Imaging of salivary gland pathologies by Dr. Bishnu Khatiwada

1. IMAGING OF SALIVARY GLAND
PATHOLOGIES
DR. BISHNU KHATIWADA
2ND YEAR RESIDENT, MDRD
NAMS

2. Presentation Outline
• Anatomy
• Neck spaces
• Imaging modalities
• Common pathologies of salivary glands
• Salivary gland neoplasms

3. ANATOMY
• CONSISTS OF MAJOR AND MINOR SALIVARY GLAND
• 3 MAJOR SALIVARY GLAND. ALL BRANCHED TUBULOALVEOLAR
GLAND.
• PAROTID GLAND-SEROUS-STENSENS DUCT-ABOVE THE 2ND MOLAR
TOOTH. 25% OF TOTAL
• SUBMANDIBULAR- MIXED SEROUS AND MUCUS-PREDOM- SEROUS-
ON EACH SIDE OF FRENULUM-WHARTSONS DUCT- 70% OF TOTAL
• SUBLINGUAL-MIXED SEROUS AND MUCUS- PREDOM(MUCUS)-
MULTIPLE DUCT -5% OF SECRETION

4. SPACES OF THE NECK
• PAROTID SPACE- PAROTID
GLAND, RETROMANDIBULAR
VEIN FACIAL NERVE, EXTERNAL
CAROTID ARTERY, 20- 30 LNS
IN PAROTID GLAND (METS
FROMSCALP,EAC AND FACE)
PAROTID GLAND DIVISION-
SUP VS DEEP-PLANE-FACIAL
NERVE-PLANE BETWEEN BACK
OF MANDIBULAR RAMUS AND
RETROMANDIBULAR VEIN.
• PARAPHARYNGEAL SPACE-
EXTENSION-(SKULL BASE-
SUPERIOR CORNU OF HYOID),
• CT- TRIANGLE OF FAT
• MINOR SALIVARY GLANDS.
• PRIMARY PATHOLOGY-
UNUSAL
• EXTENSION OF PATHOLOGY
FROM PAROTID SPACE CAN
OCCUR

5. SPACES

6. Imaging modalities
• Plain x-ray
• Sialography
• USG
• CT
• MRI
• Radionuclide studies

7. Plain films
• Anteroposterior (normal & soft-
tissue exposure), tangential, lateral
and lateral oblique plain radiographs
 calculi & soft-tissue swelling of
parotid gland.
• Submandibular gland lateral
oblique view.
• Suppl emented by lateral view with
pt's finger in mouth, depressing
tongue & pushing submandibular
gland into sight beneath mandible.
• Stones in anterior part of duct are
best demonstrated by placing occlusal
film in mouth & submentovertical
type of projection
Lateral plain film (A) with
the patient’s index finger
depressing the tongue
Intraoral Occlusal film (B)
shows a large calculus in
Wharton’s duct.

8. Sialography - Conventional
• Performed on parotid &
submandibular glands
• Retains role in chronic inflammation &
autoimmune disease in parotid &
submandibular glands.
• Contraindicated in acute sialadenitis
for fear of exacerbation by:
 retrograde inj of contrast agents force
inflammatory products into more
peripheral parenchyma
 Instrumenting duct may irritate it,
cause narrowing from posttraumatic
edema or stricture formation & lead to
reduced drainage
 MR sialography safe in acute
sialadenitis
• Immediate & post secretory films (to
diagnose sialectasis)
Parotid
Submandibular

9. Ultrasound
• Parotid and submandibular glands are examined
using a 7.5 MHz or higher frequency linear array
transducer with patient's chin turned away from
side being examined.
• Useful for superficial salivary gland lesions
• Homogenous, echogenic (marked to slightly
compared to adjacent muscle d/o fat component)
• scattered echogenic streaks produced by branch
ducts converging to join main duct.
• Parotid: the external carotid artery and
retromandibular vein can both be seen, allowing
the position of the facial nerve to be inferred.

10. Parotid- transverse view
1. Retromandibular
vein
2. External carotid
artery
3. Echo from the
surface of the
mandible,
4. Parotid gland
5. Masseter muscle

11. Parotid- longitudinal view
1 Retromandibular
vein
2 External carotid
artery
4 Parotid gland

12. Stensen’s/ Stenon duct
1 parotid gland, 2 Stenon
duct, 4 masseter muscle, 5
surface of the mandible,
6 buccal muscle, large
arrow retromandibular vein
and external carotid
artery.
A nondilated duct is
usually not visible during
US examination.

