Rotator cuff interval - Anatomy

Rotator cuff interval
Triangular shape. Bordered by:
1. Coracoid process
2. Subscapularis muscle/tendon (SSc)
3. Supraspinatus muscle/tendon (SSp)

Houses:
1. (Intra-articular portion of) Long head of biceps tendon (LHBT)
2. Coracohumeral ligament (CHL) (superficial)
     - Variants: absent CHL
     - Originate from postero-lateral of coracoid process
3. Superior glenohumeral ligament (SGHL) (deep)
     - Variants: absent SGHL

Important structures:
1. Medial-pulley-complex (MPC)
     - Medial bundle of CHL + SSc + SGHL
     - Medial to the LHBT
     *Disruption causes subluxation of the LHBT medially

2. Lateral-pulley-complex (LPC)
     - Lateral bundle of CHL + SSp
     - Lateral to the LHBT

3. Rotator cable (part of lateral-pulley-complex)
     - Suspense and stabilise the shoulder joint
     - Thin fibrous band extension from CHL and some of SGHL
     - Traverse deep to SSp and ISp, superficial to joint capsule

4. Capsulo-ligamentous biceps pulley / Superior-complex layer (SCL)
     - CHL + SGHL + Capsule
     - Forms the roof of intra-articular portion of LHBT (proximal to the transverse humeral ligament)

5. Rotator crescent
     - An area between rotator cable and the SSp insertion
     - Poorly vascularised area
     - Gets thinner with age




Reference: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5568533/

Developmental Dysplastic Hip

DDH:
- Acetabular dysplasia AND/OR ligamentous laxity, resulting in recurrent hip subluxation / dislocation
- Left hip affected more than Right hip

Risk factors for DDH:
1. Breech presentation
2. Female (?estrogen contributing to ligamentous laxity?)
3. Firstborn
4. Family Hx
5. Oligohydramnios , Multiple gestation - abnormal posture due to crowding in-utero

Clinical features:
1. Asymmetric thigh skin folds
2. Shortened leg
3. Decreased hip ROM when Flexed and ABducted
4. Positive Ortolani and Barlow signs

Ultrasound used to assess the hips - the cartilaginous components can be seen. ie not ossified yet

Contraindications to US Hips:
1. Generally avoid if patient <3-4/52 old, as the ligaments are normally lax. Usually done at 6/52 and after.
2. Not suitable after 6mo. Femoral head ossifies, starts around 2-3mo.
Radiographs are a better modality of choice when the bone ossifies (>12mo) - AP radiographs, not frog leg view.

Ultrasound:
Done when patient is relaxed. eg. whilst feeding
Use high-resolution linear probe.

1. Coronal view
Hip slightly flexed. (~15-20degrees)
These structures should be seen, in addition to the femoral head, greater trochanter, acetabular roof.
a. Ossified ilium is horizontally orientated
b. Triradiate cartilage
c. Labrum

Look for:
1. Morphology of the hip joint
2. Coverage of femoral head using the straight ilium line (Position)
3. Alpha angle

2. Transverse view
Hip flexed. (90 degrees)
Look for: Hip joint stability
Visualisation of the hip joint whilst performing
- Barlow maneuvre
- If dislocatin/subluxation present, perform Ortolani maneuvre

Graf system (US hip for DDH introduced by Graf - Orthopaedic Surgeon)
- To grade severity of DDH and appropriate management

Graf system		Acetabular rim	Labrum	Ossified ilium line	Alpha angle
Type I	-	Normal angular	Normal	Crosses >50% of femoral head	>60	Normal
Type IIa	Age: <3mo	Rounded	Normal	Crosses <50% of femoral head, but not displaced	50-59	Physiologic immaturity. Repeat scan in 6-8/52
Type IIb	Age: >3mo	Same finding as IIa				Refer orthopaedic
Type IIc		Same finding as IIa	Everted / horizontal position	Same finding as IIa	43-49
Type IIIa	Normal acetabular roof cartilage	Flattened	-	Displaced (<50%)	<43	Refer orthopaedic
Type IIIb	Abnormalechogenic acetabular roof cartilage	Same finding as IIIa
Type IV	-	Flattened		Complete displacement	<43	Urgent orthopaedic referral

Radiographs:
1. Asymmetric hip joints
2. Asymmetric femoral epiphysis ossification: As a complication of DDH where there is delayed ossification
3. Femoral head crossing the Perkin's line laterally
4. Acetabular angle >30degree
5. Disruption of Shenton's line

Hilgenreiner's line:
Transverse line touching the triradiate cartilage superiorly and bilaterally on AP pelvis view

Perkin's line:
Line perpendicular to Hilgenreiner's line, touching lateral margin of the ossified acetabular roof on AP pelvis view.

