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Halitosis

AUTHOR: JAMIE G. ANDERSON

EDITOR: ALEXANDER M. REITER

BASIC INFORMATION image

DEFINITION

An offensive odor emanating from the oral cavity, which may arise from intraoral or extraoral causes

SYNONYMS

Bad breath, oral malodor

EPIDEMIOLOGY

SPECIES, AGE, SEX: Any species, age, and sex may be affected.

CLINICAL PRESENTATION

HISTORY, CHIEF COMPLAINT: Halitosis is a leading concern of pet owners, as it can negatively affect their relationship with the beloved pet.

PHYSICAL EXAM FINDINGS

• A complete physical examination must always include a thorough oral examination.
• Most intraoral disorders that cause halitosis are apparent upon examination of the oral cavity and surrounding tissues.
• General physical findings can vary greatly depending on the underlying disease process. For example, oral manifestations of leptospirosis vary depending on the serovar and may include halitosis, petechiae, oral hemorrhages, ulceration, glossitis with necrosis, and sloughing of the tongue.
• Attention should also be paid to the prepuce/vulva via inspection and to the anal sacs via palpation, because licking of these structures or their secretions is a recognized cause of halitosis in dogs and cats.

ETIOLOGY AND PATHOPHYSIOLOGY

• Intraoral causes:
○ Plaque and calculus accumulation, gingivitis, periodontitis, stomatitis
○ Cheilitis, lip fold pyoderma
○ Osteomyelitis, osteonecrosis
○ Oral tumors (particularly those that outgrow their blood supply and become necrotic, e.g., malignant melanoma, osteosarcoma)
○ Foreign bodies, oral implants
○ Oronasal communications
• Extraoral causes: see Differential Diagnosis

DIAGNOSIS image

DIAGNOSTIC OVERVIEW

Physical examination helps differentiate between intraoral and extraoral causes; further diagnostic tests are selected accordingly.

DIFFERENTIAL DIAGNOSIS

The DAMNIT scheme can be utilized as a guide to differential diagnosis:

• Developmental, degenerative: congenital and acquired palate defects/oronasal communications
• Autoimmune, anatomic, allergic: pemphigus vulgaris, systemic lupus erythematosus, erythema multiforme, drug eruption; “mouth breathing” associated with brachycephalic head conformation
• Metabolic, mechanical: diabetic ketoacidosis, uremia/renal failure, hepatic dysfunction causing hyperammonemia; retention of food debris
• Nutritional, neoplastic: gastroesophageal reflux; oral, pharyngeal, esophageal, gastric neoplasia; dietary indiscretion/consumption of spoiled food
• Infectious, inflammatory or idiopathic: dental plaque/calculus (oral bacteria), periodontal disease (gingivitis and periodontitis), gingival hyperplasia, contact mucositis and contact mucosal ulceration, stomatitis; leptospirosis; local and systemic fungal diseases; cheilitis and lip fold pyoderma; bronchitis, pneumonia; infection with feline leukemia virus (FeLV), feline immunodeficiency virus (FIV), feline calicivirus (FCV) or feline herpesvirus (FHV)
• Toxic, traumatic: toxic epidermal necrolysis, trauma from malocclusion, tooth fracture, jaw fracture, nonhealing oral wounds, oral foreign body

INITIAL DATABASE

Sensory evaluation and complete physical examination (including oral examination in the awake patient)

ADVANCED OR CONFIRMATORY TESTING

• CBC, chemistry panel, urinalysis: if history and physical examination suggest an extraoral cause
• Viral testing: FeLV and FIV in cats with stomatitis (feline coronavirus and feline herpesvirus testing uncommonly performed because of great number of clinically healthy carriers, and positive results likely would not change treatment plan).
• General anesthesia, oral examination, and biopsy of suspicious lesions
• Case-specific advanced diagnostics centered on the mouth and upper airway when an intraoral cause is suspected (e.g., dental radiography, CT, thoracic radiographs for metastasis check of suspected oral neoplasms) and systemic evaluations (e.g., leptospirosis testing) when an extraoral diagnosis is suspected.
• Identify and quantify volatile sulfur compounds or volatile organic compounds with gas chromatography, mass spectroscopy, and sulfide meters (in research settings).

