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Tail Paralysis



AUTHOR: BERTRAND. LUSSIER



EDITOR: ETIENNE. CÔTÉ



BASIC INFORMATION image



DEFINITION


Severe impairment or loss of tail motor function



EPIDEMIOLOGY


SPECIES, AGE, SEX: Dependent on underlying cause



GENETICS & BREED PREDISPOSITION



• Pugs, bulldogs (spina bifida, sacrocaudal dysgenesis)

• Chondrodystrophic breeds (disk herniation)


RISK FACTORS



• Outdoor cats (trauma)

• Free-roaming dogs

• Cardiomyopathies in cats (aortic thromboembolism)

• Type I disk herniation with severe paraparesis

• Degenerative lumbosacral stenosis (cauda equina syndrome)


ASSOCIATED CONDITIONS & DISORDERS



• Cutaneous wounds of the tail:
○ Self-inflicted if sensation altered by neurologic disease

○ Secondary to external trauma (hit by car, falls, etc.)

• Tail fracture


CLINICAL PRESENTATION



HISTORY, CHIEF COMPLAINT



• Trauma involving the hind quarters (hit by car, falls, stepped on, etc.)

• Trauma involving traction injury on the tail (exercise-related, malicious, caught in door, etc.)

• Unwillingness to jump up (e.g., lumbosacral diseases)

• Acute-onset vocalization and hind limb paresis/paralysis (aortic thromboembolism)


PHYSICAL EXAM FINDINGS



• Impaired tail motility with or without hind limb paresis

• Skin wounds (limbs, trunk, abdomen and/or tail)

• Concurrent fractures of the axial skeleton, pelvis, pelvic limbs, and/or thoracic limbs

• Urinary and/or fecal incontinence, urine- or feces-soiled tail

• Pain originating from the pelvic area

• Weakness, pale mucous membranes, dyspnea (if cat with thromboembolic disease)

• Shock if massive trauma

• Tachycardia, heart murmur, gallop, weak or absent pulses, cyanosis of the pelvic limbs (if feline cardiomyopathy)

• Transverse myelopathy (T3-L3 or L4-S3 or Cd1-Cd5 only)

• Large, distended bladder:
○ Easy to empty if spinal lesion involves lumbar intumescence (“lower motor neuron bladder”)

○ Difficult to empty if spinal lesion is cranial to lumbar intumescence (“upper motor neuron bladder”)

• Rectal exam: painful and might induce sacrocaudal instability if associated with trauma


ETIOLOGY AND PATHOPHYSIOLOGY



• Orthopedic:
○ Spinal/coccygeal fracture

○ Degenerative lumbosacral stenosis

• Neurologic:
○ Spinal malformations

○ Spinal fracture

○ Nerve root avulsion (lumbar intumescence/coccygeal)

○ Disk herniation (with or without paraparesis)

○ Tumor of the spine/spinal canal/cord

• Cardiac/vascular:
○ Feline thromboembolic disease

○ Vascular compromise secondary to trauma (arterial avulsion or thrombosis)

○ Fibrocartilaginous embolism


DIAGNOSIS image



DIAGNOSTIC OVERVIEW


Tail paralysis is apparent on physical exam. A complete neurologic exam helps identify the extent of the causative lesion, which in turn contributes to determining the prognosis, and whether or not treatment is likely to require tail amputation.



DIFFERENTIAL DIAGNOSIS



• Anomalous (spina bifida, hemivertebra, sacrocaudal dysgenesis, dermoid sinus)

• Degenerative lumbosacral stenosis (stenosis of vertebral canal, type II disk at L7-S1 space, sacral osteochondrosis, instability and misalignment of L7-S1, articular facet arthritis)

• Intervertebral disk disease (type I or type II)

• Spinal trauma/fracture/avulsion

• Vascular (feline thromboembolism, fibrocartilaginous embolism)

• Neoplasia

• Diskospondylitis


INITIAL DATABASE



• Rectal exam to document pain, swelling, instability, mass effect

• Complete neurologic examination to localize the lesion (see p. 1311)

