Dacryocystitis

BASIC INFORMATION

DEFINITION

Although dacryocystitis is technically inflammation of the lacrimal sac, the term is commonly used for describing inflammation anywhere along the tear drainage (i.e., nasolacrimal) system, including the lacrimal puncta, canaliculi, lacrimal sac, and nasolacrimal duct. Dacryocystitis is an acquired condition resulting in ocular discharge (see 777).

ETIOLOGY AND PATHOPHYSIOLOGY

• Most common cause of dacryocystitis is migration of foreign bodies, most frequently plant material, into the nasolacrimal system.

• Descending infections from ocular surface flora, often associated with poor tear drainage and lacrimal stasis, also incriminated with initiating inflammation.

DIAGNOSIS

DIAGNOSTIC OVERVIEW

Suspicion for the diagnosis arises based on chief complaint and physical exam findings indicative of ocular abnormalities including ocular discharge. Determination of whether dacryocystitis involves an obstruction or is secondary to inflammation is the key to diagnosis and prompt treatment. This is accomplished by checking for nasolacrimal passage of fluorescein dye and nasolacrimal flushing.

INITIAL DATABASE

• Nasolacrimal flushing if suspect complete or partial nasolacrimal duct blockage:

○ May be done under firm restraint with topical ocular anesthesia (e.g., proparacaine 0.5% [dogs]).

○ Resistant animals or signs of discomfort warrant routine preanesthetic evaluation and subsequent sedation or general anesthesia (cats have small lacrimal puncta).

○ Lacrimal puncta can be cannulated but not distal nasal puncta (dogs and cats), which are difficult to identify in many or most individuals irrespective of dacryocystitis.

○ Identify dorsal and ventral lacrimal puncta (oval in dog and round in cat, with or without circumferential pigment), 1 to 2 mm from eyelid margin in palpebral conjunctiva near medial canthus.

○ Gently insert cannula or intravenous catheter (stylet removed; 22 to 24 gauge, dogs; 24 to 26 gauge, cats), with 3-mL syringe filled with sterile saline or eyewash attached, approximately 3 mm into the dorsal lacrimal punctum.

○ Slowly inject the saline/eyewash until it flows from the ventral lacrimal punctum (confirms puncta, canaliculi, and lacrimal sac are patent).

○ Next, occlude ventral lacrimal punctum with digital pressure and flush 3-12 mL saline/eyewash through the nasolacrimal duct.

○ Collect fluid/discharge at naris in sterile basin.

• Culture and sensitivity testing of purulent discharge if present

• Consider referral to a veterinary ophthalmologist if unable to establish patency of nasolacrimal system.

ADVANCED OR CONFIRMATORY TESTING

• Dacryocystorhinography (contrast study of nasolacrimal system) with standard radiography can identify an obstruction site.

• Recently, CT-dacryocystorhinography has been demonstrated to allow highly accurate characterization of lesions obstructing the nasolacrimal duct.

TREATMENT

TREATMENT OVERVIEW

Determine character (i.e., plant material, inflammatory debris, etc.) and location of obstruction and relieve it.

ACUTE GENERAL TREATMENT

• If foreign body is lodged in canaliculi or lacrimal sac, it may be manually removed by flushing lacrimal punctum.

• If a foreign body is present in nasolacrimal duct, removal may be accomplished by dacryocystotomy (surgical incision of nasolacrimal duct; referable procedure).

CHRONIC TREATMENT

• Care after any of the preceding surgeries would include topical antibiotic/steroid combination medication (neomycin/polymyxin/dexamethasone suspension or ointment q 4-6 h) for the first 2-4 postoperative weeks.

• Dacryocystotomy requires placement and maintenance of a Silastic cannula and oral antibiotics for 3-4 weeks after surgery.

POSSIBLE COMPLICATIONS

If foreign bodies are left in the nasolacrimal drainage system, scarring, permanent occlusion, and chronic epiphora may result.