TREATMENT image

TREATMENT OVERVIEW

The goal of treatment is to control halitosis by addressing its underlying intraoral or extraoral causes. For intraoral causes, primary treatment is often followed by preventive care. For extraoral causes, treatment of the underlying disorder is the basis of therapy.

ACUTE GENERAL TREATMENT

• Improve oral hygiene via professional dental cleaning and periodontal therapy, with specific attention to treatment of oral disease associated with halitosis (e.g., extraction of teeth with severe periodontitis).
• Specific treatment for halitosis caused by extraoral disorders is directed towards the underlying disorder.

CHRONIC TREATMENT

• Maintain a healthy periodontium via routine home oral hygiene (daily tooth brushing, application of chlorhexidine products onto teeth and gums, use of diets, treats, and chew toys that help control plaque and calculus accumulation) and professional dental cleaning and periodontal therapy.
• Treat extraoral causes of halitosis.

NUTRITIONAL/DIETARY THERAPEUTICS

Home oral hygiene products, diets, treats, and toys proven to control plaque and calculus accumulation (see the Veterinary Oral Health Council website: http://vohc.org/)

RECOMMENDED MONITORING

Follow-up as indicated for routine management of underlying intraoral or extraoral cause

PROGNOSIS AND OUTCOME image

Generally depends on the ability to eliminate underlying cause

• Fair to good prognosis: periodontitis, gingival hyperplasia, anal sac disease when treatment and prophylaxis are implemented properly and maintained consistently (active disorders that usually require ongoing care)
• Guarded prognosis: oral neoplasia, leptospirosis, opportunistic infection secondary to retroviral disease; the severity of the causative problem may make halitosis difficult to control.

PEARLS & CONSIDERATIONS image

COMMENTS

A nonmalodorous oral cavity improves the human-animal bond as well as the pet’s health and well-being.

PREVENTION

• Plaque accumulation on teeth, a major cause of halitosis, can easily be prevented by daily home oral hygiene and yearly professional dental cleaning and periodontal therapy.
• Other intraoral causes of halitosis can be recognized early by means of home oral examination by the owner and professional oral examination by the veterinarian during wellness visits.

TECHNICIAN TIPS

Technicians are on the frontline of identifying oral disorders pathologies including halitosis in at least two important ways: bringing oral abnormalities to the attention of the clinician and demonstrating proper home oral hygiene techniques to the owner.

CLIENT EDUCATION

• The oral cavity can be easily assessed by most owners.
• Halitosis is obvious, abnormal, and requires appropriate veterinary intervention.
• Home oral hygiene is important to general health.

SUGGESTED READING

Tonzetich J. Production and origin of oral malodor: a review of mechanism and methods of analysis. J Periodontol. 1977;48:13.

Veterinary Oral Health Council (VOHC). http://vohc.org/.

Head Tilt

AUTHOR: JAMES B. MILLER

EDITOR: ETIENNE. CÔTÉ

BASIC INFORMATION image

DEFINITION

Tilting of the head in a clockwise or counterclockwise direction along the long axis of the body. The head may be tilted due to a disorder of balance (vestibular disease) or due to discomfort from a dermatologic problem (acute moist dermatitis of the lateral face, or otitis externa). Head tilt due to an orthopedic problem (torticollis) is rare in small animals.

EPIDEMIOLOGY

SPECIES, AGE, SEX: Idiopathic vestibular disease dogs >8 years; any age in cats

GENETICS & BREED PREDISPOSITION

• Otitis externa/dermatitis: usually “floppy eared” breeds of dogs with long pinnae (e.g., spaniels, retrievers)
• Congenital vestibular disease (uncommon): Doberman pinscher, cocker spaniel, German shepherd, others

GEOGRAPHY AND SEASONALITY: Idiopathic vestibular disease in cats may predominate in late summer/early fall

ASSOCIATED CONDITIONS & DISORDERS

• If head tilt is of vestibular origin, concurrent nystagmus, ataxia, circling, and/or vomiting may occur.
• If head tilt is associated with otitis externa/dermatitis, concurrent vigorous head shaking is common.

