Clinical Signs

Note: The CLINICAL SIGNS section of the Handbook has been designed to facilitate rapid and accurate assessment of individual presenting problems as they are likely to be interpreted by the pet owner and presented to the clinician. Each CLINICAL SIGN is listed by the common name or phrase used by owners to describe the problem. When appropriate, a descripitive medical term for that CLINICAL SIGN follows.

Proper interpretation and assessment of individual CLINICAL SIGNS is fundamental to every patient evaluation and diagnosis. It is the cornerstone of effective therapy. Failing to recognize or interpret clinical signs in patients that are not able to communicate verbally is to fail the diagnostic effort. Interpretation of signs in veterinary medicine remains a critical clinical skill that demands persistent vigilance, experience and intuition. Absolutely no laboratory test, surgical procedure, nor sophisticated imaging technology can empower a clinician more.

ABDOMINAL ENLARGEMENT: WITH ASCITES

DEFINITION

Ascites: In this instance, refers to the abnormal accumulation of fluid in the peritoneal cavity sufficient to cause observable enlargement to the appearance of the abdomen. In this case, abdominal enlargement is observable to the owner. It should be noted, however, that ascites, especially in the early, formative stages, may NOT be associated with abdominal enlargement. Fluid accumulation can result from a variety of inflammatory, infectious, metabolic, degenerative, and neoplastic disorders. Ascites must be distinguished from abdominal enlargement NOT associated with fluid accumulation.

ASSOCIATED SIGNS

Clinical signs associated with abdominal enlargement are common. Once characterized, the associated signs can provide critical information relevant to the underlying diagnosis. The history may include increased water consumption and urination, diarrhea, vomiting, increased or decreased appetite, pain, apparent or real weight gain, and loss of muscle mass.

On physical examination, verify the abdominal enlargement to determine whether or not the enlargement is caused by fluid accumulation. Examine the patient for the presence of a heart murmur and palpable arrhythmia. If fluid is not present, determine the presence or absence of a mass within the abdominal cavity. When fluid is present, analyze the fluid character biochemically and cytologically.

DIFFERENTIAL DIAGNOSIS (Figure 3-1)

Figure 3-1.

Diagnostic workup of patients with ascites.

(From King L, Gelens H: Ascites. Compend Contin Educ 14:1063, 1992.)

© 2006

 

DIAGNOSTIC PLANS

• 1.Physical examination, to establish or rule out cardiopulmonary disease. Evaluate skin and hair coat for signs supporting endocrine disease. Assess abdominal enlargement by palpation and auscultation.
• 2.Abdominal radiograph and ultrasound, to confirm the presence of fluid, fat, or organomegaly.
• 3.If fluid is present, abdominocentesis, fluid analysis, and, if available, abdominal ultrasound. A laboratory database also is recommended.
• 4.If fluid is not present, contrast radiography of the bowel (barium series), dexamethasone suppression test, abdominal laparotomy, or, if available, abdominal ultrasound (see ABDOMINAL ENLARGEMENT).

ABDOMINAL ENLARGEMENT: WITHOUT ASCITES

DEFINITION

Abdominal enlargement (not associated with ascites): Refers to any condition in a dog or cat that causes a real or apparent enlargement of the abdominal cavity as observed during the physical examination. Real abdominal enlargement can be physiologic or normal (such as postprandial enlargement in a puppy or kitten or pregnancy) or abnormal (such as that associated with organomegaly).

ASSOCIATED SIGNS

Regardless of the underlying cause, abdominal enlargement is most likely to be associated with increased respiratory effort, usually characterized as tachypnea (increased respiratory rate). Dogs are more likely than cats to vocalize during expiration (grunt). Increased heart rate, lethargy, diminished appetite, and orthopnea (positional breathing) are variably observed.

DIFFERENTIAL DIAGNOSIS (Box 3-1)

BOX 3-1. DIFFERENTIAL DIAGNOSIS OF ABDOMINAL ENLARGEMENT.

Physiologic Enlargement

Postprandial

Pregnancy

Without Fluid Accumulation

Organomegaly

Neoplasia

Obstipation

Gastric dilation

Hyperadrenocorticism

Ruptured prepubic tendon

Bladder distention

Pneumoperitoneum

With Fluid Accumulation

High protein: >2.5 g/dL

• Hepatic failure

• Right-sided congestive heart failure

• Inflammatory-infectious (e.g., FIP)

• Chemical/drug peritonitis

• Trauma

• Neoplasia

• Hepatic vein thrombosis or vascular anomaly

• Chyloabdomen

Low protein: <2.5 g/dL

• Hypoproteinemia (renal, hepatic, or gastrointestinal cause)

• Portal hypertension subsequent to primary liver disease

• Neoplasia

FIP, Feline infectious peritonitis

 

DIAGNOSTIC PLANS

• 1.History. Attempt to establish whether or not a recent meal was consumed or (in the case of adult females) whether or not pregnancy is possible.
• 2.Abdominal palpation. NOTE: Preferably accomplished with the patient in RIGHT lateral recumbency. Examination is carried out using two hands simultaneously.
• 3.Abdominal ballottement. Manipulate the abdominal wall in an attempt to determine whether or not an accumulation of fluid exists within the abdomen.
• 4.Imaging. Abdominal radiograph or abdominal ultrasound.
• 5.Laboratory profile. Generally conducted to assess patient overall health status. Coagulation profile may be indicated.
• 6.Fine needle aspiration. May be conducted to remove fluid or aspirate solid organs/masses. Samples are prepared for cytopathology.
• 7.Exploratory surgery. Laparoscopy may be a suitable alternative but requires experience and special equipment.

AGGRESSION

DEFINITION

Aggression: A behavior (either normal or abnormal) in the dog or cat that could lead to the destruction or injury of an animal or person. Furthermore, aggression can be categorized as offensive or defensive. Specific knowledge of the pattern and type of aggression is critical if effective intervention is to be accomplished. To meet the criteria of this definition, it is assumed that organic causes of aggression (e.g., pain or intracranial mass) have been ruled out.

ASSOCIATED SIGNS

Although rare, aggression may be the result of organic disease, particularly disorders affecting the brain. In these patients, the onset of aggressive behavior is usually acute and may be associated with other neurologic signs suggesting cerebral dysfunction (e.g., seizures and circling). However, animals with pain may also manifest aggressive behavior, an apparent secondary response to discomfort. Animals with unilateral or bilateral blindness or deafness may bite or manifest aggressive behavior when approached and touched from the blind, or deaf, side. This behavior is probably the result of the animal's being startled and is far less likely to be representative of abnormal behavior.

DIFFERENTIAL DIAGNOSIS (BOX 3-2, BOX 3-3)

BOX 3-2. AGGRESSIVE BEHAVIOR IN THE DOG: DIFFERENTIAL DIAGNOSIS ACCORDING TO ORIGIN.

Pathophysiologically Based Aggressive Behavior

Rabies

Intracranial neoplasia

Cerebral hypoxia

Seizure activity

Neuroendocrine disturbances

Species-Typical Aggressive Behavior*

Dominance aggression

Possessive aggression

Protective aggression

Predatory aggression

Fear-induced aggression

Intermale and interfemale aggression

Pain-induced, punishment-induced, and irritable aggression

Maternal aggression

Redirected aggression

© 2006 Churchill Livingstone

From Young MS: Aggressive behavior. In Ford RB, (ed): Clinical Signs and Diagnosis in Small Animal Practice. New York, Churchill Livingstone, 1988, p 137.

BOX 3-3. AGGRESSIVE BEHAVIOR IN THE CAT: DIFFERENTIAL DIAGNOSIS ACCORDING TO ORIGIN.

Pathophysiologically Based Aggressive Behavior

Rabies

Intracranial neoplasia and lesions

Species-Typical Aggressive Behavior*

Intermale aggression

Predatory aggression

Play aggression

Territorial aggression

Fear-induced aggression

Pain-induced aggression

Maternal aggression

Redirected aggression

 

DIAGNOSTIC PLANS

• 1.Thorough laboratory profile and neurologic examination to assess the presence of pain or underlying organic disease (such as brain tumor).
• 2.The most effective plan for diagnosis and therapy may be for the clinician to make the owners aware of the clinical signs of aggression, alert them to the usual sequelae of early patterns, and direct them to a behavior specialist.
• 3.NOTE: Administration of a psychotropic drug as empiric therapy for aggression is not recommended before determining a possible cause and attempting to modify behavior through training.

ALOPECIA (SEE HAIR LOSS)

 

ATAXIA (SEE INCOORDINATION)

 

BLINDNESS (SEE VISION LOSS)

 

BLOOD IN URINE: HEMATURIA, HEMOGLOBINURIA, MYOGLOBINURIA

DEFINITION

Hematuria: Denotes the presence of blood in the urine; the presence of trace amounts of blood in the urine will not be obvious on gross appearance of a urine sample. Therefore, any noticeable change in the color of urine observed by the owner is likely to be interpreted as “blood in the urine.” Further evaluation of the patient is necessary to determine whether or not the discoloration is associated with small blood clots in recently voided urine, blood-tinged urine, or brown or red urine. The presence of blood in the urine, whether gross or occult, is most often indicative of upper or lower urinary tract bleeding, although systemic coagulopathies and reproductive tract disorders may also cause hematuria. The presence of hemoglobin in urine (hemoglobinuria) is not necessarily a reflection of urinary tract disease. Systemic disorders (e.g., those leading to intravascular hemolysis) can be associated with significant hemoglobinuria in the presence of a normal urinary system. Owners are likely to interpret this clinical sign to be “blood in the urine.” In true hemoglobinuria, without hematuria, microscopic examination will reveal the absence of red blood cells (RBCs).

Distinguishing hemoglobinuria from hematuria is an important diagnostic consideration. Conventional urine test strips (dipsticks) do not differentiate between the two; therefore, microscopic examination of urine sediment for the presence of significant numbers of RBCs is critical.

Myoglobinuria is characterized by brown to dark-red urine, the absence of RBCs in the urine sediment, and a positive test for occult blood. Bilirubinuria can also cause dark-brown to dark-orange urine but alone will not produce a positive test for occult blood. Myoglobinuria is a serious sign and denotes generalized muscle disease.

ASSOCIATED SIGNS

Hematuria associated with the urinary tract may not be associated with any other clinical signs. In patients with significant bleeding of renal origin, evidence of systemic illness may be present but is unlikely to localize the source of hematuria. Hematuria originating from the bladder is more likely to be associated with clinical signs, particularly pollakiuria and dysuria. Reproductive tract disorders (e.g., prostatitis and vaginitis) can also cause significant hematuria. Patients with hematuria or hemoglobinuria should be examined carefully for evidence of systemic bleeding, coagulopathies, and neoplasia.

DIFFERENTIAL DIAGNOSIS (Table 3-1 and Box 3-4)

TABLE 3-1.

Causes of Hematuria in Dogs and Cats Classified by Anatomical Site of Origin

Site	Dieseases
Kidney	Pyelonephritis
	Glomerulopathy
	Neoplasia
	Calculi
	Renal cysts
	Infarction
	Trauma
	Benign renal bleeding
	Hematuria of Welsh corgis
	Dioctophyma renale infection
	Microfilaria of Dirofilaria immitis
	Chronic passive congestion
Bladder, ureter, urethra	Infection
	Calculi
	Inflammation–LUTD
	Neoplasia
	Trauma
	Thrombocytopenia
	Capillaria plica infection
	Cyclophosphamide
Any site	Coagulopathy
	Heatstroke
	DIC
Extraurinary causes (genital tract or spurious hematuria)	Prostate
		Neoplasia
		Infection
		Hypertrophy
	Uterus
		Estrus
		Subinvolution
		Infection
		Neoplasia
	Vagina
		TVT
		Trauma
	Penis
		TVT
		Trauma

DIC, Disseminated intravascular coagulation; TVT, transmissible venereal tumor; LUTD, lower urinary tract disease.

BOX 3-4. DIFFERENTIAL DIAGNOSIS OF HEMOGLOBINURIA.

Intravascular Destruction of Red Blood Cells

Immune-mediated hemolytic anemia

Transfusion hemolysis

Sepsis

Red blood cell parasites (e.g., Babesia spp.)

• Chemical-induced

• Phenothiazine

• Acetaminophen

• Methylene blue

• Copper

Hypo-osmolality

Extravascular Destruction of Red Blood Cells

Red blood cell parasites

Immune-mediated hemolytic anemia

Pyruvate kinase deficiency (basenji and beagle)

Congenital porphyria (cats)

Hereditary stomatocytosis (malamute)

Microangiopathic disease (e.g., hepatic cirrhosis, hemangiosarcoma)

Lysis of Red Blood Cells in Urine

Hematuria combined with very dilute urine

Hematuria in stored urine

 

DIAGNOSTIC PLANS

• 1.Thorough history and physical examination, with emphasis on examination of the genitalia, palpation of the prostate, and caudal abdominal palpation.
• 2. If practical, assessment of urethral patency and the patient's ability to urinate. Attempt to pass a urethral catheter if significant dysuria and evidence of lower urinary tract obstructions are present.
• 3.Complete urinalysis. Using a fresh sample, include assessment of gross appearance, specific gravity, biochemical reagent strips (dipsticks), and microscopic examination of urine sediment. Ideally, two samples should be collected: a voided urine sample followed by a urine sample collected by cystocentesis.
• 4.Culture and sensitivity, if bacteria are present.
• 5.Routine laboratory profile, to include hematology and biochemistry panel.
• 6.Coagulation profile, if hemoglobinuria is present.
• 7.Abdominal radiographs, for evidence of calculi, prostatic enlargement, and soft tissue masses.
• 8.Contrast radiography of the upper and lower urinary tracts.
• 9.Ultrasound examination of the prostate, urinary bladder, and kidneys.
• 10.Exploratory laparotomy.

COMA: LOSS OF CONSCIOUSNESS

DEFINITION

Coma: A state of complete reversible or irreversible unconsciousness that can result from neurologic as well as non-neurologic disease. Coma can be a consequence of diffuse or multifocal lesions of the cerebrum or a lesion affecting the rostral brain stem and ascending reticular activating system. A variety of organic central nervous system (CNS) disease leading to metabolic or toxic encephalopathy can also produce coma.

ASSOCIATED SIGNS

Despite the fact that the comatose patient is unconscious, a complete neuro-ophthalmologic examination should be completed. Altered pupil size and pupillary light responses usually indicate brain stem disease. Emergency cardiac assessment of the unconscious patient justifies an electrocardiogram (ECG) and thoracic radiographs. Laboratory assessment of the comatose patient includes hepatic enzymes and, when feasible, hepatic function, electrolytes, and glucose level.

DIFFERENTIAL DIAGNOSIS (Table 3-2)

TABLE 3-2.

Differential Diagnosis of Coma

	Neurogenic	Non-neurogenic
Acute, nonprogressive	Intracranial hemorrhage Brain malformations	— —
Acute, progressive	Metastatic lesions Epidural, subdural hemorrhage Meningoencephalitis Cerebral edema	Hypoglycemia Diabetic coma Heat stroke Hepatic/uremic encephalopathy Infectious Hypoxia Thiamine deficiency (cat) Heavy metal and drug toxicity Carbon monoxide poisoning
Chronic, progressive	Hemorrhage (rare) Storage diseases Hydrocephalus Encephalitis	Heavy metal toxicity

 

DIAGNOSTIC PLANS

• 1. Critical: Assessment of vital signs to evaluate airway, breathing, and circulation (pulse, heartbeat, and ECG). Take thoracic radiographs if indicated. If cerebral edema is suspected, administer ventilation support, intravenous hyperosmotic agents (e.g., mannitol 20%, 1 to 2 g/kg of body weight q6h), and glucocorticoids.
• 2.Conduct careful neurologic examination directed toward evaluation of brain stem function, including motor function, pupillary light responses (or lack thereof), and eye movement.
• 3.Comprehensive laboratory profile, to include hematology, biochemical profile, and urinalysis.
• 4.
  Special diagnostic tests as appropriate:

  • a.
    Metabolic coma. Serum ammonia, bile acids, glucose, blood and urine lead levels.
  • b.
    Neurologic coma. Skull radiographs, cerebral spinal fluid analysis, electroencephalography.
  • c.
    Assessment of response to IV Mannitol.

CONSTIPATION (OBSTIPATION) (SEE ALSO STRAINING TO DEFECATE)

DEFINITION

Constipation: The infrequent or difficult passage of feces. Obstipation: Intractable constipation resulting in fecal impaction through the rectum and possibly the colon. In both dogs and cats, either state is most likely to be acquired.

The act of straining to defecate or painful defecation, the likely manifestation of constipation or obstipation, typically represents the reason for which a constipated dog or cat is presented (see STRAINING TO DEFECATE: DYSCHEZIA).

There is no strict definition of bowel regularity; therefore, there is no “normal” number of daily or weekly bowel movements, deviations from which constitute constipation. Practically, constipation can be considered to exist when a significant delay in frequency of passing formed stools has been noted or when the stool is observed to be of unusually hard or dry consistency. Constipation is categorized under one of the following headings: Neurogenic; Mechanical (physical); Muscular (smooth muscle); Iatrogenic (drug-induced).

The owner who perceives a pet as straining to defecate may, in fact, be observing a pet that is straining to urinate. This is particularly true among cats with disorders of the lower urinary tract, such as feline urologic syndrome (FUS). In the context of this discussion, dyschezia is discussed only insofar as it is associated with constipation and obstipation (see Figure 3-2 ).

Figure 3-2.

Clinical algorithm for constipation in the dog or cat. EMG, Electromyogram.

ASSOCIATED SIGNS

Assessment of the patient presented for constipation/obstipation can represent a significant medical challenge due to the complex and varied pathogenic mechanisms involved. Animals with neurogenic causes of constipation may have significant perianal or rectal pain associated with focal lesions. Other patients may present with nonpainful neurologic disease or long-term complications stemming from previous pelvic or spinal trauma.

Mechanical causes are either extraluminal or intraluminal. Abdominal and rectal palpation is indicated in both male and female dogs and cats. Narrow or blood-tinged feces may signal the presence of an intraluminal lesion, whereas in patients with extraluminal lesions, associated clinical signs may not be manifested.

