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Conditions of the Lymph System

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Lymphedema does not respond significantly to overnight elevation, whereas edema secondary to central organ failure or venous insufficiency does. – PowerPoint PPT presentation

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Title: Conditions of the Lymph System


1
Conditions of the Lymph System
Anatomy of axillary lymph nodes
Anatomy of head neck lymph nodes
Anatomy of inguinal lymph nodes
  • Generalized adenopathy has been defined as
  • involvement of three or more
  • noncontiguous lymph node areas.

CAUSES OF LYMPHADENOPATHY Infection Bacterial
(e.g., all pyogenic bacteria, cat-scratch
disease, syphilis) Mycobacterial (e.g.,
tuberculosis, leprosy) Fungal (e.g.,
histoplasmosis ) Chlamydial (e.g.,
lymphogranuloma venereum) Parasitic (e.g.,
toxoplasmosis, filariasis)
Viral (e.g., Epstein-Barr virus, cytomegalovirus,
rubella, HIV) Benign disorders of the immune
system (e.g., rheumatoid arthritis,
SLE) Malignant disorders of the immune system
(e.g., chronic and acute myeloid and lymphoid
leukemia, non-Hodgkin's lymphoma, Hodgkin's
disease, angioimmunoblastic-like T-cell lymphoma,
multiple myeloma with amyloidosis, malignant
histiocytosis) Other malignancies (e.g., breast
carcinoma, lung carcinoma, melanoma, head and
neck cancer, gastrointestinal malignancies, germ
cell tumors, Kaposi's sarcoma) Storage diseases
(e.g., Gaucher's disease)
Acute lymphadenitis It is painful Localizing
symptoms suggest infection in specific site(
primary focus ) Constitutional symptoms may be
present e.g. Fever, malaise Treatment is
directed to the cause ,antibiotics, derange if
abscess occur
Chronic non specific lymphadenitis Mild
recurrent lymphadenitis Common sites are upper
deep cervical LN and inguinal Chronic
enlargement of affected LN, which is firm
slightly tender and mobile Primary focus is
there Treatment is directed to the cause
2
  • Specific lymphadenitis
  • Bacterial (cat-scratch disease, syphilis)
  • Mycobacterial (e.g., tuberculosis, leprosy)
  • Fungal (e.g., histoplasmosis, coccidioidomycosis)
  • Chlamydial (e.g., lymphogranuloma venereum)
  • Parasitic (e.g., toxoplasmosis, filariasis)
  • Viral (e.g., Epstein-Barr virus, cytomegalovirus,
    HIV)
  • HIV- related.Persistent Generalized
    Lymphadenopathy (PGL)
  • Lymph nodes larger than 1.5 cm in diameter in 2
    or more extrainguinal sites of 3 or more months
    duration
  • Nodes are non-tender, symmetrical, and often
    involve the posterior cervical, axillary,
    occipital, and epitrochlear nodes
  • Develops in up to 50 of HIV-infected individuals
  • Up to one-third do not have any other symptom on
    presentation (stage 1)
  • In HIV-positive patients, PGL is a clinical
    diagnosis.
  •  PGL may slowly regress during the course of HIV
    infection and may disappear before the onset of
    AIDS
  • Tuberculosis lymphadenopathy
  • Cervical nodes most commonly involved
  • Organism
  • Root lymph Vs blood