• Radiographs of the spine, including sacrocaudal region (malformations, fracture/trauma/avulsion, diskospondylitis, osteolytic/osteoproliferative tumor, intervertebral disk disease)

• CBC, serum biochemistry panel, urinalysis depending on patient stability and systemic involvement

• Thoracic radiographs:
○ To evaluate the presence of thoracic lesions secondary to trauma

○ To assess for metastases if neoplasia is suspected

• Ultrasound:
○ Thoracic (for feline cardiomyopathy)

○ Abdominal if suspected pelvic canal tumor


ADVANCED OR CONFIRMATORY TESTING



• Advanced imaging modalities: myelography (see p. 1306), CT (see p. 1233), MRI (see p. 1302)
○ May be indicated for assessing underlying spinal abnormalities

• Electromyography (rare instances of neuromuscular disease)

• Fine-needle aspiration if possible for cytologic evaluation (masses, diskospondylitis)

• Ultrasound-guided biopsy (masses)


TREATMENT image



TREATMENT OVERVIEW



• Orthopedic or neurologic:
○ Treatment limited to addressing underlying cause if no vascular compromise

○ Medical management of fractures, using pain management, bandages for immobilization

○ Amputate tail if vascular compromise:
▪ Leave 3-4 coccygeal vertebrae if well vascularized.

▪ Amputate to the level of the skin if tail is devascularized.

• Cardiac/vascular:
○ Tail amputation if tail is soiled by urine and/or feces or if tail has not revascularized well

○ Address underlying cardiac disease.

• Neoplasia:
○ Wide surgical excision if possible

○ Radiation therapy or chemotherapy if indicated and if possible

• Skin wound of the tail (see p. 1016):
○ With vascular compromise, amputate tail at appropriate level.

○ Without vascular compromise, treat accordingly by local débridement (wet-to-dry bandaging or surgical débridement).

○ Use second-intention healing (bandages with hydrogel).

○ If wound closure impossible via second-intention healing, use secondary closure (local skin flaps, free skin grafts).


ACUTE GENERAL TREATMENT



• Treat shock if present.

• Treat underlying cardiac cause.

• Administer corticosteroids if tail paralysis is secondary to spinal cord/nerve compression (controversial; see p. 1039).

• Once patient is stable, treatment depends on underlying cause.


CHRONIC TREATMENT



• Hygiene and topical care to prevent urine/fecal contact dermatitis:
○ Bathing, keeping area dry and clean, clipping perianal region, and protective ointment if necessary

• Bladder catheterization if necessary

• Physical therapy for paraparetic patients

• As indicated by underlying cardiac disease


POSSIBLE COMPLICATIONS



• Dependent on therapeutic options

• Beware of corticosteroid administration:
○ Associated with gastrointestinal ulceration, colonic perforation


RECOMMENDED MONITORING


Dependent on primary cause and therapeutic options



PROGNOSIS AND OUTCOME image



• Trauma:
○ Intact deep pain perception and normal vascularization: guarded. Generally these patients will regain enough motor activity to avoid lack of hygiene.

○ Absence of deep pain for more than 48 hours: poor prognosis for return of motor activity, but good if tau amputated and normal voluntary hind limb activity and bladder control

• Guarded to poor if feline thromboembolic disease (recurrence risk)


PEARLS & CONSIDERATIONS image



COMMENTS



• The most common causes of tail paralysis are trauma and degenerative lumbosacral stenosis:
○ Prognosis depends on deep pain perception and vascular supply.

• In dogs and cats, the tail is not essential to life:
○ Tail amputation in patients with normal limb function and bladder control provides excellent quality of life.

• Beware: pain originating from the pelvic canal (e.g., prostatic abscess, degenerative lumbosacral stenosis) can mimic tail paralysis.


CLIENT EDUCATION


Variable: depends on primary cause of tail paralysis



SUGGESTED READING



De Lahunta A, Glass EC. Veterinary neuroanatomy and clinical neurology, ed 3. St Louis: Saunders Elsevier, 2009.



