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Lymphadenopathy

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  1. Read book excerpt
  2. Lymphadenitis: Introduction
  3. Latest treatments
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  5. Lymphadenitis Overview
  6. More book excerpts for Lymphadenitis

Lymphadenopathy: Excerpt from The Diagnostic Approach to Symptoms and Signs in Pediatrics

  • Normal lymphnodes are discrete, nontender, and mobile without fixation to underlyingtissues. Normally palpable in cervical, axillary, and inguinal regions.
  • Bamji et al. (1986) reported that normallymph nodes have diameter of 3–12 mm in neonatal periodand 3–16 mm in infants up to 1 yr of age.
  • Barness (1998) noted that cervicaland inguinal lymph nodes up to 1 cm in diameter are normal in childrenup to 12 yrs of age. Larger lymph nodes in these and other areasare abnormal.
  • Lymphadenopathy may be localized (enlargedlymph node or nodes in single area) or generalized (enlarged lymphnodes in 2 or more noncontiguous areas).

    • Principal Causes of Localized Lymphadenopathy

    1. Localizedlymphadenopathy
      1. Cervical
      2. Submandibular/submental
      3. Preauricular
      4. Postauricular
      5. Occipital
      6. Supraclavicular
      7. Axillary
      8. Epitrochlear
      9. Inguinal
      10. Femoral
      11. Popliteal

    Clinical Features and Diagnosis: Localized Lymphadenopathy

    Cervical

  • Cervicallymph nodes, which drain head and neck structures, include superficialand deep cervical chains.
  • Reactive hyperplasia (usually secondaryto viral upper respiratory infections [URIs] and pharyngitis)and cervical adenitis are most common causes of cervical node enlargement.Less common causes include Kawasaki disease and neoplastic disorders(leukemia, Hodgkin disease, non-Hodgkin lymphoma, neuroblastoma,rhabdomyosarcoma, thyroid carcinoma).
  • See Chap.42, Neck Masses.

    • Submandibular/Submental

  • Submandibularnodes drain buccal mucosa, side of nose, gums, upper lip, lateralpart of lower lip, and anterior part of tongue margin.
  • Submental nodes drain center portionsof lip and floor of mouth as well as skin of chin.
  • Reactive hyperplasia (viral URIs, pharyngitis,tonsillitis, herpetic gingivostomatitis, dental abscesses) and primaryadenitis (usually secondary to pyogenic infection with group A Streptococcusor S. aureus) are most common causes of lymph node enlargement inthese areas.

    • Preauricular

  • Preauricularnodes drain anterior and temporal regions of scalp, anterior aspectof external auditory canal, pinna, and lateral conjunctivae.
  • Causes of preauricular adenopathy includeoculoglandular syndrome (conjunctivitis and ipsilateral preauricularadenopathy), adenoviral infection (epidemic keratoconjunctivitis,pharyngoconjunctival fever), cat scratch disease (B. henselae infection),and tularemia.

    • Postauricular

  • Postauricularnodes drain temporal and parietal scalp, posterior wall of externalauditory canal, and upper half of pinna.
  • Causes of node enlargement are infectionsof scalp and infections caused by human herpesviruses 6 and 7, rubellavirus, and parvovirus B19.

    • Occipital

  • Occipitalnodes drain occipital region of scalp.
  • Common causes of occipital adenopathyare tinea capitis, seborrheic dermatitis, and scalp cellulitis/abscess.
  • Isolated adenopathy in this area mayoccur secondary to rubella infection and toxoplasmosis.

    • Supraclavicular

  • Supraclavicularnodes are located in supraclavicular triangle and drain entire head andneck, arms, superficial thorax, abdomen, lungs, and mediastinum.
  • Enlarged nodes without other cervicaladenopathy suggest mediastinal, lung, or abdominal disease, whichcan be infectious, inflammatory, or neoplastic.
  • Chest radiography may demonstrate enlargedmediastinal nodes, and chest CT can define location and extent.
  • Common causes of supraclavicular andmediastinal adenopathy include histoplasmosis, tuberculosis, catscratch disease, Hodgkin disease, non-Hodgkin lymphoma, and sarcoidosis.

    • Axillary

  • Axillarylymph nodes drain arm, chest wall, and upper lateral abdominal wall.Any local inflammation or infection in these areas may cause lymphnode enlargement.
  • Enlarged tender nodes may occur withcat scratch disease after bite or scratch by kitten or cat to fingers,hand, or forearm.
  • Rapid enlargement of firm, painlesslymph node in axilla with no identifiable inflammatory or infectiouscause suggests neoplastic process (e.g., Hodgkin disease or non-Hodgkinlymphoma). In this circumstance, lymph node biopsy is diagnostic.