3
  • syphilis
  • Clinical Symptoms may evolve
  • Generalized painless lymphadenopathy
  • Maculo-papular, papular, or pustular rash on
    entire body, especially on palms and soles
  • Highly infectious lesions on mucous membranes
    (lips, mouth, pharynx, vulva, glans penis) which
    are silvery grey superficial erosions with a red
    halo and not painful unless there is a secondary
    infection.
  • 40 of these patients will have CNS involvement
    with headache and meningismus
  • 1-2 will develop acute aseptic meningitis
  • benzathine penicillin 2.4 million units IM single
    dose
  • Lymphoma
  • Lymphoma is a malignant disease that affects
    blood cells called lymphocytes immune cells
    that normally protect you from illness.
  • Damage to genes in these cells can sometimes lead
    to abnormal cell behavior which makes the cells
    immortal unable to die when they should or
    causes sustained rapid cell division..
  • These malignant cells then may accumulate to form
    tumors that enlarge the lymph nodes or spread to
    other areas of the lymphatic system, such as the
    spleen or bone marrow, or outside the lymphatic
    system to the skin, or mucosal linings of the
    stomach.
  • They arise as the result of abnormal
    proliferation of the lymphoid system, and hence
    occur at any site where lymphoid tissue is found.
    Most commonly they are manifest by the
    development of lymphadenopathy at single or
    multiple sites, although primary extranodal
    presentations account for up to 20 of
    non-Hodgkin's lymphoma.
  • The prognosis is determined by the specific
    subtype of lymphoma and the anatomical extent of
    disease and its bulk, the clinical course ranging
    from months to years.
  • Lymphomas are currently classified on the basis
    of histological appearance into
  • Hodgkin's
    lymphoma
  • non-Hodgkin's
    lymphoma.
  • The two types not only have different morphologic
    characteristics but differ also in their clinical
    behavior and their response to various
    therapeutic regimens.
  • HODGKIN'S LYMPHOMA (HL)
  • Aetiology
  • There is epidemiological evidence linking
    previous infective mononucleosis with HL and up
    to 40 of patients with HL have increased EBV
    antibody titres at the time of diagnosis and
    several years prior to the clinical development
    of HL.
  • Other environmental and occupational exposure to
    pathogens have been postulated.
  • ?? Chronic infection,?? Depressed immunity,??
    Chemical exposure pesticides,cancer therapies,
    herbicides ,?? Viral exposures
  • Pathology
  • The hallmark of HL is the Reed-Sternberg cell)
    which is usually derived from germinal centre B
    cells or, rarely, peripheral T cells.
  • Pathological classification of Hodgkin's lymphoma
  • Nodular lymphocyte-predominant Hodgkin's
    lymphoma
  • Classical Hodgkin's lymphoma  
  • Nodular sclerosis HL(young females,
    involving particularly lymph nodes in the
    mediastinum and neck ).
  •   Lymphocyte-rich HL(It often occurs in
    peripheral lymph nodes. It is often an indolent
    disease(.  
  •   Mixed cellularity HL) more common in
    men and is associated with B symptoms ( 
  •   Lymphocyte-depleted HL) It is seen in
    HL associated with HIV (

4
  • Clinical features
  • Lymph node enlargement, most often of the
    cervical nodes (other causes are shown in, these
    are usually painless and with a rubbery
    consistency.
  • Enlargement of the spleen/liver.
  • 'B' symptoms fever, (25) drenching night
    sweats, weight loss of gt 10 bodyweight
  • Other constitutional symptoms, such as pruritus,
    fatigue, anorexia and, occasionally,
    alcohol-induced pain at the site of enlarged
    lymph nodes.
  • Symptoms due to involvement of other organs (e.g.
    lung - cough and breathlessness (
  • Investigations
  • Blood count may be normal, or there can be a
    normochromic, normocytic anaemia. Lymphopenia and
    occasionally eosinophilia are present.
  • Erythrocyte sedimentation rate )ESR) is usually
    raised and is an indicator of disease activity.
  • Liver biochemistry is often abnormal, with or
    without liver involvement.
  • Serum lactate dehydrogenase raised level is
    adverse prognostic factor.
  • Chest X-ray may show mediastinal widening, with
    or without lung involvement.
  • CT scans show involvement of intrathoracic nodes
    in 70 of cases. Abdominal or pelvic lymph nodes
    are also found. It is the investigation of choice
    for staging although PET scanning is increasingly
    being used.
  • Lymph node biopsy is required for a definitive
    diagnosis
  • Cotswolds modification of Ann Arbor staging
    classification
  • Stage I Involvement of a single lymph-node region
    or lymphoid structure (e.g. spleen, thymus,
    Waldeyer's ring) or involvement of a single
    extralymphatic site
  • Stage II Involvement of two or more lymph-node
    regions on the same side of the diaphragm (hilar
    nodes, when involved on both sides, constitute
    stage II disease) localized contiguous
    involvement of only one extranodal organ or site
    and lymph-node region(s) on the same side of the
    diaphragm (IIE). The number of anatomic regions
    involved should be indicated by a subscript (e.g.
    II3)

