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Fig. 2C.19: Image depicting profile sign and Schamroth’s sign.
Atypical presentation of clubbing
Acute clubbing Subacute bacterial endocarditis
Lung abscess
Empyema
Unilateral clubbing Hemiplegia
Aneurysm of subclavian artery
Pancoast tumor
Pseudoclubbing Leprosy
Leukemic infiltration
Hyperparathyroidism
Thyroid acropachy
Sclerodactyly
Exposure to vinyl chloride
Subungual tumors or cysts
Painful clubbing Bronchogenic carcinoma
Subacute bacterial endocarditis
Lung abscess
Reversible clubbing Lung abscess
Empyema
Unidigital clubbing Median nerve injury
Trauma
Clubbing with cyanosis Cyanotic congenital heart diseases
ILD
Differential clubbing:
Upper limb (N)
Lower limb (clubbing)
Patent ductus arteriosus (PDA) with reversal of shunt
Reverse differential clubbing:
Upper limb (clubbing)
Lower limb (N)
PDA + transposition of the great arteries (TGA) + reversal of shunt
Phalangeal Depth Ratio (Fig. 2C.20)
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Ratio of distal phalangeal depth (DPD) with interphalangeal depth (IPD).
<1 is normal, >1 is suggestive of clubbing.
Fig. 2C.20: Picture depicting the phalangeal depth at proximal and distal interphalangeal joints.
Digital Index
Sum of phalangeal depth ratios of 10 fingers
A digital index of 10.2 or higher is indicative of clubbing. Although, a phalangeal depth ratio of 1.0 or
greater in any finger is suggestive of clubbing, digital index is more specific for clubbing.
Other Nail Changes
Nail changes Causes
Koilonychia Iron deficiency anemia (IDA)
Hemochromatosis
Beaus lines Measles
Pneumonia
Pulmonary infarction
Plummer nails Seen in hyperthyroidism
Red nails Congestive cardiac failure (CCF)
Blue nails Copper or silver deposit
Black nails Peutz-Jegher’s syndrome
Cushing’s disease
Addison’s disease
White nails Anemia
Hypoalbuminemia
Diabetes mellitus (DM)
CCF
Rheumatoid arthritis
EDEMA
Definition
Abnormal accumulation of fluid in interstitium.
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Sites of Examination of Edema
In mobile patient Legs 2–3 cm above the medial malleolus
In bed ridden supine patient Sacrum
Back over the scapula
To check for abdominal wall edema Pinch the skin over the abdomen
Technique (Fig. 2C.21)
Press the skin and subcutaneous tissue for at least 15–20 seconds against a bony prominence (except
for abdominal wall edema where we pinch the skin and subcutaneous tissue).
Grading of Pitting Edema (Fig. 2C.22)
1+ 2-mm depression, immediate rebound
2+ 4-mm deep pit, a few seconds to rebound
3+ 6-mm deep pit, 10–12 seconds to rebound
4+ 8-mm deep pit, >20 seconds to rebound
Fig. 2C.21: Method of eliciting pedal edema.
Fig. 2C.22: Grading of pitting edema.
Edema
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Pitting Nonpitting (Brawny edema)
Rapid recovery Slow recovery
Recovers in <40 seconds Recovery takes >40 seconds Does not pit or recover in few seconds
Nontender
Skin shows hyperkeratosis
Mechanism: ↓oncotic
pressure
Mechanism: ↑hydrostatic pressure Mechanism: Lymphedema
Low serum protein (N) serum protein Lymphatic obstruction
Causes:
Increased protein loss
Burns
Nephrotic syndrome
Bowel disease
Decreased intake or
synthesis
Kwashiorkor
Malabsorption
Liver disease
Causes:
Systemic venous hypertension (HTN)
Congestive heart failure (CHF) (Fig.