Tarsal Trauma



AUTHOR: JOHN J. HABURJAK



EDITOR: JOSEPH. HARARI



BASIC INFORMATION image



DEFINITION


Includes ligament damage, luxation/subluxation of individual tarsal bones, fractures, or shearing injuries



SYNONYM


Tarsal breakdown



EPIDEMIOLOGY


GENETICS & BREED PREDISPOSITION: Racing greyhounds: central tarsal bone fractures. Border collies: central tarsal bone fracture with luxation. Shelties and collies: luxation of superficial digital flexor tendon.


RISK FACTORS: Racing or agility activities; distal hind limb trauma



CLINICAL PRESENTATION


DISEASE FORMS/SUBTYPES: Sprains, fractures, and shearing or degloving wounds; coaptation-related injuries, including pressure sores from casts or splints, dermatitis from soiled bandages, and wound infection or dehiscence from contaminated dressings


HISTORY, CHIEF COMPLAINT: Hind limb trauma; lameness after competition or exercise



PHYSICAL EXAM FINDINGS



• Lameness

• Swelling

• Open wounds around the tarsus

• Pain or crepitation on palpation of the tarsus

• Gross instability characterized by a plantigrade stance

• Tarsal deformity


ETIOLOGY AND PATHOPHYSIOLOGY



• Racing animals on counterclockwise tracks are predisposed to right-sided injuries.

• In racing greyhounds, there is a classic triad of fractures involving the central tarsal bone, calcaneus, and base of metatarsal V.

• In border collies, unknown etiology for exercise induced subluxation with central tarsal bone fracture

• In pets, fractures often occur in the calcaneus.


DIAGNOSIS image



DIAGNOSTIC OVERVIEW


Tarsal injuries are best diagnosed by physical and radiographic examinations.



DIFFERENTIAL DIAGNOSIS



• Autoimmune polyarthropathy (systemic lupus erythematosus [SLE], rheumatoid arthritis)

• Infectious (Lyme borreliosis, rickettsial disease)


INITIAL DATABASE



• Mediolateral and dorsopalmar radiographic projections of the tarsus

• CBC, chemistry panel, and urinalysis based on the animal’s stability and the American Society of Anesthesiologists (ASA) classification (see p. 1372)

• Thoracic/abdominal radiographs, abdominal ultrasound, electrocardiogram (ECG) for animals that have undergone severe trauma


ADVANCED OR CONFIRMATORY TESTING



• Oblique radiography (nondisplaced fractures); skyline views (trochlea of the talus)

• Stress-film radiography (mediolateral radiograph with tarsus manually forced into dorsal and plantar extension and a dorsoplantar radiograph with a medial to lateral stress applied) to identify location of joint instability


TREATMENT image



TREATMENT OVERVIEW


The goal of therapy is anatomic and functional restoration of tarsal functions:


• Fractures: stabilization and anatomic reduction
○ Buttress repair of comminuted tarsal bone fractures to prevent joint collapse

• Ligamentous injuries: reestablishment of joint support by repairing collateral ligaments or arthrodesis/ankylosis

• Shearing injuries: wound management


ACUTE GENERAL TREATMENT



• Minimally displaced, nonarticular fractures and grade I and most grade II sprains can be stabilized for 6-8 weeks with an external splint (see p. 1336):
○ Luxated joints, intraarticular fractures, and grade III sprains are supported in a modified Robert-Jones bandage until surgery.

• Shearing injuries require initial wound-management treatment (see p. 1016):
○ Gentle lavage of open wounds using warm saline, lactated Ringer’s solution, and dilute chlorhexidine solutions to reduce gross contamination. (Animals are sedated and given analgesics.)

○ Coverage of tissues with moistened (above solutions) gauze sponges useful in débridement (wet-to-dry-bandages) as they are changed daily.

○ Alternatively, direct application of sugar or honey has been used for reducing infection and promoting healing for highly contaminated, traumatic open wounds, but the role of such treatment in the joint is unclear.

○ Final surgical débridement and joint lavage can be performed during orthopedic stabilization surgery.