5
  • NON-HODGKIN'S LYMPHOMA (NHL)
  • These are malignant tumours of the lymphoid
    system classified separately from Hodgkin's
    lymphoma. Most (70) are of B cell origin
    although T cell tumours are increasingly being
    recognized.
  • NHL is associated with the EBV virus (Burkitt's
    lymphoma) and the human T cell lymphotropic virus
    which is prevalent in Japan, Africa, South
    America and the Caribbean. Herpes virus 8 is
    associated with primary effusion lymphomas and
    Castleman's disease there is an increase in
    lymphoma in patients with AIDS. Helicobacter
    pylori is an aetiological factor in gastric
    lymphoma.
  • Lymphomas also occur in congenital
    immunodeficiency, post-transplantation and in
    autosomal family cancer syndromes .
  • Other causes, e.g. occupation, dietary and
    exposure to chemicals, have been linked to the
    increasing incidence but the evidence is
    unconfirmed
  • Types
  • Follicular
  • Lymphoplasmacytict
  • Mantle cell
  • Diffuse large B cell
  • Burkitts
  • Anaplastic
  • MALT (mucosal associated lymphoid tissue)
  • WHO classification of lymphoid neoplasms
  • B cell lymphomas
  • Precursor B cell lymphoma Precursor B
    lymphoblastic lymphoma/leukaemia (highly
    (aggressive)
  • Mature B cell lymphoma

6
The Lymphatics
  • Treatment options
  • Aggressive combination chemotherapy gives high
    complete remission rates and molecular remission.
  • Antibody therapy. The monoclonal antibody
    rituximab induces remission (partial) in 30-70
    of patients, almost without toxicity. Molecular
    remissions are observed. Complications include
    the cytokine release syndrome, with fever,
    vomiting and allergic reactions (angio-oedema,
    bronchospasm and dyspnoea).
  • Rituximab/chemotherapy combination. These have
    now been reported to improve the complete
    remission rate (with disappearance of Bcl-2
    positive cells from the bone marrow in 100 of
    patients), freedom from progression and
    event-free survival, even though there is (as
    yet) no effect on overall survival. This may
    become the standard therapy for CD20 positive
    lymphoma.
  • Antibody-targeted irradiation
  • Clinical approach
  • A careful history
  • , -Age of the patient.
  • -The occurrence of fever, sweats, or
    weight loss
  • Site of infection, a particular medication, a
    travel history, or a previous malignancy.
  • physical examination
  • localized or generalized
  • size of nodes
  • Texture
  • Mobility
  • presence or absence of nodal tenderness
  • signs of inflammation over the node
  • skin lesions

7
  • Clinical picture
  • The edematous limb has a firm and hardened
    consistency.
  • There is loss of the normal perimalleolar shape,
    resulting in a tree trunk pattern.
  • The dorsum of the foot is characteristically
    swollen, resulting in the appearance of the
    buffalo hump, and the toes become thick and
    squared .
  • In advanced lymphedema, the skin undergoes
    characteristic changes, such as lichenification,
    development of peau dorange, and
    hyperkeratosis.Additionally, the patients give a
    history of recurrent episodes of cellulitis and
    lymphangitis after trivial trauma and frequently
    present with fungal infections affecting the
    forefoot and toes.
  • Patients with isolated lymphedema usually do not
    have the hyperpigmentation or ulceration one
    typically sees in patients with chronic venous
    insufficiency.
  • Lymphedema does not respond significantly to
    overnight elevation, whereas edema secondary to
    central organ failure or venous insufficiency
    does.