13. Submandibular gland- oblique US

14. • Major advantage both parenchymal fuction & excretion
fraction of both parotid and submandibular glands can be
quantified simultaneously
• Normally conc 99mTc pertechnetate generalized
decreased uptake with aging
• Hyperfunction acute sialoadenitis, granulomatous
disease, lymphoma, and sialosis.
• Hypofunction Sjogren’s syndrome, most primary &
metastatic tumors; viral sialadenitis causes generalized
decreased uptake, and ductal obstruction can be estimated
by degree of prolongation of secretory phase of
radionuclide study.
• Most often examined lesions are those that are suspected
of highly concentrating 99mTc i.e. Warthin’s tumors and
oncocytomas. Role of scintigraphy usually limited to
confirming clinical dx of Warthin tumors in patients with
multiple parotid masses
Radionuclide Studies
Oblique frontal technetium
sialogram shows multiple masses
with intense uptake in both
parotid glands. This patient had
bilateral Warthin's tumors.
Panda sign

15. CT and MRI
• Parotid & submandibular salivary glands well
demonstrated
• Parotid glands variable amounts of fatty
stroma lower CT attenuation (-25 to +15 HU)
than adjacent muscles, lymph nodes & vessels
(increasing fatty infiltration with age)
• Higher density of gland in childhood not be
misinterpreted as pathology.
• Submandibular glands have higher attenuation
than parotid glands but still easily distinguished
from adjacent musculature.
• Sublingual & minor salivary glands line upper
aerodigestive tract are not routinely visualised.
The minor salivary glands may give rise to masses
in the parapharyngeal space.

16. CT &MRI
• Some advocate MR as first (and only)
technique to evaluate neoplasm of major
salivary glands
• If there is even a slight chance that mass may
in some way be related to sialolithiasis, CT
should be recommended first, since MR
imaging is not as reliable in detecting small
calculi, and ‘‘pseudomasses’ may accompany
sialolithiasis.
• Virtually all parotid lesions are well visualized
on T1WI because of hyperintense (fatty)
background of gland . T1WI gives excellent
assessment of tumour margin, its deep
extent, and its pattern of infiltration. (CT for
inflammatory lesion; MR for neoplastic
lesion)

17. Pathology
Obstructive & inflammatory lesions:
• Sialolithiasis
• Acute parotitis including sialdenitis
• Chronic sialdenitis
• Sialosis
• Strictures
• Sialectasis
• Ranula
Neoplastic:
• Adenoma
• Carcinoma
Systemic Conditions with Salivary Gland Involvement:
• Infectious
• Viral
• Metabolic

18. Sialolithiasis
• Formation of concrements (sialoliths)
inside ducts or parenchyma of salivary
glands.
Submandibular gland- 80-90%
(secretion: more thicker, viscous,
alkaline; Wharton: dependent gland,
uphill course, wider lumen, tight
orifice)
Parotid gland-10-20%
Sublingual gland-1-7%
Minor salivary gland – rare (often in
upper lip and buccal mucosa)
• 75% stones solitary; 25% multiple.
• In patients with chronic sialadenitis, at
least one calculus is present in two thirds
of the cases.

19. Plain film
• Able to visualise only 80-90% of
submandibular stones & approx
60% of parotid duct stones,
presumably due to differences in
composition of secretion of parent
glands
• Oblique views often required to
project stones away from adj.
bone & teeth.
• For plain film (and CT), differential
is that of other calcific foci:
 Haemangioma / phlebolith
 Atherosclerotic calcification

20. Sialography
• Delineates exact size &
location of stones within
salivary gland ducts.
• Stone visualised as filling
defect within duct. In some
cases, contrast will not be
able to pass beyond stone.
• CI if active infection is
suspected,
• Filling defects on sialography,
DDx:
Injected bubble of air
Tumour
Blood clot
FILLING
DEFECT

21. Ultrasound
• Able to visualise radiolucent
stones
• Stone: strongly hyperechoic
lines or points with distal
acoustic shadowing; small
stones (<2mm) may however
not shadow
• Acute obstructive cases, gland
appears enlarged & excretory
ducts proximal to stone may
be visibly dilated.
• Examination is best performed
with small high frequency
intra-oral probes
Fig. Stone in
submandibular duct
causing proximal duct
dilatation.

