STROKE IMAGING

STROKE IMAGING IS EASY TO UNDERSTAND , YET VERY IMPORTANT TO EVERY DOCTOR

Stroke :

 A term that describes an acute episode of neurologic deficit.
 80% of strokes are due to cerebral ischemia (embolic or thrombotic).
 Transient ischemic attacks (TIAs) are focal neurologic events that resolve within 24 hours.
 Those that resolve after 24 hours are called reversible ischemic neurologic deficits (RINDs).

Causes:

1) Cerebral infarction, 80%: o   Atherosclerosis-related occlusion of vessels, 60%

o   Cardiac emboli, 15%

o   Other, 5%

2) Intracranial hemorrhage, 15%
3) Non-traumatic SAH, 5%
4) Venous occlusion, 1%

 

  • Atherosclerotic disease:
  • Atherosclerosis represents the most common cause of cerebral ischemia/infarction.
  • Carotid atherosclerosis causes embolic ischemia;
  • Intracranial atherosclerosis causes in-situ thrombotic or distal embolic ischemia.
  • Location:
  • ICA origin > distal basilar > carotid siphon, MCA.
  • Critical carotid stenosis:
  • Defined as a stenosis of >70% in luminal diameter.
  • Patients with critical stenosis & symptoms have an é risk of stroke & benefit from carotid endarterectomy.
  • Patients with stenosis < 70% or who are asymptomatic are usually treated medically.
  • Imaging Features:
Gray-scale imaging (B-scan) of carotid arteries: o   Evaluate plaque morphology/extent

o   Determine severity of stenosis (residual lumen)

o   Other features:

§  Slim sign à collapse of ICA above stenosis

§  Collateral circulation

Doppler imaging of carotid arteries:

 

o   Severity of stenosis determined by measuring peak systolic velocity:

§  50 70% à velocity 125 to 250 cm/sec

§  70 90% à velocity 250 to 400 cm/sec

§  > 90% à velocity >400 cm/sec

o   Stenoses > 95% may result in decreased velocity (<25 cm/sec)

o   90% accuracy for >50% stenoses

o   Other measures used for quantifying stenosis:

§  End diastolic velocity (severe stenosis à >100 cm/sec)

§  ICA/CCA peak systolic velocity ratio (severe stenosis à >4)

§  ICA/CCA peak end-diastolic velocity ratio

o   Innominate artery stenosis may cause right CCA/ICA parvus tardus

o   CCA occlusion may result in reversal of flow in ECA

Color Doppler flow imaging of carotid arteries: o   High-grade stenosis with minimal flow (string sign in angiography) is detected more reliably than with conventional Doppler US.
CT and MR angiography Are used for confirmation of US diagnosis of carotid stenosis:

o   On CTA, 1.0- to 1.5-mm residual lumen corresponds to 70%-90% stenosis.

o   To determine complete occlusion versus a string sign (near but not complete occlusion), delayed images must be obtained immediately after the initial contrast images.

o   At some institutions, carotid endarterectomy is performed on the basis of US and CTA/MRA if the results are concordant.

o   Pitfalls of US and MRA in the diagnosis of carotid stenosis:

§  Near occlusions (may be over diagnosed as occluded)

§  Post-endarterectomy (complex flow, clip artifacts)

§  Ulcerated plaques (suboptimal detection)

§  Tandem lesions (easily missed)

Carotid arteriography: The gold standard is primarily used for:

o   Post-endarterectomy patient

o   Accurate evaluation of tandem lesions and collateral circulation

o   Evaluation of aortic arch and great vessels

o   Discordant MRA/CTA & US results

  • Cerebral ischemia & infarction:
  • Cerebral ischemia:
  • Refers to a diminished blood supply to the brain.
  • Infarction:
  • Refers to brain damage, being the result of ischemia.
  • Causes:
Large vessel occlusion, 50%
Small vessel occlusion (lacunar infarcts), 20%
Emboli: o   Cardiac, 15%:

§  Arrhythmia, atrial fibrillation

§  Endocarditis

§  Atrial myxoma

§  MI (anterior infarction)

§  Left ventricular aneurysm

o   Non-cardiac:

§  Atherosclerosis

§  Fat, air embolism

Vasculitis: o   SLE

o   Polyarteritis nodosa

Other:

 

 

 

 

 

 

 

o   Hypo-perfusion (border-zone or watershed infarcts)

o   Vasospasm: ruptured aneurysm, SAH

o   Hematologic abnormalities:

§  Hypercoagulable states

§  Hb abnormalities (CO poisoning, sickle cell)

o   Venous occlusion

o   Moyamoya disease

  • Imaging Features:
Angiographic signs of cerebral infarction: o   Vessel occlusion, 50%

o   Slow antegrade flow, delayed arterial emptying, 15%

o   Collateral filling, 20%

o   Non-perfused areas, 5%

o   Vascular blush (luxury perfusion), 20%

o   AV shunting, 10%

o   Mass effect, 40%

Cross-sectional imaging: Ø CT à the 1.st study of choice in acute stroke in order to exclude:

ü Intracranial hemorrhage.

ü Underlying mass/AVM.

Ø Most CT examinations are normal in early stroke.

Ø Early CT signs of cerebral infarction include:

·        Loss of gray-white interfaces (insular ribbon sign)

·        Sulcal effacement

·        Hyper-dense clot in artery on NCCT (dense MCA sign)

Ø Edema (maximum edema occurs 3 5 days after infarction):

§  Cytotoxic edema àdevelops within 6 hours (detectable by MRI).

§  Vasogenic edema àdevelops later (first detectable by CT at 12 24 hours).

Ø Characteristic differences () distributions of infarcts:

§  Embolic à periphery, wedge shaped

§  Hypo-perfusion in watershed areas of ACA/ MCA and MCA/PCA

§  Border-zone infarcts

§  Basal ganglia infarcts

§  Generalized cortical laminar necrosis

Ø Reperfusion hemorrhage is not uncommon after 48 hours:

§  MRI much more sensitive than CT in detection

§  Most hemorrhages are petechial or gyral.

Ø Mass effect in acute infarction:

ü Sulcal effacement

ü Ventricular compression

Ø Sub-acute infarcts:

ü Hemorrhagic component, 40%

ü Gyral or patchy contrast enhancement (1 3 weeks)

ü GWM edema

Ø Chronic infarcts:

ü Focal tissue loss à atrophy, porencephaly, cavitation, focal ventricular dilatation

ü Wallerian degeneration à distal axonal breakdown along white-matter tracks

 

CT & MRI appearances of infarcts:

Factor 1st Day 1st Week 1st Month > 1 Month
Stage: Acute Early subacute Late subacute Chronic
CT density:  Subtle decrease Decrease Hypodense Hypodense
MRI: T2W: edema T2W: edema Varied T1W dark, T2W bright
Mass effect: Mild Maximum Resolving Encephalomalacia
Hemorrhage: No Most likely here Variable MRI detectable
Enhancement: No Yes; maximum at 2-3 weeks Decreasing No
  • Pearls:
  • Cerebral infarcts cannot be excluded on the basis of a negative CT.
  • MRI with diffusion weighted imaging (DWI) & perfusion weighted imaging (PWI) should be performed immediately if an acute infarct is suspected.
  • CM administration is àreserved for clinical problem cases & should not be routinely given, particularly on the first examination.
  • Luxury perfusion refers to hyperemia of an ischemic area:
  • The increased blood flow is thought to be due to compensatory vasodilatation 2.ry to parenchymal lactic acidosis.
  • Cerebral infarcts have à a peripheral rim of viable but ischemic tissue (penumbra).
§  Acute cerebral ischemia may result in a central irreversibly infarcted tissue core surrounded by peripheral region of stunned cells that is called àa penumbra

§  These cells have ceased to function, but this region is potentially salvageable with early re-canalization.

  • Thrombotic & embolic infarcts occur in vascular distributions àe., MCA, ACA, PCA, etc.
  • MR perfusion/diffusion studies are àimaging studies of choice in acute stroke:
  • DWI detects reduced diffusion coefficient in acute infarction, which is thought to reflect cytotoxic edema.
  • In patients with multiple T2W signal abnormalities from a variety of causes, DWI can identify those signal abnormalities that arise from acute infarction.
  • 50% of patients with TIA have DWI abnormality.
  • MRI in acute stroke:
  • On PD/T2WI and FLAIR infarction is seen as àhigh
  • These sequences detect 80% of infarctions before à24 hours.
  • They may be negative up to à2 4hours post-ictus!
  • High signal on conventional MR-sequences is comparable to àhypo-density on CT.
  • It is the result of irreversible injury with cell death.
  • So hyper-intensity means BAD news à dead brain.
Hyper-intensity on MR = irreversible ischemic brain damage
  • Comprehensive Stroke Protocol: MR
MRI: o   Sag T1, Ax T2, Ax DWI
MRA: o   TOF head & neck
MRA: o   elliptic-centric arch /carotids
Perfusion: ü Single dose Gad

ü GRE-EPI

ü Automated arterial input function

ü Parameter maps: CBV, MTT, CBF

 

Post Gad: o   ax T1, coronal T2 FLAIR
  • Imaging features:
Loss of flow voids: o   Artery or vein.
Loss of Flow-Related Enhancement
Intravascular enhancement: o   DD of intra-vscular enhancement:

ü Meningitis

ü Sturge-Weber syndrome

ü Sarcoid

ü Tumor

Parenchymal Enhancement: o   Rule of 3’s à starts 3days, peaks 3 weeks, gone 3 months.

o   Parenchymal MR Imaging in Stroke:

ü Confirm diagnosis

ü Ischemic vs. hemorrhagic

ü Underlying cause

ü Risk of progression:

v Location

v Size

v Complications

ü Mass effect / herniation

ü Hemorrhagic transformation

Pearl:

  • MRI is better than CT for Hemorrhage:
  • MRI may be as accurate as CT for the detection of acute hemorrhage in patients presenting with acute focal stroke symptoms.
  • MRI is more accurate than CT for the detection of chronic intra-cerebral hemorrhage.
  • Diffusion & perfusion imaging in stroke:
  • Standard diffusion protocol includes a DWI & an apparent diffusion coefficient (ADC) image àusually interpreted side by side:
DWI: o   Summation of diffusion + T2 effects.

o   Abnormalities appear as à high signal.

ADC: o   Diffusion effects only.

o   Abnormalities appear as àlow signal.

Perfusion imaging:

  • Performed using the susceptibility effects of a rapid bolus injection of gadolinium administered intravenously.
  • Rapid continuous scanning during this injection allows the signal changes associated with the gadolinium to be plotted over time for a selected brain volume.
  • These time-signal plots can be processed to yield several possible parameters relating to cerebral perfusion.

 

  • Vascular (perfusion) parameters:
Mean Transit Time: (MTT) §  Measured in àseconds.

§  A measure of how long it takes blood to reach the particular region of the brain.

Cerebral Blood Volume: (CBV) §  Measured in àrelative units &

§  Correlates to the total volume of circulating blood in the voxel.

Cerebral Blood Flow: (CBF) §  Measured in àrelative units &

§  Correlates to the flow of blood in the voxel.

 

 

  • Interpretation:
  • Stroke Evolution on MRI: 
Sequence Hyper-acute

(< 6hours)

Acute

(> 6 hours)

Sub-acute

(Days to weeks)

Chronic
DWI High High High (ê with time) Iso-intense to bright
ADC Low Low Low to iso-intense Iso-intense to bright
TW2/Flair Iso-intense Slightly bright to bright Bright Bright
  • A typical infarct is DWI bright & ADC dark.
  • Gliosis appears DWI bright due to T2 shine-through but is also bright on ADC.
  • DWI:
  • Very sensitive for detecting disease àwill pick up infarcts from about 30 minutes onward.
  • But is non-specific & will also detect non-ischemic disease.
  • ADC:
  • Less sensitive than DWI.
  • But dark signal is fairly specific for restricted diffusion, which usually means ischemia.
  • Significance of a DWI-bright, ADC-dark lesion:
  • This tissue will almost certainly go on to infarct & full necrosis.
  • Rare instances of reversible lesions have been reported àvenous thrombosis, seizures, hemiplegic migraine and hyper-acute arterial thrombosis.
  • Match and mismatch:
  • In the acute stroke setting, a region that shows àmatched both diffusion and perfusion abnormalities is thought to represent irreversibly infarcted tissue,
  • While a region that shows àmismatched perfusion abnormalities and diffusion likely represents viable ischemic tissue, or a penumbra
EXP: (exponential) o   The map that “subtracts” the T2 effect.

o   In equivocal cases, use EXP map as àa problem solver:

ü If it stays bright on the EXP map, then it is àtrue restricted diffusion.

MTT: o   Highly sensitive for disturbances in perfusion.

o   But not good for prediction of later events.

ü For example à an asymptomatic carotid occlusion would have a dramatically abnormal MTT, without the patient being distressed.

CBV: o   A parameter that changes late in the ischemic cascade, &

o   Usually reduced CBV is also accompanied by restricted diffusion..

o   Reduced CBV + restricted diffusion àcorrelate well with tissue that goes on to infarction.

CBF: o   In experimental setting:

ü Can be used to predict the likelihood of brain tissue infarcting.

o   In current clinical practice:

ü If a CBF abnormality exceeding the DWI abnormality (diffusion- perfusion mismatch):

§  This implies that there is brain at risk that has not infracted yet.

§  This brain at risk is the target of therapeutic interventions.

Role of CT/CTA in acute stroke:

Value:

1)    Important in early stages of stroke evaluation to facilitate thrombolytic therapy.

2)    CTA:

§  Demonstrates the anatomic details of the neuro-vasculature from the great vessel origins at the aortic arch to their intracranial termination.

§  Highly accurate in the identification of proximal large vessel circle of Willis occlusions &

§  Therefore in the rapid triage of patients to intra-arterial (IA) or intravenous (IV) thrombolytic therapy.

 

 

CT Early signs of ischemia:

Hypo attenuating brain tissue: o   The reason we see ischemia on CT is that in ischemia cytotoxic edema develops as a result of failure of the ion-pumps.

o   These fail due to an inadequate supply of ATP.

o   An increase of brain water content by 1% will result in a CT attenuation decrease of 2.5 HU.

o   Hypo-attenuation on CT is highly specific for irreversible ischemic brain damage if it is detected within first 6 hours.

o   Patients who present with symptoms of stroke and who demonstrate hypo-density on CT within first 6 hours were proven to have larger infarct volumes, more severe symptoms, less favorable clinical courses and they even have a higher risk of hemorrhage.

o   Therefore whenever you see hypo-density in a patient with stroke this means bad news.

o   No hypodensity on CT is a good sign.

Hypo-density on CT = irreversible ischemic brain damage
Obscuration of the lentiform nucleus: o   Obscuration of the lentiform nucleus, also called blurred basal ganglia, is an important sign of infarction.

o   It is seen in MCA infarction & is one of the earliest & most frequently seen signs.

o   The basal ganglia are almost always involved in MCA infarction.

Insular Ribbon sign: o   This refers to hypo-density & swelling of insular cortex.

o   It is a very indicative & subtle early CT-sign of infarction in the territory of MCA.

o   This region is very sensitive to ischemia because it is the furthest removed from collateral flow.

o   It has to be differentiated from herpes encephalitis.

Dense MCA sign: o   This is a result of thrombus or embolus in the MCA.

o   On CT-angiography occlusion of the MCA is visible.

Loss of sulcal effacement
  • Technique:
  • Stroke protocol (CT/CTP/CTA):
NCCT:

(done first)

§  Value:

o   To exclude hemorrhage àan absolute contraindication to thrombolytic therapy.

o   To detect irreversible “core” of infarction (>1⁄3 of a vascular territory) à a relative contraindication to thrombolysis.

§  Scanning parameters:

o   140 kV, 170 mA, pitch = “high quality” (3: 1)

o   Table speed à 7.5 mm/sec.

o   Scanning from à skull base to vertex.

o   Slice thickness à 5 mm

o   Window width ànarrow settings, with a center level of about 30 HU (width of 5 to 30 HU):

v This facilitates the detection of early, subtle, ischemic changes contiguous with normal parenchyma.

CTP: §  Scanning parameters:

o   IV contrast bolus ~ 50 cc

o   Dynamic scanning ~ 45 seconds

o   4-8 slices

o   5 mm

o   Calculate perfusion parameters:

v Cerebral blood volume CBV

v Mean transit time MTT

v Cerebral blood flow CBF

CTA: §  Scanning parameters:

Initial phase scan parameters:

o   IV contrast (non-ionic, non-osmolar CM) bolus 100 ml (90-120 ml) à   4 cc/sec

o   Scan delay of à 25 sec.

v A longer delay may be needed for patients with à compromised cardiac function & atrial fibrillation.

o   Scanning from à skull base to the vertex

o   Used parameters are as per the NCCT scan.

Second phase scan parameters:

o   Performed immediately after initial scan, with minimal possible delay.

o   Scanning from the aortic arch to the skull base.

o   Similar scan parameters except for àan é in the table speed to 15 mm/sec.

§  Note that:

o   Major advantages of first scanning the intracranial circulation include:

v obtaining the most important data first, which can be reviewed during subsequent acquisition;

v allowing time for clearance of dense IV contrast from the subclavian, axillary, and other veins at the thoracic inlet, reducing streak artifact

o   On a >16-slice scanner, CTA may be performed from the vertex to the aortic arch in one pass,

v This gets rid of the loss of contrast enhancement in the neck CTA usually seen with a two-stack protocol

  • Lacunar infarcts:
  • Lacunar infarcts:
  • Account for à20% of all strokes.
  • The term refers to à occlusion of penetrating cerebral arterioles
  • Commonly affected are:
§  Thalamoperforators (thalamus)

§  Lenticulostriates (caudate, putamen, internal capsule)

§  Brainstem perforator (pons)

  • Usually cause characteristic clinical syndromes:
  • Pure motor hemiparesis, pure hemisensory deficit, hemiparetic ataxia, or dysarthria-hand deficit.
  • Imaging Features:
o   MRI is àthe imaging study of choice.

o   Small ovoid lesion (< 1 cm):

§  Hyper-intense on T2W & proton density–weighted (PDW) image.

o   Location of lesions is very helpful in DDx:

ü Dilated peri-vascular or Virchow-Robin (VR) space:

§  Can be large (giant VR space), can cause mass effect & can have surrounding gliosis

§  More elongated appearance on coronal images

Therapeutic options:

  • Within 3 hours of stroke onset à IV thrombolysis + recombinant tissue plasminogen activator (r-tPA)
  • If > 3 hours of stroke onset à no IV thrombolysis given (é probability of intracranial hemorrhage)
  • The time window for treatment with IA agents is:
  • Twice as long for the anterior circulation &
  • Indefinite for the posterior circulation.
  • For thrombosis localized to the posterior circulation:
  • The time window for treatment may be extended beyond 6 hours due to the extreme consequences of loss of blood flow to the brainstem, despite the risk of hemorrhage.
  • Advanced CTA/CTP imaging of acute stroke:
  • Has the potential to not only help exclude patients at high risk for hemorrhage from thrombolysis,
  • But also identify those patients most likely to benefit from thrombolysis.
  • Even without hemorrhage, treatment failure with thrombolytics is not uncommon.
  • The choice between IA & IV thrombolysis depends on a variety of factors, including:
o   the time post ictus,

o   the clinical status of the patient, &

o   whether the clot is proximal (IA) or distal (IV).

  • When typical findings of occlusive thrombus on CTA & ê tissue enhancement on CTP are not present, the DDx include:
o   Lacunar infarct.

o   Early small distal embolic infarct.

o   Transient ischemic attack.

o   Complex migraine headaches.

o   Seizure.

  • Golden points:
What you like to know? §  Is there hemorrhage?

§  How extensive is the edema?

Answer à CT
§  Where’s the occlusion?

§  What’s the blood flow?

§  How much brain is dead?

§  How much brain is at risk?

Answer à MRA-PWI-DWI- CT- CTA-CTP
4 P: o   PARENCHYMA:

§  Exclude Hge.

§  Early signs of stroke.

o   PIPES

§  Intra-cranial circulation.

§  Extra-cranial  circulation

o   PERFUSION à CBV –CBF –MTT

o   PENUMBRA       : Tissue at risk of dying

 

IMAGING OF CONGENITAL SKULL LESIONS

I-Lacunar Skull:

IMAGING OF CONGENITAL SKULL LESIONS IS A VERY RICH TOPIC TO TALK, LET’S GET A LOOK.

*Pathology:-

  • A dysplasia of the cartilage bones of the skull vault.
  • They lie in the thickest part of frontal, parietal & upper occipital bone.
  • Commonly associated with CNS anomalies: myelomeningiocele, hydrocephalus.

*Statistics:

In infants, disappear by 4-6 months.

*Radiology:-

1-Plain films:

Bilateral clusters of elliptical areas in which the vault is extremely thin are separated by thicker strands; some areas of the vault may be normal.

2-CT:

Shows that the scalloping predominantly affects the outer table.

II-Abnormalities of the Cranial Sutures:

A- Normal variation of the shape of the skull (Not pathological):

1-Dolichocephaly: longer skull in relation to width.

2-Brachycephaly: wider skull in relation to length.

3-Trigonocephaly: triangular skull due to the sharp anterior pointing of frontal bone due to premature fusion of metopic suture (in utero).

4-Bathrocephaly: square occipital bone overlapping the parietal bone at the lambdoid suture (should not be confused with traumatic lesions).

B-Premature fusion of Skull Sutures (Craniosynostosis):

Craniosynostosis

*Pathology:

  • Premature fusion of a calvarial suture.
  • Maybe primary or secondary to metabolic disease, bone dysplasia, hematological disorder or decreased intracranial pressure.

 *Statistics:

  • Most cases are detectable at birth.
  • M:F = 3:1.
  • Frequency of sutural involvement: sagittal 56%, multiple 14%, unilateral coronal. 11%, bilateral coronal 11%, metopic 17% and lambdoid 1%.

*Presentation:

Abnormally shaped head.

*Radiology:

1-Plain Film:

  • Analysis of skull shape is the best radiologic clue for diagnosis.
  • The resulting deformity depends on which suture is affected:

1-Sagittal Suture: 

Produces a long and narrow skull (dolichocephaly or scaphocephaly).

Severe craniosynostosis of the scaphocephalic type caused by premature synostosis of only a short segment of the sagittal suture of
a 2-week-old infant. A, In lateral projection, deformity resulting from the craniostenosis is clearly seen, but the sagittal suture itself is invisible (superior
black arrows). Coronal (black arrows) and lambdoid sutures (white arrow) are widened. B, In frontal projection, the sagittal suture is visible in its entirety
and is open except for a short segment (arrows) only a few millimeters long.
Caffey's Pediatric diagnostic imaging

2-Coronal suture:

May be unilateral or bilateral

-if bilateral produce a short and wide/tall skull (brachycephaly or turricephaly).

