Dr. Sandeep B S discusses the imaging findings of sarcoidosis in various organs. On thoracic CT, typical findings include bilateral hilar and right paratracheal lymphadenopathy, as well as peribronchovascular and subpleural lung nodules. Cardiac MRI can detect myocardial inflammation and scarring from sarcoidosis with high sensitivity and specificity. Hepatic and splenic sarcoidosis may appear as nodules or periportal adenopathy on abdominal imaging. Neurosarcoidosis can involve the leptomeninges, cranial nerves, dura, or spine. Bone sarcoidosis may cause lytic lesions, while musculoskeletal sarcoidosis can result

1. Dr. SANDEEP B S
ASSOCIATE CONSULTANT
APOLLO BGS HOSPITAL

2. THORAX
ABDOMEN
CNS
MSK

3. THORACIC
SARCOIDOSIS
Nodes
Lung
Cardia

4. Lymphadenopathy -typical patterns
 Most common .
 Bilateral symmetric hilar and right paratracheal lymph
node enlargement- in ~ 95%.
 Left paratracheal , subcarinal, AP window, prevascular
nodes in ~ 50%.
 DD- TB , Lymphoma.

5. 1
2
3

7. Right paratracheal
Left paratracheal
AP window
Left hilar
Bilateral hilar
Subcarinal
Homogenous enhancement
No necrosis

8. Lymphadenopathy- Atypical
patterns
 Asymmetrical hilar involvement
 Unusual locations (internal mammary, paravertebral,
and retrocrural regions).
 Isolated unilateral hilar lymph node (usually on the
right side) - < 5% of cases.
 Calcification - amorphous, punctate or eggshell-like (
TB, Histoplasmosis, Silicosis)

10. Lung manifestations - Typical
 1. Perilymphatic nodules
2-4mm round nodules
Peribronchovascular , subpleural interstitium
>> interlobular interstitium.
Bilateral symmetrical
Upper and mid zone predominance.

13. Typical lung features
 2. Bilateral perihilar opacities
Areas of consolidation with irregular edges.
Radiate from the hilum towards the periphery.
Accompanied by micronodules.

15. Bilateral parahilar opacities

16. Typical features
 3.Chronic Fibrotic changes (in 20% of patients)
Follow large airways in perihilar region
Linear opacities
Traction bronchiectasis
Architectural distortion (displacement of fissures
and bronchovascular bundles).
Upper and midzone predominance
 4.Pulmonary hypertension in extensive fibrosis.

18. Lung features- Atypical
 1.Pulmonary masses
15%–25% of patients
Ill-defined irregular opacities measuring 1–4 cm in
diameter .
Multiple and bilateral.
Small micronodules surrounding them – “Galaxy
sign”.
Multiple cluster of micronodules- “Cluster sign”.
DD- Other granulomatous disease, malignancy

19. Sarcoid
galaxy
Sarcoid cluster

20. Atypical features
 2.Patchy GGOs
40% of patients
Confluence of multiple micronodules and fibrotic
interstitial lesions.
Not an isolated finding .
Always on a background of perilymphatic nodules and
other findings.

21. Patchy GGOs –
Peribronchovascular,
sublpeural
Fibrosis,traction
bronchiectasis
Subpleural, fissural nodules
GGOs

22. Atypical lung features
Fungal ball within a cavity

23. Small Airway Abnormalities
Small airway involvement by granulomas /
fibrosis narrowing of lumen  Air trapping
(Multiple small areas of low attenuation).
Expiratory CT- Mosaic attenuation

24. Endobronchial
soft tissue
Partial segmental atelectasis

25. Rare features
 Pleural effusion
Transudative/ Exudative/ Chylous.
Minimal , resolve over 2-3 months.
 Pleural plaques
 Miliary nodules

26. Siltzbach staging /classification

27. Siltzbach staging
 Developed before the introduction of CT.
 CT/ HRCT is far more sensitive than chest radiography
in depicting subtle parenchymal abnormalities in early
stages of the disease, even in stage 1.

