Spleenomegaly Lymphnodes Enlargement BDS2017 BATCH MEDICINE THEORY LECTURE

Spleenomegaly & Lymphnodes Enlargement BDS-2017 BATCH MEDICINE THEORY LECTURE PROF. S. F. HAQUE Department of Medicine, JNMCH, AMU

INTRODUCTION: • �Anatomy & Physiology • �Classification • �Etiology • �Step-wise approach • �Associated features • �Investigation

Spleenic Functions: • Quality control over RBC – culling & pitting • Synthesis of antibodies • Removal of antibody coated bacteria & RBC MECHANISMS OF SPENOMEGALY : Reactive Reticulo-endothelial -Lymphoid hyperplasia Extramedullary hemopoeisis Proliferation of macrophages Vascular congestion

Major Causes: • INFECTIVE • Acute & subacute- IMN, infective endocarditis, CMV, AIDS • Chronic - TB, syphilis, brucellosis • Tropical splenomegaly - Malaria, kala azar, trypanosomiasis • CONGESTIVE • Portal hypertension - cirrhosis, biliary cirrhosis, • Extra-hepatic portal hypertension – • Thrombosis ofsplenic vein • Chronic passive congestion of cardiac origin

Causes cont. • HYPERPLASTIC : Extramedullary Hemopoeisismyeloprolif. d/s - marrow damage – marrow infiltration Reticulo endothelial hyperplasia –(abnormal RBCs) : – Sickle cell Disease Spherocytosis, Heamoglobinopathies-- Thalassemia major

Physical Examination: • NORMAL SPLEEN • Normal size – 12 cm length , 7 cm width • weight- < 250 gm • Located along- 9 th, 10 th, 11 th ribs mid-axillary • < Spleen should be twice the size to be PALPABLE > Important to note • Palpable spleens are not always ABNORMAL •

MASSIVE SPLENOMEGALY : (>8 CM, >1000 GM) Common Causes: • Myeloproliferative disorder • Chronic malaria, kala-azar (Trop. Splenomegaly Syndrome) • Storage disorders • Thalassemia major • MODERATE SPLENOMEGALY(4 -8 CM): D/D • Cirrhosis , Lymphomas, Amyloidosis • Hemolytic anemias • MILD SPLENOMEGALY (1 -3 CM) • Acute infections: Acute malaria, Typhoid, Kala-azar, septicemias

HYPERSPLEENISM: • Splenomegaly • Pancytopenia • Presence of hypercellular marrow • Reversal with splenectomy

DIFFERENCES : SPLEEN AND KIDNEY • • Spleen: Sharp edge Notch –med border Cross midline Towards RT. Iliac fossa Moves with respiration Cannot get above it KIDNEY: Ballotable , Can get above it Round edge No notch Not cross midline Not moves with resp.

STEP-WISE APPROACH TO SPLENOMEGALY: • HISTORY : • Age , gender , Race • Recent infections like malaria • Fever, weight loss, s weating (lymphomas, infections) • Jundice, Pruritis • Abnormal bleeding/bruising • Joint pain • H/o Alcholism , • High risk sexual behaviour: Hepatitis B, C, AIDS,

PHYSICAL EXAMINATION : • • • Points to consider: Size of the spleen Hepatomegaly i. e a case of Hepatospleenomegaly? Lymphadenopathy Fever Icterus, Purpura, Bleeding diathesis Stigmata of Chronic Liver Disease Stigmata of RA/SLE Splinter hemorrhage, Retinal hemorrhage , Cardiac murmurs

INVESTIGATIONS: • CBC Blood smear • Retic count • Blood C/S • Serology (fungal, viral, parasitic) • LFT • Hb electrophoresis / coombs test • Coagulation Profile: BT, CT, PT. INR • Amylase/lipase • AMA, Anti CCP, RA factor • Bone marrow analysis

IMAGING: • USG- sensitive & specific non-invasive • CT scan – etiology of splenomegaly, - liver size, heterogenecity, splenic mets, abscess- retro peritoneal LN • - Craniocaudal length > 10 cm • Liver- spleen colloid scan- (RBC –Cr 51, Tc 99) • - MRI/ Doppler usg- portal/splenic vein thrombosis • - cavernomas • MRI scan- liver hemangioma

