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MISC 1
GYNAECOMASTIA (GYNAECOMAZIA-enlargement of the male breast)
What is this?
     This is a condition where the male breast looks like that of a female. On inspection. even the nipple and
areola assume a feminine appearance. Gynaecomastia means ―a woman‘s breast‖, and is therefore an
abnormality only in men. This is ‗true‘ enlargement of the male breast.
     Early gynaecomastia is characterized by proliferation of both the fibroblastic stroma and the duct
system, which elongates, buds and duplicates. As gynaecomastia persists, progressive fibrosis and
hyalinization are associated with regression of epithelial proliferation. Eventually the number of ducts
decreases. Resolution occurs by reduction in size and epithelial content with gradual disappearance of the
ducts, leaving hyaline bands that eventually disappear.
     It is usually painless but elderly person with gynaecomastia may have little pain. Gynaecomastia may
range from minor degrees of subareolar glandular enlargement to substantial breast prominence; breast
enlargement associated with generalized adiposity should not be confused with true gynaecomastia.
     Growth of breast in men, as in women, is mediated by estrogen and results from disturbances of the
normal ratio of active androgen to estrogen in plasma or within the breast itself. Estradiol formation in the
normal man occurs principally by the conversion of circulating androgens to estrogens in extra- glandular
tissues; the normal ratio of production of testosterone to estradiol in adult men is approx. 100:1(6 mg
versus 45μg), and the normal ratio of the two hormones in plasma is about 300:1. Growth of the breast
tissue ensues in men when this effective ratio decreases significantly as the result of diminished
testosterone production or action, enhanced estrogen formation, or both processes occurring
simultaneously.
Examination of the patient:
I) Examine the breast tissue with fingers and then with the f1at of the hand. It has been said that breast
tissue cannot be palpated in normal adult men. A modified approach: place finger in the nipple and invert
it. If the finger does not encounter a bud of glandular tissue (not fat), do not describe the patient having
gynaecomastia, no matter what the external contour.
2) Unilateral or bilateral.
3) Age of the patient.
4) Stature of the patient.-Klienfelter‘s syndrome-patients are tall and thin with poorly developed secondary
sexual characteristics.
5) h/o taking drugs (producing gynaecomastia) or alcoholism.
6) h/o mumps or castration.
7) Examine both the testis.
8) Examine the liver, spleen and search for any hepato-celullar failure.
9) Look for the signs of carcinoma of the lung in the form of SVC obstruction, collapse of the lung etc.
10) Examine the spine for any tenderness or gibbus (caries spine).
II) Signs of leprosy-nodules. Hypopigmented spots in skin or thickened peripheral nerves etc.
12) P/IR examination to exclude carcinoma of the prostrate for which the patient is being treated by
stilboesterol.
Clinical assessment of the patient with gynaecomastia should include enquiry concerning any change in
libido and examination of thyroid status, the genitalia (sexual ambiguity-hermaphroditism), the muscles
and for stigmata of chronic liver disease.
In males, gynaecomastia is a sign of chronic liver disease. It may be unilateral or bilateral and the breasts
may be tender. This may be a sign of cirrhosis, particularly alcoholic cirrhosis, or of chronic active
hepatitis. In chronic liver disease changes in the estradiol to testosterone may be responsible. In cirrhotic
patients, spironolactone, used to treat ascites, is also a common cause. Gynaecomastia may also occur in
alcoholics without liver disease because of damage to Leydig cells of the testis from alcohol.
Finally, examine the visual fields for evidence of a pituitary tumor.
DRUGS PRODUCING GYNAECOMASTIA:
     l) Estrogens (used in treatment of prostatic cancer). Estrogen contaminated foods-boys and young men
     are particularly sensitive to estrogen and can develop gynaecomastia after the use of dermal ointments
     containing estrogen or after the ingestion of milk or meat from estrogen treated animals.
     2) Digitalis (due to estrogen-like effect).usually occurs in men with abnormal liver function.
     3) Spironolactone (reduces serum testosterone level) - Often the breasts are tender.
     4) Cimetidine (anti-androgenic).
     5) INH (cause not known).
     6) Methyldopa (cause not known).
     7) Marijuana or heroin abuse (associated with high estrogen and low testosterone).
     8) Busulphan, ethionamide, tricyclic antidepressants. D-penicillamine, diazepam, ketoconazole (by
     blocking testosterone synthesis), Phenytoin.-unknown mechanism.
Explanation of your method of examination:
l) Age of the patient-
Newborn (a common finding in male neonate due to the effect of maternal/placental estrogen; the
enlargement usually disappears in a few weeks but may persist longer); adolescence and old age may have
physiological gynaccomastia.
Mild breast enlargement in the male may occur as a temporary phenomenon in puberty (about 50% of
pubertal boys)-because of the relatively high estradiol levels; breast stimulation by unopposed action of
estrogen at the beginning of puberty-this happens before androgen level rise; median age of onset is 14 yrs
-it regresses spontaneously so that by age 20 only a small number of men have palpable vestiges of
gynaccomastia in one or both breasts but may persist for several years, or sometimes indefinitely. It may be
more pronounced unilaterally. In one study of hospitalized patients, the prevalence of gynaecomastia wss
highest (72%) in men aged 50-96 years, and increasing with body mass index. A likely explanation is the
increase, with age in the conversion of androgens to estrogens in the extraglandular tissue and also due to
falling testosterone levels. As also adipose tissue increases, more androstenedione is converted to estrone,
explaining the relationship to bodies mass index.
 2) Stature of the patient- Klinefelter's syndrome and hypogonadism may have tall stature
3) Drugs, mumps orchitis, Castration- all produce gynaecomastia.
4) Examination of testis:
          a) Testicular tumor- Asymmetry of testis, smooth or lobulated. Teratoma, chorionepithelioma etc.
          b) Klinefelter's syndrome- Small and firm testis.
          c) Cirrhosis of liver with hepato-cellular failure- Small and soft testis.
          d) Lepromatous leprosy- Atrophied small and soft testis.
          e) Congenital small testis
5) Examination for hepatosplenomegaly:
           a) Cirrhosis of liver.
           b) Leprosy.
           c) Acute leukemia (leukaemic deposits in breast).
6) Facies:
           a) Puffy, bloated and congested- SVC obstruction due to carcinoma of the lung.
           b) Leonine facies- Lepromatous leprosy.
           c) Hepatic facies- Cirrhosis of liver with hepato-cellular failure.
           d) Rarely true hermaphroditism.
7) Spine- Occasionally cold abscess may form behind the breast tissue in a patient suffering from caries
spine. This is not true gynaecomastia and usually produces unilateral painless swelling of the breast
8) Examination of the skin is done for hypo pigmented anesthetic spots, fall of body hairs and eye
         brows, and subcutaneous nodules for lepromatous leprosy, which causes gynaecomastia.
9) P /R examination - If the patient gives the history of taking stilboesterol (probably suffering from
         Carcinoma of the prostrate).
10) Unilateral or bilateral- Gynaecomastia may be unilateral to start with.
Klinefelter's syndrome, physiological Gynaecomastia are bilateral
COMMON CAUSES OF GYNAECOMASTIA:
    1) Physiological- Newborn, adolescence and old age.
    2) Klinefelter's syndrome (47. XXY).-decreased androgen production(hypogonadal state)
    3) Hepato-cellular failure commonly from alcoholic cirrhosis.
    4) Drug induced.
    5) Bronchogenic carcinoma (HCG).
    6) Lepromatous leprosy.
   7) Leukaemic deposits in breasts (not true gynaecomastia).
   8) Starvation(increased estrogen production)
When there is no cause the condition is said to be idiopathic. A satisfactory diagnosis can be made in only
half or less of patients referred for gynaecomastia. Gynaecomastia may in some instances be normal rather
than due to pathological state.
Gynaecomastia in the adult male may result from:
      Excess estrogen stimulation
      Reduction in circulating androgen
      Antagonism of androgen action
      Androgen insensitivity.
CAUSES OF GYNAECOMASTIA:
Increased estrogen/testosterone ratio
      Chronic liver disease, including liver cancer (increased conversion of estrogen from androgen).
      Thyrotoxicosis-increased peripheral conversion of androstenidione to estrogens, increased
          production of androstenidione,high sex hormone binding globulin(SHBG) concentration which
          will amplify the effects of the altered androgen/estrogen ratio.
      Phenytoin therapy
Androgen receptor antagonist
      Spironolactone, digoxin.
Inherited androgen receptor defects
      Testicular feminization syndrome
Testosterone deficiency or estrogen excess
      Primary and secondary hypogonadism
      Tumor production of HCG (inappropriate HCG production by testicular tumor-chorionepithelioma
          or lung cancer may cause unilateral or bilateral breast enlargement in male-HCG causes enhanced
          testicular secretion of estrogen)
      Estrogen production of Leydig cell tumor of testis, some adrenal tumors.
      Decreased testosterone production-orchitis, trauma, castration, neurologic and granulomatous
          diseases, renal failure (secondary testicular failure), Klienfelter‘s syndrome
Congenital and hereditary
      X-linked spinal muscular atrophy (Kennedy syndrome)
      Klienfelter‘s syndrome (karyotype XXY).
Prolactinoma –a high plasma prolactin level per s e is not responsible for gynaecomastia but combined with
the associated androgen deficiency secondary to low gonadotrophins can result in breast development.

Causes of pathological gynaecomastia
    Increased estrogen production
     Leydig cell tumor (estrogen)
     Adrenal carcinoma (estrogen)
     Bronchogenic carcinoma (HCG)
     Liver disease(increased conversion of estrogen from androgens)
     Thyrotoxicosis (increased conversion of estrogen from androgens)
     Starvation
    Decreased androgen production (hypogonadal state)
          Klienfelter‘s syndrome
          Secondary testicular failure: orchitis, castration, trauma.
    Testicular feminization syndrome
    Drugs
          Estrogen receptor binders: estrogen, digoxin.marijuana
          Antiandrogens: spironolactone, cimetidine.
Significance of gynaecomastia
Gynaecomastia is such a common finding; the issue is not whether it is present, but whether it requires a
work-up.
Symptoms and signs that point to a need to investigate gynaecomastia include
       Drug history is negative,
       Pain & tenderness (rapid breast enlargement),
       Breast mass> 4 cm in diameter, an eccentric or hard irregular breast mass
       or a testicular mass.
.How to proceed for diagnostic evaluation?
After proper clinical evaluation:
1) A careful drug history is taken.
2) Measurement and examination of testis (if both are small and firm, a karyotype is indicated; if testis are
asymmetric an evaluation for testicular tumor is instituted).
3) Liver function tests.
 4) 24-hrs Urinary 17-ketosteroid; plasma oestradiol, LH and testosterone measurement.
 Explanation:
        If there is ↑ LH and testosterone ↓. = testicular failure.
        LH ↓ and testosterone ↓. = most likely there is increased primary estrogen production (e.g. Sertoli
           cell tumor of the testis).
        LH and testosterone ↑ = androgen resistance state or gonadotropin-secreting tumor.
        ↑ Urinary 17-ketosteroid = feminizing adrenal tumor.
       Mammography/sonography-it may be difficulty to distinguish true breast tissue from masses of
          adipose tissue without true breast enlargement (lipomastia); in such cases true gynaecomastia can
          be separated from lipomastia by Mammography/sonography.
How do you like to treat your patient?
I) Treatment of the cause like leprosy, hepato-cellular failure, withdrawing the offending drug etc.
 2) Painful who are not candidates for other therapy - Treatment with antioestrogens e.g. Tamoxifen should
be tried.
3) Indication for surgery (simple mastectomy)
i) Severe psychological problem.
ii) Cosmetic problem.
iii) Continued growth.
iv) Suspicion of malignancy.
 In gynaecomastia, although there is relatively increased risk of carcinoma of the breast, as a whole it is
very very rare.




SPIDER NAEVI
WHAT ARE THESE?
Punctiform flat or little elevated with sharp margin.
These are formed by centrally dilated arteriole from which numerous small vessels radiate resembling the
legs of a spider. Usually it is a sign of hepato-cellular failure.
COMMON SITES In the upper half of thorax (necklace area-chest & upper arms), back. face, forearms and
dorsum of hands. Rarely, they are seen in mucous membrane of oral cavity and nose.
METHOD OF DEMONSTRATION: The central arteriole (central prominence) is occluded by giving
pressure with a pinhead and the response is immediate blanching of the whole naevus. If the pressure is
released, the naevus goes back to its original shape and color. Also can be demonstrated with cover slide. If
a glass slide is placed on the top of the spider, the pressure can be gradually increased to a point at which
the spider will blanch only during diastole, and will be seen to pulsate in time with the heart beat. If the
lesion is blanched completely and the pressure is gradually reduced, the central part will fill with blood
first.
SIZE OF SPIDERS:
Generally from a pinhead to 0.5 cm in diameter. When it attains a large size, it may be seen or felt to
pulsate.
OTHER NAMES OF SPIDER NAEVI : Arterial spider, spider telengectasia, spider angioma, vascular
spider.
CLINICAL ASSOCIATIONS:
          1. Hepato-cellular failure (commonest and principal cause).
          2. Alcoholic cirrhosis.
          3. Viral hepatitis (transient).
          4. During third trimester of pregnancy (2nd to 5th months)/female on prolonged oral
               contraceptives. Disappears within 8 weeks of delivery.
          5. Occasionally in children.
          6. Sometimes in thyrotoxicosis.
          7. In some healthy people (2%). Many young people have up to seven naevi on the face,
               shoulders or arms.
     However, finding of more than two spider naevi any where on the body is considered to be abnormal.
                     It is more prominent when there is hypertension.
                     It increases with progression of disease.
                     It decreases with regression of disease.
                     It disappears with death.
                     They can occasionally bleed profusely.
‗Paper money‘ skin may occur in a similar distribution to spiders. This consists of numerous small vessels
scattered randomly throughout the skin. These resemble the silk threads in American dollar notes, which
accounts for the name.
AETIOPATHOGENESIS:
Like palmar erythema, spiders are formed due to hyperoestrogenaemia (as it is not metabolized by the liver;
part of the normal hepatic function is the inactivation of estrogens which is impaired in chronic liver
disease). It is known that estrogen has a dilating effect on spiral arteries of endometrium and such a
mechanism may be responsible for the production of cutaneous spiders. Now a days, it is said that the ratio
of (high) estrogen and (low) testosterone level is the main factor for production of spiders. Changes in the
plasma estradiol level, however, have not been found to correlate with the appearance and disappearance of
spiders.
DIFFERENTIAL DIAGNOSIS:
      1. Mosquito bile-The fresh mosquito bite marks blanch like spiders. H/O using mosquito net in night
           should be taken. Mosquito bite marks may present anywhere in the body.
      2. Hereditary hemorrhagic telengectasia (HHT)-Telengectasia (greek-dialation of the ends of the
           vessels) are small dilated blood vessels which may be visible on the skin surface, particularly in
           the lips and they blanch on pressure Common sites of HHT are mucosal surfaces like tongue, lips,
           nose, palate, pharynx, esophagus and stomach. It is generally connected with a single vessel.
           Telengectasia may be seen in CREST syndrome.
      3. Hemorrhagic spots-Petechiae and purpura never blanch on pressure.
      4. Venous star-It is seen in persons with high venous pressure and it never blanches on pressure. It is
           2-3 cm in diameter.Common sites are back, legs, lower part of anterior chest wall and dorsum of
           foot. Here the blood flows from the periphery to the central part in contrast to vascular spiders
           where blood flows from the centre to the periphery
      5. Campbell de Morgan's spots (cherry angioma) - bright red elevated, non-compressible spots; these
           are very common in aged persons (size 1 to 2 mm in diameter). It is commonly seen in anterior
           abdominal wall and front of the chest.They do not blanch on pressure and usually elevated from
           the skin surface
WHY THE SPIDERS ARE MOSTLY SEEN IN NECKLACE AREA?
It is said that spiders are seen in the area drained by superior vena cava (above the line joining both
nipples). Actually the basic cause is not known but it is expected that exposure of the necklace area to
sunlight may damage the skin in such a way that appropriate internal stimulus may provoke the devel-
opment of spiders in the said area
DRAW INFERENCE IF A PREVIOUSLY SEEN SPIDER DISAPPEARS:
      1. The Hepato-cellular failure is corrected (good prognosis), or
      2. The fall of blood pressure in a case of hepato-cellular failure (commonly due to fresh hae-
           matemesis or melaena) may be responsible for the disappearance of spiders (bad prognosis).
CONCLUSION: Students should search spiders meticulously in its area of distribution. Spiders are very
often missed if a clinician is not careful. Always confirm it by 'blanching response' after application of
pressure by a pinhead.
PALMAR ERYTHEMA
WHA T IS THIS?
Palmar erythema is mottled, bright red cutaneous vasodilatation seen mainly over the thenar and
hypothenar eminences. It is commonly seen in a setting of hepato-cellular failure. The palms become
bright red in color [and also warm). Thus another name of palmar erythema is 'liver palms'. The soles of the
feet may be affected
SITES AFFECTED WITHIN THE PALM: I) Thenar eminence, 2) Hypothenar eminence, 3) Pulp of the
fingers, and 4) Bases of the fingers.
 METHOD OF DEMONSTRATION: Like the spider naevi, palmar erythema blanches on pressure. Here, a
glass slide is used for application of pressure and the redness of palm reappears after release of pressure. ]n
the absence of glass slide press the patient‘s palm with your thumb. Often the palm f1ushes synchronously
with the pulse rate after being pressed by a glass slide.
 CLINICAL ASSOCIATIONS:
     1. Hepato-cellular failure.
     2. Alcoholic cirrhosis.
     3. Long-continued rheumatoid arthritis.
     4. Pregnancy.
     5. Thyrotoxicosis.
     6. Chronic leukaemias.
     7. Rarely in some normal persons (familial).
     8. Sometimes seen in conditions associated with hyperdynamic circulation e.g. high fever.
* Remember, POLYCYTHEMIA causes redness of the palm and sole; so, search for plethoric face and
dusky conjunctiva.
AETIOPATHOGENESIS: Same as spider naevi.
SKIN AND APPENDICULAR CHANGES IN HEPATO-CELLULAR FAILURE:
     1. Spider naevi.
     2. Palmar erythema.
     3. Bleeding manifestations- Due to coagulation disorder (increased prothrombin time) and defects in
          the platelet (number and functional abnormalities) petechiae, purpura, ecchymosis may be seen.
     4. 'Paper money skin'-Jt is usually seen in upper arms and also observed in the common sites for
          spider naevi. These are nothing but small blood vessels and resemble silk threads in United States'
          dollar bills.
     5. White spots- Seen in arms and buttocks (demonstrated after cooling the skin). These are fore-
          runners of a spider.
     6. White nails- This is due to opacity of the nail bed. All the fingers may be affected but thumb and
          index fingers are especially involved. Hypoalbuminaemia is thought to be responsible for pro-
          duction of white nails (thus, sometimes seen in nephrotic syndrome).
     7. Gynaecomastia- May be unilateral and is produced due to hyperoestrogenaemia. It is said that
          spironolactone therapy is the commonest cause of gynaecomastia in a patient of cirrhosis of liver.
     8. Clubbing- Specially seen in biliary cirrhosis.
     9. Jaundice-In case of severe jaundice, skin may become yellow. Jaundice gives some guide to the
          severity of hepato-cellular failure.
     10. Diffuse pigmentation of the body, particularly over the face.
     11. Scanty pubic and axillary hair




                                    EXAMINATION OF THE HANDS
THE HANDS
After the initial appraisal of the patient, the formal physical assessment often begins with examination of
the hands and pulse.
Anatomy.
The hand is a highly developed structure and its area of representation in the cerebral cortex is
appropriately extensive Whilst the palmist may claim to read more from the hand than is justified, critical
examination can indeed provide much reliable information Attention should be paid first to general features
and then to detailed consideration of individual structures on an anatomical basis
The keratinous nail plate is produced mainly m the nail matrix, which lies in an invagination of the
epidermis, the nailfold, on the back of the terminal phalanx of each digit The matrix runs from the end of
the floor of the nailfold to the distal margin of the lunula ('half moon'), and from it the nail plate grows
forward covering the nail bed A small part of the nail, the undersurface, is formed from cells in the nail bed.
Nails grow throughout life.' Fingernails grow more quickly than toenails, the growth in fingernails being
approximately I cm in 3 months.
The hand is a precision tool and a power tool. The flexor and extensor muscles of the forearm
provide the powerhouse of the hand and wrist. However, without the use of intrinsic muscles
of the hand, neither proper grip nor fine movements are possible. The interphalangeal joints
allow only flexion and extension, with the metacarpophalangeal joints also allowing a little
abduction and adduction when they are extended. The wrist provides flexion, extension, radial
and ulnar deviation and circumduction .The radial, ulnar and median nerves are all essential
for normal hand function. The radial nerve innervates the wrist and finger extensors. The
ulnar nerve innervates the adductor of the thumb and most of the interossei and lumbricals.
The median nerve innervates the bulk of the flexor muscles in the forearm and the opponens
and abductor muscles of the thumb.

Examination sequence
    Inspect the general features of the dorsal and then the palmar aspects of both hands.
    Note specific changes in the skin, nails, tendons (sheath or surrounding tissue) and
       joints(deformity and swelling).
    Look for evidence of muscle wasting.
    Assess the temperature and degree of sweating.
    Test hand function especially power and fine pinch and look for any sensory disturbance
    Palpate the joints of the hands and wrists and periarticular soft tissues to elicit tenderness and to
       identify the bony or soft tissue nature of any swelling.
    Palpate the flexor tendon sheath, by placing the examining index fingers across the volar aspect of
       the patient‘s fully extended fingers and then asking the patient to open and close the fingers,
       allowing crepitus to be detected.
    Palpate the flexor tendons from the sides to detect synovial swelling (the Savill pinch test).
    Palpate for local swellings of tendons, especially at the mouth of the fibrous flexor sheath. If a
       swelling on the tendon is felt, look for triggering of the finger (i.e. locking of the finger in flexion
       as the tendon nodule engages in the mouth of the fibrous sheath).
    Ask the patient to perform fine pinch (as if threading a needle). Pinch grip may be decreased in
       lesion in the line of action of the thumb metacarpal, particularly scaphoid fractures.
    Assess the range of joint movements.
    Note the range of wrist dorsiflexion (0-90º).
    Note the range of wrist flexion (0-90º).
    Note the grip strength by asking the patient to grasp two of the examiner‘s fingers. If the range of
       movements of the joints is not full, the patient may be unable to grip two or even three of the
       examiner‘s fingers

POINTS TO NOTE:
   A. Shake hand with the patient (to assess surface temperature. skin and the grip strength) may reveal:
        i. Warm and moist hand-thyrotoxicosis, type II respiratory failure.
        ii. Cold and moist hand-anxiety neurosis. In a cold or cool climate the temperature of the
            patient‘s hand is a good guide to the blood flow. If the hand is warm and cyanosed, it can
            be deduced that arterial oxygen saturation is reduced. In most patients with heart failure the
            hands tend to be cold and cyanosed due to vasoconstriction in response to a low cardiac
            output. If they are warm the cause of the heart failure may be thyrotoxicosis or cor
            pulmonale.
      iii. Cold and dry hand-myxedema. Hands are broad and fingers appear short and stubby from
            thickening of the subcutaneous tissues. Square palm, short,fat and blunt fingers and short
            radius-cretinism.
      iv. Patient may not relax his hand after handshake-Myotonia.
      v. Weak grip strength-weakness of small muscles of the hand or weakness of flexor muscles.
      vi. Rough, thick palm-phrenoderma (vitamin A or essential fatty acid deficiency), arsenic
            poisoning,
      vii. Tylosis (hyperkeratosis of palm often associated with esophageal carcinoma-a rare inherited
            form of esophageal cancer is associated with tylosis, a thickening of the skin on the soles of
            the feet and palms of the hands).Palmar keratoses, especially when multiple may be
            associated with arsenic toxicity. Skin, bladder and lung cancer may also be associated with
            palmar keratoses, but here the keratoses may be few or single.
      viii. Part of generalized eruption to palm and soles-secondary syphilis, Reiter‘s syndrome, rare
            case of disseminated gonococcaemia, erythema multiforme (from any of its causes).

B. Color changes:
    i. Anemia or pallor (the palmar creases become pale when the Hb level is <7 gm/dl).
    ii. Jaundice-mainly the palms, dorsum rarely.
    iii. Cyanosis-tips of fingers nail beds and palm.
    iv. Palmar erythema.
    v. Janeway's lesion (non-tender erythematous maculopapular lesion present in thenar
          eminence-in SBE).
    vi. Carotenaemia (orange-yellow or lemon yellow color of palm).
    vii. Coal miners may have small blue tattoo marks in the skin of their hands and in other sites
          where particles of coal dust have been embedded in the scars of minor injuries. In miners
          and in those with professional tattoos, the blue color in the skin is due to black particles
          (carbon or Indian ink) changed in appearance by the scatter of light as it passes through and
          is reflected back from the skin. This explains why veins normally look blue, while in the
          elderly, with very thin skin, the true red color of the blood may be seen.
    viii. Purple discoloration of the finger tips-atheroembolism from a proximal subclavian
          aneurysm.

C. Finger deformities
     i. Arachnodactily (the hand is long with tapering, long slender fingers-the word literally
          means ―spider fingers‖)-Marfan's syndrome [.Arachnodactily is no longer part of the
          criteria for diagnosis of Marfan‘s syndrome- the criteria are as follows: an upper segment to
          lower segment (crown to pubis/pubis to floor) ratio of 0.85 or less, dislocated lens , a
          substantial family history of the disorder, and aortic root disease]. Arachnodactily are
          sometimes associated with ASD or other congenital cardiac anomalies. In hypogonadism
          the fingers are often slender and feminine.
          Causes:
             a). Marfan's syndrome
             b). Hypogonadism
             c). Hypo-pituitarism
             d). Homocystinuria
             e). Normal individuals
     ii. Enuchoidal hand: the hand is long and narrow and thin-skinned, with delicate and tapering
          fingers.
     iii. Polydactyly (extra finger/super numery fingers)-
             Causes:
             a). Congenital
             b). Familial
             c). Associated with VSD
             d). Laurence-Moon-Biedl syndrome.
             e). Turner's syndrome
     iv. Syndactyly (joined /webbed fingers)-often associated with underlying congenital heart
           disease. May occur in normal individuals or in those with, certain congenital abnormalities.
           It is seen in Poland's syndrome (absent unilateral pectoralis major muscle with TOF).
     v. Clinodactyly (incurved finger)-commonly affects the little finger in Down's syndrome
           (short and thick hand. short thumb arising at a level lower than normal from the palm with
           incurving of the distal phalanx of the little finger and a single palmar crease is seen over the
           palm) .
     vi. Sclerodactyly (tight skin over the phalanges)-Scleroderma the distal inter-phalangeal folds
           are lost. To make this more clear, have the patient maximally flex all inter-phalangeal
           joints.( many patients with severe Scleroderma are unable to do this).if one examines one‘s
           own distal inter-phalangeal skin lines, one will see that they are retained during flexion.
     vii. Broad massive hand with thick, large, square/blunt-tip fingers with broad and square nails–
           'paw like hand' (spade-shaped hand)-acromegaly. The increase in bulk consists of largely
           soft tisues.The diagnosis of acral enlargement may also be based on the history of an
           increase in size glove, ring, shoe, and /or hat.
     viii. Bradydactyly (short fingers)-Down‘s syndrome, Turner's syndrome,
           mucopolysaccharidosis.
     ix. Short fourth metacarpal-one can diagnose, a short fourth metacarpal without taking a x-ray
           by having the patient make a fist and noticing that the fourth knuckle is dimpled inward.
           Short fourth and fifth metacarpals producing 'dimpling sign'(knuckle-knuckle-dimple-
           dimple sign).Shortening of this bone is seen in pseudo-hypoparathyroidism -& pseudo-
           pseudo- hypoparathyroidism, gonadal dysgenesis (turner‘s syndrome) and 10% of normals
     x. Metacarpal index-by palpation one can estimate the metacarpal length to width ratio
           (metacarpal index) as a method of quantitating the elongation of the metacarpal bones in
           Marfan‘s syndrome. The independent co variable is postero-anterior hand films taken with
           the hands flat on the plate against the plate, which are used for measurement of the second
           through fifth metacarpals. The ratio of the length of the bone divided by the width (at the
           midpoint of the length) is used to generate an average, whose upper limit of normal is 8.8
           for men and 9.4 for women.
     xi. Holt-Oram syndrome: the thumb is hypoplastic and in the same plane as the rest of the
           fingers. Thumb may be tri-phalangeal. Fifth fingers may be missing. There may be radio-
           ulnar synostosis. The radius may be absent.
     xii. Absence of digits: absence of one or more fingers may be congenital. Thumb may be absent
           in Fanconi's congenital aplastic anemia.
D. Clubbing
E. Wasting of the small muscles of hand: leprosy, MND, syringomyelia, rheumatoid arthritis etc.
F. Hand in syringomyelia--burns and whitlows; resorption of the terminal phalnges, puffy
   appearance of the hands (the ‗succulent‘ hand/ ‗sausage fingers‘); weakness and wasting of small
   muscles of the hand.
   Thick and fleshy (‗sausage fingers‘) seen in
      Syringomyelia
      Acromegaly
      Myxedema
      Psoriatic arthropathy
G. Pulsation
     i.       Capillary pulsation. In cases of aortic incompetence Quincke‘s sign may occasionally be
              present. It is elicited by compressing lightly the end of the finger nail until the capillary
              bed blanches. The wide pulse pressure in aortic incompetence causes alternate blanching
              and reddening of the nail bed.
     ii.      Digital artery pulsation.
     iii.     Pulse-give the classical description (some clinicians may not like to include 'examination
              of pulse' under examination of the hand).

H. Tremor:
     i.    Static tremor.
     ii.   Action tremor.
       iii.    Intention tremor, and
       iv.     Flapping tremor-

I.   Swellings
       i.      Osler's node (red, raised tender nodules mainly on the pulp of fingers, or on thenar or
               hypothenar eminences)-seen in SBE.
       ii.     Heberden's node (marginal osteophytes)-small hard bony nodules seen at the dorsal
               aspect (lateral & medial) of distal interphalangeal (DIP) joints (at bases of terminal
               phalanges) in osteoarthritis (nodal OA).
       iii.    Bouchard's node-small hard bony nodules seen at the dorsal aspect of proximal
               interphalangeal (PIP)
       iv.     Joints in osteoarthritis. OA tends to spare MCP joints. In OA distal interphalangeal and
               first carpometacarpal joints are usually involved.
       v.      Rarely, rheumatoid nodules-fleshy and firm on extensor surface of knuckles.
       vi.     Gouty tophi-rare in hands. White subcutaneous-juxta-articular. These occur more
               frequently on the ears and feet.
       vii.  Calcinosis-scleroderma. Calcific deposits-white subcutaneous on finger pulp in
             Scleroderma, dermatomyositis.
      viii. Edema over dorsum of the hand. Edema may be part of generalized process or may arise
             from local veins or lymphatic obstruction or disuse as with a hemiplegia.
J.   Deformities
       i.      Spindle-shaped fingers (due to swelling of PIP joints)-in rheumatoid arthritis,
               Scleroderma,
       ii.     Swan neck deformity (hyperextended PIP joints and fixed flexed DIP joints)-rheumatoid
               arthritis. It is due to subluxation at the proximal interphalangeal joint and tendon
               shortening at the distal interphalangeal joint.
       iii.    'Boutonniere' or button-hole deformity (fixed flexed PIP joints and hyperextended DIP
               joints) -Rheumatoid arthritis. This is due to head of the phalanx sliding dorsally between
               the lateral slips of the extensor tendon, the middle slip having been damaged.
       iv.     Volar subluxation with ulnar deviation of hand-rheumatoid arthritis.
       v.      Z-deformity of thumb (hitchhiker's thumb)-rheumatoid arthritis.
       vi.     Swelling of DIP joints only-osteoarthritis, psoriatic arthropathy.
       vii.    In psoriasis ‗telescoped' phalanges may produce shortening of fingers with gross
               impairment of function. Finger shortening due to severe destructive arthritis in psoriatic
               disease is called arthritis mutilans. The hand may take up a main en lorgnette appearance
               due to a combination of shortening and telescoping of the digits.
       viii.   Dupuytren's contractures (flexion contractures of ring and little fingers due to thickening
               and shortening /contraction of palmar fascia/aponeuorsis-commonly involving the ulnar
               side). This initially affects the proximal and middle phalanx of the ring finger and later
               the little finger may be affected. It almost always spares the index and thumb. It is often
               bilateral and occasionally may affect the soles of the feet. This is usually inherited but
               may accompany other conditions.
               Causes are:
                    a. Repeated trauma to palm.
                    b. Alcoholic cirrhosis.
                    c. Phenytoin sodium therapy in epileptics.
                    d. intake of oral contraceptive pills.
                    e. Working with vibrating tools.
                    f. Diabetes mellitus.
                    g. May be familial
                    h. idiopathic
       ix.     Surgical deformities like club hand, MadeIung's deformity, mallet finger etc.
       x.      Claw hand-
      xi.  Main d' accoucheur-metacarpophalangeal (MCP) joints are flexed; the PIP and DIP joints
           are extended with opposition of the thumb. It is commonly seen in tetany and is also
           known as carpal spasm.
    xii. The method of demonstration of carpal spasm is known as Trousseau's sign.There is
           another Trousseau's sign in medicine which is characterized by migratory
           thrombophlebitis in a patient with carcinoma of the pancreas.
    xiii. Jaccoud's arthritis-rheumatic arthritis usually heals without deformity.
    xiv. Very rarely, minor deformity of hand may persist.
K. Nail changes
    i.     Growth is slowed by acute illness and ischemia. It is increased in psoriasis. Injury to the
           nail matrix is by far the most common cause of changes in the nails and may permanently
           impair their growth. Longitudinal ridging and beading of the nail plate increases with age
           and is not abnormal. Similarly, occasional white transverse flecks (striate leukonychia)
           are seen frequently in normal nails; they are probably caused by minor and repeated
           trauma to the nail matrix and, contrary to the popular lay belief, are not due to insufficient
           calcium. Excessively shiny or polished nails are evidence of frequent rubbing of the skin
           by the nails.
    ii.    Pitting nails (terminal IP joint swelling may occur with psoriatic pitting i.e. small
           depressions in the nail and ridging of the nail on that digit-onychopathy)-psoriasis,
           eczema when affects the proximal nail fold, alopecia areata(rare) etc.
    iii.   Beau's line, due to temporary arrest of nail growth-transverse ridge/grooves develops
           after recovery (a few weeks) from any febrile illness at the same time on all nails and
           which move out to the free margins as the nail grows or in zinc deficiency.
           Causes:
                   o Acute febrile illness
                   o Pneumonia
                   o Exanthems-measles,mumps
                   o Myocardial infarction, pulmonary infarction
                   o Child-birth
                   o Drug reaction

      iv.     Horder's line or splinter hemorrhage (linear longitudinal hemorrhage underneath the
              nails, lying parallel to the long axis of the nail)-SBE(probably the result of vasculitis in
              the nail bed), trauma(one or two are commonly seen under the nails of manual workers),
              trichinosis, systemic vasculitis(rheumatoid arthritis,SLE) ,sepsis elsewhere in the body
              ,hematological malignancy or profound anemia etc.
      v.      Mee‘s line-white line of 1-2 mm width appears above lunula (the white part at base of
              nail) in arsenic poisoning.
      vi.     Koilonychia- chronic iron deficiency anemia. The nail becomes soft, thin brittle and flat,
              and ultimately spoon-shaped. The normal convexity is lost and replaced by a concavity.
      vii.    Onycholysis (separation of the nail plate from the nail bed)-Candidiasis, ringworm
              infection, psoriasis, lichen planus, minor trauma (especially if the nails are left long) etc.
              It may also occur in thyroid disease (hypothyroidism, hyperthyroidism); photo-
              Onycholysis-doxycycline, chlortetracycline and chloramphenicol.
      viii.   Nail changes in psoriasis-pitting (small depressions in the nail), onycholysis,
              hyperkeratosis (thickening of nail), ridging and discoloration.
      ix.     Nail may be missing in nail-patella syndrome - presents with (hereditary) nephrotic
              syndrome.
      x.       Nail-fold thrombi- Scleroderma and other collagen vascular diseases.
      xi.     Green nail- severe pseudomonas infection.
      xii.    Blue lunula/blue-half moons- seen in CuS04 poisoning and hepatocellular degeneration;
              Wilson‘s disease. Blue to black nail bed with a subungual hematoma, melanoma or
              fungal infection.
      xiii.   Red lunula/red half-moons-seen in CCF.
      xiv.    Red nail:CCF
      xv.     Black nail:: Peutz-Jeghers syndrome, Cushing's syndrome, Addison's disease
      xvi.     Bitten nails-patients with anxious personality. The short, irregular nails of the nail-biter
               may suggest some instability of personality.
      xvii.    Fungal infection of nails-thickening, crumbling, discoloration-Candidiasis, ringworm
               (tinea unguium).
      xviii.   Shiny nails- indirect evidence of Pruritus.
      xix.     Leukonychia (white nails) - seen in hypoalbuminaemic conditions like cirrhosis of liver,
               nephrotic syndrome, severe malnutrition, other wasting diseases etc. the nail beds
               opacify,often leaving only a rim of pink nail bed at the top of the nail. The thumb and
               index nails bilaterally are most often involved. The exact mechanism is uncertain. It may
               be that compression of capillary flow by extracellular fluid is the explanation.
               Leuchonychia is not unique to hypoalbuminic states, but can also occur with renal failure,
               lymphoma or fungal infection, anemia, CCF, rheumatoid arthritis or be congenital.
      xx.      Yellow nails in yellow nail syndrome; it is characterized by yellow finger and toe nails,
               clubbing and onycholysis; other components of the syndrome are lymphedema of the
               extremities and pleural effusion, edema of finger, ankle, and face,infection-
               sinusitis,bronchitis,bronchiectasis,carcinoma of skin, larynx ,endometrium ,lymphoma,
               agamma-globulinaemia ,psoriasis..
      xxi.     Ribbing of the nails associated with Malabsorption syndrome.
      xxii.    Half and half nails/Lindsay nail (white proximally and red-brown distally) are seen in
               patients with chronic renal failure. Brown lines near the end of the nails occur in CRF,
               but the mechanism is uncertain.
      xxiii.   Drugs- rarely drugs like anti malarials and phenothiazines discolor nails.

L. Skin changes (mainly dorsum of the hand)
     i.    Hyperpigmentation.
     ii.   Hypopigmentation. Vitiligo may be restricted to the hands or face or widespread.
     iii.  Icthyosis (fish skin).
     iv.   Palmar xanthoma and tubo eruptive xanthomata over the elbows and knees are
           characteristic of type III hyperlipidaemia. Tendon xanthomata are yellow or orange
           deposits of lipid in the tendons which occur in type II a hyperlipidaemia. These can be
           seen over the tendons of the hand and arm.
     v.    Lilac-colored knuckles in dermatomyositis (Gordon's sign).
     vi.   Petechiae, purpura, ecchymoses. Purpura is really any short of bruising, due to
           hemorrhage into the skin. The lesions can vary in size from pinheads called petechiae to
           large bruises called ecchymoses. If the petechiae are raised (palpable purpura), this
           suggests an underlying systematic vasculitis, dysglobulinaemia (e.g. cryo globulinaemia,
           where the lesions are painful) or bacteraemia.
     vii. Rash (from diseases or drugs)
     viii. The smooth hairless hands of a child become lined and hairy in the adult male unless
           hypogonadism is present. Manual work may produce specific callosities due to pressure
           at characteristic sites. In contrast, disuse results in a soft, smooth palmar skin and
           prolonged recumbency affects the soles likewise.