28. HRCT- Reversible vs irreversible
 Reversible / Inflammatory
signs
Nodules
Airspace consolidation
Ground-glass opacities
 Irreversible changes
Architectural distortion
Traction bronchiectasis
Honeycombing , cysts, bullae
Volume loss in upper lobes
Mycetoma within a cavity

30. Is it TB or Sarcoidosis ??
 Similar clinicoradiological manifestations.
 Uncommon manifestations of TB may be commoner
than typical presentation of Sarcoidosis.
 Differentiating the two is important as treatments are
different.
 CT plays a major role .

31. Well defined
Discrete
Homogenous
enhancement
Conglomerate
Necrotic
Rim enhancement
SARCOIDOSIS
TB
Vs

33. SARCOIDOSIS TB
 Peribronchovascular,
subpleural
 Consolidation- less
common
(peribronchovascular/
UZ, MZ)
 B/l parahilar mass-like
 Non necrotic LNs
 Centrilobular,
miliary, random.
 Consolidation- more
common(Apico-post
UL, Supr seg of LL)
 Less common
 Necrotic LNs

35.  Asymptomatic throughout life.
 Few present with nonspecific features–
Conduction disorders
Congestive heart failure
Ventricular arrhythmias
Sudden cardiac death.

36.  Demonstration of non caseating granulomas in
Endomyocardial biopsy is the criterion standard.
Invasive.
Small tissue sample taken from right side
Diagnostic yield is ~30%.
Cannot give data on distribution of disease.
 CMR has good sensitivity (75-90%) and specificty (70-
80 %) for diagnosis

37. Important sequences
 T2 weighted sequence (water sensitive sequence)-
For detecting edema – bright signal
 Late Gad enhancement sequence-
10 min post contrast injection
Gad is an extracellular contrast
Accumulates in areas of increased extracellular space-
inflammation and fibrosis.
For detecting active inflammation and scars .

38. LVRV IVS
Enhancement patterns
LVRV
IVS, LV free wall and RV free wall are most common sites of
involvement

39. 1.Acute myocardial inflammation
 Granulomatous
infiltration of myocardiu
Myocardial edema
Myocardial thickening,
T2 hyperintense signal,
Late Gad enhancement

40.  Patchy mid myocardial
enhancement
 Septum

41. Mid myocardial patchy LGE

43. 2.Post inflammatory pattern
 Replacement fibrosis / scar.
 Loss of myocytes  Increase in extracellular space 
Late gadolinium enhancement.
 Mid myocardial , subepicardial region .
 Associated with myocardial thinning.

44. Mid myocardial LGE in IVS

45. Importance of LGE
 Extent of LGE is an important prognostic marker .
 Strongest independent risk factor for sudden cardiac
death.
 LGE > 20% of LV mass is a strong predictor of life
threatening arrythmias, cardiac failure .

47.  Liver
 Lymphnodes
 Spleen
 Gastro-intestinal tract (very rare )

48. Hepatic sarcoidosis
 50-75% of pateints.
 Hepatomegaly
 Focal parenchymal nodules
 Periportal soft tissue (granulomas)
 Associated with splenic nodules, portal adenopathy.
 Biliary duct involvement - strictures

49. Nodules
Periportal LNs
Splenic nodules
Periportal hypodensity

50. Splenic sarcoidosis
 25-50% of patients.
 Splenomegaly
 Multiple hypodense nodules
 Isolated splenic involvement is more common than
isolated hepatic involvement.
 DD- TB, fungal infection, secondaries, lymphoma

51. T2 Hypointense lesions
Metastases / other
inflammatory lesions-
Hyperintense
No enhancement

52. Abdominal adenopathy
 2 or more nodes with SAD of >1cm
 ~30% of patients
 Periportal, periceliac, mesentric, paraaortic.
 Retrocrural and pelvic nodes- less common ( more
common in Lymphoma).