-if unilateral produce lopsided skull (plagiocephalic).

3-Metopic suture: 

produces a pointed forehead (trigonocephaly) and hypotelorism.

4-Lambdoid suture:

-if unilateral causes flattening of the occipital region (plagiocephaly)

-if bilateral, causes flattening of the entire occiput.

5-All sutures: produce sharp peaked crown (oxycephaly).

  • ‘Harlequin eye’ appearance is seen with complete coronal craniosynostosis which extends to the sphenoethmoidal synchondrosis
  • Cloverleaf skull (Kleeblattschadel) is caused by intrauterine premature closure of the coronal, lambdoid and sagittal sutures and is associated with lacunar skull (Luckenschadel) and brain dysgenesis or hydrocephalus.as figure below.

Rudlof - Atlas of newborn - volume III

NB: In microcephaly: small head due to premature closure of all the sutures+ primary mental defect.

2-CT:

  • Sutural narrowing, parasutural sclerosis, sharpening of suture edges and bony bridging across the sutures.
  • May only see buckling of suture with fibrous (non-bony) fusion.

3-US:

Delayed growth of biparietal diameter in early pregnancy

*Management:

  • Strip craniectomy in cases of single craniosynostosis is for cosmetic purposes as brain growth is not impaired
  • With universal craniosynostosis, strip craniectomy is mandatory to prevent complications of increased intracranial pressure and to allow brain growth.

NB: Prevent premature closure of sutures before 9 months:

                            – prevent mental defect.

                            –regain normal shape.

C-Widening of the sutures

  • occurs most commonly with raised intracranial pressure.
  • It is also seen with neoplastic infiltration of the sutures by, e.g., neuroblastoma, in which case the adjacent bone is often clearly eroded.

III-Abnormalities of skull base& foramen magnum:

 A-Platybasia:

*Definition:

A condition in which the base of skull appears relatively flattened

*Pathology:

  • There is an increase in the basal angle, as measured on a true lateral skull film.
  • The basal angle: lies between the two lines drawn from the anterior lip of the foramen magnum and the nasion to a point at or near the tuberculum sellae: the normal range is 120–140º; when the angle exceeds 148º the base of the skull is abnormally flat.
  • The term platybasia is sometimes used rather loosely to include basilar impression and basilar invagination.

B-Basilar Impression:

  • Indicates an elevation of floor of the posterior fossa.
  • Commonly associated with congenital anomalies of cervical spine.
  • The foramen magnum may be abnormal in shape and size.

C-Basilar Invagination:

Definition:

This is a term reserved for conditions in which the margins of the foramen magnum are inverted.

Etiology:

it is usually developmental, but similar changes may complicate rickets, Paget’s disease or other conditions in which the bone is softened.

Radiology:

The following lines may be used for assessment of basilar invagination on either plain films or CT scout topogram film:

1-Chamberlain’s line: drawn on the true lateral projection of the craniocervical junction, from the posterior end of the hard palate to the posterior border of the foramen magnum. Not more than 2 mm of the odontoid process should lie above this line

.2-MacGregor’s modification: as above, but using the occipital squama as the posterior landmark when the posterior lip of the foramen is not identified with ease. This line is vitiated if the head is tilted to one side. Not more than half the odontoid should be above this line.

3-The digastric line: on the occipitofrontal projection, between the two digastric notches. The atlanto-occipital joints should be below this line.=Basilar invagination is not the only condition in which the odontoid is unduly high: an abnormally short clivus and/or occipitalization of the atlas can give similar appearances.

NB: Both basilar invagination and platybasia are best assessed by mid-line sagittal MRI, when the effects on the neuraxis are also displayed.

III-Occipitalization of the Atlas:

*Definition:

The first cervical vertebra is fused to the skull base.

*Incidence:

1% of the population.

*Pathology:

  • In its mildest degree, the distance between the 2 posterior arch of the atlas and occipital bone is reduced and does not change with flexion and extension.
  • In ‘assimilation’ of the atlas, bony fusion is complete, and no separate components of the atlas can be identified.
  • The normal relationship of atlas and axis is, however, preserved, so that the odontoid is abnormally high.
  • The potential significance of this anomaly lies in its association with the Chiari malformation.

IV-Defective ossification:

in conditions such as:

1-Cleidocranial dysostosis.

2-Osteogenesis imperfecta.

 *Result in:

  • Very wide sutures, without other signs of raised intracranial pressure.
  • Wormian bones are prominent.
  • It is usually evident that the patient has a generalized bone disorder.

V-Hypertelorism:

  • A condition in which the orbits seem widely separated.
  • Usually associated with well developed ethmoid cells occupying the gap between the orbits.
  • Present in:

             1-Isolated congenital lesion (Grieg’s disease).

              2- Osteogenesis imperfecta.

              3- Cleidocranial dystosis.

              4- Fibrous dysplasia.

              5- Craniostenosis.

              6- Secondary to mucocele of ethmoid sinus (acquired).

 

**NOTES:-

*Apeurt’s syndrome = Syndactyly + oxycephally.        

*Acrocephally = Summit skull (brachycephally) (same as tower skull).

*Crourzon’s disease = (hereditary craniofacial dysostosis) is a form of acrocephally + facial bone hypoplasia, hypertelorism, exophthalmos, parrot-beak nose, prognathism, MR & corepulmonale .

*Carpenter’s syndrome = acrocephalopolysyndactyly

 

 

 

Dangers of Radiation in Diagnostic Imaging

Introduction

       DANGERS OF RADIATION IN DIAGNOSTIC IMAGING is very important in oir life , let’s talk first about Radiation.

Radiation is a fact of life. Light and heat from the sun are natural forms of radiation essential to our existence.There are also other forms, which we generate in everyday life, such as microwaves for cooking, radio waves for communication, radar for navigation, and X-rays for medical examinations.

Radioactive materials also emit radiation.These materials occur naturally throughout the environment, but we have also produced others artificially.

We can classify radiation according to the effects it produces on the matter. There are two categories, ionizing and non-ionising radiations.

Ionizing radiation includes cosmic rays, X-rays, and the radiation from radioactive materials.

Non-ionising radiation includes ultraviolet light, radiant heat, radio waves, and microwaves.

we can also classify radiation in terms of its origin as natural radiation or artificial radiation.(1)

The benefits from natural non-ionising radiation, mainly heat, and light from the sun, are enormous, but there are no clear benefits from exposure to natural ionizing radiation.

We make considerable use of both lionizing and non-ionising radiation, however, Artificial radiations have led to dramatic advances In medical diagnosis and treatment, and are used for a wide range of procedures In Industry, agriculture, and research.

Nevertheless, they can be harmful to human beings and people must be protected from unnecessary or excessive exposures.

The greatest concern about ionizing  radiation stems from the way In which it can cause malignant diseases in people exposed to it and inherited defects In later generations.(2)

The likelihood of such effects depends on the amount of radiation that a person receives: this is equally true whether the radiation is natural or artificial.

So in circumstances that we can control, we need to make a careful balance between the risks and the benefits of the procedures that expose people to radiation.

The effects of non-ionising radiation depend on the type and intensity of the radiation.

Non-ionising radiation can damage the skin and the eyes, If it penetrates body tissues, It can damage internal organs by heating them in the long term, exposure to ultraviolet radiation may cause skin cancer and cataracts. Again we need measures to protect people from such effects.

As the effects of Ionising and non-ionising radiations have become better understood during recent decades, a system of radiological protection has been developed to protect people from sources of radiation.

The subject of radiation safety receives much attention In our society partly because radiation is one cause, among many, of cancer. Moreover, our senses cannot detect most forms of radiation; this undoubtedly adds to our anxiety.

Another reason for general concern may be the lack of reliable and accessible information about radiation. (3)

The Human Cell

The cell is the base unit of the life that reflect all its features (7).

It’s formed from the organic structure which is formed from macro-molecules, formed by a molecule which consists of atoms. In humans, there are approximately 1014 cells [8].

Cells can be simply divided into two categories: prokaryotic cells and eukaryotic cells [9].

The Prokaryotic cells don’t have a nucleus or membranous organelle (e.g mitochondria) but have nuclear membrane and ribosomes, so the DNA is found in the cytoplasm scattered, where they do their viral function. on the other side, The Eukaryotic cells have a nucleus and membranous organelles and, so divide by mitosis. [9].

To understand the effects of radiation on human beings. We should first study the human cell and its components very well.

Typical cell composed of a single nucleus (containing DNA molecules) embedded in cytoplasm and enclosed a cell membrane that selectively regulates the interchange of materials between the cell and its environment.(7)

 

Spiral staircase shape structure of The DNA27

DNA Structure: DNA is made up of subunits called Nucleotides, Each Nucleotide is made up of a sugar, phosphate and a base. There are 4 different bases in a DNA molecule: the first is Adenine (a Purine), the second is Cytosine (a Pyrimidine), the third is Guanine (a Purine), the fourth and the last is Thymine (a Pyrimidine).

We should note that number of Purine bases equals a number of Pyrimidine bases, and a number of Adenine bases equals the number of Thymine bases, also a number of Guanine bases equals the number of Cytosine bases.

The basic structure of DNA molecule is helical, with the bases being stacked on top of each other.

Cell Cycle

During its life, a cell generally exhibits a long period or phase (interphase) during which no division occurs, and a division phase (mitosis). This is called the cell cycle (10)

Cell Cycle can be divided into phases: G1 (gap), S (synthesis), G2 (gap), and M (mitosis).

Cells not actively growing to occupy a fifth phase known as G0, in which they can be stimulated to enter active cycle by environmental stresses. Cells are least sensitive when in the S phase (Resistance in

S phase may be due to the presence of synthetic enzymes capable of prompt repair of DNA breaks), then the G1 phase, then G2 phase as well as all cells in G0 phase and most sensitive in the M phase of the cell cycle. This is described by the law of Bergonie and Tribondeau, formulated in 1906. [10.11]

 

Active eukaryote cell divide through cell cycle stages28

 

BASIC INTERACTIONS OF RADIATION WITH MATTER:

We can classify the interaction according to two forms, either by energy of radiation or by site of energy deposition and interaction.

 

First, interactions according to the energy of radiation:  when radiation interacts with target atoms, energy is deposited, resulting in Ionization or excitation.

 

Now we will talk about interactions according to the site of energy deposition & interaction:

absorption of energy from ionizing radiation produces damage to molecules by direct and indirect actions, that will result in :

Direct Effects:

Damage occurs as a result of Ionization of atoms on target molecules in the biologic system e.g. DNA, RNA, ribosomes…

IONIZATION occurs at all radiation qualities but is predominant with High LET radiation, e.g. Alpha particles and Neutrons.there is considerable evidence suggesting that DNA is the primary target for Cell Damage from Ionizing Radiation.

Indirect Effects:

involves the production of reactive free Radicals in the medium in which cell organelles are suspended, whose toxic damage on Target molecule results in a Biologic effect. It’s is Predominant with Low LET radiation, e.g. X and Gamma rays. These are effects mediated by free radicals.

A free radical is an electrically Neutral atom with an Unshared (uneven) electron in the orbital position. The radical is electrophilic and highly reactive. Since the Predominant molecule in biological systems is Water, it is usually the intermediary of the radical formation and propagation.

Radiolysis Of Water:

 

Fate Of Free Radicals is one of the following: first rejoining each other causing no effect, as :

H0+ OH0 (free radicals) à H-O-H (H2o) which is not harmful

Secondly, Joining with other free radicals, as follows: Formation of Toxic Hydrogen Peroxide

(H2O2)which is very toxic; i.e. OH0 + OH0 à H2O2 (peroxide dimer)

Lastly, It can be transferred to an Organic molecule in the cell and Damaging it.

The Presence of dissolved oxygen can modify the reaction by enabling the creation of other free

radical species with greater stability and lifetimes.

 

Lifetimes of simple free radicals (H0 or OH0) are very short, on order of 10-10 sec.While generally highly reactive à they do not exist long enough to migrate from site of  formation to cell nucleus

However, Oxygen-Derived Species such as Hydroperoxy free radical does not readily, recombine into neutral forms. These more stable forms have a lifetime long enough to migrate to the nucleus where serious damage can occur.

FATE (RESPONSE) OF IRRADIATED CELLS ·

Irradiation of a cell will usually result in one of the following possible outcomes (responses):

First Division delay (Mitotic delay) in which Cell is delayed from going through division.

Secondly, Inter-phase death which occurs with high dose and insensitive phases.

Third , Reproductive failure in which Cell becomes incapable to undergo repeated division.

A) Division delay (Mitotic delay):

The cell is delayed from going through division; Length of delay depends on Cell Type, Dose Of Radiation and Dose Rate.the Cause of this delay is not Fully Understood but may be due to decreased DNA synthesis, or Prevention of Protein Synthesis needed for division. Alteration of Chemicals needed in the division process is also can be a cause. Another cause is mitotic Index, In a population of cells, Ratio Of No of cells undergoing mitosis (cell division) to No of cells not undergoing mitosis.

– Pre-Irradiation:

Mitotic Index shows Straight Line (Horizontal) and is Constant, this is because as some cells Complete mitosis, other cells Enter Division (same number).

– Post-Irradiation:

Radiation disturbs  Constant Ratio between  Dividing (Mitotic) Cells and  Non-Dividing (Non-Mitotic) Cells, this disturbance takes one of two forms;  Mitotic Delay (Decreased mitotic index), and Mitotic Overshot (Increased mitotic index). The mitotic delay is dose-dependent, At Low Doses After Irradiation Mitotic Delay occurs, followed by Mitotic Overshooting, then Mitotic Index Return to Pre-Irradiation state.

At High Doses, After Irradiation Mitotic Delay occurs and Mitotic Index Decreased and Cannot Return to Pre-irradiation state; because Reproductive Failure Occurs.

B) Interphase death:

The cell dies before entering the mitotic division.This occurs in non-dividing cells as well as rapidly dividing cells with high doses of radiation. The cell breaks fragmented into Smaller Bodies, taken up by Neighboring Phagocytes.

C. Reproductive failure:

It is the Inability of the Cell to undergo Repeated Division after irradiation. The Mechanism is due DNA and chromosomal damage.This Occurs With High doses of radiation.

CLASSIFICATION OF RADIATION DAMAGE14.15

Radiation damage to mammalian cells is divided into three categories Lethal, Sub-Lethal and Potential Lethal Damage.

A) Lethal Damage

It’s irreversible and Irreparable and can lead To cell death.(14,15)

B) Sub-Lethal Damage (SLD):

It is damages caused by a Sub-lethal dose of ionizing radiation, which can usually be repaired in hours Unless the additional sublethal damage is added.

It occurs when radiation is divided into small equal doses given to cell at separate time intervals (fractionation).

The Sub-lethal damage repair is a term used to describe the increase in cell survival seen if a given radiation dose is split into 2 equal fractions separated by a time interval.

If Dose is Split into 2 fractions separated by a time Interval, this leads to more cells survive than for the same total dose given in a single fraction, because the shoulder of the curve must be repeated each time.

High LET radiation, e.g., neutrons, is associated with little repair of SLD. Since Presence of a shoulder on a Cell Survival Curve is dependent on Quality of radiation used à Amount Of SLD Repair is similarly dependent on Quality Of Radiation.

Applications:

Sublethal damage repair is Of Significant Importance in the radiotherapy fields, as we can spare normal tissues from the effect of the therapeutic irradiation by fractionating the dose.

Example: Cells and Tissues with broad shoulder survival curves e.g. jejunum: shows a large amount of Sublethal damage and Repair: While other tissues e.g. bone marrow stem cells have Narrow shoulder survival curves, so they are more sensitive to irradiation & less amount of Sublethal Damage and Repair. (14,15)

diagram32

C) Potentially Lethal damage:

Component of radiation damage that modified by Post-Irradiation Environmental Conditions. It manipulated by Repair when cells are allowed to remain in a nondividing state.  Varying environmental conditions after exposing cells to X-rays: can Influence Proportion of cells that Survive a given dose due to Repair of PLD.

Damage considered Potentially Lethal since under ordinary circumstances leads to cell death. However, if Survival is increased following manipulation of the Post-irradiation environment, PLD is considered to have been repaired. (15)

 

FACTORS AFFECTING RADIOSENSITIVITY (RESPONSE) OF CELLS:

the response of the cells to radiation is affected by multiple factors, physical or biological or chemical …. In the following we will discuss some of it in few words:

 A) Physical Factors

1) LET (Linear Energy Transfer):

It is Rate at which energy is lost while traveling through matter; it differs according to the type of radiation ( the average amount of energy lost per unit of matter length).Measurement of the number of ionization which radiation causes per unit distance as it traverses the living cell or tissue.

In General, ALPHA Particles, which are relatively slow moving, have

a much higher LET than beta particles or GAMMA rays.BIOLOGICAL EFFECTS of High LET Radiations is higher than those of Low LET Radiations with the same energy. WHY?? This is because High LET radiation can deposit most of its energy within Volume Of One Cell of the body, Chance Of Damage to the cell is therefore Larger.Shoulder Region (in cell survival curve) is more Prominent with Low LET radiations.and is reduced and Slope becomes steeper with High LET radiations.(29)

diagram32

 

2) RBE (Relative Biological Effectiveness):

it’s comparison of a dose of some test radiation to a dose of 250 kV x-rays that produce a same biologic response. It’s used in Comparing effects of different types of radiation. e.x. RBE of Alpha Particles has been determined to be 20 -> This means that 1 Gy of ALPHA is equivalent to 20 Gy of GAMMAS/X-RAYS

RBE depends on LET (i.e. radiation quality), and Dose of radiation, Dose rate, Biologic system or endpoint, and Oxygen enhancement ratio (OER).Diagnostic X-ray has RBE of 1. RBE and LET have a relation as follow: increase LET, lead to increase  RBE,  till maximum effect (cell death) occur, then decrease RBE. If LET increases (with Constant factors), RBE will increase slowly at first, then more rapidly as LET > 10 keV/μm, RBE then increases rapidly to a peak value of 100 keV/μm, after which RBE decreases rapidly. (16,17).

diagram32

 

3) Dose rate (Protraction):

It is RATE the by which the radiation is delivered.it occurs with low LET radiations (with large shoulder curves) Only .in case of low dose rate, it allows Repair to occur before accumulated damages to the cell occur.If dose is Split into 2 fractions separated by time interval à More Cells Survive than for Same Total Dose given in a single fraction because shoulder of curve must be repeated each time.(7)

B) Biological Factors

 1) Stage of Cell Cycle:

Position of Cell in Its Cycle has a role in its response to radiation (Radiosensitivity). Cells are least sensitive when in S phase and most sensitive in M phase of cell cycle.

2) Intracellular Repair.

3) The degree of Differentiation:

Most Sensitive cells are those that are Undifferentiated, and Well Nourished, and Divide Quickly and is Highly Metabolically Active.

Most Sensitive body cells are Erythroblasts, Epidermal stem cells, and GIT stem cells. The Least Sensitives are Nerve Cells and Muscle fibers.

According to Law of Bergonie and Tribondeau that was set at 1906 by Bergonie and Tribondeau when they realized that cells were most sensitive to radiation when they are Rapidly dividing, Undifferentiated and have a long mitotic future

C) Chemical Factors

1) Oxygen effect:

Well, oxygenated tissues are more sensitive to radiation than Hypoxic Or Anoxic tissues.Oxygen enhances Cell Killing Effect of radiation.

Oxygen Enhancement Ratio (OER): it’s Ratio between Hypoxic and Aerated doses à to obtain the same biological effect.

Mammalian cells reach full Radiosensitivity before their full capacity of oxygen.

Effects of Oxygen are  Enhancement of free radicals formation, Increasing of stability and toxicity of free radicals, and Enhancement of cell division (mitosis), making the cell more sensitive.

OER is LET dependant: as ↑LET  → ↓OER.Effect of oxygen is More Obvious with Low LET radiations e.g. X-ray, Less Obvious with High LET radiations e.g. neutrons. Oxygenation of tissues à leads to shifting of Survival Curve to Left,

Hypoxia → leads to shifting Curve to Right.This effect is used to increase the effect of radiation therapy in Oncology Treatments.In Solid Tumors, the Inner parts become Less Oxygenated Than Normal Tissue.And Up to Three Times, higher dose is needed to Achieve the Same Tumor Control probability as In Tissue With Normal Oxygenation.(18)

Oxygenation and SF(7)

2) Radio-Sensitizing Agents:

drugs that make tumor cells more sensitive to radiation therapy e.g. Nitroimidazoles. (7).

3) Radioprotective agents:

Scavenging free radicals & producing hypoxia e.g. Thiols, do it can even worse than radiation. (29)

THE CELL SURVIVAL CURVE        

Cell Survival Curve is a curve that describes Relationship between Radiation Dose and Fraction of cells that survive. (i.e. fraction of irradiated cells that maintain their reproductive Integrity).

When Radiation Dose increases ⇒ Surviving cell fracture decreases constantly.Conventionally, the Surviving fraction is depicted on a logarithmic scale and is Plotted on the y-axis against dose on the x-axis.

Low Mammalian Cells:

Survival Curve shows constant slope i.e. equal increases of the dose causing a corresponding an equal decrease in Surviving Cell Fraction.

Every radiation dose is efficient to kill a fraction of cells, so the Response Curve is Linear.

Most Mammalian Cells:

Survival Curve exhibits a broad initial shoulder followed by a Steep Straight Slope. In Shoulder Region: Equal increases of the dose do not cause a corresponding equal decrease in the surviving cell fraction e.g. in the below curve < 2 Gy are inefficient to produce cell kill, indicating that damage must be accumulated before cell death.Below 2Gy dose, the curve show shoulder region.After a 2Gy dose, the curve becomes straight. (19,29,21)

                                                                                     

  diagram32

 Factors affecting the survival curve:

Linear Energy Transfer (LET) :

the first important factor as when it increases, the survival curves become steeper and decrease shoulder(progressively smaller).

The Second Important factor is RBE.

The Third Factor is Oxygen effect:

As Oxygenation of tissues leads to Shifting of the survival curve to the Left, while Hypoxia leads to shifting the curve to the right.the fourth and last factor is the dose Rate (Protraction) as follows: if the dose is split into 2 fractions separated by a time interval, this leads to more cells survive than for same total dose given in a single fraction, Because Shoulder of the curve must be repeated each time. (29)

TARGET THEORY

When Ionizing Radiation interacts with one of the essential (key) molecules, this is called Target.