CLINICAL PRESENCE WITH SPLENOMEGALY : D/D to Consider: Ø Fever - Typhoid, malaria, kaalazar, infect. endocarditis, leukemia Tender spleen- Rupture, Abscess, infarct Acute illness+ anemia - AIHA, leukemia Fever + LN- IMN, leukemia, lymhomas, SLE, sarcoid Anemia- hemolytic anemia, hemoglobinopathies Jaundice – cirrhosis, hemolytic anemia Pulsatile spleen- aneurysm �High ESR- connective tissue disorder Leukopenia- felty‟s syndrome, septicemia

TROPICAL SPLENOMEGALY syndrome: Ø Massive splenomegaly � Ø Endemic areas of malaria, kala-azar ØIg. M antibodies +ve ØNo parasite in blood Ø Lymhocytic infiltration of splenic sinusoids Ø Long term anti-malarials

SUMMARY • Splenomegaly – major physical finding • Step wise approach • History, • Physical exam: D/D of Spleenomegaly • Look for associated features • Lab investigation & Imaging • Search for etiology • Specific Treatment

LYMPH NODES ENLARGEMENT: • • • • Lymph nodes, in conjunction with the spleen, tonsils, adenoids, and Peyer patches, are highly organized centers of immune cells that filter antigen from the extracellular fluid. �The lymph node, with its high concentration of lymphocytes and antigen-presenting cells, is an ideal organ for receiving antigens that gain access through the skin or gastrointestinal tract. Nodes have considerable capacity for growth and change. Lymph node size depends on the person's age, the location of the lymph node in the body, and antecedent immunological events. In neonates, lymph nodes are barely perceptible, but a progressive increase in total lymph node mass is observed until later childhood. Lymph node atrophy begins during adolescence and continues through later life. Diagnostic Approach

Clinical Approach : Lymphadenopathy • A careful history and physical examination will identify a readily diagnosable cause of the lymphadenopathy: • upper respiratory tract infection, • pharyngitis, • periodontal disease, • no further assessment is necessary

Generalized lymphadenopathy: • Generalized lymphadenopathy is defined as enlargement of more than 2 noncontiguous lymph node groups. • A thorough history and physical examination are critical in establishing a diagnosis. • Causes : • infections, autoimmune diseases, malignancies, • histiocytoses, storage diseases, benign hyperplasia, • and drug reactions.

Cervical lymphadenopathy is a common problem in children. Cervical nodes drain the tongue, external ear, parotid gland, and deeper structures of the neck, including the larynx, thyroid, and trachea. Inflammation or direct infection of these areas causes subsequent engorgement and hyperplasia of their respective node groups. Adenopathy is most common in cervical nodes in children and is usually related to infectious etiologies.

Infectious etiologies Cervical adenopathy is a common feature of many viral infections. The classic manifestation of group A streptococcal pharyngitis is sore throat, fever, and anterior cervical lymphadenopathy. Atypical mycobacteria cause subacute cervical lymphadenitis, with nodes that are large and indurated but not tender. The only definitive cure is removal of the infected node. Mycobacterium tuberculosis may manifest with a suppurative lymph node identical to that of atypical mycobacterium. . Lymphadenopathy posterior to the sternocleidomastoid is typically a more ominous finding, with a higher risk of serious underlying disease.

PHYSICAL EXAMINATION • When lymphadenopathy is localized, the clinician should • examine the region drained by the nodes for evidence of • infection, skin lesions or tumors • Other nodal sites should also be carefully examined to exclude the possibility of generalized rather than localized lymphadenopathy. • Careful palpation of the submandibular, anterior and posterior cervical, supraclavicular, axillary and inguinal nodes can be accomplished in a short time and will identify patients with generalized lymphadenopathy

Examination L. N cont. If lymph nodes are detected, the following five characteristics should be noted and described: • 1. Size • 2. Pain/Tenderness • 3. Consistency • 4. Matting • 5. Location • 6. Mobility • 7. Tissue Invasion