Muscular causes are the least common and are generally the result of extreme metabolic aberrations. Idiopathic colonic atony is reported, but constipation may also result from severe catabolic states. Laboratory evidence of endocrine disease and electrolyte abnormalities should be assessed (see p. 630).

DIFFERENTIAL DIAGNOSIS (See Box 3-5 on p. 400)

BOX 3-5. DIFFERENTIAL DIAGNOSIS OF CONSTIPATION.

Neurogenic causes

Cortical (pain-induced)

• Perianal neoplasia

• Anal sac disease

• Perianal fistulas

• Myiasis

CNS disease

• Spinal trauma

• Spinal neoplasia

• Degenerative myelopathy

Peripheral nerve disease (e.g., complication following pelvic trauma)

Mechanical causes

Extraluminal

• Prostate (neoplasia or hyperplasia)

• Large intra-abdominal tumors

• Pregnancy (?)

• Pelvic fracture

Intraluminal

• Rectal stricture (e.g., adenocarcinoma)

• Colonic stricture

• Granulomas (e.g., histoplasmosis)

• Benign colorectal tumors

• Fecalith

• Rectal-colonic prolapse

• Intussusception

Muscular causes

Colonic atony

Severe malnutrition and cachexia

Hypothyroidism

Hypercalcemia

Hyperkalemia

Hyperparathyroidism

Segmental dilation subsequent to surgery

Drug-Induced Causes

Anesthetics

Anticholinergics (e.g., atropine)

Anticonvulsants

Barium sulfate

Diuretics

Prolonged laxative therapy

Monoamine oxidase inhibitors

Heavy metal toxicity (e.g., lead)

Behavioral

Soiled or odiferous litter

No litter available

 

DIAGNOSTIC PLANS (See Figure 3-2)

 

COUGH

DEFINITION

Cough: A sudden, forceful expiratory response to irritating stimuli (e.g., secretions) situated in the tracheobronchial tree. Cough is the most frequent clinical problem (followed by dyspnea and hemoptysis) that is referable to the lower respiratory tract. At presentation, cough should be characterized as “acute-onset” (duration of only a few days) or “chronic” (duration ≥ week). It should be noted that attempting to define cough as productive or nonproductive can be difficult in animals and, furthermore, seems to have little value in the overall diagnostic plan.

ASSOCIATED SIGNS

Although cough is a principal sign of lower respiratory tract disease, particularly lower airway (tracheal and bronchial) disease, it may also occur in animals with nonpulmonary disease, particularly cardiac and intrathoracic diseases. Associated signs, therefore, may include a wide spectrum of findings; there may also be no associated signs. Particular attention should be given to determining the character of the cough: it can be paroxysmal and severe, which usually indicates the need for immediate intervention, or mild but persistent. Animals in need of immediate attention are those with cough associated with syncope, dyspnea, or hemoptysis. Orthopnea, the inability to breathe without assuming a particular (usually upright) position, is a serious sign that suggests compromised respiratory function and also warrants immediate attention. Nasal discharge, tachypnea, and hyperpnea are less commonly associated with cough.

Cough can be misinterpreted as vomiting, particularly in dogs with tracheobronchitis. Coughing episodes in affected dogs typically terminate in the expectoration of tracheal secretions. The white, foamy phlegm expelled as the dog retches may appear to the untrained eye as vomitus.

DIFFERENTIAL DIAGNOSIS (Box 3-6)

BOX 3-6. DIFFERENTIAL DIAGNOSIS OF COUGH.

Primary Respiratory Tract Disease

Airway diseases

Tonsillitis and pharyngitis

Tonsillar neoplasm

Pharyngeal polyp (cat)

Laryngeal cyst

Laryngeal neoplasm

Laryngeal paralysis

Tracheobronchitis and tracheitis

Tracheal hypoplasia

Segmental tracheal stenosis

Tracheal collapse—acquired and congenital

Tracheal neoplasia

Tracheal osteochondral dysplasia

Foreign body

Bronchiectasis

Bronchial collapse

Immotile cilia syndrome

Aspiration

Respiratory parasites (e.g., Capillaria aerophila in cats; Filaroides osleri in dogs)

Pulmonary Vascular Disease

Pulmonary edema (multiple causes)

Pulmonary hypertension, esp. heartworm disease

Pulmonary Parenchymal Disease

Bacterial pneumonia

Systemic mycoses (e.g., histoplasmosis)

Pulmonary neoplasia

Pulmonary abscess

Protozoan pneumonia (e.g., feline toxoplasmosis)

Viral pneumonia

Allergic pneumonitis (e.g., feline asthma)

Metabolic and endocrine (e.g., hyperadrenocorticism)

Cardiovascular Diseases

Left heart disease

Left heart failure (cardiogenic pulmonary edema)

Intrathoracic Disease

Mediastinal abscess

Mediastinal neoplasia

 

DIAGNOSTIC PLANS

• 1.History and physical examination. Focus on known breed and age predispositions. Physical examination is particularly valuable in determining the extent of respiratory tract involvement and characterizing the type of cough present, particularly when the cough can be elicited by manipulation of the cervical trachea.
• 2.Careful thoracic auscultation, to determine the presence or absence of murmur or abnormal lung or airway sounds.
• 3.Thoracic radiographs, using lateral and ventrodorsal projections. These are critical, particularly when the patient has associated signs compatible with respiratory distress. Oxygen should be available to the dyspneic patient throughout the radiographic procedure. Patients with suspected tracheal collapse should be radiographed twice in the lateral position to assess changes in the intrathoracic tracheal and bronchial diameters between inspiration (open) and expiration (closed). In addition to obtaining a ventrodorsal (VD) projection, patients suspected of having thoracic neoplasia should have LEFT and RIGHT lateral thoracic radiographs assessed.
• 4.A laboratory profile, to include hematology, biochemistry panel, fecal flotation, urinalysis, heartworm test, and the feline leukemia virus/feline immunodeficiency virus (FeLV/FIV) test in the cat.
• 5.
  Special diagnostics:

  • a.
    Primary respiratory disease: transtracheal aspiration, bronchial lavage, bronchoscopy, contrast bronchography, fluoroscopy, and radionuclide assessment of mucociliary transport.
  • b.
    Primary pulmonary disease: fine-needle lung aspiration, arterial blood gases, fungal serology, nuclear studies (perfusion-ventilation), lung biopsy.
  • c.
    Primary cardiac disease: ECG, echocardiogram (M-mode and two-dimensional) and nonselective angiography.

COUGHING BLOOD: HEMOPTYSIS (SEE ALSO DIFFICULTY BREATHING)

DEFINITION

Hemoptysis is the expectoration, during cough, of blood. Seldom is the volume of blood loss sufficient to cause anemia; however, once confirmed, hemoptysis is a severe clinical finding indicative of bleeding into or from the lower airways. Hemoptysis can be attributed to direct injury of the pulmonary or, less commonly, the tracheobronchial blood vessels, pulmonary hypertension, or coagulopathy. Although an uncommon presenting sign, hemoptysis is more prevalent in dogs than in cats.

Since vomiting can be mistaken by the owner for coughing, it becomes essential to differentiate between hemoptysis and hematemesis during the initial examination. Hemoptysis is regarded as an emergency presentation.

ASSOCIATED SIGNS

The most common, and least significant, sign associated with hemoptysis is melena, or dark-red or black discoloration of stool that occurs subsequent to swallowing expectorated blood. More serious associated signs include coughing, hyperpnea, orthopnea, and cyanosis. Apparent episodic weakness and collapse may also be reported.

DIFFERENTIAL DIAGNOSIS (Box 3-7)

BOX 3-7. DIFFERENTIAL DIAGNOSIS OF HEMOPTYSIS.

Cardiovascular Hemoptysis

Thromboembolic disease

• Heartworm disease (in the dog and cat)

• Hyperadrenocorticism

• Cardiomyopathy

• Renal amyloidosis (in the dog)

• Idiopathic

Acute pulmonary edema

Arteriovenous fistula

Parasitic Hemoptysis

Lung flukes (e.g., Paragonimus spp.)

Lungworms (e.g., Aelurostrongylus spp.)

Inflammation-Induced Hemoptysis

Chronic bronchitis

Pneumonia

Mycotic lung infection

Lung abscess

Neoplasia

Either primary or metastatic

Miscellaneous

Coagulation disorder

Direct injury or trauma

Transtracheal aspirate

 

DIAGNOSTIC PLANS

• 1.Thorough history and physical examination. In addition, an attempt should be made to determine that the sign for which the patient was presented is, in fact, expectoration of blood during coughing and not bloody vomitus.
• 2.Routine laboratory profile, to assess the patient's overall health status. Emphasis should be placed on the fecal examination and heartworm tests. Multiple attempts to locate parasite ova in the stool should be made, since lung parasites may be few in number and ova shed intermittently.
• 3.Thoracic radiographs.
• 4.Coagulation profile, particularly in those animals with significant bleeding from other sites.
• 5.Transtracheal aspiration with cytologic studies or bacterial culture and sensitivity tests, or both.
• 6.Special procedures, including ultrasonography of the lung, particularly when discrete masses are seen on radiographs; echocardiography; blood gas analysis; bronchoscopy; bronchography; and angiography.
• 7.Radionuclide scans. Although availability is limited, studies may detect areas of pulmonary embolization.

DEAFNESS OR HEARING LOSS

DEFINITION

Deafness is the detectable lack or loss, complete or partial, of the sense of hearing. Deafness can result from abnormalities at any one of several levels from the ear to the brain. Peripheral deafness is categorized as either conduction deafness, involving abnormalities of the transduction apparatus (external ear canal, tympanic membrane, auditory ossicles in the middle ear), or nerve deafness, involving the hearing receptors in the cochlea or the auditory branch of the eighth cranial nerve. Congenital deafness is usually nerve deafness and is the result of abnormal development of the spiral organ or auditory receptors in the middle ear. Central hearing loss (intracranial cause) is uncommon, since auditory pathways in the brain are multisynaptic.

Loss of hearing, either partial or complete, in one or both ears does occur in both dogs and cats but is particularly difficult to confirm. Partial loss of hearing occurs most commonly in older animals but is rarely confirmed. Deafness is generally first detected by astute owners who observe diminished or absent responses to noise in an animal with no previous history of hearing difficulty.

ASSOCIATED SIGNS

Although rare, invasive lesions or panencephalitis could conceivably cause central hearing loss. However, the associated neurologic signs would be extensive, and hearing loss becomes a secondary or insignificant clinical issue.

Animals with peripheral hearing loss due to acquired unilateral lesions may manifest a variety of signs referable to the vestibular apparatus, particularly head tilt and, less often, circling. Pain or increased sensitivity may be associated with invasive lesions affecting hearing in either ear. Physical evidence of otitis externa is readily detected during routine examinations. Severe swelling associated with a chronic inflammation, a ruptured or damaged tympanic membrane, and infections of the middle ear may effectively decrease hearing acuity. Hypothyroidism may also be associated with degeneration of the cochlea and subsequent decrease in hearing acuity. The clinical history is important and should include any prior exposure to drugs known to be toxic to the cochlear nerve and organ of Corti (e.g., aminoglycosides).

Congenital (hereditary) deafness is associated with a white or merle hair coat in both dogs and cats. In dogs, the highest incidence is in the Dalmatian. However, several breeds are reported to be affected.

DIFFERENTIAL DIAGNOSIS (Box 3-8)

BOX 3-8. DIFFERENTIAL DIAGNOSIS OF DEAFNESS.

Acquired Hearing Loss

Degenerative causes

• Neurogenic deafness in the geriatric dog and cat

• Subsequent to chronic inflammatory disease (?)

Metabolic (endocrine) causes

• Hypothyroidism

• Neoplastic causes

• Invasive tumors of the pharynx and retropharyngeal tissue

Infectious-inflammatory causes

• Otitis externa and media

• Canine distemper virus infection

• Protothecosis (in the dog)

Toxic

• Aminoglycoside antimicrobials, especially gentamicin, streptomycin, and neomycin

Traumatic

Idiopathic

Congenital Hearing Loss—Breed Predisposition

White, blue-eyed cats (may be unilateral or bilateral)

Several breeds affected, particularly those with a white or merle hair coat

 

DIAGNOSTIC PLANS

• 1.Assessment of response to noise while the animal is relaxed or asleep.
• 2.Thorough physical examination, particularly of the external ear canal and tympanic membrane.
• 3.Neurologic examination.
• 4.Assessment of thyroid hormone levels.
• 5. Radiography of the head, with particular emphasis on the tympanic bullae, for evidence of otitis media.
• 6.Electrophysiologic studies, including electroencephalography, tympanometry, and brain stem auditory evoked potentials (BAER test).

DECREASED URINE PRODUCTION: OLIGURIA AND ANURIA

DEFINITION

Oliguria: Reduced amount of urine production and output in relation to fluid intake. Patients in which urine production ceases have anuria and are considered to be anuric. In contrast to polyuric states, neither oliguria nor anuria is likely to be the primary problem for which a dog or cat is presented to a veterinarian. The metabolic consequences of decreased urine production are severe and generally represent significant compromises in renal blood flow or in the functional status of a critical nephron mass. The daily urine volume at which oliguria begin is a function of solute load and renal concentrating ability. In general, oliguria exists when daily urine production is reduced by 75% or more. Production of 0.5 to 1.0 mL/kg/hr of urine indicates adequate renal perfusion in the dog. Anuria begins or terminates with oliguria; therefore, early detection and treatment of the underlying cause are critical to the overall prognosis.

ASSOCIATED SIGNS

The problem(s) for which an oliguric or anuric patient is presented will likely be related to the metabolic consequences of compromised renal function. Uremia, characterized by vomiting, hematemesis, diarrhea, lethargy, or anorexia, predominates. Any one or a combination of signs may present at the time of initial examination. Some patients may present in a comatose or semiconscious state, in which case it is essential that renal function and urinary output be established immediately.

Since acute renal failure (ARF) is the principal differential diagnosis in oliguria and anuria, once it has been established the clinician must obtain a thorough clinical history and laboratory profile, including urinalysis if possible, in an attempt to determine the cause of renal failure and to institute corrective therapy.

DIFFERENTIAL DIAGNOSIS (Box 3-9)

BOX 3-9. DIFFERENTIAL DIAGNOSIS OF ACUTE RENAL FAILURE.

Inflammatory-Infectious Causes

Leptospirosis

Pyelonephritis

Immune complex glomerulonephritis

• Systemic lupus erythematosus

• Heartworm disease

• Pyometra

• Endocarditis

• Feline leukemia virus infection

Viral

• Canine distemper virus infection

• Infectious canine hepatitis infection (rare)

• Canine herpesvirus infection (rare)

Primary Renal Causes (Nephroses)

Hypoperfusion (ischemia)

Extreme dehydration

Hemorrhage

Trauma

Sepsis

Surgery

Thromboembolic diseases

Nephrotoxins

Heavy metals (lead, arsenic, thallium, mercury)

Carbon tetrachloride

Ethylene glycol (antifreeze)

Aminoglycoside antibacterials (amikacin, gentamicin)

Antibiotics (cephaloridine, amphotericin B)

Hypercalcemia

Anesthetics (fluoride metabolites of methoxyflurane)

 

DIAGNOSTIC PLANS

• 1.Initiation of fluid therapy and placement of an indwelling urinary catheter, to establish the rate of urine production.
• 2.History, to address any possible exposure to toxins, particularly antifreeze, as well as recent drug treatment.
• 3.Radiographs of the abdomen. These may reveal enlarged kidneys, thereby supporting a diagnosis of ARF. Do not rule out the diagnosis of ARF if kidney size appears normal. Ultrasound imaging of kidneys is also helpful in establishing diagnosis.
• 4.Complete blood count (CBC). The biochemical profile should include electrolytes as well as blood urea nitrogen (BUN) and creatinine levels. Urinalysis (must include urine specific gravity) with microscopic examination of sediment for evidence of crystaluria, RBCs, white blood cells (WBCs), and casts is essential even if only a small volume of urine can be obtained.
• 5.Blood gases, to assess for metabolic acidosis, which may be severe in ARF.
• 6.Urine protein-creatinine ratio, to assess proteinuria.
• 7.If possible, determinations of serum osmolality and serum osmole gap.
• 8.Special diagnostics: intravenous pyelogram (IVP), renal biopsy, and determinations of lead and other heavy metals in the blood as indicated.

DIARRHEA, ACUTE-ONSET

DEFINITION

Acute diarrhea: A sudden change in bowel pattern, characterized as increased fluidity, frequency, or volume, that is sustained despite empiric or supportive therapy (see also Diarrhea, chronic). Fundamentally, diarrhea occurs when the amount of water and other intestinal contents reaching the colon exceed the ability of the colon to store the feces and adequately remove the excess water. The pathogenesis of acute diarrhea may be categorized:

Osmotic diarrhea: Development of an osmotic gradient in the bowel that favors movement of water into the gut lumen. Disorders of digestion and absorption readily generate such an intraluminal osmotic gradient. In simple osmotic diarrhea, clinical signs should resolve when the patient is fasted and the osmotic gradient equilibrates.

Abnormal gut permeability may be associated with infiltrative disease of the bowel (e.g., inflammatory bowel disease or neoplasia). Inflammatory lesions of the intestine alter mucosal permeability and promote exudation into the gut lumen.

Secretory diarrhea results from the effect of various substances (e.g., enterotoxins, gut hormones) that act as secretagogues. The gut is stimulated to secrete fluids without concurrent changes in permeability, absorptive capacity, motility, or osmotic gradients.

Abnormal bowel motility may occur in several primary disorders of the gastrointestinal (GI) tract, but it appears unlikely that abnormal motility is a primary cause of diarrhea. Normally, peristaltic contractions move chyme aborally, whereas segmental activity retards the movement of chyme, thereby performing the important functions of mixing intestinal contents and maximizing contact with the brush border enzyme systems. As segmental contractions are diminished, intestinal contents flow freely through the flaccid gut.

In the patient with acute diarrhea, it is conceivable that only one of these mechanisms is involved. However, the longer the underlying cause of the diarrhea persists, the more likely that homeostatic and compensatory mechanisms will be overwhelmed. The pathogenesis of the patient's diarrhea is then related to a combination of events.