The nucleus is more sensitive to radiation damage than Cytoplasm, thus implying that the Target for radiation is a Nuclear Constituent.

Since DNA is a molecule that controls all cellular activities, therefore DNA is the most likely target for radiation action.

Target Theory explains shoulder region in cell survival curve, AS Each cell, have a certain number of targets all of which must be hit to kill the cell. if one target is not hit à Cell will survive and repair the damage.13

STOCHASTIC AND DETERMINISTIC (NON-STOCHASTIC) EFFECTS                             

harmful effects of radiation may be classified into two general categories: STOCHASTIC and DETERMINISTIC (non-stochastic).

Stochastic Effect:

It’s Effect in which Probability Of Occurrence increases with increasing dose. Its severity in affected individuals does not depend on Dose.No Threshold The dose for stochastic effects, As these effects Arise In Single Cells.

Assumed that there is always Some Small Probability of the event occurring even at very small doses.Its Dose-Response Curve is a linear Quadratic relationship with No Threshold, it’s also Called Probabilistic.Examples: Induction Of Cancer, Radiation Carcinogenesis and Genetic Effects.12

Deterministic (Non-Stochastic)System:

It’s Effect on which The Occurrence depend On Threshold Dose i.e Below this Threshold Dose, the effect does

not occur.its severity increase with increasing dose,(above a threshold dose) in affected individuals.Threshold Value is variable for different cell systems & from one person to another.

These are events caused by damage to populations of cells, hence the presence of a threshold dose.

Its Dose-Response Curve is a Sigmoid relationship with a threshold. Examples: Fibrosis, Cataract, Acute Radiation Syndrome, Blood Changes and Decrease in Sperm Count (sterility).12

                                                                                                                                               

 diagram32

 

 

                                                                     

diagram32

Effects of Radiation on Developing Fetus.

Principal Effects of radiation on a fetus are: first, fetal or neonatal death. second Malformations. Thirdly, Growth Retardation. Fourthly, Congenital Defects. Fifthly, Cancer Induction. (31)

Between Conception and Birth, the fetus passes through three basic stages of development: Pre-implantation (day 1 to 10).Organogenesis (day 11 to 42).Growth stage (day 43 to birth). Effects of radiation on fetus depend on two factors, The dose and the Stage Of Development at the time of exposure. (6)

Pre-implantation ٍStage:

It is a stage from Concept (fertilization) up to 10 days (time of implantation), it is characterized by very rapid cell division making the stage very sensitive to radiation. (6)Effects of radiation in this stage are the Lethal effect (prenatal death), and Congenital anomalies (few).

Organogenesis Stage: (6)

It is a stage from the 10th day to 40 days; characterized by Organs Formation and Differentiation. During this stage: Incidence of Congenital Anomalies is increased especially in organs formed during this stage.

CNS and Special sense organs, and Skeletal and Muscular systems. Effects of radiation in this stage are Anomalies and malformations (mainly): e.g. CNS anomalies as microcephaly, spina bifida, hydrocephalus…. Etc. If these anomalies are Severe Enough, they lead to Abortion. (6)

 

Growth Stage:

It is the stage of fetal life after 40 days.Effects of radiation include Carcinogenesis (mainly): e.g. leukemia, retinoblastoma.Effects on developing fetus depend mainly on the dose of radiation and age of fetus when irradiated (stage). (6)

 

ABORTION: 

as a choice to avoid the possibility of radiation-induced congenital abnormalities should be considered only when the fatal dose has exceeded 10 cGy.Effect of 2-5 Gy of radiation differ as follows:

From 2nd to 3rd week: Prenatal Death.

From 4th to 11th week: severe congenital anomalies especially CNS and MSK system.

From 11th to 16th week: Mental Retardation, Microcephaly. After 20th week: Functional Defect.(6)

Acute Radiation Syndrome “ARS” (Whole Body Radiation).

Acute illness caused by a dose greater than 1 Gy of penetrating radiation to most or all of the body in a short time, usually a matter of minutes. ·

Hence, This syndrome needs 3 conditions to occur, Short exposure time (minutes), Total body exposure. External penetrating Radiation.

This syndrome includes a number of characteristic signs and symptoms whose severity depends on the magnitude of dose and duration of exposure.

Stages of ARS: according to the progression of illness through 4 stages:

Prodrome (the Prodromal stage):

Prodromal Symptoms has the following characters, it Occurs shortly after irradiation, Dose of exposure determine severity, duration, & onset. It may Last (episodically) for minutes up to several days. Its common prodromal symptoms include nausea, vomiting, anorexia, fatigue, diarrhea, abdominal cramping, and dehydration.severe and early onset of prodromal symptoms indicates higher dosage of exposure and a poor prognosis.it’s Progression through the other phases depends on the dosage of exposure.

Clinical latency (Latent stage):

In this stage, the Patient looks and feels generally Healthy for a few hours or even up to a  few weeks.

Manifest illness:

In this stage, the symptoms depend on the specific ARS syndrome.It Last from hours up to several months.

It ends in  Recovery or death.

Classic ARS syndromes  :

3 classic sub-syndromes:

1) Bone marrow syndrome (Hematopoietic system failure), It typically occurs after exposures of 2-10 Gy, death happened due to infection or huge at 4.5–6 Gy without supportive care. (23)At these doses, Lymphocytes and Precursor cells in Bone Marrow are destroyed, so preventing the new production of leukocytes and platelets.

2) During Few weeks (Clinical Latency), Circulating cells Die off with no replacements.

3) Manifest clinical stage, development of Infections.Possible Hemorrhage. Anemia from red cell depression. Management includes prevention of Infections: Antibiotics for infection, Isolation may be needed. Anemia: Transfusions as needed, Bone Marrow Transplantation.

Gastrointestinal syndrome:

Occurs after exposures of doses of 6-15 Gy. (23) Death of Intestinal mucosal stem cells in the crypts. (22)Common symptoms (manifest stage) include Anorexia, Nausea, Vomiting, Prolonged Bloody Diarrhea, Abdominal Cramps, Dehydration, and Weight Loss.m management: mainstays of treatment are Fluid and Electrolyte Balance and Infection.Prevention, but Death often follows in 7-10 days. (23)

CNS syndrome,

Occurs after exposures of more than 20 Gy. (23) If doses more than 100, so Death occurs within hours. Prodromal stage last few minutes. Symptoms include: Nausea, Vomiting, Hypotension, Ataxia, and Convulsions, and Death follow in a few days.Although the Exact mechanism of death is not fully understood, Vascular Damage is thought to lead to significant Cerebral Edema, producing Neurologic and Cardiovascular collapse. (23)

Effect of Radiation On Mammalian (Reproductive) Systems                          

Male Reproductive System

The sensitive reproductive organ is TESTES. The tissue of Testes is highly Radio-Sensitive as cells are rapidly dividing and are undifferentiated.

Main effects on testis are Infertility.Primary Effect of irradiation to Testes is Depletion Of Spermatogonia (especially type B), this leads to decreased Mature Sperms Count.

Temporary Sterility occurs if acute Dose of 2 Gy to Gonads of Adult Male, induces a temporary sterility which lasts a few months. Permanent Sterility: Acute Dose of 5 Gy to Gonads of Adult Male, induce Permanent sterility.

Of course, this is only for a Local Exposure because a whole-body dose of this magnitude would be Lethal. Chromosomal aberrations and genetic mutations occur in Spermatozoa and immature spermatogonia.

The Altered Genetic Information can be transmitted to the Next Generations.Note that The Male still retains the ability to engage in sexual intercourse, i.e. no impotence, so after radiation exposure to testis Patient should avoid sexual activity for 4 months till all cells at the time of irradiation disappear. (29)

 

Female Reproductive System:

The sensitive reproductive organ is OVARY.The tissue of Ovary is highly Radio-Sensitive as: cells are rapidly dividing and are undifferentiated.

Radio-Sensitivity of Ovary is Age-Dependent. Main effects on Ovary are Infertility, Temporary Sterility occurs when acute Dose of 2 Gy to Gonads of Adult Female, which leads to induces a temporary sterility, then start  Two months after irradiation (initial period of Fertility due to the presence of mature follicles that can give an Ovum).

Permanent Sterility occurs when Acute Dose of 6 Gy to Gonads of Adult Female, this induces Permanent sterility. Of course, this is only for a Local Exposure because a whole-body dose of this magnitude would be Lethal.

Chromosomal aberrations and genetic mutations occur in Oozoa and immature follicles.

The Altered Genetic Information can be transmitted to the Next Generations. Note that  Doses Causing Sterility in Females are higher than in Males, IRRADIATION of female genital system affect 2ry Sexual Characters e.g. causing menopause (due to Hormonal Disturbances). (29)

 

EFFECTS OF RADIATION ON THE EYE.   

EYE LENS is peculiar in that, as there is no cell replacement system, therefore damaged cells that have become opaque are not replaced naturally.

Radiation damage to EYE LENS shows a definite threshold effect (Deterministic =non-stochastic); does not occur below the threshold, but above threshold, increases Severity of the effect with increasing dose. Threshold Dose, Cataracts are induced, when dose more than 250-650 cGy is delivered to EYE LENS.

Above Threshold, increases  Severity of Cataract increases with increasing dose.Latent period, Radiation-induced cataracts may take many months to years (8 years) to appear.

Latent Period is Dose-Dependent; increasing dose will decrease the period.Features include Radiation-induced cataracts have Unique Features that distinguish them from senile cataracts.

The Earliest Changes include Diffuse Opacities (dots) around the Suture in the Posterior region.

Severity Of Opacities will Increase Gradually.Progression of Posterior Changes and involvement of the anterior sub epithelial region.Continued cataract development lead to entire Cortex is involved, but Posterior Capsule can still be discerned.

A 4+ cataract stage is one with Complete Anterior Opacification preventing visualization of the remainder of the lens.

The Pluses after the Score indicate the reality that a particular score at some given examination time reflects a cataract stage that was reached during the interval between the Previous and Current examinations.

Threshold Of Cataract Formation, Radio-sensitivity of the lens increases with age .24

 

Radiation Effect on DNA.  4

The BASE DAMAGE is Loss or change in The base of DNA which leads to Mutation.

SINGLE STRAND STREAK is Break in the Backbone of One Chain of DNA (mostly Easy repair), As the other chain act as a Template upon which the other chain repaired. DOUBLE STRAND STREAK is a  Break in both chains of DNA which leads to cell Killing, it’s difficult to be repaired.

Cross-Linking Occur Either within DNA molecule Or from One molecule to Another, which is Important of that lesion in Cell Killing is Un-Clear, But maybe important if not probably repaired.(4)

 

Radiation Effect on Chromosome. 

Chromosomal Damage Is Evident during Metaphase, Anaphase as chromosome is shortened & thickened.Radiation-Induced Chromosomal Breaks: Can Occur in both “Somatic & Germ cell”, and transmitted during Miosis & Mitosis.(4)

I) General Chromosomal Effect:

When Chromosome is exposed to Radiation, Breaking Occurs 2 or more chromosomal Fragments each of them having a broken end, then the broken end joins with the other end.

This will Possibly Produce New Chromosome, The new Chromosome May or May not appear structurally different from chromosome prior to radiation.

If It Occur, It occurs Either Before DNA Synthesis, this leads to Chromosomal Aberration “ Both daughter cells are affected”. or After DNA Synthesis: (G2-S Stage), this leads to Chromatid Aberration because Only One chromatid of pair has been damaged ⇒ One daughter Cell Affected. (29)

2) Types of Break:  

The first type is Single Break which occurs in One chromosome or chromatid.second type is Single Break occurring in Separate chromosome or chromatid.third type is Two or More Breaks occurring in the same chromosome or chromatid.last type is Stickiness or Climbing of chromosome or chromatid.

This Results In Consequences To the cells of these Structural changes may be one of the following.

First Restitution as Broken ends region with no visible damage. Secondly,  Deletion as Loss of a Part of chromosome or Chromatide, at the next mitosis gives rise to aberration.

Thirdly Re-arrangement of broken ends with Visible damage can produce grossly distorted chromosome. ( E.X 1) ACenteric Chromosome. ring Chromosome, Di-Centric Chromosome, and Anaphase Bridge.Re-arrangement of broken ends without Visible damage, this leads to Trans-location of Genetic Material Re-arrangement, which leads to Mutation. (29)

3) Chromosomal Sticking:

this occurs in a cell already in the division at Time Of Radiation.which leads to alteration of chemical composition Of Protein Chromosome, this results in Inability of Separation of Chromosome at Meta and Anaphase, Then Obride Formation between two opposite Poles.All lead to Error of Transmission of Genetic Materials of Daughter Cells.Change to the sequences of Genetic information, this occurs by “Trans-location and Inversion”. Both Processes requires 2 breaks either in the same chromosomal or different chromosomes. (29)

 

Radiation Effect on SKin.

LAYERS OF SKIN

Epidermis Outer layer of skin has two types of cell, Mature: Non-Dividing Cells, at the surface. And Immature: Dividing Cell of the base (Basal Layer). Cells lost from surface replaced by cells from the base layer which is Dividing, SO Skin is SENSITIVE TO RADIATION Dermis.: A layer of C.T which contain hair follicles, sebaceous gland, sweat gland, Bl.Vessels, Nutrition of skin.Sub-Cutaneous layer of C.T & Fat .(29)

 

I) Acute Effects:

when exposure to dose of 4-10 Gy, 2-3 Wks  after Radiation, this leads to Erythema & Inflammation, Dry Desquamation, and Moist Wet Desquamation.25,26

2) Chronic Effects:

Atrophy & Thinning of the epidermis, and Fibrosis, and increase pigmentation, ulceration, necrosis.Note that Fractionated dose of 60 Gy in 60 wks with high energy unit Radiation Produce Minimal Skin Effect in Chronic Changes, this leads to  Atrophy of Irradiated area. Severe Necrosis Rare to occur at practice.

 

Hair Follicles

it is actively growing tissue which is Radio-Sensitive.Temporary Hair Loss Occur at a moderate dose of 7 Gy.Permanent Hair Loss Occur at High Dose more than  7 Gy.Hair Loss Occur on the 7th day of radiation.

 

Salivary Glands

when exposed to  40 Gy. As they are sensitive to radiation after 1st Wk of radiation. Saliva is reduced frequently after a transient phase of hyper-salinization. Total Dose of Bilateral Salivary gland 40 Gy, this will stop salivary production. Chronic Xerostomia has an impact on quality of life.

 

Radiation to Mucosa causes Erythema, Edema, Patchy mucositis. Mucositis start after 3 Gy.26

 

EFFECT OF RADIATION ON SKIN(4)

 

 

RADIATION PROTECTION:

AFTER their discovery, x-rays were applied to the healing arts. It was recognized within months, however, that radiation could cause harmful effects.

The first American fatality that resulted from radiation exposure was Thomas Edison’s assistant, Clarence Dally.

Since that event, a great deal of the effort has been devoted to developing equipment, techniques, and procedures to control radiation levels and reduce unnecessary radiation exposure to radiation workers and the public.

The cardinal principles for radiation protection are simplified rules designed to ensure safety in radiation areas for occupational workers. In 1931, the first dose-limiting recommendations were made.

Today, the National Council on Radiation Protection and Measurements (NCRP) continuously reviews the recommended dose limits.

Providing radiation protection for workers and the public is the practice of health physics. Health physicists design equipment, calculate and construct barriers, and develop administrative protocols to maintain radiation exposures as low as reasonably achievable (ALARA).(29)

Structure materials, air, coolant waters etc. are activated in neutron fields. The induced activity has to be considered in radiation protection design of nuclear reactors, fusion experimental reactors, and high energy accelerators. (30)

The term health physics was coined during the early days of the Manhattan Project, the secret wartime effort undertaken to develop the atomic bomb.

The group of physicists and physicians responsible for the radiation safety of persons involved in the production of atomic bombs were the first health physicists.

Thus, the health physicist is a radiation scientist who is concerned with the research, teaching, or operational aspects of radiation safety At the turn of the Millennium, the year 2000, the National Academy of Sciences identified the 20 greatest scientific and technical accomplishments of the 20th century.

Medical imaging was number 14 on this list.This is important to point out to our patients, many of whom remain wary of radiation. One never reads the word “radiation” in a newspaper or a magazine without the modifier “dangerous,” “deadly,” or “harmful.”

We practice ALARA because of the linear no-threshold radiation dose-response relationship (LNT) for stochastic effects—cancer, leukemia, and genetic effects.

Yet we should also recognize that we actually employ low levels of radiation in diagnostic imaging.Unquestionably, the application of this radiation has had a major impact on our health and increasing longevity.

If you had been born in the United States in 1900, your life expectancy was 47 years. During the first century of diagnostic x-ray imaging, life expectancy has soared.

Life expectancy is now 78 years (Figure BELOW).Nevertheless, because of LNT, we must continue to be aware of patient and occupational radiation dose and must take those steps necessary to implement ALARA.(29)

Life expectancy as a function of year of birth.(29)

Conclusion

We can summarize the previous article that Radiation is a double way weapon, it can be used in the diagnosis and treatment of different body diseases. but it must be used carefully as it has many side effects that may turn the simple diagnosis maneuver into fatal disease . to reach to good knowledge of the harmful effect of radiation on human body we discuss the basic unit of the body, the cell. and we discuss the radiation interaction, effect of radiation on different body systems.

 

 

References:

  1. Types of radiation, Introduction, Living with radiation by Roger Clark, NRPB, 5th; 1.
  2. Benefits and risks, Introduction, Living with radiation by Roger Clark, NRPB, 5th; 1.
  3. Public Anxiety, Introduction, Living with radiation by Roger Clark, NRPB, 5th; 2.
  4. Kelsey C. Radiation biology of medical imaging. Hoboken, NJ: Wiley-Blackwell; 2014.
  5. William R. Hendee, Ph.D., Michael K. O’Connor, Ph.D. Radiation Risks of Medical
    Imaging: Separating Fact from Fantasy. Radiology: Volume 264: Number 2—August 2012.
  6. Cynthia H. McCollough, Ph.D. et al, Radiation Exposure and Pregnancy: When Should We Be Concerned?, RadioGraphics 2007; 27:909–918 ● Published online 10.1148/rg.274065149.
  7. Beyzadeoglu M, Ozyigit G, Ebruli C. Basic radiation oncology. Ch.2 Radiobiology. Springer-Verlag Berlin Heidelberg 2010. ISBN 978-3-642-11666-7.
  8. de Pouplana LR (ed) (2005) The genetic code and the origin of life. Springer, Berlin, pp 75–91.
  9. Thomas DP, William CE (2007) Cell biology. Saunders, Philadelphia, pp 20–47.

10.Moeller SJ, Sheaff RJ (2006) G1 phase: components, conundrums, context. In: Kaldis P (ed)
Cell cycle regulation. Springer, Berlin, pp 1–29.

  1. Hartwell LH, Culotti J, Pringle JR et al (1974) Genetic control of the cell division cycle in
    yeast. Science 183:46.
  2. Awwad HK (2005) Normal tissue radiosensitivity: prediction on deterministic or stochastic
    basis? J Egypt Natl Canc Inst 17(4):221–230 (review).
  3. Katz R, Cucinotta FA (1999) Tracks to therapy. Radiat Meas 31(1–6):379–388 (review).

14. Goitein M (2008) Radiation oncology: a physicist’s-eye view. Springer, New York, pp 3–4
15. Podgorsak EB (2005) Radiation oncology physics: a handbook for teachers and students.
International Atomic Energy Agency, Vienna, pp 485–491.

16. Beck-Bornholdt HP (1993) Quantification of relative biological effectiveness, dose modification factor, and                    therapeutic gain factor. Strahlentherapie Onkol 169(1):42–47
17. Magill J, Galy J (2005) Radioactivity, radionuclides, radiation. Springer, Heidelberg, pp 102–103.

18.Barendsen GW, Koot CJ, Van Kersen GR, Bewley DK, Field SB, Parnell CJ (1966) The effect
of oxygen on impairment of the proliferative capacity of human cells in culture by ionizing
radiations of different LET. Int J Radiat Biol Relat Stud Phys Chem Med 10(4):317–327.

19. Bond VP (1995) Dose, effect severity, and imparted energy in assessing biological effects.
Stem Cells 13(suppl 1):21–29 (review)
20. Podgorsak EB (2005) Radiation oncology physics: a handbook for teachers and students.
Vienna, International Atomic Energy Agency, p 492
21. Stabin MG (2008) Quantities and units in radiation protection In Stabin MG (ed) Radiation
protection and dosimetry. Springer, New York, pp 100–102.

22. Lutgens LC, Deutz N, Granzier-Peeters R, et al. Plasma.citrulline concentration: a surrogate end point for           radiation-induced mucosal atrophy of the small bowel. A feasibility study in 23 patients. Int J Radiat Oncol Biol                  Phys 2004;60:275–85.

23. Miquel Macià I Garau, Anna Lucas Calduch, Enric Casanovas López. Radiobiology of the acute radiation                   syndrome. reports of practical oncology and radiotherapy 1 6 ( 2 0 1 1 ) 123–130.

24.Gordon K, Char D, Sagerman R. Late effects of radiation on the eye and ocular adnexa. International                        Journal of Radiation Oncology*Biology*Physics. 1995;31(5):1123-1139.

25.Collen EB, Mayer MN. Acute effects of radiation treatment: Skin reactions. The Canadian Veterinary                        Journal.  2006;47(9):931-935.

26.Bray FN, Simmons BJ, Wolfson AH, Nouri K. Acute and Chronic Cutaneous Reactions to Ionizing                           Radiation Therapy. Dermatology and Therapy. 2016;6(2):185-206. doi:10.1007/s13555-016-0120-y.

  1. Genetics Home Reference, U.S National Library of medicine, available at https://ghr.nlm.nih.gov/.
  2. The Cell Cycle, Mitosis, and Meiosis, Virtual Genetics Education Centre, University of Leicester.
  3. Bushong S. Studyguide for radiologic science for technologists. Printed in the United States of America: Academic Internet Publish; 2012.
  4. Kaul A, Becker D. Radiological protection. Berlin: Springer; 2006.
  5. Hall, Eric J.; Giaccia, Amato J. Radiobiology for the Radiologist, 6th Edition.Copyright ©2006 Lippincott Williams & Wilkins.
  6. Tubiana M, Dutreix J, Wambersie A. Introduction to radiobiology. London: Taylor & Francis; First published 1990., 2005 edition.

