Lymphadenitis

Reading File

Finding Sources

Searching PubMed

lymphadenitis diagnosis management

Reading File

Loading Image

I now have excellent content from multiple authoritative sources. Let me compile a comprehensive answer.

Lymphadenitis

Lymphadenitis is inflammation of lymph nodes, resulting from immune activation by infectious or inflammatory stimuli. It is classified as acute or chronic, and further as nonspecific (reactive) or specific (granulomatous, etc.).

Normal Lymph Node Physiology (Background)

Lymph nodes are discrete encapsulated structures containing separate B-cell zones (cortical follicles) and T-cell zones (paracortex), richly supplied with phagocytes and antigen-presenting cells. On antigenic stimulation, primary follicles enlarge to form secondary follicles with pale germinal centers within days. Lymph nodes in adults are almost never truly "resting," making it necessary to distinguish past residual changes from active disease.

Robbins & Cotran Pathologic Basis of Disease

1. Acute Nonspecific Lymphadenitis

Causes

Cervical region: drainage from dental or tonsillar infections (Streptococcus, Staphylococcus, Actinomycosis)
Axillary / inguinal: infections of the extremities
Mesenteric: acute appendicitis, inflammatory gut conditions, self-limiting viral infections
Generalized: systemic viral infections (especially in children) and bacteremia

Morphology

Nodes are swollen, gray-red, and engorged
Microscopically: enlarged reactive germinal centers with numerous mitotic figures
Macrophages contain particulate debris from dead bacteria/necrotic cells
Pyogenic organisms → neutrophilic infiltration, follicle center necrosis, possible conversion of entire node to pus
Activated, enlarged endothelial cells line the sinuses
With abscess formation: nodes become fluctuant, overlying skin becomes red
Suppurative infections may track through the capsule to form draining sinuses
Healing may leave residual scarring

Follicular hyperplasia in reactive lymphadenitis. (A) Low-power: reactive follicle with surrounding mantle zone - dark zone on right, light zone on left. (B) High-power: germinal center dark zone showing mitotic figures and tangible body macrophages with phagocytosed apoptotic cells.

Fig. 13.3 - Follicular hyperplasia in reactive lymphadenitis. Robbins & Cotran Pathologic Basis of Disease.

Clinical Features

Enlarged, tender nodes
Systemic: pyrexia, anorexia, malaise
Fluctuance when abscess formation is extensive

Treatment

Directed at the primary focus of infection (e.g., treat tonsillitis or dental abscess)

2. Chronic Nonspecific Lymphadenitis

Various chronic immunological stimuli produce three distinct histological patterns (often coexisting):

Pattern	Mechanism	Causes	Histology
Follicular hyperplasia	Humoral immune activation	Rheumatoid arthritis, toxoplasmosis, early HIV	Large oblong secondary follicles with polarized germinal centers (dark zone of centroblasts + light zone of centrocytes); tangible body macrophages
Paracortical hyperplasia	T-cell mediated	Acute viral infections (e.g., EBV/infectious mononucleosis)	Expanded T-cell zones with immunoblasts (3-4x size of resting lymphocytes), can efface B-cell follicles
Sinus histiocytosis	Sinusoidal macrophage proliferation	Lymph nodes draining cancers (e.g., breast carcinoma)	Increased endothelial cells and intrasinusoidal macrophages distending sinusoids

Distinguishing reactive hyperplasia from follicular lymphoma:

Preserved lymph node architecture (T-cell zones, sinusoids intact)
Marked variation in follicle shape/size
Frequent mitotic figures, phagocytic macrophages, and recognizable light/dark zones (all tend to be absent from neoplastic follicles)

3. Specific (Granulomatous) Lymphadenitis

TB Lymphadenitis (Scrofula)

This is the most common form of extrapulmonary TB.

Epidemiology:

Most common in young women and children
In the USA, scrofula is more often caused by non-tuberculous mycobacteria than M. tuberculosis
More common in HIV-coinfected individuals (tends to be generalized in HIV+)
Pulmonary disease coexists in only a minority of isolated TB lymphadenitis cases

Clinical features:

Painless, enlarging, firm, red mass - most commonly anterior/posterior cervical chain or supraclavicular fossa
Early: discrete, rubbery, freely mobile nodes with normal overlying skin
Late: matted, harder nodes with inflamed skin; fluctuance, abscess, or sinus tract if node erodes through skin
Systemic symptoms (fever, night sweats) uncommon in immunocompetent patients

Secondary effects by nodal location:

Intrathoracic adenopathy → bronchial compression, upper airway obstruction
Intrathoracic/intraabdominal nodes → chylothorax, chylous ascites (from lymphatic disruption)

Diagnosis:

Fine-needle aspiration (FNA) of the affected node is the preferred method
- AFB smear: positive in only ~20% of cases
- Granulomatous inflammation may be apparent on cytology
- FNA sensitivity 77%, specificity 93% for TB

Treatment:

First-line: standard anti-tuberculous drug therapy
Surgical excision: reserved for failure of medical therapy or diagnostic uncertainty
Incision and drainage is contraindicated - results in permanent sinuses and prolonged drainage

4. Filarial Lymphadenitis (Special Form - Acute Retrograde)

Seen in endemic areas (bancroftian/Malayan filariasis), caused by dying adult worms.

Inguinal lymphadenitis most common; painful, with overlying skin erythema
Precedes lymphangitis; accompanied by fever and chills
Episodes last ~1 week, frequently recur
Can be complicated by epididymitis, orchitis in men
Repeated episodes → lymphatic vessel dilation → chronic lymphedema (elephantiasis)

Causes of Cervical Lymphadenopathy - Summary

Category	Examples
Reactive hyperplasia	Non-specific stimuli
Viral	Infectious mononucleosis (EBV), HIV
Bacterial	Streptococcus, Staphylococcus, actinomycosis, TB, brucellosis
Protozoan	Toxoplasmosis
Primary malignancy	Lymphoma (Hodgkin and non-Hodgkin)
Metastatic malignancy	Squamous cell carcinoma (common in older adults), other carcinomas

Key Differentiating Points

Feature	Acute Bacterial	Reactive (Viral)	TB	Lymphoma
Pain	Tender	Mild tenderness	Painless	Painless
Consistency	Soft/fluctuant	Rubbery	Firm, matted	Rubbery/"rubbery-hard"
Skin changes	Erythema	None	May perforate	None
Systemic	Fever, malaise	Pharyngitis, rash	Rare (unless HIV+)	B-symptoms (drenching sweats, weight loss, fever)
Treatment	Antibiotics	Supportive	Anti-TB drugs	Chemotherapy/radiotherapy

Sources: Robbins & Cotran Pathologic Basis of Disease, p.552 | Robbins & Kumar Basic Pathology | Rosen's Emergency Medicine | Goldman-Cecil Medicine | Bailey and Love's Short Practice of Surgery, 28th Ed.

This is a shared conversation. Sign in to Orris to start your own chat.