ASSOCIATED SIGNS

Acute diarrhea is a common presenting sign for which multitudes of diagnostic possibilities exist. The list of associated signs can be, in the clinical setting, extensive. Among the most common signs encountered in an animal presented for acute diarrhea are vomiting, dehydration, slight weight loss, and hematochezia. Abdominal pain, halitosis, flatulence, and borborygmus are other gut-associated signs. However, not all patients with acute diarrhea have primary intestinal disease, such as those with renal or hepatic failure or hypoadrenocorticism. Therefore, icterus, oral ulcers, muscle weakness, and so on may also be encountered. Fever, anorexia, and lethargy may also accompany acute diarrhea in the dog and cat.

DIFFERENTIAL DIAGNOSIS (Box 3-10)

BOX 3-10. DIFFERENTIAL DIAGNOSIS FOR ACUTE-ONSET DIARRHEA.

Infectious Causes

Intestinal parasites: nematodes (e.g., ascarids, hookworms, whipworms, Strongyloides spp., Trichinella spp.); protozoa (e.g., coccidian, giardia, Cryptosporidium spp., Pentatrichomas).

Bacterial: E. coli. Salmonella spp., Pseudomonas spp., Clostridium spp., Campylobacter spp., Yersinia entercolitica, Staphylococcus spp., Helicobacter spp (?).

Viral: paramyxovirus (canine distemper), parvovirus (feline and canine), adenovirus-1, (coronavirus and reovirus-minor or insignificant).

Rickettsial: salmon poisoning.

Toxic Causes

Antimicrobials/antibiotics, parasiticides, antineoplastic agents, heavy metals, insecticides, organophosphate-containing compounds, anti-inflammatory drugs.

Dietary Causes

Dietary indiscretion, engorgement, food hypersensitivity, sudden change in diet.

Bowel Obstruction

Foreign body, intussusception, volvulus, neoplasia.

Extraintestinal Causes*

Renal failure, hepatic disease, hypoadrenocorticism (Addison's Disease), pancreatitis (acute and chronic).

Idiopathic Causes

 

DIAGNOSTIC PLANS

• 1.History and physical examination, including abdominal palpation. Establish possible exposure to infectious agents and associated signs.
• 2.Intravenous fluids containing NaCl may be a critical part of the early evaluation (signs associated with hypoadrenocorticism or Addison's disease may resolve within minutes to hours) in severely dehydrated patients presented for acute diarrhea.
• 3.Laboratory profile (to include routine hematology), biochemistry profile (to include amylase or lipase and sodium and potassium), urinalysis, examination of feces (direct and flotation). Perform several examinations before ruling out parasitic disease. Cats should be tested for both FeLV and FIV. Dogs should be tested for parvovirus antigen in stool.
• 4.Abdominal radiographs.
• 5.Special diagnostic tests as indicated: abdominal ultrasound; duodenoscopy and mucosal biopsy; stool culture for viruses or bacteria; serologic studies for rickettsial, viral, and fungal disease; and abdominal laparotomy.

DIARRHEA, CHRONIC

DEFINITION

Chronic diarrhea: Persistent or gradual change in bowel pattern—characterized by increased fluidity, frequency, or volume of stool—that is sustained for more than 1 to 2 weeks despite empiric or supportive therapy (see also Diarrhea, Acute-Onset). In the clinical setting, the clinical history and associated signs should be used to further characterize chronic diarrhea as large bowel or small bowel.

ASSOCIATED SIGNS

Clinical differentiation of small bowel and large bowel diarrhea is fundamentally important for the diagnosis and treatment of chronic diarrhea (Table 3-3 ).

TABLE 3-3.

Clinical Differentiation of Diarrhea of the Small Bowel and Large Bowel Types

Clinical signs	Small bowel	Large bowel
Fecal volume	Markedly increased daily output (large quantity of bulky or watery feces with each defecation)	Normal or slightly increased daily output (small quantities with each defecation)
Frequency of defecation	Normal or slightly increased	Very frequent: 4–10 times/day
Urgency of tenesmus	Rare	Common
Mucus in feces	Rare	Common
Blood in feces	Dark black (digested)	Red (fresh)
Steatorrhea (malassimilation)	May be present	Absent
Weight loss and emaciation	Usual	Rare
Flatulence	May be present	Absent
Vomiting	Occasional	Occasional

From Sherding RG: Chronic diarrhea. In Ford RB, editor: Clinical signs and diagnosis in small animal practice. New York, 1988, Churchill Livingstone, p 466.

© 2006 Churchill Livingstone

Less specific signs associated with chronic diarrheal diseases include dehydration, poor-quality hair coat, and fever. On abdominal palpation, discrete masses, thickened bowel loops, pain, or gas may occasionally be detected. Edema, ascites, and pleural effusion in patients with chronic diarrhea suggest substantial protein losses through the bowel. The patient with pallor should be assessed for intestinal bleeding, as well as for an anemia of chronic inflammatory disease.

Hematologic signs of most significance include eosinophilia (allergic or inflammatory) and lymphopenia (lymphangiectasia). Hypoproteinemia is associated with extreme malnutrition, protein-losing enteropathies, and enteric blood loss. Hyperglobulinemia is associated with basenji enteropathy.

DIFFERENTIAL DIAGNOSIS (Table 3-4)

TABLE 3-4.

Diagnosis of Specific Chronic Diarrheal Disorders

Diarrhea		Diagnostic test/procedure
Small Bowel Type
Exocrine, pancreatic insufficiency		Serum trypsin-like immunoreactivity (TLI)
Chronic inflammatory small bowel disease
	Eosinophilic enteritis	Eosinophilia, biopsy
	Lymphocytic-plasmacytic enteritis	Biopsy
		Serum protein electrophoresis
	Immunoproliferative enteropathy of basenjis	Radiography, biopsy
	Granulomatous enteritis
Lymphangiectasia		Lymphopenia, biopsy
Villous atrophy
	Gluten enteropathy	Response to gluten-free diet
	Idiopathic	Biopsy
Histoplasmosis		Serology, cytology, biopsy
Lymphosarcoma		Biopsy
Small intestinal bacterial overgrowth (SIBO)		Culture intestinal aspirate, folate, response to antibiotics
Giardiasis		Fecal examinations, response to parasiticides
Lactase deficiency		Response to lactose-free diet
Large Bowel Type
Chronic colitis		Colonoscopy, colon biopsy
	Idiopathic
	Histiocytic
	Eosinophilic
Abrasive colitis		Dietary history, inspection of feces
Whipworm colitis		Fecal flotation, colonoscopy, response to fenbendazole
Protozoan colitis		Saline fecal smears
	Amebiasis
	Balantidiasis
	Trichomoniasis
Histoplasma colitis		Fecal cytology, colon biopsy, serology, culture
Salmonella colitis		Culture
Campylobacter colitis		Culture
Protothecal colitis		Colon biopsy
Rectocolonic polyps		Digital palpation, barium enema
Colonic adenocarcinoma		Colonoscopy, barium enema, possibly abdominal ultrasound
Colonic lymphosarcoma		Barium enema, colonoscopy
Functional diarrhea (irritable colon)		History, diagnostic workup excludes all other diseases

 

DIAGNOSTIC PLANS

• 1.Clinical history and physical examination findings, to classify the diarrhea as small bowel or large bowel. Routine patient screening should include hematologic studies, biochemical profile, fecal flotation and direct examination, and urinalysis.
• 2. Diagnosis of intestinal parasites. Perform a visual examination of the feces and anus for proglottids, a zinc sulfate flotation test for Giardia and Coccidia cysts, a saline suspension for protozoan trophozoites, and a sedimentation or Baermann determination for Strongyloides larvae. Adult whipworms can be seen in the colon on colonoscopy.
• 3.Additional fecal studies. Beyond routine fecal flotation and direct examination, several other fecal tests are indicated, including microscopic examinations for fat (Sudan preparation), starch (iodine preparation), and cytologic staining (Gram stain and Wright's stain) to assess for presence of leukocytes and infectious agents. Malassimilation can be assessed through quantitative fecal fat analysis and fecal weight (daily output), although in clinical practice these tests are seldom performed. Several special biochemical and physical tests can also be carried out on feces: fecal water content, nitrogen content (for azotorrhea and malassimilation), electrolytes, pH, osmolality, fecal occult blood, and cultures for both fungi and bacteria.
• 4.Tests of absorptive and digestive function, such as trypsin-like immunoreactivity (TLI), serum folate, and vitamin B₁₂ assay.
• 5.GI radiography and ultrasonography.
• 6.GI endoscopy (gastroscopy, duodenoscopy, and colonoscopy), with biopsy of intestinal mucosa. Duodenal intubation and aspiration can be performed to obtain specimens for cytologic examination and culture.
• 7.Exploratory laparotomy and intestinal biopsy.
• 8.Response to empiric treatment: Enzyme replacement or treatment of occult parasite infections.

DIFFICULTY BREATHING OR RESPIRATORY DISTRESS: CYANOSIS (SEE ALSO DYSPNEA)

DEFINITION

Cyanosis: Bluish discoloration of the skin and mucous membranes resulting from excessive concentration (>5 g/dL) of reduced hemoglobin in the blood. In dogs and cats, cyanosis may develop acutely in hypoxic states or may be chronic. Although cyanosis can develop during hypoxia, the terms are not synonymous.

NOTE: The increased concentration of reduced hemoglobin in blood is the result of either an increase in the quantity of venous blood in the cutaneous tissues (passive venous congestion) or a decrease in oxygen saturation in capillary blood. It is the absolute, rather than the relative, amount of reduced hemoglobin that actually causes the cyanosis to develop. If the concentration of hemoglobin is also reduced, the absolute concentration of reduced hemoglobin is also decreased. Therefore, even in severe anemia, cyanosis is not evident. On the other hand, patients with an elevated red blood cell (RBC) mass, or polycythemia, tend to be cyanotic at higher levels of arterial oxygen saturation than patients with a normal RBC mass. Cyanosis also occurs when functional abnormalities of hemoglobin (e.g., methemoglobinemia [dark-brown blood]) exist. In the dog and cat, disorders affecting the oxygen-carrying capacity of hemoglobin are usually drug- or chemical-induced. As little as 1.5 g/dL of methemoglobin or 0.5 g/dL of sulfhemoglobin will produce cyanosis.

ASSOCIATED SIGNS

Cyanosis can result from disorders affecting the cardiovascular system, ventilation, or oxygen-carrying capacity of RBCs. Several cardiovascular diseases, particularly those that compromise cardiac output or are associated with right-to-left vascular shunts, predispose to cyanosis. Therefore, animals with both acquired and congenital cardiac disease are susceptible. Associated signs include cough, respiratory distress, and syncope. The most common congenital heart defects associated with right-to-left shunts are (1) pulmonary valve stenosis as seen in tetralogy of Fallot, stenosis, and ventricular septal defect (VSD) and (2) pulmonary hypertension as seen in patent ductus arteriosus (PDA) and VSD.

Respiratory disorders affecting ventilation predispose to cyanosis. Severe infiltrative lung disease (e.g., neoplasia, pulmonary edema, or generalized pneumonia) can produce cyanosis associated with increased respiratory effort.

Animals that do present with cyanosis not associated with clinical signs other than increased respiratory rate may have abnormal hemoglobin levels, which, if present in sufficient concentration, will cause cyanosis. Associated signs include methemoglobinuria and methemoglobinemia.

Central cyanosis is defined as compromised oxygen saturation or abnormal hemoglobin; peripheral cyanosis is compromised blood flow.

DIFFERENTIAL DIAGNOSIS (Box 3-11)

BOX 3-11. DIFFERENTIAL DIAGNOSIS FOR CYANOSIS.

Cardiovascular Causes

Right-to-left shunting congential heart defect (e.g., R-to-L shunting patent ductus arteriosis)

Pulmonary embolism

Decreased cardiac output

Arterial obstruction

Pulmonary Causes

Airway collapse/obstruction (multiple causes)

Hypoxia

Pulmonary edema

Oxygen diffusion-alveolar ventilation abnormalities

Pulmonary arterial-venous shunts/fistulae

Restrictive lung disease (e.g., hydrothorax, diaphragmatic hernia)

Toxic/Drug Causes

Paraquat poisoning

Acetaminophen (cats)

 

DIAGNOSTIC PLANS

• 1.Provide 100% oxygen, particularly in patients with respiratory distress. Reassess color of the mucous membranes at 2- or 3-minute intervals. Auscultate the heart and lungs.
• 2.Thoracic radiographs. Oxygen should be available at all times.
• 3.Hematology, with particular emphasis on RBC morphology (Heinz bodies in the cat and hematocrit values), biochemical profile, and urinalysis.
• 4.Special diagnostics: arterial blood gases (with and without 100% oxygen), ECG, echocardiogram, and nonselective angiogram.

DIFFICULTY BREATHING OR RESPIRATORY DISTRESS: DYSPNEA

DEFINITION

True dyspnea: Pathologic breathlessness ascribed to the unpleasant, distressful sensation of labored breathing most commonly associated with cardiac or pulmonary disease. What actually is and is not true breathlessness in veterinary medicine is difficult to define in clinical practice. Serious respiratory distress associated with substantive respiratory compromise may appear, to the owner at least, as only a minor problem. Physical examination and patient assessment are critical to the recognition and interpretation of this clinical sign.

Respiratory distress may result from (1) the need for oxygen, (2) metabolic aberrations leading to acidosis (a compensatory mechanism), (3) high environmental temperatures (heat stroke), (4) CNS disease, (5) disorders affecting motor innervation to the muscles of respiration, and (6) pain. In any event, once confirmed, diagnostic evaluation of the patient presented in respiratory distress should not be delayed.

ASSOCIATED SIGNS

The most common respiratory signs that characterize distress or dyspnea include (1) tachypnea (increased respiratory rate), (2) hyperpnea (increased respiratory rate and depth), (3) orthopnea, and (4) cough. In obstructive upper airway diseases, stridor and stertorous breathing may be present on the initial examination.

Fluid accumulation in the thoracic cavity may be accompanied by ascites and hepatomegaly. Physical evidence of hyperadrenocorticism supports thrombolic pulmonary disease. Cyanosis, pallor, evidence of physical trauma, shock, and coma are serious signs often associated with respiratory distress.

DIFFERENTIAL DIAGNOSIS (see Table 3-5 on p. 412)

TABLE 3-5.

Differential Diagnoses of Dogs and Cats Presented for Dyspnea

Upper Airway		Lower Airway		Restrictive		Miscellaneous
Stenotic nares		Bronchial diseases		Pneumothorax		Anemia
Rhinitis/sinusitis			COPD	Pleural effusion		Methemoglobinemia
Laryngeal diseases			Allergic bronchitis (asthma, PIE)		Right heart failure	Compensation for metabolic acidosis
Nasopharygeal tumor or foreign body			Lungworms		Neoplasia
	Necrotic laryngitis	Pneumonia			Hypoalbuminemia	Heatstroke
	Edema	Pulmonary edema			Hemothorax	Damage to respiratory center
	Paralysis of vocal folds		Left heart failure		Chylothorax		Head trauma
	Everted saccules		Hypoalbuminemia		Pyothorax		Encephalitis
	Laryngeal collapse		Others		Feline infectious peritonitis		Neoplasia
	Neoplasia	Pulmonary thromboembolism		Pericardial effusion		Neuromuscular weakness
Intraluminal tracheal or bronchial foreign body or mass			Heartworm disease	Diaphragmatic hernia			Polyradiculoneuritis (coonhound paralysis)
			Hyperadrenocorticism	Intrathoracic neoplastic mass		Diaphragmatic paralysis
Extraluminal tracheal or bronchial obstruction			Others	Thoracic wall trauma			Others
		Pulmonary contusions (trauma)			Flail chest	Pain
	Mediastinal mass Tracheal or bronchial collapse Hilar lymphadenopathy	Pulmonary fibrosis		Extreme obesity			Fractured ribs or vertebrae
		Pulmonary granulomatosis		Severe hepatomegaly			Pleuritis
		Deep mycosis		Marked ascites			Others
				Large intra-abdominal mass		Paraquat poisoning
				Severe gastric distention (gastric volvulus)

COPD, Chronic obstructive pulmonary disease; PIE, pulmonary infiltrates with eosinophils

 

DIAGNOSTIC PLANS

• 1.Physical examination. This is justified even before a comprehensive history is completed. Patient stabilization, as required, must be accomplished.
• 2.History. Historical information relevant to duration, progression, and exposure to noxious substances or trauma is indicated. Knowledge of all current medications, including heartworm preventative, is established.
• 3.Laboratory profile, to include a CBC, biochemistry panel, urinalysis, heartworm test (in dogs), and FeLV and FIV tests (in cats). Cytologic, bacteriologic, and biochemical assessments of body cavity effusions are indicated.
• 4.Thoracic and cervical radiographs. Presence of a heart murmur, cardiac arrhythmia, or both, should be further evaluated by electrocardiography and echocardiography.
• 5.Examination of the upper respiratory tract in the anesthetized patient and endoscopy when signs of tracheal and bronchial disease exist.

DIFFICULTY SWALLOWING: DYSPHAGIA

DEFINITION

Dysphagia is painful or difficult swallowing. Clinically, dysphagic animals characteristically are presented for making frequent and forced attempts to swallow with or without regurgitation. Signs are most apparent immediately following prehension of food or water.

Swallowing is a complex reflex requiring coordination of multiple muscular and neurologic reactions involving the tongue, palate, pharynx, larynx, esophagus, and gastroesophageal junction. The swallowing reflex is coordinated by cranial nerves V, VII, IX, X, and XI; therefore, neurologic lesions affecting nuclei in the brain stem and reticular formation can alter normal swallowing. Dysphagia may occur as a result of disorders affecting any one of the three swallowing phases: oropharyngeal, esophageal, and gastroesophageal.

Both morphologic as well as functional lesions affecting the oropharynx, esophagus, stomach, and brain or brain stem may result in dysphagia.

Functional or motility disorders that affect swallowing include spasticity, incoordination, or failure of muscular contractions, and they result from neurologic disorders, disorders of neuromuscular transmission, or primary muscle disease. Such disorders may be either congenital or acquired. Disorders affecting the oropharyngeal phase of swallowing are responsible for causing pronounced dysphagia, whereas disorders affecting the esophageal and gastroesophageal phases of swallowing are associated with regurgitation.