53. Periportal, periceliac nodes
Extrinsic bile duct
compression

55.  5-10% of patients with systemic sarcoidosis.
 Facial nerve paralysis
 Vision loss
 Headache, seizure, and signs of meningeal irritation

56. 1.Leptomeninges
 Most typical, 40%.
 Enhancing thickening with predilection to basal
meninges.
 Spread along the leptomeninges into parenchyma.

57. Basal meningeal ,
Sylian fissural
Enhancement.
DD-
TB
Lymphoma
Metastases

58. 2. Pitutary- Infundibulum
 Features of Diabetes insipidus.
 DD - Histiocytosis

59. 3.Cranial nerves
 7th , 2nd and 5th cranial nerves – mc.
 Isolated finding / along with leptomeningeal
involvement.
 MRI- neural/ perineural emhancement

62. 4.Dura
 Focal dural masses/ diffuse dural thickening.
 T2 hypointense lesions, show enhancement.

63. FOCAL DURAL INVOLVEMENT
DDs – Metastases/ Meningiomas.

64. DIFFUSE DURAL INVOLVEMENT
DDs-
Lymphoma ,
Idiopathic pachymeningitis.

65. Spine
 Leptomeningeal and dural – mc
 Intramedullary – relatively less common

67. Parenchymal nodules
Nerve root enhancement

69.  1% – 13% of sarcoidosis patients.
 Osseous lesions (small >>large bone sarcoidosis)
 Sarcoid arthropathy.
 Sarcoid myopathy.

70. Small bone sarcoidosis
 Bones of hands and foot.
 Lace like lytic appearance
(honeycombing)
 Punched out lesions
 Pathological # and bone
collapse

72. Sarcoid Arthropathy
 Arthralgia due to
cytokines
 Lofgren’s syndrome
 Polyarticular ( Knee,
ankle, wrist, elbow, PIP)
 Self-limiting
 X ray- osteopenia, soft
tissue swelling
 Granulomatous
arthritis, synovitis
 2 or more joints (Knee,
ankle, PIP )
 Chronic relapsing course
 X ray- Mild joint space
narrowing, subchondral
cysts

73. Role of MRI
 Synovitis
 Tenosynovitis
 Bursitis
 Tendonitis
 Findings are non- specific .
 USG can also pick these lesions

74. Sarcoid Myopathy- Nodular
 Soft tissue nodular masses
 Multiple, bilateral
 Lower limbs

75. Sarcoid Myopathy - Diffuse
 Proximal muscle atrophy
with fatty replacement
 Post treatment
corticosteroid myopathy-
similar imaging
appearance.

76. Role of PET in Sarcoidosis
 PET is a metabolic study which shows areas of
increased metabolism as bright spots (infection,
inflammation, malignancy ).
 Not useful for diagnosis of Sarcoidosis.
 Used to assess the activity in proven cases of
sarcoidosis / for follow up.

77. PRE TREATMENT
POST TREATMENT

78. TAKE HOME POINTS
 B/l hilar and right paratracheal LNs.
 Peribronchovascular / subpleural nodules.
 Very important to differentiate from TB.
 CMRI is powerful tool to assess cardiac sarcoidosis /
risk stratification .
 PET – useful to assess the activity and response to
treatment .

79. References
 Pulmonary Sarcoidosis: Typical and Atypical Manifestations
at HighResolution CT with Pathologic Correlation .
RadioGraphics 2010; 30:1567–1586 .
 Radiologic Manifestations of Sarcoidosis inVarious Organs.
RadioGraphics 2004; 24:87–104.
 Dilemma of diagnosing thoracic sarcoidosis in
tuberculosisendemic regions: An imaging-based approach.
Part 1. Indian J Radiol Imaging2017;27:369-79.
 Cardiac Sarcoidosis: Spectrum of MRI Features. AJR
2005;184:249–254 0361–803X/05/1841–249

80. THANK YOU