 

 

MRI ANATOMICAL POSITIONING

Introduction

Magnetic Resonance Imaging could be identified as a medical diagnostic procedure that makes different organs images by using the principle of nuclear magnetic resonance.

It generates thin-sections of any a part of the body – from any angle and direction, So Imaging can form such an image once the body is exposed to electromagnetic field.

MRI creates a powerful magnetic field and also the tiny biological “magnets” within the body consisting of protons set within the nucleus of the atom are attractable, As the nucleon possesses basic magnetic properties.

First, imaging creates a gentle state of magnetism inside the body by inserting it in a very steady magnetic field.

Second, the imaging stimulates the body with radio waves to vary the steady-state orientation of protons.

Third, the imaging machine stops the radio waves and registers the body’s magnetic force transmission.

Fourth, the transmitted signal is accustomed construct internal pictures of the body by computerized axial imaging.

An imaging image isn’t a photograph. it’s truly a computerized map or image of radio signals emitted by the organs. imaging is superior to CAT scan as a result of CAT scan is mistreatment radiation, imaging uses harmless radio waves.

The sole uncommon preparation is that every one removable golden objects should be left outside the scanning space, together with removable hearing aids, dentures, and different prosthetic devices.

Credit cards may be broken by the imaging as a result of magnetic codes may be full of the imaging magnet.

Magnetic Resonance Imaging could be a powerful diagnostic tool within the medical imaging market place because of the procedure of alternative for the visualization of sentimental tissue.

The imaging business is manufacturing over a pair of,000 units p.a. U. s. is portrayed with four-hundredth of the planet promoting and production of imaging. there’s associate degree rising agreement that the imaging incorporates a broad application in smaller hospital and clinics. (1)

 

History of MRI

1882 – Nikola Tesla discovered the Rotating magnetic field in the national capital, Hungary. This was a basic discovery in physics.

Figure (1); Nikole Tesla The genius who lit the world,
The Discoverer of Magnetic Field and the God father of The current MRI (2)

 

1937 – Columbia University prof Isidor I. Rabi operating within the Pupin physic Laboratory in NY town, discovered the quantum phenomenon dubbed nuclear magnetic resonance (NMR).

1950’s – Herman Carr creates a one-dimensional MR image.

1956 – International Electro-technical Commission-Committee of Action declared the MR creation of The at Munich, Deutschland by.

All magnetic resonance imaging machines are a label in “Tesla Units”. The strength of a magnetic field is measured in Tesla or Gauss Units.

The strength of a field is measured in Tesla or Gauss Units. The more sturdy the field, the more sturdy the quantity of radio signals which might be evoked from the body’s atoms and so the higher the standard of resonance imaging footage.

1972 – Raymond Damadian applies for a patent, that describes the idea of nuclear magnetic resonance being employed for the higher purpose. He illustrates major components of magnetic resonance imaging machine in his application.

1973– Paul Lauterbur, a chemist Associate in Nursingd a nuclear resonance pioneer at the State University N Y, Stony Brook, created the first nuclear resonance image. it completely was of a tubing.1974 – Raymond Damadian receives his patent.

1977  Raymond Damadian with his two post-doctoral students, Michael Goldsmith and Larry Minkoff build the first MRI scanner at New York’s Downstate Medical Center. And They do first MRI scan.

Figure (2): shows First MR image ever of the Human organ. 1977 (3)

last 40 years:

1983 – Ljunggren and Tweig introduce k-space.

1986 – Le Bihan writes about diffusion weighted imaging (DWI).

1987 – Real time MR imaging of the heart is developed.

1991 – Filler and colleagues describe imaging of axonal transport of super magnetic metal oxide particles, a technique, which later becomes important in imaging of neural tracts.

1993 – Functional MR imaging of the brain is introduced.

1994 – The first intraoperative MR unit developed by GE and Harvard is installed at the Brigham and Women’s Hospital in Boston.

2000‘s – Cardiac MRI, Body MRI, fetal imaging, practical MR imaging is more developed and become routine in several imaging centers. analysis centers create important strides forward in imaging cartilage on high field scanners. the amount of free standing magnetic resonance imaging centers, most of that utilize low or moderate field MR scanners considerably will increase.(4)

HEAD Imaging

Figure (3): shows A sample patient positioning in an eight channel brain coil (5).

Head is considered the first Organ that MRI was practically used to scan. The brain is the most complicated organ in the body.

MRI has made an advanced progress in the diagnosis of many diseases. Here we are, we will go A step-by-step approach to head and brain MR imaging as given below:

Patient Preparation:

 

Routine Procedure :

The patient consent form should be given to the patient with a detailed explanation of the content. The form should be carefully read, all questions must be answered with clear answers such as “YES” or “NO,” and additional clarifications should be written. It must be signed by the patient or legal guardians and confirmed by MR personnel.

If there are any surgical implants, radiologist on duty has to make a decision based on implant type and MR compatibility.

If there is any suspicion or lack of information on the implant, do not take any risk with the patient safety and do not scan the patient.

If the form is complete with all the information, the patient should change to MR gown and remove any clothing with any metal. It is always a good practice to remove the jewelry as well.

As the last line of patient safety, it is also a good practice to scan patient with a handheld metal detector before taking the patient to MRI room.

Patient Positioning:

The patient head should be centered at the brain coil, chin pointing upward as shown in the figure (3).

The patient should use earplugs for hearing protection with additional headsets and/or immobilization pads should be placed around the head to reduce the noise and gross patient motion.

The head should also be fixed with additional straps for further patient motion reduction while keeping patient safety and comfort as a priority.

We also recommend placing the leg support pads for patient comfort. An alarm bell should be given to the patient and tested.

After landmarking the center of the brain coil or just below the eyes using laser marker lights (while the eyes are closed) or touch sensors, you can send the patient in and start the exam(6).

Routine Brain

Sample Imaging Protocols: Routine brain imaging is used for the patients referred to MRI without any specific diagnosis and it can be applied for general nonspecific headache or even checkup.

Figure (4) show Routine Brain Sequences (7)

Tips and Tricks

Sagittal T1 can be replaced by a sagittal T2 sequence that might be more informative for visualizing craniocervical lesions.
Recently, diffusion weighted imaging (DWI) has been added to routine brain imaging as well. It can also be routinely acquired for older patients.
It is also important to remind that T1 flair as an alternative to T1 imaging can be used for routine brain imaging.

T1 flair sequence provides better gray-white matter contrast and has shorter acquisition times due to higher echo train length. It also further suppresses the CSF resulting in better image quality. However, due to inversion pulse associated with the T1 flair sequence, there are considerable worries regarding postcontrast use of T1 flair sequence.

 

Temporomandibular Joint (TMJ)

Temporomandibular joints (TMJ) joint imaging , we can doe it  with a number of different coils depending on the availability at your site.

Even though today high-density coils with eight channel of above can give you good quality, the TMJ imaging dedicated coils do produce a very nice image quality.

The TMJ dedicated coils usually has a holder device to fix them in the desired position and can be used for bilateral joint imaging with small loop coils as shown in the figure below.                                                                            These loop coils are practically surface coils and can have different diameters. The coil shown in this book is two 3 in. diameter coil.

These coils will get relatively uniform signal within the 3 in. in diameter and 3 in. in depth. Therefore, they provide a high signal for the TMJ joints.

If you have one of the new multichannel brain coils but not the loop coils, you can still follow the guidance in the book to acquire very nice TMJ images.

Quite often TMJ imaging can be done in dynamic imaging or so-called kinematic imaging.

Kinematic imaging requires imaging TMJ joint while the mouth is closed and opened at different levels so that the joint and disc position can be imaged dynamically.

To keep the mouth open at different levels without motion is possible by using kinematic devices from different companies.

However, if you do not have any special hardware for this type of exam, you can still do the kinematic exam by explaining the patient the procedure and give instructions during the scan accordingly.                                              The kinematic exam starts with the mouth shut. Then, we repeat the scan while the patient opens his/her mouth 1–2 cm in each time until we reach the maximum opening.

A step-by-step approach to TMJ MR imaging is given below.

Patient Preparation:

The patient consent form should be given to the patient with a detailed explanation of the content. The form should be carefully read, all questions must be answered with clear answers such as “YES” or “NO,” and additional clarifications should be written.

It must be signed by the patient or legal guardians and confirmed by MR personnel.

Plus Routine Procedure :

As the last line of patient safety, it is also a good practice to scan patient with a handheld metal detector before taking the patient to MRI room.

Patient Positioning:

The TMJ coil is shown in figure (5). The holder enables you to position the coil in the desired location and can be fixed in this location so that it does not move during the scan.

When you position the coil, ask the patient to open and close the mouth while you feel exactly where the TMJ joint is with your hand. The loop coil center should be placed directly at the TMJ joint.

The coils should be as close to the face as possible without disturbing the patient. If you do not have the TMJ dedicated coils, you can use general purpose brain coil for imaging.

Please make sure that you give the patient alarm/buzzer to patient’s hand and test it before sending in. The landmarking should be at the center of loop coils using laser lights or touch sensor.

It is always recommended to let the patient know how long the scan is going to take and also keep communicating frequently to make them as comfortable as possible in the MR bore (8).

Figure (5): A sample patient positioning in a TMJ dedicated loop coils (9)

 

Elbow Imaging

Elbow imaging can be done with several different coils.

If you have a general flexible coil available at your site, you can put the patient feet first on supine position and let the arms at the side. Then you can wrap the coil around the elbow. This is the most comfortable position for the patient.

However, if you do not have any working flexible coils, you can use one of the smaller diameter coils such as the knee, foot, or loop coils to scan the patient head first on prone position. This is also called superman position.

Somewhat contrary to the position name, it is a super uncomfortable position for the patient though. If you have to scan a patient in a cast and cannot be placed straight, you can also use other coils such as shoulder coil for an efficient scan.

Patient Preparation:

Routine Procedure

Patient Positioning:

If you do have a flexible coil, you can position the patient supine, feet first or head first and you can wrap the coil around the elbow of interest. Quite similar to shoulder imaging patient preparation, place additional pads under the patient’s arm to make humerus almost parallel to the table.

The palm of the hand should be pointing upward as well for the best patient position as shown in Figure (6). However, if the patient is unable to stay in this position due to injury or pain, you can position the arm in a more comfortable way.

To reduce gross patient motion artifacts, immobilization straps should be placed over the patient arm at the elbow level or a bit more inferior.

Please make sure that you give the patient alarm/buzzer to patient’s hand and test it. After landmarking the center of the coil using laser lights or touch sensors, you can send the patient in and start the exam.

It is always recommended to let the patient know how long the scan is going to take and also keep communicating frequently to make them as comfortable as possible in the MR bore (10).

Figure (6) shows: A sample patient positioning for an elbow in a general purpose flexible coil. Please
note that the patient palm point upward in this position (external rotation)(11).

Knee Imaging

Knee joints are usually imaged unilaterally using dedicated coils.

The knee and foot coils are usually what we call transmit/receive coils rather than receive only coils.

Transmit/receive coils have the design features to be able to transmit the RF pulse directly from a transmitter element in the coil and receives the signal with receiver elements. This way, we can eliminate possible wrap around
or aliasing artifacts from the other knee.

Most of the MR systems use dedicated single channel (quadrature) transmit-receive knee coils. However, most of the recent MR systems come with multichannel (8 or 16) dedicated transmit/receive knee and/or foot coils.

The utilization of dedicated multichannel knee coils can make significant improvements in MR image SNR and We can use it for either shorter scan time or increased spatial resolution.

If you do not have a dedicated knee coil,So you can use other available coils. However, the image parameters should be modified to compensate for the SNR loss.

Patient Preparation:

Routine Procedures.

Finally, have the patient go to the restroom before the exam.

Patient Positioning:

Place the knee coil straight at the center of the MR table.

When you place the patient’s knee in the coil, insert a small pad under the knee joint to slightly bend the knee (about 15°).

The patella should be aligned with the center of the coil for good positioning.

When the coil top is attached and locked, place additional pads between the knee and coil to further immobilize the knee. These pads can significantly reduce the motion artifacts.

The other knee should be placed as further ways from the coil as possible to prevent any wrapping or aliasing, especially with the receive-only coil.

Please make sure that you give the patient alarm bell to the patient and ask them to test it before sending in.

Mark center of the coil by using laser lights then send the patient in and start the exam.

It is always recommended to let the patient know how long the scan is going to take and also keep communicating frequently to make them as comfortable as possible in the MR bore (12).

Figure (7): shows A sample for feet first and supine patient positioning in a multichannel transmit/ receive knee coil is shown. Please note that this coil design includes a small pad under the knee joint (13).

Figure (8): shows A sample for feet first and supine patient positioning in a multichannel transmit/receive knee coil is shown. Please note that this coil design includes a small angulation around 15°(14).

Liver and biliary system

.
Indications
Why the physician would ask for MRI on Liver and biliary system.

first, if he is looking for Focal lesions or staging of neoplasms, or even benign hepatic disease, especially haemangioma and focal nodular hyperplasia. hemochromatosis.

Gallbladder disease and biliary duct obstruction are also of the important indications.

Finally evaluation of liver infiltrants such as iron or fat.

Equipment

we will need Body coil/volume torso array or multi-coil and  RC bellows. Also, Ear plugs and Pe gating leads are required.

Patient positioning

The patient lies supine on the examination couch with the RC bellows (if required) securely attached.

The patient is positioned so that the longitudinal alignment light lies in the midline, and the horizontal alignment light passes through the level of the third lumbar vertebra or the lower costal margin(15) .

Suggested protocol:

Coronal breath-hold incoherent (spoiled) GRE/SE T1 (Figure 9)

Acts as a localizer if three-plane localization is unavailable, or as a diagnostic sequence.

Thick slices/gap are prescribed relative to the vertical alignment light, from the posterior abdominal muscles to the anterior abdominal wall.

The area from the pubic symphysis to the diaphragm is included in the image.

P 60 mm to A 40 mm

Axial SE/FSE/incoherent (spoiled) GRE T1 and out of phase (Figures 10 and 11)

As for Coronal T1, except prescribe slices from the inferior margin of the liver to the diaphragm.

Figure 11.2 Coronal SE T1 weighted image through the abdomen demonstrating slice prescription boundaries and orientation for axial imaging of the liver.

Delayed scans after contrast enhancement using chemical/spectral presaturation techniques are sometimes necessary to evaluate arterial and venous phases.

Figure (9): Coronal SE T1 weighted image through the abdomen demonstrating slice prescription boundaries and orientation for axial imaging of the liver(16).

Figure (10): Axial FSE T1 weighted image through the liver (17).

Figure (11): Axial incoherent (spoiled) T1 weighted breath-hold image of the liver (18).

 

Additional sequences

SS-FSE (MRCP) (Figure 11)

This sequence provides images in which only fluid-filled spaces such as the gall bladder and biliary ducts return signal.

It is necessary to use very long TEs and TRs to effectively nullify the signal from all tissues except those that have long T2 decay times.

TEs in excess of 200 ms and TRs of more than 10 s are required (see also Pancreas and Salivary glands). If SS-FSE is unavailable then an FSE sequence may be substituted.

Figure (12) Coronal SS-FSE image of the gallbladder (MRCP). Very long values of TR and TE were used to acquire images in which only fluid is seen (19).

 

SS-FSE/GRE-EPI/SE-EPI/diffusion imaging

The use of real-time imaging has applications in the liver and biliary system. This includes biopsies and thermal ablations of liver lesions under real-time MR control.

In addition, diffusion and perfusion techniques of the liver have been developed that may negate the use of contrast agents in the future.

DWI images are overlaid onto T1 weighted acquisitions.

The DWI image set provides pathology information, whereas the T1 weighted acquisition provides anatomical data.

The images produced are not dissimilar to a PET/CT scan.

In addition diffusion tensor imaging used in conjunction with parallel imaging techniques enables differentiation of benign from malignant hepatic lesions and may also assist in the quantification of hepatic fibrosis.

Image optimization

TECHNIQUE ISSUE:

The inherent SNR and CNR of the abdominal contents are usually excellent due to their high proton density, and the use of a torso array coil increases this even further.

In addition, parallel imaging techniques using multi-array coils reduce scan time significantly.

Due to the respiratory artifact, RC or respiratory triggering may be necessary. Alternatively, breath-hold techniques may be used to suspend respiratory motion.

In axial T1 sequences, it is necessary to shorten the TR to less than 400 ms in SE sequences as this is considered the optimum value for demonstrating liver contrast.

As the slice number available per acquisition is reduced with a short TR, two or three acquisitions may be required to cover the whole liver.

Two FSE sequences using TEs of 80 ms and 160 ms are required to characterize haemangiomas, which retain a high signal intensity on late echo images.

Artefact problems

The main source of artifact in the liver is motion caused by respiration, flow and peristalsis.

RC or respiratory triggering is often required, especially on the superior axial slices, due to the proximity of the diaphragm.

However, breath-hold techniques may also be utilized. Pe gating is sometimes used but it often increases the scan time, especially if the patient’s heart rate is slow or cardiac output poor, so that the system cannot trigger efficiently off each R wave.

Commonly, Pe gating does not significantly increase image quality and only serves to lengthen the scan time. Under these circumstances it is advisable to dispense with it.

Spatial presaturation pulses placed S and I to the FOV are necessary to decrease flow motion artifact in the aorta and IVC.

GMN also minimizes flow artifact but, as it increases the signal in vessels and the minimum TE, it is not usually beneficial in T1 weighted sequences.

Bowel motion is often a problem on the lower axial slices of the liver, whereas gastric motion artifact is sometimes evident on the more superior slices. Antispasmodic agents, given IV, IM or subcutaneously prior to the examination, effectively reduce this.

Patient considerations

Careful explanation of the procedure is important.

Ensure that the patient is as comfortable as possible. Some antispasmodic agents given IM may cause nausea but fruit juice given after the study can alleviate this.

Due to excessively loud gradient noise associated with some sequences, ear plugs must always be provided to prevent hearing impairment.

Contrast usage;

Contrast is often beneficial to demonstrate liver metastases.

Weighting depends on the type of contrast media used.

T1 shortening agents such as gadolinium require T1 weighted post-contrast scans.

These can be acquired in conjunction with chemical/spectral presaturation pulses and acquired in multiple phases to evaluate the dynamic contrast enhancement characteristics of hepatic lesions.

T2 weighting is necessary after injection of superparamagnetic T2 shortening (liver specific) agents (see Contrast agents in Part 1).

Scans should be delayed for approximately 1 hour after injection to allow time for uptake of contrast by the liver.

The use of contrast and dynamic imaging to visualize liver vasculature and the biliary system is gaining in popularity. Oral and rectal contrast agents,for evaluation of gastrointestinal disease, are also used

Kidneys and adrenal glands

Indications:

Why the physician asks for MRI on Kidneys and adrenal glands. this happens when we we are looking for: Adrenal masses and hemorrhage Or  Renal masses and haemorrhage.Or renal cell carcinoma.Or Renal transplant rejection.Or Ureteric obstruction.

Equipment

 we will need Body coil/multi-phased array or multi-coil array, RC bellows and  Ear plugs.

Patient positioning

The patient lies supine on the examination couch with the RC bellows securely attached (if required).

The patient is positioned so that the longitudinal alignment light lies in the midline, and the horizontal alignment light passes through the level of the third lumbar vertebra, or the lower costal margin. The kidneys are generally located about four fingers inferior to the xiphoid (20).
 

Suggested protocol

Coronal breath-hold fast incoherent (spoiled) GRE/SE/FSE T1 (Figure 13)

Acts as a localizer if three-plane localization is unavailable. Alternatively it can be used as a diagnostic sequence. Medium slices/gap are prescribed on either side of the vertical alignment light, from the posterior abdominal muscles to the anterior abdominal wall. The area from the pubis symphysis to the diaphragm is included in the image.

Axial incoherent (spoiled) GRE T1 in and out of phase .contrast chemical/spectral presaturation

As for Coronal SE/FSE T1, except medium slices/gap are prescribed from the inferior margin of the kidneys to the superior aspect of the adrenals (Figure 14). The coronal plane may also be useful depending on lesion location. Slices may also be offset to specifically image the adrenals.

 

Figure (13) Coronal incoherent (spoiled) GRE T1 weighted image through the abdomen demonstrating the kidneys(21)

 

Figure (14) Coronal incoherent (spoiled) GRE T1 weighted through the abdomen demonstrating slice prescription boundaries and orientation for axial imaging of the kidneys(22)

Additional sequences

MR urography:

Either FSE or SS-FSE sequences may be used with very long TEs and TRs to produce heavily T2 weighted images in which only fluid that has a very Figure 11.10 Coronal incoherent (spoiled) GRE T1 weighted through the abdomen demonstrating slice prescription boundaries and orientation for axial imaging of the kidneys.for use in the urinary system to visualize the renal collecting system, the ureters, and the bladder.

Diffusion imaging

DWI using SS-EPI acquisition in conjunction with parallel imaging techniques may be useful in the differentiation of malignant adrenal lesions from hyperplasia or adenomas and renal cysts from renal cell carcinomas.

Image Optimization

Technical issues

The inherent SNR and CNR of the abdominal contents are usually excellent due to their high proton density, and the use of a torso array coil increases this even further. In addition, parallel imaging techniques using multi-array coils reduce scan times significantly. Spatial resolution is important, especially when imaging relatively small structures such as the kidneys and adrenal glands, which therefore require thin slices/gap.

However, this is often difficult to achieve when using the body coil, a large FOV and in the presence of respiratory and flow artifact. The use of a torso array coil greatly improves resolution in the abdomen. In addition, parallel imaging techniques can be used to improve resolution whilst

keeping scan times short. SE sequences usually produce the best contrast in the abdomen, but result in fairly lengthy scan times. For this reason, breath-hold GRE or SS-FSE sequences are often preferred. FSE used in conjunction with a rectangular/asymmetric FOV allows PD and T2 images to be obtained in a shorter scan time.

Artefact problems

The main source of artifact in this area is from respiratory movement and flow in the aorta and the IVC. RC or respiratory triggering is often required and significantly reduces respiratory ghosting.

Alternatively, breath-hold techniques may be utilized. Spatial presaturation pulses placed S and I to the FOV are necessary to reduce flow motion artifact arising from the aorta and IVC.

As the kidneys and adrenals are retroperitoneal structures, a spatial presaturation band brought into the FOV and placed over the anterior abdominal wall reduces respiratory artifact significantly without obscuring important anatomy.

GMN also minimizes flow and, in some cases, respiratory motion but it increases the signal in vessels and the minimum TE.