M. Miscellaneous:
    i.     Nicotine staining (actually caused by tar as nicotine is colorless) in right index and
           middle fingers in chronic smoker. This does not indicate the number of cigarettes
           smoked.
    ii.    Palmar dermatoglyphics-Single palmar crease (simian crease-bilateral ) in Down's
           syndrome. Normal two transverse palmar lines are replaced by a single line that
           completely crosses the palm.
    iii.   If both transverse lines are maintained, but the proximal one completely crosses the palm,
           it is referred to as Sydney crease.
    iv.    Involuntary movements like chorea, athetosis etc.
    v.     Power of individual small muscles should be tested; sensory loss. if any. should be
           detected
    vi.    Paronychia or whitlow. Paronychia is the term used to describe inflamed, bolstered and
           swollen nail folds. Chronic paronychia is seen most commonly in those with a poor
                   peripheral circulation, in those involved in wet work, in diabetes and those who are
                   overenthusiastic when manicuring the cuticles.
           vii.    Movement at different joints- to find out any restriction of movement.
           viii.   Loose-jointedness -tested by passive hyperextension of fingers and even hyperextended
                   fingers may touch the forearm. It is commonly seen in Osteogenesis imperfecta, Marfan's
                   syndrome, Ehlers-Danlos syndrome and in some normal persons.
           ix.     Pulp atrophy. Telengectasia, digital infarction, digital ulceration, digital gangrene,
                   triphasic color response of Raynaud's phenomenon-in Scleroderma or SLE (features of
                   vasculitis-vasculitic changes around the nail folds consists of black to brown 1 to 2 mm
                   lesions due to skin infarction and occur typically in rheumatoid arthritis ). Pits and healed
                   scars in the finger pulps-secondary Raynaud‘s syndrome. Ragged cuticles and dilated or
                   thrombosed capillaries in the proximal nailfold are an important pointer to connective
                   tissue disease. Dilated capillaries (periungual telengectasia) in the proximal nailfold is
                   characteristic of SLE, Scleroderma, Dermatomyositis (use magnifying glass).
           x.      Test for finger-flexion jerk.
           xi.     Posture. This may be almost diagnostic. Examples include the flexed hand and arm of
                   hemiplegia, wrist drop or radial nerve palsy and ulnar deviation in long-standing
                   rheumatoid arthritis
           xii.    In fractures of the scaphoid the only finding may be tenderness localized in the
                   anatomical snuff-box. Occasionally the bones of the hand, particularly the phalanges,
                   may be involved in granulomatous or other generalized disorders such as Sarcoidosis,
                   Paget‘s disease or thyrotoxicosis. Acute dactylitis is characteristic of sickle cell disease in
                   children, grave‘s disease, autoimmune hyperthyroidism may be associated with finger
                   clubbing and periosteal new bone formation in the phalanges.
           xiii.   Some people speak with their hands. For example, the hand pressed flat on the top of the
                   head accompanying a complain of headache suggests a psychogenic symptom ‗something
                   weighing on the mind‘.
X-RAY HANDS:
Soft tissues
      Generalized increase in thickness-spade like hands in acromegaly, sausage digit in psoriatic
          arthropathy
      Soft tissue calcification- CREST –scleroderma, dermatomyosistis
      Localized thickness-gout, pericapsular inflammation, soft tissue tophus in gout, rheumatoid
          nodules, Bouchard and Heberden's nodes in osteoarthritis.
Joints:
      Symmetrical peripheral small joints except DIP-rheumatoid arthritis
      Pitting in nails with DIP and skin lesions-psoriasis
      Osteoarthritis-DIP (Heberden's nodes)/ PIP (Bouchard's nodes) with osteoporosis.
Deformities:
      Ulnar deviation and subluxation-rheumatoid arthritis-swan neck, boutonnière deformity
      Look for syndacyly or polydactyly-pulmonary stenosis/ ASD /Laurence-Moon-Biedl syndrome
      Short metacarpals-pseudo-hypoparathyroidism (knuckle-knuckle-dimple-dimple syndrome),
          pseudo- pseudo hypoparathyroidism, Turner's syndrome.
Erosion of terminal phalanageal tufts
      Seen in sarcoidosis, hyperparathyroidism, scleroderma with 'pseudo-clubbing' and psoriasis.
Coarse trabeculations:
      Chronic hemolytic anemia, Paget's disease, lipoidoses-Gaucher's syndrome.
Middle phalanx:
      Subperoosteal erosion along the radial border is an early sign of hyperparathyroidism.
EXAMINATION OF THE HAND IN SLE AND SCLERODERMA:
EXAMINATION OF THE HAND IN LEPROSY:
     1. Skin changes in TT and LL
     2. Claw hand with wasting of the small muscles of hand, and
     3. Trophic changes - dry and rough skin, brittle nails, loss of hair, digital ulceration and gangrene,
          tapering and conical fingertips with trophic ulcers.
EXAMINATION OF THE HAND IN RHEUMATOID ARTHRITIS:
First sit the patient over the side of the bed and place the hands on the pillow with palms down.
     1. Spindle-shaped fingers.
     2. Swelling of the wrist and different joints (MCP and PIP) in the hand- No swelling at DIP joints. It
           is worth remembering that rheumatoid arthritis of the wrist tends to spare the radial side of the
           joint. In fact a severe arthritis of the wrist that spares the ulnar side and vigorously attacks the
           radial side is likely to be OA (degenerative). ‗Square hand of OA‘-OA of the Ist MCP joint-joint
           stiffened and adducted. In rheumatoid arthritis joint feels warm, differentiating it from the ‗cool‘
           synovitis of ‗OA‘ or trauma.
     3. Swan neck deformity (described earlier)- Due to disruption of the volar plate of PIP joints, often
           with associated rupture of the insertion of flexor sublimis.
     4. Button-hole deformity (described earlier)- Chronic sinuvitis of PIP joints lead to protrusion of
           joint between two lateral slips of extensor tendon.
     5. Volar (palmar) subluxation with ulnar deviation of hand- MCP joint subluxation;Due to bowstring
           action of displaced extensor tendons. The whole hand, but specially the fingers from the MCP
           joints, is deflected to the ulnar side. Ulnar deviation is deviation of the phalanges at the MCP
           joints towards the lateral(ulnar) side of the hand. The best fingers to check ulnar deviation are the
           third and index fingers since many normal older persons will appear to have mild ulnar deviation
           of the other fingers. However, in severe carpal rheumatoid arthritis, all the fingers show a clear
           ulnar deviation.
     6. Z-deformity of thumb-consists of hyperextension of the interphalangeal joint and fixed flexion and
           subluxation of the MCP joint. Due to muscle wasting, rupture of tendon and weakened joint
           capsule.
     7. Palmar erythema
     8. Joint movements are painful and restricted.
     9. Function of the hand-
                i. Grip-strength is poor. Tested by getting the patient to squeeze two of the examiner‘s
                      fingers.
                ii. Key grip-is the grip with which a key is held between the pulps of the thumb and
                      forefinger. Ask the patient to hold this grip tightly and try to open up his fingers.
                iii. Opposition strength-is where the patient opposes the thumb and little finger and the
                      difficulty with which these can be forced apart is assessed.
                iv. Practical test -such as asking the patient to undo a button or write with a pen, should be
                      performed.
     10. Wasting of the small muscles of hand (gives the hand a flattened appearance) - Chiefly due to
           disuse atrophy or carpal tunnel syndrome or rarely by prolonged use of Corticosteroids.
           Interosseous atrophy, best noted by inspecting the dorsum of the hand in oblique lighting, which
           results in hollow ridges appearing between the metacarpal bones.
     11. Digital infarction, digital gangrene, splinter hemorrhage..
     12. Nail-fold thrombi.
     13. Carpal tunnel syndrome.
     14. Rheumatoid nodule (rare in hands). The extensor surfaces of the upper extremities are the best
           places to find rheumatoid nodules. The presence of rheumatoid nodules predicts 90%chance of
           having rheumatoid factor. Rheumatoid nodules may be found in the subcutaneous tissues,
           especially over the elbow/upper end of ulna, forearm and hand, but also in the lungs, pleura and
           other organs (heart valves, myocardium or vocal cords). Rheumatoid nodules are areas of fibrinoid
           necrosis with a characteristic histological appearance and are probably initiated by a small vessel
           vasculitis. They are localized by trauma but can occur elsewhere, especially attached to tendons,
           over pressure areas in the feet or hands.

    15. Causes of arthritis with nodules
            i. Rheumatoid arthritis
            ii. SLE ( rare )
            iii. Rheumatic fever (Jaccoud‘s arthritis)-very rare )
            iv. Granulomas e.g. sarcoidosis ( very rare )
    16. Rheumatoid nodules are quite hard, may be tender and are attached to underlying structures.
    17. Gouty tophi have a firm feeling and often appear yellow-colored under the skin.
    18. Trigger finger (flexion deformity from which the finger can be extended only by force due to
        thickening of a section of digital flexor tendon; it tends to jam when passing through a narrowed
        part of its tendon sheath). Rheumatoid arthritis is an important cause. Typically, flexion of the
        finger occurs freely up to a certain point where it sticks and cannot be extended (as flexors are
        more powerful than extensors). The application of greater force overcomes the resistance with a
        snap.
    19. Rupture of the extensor tendons of ring and little fingers (rare). Excessive use of the tendon may
        result in tenosynovitis. This commonly produces a sensation of local crepitus and swelling over
        the tendon sheath. A common site is the extensor pollicis tendon at the wrist where it crosses the
        radial styloid (de Quervain‘s tenosynovitis).
    20. Palmar tendon crepitus-the palmar aspects of the examiner‘s fingers are placed against the palm of
        the patient‘s hand while he flexes and extends the MCP joints. Inflamed palmar tendons can be
        felt creaking in their thickened sheaths and nodules can be palpated.

    21. Purpuric rash (thrombocytopenia due to Felty's syndrome).
    22. Raynaud's phenomenon
    23. Feel and move: turn the hands back again to the palm down position. Palpate wrists with both
         thumbs placed on the dorsal surface with the wrists supported underneath with the index fingers.
         Feel gently for synovitis (boggy swelling) and effusions. The wrist should be gently flexed
         (normally possible to 75 degrees) and extended (also possible to 75 degrees) with the examiner‘s
         thumbs. The radial deviation (20 degree) is tested. Note any tenderness or limitation of movement
         or joint crepitus. Palpate the ulnar styloid for tenderness which can occur in rheumatoid arthritis.
    24. Go on to MCP joints which are palpated in a similar way with the two thumbs. Again passive
         movement is tested. Volar subluxation can be demonstrated by flexing the MCP joint with the
         proximal phalanx held between the thumb and fore finger and rocking the MCP joint backwards
         and forward. In a normal joint there is very little movement possible with this maneuver.
         Considerable movement may be present with ligamntous laxity or subluxation.
    25. Tinel‘s sign-tap over the flexor retinaculum which lies at the proximal part of the palm. This may
         cause paraesthesiae (pins and needles) in the distribution of the median nerve, when thickening of
         the flexor retinaculum has entrapped the nerve in the carpal tunnel. If the carpal tunnel syndrome
         is suspected, ask the patient to flex both wrists for 30 seconds-parasthesiae will often be
         precipitated in the affected hand if the syndrome is present (wrist flexion test ).
    26. Arthritis frequently involves the small joints of the hands. Common conditions include OA,
         rheumatoid arthritis and psoriatic arthropathy.
    27. The seronegative (non-rheumatoid) spondyloarthropathies (e.g. Reiter‘s disease) tend
         predominantly to involve the joints of the lower limb. Acute synovitis of the IP joint of Hallux in
         Reiter‘s disease; differential diagnosis-gout.
Differential diagnosis of a Deforming polyarthropathy
    a) Rheumatoid arthritis
    b) Seronegative spondyloarthropathy,particularly psoriatic arthritis,Ankylosing spondylitis or
         Reiter‘s disease
    c) Chronic tophaceous gout
    d) Primary generalized osteoarthritis

Sausage shaped phalanges-due to interphalangeal arthritis and flexor tendon sheath
edema.
Causes:
     a) Psoriatic arhtropathy
     b) Ankylosing spondylitis
     c) Reiter‘s disease
RAYNAUD PHENOMENON
This condition is characterized by intermittent spasm of digital arteries induced by cold and relieved by
heat. Young women are most often affected and usually no underlying cause can be found (Raynaud's
disease), but some cases are associated with occlusive arterial disease, arteritis, blood disorders, neurogenic
lesions or repeated trauma to the hands. The patient complains that, when exposed to cold, the fingers and
less commonly the toes go numb and white, sometimes with patchy cyanosis. This is followed by redness,
throbbing and tingling due to a reactive hyperemia occurring either spontaneously or on rewarming. The
hands may appear normal between attacks but trophic lesions develop in long-standing cases, especially
those associated with organic disease. The fingers may then become thin and tapered with tight shiny skin
('scleroderma'}, telengectasia, deformed atrophic nails and infarcts causing painful ulcers at the fingertips.

Feet and toes:
Genu varum (bow legs)
Causes:
      a). Rickets
      b). Osteomalacia
      c). Osteitis deformans (Paget's disease)
      d). Achondroplasia
Genu valgum (knock knees)
Causes:
      a). Congenital
      b). Rickets
Large feet
It is seen in acromegaly
Short and broad feet
It is seen in Achondroplasia
"Rocker bottom" feet
This is a severe type of flat foot with a protuberant heel. Seen in trisomy-18 (Edward's syndrome, which
may be associated with PDA)
Pes cavus (claw foot)
Causes:
      a). Familial
      b). Peroneal muscular atrophy
      c). Fredrick's ataxia
      d). Syringomyelia
      e). Spina bifida occulta
      f). Anterior poliomyelitis
Clawed toes:
It is seen in
      a). Fredrick's ataxia
      b). Peroneal muscular atrophy
Heel pad thickness:
It is the distance measured in a X-ray film of the patient's foot taken laterally from the lower most point of
the calcaneum to the lower most point of the heel PAD soft tissue shadow.
Heel PAD thickness is said to be increased when
      a). It is more than 23 mm in males
      b). It is more than 21 mm in females
Causes of increased Heel pad thickness:
      a). Acromegaly
      b). Myxedema
      c). Obesity
      d). Peripheral edema
      e). Infection or injury to heel
      f). Eptoin therapy

'VASCULITIS' AND ITS CHARACTERISTIC SKIN CHANGES:
Vasculitis is the necrotizing inflammation of blood vessels.
Endothelial edema and proliferation with hemorrhage contribute to the occlusion of the vascular lumen and
subsequent ischemic changes.
Examples:
             A). Large and medium arteries: Giant cell arteritis or cranial arteritis.
             B). Medium and small arteries: Polyarteritis nodosa.
             C). Small arteries: Allergic granulomatosis.
             D). Small arteries, arterioles and venules, Wegener's granulomatosis.
             E). Capillaries, arterioles and venules: Hypersensitivity vasculitis.
             F). Dermatological manifestations:
               1. Large arteries - Digital gangrene.
               2. Small arteries
                          a). Palpable purpura.
                          b). Urticarial rashes.
                          c). Morbilliform eruptions (look like measles rashes).
                          d). Maculopapular eruptions.
               3. Arterioles and very small arteries –
                          a). Digital infarction
                          b). Digital ulceration
                          c). Nail-fold thrombi
                          d). Bullous lesion
                          e). Splinter hemorrhage
                          f). Raynaud‘s phenomenon
                          g). Vasculitis in collagen vascular disease is responsible for the characteristic skin
                               lesions.

ABNORMALITIES OF THE CHEST WALL

Abnormalities of the chest wall are not infrequently present without disease of the thoracic contents. The
softness of the bones in childhood renders the chest liable to deformities if the normal relationship between
intra thoracic pressure and that of the atmosphere is disturbed.
Mention the common chest deformities-
  1.       Kyphoscoliosis
  2.       Barrel-shaped chest
  3.       Pigeon chest(Pectus carinatum)
  4.       Funnel chest(Pectus excavatum)
  5.       Alar chest
  6.       Unilateral or bilateral, depression or fullness of the chest
  7.       Deformity associated with ankylosing spondylitis.
  Kyphoscoliosis-
        The curvature of the spine is normally concave forward (kyphotic) in the thoracic and sacral regions
        and convex forward (lordotic) in the lumbar and cervical regions.
        The normal shape of the thoraco-lumbar spine is an S-shaped curve. Examine the patient standing
        and sitting in the erect posture. If there is an abnormality, note which vertebrae are involved and at
        what level any vertebral projection is prominent. Note the presence of any local projections or
        angular deformity of the spine.
        Palpation:the major landmarks are the spinous processes of C7(the vertebra prominens) and the last
        rib, which articulates with the 12th thoracic vertebra. In many patients, however, the last rib cannot
        be distinctly felt and this is therefore rather untrustworthy as a guide to this level.
        The neutral position of the spine is a normal upright stance with head erect and chin drawn in. note
        any curvature of the spinal column, whether as a whole or of part of it. The curvature may be an
        anterior, posterior, or lateral direction.
        Kyphosis means backward bending of vertebral column with its convexity posteriorly(posterior
        curvature).
Scoliosis means lateral bending of the vertebral column and may be towards either side. It is always
accompanied by rotation of the bodies of the vertebrae in such a way that the posterior spinous
processes come to point towards the concavity of the curve. The curvature is always greater than
appears from inspection of the posterior spinous processes.
Kyphosis and scoliosis are often combined, particularly when the cause is an idiopathic spinal
curvature, beginning in adolescence.
These are abnormalities of alignment of the dorsal and lumbar spines. They may lead to asymmetry
of the chest wall, and cause maldistribution of ventilation and blood flow in the lungs. Abnormalities
of thoracic spine curvature are common. Kyphosis or scoliosis by itself rarely leads to respiratory or
cardio-vascular complications. Severe kyphoscoliosis may have profound effects on pulmonary
function, as the chest deformity may diminish the volume of the lungs & reduce the ventillatory
capacity of the lungs (may significantly restrict lung movement), and increases the work of
breathing. Ultimately type II respiratory failure (hypoxia, hypercapnea), pulmonary hypertension,
RVF and chronic cor pulmonale develop (at an early age-middle life-symptoms & signs usually do
not appear until the fourth or fifth decade). Thoracic kyphoscoliosis ranges in degree from the minor
changes in spinal curvature seen in many otherwise healthy subjects to grossly disfiguring and
disabling deformities.
The thoracic spine usually exhibits a slight smooth kyphosis, which increases in the elderly and
especially in osteoporosis.
Common causes of kyphoscoliosis are:
     1. Congenital
     2. Vertebral diseases like ankylosing spondylitis, senile osteoporosis, osteoarthritis,
         rheumatoid arthritis etc. Ankylosing spondylitis restricts the expansion of the chest by
         immobilizing the costo-vertebral joints, while kyphoscoliosis may so diminish the volume
         of the lungs as to cause cardiac and respiratory failure in middle life.
     3. Carie‘s spine-with gibbus (acute angualtion in the spine) formation.
     4. Neurological causes-neurofibroamtosis, friedrich‘s ataxia, syringomyelia.poliomyelitis and
         cerbral palsy.
     5. Occupational or postural.
     6. Miscellaneous-Marfan‘s syndrome(congenital kyphoscoliosis & sternal deformity0,
         Turner‘s syndrome, after throracoplasty etc. Extensive unilateral fibrosis or collapse of the
         lung in childhood may give rise to scoliosis.
  Gibbus-localized angular deformity (in contrast to a gentle curve)-causes-fracture, Pott‘s disease
  (spinal TB), or by a metastatic malignant deposit.
  Thoracic scoliosis may alter the position of the mediastinum in relation to the anterior chest wall,
  with the result that abnormalities in the position of the trachea and the apex beat may be
  mistakenly attributed to heart or pulmonary disease. The common form of scoliosis with convexity
  to the RT side displaces the apex beat towards the concavity i.e. to the LT side. Trachea may be
  displaced in simple scoliosis. It should be remembered that the commonest cause of displacement
  of the apex beat is deformity of thoracic cage, usually scoliosis.
  Method of diagnosis-
       1. Scoliosis-the patient will stand straight (chest must be exposed fully ) and the observer
            looks for scoliosis from his back. Observe whether the convexity is present in the LT or
            RT side. After wards it may be corroborated by palpation of the spine.
            In scoliosis due to muscle spasm (e.g. with lumbo-sacral disc protrusion syndromes), the
            spinal curvature and rotational deformities decrease in flexion. When scoliosis is caused
            by inequality of leg length it disappears on sitting because the buttocks then become
            level. Scoliosis secondary to skeletal anomalies shows in a spinal flexion as a ‗rib hump‘
            due to rotation. The curve may be either S shaped or C shaped. The former is more
            likely to be structural, and the latter to result from a paralytic condition. Look for high
            shoulder, a prominent hip or a projecting shoulder blade. Have the patient lean forward as
            you observe from behind, with his shoulder blades at your eye level. Look for asymmetry
            in the scapulae and the erector spinae muscle masses.
            Scoliosis is a lateral curvature of the spine that usually becomes apparent during the years
            of growth. If neglected it can progress to cause severe deformity and impairment in
          respiratory mechanics. Therefore, a check for this condition is part of the screening
          physical examination of children and adolescents.
          Structural scoliosis may be congenital, resulting from developmental anomalies such as
          hemivertebra or asymmetric fusion of two or more vertebrae. Cryptogenic scoliosis might
          result from a slight unilateral weakness of the trunk musculature , or asymmetric growth
          at the epiphysis plates of the vertebral bodies.
          Known causes of structural scoliosis include Neurofibromatosis, osteogenesis imperfecta,
          osteomalacia, or unilateral thoracic conditions such as chronic empyema. Paralytic
          scoliosis may be sequelae of poliomyelitis, progressive muscular dystrophy, friedrich‘s
          ataxia, or syringomyelia. Compensatory scoliosis is due to muscle spasm and /or pain in
          the spine or its associated soft tissues.
          Idiopathic scoliosis is disorder of puberty of unknown etiology, which may result in
          progressive and serious deformity with significant long term morbidity. It is more
          common in girls. Since it is frequently difficult to detect in standing or lying position
          ,the young patient should be asked to touch their toes, with the observer directly behind
          them. Scoliosis is seen as a curve in the trunk and asymmetry of the posterior ribs.
     2. Kyphosis-the observer inspects the back from the sides in profile i.e. in a tangential view
          from both sides are necessary. The patient will stand straight with fully exposed chest. In
          kyphosis, there is increase in the antero-posterior diameter of the chest.
‗Lordosis‘ means forward bending of the vertebral column with its convexity anteriorly. There are
natural lordotic curves in the cervical and lumbar regions. It is commonly seen in pregnancy, poor
posture, wearing high heels, secondary to hip joint disorders, in large abdominal tumors or
massive ascites. Flattening of lumbar lordosis may occur in painful conditions of the lower back
such as sacrolilitits, or a herniated intervertebral disc. An exaggerated lordosis can be primary (as
in rickets, cretinism or spondylolisthesis), but is usually compensatory for other deformity of the
spine or diseases in the lower limbs [flexion contractures of the hip, congenital dislocation of the
hip, progressive muscular dystrophy, paralysis from poliomyelitis, obesity of the abdomen, dorsal
kyphosis, and shortening of the Achilles‘ tendon].
Describe the normal chest:
     1. Elliptical in cross section i.e. transvrerse: antero-posterior diameter =7:5; in infancy and
          early childhood the ratio is 1:1(circular)
     2. Bilaterally symmetrical and without undue elevation or depression
     3. Both the sides of the chest move simultaneously and symmetrically.
     4. Subcostal angle is acute i.e.<90º (males having a narrower angle than females).

Abnormality chest:
A. Symmetrical

    o    Barrel shaped chest (pulmonary kyphosis)-

             1.   Antero-posterior diameter of the chest is increased (A P: T R=1:1) and it is
                  circular in cross-section. Thoracic cage becomes cylindrical or barrel like and
                  cross section appears circular (Antero-posterior diameter is equal to the
                  transverse diameter).

             2.   The whole chest is relatively fixed in full inspiration.

             3.   Intercostal spaces are full, ribs less obliquely set and wide apart.

             4.   There may be kyphosis of thoracic vertebrae. Fullness of supraclavicular fossae.

             5.   The chest tends to move upwards in one piece.

             6.   Wide subcostal angle.
                       7.   Prominence of sternal angle. The sternum is displaced outwards and the ribs and
                            clavicles are more horizontal than normal. Expansion is limited and inspiration
                            can only be achieved with the aid of accessory muscles of the neck elevating the
                            clavicles.

                       8.   Rarely encircling prominent veins are seen in the lower part of the chest.

                       9.   Causes-severe obstructive airway disease or emphysema. However the barrel
                            chest is not evident in all cases and may be found in healthy subjects. Increased
                            A P diameter does occur in acromegaly, along with kyphosis.

         The degree of chest deformity in emphysema is not a reliable guide to the severity of the
         functional defect. An increase in the antero-posterior diameter may also be due to thoracic
         kyphosis unrelated to respiratory disease.
         Pigeon chest (Keel breast; pectus carinatum)-
            1.        Triangular chest(in cross section) with prominent sternum(marked bulging) & forward
                      protrusion of the adjacent costal cartilages.
            2.        Rickety rosary (bead like rounded enlargement/knob-like projections of bilateral costo-
                      chondral junctions; best demonstrated in the 4th, 5th & 6th costo-chondral junctions.
                      Scorbutic rosary in contrast have sharper rib angulation and backward sternal
                      displacement.
            3.        Harrison‘s sulcus (linear depression or sulcus present transversely from the sides of the
                      xiphoid process. It is due to pulling in effect of costal attachment of diaphragm-in
                      drawing of the ribs to form symmetrical horizontal grooves above the costal margins,
                      which are themselves are everted. These deformities are thought to result from lung
                      hyperinflation with repeated strong contractions of the diaphragm while the bony
                      thorax is still in a pliable state.).
                             Cause:
                                      a) Childhood Bronchial asthma (severe)
                                      b)Repeated lung infections since childhood
                                      c) Rickets
                                      d)Idiopathic/congenital variant.
Rachitic chest (Rickety chest): it is due to unduly soft bones found in childhood. Following deformities are
noticed
               1. Pigeon chest
               2. Harrison‘s sulcus
               3. Rickety rosary
               4. Funnel chest (pectus excavatum or cobbler‘s chest)
Funnel chest (pectus excavatum or cobbler‘s chest)-
         1.      There is an exaggeration of normal depression in the lower part of the sternum or less
                 commonly, depression of the whole length of the body of the sternum and of the costal
                 cartilages attached to it.
         2.      Antero-posterior diameter <transverse diameter
         3.      Undue prominence of the costo-chondral junction
         4.      Pectus carinatum is usually asymptomatic, but when there is marked degree of depression
                 of the sternum, the heart may be displaced to the LT, giving a spurious impression of
                 cardiac enlargement, and the ventillatory capacity of the lungs restricted.
         Cause:
                 a) Repeated lung infections since childhood
                 b) secondary to childhood rickets
                 c) occupational-in cobblers (also known as cobbler‘s chest-cobbler pressing the kneel
                           against the lower end of sternum).
                 d) Familial/hereditary-often congenital in origin.
Combinations of Harrison‘s sulcus, pigeon-chest, and funnel breast are sometimes present. Rickets favor
their production by making the bone abnormality soft, and sometimes leaves further traces as a ‗rickety
rosary‘. Deformities of the thoracic cage can also result from osteomalcia due to Malabsorption from the
bowel.
Alar chest:
     a) Drooping of both the shoulders.
     b) Winging of the scapula (i.e. prominent vertebral border of scapula).
     c) Chest is narrow and tubular.
     d) Cause: it is found in tall and thin normal persons.
Flat chest-
               In this A P diameter of the chest is reduced because the sternum is close to the spine.
               It may be associated with chronic nasal obstruction(due to adenoid hypertrophy),
                   secondary to childhood rickets or bilateral pulmonary TB.
 Cross-sectional views in different types of chest deformities:
      Normal-elliptical
      Barrel shaped-circular
      Pigeon chest-triangular.
D/D of rickety rosary (seen in scurvy)-the costo-chondral junctions are prominent and appear sharp as well
as angular. Rickety rosary-the prominence is dome-shaped and semicircular.
Abnormal chest-
Asymmetrical: it may be secondary to
      Deformity of the spine (e.g. scoliosis)
      Unilateral bulging or prominence as in
              a) Pleural effusion
              b) Pneumothorax
              c) Malignant pleural disease
              d) Compensatory unilateral lung hypertrophy
              e) Localized bulging e.g. aortic aneurysm, pericardial effusion or liver abscess, local disease
                   of the ribs or sternum & fibrotic changes in the lungs and pleura.
      Unilateral flattening or retraction as in
              a) Collapse
              b) Fibrosis
              c) Unilateral wasting of muscle as in poliomyelitis.

      Thoracic operations-surgery may result in varying degrees of chest deformity, as may severe chest
                                            trauma.
   Fullness or depression of the chest:
            A. Fullness-
                  1. Massive pleural effusion
                  2. Empyema thoracis
                  3. Pneumothorax
                  4. Hydropneumothorax or pyopneumothorax
                  5. Bronchogenic carcinoma
                  6. Pericardial effusion
                  7. Emphysema produces bilateral dullness
                  8. Empyema necessitatis or encysted pleural effusion produce localized dullness
            B. Depression-
                  1. Fibrosis of the lung
                  2. Collapse of the ling
                  3. Thickened pleura or pleural adhesions
                  4. After rib resection in thoracotomy.
INSPECTION‘ FOR SHAPE AND MOVEMENT OF THE CHEST.

             A. Inspection of the chest is best done in standing or sitting (if standing is not possible)
                position in good day light with proper exposure of front and back of chest. The patient
                should stand absolutely straight. Chest is inspected from the :

                                     i)    Front
                                      ii)      Back

                                      iii)     The sides in profile

                                     iv) Looking from above (standing behind the patient), over the
                  shoulders for the upper part of the chest.

                  Sitting means the patient will sit on a stool. If standing or sitting is not possible for the
                  patient, then inspect the chest in lying down position (patient lies absolutely straight in
                  bed in supine position) from the:

                                              i. Top

                                             ii. Foot end of bed

                                             iii. The sides in profile

                                             iv. Head end

                                             v. Back(try to turn the patient to any one side).

             B. Points to note:

                  1.   Any deformity, fullness or depression (i.e. shape of the chest), apical impulse etc.

                  2.   Back (winging of the scapula, dropping of the shoulder, kyphoscoliosis, gibbus,skin
                                                      changes, sinus etc)

                  3.   Whether both the sides of the chest are moving simultaneously and symmetrically.

Classical winged scapula is found in paralysis of nerve to serratus anterior (C5,6,7).

IN GENERAL SURVEY HOW DO YOU EXAMINE ‗RESPIRATION‘?

         A. Rate-normal respiratory rate in an adult is 14-18/minute;at birth the rate is about 40/minute.

    Variations:

             a)   Increased rate-tachypnoea; causes-exertion, hypoxia, respiratory centre stimulation e.g.
                  fever, acidosis, pain.

             b) Decreased rate-bradypnoea-respiratory centre depression e.g. poisoning and brain
                tumors, neuro-muscular paralysis e.g. myasthenia.

             Rate of respiration is counted surreptiously by placing the hand in the epigastrium or with the
             fingers held on the radial pulse to avoid patient‘s attention to breathing. The rate is counted
             for a full minute.

             Respiration/pulse=1:4

         B. Rhythm-changes in rhythm are diagnosed by inspecting the movement of the chest. There
         may be wide variation in health.

             a)   Irregularly irregular or Biot‘s breathing-it is a chaotic type of breathing-the respiration is
                  sometimes slow, sometimes rapid, sometimes superficial, sometimes deep but without
                  any constant relation of succession between the two types, with pauses at irregular
                  intervals. This is most commonly seen in meningitis (raised intracranial tension),
                  especially in children.

              b) Regularly irregular or Cheyne stoke‘s respiration. It is a gradual waxing and waning type
                 of respiration due to respiratory centre involvement. Here CO2 retention (resulting out of
                 respiratory centre depression) stimulates the respiratory centre,which washes out the CO2
                 resulting into hypocapnoea. This in turn depresses the respiratory centre. It is manifested
                 as Cheyne –stokes breathing. It occurs in
                   i) Deep sleep
                   ii) Narcotic poisoning
                   iii) Cardio-respiratory embarrassment
                   iv) Intracranial disorders.
              c) Kussmaul‘s breathing (air-hunger): it is rapid and deep breathing. It is hallmark of
                 acidosis. It occurs in
                   i) DKA
                   ii) Uremia
                   iii) Alcohol intoxication
                   iv) Starvation ketosis



         C. Type—diagnosed by inspecting the movement of the chest and abdomen.

         Variations:
         a) Thoracic-adult women, anxiety,peritonitis,huge ascites,hysteria,diaphragmatic palsy.
         b) Abdominal-adult men, young children, pleurisy,ankylosing spondylitis, intercostal muscle
               paralysis.
         c) Abdomino-thoracic-young children, sometimes in adult men.
         d) Paradoxical respiration-diaphragmatic palsy.
           In females, intercostal muscles play more (so thoracic type-thoracico-abdominal) and in males,
           diaphragm plays more (so abdominal type-Abdomino-thoracic) in normal respiration.
           If it is other way round there is a problem above or below the diaphragm.
           Females with predominantly abdominal type respiration –any painful condition in chest (e.g.
           pleurisy, chest trauma, Pneumothorax etc).
           Males with predominantly thoracic type respiration-any painful condition in abdomen ( e.g.
           acute peritonitis),huge ascites etc.

         D.       Depth- inspect the excursion of chest-

         Variations:
             a) Shallow-narcotic poisoning
             b) Deep-hyperpnoea, hyperventilation e.g. in metabolic acidosis.
             c) Bilateral diminished movements:emphysema,bronchial asthma.
             d) Unilateral diminished movements:collapse,fibrosis,pneumonia,pleural
                  effusion,Pneumothorax.


X-rays are produced by energy conversion when a fast moving stream of electrons produced by cathode
(i.e. a heated tungsten filament) strikes the anode.
The high energy electron beam when strikes the anode, produces X-ray radiation by the following
mechanisms:
The electron strikes the nucleus of the atom-in the process they lose all their energy in the form of X-ray
radiation
The high speed electrons strike the electrons within the orbits around nucleus.
                                            THE CHEST X-RAY
     A chest X-ray is the common non-invasive investigation that helps not only in the diagnosis of
      respiratory disease but also in cardiac-vascular disease too, hence, should be performed routinely in
      these disorders. The chest film is the mirror of many systemic disorders in addition to the
      information it reveals for respiratory and cardiovascular disorders.
   Analysis of the chest X-ray is complimentary to the patient's physical examination. It provides much
      information about the heart and lungs.
   One should feel personally responsible for viewing a patient‘s radiograph.
   The X-ray plate should be examined in a view box, usually from a distance of 2 feet.
   The plate should be correctly mounted in the view-box.
   Plain radiography was first used in 1896.
   Most medical students faced with giving their interpretation of a chest X-ray either opt for a 'spot
      diagnosis'(usually wrong) or raise their eyes to heaven, hoping for divine inspiration. However, a
      systematic approach is generally more useful! More is missed by not looking than by not knowing.
              Note the name of the patient, sex and age and to be sure that it is the correct patient's
                  film.
              Checking the Lt or Rt marker prevents missing Dextrocardia.
Older patients tend to have
              An enlarged heart
              Emphysema
              Calcification in the bronchi, costal cartilages, or coronary arteries.

     The standard Chest X-ray is postero-anterior (PA) view of an erect patient, which is taken with the
      film against the front of the patient‘s chest and the X-ray source 2 m (6 feet) behind the patient; the
      hands placed on the waist and the elbows drawn a bit anteriorly. This minimizes the magnification of
      the cardiac silhouette and distortion of images. By placing the elbows in a forward direction, the
      scapulae go apart and thus they never produce obstruction to the lung fields.
     P-A chest X-ray –anteriorly situated heart is as close to the film as possible and its image will be
      minimally enlarged.
     The patient is made to stand straight facing the cassette. The chin is raised with the shoulder rotated
      forward so as to displace the scapula out of lung fields.
     Centering of the X-ray beam is done at D4 vertebrae level, perpendicular to the film and exposure is
      made with the subject holding breath in full inspiration.
     A well-centered film is one where medial ends of the clavicles are equidistant from the vertebral
      spinous process at T4-T5 level. If the patient is rotated, this will accentuate the hilum that is turned
      forwards.

Properly taken X-ray should satisfy the following 4 points:
     Size-it should include some portion of the neck above and some portion of the abdomen below to
         find cervical rib and gastric bubble respectively. The sides should include costo-phrenic angles on
         both sides. Apices and C P angles should be on the film.
     Inspiration-
              1. It should be taken while breath is held during deep inspiration, not too deep inspiration.
                  This is known by finding the costo phrenic angles at or below the 7 th or 8th rib. If the
                  angles are at 4th or 5th space, one may see pseudo-cardiomegaly. At least six posterior
                  ribs should be seen above RT diaphragm.
             2.   It normally shows anterior portion of 6 ± 1 ribs and posterior portion of 9 ± 1 ribs. More
                  ribs/intercostal space can be seen in COPD, bronchial asthma and emphysema.
             3.   To judge the degree of inspiration, count the number of ribs above the diaphragm. The
                  anterior end of the 6th rib should be above the diaphragm as should be the posterior end
                  of 10th rib.
             4.   If more ribs are visible then the lung is hyperinflated. If fewer ribs are visible, then
                  patient has not held the breath during full inspiration. It is important to note this because
                  poor inspiration will make the heart size to look larger and cause the trachea to appear
                  deviated to Rt.

       Symmetry: both sterno-clavicular joints should be in the same line. Scapula should be out.
       Penetration /proper exposure i.e. dose of radiation -normally some vertebrae should be visible
        behind the cardiac shadow, but not every one. Mid-cardiac inter-vertebral disc spaces should be
        visible. A good exposure in P-A view is one in which upper thoracic vertebrae can just be
        identified. Normally four thoracic vertebrae are seen. If less then four thoracic vertebrae are
        visualized it is an under-exposed film (the film will be too white). No vertebra is seen behind the
        heart shadow when it is underexposed. Every vertebra is seen in over exposed film and the lung
        fields appear more black. In over-penetrated X-rays you are likely to miss low density shadows.
        Under exposure makes the lung fields hazy. Ideally films should be of medium contrast.
     The film needs to be exposed in full inspiration, so that there is no basal crowding of the
        pulmonary vessels and so that the estimation of CT ratio is accurate. Heart size can be reliably
        assessed only from a P-A chest film. On full inspiration the diaphragm lies at level of the tenth or
        eleventh rib posteriorly, or at the level of 6 th costal cartilage anteriorly (mid-clavicular line). The
        RT hemi-diaphragm lies about 2 cm higher than the LT. The Rt hemi-diaphragm is higher then Lt
        Diaphragm by 3 cm in 95 % of cases. This apparent elevation of the Rt diaphragm (not due to
        liver) is due to the downward displacement of the Lt side of the diaphragm by the heart.
     Rotation-medial end of clavicles should be equidistant from spinous process (mid-line). In other
        words the gap in the sternoclavicular articulation should be equidistant from mid-line. Rotation of
        the patient may make the mediastinum appear distorted.
     If the breast shadows are visualized, the plate is of a female patient.
     Soft tissue shadow: it is widened in case of subcutaneous emphysema and is more prominent in
        supra-clavicular and axillary region.
     Chest X-ray PA view- anteriorly situated heart is as close to the film as possible and its image will
        be minimally enlarged. The Chest X-ray PA view is the common view in use.
     Correct orientation- do not miss dextrocardia-the heart apex will be to the Rt and the stomach gas
        to the lt. Do not be misled by Lt or Rt markers wrongly placed by a sleepy radiographer.
    The side-determination (maintaining anatomical position) is done by the following methods:
             1. Label put by the radiology technician ( L or R). He should label the plate properly with
                   the date of exposure.
             2. Apex of the heart should be on the Lt side
             3. Fundal gas shadow should be on the Lt side
             4. Rt dome of the diaphragm is placed at a higher level than the Lt
             5. Aortic knuckle should be on the Lt side.
             In case of rotation of viscera (dextrocardia with situs inversus), the above formula does not
             serve the purpose and one has to depend only on radiographer‘s labeling.