8
  • Differential Diagnosis
  • The most common causes of bilateral extremity
    edema are of systemic origin. The most common
    etiology is cardiac failure, followed by renal
    failure. Hypoproteinemia secondary to cirrhosis,
    nephrotic syndrome, and malnutrition can also
    produce bilateral lower extremity edema.
  • Another important cause to consider with
    bilateral leg enlargement is lipedema. Lipedema
    is not true edema but rather excessive
    subcutaneous fat found in obese women. It is
    bilateral, nonpitting, and greatest at the ankle
    and legs, with characteristic sparing of the
    feet. There are no skin changes,and the
    enlargement is not affected by elevation. The
    history usually indicates that this has been a
    lifelong problem that runs in the family.
  • Once the systemic causes of edema are excluded,
    in the patient with unilateral extremity
    involvement, edema secondary to venous and
    lymphatic pathology should be entertained. The
    edema responds promptly to overnight leg
    elevation. In the later stages, the skin is
    atrophic with brawny pigmentation. Ulceration
    associated with venous insufficiency occurs above
    or posterior and beneath the malleoli.
  • CLASSIFICATION of lymph- edema
  • Lymphedema is generally classified as primary
    when there is no known etiology and secondary
    when its cause is a known disease or disorder.
  • Primary lymphedema has generally been classified
    on the basis of the age at onset and presence of
    familial clustering.
  • Primary lymphedema with onset before the first
    year of life is called congenital. The familial
    version of congenital lymphedema is known as
    Milroys disease and is inherited as a dominant
    trait.
  • Primary lymphedema with onset between the ages of
    1 and 35 years is called lymphedema praecox. The
    familial version of lymphedema praecox is known
    as Meiges disease.
  • Finally, primary lymphedema with onset after the
    age of 35 is called lymphedema tarda.
  • Worldwide the most common cause of secondary
    lymphedema is infestation of the lymph nodes by
    the parasite Wuchereria bancrofti in the disease
    state called filariasis. In the developed
    countries the most common causes of secondary
    lymphedema involve resection or ablation of
    regional lymph nodes by surgery, radiation
    therapy, tumor invasion, direct trauma, or, less
    commonly, an infectious process.
  • Investigation
  • The diagnosis of lymphedema is relatively easy in
    the patient who presents in the second and third
    stages of the disease. It can however, be a
    difficult diagnosis to make in the first stage,
    particularly when the edema is mild, pitting, and
    relieved with simple maneuvers such as elevation.
    For patients with suspected secondary forms of
    lymphedema, computed tomography (CT) and magnetic
    resonance imaging (MRI) are valuable and indeed
    essential for exclusion of underlying oncologic
    disease
  • In patients with known lymph node excision and
    radiation treatment as the underlying problem of
    their lymphedema, additional diagnostic studies
    are rarely needed except as these studies relate
    to follow-up of an underlying malignancy.
  • For patients with edema of unknown etiology and a
    suspicion for lymphedema, lymphoscintigraphy is
    the diagnostic test of choice.
  • When lymphoscintigraphy confirms that lymphatic
    drainage is delayed, the diagnosis of primary
    lymphedema should never be made until neoplasia
    involving the regional and central lymphatic
    drainage of the limb has been excluded through CT
    or MRI.
  • If a more detailed diagnostic interpretation of
    lymphatic channels is needed for operative
    planning, then contrast lymphangiography may be
    considered.

9
pleomorphic adenomaof parroted gland
Neck lump
Ludwigs angina
Multiple cervical metastases visible in the nodal
basins that drain the site of the primary
malignancy
Virchows lymph node
Ranula
Branchial cyst
Thyroglossal cyst
10
Neck lumpThyroid, lymph node ,carotid ,salivary
gland , sternomastoid muscle
Cystic Hygroma
  • Goitre.
  • Neoplasm
  • Thyroid neoplasms
  • Metastatic carcinoma.
  • Primary lymphoma.
  • Salivary gland tumour.
  • Sternocleidomastoid tumour.
  • Carotid body tumour.
  • Inflammatory
  • Acute infective adenopathy.
  • Collar stud abscess.
  • Parotitis.,submandibular sialadinitis
  • Congenital
  • Thyroglossal duct cyst.
  • Cystic hygroma.
  • Branchial cyst.
  • Dermoid cyst.
  • Torticollis.
  • Vascular
  • .Caroted body tumors
  • Subclavian aneurysm.
  • Subclavian ectasia.

Children
Congenital and inflammatory lesions are common.
Cystic hygroma in infants, base of the neck,
brilliant transillumination. Thyroglossal or
dermoid cyst midline, discrete, elevates
with tongue protrusion. Torticollis rock-hard
mass, more prominent with head flexed, associated
with fixed rotation (a fibrous mass in the
sternocleidomastoid muscle). Branchial cyst
anterior to the upper third of the
sternocleidomastoid. Viral/bacterial adenitis
usually affects jugular nodes, multiple, tender
masses. Neoplasms (lymphoma most
common). Young adults Inflammatory neck masses
and thyroid malignancy are common. Viral (e.g.
infectious mononucleosis) or bacterial
(tonsillitis/pharyngitis) adenitis. Papillary
thyroid cancer isolated, non-tender, thyroid
mass, possible lymphadenopathy. Older age group
Neck lumps are malignant until proven
otherwise. Metastatic lymphadenopathy
multiple, hard, nontender, tendency to be
fixed. 75 in primary head and neck (thyroid,
nasopharynx, tonsils, larynx, pharynx), 25 from
infraclavicular primary (stomach, pancreas,
lung). Primary lymphadenopathy (thyroid,
lymphoma) fleshy,rubbery, large size. Primary
neoplasm (thyroid, salivary tumour) firm,
nontender, fixed to tissue of origin.
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