ASSOCIATED SIGNS

Dysphagia is observed in young animals, particularly in association with congenital esophageal motility disorders and as an acquired condition in older animals. This is more common as a presenting sign in dogs than in cats. There is no sex predisposition.

Prehension of food in animals presented for dysphagia is characteristically normal. Hypersalivation may occasionally be reported, particularly in animals with nasal discharge associated with regurgitation.

Regurgitation is an inconsistent sign associated with dysphagia that does not necessarily correlate with the severity of the underlying disorder. Generally, regurgitation is a consequence of abnormalities of the esophageal and gastroesophageal phases of swallowing. Although most dysphagic patients have a normal to increased appetite (polyphagia), anorexia, weight loss, and coughing may be associated with severe or chronic obstructive esophageal disease or esophageal ulceration.

CAUTION: Assessment of affected patients for evidence of neurologic signs is of paramount importance, since dysphagia is a principal neurologic complication associated with rabies virus infection.

DIFFERENTIAL DIAGNOSIS (Box 3-12)

BOX 3-12. DIFFERENTIAL DIAGNOSIS OF DYSPHAGIA.

Cardiovascular

Megaesophagus secondary to congenital persistent fourth aortic arch

Lymphatic and immune

Mandibular, retropharyngeal, and less commonly bronchial lymphadenopathy associated with lymphosarcoma, thymic neoplasia in FeLV-positive cats, and systemic mycoses (histoplasmosis or blastomycosis)

Epidermolysis bullosa-induced esophagitis (rare)

Gastrointestinal

Esophageal obstruction due to foreign body, parasitic granuloma (Spirocerca lupi), stricture, esophageal neoplasia

Cricopharyngeal achalasia (young dogs)

Megaesophagus secondary to pyloric obstruction in cats

Esophageal diverticula

Traumatic esophageal rupture

Reflux esophagitis

Doxycycline-induced esophagitis

Feline herpesvirus-induced esophagitis (rare)

Neurologic

Congenital and acquired megaesophagus

Myasthenia gravis in dogs

Rabies virus infection

FeLV, feline leukemia virus.

 

DIAGNOSTIC PLANS

• 1.Observation of the patient's attempt to swallow food and water.
• 2.Hematologic studies, a biochemistry profile, and urinalysis. Findings are usually of little diagnostic value but are important in assessing overall patient status. A fecal flotation test for parasite ova can be diagnostic for Spirocerca lupi.
• 3.Special laboratory tests, including antinuclear antibody (ANA) titer and lupus erythematosus (LE) cell results, to assess for the presence of immune-mediated disease. Serum thyroxine (T₄) and thyroid-stimulating hormone (TSH) tests are indicated to rule out peripheral neuropathy due to primary hypothyroidism.
• 4.Noncontrast thoracic and cervical radiographs.
• 5.Positive contrast esophogram, both thoracic and cervical.
• 6.Esophagoscopy, which may be therapeutic if esophageal foreign body can be retrieved. Esophageal endoscopy is not a reliable means for diagnosing megaesophagus.
• 7.Fluoroscopic evaluation of esophageal motility.
• 8.Visual examination of the oropharynx in the anesthetized patient. (Findings are of low diagnostic value.)

HAIR LOSS: ALOPECIA

DEFINITION

Hair loss, also called alopecia: Loss or absence of hair in any amounts and any distribution that is the result of one or a combination of disorders affecting the integrity of the hair coat. Therefore, physiologic loss of hair (e.g., normal shedding or hereditary hair loss such as in the Rex cat breed) is excluded from this definition. In clinical practice, hair loss, with and without pruritus, is among the most common reasons a cat, and particularly a dog, is presented. In most cases, the loss of hair is secondary to some underlying disorder rather than being a primary event. The distribution of hair loss is important in that it can be characteristic of the underlying etiology.

Alopecia can be classified on the basis of distribution as (1) diffuse, (2) regional, (3) multifocal, and (4) focal. The causes for hair loss are varied and often complex. Abnormalities of follicular structure may be inherited, ranging from complete absence of hair follicles to selective absence of follicles that produce hair of a specific color. Inflammatory skin diseases that incorporate the hair follicle may disrupt hair growth and maintenance. Bacterial folliculitis, demodectic mange, and follicular hyperkeratosis are examples.

Disorders disrupting the normal follicular cycles can interrupt hair growth without loss or injury to the hair follicle. The cycle is as follows: Anagen (growth phase), Catagen (transitional phase), Telogen (resting phase).

ASSOCIATED SIGNS

The complex pathogenesis of alopecia supports a multitude of associated clinical signs in any animal presented for hair loss. Pruritus is an important associated sign if present. Allergic, inflammatory, and parasitic skin diseases are likely to cause pruritus. Secondary traumatic excoriation of the skin may further provoke cutaneous injury, thereby intensifying the pruritus. Alopecia caused by endocrine, genetic, and metabolic factors is less likely to be associated with pruritus, although pruritus may become a factor if the exposed skin becomes particularly dry or sunburned. Immune-mediated diseases leading to alopecia are variably pruritic, depending on the distribution and type of skin injury. Nutritional alopecia is rarely confirmed but can be a source of dermatitis and associated pruritus.

Alopecia without pruritus may be associated with dramatic physical signs resulting from endocrine or metabolic disorders. Dermatologic signs include thickened skin, hyperpigmentation, and dry and brittle hair coat (hypothyroidism). On the other hand, skin may appear thin and lack elasticity (canine Cushing's syndrome, Sertoli cell tumor). Gynecomastia, skin softness, calcinosis cutis, and pigmented macules are other dermatologic signs associated with alopecia.

DIFFERENTIAL DIAGNOSIS

Virtually all dogs and cats with primary skin disease manifest some degree of alopecia. The pattern of hair loss is typically asymmetric, and primary skin disease can appear to be symmetric (e.g., parasitic dermatoses). In pursuing the diagnosis in dogs or cats presented for hair loss, thorough systemic and skin examinations are indicated. The clinician may find it helpful to characterize a patient's hair loss according to various etiologic categories:

Primary cutaneous causes of hair loss include the following:

• •Infectious
• •Bacterial
• •Ectoparasitic
• •Dermatophytoses
• •Dermatomycoses
• •Neoplastic
• •Keratinization

Secondary causes of hair loss include the following:

• •Genetic (Box 3-13 )
• •Nutritional
• •Endocrine (e.g., hypothyroidism, hypoadrenocorticism)
• •Keratinization
• •Atopic (allergenic)/contact hypersensitivity
• •Drug therapy (especially corticosteroids and chemotherapeutic agents)
• •Environmental factors
• •Neoplasia
• •Psychogenic

BOX 3-13. DIFFERENTIAL DIAGNOSIS OF GENETIC DISORDERS CAUSING ALOPECIA.

• •Hairless breeds (e.g., African Sand Dog, Abyssinian Dog, Chinese Crested, xoloitzcuintli, Turkish Naked Dog; Sphinx Cat, Rex Cat [seasonal alopecial])
• •Ectodermal and follicular dysplasias (e.g., Miniature Poodles)
• •Hypotrichosis
• •Black hair follicular dysplasia
• •Color-mutant alopecia
• •Pattern baldness
• •Feline alopecia universalis
• •Demodicosis

DIAGNOSTIC PLANS

• 1.History and physical examination, to determine the nature and extent of primary and secondary skin lesions. Distribution, pattern of alopecia, and associated cutaneous lesions should be characterized. Use the physical examination to determine whether or not evidence of systemic disease is present. Time of onset or the seasonal nature of alopecia may be significant, particularly when accompanied by pruritus.
• 2.Examination (macroscopic and microscopic) of affected and nonaffected hair.
• 3.Skin scraping (multiple), fungal cultures, and bacterial cultures (particularly of pustules).
  • a.
    Fine-needle aspiration of discrete intracutaneous masses.
  • b.
    Skin biopsy, to include normal and affected skin.
• 4.Laboratory database, to include hematology, biochemical profile, urinalysis, and fecal flotation. In addition, cats should be tested for FeLV and FIV.
• 5.
  Special diagnostics:

  • a.
    Allergic skin disease: Intradermal antigen inoculation, radioallergosorbent test (RAST) (IgE).
  • b.
    Endocrine alopecia: T₄ before and after TSH stimulation, adrenocorticotropic hormone (ACTH) stimulation, dexamethasone suppression, serum testosterone.
• 6.Implementation of an elimination diet trial (minimum 6 weeks duration).
• 7.Environmental allergen or irritant.

HEMORRHAGE (SEE SPONTANEOUS BLEEDING)

 

ICTERUS (SEE YELLOW SKIN)

 

INCOORDINATION: ATAXIA

DEFINITION

Ataxia: The loss of coordination without spasticity, paresis, or involuntary movement. In practice, however, it is possible for ataxia to be accompanied by additional neurologic signs. Ataxia is the result of disorders of the conscious or unconscious proprioceptive system, disorders of the cerebellum, or disorders of the vestibular system.

ASSOCIATED SIGNS

In the spectrum of disorders causing ataxia, lesions of the vestibular system predominate. However, vestibular signs may result from other brain disorders and spinal cord syndromes. Associated signs include head tilt, nystagmus, circling, and hemiparesis. Patients with cerebellar lesions typically have symmetric signs: hypermetria, abnormally long range of movement (goose-stepping gait); hypometria, abnormally short range of movement; or tremor, particularly of the head.

DIFFERENTIAL DIAGNOSIS (Box 3-14)

BOX 3-14. DIFFERENTIAL DIAGNOSIS OF ATAXIA.

Congenital (Signs Present Before 3 Months of Age)

Reported in Siamese and Burmese cats and several dog breeds. Multiple congenital disorders are present with multiple neurologic signs, including ataxia. Bilateral congenital vestibular disorders have been observed in Doberman Pinschers, Beagles, and Akitas.

Inflammatory

Otitis interna, as an extension of otitis externa and media

Neuritis of the eighth cranial nerve

Infections

Toxic

Drug-induced aminoglycoside therapy

Nutritional

Thiamine deficiency (cat only–rare)

Metabolic

CNS signs secondary to other diseases (e.g., hepatic, renal)

Traumatic-Vascular

Head trauma with concussive injury to the cerebellum and brain stem

Neoplastic

Any tumor

Degenerative

Storage diseases

Demyelinating diseases

Neuropathies

Cerebellar abiotrophy

Idiopathic (Particularly Common Cause of Vestibular Signs)

Feline vestibular syndrome

Geriatric canine vestibular syndrome

Acute labyrinthitis

 

DIAGNOSTIC PLANS

• 1.Physical examination, with particular attention to the external ear and tympanic membrane.
• 2.Neurologic examination, to include assessment of the cranial nerves with the intent of localizing the lesion.
• 3. Laboratory profile, to assess metabolic or infectious causes.
• 4.Skull radiographs, to include the tympanic bullae.
• 5.Collection and examination of cerebrospinal fluid (CSF).
• 6.Special diagnostics, depending on availability (e.g., electroencephalogram [EEG], computed tomography [CT], or magnetic resonance imaging).

INCREASED URINATION AND WATER CONSUMPTION: POLYURIA AND POLYDIPSIA

DEFINITION

In practice, polyuria (PU) and polydipsia (PD) are loosely interpreted to mean an increase in urination and water consumption, respectively. The fact that polyuria is an abnormal increase in urine production, usually of low specific gravity, is seldom confirmed in practice. Likewise, although polydipsia is an abnormal or absolute increase in water consumption usually associated with increased thirst, water intake is seldom quantitated. Use of the terms polyuria and polydipsia is usually justified when a client presents a dog or cat for subjective increases in urination frequency and water intake as the primary problem. When clear evidence of increased urination and increased thirst is not present, actual documentation of 24-hour urinary output and water intake may be necessary.

Polydipsia is a compensatory sign that develops subsequent to polyuria. Primary polydipsia with compensatory polyuria is uncommon.

The pathophysiology behind polyuria is complex in that several renal and nonrenal mechanisms can be involved. Diseases affecting proximal tubules (e.g., primary renal failure, renal glycosuria) or those causing high solute loads overwhelming proximal tubule absorptive capacity (e.g., diabetes mellitus) cause osmotic diuresis. Water conservation is also affected at the level of the loop of Henle (e.g., primary renal disease, diuretics) and in the distal tubules and collecting ducts. Disorders of the distal tubule and collecting duct are frequently responsible for polyuria, including diabetes insipidus, pyometra, hyperadrenocorticism, liver failure, and hypercalcemia.

Polyuria does result in subsequent failure of the sodium chloride pump in the loop of Henle, leading to significant decreases in the renal medullary osmotic gradient. Liver failure resulting in urea depletion and prolonged polyuria can cause medullary washout.

Primary polydipsia subsequent to increased thirst can cause secondary polyuria but is an uncommon clinical finding. Compulsive water drinking (pseudopsychogenic polydipsia) is probably the most important type of primary polydipsia, although the underlying cause is not known. Hypothalamic lesions, hypercalcemia, and increased levels of plasma renin are less common causes of primary polydipsia.

ASSOCIATED SIGNS

Signs associated with PU or PD are varied and dependent on the underlying disease. Generalized signs include weakness, decreased appetite, weight loss, diarrhea, and fever. Polyphagia with weight loss occurs in animals with diabetes mellitus and in cats with hyperthyroidism. Paraneoplastic syndromes, particularly hypercalcemia, may develop in conjunction with PU or PD. A comprehensive physical examination and a laboratory assessment are justified in all patients presented with PU or PD as the primary complaint.

DIFFERENTIAL DIAGNOSIS (Box 3-15)

BOX 3-15. DIFFERENTIAL DIAGNOSIS OF POLYURIA AND POLYDIPSIA.

Polyuria of Renal Origin

Renal failure

• Glomerulonephritis

• Tubular dysfunction

• Renal medullary dysfunction

Postobstructive diuresis (e.g., feline urologic syndrome)

Diabetes insipidus (nephrogenic)

Hypercalcemic nephropathy

Fanconi's syndrome

Medullary washout

Polyuria of Nonrenal Causes

Diabetes insipidus (neurogenic)

Diabetes mellitus

Hyperadrenocorticism

Liver disease (nonspecific)

Pyometra

Pseudopsychogenic polydipsia

Drug-Induced Polyuria

Glucocorticoids (esp. in dogs)

Mannitol, IV

Dextrose, concentrations >50 mg/dL (5.0%)

Alcohol

Diuretic therapy (e.g., furosemide)

Phenytoin

Vitamin D intoxication

 

DIAGNOSTIC PLANS (Figure 3-3)

Figure 3-3.

Clinical approach to the patient with polydipsia and polyuria. CBC, complete blood count; ADH, antidiuretic hormone.

(From Fenner WR: Quick reference to veterinary medicine, ed. 2, Philadelphia, 1991, JB Lippincott, p. 110.)

© 2006 JB Lippincott

• 1.History and physical examination, to facilitate verification of the problem in addition to determining the duration of the problem and associated signs. Of particular importance is knowledge of the recent administration of medication.
• 2. Laboratory database. The primary focus of the diagnostic plan is interpreting results from a laboratory database, including a CBC, biochemistry profile, urinalysis, fecal culture, heartworm test (in dogs), FeLV and FIV tests (in cats), and urine culture.
• 3.Collecting urine and measuring water intake over a 24-hour period, to document the problem, if necessary.
• 4.Abdominal radiographs, if indicated.
• 5.
  Special diagnostic tests, if indicated, based on results from a laboratory database:

  • a.
    Water deprivation and modified-water deprivation tests (contraindicated in the presence of azotemia, dehydration, or hypercalcemia).
  • b.
    Antidiuretic hormone (ADH, vasopressin) response test.
  • c.
    Glucose tolerance test.
  • d.
    ACTH stimulation or dexamethasone suppression.
  • e.
    Serum T₄.
  • f.
    Liver function studies (e.g., serum ammonia, bile acids).
  • g.
    Abdominal ultrasound.
  • h.
    Tissue biopsy (e.g., renal and hepatic).
  • i.
    Exploratory laparotomy.

ITCHING OR SCRATCHING: PRURITUS (See Also Hair Loss)

DEFINITION

Pruritus: Abnormally frequent scratching or biting that results from unpleasant, sometimes intense, epidermal stimulation. Histamine, endopeptidases, and other polypeptides liberated from skin cells serve as mediators of pruritus. Histamine is the primary mediator of itch associated with wheal-and-flare reaction. Histamine-mediated itching cannot be completely inhibited by either H₁- or H₂-receptor antagonists (blockers). Other polypeptides (such as bradykinin), β-endorphin, and neuropeptides, such as substance P, can induce itching when applied directly to skin. The close association between itching and inflammation of the skin is attributed to the fact that many of the endogenous mediators and potentiators are released in situ during inflammatory events.

Itching, although a protective response, can become more harmful than helpful. As a feature of dermatitis, itch mediators cannot be removed by the patient. In fact, scratching and biting eventually promote more inflammation and subsequently perpetuate the itching.

ASSOCIATED SIGNS

Skin lesions are commonly associated with pruritus; however, it becomes important to characterize the lesion and to distinguish those that are primary from those that are secondary to scratching or biting. Papules and pustules are characteristic primary lesions that may ultimately develop into secondary lesions, such as crusts, ulcers, scale in collarettes, and pigmented macules. Vesicules and bullae, plaques, and urticaria (wheals) can also occur as primary skin lesions. Linear crusts, irregular ulceration, lichenification, diffuse scaling and pigmentation, and patchy alopecia are characteristic lesions that develop secondary to excoriation.

Pruritus can also occur without primary lesions (i.e., “essential” pruritus). This type of itching is a manifestation of systemic disease, although mediation may be central or cutaneous. Causes include atopy, dry skin, and neurogenic and psychogenic disorders. A spectrum of renal, hepatic, hematopoietic, allergic, and endocrine diseases are associated with essential pruritus.

DIFFERENTIAL DIAGNOSIS (Box 3-16)

BOX 3-16. DIFFERENTIAL DIAGNOSIS OF PRURITUS.