The standard frontal film is taken by a posteroanterior (PA) projection of an erect patient. A P and supine
films are second best.
An antero-posterior view (A- P view) chest X-ray is normally taken in emergency conditions mostly at the
bed side; while the other view is postero-anterior (PA view) which is common in routine use. These views
in fact reflect the direction of the rays from the source to the plate.
X-ray chest A-P view (patient too ill to stand or sit for standard X-ray) differs from P-A view in the
following:
      Apparent enlargement of the heart due to magnification
      Ribs are more horizontally placed
      Clavicles are straighter
         Lung fields are not well evaluated as the diaphragm is high and scapulae obscure part of the lung
          fields.
      Intervertebral disc spaces are seen better.
      In supine film there is distension of all the posterior (gravity-dependent) vessels & thus the lung
          fields appear more plethoric.
      Spines and ribs (skeletal structures) are best seen in A P view.
      A small pleural effusion may not be visible if it is lying posteriorly.
Chest X-ray PA view is preferred because:
               o This view gives a wider lung field as well as a clear picture of broncho-vascular shadow
                   ( in an A P view, cardiac size is more exaggerated and obstructs part of lung fields)
               o Radiation risk to eyes is negligible.
The scapula should not project over lung fields. It should be remembered that approximately 75 % of the
lung fields are seen in routine PA view of the chest (25 % of lung fields are obstructed by clavicles, ribs,
cardio-vascular shadow and sub-diaphragmatic tissue). While taking an X-ray, the patient should be
unclothed, long hairs should be pinned up, radio-opaque materials e.g. jewelleries should be removed.
When distinction between P A/A P is difficult, it is better to describe as frontal view.
Apicogram: -
Useful for visualization of apical and upper zone lesions, which are partly obscured by the ribs or clavicles
in P-A view. A lordotic view is an A-P view taken with the patient leaning backwards or the patient is
straight and tube is angled upwards. The clavicles and the first rib are projected above the lungs and the
apices are not obscured by bony structures.
Expiratory film (X-ray in full expiration)
This helps to demonstrate
      Small Pneumothorax, which is not obvious on a conventional P-A view. However, most
          pneumothoraces, which are clinically important, are readily seen on inspiration views.
      Localized hyperinflation due to partial obstruction caused by a foreign body, tumor etc. A view in
          expiration is particularly important with a non-opaque inhaled foreign body since the diameter of
          the bronchial wall will be less in expiration and hence the obstruction greater.
      Diaphragmatic movements (films are taken at end of inspiration & expiration)
      Interstitial lesions are better evaluated in expiratory film.
**Radiological findings of foreign body inhalation:
                Hyperinflation of affected lobe (50 %)
                Atelectasis (collapse) i.e. radio-opaque (45 %)
                Pneumonia (5 %)
**AIPGME 2002
Lateral decubitus view –
     This is an A-P view taken with the patient lying on one side using a horizontal X-ray beam. It is useful
     in the following situations: -
           To demonstrate a small amount of free pleural fluid, which collects along the dependent chest
               wall in, the decubitus view.
           To confirm gravitational mobility of larger collection
           To visualize small Pneumothorax not appreciated in P-A view.
           To visualize wall of a cavity or to reveal pulmonary areas obscured by fluid in P-A view.
           To distinguish raised diaphragm from sub-pulmonary effusion.
The X-ray is examined systematically on a viewing box according to the following plan.
Costo-phrenic angle: normally clear, sharp and well defined (acute in angle) in PA view of the chest.
Obliteration indicates
     1. Effusion
     2. Fibrosis
Cardio-phrenic angle (junction of heart and diaphragm): RT cardio-phrenic angle is the place of insertion of
inferior vena cava into the RT atrium. In health, the Rt cardio-phrenic angle is acute or near about right
angle. This angle becomes more acute in RT atrial enlargement and becomes obtuse in LT atrial
enlargement. In pericardial effusion the angle also becomes more acute (Rotch‘s sign).The Lt sided cardio-
phrenic angle cannot be distinctly seen due to presence of epicardial fat pad (especially in elderly fatty
people) and thus it is of no importance radiologically.
View (PA, Lateral, oblique)
Recumbent view:
X-ray taken in lying down position, usually supine when the patient is unable to stand due to serious
illness.
Exposure
Centralization
The position of the patient. Is the patient straight or rotated? If straight the inner ends of the clavicles will
be disposed symmetrically with reference to the vertebral column. Look at the clavicles; if they are at the
same level, then X-ray is centralized and if not, then it is poorly centralized. Any rotation will tend
particularly to alert the appearance of the mediastinum and hilar shadows.
The outline of the heart and the mediastinum-is this normal in size, shape and position?
The descending aorta normally descends on the LT side of the posterior mediastinum. It may be tortuous in
the elderly. Dilatation may be uniform or more localized as with an aneurysm. Dissecting aneurysm may
‗leak‘ causing mediastinal swelling, and a bloodstained or serous ‗sympathetic‘ LT pleural effusion.
Heart casts a homogenous shadow on the chest film. No internal details can be seen within its contour
because the radiodensities of blood, myocardium and or cardiac tissues are so similar that one cannot be
distinguished from the others. Only two borders of the heart, where it contacts the radiolucent air-
containing lung, can be discerned in any one projection.
The mediastinum including the trachea can be deviated by a large pleural effusion, a tension pneumothorax
or pulmonary collapse.
Rotation of the patient may make the mediastinum appear distorted.
The position of the trachea-this is seen as dark column representing the air within the trachea (black airy
tube). The cartilaginous rings are not visible. The trachea is not usually straight and is commonly a little
over to the RT of the mid-line at the thoracic inlet. Commonly in the elderly it is somewhat too long and
becomes tortuous. The RT main bronchus is shorter and more horizontal than the LT. The trachea may be
deviated a little to the Lt as it passes the aortic knuckle. (The aortic arch becomes wider and unfolded with
age because of loss of elasticity).

The carina should be seen through the heart shadow and normally has an angle of about 90º, but may be
widened due to subcarinal node enlargement or LT atrial enlargement as with mitral stenosis.
The diaphragm –can the diaphragm be seen on each side? Is it normal in shape and position? Normally the
anterior end of the sixth or seventh rib crosses the mid-part of the diaphragm on each side, although the
diaphragm on the RT may be a little higher than on the LT. Are the cardio-phrenic angles are clearly seen?
The hemi-diaphragms visualized on the frontal films are the top of the domes seen tangentially. Much lung
in the posterior costophrenic angle is not seen in on the frontal film.
The Rt and Lt dome the diaphragm are convex upwards and sharp in outline. The Rt dome is placed high-
up (0.5-2 cm) than the Lt dome.
In the mid-clavicular line, the upper limit of the Rt dome should be between 6 th and 7th intercostal space
anteriorly and 10 the intercostal space posteriorly.
Minor eventrations or a lobulated appearance are common but may also be due to masses below the
diaphragm. Interposition of the colon may also occur in front of and above the liver; this is a feature, which
is common in children and the elderly, sometimes known as the Beclere or Chilaiditi syndrome (colonic
haustrations seen as distinguishing feature).
If the hemi-diaphragms are low and flat, emphysema may be present. A critical look must be made beneath
the diaphragm to see if there is free peritoneal gas.
      Elevated diaphragm-collapse or fibrosis of the lung (basal ),ascites,pregnancy,diaphragmatic
          palsy, abdominal mass, amebic liver abscess (Rt dome)
      Depressed or flat dome-emphysema (bilateral),pneumothorax (unilateral)
      Localized bulge or tenting- amebic liver abscess, sub diaphragmatic abscess, pleural tumor.

 The lung fields- for radiological purposes, the lung fields are divided into three zones on the frontal field.
It is easy then to compare one zone with another for density differences and the distribution of the vascular
'markings'. Zones in the X-ray plate do not correspond with the lobes of the lungs.
       The upper zone extends from the apex to a transverse line drawn through the lower borders of the
          anterior ends of the second costal cartilages.
   The mid-zone extends from this line to another line drawn through lower borders of the fourth
    costal cartilages.
   The lower zone extends from this second line to the bases of the lungs (between fourth and sixth
    costal cartilages) or to the dome of the diaphragm .

Each zone is systematically examined on both sides and any area which appears abnormal is carefully
compared with the corresponding area on the opposite side.

   The minor inter lobar fissure, which separates the RT, upper and middle lobes, may sometimes be
    seen running horizontally in the third and fourth intercostal space on the RT side.

   The apices lie above the level of the clavicles. The upper zones include the apices.

   The transradiancy of the lung field is due to the air filling the lung. The greyness is due to blood in
    the pulmonary vessels. The upper zones of the lungs are normally less well perfused, resulting in
    smaller blood vessels. With raised Lt atrial pressure, there is upper zone blood diversion and the
    vessels are congested.

   Normally lung fields are translucent and look reticular too (due to broncho-vascular markings).
    The vascular shadows (looks white linear) in the lung are casted by branches of pulmonary artery.
    Pulmonary veins (often seen in upper lobes) produce low-density shadow. Branches of pulmonary
    artery (form major bulk of hilar density) and vein are accompanied by a corresponding branch of
    the bronchus. The alveoli, pleura, interstitium and lymphatics produce a very low density shadow
    which is rarely identified in the X-ray film.

    Increase in the white linear shadows ( i.e. broncho-vascular markings radiating from the hilar
     region to the periphery ) may be seen in:
          o Accentuated pulmonary arteries –Lt to Rt shunt in ASD, VSD , PDA .
          o Distension of pulmonary veins -in the Lt sided heart failure ( Lt ventricular or Lt atrial
              failure).
          o Accentuation of bronchial pattern-seen in chronic bronchitis,bronchiectasis
          o Prominence of lymphatic vessels-commonly seen in Bronchogenic carcinoma
          o Thickened alveolar septum-seen in pneumoconiosis, pulmonary fibrosis (ILD).
     Broncho-vascular markings become less prominent in
                   – Pulmonary stenosis
                   – Pericardial effusion
     Linear opacities: atelectasis, septal lines (Kerley B lines -inter-lobar lymphatics), tumor,
     lymphangitis carcinomatosis
 Increase in lung radiolucency occurs with pulmonary vessels loss, as also happens with
     emphysema. Lung radiolucency is lost with an effusion or consolidation.
The bony skeleton-is the chest symmetrical? Is scoliosis present? Are the ribs unduly crowded
(collapse or fibrosis of the lung) or widely spaced (emphysema) in any area? Are cervical ribs present?
Are any ribs eroded or absent? Check that there are no rib fractures or lesions. Erosions or arthritis
around the shoulder joints should be looked for.
Erosion of clavicle:
      Bronchogenic carcinoma
      Multiple myeloma
Absence of clavicle-cleido-cranial dysostosis.
Soft tissue:
         –     Soft tissue abnormalities of the chest wall (wart, angioma, neurofibroma), upper
               abdomen, neck (calcified lymph nodes) and shoulder ,sternomastoid shadows (especially
               in male) may be visible in the Chest X-ray.
         –    Breast and nipple shadow in female; Look carefully for a missing breast shadow in a
              female patient. A mastectomy may provide a diagnostic clue to explain bony or
              pulmonary metastasis, or upper zone post-radiation fibrosis.
         –    Soft tissue gas (sub-cutaneous emphysema) may accompany a pneumothorax or be
              present after a thoracotomy.
         –    Calcified tuberculous glands in the neck should be looked for in patients with lung
              scarring or calcified hilar lymph nodes.
         –    Artifacts (errors in film handling by technician may give rise to white linear shadows or
              hair balls may cast rounded shadows in female ) should be carefully identified.

LATERAL VIEWS:-
        Lateral view of the chest is essential for identification of the lobes and
         segmental details of the lung affected and also to note the cardiac chamber
         hypertrophy. This view is most useful in localizing the lung lesion already
         visible on the frontal film, because interlobar fissures are clearly seen in this
         view
        The Rt hemi-diaphragm crosses through the heart shadow to the anterior chest
         wall and the Lt hemi-diaphragm ends at the posterior cardiac border in lateral
         views of the chest X-ray.
        When taking a lateral view the side to be evaluated should be kept close to the
         cassette to avoid magnification. For lateral view, the patient‘s arms are folded
         and extended above the head.
        Lateral views are indispensable in the localization of lung lesions for the
         postero-anterior view does not show whether a shadow is situated in the
         anterior or posterior part of the chest or (if in the mid-zone) whether in the
         upper or lower lobe. Sometimes a lesion is only seen in the lateral view.
        In examining a lateral view the following is the plan:
Bony cage:
Identify the sternum anteriorly and vertebral bodies posteriorly. The cardiac shadows lie anteriorly and
inferiorly.
Anterior border of the cardiac silhouette-body and outflow tract of RV
RV abuts the lower 1/3rd of sternum.
Posterior border extends from carina to the diaphragm-upper half-back of LA; lower half-posterior
wall of LV.
There should be a lucent (dark) area retrosternally, which has approx. the same density as the area
posterior to the heart and anterior to the vertebral bodies i.e. retro-sternal & retro-cardiac triangles are
normally of similar radio-density. Check for any difference between the two, or for any discrete lesion
in either area. Check for any collapsed vertebrae.
In Lt lateral view Lt ventricular hypertrophy is best visualized as it encroaches the spine and the Rt
ventricular hypertrophy is well visualized as it encroaches the retro-sternal space.
The thoracic vertebrae become less opaque lower down the spine; unless there is pulmonary or pleural
disease. The lowest vertebrae should appear darkest, becoming whiter as they progress superiorly, due
to the thickness of the shoulders and associated muscles. When this picture is reversed think of a lower
lobe collapse or pleural fluid. Interruption of this smooth gradation suggests an abnormality overlying
the vertebral bodies involved.
The posterior costophrenic angle is sharp unless there is fluid or adjacent consolidation.
The hilar shadows are different on the two sides. Note that the LT pulmonary artery lies posterior to
the trachea and carina, whilst the RT pulmonary artery lies anterior. This means that any mass lying
anteriorly in the LT hilum or posteriorly on the RT cannot be a vascular mass, and is most likely to be
due to enlarged nodes.
The diaphragm-as the level of the diaphragm differs on the two sides, a double outline may be seen,
that of the side nearer the film being the clearer. The RT dome is normally higher than the LT. the
hemi-diaphragms are well-defined unless there is pleural or pulmonary disease.
Position of trachea
The lung fields are obscured by two relatively opaque areas, one above and behind, due to the shoulder
joint, and one below and in front due to the heart, which rests on the anterior part of the diaphragm.
There are thus two relatively clear areas-one above and in front, behind the upper part of the sternum,
one below and behind including the angle between the diaphragm and the spine.
Fissures:
                The abnormality on lateral view is detected by distortion of interlobar fissures which
                   are seen as lines.
                The fissures are seen as hairline shadows. The horizontal fissure is at the level of RT
                   fourth costal cartilage.
                The shrinkage of a lobe from collapse or fibrosis distorts this fissures/lines.With
                   collapse its position may be altered, being elevated with upper lobe collapse or
                   depressed with middle or lower lobe collapse.
                The oblique fissures are not seen on the frontal view. The oblique fissure placement
                   is ‗4‘ to ‗4‘. It passes from approx 4 cm behind the anterior costo-phrenic angle
                   through the hilum to T4 vertebral body level.
Remember that chest wall lumps may cause a chest X-ray shadow simulating as intra-pulmonary lesion
e.g. lipomata.
Heart:
The Rt ventricle forms the anterior heart border on the lateral film. The Lt atrium forms the upper
posterior border.
Review: certain parts of the film should be double checked if the x-ray appears normal.
The retro cardiac region should be looked at again. A collapsed Lt Lower lobe will reveal itself as a
triangular opacity behind the heart shadow.
Both apices should be rechecked for lesions, especially pancoast tumors or tuberculosis.
Has the patient a pneumothorax? There will be difference between the tranradiancy of the two lungs.

4 useful points in LT lateral view: it is particularly useful for the evaluation of
      Pericardial disease-pericardial calcification
      RT coronary artery calcification
      Aortic arch anomalies
      LT atrial enlargement–barium filled esophagus helps to diagnose
4 useful points in RT anterior oblique (RAO) view at 45 degrees: -useful in studying the following
structures:
      LT atrium
      Pulmonary conus
      First part of the aorta
      Barium filled esophagus.
4 useful points in LT anterior oblique (LAO) view at 60 degrees: -useful in studying the following
structures:
      Ventricular enlargement
      LT coronary artery calcification
      Thoracic aorta which is seen entirely
      Tracheal bifurcation-it evaluates the effect of enlarged LT atrium on LT bronchus.
4 chambers of the heart are better seen in 4 views:-
      P-A view for LT ventricular enlargement-when it enlarges it moves downwards, posteriorly
         and to the LT.
      RAO view with barium swallow for LT atrial enlargement. Seen as an indentation of barium
         filled esophagus (the sickling effect of compression on esophagus by the Lt atrium). LT
         atrium enlargement is suspected when a bulge is noticed beneath the pulmonary artery in the
         P-A view.
      RT lateral view for RT ventricular enlargement-anterior wall of the RT ventricle is directly
         behind the lower third of the sternum.
         LT anterior oblique view for RT atrial enlargement-it is seen as a bulging of the cardiac
          silhouette to the RT along with increase in curvature of RT border. Estimation of the RT
          atrial size is the least reliable of all the cardiac chambers by X-ray chest.
    Now-a-days cardiac series are not taken. Echo provides a comprehensive assessment of the size of
    individual chambers.
    X-ray chest in an obese individual looks as any /all of the following 4
           The heart is transverse
           The diaphragm is raised
           The intercostal spaces are narrowed
           The chest is broad and short.
    X-ray chest in a thin and tall individual looks as any /all of the following 4
           The heart is vertical
           The diaphragm is low
           The intercostal spaces are wide
           The chest is long and narrow.
    Points to note when assessing the Chest X-ray
          1. Bony skeleton
          2. Position of the patient
          3. Position of the trachea
          4. Outline of the heart
          5. Outline of the mediastinum
          6. Diaphragm
          7. Lung fields.
Systematic examination of the Chest X-ray.
                        Size of the heart
                        Hilar mediastinal contours
                        Lungs –upper. middle and lower zones
                        Review areas.
                          A. Apices
                          B. Behind first rib and medial end of the clavicles
                          C. Behind the heart (cardiac)
                          D. Below the diaphragm; pleural spaces
                          E. Soft tissues
                          F. Skeleton (ribs, vertebrae, sternum, clavicles)
Always search for the following, in an apparently normal looking chest X-ray
                    i)    Small apical pneumonia
                   ii)    Very small collection of pleural fluid.
                 iii)     Fluid level[e.g. hiatus hernia or air/fluid level (e.g. atelectasis)] behind the
                          cardiac shadow
                  iv)     Rib-notching, rib erosion
                   v)     Gas-shadow under the diaphragm
                  vi)     Deviation of trachea
                 vii)     Paratracheal lymph node enlargement
                viii)     Cervical ribs
                  ix)     Mastectomy
                   x)     Rt middle lobe collapse (with loss of clear outline of Rt cardiac border).
A case of diaphragmatic hernia typically presents with:
  –       Severe respiratory distress within the first few hours of life (neonatal period)
  –       Absence of breath sounds and shift of heart sounds (mediastinal shift)
  –       Accompanied by a scaphoid abdomen in infants.
Congenital diaphragmatic hernia: Chest X-ray is usually diagnostic:
A lateral film shows the intestine passing through the posterior portion of the diaphragm. As a result of
swallowed air, coils of air filled small bowel may appear as multiple cystic air filed spaces in the chest.
Occasionally congenital cystic lesion in the lung may produce a similar radiographic picture.
Chest X-ray check-list:
A- Air-way (mid-line, no obvious deformities, no para-tracheal masses)
B- Bones and soft tissue (no fractures, sub-cutaneous emphysema)
C- Cardiac size, silhouette and retro-cardiac density normal
D Diaphragms (Rt above Lt by 1 cm to 3 cm, costo-phrenic angles sharp, diaphragmatic contrast
    with lung sharp)
E- Equal volume (count ribs, look for mediastinal shift)
F- Fine detail (pleura and lung parenchyma)
G- Gastric bubble (above the air bubble one should not see an opacity of any more than 0.5 cm width)
H- Hilum ( Lt normally above Rt by up to 3 cm, no larger than a thumb),hardware(in intensive care
    unit;endo-tracheal tube, central venous catheters)
Read Chest X-ray in six components:
ATTMLL (Are There Ten or More Lung Lesions)
         – Abdomen:
              Liver
              Splenic enlargement (splenic flexure of colon)
              Stomach bubble
              Diaphragmatic position
         – Thorax -soft tissue:
              Apex of chest wall (a symmetry-Pan coast)
              Extra-thoracic trachea and neck
              Breasts
              Pleural thickening or calcification
              Costo-phrenic angina-blunting
         – Thorax -bones
         – Mediastinum
         – Lung-unilateral
         – Lungs-bilateral

The normal cardiac outline-the heart is seen as a flask shaped shadow or ovoid with the apex pointing
to the Lt , lying between the translucent lungs, about 1/3rd of its area to RT of the midline and 2/3rd to
the LT. The apex of the heart is internal to the mid-clavicular line. The mediastinum projects a little
more to the LT than to the RT of the midline.
Triangular masses at either of the lower aspects of the heart may be due to fat, especially in obese
patients. These are very common and are termed ‗fat pads‘.
The RT border of the cardiac shadow is smooth and formed, from above downwards, by two curves:
              1.   A slightly curved portion, the outer edge of the superior vena cava with the
                   ascending arch of the aorta.
              2.   A more convex portion, the outer border of the RT atrium, which ends at the
                   diaphragm.
Some patients are able to lower the diaphragm sufficiently during inspiration to uncover a small,
straight segment of inferior vena cava between the diaphragm and the RT atrium.
The LT border is made from above downwards by (4 step like convexities):
              1.   The prominent knuckle produced by the arch of the aorta as it passes backwards,
                   slightly to the Lt, then downwards (aortic knob-the most distal portion of aortic
                   arch)-a convexity.
              2.   The straighter line of the pulmonary artery (LT branch of the pulmonary artery) or a
                   concavity ( known as ‗pulmonary bay‘/conus)
              3.   LT atrial appendage seen especially if enlarged in penetrated P-A view (short
                   straight portion).
              4.   The wide sweep of the LT ventricle, ending at the apex, where it rests on the
                   diaphragm- the convexity in the lower part.
    The LT atrium lies at the back of the heart and does not form part of the cardiac silhouette seen from
    the front. In the side view it forms the upper part of the posterior border and is adjacent to the
    esophagus.
    The LT margin of the RT ventricle lies about a thumb‘s breadth in from the LT heart border. On the
    surface of the heart it is marked by LAD.
     A *bulge on the Lt cardiac border may be caused by
         1. Lt atrial appendage enlargement
         2. Coronary artery aneurysm
         3. Pericardial defect
     *AIPGME 2000.
     A normal chest X-ray should be described in the following way:
           This is a PA view of the chest with normal exposure, proper centering and without any
                apparent bony abnormality.
           The lung fields are clear with normal broncho-vascular markings; cardio-vascular silhouette is
                within normal limit with normal cardio-thoracic ratio.
                Mediastinum, costophrenic and cardiophrenic angles, domes of the diaphragm and soft tissue
                show no abnormality.
     While describing an X-ray chest, try to maintain the frame of words described in conclusion, along
     with the abnormalities seen.
     THE ABNORMAL HEART SHADOW:
The major part of the heart shadow may lie on the Rt side than Lt, indicates either shift of the mediastinum
to the Rt or meso-cardium (heart lies in the centre) or Dextrocardia (heart lies on the Rt side instead of Lt).
Differential radiological features
First of all, always look for radiographer marking e.g. Lt or Rt at the top of X-ray. Incorrect marking can
produce iatrogenic Dextrocardia. If there is doubt, repeat the film.
Look for the trachea. Shift of the mediastinum indicates shift of the heart due to collapse, fibrosis,
Pneumonectomy.
If marking is correct, and trachea is central, look at apex of the heart; if it lies on the Rt then it is
Dextrocardia. Dextrocardia will be further confirmed by absence of aortic knuckle on the Lt. it will be
present on the Rt side.
Now look at the domes of the diaphragm, higher Lt dome than Rt with air bubble below it confirms situs
inversus.
The heart shadow is said to be enlarged if it occupies more than half of the trans-thoracic diameter.
Causes of enlargement of heart shadow:
              Lt to Rt shunt e.g. ASD, VSD,PDA. This is associated with increased pulmonary
                 plethora.
              Ventricular enlargement.
              Ventricular aneurysm
              Pericardial effusion
Lt to Rt shunt (L→R)
Radiological features
               Look at the X-ray for cardiomegaly. Confirm cardiomegaly by measurement.
               Look at the pulmonary conus. If full and convex, indicates pulmonary hypertension.
               Now look at the shape of the heart. See the apex of the heart which is rounded due to
                  enlargement of Rt ventricle and is being lifted up clear off the diaphragm. As Rt atrium
                  enlarges in Lt to Rt shunt, the Rt border looks also rounded and fuller than normal
               Determine the position of the heart with reference to position of the vertebrae; in Lt to Rt
                  shunt (e.g. ASD,VSD) the heart is sometimes shifted transversely to the Lt and so the Rt
                  edge of the vertebral column is revealed.
               Pulmonary plethora. i.e. Lt to Rt shunt, there is increased blood flow through pulmonary
                  vessels leading to their dilatation called-pulmonary plethora. On X-ray, the vessels
                  especially the pulmonary artery and lung vasculature are prominent ( i.e. broncho-
             vascular markings are visible up to the periphery) and increased pulsations of these
             vessels may be seen on fluoroscopy.
            Look at the aortic knuckle and arch of aorta. It is often smaller due to shunting of blood
             from Lt side to Rt side rather than passing through aorta.




Bulge on the LT heart border is seen in four conditions -
      Enlarged LT atrial appendage
      Ventricular aneurysm (LT ventricular aneurysm produces a distinct bulge or distortion of the
          LT heart border)
      Pericardial cyst
      Myocardial mass.
LT ventricular aneurysm:
A Lt ventricular aneurysm is a cause of heart enlargement on chest X-ray. It can often cause
generalized enlargement of Lt ventricle and be indistinguishable from Lt ventricular dilatation.
                Bulging of a part of the wall of the LT ventricle, which appears as a distinct bulge
                    from the smooth outline of the LT border of the heart, which may be enlarged. If a
                    bulge is noticed, follow it to determine whether it imperceptibly merges with the
                    heart border; if yes, then it is suggestive of ventricular aneurysm.
                Sometimes, a rim of calcification along the heart border may be seen, in long-
                    standing aneurysm .
Cardiac failure:
1. Heart size is enlarged
2. Pulmonary markings are prominent at the apex
3. Kerley B lines may be present.
4. Evidence of pulmonary edema or phantom tumor opacity (which disappears once failure is
     treated) may be present
5. Hydrothorax
Rib notching:
Causes:
1. Arterial:
     a) Aortic: Coarctation of aorta (lower border). This is due to hypertrophy of the intercostal
          arteries in which retrograde flow from the axillary collaterals is taking blood back to the
          descending aorta.
     b) Subclavian: Blalock-Taussig operation (done in TOF)
2. Venous: superior and inferior venae cava blocks
3. Arterio-venous fistula/A-V mal-formation of intercostal vessels
4. Nerves: Neurofibromatosis (upper border of rib) of intercostal nerves
5. Idiopathic
Rib notching:
Superior rib notching:
     Mnemonic=porn-MCH
      Poliomyelitis
      Osteogenesis imperfecta
      Restrictive lung disease
      Neurofibromatosis
      Marfan‘s syndrome
      Connective tissue disease-rheumatoid arthritis,SLE,scleroderma,sjogren‘s syndrome
      Hyper parathyroidism
Inferior rib notching:
     Mnemonic= C-PAST
      Coarctation of Aorta
      Pulmonary-oligaemia/A-V mal formation
        Aortic thrombosis
        Subclavian obstruction
        Blalock-Taussig operation (done in TOF)

Rib erosion (ribs may look moth-eaten):
      i)    Multiple myeloma
     ii)    Bronchogenic carcinoma
    iii)    Hyperparathyroidism(random)
    iv)     Histiocytosis X disease.
Ribs
Sclerotic rib border: benign nature of lesion
Rib destruction
Tumors:
Primary
      Lung
      Breast
      Renal
Round cell tumor:
Ewing-child
Adult
         – Multi myeloma
         – Plasmacytoma
Inflammatory
      TB
      Actinomycosis
      Nocardia
      Blastomycosis
In overpenetrated postero-anterior film the LT atrium can be seen, especially if enlarged, and the aorta
is particularly well shown. Calcification in the pericardium or valves is usually apparent.
The RT lateral film is also of value in showing calcification and in addition is helpful in RT ventricular
hypertrophy when the cardiac shadow comes closer to and higher up the sternum than usual.
Valve calcification is better seen in the lateral view. On the frontal view, the valve calcification cannot
be seen over the spine. Mitral valve calcification is seen below an imaginary line drawn from the
anterior costo-phrenic angle to the hilum (mid-point), whereas aortic valve calcification lies above the
line. On the PA view, the line passes from the Rt cardio-phrenic angle to the inferior aspect of the Lt
hilum.
Heart size-measure the heart size across its widest point in the horizontal plane. Measure the pleural
size across its widest point from the inner rib margins on each side. Cardio-thoracic ratio is a ratio of
maximum cardiac diameter to maximum transverse diameter of the chest. The cardio-thoracic ratio
(CTR) should be less than 0.5, except in neonates, infants, athletes, and patient with skeletal
abnormalities e.g. scoliosis, funnel chest. If the cardiac shadow occupies more than 50 % of the trans-
thoracic diameter, then heart is said to be enlarged. Pericardial effusion or cardiac dilatation increases
the ratio. The maximum transverse diameter of the heart is <15.5 cm in male and < 15 cm in female.
This is the sum of the maximum projections of the RT and LT border of the heart from the mid-line.
Transverse cardiac diameter >15.5 cm is abnormal. The thoracic measurement (maximum width of the
thorax) is the widest diameter measured from the inner edges of the ribs above the costo-phrenic
angles, usually at the level of the RT hemi-diaphragm. An increase of > 1 cm of cardiac diameter from
a prior film is a more reliable index. CT ratio is slightly decreased in emphysema.
In a PA view of the chest, 2/3rd of the cardiac shadow lies on the Lt and 1/3rd on the Rt from the mid-
line.
 A cardiothoracic ratio at the upper limit of normal should not cause alarm if the patient has no reason
to have cardiac failure and no symptoms of it.
Hila: the hila are mostly formed by the pulmonary arteries with the upper lobe veins superimposed.
The Lt hilum is formed mostly by the Lt main pulmonary artery and partly by the Lt upper pulmonary
veins. The RT hilum (at horizontal fissure) of the lung is lower or at the same level as the LT (0-2.5
cm higher-usually 1 cm higher ). The LT has a squarish shape whereas the RT has a V shape. They are
concave in shape and look similar to each other (density similar). A hilum can be more prominent if
the patient is rotated. Change in density denotes rotated film or tumor or lymph
nodes.Lymphadenopathy or a large pulmonary artery will cause hilar enlargement
Cardiac enlargement is caused either by dilatation of the cardiac chambers or by pericardial effusion.
Myocardial hypertrophy only affects the heart size if very severe.
Chest films are most sensitive for detecting chamber dilatation. Cardiac hypertrophy –most difficult to
recognize, as the thickened myocardium tends to encroach on ventricular lumen more than extending
outward and enlarging the chamber silhouette.

Heart size-normal size heart does not guarantee the absence of cardiac disease e.g. angina does not
affect heart size until LV decompensates. Restrictive Cardiomyopathy may be in severe CCF with a
normal appearance heart. In most cases, exact measurement of the cardiac silhouette is not necessary,
as a reasonably experienced observer can achieve an acceptable degree of accuracy by visual
estimation.
The single greatest effect on apparent cardiac size is the degree of inspiration. On a properly positioned
frontal chest film, a reasonable degree of inspiration is indicated if the diaphragm is lowered to at least
to the level of the posterior portion of 9th rib.
With expiration, as the diaphragm moves up, the vertical diameter of the heart is shortened and its
transverse diameter increases. Hence the heart appears larger on expiratory film.
When A P diameter of the chest is small, the heart may be compressed between the sternum and the
spine so that it splays to one or both sides. For this reason the heart often appears enlarged in patients
with straight back syndrome and with pectus excavatum deformity of the sternum. The epicardial fat
pad (actually it is truly extra pleural fat outside the pericardium) can occur in one or both cardiophrenic
angle and make the heart appear larger than actually it is. The cardiophrenic angle often appears obtuse
or the cardiac apex is indistinct. Slightly more radiolucent image of the fat can be easily distinguished
from the greater density of the heart.


Size of the cardiac silhouette and cardiac cycle:
Change in size of the cardiac silhouette can occur between systole and diastole. Chest films are
exposed at random with reference to the cardiac cycle. In the majority of the cases, the difference in
transverse cardiac diameter between systole and diastole is small, no more than several millimeters.
However, in younger patients, especially the male athlete with a slow heart rate and a large stroke
volume phasic change in the normal cardiac diameter can be as much as 2 cm.
Pericardial effusion: means collection of fluid in the pericardial sac leading to enlargement of cardiac
shadow on chest X-ray.
     Causes of pericardial effusion:
          1. Transudative
               CCF
          2. Exudative
                      Infection e.g. viral, bacterial (tuberculosis, Pyogenic), amoebic (rupture of
                          amebic liver abscess into pericardium), fungal (Actinomycosis,
                          Histoplasmosis)
                      Post-myocardial infarction
                      Neoplastic infiltration
                      Collagen vascular disorders e.g. rheumatoid arthritis,SLE
                      Trauma, post-radiation
                      Iatrogenic e.g. post-cardiac surgery
                      Metabolic e.g. uremia
                      Endocrine e.g. myxedema
          3. Hemo-pericardium
                      Trauma
                      Neoplastic infiltration
                      Aortic dissection
                         Bleeding diathesis e.g. leukaemia, anti-coagulation
Radiological features:
                                  Cardiac shadow is enlarged; look at the X-ray and confirm the
                                   enlargement of cardiac shadow by measurements.
                               Globular sharp edged shadow (‗water-bottle configuration‘ or ‗pear
                                   shaped heart‘ or 'Moneybag appearance') with the straightening of both
                                   the borders of the heart. Both the hila are covered by the heart shadow .
                               Enlargement may occur quite suddenly & unlike heart failure –no
                                   associated change in pulmonary vasculature. Lung fields are oligaemic
                                   in pericardial effusion.
               -Echo more specific than X-ray. At least 250 ml of fluid must accumulate before X-ray
               changes are apparent. Echocardiography can detect pericardial effusion as small as 15 ml.
               -The cardio-thoracic ratio is increased. The cardiac landmarks (indentations) on the
               border of the heart (i.e. ups and downs, or convexity-concavity) are obliterated. Rt
               cardio-phrenic angle is obtuse (Rotch‘s sign). In a patient of pericardial effusion, if the X-
               ray is taken in Trendelberg‘s position there is widening of superior mediastinal shadow.
Ventricular dilatation-the PA Chest X-ray does not reliably distinguish LT from RT ventricular
dilatation. For this, the lateral Chest X-ray is more helpful. Dilatation of the posteriorly located LT
ventricle encroaches on the retro-cardiac space, while dilatation of the anteriorly located RT ventricle
encroaches on the retro-sternal space.
In LT ventricular enlargement, as found with aortic valve disease or hypertension there is a prominent
convexity curving below the diaphragm and forming an obtuse angle. The normal concavity below the
aortic knuckle is exaggerated. There is increase in CT ratio; smooth elongation and increased
convexity of the LT heart border. Lt ventricular enlargement causes the heart shadow to enlarge down
and out giving an appearance of boot-shaped heart. In LAO, the LT ventricle enlargement causes
posterior displacement of cardiac contour so that the heart shadow may project far enough back to
overlie the spine.
In RT ventricular enlargement the outline of the apex is turned up and the heart shadow makes an acute
angle with the diaphragm, for example in congenital heart disease. There is increase in CT ratio. The
enlarged RT ventricle pushes LT ventricle leftward, upward and eventually backward. The Rt
ventricular enlargement produces enlargement of cardiac shadow outwards.
Enlargement of the ventricular outflow tract causes filling in and results in convexity of the normal
concavity of the LT heart border below the aortic knuckle.
Concavity of the pulmonary trunk becomes convex:
          – Pulmonary hypertension
          – Lt to Rt shunt in the heart e.g. ASD,VSD,PDA.
Absent pulmonary artery shadow:
          – Pulmonary stenosis
          – Pulmonary atresia
 In LAO view anterior displacement of cardiac outline is considered to indicate RT ventricular
enlargement.
More commonly it is only possible to indicate that there is an increase in ventricular mass without
being able to accurately predict which chamber is responsible. Differentiation of LT from RT
ventricular enlargement may be difficult from the shape of the LT heart border.
Lateral view
-enlargement anteriorly from RT ventricle-obliteration of retro-sternal space from below upwards
-enlargement posteriorly from LT ventricle.
Atrial dilatation- RT atrial dilatation is usually due to RT ventricular failure but occurs as an isolated
finding in tricuspid stenosis and Ebstein‘s anomaly. It produces cardiac enlargement without specific
radiographic signs.
Mitral valve disease:
Mitral stenosis produces a combination of Lt atrial and Rt ventricular enlargement; while mitral
regurgitation produces Lt atrial and Lt ventricular enlargement; other radiological signs are common to
both. The heart in mitral valve disease is called mitralised heart.
Radiological features
         Look at the cardiac shadow which is enlarged in mitral valve disease
        Look at the Lt border. Straightening of the Lt border is due to Lt atrial enlargement.
         Sometimes the Lt atrial enlargement is so great (giant Lt atrium in mitral regurgitation) that
         part of the heart bulges outward (third mogul sign)
        Now look at the Rt border of the heart. Look carefully for a double atrial shadow which is
         best seen in well-penetrated film and is due to Lt atrial enlargement (mitralised heart). The Lt
         atrium also causes the Rt heart border to shift further over to the Rt than usual. For Lt atrial
         shadow, hold the X-ray in Rt hand in horizontal or oblique position in front of you in bright
         light; the double shadow i.e. Double Rt border will be visible as peripheral less opaque and
         inner dense opaque area.
        Look at the carina by following the tracheal shadow to its bifurcation into Rt and Lt bronchi.
         The angle between the two bronchi is < 90°.widenming of this angle suggest Lt atrial
         enlargement.
        Look at the apex. If it is lifted up clear off the diaphragm, the heart enlargement is Rt
         ventricular type (boot-shaped). If the heart lies on the diaphragm, then it is Lt ventricular
         enlargement.
        Look at the pulmonary area. Prominent pulmonary conus indicates pulmonary hypertension.
        Look at the lung fields and pulmonary vasculature. Prominent upper lobe veins (inverted
         moustache sign), haziness of lung field from hilum towards periphery and the transverse
         Kerley's B line indicating interstitial edema and acute pulmonary edema or congestive cardiac
         failure
        Look at the mitral valvular orifice area for flecks of calcification.
LT atrial dilatation occurs in LT ventricular failure and mitral valve disease. Radiographic signs are:
     Flattening and later bulging of the LT heart border below the main pulmonary artery.(the LT
         atrial appendix shows in chest X-ray as a straightening or convexity of the normally concave
         LT border of the heart below the pulmonary artery)-straightening of the Lt border of the heart
         (the base of the pulmonary bay).
     Elevation of the LT main bronchus (displaced upwards by the enlarged LT atrium and lies
         more horizontally), with widening/splaying of the carina.
     Appearance of the medial border (RT border) of the LT atrium behind the RT side of the heart
         /identified through the shadow of the RT atrium (double-density sign/double contour); the
         outer and upper border is due to Lt atrium and the inner and lower border is due to Rt atrial
         enlargement.
     LT atrial enlargement can also be assessed by giving the patient a barium paste to swallow
         and screening him in the RT oblique position. The esophagus is displaced backwards and to
         the RT by the enlarged LT atrium .RAO with barium swallow-demonstrates even slight
         degree of LT atrial enlargement, which cannot be identified by a P-A view.
    Atrial enlargement (Rt or Lt) is often better seen in the lateral view as a posterior bulge.
    ‗Mitralisation‘ of heart or straightening of the Lt border of the heart is due to from above
    downwards:
          i) Small aortic knuckle
         ii) Conspicuous convexity due to dilated pulmonary artery
        iii) Convexity produced due to prominent Lt atrial appendage
        iv) Normal Lt border of Lt ventricle.