22. CT
• NECT: Excellent at visualizing
stones both within duct &
within gland
• CECT: Additionally assess
gland (although not as well
as MRI)
• Acute obstruction: gland
enlarged, hyperdense & a/w
stranding & enhances on
contrast
• Chronic cases: fatty atrophy,
parenchyma replaced by fat.
Stenson’s Duct
Wharton’s Duct

23. MRI
• Visualize larger stones, map ductal anatomy &
assess gland
• Acute obstruction: enlarged glands &
inflammatory changes:
 T1 : reduced signal compared to other side
 T2 : increased signal (best seen on fat
suppressed sequences)
• Chronic: gland is reduced in size & fatty atrophy :
 T1 : increased signal compared to other side
 T2 : reduced signal of gland parenchyma
which is itself reduced in amount
Submandibular calculi (a) Transverse T1WI: two areas of
low SI (arrows) in mouth floor on left. (b) Confirmed on
transverse T2WI: obstructed duct (arrowhead) is evident

24. Acute parotitis inc sialadenitis
• Etiology: viral, mumps, EBV, CMV,
sialolithiasis, Staphylococcal and
streptococcal (infections may
develop in debilitated, dehydrated
patients with poor oral hygiene),
tuberculosis, candidiasis and cat
scratch disease.
US:
• Enlarged & round edges
• Hypoechoic, may be
inhomogeneous rough echotexture;
may contain multiple small, oval,
hypoechoic areas
• May have increased blood flow.
• Enlarged lymph nodes with
increased central blood flow

25. CT: swollen gland, increased enhancement,
surrounding inflammatory stranding & local
lymphadenopathy.
MR: increased signal on T2WI
Complications:
Abscess (avascular area with irregular enhancing
rim, on US hypo to anechoic lesion with irregular
margins with pos. enhancement & increase
peripheral vascularity, can see mobile internal
echoes, gas)
Deep parotid infection may extend to
parapharyngeal space

27. Chronic Sialadenitis
• intermittent swelling often painful,with or
without a/w food intake
US:
normal sized or smaller
coarse echotexture
hypoechoic & inhomogeneous.
Small cystic echo free domains.
Usually no increased blood flow.
Occasionally intraglandular concretions.

29. Chronic sclerosing sialdenitis
Aka Kuttner Pseudotumour
• Predominantly seen in submandibular glands & in adult
females.
• firm on palpation and are therefore easily mistaken as
‘tumour’ on clinical examination and also referred to as
cirrhosis of the submandibular gland.
• US- well-defined, hypoechoic areas involving part of one or
both submandibular glands with geographical pattern and
rounded contour. Doppler reveals hypervascularity of the
involved areas without vascular displacement.
• The characteristic sonographic appearances usually suffice
to support the diagnosis without the need of an FNAC.

31. Kimura Disease
• Chronic inflammatory condition
predominantly affecting young Asian male
patients.
• Characterized by unilateral, painless, slowly
enlarging intraparotid lymphadenopathy
often affecting the neck.
• The adjacent parotid parenchyma may be
heterogenous in appearance.

33. Ranula
• Aka mucous escape cyst/mucous retention
cyst/mucocele of sublingual or neighboring
minor salivary glands
• High in T2WI & no enhancement in Fat Sat
T1C+
• Types: Simple vs Plunging

34. Simple Plunging/pseudocyst
Relation to mylohyoid
muscle
Superficial Plunges through
mylohyoid
Epithelium lined Yes No
Surgical approach transoral-
resection/marsupialisati
on
transcervical
Risk of Nerve damage
(lingual/CN XII)
Yes No

36. Sialosis
• Diffuse, non-inflammatory, non-
neoplastic recurrent enlargement
of major salivary glands
• Common causes: diabetes mellitus
& alcoholism; malnutrition,
hormonal insufficiency and
radiation therapy
 enlarged hyperechoic glands
without focal lesions or increased
blood flow

37. Strictures
• Usually result from a combination
of obstruction & infection
• Strictures involving main parotid
or submandibular duct may be
single or multiple.
• Site - orifice of parotid or
submandibular duct - result of
trauma from ill-fitting dentures,
Cheek biting
• Ducts proximal to stricture dilate
& contrast medium is retained on
postsialogogue film.
• Localized strictures can be dilated
using a guide-wire and a small
balloon catheter
PAROTID DUCT
STRICTURE
BALLOON DILATATION
POSTPROCEDURE