Pustular Dermatitis

Infectious

• Puppy pyoderma

• Folliculitis and furunculosis

Immune-mediated

• Pemphigus foliaceus

• Vesicle-forming disorders (e.g., drug eruption)

• Linear IgA γ dermatosis

Idiopathic

• Puppy strangles

• Subcorneal pustular dermatosis

Vesicular/Bullous Eruption

Bullous dermatoses

Systemic lupus erythematosus (SLE)

Toxic epidermal necrolysis

Drug eruption

Acute contact dermatitis

Plaque Formation

Infectious dermatitis

Immune-mediated dermatitis

Neoplasia (e.g., mast cell tumor)

Papular Eruption (Dog)

Infectious

• Folliculitis (bacterial, fungal, demodectic)

• Parasitic (Sarcoptes, Cheyletiella, lice, fleas)

• Vasculitis (Rocky Mountain spotted fever)

Immune

• Allergy (atopy)

• Autoimmune (pemphigus foliaceus, SLE)

• Idiopathic

Papular Eruption (Cat)

Infectious (bacterial folliculitis)

Dermatophytosis

Parasitic (otodectic and notoedric mange, Cheyletiella, lice)

Immune-mediated (hypersensitivity to food)

Idiopathic military dermatitis

Ulcerative Dermatitis

SLE

Leukocytoclastic vasculitis

Erythema multiforme

Toxic epidermal necrolysis

Mycosis fungoides

Epidermolysis bullosa complex

Dermatomyositis

Acute contact dermatitis

Vogt-Koyanagi-Harada syndrome

 

DIAGNOSTIC PLANS

• 1.History and physical examination, to characterize the skin lesion and its distribution, to determine whether or not the condition appears to be contagious, and to determine whether or not systemic disease is present.
• 2.Laboratory database, if evidence of systemic disease is present.
• 3. Skin and coat examination. Perform multiple skin scrapings, and examine skin and hair coat with Wood's light.
• 4.Microbiologic testing for bacteria and dermatophytes.
• 5.Immunologic testing, to include intradermal skin testing and direct fluorescent antibody testing of skin (both normal and affected) biopsy specimens.
• 6.Skin biopsy with dermatohistopathology.
• 7.Provocative exposure to selected environmental agents, diet, and drugs.

JAUNDICE (SEE YELLOW SKIN)

 

JOINT SWELLING: ARTHROPATHY (SEE ALSO LAMENESS)

DEFINITION

Joint swelling, or joint enlargement: Any abnormal increase in size, either visible or palpable, of any joint that is not directly caused by a proliferation of tissue. In practice, joint swelling is the primary presenting sign only occasionally. Pain and associated lameness are more likely causes for presentation, whereas actual enlargement of a joint is detected during physical examination. However, there is not necessarily an association between joint swelling and pain.

Joint swelling, or effusion, occurs subsequent to injury to the synovial membrane in which there is not only an increase in volume of synovial fluid produced, but quantitative biochemical and cellular changes as well. Most joint swelling is attributed to inflammation of the synovial membrane, or synovitis. Abnormal synovial fluid accumulation (effusion) may be classified as serous, fibrinous, purulent, septic, or hemorrhagic.

ASSOCIATED SIGNS

Although lameness is the most common clinical sign associated with joint swelling, it is not consistently present. Joint swelling may also be associated with, or mistaken for, hyperplasia, metaplasia, or neoplasia of the synovium, joint capsule, articular cartilage, or periarticular bone. Hemorrhagic joint effusion (hemarthrosis) may be associated with coagulopathy and spontaneous bleeding from the respiratory, GI, or urinary tract. Subluxation or fracture of a carpus, tarsus, or stifle may also be associated with detectable joint swelling. Arthritis associated with systemic disease (e.g., infectious or immune mediated) can also be accompanied by significant joint swelling.

DIFFERENTIAL DIAGNOSIS (Box 3-17)

BOX 3-17. ARTHROPATHIES IN THE DOG AND CAT.

Noninflammatory

Degenerative joint disease (osteoarthritis, osteoarthrosis)

• Primary

• Secondary

• As a sequel to acquired or congenital defects of the joints and supporting structures

Traumatic

Neoplastic involvement

Drug-induced

Inflammatory

Infectious

• Bacterial

• Caliciviral (cat)

• Mycoplasmal

• Fungal

• Protozoal

• Rickettsial (neurophilic erlichiosis, Rocky Mountain spotted fever)

• Spirochetal (Lyme disease)

Noninfectious

• Immunologic

  • Erosive (deforming)

    • Rheumatoid arthritis
  • Nonerosive (nondeforming)

    • Systemic lupus erythematosus
    • Arthritis resulting from chronic infectious disease
    • Idiopathic nonerosive arthritis
    • Drug reactions (sulfadiazine reaction)

Nonimmunologic

• Crystal-induced arthritis (gout, pseudogout)

• Chronic hemarthrosis (coagulation defects, congenital or acquired)

 

DIAGNOSTIC PLANS

• 1.History. The history generally focuses on associated signs rather than primary joint swelling and should address duration, exposure to ticks, known injury, and evidence of spontaneous bleeding. Physical examination establishes the presence of joint swelling and the number of joints involved. Evidence of inflammation, crepitus, joint laxity, abnormal range of motion, a drawer sign, luxations, or fractures should be determined.
• 2.Radiography of the affected joint(s).
• 3.Synovial fluid analysis, including biochemical, cytologic, and culture findings.
• 4.Coagulation profile in the presence of hemarthrosis.
• 5.Immune function testing: ANA titer, rheumatoid factor, and LE cell preparation.
• 6.Contrast arthrography.
• 7.Joint capsule–synovial membrane biopsy.
• 8.Periarticular bone biopsy.
• 9.Surgical exploration of the affected joint.

LOSS OF APPETITE: ANOREXIA

DEFINITION

Anorexia: Strictly speaking, anorexia is the lack or loss of appetite for food. In veterinary medicine, this term is loosely used to describe diminished or partial, as opposed to complete loss of, interest in eating. In addition, part of the difficulty in assessing the patient that is presented for loss of appetite is grounded in owner expectation of what is and what is not a normal appetite in a dog or cat. While domesticated pets do tend to eat at regular intervals throughout the day, some do experience transient periods of sustained inappetence that may, in fact, be entirely normal and not associated with underlying disease. When assessing a dog or cat for partial loss of appetite, careful history and physical evaluation are indicated to determine whether or not underlying disease may be the cause of this vague clinical sign. In addition, the clinical history must establish the duration of the anorexia and whether the loss of appetite is complete or partial.

Note: What makes anorexia such an important clinical sign is the fact that loss of appetite is the very first outward sign the owner may notice when a pet is ill.

ASSOCIATED SIGNS

What makes anorexia such an important clinical sign is the fact that loss of appetite is the first outward sign the owner may notice when a pet is ill. Anorexia is regarded as a low-yield clinical sign—that is, it is not a discrete sign and, like pain, may be associated with numerous underlying disorders.

Historical evidence of a significant change in the pet's environment (e.g., a new child in the family) or daily routine (e.g., the dog is home alone during the day for the first time) is important to assess. Knowledge of current drug therapy, whether the pet eats sticks or other foreign material, whether or not the pet food type recently changed or may not be fresh (moldy canned and dry food will generally not be consumed) is important.

Physical examination should determine overall body conformation, body weight, extent of weight loss (if present), and any obvious external injuries that might contribute. Age is an important factor in the assessment of anorexia. Diminished sense of smell, neoplasia, joint disease, and dental disease are common age-related disorders that may contribute to anorexia.

DIFFERENTIAL DIAGNOSIS

Differential diagnoses associated with anorexia are too numerous to be of assistance in resolving to a diagnosis. The clinician faced with a patient that has only anorexia is faced with a significant clinical challenge in defining the underlying disorder. Even the categories of disease that could be associated with inappetence are wide ranging and include psychologic, metabolic, orthopedic, infectious, inflammatory, and neoplastic causes.

DIAGNOSTIC PLANS

• 1.Careful observation of the patient on and off the examination table is important.
• 2.A methodical physical examination.
• 3.A standard laboratory profile to include hematology, biochemistry, and urinalysis (fecal is optional depending on the presenting signs.
• 4.Radiography or other imaging study is indicated if the pain can be localized to a discrete region of the body (e.g., abdominal cavity).
• 5.Special diagnostic tests are indicated if specific abnormalities can be detected (e.g., biopsy, aspiration and cytopathology, myelography).

LYMPH NODE ENLARGEMENT: LYMPHADENOMEGALY

DEFINITION

Lymphadenomegaly: Any change in the size or consistency of a lymph node or group of lymph nodes. Lymphadenomegaly refers to those lymph nodes that are larger than expected with or without commensurate changes in consistency. Involved nodes may be unusually soft, firm, or painful, suggestive of inflammation; whereas enlarged, firm, nonpainful lymph nodes suggest neoplasia. Lymphadenomegaly is usually not a presenting problem, with the possible exception of generalized enlargements of all superficial lymph nodes.

Lymph nodes become enlarged as a result of inflammation (pyogenic or granulomatous), reactive lymphoid hyperplasia, or neoplasia (primary or neoplastic). In pyogenic inflammation, neutrophils dilate and engorge the sinuses; whereas in granulomatous inflammation, an infiltrate or macrophages is present (e.g., systemic mycoses). Reactive lymphoid hyperplasia is associated with an increase in the number of germinal centers within the lymph node and an infiltrate of plasma cells. In neoplastic lymph nodes, tumor cells may invade the sinuses (metastatic), gradually destroying the normal node architecture, or the architecture of the lymph node is entirely replaced by malignant lymphocytes (lymphosarsoma)—that is, histologically, the sinuses are obliterated and germinal centers cannot be found.

ASSOCIATED SIGNS

Characterize the consistency and number of affected nodes as well as their location (i.e., generalized or regional). Lymph node pain is an inconsistent finding usually associated with inflammatory disease rather than neoplasia. Associated signs are likely to be regional, as is the lymph node enlargement (i.e., tissue injury or infection). Patients with generalized lymphadenomegaly may not have associated signs, or there may be nonspecific signs, including weight loss, fever, decreased appetite, and lassitude as a result of systemic illness.

DIFFERENTIAL DIAGNOSIS (Box 3-18)

BOX 3-18. DIFFERENTIAL DIAGNOSIS FOR LYMPHADENOMEGALY.

Generalized

Lymphosarcoma

Diffuse, generalized skin disease

Infectious diseases (numerous infections are known to cause lymph node enlargement)

Parasitic (especially severe ectoparasitism, e.g., demodicosis with secondary pyoderma)

Vaccination

Localized

Any of the causes of GENERALIZED

Localized infection, especially in the skin or subcutaneous tissues

Cutaneous neoplasia, other than lymphoma

 

DIAGNOSTIC PLANS

• 1.History and physical examination, to determine the duration and type of associated signs, if any, and the duration of lymph node enlargement, if known.
• 2. Laboratory profile, with emphasis on CBC, including platelet count; biochemistry panel; and urinalysis.
• 3.Specific tests for infectious diseases, as indicated (e.g., FeLV antigen and FIV antibody).
• 4.Thoracic and abdominal radiographs, as indicated.
• 5.Fine-needle aspiration of affected lymph node(s).
• 6.Serum protein electrophoresis.
• 7.Bone marrow aspirate.
• 8.Lymph node biopsy and, if indicated, culture.

PAIN

DEFINITION

Pain: The perception of an unpleasant sensation; may be generalized or localized. While pain may be the single most common presenting complaint of humans who seek medical attention from a physician, the ability of a dog or cat to communicate pain and the ability of the owner to interpret the signs correctly make this a particularly complex clinical sign in animals.

ASSOCIATED SIGNS

As in humans, the actual perception and manifestation of pain varies from one animal to another. Fundamental to the ability to interpret the presence of pain in an animal is the ability to recognize a change in behavior. Acute injury and associated pain is relatively simple to ascertain. However, chronic pain emanating from a specific organ or tissue (e.g., liver or bone) can be extremely difficult to define and localize. Other signs that may be associated with pain include sleeplessness; unusual posture; decreased activity; decreased appetite; reluctance to play, walk, or run; agitation; or altered grooming behavior. Physical findings are also highly varied and may include such findings as hypersalivation, mydriasis, tachycardia, shivering, or increased respiratory rate. Unfortunately, despite efforts to objectively measure pain in animals, there are no tests that clearly define whether or not an individual animal is experiencing pain.

Note: Pain Management has become increasingly recognized as an essential part of clinical practice today. Section 1 (Tables 1-17 to 1-22) addresses indications of the drugs and doses most commonly employed in pain management of dogs and cats.

DIFFERENTIAL DIAGNOSIS

Many disorders are associated with pain. Hence, developing a list of differential diagnoses becomes impractical. Since pain is characteristically associated with inflammation or tissue trauma, every effort should be made to localize the source of the pain in order to focus the diagnostic search. Localizing acute-onset pain is generally less problematic than localizing chronic pain. Particularly in the patient with nonlocalizing, chronic pain, developing a clear diagnostic plan is essential in establishing a diagnosis.

DIAGNOSTIC PLANS

• 1.Careful observation of the patient as it moves, stands, sits, lies down, and so on is critical.
• 2.A methodical physical examination.
• 3.A standard laboratory profile to include hematology, biochemistry, and urinalysis (fecal is optional depending on the presenting signs).
• 4.Radiography or other imaging study is indicated if the pain can be localized to a discrete region of the body (e.g., abdominal cavity).
• 5.Special diagnostic tests are indicated if specific abnormalities can be detected (e.g., biopsy, aspiration and cytopathology, myelography).
• 6.In some patients, empiric treatment with anagesics or nonsteroidal antiinflammatory drugs may be indicated. However, utilizing this method for managing pain requires the ability to provide follow-up care to that patient.

PAINFUL URINATION: DYSURIA (SEE STRAINING TO URINATE)

 

PAINFUL DEFECATION: DYSCHEZIA (SEE STRAINING TO DEFECATE)

 

RECTAL AND ANAL PAIN (SEE STRAINING TO DEFECATE)

 

REGURGITATION (SEE ALSO DIFFICULTY SWALLOWING AND VOMITING)

DEFINITION

Regurgitation: Retrograde esophageal transport of ingesta subsequent to a mechanical, neurogenic, or myogenic swallowing disorder. Owners most often describe regurgitation as “vomiting.” Both regurgitation and vomiting imply a backward flowing of ingesta through the esophagus; however, regurgitation is a relatively effortless act in contrast to the retching and abdominal pressure characteristic of vomiting. Regurgitation localizes the problem to the esophagus.

The pathophysiology of esophageal function is addressed and referenced in the article on dysphagia. Both acquired (e.g., foreign body) and congenital (e.g., familial megaesophagus) forms and esophageal disease can lead to regurgitation. Many esophageal problems remain undiagnosed if regurgitation is not present.

ASSOCIATED SIGNS

Physical signs recognized by owners of dogs or cats with regurgitation include dysphagia characterized by difficulty swallowing food, frequent attempts to swallow food, and hypersalivation. Belching may also be reported subsequent to the entrapment of air in the esophagus. Inappetence and weight loss subsequently develop. Esophageal dilatation may be observed at the level of the lower cervical esophagus or thoracic inlet.

Owners may report expulsion of blood-tinged saliva subsequent to esophageal mucosal injury. Paroxysms of coughing and retching, particularly when eating, may be present along with difficult breathing in animals with significant pneumonia. Nasal discharge may consist of mucoid to mucopurulent exudates or of food and liquid recently consumed.

Rarely, affected animals present with swollen joints, lameness, and severe weakness associated with hypertrophic osteodystrophy subsequent to an intrathoracic lesion. Atypical signs include inspiratory dyspnea, regurgitation unrelated to eating, and recurrent gastric bloating associated with aerophagia.

DIFFERENTIAL DIAGNOSIS (Box 3-19)

BOX 3-19. DIFFERENTIAL DIAGNOSIS OF REGURGITATION.

Functional Megaesophagus*

Primary (or congenital)

Secondary (or acquired)

• Foreign body

• Esophageal stricture

• Esophageal diverticula

• Neurogenic (e.g., myasthenia gravis, rabies)

• Myopathy, smooth muscle

• Extraesophageal compressive lesion (e.g., neoplasia)

• Vascular anomaly

Esophagitis

Gastric reflux

Neoplastic

Restrictive Lesion Without Megaesophagus

Foreign body obstruction

Intrathoracic mass

Vascular ring anomaly

Esophageal stricture

 

DIAGNOSTIC PLANS

• 1.History and physical examination, to characterize the nature of the problem, to distinguish between vomiting and regurgitation, and to establish the character of the regurgitated material.
• 2.Laboratory database, to assess patient status, particularly if secondary complications are present.
• 3.Survey thoracic and cervical radiography, to assess presence of megaesophagus, radiopaque intraesophageal lesion, or both.
• 4.Contrast esophagram, to confirm any interference with normal bolus transport at the point of obstruction, changes in mucosal integrity or luminal displacement, and the presence of extraluminal gas. (Oral suspension of barium sulfate is recommended over other contrast materials.) NOTE: Contrast medium retention in the esophagus is the hallmark of a motor disorder and often localizes the site of dysmotility.
• 5.Endoscopy and, as indicated, biopsy, to determine the cause of megaesophagus rather than to diagnose megaesophagus. In some instances, especially foreign body obstruction, endoscopy may be therapeutic.
• 6.Special procedures, to include contrast esophagram during fluoroscopy, CT, and exploratory laparotomy.

SEIZURES (CONVULSIONS OR EPILEPSY)

DEFINITION

The terms seizure, convulsion, epilepsy, epileptic attack, and fit all describe a clinical sign that is characterized by involuntary contraction of a series of voluntary muscles. Seizures result from disorders of the brain that cause spontaneous depolarizations and excitation of cerebral neurons. As a presenting problem, seizures are much more common in the dog than in the cat. Such disorders may originate from extracranial causes, metabolic or toxic diseases, and intracranial causes (e.g., organic brain disease). When seizures occur in the absence of detectable organic or metabolic CNS abnormalities, the seizures are described as idiopathic. Idiopathic epilepsy is the most common type of seizure reported in companion animal species.

A distinction is made between partial seizures (also called focal seizures) and generalized seizures. Three classes of partial seizure are recognized: partial motor seizures (the most common type of seizure in animals), psychomotor seizures, and sensory seizures.

Partial seizures are caused by a cortical lesion or focus that periodically disrupts cerebral function. Generalized motor seizures represent a widespread disorder not referable to any single anatomic or functional system. Clinical manifestations suggest widespread activation of the brain.