Double density shadow cast by LT atrial enlargement may be found within the confines of the heart in
some other conditions also indicating a variety of dilated vascular structures such as these four
     Tortuous descending aorta
     Aortic aneurysm
     Coronary artery aneurysm
     Pulmonary varix.
    In achalasia the esophagus may be considerably dilated, and since it lies in the posterior
    mediastinum behind the heart, its border may be seen through the heart or even to its RT giving an
    apparent ‗double shadow‘ to the RT side of the heart.
RT atrial enlargement –RT border of the heart projects into RT lower lung field.
Prominent ascending aorta is seen in 4 conditions
     Aortic unfolding
     Aortic regurgitation
     Aortic aneurysm
     Post-stenotic dilatation
Enlarged aortic knuckle is seen in 4 conditions:
     Systemic hypertension/atherosclerosis of the aorta
     Aneurysm of aorta
     Aortic regurgitation/aortitis
     PDA.
Prominent aortic knuckle:
     Old age (unfolding of the aorta and atherosclerosis)
     Aortic aneurysm
     Aortitis.
     Post-stenotic dilatation
Small aortic knuckle is seen in 4 conditions:
     Decreased cardiac output
     Mitral stenosis
     Coarctation of aorta
     Intra-cardiac LT to RT shunts.
Prominent pulmonary conus:
               idiopathic dilatation of pulmonary artery
               Post-stenotic dilatation
               pulmonary hypertension

Prominence of the pulmonary trunk is a reliable secondary sign of RT ventricular enlargement with the
following 4 exceptions-
      TOF with hypoplasia of pulmonary trunk
      Idiopathic dilatation of the pulmonary artery
      PDA earlier to the development of Eisenmenger‘s complex
      Straight-back syndrome, pectus excavatum and scoliosis with narrowed antero-posterior
        diameter of the chest. In these conditions heart is compressed, displaced, rotated to the LT
        giving a falsely enlarged pulmonary artery shadow.
Pulmonary artery shadow is absent in:
              Pulmonary valvular stenosis
              Pulmonary artery atresia
              TOF
4 common causes of small cardiac shadow are:
     1. Constrictive pericarditis
     2. Emphysema
     3. Addison‘s disease
     4. Wasting diseases-malnutrition, dehydration, starvation, and anorexia nervosa.

A smaller heart than average heart is difficult to define unless it is seen in a retrospective manner when
it returns to normal size following successful treatment e.g. heart response to steroid treatment in
Addison‘s disease results in enlargement of the heart significantly.




In clinical practice common causes of enlarged cardiac shadow /Cardiomegaly:
      Pericardial effusion
      Cardiomyopathy
      Systemic hypertension
      Valvular heart disease present singly or combination. e.g. AI,M I,MS with M I,etc
      IHD
Enlarged cardiac shadow in radiology:
      Cardiomyopathy (indentations at cardiac border are retained; absence of pulmonary
          oligaemia, Rt cardio-phrenic angle remains acute).
      Pericardial effusion (indentations at cardiac border are lost, pulmonary oligaemia, obtuse Rt
          cardio-phrenic angle )
      Enlargement of heart chambers :
           i) Enlargement of transverse diameter-RVH
          ii) Enlargement in oblique diameter with boot shaped heart-LVH
         iii) Double contour of Rt border-Lt atrial dilatation /hypertrophy.
         iv) Extension of Rt atrial border with increased convexity-Rt atrial dilatation/hypertrophy (
                    a bulge is seen).
      Heart failure (upper lobar veins prominent,Kerley B lines ,phantom tumor/interlobar effusion
          or even hydro-thorax)
      Lt ventricular aneurysm ( a distinct bulge is seen from the wall of the Lt ventricle)
      Chest X-ray taken in full expiration or in lying down position, patients with high diaphragm
          or with cardiac pad of fat, or with skeletal deformity ( e.g. depressed sternum ,scoliosis)- may
          give a false impression of Cardiomegaly (spurious)
Vascular dilatation-
 Aortic dilatation caused by aneurysm or dissection may produce widening of the
     entire upper mediastinum.
 Dissection of ascending aorta causes widening of mediastinum, a LT sided pleural effusion (if
     aneurysm leaks), blood around the apex of the lung(capping).
 Localized dilatation of the proximal aorta occurs in aortic valve disease and produces a
     prominence in the RT upper mediastinum.
 Enlargement of the ascending aorta occurs in syphilitic aortitis with aneurysm, in aortic stenosis
     (post-stenotic dilatation) and in aortic regurgitation.
     Ascending aorta dilatation causes prominence of aortic shadow to the RT of the mediastinum
     between R A & SVC.
 Unfolding of the aorta is seen in atheroma, especially when hypertension is associated. Aortic arch
     becomes wider and unfolded with age because of loss of elasticity.
 The shadow of the superior vena cava is widened in congestive cardiac failure.
 Dilatation of the main pulmonary artery occurs in pulmonary hypertension and pulmonary stenosis
     ,LT to RT shunt and produces a prominence below the aortic knuckle, on the LT heart border .
Intra-cardiac calcification- because the radio-density of cardiac tissue is similar to that of blood, intra-
cardiac structure can rarely be identified unless they are calcified. Valvular, pericardial or myocardial
calcification may occur, and usually indicates important disease of these structures . Calcification of
cardio-vascular system occurs due to tissue degeneration.
Pericardial calcification-plaque like opacities over the surface of the heart, particularly concentrated in
A-V groove, e.g. TB pericarditis (constrictive pericarditis).
Valvular calcification: long standing rheumatic/bicuspid aortic valve disease; aortic and mitral valves
are most commonly affected.
Lateral film-calcified aortic valve is seen on or above a line joining the carina to sterno-phrenic angle.
Mitral valve calcification below and behind this line.
Myocardial calcification after MI, especially in association with LV aneurysm.
Calcification of aorta-common normal finding in-patient >40 years; curvilinear opacity around the
circumference of the aortic knuckle. Coma shaped calcification of the aortic knuckle indicates
atherosclerosis.
Calcification in ascending aorta- is diagnostic of syphilitic aortitis
Descending aorta-atheroma; young patient-non-specific aortitis.
Coronary artery calcification-specially proximal LT coronary artery with atheroma, but does not
necessarily correspond to the site of maximal stenosis.
Position of the heart in the chest-
Displacement of the heart as a whole is seen in pleural effusion, Pneumothorax and fibrosis of the
lung. In distension of the stomach and obesity, the heart is raised with the diaphragm and the apex
tilted upwards. The common type of scoliosis (convexity of the curve to the RT) is frequent cause of
displacement of the heart to the LT. In narrow chests the heart often lies centrally and seems smaller
and slender.
LUNG FIELDS-
Normally lung shadows are translucent. Most of the vascular shadows (white linear) in the lung fields
are due to branches of the pulmonary artery. They are usually accompanied by a corresponding branch
of the bronchus. The pulmonary arteries form the major bulk of the hilar density. In contrast,
pulmonary veins have low density. They may be seen in the upper lobes just lateral to the upper lobe
artery. The lymphatics, interstium, alveoli and pleura cast a very low density and are difficult to
identify. The normal pleural structures are seldom visible. Pleura may be visible, if thickened or
calcified.
In normal person , the ‗hilar shadows ‗ are made up of pulmonary arteries, pulmonary veins
,bronchi,hilar lymph glands ,lymphatics and connective tissue components.
Common lung field abnormalities in cardio-vascular disease are caused either by altered pulmonary
flow or by increased LT atrial pressure.
Altered pulmonary flow
Increments in pulmonary flow sufficient to cause radiographic abnormalities are caused by LT to RT
intra-cardiac shunts (e.g. ASD,VSD,PDA); generalized increase in vascularity of lung fields and
increase in size of hilar vessels ( e.g. RT lower lobe arteries),which normally should not exceed 16 mm
in diameter.
Prominence of the vascular markings give the lung fields a plethoric appearance. This is specially
obvious when some of the branches are seen end-on near the hilum.
Reduction in the pulmonary flow, on the other hand, cause reduced vascular markings. This may be
regional (e.g. pulmonary embolism) or global (e.g. severe pulmonary hypertension). In Fallot‘s
 tetralogy the vascular markings in the lung fields are inconspicuous- (paucity of vascular markings,
decrease in width of the arteries, decrease in pulmonary blood flow).
Pulmonary oligaemia (lung vessels are of diminished caliber)-pericardial effusion, severe pulmonary
stenosis, TOF.
Pulmonary plethora (dilated vessels through out the lung field)-LT ventricular failure, valvular heart
disease: MS, M I, AS, AI. Lt to Rt shunt (ASD, VSD, PDA). ASD is an important cause of pulmonary
plethora in clinical practice.
Pulmonary vessels
               - Large in intra-cardiac (LT to RT e.g. ASD, VSD, PDA) or peripheral shunts-
                   prominent in outer third (plethora).
               - Large/prominent (close to the hila) in pulmonary hypertension with small vessels in
                   outer third (pruning); cause: COAD, chronic LT heart disease e.g. MS, VSD.
               - **Diameter of descending Rt pulmonary artery >16 mm for males & > 15 mm for
                   females denotes pulmonary hypertension (Sutton 7 th edn).
               - Segmental avascualrity (pulmonary embolism)
               - Small in congenital heart disease (pulmonary stenosis), RT ventricle or pulmonary
                   artery atresia.
**AIPGME 2006
Increased LT atrial pressure- this occurs in mitral stenosis and LT ventricular failure and produces
corresponding rises in pulmonary venous and pulmonary capillary pressures.
Prominence of the upper lobe veins is an early radiographic finding. As the LT atrial and pulmonary
capillary pressures rises above 18 mm hg (normal- 4-12 mm hg) transudation into the lung produces
interstitial pulmonary edema , characterized by prominence of the interlobular septa,particularly at the
lung bases(Kerley B lines). The interstitial edema causes diffuse shadowing in the lung fields with
blurring of the vessel margins. The escape of fluid into the interstitial tissue occurs when the capillary
pressure exceeds the plasma oncotic pressure of 25 mm hg.Further elevation of pressure leads to
alveolar edema characterized by perihilar ‗bat‘s wing‘ shadowing. When the pulmonary venous
pressure reaches 30 mm hg edema fluid will pass into the alveoli. This causes shadowing (patchy to
confluent depending on the extent) in the lung fields. This usually occurs first around the hila and gives
a bat‘s wing appearance. These changes are usually superimposed on the interstitial edema.
 Normal pulmonary venous pressure-5-14 mm hg.
 Mild pulmonary venous hypertension-15-20 mm hg-isolated dilatation of upper zone vessels.
                                                  -21-30 mm hg –interstitial pulmonary edema-fluid collects in
                                                 interlobar fissure, interlobular septa (Kerley B lines)? Pleural
                                               space, indistinction of hilar regions, haziness of lung fields.
                                                >30 mm hg –alveolar edema-appears as areas of consolidation
                                                & mottling of lung fields & pleural effusion.
    Interstitial edema is shown by septal enlargement. Pulmonary septa are connective tissue planes
    containing lymph vessels and are normally invisible; when thickened they give rise to lines on Chest
    X- ray .
                    Q.What are the various grades of pulmonary venous hypertension?
                       o Grade I: cephalisation of pulmonary venous markings (upper lobe re-
                            distribution) or inverted moustache sign or Antler's sign
                       o Grade II: interstitial edema or Kerley B lines (suggest LA pressure >20 mm hg
                            in 70 % of the patients )
                       o Grade III:pulmonary alveolar edema or Bats-Wing appearance
Pressure changes in Lt Atrium in evolution of pulmonary edema:
   Normal Lt atrial pressure:6-10 mm hg
   Prominence of upper lobar pulmonary veins in X-ray:12 mm hg.
   Interstitial edema:>15 mm hg
   Kerley‘s B lines in Chest X-ray:>20 mm hg
   Pulmonary edema:>25 m hg.
PERI HILAR BAT-WING INFILTRATION :
Please Please Study Light, Don‘t Get All Uptight
P: Pulmonary edema
P: Pulmonary alveolar proteinosis
S: Sarcoidosis
L: Lymphoma
D: Drug
G: Goodpasture syndrome
A: Alveolar cell carcinoma
U: Uraemia

Kerley‘s ‗A‘ lines radiate from the hila especially in the upper and mid-zones and do not reach the lung
edge (unbranched lines).
Kerley‘s ‗B‘ lines (which are edematous interlobular septa) are horizontal about 1-2 cm in length and are
best seen at the periphery of the lung bases (near costophrenic angles-Rt CP angle). Commonly seen in
patients with chronic cardiac failure (e.g. mitral stenosis). They contain the engorged lymphatics, which
were originally thought by Kerley to be the sole cause of the 'B' lines.
Kerley‘s ‗A‘ and ‗B‘ lines may also be found in acute cardiac failure (e.g. myocardial Infarction) and are
very prominent in lymphangitis carcinomatosa.
Kerley‘s ‗C‘ lines are short lines radiating at different angles to give a network pattern (interlacing lines).
Commonly present in dust diseases. Commonly seen in central area and perihilar regions.
Kerley‘s ‗D‘ lines similar to ‗A‘ and ‗B‘ lines are specially seen in the RT middle lobe and lingula
overlying the shadow of the heart on lateral view.
Kerley ‗A‘ line stands for apex.
Kerley ‗B‘ line stands for base.
Kerley ‗C‘ line stands for central region.
'A‘, ‗B‘ and ‗C lines are also known as septal lines. These lines represent dilated lymphatics and distended
interlobar septa. Kerley ‗B‘ line is most commonly seen. They occur most often in pulmonary edema as a
result of chronic pulmonary venous hypertension. Kerley‘s ‗B‘ line has a relation with Lt atrial pressure
(‗B‘ lines are invariably present if Lt atrial pressure goes above 20 mm hg). These lines are actually found
in Lt heart failure.
         A

                         ….
        B                ….C

Kerley ‗B‘ lines are found in
    1. Pulmonary venous hypertension e.g. LVF, LAF ( from MS)
    2. Dilated lymphatics due to lymphatic obstruction e.g. lymphangitis carcinomatosa.

       Long standing pulmonary venous hypertension-reactive thickening of pulmonary arteriolar intima-
        which protects the patient from pulmonary edema. Thus in this patient pulmonary venous pressure
        may increase well above 30 mm hg before frank edema develops.
          Pulmonary arterial hypertension:
    Bulging central arteries, abruptly tapering to small peripheral branches.
                Bulging pulmonary arteries at hilum (para hilar prominence)
                Peripheral pruning (peripheral pulmonary arteries taper sharply)
                Kerley ‗B‘ lines disappear.
    Causes:
    1. Recurrent pulmonary emboli
    2. Chronic pulmonary disease
    3. Long standing LT heart disease
    4. LT to RT shunt
          Pulmonary venous congestion
    Increased vascular markings due to venous congestion in lungs.
    Causes:
    1. Lt sided heart failure (LAF,LVF) i.e. Mitral or aortic valve disease,IHD,cardiomyopathy
    2. Cor pulmonale
    3. Pulmonary emboli
    4. Pulmonary venous obstruction (Veno-occlusive disease)
    A patient of mitral stenosis suddenly becomes symptomatic or within few days-possibilities:
                  1. Lt atrial failure and pulmonary edema
                  2. Atrial fibrillation
                  3. Pulmonary embolism
                  4. Unaccustomed exercise
                  5. Severe anemia,intercurrent illnesses e.g. infection, thyrotoxicosis
                  6. Pregnancy
                  7. Acute rheumatic carditis.
    Differential diagnosis of widespread alveolar opacities:
        1. Pneumonia
        2. ALI or ARDS
        3. Alveolar cell carcinoma
        4. Uraemic pneumonitis
        5. Intra-alveolar hemorrhage
        6. Fat embolism.
        7. Metastasis by hematogenous route.
    X-ray shows pulmonary edema without any cardiac enlargement:
        1. MS ( particularly LAF)
        2. Constrictive pericarditis
        3. Causes of non-cardiogenic pulmonary edema (drowning, inhalation of toxins, gram negative
             septicaemia,fluid over load, insecticide poisoning, narcotic overdose, hemorrhagic
             pancreatitis,high altitude)
    Pulmonary edema without cardiomegaly:
    U DOPA
    U: Uraemia
    D: Drugs
O: Over-hydration
P: Pulmonary hemorrhage
A: Acute MI/Arrhythmias
X-ray shows ‗mitralisation‘ but the apex is down and out. MS does not produce LVH, so other causes
of LVH should be considered to be associated with
     1. M I, AI,AS
     2. Systemic hypertension
     3. IHD
     4. Severe anemia
     5. Cardiomyopathy
     6. Thyrotoxicosis
The position of the cardiac apex is done by counting intercostal spaces (whether outwards or
downwards as well as outwards) in chest X-ray PA view.
LT to RT shunt (ASD, VSD and PDA)
                           ASD VSD                       PDA
Pulmonary plethora         +        +                    +
Aortic knuckle             Small Small or normal Large or normal
Chamber enlargement RVH LVH, RAH                         LVH, RVH
Alteration in size of one pulmonary artery relative to the other.
This will happen if the blood flow to one lung is severely impaired, e.g. with fibrosis, unilateral
transradiant lung (Macleod‘s syndrome), pulmonary embolism blocking the blood supply to one lung,
or sometimes with bronchial neoplasm involving or stimulating a narrowing of one pulmonary artery.
In the latter instance dilatation of the contra-lateral artery will give rise to the ‗paradoxical hilar
enlargement sign‘.
Blood diversion-
One has also to consider blood diversion not only in a contralateral direction but also vertically. With
our upright posture the apices of the lungs rather are poorly perfused,which is one reason for the
development of apical bullae. Diversion of blood from lower to upper lobes ( vessels above the hilum
appear wider than those below) occur with increased pulmonary venous pressure (mitral stenosis or
CCF), basal emphysema or embolism. The mechanism of this blood diversion is not fully understood.
These changes are seen when the pulmonary venous pressure is about 15-20 mm hg.
Re-distribution of pulmonary vasculature to the upper lobe.
Usually the normal Chest X-ray shows the pulmonary blood vessels prominent in the lower lobes.
With CCF fluid collects in the dependent portion of the lungs. The ability to exchange O 2 in these
lower lung fields is impeded. To compensate for this altered physiology, the blood flow is re-directed
to the upper lung fields, where the lung tissue is still free of edema fluid. With CCF, the chest films
shows enlarged prominent blood vessels in the upper lobes, where they should be small and barely
noticeable.
Other lung field abnormalities-
A water density lesion which obliterates the RT border of the heart must lie in the RT middle lobe and
not RLL.
Pulmonary Infarction- localized and typically wedge shaped areas of consolidation are occasionally
seen in pulmonary embolic disease, although more often the bronchial circulation protects against
ischaemic damage.
Pneumonic consolidation and abscess
In patients with RT-sided endocarditis infected pulmonary emboli commonly cause septic foci within
the lung fields.
Fluid –filled bronchi or Mucocele may be seen distal to the blocked segmental bronchi, due to air
passing from one segment to another by ‗collateral air drift‘ through the inter-alveolar pores of Kuhn.
These mucocoeles are particularly seen with slowly growing endobronchial tumors-adenomas and
some malignant tumors.
Interstitial lung disease- in long standing pulmonary hypertension complicating rheumatic mitral valve
disease,haemosiderosis(stippled shadowing through out the lung fields) was once a common X-ray
finding. It is now rarely seen.
The nipple shadowing are often seen over the lower zones and are about 5 mm in diameter. This can be
confused with coin lesion. Nipple markers may be helpful.
Bony abnormalities- bony abnormalities are unusual in cardiovascular disease, apart from Coarctation
of aorta and thoracic outlet syndromes. In Coarctation of aorta dilatated bronchial collateral vessels
erode the inferior aspect of the ribs to produce notches although they are rarely present before
adolescence. Cervical ribs may compress the neuro-vascular bundle in the thoracic outlet, and special
thoracic outlet views are necessary for radiographic diagnosis.
      Evaluate the density of the lung fields on the two sides; it should be the same, allowing for the
          superimposed density of breast tissue. Check the review areas. Try to, localize the origin of
          any abnormalities: lung, lymph node, pleura, heart, blood vessel or bone? Shadowing in the
          lung field has several possible causes :
Chest X-ray in pulmonary disorders:
Certain patterns encountered on chest X-ray in pulmonary diseases are:
Infiltrate:
               It is an abnormal shadow in the lung which does not have any pattern-a vague term.
                    If these infiltrates involve the alveoli such as in pneumonia and lymphoma, a
                    homogenous dense opacity is produced.
               When this opacity is confined to one lobe, it is called lobar consolidation and this is
                    seen in bacterial pneumonia. An air-bronchogram is also seen.
               Multiple such opacities when present in the lung constitute broncho-pneumonia. The
                    alveolar exudates may coalesce to produce nodular opacities or large fluffy cotton
                    wool like shadows.
               Alveolar infiltrates are patchy, homogenous and have air- bronchogram. They may
                    be segmental or lobar.
               Interstitial infiltrates occur when there is involvement of interstitium as in viral
                    pneumonia, interstitial pneumonitis and occupational disorders. The radiological
                    patterns that arise from these infiltrates reflect as micro-nodular, reticular, reticulo-
                    nodular and multiple linear shadows.
               On occasion both alveolar and interstitial infiltrates get superimposed on each other
                    such as occur in pulmonary edema.
CHRONIC ALVEOLAR INFILTRATION
PAL GETS MOD
P: Pulmonary alveolar proteinosis
A: Alveolar cell carcinoma
L; Lymphoma
S; Sarcoidosis
G: Granuloma
E: Eosinophilic granuloma
T: Tuberculosis
M: Microlithiasis
O: Oil pneumonia
D: Desquamative interstitial pneumonitis
RETICULO-NODULAR INFILTRATION
Please Don‘t Eat Stale Fish Sandwich Every Morning
P: Pneumoconiosis
D: Drug
E: Eosinophilic granuloma
S: Sarcoidosis
T: TB
F: Fungal
S: Schistosomiasis
E: Exanthems (Measles, Chicken-pox)
M; Metastasis
MULTIPLE LUCENT LESIONS
Can‘t BAN WHIPS In Court
C: Coccido mycosis
B;Bronchogenic cyst,Bronchiectasis,Bowel (Diaphragmatic hernia)
    A: Abscess
    N: Neoplasm
    W: Wegener‘s
    H: Histocytosis
    I: Infection
    P: Pneumatocoele
    S: Sequestration
    I: Infection (Necrotizing pneumonia)
    C: Cyst adenomatoid mal-formation
    The whiteness (opacification) of the lungs
    Acute pulmonary edema:
    In pulmonary edema, there is leakage of fluid from the pulmonary venous circulation into the alveoli
    and the lung interstitium producing haziness of the lungs from the centre towards the periphery on both
    the sides.
    Acute pulmonary edema may be cardiogenic (heart size is enlarged due to Lt heart failure )or non-
    cardiogenic (ARDS-type I respiratory failure) in which there is opacification of peripheral fields of the
    lung with normal cardiac size.
    Radiological findings :
    Radiological findings in the cardiogenic pulmonary edema are:
                   Haziness of the lung. severe pulmonary edema due to LVF gives confluent alveolar
                      shadowing (haziness) which spreads from the hilum towards periphery giving a
                      "bat's wing appearance". In ARDS, the haziness is more peripheral than central.
                   Upper lobe veins are prominent. In PA view in erect position, normal blood flow is
                      greater in the lower lobes than the upper due to gravity; hence lower blood vessels
                      are more prominent. In heart failure (pulmonary edema), the upper lobe veins are
                      dilated due to diversion of blood flow-the first sign of the heart failure.
                   Size of the heart. heart size is enlarged
                   Kerley's B lines these are caused by edema of the interlobar septa. They are
                      horizontal, non branching white lines best seen at the periphery of the lungs just
                      above the costo-phrenic angle.
                   Pleural effusion or hydro-thorax. A small pleural effusion obliterating the costo-
                      phrenic angle is common.


    Radiological comparison of cardiogenic vs. non-cardiogenic pulmonary edema
Features               Cardiogenic                                    Non-cardiogenic
Distribution of        Bilateral haze is more central than            Bilateral haze is more peripheral than
haze                   peripheral                                     central
Heart size             Enlarged                                       Normal
Upper lobe veins       Dilated and enlarged                           Normal
Kerley B lines         Far more common                                Less common
Pleural effusion       Common                                         Less common
    Reticulo-nodular shadows (fibrosis or edema of the lungs)
    The reticulo-nodular shadowing simply means a meshwork of lines that combines to form nodules and
    ring shadows of < 5 mm in diameter. Sometimes this meshwork is very fine giving a ground-glass
    appearance, said to look like a thin veil over the lung. Later it gives a more coarse appearance and is
    said to look like a honey-comb. Honey-combing is a feature of interstitial lung disease/pulmonary
    fibrosis. The causes of reticulo-nodular opacities are:
                    Pulmonary edema
                    Broncho-pneumonia
                    Lymphangitis carcinomatosa
    Differentiating features:
                    Bilateral basal reticulo-nodular shadowing could be either due to edema or fibrosis.
                       Shadowing that is confined to midzone or apical region is more likely to be fibrosis.
                The presence of small lung indicates fibrosis rather than pulmonary/interstitial
                 edema
                Shifting of mediastinum to the side of shadowing is due to fibrosis rather than due to
                 edema
                In fibrosis, heart border and diaphragm on the side involved appear blurred
                Vascular markings are less distinct in areas of fibrosis.




End stage lung disease(Honey-comb)
CHIPS
C: Collagen Vascular Disease, Cystic fibrosis
H: Histiocytosis
I: ILD
P: Pneumconiosis
S: Sarcoidosis



INTERSTITIAL LUNG DISEASE:
UPPER LOBE:
CASSET
C: Cystic fibrosis
A: Ankylosing spondylitis
S: Silicosis
S: Sarcoidosis
E:Eosinophilic granuloma
T: TB
LOWER LOBE
BASILAR
B: Bronchiectasis
A: Asbestosis
S: Scleroderma
I: Interstitial pulmonary fibrosis-lymphangetic carcinomatosis
A: Aspiration pneumonia
R: Rheumatoid arthritis

Coin lesion-coin shaped lesion with circumscribed margin which is completely surrounded by normal
aerated lung.
     This is the routine pre-operative film of a 65 year old male smoker. There is a mass in the Lt upper
     lobe with a well-defined slightly lobulated border. This is a carcinoma.
                             Causes of a single coin lesion
                              Benign tumor e.g. hamartoma
                              Malignant tumor e.g. bronchogenic carcinoma, single secondary infection
                                 e.g. pneumonia, abscess, tuberculosis, hydatid cyst, infarction
                              Rheumatoid nodule
A solitary pulmonary nodule (SPN) by definition is a well-circumscribed opacity less than 3 cm in
diameter. Initial evaluation of the SPN may be done in a stepwise fashion. Is this truly an intrapulmonary
nodule? Bony shadows such as those originating from the ribs, or soft tissue shadows such as of the
nipples, may mimic an SPN. Is this SPN truly solitary? If this is not clear from the chest radiograph or
patient examination, a *CT scan can be helpful. CT scan provides conclusive evidence of calcification
within the nodule. This helps in differentiating malignant lesions from benign ones and thus avoid un-
necessary invasive procedures for benign conditions and concomitantly identify low stage, potentially
curable malignant lesions. CT scan is far more superior to MRI in seeing calcification. Comparison with a
previous CXR helps avoid unnecessary further workup, as a stable lesion seen on a previous x-ray taken 2
years ago virtually confirms benignity. Small nodules 10 mm or less in size are usually not seen
prospectively and may be difficult to find retrospectively on a CXR. Approximately 33% of all SPNs are
not detected on an initial radiograph. Evaluation of rate of growth to assess stability of a lesion is helpful to
determine benignity. Estimation of doubling time (a 25% increase in diameter is equivalent to doubling of
volume) aids in diagnosis. Most bronchogenic carcinomas double within 2 years. Once the diagnosis of
SPN has been established, the nodule‘s characteristics should be evaluated. Characteristics within the
nodule such as air bronchograms or cavitation are nonspecific diagnostically. Sharply marginated SPNs are
detected more easily. In general, spiculated or ill-defined nodules have a higher incidence of malignancy
compared to rounded, smooth-edged nodules. Multilobulated nodules are frequently seen in malignant
lesions. Calcification of an SPN is a very helpful feature in differentiating between malignant and benign
nodules. The presence of a central or complete calcification virtually excludes malignancy, although
eccentric or peripheral calcification may be seen in scar carcinomas. The most common cause of calcified
SPNs is old healed granulomatous disease such as TB or fungal disease. Diffuse, stippled ―popcorn‖
calcifications are seen in hamartomas. These are benign mesenchymal lesions of connective tissue origin
with mixed fibromuscular/cartilaginous and adipose tissue and are usually discovered as incidental
findings in asymptomatic patients. These lesions can grow slowly. Diagnosis is confirmed by thoracotomy.
Further evaluation of SPNs depends on patient-related factors such as age and risk factors for cancer. Most
cancer is detected after age 55 and is rare before age 35. Diagnostic tests such as CTguided transthoracic
biopsy or fiberoptic bronchoscopy are done based on the accessibility of the lesion by these approaches.
Central lesions with air bronchograms leading to them are more accessible by bronchoscopy, whereas a
CT-guided needle aspiration/biopsy has a better yield in peripheral lesions.
*AIIMS May 2002.
This chest x-ray shows a radiographically dense      This chest x-ray shows a normal heart size.
nodule in the left hilum. Cardiophrenic and           No pleural or mediastinal disease is noted.
costophrenic angles are clear. An 0.8 x 1-cm          Cardiophrenic and costophrenic angles are
circular solitary pulmonary nodule with peripheral clear. A dense, rounded solitary pulmonary
yet distinct calcification in the superior aspect is  nodule is noted in the right lung.
seen overlying the 5th posterior rib in the right
upper lung zone.
.PULMONARY NODULE WITH PNEUMOTHORAX
WHO
W: Wilm‘s tumor
H: Hisocytosis X
O: Osteosarcoma
     Solitary pulmonary nodule: spherical 1-6 cm in diameter, intra-pulmonary radiographic density.
     Mass lesion: > 6 cm in diameter.

    Feature                                          causes

    Mass lesion (>3.5 mm)
                                                    Bronchogenic carcinoma
                                                    Abscess
                                                    Solitary metastasis
                                                    Grannuloma
                                                    Arterio-venous malformation
                                                    Haematoma
                                                    Pulmonary Infarct



    Solid round focus              differential diagnosis
                                             o Carcinoma
                                             o Tuberculoma
                                             o Adenoma
                                          o   Hamartoma
                                          o   Metastasis especially if multiple
                                          o   Rare causes such as rheumatoid nodule, polyarteritis or
                                              Infarct
   Spiculation or scalloping
                                             Carcinoma
                                             Tuberculoma
  Notching or umblication
                                             Carcinoma
                                             Adenoma
                                             Hamartoma
  Vessels entering or radiating vessels
                                             Carcinoma, A-V malformation

  Satellite sign                          carcinoma


  Peribronchial infiltration
  or ‗track to hilum‘                     carcinoma, Infection




  Mass with calcification
                                             Tuberculoma
                                             Adenoma
                                             Hamartoma (‗popcorn‘ calcification)
                                             Metastasis (bone sarcoma)
                                             Carcinoma unlikely unless old tuberculous focus
                                                  incorporated in tumor.
Large round mass
                                             Carcinoma
                                             Bronchogenic cyst
                                             Hydatid cyst
                                             Secondary deposit (e.g. from sarcoma)
                                             Adenoma
Mass with cavity,
often eccentric
                                             Carcinoma
                                             Infarct (especially if infected)
                                             Fungus infection (may contain a fungus ball or
                                              mycetoma)
                                             Rarely metastasis (squamous primary or rapidly growing
                                              tumor e.g. sarcoma)
                                             Lung abscess (if acute)
Thin walled cavity
(May have nodule on its inner wall)
                                             Emphysematous bullae
                                             Tuberculosis
                                             Bronchial carcinoma (very occasionally), perhaps due to
                                                      check valve mechanism as also occurs in
                                                      staphylococcal pneumonia
  A large, 7x11-cm mass is seen in the left          This chest x-ray shows a 3x 2.5-cm
parahilar area. This has a well-defined edge         shadow in the right middle zone
and silhouettes out the hilar structures. The        with slightly irregular margins.
diaphragms are flattened, and there is no            There is an area of nonspecific
pleural disease. There are mediastinal               infiltrate above this mass
(sternal) wires from prior CABG.                     with air bronchograms.
rounded masslike                                     Increased vascular markings are seen
.                                                    in the right lower zone and the hilar
                                                     area reveals calcified lymph nodes.



Cigarette smoking is commonly associated with squamous cell carcinoma, small cell carcinoma,
and, to a lesser degree, adenocarcinoma. Other carcinogens include asbestos, heavy metal, radiation, and
urban pollutants. Radio graphically, a peripheral mass is the most common manifestation of
adenocarcinoma. Squamous cell carcinomas attain large size and frequently cavitate, and
patients may present with lung collapse and consolidation distal to a central obstruction. Small cell
carcinoma typically presents with a proximal mass, lymphadenopathy, and mediastinal invasion.
This chest x-ray shows right upper zone opacity with         This PA chest x-ray shows a large Rt
multiple air-fluid levels. Surrounding this opacity and upper lobe mass with an air-fluid level.
the air-fluid levels is an ill-defined infiltrate. Note that This mass has a very thick wall with irregular
 the right apex and lower lung zones are clear. The left inner margins and is abutting the mediastinum
lung is also clear, and no pleural or mediastinal disease.         Differential diagnosis in
 is noted. This x-ray is consistent with a necrotizing             this case would include lung abscess
process in the posterior segment of the right upper lobe,          or cavitary squamous cell carcinoma
with an air-fluid level such as in a lung
abscess.
Causes of Cavitating lung lesions:
      Abscess
      Neoplasm
      Cavitation around a pneumonia
      Infarct
      Rheumatoid nodule (rare)
The x-ray differential for infiltrates with areas of breakdown or cavitation and signs of loss of volume or
retraction includes primarily inflammatory diseases such as TB, sarcoidosis, nontuberculous mycobacterial
diseases (MOTT/ NTM), nocardia, fungal diseases, and gram-negative necrotizing pneumonia.
Postobstructive pneumonia secondary to tumor or foreign body may cavitate and cause volume loss.
Cavitary cancer usually does not retract lung tissue but may push adjacent structures. An ―air-crescent
sign‖ on a chest x-ray or a ―halo sign‖ on CT scan suggests a fungus ball in a patient with underlying
bullous/fibrotic/cavitary disease. Clinical hints that may be helpful include
clubbing that may suggest lung abscess or a cavitary carcinoma and fluctuating
fluid level suggesting instability due to infection or ongoing hemo

    Tiny multiple nodules: these are seen because multiple tiny opacities augment one another, and a few
                                            may not be seen at all.
    Micronodules (< 1 mm)
                                             Pneumoconiosis, stage 1-2;coal miners; fettlers; quarry
                                                              workers etc.
                                             Inhaled metal, Fe: hematite workers; knife and lens
                                                              polishers using rouge (ferric oxide)
    Miliary nodules (1-2 mm)
                                             o    Miliary tuberculosis
                                             o    Sarcoidosis
                                             o    Miliary carcinoma
                                             o    Acute alveolitis or Bronchiolitis: infection or allergic.
                                             o    Acute chicken pox pneumonia: especially in adolescents
                                                  or adults.




This x-ray shows a bilateral diffuse miliary A bilateral nodular pattern is seen in both
nodular pattern involving both lung fields with       lung fields. However, these nodules are
no loss of volume                                     predominantly in the upper zones
Diagnosis: Miliary tuberculosis                        with some patchy areas of confluence.
                                                      The bases are clear and there is no pleural disease.
                                                      Diagnosis: Silicosis.
                                                      Silicosis is caused by inhalation of silica dioxide
                                                      dust. Exposed populations include sandblasters, stone
                                                      grinders, ceramic workers, and mine workers.
                                                      Acute silicosis, also called silicoproteinosis, can
                                                      rarely develop after a single
                                                      massive exposure and results in pulmonary
                                                      consolidation. Simple silicosis causes multiple
                                                      discrete pulmonary nodules occurring with upper
                                                      zone predominance. Mediastinal adenopathy is
                                                      common and classically seen with ―eggshell‖
                                                      calcification. Complicated silicosis or progressive
                                                      massive fibrosis refers to larger confluent densities or
                                                      conglomerate upper lobe masses.
Miliary disease:
TEMPEST
T:TB+Fungal infection(rarely nocardia or salmonella)
E:Eosinophilic granuloma (>2 mm usually in size< 4 mm)
M: Metastasis(thyroid)
P: Pneumoconiosis (silicosis/siderosis)
E: Embolism
S: Sarcoidosis (1-2 mm in size)
T: Tuberous sclerosis
This Chest x-ray shows opacification of the left      This x-ray shows a bilateral generalized nodular
lung field with surgical rib changes and clips seen    pattern in all lung fields. There is an area of a
 near the left main stem secondary to a left          mass like confluence in the left upper zone.
 pneumonectomy. Multiple nodular opacities of         The superior mediastinum appears widened
varying sizes are seen in the right lung field.       primarily on the left side with
These changes are characteristic of metastatic        a prominent right paratracheal node.
disease.                                              Cardiophrenic and costo-phrenic
                                                      angles are clear. This x-ray is consistent with left
                                                      upper lobe mass with metastatic disease.