38. Sialectasis
• Change in calibre of salivary ducts & is most often
caused by a stricture or stone.
• Causes -past infection in childhood or if there is
Sjogren's syndrome, RA, SLE, scleroderma
• Sialectasis varies in severity:
Punctate sialectasis: punctate glandular
collections (<1mm)
Globular sialectasis: collections of 1-2mm in size
with intraglandular ducts that are irregular,
deformed & sparse
Cavitating sialectasis results from coalescence of
globules into cavities
Destructive sialectasis contrast medium
extravasates into large cavities

39. Punctate sialectasis Globular sialectasis
Cavitating and destructive sialectasis Ultrasound

40. Salivary gland Neoplasms
ADENOMAS (65%)
• Pleomorphic adenoma
(mixed parotid tumour) -
50%
• Adenolymphoma
(Warthin's tumour) - 10%
• Basal cell (monomorphic)
adenoma - 3%
• Myoepithelioma - 1%
• Oncocytoma -1%
CARCINOMAS (35%)
• Mucoepidermoid tumour-
15%
• Adenocarcinoma - 7 %
• Adenoid cystic carcinoma
- 3%
• Acinic cell carcinoma – 6%
• Carcinoma in mixed
tumour – 3%
• Undifferentiated
carcinoma – 1%

41. • Enlarging mass- painful or not
 Painful obstructive/inflammatory
 Painless neoplasm, cyst, LN
• Neoplasm: Benign vs malignant
(Regional Lymphadenopathy; facial N palsy, Skin
infiltration, deep infiltration into the parapharyngeal
space, muscles, and bone, well seen on T1WI; low to
intermediate SI on T2WI (25% error), ill defined
margins, diffuse growth favor malignancy)
• The smaller the salivary gland, the higher the rate of
malignancy.
 20%–25% in parotid gland
 40%–50% in submandibular gland
 50%–80% in sublingual glands & minor salivary glands
• Multiple parotid masses: Lymphadenopathy, Warthin

42. Commonest benign Commonest malignant
Parotid (B>>M) Pleomorphic adenoma Mucoepidermoid Ca
Submandibular (B>M) Pleomorphic adenoma Adenoid cystic Ca
Sublingual & minor (M>B) Pleomorphic adenoma Adenoid cystic Ca

43. Pleomorphic Adenoma (Mixed Tumor of Salivary Glands)
• Most common salivary gland tumour
• 70 - 80% of benign salivary gland tumour
• Middle age women
• Prior head & neck irradiation is a risk factor
• Typically present with a smooth painless enlarging mass.
• Distribution
 Parotid gland: 84% (commoner in the superficial
lobe)
 Submandibular gland : 8%
 Minor salivary glands : 6.5% (widely distributed
including the nasal cavity, pharynx, larynx, trachea)
 Sublingual glands : 0.5%
• Also commonly found in lacrimal glands (approx 50% of
lacrimal gland tumours)

44. 80% rule of parotid gland
• 80%-Tumour of parotid gland are benign.
• 80% benign tumour of parotid gland are
pleomorphic adenoma.
• 80% salivary gland pleomorphic adenoma occur
in parotid gland.
• 80% parotid pleomorphic adenoma occur in
superficial lobe.
• 80% untreated pleomorphic adenoma remain
benign and 20% ultimate undergo malignant
change.

45. Pathology
• Wide cytomorphologic and
architectural diversity.
• 3 components:
 Epithelial cell component
 Myoepithelial cell component
 Stromal (mesenchymal) component
• Types-
1. Myxoid.
2. Cellular
3. classic

46. USG
• Typically hypoechoic with
lobulated distinct border
with posterior acoustic
enhancement+
calcification
• Vascularization in
pleomorphic adenomas is
often poor or absent (even
when the sensitive power
Doppler mode is used)

47. CT
• Most small benign mixed
tumors smoothly marginated,
spherical tumors & higher
attenuation than surrounding
parotid parenchyma.
• Larger masses most often
nonhomogeneous appearance,
with sites of lower attenuation
representing areas of necrosis,
old hemorrhage, and cystic
change. Small regions of
calcification are common.
• Larger tumors tend to develop a
lobulated contour highly
suggestive of the diagnosis
• All of these tumors enhance
variably on contrast-enhanced
studies.
C+ DELAYED PHASE
C+ EARLY PHASE