CLINICAL PRESENTATION

DISEASE FORMS/SUBTYPES

• Vestibular disease (peripheral or central)
• Associated with discomfort (e.g., otitis externa or dermatitis ventral to the ear)

HISTORY, CHIEF COMPLAINT

• Head tilt associated with idiopathic vestibular disease; usually acute onset:
○ Vomiting followed by head tilt, ataxia, and circling/rolling for the next 1-2 hours is common
○ Owners may not report nystagmus.
• Head tilt associated with otitis externa/dermatitis:
○ Signs of pain of the affected ear/dermatitis lesion
○ Scratching of ear/affected skin
○ Rubbing of face on the floor

PHYSICAL EXAM FINDINGS

• Head tilt associated with peripheral vestibular disease (one or more maybe present):
○ Head tilt is always toward the side of the lesion.
○ Nystagmus (horizontal or rotary) with fast phase away from the side of the head tilt (see p. 772).
○ Circling
○ Ataxia with falling to the side of the head tilt
• Head tilt associated with central vestibular disease (one or more may be present):
○ Head tilt is toward the side of the lesion.
○ Nystagmus (horizontal, rotary, or vertical) with fast phase away from the side of the head tilt (see p. 772)
○ Circling
○ Ataxia
○ Proprioceptive deficits, motor weakness on the side of the lesion
○ Rarely, central vestibular disease may cause paradoxical signs (head tilt away from the side of the lesion). Proprioceptive deficits indicate the true side of the lesion (ipsilateral).
○ Other cranial nerve deficits (V, VI, VII)
• Head tilt associated with otitis externa/dermatitis:
○ Otitis externa (frequently suppurative)
○ Moist dermatitis (“hot spot”) just ventral to the ear but covered by the pinna

ETIOLOGY AND PATHOPHYSIOLOGY

• Peripheral vestibular disease:
○ Idiopathic
○ Infection (otitis media/interna)
○ Neoplasia
○ Hypothyroidism (rare)
○ Post middle ear surgery
○ Intoxication (e.g., aminoglycoside antibiotics; rare)
○ Congenital/hereditary
• Central vestibular disease:
○ Infection
○ Inflammation
○ Neoplasia
○ Trauma
• Otitis externa/dermatitis:
○ Dogs: secondary to atopy, food hypersensitivity/allergy, hypothyroidism
○ Bacterial
○ Yeast
○ Mites (cats)

DIAGNOSIS image

DIAGNOSTIC OVERVIEW

Head tilt is most commonly caused by vestibular dysfunction. Therefore, the diagnostic process should seek to identify whether the brain (central) or inner/middle ear (peripheral) is the site of the lesion, which can usually be determined with a clinical neurologic exam. Further testing is selected based on a differential diagnosis list elaborated from history, physical exam, and neurologic exam findings.

INITIAL DATABASE

• CBC, serum chemistry profile, and urinalysis: usually normal
• Otoscopic exam:
○ Otitis externa, polyp, blood (head trauma) are possible.
○ Careful examination may reveal fluid in the middle ear with infectious causes.
• Tympanic bulla radiographs
• In otitis externa, consider evaluation for atopy, food hypersensitivity/allergy, and hypothyroidism

ADVANCED OR CONFIRMATORY TESTING

• Serum thyroid assays if cutaneous, biochemical, or other signs suggesting hypothyroidism are present (dogs).
• MRI or CT if inner ear or intracranial lesion is suspected based on case information to date.
• Cerebrospinal fluid analysis if intracranial disease is considered.

TREATMENT image

TREATMENT OVERVIEW

• Improve the clinical condition by decreasing nausea, anorexia, skin and external ear irritation, and pain.
• Treat primary cause when possible.

ACUTE GENERAL TREATMENT

• Vestibular:
○ No specific therapy is available for treatment of idiopathic vestibular syndrome in dogs or cats. Glucocorticoids do not appear to help.
○ Other specific causes will require treatment based on etiology.
○ It may be difficult for the animal to walk or stand, so good nursing care including ability for the animal to get to food and water as well as appropriate care to prevent urine or fecal scalding are very important.
• Dermatologic:
○ In cases of moist dermatitis, clipping the hair of the affected area and gentle cleaning with an antiseptic are recommended (see p. 30).