Seizures may be repeated frequently in groups of two or three, or they may occur singly. If a series of seizures occurs and the patient fails to regain consciousness during the interictal period, the term status epilepticus applies. In contrast to a single seizure, status epilepticus is a serious, life-threatening condition that justifies emergency intervention.

ASSOCIATED SIGNS

Generalized motor seizures are the most prevalent type of seizure encountered in veterinary medicine. Most cases are diagnosed as idiopathic epilepsy on the basis that organic causes of seizure activity cannot be identified. The interictal period in animals with a history of generalized motor seizures is characteristically described by owners as normal. The immediate postictal period, regardless of the cause of the seizure activity, is often associated with transient disorientation, blindness, stumbling, polydipsia, or polyphagia.

The spectrum of possible clinical signs associated with seizure activity is extensive. Before a diagnosis of idiopathic epilepsy is reached, it is important that the patient be evaluated for cardiovascular disease, trauma, toxicity, infectious disease, parasites, neoplasia, and metabolic disorders, particularly those affecting the kidney, liver, and endocrine pancreas.

Age of Animal

Seizures in young animals (<1 year old) are commonly caused by developmental abnormalities, hydrocephalus, lissencephaly, encephalitis (infectious), lead poisoning, severe intestinal parasitism, portacaval shunt abnormalities, and juvenile hypoglycemia. Idiopathic epilepsy usually begins when animals are 1 to 3 years of age. Animals over 5 years of age are more likely to have CNS tumors or hypoglycemia from insulin-secreting beta cell pancreatic neoplasms.

Breed Predisposition

Some basic knowledge about breed predisposition to seizure disorders may be helpful in establishing a diagnosis. Idiopathic epilepsy has been seen in numerous dog breeds, particularly German Shepherd Dogs, Belgian Tervurens, Keeshonds, Saint Bernards, Standard and Miniature Poodles, Beagles, Irish Setters, Cocker Spaniels, Alaskan Malamutes, Siberian Huskies, and Labrador and Golden Retrievers. Juvenile hypoglycemia is most prevalent in toy breeds. Hydrocephalus is common in the toy and brachycephalic breeds. Neoplastic diseases are common in brachycephalic breeds over 5 years of age.

Concerning disorders of CNS metabolism, leukodystrophy is most common in Cairn and West Highland whites; lipodystrophy in German Short-Haired Pointers and English Setters; lissencephaly in the Lhasa Apso; and portacaval shunts and hyperlipoproteinemia in Miniature Schnauzers. A unique, usually fatal, encephalitis occurs in Pugs.

Environment

Exposure to infectious agents or other sick animals may be important, as is exposure to sources of intoxicants, such as lead in paints, linoleum, tar, batteries, or roofing material; hexachlorophene soap; ethylene glycol (antifreeze); metaldehyde snail bait; and various other insecticides, including chlorinated hydrocarbons, organophosphates, and rodenticides. Dogs and cats on the same premises with swine may be exposed to Herpesvirus suis (pseudorabies, or Auzjesky's disease). A high protein diet exacerbates hepatic encephalopathy. Thiamine deficiency may result from long-term consumption of certain fish diets or from cooking pet food.

DIFFERENTIAL DIAGNOSIS (Table 3-6)

TABLE 3-6.

Differential Diagnoses for Seizure Disorders

Intracranial		Extracranial
Congenital		Intoxication
	Hydrocephalus		Lead
	Lissencephaly		Organophosphates
	Other malformations		Chlorinated hydrocarbons
	Storage diseases		Strychnine
	Vascular anomaly		Drugs
Traumatic			Garbage
	Immediate	Metabolic
	Post trauma		Hypoglycemia
Inflammatory			Hypocalcemia
	Distemper		Hyperkalemia
	Rabies		Acid-base
	Feline infectious peritonitis		Hepatic encephalopathy
	Feline leukemia virus		Uremia
	Toxoplasmosis		Hyperlipoproteinemia
	Mycosis	Nutritional
	Bacteria		Thiamine
	Reticulosis		Parasites?
	Parasites	Hypoxia
Neoplasia			Cardiovascular disease
	Primary		Respiratory disease
	Metastatic		Birth
Vascular–cerebrovascular accident			Anesthetic accident
		Hyperthermia

From Russo ME: Seizures. In Ford RB, ed: Clinical Signs and Diagnosis in Small Animal Practice. New York, Churchill Livingstone, 1988, p 290.

© 2006 Churchill Livingstone

 

DIAGNOSTIC PLANS

• 1.History, to take into consideration breed predisposition, environmental exposures, past medical illnesses, and medication. Because most seizures are of short duration and the physical (tonic-clonic) manifestations of a seizure are so dramatic, requesting the owner to describe the type and duration of seizure may elicit unreliable information.
• 2.Thorough physical examination, to include careful neurologic examination, with particular attention to cranial nerves, funduscopic examination, and cardiac auscultation.
• 3.Laboratory database, essential to rule out metabolic causes. In addition to a CBC, biochemistry profile, urinalysis, and fecal culture, any or all of the following tests are indicated: serum ammonia, bile acids, serum insulin in hypoglycemic patients, blood lead test, and serial blood cultures.
• 4.Survey radiographs of the skull. These are rarely helpful, as intracranial neoplasms are not detectable on conventional skull radiographs.
• 5. In special circumstances, limited ultrasound examination of the brain may be possible in young dogs through a cranial fontanelle. Evidence of hydrocephalus may be seen.
• 6.Computed tomography or magnetic resonance imaging (special facilities required).
• 7.Electrocardiogram or echocardiogram, if indicated.
• 8.Serologic studies for canine distemper, rabies, feline infectious peritonitis (FIP), FeLV, FIV, toxoplasmosis, and systemic (deep) mycoses.
• 9.CSF analysis, including biochemistries, antibody titers, and cytologic parameters.
• 10.EEG. Although limited in availability, the EEG may be useful in detecting inflammatory brain disease and congenital intracranial abnormalities (e.g., hydrocephalus).
• 11.Contrast studies, requiring special equipment or facilities: radioisotope brain scan, cerebral angiography, pneumoencephalography, and CT scan.

SNEEZING AND NASAL DISCHARGE

DEFINITION

Sneezing: A protective reflex described as a sudden, involuntary, and forceful, even violent, expulsion of air from the upper respiratory tract; may or may not be accompanied by significant nasal discharge. Clients easily recognize sneezing. Although sneezing is a physiologic response to irritating stimuli, increased frequency and paroxysmal sneezing episodes are readily recognized as abnormal. Like sneezing, a nasal discharge, regardless of its consistency, is a clinical sign that clients accurately interpret and reliably describe to the clinician.

Sneezing is the outward manifestation of nasal passage irritation by extraneous (foreign material) or endogenous (antigen-antibody interaction) agents. Afferent impulses travel via the fifth cranial nerve to the medulla, where the initial reflex is triggered. Chronic nasal discharge is a clinical sign that localizes a disorder to the upper respiratory passages, particularly the nasal cavity and frontal sinuses.

ASSOCIATED SIGNS

Important associated signs suggesting systemic involvement include facial asymmetry (neoplasia or fungal infection), atrophy of the masseter and temporal muscles, difficulty prehending or masticating food, conjunctivitis, and ocular discharge. Epistaxis, which is distinguished from blood-tinged nasal discharge, is an important associated sign that further supports intranasal disease or coagulopathy. Cleft palate is a common cause of nasal discharge in neonates. Erosion and depigmentation of the planum nasale is often associated with nasal aspergillosis in dogs, whereas cats with nasal cryptococosis may have a detectable granuloma at the rostral aspect of the nose. Occasionally, cough is associated with purulent nasal discharges and sneezing.

DIFFERENTIAL DIAGNOSIS (Box 3-20)

BOX 3-20. DIFFERENTIAL DIAGNOSIS FOR SNEEZING AND NASAL DISCHARGE.

Intranasal Causes

Serous Nasal Discharge

• Acute viral upper respiratory infection (feline)

• Feline chlamydiosis

• Intranasal parasites

• Oronasal fistula (canine tooth)

• Rhinosporidiosis (canine, rare)

Purulent Nasal Discharge

• Viral upper respiratory infection with secondary bacterial infection (dog and cat)

• Mycotic nasal disease

• Foreign body rhinitis

• Traumatic rhinitis or sinusitis

• Cleft palate

• Neoplasia (several types possible)

• Nasopharyngeal polyps (feline, rare)

• Benign nasal polyps (canine, rare)

• Oronasal fistula

Mucoid to Mucopurulent Nasal Discharge

• Mycotic nasal disease (e.g., aspergillosis, cryptococcosis, blastomycosis)

• Neoplasia (especially adenocarcinoma)

Epistaxis

• Acute nasal trauma

• Oronasal fistula

Extranasal Causes

Purulent Nasal Discharge

• Bacterial pneumonia

• Megaesophagus with aspiration pneumonia, congenital or acquired

• Achalasia with nasal reflux of food

• Acquired esophageal stricture

Epistaxis

• von Willebrand's disease (most common canine coagulopathy)

• Factor VIII deficiency (classic hemophilia)

• Other inherited factor deficiencies

• Thrombocytopenia (infectious or immune-mediated)

• Disseminated intravascular coagulation

• Hyperviscosity syndrome

 

DIAGNOSTIC PLANS (Figure 3-4)

Figure 3-4.

Clinical algorithm for the patient presented for sneezing, nasal discharge, or both. ACT, activated clotting time; PT, prothrombin time; PTT, partial thromboplastin time; CT, clotting time; Factor VIIIR:Ag, factor VIII-related antigen; ϕ, decreased (numbers); δ, prolonged (time); N, normal; N (δ), usually normal, occasionally prolonged; ? (N), usually prolonged, occasionally normal.

 

SPONTANEOUS BLEEDING: HEMORRHAGE

DEFINITION

Spontaneous or prolonged bleeding: The visible, abnormal discharge of blood resulting from a failure of one or more hemostatic mechanisms. May result from deficiencies in platelet numbers or function, in the extrinsic or intrinsic coagulation cascades, or in vascular integrity.

The hemostatic response is a complex defense system that fulfills three basic functions: ensures that blood is confined to the vascular system of the normal animal (vascular integrity), causes the arrest of bleeding at sites of vascular injury, and maintains the patency of the vascular network.

These functions are accomplished through complex interactions between blood platelets, the blood vessel wall, and a variety of plasma enzyme systems. Disorders affecting these interactions can result in spontaneous or prolonged bleeding.

The primary phase of hemostasis occurs with platelet aggregation and the formation of the relatively unstable platelet plug. The secondary phase of hemostasis, essential to complete hemostasis, reinforces the platelet plug with fibrin. Secondary hemostasis depends on adequate plasma concentration of procoagulant proteins and on their proper interaction. Coagulation can be initiated through an intrinsic pathway, which involves components normally found within the vasculature and which is activated by contact with a foreign surface. The extrinsic pathway is an alternative mechanism through which clotting is initiated.

Secondary hemostasis is regulated by inhibitory products that limit the extent of enzymatic reaction and prevent their dissemination: antithrombin III, a potent inhibitor of kallikrein; factors IXa, XIa, XIIa, and Xa; and thrombin. The fibrinolytic system, another plasma protein-enzyme system, removes the hemostatic plug once its function has been served.

ASSOCIATED SIGNS

Bleeding disorders are most apparent when bleeding develops spontaneously from one or more body orifices and is prolonged. Bleeding from the nose (epistaxis: see Figure 3-4) is perhaps the most commonly reported outward manifestation of a bleeding disorder in dogs. Bleeding into the skin or mucous membranes (e.g., petechiation) may not be immediately apparent to even the most observant owner. Excessive or prolonged bleeding into soft tissues (hematoma) or joints (hemarthrosis) may be seen as physical enlargement of the affected tissues with pain and lameness.

There may be a history of recurrent minor bleeding episodes in some animals. The severity of clinical signs depends on such factors as type of defect, degree of clotting factor activity, and individual variation. Moderately to severely affected animals are typically young at the time of presentation. Prolonged bleeding subsequent to elective surgical procedures may be the first sign of a bleeding disorder.

DIFFERENTIAL DIAGNOSIS (see Box 3-21 on p. 433)

BOX 3-21. DIFFERENTIAL DIAGNOSIS OF SPONTANEOUS BLEEDING.

Hereditary Disorders—Factor Deficiencies

Hypoprothrombinemia (factor II)–Boxers

Hypoproconvertinemia (factor VII)–Beagles, Malamutes

Hemophilia A (factor VIII)–most dog breeds and cats

Hemophilia B (factor IX)–several dog breeds and British short-hair cats

von Willebrand's disease (vWD factor)–most dog breeds

Stuart factor deficiency (factor X)–Cocker Spaniels

Plasma thromboplastin antecedent (PTA) deficiency (factor XI)–Springer Spaniels, Great Pyrenees, Kerry Blue Terriers

Hageman factor deficiency (factor XII)–cats

Hereditary Platelet Disorders

Thromobocytopenia

Platelet dysfunction

• Thrombasthenia (Glanzmann's disease)*

• Thrombopathia (e.g., osteogenesis imperfecta, Ehlers-Danlos syndrome)*

Acquired Clotting Factor Disorders

Primary hyperfibrinolysis

Disseminated intravascular coagulation (DIC)

Chemical- or drug-induced

• Vitamin K deficiency

• Rodenticide ingestion

• Prolonged enteric antimicrobial therapy*

Circulating anticoagulants

• Heparin

• Warfarin

• Warfarin-like chemical (e.g., diphacinone)

• Plasma expander therapy*

• Antifactor antibody*

Liver disease

• DIC

• Vitamin K deficiency

• Decreased factor synthesis subsequent to severe liver disease*

Acquired Platelet Disorders

Thrombocytopenia (relatively common)

• Decreased or ineffective thrombopoiesis*

• Immunologic destruction: immune-mediated, infectious, drug-induced

• Consumption: DIC, vasculitis

• Sequestration: splenomegaly subsequent to neoplasia*

• Dilutional: IV fluid administration*

Platelet dysfunction

• Secondary to underlying disease: renal failure and uremia, hepatic failure, polycythemia*

• Drug-induced: aspirin, phenylbutazone, estrogen, phenothiazines, plasma expanders*

 

DIAGNOSTIC PLANS

• 1.History. Age (inherited versus acquired), sex (sex-linked versus autosomal), and breed (inherited versus acquired) of the bleeding patient must be carefully considered. Bleeding disorders in related animals should also be considered. A detailed history of recent or current drug administration and vaccination is critical.
• 2.Physical examination. This may be normal. However, evidence of melena, hematuria, epistaxis, and hematoma or hemarthrosis should be pursued. The skin and mucous membranes should be inspected for evidence of petechiae or ecchymoses.
• 3.Routine laboratory database, indicated in all bleeding patients to assess for the presence of underlying contributory diseases, as well as the possible consequences of bleeding within major organs.
• 4.Antibody titers for ehrlichiosis and Rocky Mountain spotted fever.
• 5.
  Coagulation screening tests:

  • a.
    Peripheral blood smear (for the presence of platelets).
  • b.
    Platelet count followed by buccal mucosal bleeding time (a test of platelet function) is the presence of adequate platelet numbers.
  • c.
    Assessment of clot retraction.
  • d.
    Prothrombin time (PT).
  • e.
    Activated partial thromboplastin time (APTT).
  • f.
    Thrombin clotting time.
  • g.
    Fibrinogen.
  • h.
    Fibrin degradation products.
  • i.
    Clot lysis.
• 6.
  Specialized laboratory tests (special facilities required):

  • a.
    Specific factor activity assays.
  • b.
    Platelet function studies (adhesion, aggregation, secretion).
  • c.
    Antiplatelet antibody.
  • d.
    Antithrombin III.
  • e.
    Kallikrein.
  • f.
    Electron microscopic assessment of platelets.

STRAINING TO DEFECATE: DYSCHEZIA

DEFINITION

Dyschezia: Painful or difficult evacuation of feces from the rectum. In the clinical setting, dyschezia may be a difficult problem to ascertain unless the owner is particularly astute and is able to distinguish effort to urinate (see Dysuria) from effort to defecate in cats and female dogs. Therefore, a concerted effort on the part of the clinician is usually necessary to differentiate disorders affecting the urinary outflow tract and micturition from disorders affecting defecation.

The most likely cause for any animal to present with dyschezia is rectal or perianal pain. The origin of the pain may be mucosal, mucocutaneous (anal), or extraluminal lesions. Rectal strictures are uncommon but may contribute to constipation and associated dyschezia. Strictures typically develop subsequent to neoplasia or deep, nonpenetrating injury to the rectum. Although uncommon, dyschezia may also occur subsequent to lesions in the lumbar spinal cord or sacrum.

ASSOCIATED SIGNS

The most common response to dyschezia is constipation, although many owners do not recognize this as a primary problem. Not uncommonly, the pain associated with rectal lesions is intense during attempts to defecate. The animal may cry or turn abruptly and lick the anus in response to the pain. Dogs may circle while assuming the position to defecate. Cats are more likely to make many attempts at defecation or may manifest inappropriate defecation in locations outside of the litter box. Unless attempting defecation, the animal is likely not to manifest pain at all.

Physical examination should include digital examination of the rectum and inspection of the perineum and each anal sac for evidence of lesions. It is important to consider shaving the perineum to assess the integrity of the skin for evidence of lesions, particularly neoplasia.

DIFFERENTIAL DIAGNOSIS (Box 3-22)

BOX 3-22. DIFFERENTIAL DIAGNOSIS OF DYSCHEZIA.

Constipation (See Box 3-5)

Idiopathic Ulcerative and Inflammatory Lesions

Colon (colitis)

Rectum (proctitis)

Anal sacs (determined at surgery)

Neoplasia

Mucosa (e.g., carcinoma)

Intestinal wall (e.g., carcinoma, sarcoma)

Extramural (intra-abdominal prostate)

Anal glands

Perineum (particularly skin/mucocutaneous tissues)

Direct Rectal Injury

With stricture formation

Without stricture formation (e.g., linear foreign body)

Perineal Hernia

 

 

DIAGNOSTIC PLANS

• 1.
  History and physical examination, to determine the ability of the patient to urinate versus defecate. Physical examination must include the following:

  • a.
    Rectal temperature, as a means of detecting source of pain.
  • b.
    Rectal examination, expressing both anal glands and assessing the character of the discharge (sedation may be required).
  • c.
    Evaluation of the perianal skin (shaving the perineum is recommended).
• 2.Fecal examination for occult blood.
• 3.Abdominal radiographs or abdominal ultrasound to assess prostate size (in male dogs), presence of intra-abdominal masses, or presence of fecalith formation.
• 4.Colonoscopy or proctoscopy, with rigid or flexible endoscope and biopsy of any obvious lesions. Recovered tissues should be examined cytologically and by histopathology. Anesthesia is rarely required for this procedure unless the integrity of the rectal mucosa is substantially compromised or pain is significant.
• 5.Rarely, exploratory laparotomy, to further elucidate the nature of abnormal intra-abdominal findings.