○ Wounds with healthy granulation tissue, reduced contamination, and early epithelialization can be closed with sutures or covered with a non-adherent dressing and allowed to heal via second intention.


CHRONIC TREATMENT



• Surgical repairs to the tarsus require 6-12 weeks of external coaptation (splints or external fixatures) and exercise restriction.

• Collateral ligament disruption requires stabilization with tension-band principle (malleolar fractures) or replacement with prosthetic suture.

• Instability of the tarsocrural joint or complete (grade III) plantar tarsal disruption necessitates pantarsal arthrodesis.

• Individual tarsal bone fractures require lag screw fixation, except for lesions of the calcaneus (tension-band principle).

• Plantar intertarsal and plantar tarso-metatarsal subluxations are unstable in weight-bearing animals and require partial tarsal arthrodesis with pins or small plates (tension-band principle).

• Dorsal intertarsal and dorsal tarso-metatarsal subluxations are rare and stable (compressed) in weight-bearing animals:
○ Establishing the diagnosis requires stress film radiography.

○ Primary ligament repair or partial tarsal arthrodesis is performed.

• Luxation of the superficial digital flexor tendon is treated by suturing of torn retinacular tissues.


POSSIBLE COMPLICATIONS



• Reduction/implant failure

• Delayed or failed arthrodesis

• Plantar necrosis (vascular injury)

• Wound infection

• Coaptation-related morbidity

• Degenerative joint disease


RECOMMENDED MONITORING



• Lameness evaluation 1-3 months following injury and treatment

• Serial radiographic studies to evaluate fracture healing or progression of arthrodesis


PROGNOSIS AND OUTCOME image



• Good to excellent for noncompeting dogs

• Variable for return to preinjury status for competing dogs

• Severe shearing injuries with neurovascular compromise may necessitate limb amputation.


PEARLS & CONSIDERATIONS image



COMMENTS



• When conservatively managed, intraarticular fractures rarely heal with osseous bridging, thus leading to degenerative joint disease. Surgical treatment is recommended to reduce the risk of such adverse consequences.

• Severe shearing injuries are commonly due to motor vehicle trauma. Despite significant damage, acceptable function is possible with various reconstructive efforts.

• In noncompeting animals, solitary intertarsal joint fusion/ankylosis (i.e., calcaneotarsal, calcaneoquartal, quartalmetatarsal) can lead to near normal function.


SUGGESTED READING



Dee JF. Tarsal injuries. In: Bloomberg MS, Dee JF, Taylor RA, editors. Canine sports medicine and surgery. Philadelphia: WB Saunders; 1998:120-137.


Piermattei DL, Flo GL, DeCamp CE. Fractures and other orthopedic injuries of the tarsus. In Brinker, Piermattei, and Flo’s handbook of small animal orthopedics and fracture repair, ed 4, St Louis: Elsevier; 2006:661-713.



Taurine Deficiency



AUTHOR: KATHRYN M. MEURS



EDITOR: KATHRYN. MICHEL



BASIC INFORMATION image



DEFINITION


Inadequate intake or availability of dietary taurine



EPIDEMIOLOGY


SPECIES, AGE, SEX: Taurine is an essential nutrient for cats but not for dogs under most circumstances. Deficiency can occur in cats that cannot meet metabolic needs from dietary sources and occasionally in dogs, particularly if on restricted diets.



GENETICS & BREED PREDISPOSITION



• None reported in cats

• In dogs, isolated occurrences of taurine-deficient dilated cardiomyopathy have been identified in a variety of breeds, including American cocker spaniels, golden retrievers, and Newfoundlands.


RISK FACTORS



• Cats: inadequately supplemented commercial or home-prepared diets

• Dogs: breed predisposition, inadequate protein and sulfur-containing amino acid intake (restricted diets), possible impact of diet composition on intestinal availability


CLINICAL PRESENTATION



DISEASE FORMS/SUBTYPES



• Cats: central retinal degeneration (CRD), reproductive failure, growth retardation, and dilated cardiomyopathy (DCM)

• Dogs: DCM in susceptible breeds or individuals


HISTORY, CHIEF COMPLAINT



• Cats: compatible diet history (poorly formulated commercial or home-prepared diet) is suggestive but not pathognomonic; dyspnea, respiratory distress.