PROGNOSIS AND OUTCOME image

• Vestibular:
○ The prognosis for idiopathic vestibular disease is excellent (dog and cat), but recurrence is possible.
○ With idiopathic vestibular disease, a head tilt may remain after resolution of all other signs.
○ The prognosis for neoplasia and all causes of central vestibular nystagmus is guarded to poor, depending on the exact cause, ability to treat, and response to therapy.
• Dermatologic:
○ The prognosis for otitis externa is good, but chronic cases may require advanced treatment or occasionally surgery.
○ Moist dermatitis ventral to the ear has an excellent prognosis.

PEARLS & CONSIDERATIONS image

COMMENTS

• In a majority of cases in dogs and cats, acute-onset head tilt is caused by idiopathic peripheral disease and will resolve spontaneously in 1-2 weeks.
• Idiopathic vestibular disease is a diagnosis of exclusion.
• Nearly all central vestibular disease cases will have other central nervous system signs (proprioceptive defects, weakness, other cranial nerve involvement).

CLIENT EDUCATION

• When idiopathic vestibular disease is the primary consideration, the owners need to know that the problem will usually resolve with time.
• Otitis externa may become a chronic problem; owners should be advised that rechecks are needed even if the animal appears normal.

SUGGESTED READING

Lorenz M, Kornegay J. Ataxia of the head and the limbs. In: Lorenz M, Kornegay J, editors. Handbook of veterinary neurology. Philadelphia: WB Saunders; 2004:219-243.

Head Trauma

AUTHOR: ELIZABETH M. STREETER

EDITOR: ELIZABETH. ROZANSKI

BASIC INFORMATION image

DEFINITION

Traumatic injury resulting in damage to soft tissues of the head, the skull, intracranial structures, or some combination of these

EPIDEMIOLOGY

SPECIES, AGE, SEX: Animals of any age or breed. Young animals may be overrepresented (lifestyle, increased risk of traumatic injury).

ASSOCIATED CONDITIONS & DISORDERS

• Traumatic injuries affecting other body systems
• Head trauma may increase the risk for future seizure disorders.

CLINICAL PRESENTATION

HISTORY, CHIEF COMPLAINT

• History of traumatic event
• Owners may report loss of consciousness, inappropriate behavior, or seizure activity.

PHYSICAL EXAM FINDINGS

• Signs of hypotensive shock (e.g., tachycardia, hypotension, pale mucous membranes) may be present.
• Neurologic exam (see p. 1311): indicators of intracranial injury:
○ Pupil asymmetry, abnormal pupil reactivity (excluding ocular trauma).

Dilated unresponsive pupils (in the absence of ocular trauma or atropine) indicate severe neurologic injury and a poor outcome.

○ Diminished or absent oculocephalic (doll’s eye) reflex
○ Postural reaction deficits (may be due to spinal injury [see p. 1039]; note remainder of neurologic findings).
○ Diminished or altered consciousness (may be due to shock; note remainder of physical exam).
• Skull fractures may be palpable.
• Respiratory, musculoskeletal, and other body systems may show signs of traumatic injury.

ETIOLOGY AND PATHOPHYSIOLOGY

• Cerebral blood flow (CBF) is mainly determined by blood pressure. Auto-regulation maintains blood flow to brain over a variety of pressures but is lost when systolic arterial blood pressure <50 mm Hg or during neuronal injury (at which time arterial blood pressure dominates control of blood flow to the brain).
• Cerebral perfusion pressure (CPP = mean arterial pressure [MAP] – intracranial pressure [ICP]) is used for estimating CBF. As ICP rises or MAP drops, cerebral perfusion decreases.
• Trauma can result in primary (at the time of incident, due to direct neuronal damage and hemorrhage) or secondary (hours or days after the incident, due to energy depletion, free radical generation, cytokine release) insults to the brain. Treatment aims to prevent or limit secondary effects.

DIAGNOSIS image

DIAGNOSTIC OVERVIEW

Diagnosis is based on a history of trauma with physical signs of intracranial injury. Complete neurologic evaluation is essential for establishing treatment plan and prognosis. Concurrent traumatic injuries affecting other body systems are common and should be ruled out as part of the diagnostic plan.