STRAINING TO URINATE: DYSURIA

DEFINITION

Dysuria: Painful or difficult urination. A relatively common presenting sign in both dogs and cats, dysuria should be regarded as an urgent situation worthy of immediate attention. Owner observations are not entirely reliable in describing dysuria. Therefore, physical examination is usually necessary to differentiate attempts to defecate from attempts to urinate and to distinguish between incontinence and dysuria.

Dysuria generally results from disorders of the lower urinary tract (bladder or urethra), genital tract (prostate or vagina), or both that induce an impediment to urinary outflow resulting in abnormal micturition or inappropriate urination. However, a variety of neurologic lesions, particularly lesions in the caudal lumbar spine and sacrum affecting either parasympathetic or sympathetic innervation to the lower urinary tract, can result in dysuria. Neurologic dysurias are among the most difficult to characterize and to treat.

ASSOCIATED SIGNS

Clinical signs associated with dysuria can often be localized to the point of the primary lesion in the lower genitourinary tract. Dysuria is commonly associated with discolored urine (particularly hematuria), pyuria, or both, subsequent to mucosal inflammation and infection. Certain causes of urinary incontinence may also result in dysuria. The owner may also report frequent attempts at urination by the animal.

Distinguish between two additional clinical signs associated with dysuria: polyuria (increased volume) versus pollakiuria (increased frequency). Patients with dysuria may also manifest strangury, defined as a slow, painful discharge of urine caused by spasm of the bladder and urethra. In male dogs, dysuria caused by an enlarged prostate may also be associated with constipation.

DIFFERENTIAL DIAGNOSIS (Box 3-23)

BOX 3-23. DIFFERENTIAL DIAGNOSIS OF DYSURIA.

Infectious and Inflammatory Causes

Bacterial cystitis

Urethritis

Prostatitis/benign prostatic hyperplasia (male dog)

Vaginitis

Feline urologic syndrome

Cystic and Urethral Calculi

 

Neoplasia

Urinary bladder

• Transitional cell carcinoma

• Rhabdomyoma or fibrosarcoma

Prostatic carcinoma

Congenital

Ectopic ureters (esp. female)

Various vaginal malformations

Urethra

• Transitional cell carcinoma

• Transmissible venereal tumor

Vagina and penis

• Transmissible venereal tumor

• Fibroma

• Sarcoma

• Carcinoma

Trauma

Ruptured bladder

Urethral laceration (bite wound, calculus)

Urethral stricture

Neurologic Causes

Reflex dyssynergia

Vesicular-urethral asynchronization

 

DIAGNOSTIC PLANS

• 1.Preliminary measures. The initial diagnostic plan depends on confirmation of dysuria at presentation and whether, on abdominal palpation, the urinary bladder is empty or distended (Figure 3-5 ).
• 2.Routine hematology and biochemical profile.
• 3.Urinalysis, with specific attention to color, specific gravity, protein, glucose, occult blood, and microscopic evaluation of urine sediment.
• 4.Radiography of the abdomen, including the lower urinary tract. Follow nondiagnostic studies with contrast radiography of the lower urinary tract (contrast urethrography, contrast cystography, and double-contrast cystography).

Figure 3-5.

Algorithm for the differential diagnosis of dysuria. LUTD: lower urinary tract disease.

SWELLING OF THE LIMBS: PERIPHERAL EDEMA

DEFINITION

Peripheral edema: A pathologic increase in the fluid volume of the interstitium of soft tissue typically affecting the head and neck, forelimbs, or hind limbs. The distribution pattern of peripheral edema can be characterized as generalized, regional, or focal. Peripheral edema may or may not be associated with other forms of edema, such as cerebral edema or pulmonary edema.

The distinction between normal and abnormal increases in interstitial fluid volumes is difficult to establish clinically. Moderate to severe increases (30%) in interstitial fluid volume are evident on visual examination of the patient as a result of the physical changes in the tissue caused by the fluid. Any increase in the interstitial fluid volume identified by any means (e.g., histopathology, physical examination) constitutes peripheral edema.

Albumin is the smallest plasma protein and is the primary source of plasma colloidal oncotic pressure. Edema may become clinically evident as the serum albumin concentration falls below 2 g/dL. However, other factors are also involved in the formation of edema, such as decreased plasma volume and increased extracellular space associated with decreased renal excretion of sodium.

ASSOCIATED SIGNS

Patients that are presented with peripheral edema may manifest other signs. Evidence of chronic inflammatory disease, vasculitis, ecchymoses, cardiac disease, allergy, or trauma (including burns) should be considered. Patients with peripheral edema may also have primary protein-losing (renal or GI) disorders. These patients may be presented with increased water consumption or urination or diarrhea and weight loss. Severe hepatic disease may result in diminished synthesis of albumin, thereby contributing to the formation of edema.

DIFFERENTIAL DIAGNOSIS (Box 3-24)

BOX 3-24. DIFFERENTIAL DIAGNOSIS OF EDEMA.

Increased Capillary Hydrostatic Pressure

Functional or structural obstruction to blood flow

• Congestive heart failure

• Venous obstruction

• Compression of a vessel by a mass lesion

Arteriovenous fistula

Decreased Capillary Oncotic Pressure (Hypoalbuminemia)

Protein-losing enteropathies

Protein-losing nephropathies

Decreased hepatic synthesis

Decreased dietary intake (protein malnutrition)

Chronic hemorrhage

Exudative lesion with large surface (e.g., burns, peritonitis)

Permeability

Chronic inflammatory disease

Vasculitis

Vascular trauma

Toxins

Infections

(esp. tick-borne disease, e.g., ehrlichiosis)

Neurogenic, physical, or other vasoactive stimuli

Decreased Lymphatic Drainage (Lymphedema)

Congenital (primary) lymphedema–an autosomal dominant trait primarily affecting the hindlimbs by 3-6 mo of age

Acquired (secondary) lymphedema (focal or regional)

Infectious, granulomatous, neoplastic, traumatic injury, or compression of lymphatics

Increased Interstitial Gel Matrix

Myxedema (hypothyroidism)–rare

 

DIAGNOSTIC PLANS

• 1.History and physical examination, to focus on cardiac, hepatic, GI, and urinary system disease. Particular attention is given to the presence of jugular vein distention or pulsations, tachycardia, and ascites.
• 2.
  Clinical pathology.

  • a.
    Routine hematology.
  • b.
    Biochemical profile, including electrolytes, total protein, and albumin.
  • c.
    Urinalysis.
  • d.
    Urine protein-creatinine ratio.
• 3.
  Special laboratory testing, as indicated:

  • a.
    Bile acids.
  • b.
    Quantitative urinary clearance studies.
  • c.
    Serology—viral or rickettsial infections.
  • d.
    ANA titer, LE cell preparation, and rheumatoid factor assay.
• 4.Central venous pressure (CVP).
• 5.
  Radiography:

  • a.
    Thorax. Look for evidence of pericardial effusion, pleural effusion, or cardiac disease.
  • b.
    Abdomen. Look for liver or mass lesions in particular, and peritonitis.
  • c.
    Abdominal ultrasound.
• 6.Contrast radiography. Angiograms or lymphangiograms are indicated to confirm an obstructive lesion or the presence of an arteriovenous fistula.
• 7.Serologic studies, particularly for ehrlichiosis and Rocky Mountain spotted fever.
• 8.Edema fluid analysis. Collect by direct insertion of a 22-gauge needle into edematous tissue. A sample is collected into plain and edetic acid (EDTA)-containing tubes. Fluid is analyzed for color, consistency, and turbidity as well as protein and cellularity.
• 9.Postcapillary venous pressure and oxygen saturation, to confirm proximal obstruction to venous drainage or an arteriovenous fistula. (Normal postcapillary venous pressure = 13 ± 4 mm Hg).
• 10.Cytology and histopathology. Studies are particularly useful in evaluating mass lesions associated with edematous tissue. Indirect fluorescent antibody (IFA) staining of affected tissue may facilitate detection of immune-mediated disorders.

UNCONTROLLED URINATION: URINARY INCONTINENCE

DEFINITION

Urinary incontinence: The lack of normal ability to prevent discharge of urine from the bladder. Urinary incontinence is suspected when an animal that previously exhibited normal control of urination begins passing urine at times or in places that are inappropriate. Determining whether or not the presenting complaint of inappropriate urinary behavior is involuntary can be a formidable task in a dog or cat. Distinguishing between voluntary and involuntary urination is fundamental to the diagnostic plan.

The normal micturition reflex is a result of the complex interaction of the autonomic and somatic nervous systems. Normal control of micturition can be divided into a series of nervous pathways:

• 1.Sensory neurons have stretch receptors in the bladder wall that relay information through ascending spinal cord tracts to the brain stem and somesthetic cortex of the frontoparietal lobes. This pathway is the basis for the perception of a full bladder.
• 2.Frontoparietal motor cortex projects to the brain stem reticular formation centers for micturition that are responsible for storage and evacuation of urine.
• 3.From these centers, reticulospinal tracts descend the spinal cord to influence gray matter centers responsible for the storage or evacuation of urine. For evacuation, the visceral efferent neurons in the sacral segments that innervate the detrusor muscle via the pelvic nerves are facilitated. The somatic efferent neurons in the sacral segments that innervate the striate urethralis muscle via the pudendal nerve are inhibited. Facilitation of these pudendal somatic neurons prevents urination.

Urinary incontinence is the physical manifestation of any one of several disorders affecting voluntary urine retention in the bladder. Neurologic lesions involving either upper motor or lower motor neuron segments of the micturition reflex arc result in urinary incontinence. A paralytic bladder usually results in bladder overdistention and urine dribbling. Urine can be easily expressed by manual compression of the bladder in affected patients. A “cord bladder” is caused by a lesion between the brain and the spinal reflex center of micturition. There is usually temporary bladder paralysis followed by involuntary reflex micturition subsequent to manual compression.

Non-neurogenic urinary incontinence may be due to anatomic or functional disorders (e.g., ectopic ureters) affecting the storage phase of micturition. Hormone-responsive incontinence is also a common form of non-neurogenic urinary incontinence. In these patients, the detrusor reflex is normal and the animal exhibits normal urination behavior in addition to urine dribbling.

A number of disorders of micturition are associated with excessive outlet resistance (e.g., urethral calculi, neoplasia) during voiding. Bladder overdistention and urine dribbling are frequently accompanied by dysuria and hematuria.

ASSOCIATED SIGNS

Evidence of urine or blood-tinged urine on the hair coat around the genitalia or on the patient's sleeping surface is frequently the first sign of a micturition disorder that owners recognize. Patients with neurogenic urinary incompetence may show evidence of spinal cord disease with conscious proprioceptive deficits in the hindlimbs, foot drag, and abrasions on the dorsal aspect of the hindfeet. However, lesions involving the cerebral cortex and cerebellum may also be associated with incontinence, as can behavioral disorders.

Obvious straining to urinate, particularly if associated with an enlarged abdomen, may indicate obstructive disease. Affected patients may be uremic, manifesting characteristic signs of lethargy, anorexia, and vomiting.

DIFFERENTIAL DIAGNOSIS (Box 3-25)

BOX 3-25. DIFFERENTIAL DIAGNOSIS OF URINARY INCONTINENCE.

Neurogenic

Cerebral lesions

Cerebellar lesions

Brain stem lesions

Spinal cord lesions

Spinal nerve root lesions

Non-neurogenic without Distended Bladder

Ectopic ureter(s)

Patent urachus

Hormone-responsive incontinence

Urethral incompetence

Neoplasia

Reduced bladder capacity

Cystitis

Non-neurogenic with Distended Bladder

Urethral obstruction, calculi, or neoplasia

Detrusor-urethral dyssynergia

Overflow incontinence (associated with polyuric states)

 

DIAGNOSTIC PLANS

• 1.History and physical examination. The size of the urinary bladder must also be determined.
• 2.Neurologic examination. A thorough neurologic examination should be performed in an attempt to establish or rule out a neurogenic cause. Particular emphasis is given to the spinal cord and sacral nerve roots. The bulbourethral and perineal reflexes should be assessed.
• 3. Catheterization of urinary bladder, to determine residual urine (normal=0.2 to 0.4 mL/kg in the dog and cat). Urine collected is submitted for urinalysis and, as indicated, for culture and sensitivity.
• 4.Laboratory database, to evaluate patient health status.
• 5.Survey radiographs of the caudal abdomen and spinal cord.
• 6.Contrast studies, as needed, including, pneumocystogram (only in the absence of hematuria), contrast urethrogram, and excretory urogram (also called intravenous pyelogram).
• 7.Cystometrogram. Special equipment is required.

VISION LOSS: TOTAL BLINDNESS

DEFINITION

Blindness: The inability to perceive visual stimuli. Because loss of visual function in animals is typically characterized by a change in behavior, the ability of pet owners to detect vision loss depends on their perception of changes in the animal's awareness of and interaction with its surroundings. Vision loss is likely to be apparent to owners only when there is complete loss of vision. An owner is unlikely to detect visual deficits, such as partial vision loss or unilateral blindness, because of the animal's ability to compensate.

Blindness can occur in any of four ways: lesions causing opacification of clear ocular media (e.g., cornea, aqueous humor, or lens); failure of the retina to process visual images; failure of neurologic transmission; and failure in the final image processing (i.e., cortical blindness).

DIFFERENTIAL DIAGNOSIS

When an animal is presented with acute visual loss, the owner is usually describing a bilateral ocular disease problem or the possibility of a CNS problem. Acute unilateral visual loss problems are not often recognized except by the very astute animal owner or observer. For the veterinarian, initial assessment of the animal with acute visual loss depends initially on confirming that the ocular media are clear and allow light to pass from the anterior ocular segment and reach the photoreceptor cells (rods and cones) in the posterior ocular segment. Transillumination should be used to evaluate the ocular media. Such conditions as acute bilateral uveitis, severe corneal edema, bilateral acute keratitis, rapidly developing metabolic cataracts, or acute cyclitis with vitreous involvement may alter the ocular media to interfere with light transmission. Both direct and indirect pupillary responses should be evaluated while evaluating the anterior ocular media. Once it has been determined that light can reach the posterior ocular segment, a fundus evaluation should be done. Fundic abnormalities associated with acute visual loss may include acute chorioretinitis, often with exudative retinal detachments; acute choroidal hemorrhages, often associated with abnormal blood pressure in chronic renal disease; and acute optic neuritis.

Acute visual loss in the dog without accompanying fundic lesions that can be seen on ophthalmoscopic examination may be associated with a retrobulbar optic neuritis or with the syndrome of sudden acquired retinal degeneration in the dog (SARDS). SARDS is poorly understood. The syndrome appears to involve middle-aged to old female dogs and there is a breed predilection for the dachshund. The visual loss may first start as a nyctalopia and progress over a period of weeks to complete visual loss. In some cases the visual loss is generalized and acute. Associated systemic signs of polydipsia, polyuria, polyphagia, obesity, and hepatomegaly may be present. Laboratory profiles may show abnormal differentials in the WBC count, elevated liver enzymes, an abnormal response to ACTH stimulation testing, or an abnormal response to low-dose dexamethasone suppression testing. The fundus may appear absolutely normal or early signs of retinal thinning and atrophy may be evident. Differential diagnosis with an optic neuritis is based on electroretinography (ERG) testing in which the ERG response is flat in SARDS but the ERG response is normal in optic neuritis. The cause of SARDS is unknown.

Acute visual loss associated with tumors of the CNS, particularly CNS tumors that involve the optic chiasm, are infrequently reported in the dog. Pituitary tumors are most likely to be the source. Pituitary tumors must become macroadenomas before invading and involving midbrain structures and the optic chiasm region. It is not uncommon for macroadenomas to be nonfunctional; thus, the affected animal may not develop any clinical metabolic abnormalities. Papilledema is rarely observed with brain tumors in dogs. Although pituitary macroadenomas that produce chiasmal compression and visual loss are rare in dogs, the differential diagnosis must still be considered.

The availability of CT has provided the ability to diagnose tumors of the hypophysis that may be associated with acute visual loss. Additionally, the use of the same technique has made visualization of the adrenal glands and the ability to diagnose bilateral adrenal gland hyperplasia easier. Pituitary macroadenomas are larger than 1 cm in diameter.

Optic neuritis may present as an acute visual loss problem. There may or may not be observable ophthalmoscopic changes of the optic nerve. Ophthalmoscopic abnormalities are characterized by edema of the disk, hemorrhages in and around the disk, edema, and inflammation of the surrounding retinal tissue. Acute optic neuritis often persists as a retrobulbar lesion without any ophthalmoscopically observable lesions. Pupils are widely dilated and nonresponsive or poorly responsive to light. In suspected acute optic neuritis, a complete physical examination, including a neurologic evaluation, peripheral blood count, and CSF analysis, should be performed, if possible. The presence of pleiocytosis and increased protein content in the CSF is of significance. It may be difficult to specifically diagnose the cause of acute optic neuritis.

DIAGNOSTIC PLANS (Box 3-26)

BOX 3-26. DIFFERENTIAL DIAGNOSIS FOR THE PATIENT PRESENTED FOR SUDDEN ACQUIRED BLINDNESS.