PROGNOSIS AND OUTCOME

• Depends on underlying cause

• Good prognosis with successful removal of foreign body

BASIC INFORMATION

EPIDEMIOLOGY

ASSOCIATED CONDITIONS & DISORDERS

• Otitis externa and/or media

• External or middle ear canal neoplasia

• Nasopharyngeal polyps (cats)

CLINICAL PRESENTATION

DISEASE FORMS/SUBTYPES: Described as:

• Congenital or adult-onset

• Inherited or noninherited

• Sensorineural or conduction deafness

ETIOLOGY AND PATHOPHYSIOLOGY

• Acquired conduction deafness resulting from otitis externa/media

○ Impaired conduction of sound waves to the tympanic membrane from hyperplasia and exuberant cerumen production or the presence of pus in the external ear canal

○ Impaired transduction of sound waves to the otic ossicles due to stiffened, fibrotic, or ruptured tympanic membrane

○ Impaired mechanoelectrical transduction due to sclerosis of otic ossicles

• Acquired conduction deafness from external or middle ear masses

○ Obstruction of sound waves to the tympanic membrane

○ Destruction of middle ear structures

• Presbycusis (senile deafness)

○ Degeneration of the neural components of the inner ear

○ ± Stiffening of the tympanic membrane

○ ± Ankylosis of the otic ossicles

• Loud noise exposure

○ Damage to inner ear hair cells and/or ossicles and/or tympanic membrane

• Congenital hereditary deafness associated with coat color

○ Associated with coat-color genes

○ Abnormal migration of neural crest cells (precursor to melanocytes) to the inner ear (thought to provide nourishment to inner ear); associated with sacculocochlear-type degeneration

PROGNOSIS AND OUTCOME

• Inherited sensorineural deafness and deafness resulting from degeneration of inner ear is permanent.

• Variable prognosis for animals with conduction deafness (depends on chronicity and/or severity of the disease)

PEARLS & CONSIDERATIONS

PREVENTION

• Use non-deaf animals for breeding.

• For breeds predisposed to congenital deafness, use animals with non-blue irides for breeding.

BASIC INFORMATION

DEFINITION

Deciduous teeth that failed to exfoliate

SYNONYM

Retained deciduous teeth: retained refers to failure to erupt (emerge through the gingival surface); persistent is more accurate because it refers to failure to exfoliate (cause shedding of the deciduous tooth).

EPIDEMIOLOGY

Dogs and cats. Permanent dentition eruption schedules dictate when a deciduous tooth is considered persistent (use table cautiously; breed and individual variation can be significant [±1 to 2 months]):

GENETICS & BREED PREDISPOSITION

High prevalence in toy dog breeds (Yorkshire terriers, miniature poodles, Pomeranians) suggests inheritance. Recent advances in the understanding of eruption and exfoliation suggest familial and/or genetic influence.

Permanent Dentition Eruption Times in the Dog and Cat

	Dog	Cat
Incisors	3-5 months	3-4 months
Canines	4-6 months	4-5 months
Premolars	4-6 months	4-6 months
Molars	5-7 months	4-5 months

ETIOLOGY AND PATHOPHYSIOLOGY

• Pathophysiologically important information includes:

○ Persistent deciduous teeth may result in malpositioned permanent teeth.

○ Permanent mandibular incisors, canines, and premolars erupt lingual (i.e., toward the tongue) to persistent deciduous teeth; lingually deviated permanent mandibular canine teeth may cause palatal trauma.

○ Permanent maxillary incisors and premolars erupt palatal (i.e., toward the palate) to persistent deciduous teeth.

○ Permanent maxillary fourth premolars erupt buccal/labial (i.e., toward the cheek/lip) and distal (i.e., away from the midline of the dental arch) to persistent deciduous teeth.

○ Permanent maxillary canine teeth erupt mesial (i.e., toward the midline of the dental arch) to persistent deciduous teeth.

○ Food, debris, plaque, and calculus accumulating on and between deciduous and permanent teeth may cause periodontal disease even in young animals.

DIFFERENTIAL DIAGNOSIS

• Missing, malformed, malpositioned or unerupted permanent tooth

• Supernumerary permanent tooth

• Malocclusion

INITIAL DATABASE

• CBC, serum chemistry panel, urinalysis: preoperative, generally unremarkable

• Full-mouth dental radiographs: evaluate root structures, confirm and document presence of healthy permanent teeth.

ADVANCED OR CONFIRMATORY TESTING

Hormone levels if metabolic/endocrine disease is suspected

TREATMENT

TREATMENT OVERVIEW

Extraction is indicated in virtually all cases (exception: no equivalent permanent tooth) to alleviate dental crowding, soft-tissue trauma, and/or dental interlock; prevent periodontal disease; prevent malpositioning of permanent teeth and malocclusion; and correct existing malocclusion.

