount of virus present in salivary glands, where it is shed. Salivary virus excretion begins up to 2 weeks before the onset of neurologic signs.
• The incubation period varies and depends on the innervation at the bite site, distance of the bite site to the CNS, and virus variant and amount of virus in the exposure; can range from 2 weeks to as long as 6 months or more.
DIAGNOSIS 
DIFFERENTIAL DIAGNOSIS
• Encephalitis: viral (canine distemper, feline leukemia virus, feline immunodeficiency virus, feline infectious peritonitis); immune-mediated (e.g., granulomatous meningoencephalitis); rarely, protozoal, rickettsial, bacterial, fungal
TREATMENT 
TREATMENT OVERVIEW
• The first reported survival of a human who did not receive rabies pre- or postexposure prophylaxis was recently described. The case has prompted further exploration of the treatment she received, termed the “Wisconsin Protocol.” Rifampin, amantadine, and the induction of a ketamine/mid-azolam coma were the mainstays of treatment.
RECOMMENDED MONITORING
• Management of rabies suspects varies with immunization status and local laws. The attending veterinarian should contact the local state veterinarian.
• Most public health laws require a 10-day confined observation period after human exposure from a suspected dog or cat:
• All rabies suspects must be securely confined and monitored for behavioral changes and/or neurologic signs suggestive of rabies.
• A healthy dog or cat that bites or scratches an individual should be confined and monitored for 10 days:
○ If clinical signs do not develop within 10 days of bite/scratch, there has been no exposure to rabies virus.
• Unvaccinated dogs or cats that are exposed to a known rabid animal or to any bat or wild, carnivorous mammal:
PEARLS & CONSIDERATIONS 
COMMENTS
• If clients are concerned regarding possible or known human exposure to rabies, they must see their physician immediately.
• Signs take weeks to months to develop after exposure, but once signs are present, death ensues quickly (<2 weeks).
• Travel to rabies-free areas has been facilitated by a vaccinate-microchip-and-blood test protocol that shows adequate neutralizing antibody levels (e.g., >0.5 IU/mL) and no clinical signs of rabies typically over a 6-month period prior to departure. This reduces the burden of travel on the pet (previously a 6-month quarantine in the destination country/state). The specific jurisdiction can provide detailed requirements (e.g., for the United Kingdom: http://www.defra.gov.uk/wildlife-pets/pets/travel/pets/index.htm).
PREVENTION
• All dogs and cats should be vaccinated for rabies after 12 weeks of age, again at 12 months of age, and then every 3 years or yearly depending on state regulations.
• Cats should only receive inactivated vaccines; do not use modified live virus (MLV) vaccines in cats.
TECHNICIAN TIPS
• Gloves should be worn during examination of all unknown or unvaccinated animals and during examination of bite wounds of unknown origin as a protection against rabies.
Centers for Disease Control and Prevention. http://www.cdc.gov/ncidod/dvrd/rabies/.
Greene CE, Rupprecht CE. Rabies and other lyssavirus infections. In: Greene CE, editor. Infectious diseases of the dog and cat. ed 3. St Louis: Saunders-Elsevier; 2006:167-183.
Lackay SN, Kuang Yi, Fu Zhen F. Rabies in small animals. Vet Clin Small Anim. 2008;38:851-861.
Radiation Therapy: Adverse Reactions
BASIC INFORMATION 
EPIDEMIOLOGY
RISK FACTORS
• Radiation dose, fraction size, radiation energy, overall treatment time, field size, previous surgery, concurrent administration of chemotherapy, and necrotic or unhealthy tissues may influence a patient’s risk for the development of adverse radiation reactions. Cats are less likely to have radiation side effects than dogs.
CLINICAL PRESENTATION
DISEASE FORMS/SUBTYPES
• Skin effects:
○ Acute: hyperemia, dry desquamation, moist desquamation, ulceration, necrosis, hair loss, lymphedema, pain
• Head/neck effects:
○ Acute: stomatitis, mucositis, pharyngitis, esophagitis (erythema, edema, confluent or patchy white/yellow membrane formation), xerostomia, dry/cracked lips, ulceration, pain, difficulty swallowing, secondary infection with bacteria or fungi (soft, curdlike white patches), swelling of parotid/submandibular salivary glands, keratitis, keratoconjunctivitis sicca, blepharospasm, periocular crusting, corneal edema
• Bone effects (chronic): clinical/radiographic evidence of fracture, necrosis, infection, or secondary tumor
• Heart effects (acute/chronic): signs relative to pericarditis, chronic constrictive pericarditis, or restrictive cardiomyopathy due to myocardial fibrosis, such as fever, tachycardia, presence of pericardial effusion, cardiac tamponade, pleural effusion, dyspnea, conduction abnormalities, exercise intolerance, subclinical valvular defects
• Bladder effects (acute/chronic): pain on palpation, clinicopathologic evidence of cystitis (pollakiuria, nocturia, dysuria, hematuria)
• Lung effects (acute/chronic): clinical and radiograph signs compatible with acute pneumonitis and chronic fibrosis (fever, dyspnea, cough, production of sputum, signs of right heart failure if pulmonary hypertension exists). Fibrosis usually, not always, preceded by pneumonitis.
