Exposure to antigen through a break in the skin or mucosa results in antigen being taken up by an antigen-presenting cell and carried via lymphatic channels to the nearest lymph node. Lymph channels course throughout the body except for the brain and the bones. Lymph enters the node through the afferent vessel and leaves through an efferent vessel. Because antigen-presenting cells pass through lymph nodes, they present antigen to lymphocytes residing there. Lymphocytes in a node are constantly being replaced by antigen-naïve lymphocytes from the blood. They are retained in the node via special homing receptors. B cells populate the lymphoid follicles in the cortex; T cells populate the paracortical regions. When a B cell encounters an antigen to which its surface immunoglobulin can bind, it stays in the follicle for a few days and forms a germinal center where the immunoglobulin gene is mutated in an effort to make an antibody with higher affinity for the antigen. The B cell then migrates to the medullary region, differentiates into a plasma cell, and secretes immunoglobulin into the efferent lymph.
When a T cell in the node encounters an antigen it recognizes, it proliferates and joins the efferent lymph. The efferent lymph laden with antibodies and T cells specific for the inciting antigen passes through several nodes on its way to the thoracic duct, which drains lymph from most of the body. From the thoracic duct, lymph enters the bloodstream at the left subclavian vein. Lymph from the head and neck and the right arm drains into the right subclavian vein. From the bloodstream, the antibody and T cells localize to the site of infection.
Lymphadenopathy may be caused by infections, immunologic diseases, malignancies, lipid storage diseases, or other disorders of uncertain etiology (e.g., sarcoidosis, Castleman's disease; Table 46-1 Diseases Associated with Lymphadenopathy). The two major mechanisms of lymphadenopathy are hyperplasia, in response to immunologic or infectious stimuli, and infiltration, by cancer cells or lipid- or glycoprotein-laden macrophages.
| APPROACH TO THE PATIENT | ||
LymphadenopathyHistoryAge, occupation, animal exposures, sexual orientation, substance abuse history, medication history, and concomitant symptoms influence diagnostic workup. Adenopathy is more commonly malignant in origin in those over age 40 years. Farmers have an increased incidence of brucellosis and lymphoma. Male homosexuals may have AIDS-associated adenopathy. Alcohol and tobacco abuse increase risk of malignancy. Phenytoin may induce adenopathy. The concomitant presence of cervical adenopathy with sore throat or with fever, night sweats, and weight loss suggests particular diagnoses (mononucleosis in the former instance, Hodgkin's disease in the latter). Physical ExaminationLocation of adenopathy, size, node texture, and the presence of tenderness are important in differential diagnosis. Generalized adenopathy (three or more anatomic regions) implies systemic infection or lymphoma. Subclavian or scalene adenopathy is always abnormal and should be biopsied. Nodes >4 cm should be biopsied immediately. Rock-hard nodes fixed to surrounding soft tissue are usually a sign of metastatic carcinoma. Tender nodes are most often benign. Laboratory TestsUsually laboratory tests are not required in the setting of localized adenopathy. If generalized adenopathy is noted, an excisional node biopsy should be performed for diagnosis, rather than a panoply of laboratory tests. |
| TREATMENT | ||
LymphadenopathyPts over age 40 years, those with scalene or supraclavicular adenopathy, those with lymph nodes >4 cm in diameter, and those with hard nontender nodes should undergo immediate excisional biopsy. In younger pts with smaller nodes that are rubbery in consistency or tender, a period of observation for 7-14 days is reasonable. Empirical antibiotics are not indicated. If the nodes shrink, no further evaluation is necessary. If they enlarge, excisional biopsy is indicated. |
Section 3. Common Patient Presentations