DIFFERENTIAL DIAGNOSIS

• Rule out other causes of intracranial disease (i.e., neoplasia, infectious, inflammatory, congenital), especially when trauma is suspected but was not witnessed.
• Animals in hypotensive shock may manifest altered consciousness without neurologic damage. Await full neurologic assessment until initial stabilization has been completed.
• Metabolic diseases (e.g., hypoglycemia, liver disease) may also affect neurologic exam and should be considered as differentials if no traumatic event is reported or if the history is uncertain.

INITIAL DATABASE

• Baseline tests (packed cell volume/total solids, blood glucose, blood urea nitrogen); initial assessment of some metabolic causes of altered mentation:
○ Consider transfusion if necessary (severe anemia/hemorrhage) to support adequate oxygen delivery to tissues.
○ Avoid causing hyperglycemia, which may be associated with poor outcome in head injury.
○ With azotemia or dehydration, diuretics (mannitol/furosemide) should be used with caution if at all; tissue perfusion (normotension) is most important.
• Blood pressure:
○ Identify and correct hypotension.
○ Systemic hypertension may be seen with elevated intracranial pressures or a consequence of pain or anxiety.
• Blood gas or pulse oximetry:
○ Identify hypoxemia (e.g., Pao2 <80 mm Hg when breathing room air) to provide supplemental oxygen.
○ Identify and correct hypercarbia (elevated PaCO2, e.g., >35 mm Hg).
• Heart rate/electrocardiogram
○ Sinus tachycardia common with shock or volume depletion; ventricular arrhythmias possible (see p. 1165)
○ Bradycardia may be seen with elevated ICP; in a comatose patient, it suggests brain herniation.

ADVANCED OR CONFIRMATORY TESTING

• Radiographs
○ May be useful in identifying skull fractures
○ Of limited value in the overall assessment of intracranial injury
• CT
○ Ideal imaging modality if available; requires general anesthesia, but some comatose/obtunded patients have been imaged without anesthesia.
○ Evaluate for skull fractures, hemorrhage, or other injuries
• ICP monitoring
○ Useful for directing therapies and limiting consequences of elevated intracranial pressures
○ May also be prognostic
○ Infrequently used in veterinary medicine
○ Requires skill and advanced care

TREATMENT image

TREATMENT OVERVIEW

Treatment is aimed at ensuring adequate cerebral perfusion. Important goals include maintaining adequate systemic blood pressure and systemic oxygenation (oxygen delivery to tissues).