Ocular Causes

Cornea

Edema (keratitis, herpesvirus-1 recrudescence [cats], corneal dystrophy)

Infection (bacterial, viral, fungal)

Fibrosis

Neovascularization (keratoconjunctivitis sicca-advanced)

Corneal dystrophy (lipid or congenital)

Anterior Chamber

Anterior uveitis-multiple causes

Hyphema

Lens

Cataract

Subluxation

Vitreal Humor

Hemorrhage

Hyalitis (inflmmation associated with infection [FIP], spontaneous bleeding, trauma)

Retinal Injury

Glaucoma

SARD (sudden acquired retinal degeneration syndrome)

Retinal atrophy-progressive or central progressive

Feline central retinal degeneration

Drug–induced (fluoroquinolone administration in cats)

Extraocular Causes

Viral infections (canine distemper, FIP)

Fungal infections (deep mycoses)

Intracranial tumor

Brain trauma

Hydrocephalus

Immune-mediated optic neuritis

Sustained hypoxia

Seizure disorder (postictal, transient blindness)

Heat stroke

Granulomatous meningoencephalitis (GME)

Retinal Detachment

Hypertension, especially in cats with renal failure

Neoplasia

Retinal dysplasia

Congenital detachment (collie eye anomaly)

Infection (FIP)

• 1.Evaluate pupillary light responses and vision by evaluating the animal's vision in an obstacle course and in altered light conditions.
• 2. Perform an ophthalmic examination to evaluate the clarity of the ocular media and the ability of light to reach the photoreceptor cells. Evaluate the posterior ocular segment by performing an ophthalmoscopic examination.
• 3.
  Evaluate the general physical condition of the animal including a basic neurologic examination:

  • a.
    If acute retinal or vitreal hemorrhage is present, determine if the bleeding involves only the eyes or if there is evidence of bleeding elsewhere in the body. Determine if blood pressure is normal and if there is evidence of chronic renal disease, hyperadrenocorticism, or hyperthyroidism.
  • b.
    If active chorioretinitis with or without exudative retinal detachment is present, determine if the inflammation appears granulomatous; if it does, consider systemic fungal infections and consider performing a vitreal or subretinal aspiration and cytologic examination to look for fungal agents. If inflammation is not granulomatous, perform a complete physical examination, CBC, and chemistry panel, and look for evidence of other systemic inflammatory diseases.
  • c.
    If acute visual loss is unaccompanied by any fundus abnormalities, perform a complete physical examination, including a basic neurologic evaluation; if acute retrobulbar optic neuritis is suspected, a CBC and CSF examination should be considered; an ERG may be indicated to distinguish between SARDS and acute optic neuritis.

VOMITING (SEE ALSO REGURGITATION)

DEFINITION

Vomiting: Forceful ejection of food or fluid through the mouth from the stomach and, occasionally, the proximal duodenum. The term applies to those animals with overt evidence of effort associated with the expulsion of food and is characterized by vigorous abdominal pressing, arched back, gagging or retching, and hypersalivation. Projectile vomiting is the term used to describe the violent ejection of stomach contents without nausea or retching. Regurgitation, on the other hand, denotes expulsion of food or fluid from the esophagus and is a considerably more passive act than in vomiting.

Note: Cough-induced gagging associated with tracheitis or tracheobronchitis is often accompanied by the expulsion of mucus from the respiratory tract and can be a forceful act. As such, productive coughs may appear to the owner to be vomiting.

Vomiting is a complex reflex that entails coordination of the GI tract, musculoskeletal system, and nervous system. Although the CNS vomiting center initiates vomiting, it must first be stimulated. Even when vomiting is drug induced, stimulation of the vomiting center is accomplished subsequent to stimulation of a medullary chemoreceptor trigger zone that forwards impulses to the vomiting center. Many sensory nerves can mediate emetic impulses. Therefore, intense pain (especially abdominal); nervous (psychogenic) stimuli; disagreeable odors, tastes, and smells; sensations from the labyrinth and pharyngeal areas; various toxins and drugs; and, presumably, the retention of metabolic waste products all may lead to vomiting. Numerous receptors for vomiting are located in the abdominal viscera, especially the duodenum. Afferent nerve fibers are found in the vagal and sympathetic nerves.

Vomiting can be quite debilitating. When excessive, it causes severe extracellular fluid deficits, particularly of sodium, potassium, and chloride ions and water. Loss of mainly gastric contents results in loss of hydrogen ions, a high serum bicarbonate concentration, and metabolic alkalosis. Vomited material from the proximal intestinal tract contains high concentrations of bicarbonate.

Clinically, vomiting should be addressed as a problem that originates from the GI tract (primary causes) or from causes outside the GI tract (i.e., metabolic causes [secondary]).

ASSOCIATED SIGNS

Depending on the underlying cause, vomiting may be associated with a number of significant clinical signs. Primary causes of vomiting are generally associated with other GI signs, such as diarrhea, abdominal pain, obvious foreign bodies (e.g., a linear foreign body entrapped proximally under the tongue), ingestion of known irritant materials or drugs, hematochezia, or palpable abdominal tumors. Animals with metabolic or secondary causes of vomiting may appear lethargic, anorectic, and weak, particularly when the vomiting episodes have been sustained for several days. In some animals, polyuria or polydipsia, anuria, icterus, cough, and anemia are present.

DIFFERENTIAL DIAGNOSIS (Box 3-27)

BOX 3-27. DIFFERENTIAL DIAGNOSIS OF VOMITING.

Infectious Causes

Feline panleukopenia virus infection

Canine parvovirus infection

Canine coronavirus infection

Infectious canine hepatitis

Leptospirosis

Bacterial enteritis

Parasitic enteritis

Heartworm disease (cats)

Inflammatory

Pyometra

Prostatitis

Peritonitis

Acute pancreatitis

Gastritis and enteritis

Gastric ulcers

Obstructive Causes

Intestinal foreign body

Gastrointestinal neoplasia

Gastric dilation–volvulus syndrome

Pyloric stenosis

Trichobezoar (hairballs)

Diaphragmatic hernia

Metabolic Causes

Renal failure (uremia)

Hepatic disease

Diabetic ketoacidosis

Hypoadrenocorticism (Addison's disease)

Hypokalemia, regardless of cause

Hyperthyroidism (cats)

Chemical Causes

Heavy metals, pesticides, solvents

Digitalis, salicylates, mebendazole, penicillamine, chloramphenicol, morphine, antineoplastic drugs, others

Idiopathic/Miscellaneous Causes

Psychogenic, vestibular (car sickness)

Overconsumption of food, especially in puppies

Various CNS diseases

Bilious vomiting syndrome

Autonomic epilepsy

Constipation/obstipation

Ileus, paralytic

 

DIAGNOSTIC PLANS

• 1.Verification that the patient is vomiting, not gagging or retching subsequent to tracheal disease. Determine duration, precipitating causes, and current drug therapy. Assess associated signs.
• 2.Laboratory database, fundamental to the diagnostic plan. It must include CBC, biochemistry profile, urinalysis, and fecal flotation. Cats should also be tested for heartworm disease, FeLV, FIV, and hyperthyroidism. Perform serologic studies, as needed, to rule out systemic infections (e.g., systemic mycoses).
• 3.Radiographs of the thorax and abdomen; abdominal ultrasound.
• 4.Contrast radiographic studies of the stomach and small bowel (e.g., barium series).
• 5.Exploratory laparotomy, depending on patient condition.
• 6. Special diagnostic procedures: endoscopy, GI biopsy, double-contrast studies of the stomach and small bowel, and gastric motility studies (fluoroscopy).

VOMITING BLOOD: HEMATEMESIS (SEE ALSO VOMITING)

DEFINITION

Hematemesis: The vomiting of blood. An uncommon presentation in the dog and particularly rare in the cat. Although the presence of blood in the vomitus is, by strict definition, hematemesis, repeated episodes of vomiting in which the vomitus is composed of large blood clots, frank, uncoagulated blood, or the so-called coffee-ground appearance of blood denatured by gastric acid represents a serious clinical finding.

ASSOCIATED SIGNS

Hematemesis does not localize the diagnosis to the stomach or GI tract. Since a variety of metabolic and coagulation disorders may result in severe hematemesis, a wide spectrum of physical signs may also be present in affected animals. In addition, blood emanating from the upper respiratory tract may be swallowed and, subsequently, vomited, giving the appearance that bleeding is from the stomach.

Anorexia and vomiting are the most common associated, but nonspecific, signs. Weight loss, weakness, dark stool (melena), dehydration, and inactivity are other related signs having low diagnostic yield. Severe anemia can result from sustained gastric hemorrhage and, if acute, may justify exploratory laparotomy to identify the source of the bleeding.

Increased water consumption and urination may suggest underlying renal or hepatic disease. Intracutaneous or subcutaneous tumors, specifically mast cell tumors, can be associated with severe gastric ulceration and bleeding. Ulcerative lesions in the mouth may indicate recent ingestion of caustic or toxic compounds. The frenulum in the mouth should always be examined to rule out linear foreign bodies.

DIFFERENTIAL DIAGNOSIS (Table 3-7)

TABLE 3-7.

Differential Diagnosis of Hematemesis

Primary gastric disorders		Systemic metabolic disorders
Gastritis		Acute pancreatitis
	Infectious (e.g., parvovirus)	Adrenocortical insufficiency (Addison's disease)
	Toxic
	Bile reflux-bilious vomiting syndrome	Toxins (e.g., lead, ethylene glycol)
	Foreign body	Hepatic failure
Gastric ulcers		Renal failure
	Drug-induced (e.g., aspirin)	Neoplasia
	Idiopathic
	Metabolic (e.g., renal failure)
	Neoplastic

 

DIAGNOSTIC PLANS

• 1.
  Comprehensive history. This is critical and should focus on the following:

  • a.
    Recent medications administered, both prescription and nonprescription.
  • b.
    Known and potential exposure to toxic or poisonous substances.
  • c.
    Duration of the primary and associated signs.
  • d.
    Physical appearance of the vomitus.
  • e.
    Physical status of other pets in the family, if applicable.
• 2.Laboratory profile, including, as a minimum, hematologic values, particularly in anemic patients; biochemistry findings; urinalysis; and fecal flotation. Emphasis should be placed on renal, adrenal, and hepatic function.
• 3.Testing of feces for the presence of parvovirus antigen.
• 4.Activated coagulation time (ACT). A coagulation panel—including partial thromboplastin time (PTT), prothrombin time (PT), fibrin degradation products (FDPs), fibrinogen, and total platelet count—is indicated as appropriate.
• 5.Fine-needle aspiration of any intracutaneous or subcutaneous tumors.
• 6.Abdominal and thoracic radiographs; abdominal ultrasound.
• 7.Gastroscopy and esophagoscopy.
• 8.Exploratory laparotomy and gastrotomy.

NOTE: In patients with severe hematemesis, surgery may be indicated before obtaining results from the laboratory profile.

WEIGHT LOSS: EMACIATION/CACHEXIA

DEFINITION

Emaciation: A serious, usually chronic and progressive condition characterized by significant (>20%) body weight loss. Cachexia is the termed used to describe the end stage of emaciation. Significant weight loss, associated with emaciation or cachexia, typically results from catabolism of body fat and protein in excess of caloric intake. Increased metabolism (hypermetabolic), inadequate consumption or assimilation of nutrient, or excessive nutrient loss contributes to significant weight loss.

ASSOCIATED SIGNS

The clinical history should center on diet, appetite, and known health status (i.e., evidence of vomiting, diarrhea, etc). The duration of time over which the owner perceives weight loss occurring is important. Emaciation developing within a month (e.g., neoplasia) may carry a poorer prognosis than animals with emaciation developing over several months. The physical examination should focus on the presence of fever, gastrointestinal disease, and overt changes in size and consistency of internal organs.

DIFFERENTIAL DIAGNOSIS

A spectrum of differential diagnoses must be considered in the patient that presents with emaciation or cachexia. Several categories of illness should be considered evaluating patients with emaciation/cachexia associated with the following:

• Malnutrition. Quality and quantity of food, availability of food, evidence of neglect/abuse.

• Polyphagia. Malassimilation (i.e., either maldigestion or malabsorption), hypermetabolic states (e.g., hyperthyroidism, pregnancy), excessive nutrient losses (e.g., diabetes mellitus, glomerulonephropathy).

• Anorexia. Infectious diseases, neoplasia, neurologic disease, toxicity (e.g., chronic lead poisoning), dental disease (pseudoanorexia).

• Gastrointestinal signs. Malassimilation (i.e., either maldigestion or malabsorption); parasitism.

• Urinary tract signs. Excess renal loss of fluid and nutrients (polyuric states).

• Fever. Infectious diseases.

DIAGNOSTIC PLANS (Figure 3-6)

Figure 3-6.

Differential diagnosis of weight loss/cachexia.

(From Greco DS: Cachexia. In Ettinger SJ, Feldman EC, editors: Textbook of veterinary internal medicine, ed 5, Philadelphia, 2000, WB Saunders, pp. 72-74.)

 

YELLOW SKIN OR MUCOUS MEMBRANES: ICTERUS (OR JAUNDICE)

DEFINITION

Icterus, or jaundice: Yellow discoloration of tissue (especially skin, mucous membranes, and sclera) caused by an increased serum concentration of bilirubin. Is indicative of underlying hepatocellular disease or intravascular hemolytic disease. Hyperbilirubinemia is required for icterus to develop but may not occur concurrently with icterus.

In practice, icterus is an uncommon presenting complaint, since the dense hair coat of cats and dogs precludes early detection of bile pigment in skin. Icteric tissues are most evident in the sclera and in the oral, vaginal, and preputial mucous membranes, particularly in anemic patients. Icterus can occur subsequent to the accumulation of either unconjugated (lipid-soluble) or conjugated (water-soluble) bilirubin in the blood.

Icterus can originate at any of three levels: prehepatic (hemolytic disease), hepatic (hepatocellular disease), posthepatic (obstructive or reduced bile flow).

Unconjugated hyperbilirubinemia results from rapid hemolysis (a common cause in the dog and cat), ineffective erythropoiesis, impaired hepatic uptake of conjugated bilirubin, or impaired conjugation. Conjugated (water-soluble) hyperbilirubinemia is generally the result of disorders intrinsic to the liver that affect bilirubin transport. Cholestatic disease is associated with reduced bile flow and can be characterized by significant bile acidemia and icterus.

ASSOCIATED SIGNS

Icterus can be detected in a dog or cat without overt clinical signs; however, RBC values and hepatic function should be assessed. Prehepatic icterus is characteristically associated with rapid-onset anemia and with generalized weakness, lassitude or acute collapse (caval syndrome), and bright orange urine. Pallor can be difficult to assess in patients with marked icterus. Hepatic icterus and posthepatic icterus are generally associated with lethargy and decreased appetite and are therefore difficult to distinguish clinically. Depending on the type of hepatic injury or the level of obstruction, episodic vomiting or diarrhea, weight loss, abdominal distention, polyuria or polydipsia, peripheral edema associated with hypoproteinemia, and prolonged bleeding (uncommon) may be reported.

DIFFERENTIAL DIAGNOSIS (Box 3-28)

BOX 3-28. DIFFERENTIAL DIAGNOSIS OF ICTERUS.

Prehepatic (Hemolytic)

Immune-mediated hemolytic anemia (Coombs'-positive anemia)

Heartworm disease, especially postcaval syndrome

Hemolytic septicemia

Transfusion-induced hemolysis

Hepatic (Hepatocellular)

Cholangitis/cholangiohepatitis

Chronic active liver disease

Copper storage disease (Bedlington terriers and Doberman pinschers)

Drug-induced/vaccine-induced

• Thiacetarsamide–sporadic occurrence

• Imidazole anthelmintics–sporadic occurrence

• Anticonvulsants, especially primidone

• Acetaminophen/methylene blue (in cats)

Hepatic fibrosis

Septicemia

• Gram-negative bacteremia

• Leptospirosis

Viral

• Canine viral hepatitis

• Feline leukemia

• Feline infectious hepatitis

Neoplasia, primary or metastatic

Posthepatic (Obstructive)

Cholangitis/cholangiohepatitis

Hepatic fibrosis

Neoplasia

Acute pancreatitis

Extrahepatic neoplasm (by compression)

Bile duct trauma

Ruptured gallbladder (usually traumatic)

Cholelithiasis

 

DIAGNOSTIC PLANS

• 1.Thorough history. This should focus on current and previous drug therapy, including heartworm preventative, as well as duration of illness and associated signs. Physical examination confirms the presence of icterus but is unlikely to reveal the underlying cause. Abdominal palpation may reveal hepatomegaly, a discrete mass, or the presence of fluid.

In obviously anemic patients, when practical, transfusion should be avoided until laboratory test results have been interpreted.

• 2.Laboratory evaluation of the icteric patient. This is essential and should initially include a CBC, biochemistry panel (to include total and direct bilirubin), fecal analysis, urinalysis, heartworm test (in dogs), serum electrophoresis (in cats), and a test for FeLV antigen and FIV antibody.
• 3. Anemic patient. Coombs' test; ANA titer; peripheral blood smear for the presence of parasites; blood cultures, particularly if the patient is febrile; and IFA test on bone marrow for FeLV antigen (in cats).
• 4.Nonanemic patient. Abdominal radiographs, abdominocentesis with fluid analysis and cytologic study, fine-needle aspiration of liver, plasma ammonia, bile acids, serum amylase, and lipase if not included in the biochemistry panel.
• 5.Special diagnostic tests. Coagulation profile, followed by liver biopsy (percutaneous or at laparotomy) or exploratory celiotomy with biopsy.
• 6.Abdominal ultrasound, CT, and perfusion scintigraphy (special facilities required).

Additional Reading

Ettinger SJ, Feldman EC (editors): Textbook of veterinary internal medicine, ed 6, vol 1, Section 1: Clinical manifestations of disease. St. Louis, 2005, Elsevier Saunders, pp. 1-240.

Grauer GF: Clinical manifestations of urinary disorders. In Nelson RW, Couto CG, editors: Small animal internal medicine, ed 3, St. Louis, 2003, Mosby, pp. 568-583.

Guilford WG, Center SA, Strombeck DR, et al: Strombeck's small animal gastroenterology, ed 2, Philadelphia, 1996, WB Saunders.

Hawkins EC: Respiratory system disorders. In Nelson RW, Couto CG, editors: Small animal internal medicine, ed 3, St. Louis, 2003, Mosby, pp. 210-343.

Tams TR: Gastrointestinal symptoms. In TR Tams, editor: Handbook of small animal gastroenterology, ed 2, St. Louis, 2003, Saunders, pp. 1-50.

Ware WA: The cardiovascular examination. In Nelson RW, Couto CG, editors: Small animal internal medicine, ed 3, St. Louis, 2003, Mosby, pp. 1-11.