In considering the differential diagnosis of fine nodules, note that
      Tuberculosis tends to affect the upper two thirds of both lungs,
      Sarcoidosis tends to affect the middle two thirds,
      Pneumoconiosis will spare the apices (because of bullae there), and that
      When all parts of the lungs are affected one should think of miliary carcinomatosis.
Note: Small nodules of pulmonary sarcoidosis tend to be mid-zone and peri-hilar whereas hematogenous
metastasis are generally of varying sizes and have a predilection for the lower lobes ( probably because of
increased blood flow to these regions).
     If calcified
                                                     Previous chicken pox pneumonia
                                                     Histoplasmosis
                                                     Microlithiasis pulmonale in mitral stenosis
                                                     Rarely, stony lung disease
       Multiple calcified nodules:
       HAM TV Station
      H: Histoplasmosis,Hamartoma
     A: Amyloid,Alveolar microlithiasis
     M:Mitral stenosis,Metastasis (BOTTOM)
     Breast
     Osteosarcoma
     Thyroid
     Testicular
    Ovarian
    Mucinous adeno-carcinoma
    T:treated lymphoma, tuberculosis
    V:Varicella
    S: Silicosis
    3-4 mm nodules
                                             Sarcoidosis
                                             Metastasis
                                             Alveolar microlithiais
                                             Broncho-pneumonia
                                             Drug effect


Multiple rounded opacities (both lungs)
                                             Multiple pulmonary metastases
                                             Hydatid cysts
                                             Large sarcoid nodules
                                             Large rheumatoid nodules

Multiple nodules:
GAMMA WRAPPS BIKE
G: Granuloma
A: Abscess
M: Metastasis
M: Multiple myeloma
A: AVM
W: Wegener‘s
R: Rheumatoid Lung
A: Amyloid
P: Paragonimus
P: Papillomatosis
S: Sarcoidosis
B: Bronchoalveolar carcinoma
I: Infarcts (Organizing)
K: Kaposis‘s
E: Eosinophilic granuloma



Multiple ill-defined nodules:
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S: Sarcoidosis
S: Septic emboli
M: Metastatic lesions
L: Lymphoma,LIP,Lung primary,lymphomatoid granulomatosis
A: Alveolar cell carcinoma
R: Rheumatoid arthritis
W: Wegener‘s granulomatosis
F: Fungal infection
T: TB
Metastasis with cavitation:
Squamous Cell Mets Tend To Cavitate:
S: Squamous cell carcinoma, Sarcoma
C: Colonic cancers
M: Melanoma
T: Transitional cell carcinoma
C:Cervical cancer
Hemorrhagic metastasis:
Can‘t Run Marathon Today
C: Chorio-carcinoma
R: Renal Cell
M: Melanoma
T: Thyroid
Endo-Bronchial Metastasis
Long Range BBC
L:Lymphoma
R: Renal cell
B: Breast
B: Bronchoalveolar carcinoma
C: Colon
CAPLAN‘S SYNDROME: first described in coal miners but subsequently found in patients with
silicosis, includes seropositive rheumatoid arthritis with characteristic pneumoconiotic nodules. Silica has
immuno adjuvant properties and is often present in anthracitic coal dust.
          It is a rare condition.
          Characterized by the presence of necro-biotic nodules in the periphery of the lung in coal
           worker‘s with rheumatoid arthritis (Coal worker‘s pneumoconiosis + rheumatoid arthritis)
Differential diagnosis of multiple pulmonary nodules:
Caplan‘s syndrome:
      Nodules are well-defined.
      Develop in crops
      Calcification with cavitation occur
      Background stippling of pneumoconiosis
Wegener‘s granulomatosis:
      Wide spread distribution
      5-10 cm in size
      Round and well-defined
      No calcification
      Cavitation in 30-50 % of cases
       Focal pneumonitis
Silicosis:
      First seen around Rt Hilum later disseminated throughout both lungs
      Sparing of bases and apices
      Cavitation and calcification may occur
Sjogren‘s syndrome: pulmonary nodules are not seen.
Egg shell calcification is seen in:
     a) Silicosis
     b) Sarcoidosis
     c) Scleroderma
     d) Histoplasmosis
     e) Amyloidosis
      f) Lymphoma following radio-therapy
      g) Coal worker‘s pneumoconiosis
Pulmonary involvement in asbestosis:
           – Plaques or pleural thickening in lower half
           – Calcified plaques usually diaphragmatic
           – Bilateral pleural effusion in 20 % cases
Pulmonary involvement in Silicosis:
           – Multiple pulmonary nodule restricted to upper zone
           – Nodules can cavitate or calcify if progressive massive fibrosis is superimposed in them
           – Hilar lymph node calcification
Pulmonary involvement in sarcoidosis
           – Bilateral hilar Lymphadenopathy
           – Nodules mainly in mid-zones
           – Pleural involvement in 5-7 % of cases, effusion in 2 %
           – Pneumothorax
           – Broncho-stenosis in 1-2 %.
Characteristically, miliary nodules are less than 4 mm in size. They are generally non-calcified and diffuse
and are seen in many conditions, such as TB/fungal infections/pneumoconiosis and certain malignancies
such as melanomas/thyroid cancer. Larger, more confluent lesions can be seen in alveolar sarcoid,
Wegener‘s granulomatosis, and metastatic disease. The clinical hints that aid diagnosis include:
• An occupational history without constitutional symptoms.
• X-ray that looks worse than the patient‘s complaints, as in sarcoidosis.
• History of thrombo-embolic disease or sepsis, as in septic emboli or pulmonary infarcts. These are
generally seen in the lower lung zones.
• History of arthritis; may suggest rheumatoid nodules.
• Presence of eosinophilia in the peripheral smear with fleeting infiltrates; provides clue for pulmonary
infiltrates with eosinophilia (PIE) syndrome, in which case history of travel or use of medications/drugs
may be helpful and a stool exam may aid in the diagnosis.
• Immune-compromised patients may have opportunistic infections such
as herpes or CMV.
The lungs have a spotted appearance. This may be due to miliary shadowing but sometimes ground glass
appearance can look similar. Also the normal lung can sometimes have a mottled appearance. You must
first need to distinguish between these.
      1. Look at the distribution of the shadowing. Look carefully at the periphery. If the shadowing is
           present in the periphery it is more likely to be pathological. Sometimes normal vasculature can
           mimic interstitial shadowing but this usually occurs only towards the centre of the lung fields.
      2. Move close to the X-ray and carefully examine the shadowing. With miliary shadowing the
           opacities should be discrete.
      3. Compare a number of opacities. If the shadowing is miliary they should be of similar density and
           size. If the shadowing is ground glass their size and density will vary.
      4. Look at the underlying lung field. The normal anatomy of the lung should be visible with miliary
           shadowing but may be obscured with a ground glass appearance.
      If you feel the shadowing is miliary then look for clues as to its cause. Likely possibilities are miliary
      tuberculosis, sarcoidosis, or malignant miliary metastasis.
.
      1. Look again at the distribution .With miliary tuberculosis, the opacities are most profuse in the
           upper zone, with sarcoidosis they are most profuse in the per-hilar and mid-zones and with miliary
           metastasis there is a profusion of opacities in the lower zone.
      2. Look again at the density. Very white shadows are likely to be dust related industrial disease or
           calcified tuberculosis. Less dense changes could be multiple secondaries, sarcoidosis or any other
           cause s of miliary mottling.
      3. Look at the rest of the X-ray for signs of other disease processes. Look at the hilum.
           Unilateral hilar enlargement suggests tuberculosis and bilateral hilar enlargement sarcoidosis.
           Look at the upper part of the mediastinum for thyroid enlargement which could suggest
           secondaries from a thyroid carcinoma.
           Look at the apices for subtle cavitating lesions suggestive of tuberculosis.
    Note however that the presence of apical shadowing, although suggestive of tuberculosis, is in fact
    very rare in patients with miliary spread.




Air/water interface                        pulmonary edema
                                           Pus
                                           Necrotic cancer and lymphoma
                                           Vasculitis
Interstitial lesions                       Pulmonary edema
                                           Fibrosing alveolitis
                                           Lymphangitis carcinomatosis
                                           Bronchiectasis
Pulmonary collapse                         Blockage of a bronchus by mucus or tumor
                                           Foreign body in bronchus.
Solid lesions that have not changed in size over a year or more are probably benign, for example a
hamartoma, an arterio-venous malformation (AVM), or a grannuloma, but recent solid masses,
especially if multiple, are likely to be malignant, or, rarely, abscesses ( multiple abscesses are
extremely unlikely in the absence of cavitation). A CT scan will help to differentiate these possibilities,
and will aid localization for needle biopsy.

Air in the pleural space (Pneumothorax) can be difficult to detect, and is easily missed. Look carefully
at the apex and edges of the lung. In addition to air, the pleura may contain blood (hemothorax),
inflammatory (empyema) or neoplastic effusion, or lymphatic fluid (chylothorax).
The mediastinum should be examined next. Disease in any of the tissues found in the mediastinum can
cause abnormalities in this space, including thyroid, lymph nodes, thymus, aorta, heart, vertebrae and
nerves.
Check each rib for fracture, texture or abnormal bone density. Look carefully at the vertebral bodies
and their laminae. In women check that both breast are present and symmetrical.
In the chest, CT imaging is useful in detecting and staging primary cancer and metastases, in the
investigation of bronchiectasis and infiltrative lung disease, in the investigation of pleural lesions, and
in the diagnosis of pulmonary emboli.
Severe airway obstruction, particularly long term, as in COPD may lead to an overinflated and barrel-
shaped chest. The ribs are less obliquely set than normal.
Chest trauma- a plain chest X-ray is useful for identifying:
        Lung contusions or mediastinal injury not suspected clinically.
        Bony injury such as fractured ribs or flail chest.
        Simple Pneumothorax and/or hemothorax
        Diaphragmatic injury
        Correct placement of chest drains and CVP line can be confirmed.

Interpretation is surprisingly difficult because this is an antero-posterior film taken with the patient
lying flat and the normal appearances are quite different from the standard postero-anterior erect chest
X-ray.

The discovery of a tension Pneumothorax on X-ray means that the patient has not been properly
assessed clinically.

The diagnosis of a ruptured diaphragm may be quite difficult to make unless a naso-gastric tube has
been placed and is seen inside the stomach, but within the thoracic cavity. Placing a Nasogastric tube
in situ before the chest X-ray is helpful since it often appears in the chest if the diaphragm is ruptured.
    Radiographic appearances of a pleural effusion-a horizontal section of hemithorax close to the upper
    margin of the effusion shows that there is at this site a similar amount of liquid anteriorly, posteriorly
    and laterally. However, because of the shape of the hemithorax, the X-ray beam traverses more liquid
    laterally than they do centrally. This produces the characteristic radiographic shape of a pleural
    effusion shadow with curved upper margin ascending towards the axilla (‗meniscus sign‘).

    Pulmonary tuberculosis and bronchial carcinoma are two important diseases, which may not give rise
    to any clinical abnormality in the early stages. It is therefore essential to advise chest radiological
    examination whenever one of these conditions is suspected from the history.

    It is not possible to determine accurately the site of most abnormality visible on postero-anterior or
    antero-posterior X-ray and lateral should be used to elucidate any abnormality shown on a PA film.
    A comparison between current and previous films, if they can be obtained, may provide vital
    diagnostic information:
           If a pulmonary opacity has not increased in size over a period of a year or longer, a diagnosis
               of bronchial carcinoma is highly improbable.
           If an opacity has become smaller or less dense in the course of a few days or weeks,
               pneumonia or pulmonary Infarction is most likely the cause.
           If a lesion was not present on an earlier film, or has become larger, it is almost certainly a
               tumor or an active tuberculous infection.




         Silhouette sign: the cardiac and diaphragmatic outlines are entirely dependent on air filling lung
         being adjacent to them. When fluid is present in the pleura or if the adjacent lung is opaque i.e.
         collapsed or consolidated, then these outlines may be obscured or lost. This is known as the
         Silhouette sign (American positive when the Silhouette is lost). Thus loss of the RT lower cardiac
         outline implies that the middle lobe is opaque or on the LT the lingula. Note that a collapsed and
         opaque lower lobe will lie behind the heart shadow and not affect its outline.




         Fan sign‘: blood vessels are usually visible as far as the outer third of the lungs (normally no
         vessels are visible in the outermost 1-2 cm of lung), but may be seen right out to the periphery in
         congestion or with other causes of pulmonary plethora. Pulmonary artery enlargement may occur
         in both hila, as with emphysema or corpulmonale,or be unilateral if the blood supply to the contra-
         lateral lung is impaired. The number of vessels on either side should be roughly equal-if not
         suspect a collapsed lobe or a previous lobectomy, the fan sign-i.e. the vessels splayed apart. There
         is compensatory over expansion of the rest of the lung and only half the number of vessels is seen
         in a given area.




normal                      crowded                                       vessels splayed apart

Differential diagnosis of mediastinal widening:
    1. lymph node enlargement as a result of Bronchogenic carcinoma ( primary or
         secondary),lymphoma,tuberculosis,sarcoidosis,fungal infection of the lung
    2. Mediastinal mass-
            i)       Anterior and middle mediastinum-teratodermoid, lymphoma, metastatic carcinoma, aortic
                     aneurysm, bronchogenic cyst, pericardial cyst.
           ii)       Superior mediastinum-thymoma,retro-sternal thyroid,metastatic carcinoma, aortic
                     aneurysm,Zenker‘s diverticulum, tumors of the parathyroid
          iii)       Posterior mediastinum-neurogenic (neurofibroma),lymphoma, aortic aneurysm,achalasia
                     cardia,hiatus hernia, Paravertebral abscess.

Homogenous opacity of one hemi-thorax
Causes:
   1. Pleural effusion
   2. Consolidation :opacity +air bronchogram within it (Silhouette sign)
   3. Atelectasis/collapse: loss of volume causes shift of the normal landmarks
        (mediastinum,hila,fissures etc)
   4. Pulmonary agenesis
   5. Destroyed lung (chronic infection, fibrosis)
   6. Pneumonectomy.
   7. Pulmonary agenesis

                  Ipsilateral shift of trachea and mediastinum, narrowing of intercostal spaces, elevation of
                   dome of diaphragm and compensatory emphysema of the uninvolved side indicates
                   atelectasis or collapse, fibrosis, pneumonectomy and pulmonary agenesis.
               The contra-lateral shift of the trachea and mediastinum,the homogenous opacification in
                   the peripheral lung field with concave border towards the lung, widening of intercostal
                   spaces, obliteration of costo-phrenic angle and non-visibility of the dome of the
                   diaphragm on the involved side indicate pleural effusion.
               In mild pleural effusion, there may just obliteration of costo-phrenic angle; while a
                   localized effusion produces a homogenous opacification similar to a tumor with no shift
                   of trachea or mediastinum.
               In massive consolidation, a rim of normal lung tissue at costo-phrenic angle may be seen.
                   There may be no shift of trachea or mediastinum. No compensatory emphysema is seen.
A lobar homogenous opacity:
A homogenous opacity looks like an area of white lung. If there is a patch of opacity, it could be due to
collapse, pleural effusion or consolidation.
               if the opacity is uniform with a well demarcated border, then it is either a lobar collapse
                   or pleural effusion which can be differentiated by shift of trachea and mediastinum with
                   crowding of the ribs and elevated dome of the diaphragm on the side involved in case of
                   collapse but reverse will happen in pleural effusion (shift of trachea and mediastinum to
                   opposite side, widening of intercostal spaces and flattening of dome of the diaphragm).
               If the shadow is not uniform and the border is not well defined then it could be either
                   consolidation or fibrosis.
               In fibrosis, the signs are similar to collapse of the lung.
               In consolidation note the following:
                        1. Presence of air- bronchogram within opacity confirms the diagnosis of
                             consolidation. In consolidation, the air spaces are filled with fluid or exudates
                             making them appear as white whereas air-ways within opacity retain air, making
                             them appear black. The areas of blackness within white back-ground suggest air-
                             bronchogram
                        2. The shadowing in consolidation gets denser as one move down the lung because
                             fluid sinks and makes the lower border denser and well-defined.
               Pulmonary TB: classically sharply-defined consolidation is rarel; pleural reaction is
                   common.
               Pulmonary infarction: wedge-shaped homogenous, poorly defined opacity is produced,
                   attached against pleura; thus blunting of CP angle is commonly seen here.
               Bronchogenic carcinoma: pleural reaction i.e. pleural effusion is commonly seen; absence
                   of air-bronchogram and there may be presence of rib erosion.
Pneumonia:
Radiological criteria for diagnosis:
    1. Homogenous opacity
    2. Segmental or lobar distribution
    3. Presence of air-bronchogram/air –alveolar gram-the lung is opaque but the bronchi are patent and
         air-filled bronchi giving rise to the air-bronchogram sign.
    4. Clear C P angle.
    5. No shift of mediastinum is the outstanding feature.
    Air-bronchogram: bronchus contains air and the air is not visible separately in a normal chest X-ray;
    but in consolidation of the lung (pneumonia), the air within the bronchus casts linear translucency
    (black) over the background of homogenous opacity (consolidation). These are commonly seen as
    scattered linear translucencies rather than continuous branching structures. Air-bronchogram reflects
    that an opacity is intra-pulmonary. It needs a good quality of X-ray film and the observer should have
    an eagle‘s eye.
Pneumatocoele:
These are one or more air-filled cysts generally infective in origin and resulting due to check valve
obstruction of a communication between cavity and bronchus.
Causes:
    1. Staphylococcus aureus
    2. Streptococcus pneumoniae
    3. Klebsiella
    4. H.influenza

Pleural Effusion :
         Chest X-ray PA view:
       a) Triangular homogenous opacity with a curved upper border, which is concave medially (facing
            mediastinum) & upwards and extends up to axilla.
       b) Obliteration of costophrenic angle (earliest site of fluid collection-150 ml of fluid)
       c) Massive effusion produces unilateral homogenous opacity.
       d) Displacement of mediastinum to opposite side
       e) Lateral view is often done to differentiate from lobar consolidation.
       Encysted pleural effusion may not obliterate the costo phrenic angle.
       Radiologically, pleural effusion can be classified as free or loculated as given below:
                   1. Free classical: mild (blunting of costo phrenic angle on lateral decubitus view) or
                        moderate or severe (homogenous opacity with classical lateral-medial, superior-
                        inferior curve with mediastinal shift to the opposite side)
                   2. Free subpulmonic: additional elevation of diaphragm
                   3. Loculated fissural: phantom/vanishing tumor
                   4. Loculated along the chest wall.
Pleural effusion: differential diagnosis-
    1. Thickened pleura-
               Usually no mediastinal shift unless associated with gross thickening when mediastinum is
                   shifted to the same side.
               Ribs may be visible within the opacity i.e. the opacity is not truly dense
               Upper margin is fading and not concave.

   2. Empyema thoracis
   3. Bronchogenic carcinoma or consolidation ( with synpneumonic effusion)
   4. Fibrosis or collapse of the lung ( mediastinum shifted to the diseased side)
Causes of pleural effusion with large cardiac size:
                  1. CCF
                  2. Pulmonary embolism with heart failure
                  3. Myocarditis or pericarditis-T.B. or rheumatic
                  4. Metastasis
Causes of pleural effusion with hilar Lymphadenopathy:
   1. Bronchogenic carcinoma
   2. Lymphoma
   3. Metastasis
   4. Tuberculosis
   5. Sarcoidosis
   6. Fungal infection
Causes of pleural effusion with fine reticular shadows:
   1. Pulmonary edema
   2. Infection
   3. CCF
   4. Lymphoma
   5. Lymphangitis carcinomatosis
   6. Rheumatoid arthritis
How malignant pleural effusion is suspected?
   1. A convex bulge may be seen above the concave fluid level
   2. Collapse (absorption) of the lung may be associated with (in any part of either lung)
   3. Trachea may be shifted to the same side ( due to associated absorption collapse)
   4. Elevated hemi-diaphragm may indicate diaphragmatic palsy
   5. Prominence of hilar or para hilar shadow; erosion of ribs may be seen
   6. Recurrent, rapid collection of fluid.




Consolidation:
Differential diagnosis-
    1. Collapse of the lung (mediastinum moves to the diseased side)
    2. Bronchogenic carcinoma (pleural reaction i.e. pleural effusion is commonly seen; absence of ‗air-
         bronchogram‘ and there may be presence of rib erosion)
    3. Pulmonary tuberculosis ( classically sharply defined consolidation is rare; pleural reaction is more
         common)
    4. Pulmonary infarction ( may be a possibility because in pulmonary infarction wedge-
         shaped,homogenous,poorly defined opacity is produced attached against pleura; thus blunting of
         costophrenic angle is commonly seen here).
Pneumothorax:
Radiological features:
    a) Complete radiolucency with absence of lung markings
    b) Collapsed lung is seen as a homogenous opacity with razor sharp outline (present paravertebrally)
    c) Shifting of mediastinum towards opposite side
    d) Costophrenic angles clear
To diagnose the type of pneumothorax, history of onset and progress of symptoms are the two most
important determinants. In pneumothorax always look for stigmata of tuberculosis in the other lung.
Hydropneumothorax:
Chest X-ray PA view in erect posture shows:
    1. Horizontal fluid level
    2. Increased radiolucency above the horizontal fluid level which lacks in lung markings (pneumo
         component) and there is homogenous opacity below the horizontal level (hydro component)
    3. Shifting of trachea and cardiac shadow towards the opposite side.
Differential diagnosis:
     Hemopneumothorax,pyopneumothorax
     Infected lung cyst
     Very big lung abscess
Cardinal features of hydro-pneumothorax:
    1. Shifting dullness
    2. Succussion splash
    3. Horizontal fluid level ( upper limit of dullness is horizontal)
Collapse of the lung:
Collapse of the lung means an area of the lung devoid of air, hence, is detected as white area within lung
fields.
Radiological features:
Lung fields: look at the lung fields. The Rt lung is normally larger than the Lt-if it is not, then suspect an
area of Rt lung collapse
Position of diaphragm: normally,Lt dome should be lower than the Rt. if it is not( e.g. Lt dome elevated)
then Lt lung collapse may be suspected.
Position of the horizontal fissure in the Rt lung. The horizontal fissure normally on the Rt should run from
the centre of the hilum to the level of the 6 th rib in the axillary line. If this is pulled up, it suggests Rt upper
lobe collapse and if pulled down then Rt lower lobe collapse should be suspected.
Position of the heart: the heart shadow lies in the middle with one-third to the Rt and two-thirds to the Lt.
The heart shadow gets deviated to the side of collapse.
Heart borders: define the heart borders. Normally the borders are distinct. If the adjacent lung is collapsed,
then heart border will appear blurred. For example, if Rt heart border is blurred this indicates Rt middle
lobe collapse; and if Lt is indistinct or blurred, then suspect Lingular collapse. Chest X-ray lateral view
shows a triangular opacity with apex towards hilum and base between sternum and diaphragm.
Position of trachea: normally trachea is central; it gets deviated if there is pathology in the upper lobes.
Collapse of Rt or Lt upper lobe will pull the trachea towards the area of collapse. Lateral lines: check the
position of oblique and horizontal fissures. The horizontal fissure appears as faint white line which should
pass horizontally from the hilum to the anterior chest walls. If this line is not horizontal, the fissure is
displaced. The oblique fissure should pass obliquely downward from T4/T5 vertebrae, through the
hilum,ending at the anterior third of the diaphragm.
To determine the collapse of the lung both PA view and lateral chest X-ray must be taken and examined.
Collapse of any of the lobes of the lungs gives a distinct appearance on X-ray.
Collapse of the lung:
Chest X-ray PA view and lateral view shows shrunken lung as manifested by
                           a) Mediastinal shift on same side
                           b) Displacement of inter-lobar fissure
                           c) Ipsilateral elevation of diaphragm/tenting of diaphragm in basal collapse
                           d) Crowding of ribs/retraction of hemithorax on the affected side.
                           e) Homogenous shadow of the collapsed lung /opacity of the involved area
                           f) Compensatory emphysema elsewhere.
                           g) In compression collapse-the etiology of compression is seen e.g.
                                Pneumothorax/pleural effusion.
                           h) In long-standing massive collapse, scoliosis of the spine with concavity
                                towards the affected side.
     Lateral view is needed to determine the segment or lobe involved.
Collapse of whole Lt lung vs. Pneumonectomy
The distinct features are:
                In Pneumonectomy , the Lt hemithorax is homogenously opaque with no lung markings
                   while in collapse, lung markings are visible
                In Pneumonectomy, the whole mediastinum and even a portion of Rt lung lies in the Lt
                   hemi-thorax while in collapse only mediastinum is shifted
Pulmonary embolism:
Chest X-ray-often subtle, oligaemic lung fields/hypervascularity often difficult to detect, slight↑hilar
shadows.
The common findings in P E include focal infiltrates, segmental collapse, raised hemidiaphragm and
pleural effusion (usually blood stained); a wedge shaped or triangular opacity situated in the periphery
(pleural-based), though well described, is rare. It may lead to a small pleural effusion. There may be
collapse or linear atelectasis.
Valuable in excluding other diagnoses such as heart failure, pneumonia, pneumothorax or tumor.
 A normal chest X-ray in acutely breathless and hypoxemic patients increases the likelihood of P E.
Salient features-
     1. Opacity produced by Infarction (wedge shaped)
     2. Raised diaphragm, which moves poorly on inspiration.
Pulmonary embolism can also lead to black area of under perfused lung which is difficult to detect on plain
X-ray. CT scan and MRI are diagnostic. The enlargement of heart and prominent pulmonary conus
suggests acute cor pulmonale.




Hemi thorax opacity without any mediastinal shift:
    1. Consolidation of the lung
    2. Small pleural effusion
    3. Mesothelioma of pleura
Unilateral hypertrnslucency in X-ray film:
    9. Pneumothorax
    10. Bullae
    11. Lung cyst
    12. Eventration of Lt dome of the diaphragm
    13. Partial bronchial obstruction (unilateral)-obstructive emphysema
    14. Compensatory emphysema
    15. Contra-lateral thickened pleura (produces apparent increased translucency)
    16. Mastectomy; congenital absence or atrophy ( e.g. poliomyelitis) of pectoral muscle
    17. Poor technique, scoliosis.
BRONCHIAL OBSTRUCTION:
MEAT FACE
M: Mucous plug
E: Endo-bronchial granulomatous disease(Wegener‘s sarcoid)
A: Adenoma
T: Tuberculosis
F: Foreign body
A: Atresia,Amyloid-primary
C:Cancer 1°
E: Endo-bronchial mass
Pulmonary edema:
Features: ―bats wing appearance‖ of confluent shadows extending from the hilum into midzone.
PERI HILAR BAT-WING INFILTRATION :
Please Please Study Light, Don‘t Get All Uptight
P: Pulmonary edema
P: Pulmonary alveolar proteinosis
S: Sarcoidosis
L: Lymphoma
D: Drug
G: Goodpasture syndrome
A: Alveolar cell carcinoma
U: Uraemia




Homogenous rounded opacity (solitary pulmonary nodule or coin lesion in lung)
it needs not be strictly circular.
Causes:
A. Infectious: tuberculosis, histoplasmosis, coccidoidomycosis, pneumonia etc.
B. Neoplasms: bronchogenic carcinoma, adenoma, metastatic nodule, mesothelioma or fibroma of the
    pleura, hamartoma etc.
C. Cysts: hydatid, bronchial
D. Vascular: pulmonary Infarction and A V fistula
E. Occupational diseases: silicosis, anthracosis etc.
The causes of single coin lesion:
               Benign tumor e.g. hamartoma
               Malignant tumor e.g. Bronchogenic carcinoma, solitary secondary
               Infection e.g. consolidation,abscess,Tuberculoma
               Hydatid cyst
               Pulmonary infarction
               Rheumatoid nodule
Differentiating features:
               A speckled irregular or lobulated edge of the lesion suggests malignancy
               Calcification within the lesion indicates tuberculosis or infection
               More than one coin shaped lesion suggest metastatic disease
               Air –bronchogram suggests consolidation rather than a tumor
               Surrounding the lesion, the area of consolidation or collapse may indicate a tumor
               Malignant tumors are associated with mediastinal lymphadenopathy,rib erosion and
                   pleural effusion

Miliary mottling: 1-2 mm miliary opacities mimic millet seeds and it is why these types of shadows are
known as ‗miliary mottlings‘.
             Miliary shadowing refers to small miliary opacities having similar density and size
                 distributed in the lung(s) giving a spotted or mottled appearance.
             They sometimes can be confused with a ground glass appearance or normal vascular
                 markings of the lung.
             To differentiate between them, move close to the X-ray and examine the shadowing
                 carefully.
             In miliary mottling the opacities are dicrete, small and have similar size and density, are
                 mainly distributed in the peripheral lung fields.
Main causes:
    1.  Miliary tuberculosis ( generalized ,uniform size, smaller shadows, usually hilar lymph nodes are
        not affected and common in children)
    2. Tropical eosinophilia( usually involves mid and lower zones,non-uniform,larger shadows with
        hilar lymph node involvement ,persons of any age are affected)
    3. Alveolar cell carcinoma
    4. Histoplasmosis,coccidomycosis
    5. Pulmonary haemosiderosis ( smaller but dense shadows)
    6. Sarcoidosis ( larger shadows, spare apices and hilar lymph nodes may be enlarged)
    7. Pneumoconiosis ( size 3-5 mm;coal-miners commonly)
    8. Fibrosing alveolitis
    9. Silicosis
    10. Lymphangitis carcinomatosis [ a form of metastatic carcinoma where the pulmonary lymphatics
        are involved and often blocked by malignant cells; 2-3 mm nodules with thickening of pulmonary
        septa ( Kerley ‗s A and B line);may be primary source in bronchus,stomach,breast,colon or
        prostate].
    11. Disseminated metastasis in the lungs
    12. Interstitial lung disease
Miliary mottling:
A. Infection:
    1. Bacterial: disseminated tuberculosis, broncho-pneumonia, Brucellosis
    2. Fungal: Histoplasmosis, coccidiodomycosis, blastomycosis etc
B. Allergic: tropical eosinophilia, Loeffler‘s syndrome, drug reaction
C. Neoplastic: lymphangitis carcinomatosis, alveolar cell carcinoma, leukaemia, lymphoma
D. Pneumoconiosis:
E. Cardiac: multiple pulmonary Infarction, pulmonary edema
F. Miscellaneous: rheumatoid arthritis, Sarcoidosis, haemosiderosis, interstitial pulmonary fibrosis,
                            hyaline membrane disease, chicken-pox pneumonia, after lipoid
                            bronchography
G. Artifacts: skinwarts (multiple),neurofibromatosis etc.
Miliary mottling:
A. Extremely numerous opacities:
    Causes: tuberculosis, Histoplasmosis, metastases, alveolar microlithiasis
B. Opacities few in number:
    Causes: Varicella, metastases, Sarcoidosis.
C. Opacities in mid and lower zones:
    Causes: Sarcoidosis, Pneumoconiosis, alveolar microlithiasis, metastases
D. Confluent opacities:
    Causes: alveolar microlithiasis, hyaline membrane disease, Pneumoconiosis
E. Fine pin-point opacities:
    Causes: alveolar microlithiasis, post- lymphangiography, stannosis,Bartosis
F. Opacities with associated lymph nodes
    Causes: tuberculosis, Sarcoidosis, Histoplasmosis, metastasis, silicosis.
"Snow-storm" motlings: Disseminated Hematogenous Metastasis.Miliary Tuberculosis and Dust Diseases
Differentiating features:
Distribution of opacities:
               In miliary tuberculosis, the opacities are most marked in the upper zone,
               In sarcoidosis these are most marked in perihilar regions and mid-zones
               While in miliary metastasis these are limited to lower zones.
Density:
               Higher dense white opacities are likely to be due to dust related industrial/occupational
                   disorders or calcified tuberculosis.
               Less dense changes could either be multiple secondaries or sarcoidosis or any other cause
                   of miliary mottling.
Other associated signs:
               Unilateral hilar enlargement suggests tuberculosis
               While bilateral hilar enlargement (Lymphadenopathy) indicates sarcoidosis.
               Presences of subtle cavitating lesions suggest tuberculosis.
Ring shadows ( e.g. Bronchiectasis):
    1. Multiple ring shadows of any size up to 1 cm in diameter occurring in groups giving a honey-
         comb or "bunches of grapes" appearance on chest X-ray may suggest bronchiectasis.
    2. Other lesions described in bronchiectasis are:
               Tubular shadows: these are thick white shadows up to 8 mm wide, represent bronchi
                   filled with secretions (end-on-bronchus)
               Glove-finger shadows. These re-present a group of tubular shadows seen head on and
                   look like the finger of a glove.
The presence of any of these features suggests bronchiectasis but a normal chest X-ray does not, however,
exclude the diagnosis. The CT scan is most sensitive diagnostic test available for bronchiectasis.

Bronchiectasis:
              a. Multiple ring-shaped shadows, especially at the base
              b. Areas of fibrosis or haziness.
Ring shadows: Bronchiectasis, Cavitating lesion, tumor, abscess,hydatid cyst, pulmonary infarct(triangular
with a pleural base-Hampton's hump)
Fever with nodular patterns in the lung:
  1. Miliary tuberculosis
  2. Eosinophilic grannuloma
  3. Sarcoidosis
  4. Inhalational disease(fume inhalation)
  5. Metastasis
  6. Viral pneumonia
  7. Fungal lung disease
Hypertranslucency: it refers to increased blackness of the lung fields due to trapping of air either in the
pleural space or in the lungs. It may be unilateral or bilateral.
Caution: before commenting upon hypertranslucency, check the penetration of X-ray. If the vertebral
bodies are just hardly visible behind the heart, it is a good quality X-ray while if they are clearly visible,
then the film is over-penetrated and makes the lungs appear black (hypertranslucenct)
Causes:
Unilateral
1. Pleural:
    a) Pneumothorax-absent vascular marking with visible collapsed lung.
    b) Contra-lateral pleural thickening (apparent hyper-translucency)
2. Pulmonary artery :
    a) Congenital absence
    b) Embolic occlusion-Westermark's sign
3. Lung parenchyma
    a) Bullous emphysema
    b) Eventration of the LT dome of the diaphragm
    c) Unilateral emphysema /compensatory overinflation
4. Air ways:
    a) Obstructive overinflation
    b) Macleod‘s syndrome
5. Chest wall:
    a) Mastectomy
    b) Absent pectoral muscle c) Scoliosis d) Contralateral lipoma.
Bilateral:
Causes:
1. Pleural: bilateral Pneumothorax
2. Pulmonary:
    a) Emphysema
    b) Bronchial asthma
    c) Bullae (multiple)
3. Cardiac:
    a) Primary pulmonary hypertension(if vascular shadow disappears, the lung is replaced by air)
    b) Ebstein‘s anomaly
    c) Fallot‘s tetrad with pulmonary atresia.
4. Chest wall: bilateral mastectomy
5. Overexposed Film

Emphysema
The radiological findings in COPD are due to hyperinflation of the lungs with constriction of the cardiac
shadow.
              The lungs are large and voluminous due to hyperinflation which can be checked by
                  counting the ribs anteriorly. If you can count more than 7 ribs above the diaphragm, then
                  lungs are hyperinflated. This can be a normal finding in some individuals also.
                  The domes of the diaphragm are low and flat instead of being convex due to
                   hyperexpansion of the lungs.
                The heart is tubular (elongated and narrow) due to over-expansion of both the lungs. The
                   heart, instead of sitting on the diaphragm often appears to "swing in the wind".
                Hypertranslucency of both the lungs is characteristic. Bullae (densely black areas of lung,
                   usually round, surrounded by hair-line shadows) may be seen which may compress the
                   normal lung and distort the surrounding vasculature. Thus, to find out the bullae, look out
                   for areas for decreased vascular markings.
                The lung vascular markings are reduced bilaterally (oligaemic lungs) and fan out as
                   straight lines from the hilum but stop two-thirds of the way out i.e. peripheral pruning
                   (peripheral fields appear without vascular markings)
                The ribs are more horizontal and the intercostal spaces appear widened.
X-ray chest in COPD:
     1. Hyper translucency of lung fluid
     2. Widened intercostal spaces
     3. Low flat diaphragm
     4. Increased retro-sternal translucency
     5. Narrow vertical heart(tear drop heart)
     6. Large hilar shadows
     7. Diminished peripheral vascular pattern
     8. Bullae: rounded areas of hyper translucency with thin hairline shadow forming the margin.
     9. No mediastinal shift
MULTIPLE-THIN-WALLED CAVITIES
B: Bulllae (+ pneumatocoele)
I: Infections-Tuberculosis, Coccidomycosis, Staphylococcus Aureus
T: Tumors
C: Bronchogenic,Traumatic Cysts
H: Hydrocarbon
Bullae and emphysema-
Bullae are thin-walled air spaces more than 1 cm in diameter, produced by rupture of alveolar walls.Bullae
may occur anywhere, but are most commonly seen at the apices. They seem to result from lung atrophy,
either physiological (at the apices) or in relation to a disease process. Such cavities may become large,
forming pneumatocoeles, which compress the remaining lung tissue to cause severe respiratory distress.
Bullae may also become infected and contain fluid levels.
Emphysema is not synonymous with overdistension, which occurs in bronchial asthma and may be present
with normal or only slightly overinflated lungs especially in emphysema of centrilobular type. One should
look for signs of lung destruction-smaller and fewer the normal pulmonary vessels, fibrosis, and bullae
which may occupy part or even a whole lung.
Pneumothorax (unilateral black lung):
Before commenting on unilateral blackness, check the technical quality of film. A rotated film (one clavicle
 is nearer the mid-line than the other ) may make one side less dense than the other.
Chest X-ray PA view done in erect posture.

Features:
     a). Complete radiolucency with absence of lung markings. This is due to air trapped in pleural space.
     b). Collapsed lung is seen as a homogenous opacity with razor sharp outline (present paravertebrally).
         The sharply defined edge of the deflated lung is seen as a vertical line when X-ray is turned on its
         side which is convex towards periphery. In a large pneumothorax, deflated lung appears small
         towards the centre with convex borders.
     c). Shifting of mediastinum towards opposite side indicating tension pneumothorax which returns to
         normal after removal of air on expansion of lung.
     d). Costo phrenic angles clear
Differentiation between a bullae and pneumothorax is sometimes difficult and often impossible.
However, if lung markings are seen either crossing the area of blackness or are limited to the periphery of
the blackness, then it is a bullae rather than pneumothorax. Bullae are usually multiple if bullous disease is
suspected.
Honey combing of lung (multiple air containing cyst like shadows or ring shadows measuring 0.5-2 cm in
   diameter)
   a) Cystic bronchiectasis
   b) Sarcoidosis
   c) Interstitial fibrosis, fibrosing alvelolitis, extrinsic allergic alveolitis.
   d) Rheumatoid lung
   e) Scleroderma, SLE
   f) Drug treatment
             i) NFT
             ii) Busulphan
             iii) Bleomycinor melphalan.
   g) Neurofibromatosis
   h) Histiocytosis
   i) Adenoma sebaceum (tuberous sclerosis)
   Elevation of the diaphragm:
   Causes:
   Unilateral:
       1. Amebic abscess
       2. Subphrenic infections/abscess
       3. Sub-diaphragmatic tumor/splenic cyst
       4. Basal pleural or pulmonary infection
       5. Basal collapse of lung /fibrosis.
       6. Subpulmonic pleural effusion
       7. Basal pulmonary Infarction
       8. Eventration of the diaphragm
       9. Phrenic nerve palsy
       10. Scoliosis
       11. Hemiplegia
       12. Gas in the colon or fundus of the stomach
   Raised RT dome of the diaphragm:
       1. Subpulmonic effusion
       2. Eventration of diaphragm
       3. Paralysis of dome of diaphragm (phrenic nerve palsy)
       4. Subphrenic abscess
   Bilateral:
       1. Pregnancy
       2. Obesity
       3. Ascites
       4. Large abdominal mass
       5. Abdominal distension
       6. Infants.
       7. Hepatosplenomegaly
       8. Pneumoperitoneum
       9. Fibrosis in both the lungs/bilateral basal collapse.
       10. Bilateral subphrenic abscess
       11. Bilateral phrenic nerve palsy
   Unilateral hilar shadow enlargement
   Due to lymph node enlargement
                   Infective e.g. tuberculosis,Histoplasmosis
                   Sarcoidosis
                   Neoplasm e.g. lymphoma, metastasis from Bronchogenic carcinoma
                      Due to vascular enlargement
                   Pulmonary artery aneurysm
                   Post-stenotic dilatation of pulmonary artery
       1. Bronchogenic carcinoma
    2. Sarcoidosis
    3. Lymphoma
    4. Tuberculosis
Bilateral hilar Lymphadenopathy
(More than 5 mm is pathological)
Causes:
    A. Infection
               1. Tuberculosis
               2. Histoplasmosis
               3. Recurrent chest infections
               4. AIDS
    B. Neoplasms
               1. Lymphomas
               2. Metastasis
    C. Occupational lung diseases and other
               1. Silicosis
               2. Berylosis
               3. Sarcoidosis
Bilateral hilar shadow enlargement:
Above causes +
     Increased pulmonary blood flow due to septal defect
     Pulmonary hypertension.

Differential features of hilar enlargement:
              a). Smooth enlargement of hilum is due to vascular lesion while lobulated appearance
                   indicates lymphadenopathy and spiculated irregular or indistinct margins suggest
                   malignancy.
              b). Presence of calcification within the mass indicates lymph node enlargement usually
                   tuberculosis. Egg shell calcification indicates lymphadenopathy due to silicosis.
              c). Hilar enlargement due to malignant lung lesion is also associated with superior
                   mediastinal lymphadenopathy
              d). Look at the lung fields ( for presence of tumor or tubercular infiltration) and bone/ribs for
                   metastasis.
Mediastinal shadow widening (enlargement)
                        – The mediastinum comprises the central area between the two lungs and their
                             pleural coverings.
                        – Laterally on either side, it is bounded by mediastinal pleura. It extends from the
                             thoracic inlet (above) to the diaphragm (below) and from the sternum (front) to
                             the spine(back). The structures present in the mediastinum include lymph nodes,
                             heart and great vessels (aorta and its branches), SVC, thymus, esophagus, and
                             fatty areolar tissue.
                        – In a normal Chest X-ray, trachea remains central (the black airy tube) or slightly
                             deviated to Rt and evenly calibrated. The thymus, pleural reflections and fibro
                             fatty tissue may or may not be visible.
                        – Position of the cardiac apex (outwards, or out and downwards) and the trachea
                             indirectly indicates shifting of the mediastinum.
                        – Observe, whether the mediastinum is widened or not.
                        – On PA view, measure the width of the mediastinum (white area) at its maximum
                             convexity and compare it to the width of the chest at that point; if it is >30 % of
                             the width of the chest, then mediastinum is said to be enlarged/widened.
Causes:
    A. Lymphadenopathy
              1. Tuberculosis
              2. Sarcoidosis
              3. Lymphomas
              4. Leukaemias
                5. Metastasis
     B. Aorta
                1. Aneurysm
                2. Unfolding
                3. Anomalous origin of the great vessels
     C. Cysts
                1. Dermoid Teratoma
                2. Cystic hygroma
                3. Bronchogenic cyst
                4. Pleuro-pericardial cyst
                5. Meningocoele
     D. Thymus
                1. Enlargement
                2. Tumor
     E. Esophagus
                1. Achalasia cardia
                2. Hiatus hernia
                3. Enterogenous cyst
     F. Miscellaneous
                1. Lipoma, mesothelioma
                2. Mediastinal abscess
                3. Cardiac aneurysm or tumor
Differentiating radiological features:
     a). Site of enlargement/widening: look at the X-ray and note whether widening is at the top, in the
          middle or lower part of mediastinum.
Widening at the top could either be due to thyroid, thymus or innominate artery
Widening of the middle or bottom of the mediastinum could be due to lymphadenopathy, aortic aneurysm,
dilatation of esophagus (cardia achalasia) or a Hiatal hernia
                   If widening is at the top, then look at the position of the trachea. An enlarged thyroid
                       displaces or narrows the trachea while tortuous innominate artery or thymus does not.
     b). If you suspect an enlarged thyroid then look at the out-line of the shadow. A thyroid has a well-
          defined shadow that tends to become less clear as one moves up to the neck.
     c). Look at the Rt side of the trachea. A white edge of trachea is 2-3 mm wide, its further widening
          suggest either enlarged SVC or a para-tracheal mass.
     d). If you suspect widening of aorta, follow the outer edge of the aorta downward, you may be able to
          detect a continuous edge which widens to form the edge of enlarged mediastinum. This would
          suggest that the widening is due to dilatation of the aorta.
     e). Look at the calcification in the wall of aorta. If you detect a line of calcification, then follow it. If
          it leads into an area of aortic knuckle, then this strongly suggests aortic aneurysm or
          atherosclerosis of aorta. If the line of calcification is separated from the edge of aortic shadow this
          strongly suggests aortic dissection.
     f). To differentiate aortic aneurysm from unfolding of aorta ,follow both the edges of aorta and note
          for any widening which will suggest the aneurysm. Obtain lateral film. If the edges of the aorta are
          parallel then you are probably dealing with unfolding of the aorta on the PA view of chest X-ray.