2C.23)
Pericarditis
Tricuspid valve diseases
Local venous HTN
Deep venous thrombosis (DVT)
Inferior vena cava syndrome
Causes:
Myxedema (Fig. 2C.24)—hypothyroidism
Pretibial myxedema—Graves’s disease
Upper limb
Breast cancer
Radiation induced
Lower limb
Aplasia cutis
Congenital (praecox, tarda, milroy’s disease, and Meigs
disease)
Filariasis (Fig. 2C.25)
Recurred streptococcal infection
Malignancies
Facial edema: Trichinosis, hypothyroidism, allergies, nephrotic syndrome, and angioedema (Quincke’s edema)
Neurogenic edema: Secondary to autonomic dysfunction
Drug-induced edema: Nifedipine, corticosteroids, estrogen, nonsteroidal anti-inflammatory drugs (NSAIDs), and insulin
May-Thurner syndrome—chronic, unilateral, pitting edema due to compression of the left iliac vein by the right common iliac
artery against the lumbar spine
Idiopathic edema—chronic, bilateral, and pitting
In females <50 age, more during menstrual cycles.
Fig. 2C.23: Pitting type of pedal edema seen in congestive cardiac failure.
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Fig. 2C.24: Nonpitting type of pedal edema seen in myxedema.
Fig. 2C.25: Nonpitting type of pedal edema seen in filariasis.
LYMPHADENOPATHY
Definitions
Generalized Lymphadenopathy
Generalized lymphadenopathy is defined as involvement of ≥2 noncontiguous lymph node groups and is
typically indicative of systemic disease.
Significant Lymphadenopathy (based on Size, Fixity and Consistency)
Size >2 cm in Inguinal region
Size >1 cm in Extrainguinal region
Any size Supraclavicular
Epitrochlear
Popliteal
Any lymph node with a lesion in the draining area
Based on fixity Fixed to each other (matting)
Fixed to underlying tissues
Fixed to skin
Based on consistency Hard/firm lymph nodes
Persistent Generalized Lymphadenopathy
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It is defined as lymph nodes of more than 1 cm in size, in 2 or more areas persisting for 3 or more
months (mnemonic 1-2-3). Seen in human immunodeficiency virus/acquired immune deficiency
syndrome (HIV/AIDS).
Causes of generalized lymphadenopathy
Infections Bacterial Disseminated TB
Secondary syphilis
Viral HIV
Infectious mononucleosis
Parasitic Toxoplasmosis
Fungal Histoplasmosis
Coccidioidomycosis
Paracoccidioidomycosis
Malignancy Lymphomas
Acute leukemias
Chronic lymphocytic leukemia (CLL)
Chronic myeloid leukemia (CML) (in blast crisis)
Immunological Systemic lupus erythematosus (SLE)
Adult-onset Still’s disease
Juvenile rheumatoid arthritis (JRA)
Sjogren’s syndrome
Kawasaki disease
Serum sickness (postzone phenomenon—excess of antibody)
Granulomatous Sarcoidosis
Amyloidosis
Histiocytosis X
Endocrine Hyperthyroidism
Drugs Phenytoin (pseudolymphoma)
Primidone
Carbamazepine
Allopurinol
Captopril
Cotrimoxazole
Sulindac (NSAIDs)
Hydralazine
Beta-blockers
Syndromic lymphadenopathy Kikuchi-Fujimoto disease
Castleman’s disease
Kimura disease
Rosai–Dorfman syndrome
Familial Mediterranean fever
Miscellaneous Niemann-pick disease
Describing a Lymph Node
Size (significant or not)
Site
Number
Consistency
Overlying skin
Mobility
Tenderness
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Draining area.
Consistency
Soft Normal consistency
Hard Malignancy
Indian rubber Hodgkin’s lymphoma
Shotty lymph node Syphilis
Bubo (large node with central necrosis) Lymphogranuloma venereum
Matted Tuberculosis (due to periadenitis)
Hard lymph nodes in tuberculosis Hyperplastic tuberculosis lymphadenopathy
Different Group of Lymph Nodes (Fig. 2C.26)
Fig. 2C.26: Image showing different groups of lymph nodes.