    • Epitrochlear

  • Epitrochlearnodes drain distal arm and third, fourth, and fifth fingers.
  • Common causes of epitrochlear adenopathyare staphylococcal and streptococcal skin infections, infectiousmononucleosis, and cat scratch disease. Hodgkin disease also maypresent with enlarged epitrochlear nodes.

    • Inguinal

  • Inguinalnodes drain skin of lower extremities, penis, scrotum, perineum,gluteal region, and abdominal wall below umbilicus.
  • Most common cause of inguinal adenopathyis skin infection involving lower extremities. Genital infections(herpes simplex, lymphogranuloma venereum, chancroid, primary syphilis)also may cause enlarged inguinal nodes. Other causes of inguinaladenopathy include testicular tumors, metastatic lower extremitybone tumors, Hodgkin disease, cat scratch disease, and mycobacterialinfection.

    • Femoral

    Enlarged femoral nodes are palpable on legbelow inguinal ligament and may enlarge secondary to superficialor deep infection of lower extremity.

    Popliteal

  • Poplitealnodes drain knee joint and skin of lateral side of lower leg and foot.
  • Common cause of enlarged poplitealnodes are infections of lower leg, foot, or knee joint.

    • Principal Causes of Generalized Lymphadenopathy

    1. Generalizedlymphadenopathy
      1. Infection
        1. Viral
        2. Bacterial
        3. Fungal
        4. Parasitic
      2. Neoplasia
        1. Leukemia
        2. Hodgkin disease
        3. Non-Hodgkin lymphoma
        4. Neuroblastoma
      3. Histiocytoses
        1. Class I (Langerhans histiocytosis)
        2. Class II histiocytoses
          1. Familialerythrophagocytic lymphohistiocytosis
          2. Infection-associated hemophagocyticsyndrome
          3. Sinus histiocytosis with massive lymphadenopathy
          4. Histiocytic necrotizing lymphadenitis(Kikuchi-Fujimoto disease)
        3. Class III histiocytoses
      4. Lymphoproliferative disorders
      5. Immunodeficiency diseases
      6. Collagen vascular diseases
      7. Storage diseases
      8. Sarcoidosis
      9. Drugs
      10. Serum sickness
      11. Reactive hyperplasia

    Clinical Features and Diagnosis: Generalized Lymphadenopathy

    Most common causes are infection, neoplasia,and reactive hyperplasia.

    Infection

    Viral

  • Viral infectionsmay produce generalized adenopathy.
  • Postauricular and occipital adenopathyoften occur with rubella, rubeola, and human herpesvirus 6.
  • Bilateral cervical, axillary, and inguinaladenopathy is frequently seen with Epstein-Barr virus (EBV) andcytomegalovirus infections.
  • Generalized adenopathy often occurswith HIV infection.

    • Bacterial

  • Generalizedadenopathy may occur with septicemia caused by S. aureus, S. pneumoniae,group A Streptococcus, H. influenzae type b, and gram-negative entericbacteria. These children are ill appearing and have fever. Positiveblood culture is diagnostic.
  • Tuberculosis, brucellosis, tularemia,and leptospirosis also may cause generalized adenopathy.

    • Fungal

  • Pulmonaryhistoplasmosis may produce cough, respiratory distress, and hilaradenopathy. Clinical manifestations of disseminated disease includefever, generalized adenopathy, hepatosplenomegaly, endocarditis,and pericarditis.
  • Coccidioidomycosis is most common inSan Joaquin Valley of California. Inhalation of airborne sporesproduces this infection, and hilar adenopathy is prominent finding.Generalized adenopathy, skin abscesses, osteomyelitis, and meningitismay occur with disseminated disease.
  • See Chap.10, Cough.

    • Parasitic

  • Common presentationof toxoplasmosis is localized or generalized adenopathy, sometimesassociated with fever and malaise.
  • Ingestion of poorly cooked meat thatcontains cysts or accidental ingestion of oocysts in contaminatedfood transmit infection.
  • Atypical lymphocytes may be seen onblood smear. Presence of T. gondii–specific IgM antibodies,4-fold rise in specific IgG antibody titer, or biopsy of node withidentification or culture of organism is diagnostic.