48. MRI
• Well-circumscribed
homogeneous when small;
heterogeneous when larger
• T1: low SI
• T2:
– Usually very high SI (esp
myxoid type)
– Often rim of low SI on T2WI
(surrounding fibrous capsule)
• T1 C+ (Gd) : usually
homogeneous
enhancement
T1
T2 T1 C+

50. Treatment & prognosis
• Surgical excision is curative, however as
tumour is poorly encapsulated (despite
imaging suggesting otherwise), there is a
significant rate of recurrence (1-50%)
• Percutaneous ultrasound biopsy (both FNAC
and core biopsy) can be performed safely and
a/w very low tumour seeding rates & without
facial nerve injury provided meticulous
technique is used

51. Complications
• Small risk of malignant transformation into
carcinoma ex pleomorphic adenoma which is
proportional to time the lesion is in situ (1.5% in
first 5 years, 9.5% after 15 years), thus excision is
recommended in essentially all cases.
• Additional risk factors for malignancy include
advanced age, large size, radiation therapy and
recurrent tumours.
• True malignant mixed tumours
• Metastasising pleomorphic adenoma (rarest). It
presents with metastases to lung bone and soft
tissues despite having 'benign' histology .

53. Warthin tumour (adenolymphoma)
• Aka papillary cystadenoma lymphomatosum
• Second most common benign tumour
• Occurs virtually only in parotid gland (superficial part, tail) &
is thought to arise from heterotopic salivary tissue trapped
within a regional lymph node during embryogenesis
• 5th-6th decade males
• Smoking and development of Warthin tumors related
• Bilateral in up to 15% of cases.
• most common lesion to manifest as unilateral, multifocal
masses and is the most common salivary neoplasm to
manifest as multiple masses in one or both parotid glands
• Lower attenuation than pleomorphic adenoma & more
homogeneous on MRI. They may be multifocal.

54. At US, Warthin tumors are oval,
hypoechoic, well-defined tumors
and often contain multiple
anechoic areas . Warthin tumors
are often hypervascularized. No
calcification.
Multiple or bilateral parotid or
periparotid masses strongly
suggest the diagnosis

56. • Role of scintigraphy is usually
limited to confirming clinical
diagnosis of Warthin tumors in
those patients with multiple
parotid masses.
• unique in that they (including
oncocytoma) show increased
radiotracer uptake at
technetium pertechnetate
imaging
• No malignant potential
course of observation (no
aggressive management)

57. Benign masses
• Other benign tumors (eg, oncocytoma, basal cell
adenoma) occur less frequently in the salivary
glands.
• Haemangioma
• Lymphangioma
• Branchial cleft cysts: rare but may occur
superficial to, within, or deep to the parotid
gland.
• Among nonepithelial lesions, lipomas, and
neuromas or schwannomas may be found in
salivary glands

58. Mucoepidermoid carcinoma
• All adult age groups, most common in middle age (35-
65 years)
• Most common malignant salivary gland tumour of
childhood
• In the parotid gland they are the most common
malignant primary neoplasm (Vs Adenoid cystic Ca in
submandibular gland and sublingual gland).
• A slight female predilection has been described, and
radiation has been implicated as a risk factor .

59. Clinical presentation
• Most frequently arise in parotid gland, and presents as a
painless swelling, with or without facial nerve
involvement.
• Overall distribution across various glands is as follows
Minor salivary glands : ~ 50%
Palate : most common
Retromolar area
Floor of the mouth
Buccal mucosa
Lip
Tongue
Other : anywhere in the proximal
aerodigestive tract, the lacrimal glands and
even in the bronchi
Major salivary glands : ~ 50%
Parotid gland : ~ 40%
Submandibular gland : ~ 7%
Sublingual gland : ~ 3%

60. CT
• Low grade tumours: well
circumscribed, cystic
component
• High grade tumours:
poorly defined , solid
infiltrate locally
• Solid components
enhance, and
calcification is
sometimes seen.
• Low grade tumor
appears similar to
benign mixed tumours.