Pneumo-mediastinum
Differential diagnosis of focal mediastinal gas:
                        Locally or diffusely dilated esophagus
                        Esophageal diverticulum
                        Hernia
                        Communicating duplicating cyst

Differential diagnosis of diffuse mediastinal gas:
Sources
     Esophagus
        Trachea
        Bronchus
        Perforation of duodenum or colon
        Neck
        Tooth-dental drilling

     Lung
Pneumo-pericardium
Differentiation of pneumo-mediastinum and pneumo-pericardium radiologically
Obtain frontal views with patient in Rt and Lt lateral positions.
Pneumo-pericardium                        Pneumo-mediastinum
Air may cross the mid-line                Air does not cross the mid-line
Air does not rise to level of aortic knob Air rises to level of aortic arch, neck etc
Air out-lines pulmonary artery            Air does not out-line pulmonary artery


Calcification of aorta (aortic aneurysm)
Calcification of aorta (aortic aneurysm) is common in old, in patients with diabetes mellitus and chronic
renal failure
NB:
                  Always look for abdominal aorta when you are looking at plain X-ray of abdomen
                     because calcification of aorta/aortic aneurysm may be an incidental finding.
                  Secondly it is important from therapeutic point of view as this condition is potentially and
                     eminently treatable by surgery or stenting.
                  Most aneurysms bulge to the Lt or to the Rt (occasionally ) or lie in the middle over the
                     spine (uncommonly)
Clinical tip: a normally calcified aorta (due to atherosclerosis) over the spine with parallel or converging
walls excludes an aortic aneurysm (e.g. aortic aneurysmal calcification means loss of parallelism in its
walls). Therefore, always look at the walls of aorta for parallelism.
 Q.What are the causes of aneurysm of aorta and other vessels?
                Atherosclerosis
                Hypertension
                Infection (mycotic)
                Traumatic
                Congenital
                Fibro-muscular dyspalsia
                Polyarteritis nodosa
Caution; the absence of a visible aneurysm on the plain film does not mean the patient has not got one.
Always try other sophisticated investigations to confirm its presence or absence.
Calcification in chest:
Causes:
A.        Pulmonary/parenchymal calcification
          I. Diffuse
               1. Infection: tuberculosis, abscess, Histoplasmosis, Varicella, pneumonia.
               2. Tumor: hamartoma, pulmonary A-V aneurysm, metastasis from osteogenic sarcoma
               3. Unknown: Bronchiolitis, alveolar microlithiasis
               4. Silicosis
               5. Haemosiderosis (following hemoptysis in long standing mitral stenosis)
               6. High density (post lymphangiography, baritosis, stannosis)
          II. Solitary
               1. Infection: tuberculosis, Histoplasmosis
               2. Hamartoma (pop corn calcification)
B.        Cardiac calcification
               1. Aortic arch (ring shaped or annular calcification in atherosclerosis)
               2. Constrictive pericarditis (pericardial calcification)
         3. Valves or valve rings (mitral and aortic valve)
         4. Thrombi and myxomas
         5. Coronary arteries calcification
C.   Mediastinal calcification
         1. Lymph glands: tuberculosis, sarcoid, pneumoconiosis
         2. Tumors: Teratoma, dermoid, thyroid adenoma
D.   Pleural calcification
         I. Diffuse
              1. Infection: tuberculosis, Pyogenic empyema (healed),Histoplasmosis
              2. Asbestosis

         II. Focal (subpulmonic plaques)
             1. Asbestosis-asbestos causes pleural plaques especially antero-laterally, in the inter-
                 lobar fissures, and over the diaphragm where their calcification looks similar to
                 ‗icing sugar on a cake‘.
             2. Talcosis
             3. Trauma –hemothorax may also calcify.
E.         Chest wall calcification
               1. Ribs (bone islands, costal cartilages)
               2. Muscles and soft tissue (cysticercosis, Guineaworm, dermatomyositis)
               3. Phleboliths
F.         Egg-shell calcification
               1. Silicosis (commonest)-calcification of the hilar lymph nodes may occur in a s many as 20
                    % of cases and produces the characteristic ‗egg shell pattern‘.
               2. Sarcoidosis-some of unusual chest X-ray findings in sarcoidosis include ‗egg shell
                    calcification of hilar nodes‘, pleural effusions.
               3. Scleroderma
               4. Histoplasmosis
               5. Amyloidosis
               6. Lymphoma following radio-therapy
               7. Coal worker‘s pneumoconiosis
               Mnemonic: SHALL for shell calcification
Distinction between the following lesions-
       Extra-thoracic and intra-thoracic
           -Extra-pulmonary and intra-pulmonary
       Benign and malignant chest wall lesions
Tapered border sign:
       Indicates displacement of the pleura inward by the mass.
       Suggests intra-thoracic, extra-pulmonary location, not cutaneous or parenchymal
       Pitfalls: not seen in en face lesions.
Extra-pulmonary lesions
This space includes connective tissue, nerves, vessels, muscles and ribs.
It lies between the parietal pleura and thoracic cage.
Lesions typically show:
       Sharp, convex contour facing lung
       Smooth outline
       Horizontal diameter as great as vertical
     Superior and inferior edges are usually tapered
     Widest part is usually opposite the centre of attachment
Incomplete border sign:
     A lesion‘s border is produced by the inter-face of mass and air.
     If the mass is continuous with soft tissue, the border is lost.
     An incomplete border is suggestive of extra-pulmonary process.
     It may, therefore, signify an extra-thoracic (cutaneous) or intra-thoracic chest wall lesion.


Pleural thickening:
     1. Tuberculosis
     2. Empyema
     3. Metastasis
     4. Trauma
     5. Rheumatoid arthritis
Solitary pleural mass
     1. Localized pleural effusion
     2. Mesothelioma
     3. Organized empyema
     4. Metastasis
     5. Lipoma.
Causes of pericardial calcification:
     1. Post-tuberculous
     2. Post-traumatic
     3. Uremia
Calcification in myocardium
     1. Infarction
     2. Aneurysm
     3. Hydatid disease
     4. Aortic valve calcification
          a) Bicuspid aortic valve
          b) Rheumatoid valvulitis
          c) Syphilis
          d) Old age
Eggshell calcification of lymph nodes:
     1. Silicosis
     2. Coal worker‘s pneumoconiosis
Calcification inside the lungs:
     1. Malignancy
     2. Tuberculosis
     3. A-V fistula
     4. Hydatid cyst
     5. Haemochromatosis
Fine reticular patterns with hilar Lymphadenopathy
     1. Viral pneumonia
     2. Sarcoidosis
     3. Lymphoma
     4. Primary bronchogenic carcinoma
     5. Metastasis
     6. Silicosis
Unilateral hilar lymphadenopathy
     1. Tuberculosis
     2. Carcinoma
     3. Pneumonia
     4. Mediastinal mass
    5. Whooping cough
Bilateral hilar lymphadenopathy
Main causes:
     1. Viral infection
     2. Tuberculosis
     3. Lymphoma
     4. Silicosis
X-ray of small heart
     1. Normal variant
     2. Emphysema
     3. Addison‘s disease
     4. Dehydration
     5. Constrictive pericarditis.
Cardiomegaly
     1. Multi-valvular heart disease
     2. Pericardial effusion
     3. Cardiomyopathy
     4. CCF
Enlargement of SVC:
     1. Tricuspid incompetence
     2. Mediastinal mass
     3. Bronchogenic carcinoma
     4. Constrictive pericarditis
The azygos vein is usually situated above the RT main bronchus, but may lie within an accessory fissure in
the RT upper lobe. when it forms an ‗azygos lobe‘.
Enlargement of azygos vein:
     1. Heart failure
     2. Superior vena cava obstruction
     3. Pregnancy
     4. Pericardial effusion
     5. In normal people tends to be larger on views taken with the patient lying down compared with
          those in the erect position.
Causes of cavitatory nodules
     1. Lung malignancies
          a) Squamous cell carcinoma
          b) Sarcoma
          c) Melanoma
     2. Metastasis
     3. Septic embolism
     4. Cryptococcal infection
     5. Collagenosis.
Cavity-liquefaction necrosis within the lung (may remain empty or filled with secretion) and
communicating with the bronchus. A cavity is walled off area of the lung which is darker in the centre than
the periphery. Some coin shaped lesion may cavitate.
Pseudo-cavity-radiological appearance of pulmonary cavity as a result of summation shadows of ribs,
vessels, fibrotic bands, calcification or artefacts.
Cavitating lung lesions –any lung lesion, which becomes infected or outgrows its blood supply may
cavitate, but certain features may suggest the underlying cause:
     1. Bullae are the commonest cavities
     2. Pneumonia with lung abscess appears as an area of lung consolidation with a cavity. In
          staphylococcal pneumonia cavitation may be real and due to lung break-down or be apparent and
          due to pneumatocoele or bullae, as a result of bronchial distortion and air trapping.
     3. Tuberculosis-suggested by multiple cavities and lung infiltration especially in the upper lobes or
          apices of lower lobes. There may also be associated chronic lesion containing calcification.
         4.  Neoplasm with secondary degeneration and cavitation–commonly primary lung tumor masses
             break down to give an eccentric irregular cavity within the mass. Squamous tumors commonly
             produce a thick walled cavity having an irregular inner border
        5. Pulmonary Infarct-may cavitate especially if infected as in drug addicts, diabetes mellitus or
             patients with infected shunt (undergoing hemodialysis)-rare.
        6. Cavitating pneumoconiotic nodules-suggested if there are smaller nodules and pulmonary
             fibrosis.
        7. Rheumatoid and other necrobiotic or granulomatous nodules may also cavitate-rare .
        8. Fungus infection in which the cavities may contain a mycetoma or fungus ball.
    Differentiating features:
                   The cavity may contain a horizontal fluid level- a line within lesion. There will be
                       whiteness (fluid) below the line with an area of blackness (air) above. This is common in
                       Pyogenic infection i.e. lung abscess
                   If the walls of the cavity are thick (>5 mm) and irregular, infiltrating into the surrounding
                       lung, then it is neoplasm as opposed to an abscess. Staphylococcal lung abscess
                       especially is a thin-walled called pneumatocoele. This rule does not always hold true.
                   A white ball within a cavity is characteristic of an aspergilloma which can be seen
                       floating in the cavity.

    CAVITY
    C: Carcinoma
    A: Abscess
    V: Vascular-metastasis and septic emboli
    I: Infections-fungal; immune –rheumatoid
    T: Trauma
    Y: Young patient (sequestration)

     Lesions of bone especially secondary deposits (lytic or sclerotic), in the spine, or ribs.
a) Lytic deposits-metastasis primary with bronchus, kidney, bowel, myeloma, or thyroid.
b) Sclerotic or mixed deposits with reticuloses, breast or prostrate (specially after treatment),also rarely with
     other tumors such as villous papilloma of rectum or medulloblastoma.
Unilateral dense homogenous opacity of one hemithorax:
          1. Massive pleural effusion
          2. Empyema thoracis
          3. Collapse of the lung
          4. Massive consolidation
          5. Thickened pleura
          6. Pleural mesothelioma
          7. Asbestosis of lung
          8. Pneumonectomy
          9. Destroyed lung ( from chronic inflammation and fibrosis)
     Shifting of mediastinum (trachea and cardiac shadow):
          1. Pleural effusion- opposite side
          2. Empyema-opposite side
          3. Collapse of lung-same side
          4. Consolidation-no shifting
          5. Thickened pleura-same side ( in gross thickening)
          6. Pleural mesothelioma-usually no shifting
          7. Agenesis of lung, pneumonectomy and destroyed lung- same side.
Intra-thoracic lymph nodes:
Nodes should be, if possible, differentiated from vessels on plain X-ray
      By their nodualrity
      By overlapping the vessels
      In difficult cases by opacifying the vessels with contrast medium at angiography/CT.
     Sarcoidosis:
                 Nodal enlargement particularly seen in the broncho-pulmonary (hilar nodes), the azygos region,
                  and the subcarinal nodes.
              Disease is symmetrical on either side of chest.
         Reticulosis:
              Nodal enlargement tends to asymmetrical
              Enlargement of anterior mediastinal or thymic nodes is common and may be massive




         Tuberculosis:
               Primary tuberculosis in children (the typical ghon focus with a small peripheral lesion/focal
                  pneumonia and central lymph node enlargement-primary complex)[ in contrast, with tuberculous
                  reactivation or reinfection local destructive pneumonia with caviation occurs and there is no
                  lymphadenopathy ].
         Azygos node enlargement may be seen with tuberculosis, Sarcoidosis and tumors. It is often readily
         distinguished from distension of azygos vein by being
               Very large
               Associated with other lymphadenopathy
               Distended with the patient supine and much smaller when sitting or standing.




         azygos vein in azygos fissure ; enlarged azygos node.

Surgical emphysema:
Collection of air in the soft tissue structure is called surgical emphysema because mostly it is due to either a
complication of surgery or chest tube drainage.
Radiological characteristic:
Look at the soft tissue shadow around the chest X-ray. Lozenge -shaped areas of blackness which re-presents
pockets of air in the soft tissue indicate surgical emphysema. These areas lie in the same plane as the soft tissue
structures. In severe cases, orientation of the planes is lost and dark and white lines are produced which cross a part
or whole of the film
Causes of surgical emphysema:
                Trauma
                Iatrogenic e.g. surgery, chest tube drainage
                COPD, asthma
                Esophageal rupture
                Gas gangrene




                                           PLAIN-X-RAY –ABDOMEN
The diagnostic potential of X-ray chest because of the superb natural contrast of air is less generously available.
              Every abdominal X-ray is an A-P film because beam passed from the front to the back with the
                 film behind the patient who is lying down with X-ray machine over-head.
              On demand, you can have an erect film or even decubitus views. Usually the radiographer will
                 mark the film with a badge or write on it by hand "supine" or "erect" to guide you.
                Otherwise, also you can guess how a given film was taken from the relatively positions of organs,
                 fluid and gas etc.
        Penetration:
                       Under- penetration (film is less dark) is not a problem because if you can see the bones in
                          the spine, the most of every thing else you need to see will probably be visible well.
                       However, in any over-exposed film (excessively dark) areas on an X-ray must be
                          inspected with a bright light behind them (there is provision in certain view-boxes to see
                          such area (s) or a separate device may be available).
                       However, in case of doubt, a good film after full preparation of the patient may be got
                          done again because certain important information such as air under diaphragm which
                          indicates a potential fatal condition is likely to be missed.
        Shadows on the X-ray: it is worth knowing that only five basic densities are visible such as:
                       Gas: black
                       Fat: dark grey
                       Soft tissue/fluid: light grey
                       Bone/calcification-white
                       Metal-intense white



Normal adult supine A-P X-ray abdomen:
This is the film frequently taken as it shows most of the structures to the best advantage
An X-ray should always be inspected on a view box as irregular illumination and reflection will prevent 10-20 % of
the useful information on it being visualized.
Always look for 'R' mark written any where on the film, usually low down on the Rt side. All references to Rt or Lt
refers to patient's Rt and Lt.
Lastly check that 'R' marker is compatible with visible anatomy e.g.
                Liver on the Rt
                Lt kidney higher than Rt
                Stomach bubble on the Lt
                Spleen on the Lt
                Heart on the Lt if visible
                Dark skin fold going across the upper abdomen is normal.
In an emergency, plain X-ray of the abdomen is taken without prior preparation.
Plain-X-ray-abdomen must be evaluated as follows:
1. Lung bases and diaphragm: for basal pneumonia, pleurisy, gas under the diaphragm (in erect film denotes bowel
     perforation)
2. Extra-abdominal soft tissues (an incarcerated hernia may be the cause of patient‘s bowel obstruction)
3. Skeletal structures: lumbar vertebra, vertebral pedicles, lower ribs and sacro-iliac joints; the wide pelvis
     indicating the X-ray belong to a female. Joint spaces of the hip-look for any narrowing or any other
     abnormality.
4. Fat and muscle plane; psoas muscle
5. Solid organs: the dark margins outlining the liver, spleen and kidneys (try to find as many organ outlines),
     bladder and psoas muscles
6. Hollow organs: G.I. tracts; small bowel is recognized by its central position and valvulae conniventes which
     reach from one wall to other. Displacement of bowel denotes space occupying lesion (tumor) or massive
     organomegaly.
7. Gas shadow in stomach and descending colon: large bowel is peripheral in position with its haustrations.
8. Calcification; pelvic phleboliths- a common normal finding
9. Intraperitoneal air and fluid
                Liver-< 18 cm long usually inferior surface outlined by fat.
                Spleen-enlargement displaces stomach gas bubble to mid-line.
                Kidneys-normally 3-3.5 vertebra long.
Solid, hollow organs and bones:
These structures can be classified as:
                                                  1.   Visible or not visible and therefore whether present or
                                                       potentially absent
                                                  2.   Too large or too small
                                                  3.   Distorted or displaced
                                                  4.   Abnormaly calcified
                                                  5.   Containing abnormal gas, fluid or discrete calculi
Indications of plain X-ray abdomen:
              1. For stone and calcification in the genito-urinary area, pancreas, solid organ, hematomas, abnormal
                   mass (lymph nodes), vascular structures etc
              2. Perforation of hollow organ e.g. stomach, colon, appendix etc. erect film will show air under
                   diaphragm.
              3. Duodenal or Paralytic ileus/ or gall stone ileus. dilated intestinal loops are seen.
              4. Sub-diaphragmatic pathology. An amebic liver abscess may push RT dome of the diaphragm and
                   a big splenic will push Lt Dome. In ascites, both domes are raised on supine X-ray .
              5. Eventration of diaphragm: the gastric contents are seen in thoracic cavity in eventration of Lt
                   dome.
              6. Certain soft tissue masses e.g. psoas abscess, Para-vertebral abscess.
Importance of X-ray abdomen:
                         Remember that X-ray is only a snap shot of the patient and that serious disease may still
                             be present despite a normal initial X-ray. Follow-up films are thus necessary to come at a
                             correct diagnosis as the radiological signs evolve.
                         Never forget to get the X-ray reported by a radiologist because he/she is trained to see
                             and extract the maximum amount of useful information from every film that can
                             frequently help to optimize the care of your patient.
                         Never try to subject the pregnant female to X-ray examination. If in doubt, either delay
                             the investigation or use USG to investigate the problem.
Hollow organs:
           1. Stomach (X-ray to be taken in erect position-A P erect):
                    In the supine position, the gas in the stomach will rise anteriorly and the fluid in the stomach
                        will pool posteriorly creating a circular out-line which can be confused with gastric pseudo-
                        tumor. This mass can be made to disappear by taking X-ray in upright or erect position.
                    In the erect film, the gas bubble will be seen with a fluid level beneath the Lt dome of the
                        diaphragm.
           Abnormalities:
           A gastric outlet obstruction
           Look at the X-ray and note:
                           Abnormal large size of the gastric out-line
                           Excessive quantities of semi-digested food in the stomach
                           Small quantity of gas in the small bowel
                           Two fluid levels, one on the Lt under the Lt dome of diaphragm and other on the Rt in the
                             Rt hypochondriac region re-presenting the duodenum. This double-bubble sign indicates
                             high gut obstruction probably in the duodenum.
                           The semi-digested food residue and a fluid level confirm obstruction.
                   A bezoar looks like semi-digested food e.g. phytobezoar-means retained vegetable matter and
                   trico-bezoar means hair ball in the stomach.
                    Q.What are the causes of gastric outlet obstruction?
                           Healed peptic ulcer
                           Antral gastric carcinoma
                           Lymphoma
                           Gastritis
                           Tuberculosis (lymph nodes-producing obstruction from out-side)
                           Impacted foreign body
                           Bezoar (hairball, vegetable matter)
                           Metastasis producing compression from out-side
                    Q.What are the clinical signs of pyloric obstruction?
                   The signs are:
                          Increased peristalsis from Lt to Rt
                          Abdominal distension
                          Vomiting
                          Succussion splash
Paralytic ileus:
                   Diffuse fluid and gaseous distension of small and large bowels and if the plate is taken in upright
                    position, air and fluid levels may be present at the same level (< 5 AFL/air fluid level –normal;
                    many-obstruction).
                The longer the duration of obstruction, the bigger the fluid levels.
                It is not necessary for obstruction to have fluid levels.
Pyloric stenosis-single bubble appearance. In pyloris obstruction there will be only **single air-fluid level.
Duodenal atresia-double bubble appearance.
Ileal atresia- multiple air-fluid levels.
**AIPGME 2002.
 Q.What are the causes of paralytic ileus?
The causes are:
                Post-operative e.g. following excessive handling of the gut
                Hypokalaemia
                Drugs e.g. L-dopa
                Peritonitis
                Infarction of the gut
                Trauma
                Reflex ileus from acute abdomen (renal colic, leaking aorta)
In inflammatory or ischaemic colitis the swollen bowel mucosa will be outlined by gas (‗thumb-printing‘)
Bowel obstruction:
Proximal to the lesion the gut is distended with gas and fluid, distally the gut is empty. The upright X-ray shows
step-ladder distribution.
 Q.What are the causes of small bowel obstruction?
Causes in different age groups are:
In adults                                 in children


                   .

  1.   Adhesions (post-operative)      1.   Hypertrophic pyloric stenosis
  2.   Bowel strangulation             2.   Intussuception
       (band, internal hernia)         3.   Duodenal atresia
                                       4.   Meconium ileus
  3. Tumor-lymphoma
  4. Gallstone ileus
  5. Crohn's disease
  6. Hernia
  7. Volvulus
Local vascular accidents like mesenteric artery occlusion may also cause distended loops, but here loops have thick
walls because of the gross edema and the gas trans-radiancies in adjacent loops may be separated by 1 cm wide
areas of opacity.
 Q.What are the causes of large gut (colonic) obstruction?
The causes are:
              Colon carcinoma
              Diverticulosis
              Volvulus
              Inflammatory bowel disease
              Appendicular abscess
                 Metastasis
                 Lymphoma
                 Pelvic masses

 Q.What are the causes of pseudo-intestinal obstruction?
The causes are:
               Myocardial infarction with pulmonary edema
               Pneumonia
               Myxedema
Sigmoid volvulus:
Sigmoid volvulus is grossly dilated sigmoid colon; occurs in elderly patients who have redundant loops of sigmoid
colon and a history of constipation. Acute volvulus present with severe pain, constipation and on P R examination
the rectum is empty.
The radiological signs are:
     1. A grossly dilated loop of sigmoid colon filling the whole abdomen extending from the pelvis to diaphragm
         is seen. Compression together of two medial walls is producing "coffee bean sign"
     2. There is lack of haustra due to enormous distension.
The following signs help to the diagnosis and indicate severity of distension.
               The apex of distension of colon lies above the 10th thoracic vertebra
               Convergence of lower margins of the distended loops on the Lt
               Liver over lap sign indicates presence of distended colon above the liver on the Rt.
               Lt flank overlap sign indicates distended loop in the Lt flank.
The diagnosis is confirmed by retrograde contrast study (barium enema) which will show a "twisted beak-like" or
"bird of prey" sign at the point of convergence.
NB: absence of free air under the diaphragm rules out perforation.

Bowel dilatation:
When an ileus or obstruction is present, it is possible to distinguish small from large bowel dilatation.
      The large bowel loops are peripheral, few in number, have diameter greater than 5 cm, contain faeces and
          have haustral margins. Vertical in flanks and across top of abdomen. Haustral folds do not cross
          lumen.>5.5 cm-suggests obstruction ;> 9 cm –suggests perforation risk.
      The small bowel loops are central, multiple, between 3 and 5 cm in diameter, and do not contain faeces.
          Vulvulae conniventes (transverse mucosal bands across lumen) are seen in the jejunal loops. Dilated when
          >3.5 cm proximally and >2.5 cm distally –suggests obstruction.
      The more distal the obstruction (large bowel obstruction), the more distended loops will be seen.
With gastric dilatation the stomach may be massively enlarged and distended with air. Mechanical obstruction –due
to a pyloric ulcer or carcinoma. Atonic dilatation is usually a post-operative complication, but may occur with
diabetic coma, trauma, pancreatitis or hypokalemia.
Air under the diaphragm
The area immediately under the diaphragm will usually be white due to presence of solid structures (liver and
spleen) except a darker round area under Lt dome of the diaphragm due to presence of air-bubble in the stomach.
On the RT side, normally diaphragm and liver shadows merge with each other. If there is free gas in the peritoneal
cavity it will ascend in standing position and lie between the diaphragm and the liver density.
Causes:
      Perforation of a viscus ( hollow)
      Following abdominal surgery
      Tubal insufflation test
      Peritoneal dialysis
      Infection of peritoneum by gas forming organisms.
          Air under the diaphragm is an important sign, since it indicates an intra-abdominal perforation ( e.g.
          intensity,stomach,colon etc). The air under Rt dome of diaphragm can be easily be recognized as a rim of
          blackness immediately under the diaphragm. However, it is difficult to differentiate air under Lt dome from
          the normal stomach bubble as both produce blackness under diaphragm. The differences between the two
          are:
         Thickness of diaphragm: the diaphragm appears as a thin white line between the white area below and the
         black lungs above. In the presence of air under Lt dome, this line becomes very thin (<5 mm) as it consists
         of diaphragm only. Normally due to the presence of air bubble in the stomach, this line is thicker (> 5 mm)
         as it consists of diaphragm and the walls of the stomach.
         Length of air bubble: measure the length of air bubble. If it is longer than the half of the length of the
         diaphragm, it is likely to be free air than stomach air bubble.
         Look at the other dome i.e. Rt hemi-diaphragm. If there is air bubble below the Rt and Lt hemi-diaphragm,
         it is likely to be free air in the abdomen.
Clinically how to detect the presence of gas under the diaphragm?
Percussion of the liver is done from above downwards along rt M CL. Loss of liver dullness clinches the above
    diagnosis in a patient with acute abdomen.
Abnormal gas:
     Pneumoperitoneum
     Both sides of bowel defined as thin lines
     Loss of liver density from gas anteriorly
     Bowel wall-thin streaks of gas suggest infarction or gas-producing bacteria.


Although obstruction and perforation, usually present separately and clinically differently, but it is hard to
differentiate between the two on radiological grounds. The clinical context is essential to differentiate between them.
However, remember:
                Paralytic ileus produces air and fluid levels are one level (i.e. same level); while in the intestinal
                  obstruction, air and fluid level follow a step-ladder pattern or there are rising fluid levels.
                Combined small and large bowel dilatation form the classical radiological signs of paralytic ileus
                  while a gas under diaphragm indicates perforation.
Extra-luminal gas:
                In the liver or biliary system-gas forming infection, after ERCP, after passing stone.
                In the genito-urinary system -entero-vesical fistula, emphysematous pyelonephritis (diagnostic of
                  DM with E.Coli infection)
                In the colonic wall-Pneumatosis coli/infective colitis
                In the sub-phrenic abscess.

Elevation of hemi-diaphragm:
The mid-point of Rt hemi-diaphragm should be between the 5th and 7th ribs anteriorly; while the Lt dome is lower
than Rt by about 3 cms. The diaphragm placed above the 5th rib is said to be elevated which may be unilateral or
bilateral.
Calcification in abdomen: calcification shows up well against the grey soft tissue densities.
Causes:
1. Faecoliths in diverticulitis.
2. Phleboliths are rounded opacities seen in the pelvis below the level of the ischial spines, whereas ureteric calculi
     lie above this level, in the line of the ureters.
3. Calcified lymph nodes (Tuberculosis-abdomen), calcified aorta.
4. Calculi: renal(about 90% of renal stones are calcified), ureteric calculi,biliary (only 10% of gall stones are
     calcified), pancreatic, splenic
5. Calcified fetus/dermoid cyst(may contain teeth)/fibroid.
6. Liver: amebic abscess, tuberculosis, calcified hydatid cyst (rim of calcification outlining the hydatid cyst ),
     Histoplasmosis, Brucellosis
7. Calcification of abdominal wall, cysticercosis
8. Pancreas: chronic pancreatitis-pancreatic calculi
9. Suprarenal: Addison‘s disease, neuroblastoma
10. Splenic: splenic cyst.
11. Costal cartilage calcification commonly seen in elderly patients, projected over the hypochondrial regions.
12. Egg-shell calcification in an aneurysm
Calcified lymph nodes:
     A. Mesenteric lymph nodes:
               These are numerous
               They lie in line with mesentery
               They tend to be quite mobile and show dramatic change in position from film to film
    B. Para-aortic lymph nodes:
               These are seen as spotty calcification along the para-vertebral gutter in the upper part of abdomen.
               In lateral view these calcified retro-peritoneal lymph nodes may over-lie the spine, require to be
                   differentiated from calculi or renal calcification.
Pancreatic calcification: plain X-ray abdomen shows fine punctate foci of calcification lying from Rt of the upper
lumbar spines passing upwards and obliquely to the Lt to the region of the splenic hilum.
Causes:
1. Chronic pancreatitis
2. Alcoholism
3. Pseudocyst
4. Hyperparathyroidism
5. Pancreatic tumors (occasionally)
6. Cystic fibrosis.
Calcification of adrenals:
1. Tuberculosis
2. Phaeochromocytoma
3. Carcinoma.

Calcification inside the liver:
1. Malignancy
2. Tuberculosis
3. A-V fistula
4. Hydatid cysts
5. Haemochromatosis.
Nephrocalcinosis:medullary sponge kidney or metabolic acidosis.

Calcification in spleen:
    1. Phleboliths
    2. Tuberculosis
    3. Arterial calcification
    4. Venous calcification
    5. Hydatid cysts
    6. Splenic Infarction
    7. Histoplasmosis.
The kidneys:
               These are usually visible as bean-shaped objects of soft tissue density high in the abdomen-
                   parallel to the psoas line.
               These are smooth in out-line extending from the upper border of T12 on the Lt side to the lower
                   border of L3 on the Rt side, with the Lt kidney lying slightly higher than the Rt by about 1.5 cm.
                   Both kidneys are inclined medially.
               Length of kidney is equal to 2-3.5 vertebral bodies (T12 to L2).
               Normally, they move down with inspiration and dropping several cms in the erect position.
               Usually, however, only parts of their out-lines are visible and you have to make or deduce its
                   outlines.
Preparation:
         For X-ray of uro-genital system, the patient is put on low residue diet for 2-3 days. On the night previous to
         X-ray patient is given purgative and a deflatulant e.g. methyl polysiloxane or activated charcoal. Patient is
         kept on over night fasting.
Abnormalities of kidneys:
Big kidneys:
Causes of enlarged kidneys:
         Bilateral                                    Unilateral
     Acute glomerulonephritis                Acute obstruction
     Diabetic glomerulosclerosis             Renal vein thrombosis
     Adult polycystic kidney disease         Acute Pyelonephritis
     ATN                                     Radiation nephritis
     Acute cortical necrosis                 Duplex system
     Bilateral acute Pyelonephritis          Compensatory hypertrophy from contralateral
     Leukaemic infiltration                   nephrectomy or dysfunction
     Amyloid kidneys                         Renal mass
     Secondary renal disease
     Excessive beer drinking

                  The importance of detecting large kidneys is that there may be potential for recovery
                   when this finding is associated with renal failure. Biopsy is required for confirmation of
                   the diagnosis. USG is done to exclude renal obstruction and to assess renal parenchyma
                   before biopsy.
Causes of small kidneys:
               Chronic glomerulonephritis
               Chronic renal ischemia (renal artery atherosclerosis)
               Chronic Pyelonephritis
               Reflux nephropathy
               Infarctions of kidneys
               Senile atrophy
               Bilateral congenital hypoplasia
               Smaller kidneys re-present end-stage renal disease (e.g. irreversible state), making biopsy
                   potentially hazardous; hence small kidney constitute contra-indication for biopsy.
               Look at the edges of the kidneys whether smooth or lobulated. Irregular kidney out-lines
                   indicates scarring of kidneys due to pyelo-nephritis or glomerulonephritis.
Abnormally placed kidney
Horse-shoe kidney tends to lie lower than nth normal. The pathognomic radiological sign is to see the renal
cortices of the lower kidneys on plain X-ray crossing the margins of the psoas muscles medially to connect
with the other side with isthmus. The drainage system is malrotated forwards, best seen on IVP.
Renal stone/calculi:
               The majority of stone (90 % approximately) that form in kidneys are radio-opaque due to
                   their calcium content.
               They are seen on plain X-ray as radio-opaque opacity /opacities ranging form tiny
                   (nephrocalcinosis) to one big calculus blocking the collecting system (stag-horn).
               A renal stone maintains a constant position in relation to the kidney when erect or oblique
                   films or control tomography films are taken.
               The renal stone has to be differentiated from calcified costal cartilage or a gallstone (both
                   of which are anteriorly placed structures).
               Always remember that gallstones are anterior to the spine while the shadow of renal stone
                   is superimposed on vertebral column in lateral film.
               Only calculi of pure uric acid, xanthine, dihydroxyadenine, indinavir, triamterine, or
                   matrix can be considered truly radiolucent. Allopurinol treatment may form xanthine
                   stones that are radiolucent. *Cysteine calculi are slightly radio dense because of their
                   sulfur content.
              *AIIMS May 2003.
The test of choice at most centers for diagnosing an acute stone is **non-contrast CT scan of the abdomen .
Spiral CT (non contrast) has become the study of choice in emergent situation as the entire urinary tract can
be scanned rapidly and without contrast injection.
**AIPGME 2005.
 Q.What are the causes of renal calculi?
The causes are:
               Hyperparathyroidism
                        Infection
                        Urinary tract obstruction
                        Dehydration
                        Hyper-vitaminosis D
                        Medullary sponge kidney
                        Uric acid stones
                        Renal tubular acidosis
                        Milk-alkali syndrome
                        Renal tuberculosis
         Ascites: with accumulation of peritoneal fluid within the peritoneal cavity ,the film looks generally grey
         and lacks detail. On the supine film the bowel loops float towards the middle of the abdomen.
Psoas lines-
     Outlined by retro-peritoneal fat
     Absent in 20 % of individuals
     Obliterated in retro-peritoneal inflammation, hemorrhage or peritonitis.
     Unilateral absence–suggests retro-peritoneal mass or hematoma.
         Meteorism:
         Localized peritoneal inflammation can cause a localized ileus. It can be seen as a 'sentinel loop' of intra-
         luminal gas and can provide a clue to the site of pathology-such as cholecystitis, pancreatitis, appendicits
         and diverticulitis. However, at times even localized infection can produce generalized ileus.
    Abnormalities of supine X-ray film:
    Vertebral column and pelvis
    The causes of increased bone densities:
                   Flurosis
                   Chronic renal failure
                   Paget's disease of the bone
                   Osteosclerotic secondaries from prostrate
                   Milk-alkali syndrome

    Spine:
                      Bi-concave vertebrae (cod-fish)-biconcave because of weakening of subchondral plates and
                       expansion of inter-vertebral discs.
                  Bamboo-spine (due to calcification of interspinous ligaments)
                  Degenerative changes(osteoarthritis)
                  Metastasis (Osteolytic/osteoblastic)
                  Collapse
                  Looser zones (osteomalacia-'rugger-jersey' spine)
                  Paget's disease
    *Calcification of intervertebral disc is seen in Alkaptonuria. *AIPGME 2000.

                                                   X-RAY OF BONES
    X-ray of the born must be viewed as follows:
        1. Soft tissues: swelling or muscle wasting
        2. Bony surfaces
                  a) Periosteal new bone formation: this is seen as a linear density, parallel to the cortex. It is seen
                      in healing scurvy, hypervitaminosis A and D and infantile cortical hyperostosis
                  b) Juxta articular erosions
                  c) Diffuse cortical resorption: this is the typical loss of diaphysial cortex seen in
                      hyperparathyroidism
        3. Shape and size of the bone: fractures, dislocation and congenital anomalies
        4. Internal structure of the bone:minerilastion,localized destruction etc.
        Osteomyelitis
        A.        Acute osteomyelitis
                      i)       Slight focal de-calcification
                    ii)      Soft-tissue swelling
                    iii)     Faint periosteal new bone formation

      B.       Chronic osteomyelitis
                   i)       Bone destruction with sclerotic reaction
                   ii)      Sequestrum: dense, devascularized bony fragments lying within the pus and
                                 granulation
                   iii)     Involucrum: peripheral shell of new supporting bone laid down by the periosteum
 Tuberculosis of bone:
      1. Diffuse loss of bone density
      2. Slight diminution of joint space
      3. Tuberculae become indistinct and cortex is thinned out
      4. Periosteal new bone formation is absent and there is no massive sequestrum formation.
Aneurysmal bone cyst
  These are seen in several disorders. It usually indicates an autonomous parathyroid gland (primary or tertiary
      hyperparathyroidism).




  Osteomalacia: a disorder characterized by failure of the bone matrix to mineralize normally and promptly.
  Features:
      1. Generalized de-calcification of the bone
      2. Vertebral bodies are biconcave (cod-fish vertebrae)
      3. Looser‘s zones or pseudo-fracture may be present. They are 1-3 mm wide transradiant zones extending
           1 cm into the bone at RT angle to the cortex and look like incomplete fracture. They occur in ischio-
           pubic rami, axillary borders of the scapula, ribs, femur, humerus and lower third of tibia and fibula
      4. Deformities of the limb and pelvis (tri-radiate pelvis) may be present
      5. If chronic renal failure is the cause of osteomalacia there may be subperiosteal bony erosions in middle
           phalanges and sclerosis of the vertebral end plate (rugger jersey spine).
  Osteoporosis:
      1. Demineralization of bone with thin cortices and delicate medullary trabecullae.
      Causes:
               1. Endocrine: Cushing‘s syndrome, thyrotoxicosis, hypogonadism
               2. Metabolic: mucoplysaccharoidosis, Homocystinuria
               3. Deficiency: famine, scurvy, hypocalcaemia
               4. Blood diseases: leukaemia, myeloma, lymphosarcoma, secondaries, histiocytosis
               5. Drugs: heparin, steroids
               6. Idiopathic
               7. Osteomalcia.
      Osteosclerosis: ( bones turn absolutely whitish)
      Causes:
               1. Flurosis
               2. Secondaries from malignancy of prostrate( commonly),breast,bronchus ,gut and lymphoma
                                  (Hodgkin-ivory vertebra )
               3. Marble bone disease ( osteopetrosis)
               4. Osteopoikilosis
      Bony metastasis:
               1. Erosion without bone reaction or periosteal new bone formation
               2. In the vertebrae it may cause vertebral collapse with intact disc space
               3. Sclerosing bony metastases have to be distinguished from Paget‘s disease.
                             Sclerosing bony metastases Paget‘s disease
      Width of bone          Normal                         Increased
      Trabeculase            Normal                         Wider and spaced at greater intervals
      Softening of bones absent                             present, causing deformities
             –    **Most common cause of single vertebral body collapse in child with maintained disc space
                  is
              – Eosinopphilic granuloma: most common cause.
              – Trauma
              – Tumor (primary tumors like ABC and GCT as well as secondary)
              – Tumor like condition as Hydatid cyst
              – Hemi-vertebrae
              – Pott‘s spine
    In pott‘s spine decreased disc space is late manifestation.
    ** AIPGME 2003.
Flurosis:
              1. Osteosclerosis of the spine and pelvis
              2. Ground glass appearance of the bones
              3. Calcification of the interosseous membrane of the forearm, intervertebral ligaments,
                           sacrospinous and sacrotuberous ligaments.
Cretinism:
              1. Delayed appearance of the epiphysis which may be hypoplastic or stippled
              2. X-ray spine: intervertebral disc and the vertebral bodies are of same size
              3. Mandible is ill-formed
                                             Plain X-ray of spine:
In majority of cases X-ray of spine may be adequate to reach reasonable diagnosis in suspected lesion of the
spinal cord. The varied views taken include:
1. A-P view
2. Lateral view
3. Oblique view
4. Bending views
5. Tomogram in selected cases.