    • Neoplasia

    Leukemia

  • Most commonform of cancer in childhood. Always disseminated at time of diagnosis andmay affect any organ system.
  • 2 major types occur: acute lymphoblasticleukemia (ALL), which accounts for about 80% of childhoodleukemia, and acute myeloid leukemia (AML).
  • Clinical presentations of ALL and AML,which are similar, vary from acute, often explosive onset to moreinsidious one. Clinical manifestations include fatigue, pallor,fever, purpura, bone or joint pain, lymphadenopathy, and hepatosplenomegaly.
  • CBC usually reveals anemia, thrombocytopenia,and abnormal leukocyte and differential counts. Leukocyte countsrange from 102 to 106/mm3,often with absolute granulocytopenia. Blood smear may show many blasts;however, many children with ALL have low leukocyte counts and noblasts. Bone marrow aspirate or biopsy confirms diagnosis.
  • Next step is to determine specifictype of leukemia, but this is beyond the scope of this discussion.

    • Hodgkin Disease

  • Usuallyaffects adolescents and young adults. Rare before 5 yrs of age.
  • Progressive painless enlargement ofcervical or supraclavicular nodes is characteristic. Mediastinalnodes also may be enlarged. Fever, night sweats, and weight lossmay be noted at time of presentation but occur in <50% ofcases.
  • With localized disease, CBC may benormal. With more extensive disease, hepatosplenomegaly, anemia,and either neutrophilic leukocytosis or lymphopenia may occur.
  • Lymph node biopsy is diagnostic.

    • Non-Hodgkin Lymphoma

  • Usual manifestationis painless enlargement of lymph nodes in cervical or supraclavicularchains. However, this disease also may arise in tonsils, adenoids,sinuses, mediastinum, abdomen, or other peripheral lymph nodes.
  • Generalized adenopathy suggests bonemarrow involvement. Other findings include fever, malaise, and anorexia.
  • Biopsy of involved lymph node or tumormass confirms diagnosis.

    • Neuroblastoma

    Can be associated with generalized adenopathy,but usually there are other signs of involvement (e.g., chest orabdominal mass, liver disease, and anemia). See Chap. 1, Abdominal Masses.

    Histiocytoses

  • Group ofdisorders in which primary process is infiltration and accumulationof cells of monocyte-macrophage series in involved tissues.
  • 3 major forms in childhood are classI (Langerhans cell histiocytosis), class II (familial erythrophagocyticsyndrome, infection-associated hemophagocytic syndrome, sinus histiocytosis,histiocytic necrotizing lymphadenitis), and class III (malignantdisorders of mononuclear phagocytes including acute monocytic leukemia,malignant histiocytosis, and true histiocytic sarcoma).

    • Class I (Langerhans Histiocytosis)

  • Langerhanscell histiocytosis is the principal disease in this class and themain proliferative disorder of the Langerhans cell.
  • Although clinical presentation is variable,hallmark is presence of lytic bone lesions. Fever and weight lossalso may occur. In disseminated form, which usually occurs in children <2yrs of age, clinical features include generalized adenopathy, hepatosplenomegaly,seborrheic dermatitis, anemia, and sometimes pancytopenia.
  • Detection of Birbeck granules by electronmicroscopy in cells of lesions confirms diagnosis.

    • Class II Histiocytoses

    2 major disorders are familial erythrophagocyticlymphohistiocytosis (FEL) and infection-associated hemophagocyticsyndrome. Other class II histiocytoses associated with generalizedadenopathy include sinus histiocytosis with massive lymphadenopathyand histiocytic necrotizing lymphadenitis (Kikuchi-Fujimoto disease).

    Familial Erythrophagocytic Lymphohistiocytosis

  • Autosomal-recessivedisorder characterized by uncontrolled T-lymphocyte and macrophageactivation.
  • Clinical features include fever, failureto thrive, generalized adenopathy, hepatosplenomegaly, and macularor papular skin rash. Involvement of CNS may produce seizures andalteration in consciousness.
  • Lab findings include pancytopenia,hyperlipidemia, hypofibrinogenemia, and evidence of cellular immunologicdysfunction.
  • Bone marrow aspirate that shows normal-appearinghistiocytes containing red cells and platelets is diagnostic.

    • Infection-Associated Hemophagocytic Syndrome

  • Has occurredin association with viral, bacterial, fungal, and parasitic infections.
  • Clinical features are similar to thoseof FEL.
  • Diagnosis is confirmed by bone marrowaspirate, but search for triggering infectious pathogen should beundertaken.