ACUTE TREATMENT

• Maintain mean blood pressure above 60 mm Hg (generally signifies that systolic blood pressure >90 mm Hg): essential in management of head trauma, managed via titration of intravenous fluids. Options:
○ Crystalloids (e.g., 0.9% NaCl or lactated Ringer’s solution) at shock doses IV (60-90 mL/kg for dog, 45-60 mL/kg for cat), unless renal/cardiovascular/dilutional contraindication; exact dose is titrated to blood pressure.
▪ Concurrent use of colloids or hypertonic saline may limit cerebral edema that can occur with aggressive fluid administration.
▪ Avoid fluids with excessive free water (maintenance fluids, 5% dextrose in water, 0.45% saline).
○ Colloids, e.g., hetastarch, pentastarch (10-20 mL/kg/d IV). Oncotic effect draws free water from the interstitium into the vasculature. May potentiate effects of lower molecular weight substances (i.e., mannitol). Useful for intravascular support with limited fluid volumes.
○ Hypertonic saline (7.5%), 4 mL/kg IV slowly. Short-lived osmotic action draws fluid from cerebral interstitium; combination with crystalloids prolongs osmotic effect.
▪ May also limit other secondary effects of head injury. Only used if patient is adequately hydrated.
• Decrease intracranial pressure:
○ Mannitol (0.5-1 g/kg IV q 6-8 h; limit to three bolus injections/24-h period). Osmotic diuretic with free-radical scavenging properties. Increases intravascular osmolarity and draws fluid in from cerebral tissue. Decreases blood viscosity, increases cerebral blood flow. Potential adverse effects:
▪ Diuresis may decrease blood volume and consequently blood pressure (ensure adequate blood pressure and volume status before administration).
▪ May result in “reverse osmotic shift.” In areas of hemorrhage, mannitol may leak into interstitium, worsening cerebral edema. The effects of mannitol on lowering ICP may outweigh these potential effects on damaged areas.
○ Furosemide (2-5 mg/kg IV in coordination with mannitol). Decreases production of cerebrospinal fluid and causes diuresis; may potentiate effects of mannitol and decrease ICP. Caution: diuretic action may also worsen intravascular volume contraction and lead to hypovolemia.
• Maintain adequate oxygenation:
○ Supplemental oxygen as needed (see p. 1318)
○ Ensure adequate oxygen-carrying capacity (hematocrit/hemoglobin) and delivery (adequate blood pressure).
• Miscellaneous therapies:
○ Surgery:
▪ Craniotomy may be indicated for removal of hematomas, control of hemorrhage in the case of depressed skull fractures, or for removal of penetrating objects.
▪ Results in a substantial decrease in ICP (15% with craniotomy and an additional 65% reduction with durotomy) and is superior in relief of elevated ICP compared to any medical therapy.
▪ CT is useful for evaluation of injuries and determining need for surgical intervention.
○ Hyperventilation:
▪ Has been advocated in head injury, although its use is controversial
▪ Lowers CO2. Resultant vasoconstriction decreases cerebral perfusion pressure and decreases ICP. However, decreased perfusion to brain parenchyma may have deleterious consequences.
▪ Current recommendation: ventilate patient such that Paco2 = 30-35 mm Hg.
○ Barbiturates:
▪ Can use pentobarbital to effect (4-16 mg/kg IV titrated for induction, then 0.2-1 mg/kg/h to maintain sedation
□ Decreases cerebral metabolic rate and vasoconstricts, decreasing ICP
□ Studies evaluating efficacy controversial
□ May cause respiratory or cardiac depression, which is severely problematic in the head-injured patient
□ If used, intensive nursing care is essential to monitor respiration (intubation and mechanical ventilation may be necessary) as well as blood pressure and temperature.
□ Often discussed as “last resort”
□ May be beneficial for seizure control or in an extremely agitated animal
○ Hypothermia:
▪ Results in decreased cerebral metabolic rate, decreased cerebral perfusion via reflex vasoconstriction, and consequently decreases ICP
▪ May also limit secondary brain injury by limiting neuroexcitatory activities and suppression of local inflammatory response
▪ Can be associated with coagulation abnormalities, cardiac disturbances, and hypotension
▪ Moderate hypothermia (32-33°C) has been reported to be efficacious in human trials and animal models of brain injury. Clinical use in veterinary patients is uncertain
○ Glucocorticoids:
▪ Methylprednisolone sodium succinate (30 mg/kg slow IV over 10 minutes) after initial resuscitation may be best choice
▪ Use of corticosteroids in head injury is highly controversial and generally not recommended. Human studies have failed to show benefit.
▪ Potential benefits due to antiinflammatory and free radical scavenging effects
▪ May be associated with several complications (hyperglycemia, gastric ulceration, decreased wound healing, and infection)

NUTRITION/DIET

• Supplemental nutrition may be needed in severely compromised patients.
○ Enteral route preferred if possible/safe (see p. 1267)
○ Parenteral nutrition (see p. 1322) may be needed in patients at risk for aspiration pneumonia.

BEHAVIOR/EXERCISE

• Animals with severe neurologic deficits may be recumbent with limited mobility.
○ Range-of-motion exercises and physical rehabilitation (see p. 1329) may be beneficial for these patients.

POSSIBLE COMPLICATIONS

• Infection (aspiration pneumonia, nosocomial infection)
• Seizures
• Renal failure
• Persistent neurologic deficits

RECOMMENDED MONITORING

• Assess neurologic status:
○ Repeated examination may aid in the evaluation of efficacy of therapy.
○ Imaging (CT scan) may be helpful in assessing injury.
○ Therapy to decrease intracranial pressure if indicated
• Monitor oxygenation (arterial blood gas/pulse oximetry).
• Ensure adequate blood pressure.

PROGNOSIS AND OUTCOME image

• Prognosis is dependent on severity and type of injury:
○ Fair to good with minor, nonprogressive injury
○ Severely injured animals have poorer short-term recovery rates and may have longer rehabilitation/recovery periods if they survive.
• Modified Glasgow Coma Score (MGCS; see box) has been used for scoring injury severity in head trauma and has been correlated to outcome.