Cervical Lymph Nodes
Divided into:
Superficial or deep (based on whether above or below deep cervical fascia)
Vertical or horizontal
Superficial Cervical Lymph Nodes
They are superficial to deep cervical fascia
They include:
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External Waldeyer ring
Submental
Submandibular bilateral
Preauricular bilateral
Postauricular bilateral
Occipital lymph nodes.
Pretracheal
Paratracheal
Posterior triangle lymph nodes.
Deep Cervical Lymph Nodes
Horizontal: Supraclavicular lymph nodes
Vertical: Jugulodigastric and jugulo-omohyoid lymph nodes.
Examination of Cervical Lymph Nodes
Examination of anterior group of lymph nodes is done by standing behind the patient→flex the neck
to relax the fascia→first feel for the submental group (using a single finger) (Fig. 2C.27) and
then→bilateral submandibular (Fig. 2C.28) → bilateral preauricular (Fig. 2C.29) → jugulodigastric
(Fig. 2C.30) → juguloomohyoid (Fig. 2C.31) →supraclavicular groups (Fig. 2C.32) (± pre- and
paratracheal).
Examination of posterior group of lymph nodes is done by standing in front of the patient→feel for
the post auricular (Fig. 2C.33) → occipital (Fig. 2C.34) → posterior triangle group of lymph nodes
(Fig. 2C.35).
Fig. 2C.27: Method of examining submental group of lymph node.
Fig. 2C.28: Method of examining submandibular lymph nodes.
Fig. 2C.29: Method of examining preauricular lymph nodes.
Fig. 2C.30: Method of examining jugulodigastric lymph nodes.
Fig. 2C.31: Method of examining jugulo-omohyoid lymph nodes. Fig. 2C.34: Method of examining occipital lymph nodes.
Fig. 2C.32: Method of examining supraclavicular lymph nodes. Fig. 2C.35: Method of examining posterior triangle lymph node
Fig. 2C.33: Method of examining postauricular lymph nodes.
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Supraclavicular Lymph Nodes and Drainage
Right supraclavicular Left supraclavicular
Right lung (all three lobes)
Left lung lower lobe
Left lung upper lobe
4 B’s and Gonads:
Breast
Bronchus
Bowel
Bladder, and
Gonads (testis/ovaries)
Note: mechanism of left supraclavicular lymphadenopathy in GI and other malignancies—reflux of tumor cells from the
thoracic duct into left supraclavicular node at the junction of thoracic duct and left subclavian
Trousseau sign of tetany: Carpopedal spasms
Trousseaus syndrome: Migratory thrombophlebitis in malignancy
Troisier’s sign: Enlarged hard left supraclavicular lymphnode (Virchow’s node).
Other named lymph nodes
Virchow node Left supraclavicular node
Scalene node
(Fig. 2C.36)
Sentinel node of bronchogenic carcinoma
Relax neck
Palpate (deep) between the two heads of SCM
Winterbottom sign Posterior triangle lymph node enlargement
Seen in early phase of African trypanosomiasis
Causes of posterior triangle lymph node
enlargement
Scalp infection
Measles
Rubella
Infectious mononucleosis
Trypanosomiasis.
Node of Woods Jugulodigastric lymph node enlargement seen in TB when spread via
tonsils
Delphian node Pretracheal node
External Waldeyer ring Commonly seen to be enlarged in non-Hodgkin’s lymphoma
Berry’s node Jugulo-omohyoid lymph nodes seen in thyroid malignancy
Axillary Group of Lymph Nodes
There are five axillary lymph node groups
Lymph nodes include:
Lateral (humeral),
Anterior (pectoral),
Posterior (subscapular),
Central and
Apical nodes.
The apical nodes are the final common pathway for all of the axillary lymph nodes.
Note: Examine the right axillary lymph nodes with the left hand except for humeral (lateral) group (which
is examined with right hand).
Examination of Right Axillary Lymph Nodes (Figs. 2C.37 to 2C.46)
Hyperabduct the right arm of patient
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Place the right forearm of patient on your left forearm
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