    • Sinus Histiocytosis with Massive Lymphadenopathy

  • In thisdisorder of unknown cause, usual finding is massive, painless, bilateral,cervical adenopathy. Lymph nodes also may be enlarged in other regionsof neck, as well as in axillary and inguinal regions. Other sitesof involvement include skin, salivary glands, bone, respiratorytract, and CNS.
  • Lab abnormalities include mild normochromicanemia, leukocytosis, hypoalbuminemia, reversal of CD4:CD8 ratioin circulating lymphocytes, polyclonal hypergammaglobulinemia, andincreased sedimentation rate.
  • Some children also may have associatedglomerulonephritis or joint disease that may precede or occur withonset of histiocytosis.
  • Pathologic appearance is distinctivewith proliferation of histiocytes and phagocytosis of lymphocytes,plasma cells, and red cells.

    • Histiocytic Necrotizing Lymphadenitis (Kikuchi-Fujimoto Disease)

  • Cause ofthis rare disorder is unknown.
  • Usual presentation is localized orgeneralized adenopathy with or without fever. Associated findingsinclude hepatosplenomegaly, weight loss, and leukopenia. Lymph nodebiopsy shows focal necrotizing lesion.
  • Spontaneous resolution usually occursover several months.

    • Class III Histiocytoses

  • Histiocytosesthat are true neoplasms comprise this category and include acutemonocytic leukemia, malignant histiocytosis, and true histiocyticsarcoma.
  • In each of these disorders generalizedadenopathy, hepatosplenomegaly, fever, and weight loss may occur.
  • Diagnosis is made by lymph node biopsy.

    • Lymphoproliferative Disorders

  • Infectionwith EBV triggers the onset of the X-linked lymphoproliferativesyndrome.
  • Usual presentation is severe infectiousmononucleosis.
  • Identification of susceptible individualsbefore infection is possible by molecular genetic analysis. See Chap. 53, Recurrent Infection.

    • Immunodeficiency Diseases

    Generalized adenopathy may occur with someimmunodeficiency diseases (e.g., Wiskott-Aldrich syndrome, commonvariable immunodeficiency, Chediak-Higashi disease, chronic granulomatousdisease, and HIV). See Chap.53, Recurrent Infection.

    Collagen Vascular Diseases

    Generalized adenopathy may occur with juvenilerheumatoid arthritis and systemic lupus erythematosus. See Chap. 37, Limp.

    Storage Diseases

    In Gaucher, Niemann-Pick, and Wolman diseases,accumulation of lipid-containing histiocytes can produce enlargementof lymph nodes, liver, and spleen. See Chap. 13, Developmental Delay and Chap. 30, Hepatomegaly.

    Sarcoidosis

  • Chronicmultisystem granulomatous disease of unknown cause. Lung is mostfrequent site of involvement, and chest radiography may show parenchymalinfiltrates and miliary nodules as well as hilar and paratrachealadenopathy. Generalized adenopathy with enlarged cervical nodesis also common. Other clinical features include fever, cough, weightloss, night sweats, uveitis, and hepatosplenomegaly.
  • Lab findings include increased sedimentationrate, peripheral eosinophilia, hypercalcemia, and increase in angiotensin-convertingenzyme concentration.
  • Biopsy shows characteristic noncaseatinggranulomatous lesions.

    • Drugs

    Localized or generalized adenopathy can occur1–2 wks after administration of drugs (e.g., phenytoin,isoniazid, aspirin, penicillin, tetracycline, iodides, sulfonamides,or allopurinol). Fever, macular or papular rash, pruritus, and hepatosplenomegalyalso may be found.

    Serum Sickness

  • Hypersensitivityresponse to foreign proteins.
  • Onset is usually 1–2 wks afterinjection of foreign material (e.g., antitoxin for snake envenomation).
  • Previous exposure may result in immediateanaphylaxis or illness 1–3 days after exposure.
  • Common findings include fever, urticaria,edema, arthralgias, and generalized lymphadenopathy.

    • Reactive Hyperplasia

  • Lymph nodeenlargement that follows recognition of foreign antigens and lymphocyteproliferation is known as reactive hyperplasia.
  • Occurs commonly with viral and bacterialinfections. In most cases localized or generalized adenopathy diminishesor disappears after a few weeks. If lymph node enlargement persistsfor 6–8 wks, and diagnosis is uncertain, biopsy may needto be performed to determine presence of any malignancy.

    • Diagnostic Approach

  • First stepis to determine whether lymph nodes are enlarged.
  • If they are enlarged, next step isto determine whether adenopathy is localized or generalized.