PEARLS & CONSIDERATIONS image

COMMENTS

• Head trauma is a common and serious injury in dogs and cats.
• Clinicians must recognize the signs of progressive neurologic injury.
○ The MGCS may be helpful as a monitoring tool.

Modified Glasgow Coma Score

Motor Activity
Normal gait, normal spinal reflexes 6
Hemiparesis, tetraparesis, or decerebrate activity 5
Recumbent, intermittent extensor rigidity 4
Recumbent, constant extensor rigidity 3
Recumbent, constant extensor rigidity with opisthotonos 2
Recumbent, hypotonia of muscles, depressed or absent spinal reflexes 1
Brainstem Reflexes
Normal pupillary light reflexes and oculocephalic reflexes 6
Slow pupillary light reflexes and normal to reduced oculocephalic reflexes 5
Bilateral unresponsive miosis with normal to reduced oculocephalic reflexes 4
Pinpoint pupils with reduced to absent oculocephalic reflexes 3
Unilateral unresponsive mydriasis with reduced to absent oculocephalic reflexes 2
Bilateral unresponsive mydriasis with reduced to absent oculocephalic reflexes 1
Level of Consciousness
Occasional periods of alertness, responsive to environment 6
Depression or delirium, capable of responding to environment but response may be inappropriate 5
Stupor, responsive to visual stimuli 4
Stupor, responsive to auditory stimuli 3
Stupor, responsive only to repeated noxious stimuli 2
Coma, unresponsive to repeated noxious stimuli 1
Total: _____
Assessment
Good prognosis 15-18
Guarded prognosis 9-14
Grave prognosis 3-8
  

TECHNICIAN TIPS

• Diligent monitoring and nursing care are important for an optimal outcome.
○ Even subtle changes in neurologic assessment can be important and should be brought up with the attending veterinarian.
○ Comprehensive nursing care is important to prevent complications such as nosocomial infection or aspiration pneumonia.

CLIENT EDUCATION

• Clients must be informed of the potential for long recovery periods with severely injured animals.
• Clients should also be made aware of the need for intensive treatment and monitoring of animals with head injury.
• The MGCS may be helpful in quantitating injury severity in order to provide the client with a prognosis.

SUGGESTED READING

Dewey CW. Brain trauma. In: Wingfield WE, Raffe MR, editors. The veterinary ICU book. Jackson Hole: Teton New Media; 2002:910-920.

Dewey CW. Emergency management of the head trauma patient. Principles and practice. Vet Clin North Am Small Anim Pract. 2000;30:207.

Platt SR, Radaelli ST, McDonnell JJ. The prognostic value of the Modified Glasgow Coma Scale in head trauma in dogs. J Vet Intern Med. 2001;15:581.

Heart Base Tumor

AUTHOR: HERBERT W. MAISENBACHER, III

EDITOR: ETIENNE. Côtĺ

1ST EDITION AUTHOR: ERIN. VICARI

BASIC INFORMATION image

DEFINITION

A general term describing a cardiac tumor of any type located at the base of the heart in association with the ascending aorta and/or pulmonary trunk, but without right atrial involvement

SYNONYMS

Chemoreceptor cell tumor: chemodectoma, aortic body tumor, nonchromaffin paraganglioma

EPIDEMIOLOGY

SPECIES, AGE, SEX

• Dogs: second most common cardiac tumor, mean age 10 years (range (5-15 years), males may be overrepresented in predisposed breeds.
• Cats: reported but rare

GENETICS & BREED PREDISPOSITION: Brachycephalic breeds (English bulldogs, boxers, Boston terriers) appear to be predisposed.

RISK FACTORS: Chronic hypoxemia may be a contributing factor.