Chemical shift artifact is often troublesome in the kidneys, especially at higher field strengths. This is due to retroperitoneal fat being adjacent to fluid-filled kidneys.

Narrowing the receive bandwidth increases this artifact but, if used in conjunction with fat suppression techniques, results in a significant improvement in SNR and a reduction in chemical shift.

However, this strategy increases the minimum TE and is therefore reserved for T2 weighted sequences.

Bowel motion is also troublesome but is effectively reduced by the administration of antispasmodic agents given IV, IM or subcutaneously prior to the examination.

Patient considerations

Careful explanation of the procedure is important. Ensure that the patient is as comfortable as possible. Some antispasmodic agents given IM may cause nausea but fruit juice given after the study can alleviate this. Due to excessively loud gradient noise associated with some sequences, ear plugs must always be provided to prevent hearing impairment.

Contrast usage

Contrast is sometimes used in conjunction with dynamic imaging to visualize the uptake of contrast in the kidneys (see Dynamic imaging under Pulse sequences in Part 1).

Vascular imaging of the renal arteries is a common technique discussed later (see Vascular imaging later in this chapter). Contrast may also be necessary to increase the conspicuity of the adrenal glands.

Recently functional imaging of the kidneys after the administration of macromolecular contrast agents have been advocated in the evaluation of a variety of renal diseases.

These agents are almost totally excreted by the kidneys, thereby improving the conspicuity of lesions that have different perfusion characteristics.
 

Pancreas

Common indications

Why the physician asks for MRI on Pancreas. if he is looking for Pancreatic Tumors.or Pancreatic duct obstruction.

Equipment

In this examination, we will need Body coil or multi-phased array or multi-array coil.An RC bellows is also needed.and finally,  Ear plugs is requested in this examination.

Patient positioning

The patient lies supine on the examination couch with the RC bellows securely attached.

The patient is positioned so that the longitudinal alignment light lies in the midline, and the horizontal alignment light passes through the level of the third lumbar vertebra, or the lower costal margin (23).

Suggested protocol

Coronal breath-hold fast incoherent (spoiled) GRE/SE T1 Acts as a localizer if three-plane localization is unavailable, or as a diagnostic sequence.

Thick slices/gap are prescribed on either side of the vertical alignment light, from the posterior abdominal muscles to the anterior abdominal wall. The area from the pubic symphysis to the diaphragm is included in the image.

Figure (15): Coronal FSE T1 weighted image through the abdomen demonstrating slice prescription boundaries and orientation for axial imaging of the pancreas (24).

Figure (16): Axial high-resolution FSE T2 of the pancreas (25).

Figure (17): Axial SS-FSE T2 of the pancreas during free breathing(26).

 

Figure (18): Axial fast incoherent (spoiled) T1 weighted image of the pancreas(27).

Diffusion imaging

Diffusion imaging used in conjunction with parallel imaging techniques may be useful to detect pancreatic adenocarcinoma and for differentiation from benign and cystic lesions.

Image optimization: Technical issues

The inherent SNR and CNR of the abdominal contents are usually excellent due to their high proton density, and the use of a torso array coil increases this even further. In addition, parallel imaging techniques using multi-array coils reduce scan times significantly.

Spatial resolution is also important, especially when imaging relatively small structures such as the pancreas that require thin slices/gap. However, good resolution is often difficult to achieve when using the body coil and a large FOV, and in the presence of respiratory and flow artifact.

A torso phased array coil greatly improves the SNR that can then be traded for resolution. In addition, parallel imaging techniques can be used to improve resolution whilst keeping scan times short.

SE sequences usually produce the best contrast in this region, but result in fairly lengthy scan times and therefore FSE is usually used.

Artefact problems

The main source of artifact in this region is from respiratory and flow motion in the aorta and IVC. RC or other respiratory gating techniques are often required and significantly reduce respiratory ghosting.

Alternatively, breath-hold techniques may be utilized. Spatial presaturation pulses placed S and I to the FOV are necessary to reduce flow motion artifact in the aorta and IVC.

GMN also minimizes flow motion but, as it increases the signal in vessels and the minimum TE, it is not usually
beneficial in T1 weighted sequences.

Additional shimming may be required before chemical/spectral presaturation sequences.

Gastric and bowel motion is also troublesome in this area due to the proximity of the stomach and the duodenum to the pancreas.

This artifact is effectively reduced by the administration of antispasmodic agents given IV, IM or subcutaneously prior to the examination.

Patient considerations

The careful explanation is essential if breath-holding sequences are to be performed. Some antispasmodics given IM may cause nausea, which can be remedied by giving the patient fruit juice after the scan. Due to excessively loud gradient noise associated with some sequences, ear plugs must always be provided to prevent hearing impairment.

Contrast usage

Contrast is often necessary for conjunction with dynamic imaging to visualize small pancreatic lesions.

Positive and negative oral contrast agents to delineate bowel, and therefore the pancreas can be useful.

Recently studies have been performed using secretin as an enhancement agent.

This stimulates the release of fluid into the pancreatic duct, thereby improving visualization on T2 weighted images. There may also be a role for secretin in the evaluation of the pancreatic function.

TESTES

Patient Preparation

Firstly The patient has to go to the toilet before the study. Then you should explain the procedure to the patient and then Offer him/her ear protectors or ear plug.

Ask the patient to undress except for underwear and  Ask him/her to remove anything containing metal (hearing aids, hairpins, body jewelry, etc.). finally, you must have an intravenous line placed

Positioning

The Patient is Supine. The  Body array coil (wraparound coil, surface coil, e.g., circular surface
coil) and we don’t forget to cushion the legs.

Sequences

The Scout: coronal, sagittal, and axial.

Sequence 1 coronal T2-weighted.

Slice thickness of 4 mm is determined with slice gap of 0–20 % of slice thickness (0–0.8 mm or factor 1.0–1.2). The  FOV should be small ( e.g., 200 mm) with  Matrix about  512 ( but then with NSA 3–4). we also should do Phase oversampling. Finally, saturation slab is axial superior to the slices for saturation of the vessels

Sequence 2 coronal T1-weighted

Slice thickness of 4 mm is determined with slice gap of 0–20 % of slice thickness (! 0–0.8 mm or factor 1.0–1.2). The FOV should be small (e.g., 200 mm). Phase oversampling should be done. finally, saturation slab is axial superior to the slices for saturation of the vessels.

Figure (19): Testes, coronal, sequences 1 and 2(28)

Figure (20): Testes, axial, sequence 4(29)

Sequence 3 coronal

As sequence 2 but after administration of contrast agent (Gd-DTPA)

Sequence 4 axial

T1-weighted after administration of contrast agent.

slice thickness of 4 mm is determined with slice gap about 20 % of slice thickness ( 0.8 mm or factor 1.2).

The FOV should be small (e.g., 200 mm). Saturation slab is axial superior to the slices for saturation of the vessels (30).
Tips & Tricks

Positioning aid: leave tight-fitting underpants in place (immobilizes the testes).

If necessary, cushion the testes. If a surface coil is used, perhaps place a thin foam pad between testes and coil to prevent too strong a signal in the vicinity of the coil.

BREAST

Patient Preparation

Firstly The patient has to go to the toilet before the study. Then you should explain the procedure to the patient and then Offer him/her ear protectors or ear plug.

Ask the patient to undress completely above the waist and  Ask him/her to remove anything containing metal (hearing aids, hairpins, body jewelry, etc.). finally, you must have an intravenous line placed.

Positioning

The Patient is Prone. We will use the Breast coil. Arms will be alongside the body or in front of the head, forehead resting on the hands(31).

Sequences

Scout: axial, coronal, and parasagittal

Sequence 1 axial T2-weighted

Slice thickness of 4 mm with slice gap: 0–20 % ( 0–0.8 mm or factor 1.0–1.2). Phase encoding gradient should be LR (because of cardiac motion). No Saturation slab.

Figure (21): Breast, axial, sequence 1(32).

Sequence 2 axial T2-weighted 3-D GRE

With Flip angle 25° 1.0 T , TR = 8.5–12 and TE = 5.3–6.1. With Flip angle 20–25° 0.5 T , TR = 7.7–10
and TE = 2.5–3. with Flip angle 25, TR = 24 and TE = 13. with Flip angle 50° and  Slab thickness: 128 mm, Number of partitions: 32. (Effective) slice thickness:  4 mm. The FOV: 30–35 mm. Phase encoding gradient: LR. No Saturation slab.

Sequences 3–8 T1-weighted axial

as sequence 2 but after administration of contrast agent (Gd-DTPA 0.1 mmol/kg body weight), no delay between the sequences (sequence duration 50–90 seconds), and possibly coronal images.

Sequence 9 coronal T1-weighted 3-D GRE

With  Flip angle 20–25°, Slab thickness: 128 mm. A number of partitions: 32. (Effective) slice thickness: 4 mm. The FOV: 30–35 mm. Phase encoding gradient: cephalocaudal. No Saturation slab.

Figure (22): Breast, coronal, sequence 9(33).

Postprocessing

Subtract sequence 2 from, e.g., sequence 4. Dynamic assessment of pathologic contrast enhancements.

Tips & Tricks

For a small breast, cushion the inside of the coil with some padding (reduces motion artifacts)
A tight-fitting T-shirt can also be quite effective in immobilizing the breast

SOFT TISSUES OF THE NECK

Patient Preparation

Firstly The patient has to go to the toilet before the study. Then you should explain the procedure to the patient and then Offer him/her ear protectors or ear plug.

Ask the patient to undress completely above the waist except for underwear and  Ask him/her to remove anything containing metal (hearing aids, hairpins, body jewelry, etc.).

finally necessary, have an intravenous line placed (e.g., if the investigation is for possible tumor)

— Note: Before starting the study ask the patient to swallow mostly during the pauses and to try not to swallow at all during acquisition (i.e., when the scanner is loud) (34).

Positioning

The patient is Supine. We would use the Neck coil, and we shouldn’t forget Cushion of the legs

Sequences

Scout: sagittal and axial (three planes are best)

Figure (23): Soft tissues of the neck, coronal, sequence 1(35).
  

Sequence 1 coronal:

T2-weighted fat-saturated (plot on sagittal slice: more central or more dorsal depending on the purpose of the investigation; outline FOV on axial slice)

Slice thickness: 6 mm with Slice gap: 20 % of it ( 1.2 mm or factor 1.2). FOV:  250 mm

— Saturation slab: axial below the slices for saturation of the blood vessels (if necessary with flow compensation)

Sequence 2 axial (from jugular fossa to base of skull) T2-weighted

Slice thickness: 6 mm with slice gap: 20 % of it ( 1.2 mm or factor 1.2). FOV: approx. 180–200 mm. Saturation slab: axial (parallel) below the slices for saturation of the vessels (if necessary with flow compensation)

Sequence 3 sagittal T2-weighted

Slice thickness: 6 mm with slice gap: 20 % of it (1.2 mm or factor 1.2).saturation slab: axial below the slices for saturation of the blood vessels (if necessary with flow compensation)

Figure (24): Soft tissues of the neck, sagittal, sequence 3(36).
 

Sequence 4 axial T1-weighted

Example:  TR = 450–600     TE = 12–25 otherwise as sequence 2 If contrast agent is administered:

Sequence 5 axial T1-weighted

(as sequence 4 but after administration of contrast agent, e.g., Gd-DTPA)

Sequence 6 coronal

T1-weighted (after administration of contrast agent)
Example:  TR = 450–600   TE = 12–25 otherwise as sequence 1

Tips & Tricks

Positioning aid: center on the upper border of the larynx. For really obese patients use either large flexible wraparound coil or spinal array coil (select upper section)

Conclusion

MRI Invention was considered a revolution in the science of radiological diagnosis, especially in soft tissue pathology. Anatomical positions are variable and all depend on requested examination and condition of the patient. patient preparations in every examination are very important and just very vital in patient survival and keep the Technology and machines well. sequences of every examination are important to cover up all different pathologies from a different view.

.

References:

  1. The article How MRI works? Available at site http://www.teslasociety.com/mri.htm
  2. The Genius Who Lit the World (Nikola Tesla) available at http://www.teslasociety.com/index.html
  3. Figure 20. The interpolated image of the Minkoff scan and the first ever MRI scan of a live human being (4:45 AM July 3, 1977). Major Diagnostic Breakthrough in Multiple Sclerosis Achieved With Advanced UPRIGHT® MRI available at http://www.fonar.com/news/100511.htm.
  4. A quick history of the MRI, available at http://two-views.com/mri-imaging/history.html#sthash.kqJYI7wV.dpbs

5.  Figure 7.1 patient positioning available at M. Elmaoğlu and A. Çelik, MRI Handbook: MR Physics, Patient                     Positioning, and Protocols(1st e); 106.

 

  1. The patient positioning of Head Imaging, MRI CNS available at Elmaoglu – MRI Handbook – MR Physics, Patient Positioning, and Protocols (1st e); 106.
  2. Table 7.1 Routine brain protocols and prescription plans, CENTRAL NERVOUS SYSTEM: MRI PROTOCOLS, IMAGING PARAMETERS available at Elmaoglu – MRI Handbook – MR Physics, Patient Positioning, and Protocols (1st e); 107.

8.. Patient preparation and positioning, Tempo-mandibular joint available at Elmaoglu – MRI Handbook – MR                   Physics, Patient Positioning, and Protocols (1st e); 182.

  1. Figure (8.2 & 8.3) patient positioning in a TMJ dedicated loop coils, TMJ MRI available at Elmaoglu – MRI Handbook – MR Physics, Patient Positioning, and Protocols (1st e); 183.
  2. Patient Positioning, Elbow Imaging available at Elmaoglu – MRI Handbook – MR Physics, Patient Positioning, and Protocols (1st e); 191.
  3. Figure (8.12 & 8.13) patient positioning for the elbow, available at Elmaoglu – MRI Handbook – MR Physics, Patient Positioning, and Protocols (1st e); 192.
  4. Patient Positioning, Knee Imaging available at Elmaoglu – MRI Handbook – MR Physics, Patient Positioning, and Protocols (1st e); 209.
  5. Figure (8.32) feet first and supine patient positioning in a multi-channel transmit/receive knee coil, available at Elmaoglu – MRI Handbook – MR Physics, Patient Positioning, and Protocols (1st e); 210.
  6. Figure (8.32) feet first and supine patient positioning in a multi-channel transmit/receive knee coil, available at Elmaoglu – MRI Handbook – MR Physics, Patient Positioning, and Protocols (1st e); 210.

15.Patient positioning, MRI of Liver and biliary system . available at Handbook of MRI Technique (3rd e) by Catherine Westbrook;219.

  1. Figure (11.2) Coronal SE T1 weighted image through the abdomen demonstrating slice
    prescription boundaries and orientation for axial imaging of the liver, MRI of Liver and biliary system . available at Handbook of MRI Technique (3rd e) by Catherine Westbrook;220.

17. Figure (11.3) Axial FSE T1 weighted image through the liver, MRI of Liver and biliary system . available at Handbook of MRI Technique (3rd e) by Catherine Westbrook;221.

 

18. Figure (11.4) Axial incoherent (spoiled) T1 weighted breath-hold image of the liver, available at Handbook of MRI Technique (3rd e) by Catherine Westbrook;221.

 

19. Figure (11.7) Coronal SS-FSE image of the gallbladder (MRCP). Very long values of TR and TE were used to acquire images in which only fluid is seen, available at Handbook of MRI Technique (3rd e) by Catherine Westbrook;223.

 

20.Patient Positioning, MRI of Kidneys and adrenal glands available at Handbook of MRI Technique (3rd e) by Catherine Westbrook;227.

 

21. Figure 11.9 Coronal incoherent (spoiled) GRE T1 weighted image through the abdomen demonstrating the kidney, MRI Kidney available at Handbook of MRI Technique (3rd e) by Catherine Westbrook;227.

 

22. Figure 11.10 Coronal incoherent (spoiled) GRE T1 weighted through the abdomen, MRI Kidney available at Handbook of MRI Technique (3rd e) by Catherine Westbrook;228.

 

23. Patient positioning, MRI of the pancreas available at Handbook of MRI Technique (3rd e) by Catherine Westbrook;233.

 

24. Figure 11.16 Coronal FSE T1 weighted image through the abdomen.MRI of the Pancreas, available at Handbook of MRI Technique (3rd e) by Catherine Westbrook;234.

 

25. Figure 11.17 Axial high-resolution FSE T2 of the pancreas, MRI of the Pancreas, available at Handbook of MRI Technique (3rd e) by Catherine Westbrook;235.

 

26. Figure 11.18 Axial SS-FSE T2 of the pancreas during free breathing, MRI of the Pancreas, available at Handbook of MRI Technique (3rd e) by Catherine Westbrook;235.

 

27. Figure 11.19 Axial fast incoherent (spoiled) T1 weighted image of the pancreas, MRI of the Pancreas, available at Handbook of MRI Technique (3rd e) by Catherine Westbrook;236.

 

28. Testes, coronal, sequences 1 and 2, MRI of Tests available at MRI Parameters and Positioning by Torsten B. Moeller, M.D (1st e); 73.

 

29. Testes, axial, sequence 4, MRI of Tests available at: MRI Parameters and Positioning  by Torsten B. Moeller, M.D (1st e); 73.

 

30. Patient Positioning, MRI of Testis, available at MRI Parameters and Positioning by Torsten B. Moeller, M.D (1st e); 72.

 

31. Patient Positioning, MRI of the breast, available at MRI Parameters and Positioning by Torsten B. Moeller, M.D (1st e); 30.

 

32. Breast, axial, sequence 1, MRI of the breast, available at MRI Parameters and Positioning by Torsten B. Moeller, M.D (1st e); 31.

 

33. Breast, coronal, sequence 9, MRI of the breast, available at MRI Parameters and Positioning by Torsten B. Moeller, M.D (1st e); 32.

34. Patient preparations, MRI of the soft tissue of the neck, available at MRI Parameters and Positioning by               Torsten  B. Moeller, M.D (1st e); 17.

  1. Soft tissues of the neck, coronal, sequence 1, MRI of the soft tissue of the neck, available at MRI Parameters and Positioning by Torsten B. Moeller, M.D (1st e); 18.
  2. Soft tissues of the neck, sagittal, sequence 3, MRI of the soft tissue of the neck, available at MRI Parameters and Positioning by Torsten B. Moeller, M.D (1st e); 19.

 

MRI of HEPATOCELLULAR CARCINOMA

Pathology and clinical condition of HCC

This is a well-known medical truth that Hepatocellular carcinoma (HCC) now involving about the fifth of all malignant tumors in the world, and it’s one of the most common causes of deaths resulting from cancer in the world and USA (1).

It causes about 250.000 to 1000.000 deaths/year (2).

HCC develop mainly in the cirrhotic liver.

Liver damage which eventually leads to liver illness (cirrhosis or fibrosis ) can occur due to several causes.

We can numerate Viral infections, Alcoholism, Obesity, Toxic agents, metabolic function disease. In Asia and Africa (3), HCC has higher incidence more than other regions.

The main cause of HCC in there are endemic Hepatitis B, C, and Aflatoxins. In the USA and Europa HCC has a lower incidence (5), however, it still has a high incidence. Hepatitis C consider causing more than 30% of HCC in the state, either alone or with other cause like alcohol, others (4).

Another noncirrhotic cause is found to spread nowadays, especially in western countries. We can mention hemochromatosis,
Primary biliary cirrhosis, autoimmune hepatitis, and obesity with nonalcoholic steatohepatitis, or can also call (NASH) (4).

NASH now considered one of the most important causes of HCC in the states and Europe.the end result of NASH is called cryptogenic cirrhosis which increases HCC incidence. (4)

As the clinical presentation of HCC is variable and limited mainly to the underlying cause. so it’s mostly discovered late during the patient survey and that affects the disease prognosis. so the surveillance in cirrhotic and hepatitis patients is very important in reducing the incidence and deaths of HCC (2).

HCC has a male predominance(2). typical usual presentation of HCC is an old man with cirrhosis and Ascites with splenomegaly and weight loss, increase alpha-fetoprotein (2). However acute presentation of acute RUQ pain may occur due to rupture of liver capsule.(2)

In cirrhotic patients the pathology of HCC  evolute form necrosis and fibrosis of hepatocytes to the neoplasm. This evolution takes multiple steps from regeneration nodules to low-grade dysplastic nodules to high-grade dysplastic nodules to early HCC and finally advanced HCC (6).

This figure shows a high vascular heterogenous mass lesion which invades the adjacent portal vein in cirrhotic liver. (2)

 

MRI sequences of Localize and characterizations of HCC:

Hepatocellular Carcinoma is typically a hyper-vascular spherical heterogenous mass with contrast enhancement wash-out and portal vein invasion. The size of HCC may be small, less than 2 cm, or large, more than 5 cm.

The smaller ones are more liable to be cured by ablation or resection, or transplantation. While the larger ones especially if associated with venous invasion, those are more able to TACE (trans-arterial chemo-embolization) (2).

If HCC invades the portal vein, the following imaging signs are detected; first  the lumen of the portal vein is seen expanded, Second the tumor is seen enhanced within the vein, third the tumor and portal vein is fused with each other.(2)

Now let’s talk a look at sequences of MRI used to localize and characterize HCC, we should note that variable intensity of HCC depends mainly on necrosis, fibrosis and fatty changes degree:

T1 Weighted Image:

In this sequnce, HCC usually appears as a hypointense mass in compared to surroundings. As the cell increases in number, which means increase water amount. but in small HCC, it may appear hyper or iso  due to increase fat and glycogen content.(7)

T2 Weighted Image:

in T2 HCC is usually have a hyper-intense appearance to the liver density.

on the other side, the regenerative nodule usually appeared hypo-intense to the liver.

In this sequence, we can discriminate The HCC which arise inside the dysplastic nodule, as it has a pattern of (Nodule within the module) as it appears as small increase signal intensity focus within nodule of decreased intensity. (2)

T1 plus gadolinium contrast:

on this sequence, HCC appears as hyperintense heterogenous mass, associated with washout on delayed and venous phase.