Acetabular angle:
Angle between Hilgenreiner's line and the acetabular roof.
Normal: <30degree

Shenton's line:
Smooth curve lining the inferior margin of the superior pubic ramus and the medial margin of the proximal femur.

Putti's triad:
1. Femoral head displace superolaterally
2. Small femoral epiphysis
3. Acetabular angle > 35degrees

Bonescan lesions

3 +/- 1 phase Bone scan
1st phase: Arterial blood flow; immediately after injection
2nd phase: Blood pool (tissue phase) 10min after injection
3rd phase: Delayed phase (Skeletal phase) 2-5hr after injection
4th phase: 24hr delayed phase if renal insufficiency and as a result suboptimal image on 3rd phase

Standard whole body bone scan: Acquire at delayed phase (skeletal phase)
Mechanism: Radiotracer adsorbed on hydroxyapatite matrix of the bone, where the mineral phase is active.

Superscan:
Increased radiotracer uptake of bone in relative to the soft tissue background and (almost) absent renal activity.
Causes:

1. Widespread metastasis in: Breast / Lung / Prostate CA, +/- Lymphoma +/- Bladder CA
2. Metabolic bone disease: Renal osteodystrophy, Osteomalacia, Hyperparathyroidism
3. Myelofibrosis, Systemic mastocytosis

Hot lesions:

1. Fibrous dysplasia
2. Paget's disease
3. Brown tumors
4. ABC (because it is very vascular)
5. Osteoid osteoma
6. Chondroblastoma
7. Metastasis (Osteoblastic activities ie Sclerotic eg Prostate CA mets)
8. Joint diseases
9. Dental infection
10. Acute fracture (after 24 - 48hr)

3 phase positive lesions: (lesions that causes bone remodelling)

1. Osteomyelitis
2. Healing fracture
3. Orthopaedic implant
4. Neuropathic osteoarthropathy

Normal scan: (no increased or decreased uptake)

1. Acute fracture (acute phase)
2. Bone cyst, bone island, exostoses
3. Multiple myeloma ** there for this condition is monitored by skeletal survey radiograph**
4. Osteoporosis

Cold lesions:

1. Radiotherapy
2. Avascular lesion
3. Multiple myeloma 
4. Haemangioma
5. Advanced carcinoma

Varying lesions

Mixed lytic/sclerotic metastasis (Breast, Lung etc) may show hot or cold (with hot margins).

Enostosis - Bone island

Commonly known as bone island

Mature cortical bone within the medulla
Due to failure of resorption during endochondral ossification
Asymptomatic

Features:
CT/Radiograph: 
- Spiculated margin - blends with the surrounding trabecular bone
- Dense sclerotic focus
MR:
- All sequences: Very low SI
Scintigraphy
- Typically no activity. Some may have increased activity

DDx:
- Dense osteoid osteoma
- Osteoblastoma

PVNS

Pigmented villonodular synovitis
- Unknown aetiology
- Synovial proliferation disorder
- intracellular Haemosiderin deposition (thus "Pigmented")

Monoarticular
Age 30-40s

Benign proliferation of synovium in the joint or in bursa/tendon sheath +/- hemorrhagic effusion
If occurs in the tendon sheath => then it is known as Giant Cell Tumor of the tendon sheath

Clinical features:
- Insidious onset
- Monoarticular arthropathy
- Swelling
- Stiffness
- Pain

Pathology:
- Hyperplastic synovium
- Lipid-laden foam cells, histiocytes, giant cells, haemosiderin deposits

Distribution:
- Knee > Hip > Ankle > Shoulder

Radiograph:
- Dense effusion
- Dense soft tissue mass (due to haemosiderin)
- Bone erosion
- Large subchondral cysts
- Preserved joint space
- Typically normal in the early stage