• Colon/rectal effects (acute/chronic): diarrhea secondary to acute enteritis, hematochezia, sense of urgency, chronic diarrhea, proctitis, stricture, fistula formation secondary to chronic colorectal/anorectal injury
ETIOLOGY AND PATHOPHYSIOLOGY
• Radiation lesions induced in normal tissues are attributed primarily to loss of specific target cells or clonogenic cells. Hence, acute effects develop in rapidly renewing tissues such as skin, gastrointestinal (GI) tract, or bone marrow.
• This target cell theory also applies to vascular damage as the predominant lesion in chronic effects, as endothelial cells are slowly lost to mitotic death.
DIAGNOSIS 
ADVANCED OR CONFIRMATORY TESTING
Generally not necessary. In people:
• Chronic skin fibrosis measured by tissue compliance meter, ultrasound measurement, or BTC-2000 suction device in humans
• Xerostomia measured by functional radioisotope imaging, salivary flow output, and patient assessment in humans
TREATMENT 
TREATMENT OVERVIEW
• Improving patient quality of life by minimizing pain, establishing return to function, and ruling out tumor recurrence
ACUTE TREATMENT
• Skin effects:
○ Clean moist desquamation with aluminum subacetate (Domeboro) soaks, 1/3 strength hydrogen peroxide (1%), or diluted chlorhexidine solution.
○ Use of skin care products anecdotal but include: Aquaphor, Collasate, vitamin A/E ointment, aloe vera gel, Theracare, 1% hydrocortisone ointment, silver sulfadiazine, Miaderm, Biafine, Radioplex.
○ Bandages promote moist environment and are not advised when possible. If necessary, use moisture vapor–permeable dressings (Tegaderm, Mepilex).
• Head/neck effects:
○ Stomatitis/mucositis/esophagitis:
▪ Use of soft, bland diet with decreased amount, increased frequency, and room temperature. Avoidance of salty, acidic foods.
▪ Mouthwashes to cleanse and lubricate the oral cavity (saline, sodium bicarbonate solutions, dilute tea, dilute hydrogen peroxide, “magic mouthwash”; avoid alcohol preparations).
▪ Topical anesthetics and coating agents such as viscous lidocaine (Xylocaine), sucralfate suspensions, Acemannan-containing gel all proven to ameliorate mucositis. NOTE: viscous lidocaine may burn initially prior to taking effect.
▪ Omega-3 fatty acid, arginine, glutamine, and oral zinc supplementation all proven in humans to ameliorate pathologic or clinical evidence of mucositis
▪ Antibiotics (aerobic gram-negative bacteria most likely) and/or antifungals topically (chlorhexidine rinse with topical suspension of nystatin) or systemically for secondary infections
• Acute heart effects: pericarditis managed primarily by prevention. Rest, nonsteroidal antiinflammatory drugs, and mild diuretics often all that is needed during self-limiting, subclinical resolution. Subtotal parietal pericardiectomy if clinical signs do not resolve. Coenzyme Q10 used for prevention in humans.
• Acute bladder effects: maintain patient hydration; increase fluid intake to dilute urine (less irritating). Treat underlying urinary infections, treat bladder spasms (phenazopyridine hydrochloride, Urimax, flavoxate hydrochloride agents, oxybutynin used in human oncology), rule out recurrent tumor.
• Acute lung effects: glucocorticosteroids provide much clinical utility despite lack of published evidence. Rest, oxygen therapy, antibiotics as needed. Supportive care with expectorants and bronchodilators.
CHRONIC TREATMENT
• Skin effects:
○ Fibrosis: physical therapy, impedance-controlled microcurrent treatment, hyperbaric oxygen, pain management, glucocorticosteroids in the initial setting (limited usefulness for established fibrosis), pentoxifylline ± vitamin E, and superoxide dismutase all are methods to delay or reduce fibrosis in human oncology. Investigational treatments include decorin (inhibitor of transforming growth factor beta [TGF-b]), angiotensin-converting enzyme (ACE) inhibitors, and interferons.
○ Lymphedema: Manual Lymphatic Drainage (specialized massage with specific stroke duration, orientation, pressure, sequence) combined with compression bandages, exercise, skin care, pressure gradient sleeves, and/or pneumatic pumps method to ameliorate lymphedema in human oncology. Diuretics to cause acute reduction in the initial setting (limited usefulness for long-term owing to removal of lymph fluid but not proteinaceous debris from interstitial space). Benzopyrones (coumarin), autologous lymphocyte injection, and selenium proven methods to improve resolution in humans. Of interest but less usefulness, glucocorticosteroids, weight management, hyperbaric oxygen, antibiotic therapy, flavonoids, surgical intervention.
• Chronic head/neck effects:
○ Esophageal stricture (see p. 365): dilatations and semisolid diet, feeding tubes, hydrocortisone injection at the stricture site
• Chronic heart effects: antipyretics for fever, centesis for tamponade, pericardiectomy if severe. Medical management by veterinary cardiologist.