Following conditions can be diagnosed by X-rays of the spine:
        I.       Congenital and developmental abnormalities
                    a) Spina bifida, hemi-vertebrae and vertebral fusion
                    b) Kyphosis and scoliosis
        II.      Inflammatory and or infective
            a) Tuberculosis of spine
                      i)    Erosion of the affected vertebrae
                      ii)   Collapse of vertebrae
                      iii)  Anterior wedging of vertebrae and angular kyphosis
                      iv)   Two affected vertebrae fuse into single wedge shaped bone
                      v)    Decrease in the inter vertebral disc spaces
                      vi)   Para-vertebral abscess, Para vertebral soft tissue shadows well seen on frontal
                            view.
            b) Ankylosing spondylitis
            Initially changes are in both sacro-iliac joints-they are as follows:
                      i)       Slight widening of sacro-iliac joint due to bone destruction is seen initially
                               (Demineralization along the joint surface with bone).
                      ii)      Decrease in width due to cartilage destruction is seen in later on
                      iii)     Periarticualr erosions and osteoporosis are noticed.
                      iv)      Sclerosis may be noticed
                      v)       Squaring of vertebral body is very characteristic
                      vi)      Bamboo spine: Fusion of anterior and lateral ligament gives an appearance of
                               bamboo spine or railroad tract

                      vii)     Large syndesmophytes
                      viii)    Ossification of spinal ligament produces ‗tram-track‘ sign.
    III.    Degenerative
        a) Degeneration of disc spaces
        b) Osteophytes small to large size
        c) Osteoporosis
    IV.     Traumatic
        a) Vertebral collapse
        b) Fracture of various parts of vertebrae
    V.      Neoplastic
    Changes in rickets:
    Best demonstrated in rapidly growing bones like wrist and knee joints
         Epiphysis: the epiphysis lacks a bony cortical margin and appears indistinct. There may be
            epiphyseal separation which is more common in renal rickets
         Metaphysis: Fraying/saucer deformity of the metaphysis (indistinct or blurred metaphyseal
            margin). The metaphysis is splayed out and distally concave (cupping). The zone of
            calcification instead of forming a well-defined white line, is irregular and of low density. Its
            end appears arranged in longitudinal rows (fraying or streaking). Cortical spurs from the
            metaphysis may growth towards displaced epiphysis resulting in deformity. Cortical spurs
            from metaphysis growing towards displaced epiphysis (produces deformity)
         Diaphysis: there is generalized decalcification(osteoporosis) of the bones resulting in
            increased radiolucency between the diaphysis and epiphysis-because of non-calcification of
            rachitic metaphysis.
         Bowing of the legs
         Looser‘s zone may be seen
         Green-stick fractures with bending and deformities may be occur.
        Healing rickets: return of zone of provisional calcification, sclerosis, metaphyseal lucency.

Differential diagnosis of fraying of metaphysis:
    1. Rickets
    2. Hypophosphatasia
    3. Copper deficiency
Differential diagnosis of cupping of metaphysis:
    1. Rickets
    2. Hypophosphatasia
    3. Bone Dysplasia-achondroplasia,metaphysical chondrodysplasia
    4. Scurvy
    5. Metatropic and diastropic dwarfism

Radiological features of X-ray skull in rickets:
      Delayed closure of anterior fontanelle
      Frontal and parietal bossing
      Quadrate skull
      Widening of sutures
      Late appearance of temporary teeth.
Radiological signs of healing rickets:
      The radiological density is increased and roughness is diminished.
      Epiphyseal cartilage becomes horizontal
      Horizontal ‗Harrison‘s lines‘ are seen in the lower end of diaphysis (initially near the epiphysis)
     Changes in scurvy:
In scurvy there is adequate calcium but lack of osteoid tissue. Vitamin C deficiency creates a condition
where there is diminished production of and maintenance of inter cellular ground substance .
          Epiphysis: Halo‘s sign/ring sign of Wimberger. It is small epiphysis with penciling; the
              epiphysis has a dense margin with radiolucent centre
          Metaphysis; White line of Frankel the white line of.metaphysis is wider than normal. It is
              dense and prominent zone of calcification. White line of Frankel reflects impaired growth and
             continued deposition of calcium phosphate. Scurvy line (black line) reflects failure of primary
             ossification.
          Diaphysis: Generalized decrease in bone density due to uniform demineralization of the bone.
          Pencil cortex (thinning of the cortex). The cortex is thinned out giving the bone a uniformed
             ground glass appearance of the shafts with penciled outline. Angular lateral bony spurs are
             present. These are defects in the cortex at the junction of diaphysis and metaphysis (angle
             sign)
          Zone of Trummerfield. This is a radiolucent zone proximal to white line of Franknel. The
             ‗scurvy zone‘ lies between the bone and the white line.
          Pelkan‘s spurs of marginal metaphyseal Infarction protruding laterally-marginal fractures at
             the junction of metaphysis and diaphysis (Pelkan‘s sign)
          Sub periosteal hemorrhage lifting the periosteum. It may calcify sometimes.
          Osteoporosis in adults.
         Healed scurvy: metaphyseal lucency; uneven periosteum.
         Differential diagnosis of scurvy:
             1. Traumatized child syndrome ( absence of demineralization of bone)
             2. heavy metal poisoning e.g. lead poisoning ( no osteopenia and absence of zone of
                  translucency)
    X-rays of tuberculosis of spine:
    In order of decreasing frequency tuberculosis involves lower thoracic, lumbar and cervical spine.
    There are 3 main types:
         1. Anterior type: disc erosions though seen late, are uncommon features. Abscess tracts along
             the anterior longitudinal ligament
         2. Central type: there is a central abscess, which grows outwards. Usually inter vertebral disc
             remains normal.
         3. Marginal type: characteristics are:
                  a) Adjacent vertebral involvement
                  b) Articular sclerosis
                  c) Reduction of disc space
                  d) Para-vertebral abscess seen in frontal view
                  e) Collapse with anterior wedging of the vertebrae with consequent gibbus formation or
                       development of kyphosis.
    Causes of erosion/destruction/absence of pedicle of vertebra:
         a) Metastasis
         b) Tuberculosis
         c) Multiple myeloma
         d) Bony tumors
         e) Congenital absence

Causes of enlarged vertebral body:
   a) Acromegaly
   b) Gigantism
   c) Benign bone tumor
   d) Paget‘s disease.
Causes of block vertebrae:
   a) Congenital
   b) Klippel -feil syndrome
   c) Rheumatoid arthritis
   d) Ankylosing spondylitis
   e) Tuberculosis
   f) Post-operative
   g) Post-traumatic
Causes of rib notching on the inferior surface
   a) Coarctation of aorta
   b) Aortic thrombosis
    c)   Subclavian obstruction
Causes of rib notching on superior surface:
    a) Neurofibromatosis
    b) Rheumatoid arthritis
    c) SLE
    d) Hyperparathyroidism
    e) Osteogenesis imperfecta
Resorption of tuft of metacarpals:
    a) Hyperparathyroidism
    b) Raynaud‘s disease
    c) Scleroderma
    d) Psoriatic arthritis
    e) Neuropathic disease
X-RAY SKULL:
The X-ray of the skull must be viewed as follows:
    I. Calvarium and base
             A. Normal radiolucencies e.g. sutures and vascular markings
             B. Fractures: linear, depressed or basilar
    II. Sella turcica
             A. Shape and size: it is ballooned in pituitary tumors
             B. Normal size- antero-posterior diameter-11-16 mm and depth 8-12 mm.
             C. Mineralization: it is demineralixed in pituitary tumors
             D. Erosion of posterior clinoids-raised ICT
             E. Erosion of lamina dura of dorsum sellae-tumor or aneurysm.

     III. Calcification
     Normal size of pituitary fossa:
     a) Height-5-11 mm
     b) Length 9-16 mm
     c) Breadth 9-19 mm
     Causes of erosion:
          a) Raised intra-cranial pressure
          b) Pituitary adenoma
          c) Meningioma
          d) Metastasis
Intra-cranial calcification :
      Pineal body,gliomas,meningiomas,cranio-pharyngiomas
      Tram-line calcification-Sturge-Weber syndrome
      Ring calcification- cerebral aneurysm, tuberculosis, and toxoplasmosis.

Causes of unifocal intra-cranial calcification:
   a) Meningioma
   b) Glioma
   c) Chordoma
   d) Abscess
   e) Metastasis

Causes of multiple calcifications:
    a) Toxoplasmosis
    b) Cysticercossis
    c) Hydatid cysts
    d) Tuberculoma
    e) Multiple metastasis
Calcification of basal ganglia:
    a) Physiological with ageing
    b)    Infection: Congenital Toxoplasmosis, congenital rubella,CMV,cysticercosis
    c)    Chemo-therapy/radiation
    d)    Toxic: birth anoxia, Co poisoning, lead poisoning
    e)    Metabolic:Fahr‘s disease, mitochondrial defects ,Cockayne‘s syndrome(premature ageing)
    f)    Tuberous sclerosis
    g)    Vascular mal-formation
    h)    Endocrine :
               – Hypoparathyriodism
               – Pseudhypooparathyroidism
               – Hyperparathyroidism
               – Hypothyroidism
Causes of punched out areas in skull:
     a) Multiple myeloma
     b) Hyperparathyroidism
     c) Metastasis
     d) Osteomyelitis
     e) Histiocytosis ‗X‘
Signs of raised intra-cranial pressure in children:
     a) Suture separation
     b) Erosion of dorsum sellae/posterior clinoids
     c) sella turcica is shallow
     d) Pineal displacement
     e) Increased convlutional markings
Signs of raised intra-cranial pressure in adults:
     a) Erosion of dorsum sellae is the earliest sign
     b) Slight porosis of anterior cortex of dorsum and the cortex of sellar floor. Erosion starts from above
          downwards
     c) silver beaten appearance
     d) Displacement of pineal body
Intra-sellar space occupying lesions
     a) Widening and deepening of the sella.
     b) Sellar ballooning is seen in chromophobe and eosinophil adenomas.
Physiological calcification in the skull
     a) Habenualr comissure-anterior to pineal body and is ‗C‘ shaped
     b) Choroid plexus of lateral ventricles
          Site: parietal region 1º above and behind the pineal body
     c) Interclinoid ligaments may calcify e.g. petroclinoid ligament.
     d) lateral edges of diaphragm sellae.
     e) Basal ganglia
     f) Dentate nucleus
     g) Falx cerebri
     h) Pineal body
Abnormal calcification
     a) Infections: tuberculosis, hydatid cyst, cysticercosis and toxoplasmosis
     b) Vascular: subdural heamtoma, old Infarct,arterioscleosis,A V malformations
     c) Tumors: meningioma, drmoid, craniopharyngioma etc.
     d) Miscellaneous: sturge Weber syndrome, tuberous sclerois, hypoparathyroidism,
Pineal calcification:
     a) Varies from 3-5 mm in size
     b) Appearance: amorphous nodular or ring like
     c) Common in old age
     d) Displacement in intra cranial tumors



Vascular calcification in skull:
    a) Aneurysm
    b) Angioma
    c) Atheroma
    d) Subdural haematoma
    e) Intracranial Hamartoma
Radiological evidence to localize the cerebral tumors
    a) Intra-cranial calcification
    b) Abnormal vascular markings
    c) Displacement of pineal body
    d) Skull erosion
    e) Hyperostosis
Following Intra-cranial tumors calcify:
    a) Meningioma-in 10 % cases.
    b) Glioma-oligodendroglioma shows calcification in 50 % cases, posterior fossa glioma in over 20 %
        cases.
    c) Pituitary adenoma
    d) Craniopharyngioma
    e) Ependymoma-unusual if seen dense calcification.
    f) Chordoma
    g) Hamartoma
    h) Pinealoma
    i) Dermoid, epidermoid and teratoma.
    j) Lipoma (bracket calcification in lipoma of corpus callosum).
         Linear skull fracture (likelihood of intra-cranial hematoma-more frequent with
             unconscious patient than with conscious alert patient).
         Depressed skull fracture (needs elevation)
         Status of cranio-cervical junction
         Shift of calcified pineal body> 3 mm from mid-line
         Increase in vault density-Paget's disease.flurosis,diffuse increase in thickness-
             acromegaly, Thalassaemia.
         Localized increase in thickness- Paget's
             disease,meningioma,osteomyelitis,leukaemia,histiocytosis
         Lucent areas- Multiple myeloma , Paget's (osteoporosis circumscripta),malignancy,
             hyperparathyroidism

Air sinuses:
          Thickened mucosa –chronic sinusitis
          Enlarged sinuses-acromegaly
          Fluid level-after trauma (maxillary sinus-infra-orbital fracture, sphenoid sinus-fracture base of
              the skull).
Multiple myeloma:
Lesions are commonly seen in skull, ribs, vertebrae and pelvis. Earliest sign-osteopenia.
Later on one finds following changes:
     a) Osteolysis without surrounding sclerosis ―punched out‖ lesions is classically seen in skull. Single
         or multiple, small, rounded, punched out areas of radiolucency best seen in skull, sternum, ribs,
         vertebrae and pelvis. The margins of the radiolucent areas are sharply defined.
     b) A drumstick expansion of the anterior ends of some of the ribs may be present over the radiolucent
         deposit.
     c) Lesions in the jaws are pathognomic, as secondaries in jaws are rare
     d) It also affects vertebral bodies producing collapse. pathological fractures and vertebral collapse
         with spinal deformities may be present.This change is also noted in secondaries. However,
         myeloma affects body where as secondaries affects pedicles
     e) In 4% of cases lesions are osteosclerotic rather than osteolytic.
Metastatic bone disease
         Original tumor                       sex predominance
     a) Prostate                             males
     b) Breast                               females
     c) Kidneys                              both
     d) Lungs                                both
Majority of bone metastasis are osteolytic. Osteoblastic metastases are rare. They originate from the
following sites.
     a) Prostate
     b) Stomach
     c) Ovaries
     d) Breast after hormone therapy
     e) Carcinoids

      Driven-snow appearance-Pindborg tumor**
      Onion peel appearance-Ewing sarcoma
      Sunburst appearance-osteosarcoma
Pindborg tumor-is also known as calcifying epithelial odontogenic tumor. It resembles an ameloblastoma
in that it is locally invasive and commonly identified as uni-or multi-locular swelling in the molar ramus
region
Radiological features:
      The central location of the tumor in the jaw often with the expansion of the cortex and the areas of
           spotty calcification in the form of Liesegang rings.
      Scattered flecks of calcification throughout the radiolucency give rise to the term ―driven snow-
           appearance‖.
      In some instances the lesion is totally radiolucent and is associated with an impacted tooth, thus
           leading to mistaken clinical diagnosis-Dentigerous cyst.

Osteosarcoma- A plain radiograph reveals a destructive lesion with a moth-eaten appearance, a
    spiculated periosteal reaction (sunburst appearance), and a cuff of periosteal new bone formation at the
    margin of the soft tissue mass (Codman's triangle.
Ewing sarcoma- The plain radiograph may show a characteristic "onion peel" periosteal reaction with a
    generous soft tissue mass, which is better demonstrated by CT or MRI.
** AIPGME 2002


Single or multiple osteolytic lesions in skull:
             1. Multiple myeloma (classical ‗round‘/‘punched out‘ areas without surrounding
                  osteosclerosis)
             2. Metastatic carcinoma from bronchus, thyroid, breast or kidney (osteoblastic reaction i.e.
                  osteosclerosis seen at the margin of osteolytic lesions)
             3. hypoparathyroidism ( spotty de-calcification)
             4. Paget‘s disease ( Moth-eaten appearance)
             5. histiocytosis-X disease ( big mappy area of radiolucency)
             6. Leukaemic or lymphomatosis deposits ( small to large)
             7. burr-hole(iatrogenic)
             8. sarcoidosis( small to large)
             9. Miscellaneous (big diploic foramen, congenital venous lakes, haemangioma of the vault,
                  fibrous dysplasia, arachnoid granulations).
Radiological changes in rheumatoid arthritis:
These changes take 2-3 months to develop and in some cases may be delayed for 3 years. They are not seen
in asymptomatic patient.
Sites:
Bones of feet and hands, metatarsophalangeal and metacarpophalangeal joints are commonly involved.
In hand common joints affected in order of frequency are carpals, wrist and interphalangeal joint
Following changes are noticed:
     a) Erosions: usually they occur at joint margin, later on spread to the joint surface
    b) Osteopoerosis:it is initially juxta-articualr and later on generalized
    c) Soft tissue swelling: it is always symmetrical and even clinically evident
    d) Changes in the joint space.
            i)       Initial widening due to effusion
            ii)      Later on reduction due to destruction of the cartilage
            iii)     Subluxation
            iv)      Bony ankylosis

    e) Secondary osteoarthitis
Rheumatoid arthritis:
Early phase             Late phase
Slight demineralization Massive destruction
Joint effusion          Subluxation
Pericapsular swelling   Fibrous ankylosis
Marginal erosion
Osteoarthritis:
    1. Loss of joint space
    2. Bony marginal lipping may be present
    3. Sclerosis of subarticular bone

Gout:
   1.    Capsular swelling leading to gross destruction of the joint usually affecting the distal
         interphalangeal joint
    2. Small well-defined, punched out areas without a white rim of sclerotic bone near the articular ends
         of the bone. These are caused by urate deposits
    3. Tophi within the soft tissues.
Septic arthritis:
    1.      Joint effusion with joint swelling
    2.      Rapid loss of cartilage and subchondral bone
Psoriatic arthritis:
    1. Affects the distal interphalangeal joints
    2. Joint space will be narrow
    3. Marginal splaying out of the base of the terminal phalanges with punched out erosions (sharpened
         pencil appearance) may occur.

Hyperparathyroidism:
Sub-periosteal resorpton of the bone seen in hands and skull.
    1. In the hands de-calcification of the cortical bone is seen in the middle and distal phalanges.
    2. In the skull there is fine granularity with demineralization and radiolucent cystic areas.
Acromegaly:
             a) The long bones are wide, thick, with coarse bony trabecular pattern & tufting of the
                  terminal phalanges
             b) The vault of the skull is increased in thickness, paranasal sinuses are large, mandible
                  shows prognathism and malocclusion of teeth and sella turcica is widened, deep and
                  ballooned.
Hydrocephalus:
    a) Signs of raised intra cranial tension
    b) Skull may be enlarged in size. Sutures am be separated
    c) Pituitary fossa may be eroded.

Thalassaemia:
            1.    Skull: the diploic space is widened with lack of definition of the outer table. In severe
                  cases, outer table cannot be defined and the bony trabecuale tend to be arranged at RT
                  angles to the inner table giving hair on end appearance (sun ray appearance).
             2.   Long bones: the medullary cavity is wider with coarse trabecuale and thinned out cortex.
                  This is best seen in phalanges, which may lose its biconcave shape and become
                  rectangular or biconvex.
                  Usually skeletal changes are absent in Thalassaemia minor.
                  What are the other possible radiological changes in skull?
                          Obliteration of paranasal sinuses
                          Slight prominence of frontal and maxillary bones
                          Dental malposition.

Barium study:
                 Barium contrast study is useful to delineate the interior of G.I. tract when it is filled with
                  radio-opaque substance e.g. barium.
                 Barium meal is done by asking the patient to swallow a suspension of barium. The
                  radiologist observes the movements of the barium on fluorescent screen or on the TV
                  monitor of an image intensifier. Films are taken at different intervals on the site of
                  pathology detected or suspected. These films provide a permanent record of any
                  abnormality.
                 A plain X-ray of the abdomen should always be taken before barium study in patients
                  with suspected perforation or obstruction.
                 Normal barium meal study will reveal normal plica semilunaris.
                 Barium swallow is done for any pathology in the esophagus e.g. varices, stricture, carida
                  achalasia, hiatus hernia and malignancy.
                 Small bowel follow-through: The barium study is done for certain gastric disorders by
                  taking films of the abdomen at intervals after a barium meal. Abnormalities in the transit
                  time to the colon and in small bowel pattern e.g. dilatation, narrowing, flocculation of
                  barium are seen in malabsorption.
                 Areas of narrowing with proximal dilatation, fistula and mucosal abnormalities are seen
                  in Crohn's disease. Small bowel diverticula or neoplasm may also be seen.
                 Narrowing of ileo-caecal junction with caecum being pulled up indicates ileio-caecal
                  tuberculosis.
Barium enema:
                   For this study barium suspension is introduced via a tube into the rectum as an enema and
                    manipulated around the rest of the colon to fill it. The radiologist screens the barium
                    filled colon and films are taken for permanent record. The barium is then evacuated and
                    further films are taken.
                By this study obstruction, polyps, pseudopolyposis of the clon, tumors, diverticular
                    disease, fistula and other abnormalities of rectum can be recognized.
                Following evacuation, air is introduced into the colon. This facilitates visualization of the
                    mucosa by distending the colon; hence is especially useful for detecting small lesions e.g.
                    polyps and small tumors, ulcers, fistula and diverticula which may be missed on barium
                    study. This type of study in which barium and air are used for contrast is called "double
                    contrast study ".
**Barium meal study of carcinoma of head of pancreas present with:
           – Widened duodenal C-loops
           – Mucosal irregularity (speculation,nodularity,blunted, stricture)
           – Double contour to the medial border of the loop (indentation by mass)
           – Frostburg‘s reversed 3 sign
           – Indentation of duodenal cap (enlarged gall bladder due to obstruction of the duct).
** AIPGME 2004.
Barium study of chronic pancreatitis: double contour & strictures
CT scan abdomen : dilatation and beading of main pancreatic duct and its branches and calculi
(calcification) is pathognomic of chronic pancreatitis. [Seen as beaded /string of pearls/chain of lakes and
rat tail appearance in ERCP].
Barium study of acute pancreatitis:
         –    Widening or narrowing of duodenal C-loop
         –    Frostburg‘s reversed 3 sign
         –    Thickening and effacement of mucosal fold
CT findings of acute pancreatitis:
         –   Pancreatic edema and enlargement
         –   Poor contrast enhancement due to necrosis
         –   Ill-defined pancreatic out-line due to blurring of fat planes and fluid collection.
Barium    study of duodenal ileus: widened duodenal loop with regular mucosal pattern

Cholangiography: it can be performed in many ways:
  1. Oral cholecystography:
        Give oral contrast 12-24 hours prior to the study.
        Failure to visualize the gall bladder
             Acute cholecystitis
             Peritonitis
             Pancreatitis
             Gall stone disease
        This test is not useful when serum bilirubin is elevated.
  2. Intra-venous cholecystography: it is useful in suspected choledocholithiasis and is
      seldom indicated.
  3. Per-cutaneous trans-hepatic cholangiography (P.T.C.): this investigation is useful to
      demonstrate dilated ducts in obstructive jaundice. Bleeding tendency, cholangitis,
      ascites, and allergy are contraindications for this test.
  4. Endoscopic retrograde Cholangio-pancreaticography (ERCP):
             A catheter is passed with the help of endoscope through the ampulla into
                the common bile duct (CBD) and X-rays are taken after injecting the
                contrast medium.
             It demonstrates the lesion in the biliary tree and the pancreatic ducts.
             Antibiotic prophylaxis with ciprofloxacin 750 mg PO two hours prior to
                the procedure is advisable.
             Therapeutic measures:
                a. Sphincterectomy with CBD stone removal
                b. Dilatation of benign biliary strictures
                c. Palliative stents for bile duct obstruction in malignancy
             Complications:
                a. Ascending cholangitis
                b. Pancreatitis
                c. Perforation
                d. Hemorrhage
Intra –venous pyelography (IVU or IVP):
It is excretion urography in which a radio-opaque iodine compound is injected intra-venously and its
excretion through the kidney is followed at certain intervals. It is important investigation for assessing renal
functions in renal failure and for structural abnormalities such as calculi or obstruction. When renal
function is poor, the kidneys are more easily seen if tomographs and large dose of the contrast are used.
This technique provides excellent delineation of the collecting system and ureters and is superior to USG
for examining renal papillae, stones and urolithial malignancy.
A good preparation is essential for obtaining detailed clinical information after IVP
Pre-cautions:
                 Before injecting the dye, iodine sensitivity should be tested.
                 Resuscitative equipments (drugs, O2) should be made available on the side table.
                 The patient should not take water after the previous night. However, patients with
                  diabetes mellitus, myeloma, old age, compromised renal function should be well hydrated
                  to avoid nephrotoxicity due to the contrast medium.
                 If patient is taking diuretics, they should be omitted for 3 days prior to the procedure.

Procedure:
Abdominal binder is applied tightly enough to compress the ureters. 20 -40 ml of contrast medium along
with an antihistamine is injected slowly IV. Abdominal radiolographs are taken at 1,3,5,10,15 and 30
minutes intervals; the binder is then released and at 45 minutes 'prone' and 'standing' films are taken.
Bladder is visualized in the film taken when the patient gets a sensation of fullness and desires to empty it.
A radiogram (micturating cystogram) is taken during and immediately after evacuation of the bladder.
Results and interpretation:
Normal IVP visualizes both the kidneys and ureters very well.

    1.   Nephrogram:
         a) It means appearance of the contrast in the kidneys. The image of the kidneys as a result of
             contrast diffusing through them in early stage of contrast excretion. Nephrogram is the first
             phase of IVU. The 2nd phase is pyelogram.
         b) The Nephrogram phase is because of the filtration of the contrast in the nephrons i.e. in the
             proximal tubules and the distal tubules. In the Nephrogram phase the cortex of the kidney is
             visualized.
         c) Excretion of the contrast in the pelvicalyceal system gives rise to the pyelogram phase.
         d) Normally; a good nephrogram should be seen in one minute film.
         e) Usually in a normal functioning kidney the Nephrogram phase appears within a minute time
             of injection of the contrast intravenously, and passes off quickly within next 2-3 minutes.
         f) But when it persists for longer duration (i.e. for hours), it is known as ―persistent‘
             Nephrogram. If it is of increased radio-density, then it known as ‗dense‘.
         g) Nephrogram is delayed and contrast is poor if renal function is impaired.
              Absent- non-functioning kidney (infarction, severe glomerulonephritis)
              In renal artery stenosis, late appearance of the nephrogram and hyper-concentration of the
                  contrast is seen.
              Nephrogram will appear late, persist for longer period and will progressively show hyper-
                  concentration of contrast in acute unilateral urinary tract obstruction. In acute ureteral
                  obstruction, due to increased back-pressure, there is delayed filtration of the contrast in
                  the nephrons and even a more delayed excretion in the pelvicalyceal system. This leads to
                  concentration of the contrast in the nephrons and thus a dense persistent Nephrogram.
              Dehydration: a decreased renal blood flow due to dehydration, will lead to more and
                  more re-absorption of water and Na+ (along with the contrast, as contrast is mainly a salt
                  of sodium i.e. sodium ditriazoate). This contrast is again filtered into the nephrons and
                  thus gets concentrated here in the tubules leading to dense persistent Nephrogram.
              Severe Hydronephrosis: severe hydronephrosis is never a feature of acute obstruction. It
                  is seen in chronic obstruction. In cases of acute obstruction there is only mild or rarely
                  moderate hydronephrosis. With chronic obstruction, both tubular concentration ability
                  and GFR are reduced, with the result that a dense persistent (obstructive) nephrogram is
                  rarely observed during urography. Nephrographic density may be normal or faint, greater
                  degrees of obstructive atrophy leading to more impairment of nephrographic density. In
                  the extreme condition, with little residual functioning renal parenchyma, little or no
                  nephrogram and no recognizable excretion of contrast medium into the collecting system
                  is seen.
              Systemic hypertension if the systemic hypertension is due to renal artery stenosis, it
                  would then give rise to dense persistent nephrogram*.
             * AIIMS Nov 2002.
    2.   Visualization of kidneys:
The kidneys are visualized as bean-shaped organs situated each on either side in para-vertebral region
between L1 to L4. The abnormalities seen are:
         I. Pitted scars or small contracted kidney in pyelo-nephritis
         II. Polycystic kidneys give bumpy out-line with stretched pelvi-calyceal system giving a
              spidery leg appearance
         III. Cysts would cast a negative shadow.
3. Classical patterns:
          Obstruction: dense prolonged nephrogram,clubbed calyces, mega ureters
          Chronic pyelonephritis-scarred kidney with thin cortex and clubbed calyces
          Papillary necrosis-linear breaks at papillary bases.
4. Visualization of pelvi-calyceal system:
The normal calyces are cup-shaped structures. The abnormalities seen are:
Clubbed calyceal system indicate hydronephrosis (unilateral or bilateral). There may be a non-
functioning kidney.
         I. In acute papillary necrosis, sloughed off papillae may cause ring shadows on IVP.
         II. Acute papillary necrosis is seen in analgesic nephrppathy, sickle cell nephropathy,
              chronic interstitial nephritis and diabetes mellitus.

5.  Non-visualization of kidneys
         Renal agenesis
         Nephrectomy-surgical removal along with 12th rib
         Non-functioning kidney
         Obscured by bowel gas or peri-nephric abscess
6. Small kidney (< 12 cm)/contracted kidneys(<8 cm)
         Chronic pyelonephritis
         Renal artery stenosis
         Bilateral contracted kidneys (ESRD)
7. Large kidney (> 14 cm)
         Diabetes mellitus
         Renal failure
         Renal vein thrombosis
         Amyloidosis
         Polycystic kidneys
         Compensatory following contralateral nephrectomy
         Hydronephrosis
         Myeloma
         Lymphoma
         Bilateral obstruction
8. Low-lying kidney:
         Hepatomegaly
         Transplant
         Congenital
9. Visualization of ureters:
        The ureters are outlined when the contrast is excreted through the ureters to the bladder. The
        ureters are thin tubes arising from the pelvis of the kidneys and ending into the urinary
        bladder. The abnormalities are:
         Ureters(s) may be dilated proximal to the urinary tract obstruction due to stone, tumor,
             retro-peritoneal growth or pelvic masses, ureteric strictures etc. They may also look
             dilated with the use of anti-spasmodic, oral contraceptives and pregnancy.
         They are narrowed in infection. Retro-peritoneal fibrosis pulls one or both of them
             towards mid-line and produces its narrowing with proximal dilatation as described above
         The beaded appearance of the ureters is seen in renal tuberculosis.
10. Retrograde pyelogram: after catheterizing, contrast is injected into the ureters. It is useful to detect
    non-functioning kidney and to locate the site of obstruction.
     11. Visualization of bladder: the bladder is visualized as a globular structure filled with opaque
          material in the supra-pubic region, gives an accurate definition of its shape, size and condition of
          the opening of the ureters and any growth or stone. The abnormalities are:
                A small contracted thimble bladder is seen in tubercular cystitis
                A large bladder indicates neurogenic bladder
                The bladder neck is elevated and there may be convex indentation due to prostate
                    enlargement
                Trabeculations and diverticula are seen in bladder neck obstruction and spastic bladder.
                    Diverticula may also be congenital sometimes.
          Micturating cystogram is done by introducing a catheter into the bladder and injection of radio-
          opaque contrast through it. The bladder will be visualized and vesico-uereteric reflux can be
          demonstrated in which radio-opaque contrasts appear into the ureters during act of micturition or
          even before micturition. Vesico-ureteric reflux indicates chronic pyelonephritis which has certain
          additional; findings on IVP.
                The kidneys are small, and show pitted scars
                There is clubbing of the calyces adjacent to the contraction of the renal substance.
          Micturating cysto-urethrogram also demonstrates posterior urethral valves and urethral strictures,
          if present .
Contrast nephropathy classically present as rise in blood urea nitrogen and serum creatinine and is more
common in individuals with pre-existing:
          – Chronic renal insufficiency
          – Diabetes mellitus
          – CCF
          – Hypovolemia (dehydration )
          – Multiple myeloma
          – Patients on metformin: metformin is excreted by kidney as an active compound. In case of
               renal insufficiency metformin accumulate and may increase the risk of lactic acidosis. Both
               metformin and radio contrast causes renal insufficiency and should not be used together.
Investigation of choice in renal TB:
          – *Early stage: IVU. IVU is the most sensitive to detect early renal TB. In the early stages it
               shows irregularity or destruction of one or more renal papillae. USG is of limited value in the
               initial investigation of the genitor-urinary TB (Cambell). CT scan is of limited value in the
               early investigation of genitor-urinary TB because IVU gives such accurate pictures
               (Cambell). MRI has very little application in the management of genitor-urinary TB
               (Cambell).
          – Late stage: CT scan
*AIIMS May 2003.
ANGIOGRAPHY:
                For imaging aorta, major arteries and branches
                To demonstrate atheromatous stenosis,thrombosis,embolism
                To detect aneurysms, A-V fistulae,angiomatous malformations
                To delineate tumors
                Interventions-balloon dilatation (angioplasty),embolisation
Cardiac Angiography: to demonstrate cardiac pathology and valvular lesions.
Coronary Angiography: for deciding angioplasty and CABG
Pulmonary Angiography: for detecting emboli, vascular abnormalities, assessment of Rt heart pressure and
intervention in massive pulmonary emboli.
Cerebral Angiography(carotid/four-vessel): to quantify atheromatous stenosis and top detect aneurysms, A-
V malformations; for Interventional procedures.
The most preferred route to perform cerebral Angiography is the **trans-femoral route. Puncture of the
axillary artery or direct puncture of the carotid artery are only rarely performed.
**AIPGME 2005.
Renal Angiography: for investigation of renal hypertension and for embolisation of vascular tumors.
Selective visceral angiography: to locate the site of bleeding, selectively infusing drugs or embolic material
into the bleeding vessel and to assess the tumor vascularity.
Angiography is also used in peripheral vascular disease.
Radio-isotope scanning:
Any organ of the body can be imaged by using specific organ selective isotopes.
'Cold areas'-tumor tissue fails to take-up isotope.
'Hot spots'-tumor tissue may take up more of the isotope.

Cardiac scanning
99m Tc (technetium) - it is useful to demonstrate size and function of chambers (cardiac
output, ejection fraction),wall motion abnormalities, and shunts.
MUGA scan (multigated acquisition) - data collection is synchronized to the ECG to
create a dynamic picture of cardiac function. This test can be done at rest and during
exercise. It is suitable when the patient has fast irregular rhythms. The isotope
concentration is more in recently damaged myocardium(24-72 hours) with 99m Tc.pyo-
phosphate scanning.
Brain scanning with 99m Tc ():
This test was previously used to exclude brain metastasis. The test is not reliable and has
been replaced with CT scan and MRI
Ventilation/perfusion (V/Q scan):
Perfusion lung scan (Q scan) is done with 99m Tc-labeled albumin macroaggregrates or
microspheres.
Hypo-perfusion due to pulmonary embolus is shown as cold areas.
Hypo-perfusion due to other causes such as pneumonia, tuberculosis, cysts and collapse
cannot be differentiated.
Ventilation scan (V scan) is done following inhalation of radio-active xenon (133 Xe) or
krypton ( 81m Kr).
In pulmonary embolism Q scan shows filling defect whereas the V scan will be normal.
99m Tc bone scan:
Technetium labeled phosphate complexes are used to detect bone metastasis especially
from thyroid, kidney, breast, lung, and prostate cancer.
Benign lesions such as osteoarthritis, rheumatoid arthritis, fibrous dysplasia and fractures
also take up isotope and may interfere with diagnosis of metastatic bone disorders.
Renal scans:
99m Tc-DTPA is used for the assessment of renal function, renal blood flow, and
estimation of GFR and evaluation of collecting system.
99m Tc-DMSA is used for imaging renal cortex.
Reduced and uneven uptake of isotope is seen in chronic pyelonephritis, obstructive
uropathy and tuberculosis. Tumors and cysts show up as filling defects.
131 I-Hippuran is also useful for the evaluation of renal function since it is excreted
entirely in one passage.

Adrenal scan:
Imaging is done with 79 Se-cholesterol and it reveals tumors producing Cushing's and
Conn's syndrome. It fails to reveal adrenal tumor causing pheochromocytomas.
Metiodobenzylguanidine (MIBG) scanning reveals pheochromocytomas as well as
metastasis from adrenal tumors.
Hepato-biliary scan:
99m Tc colloid is used for imaging liver. Mass lesions above 2 cm diameter such as
tumor, cysts, abscesses, and hematomas appear as cold spots.
99m Tc-HIDA (hepato-imminodiacetic acid) is used to scan biliary tree. Failure to
visualize gall bladder may be either due to acute cholecystitis or due to cystic duct
obstruction. Failure to excrete into the duodenum can be due to biliary atresia.
Thyroid scan:
It can be either with 99m Tc pertechnate or with 125 I to evaluate nodules (25 % solitary
cold nodules are malignant). It is very useful to localize ectopic thyroid tissue.
Thyroid function tests, and USG imaging along with isotope scan can aid in the diagnosis
of hyper-functioning adenoma,multinodular goiter, toxic nodules, and Grave's disease
White cell scan:
Indium or Technetium labeled peripheral blood leucocytes provide the very useful non-
invasive way of localizing hidden pus and also to monitor inflammatory activity in
inflammatory bowel disorders (Crohn's and Ulcerative colitis)
Gallium-67 scan
It is very much useful to localize abscess of 5-10 days old, and chronic inflammatory
lesions. It is also useful in the assessment of spread of neoplasms and lymphoma
particularly in the mediastinum.
Amyloidosis can be diagnosed by using radio-labeled serum Amyloid P protein.

Positron emission tomography (PET):
It is most useful investigation to detect whether the cell is alive, functioning and the
status of blood flow. Molecules labeled with positron-emitting radionuclides are injected
and 3 D images are obtained to assess the blood supply (labeled ammonia) and glucose
metabolism (fluro-deoxy-glucose FDG).
Recurrent tumors:
After radiotherapy to differentiate between cell death and tumor recurrence PET scan is
very valuable. This helps in planning further management such as the need for
stereotactic radiotherapy.
Cardiology: it is useful to differentiate between hibernating and dead myocardium.
Presence of normal glucose metabolism with low blood flow denotes hibernating
myocardium. PCI like angioplasty could improve the blood supply and function
*Stereo tactic radio-surgery is a form of. radiotherapy.
Stereo tactic surgery is a type of brain surgery that use a system of 3 dimensional co-ordinates to locate the
site to be operated upon.
In it focused high dose of radiation is administered to a precisely defined volume of tissue in a single
treatment, usually using the gamma knife.
It can potentially achieve tumor ablation without invasive surgery.
Major limitation of stereotaxic surgery is that it can be used for only relatively small tumors.
*AIIMS May 2003.
Neurology:
                      It is very much useful to diagnose dementia much earlier even before
                       symptoms appear.
                      Alzheimer's dementia-symmetrical hypo-metabolism in parietal and
                       temporal lobes.
                      Pick's dementia- hypo-metabolism affecting the frontal lobes.
                     PET scan is also useful to identify epileptogenic foci when there is no
                      anatomic lesion as evidenced by MRI/CT scan.
                     PET scan is very costly and it is used mainly for research.