61. MRI
• Low grade tumors: similar
appearances to benign mixed tumours
 T1 : low to intermediate signal ;
low signal cystic spaces
 T2 : intermediate to high signal ;
cystic areas will be high signal
 T1 C+ (GAD) : heterogeneous
enhancement of solid components
• High grade tumors:
 T1 : low to intermediate signal
 T2 : intermediate to low signal

62. Adenoid Cystic Carcinoma
• Although slow growing, tendency to invade perineural
space (50-60%)
• most painful salivary gland neoplasm, Pain & mass over
several years
• Stubbornly recurrent.
• 3% of all salivary gland tumors
• Most commonly in parotid, submandibular gland &
palate.
• Very wide age range (1st-9th decade)
• F:M=3:2.

63. Imaging studies
• Parotid lesions: appear as benign, well-delineated
tumors
• Minor salivary gland neoplasms: usually have
malignant infiltrative margins
• Retrograde tumor extension to skull base often
occurs via facial nerve or mandibular nerve (MRI)
Indirect signs of perineural spread :
1. Foraminal enlargement on CT
2. Atrophy of muscles of mastication (in
mandibular nerve infiltration)
3. Obliteration of the normal fat plane in
the pterygopalatine fossa (in maxillary
nerve infiltration).
Direct signs of perineural spread:
1. Thickening & enhancement of affected
nerves (with attention also paid to
possible skip lesions).
2. Abnormal enhancement in Meckel's
cave.
3. Lateral bulging of the cavernous sinus
dural membrane.

64. T2 T1 C+ Fat sat

65. Lymphoma
• Approx 1-5% of malignant tumours of major salivary
glands
• Often difficult to determine if parotid lymphoma has a
nodal or extranodal origin.
• Most are extranodal NHL arising de novo.
• 60% of Sjogren's syndrome develop NHL
• Benign lymphoid infiltrates of myoepithelial sialadenitis
progress to lymphoma.
• Lymphoma may occur primarily in the parotid gland as
an infiltrative process or adenopathy, or as a
manifestation of systemic disease.

67. Mikulicz’s syndrome/Benign lymphoepitheial lesion
• Parotid (85%) & submandibular(15%).
• Characterised histologically by
lymphocytic infiltration, parenchymal
atrophy and myoepithelial islands.
• Swelling and pain
• Most have Sjogren's syndrome,
autoimmune dis involving lacrimal &
salivary glands, causing
keratoconjunctivitis sicca & xerostomia.
• This benign entity may be difficult to
distinguish from malignant tumours
due to its focal character, contrast
medium enhancement and its irregular
margins

68. Systemic Conditions with Salivary Gland Involvement
Infectious disorders
• Actinomycosis
• Granulomatous
disease (sarcoidosis,
tuberculosis)
Viral infection
• HIV
• Hepatitis
• CMV infection
Metabolic disorders
• Sjögren’s syndrome
• Thyroid disease
• Miscellaneous:
Alcoholism,
Malnutrition, Eating
disorders (anorexia,
bulimia), Diabetes
(uncontrolled)

69. Sjogren Syndrome
• Chronic systemic autoimmune exocrinopathy salivary & lacrimal gland
tissue destruction
• Clinical diagnosis; role of sialography is to STAGE the disease.
• primary or secondary (years after onset of associated rheumatic disorder as
RA, SLE, scleroderma, PBC, etc.
• Imaging appearance stage dependent on presence or absence of lymphocyte
aggregates within parotid
– Intermediate stage: "Miliary pattern" of small cysts diffusely
throughout both parotids
– Late stage: Bilateral enlarged parotids with multiple cystic & solid
intraparotid lesions ± intraglandular calcifications
– Chronic stage: Diffuse atrophy & fatty replacement
• Punctate calcification may be diffusely present in both parotids

70. • Conventional sialography
– Alternating areas of ductal stenosis and dilatation ("string of
beads" pattern)
– Acinar spill into enlarged acini ("apple tree" pattern)
• Increases risk of parotid lymphoma (any dominant mass in a Sjo ̈gren-
affected parotid gland must be considered lymphoma)

73. 1. Findings
2. Diagnosis

74. 1. Findings
2. Diagnosis

75. 1. Findings
2. Diagnosis.

76. References
• Textbook of Radiology and imaging, David
Sutton, 7th edition
• AIIMS-MAMC-PGI Comprehensive Textbook of
Diagnostic radiology, Niranjan Khandewal,
Veena Chaudhary
• CT and MRI of whole body, John R Haaga, 6th
edition

77. Thank You!!