MRI:
- Joint effusion
- Focal / diffuse synovial thickening: Low signal T1w and T2w, and blooming artifact on GRE (due to hemosiderin deposition)

DDx:
- (repeated) Haemarthrosis such as Haemophilics
- Septic arthritis
- Articular amyloid deposition (similar in MRI appearance)

Rx:
- Synovectomy (~50% with local recurrence)

Psoriatic arthritis

Psoriatic arthritis

Polyarticular arthritis
Skin disease: Psoriasis (Skin rash)
Chronic inflammatory
40yo, Caucasian
?Factors involved: Genetic, Immune system, Environmental
HLA-B27 +ve in 60%

Hand:
- Most commonly involved skeleton
- Interphalangeal joint (PIJ, DIJ)
- 'Fluffy periostitis'
- Bony proliferation*
- Joint erosion from articular margin* to centrally.
- Tapering of one end, saucerisation of the other end of the articular surface: Pencil-in-cup deformity
- Preserved bony mineralisation (no osteopenia), ivory phalanx
- Ankylosis
- Diffuse soft tissue swelling: Sausage digit

SIJs:
- Asymmetric sacroiliitis, sclerosis, large erosion
- Ankylosis is UNcommon

Vertebra:
- More commonly involved in MALE
- Asymmetric
- Atlanto-axial subluxation
- Squarring of vertebrae
- Enthesitis: comma-shaped ossification, paravertebral (parasyndesmophytes)
- Thoracolumbar region

Others:
- MTPJ
- TA insertion of the Calcaneum: Fluffy periostitis & Erosion

*HALLMARKS for Psoriatic arthritis

DDx:
- Ankylosing spondylitis (Ossification less bulky, symmetric sacroiliitis)
- Reactive arthritis (Genitourinary symptoms)
- Hyperparathyroidism (similarity: presence of large SIJ erosion)

Modic changes in MRI

Modic classification

Use for different endplate marrow degenerative changes (which is postulated to result from same pathological process, but at different stages) in lumbar spine MR imaging.

Modic degenerative changes often accompanies disk degenerative disease (DDD)

The Modic change can be of mix type 1 and 2, type 2 and 3.

Modic type	T1w	T2w	Pathology
1 (oedema)	Hypointense	Hyperintense Modic1. Note also disk dessication.	Oedema & Inflammation
2 (fat)	Hyperintense	Iso/Slight Hyperintense Modic2. Note also disk dessication.	Marrow ischaemia, thus red marrow converts to fatty yellow marrow
3 (sclerosis)	Hypointense	Hypointense Modic3. Note also disk dessication.	Subchondral sclerosis Radiograph of the same patient with Modic 3 degeneration. Note sclerosis (arrow).

Note:

Disciitis can mimic Modic 1 degenerative change, when the adjacent bone marrows from the inflamed/infected disk is inflamed

Look at 3 things:
(1) Whether the intervertebral disk shows corresponding degenerative change (disk dessication) or shows inflammed (disciitis)

(2) Whether the bone or adjacent structures points to infection eg bone erosion, abscess formation

(3) Last but not least, correlate clinically - Lab changes, Clinical history

	Endplates	Intervertebral disk	Others
Modic 1	Low T1w, High T2w	Iso/Low T2w Usually dessicated (modic change accompanies disk degenerative disease)	Clinically non-toxic
Diskiitis	Same as above, but with features of diskiitis ie bone erosion	High T2w Inflammed disk	Presence of inflammation / abscess in adjacent structures (eg paraspinal, epidural abscess) Clinical and laboratory findings of infection

Normal Variant: Bipartite Patella

Bipartite patella occurs due to presence of unfused ossification centre.
Other variants include

• Tripartite patella
• Multipartite patella

These normal variants can be classified using Saupe's classification.

Male : Female = 9 : 1

Occurs in 2% of population

Usually asymptomatic

Saupe type 3 Bipartite patella. About half of bipartite patellae are bilateral.

Ossification:

• Primary ossification begins at 5 - 6 years old
• 77% from one center
• 23% from two or three centers
• The ossification centers usually fuse mutually