To differentiate HCC from arterio-portal shunt, we should know that HCC takes fast central washout with residual capsular enhancement.(2)

A hepatobiliary contrast agent (gadoxetate):

the use of gadoxetate ( its trade names are Eovist, Primovist) after twenty minutes delay phase, reveal that Normal liver and some cirrhotic liver, brightly enhance m while HCC appears as hypo-intense masses.

some good differentiated HCC has proved to show persistent enhancement with gadoxetate. This technique is the most specific and sensitive technique for detection and location of HCC, it increases the incidence of small HCC diagnosis. (2)

Diffusion-weighted MR:

Diffusion restriction within HCC, usually detected as a bright signal in the focal lesion, it helps in increase MR sensitivity of HCC detection. (2)

Hepatocellular carcinoma (HCC) schematic diagram. HA, hepatic artery; HADP, hepatic artery–dominant phase; HBV, hepatitis B virus, IVC, inferior vena cava; PV, portal vein.(8) 

Large Complex HCC. A, The moderately T2-weighted image shows a large heterogeneously hyperintense lesion (arrow) bulging the liver capsule. The arterial phase (B) and delayed (C) images show variegated enhancement, often seen in large lesions.(8)

The Figure show DW MR of Cirrhotic liver. At dual-echo (a, b) and on T1-w.i (c), multiple nodules appear as iso- to hyperintense, while on T2-w.i (d) they show as slightly hypointense. On postcontrast dynamic study, no arterial nodular enhancement is detectable (e) as well as no wash-out is evident on the venous.and late phases (f, g). On hepatobiliary phase (h), acquired 20’ after contrast medium injection, all nodules show a significant uptake. (7)

This figure show : Different behavior of HCC and dysplastic nodule (DN) at MR. MR examination shows the oexistence of two differentiated nodules. At baseline (a, b), the HCC lesion (arrow) appears as hypointense on T1-w.i (a) and hyperintense in T2-w.i (b), while the DN (dotted arrow) shows the opposite signal behavior. At dynamic study (c–e), HCC presents the typical wash-in in arterial phase and wash-out in portal and late phases, while DN is iso–hypointense in all post-contrast phases. On hepatobiliary phase (f), HCC is hypointense due to the lack of intracellular contrast uptake, while DN is homogeneously hyperintense because of the
maintained hepatocyte function and cholestasis. (7)

Sequences are used to plan treatment, assess the completeness of treatment and detect a change in the lesion.

MR sequences have proved to be very effective in HCC treatment planning, monitoring the response of the lesion to treatment. Here we will enumerate the most important sequences used;

Diffusion-weighted MR:

has proven to be very effective in planning treatment either by surgical resection (ADC measurement before operations are very effective in measuring the risk of recurrence after surgery) or other treatment options as (TACE) transarterial chemo-embolization.(9.

In Trans-arterial Chemo-embolization (TACE), use of DWI to monitor ADC mapping measurements of the tumor response to treatment, as if poor response, it shows lower ADC measurements .(10)

ADC mapping can also together with venous enhancement of the lesion predict survival ration of the patient, by arranging them in survival classifications. (11)(12)

DWI, in general, is a very good factor in monitoring treatment effect and predicting survival rate as treatment cause local dynamic changes could be monitoring by DWI.(13)

 

MR Elastography.

In addition to its role in characterization of malignant liver tumors, as malignant tumor has higher stiffness than benign ones and it’s more viscous (14), the MR Elastography is very helpful in assessing the response of the tumor to chemotherapy and agents that cause vascular disruption. (15)

The technique of MR Elastography includes external vibrators that produce compression waves, that penetrate through tissue viscosity and elasticity of the tissues. This technique has been proved to be reliable in the liver in 22% for elasticity and 26% for viscosity.(16)

 

Dynamic contrast-enhanced MR imaging

in this sequence we use contrast to more visualization and detection of tumor response to treatment.

Usually, we use gadolinium contrast, then we take three phase of the liver: Arterial, Portal, and Delay (3-5 min after injection).

We can also use special hepatocyte contrast called Gadoxetate, in this case, we take additional hepato-biliary phase ( after 20 min of injection).

All phases (including arterial and portal and delayed phases) of Dynamic contrast-enhanced MR imaging should be done in routine to localize and tumor and detect its response to treatment.

so we use an especial contrast ( gadoxetate) , which in turn we get hepatobiliary phase, in which some HCC which is not good seen at classical phases of Dynamic MR imaging sequences .

and has low vascularity appears to be hypo-intense at hepato-biliary phase.Also, hyperintense lesion on these sequences predicts to prgnosed to HCC which has high vascularity. (17)

So we can say that Dynamic contrast-enhanced MR and DW MR  together can be used monitor intraarterial therapy.

There were noted survival differences between patients who their ADC level increase above 25%, their venous enhancement decrease. that’s like the difference between patients who are stable and patient who has single parameter respond, so the above text reveals the service could present the functional MR (multi-parameters) in evaluating treatment response.(18)

MRI Sequences used to grade HCC condition.

Diffusion-weighted MR:

also is useful in the grading of patients with HCC.

And almost considered the most useful sequence in this field. For example, if we had a patient with hypo-vascular liver nodule which is hyperintense on DWI. The studies proved that this nodule progress to be high vascularity HCC.

In addition, there is a correlation, but an inverse one between the level of ADC mapping and the grading of the tumor. The High differentiated tumor has more diffusion more than the poor differentiated one .(19) It’s also can predict other factors as VEGF (vascular endothelial growth factor)  (20)prognostic cell marker (21)and microvascular invasion. (22)

 

Tumor Grade ADC Potential association
High differentiation Good diffusion No reported association
Well differentiation Moderate diffusion No reported association
Poor differentiation Restricted diffusion presence of progenitor cell markers 1
Scarce differentiation Scarce diffusion presence of progenitor cell markers 1, vascular endothelial growth factor (VEGF) expression2-51, and microvascular invasion52.

Table, reveal the relation of ADC and HCC grading (23)

LI-RADS MR Grading system:  this system is the most common used and the most efficient to grade HCC.

 

This figure show LR-MR grading system of HCC. (24)

To get this we use these sequences :

MRI with extracellular contrast agents or gadobenate meglumine:

to make an HCC grading with an extra-cellular agent, we should use these sequence:

First, T1-W IP & OP sequences with no enhancement. Secondly, T2-WI (fat suppression per institutional preference).

Third Multiphase T1-WI.

Fourth Precontrast imaging.

Fifth Arterial phase, and recommended to be late.

Sixth Portal venous phase. Seventh Delayed phase.

Seventh Diffusion-weighted imaging.Eight Subtraction imaging and Multiplanar acquisition.

Lastly one to three hours hepatobiliary phase. (24)

MRI with gadoxetate disodium:

Sequenced performed with gadoxetate disodium to grade HCC.

First, T1-W IP & OP sequences with no enhancement.

Secondly, T2-WI (fat suppression per institutional preference).

Third Multiphase T1-WI.

Fourth Precontrast imaging.

Fifth Arterial phase, and recommended to be late.

Sixth Portal venous phase. Seventh Delayed phase.

Seventh Diffusion-weighted imaging.

Eight Subtraction imaging and Multiplanar acquisition.

Nine hepatobiliary phase .and we don’t forget transitional phase which we take two to five minutes after injection. (24)

 

Treatment options and outcomes for the patient

Treatment options of HCC vary according to the lesion and its nature and extent.

If the patient had a small HCC, localized peripherally and has no vascular invasion; this will be ideal for surgical resection.

So surgical resection id very optimal in previously described small peripheral avascular lesions, but its effect is limited to due to the hepatic reserve will be inadequate in the majority of patients. (2)

In patients who are not suitable for surgical resection and has an HCC isolated tumor less than 4 cm, these patients will be candidates for Radio-frequency Ablation.

On the other hand, Multi-centric HCC patients who are cannot undergo resection, they are ideal for Trans-arterial Chemo-embolization (TACE) (2).

But this procedure is limited as the hepatic reserve may be insufficient. So there is an alternative to it, The radio-embolization with Yttrium-90Y-tagged microspheres. Transplantation sill a very good choice for those who have nonmetastatic HCC tumor with no vascular invasion(2).

There are criteria called Milan Criteria used to the assessment of transplantation. these criteria are; first HCC tumor should be either solitary and less than 5 cm in diameter, or it’s more than one (up to 3 HCC nodules, each less than 3 cm in diameter).

Second, it must have no extra-hepatic metastasis and had no vascular invasion. Systemic treatment is still an option, sorafenib which is tyrosine kinase inhibitor, give good survival benefit. (2)

 

MRI Recurrence Monitoring sequences.

Diffusion-weighted MR:

It has proven to be very effective in monitoring recurrence of HCC.

As it offers a great service in distinguishing between the recurrence of the tumor, and the effect of the treatment.

The recurrent tumor gives a low ADM mapping measurements, while the necrotic tissue or the edematous area resulting as a response to treatment give high ADC mapping measurements.and as more increasing ADC level, the more successful treatment is. (25)(26)(27)

As tumor is mixed tissue components, the necrotic part could mix with the tumor part. So it can mix up in the evaluation of recurrence, so the used of Dynamic enhanced MRI with DWI is recommended to give the best precise assessment of the recurrence.(28)

Gadoxetate Disodium–Enhanced MRI:

this sequence has proved to be very effective in the assessment of recurrence of HCC after treatment especially after radio-frequency Ablation.

HCC usually when occurring as a recurrence it appears as nodular abnormal signal intensity areas or has enhanced margins especially the ablated tumor.(29)

This figure shows  70-year-old man with locally recurrent hepatocellular carcinoma after radiofrequency ablation in an anterosuperior segment of the right liver lobe.
A T2-weighted image (TR/TE, 1600/80) shows multiple areas of nodular hyperintensity (arrows) adjacent to the ablated area (arrowhead), which was hypointense on the fat-suppressed image.
B, MR image obtained during hepatic arterial phase shows area of nodular enhancement (arrow), corresponding to one of the hyperintense areas in A, adjacent to ablated
tumor. This area of enhancement showed mild washout during the portal venous phase and was due to local tumor recurrence.
C, 3D T1-weighted gradient-echo image (TR/TR, 4.0/2.1) obtained during hepatocyte phase shows area of hypointensity (solid arrow) adjacent to ablated tumor
(arrowhead), corresponding to the area of enhancement in B. This local tumor recurrence had a signal intensity ratio of 0.61. Another area of faint hypointensity (open arrow)
corresponding to a hyperintense area in A was observed adjacent to ablate the tumor. This lesion was found to be caused by reactive response to therapy and had signal
The intensity ratio of 1.65. Note area of hypointensity (asterisk) showing another ablated tumor.(30)

 

 

 

References:

  1. Hepatocellular Carcinoma by Jeong Min Lee and Byung Ihn Choi, Radiology Illustrated: Hepatobiliary and Pancreatic Radiology by Byung Ihn Choi ; SBN 978-3-642-35824-1Springer-Verlag Berlin Heidelberg 2014; 112.

 

  1. Hepatocellular Carcinoma, Malignant Tumours, Liver, Diagnostic Imaging of Gastro-intestinal Tract by Federle, Raman, 2nd  edition 2015; ISBN: 978-0-323-37755-3; 808.

 

  1. Hepato-cellular Carcinoma , Diffusion-Weighted MR Imaging by D. M. Koh · H. C. Thoeny; ISBN: 978-3-540-78575-0;112.

 

  1. Hepatocellular Carcinoma, Carlo Bartolozzi, Valentina Battaglia, and Elena Bozz, Clinical MRI
    of the Abdomen Why, How, When, Nicholas C. Gourtsoyiannis, ISBN: 978-3-540-85688-7; 95.

 

  1. Hepatocellular Carcinoma, MRI of the Liver (2nd Edition) by Günther Schneider,Luigi Grazioli, Sanjay Saini; ISBN-10 88-470-0335-0;187.

 

  1. Cirrhosis III – Dysplastic Nodules, Primary Solid Liver Lesions in Cirrhotic Liver, Liver MRI Correlation with Other Imaging Modalities and Histopathology, by Shahid M. Hussain, ISBN 3-540-25552-4; 80.

 

  1. Hepatocellular Carcinoma, Primary Malignant Neoplasms, Abdominal Imaging by Bernd Hamm and Pablo R. Ros , ISBN 978-3-642-13326-8 , 1st ed (2013).

 

  1. HCC, Focal liver lesions , Liver MRI, Fundamentals of Body MRI by Christopher G. Roth, MD, ISBN: 978-1-4160-5183-1 (2012) ; 77.

 

  1. Nakanishi M, Chuma M, Hige S. et al. Relationship between diffusion-weighted magnetic resonance imaging and histological tumor grading of hepatocellular carcinoma. Annals of surgical oncology. 2012;19:1302-9.

 

  1. Mannelli L, Kim S, Hajdu CH, Babb JS, Taouli B. Serial diffusion-weighted MRI in patients with hepatocellular carcinoma: Prediction and assessment of response to transarterial chemoembolization. Preliminary experience. European journal of radiology.2013;82:577-82.

 

  1. Bonekamp S, Li Z, Geschwind JF. et al. Unresectable hepatocellular carcinoma: MR imaging after intraarterial therapy. Part I. Identification and validation of volumetric functional response criteria. Radiology. 2013;268:420-30.

 

  1. Dong S, Ye XD, Yuan Z, Xu LC, Xiao XS. Relationship of apparent diffusion coefficient to survival for patients with unresectable primary hepatocellular carcinoma after chemoembolization. European journal of radiology. 2012;81:472-7.
  2. Corona-Villalobos CP, Halappa VG, Bonekamp S. et al. Functional Magnetic Resonance Imaging Response of Targeted Tumor Burden and Its Impact on Survival in Patients With Hepatocellular Carcinoma. Investigative radiology. 2014.

 

  1. P. Garteiser, S. Doblas, J.L. Daire, M. Wagner, H. Leitao, V. Vilgrain, et al.MR elastography of liver tumors: value of viscoelastic properties for tumor characterization

Eur Radiol, 22 (2012), pp. 2169-2177.

 

  1. L. Juge, B.T. Doan, J. Seguin, M. Albuquerque, B. Larrat, N. Mignet, et al.Colon tumor growth and antivascular treatment in mice: complementary assessment with MR elastography and diffusion-weighted MR imaging Radiology, 264 (2012), pp. 436-444.

 

  1. A.E. Bohte, P. Garteiser, A. De Niet, P.F. Groot, R. Sinkus, J. Stoker, et al.MR elastography of the liver: defining thresholds for detecting viscoelastic changes

Radiology, 269 (2013), pp. 768-776.

 

  1. Hepatocellular carcinoma: Diagnostic criteria by imaging techniques Best Pract Res Clin Gastroenterol, 28 (2014), pp. 795-812.

 

  1. S. Bonekamp, V.G. Halappa, J.F. Geschwind, Z.Li, C.P. Corona-Villalobos, D. Reyes, et al.Unresectable hepatocellular carcinoma: MR imaging after intraarterial therapy. Part II. Response stratification using volumetric functional criteria after intraarterial therapy

Radiology, 268 (2013), pp. 431-439.

 

  1. Nakanishi M, Chuma M, Hige S. et al. Relationship between diffusion-weighted magnetic resonance imaging and histological tumor grading of hepatocellular carcinoma. Annals of surgical oncology. 2012;19:1302-9.

 

  1. Inchingolo F, Tatullo M, Marrelli M, Inchingolo AM, Inchingolo AD, Dipalma G, Place P, Girolamo F, Tarullo A, Laino L, Sabatini R, Abbinante A, Caggiano R. Regenerative surgery performed with platelet-rich plasma used in sinus lift elevation before dental implant surgery: an useful aid in healing and regeneration of bone tissue. Eur Rev Med Pharmacol Sci. 2012Sep;16(9):1222-6.

 

  1. Saito K, Moriyasu F, Sugimoto K. et al. Histological grade of differentiation of hepatocellular carcinoma: comparison of the efficacy of diffusion-weighted MRI with T2-weighted imaging and angiography-assisted CT. Journal of medical imaging and radiation oncology. 2012;56:261-9.

 

  1. Suh YJ, Kim MJ, Choi JY, Park MS, Kim KW. Preoperative prediction of the microvascular invasion of hepatocellular carcinoma with diffusion-weighted imaging. Liver transplantation: official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society. 2012;18:1171-8
  2. Saito K, Moriyasu F, Sugimoto K. et al. Histological grade of differentiation of hepatocellular carcinoma: comparison of the efficacy of diffusion-weighted MRI with T2-weighted imaging and angiography-assisted CT. Journal of medical imaging and radiation oncology. 2012;56:261-9.

 

24 MR-LIRADS grading system 2017 by Mostafa Bashir and Victoria Chernyak and others published at American college of Radiology , available at:

https://www.acr.org/Quality-Safety/Resources/LIRADS/LIRADS-v2017.

 

25. Mannelli L, Kim S, Hajdu CH, Babb JS, Clark TW, Taouli B. Assessment of tumor necrosis of hepatocellular carcinoma after chemoembolization: diffusion-weighted and contrast-enhanced MRI with histopathologic correlation of the explanted liver. AJR American journal of roentgenology. 2009;193:1044-52.

 

26. Yuan Z, Ye XD, Dong S. et al. Role of magnetic resonance diffusion-weighted imaging in evaluating response after chemoembolization of hepatocellular carcinoma. European journal of radiology. 2010;75:e9-14.

 

27. Schraml C, Schwenzer NF, Clasen S. et al. Navigator respiratory-triggered diffusion-weighted imaging in the follow-up after hepatic radiofrequency ablation-initial results. Journal of magnetic resonance imaging: JMRI. 2009;29:1308-16.

 

28. Goshima S, Kanematsu M, Kondo H. et al. Evaluating local hepatocellular carcinoma recurrence post-transcatheter arterial chemoembolization: is diffusion-weighted MRI reliable as an indicator?. Journal of magnetic resonance imaging: JMRI. ;27:834-9.

 

29. Gadoxetate Disodium–Enhanced MRI Useful for Detecting Local Recurrence of Hepatocellular Carcinoma After Radiofrequency Ablation Therapy , Haruo Watanabe1, Masayuki Kanematsu1 2, Satoshi Goshima1, Mariko Yoshida1, Hiroshi Kawada1, Hiroshi Kondo1 and Noriyuki Moriyama at: American Journal of Roentgenology. 2012;198: 589-595. 10.2214/AJR.11.6844.

 

30. Fig 1: Gadoxetate Disodium–Enhanced MRI Useful for Detecting Local Recurrence of Hepatocellular Carcinoma After Radiofrequency Ablation Therapy?

Haruo Watanabe1, Masayuki Kanematsu1 2, Satoshi Goshima1, Mariko Yoshida1, Hiroshi Kawada1, Hiroshi Kondo1 and Noriyuki Moriyama, at: American Journal of Roentgenology. 2012;198: 589-595. 10.2214/AJR.11.6844.
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

ACUTE PANCREATITIS IMAGING

Introduction

This is a well known medical truth that The Pancreas is one of the largest and most important mixed (exocrine and endocrine) Gland in the body.

It lies behind Stomach and next to Small Intestine. It is considered as endocrine gland as it releases insulin and glucagon to control blood sugar level .

It acts as exocrine gland as it releases digestive enzymes that help the small intestine to do a good job in food digestion (1).

Acute Pancreatitis can be defined as Acute inflammation of the pancreas, it may be caused by reflux of the bile and pancreatic enzymes into the pancreatic parenchyma (2).

In another way, we can define pancreatitis as Pancreatic inflammation be caused by multiple etiologies that result in a final common pathway of premature activation of pancreatic enzymes that result in autodigestion of pancreatic parenchyma (3).

Acute Pancreatitis is considered a potential life threating condition.

Effective utilization of imaging in patients with acute pancreatitis needs a profound information of the natural course of disease and familiarity with the subtypes and complications of acute pancreatitis.

Imaging, primarily computerized tomography (CT), in acute pancreatitis has numerous aims. CT will ensure the diagnosing or give an alternate diagnosing, determine the etiology of pancreatitis, observe native duct gland and extrapancreatic complications, provide prognostic data, and guide therapeutic interventions.

Conventional radiography, ultrasound (US), endoscopic retrograde cholangiopancreatography (ERCP), and resonance imaging (MRI) have necessary complementary roles within the assessment and management of patients with acute pancreatitis.

This Article discusses the role of imaging in the assessment of etiology of acute pancreatitis. Also, imaging characteristics of these with expected severe disease and people with duct gland and extrapancreatic complications directly influencing individual patient management are going to be self-addressed.

Epidemiology

Among all gastrointestinal tract diseases, Acute Pancreatitis remains a commonly encountered clinical entity, with an incidence of 44 cases per 100,000 adults per year (4).

In the United States, in 2009, Acute Pancreatitis was the most common gastroenterology discharge diagnosis with a cost of 2.6 billion dollars. An increase in the annual incidence of Acute pancreatitis has been observed in most recent studies.

Epidemiologic review data from the 1988 to 2003 National Hospital Discharge Survey showed that hospital admissions increased from 40 per 100,000 in 1998 to 70 per 100,000 in 2002.

Although the case fatality rate has decreased over time, the overall population mortality rate has remained unchanged (5).

History

Before CT was widely used in cases of abdominal pain, the main cornerstone of diagnosis of Pancreatitis is clinical criteria of acute pancreatitis and by the exclusion of other causes.

X-ray signs especially cut-off signs of the pancreas could be helpfull. Detected edematous pancreas in the ultrasound and confirmation of peripancreatic fluid was a great imaging help in the diagnosis of acute pancreatitis.

The value of imaging in pancreatitis:

Using different Imaging modalities in the diagnosis of Acute Pancreatitis is very helpful in the determination of the severity of disease, the extent of involvement, local complication. It’s useful for the evaluation of fluid collection. Accompanying MRCP may help to determine the cause of pancreatitis (stone, stricture, mass, pancreatic divisum).

Radiological Anatomy:

The pancreas is mixed accessory GIT gland, it has Exocrine Function as Pancreatic acinar cells secrete pancreatic Juice that passes throughout pancreatic duct to the second part of Duodenum. It has the endocrine function as pancreatic cells of Langerhans secrete insulin, glucagon & other polypeptides reaching portal venous system (6).

The Pancreas is a retroperitoneal gland. it lies transversely across the upper part of the posterior abdominal wall, extending from concavity of duodenum on the right to the spleen on the left (7).

The Pancreas Consists of four main parts: Head, Neck, Body, Tail.

The Head of the pancreas lies in the curve of the duodenum with pylorus and duodenal bulb overlapping its upper surface, the uncinate process projects posteriorly and to the left from its lower part to lie posterior to superior mesenteric vessels.

The common bile duct passes posteriorly to pancreatic head in a tunnel till its termination in the second part of the duodenum (8).

The Pancreatic neck extends from the upper part of the anterior portion of the head . it lies just anterior to the union of the superior mesenteric vein and splenic vein to make portal vein.it lies anterior to left kidney and adrenal gland.

The splenic artery runs along the upper surface of the pancreas in the sinuously intermittent course.