• Dogs: exercise intolerance and weight loss progressing to cough, respiratory distress, and eventually ascites; possible diet history of restricted diet (very low-protein diets, vegan diets, dry dog food with lamb meal, rice, or both as the primary ingredient)


PHYSICAL EXAM FINDINGS



• Cats: variable combinations of tachypnea, dyspnea, tachycardia, lethargy, dehydration, and hypothermia. Systolic murmur at the apex on the left side, with gallop rhythm in severe cases. Peripheral vasoconstriction may result in cold extremities.

• Dogs: similar to cats; tachyarrhythmia


ETIOLOGY AND PATHOPHYSIOLOGY



• Taurine is synthesized from methionine and cysteine. It does not occur in proteins but is required for a variety of cellular homeostatic functions. Synthesis occurs in cats too slowly to maintain taurine balance in the absence of adequate intake. Dogs have a greater ability to synthesize taurine than cats but occasionally develop taurine deficiency as well. Obligatory loss also occurs in cats and dogs, because only taurine can combine with cholesterol during bile salt synthesis, whereas most other species can substitute glycine for taurine.

• In cats, excessive taurine-conjugated bile salt loss in feces occurs secondary to variable combinations of type of diet processing, protein source, changes in location and/or numbers of intestinal microflora, and/or increased secretion of bile salts due to changes in the release of cholecystokinin.


DIAGNOSIS image



DIAGNOSTIC OVERVIEW


The possibility of taurine deficiency should be considered in cats and dogs with a compatible diet history and signs of cardiac dysfunction (dogs, cats) or blindness (cats).



DIFFERENTIAL DIAGNOSIS



• Idiopathic DCM

• Other causes of myocardial failure


INITIAL DATABASE



• Cats: radiography to determine presence of heart failure (cardiomegaly plus pleural effusion, pulmonary edema, or both). Do not attempt to obtain radiographs of severely dyspneic, struggling patients, because the stress of the procedure may result in the death of the cat.

• Dogs: radiography, as for cats; electrocardiographic (ECG) signs include variable combinations of left-sided enlargement, sinus tachycardia, atrial fibrillation, and ventricular tachyarrhythmias.


ADVANCED OR CONFIRMATORY TESTING



• Echocardiography is the test of choice for diagnosis of DCM: dyskinesis (reduced systolic motion) of the left ventricular walls, increased end-diastolic diameter, and reduced shortening fraction.

• Blood and/or plasma taurine concentration (draw sample into heparin [green top] tube):
○ Animals with low taurine concentrations (whole blood: <200 nmol/mL in cats, <150 nmol/mL in dogs; plasma <40 nmol/mL in cats and dogs) should be switched to diets known to result in higher plasma concentrations or supplemented with taurine. Plasma taurine concentrations fluctuate with food intake, whereas whole blood taurine reflects long-term (weeks to months) intake.


TREATMENT image



TREATMENT OVERVIEW


The goals of treatment are to restore taurine homeostasis and improve cardiac function.



ACUTE GENERAL TREATMENT



• Supportive care for congestive heart failure (CHF; see p. 470), inotropic support (digoxin, pimobendan) and arrhythmias

• Taurine supplementation pending confirmation of diagnosis


CHRONIC TREATMENT



• Cats: recommend switching the cat to a satisfactory diet and supplementing with taurine at 250-500 mg PO or in food q 12 h for 3-6 months or until echocardiographic parameters return to normal.

• Dogs: recommend 1000 mg taurine/ day PO (divided, or once a day). Change to a diet containing more protein and sulfur-containing amino acids and less fiber if possible.


RECOMMENDED MONITORING



• Clinical condition

• Taurine levels should be reevaluated in 1-2 months.