ACUTE GENERAL TREATMENT

• No treatment is needed for uncrowded, healthy persistent deciduous teeth that have no permanent counterpart.

• Extraction of all other persistent deciduous teeth is advised.

• Closed and open extraction techniques are acceptable, depending on tooth to be extracted and degree of root resorption.

○ Closed extraction for mobile teeth

○ Open extraction via creation of a mucoperiosteal flap and alveolar bone removal for solid teeth with complete root structures

○ Slow, steady pressure with a dental elevator is key for inducing periodontal ligament fatigue and successful extraction.

○ Be sure to keep all instrumentation away from the erupting permanent tooth.

• Extraction sites should be closed using rapidly absorbable synthetic suture material while avoiding placing sutures directly over an erupting tooth.

• Postoperative dental radiographs are recommended to ensure complete extraction, evaluate surrounding structures for damage, and provide documentation.

• Antibiotics are not usually necessary post extraction.

• Pain management: intraoperative nerve block (0.5% bupivacaine hydrochloride, 0.2 to 0.3 mL near middle mental, inferior alveolar, infraorbital or maxillary nerve) followed by oral nonsteroidal antiinflammatory medication (e.g., carprofen, 2 mg/kg PO q 12 h) for 2-3 days postoperatively.

RECOMMENDED MONITORING

• Examination in 1-2 weeks to evaluate extraction sites

• Examination in 4-6 weeks to evaluate occlusion if necessary; if abnormalities persist, therapeutic recommendations are offered.

PROGNOSIS AND OUTCOME

Excellent for regional healing and reduction of risk of periodontal disease

BASIC INFORMATION

DEFINITION

Common decongestants are pseudoephedrine, ephedrine, phenylephrine, and imidazoline derivatives (oxymetazoline, naphazoline, tetrahydrozoline, xylometazoline). They are active ingredients in over-the-counter (OTC) human medications used for the treatment of cold, flu, sinusitis, and allergies. Toxicosis from other active ingredients is discussed separately (p. 87).

EPIDEMIOLOGY

SPECIES, AGE, SEX

All species, breeds, and both sexes are susceptible; dogs are more likely to be involved, based on their predilection for dietary indiscretion.

RISK FACTORS

Preexisting cardiac disease, systemic hypertension, and seizure disorders may exacerbate signs of toxicosis.

ETIOLOGY AND PATHOPHYSIOLOGY

Source:

• Toxicosis can occur either when animals accidentally ingest OTC medications or are mistakenly given the medication.

• Decongestants stimulate alpha-adrenergic receptors, resulting in vasoconstriction of arterioles in the nasal passages, thus improving air flow.

○ Pseudoephedrine, ephedrine (stereoisomer), ma huang (a herbal form of ephedra). Pseudoephedrine is available as a hydrochloride or sulfate salt. It is found as a single ingredient (30-mg or 60-mg regular pill), or extended-release (120 mg as 12-hour pill or 240 mg as 24-hour pill) or as a liquid (varying concentration). It is more commonly available in combination with other ingredients (cough suppressants, antihistamines, acetaminophen, ibuprofen). Common brand names of products that contain pseudoephedrine include Sudafed, Afrin, Tylenol, Vicks, Alka-Seltzer, and Contac.

○ Phenylephrine is available for oral use (mostly 5- to 15-mg tablets), nasal sprays (0.25%-1%), or eye drops (0.1%). It is available in combination with other medications (antihistamines, cough suppressants, pain killers).

○ Imidazoline decongestant examples are oxymetazoline, tetrahydrozoline, naphazoline, and xylometazoline. These are available as nasal and ophthalmic solutions of varying concentrations (0.01%-0.1%).

Mechanism of Toxicosis:

• Adverse effects are dose-dependent and reflect excessive stimulation of the adrenergic nervous system.

• With pseudoephedrine, the release of norepinephrine increases the potential for central nervous system stimulation. Ingestion of >3 mg/kg in an otherwise healthy dog typically warrants decontamination of the patient and close monitoring.