• Chronic bladder cystitis/fibrosis: see Acute Treatment above. Surgical intervention for fistula formation.
• Pulmonary fibrosis ameliorated by captopril in human oncology. Oxygen and glucocorticosteroids as needed.
• Chronic bowel effects: initial management with increased dietary fiber and diphenoxylate (Lomotil) or loperamide. Addition of opioid analgesics titrated to effect. Topical viscous lidocaine for anorectal irritation. Glucocorticosteroid-containing suppositories (ProctoFoam, Canasa) for acute inflammation. Sucralfate or short-chain fatty acid (butyrate) enemas for bleeding. Topical formalin, topical amifostine, coagulation with electrocautery, laser therapy, argon plasma beam coagulation, and hyperbaric oxygen for refractory bleeding in human oncology.
POSSIBLE COMPLICATIONS
• Skin effects: progression of moist desquamation to full-thickness necrosis and secondary infection, necessitating surgical débridement. Unrelenting fibrosis or lymphedema, necessitating surgical intervention.
PEARLS & CONSIDERATIONS 
PREVENTION
• Use of intensity-modulated radiation therapy/image-guided radiation therapy/conformal radiation therapy techniques, to allow increased dose to tumor while also increasing normal tissue sparing
• Acute skin effects: reduce skin folds, remove bolus where necessary, avoid topical agents immediately prior to radiation therapy, use higher-energy radiation, and ensure surgical wounds have healed prior to initiation of radiation therapy.
• Head/neck effects: preradiation therapy dental prophylaxis and removal of unhealthy teeth to decrease severity of mucositis and risk of osteonecrosis. Amifostine as a radiation protector routinely used to prevent development of xerostomia (dry mouth) in humans. Ocular: tape eyelids open for anterior megavoltage beam fields to the eye to decrease dose to cornea and conjunctiva (otherwise, the eyelids will serve as a site of radiation dose buildup, increasing the radiation dose delivered to the cornea).
CLIENT EDUCATION
• Teach family members when to expect and how to manage acute effects. Promote role of radiation therapist in client education and side-effect management.
• Prepare notebook with photographs of radiation side effects as a tool for client education. Use serial photographs to display effects as they heal with time.
Bruner DW, Haas ML, et al. Manual for radiation oncology nursing practice and education, ed 3. Pittsburgh: Oncology Nursing Society, 2005.
Cox JD, Ang KK. Radiation oncology: rationale, technique, results, ed 8. St Louis: Mosby, 2003.
Dow KD, Bucholtz JD, Iwamoto R, et al. Nursing care in radiation oncology, ed 2. Philadelphia: WB Saunders, 1997.
LaDue T, Klein MK. Toxicity criteria of the veterinary radiation therapy oncology group. Vet Radiol Ultrasound. 2001;42:475-476.
Rectal Prolapse
BASIC INFORMATION 
EPIDEMIOLOGY
SPECIES, AGE, SEX: Can occur at any age, but young dogs and cats are most frequently affected.
DIAGNOSIS 
DIFFERENTIAL DIAGNOSIS
• Prolapsed intussusception. Therapeutic importance of differentiating from rectal prolapse: prolapsed intussusception generally requires laparotomy, whereas rectal prolapse does not.
INITIAL DATABASE
• Rectal examination: insert a blunt probe between prolapsed tissue and rectal wall. The probe cannot be passed cranially with rectal prolapse but will pass at least a few centimeters into a fornix created by everted colon in cases of prolapsed intussusception.
• CBC, serum chemistry profile, urinalysis, and urine culture may identify underlying cause of straining and indicate an animal’s metabolic status.
• Abdominal radiographs may demonstrate conditions associated with rectal prolapse (i.e., neoplastic masses, prostatomegaly, urinary calculi).
(Courtesy Dr. Richard Walshaw.)
TREATMENT 
ACUTE GENERAL TREATMENT
• Acute treatment with patient under general anesthesia to prevent tenesmus during prolapse reduction.
• Place purse-string suture around rectum at mucocutaneous junction to maintain reduction. The purse-string suture should be tight enough to prevent prolapse but should still allow for passage of soft stools. Tightening the suture over a syringe case (3 mL in most small animals is adequate) may prevent overtightening.
CHRONIC TREATMENT
• If the patient undergoes resection and anastomosis, he/she should receive a low-residue diet and stool softeners to reduce postoperative straining.
PEARLS & CONSIDERATIONS 
COMMENTS
• Place a lubricated finger or small syringe case in rectum while tightening purse-string suture to prevent overtightening.
• Apply a local anesthetic to the rectal tissue after removal of the purse-string suture, which may help prevent recurrence.
Rectoanal Stricture
DIAGNOSIS 
INITIAL DATABASE
• Assessment of location (identifying possible organ of origin), symmetry (circumferential versus focal), pain, and evidence of metastasis (palpation of sublumbar lymph nodes)