ASSOCIATED CONDITIONS & DISORDERS: Pericardial effusion, right-sided congestive heart failure

CLINICAL PRESENTATION

DISEASE FORMS/SUBTYPES

• Most commonly causes clinical signs due to pericardial effusion and cardiac tamponade
• May be an incidental finding

HISTORY, CHIEF COMPLAINT

• Acute collapse
• Lethargy/exercise intolerance
• Abdominal distension
• Anorexia/inappetence
• Cough or tachypnea/dyspnea

PHYSICAL EXAM FINDINGS

• Findings associated with pericardial effusion (tachycardia, weak peripheral pulses, and muffled heart sounds)
• Findings consistent with right-sided congestive heart failure (ascites, hepatomegaly jugular distention/pulsation)
• ± Tachypnea/dyspnea

ETIOLOGY AND PATHOPHYSIOLOGY

• Chemodectoma:
○ Tumor of specialized neuroepithelial cells within the adventitia of the aortic arch; majority of heart base tumors in dogs
○ Typically benign and slow growing but may be very large at the time of diagnosis; occasionally locally invasive and rarely metastatic
• Ectopic thyroid carcinoma:
○ 5%-10% of heart base tumors in dogs; usually nonfunctional
○ Biological behavior not well characterized
• Mesothelioma may occasionally form a mass lesion at the heart base (dogs).
• Regardless of type, heart base tumors typically result in pericardial effusion, causing cardiac tamponade and right-sided congestive heart failure.
• Compression of cardiac structures and great vessels impeding inflow or outflow is possible with a large mass.

DIAGNOSIS image

DIAGNOSTIC OVERVIEW

The diagnosis is most often made with echocardiographic identification of a mass at the heart base. While a presumptive diagnosis of chemodectoma is often based on echocardiographic appearance, Definitive diagnosis of the tumor type requires histopathologic evaluation of tissue.

DIFFERENTIAL DIAGNOSIS

• Other intrapericardial tumors (hemangiosarcoma, mesothelioma, lymphoma, rare primary cardiac tumors, metastatic tumors)
• Other causes of pericardial effusion (see p. 854)

INITIAL DATABASE

• Echocardiography: diagnostic test of choice. Heart base tumors typically originate from the ascending aorta, most commonly the left cranial aspect, and lie between the aorta and the main pulmonary artery. They are usually homogeneous with smooth margins. Presence and severity of pericardial effusion is also assessed.
• Thoracic radiographs: enlarged or globoid cardiac silhouette in most but not all cases of pericardial effusion (80%). A soft-tissue mass effect at the heart base; may cause dorsal and lateral deviation of the trachea.
• Electrocardiogram: normal sinus rhythm or sinus tachycardia with low amplitude QRS complexes. Electrical alternans is suggestive but insensitive for pericardial effusion (50%).
• CBC, serum biochemistry profile, and urinalysis: often unremarkable

ADVANCED OR CONFIRMATORY TESTING

• Cytology and pH of the pericardial effusion: not generally useful. Heart base tumors typically do not exfoliate cells, reactive mesothelial cells mimic malignant cells, and there is much overlap in pH between causes.
• Histopathology of the tumor: allows a Definitive diagnosis of tumor type.

Requires surgical biopsy and often does not alter treatment plan.

TREATMENT image

TREATMENT OVERVIEW

Treatment is generally aimed at removal of pericardial fluid when cardiac tamponade occurs and eliminating recurrent effusion. When a heart base tumor is an incidental finding, initially no treatment may be necessary.

ACUTE GENERAL TREATMENT

• Pericardiocentesis (see p. 1325) is essential when cardiac tamponade is present but may not be necessary if only mild effusion is present and not causing hemodynamic effects.
• Diuretics are contraindicated in acute treatment of cardiac tamponade.

CHRONIC TREATMENT

• Repeated pericardiocentesis as needed for recurrent pericardial effusion
• Diuretics to delay effusion recurrence are controversial.
• Pericardiectomy alone is an effective palliative treatment for recurrent pericardial effusion. Less-invasive alternatives to surgical pericardiectomy include thoracoscopic pericardiectomy (see p. 1340) and percutaneous balloon pericardiotomy.
• Complete surgical resection is rarely possible owing to high vascularity of the tumor and close association with great vessels.

POSSIBLE COMPLICATIONS

• Pericardiocentesis related (see p. 1325)
• Surgical complications related to pericardiectomy. Surgical resection carries substantial risks.
• As most heart base tumors are benign, metastasis is rare but has been reported.

RECOMMENDED MONITORING

• Follow-up exams and echocardiography to assess for recurrent pericardial effusion and tumor progression

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Jul 24, 2016 | Posted by in SMALL ANIMAL | Comments Off on H

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