• With imidazoline decongestants, overdoses cause excess stimulation of central alpha-2 receptors, which results in hypotension. The margin of safety is very narrow with these agents, with ingestion of even a small amount potentially resulting in toxicosis.

DIAGNOSIS

DIAGNOSTIC OVERVIEW

Diagnosis is suspected based on a combination of evidence of exposure along with presence of consistent signs. OTC urine drug-test kits can detect pseudoephedrine, or it can be detected in plasma at a diagnostic laboratory (can help determine exposure).

INITIAL DATABASE

• CBC

• Serum biochemistry profile

• Arterial blood pressure

• ECG (heart rate and rhythm)

• Body temperature

ADVANCED OR CONFIRMATORY TESTING

Urine drug screening with OTC test kit (optional)

TREATMENT

TREATMENT OVERVIEW

Treatment is indicated based on clinical suspicion (history and physical examination), without urine test confirmation. Treatment may consist of patient decontamination alone (emesis and administration of activated charcoal) if clinical signs are absent, or decontamination and management of cardiovascular and CNS aberrations and thermoregulation if clinical signs are present.

ACUTE GENERAL TREATMENT

• Decontamination of patient:

○ Pseudoephedrine/ephedrine/phenylephrine:

▪ Induction of emesis (see p. 1364) with 3% hydrogen peroxide, 2 mL/kg PO 1-2 times to effect, maximum of 45 mL; useful only in asymptomatic animals within 1 hour of ingestion of immediate-release products and within a couple of hours of extended-release products.

▪ Activated charcoal (1-2 g/kg granules or 6.6-11 mL/kg of 10% solution with sorbitol or other cathartic PO). Repeat (3.3-5.5 mL/kg without cathartic PO) once 6-8 hours after initial administration if extended-release decongestant.

▪ Acidification of urine (use only if facility to run blood gases available): ammonium chloride, 50 mg/kg PO q 6 h; or ascorbic acid, 30 mg/kg PO q 8 h to promote excretion (ion trapping).

▪ Control CNS excitation (note: phenothiazines are drugs of choice for controlling CNS excitation: acepromazine, 0.02-0.05 mg/kg IV, IM, repeat as needed; useful for mild hypertension and CNS stimulatory signs; or chlorpromazine, 0.5-1 mg/kg IV.

▪ Control tachycardia: propranolol, 0.02-0.04 mg/kg IV, repeat in 4-8 hours; or use esmolol, 0.2-0.5 mg/kg IV or 25-200 mcg/kg/min IV as constant rate infusion.

○ Imidazoline decongestants:

▪ Due to the rapid onset of signs after imidazoline decongestant ingestion, emesis and charcoal are generally not recommended.

• Specific treatment:

○ Imidazoline decongestants:

▪ Atipamezole (50 mcg/kg IM to effect for hypotension); may be repeated as needed for life-threatening hypotension and bradycardia. A quarter to a third of the dose may be given IV for rapid effect, and the remainder IM.

▪ Yohimbine: 0.1 mg/kg IV; repeat in 2-3 hours if needed. Use if atipamezole is not available.

• Supportive care for all decongestant exposures:

○ Intravenous fluid therapy

○ Thermoregulation: cool fluids, external cooling measures as needed

○ Keep the patient calm and reduce external stimuli (quiet surroundings).

RECOMMENDED MONITORING

• Serum biochemistry profile, including electrolytes

• Acid-base status if acidifying urine

PROGNOSIS AND OUTCOME

Generally favorable with prompt presentation and appropriate care. Presence of head bobbing, circling, or DIC carries a poor prognosis. Pseudoephedrine exposures exceeding 10 mg/kg are potentially lethal without treatment.

PEARLS & CONSIDERATIONS

COMMENTS

• The use and availability of pseudoephedrine in several U.S. states has been restricted because of alleged use of this medication in illegal amphetamine synthesis. Pseudoephedrine is being replaced by phenylephrine.

• Other agents (nonsteroidal antiinflammatory drugs [p. 768], antihistamines [p. 87], cough suppressants) may also cause toxicosis if a combination product was ingested; be sure to monitor for signs and treat accordingly.

• The signs of pseudoephedrine toxicosis are very similar to amphetamine toxicosis in dogs.

• Several weight-loss OTC products contain varying levels of ma huang, a natural source of ephedrine.