Lymphadenopathy

Outline

BASICS

Overview

Disease of LNs that may be local, regional, or generalized; primary or secondary; and usually results in LN enlargement
Enlargement can be due to benign (lymphoid hyperplasia, lymphadenitis) or malignant (primary or metastatic neoplasia) causes

Signalment

Lymphoid pharyngeal hyperplasia and enlarged LNs of the anorectal region are common in young horses.

Signs

History and clinical signs depend on underlying cause and location of enlarged LNs
History may include previous or current signs of infection, wounds, and vaccination for strangles
Peripheral LNs most accessible for examination are mandibular and superficial cervical
Infected LNs may be enlarged, warm, soft, painful on palpation, and draining purulent material
Neoplastic LNs may be enlarged, firm, and often not warm or sensitive to palpation
Mandibular and retropharyngeal lymphadenopathy may cause anorexia, dysphagia, and airway obstruction; enlarged internal LNs may cause obstruction of the pharynx, esophagus, trachea, bronchi, and intestine with dyspnea, anorexia, reflux, pleural effusion, ascites, diarrhea, or other signs of organ dysfunction; dyschezia, abdominal pain, and urinary dysfunction if anorectal LNs are involved
Nonspecific signs include elevated rectal temperature, signs of depression, anorexia, weight loss, pale mucous membranes, tachypnea, and tachycardia

Causes and Risk Factors

Lymphoid hyperplasia is caused by immune stimulation associated with regional immunity of a nearby pathologic process; lymphadenitis by inflammation/infection within the LN itself (primary) or drainage of purulent site (secondary); neoplasia may be primary lymphoid neoplasia (lymphoma) or metastatic spread (e.g. melanoma, leukemia)
Risk factors include lymphoid hyperplasia—intranasal modified-live strangle vaccines; lymphadenitis—recent introduction of new horses, exposing horses to infected animals (e.g. during competition), or transporting naive horses to areas with endemic disease
Range of infectious agents associated with localized or generalized lymphadenitis

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis

If LN enlargement is primary presenting sign, lymphoid hyperplasia, lymphadenitis (primary or secondary), or neoplasia must be differentiated
If nonspecific signs, due to involvement of other body systems, are primary presenting signs, appropriate and thorough investigation of these signs is warranted

CBC/Biochemistry/Urinalysis

Variable depending on cause of LN enlargement and LNs involved
Inflammatory leukogram if lymphoid hyperplasia and lymphadenitis
Rarely, neoplastic lymphocytes in peripheral blood with lymphosarcoma cell leukemia or leukemic phase of lymphoma

Other Laboratory Tests

Cytologic evaluation of LN aspirates, blood, bone marrow, or fluids; histologic evaluation of biopsies can confirm underlying cause if cytology is equivocal
Culture of aspirate if lymphadenitis present
Serology for infectious agents
Serum protein electrophoresis if neoplastic LN and marked hyperglobulinemia

Imaging

Ultrasonography to assess size, detect fluid and infiltrative disease, and allow for guided biopsy.

Other Diagnostic Procedures

Rectal palpation to evaluate accessible internal LNs.

Pathologic Findings

Lymphoid hyperplasia—variable population of normal lymphocytes, including numerous germinal centers and plasma cells
Lymphadenitis—increased proportions of inflammatory cells, including neutrophils, macrophages, or eosinophils depending on cause and chronicity of process
Lymphoid neoplasia (lymphosarcoma)—abnormal lymphocytes among reactive normal lymphocytes; alternatively, the cells in metastatic neoplasia reflect the primary neoplasm

Treatment ⬆ ⬇

TREATMENT