• Radiography, echocardiography


PROGNOSIS AND OUTCOME image



• The prognosis is better when deficiency is identified and treated appropriately before extensive permanent change exists in the myocardium. Clinical signs of advanced heart failure, such as hypothermia or thromboembolism, suggest a poorer prognosis.

• Dogs that improve in conjunction with taurine supplementation become more energetic after a few weeks; they then also show reduction in cardiomegaly, and improvement in echocardiographic parameters should be observed in 3-6 months.


PEARLS & CONSIDERATIONS image



COMMENTS


Recovery of function and appetite occur within days to weeks after provision of taurine if deficiency of this amino acid is the cause of the signs. When they occur, reduction in cardiomegaly and improvement in echocardiographic parameters may require 3-6 months of supplementation; improvement may permit reduction or discontinuation of cardiac medications.



PREVENTION


Feeding a properly formulated diet



CLIENT EDUCATION


Explain the importance of feeding pets a properly formulated diet.



SUGGESTED READING



Buffington CAT. Nutritional diseases and nutritional therapy. In: Sherding RG, editor. The cat: diseases and clinical management. New York: Churchill Livingstone; 1994:161-190.


Meurs KM. Primary myocardial disease in the dog. In: Ettinger SJ, Feldman EC, editors. Textbook of veterinary internal medicine. St Louis: Elsevier Saunders; 2005:1077-1082.


Pion PD. Traditional and nontraditional effective and noneffective therapies for cardiac disease in dogs and cats. Vet Clin North Am Small Anim Pract. 2004;34:187.



Tear Film Abnormalities (Excluding KCS)



AUTHOR & EDITOR: CHERYL L. CULLEN



BASIC INFORMATION image



DEFINITION


A relatively common ophthalmic condition characterized by abnormal mucin (produced by goblet cells of the conjunctiva) and/or lipid (produced by meibomian [tarsal] glands) component(s) of tears. Keratoconjunctivitis (KCS) is discussed separately on p. 628.



SYNONYMS


Qualitative tear deficiencies or abnormalities



EPIDEMIOLOGY


SPECIES, AGE, SEX: Dogs and cats, any age, either sex



GENETICS & BREED PREDISPOSITION



• Cats predisposed to corneal sequestration (e.g., brachycephalic breeds) may be predisposed to tear film abnormalities (TFAs).

• Dogs predisposed to chronic eyelid and/or conjunctival irritation (e.g., breeds with inherited entropion and/or ectropion) are predisposed to developing qualitative tear deficiencies (see p. 348).


RISK FACTORS



• Disorders affecting the meibomian glands (e.g., alkali burns of the eye)

• Patients with diseases resulting in primary (e.g., feline herpesvirus-1 infection) or secondary keratoconjunctival (e.g., entropion/ectropion, keratoconjunctivitis sicca [KCS]) disorders


ASSOCIATED CONDITIONS & DISORDERS



• Conjunctivitis and TFAs commonly coexist (unclear which is causative).

• Superficial keratitis (nonulcerative or ulcerative)

• Eyelid disorders:
○ Entropion (common)

○ Ectropion (common)

○ Eyelid agenesis (rare)

○ Autoimmune disorders (rare)

○ Infectious marginal blepharitis (occasional)

• Chemical ocular burns (occasional)

• Primary or secondary skin disease involving eyelid mucocutaneous junctions (common)

• Keratoconjunctivitis sicca (common; see p. 628)

• Diabetes mellitus in dogs (common)


CLINICAL PRESENTATION


DISEASE FORMS/SUBTYPES: Mucin tear deficiency, lipid tear deficiency



HISTORY, CHIEF COMPLAINT



• Swollen eyelids

• ‘Red’ eye

• Serous or mucoid to mucopurulent ocular discharge

• Previous bout(s) of conjunctivitis responsive to standard topical medication(s) but recurrent

• Squinting

• Corneal cloudiness (see p. 245)


PHYSICAL EXAM FINDINGS



• Systemic: generally unremarkable except in those cases where systemic disease is present (e.g., diabetes mellitus; generalized seborrhea)
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