Finally the pancreatic tail.it’s related to splenic hilum where it lies in the splenorenal ligament.

Pancreatic duct begins at the tail and runs to head, it ‘s mainly located in the anterior half of the pancreas. It joins CBD at the ampulla of Vater. Its accessory duct of Santorini arises from the pancreatic head and drains via the minor papilla into the duodenum, it lies 2 cm proximal to the ampulla of Vater. It usually communicates with the main duct and it may be absent in some individuals.(9)

Figure (1) shows anatomy of pancreatic ducts and its drainage (10)

The Pancreas receives its blood supply from the Pancreatico-duodenal artery that receives its blood supply from Gastroduodenal Artery.

Also the inferior pancreaticoduodenal artery (from SMA). There are multiple anastomoses between these two vessels.The remainder of

The pancreas is supplied from the splenic artery via multiple small direct branches and arterial pancreatic manga. Another arterial supply is from the dorsal pancreatic artery, which arises from the coeliac or proximal splenic artery.

Venous drainage from the pancreatic head is to SMV and portal veins and to the splenic vein from the rest of the pancreas (11).
The Variations in Pancreatic Anatomy has wide variations:

Pancreas divisum: failure of fusion of the dorsal and ventral moieties results in the anterosuperior part of the head and the body and tail draining via the accessory papilla, while the posteroinferior part of the head drains to the ampulla; this is the commonest variation, affecting 4 – 10% population

Annular pancreas is a rare condition where the ventral pancreatic bud rotates incompletely leaving a segment of pancreatic tissue surrounding the second part of the duodenum

Agenesis of the dorsal pancreatic moiety: this results in a pancreas with a head but no body or tail and is very rare.

Figure (2) shows variation in the anatomy of the pancreatic ducts (12):

(A) atrophic accessory duct persists as a tiny accessory duct in 60%;
(B) accessory (upper) duct atrophies completely – no connection with the duodenum (20%);
(C) major and minor ducts open separately and do not communicate (pancreas divisum) (10%);
(D) both ducts persist, communicate and open separately (10%)

Pancreatic rests/ectopic pancreas (accessory nodules of pancreatic tissue) may occur in the wall of the stomach, the duodenum, the small intestine or within a Meckel ’ s diverticulum The most common site is on the wall of the duodenum closest to the pancreas and close to the opening of the pancreatic duct (13).

The neck, body, and tail of the pancreas drain to the splenic vein and the head drains to the superior mesenteric and portal veins.

Lymphatic drainage is to nodes along the course of the supplying arteries to preaortic coeliac nodes.



Now we will begin to discuss the radiological features of the pancreas in different imaging modalities:-

Plain X-ray Abdomen:

We will look First how the pancreas appears in Plain Film plain imaging of the abdomen. it’s not visible unless it’s calcified which occur mostly in chronic pancreatitis and seen as a transverse structure at first lumbar vertebrae level, with a larger head on the right side and a body and tail extending to the left and upwards.

Here we should note that acute pancreatitis may cause Ileus in the nearby intestine that will be visible in Plain Film. Another note, Acute Pancreatitis may cause fluid collection in the lesser sac which causes displacement of Stomach Gas anteriorly, visible on lateral film of the abdomen.

Figure (3) shows: Plain X-ray abdominal film of pancreatic calcification due to chronic pancreatitis (14)

Ultrasound:

Then we will discuss an important imaging module the Ultrasound. Although Ultrasound is very important in the diagnosis of abdominal Organ Pathology, Normal Pancreas seen only in 60% of abdominal ultrasound studies, this because it’s obscured by overlying Stomach and transverse colon Gas.

On transverse section, the pancreas appears anterior to the Splenic vein. Hepatic artery and bile duct are seen anterior to the portal vein and cephalad to pancreatic head.

Anteriorly we can see Stomach antrum, with the pylorus and duodenum above and be curving around the right side of the head In the upper part of the head.

Pancreatic head and neck are seen in the midline anterior to the confluence of splenic and superior mesenteric veins Just posterior to this, the left renal vein is usually seen crossing the aorta to drain into the IVC.The uncinate process is seen posterior to superior mesenteric vessels.

Pancreatic Tail can be seen by angling the transducer superolateral from midline towards the splenic hilum, or by oblique views through the spleen.

The pancreatic duct is seen within the gland closer to its anterior surface. It is seen in over 80% of cases and It is best seen in the central portion of the body where it is perpendicular to the plane of imaging. It measures approximately 1 5 mm in the tail, 2 mm in the body and 3 mm in the head(15).

Figure (4) shows : Axial ultrasound images through the pancreas centered on (A) the head and (B) the body.

The pancreas may initially be difficult to visualize but can be identifieded as it lies immediately anterior to the splenic vein. The pancreas is at least as echogenic as the liver and is more echogenic with increasing age and body fat (16).

Computed Tomography (C.T):

Before we finishing the radiological anatomy of the pancreas we should take a look at how it looks like at Computed tomography.

We should note that the pancreas lie in the abdomen at oblique position as the tail lies in a higher plane than the head . so the pancreas should be scanned in sequential thin CT slices . as we see the pancreas in the CT Cranio-caudal, on the highest slices we can see the pancreatic tail in the splenic hilum, then body.

The head and uncinate process can be seen in the lowest slices. The normal thickness of the head is 2 cm, the neck about 0 5 – 1 cm and the body and tail 1 – 2 cm.The height of the head is very variable and may measure up to 8 cm. The body and tail may measure 3 – 4 cm in height (17).

Figure (5) shows: The head of the pancreas lies lateral to the superior mesenteric vein (SMV) or SMV-portal vein confluence,while the uncinate process lies dorsal to the SMV (18).

Figure (6) shows: The uncinate process is that portion of the pancreas that extends dorsally to the superior mesenteric vein (SMV)(19).

MRI:

Finally, we have to get a look at the MRI of the pancreas. The pancreas has the shortest T1 of the abdominal organs, so it has a higher signal intensity on T1-weighted imaging, equivalent to or slightly higher than that of normal liver.

The pancreas is also well seen on T2-weighted imaging, and faster sequences, including breath-hold sequences, reduce artifact from breathing.

The pancreas is highly vascular so it enhances markedly during the arterial phase of a gadolinium bolus.

Figure (7) shows Axial T2 Image of the pancreas (20).

Figure (8) shows Coronal T2 Image of the pancreas (21).

Figure (9) shows Axial T1 Image of the pancreas (22).

Figure (10) shows Opposed Phase Axial T1 Image of the pancreas (23).




Acute Pancreatitis

By imaging, Acute Pancreatitis can be seen as enlarged edematous pancreas with or without necrosis, with pre-pancreatic fat stranding and fluid collection.

We can classify acute pancreatitis into two main sub-types: the first subtype is mild Acute pancreatitis or Interstitial Edematous Pancreatitis, the second subtype is severe acute pancreatitis or Necrotizing Pancreatitis. (24).

Interstitial Edematous Pancreatitis: It’s characterized by Enlargement and edema of the pancreas with loss of normal fatty lobulation. this type shows no necrosis .it can be associated with peri-pancreatic fat standing and fluid collection. it’s the predominant type in about 70-80 % of cases.

Necrotizing Pancreatitis: It’s characterized by parenchymal necrosis. it occurs in 20-30 % of cases.it’s associated with pancreatic and peripancreatic necrosis. at this type, complications are more liable to occur.

Embryology of the Pancreas

The pancreas Develops among the dorsal part of dorsal mesentery, that typically fuse’s with the posterior abdominal wall. It leaves solely a brief splenorenal ligament .it Carries splenic vessels and tail of pancreas and Forms left a posterior wall of lesser sac.So pancreas becomes a retroperitoneal organ.

Causes of Acute pancreatitis

The most comm Cause is Gallstones (about 50% of cases) including occult stones, microlithesis, and mud(25), large stones are more likely to cause pancreatitis as it lodges into sphincter of Oddi.

Alcohol came in the second with about 25% of cases especially if associated with the long history of alcohol drinking.
metabolic causes include hypercalcemia, hypertriglyceridemia. Trauma also can cause pancreatitis.it’s common cause of pancreatitis in children. Endoscopic Maneuvers like ERCP, Pancreatitis one of its famous complications.Other causes include Malignancy, toxicity.

Finally, Pancreatitis Occurs without any cause, in this situation we called it (idiopathic).

Pathogenesis

pathogenesis of acute pancreatitis vary according to the cause: it includes reflux of pancreatic enzymes, bile, and duodenal contents into the pancreatic duct.

It may be due to the increase in ductal pressure due to ampullary obstruction, or activation of intracellular/extracellular homeostatic factors.

Another important one is activation of pancreatic enzymes and released into surrounding soft tissues causing inflammation and autodigestive injury to pancreas

These are two phases of acute pancreatitis: Early and late: Early phase over a week and is characterized by systemic inflammatory response syndrome (SIRS).

Late phase (only seen in severe cases) occurs after 1st week and is characterized by local complications and persistent systemic inflammation

Clinical Presentation

Patients with acute Pancreatitis presented with more or less characteristic symptoms, even so, the clinical diagnosis of acute pancreatitis can he extremely difficult and, in the initial stages, other acute abdominal conditions such as a perforated peptic ulcer or acute cholecystitis have to be included in the differential diagnosis (26).

He/She is presented with Epigastric Pain radiating to the back, Vomiting while holding his belly with leaning forward and his pain increases when he/she takes a supine position.

Severe acute pancreatitis patients presented by more dramatic symptoms and signs of shock, pulmonary insufficiency, renal failure, GIT age, metabolic abnormalities. flank ecchymosis (Grey Turner’s sign), and/or periumbilical ecchymosis (Cullen’s sign) (27).

Laboratory Findings

Increase Serum Amylase and Lipase levels are specific (Lipase is more sensitive and specific) for diagnosis of Acute Pancreatitis. Increased ALT suggests biliary etiology (usually gallstones).

Clinical outcome

Identification of the severity of acute pancreatitis is incredibly helpful in the treatment of the patients.

First of all mild pancreatitis, These patients haven’t any organ failure and even several of them haven’t any fluid collections and definitely no necrosis.These patients typically recover by the end of the primary week.

Moderate or severe pancreatitis, Patient condition depend upon their body responds to the pathological process, protein cascades lead to a general inflammatory response syndrome (SIRS), that will increase the chance of organ failure. The presence of organ failure is decided by respiratory (pO2↓), urinary organ (creatinine↑) and cardiovascular failure (blood pressure↓).

The extent of morphologic changes like necrosis and fluid collections isn’t directly proportional to the severity of organ failure. several of those patients, however, can have necrotizing pancreatitis and also the mortality will increase once the necrosis becomes infected(28).

Complications of Acute Pancreatitis

Acute pancreatitis is considered a and emergency life threating condition that may progress to the variation of complications, including the following:

1. Infected Pancreatic necrosis: in which Gas enter inside the gland and result in infection necrosis.

2. Central Necrosis: in which necrosis occurs in the center portion of the pancreas and spare the rest of the gland.

3. Pancreatic Pseudocyst: it’s encapsulated fluid collection, it’s more likely to occur in lesser sac region, its capsule may be indistinguishable. it occurs in about 40% of cases. It can resolve in 50% of patients, but unlucky 20% of the patient can proceed to more complications as Peritonitis if rupture, Abscess if infected and Obstruction of duodenum and bile duct.
4. Pancreatic Abscess: it’s pus collection near or adjacent to the inflamed pancreas.

Figure (11) shows: Pancreatic abscess. The above CT image shows enhanced thick walled fluid collection. (arrowheads). Aspiration was done and reveals Pus (29).

5.Pseudoaneurysm: it occurs most commonly in splenic and gastroduodenal arteries, but can occur at any vessel, it occurs mostly due to autodigestion of arterial wall by pancreatic enzymes that result in pulsatile mass.

Figure (12) shows: CECT that shows high-density contrast collection (arrow) within a small retro-gastric pseudocyst.Angiogram was done and Pseudo-aneurysm was confirmed and embolized successfully(30).

6.Venous Thrombosis: mostly occurs in splenic, portal, SMV veins

7.hemorrhage: resulting from erosion of blood vessels and tissue necrosis

8.Fistula formation with pancreatic ascites: leakage of pancreatic secretions into the peritoneal cavity. .(31)

Acute Pancreatitis, how the imaging can show it

On X-Ray

On Abdominal X-ray erect, the film show gasless abdomen, with plus or minus ascites or intrapancreatic gas bubbles.

The Abdominal X-ray may also show dilated transverse colon with an abrupt transition to the gaseous descending colon, this is known as ‘colon cut off‘ sign.The film may also show localized segment of gas containing duodenum which known as ‘sentinel loop‘ sign (32).

As Pancreatitis cause fluid collection, a sympathetic pleural effusion may occur which appear on Chest X-ray as Pleural effusion more commonly to occur on the left side.

Figure (13) shows: Colon Cutoff Sign. White arrow on conventional radiograph points to air in colon which abruptly terminates at the splenic flexure (33).

On Ultrasound

Although CT is the technique of choice in evaluating patients with suspected acute pancreatitis, Ultrasound is often the initial test in patients presenting with abdominal pain – it may be possible to assess the inflamed pancreas or any fluid collections.

The Pancreas can be directly imaged with ultrasound, but the full length of the organ cannot be visualized in all patients either due to obesity or overlying gas.

Patient with interstitial edematous pancreatitis with mild Pancreatitis Signs may be subtle, but mostly patients presented on Ultrasound by oedematous enlarged hypoechoic spleen with blurred margins and peri-pancreatic exudates, Hypoechoic change may be diffuse or focal, the latter mimicking a tumor mass.

Accompanying dilated Pancreatic Duct may be seen due to compression or mass effect by surrounding lesion.The peripancreatic inflammatory process also can be seen.

Patients with Necrotizing Pancreatitis, imaging become more difficult because of severe tenderness and agonizing pain, but it appears on ultrasound as the Enlarged heterogeneous pancreas.

Also, we can see the cause of pancreatitis on ultrasound such as Gallstone or intraductal calculi, masses, others.

If pancreatitis is advance to complications, it can be seen as Pancreatic pseudocyst, it appears as well-circumscribed, unilocular cystic lesion within pancreas or peripancreatic tissue, it may need further follow-up ultrasound.

Pancreatic abscess can be seen as Thick-walled, mostly anechoic fluid collection with internal echoes and debris

Vascular complications as Pseudoaneurysm formation and port splenic venous thrombosis can be diagnosed by Doppler (34).Also, Portal Vein thrombosis can be seen on Color doppler Ultrasound.

Biliary pathology including common bile duct obstruction or dilatation can be seen with ultrasonography.

Figure (14) shows ultrasound of a pteint with mild interstitial edematous pancreatitis (35):

(Left) Transverse US demonstrates mild diffuse enlargement of the pancreas. The pancreatic duct is normal in size . The main sign of acute pancreatitis is fluid anterior to the pancreas as well as fluid anterior to splenic vein .

(Right) Longitudinal US of the body of the pancreas demonstrates peripancreatic fluid tracking caudally down the superior mesenteric vein . There is also fluid noted anterior to the body of the pancreas , a strong clue to the diagnosis of acute pancreatitis.

On CT

Contrast Enhanced CT is the diagnostic method of choice in acute pancreatitis, According to the main two sub-types, Acute pancreatitis can appear on Ct as the following:

Interstitial edematous pancreatitis,

in this type the pancreas appears enlarged and edematous with the loss of normal fatty lobulations. Peripancreatic fat edema and inflammation can be noted.

Fluid collection in the peripancreatic region mostly localized to Lesser sac, anterior pararenal spaces, and paracolic gutters.

normal enhancement of the gland with no necrosis is detected in this type.

Here we should mention important note that normal appearance of pancreas does not exclude pancreatitis as a mild type of pancreatitis presented with minimally elevated lipase levels can appear normal on imaging.

Figure (15) shows: CECT of a patient with Mild acute pancreatitis (36).

(A) Mild swelling of the gland that enhances uniformly but has indistinct margins because of peripancreatic edema. There is inflammatory tissue around the coeliac axis (arrow)

(B) The image at the level of the pancreatic head showing infiltration of the peripancreatic fat and fluid anterior to Gerota’s fascia (arrows).

(C) Different patient. Peripancreatic fluid with normally enhancing gland.

On the more severe type Necrotizing pancreatitis:

in this type, the necrosis in the pancreatic tissue appear as non-enhancing or severe hypoenhanced areas. Usually, it is accompanied by a greater amount of peripancreatic fluid and more sever inflammatory process (37).

Figure (16) show a patient with acute necrotizing pancreatitis. This is contrast enhanced CT image show pancreatic head enlargement with ascites and perirenal fluid collections. large necrotic nonenhancing pancreatic body and tail is noted (38).

CT technique of Pancreatitis.

Contrast-enhanced CT offers the broad spectrum of information in the diagnosis of pancreatic diseases, Thin-section spiral, and multislice CT have increased the sensitivity of CT for the detection of small lesions.

CT can be used in pancreatitis in Differentiation of exudative and necrotizing forms; and also can be used in Pretherapeutic CT to determine the extent of inflammatory spread.

It’s also used for detection and identification of pancreatic pseudocysts and in evaluation for a suspected abscess.

For pancreatitis, most Technicians perform only a contrast-enhanced scan in the parenchyma or the portal phase of enhancement.

A contrast dose of 70-100 ml is sufficient to differentiate between exudative and necrotizing pancreatitis (scan delay 40-60 s).

Thicker sections (7-8 mm) can be used for evaluation of the entire abdomen to detect spread of exudates or necrosis Because it
is a benign disease and pathology is often gross, dose reduction may be considered.

Even so that the overuse of CT in all acute pancreatitis patients can even harm rather than help the patient.So proper guidance of the clinical doctor is very helpful.

On MRI

Mild interstitial edematous pancreatitis

appears resembling normal pancreas as slightly high intensity on T1 WI and gadolinium homogenous enhancement.

Diagnostic features are stranding of peripancreatic fat tissue, which is low in signal intensity on T1-WI without fat suppression and high in signal intensity on (fat-suppressed) T2-WI.

In necrotizing pancreatitis

contrast-enhanced images, similar to the CT protocol for pancreatitis, are mandatory to define necrotic areas.

Patients with necrotizing pancreatitis may develop complications, such as abscess, bleeding, and vascular complications such as thrombosis or an aneurysm.

The assessment of pancreatitis requires a comprehensive MR protocol with MRI and MRCP, and is more difficult to perform than CT in severely ill patients.

Therefore, the most important indication for MRI in acute pancreatitis is suspected choledocholithiasis (“biliary pancreatitis”) (39).

Figure (17) shows:Axial non-enhanced magnetic resonance T1-weighted with fat-suppression image.
(A) and axial T2-weighted with fat-suppression image.
(B) show that the parenchyma of the pancreatic head, body and part of the tail is hypointense (arrows in A) and hyperintense (arrows in B) relative to the liver , it’s a case of Acute oedematous Pancreatitis(40).

PET/CT has is role in Acute Pancreatitis

The Journal of Nuclear Medicine has published a study on August 6, 2014, that say that PET/CT with FDG-labeled leukocytes has a role in detecting infection in acute pancreatitis.

A team of researchers from Chandigarh and from Postgraduate Institute of Medical Education has done a study that includes 41 patients (28 men and 13 women, ages 21-69) with acute pancreatitis and radiological evidence of fluid collection in or around the pancreas.

They separate WBCs from patients blood, labeled with FDG, and reinjected intravenously. PET/CT imaging was performed two hours later.

They make A final diagnosis of infection based on the microbiological culture of fluid aspirated from the collection. Patients were managed with supportive care and antibiotics, and percutaneous drainage was performed when indicated.

They collected LAB results and notice increased FDG uptake in the collection in 12 (29%) of the 41 patients; 10 had a culture-proven infection and underwent percutaneous drainage, and aspiration was unsuccessful in two patients.

the result of PET/CT was negative for infection in 29 patients (71%) Of the 29 patients, 25 had negative fluid cultures, and aspiration was unsuccessful in four. Sensitivity, specificity, and accuracy of the scan were 100% in the 35 patients for whom fluid culture reports were available.

Dr. Anish Bhattacharya Said that this new technique can be used to diagnose infection in patients with the pancreatic fluid collection, individuals are spared empiric antibiotic therapy or radiological intervention followed by time-consuming microbiological workup. It also could be very useful in detecting or ruling out active infection of any part of the body (41).

The Overuse of imaging modalities in Acute Pancreatitis

Acute Pancreatitis is an emergency case, so should we request a lot of imaging modalities to every patient presented with symptoms of acute pancreatitis.

According to a study published online in Radiology from researchers at Brigham and Women’s Hospital in Boston. They found that clinical assessment of acute pancreatitis, rather than advanced imaging, works just fine for most patients.

Koenraad Mortele, MD, and his colleague have done the research and his colleagues have done the study. They wrote that “Studying imaging utilization in patients with Acute Pancreatitis is appealing because of the high estimated total healthcare cost associated with the disease, the presence of well-established practice guidelines for managing the disease, and the vast array of radiologic modalities that are available to image these patients,”.

Koenraad Mortele and his team have record data of 252 adult patients admitted to the hospital with a diagnosis of acute pancreatitis between June 2005 and December 2007.

Patients who had been transferred from other hospitals or those with a history of chronic pancreatitis were not included.

The researchers defined acute pancreatitis as two or more of the following characteristics:
– Severe upper abdominal pain
– Serum amylase and/or lipase levels three or more times higher than normal
– CT or MR imaging results that demonstrated changes consistent with AP

The research team gathers all the hospital’s database of all imaging modules done with these patients and every imaging studies for each patient.

then they classify them according to modality and technique. they also gather a database of all U.S. Centers for Medicare and Medicaid Services (CMS) 2009 relative value units (RVUs) for each study to have a consistent scale with which to assess differences across exam types.

They found that among 1,324 radiologic studies were performed during the study time, the mean imaging utilization rate was 5.3 studies per patient during initial hospitalization, with an RVU of 3.9; the mean utilization rate was 9.9 exams per patient, in the one-year period after the initial admission, with an RVU of 7.8. Overall, 53% of the total imaging use occurred during a patient’s initial hospitalization.

They found that the most common imaging module done with patients with acute pancreatitis was Chest radiography, Abdomen and Pelvis Computed Tomography and Abdominal ultrasound. they make a chart of imaging modality used during the one-year period following initial hospitalization is detailed in the following chart:

Figure (18) shows: Imaging use by modality for acute pancreatitis ,Data courtesy of the Radiological Society of North America. (42)

The researchers found a 2.5-fold increase in the use of high-cost imaging modalities and a 1.4-fold increase in imaging RVUs (per case-mix-adjusted admissions), without significant improvement of patient condition.