USG:
                     Diagnostic USG is a recently developed non-invasive technique which
                      can furnish valuable clinical information and is often the first line of
                      investigation for abdomen, heart, arterial and venous system, thyroid,
                      orbit and eyes, ovaries and testicular lesions.
                     It is safe, painless, inexpensive, convenient, and repeatable and it
                      entails no ionizing radiation.
Abdominal scan:
           1. Liver size and texture-enlarged fatty liver/shrunken cirrhotic
               liver/cysts/tumor
           2. Biliary system- dilated ducts in obstruction-tumor/stone
           3. Spleen-size, evidence of portal hypertension,splenic vein thrombosis
           4. Gall bladder-thickening of wall,polyp,gall stones
           5. Pancreas-pseudo-cysts,abscesses,tumor,calculi
           6. Kidneys-enlarged or contracted,calculi,hydronephrosis,polycystic disease,
               mass lesions, adrenal mass lesions
           7. Aneurysms of aorta and major vessels
           8. Doppler studies of portal and splanchnic veins-to assess direction of flow
               and to rule out thrombosis.
           9. To monitor normal and abnormal pregnancy
           10. To monitor fetal growth and development
           11. Localization of placenta
           12. To identify ectopic pregnancy
           13. Ovarian mass lesions including PCOD
           14. Uterine mass lesions
           15. Testicular size, mass lesions, hydrocele.
Imaging intensity -USG abdomen
Organ       Hyperechoic                  Hypoechoic                   Anechoic
Liver          Stones,metastasis,granulomas     Metastasis ,abscesses               Cysts, abscesses
               ,cirrhosis,hemangiomas
Spleen         Haemangiomas, granulomas         Hematoma,lymphoma,metastasis        Cysts, abscesses
Gall           Calculi, polyps                  Carcinoma,empyema                   Cholecystitis,abscesses
bladder
Kidneys        Calculi,lipoma,angioma           Abscesses,metastasis,cancer         Cysts, dilated pelvi-
                                                                                    calyceal system
Pancreas       Chronic pancreatitis             Acute pancreatitis,carcinoma        Abscesses,cysts,pseudo-
                                                                                    cysts
ECHOCARDIOGRAPHY:
This non-invasive technique offers a wealth of anatomic and physiologic information of the heart. It is safe,
painless, repeatable, and inexpensive and it does not utilize ionizing radiation. All the modern equipments
provide the following facilitates.
    1. M-Mode
    2. B-Mode-2 D echocardiography
    3. Pulsed Doppler
    4. Continuous wave Doppler
   5. Color flow imaging
M-Mode echocardiography:
    It gives an ice-pick view of the heart and it has many limitations.
    It allows measurement of chamber size, assessment of valve and wall motion.
    Cardiac structures closer to the transducer are displayed at the top of the record and the distant
      structures are displayed below (on trans-thoracic B-mode echocardiography-the anteriorly placed
      Rt sided structures are displayed on the top and the posteriorly placed Lt sided structures
      displayed on the bottom and the order is reversed in the trans-esophageal echocardiography).
B-mode or two dimensional echocardiography:
    Useful in the diagnosis of congenital heart disease such as
          a. Septal defect
          b. Congenital valvular disease
          c. Relationship of great vessels to the cardiac chambers
          d. Fetal imaging for the ante-natal diagnosis of congenital heart disease
          e. Malposition of the heart.
    To assess the cardiac chamber hypertrophy,dilatation,systolic and diastolic
      dysfunction, type of cardiomyopathy
    To assess the type of valvular lesion-congenital,rheumatic,degenerative
    To diagnose infective endocarditis-vegetation > 2 mm size
    To diagnose pericardial thickening, effusion and impending cardiac tamponade
    Useful for the evaluation and diagnosis of coronary artery disease (including
      stress echo and pharmacological stress test)
    Doppler echocardiography is used to assess the direction and velocity of blood
      flow in the heart and great vessels ( to detect shunts, regurgitant lesions and
      quantify valvular stenosis)
    Color flow data when super-imposed on B-mode echocardiography provides more
      useful qualitative data. The color coded mapping reveals red color indicating flow
      towards and the blue away from, the transducer.

Thyroid scan:
    Useful to measure the size of thyroid enlargement and also to differentiate cyst,
       nodule/tumor.
    Not useful to differentiate benign and malignant nodule.

Orbit and eye
    Aids in the localization of foreign bodies
    Assessment of retinal and choroidal detachment
    Assessment of retro-orbital mass lesions.


Large veins and arteries:
    Assessment of blood flow in the limbs
    To assess the extent of thrombosis

Special techniques:
    Trans-esophageal echocardiography to assess mitral valve lesions and vegetations
       in infective endocarditis.
      Trans-vaginal to study uterine and ovarian lesions
      Trans-rectal to assess the lesions of prostate and rectum
      Intra-vascular USG –to study the extent of plaque, and it has a clinical role in
       coronary angioplasty and stenting.
     Endoscopic USG - assessment of depth of mucosal penetration in cancer and thus
       helpful in staging (cancer esophagus,stomach,colon and rectum).
CT scan (computerized tomography)
     The X-ray beam moves around the patient in a circular path and the slices can be
       cut at various levels.
     The detailed images are constructed from X-ray absorption data with the help of
       the computer.
     CT scan is very useful in stroke patients to differentiate infarction from
       hemorrhage since the treatment modality is different.
     In major trauma with head injury CT scan is the most important investigation of
       choice.
     CT scan is performed with or without contrast. Contrast CT scan is useful in
       abdomen, pelvis and brain. It helps in G.I. tract to delineate the bowel and in brain
       to assess the vascularity of mass lesions and in performing carotid or 4 vessel
       angiogram.
     Density measurements are essential to differentiate cyst, tumor and hematomas. it
       is expressed in "Hounsfield units" (water is 0,bone +1000,air is -1000 units, fat -
       50 to -150 and it varies for other tissues depending upon the density)
     Skeletal system disorders are better imaged by CT scan.
CT scan brain:
CT scan is useful for the diagnosis and assessment of various lesions:
     Fracture involving skull vault or base.
     Hydrocephalus-dilated ventricles with effaced sulci and thinned out cortex.
     Infarction (area of low attenuation with or without mass effect) and hemorrhage
       (high density lesion).
     Cerebral edema due to stroke or different types of metabolic coma
     Mass lesions with or without mid-line shift
     High density extra-dural or sub-dura; hematoma in acute phase
     Low density chronic sub-dural hematoma
     Various types of cerebellar lesions
     Multiple sclerosis and metastatic lesions
     Cerebral atrophy-prominence of the sulci and atrophy of the gyri.
Diffuse axonal injury:
Another type of deep white matter lesion consists of widespread acute disruption, or shearing, of axons at
the time of impact. Most characteristic are small areas of tissue disruption in the corpus callosum and
dorsolateral pons. The presence of widespread axonal damage of both hemispheres, a state called **diffuse
axonal injury, explains persistent coma and the vegetative state, but small ischemic-hemorrhagic lesions in
the midbrain and thalamus are as often the cause. Only severe shearing lesions that contain blood are
visualized byCT, usually in the corpus callosum and centrum semiovale (Fig. 357-2); however, within
days of the injury, MRI scan demonstrates such lesions throughout the white matter with the use of special
imaging sequences.
FIGURE 357-2 Multiple small areas of hemorrhage and
tissue disruption in the white matter of the frontal lobes on
noncontrast CT scan. These appear to reflect an extreme type
of the diffuse axonal shearing lesions that occur with closed
head injury.
** AIPGME 2007.
             Diffuse axonal injuries           Cerebral             Subdural hemorrhage      Multiple infarcts
                                               contusions
Etiology Axonal shear-strain are               Induced by brain     Tearing of bridging      A gradual and
             induced by sudden                 striking on          cortical veins           global reduction
             acceleration/deceleration or      statonary                                     in cortical blood
             rotational forces on brain.       calvarium                                     flow of normal
             seen in high velocity trauma. -coup                                             ageing subjects
                                               -counter-coup
Location – Lobar white matter                  Multiple Bilateral   –  Between dura and      – Often
                 Particularly at grey-white lesions commonly          arachnoid                asymmetrical
                 matter interface              in Frontal &         – 95%                    – Frontal
             – Corpus callosum                 Temporal Lobe          supratentorial(front   – Temporal
             – Dorso-lateral aspect of                                o-parietal)            – Parietal lobe
                           upper brain-                                                        with multiple
                           stem                                                                areas of
                                                                                               diminished
                                                                                               flow
Imaging     Multiple small petechial          Early:                Crescentic extra-axial   – Cortical &
CT          hemorrhage < 2 cm diameter        Patchy ill-defined    hematoma crossing           subcortical
            in cerebral hemisphere            low density lesion    suture line                 infarct
                                              (edema) mixed                                  – large
                                              with small hyper                                  ventricles
                                              dense foci of                                     and cortical
                                              petechial                                         sulci
                                              hemorrhage                                     – white matter
                                              Delayed (24-48                                    leucotasies
                                              hours):
                                              Delayed
                                         hemorrhage
                                         Edema & mass
                                         effect increases
                                         Enhance after
                                         contrast
                                         administration
MRI      Most sensitive modality         Decreased
         Multiple small foci decreased   intensity
         signal intensity of T1WI +      (hemorrhage)
         increased signal intensity on   surrounded by
         T2 WI                           hyper dense
                                         edema on T2WI

CT scan chest:
    High resolution CT scan is investigation of choice to diagnose Bronchiectasis.
    Detecting and staging primary cancer of the lungs, pleura, and mediastinum
    To diagnose metastasis of the lungs/pleura.
    To detect infiltrative lung disease
    For the diagnosis of pulmonary emboli
    Evaluation of interstitial lung disease.

CT scan coronary angiography:
    Multi-slice CT scanners are used
    Coronary angiography is performed with 64- slice technique
    80 ml of iodixanol is injected into an ante-cubital vein at a flow rate of 5
      ml/second followed by a 50 ml saline chasing bolus.
    The over-all scan time is shorter than 15 seconds and the total period of study is
      less 15 minutes.
    The main contraindications are allergy to iodine contrast and severe renal
      insufficiency.
    The technique is 95 % specific and sensitive with 85 % positive predictive value
      and negative predictive value is 99 %.
    Extensive arterial wall calcification interferes with proper vessel assessment.



CT scan abdomen:
    For accurate evaluation of pathology in obesity individuals
    To detect smaller lesions missed by USG
    Pancreas and its disorders better demonstrated
    Helpful in delineating renal and adrenal masses
    To assess par-aortic and retroperitoneal lymphadenopathy
    Spiral CT scan is useful in imaging solid organs, retro-peritoneal structures and
      small or large bowel obstruction
    For monitoring invasive procedures-biopsies, placement of drainage tubes
    Used in staging of abdominal and hematological malignancy.
CT scan bone: bony architecture is best visualized by a CT scan. The single best investigation of choice
for assessing a lesion of the temporal bone is a CT scan.
Magnetic resonance imaging (MRI)
   MRI imaging uses the disturbance induced on the resonance of protons in the
      body tissue in a uniform magnetic field.
   An image could be constructed in any chosen plane with the help of pulsed radio-
      frequency energy source.
   MRI images are constructed from the rate of decay or relaxation of proton
      resonance either in the plane longitudinal or transverse to the magnetic field.

             1. T1 images-reflects the time taken for the protons to return to the axis of
                the original field.

             2. T2 images-time for the protons to dephase.
             3. T1 weighted images-provide good anatomical planes and also useful to
                differentiate cystic or solid structures
             4. T2 weighted images-are useful to study the pathology.

Moving blood is black in T1 images and bright in GRE sequences and it is possible to
reconstruct blood vessel morphology.
This technique is very useful in non-invasive angiography of different organs.
The sensitivity of MRI images are enhanced by spino-echo sequences, and contrast
enhancement with gadolinium (a rare earth element).
Differentiating features between T1 and T2 images
Structures            T1 weighted T2 weighted
Water                 Black           White(bright)
Fat                   White(bright) White
Air                   Black           Black
Muscles               Grey            Dark grey
Tendons/ligaments Black               Black
Bone                  Black           Black
Tumors                Grey            White

MRI rooms are completely shielded by a continuous sheet or wire mesh of copper or aluminum to shield
the imager from external electromagnetic radiations etc. it is called Faraday cage*.
*AIIMS Nov 2003.

Advantages of MRI:
    No radiation
    To obtain images in any plane-sagittal/coronal/axial
    Non-invasive angiography (cerebral,coronary,renal and peripheral)
    Best images of brain/spinal cord, aorta/vena cava. MRI is now regarded as the
      investigation of choice for all space occupying lesions of the brain whether in the
      anterior, middle or posterior cranial fossa (most useful infra tentorial posterior
      fossa lesions), because it is free of ‗beam hardening‘ affect causing less brain
      artifacts and has higher contrast to noise ratio causing excellent identification and
      characterization of infratentorial neoplasm. With CT, beam hardening artifact
      cause difficulties in interpreting posterior fossa tumors. So role of CT scan
      becomes limited for posterior fossae tumors.
    Visualization of posterior fossa/cranio-cervical junction
    Best images of soft tissue lesions
    Better imaging of pancreas,adrenals,biliary tree, and lesions of pelvis
    MRI urography – bowel preparation not required and can be performed even if
      renal function is impaired (out-lines the dilated PCS even in the presence of poor
      renal function)
    MRI urography-extensive obstructions of urinary tract better visualized than in
      IVU.
Disadvantages of MRI :
    Relative high cost
    Unsuitable for patients with metal foreign bodies (pacemakers, cochlear implants,
      vascular clips)
    Difficult to image calcium
    Difficult to image critically ill patients with monitoring equipments
    Claustrophobia
    Long imaging time results in increased motion artifacts
    MRI urography-normal ureters not well visualized.
**Maximum single time radiation exposure is given by bone scan; because the radiation isotope remains in
the body for hours (according to half-life). Radiation exposure in decreasing order:
Bone scan > CT scan >X-ray
MRI & USG has no radiation risk.
**AIPGME 2006.
Maximum permissible radiation dose –is that dose which if received each year for a 50 working life-time
would not be expected to produce any harmful effect. *The maximum permissible dose for a pregnant
woman is 0.5 rads in gestation period .
The gestation period when the fetus is most sensitive to the effect of radiation t8-15 weeks of gestation.
The ‗10 day rule‘-this rule advice that any X-ray examination involving the abdomen of a woman of child-
bearing age should be carried out within 10 days of the onset of menstruation.
*AIIMS Nov 2003.
Intra-operative irradiation:*intra-operative electron beam used as boost followed by photon beam treatment
is an innnervative regimen for pancreatic, gastric and rectal cancers; retroperitoneal sarcomas; head and
neck cancers; and genitor-urinary and some gynecological cancer.
*AIIMS Nov 2003.
*Metronidazole and other nidazoles (tinidazole, nidazole,ornidazole and benzinidazole) can sensitize
hypoxic tumor cells to the effects of ionizing radiation.
Radiation therapy is a form of physical therapy that damages any tissue in its path.
Mechanism of injury of radiation in cells-
Radiation usually damages DNA
Generates free radicals from cell water. Free radicals in turn damage cell membrane proteins and
organelles. Radiation damage is dependent on oxygen. So hypoxic cells are resistant to radio-therapy.
Augmentation of oxygen is the basic of radio-sensitization.
*AIIMS Nov 2003
X-rays and Gamma rays are electromagnetic waves with highest penetrating power.
*For deep seated tumors rays with maximum penetrating power is required so X-rays and gamma rays are
used.
Megavoltage X-rays are used to irradiate internal deep seated lesions since high-energy penetrating beams
deliver a less intense superficial dose and spare the skin. *AIIMS May 2003.
Gamma radiation -the penetrating power maximum* -1000 times of α-rays
Minimum penetrating power -α-rays
* AIPGME 2002.
*Amifostine also known as WR2721 is a well-known radio-protective agent. It is believed to act by
releasing free sulphide groups which scavenge the free radicals produced due to radiation. It has also been
tried as an anti-radiation agent for astronauts. * AIPGME 2001.
Radio-sensitive tumor:
Highly sensitive                    Moderately sensitive
Lymphoma                            Small cell lung CA
Wilm                                CA breast
Myeloma                             Teratoma
Ewing‘s sarcoma                     Ovarian CA
Seminoma                            Basal cell CA
                                    Medulloblastoma
                                    Dysgerminoma
                                    Naso-pharyngeal carcinoma
Relatively resistant                Highly resistant
Squamous cell carcinoma lung        Melanoma
Hypernephroma ( renal cell CA)      Osteocsarcoma
Rectal CA/colon CA                  Pancreatic CA
Bladder CA                          Hepatoma
Soft tissue CA (Fibrosarcoma)
*Carcinoma cervix
* AIPGME 2001.

                                               HISTORY TAKING
    History taking is an art, which forms a vital part in approaching the patient's problem, and arriving at a
     diagnosis.
 History taking helps to form a healthy doctor-patient relationship.
 It also builds up the patient's confidence and trust in his doctor.
Even before going into the patient's complains, important facts can be gleaned from the following data,
asked as a routine from every patient, helping the consulting doctor to arrive a t a most probable conclusion
to the patient's problems.
1. Name:
Q.What is the importance of name in history taking?
     a. It helps in identifying patient's religion, caste (from surname), country, state and even father's
          name in Gujarat.
     b. It helps in building rapport with the patient when we call him by his name.
     c. Though certain names are ambiguous, many a times sex of the patient can be identified too.
     d. Name of the patient helps in identification of the patient ,be it for the hospital records, writing
          medication orders or administration of drugs by staff nurse (and avoiding wrong medication if the
          patient is identified by name rather than by bed no)
     Mohammed seems to be the common name in the world.

2. Age
Q.What is the importance of age of the patient?
According to age group various etiologies can be predicted to be more preponderant i.e.
   a. Problems setting in at childhood are probably congenital in origin.
   b. In neonates and infants: congenital anomalies like tracheo-esophageal fistula, congenital heart
        disease, developmental defects like cleft lip and palate etc are detected. Infectious fevers are also
        common in neonates.
   c. In adolescents: sexual promiscuity with unsafe sexual practices entails risk of STDs.
   d. In post-menopausal women: risk of ischemic heart disease increases to levels that of males.
   e. In elderly: neoplastic diseases like bronchogenic carcinoma, degenerative diseases like
        spondylosis or sclero-degenerative aortic stenosis,vascular disorders are more common in the
         middle-aged or elderly. Prevalence of atherosclerotic diseases like ischemic heart disease also
         increases with age.
Q.What are the neoplastic diseases found in children?
Neoplastic diseases of children are –neuroblastoma, retinoblastoma, Wilm's tumor, acute lymphatic
leukaemia (A.L.L.) etc.
**Wilm's tumor is described as ‗Clean lesions‘. Usually confined by renal capsule and present as well-
defined echogenic space occupying lesion.
Mean age -3 years.
** AIPGME 2002
 Q.What are the congenital disorders not manifesting at birth or even in childhood?
      Congenital heart disease-like bicuspid aortic valve without AS or AR, ASD, patent foramen ovale.
      Skeletal defects like-spina bifida occulta, protrusio acetabulae of Marfan's syndrome
      Genetic disorders manifesting in late adulthood –like HOCM, marfan's syndrome etc
      "Silent" malformations of organs like-horse kidney etc.

3. Sex
Q.What is the importance of the sex of the patient?
    a. Males have increased expression of X-linked disorders like hemophilia, color blindness
    b. Males are more likely to smoke and consume alcohol; hence they are more likely to have
         bronchogenic carcinoma and alcoholic liver disease, IHD, though women are more likely to
         develop cirrhosis at lower volume of alcohol consumed.
    c. Iron deficiency anemia is more common in females due to regular menstrual loss and poor
         nutritional supplement of dietary factors.
    d. Autoimmune disorders like SLE and diseases of thyroid are more common in females.
    e. Premenopausal women are less likely to have coronary artery disease than post-menopausal
         females or age matched male counterparts.
 Q.What is mitochondrial inheritance?
Certain genes have been found to be located on mitochondria. Since sperm lacks mitochondrial genes,
disorders are transmitted by mothers to their son, and by fathers to their daughters. example are:
                    Kearns-Sayre syndrome(external ophthalmoplegia,complete heart block, pigmentary
                       retinopathy),
                    Myopathies like MERRF (myoclonic epilepsy with ragged red fibers),
                    MELAS(metabolic encephalopathy, lactic acidosis, stroke like syndrome),
                    Leigh syndrome
                    Leber's disease.


4.   Religion
                 Q.What is the importance of religion and caste?
                 a. Rituals-burkha worn by muslims may make them susceptible to vitamin D deficiency
                    due to poor sun-light exposure.
                 b. Religious prohibition-Sikhs do not smoke while muslims are prohibited to consume
                    alcohol hence they are less likely to develop problems related to smoking 9crnm of
                    lung) and alcoholism (e.g. decompensated liver disease) respectively.
                 c. Dietary habits-Hindus do not eat beef hence T.saginata is less likely in them while
                    muslims do not eat pork hence T.solium is lees likely in them.
                 d. Certain sects of Hindus do not consume meat products and consume a high fiber diet
                    and are therefore protected from developing carcinoma of the colon.
                 e. Jews and muslims practice circumcision soon after birth hence carcinoma of penis is
                    rare in them.
                 f. Ritual fasting during ramzan or navaratras or paryushan may make patients non-
                    compliant of medicines and make diabetics prone to hypoglycemia due to fasting.
                 Importance of caste:
                 a. Consanguity is common in certain tribes and castes of southern India and in certain
                    muslims, which make them more likely to develop genetic disorders.
                  b.   Luvana-thakkars are reported to have higher incidence of thalassaemia.

5.   Address

Q.What is the importance of address of the patients?
   1. Certain diseases like filariasis is more common in coastal belts of India while iodine deficiency
        (goiter) is more common in hilly areas and so is primary pulmonary hypertension, PDA(from
        childhood).
   2. Renal stones are more common in "stone belt" of Gujarat i.e. Suarashtra and parts of north
        Gujarat.
   3. Fluorosis is more prevalent in certain pockets of Andhra Pradesh, Madhya Pradesh and Rajasthan.

     4.   People hailing from the urban region are prone to develop problems related to urbanization like
          exposure to constant stress and atmospheric pollution (industrial and vehicular) and problems
          developing consequent to this e.g. IHD,COPD,interstitial lung disease etc.

     5.  Certain infections like kala-azar is prevalent in eastern India and hence the name Dum-Dum fever.
     6.  Address helps in identifying the locality of the city or the state and hence in epidemiological
         survey and identifying the common source of infections, if any, as in case of water-borne diseases.
     7. Address helps in maintaining communications, if required with patient for future refrence,study
         and follow-up.
Occupation: enquiry must be made on all previous and present occupation, as it may give a clue to the
presence of an occupational disease in the patient and also to the plan of rehabilitation. On the other hand,
the presence of a disease in an individual makes him unfit for his occupation by proving to be hazardous to
him as well as to others e.g.
              a. Salmonella infection or carrier state in food handlers
              b. Epilepsy in drivers of public transport vehicles.
 Q.What is the importance of occupation of the patient?
     1. Occupational lung diseases can be identified in mill-workers, in form of silicosis (silica-exposure
         occurs in mine industry), anthracosis (coal dust), asbestosis (mesothelioma) etc.
     2. Organic lung disorders can also be associated with profession like farmer's lung, bysinosis (cotton
         dust) etc.
     3. Lead poisoning is known in painters and chemical workers.
     4. Industrial exposure due to chemicals can cause contact dermatitis.
     5. Aniline dye poisoning can occur in textile industries using the dye as coloring agent ( exposure to
         aromatic amines in dye stuff industry may cause carcinoma of urinary bladder ).
     6. Organo-phosphorous poisoning can occur accidentally in farmers while spraying the insecticide in
         fields.
 Q.What is the treatment of aniline dye poisoning?
Removal of the source of poisoning, ethylene blue and vitamin C is the treatment of aniline dye poisoning.
 Q.What is the commonest occupational disease in India?
Hookworm infestation and associated anemia is believed to be the commonest disease related to
occupation, because majority of India resides in villages with farming their main profession. With practice
of open defecation, hook-worm infestation by rhabditiform larva in bare-footed farmers is rampant.

Q.What is importance of status of the patient?
                 In socio-economically poor patients infectious diseases are more common while
                    urbanized rich people are more prone to atherosclerotic disorders likely IHD ,CVA
                    and to insulin resistance.
                 In socio-economically poor patients over crowding is more likely ;hence
                    transmission of infectious disorders/communicable diseases are more common.
                 Sanitation in and around the house.
 Q.How do you define various socio-economic groups?
Income groups according to family income in rupees per annum (as per statistical outlines of India, Tata
services ltd, Department of Economics and Statistics. GOI) are:
                    Low: up to Rs 20,000/-
                    Lower middle: Rs 20,000/- Rs 40,000/-
                    Upper middle Rs 40,000/- Rs 60,000/-
                    High: Rs 62,000/- Rs 86 000/-
                    Affluent high: above Rs 86,000/-
The classification has replaced classification given by Kuppuswamy et al.
 Q.How do you define overcrowding?
     1. Persons per room if exceeding the following:
                1 room-2 persons
                2 room-3 persons
                3 room-5 persons
                4 room-7 persons
                5 room-10 persons
     2. According to floor space if exceeding the following:
                ≥ 110 sq.ft.: 2 persons
                90-100 sq.ft.: 1.5 persons
                70-90 sq.ft.: 1 person
                50-70 sq.ft. : 0.5 persons
                under 50m sq.ft.: nil
          (child under 12 months is not counted between 1 to 10 years is counted as 0.5)

 Q.What is the importance of overcrowding?
Overcrowding is associated with increased spread of respiratory infections like tuberculosis, influenza and
beta streptococcal sore throat and hence rheumatic fever.
 Q.What is the importance of season in history?
Pneumonia is more common in winter and rainy season due to
     1. Lower temperature and increased survival of micro-organism
     2. Clustering of people indoors and hence increased droplet infection in co-habitants.

After having obtained the above details, the patient should be approached as follow:
Greet the patient, preferably by his name and start off the consultation with some general questions such
as," What can I do for you?", or: "How can I help you?", or "What is the problem?"
Chief complains
      Allow the patient to tell his complains in his own words.
      Do not put leading questions to the patient.
      The current complains and their duration should be noted in a chronological order.
History of present illness:
      Allow the patient to elaborate on the story of his illness from its onset to its present state.
      Take care so as not to put any leading questions to the patient which may distort the patient's
         history.
      The doctor may however, interrupt the patient to ask for the presence of 'positive' or 'negative'
         symptoms pertaining to patient's current problems.
      In analysis of the symptoms, it is important to consider the mode of onset of the illness (acute,
         subacute, or insidious) and the progression of the illness to the present state (gradually
         deteriorating, getting better, remaining the same or having remission or exacerbations).
      A re-view of all the systems can be made by questioning the patient on the presence or absence of
         symptoms pertaining to a particular system.
Q.What is the importance of the past history?
   1. History of previous illness should include all important previous illnesses, operations and injuries
       that the patient might have suffered from birth onwards.
   2. History of mode of delivery and the timing of attainment of the various developmental milestones
       in infancy may be important in some cases.
   3. It is wise to be cautious while accepting readymade diagnosis from the patient like 'typhoid fever','
       'malaria' etc unless the patient has record of the mentioned illness.
   4. History of rheumatic fever would suggest rheumatic heart disease as etiology
   5. History of risk factors like diabetes mellitus, hypertension, hyperlipidaemia etc suggests IHD as
       the etiology.
   6. History of tuberculosis would suggest it as the etiology of its sequelae like constrictive pericarditis
       or lymphadenopathy or abdominal lump.
   7. History of jaundice may suggest previously impaired liver function or hemolytic burden and may
       later the drug therapy
   8. History of similar illness would represent a recurrence and hence poorer prognosis e.g. recurrence
       of rheumatic fever is associated with higher valvular involvement. Bronchial asthma, epilepsy,
       gout are the diseases with tendency to recur.
   9. Tactful enquiry about sexually transmitted diseases and its treatment, when this is considered of
       possible relevance to the patient's problem should be made.
   10. History of a previous single painless penile ulcer with associated painless masses over the inguinal
       regions, occurring 3-4 weeks after exposure to a commercial sex worker, which may have healed
       subsequently with or without treatment with the formation of a residual papery or velvety scar
       over the penis indicates a previous affliction by syphilis. This is important as syphilis in its tertiary
       form, later in life, can present with systemic manifestations e.g. aortic aneurysm and regurgitation,
       tabes dorsalis.
   11. History of white discharge per urethra with associated dysuria, 2-3 days after exposure to a
       commercial sex worker indicates gonorrhea. This is important as gonorrhea can later lead to
       gonococcal arthritis or urethral stricture.
   12. Travel to endemic area may suggest the etiology/import of a disease by the patient .
   13. History of previous surgery may point to the etiology.
Q.What is the importance of personal history?
   1. Diet-green leafy vegetables alter the vitamin K dependent drugs like warfarin and hence can alter
       INR levels. Non-vegetarian diet is associated with certain worm infestation like Taenia and with
       higher risk of IHD. Vegetarian diet with high fiber content decreases incidence of colonic
       carcinoma and IHD.
   2. Nature of patient's work (hard work or sedentary)
   3. Bowel habits-constipation and diarrhea would suggest G.I. involvement. Various drugs can alter
       bowel habits e.g. verapamil causes constipation.
   4. Bladder habits-nocturnal frequency would suggest pathologic state like BPH, LV dysfunction etc.
       Nocturnal incontinence is often pathologic.
   5. Sleep pattern-may be disturbed due to PND. Nightmares due to drugs like non-selective beta-
       blockers etc.
   6. Drug history- would suggest etiology or the complication of drug therapy e.g. pedal edema in
       patients taking calcium channel blockers (dihydropyrilidines)
   7. Habits-tea, coffee, smoking or tobacco (whether chewed or smoked), betel nut, alcoholism may
       alter pharmacological properties of drugs and may themselves cause various disorders. an
       alcoholic consumes alcohol almost every day and develops withdrawal symptoms on abstaining
       from alcohol.
   8. Chewing betel nut or tobacco is a habit common with people living rural areas, and this increases
       the risk of developing oral malignancies.
   9. The presence of pets in the house.

Q.What are the diseases associated with smoking?
   1. CVS-IHD,hypertension,atherosclerosis,and dissection,TAO (Beurger's disease)
   2. Respiratory system -tracheitis,acute and chronic bronchitis (COPD),Bronchiectasis, Bronchogenic
       carcinoma, emphysema
     3. GIT-carcinoma lip, tongue, stomach, colon, pancreas; gastritis, peptic ulcer.
     4. Renal-renal cell carcinoma
     5. CNS-stroke, tobacco Amblyopia,tobacco related neuropathy, decreased exercise tolerance
     6. Hematological-leukaemias
     7. Pregnancy-delays conception and IUGR
     8. Hepatic enzyme inducers-hence increases drug requirement
     9. Genito-urinary -carcinoma bladder, carcinoma uterine cervix.
 Q.Which diseases are less common in smokers?
Ulcerative colitis, Parkinsonism, Sarcoidosis, Alzheimer's disease
 Q.Which is the most hazardous form of smoking?
Cigar because it is devoid of filters and has more tobacco per cigar by weight.
 Q.What is believed to be the least harmful mode of tobacco consumption?
Hookah because it contains a water trap for trapping suspended particles and long pipe which decreases
suspended particles and the water cools down the smoke. However, it does not make hookah a safe
alternative.
 Q.Which is more dangerous cigarette or bidis?
One bidi is equal to 2 cigarettes by its contents like beta naphthylamine,benzopyrene and nitrosamines
hence bidi is more dangerous.
 Q.What are acute cardio-vascular effects of nicotine?
     1. Increases myocardial oxygen demand by increasing heart rate and both systolic and diastolic BP
          and increasing peripheral vascular resistance.
     2. Causes peripheral and coronary vaso-constriction.
     3. Increases APCs and VPCs.
 Q.What is a pack year?
               It is the product of number of packs per day multiplied by number of years.
               Duration of smoking in years x number of packets of cigarettes smoked/day e.g. two
                   packs of cigarettes smoked per/day for twenty years constitutes 40 pack years .
               Risk of development of Bronchogenic carcinoma increases when pack years exceed 40.
               The lung cancer death rate is related to the total amount (often expressed in "cigarette
                   pack-years") of cigarettes smoked, such that the risk is increased 60- to 70-fold for a man
                   smoking two packs a day for 20 years as compared with a nonsmoker.
               Conversely, the chance of developing lung cancer decreases with cessation of smoking
                   but may never return to the nonsmoker level
 Q.What is smoking index?
               Smoking index is the product of number of cigarettes per day multiplied by the duration
                   in years e.g. the smoking index of a person smoking 20 cigarettes or beedis per day for 20
                   years is 400.
               Smoking index greater than 300 constitutes a risk factor for Bronchogenic carcinoma.
               Index more than 300 suggest heavy smoker while less than 100 suggest mild smoker. It is
                   better epidemiological marker of smoking than pack years.
Q.What are the drugs available to help in quitting smoking?
Nicotine replacement therapy in form of patch or chewing gum or bupropion therapy AIDS in quitting
smoking.
 Q.What are the diseases associated with alcoholism?
     1. CVS- alcohol in moderation (less than 24 gms per day by weight) is found to reduce risk of IHD.
          It when consumed more than moderation increases risk of IHD. Alcohol can cause alcoholic
          cardiomyopathy and holiday heart syndrome characterized by atrial arrhythmia after a binge of
          alcohol at weekends.
     2. CNS-alcohol can cause Wernicke's encephalopathy, withdrawal syndromes ,alcohol
          dementia,Marchiafava-Bignami syndrome( sub acute corpus callosum degeneration in crude red
          wine drinkers),cerebro-vascular disease, alcoholic cerebellar degeneration, central pontine
          myelinosis,peripheral neuropathy, Saturday night palsy, alcoholic myopathy.
     3. GIT-esophagitis,gastritis,peptic ulcer,pancreatitis,carcinoma pancreas,malabsorption
          syndrome,cirrhosis,alcoholic hepatitis ,fatty liver
     4. Hematology-macrocytic anemia due to vitamin B deficiency, hypersplenism due to cirrhosis.
 Q.How much alcohol is required to cause cirrhosis and how much is required for alcoholic
cardiomyopathy?
               For cirrhosis- 120 to 160 gms of alcohol per day for 10-12 years
               For alcoholic cardiomyopathy-80-120 gms of alcohol per day for 8-10 years.
 Q.What are the path-ways of alcohol metabolism?
               Alcohol dehydrogenase (ADH) path-way-major
               Microsomal ethanol oxidizing system (MEOS)-minor
 Q.What percent of alcoholics will develop cirrhosis?
10-15 %.
 Q.What is the mechanism of liver or cardiac injury by alcohol?
    1. Direct toxic effect
    2. Toxic effect of acetaldehyde by binding to
              a). Phospholipids and depolarizing proteins
              b). Altered mitochondrial function and cellular respiration
              c). Blocking microtubule formation and decreased transport function
              d). Neo-antigen formation by abducting with proteins
    3. MEOS path-way associated free oxygen radical formation
    4. Due to added constituents like cobalt (used as foam stabilizer)
 Q.What are the genetic factors associated with alcoholic cirrhosis?
Increased risk is found in HLA B8, HLA Dw2. LDH2 heterozygotes have impaired metabolism of
acetaldehyde.
 Q.What are the various stages of alcoholic liver diseases?
     Fatty liver defined as more than 5 G of fat per 100 gm of liver
     Alcoholic hepatitis
     Cirrhosis
 Q.What is the importance of family history?
    a). Genetic disorders run in family e.g. diabetes mellitus, neurofibromatosis, Wilson's disease,
         Huntington's chorea, hypertension.
    b). Clustering of people indoors in family can predispose to droplet infection and diseases like
         pneumonia etc.
    c). Family history can also suggest genetic susceptibility to HLA linked diseases.
    d). Recurrence of congenital diseases is more common if the parents or sibling is diseased e.g. TOF.
                        Enquire about the presence of consanguinity in the patient's parents, any disease
                            states in the patient's parents, brothers, sisters, and close relatives (presence of
                            disease states like hypertension, DM, IHD in the above may make the patient
                            more prone to develop a similar problem).
                        It is prudent to record the state of health, important illnesses, the cause and age
                            of death in any member of the patient's family (may give a clue to the presence
                            of HOCM or development of IHD).
                        Presence of a hereditary disorder prevalent in the family should be enquired for.
                        Marital status of the patient and the number of children that the patient has
                            should also be enquired for (infertility in a patient may give a clue to the
                            presence of immotile cilia syndrome, cystic fibrosis or Young's syndrome).

Q.What is the importance of menstrual and obstetric history?
   a). Menstrual history-
            i. Age of menarchy
            ii. Duration of each cycle
            iii. Regular or irregular cycles
            iv. Approximate volume of blood loss in each menstrual cycle
            v. Age of attainment of menopause
            vi. Post-menopausal bleeding
            vii. Amenorrhea if present pregnancy needs to be ruled out before starting any medication
                 with terratogenic effects e.g. Anti-arrythmics and ACE inhibitor.
   b). Obstetric history –
           i.    Number of times the patient conceived
           ii.   Number of times pregnancy was carried to term
           iii.  Number of abortions (spontaneous or therapeutic)
           iv.   Number of living children, their ages and the age of the last child delivered.
           v.    The time interval between successive pregnancies/abortions
           vi.   Mode of delivery (vaginal,forceps assisted, or caesarean)
           vii.  Development of edema legs, hypertension or seizures in the antenatal or postnatal period
                 (seizure within 48 hours of delivery is due to pregnancy induced hypertension, beyond
                 48 hours may be due to cerebral venous sinus thrombosis )
           viii. Presence of impaired glucose tolerance in the course of pregnancy or history of having
                 given birth to a large baby may give a clue to the presence of diabetes mellitus in the
                 patient.
           ix. History of abortion, premature deliveries would point to possibility of genetic
                 abnormalities in fetus
   c). Certain interventions if planned are best suited to be performed in second trimester e.g. BMV in
       severe mitral stenosis.

Importance of treatment history:
                 This should include all previous medical and surgical treatment and also any medication
                  that the patient may be continuing to take to the present date.
                 Details of drug taken, including analgesics, oral contraceptives, psychotropic drugs and
                  of previous surgery and radiotherapy are particularly important.
                 It is important to find out if the patient is allergic to or had experienced any untoward
                  reactions to any medication that he may have consumed previously, so that the same
                  medication can be avoided in the patient in future and the patient is also apprised of the
                  same.
                 Knowledge of any current therapy that the patient may be on is necessary in order to
                  avoid adverse drug reactions, when new drugs are introduced by the consulting doctor.




                                                      INDEX
INSTRUMENTS:                                                                      Page

      Endotracheal tube                                                          1
      Tracheostomy tube                                                          2
      Ambu bag                                                                   4
   Air way                                   4
   Oxygen mask                               4
   Nebuliser chamber                         4
   Metered dose inhaler                      4
   Space haler                               5
   Rotahaler                                 5
   Nelson‘s inhaler                          5
   Mouth gag                                 5
   Tongue depressor                          5
   Trocar and canula                         6
   Simple rubber catheter                    7
   Foley‘s self retaining catheter           7
   Malecot‘s catheter                        8
   Condom catheter                           8
   Urosac bag                                8
   Naso-gastric tube                         8
   Ryle‘s tube                               8
   Infant feeding tube                       11
   Stomach tube                              11
   B D needle                                11
   Tuberculin syringe                        11
   Insulin syringe                           12
   LP needle                                 13
   Sternal puncture needle                   24
   Liver biopsy needle                       28
   Tuning fork                               30
   Hammer                                    30
   Scalp vein set                            31
   Vein flow catheter                        31
   Paracentesis abdominis                    34
   Paracentesis thoracis                     35
   Pericardiocentesis                        37
   Parenteral fluid                          40
   ORS                                       43
   Feeding bottle                            46



                                      INDEX

SPECIMENS:                                    Page
Lung
 Bronchogenic carcinoma                      48
 Cavity                                      48
 Lobar pneumonia             48
 Broncho-pneumonia           49
 Lung abscess                49
 Pulmonary tuberculosis      49
 Bronchiectasis              50
Kidney
 Acute glomerulonephritis    50
 Large white kidney          50
 Flea bitten kidney          51
 Small granular kidney       51
 Polycystic kidney           52
 Hypernephroma               52
Nervous system
 Meningitis                  52
 Cerebral abscess            53
 Rheumatic heart disease     53
 Bacterial endocarditis      53
 Pericarditis                54
 Atherosclerosis             54
 Syphilitic aortitis         54
Liver
 Cirrhosis of liver          55
 Amebic liver abscess        55
 Pyogenic liver abscess      55
 Hepato-cellular carcinoma   55
 Secondary carcinoma liver   55
Intestine
 Tuberculosis of intestine   56
 Typhoid ulcer               56
 Amebic ulcer                56
 Bacillary dysentery         56

				
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