  • Most commoncauses of localized adenopathy are reactive hyperplasia and infection.
  • Most common causes of generalized adenopathyare reactive hyperplasia, infection, and neoplasia.
  • Occasionally, some disorders that causegeneralized adenopathy may present with localized adenopathy. Diagnosticapproach to cervical adenitis is discussed in Chap. 42, Neck Masses.
  • If cause of generalized adenopathyis uncertain after history and physical exam, CBC and differential,monospot test, and chest radiography should be performed.

  • Infectiousmononucleosis is still possible with negative monospot test, andEBV serologies can be performed.
  • Cytomegalovirus infection also cancause infectious mononucleosis-like syndrome, and viral isolationfrom urine is diagnostic.
  • HIV serology should be considered.
  • Bone marrow aspirate or biopsy shouldbe considered if there is pancytopenia or malignant cells are seenon blood smear.
  • If CBC is normal or mild anemia ispresent, degree of illness must be assessed. With mild illness,child may be followed for 1–2 wks and reassessed. If illnessis more severe or neoplasia is suspected, further investigationis indicated.
  • Lymph node biopsy or bone marrow aspiratemay be diagnostic.
  • In many cases, reactive hyperplasiaand not infection or neoplasia is cause of lymph node enlargement.These children should be observed to see whether regression occurs.

  • If node doesnot change in size or character in 6–8 wks, then biopsyshould be considered.
  • If node rapidly enlarges, biopsy isrecommended even if all other test results are normal. If biopsyis nondiagnostic, it is still important to follow patients closely.
  • In review by Lake and Oski (1978),of 41 children initially found to have nondiagnostic reactive hyperplasia,17% ultimately proved to have specific pathologic diagnosis.

    • References

    1. Bamji M, et al. Palpable lymph nodesin healthy newborns and infants. Pediatrics 1986;78:573–575.
    2. Barness LA. Handbook of pediatric physical diagnosis.Philadelphia: Lippincott-Raven, 1998.
    3. Behrman RE, et al., eds. Nelson textbook of pediatrics,16th ed. Philadelphia: WB Saunders, 2000.
    4. Grossman M, Shiramizu B. Evaluation of lymphadenopathyin children. Curr Opin Pediatr 1994;6:68–76.
    5. Lake AM, Oski FA. Peripheral lymphadenopathy in childhood:ten-year experience with excisional biopsy. Am J Dis Child 1978;132:357–359.
    6. Long SS, et al., eds. Principles and practice of pediatricinfectious diseases. New York: Churchill Livingstone, 1997.
    7. Malley R. Lymphadenopathy. In: Fleisher GR, Ludwig,S, eds. Textbook of pediatric emergency medicine, 4th ed. Philadelphia:Lippincott Williams & Wilkins, 2000:375–381.
    8. Online Mendelian Inheritance in Man (OMIM). McKusick-NathansInstitute for Genetic Medicine, Johns Hopkins University (Baltimore,MD) and National Center for Biotechnology Information, NationalLibrary of Medicine (Bethesda, MD), 2000. World Wide Web URL: http://www.ncbi.nlm.nih.gov/omim.
    9. Pickering LK, ed. 2000 Red book: report of the Committeeon Infectious Diseases, 25th ed. Elk Grove Village, IL: AmericanAcademy of Pediatrics, 2000.
    10. Pizzo PA, Poplack DG, eds. Principles and practiceof pediatric oncology, 3rd ed. Philadelphia: Lippincott-Raven, 1997.
    11. Rudolph AM, ed. Rudolph's pediatrics, 20thed. Stamford, CT: Appleton & Lange, 1996.
    12. Schaller RJ, Counselman FL. Infectious mononucleosisin young children. Am J Emerg Med 1995;13:438–440.
    13. Zitelli BJ. Lymphadenopathy. In: Gartner JC Jr, ZitelliBJ, eds. Common and chronic symptoms in pediatrics, St. Louis: Mosby-YearBook, 1997:365–380.
    '>>

    Book Source Details

    • Book Title: The Diagnostic Approach to Symptoms and Signs in Pediatrics
    • Author(s): Paul S. Bellet
    • Year of Publication: 2006
    • Copyright Details: The Diagnostic Approach to Symptoms and Signs in Pediatrics, Copyright © 2006 Lippincott Williams & Wilkins.

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    • Lymphadenopathy
    • "The Diagnostic Approach to Symptoms and Signs in Pediatrics" (2006)
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    Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.



    More About This Book:
    Title: The Diagnostic Approach to Symptoms and Signs in Pediatrics
    Authors: Paul S. Bellet
    Publisher: Lippincott Williams & Wilkins
    Copyright: 2006
    ISBN: 0-78172-899-1

     » Next page: Lymphadenopathy (Nursing: Interpreting Signs and Symptoms)

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