The researcher’s team wrote “In this analysis, patient outcomes were relatively stable during the study period. … Therefore, although it remains difficult to analyze the effect of imaging utilization on patient outcomes, it can probably be inferred that in our institution the increasing use of cross-sectional imaging did not result in detectable improvement in outcomes for patients with AP,”

The researchers were surprised to know that even though 90% of the patients in the study had mild disease, CT and MR use surpassed recommended Appropriateness Criteria of the American College of Radiology’s.

Despite that, there is no confirmatory evidence in existing literature that says that CT scans in patients with the milder disease would result in upstaging of disease in a significant number of patients, according to the researchers.

And there’s no value to perform early un-necessary Radiological exams to predict the clinical severity of acute pancreatitis rather than just using a clinical evaluation, they noted.

Finally, Mortele and his team wrote, “If a diagnosis of Acute Pancreatitis is established with abdominal pain and increased serum amylase and lipase activity and no systemic signs of severe disease exist, CT may not be necessary”.

So CT should be Only for Patients with an equivocal diagnosis, those who have already been established as having severe acute pancreatitis, or those who don’t improve despite conservative measures, they concluded(43).

Staging and grading

These are two ways of grading and staging of Acute Pancreatitis.

Balthazar Grading System,

in this grading system we can classify pancreatitis into

A: Normal-appearing pancreas.

B: Focal or diffuse pancreatic enlargement

C: Mild degree of inflammation in the peripancreatic area.

D: Collection of fluid Only E: Two or more fluid collections

the mortality rate is 0%, , morbidity rate is 4% for grades A, B, and C.
the mortality is 14%, the morbidity rate is 54% for grades D and E (a fluid collection is a poor prognostic indicator).

Another Grading is CT severity index (CTSI),

it integrates the Balthazar grading system with the degree of necrosis:

Assigns 0–4 points for Balthazar A–E, with 0 points for Balthazar A and 4 points for Balthazar E.

Adds 0–6 points for necrosis to create a total score from 0-10.

0 points: 0% necrosis
2 points: <30% necrosis
4 points: 30–50% necrosis
6 points: >50% necrosis
CTSI 0–3: 3% mortality, 8% morbidity
CTSI 7–10: 17% mortality, 92% morbidity (44).

Atlanta Classification of Fluid Collections

The 2012 Revised Atlanta Classification discerns 4 types of peripancreatic fluid collections in acute pancreatitis depends on the content, degree of encapsulation and time.

1.Content: it contains only fluid in the acute peripancreatic fluid collection (APFC) and Pseudocyst.A mixture of fluid and necrotic material in the acute necrotic collection (ANC) and walled-off-necrosis (WON).

2.The degree of encapsulation: None or partial wall in APFC and ANC. Complete encapsulation in pseudocyst and WON.

3.Time: Within 4 weeks: APFC and ANC.After 4 weeks: pseudocysts and WON. It takes about 4 weeks for a capsule to form.

On CT, the discrimination between an APFC and ANC may be difficult, especially in the first weeks and the term “indeterminate peripancreatic collections” can be used.Fluid collections could remain sterile or become infected. Infection is rare during the first week.

Differential Diagnosis of Acute Pancreatitis

Even so, pancreatitis has characteristic imaging appearance, it may mimic a lot of other pathologies, here are some examples:
Heterogeneous, hip enhancing mass with abrupt obstruction of the upstream pancreatic duct and upstream pancreatic atrophy. Pancreatic cancer may present with pancreatitis in about 5% of cases.

Focal pancreatitis can appear mass-like and mimic malignancy. Presence of dilated pancreatic duct or biliary obstruction should prompt further investigation for underlying mass

Pancreatic cancer infiltrates dorsally into retroperitoneum, unlike pancreatitis, which infiltrates anteriorly and laterally.other signs of malignancy, including vascular encasement, metastatic disease (most often liver), etc.

Perforated Duodenal Ulcer can cause fat stranding and edema in anterior pararenal space and mimic pancreatitis. Pancreatic head may be edematous due to adjacent inflammation which primarily centered around duodenum, not pancreas (often more apparent on coronal reformations) < 50% show extraluminal gas or contrast extravasation “Shock” Pancreas which can include infiltration of peripancreatic fat planes with pancreatic edema (similar to pancreatitis) but usually associated with the clinical history of hypotension and other imaging stigmata of shock, such as “shock bowel”. It Quickly resolves following resuscitation

Lymphoma: Lymphoma can rarely diffusely infiltrate and enlarge pancreas, superficially mimicking pancreatitis. Usually associated with regional lymphadenopathy and pancreatic involvement appears mass-like. No evidence of pancreatic or biliary ductal dilatation. Vessels encased, but not narrowed or occluded (45).

Treatment

The first line of treatment of acute pancreatitis is Conservative which includes Fluid resuscitation, Analgesics, Nothing per mouth . then nutritional support.In patient with gallstone ERCP and sphincterotomy will be helpful

Mild interstitial edematous pancreatitis patients will resolve with conservative measures alone

Severe pancreatitis with necrosis may require intensive care due to high risk of multiorgan failure and Infected pancreatic necrosis will require surgical debridement

Aspiration is used to distinguish sterile necrosis from infected necrosis if infection suspected and no response to antibiotics

Asymptomatic fluid collections do not need intervention. Symptomatic fluid collections (due to mass effect, infection, pain, etc.) need to be drained, with walled-off necrosis requiring large-bore catheter or necrosectomy (due to debris and solid components), while simpler fluid collections can be drained with standard catheters

Angiographic embolization is used for pseudoaneurysms, and anticoagulation is used for venous thrombosis either in portal vein or SMV

Prognosis

Pancreatitis has an overall mortality rate of 1-3%, even so, it has an excellent prognosis with interstitial edematous pancreatitis and Poor prognosis with Necrotizing Pancreatitis.

Mortality rate: reach up to 25% with multiorgan failure or 30% for infected necrosis (even with surgical debridement).

Conclusion

From the previous information we have listed in this long articles, we can say that acute pancreatitis is an emergency disease that needs to be well evaluated by clinical doctors and guide the patients to the appropriate radiological examination.

we can say that plain radiography, even so, it is of less value imaging modality in the confirmatory diagnosis of acute pancreatitis. Colon “cut off” sign and “Sentinal Loop” sign can be useful to help clinical doctors to diagnosis Acute pancreatitis without the need to cost the patient more radiological examinations (ultrasound will be very useful of course especially in detected peri-pancreatic fluid).

Ultrasound, I can say that ultrasound is the cornerstone here in imaging diagnosis of acute pancreatitis, as it’s low cost and is harmful the patients so it would no upgrade the condition.

Ultrasound is very useful to detect parenchymal changes of the pancreas (edema, necrosis, or any signs of inflammation), even so in mild type pancreas may appear normal, but peri-pancreatic fluid won’t’ be missed.

Also, Ultrasound is the best imaging module to detect fluid collection.The main problem of ultrasound sound in the diagnosis of acute pancreatitis is overlying gasses of the colon, this is a major problem that makes ultrasound in many cases no dependable in the diagnosis of acute pancreatitis.

Contrat Enhanced CT is the imaging modality of choice in the diagnosis of Acute Pancreatitis. CT can detect every pancreatic tissue changes either edema or necrosis or anti-inflammatory sign.

CT also can detect fluid collection. CT can overcome colonic gasses problem of the ultrasound. And it’s very accurate in detecting extension of the pathology and grading of the condition.

But even so, it has a major disadvantage, high radiation dose, and the cost makes the situation not accessible to every suspected acute pancreatitis case to perform CT scan, studies have done say that using CT in mild condition may even upgrading the condition.

So CT is recommended to use only in equivocal patients which are not confirmed by other imaging modalities and for complicated patients and finally for those who don’t respond to treatment to evaluate the cause of the problem.

MRI has been proven to be useful in the diagnosis of acute pancreatitis especially in detecting necrotic parts of the pancreas in necrotic pancreatitis. it’s very helpful when we suspect choledocholithiasis (“biliary pancreatitis”).

Finally, PET/CT is a new technique that has proved himself to become very helpful in diagnosing infection in patients with the pancreatic fluid collection.



References:

1. What Is Pancreatitis? Article at webmd.com site, available at http://www.webmd.com/digestive-disorders/digestive-diseases-pancreatitis#1

2. Acute Pancreatitis Definition, Pancreas, Diagnostic Imaging Essentials by Grainger & Allison’s; 2nd edition (2013), 3.8

3. Pancreatitis, Gastrointestinal Imaging, Core Radiology A visual approach to Diagnostic Imaging By Jacob Mandell; 1st edition 2013, 113.

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6. Overview, Gross Anatomy, Pancreas, Abdomen at Diagnostic and Surgical Imaging Anatomy Chest.Abdomen.Pelvis by Michael P. Federle (1st edition) 2006, II 370.

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8. Radiological features, the Pancreas.at: Anatomy of Diagnostic Imaging – Stephanie Ryan 3rd ed. 2004; 187.

9. Radiological features, the Pancreas.at: Applied Radiological Anatomy by Paul Butler 2nd ed. 2012; 170.

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11. Radiological features, the Pancreas, Blood Supply at: Applied Radiological Anatomy by Paul Butler 2nd ed. 2012; 170.

12. Figure 5.39, Variations in pancreatic duct anatomy, Pancreas Anatomy at: Ryan: Stephanie Ryan 3rd ed. 2004; 189.

13. Radiological features, the Pancreas, variations in pancreatic Anatomy .at: Anatomy of Diagnostic Imaging – Stephanie Ryan 3rd ed. 2004; 187.

14.Figure10.2, Plain film, The abdomen and retroperitoneum at: Applied Radiological Anatomy by Paul Butler 2nd ed. 2012; 150

15. Radiological features, the Pancreas .at: Anatomy of Diagnostic Imaging – Stephanie Ryan 2nd ed. 2004;191.

16. Figure 10.29 , Ultrasound of Pancreas, Pancreas Anatomy at: Applied Radiological Anatomy by Paul Butler 2nd ed. 2012; 170

17. Pancreatitis, Exam Technique of the Pancreas at Spiral and Multislice Computed Tomography of the body by Mathias Prokob (2001): 518.

18. Axial CT of the pancreas , Pancreas, Abdomen at: Diagnostic and surgical imaging Anatomy by Michael P. Federle,MD, FACR (1st ed);2006; II:373.

19. Axial CT of the pancreas , Pancreas, Abdomen at: Diagnostic and surgical imaging Anatomy by Michael P. Federle,MD, FACR (1st ed);2006; II:373.

20. Figure 20.11 , MRI of the pancreas and spleen at: See Right Through Me-An Imaging Anatomy Atlas (2nd Ed) 2012, by Savvas Andronikouition; 499.

21. Figure 20.12 , MRI of the pancreas and spleen at: See Right Through Me-An Imaging Anatomy Atlas (2nd Ed) 2012, by Savvas Andronikouition; 499.

22. Figure 20.13 , MRI of the pancreas and spleen at: See Right Through Me-An Imaging Anatomy Atlas (2nd Ed) 2012, by Savvas Andronikouition; 500.

23. Figure 20.14 , MRI of the pancreas and spleen at: See Right Through Me-An Imaging Anatomy Atlas (2nd Ed) 2012, by Savvas Andronikouition; 500.

24. Classifications, Acute Pancreatitis, Gastrointestinal Imaging at Primer of Diagnostic Imaging by Ralph Weissleder, MD, Ph.D. (5th ed)2011; 175.

25. Acute Pancreatitis, Aetiology at Clinical Ultrasound volume 1 by Paul L Allan (3rd ed) 2011; 300.

26. Acute Pancreatitis, the pancreas, Abdomen and gastrointestinal tract at TEXTBOOK OF
RADIOLOGY AND IMAGING by DAVID SUTTON (17th ed); 686.

27. Clinical Findings, Acute Pancreatitis, Gastrointestinal Imaging at Primer of Diagnostic Imaging by Ralph Weissleder, MD, Ph.D. (5th ed) 2011; 176.

28.Clinical Outcome at Pancreas Acute Pancreatitis by Thomas bollen available at:
http://www.radiologyassistant.nl/en/p550455dae5806/pancreas-acute-pancreatitis-20.html.

29. CT of Pancreatic Abscess, Pancreatitis,Pancreas at: Grainger & Allison’s Diagnostic Radiology
Essentials by Lee Alexander Grant BA (Oxon) FRCR (2013); 373.

30. CT of Pseudoaneurysm formation, , Pancreatitis,Pancreas at: Grainger & Allison’s Diagnostic Radiology Essentials by Lee Alexander Grant BA (Oxon) FRCR (2013); 375.

31. Complications, Acute Pancreatitis at Diagnostic Imaging – Gastrointestinal by Michael P. Federle, MD (3rd ed) 2015; 990.

32. X-Ray, Radiological Features, Acute Pancreatitis, Pancreas at Grainger & Allison’s Diagnostic Radiology Essentials by Lee Alexander Grant BA (Oxon) FRCR (3rd ed) 2013; 3.8.

33. X-ray of Colon Cut off sign , available at: http://learningradiology.com/archives2009/COW%20352-Colon%20cutoff/coloncutoffcorrect.htm.

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35. Ultrasound of acute pnacreatitis, Pancreas at: Diagnostic Imaging – Gastrointestinal by by Michael P. Federle, MD (3rd ed) 2015; 994.

36. CT of Acute mild Pancreatitis , Pancreatitis,Pancreas at: Grainger & Allison’s Diagnostic Radiology
Essentials by Lee Alexander Grant BA (Oxon) FRCR (2013); 373

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38. CT of Acute necrotizing Pancreatitis, Pancreatitis,Pancreas at: Grainger & Allison’s Diagnostic Radiology
Essentials by Lee Alexander Grant BA (Oxon) FRCR (2013); 373

39.Acute Pancreatitis, Pancreas at Clinical MR Imaging A practical approach (3rd ed) 2003 by Peter Reimer; 6.7.4.

40. Figure (2) , MRI findings of Acute Pancreatitis, available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2999333/.

41. Study: PET/CT detects infection in acute pancreatitis By AuntMinnie.com staff writers, available at: http://www.auntminnie.com/index.aspx?sec=sup&sub=mol&pag=dis&ItemID=108145.

42. Data courtesy of the Radiological Society of North America Chart, Study: PET/CT detects infection in acute pancreatitis By AuntMinnie.com staff writers, available at: http://www.auntminnie.com/index.aspx?sec=sup&sub=mol&pag=dis&ItemID=108145.

43. Advanced imaging overused in diagnosing acute pancreatitis By Kate Madden Yee, available at: http://www.auntminnie.com/index.aspx?sec=sup&sub=mri&pag=dis&ItemID=92630.

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Role of High Resolution CT in diagnosis of Interstitial Lung Diseases.

Introduction:

Role of HRCT In Interstitial Lung Diseases Diagnosis is a very important topic to discuss .

The interstitial lung diseases (ILDs) are a heterogeneous group of lung disorders that result from damage to
the lung by various forms of inflammation and fibrosis.

By definition, Interstitial Lung Diseases (ILDs) involve the lung interstitium that forms a fibrous skeleton for the lungs, However many of the conditions that traditionally included under the heading of ILDs actually associate with extensive alterations of the alveolar and airway architecture.

For this reason, the terms diffuse infiltrative lung disease or diffuse parenchymal lung disease are preferable. Still, the term ILDs remains in common clinical usage.

Interstitial Lung Diseases represent more than 200 different entities, and various and often-confusing classification systems that we can use .

One useful approach to classification is to separate the ILDs into diseases of known and unknown etiology.

ILD of unknown etiology (65% of all ILDs) , we can subdivide it into the group of idiopathic interstitial pneumonias (IIPs), and a group comprising several rare
but interesting diseases with distinctive clinicopathologic features, such as lymphangioleiomyomatosis, Langerhans cell histiocytosis, pulmonary alveolar proteinosis, and pulmonary alveolar microlithiasis.

Sarcoidosis has an exceptional position within the group of ILDs of unknown cause, as it is relatively common and can present as a systemic disease(1).

CT scanning is the most important noninvasive diagnostic key to the identification and characterization of ILD and aids the radiologist and the clinician in the management of patients who carry this disorder.

Among all noninvasive methods, it provides the highest sensitivity and specificity in the detection of ILD.Also, it has a higher accuracy in comparison to the clinical assessment, lung function tests, and chest radiography in diagnosing a specific disorder, and adds diagnostic accuracy and confidence when added to
the clinical assessment and the chest radiogram. Finally,

CT helps to identify the best location for lung biopsy , and provides an important basis for the follow-up of ILD patients.

Epidemiology

United States:

As a group, diffuse interstitial diseases of the lung are uncommon. Based on the Bernalillo County, NM, USA registry data published in 1994, the overall estimated incidence is approximately 30 cases per 100,000 persons per year.

Rates of interstitial lung disease are somewhat higher in men than in women, Age and occupational exposures affect the epidemiology . of patients referred to a pulmonary disease specialist, an estimated 10-15% have a ILD.

International:

Although little-published data exist comparing worldwide prevalence, significant differences are apparent.

The Bernalillo County study estimated a prevalence of 80.9 cases per 100,000 population in men and 67.2 cases per 100,000 population in women. In comparison, a Japanese study estimated a prevalence of 4.1 cases per 100,000 population; a study in the Czech Republic reported 7-12 cases per 100,000 population; and
data from a Finnish registry indicated 16-18 cases per 100,000 population.

Mortality/Morbidity:

The natural history of diffuse interstitial lung diseases varies among different diagnostic entities and among individuals with the same diagnosis. Note the following:

Some diseases are insidious in onset and gradual but unrelenting in progression (eg, similar to IPF), while other diseases are acute in onset but responsive to therapy (eg, COP).

Diseases that most closely approximate IPF have a similar mortality rate of approximately 50% at 5 years.

In the United States, Chronic obstructive pulmonary disease (COPD) estimate 10-15% of mortality attributed to all types of DPLDs.

Race:

Diffuse interstitial diseases of the lung sometimes show racial predilections. Examples include sarcoidosis, which is more common in those of African ancestry in the United States. In contrast, PLCH, also known as histiocytosis X, primarily affects Caucasians.

Sex:

Several diffuse interstitial diseases of the lung show sexual predilections. IPF affects men more than women (at a ratio of 1.5:1), while LAM and pulmonary tuberous sclerosis exclusively affect women.

The Bernalillo County study estimated an incidence of 31.5 cases per 100,000/year in men and 26.1 cases per 100,000/year in women.

Women are much more likely to develop rheumatologic/connective-tissue disease than men and thus are more likely to experience pulmonary manifestations of those diseases. However, when affected, men with certain rheumatologic diseases (eg, rheumatoid arthritis) are more likely to develop pulmonary manifestations than women.

The pneumoconioses (eg, silicosis) are much more common in men than in women, probably because of higher rates of occupational exposure.

Age:

Many of the diffuse parenchymal lung disease develop over many years and therefore are more prevalent in older adults. For example, most patients with IPF present in the sixth or greater decade of life.

Others forms of interstitial lung disease, such as sarcoidosis, LAM, connective-tissue disease–associated lung disease, and inherited forms of lung disease primarily present in younger adults.(2)

History and Etymology

Computed Tomography (CT) imaging is also known as “CAT scanning” (Computed Axial Tomography).

Tomography is from the Greek word “tomos” meaning “slice” or “section” and “graphia” meaning “describing”.

British engineer Godfrey Hounsfield Invent CT at  EMI Laboratories, England with the help of South Africa-born physicist Allan Cormack of Tufts University, Massachusetts.

Hounsfield and Cormack were later awarded the Nobel Peace Prize for their contributions to medicine and science.

”High resolution computed tomography” term was first used by Todo et al in 1982. He also described the usefulness of HRCT imaging in pulmonary diseases .

In 1985, Naidich et al., Nakata et al. and Zerhouni et al. described the fundamental technique of HRCT and published first report on
HRCT (3).

However, The concept of the secondary lobule and its importance in interpreting various conditions dates back to long before the advent of HRCT, a technique which merely facilitated its identification even under normal conditions.

The radiological identification of the secondary lobule came about thanks to ER Heitzman as early as 1969, who developed our understanding of the crucial role of this anatomical structure in his work “The Lung” published in 1973 – about fifteen years before the development of HRCT! (4)

Radiological Anatomy

The lungs:

The right lung has three lobes and the left has two lobes, with the lingula of the left upper lobe corresponding to the right middle lobe.

One terminal bronchiole with lung tissue forms an acinus which, together with vessels, lymphatics and nerves, forms the primary lobule, Three to
five primary lobules form a secondary lobule.

Interlobar Fissures:

The depth of fissures varies from superficial slit to complete separation of lobes. The oblique (major) fissure:

This is similar in both right and left lungs.

It extends from T4/T5 posteriorly to the diaphragm Anteroinferiorly .

The left major fissure is more vertically orientated than the right .

The fissures do not follow a straight plane from top to bottom but are undulating in their course.

The medial aspect of each fissure passes through the hilum The lateral aspect of each fissure is anterior to the medial aspect at the level of the hila and below Above the hila, the relationship changes and the lateral aspect of the fissure is more posterior than the medial aspect.

The transverse (minor) fissure:

This separates the upper and middle lobes of the right lung, It runs horizontally from the hilum to the anterior and lateral surfaces of the right lung at the level of the
fourth costal cartilage.

Its posterior limit is the right oblique fissure, which it meets at the level of the sixth rib in the midaxillary line .It is anatomically complete in only one-third of subjects and is absent in 10%.(5)

The anatomical organization of the lungs consists of the bronchovascular bundles and the secondary lobules(6).

The bronchovascular bundles are made up of the main bronchi, the pulmonary vessels and the interstitial framework around them (central interstitium).(7)

The secondary lobules are the peripheral units of parenchyma where the airways meet the capillaries within the interstitial framework supporting them (peripheral interstitium)

Secondary lobule

Knowledge of anatomy of secondary Lobule is essential for understanding HRCT.

The secondary lobule is the basic anatomic unit of pulmonary structure and function.as Interpretation of interstitial lung diseases is
based on the type of involvement of the secondary lobule.

It is the smallest lung unit that is surrounded by connective tissue septa.It measures about 1-2 cm and is made up of 5-15 pulmonary acini, that contain the alveoli for gas exchange.

The secondary lobule is supplied by a small bronchiole (terminal bronchiole) in the center, that is parallelled by the centrilobular artery.

Pulmonary veins and lymphatics run in the periphery of the lobule within the interlobular septa.

Under normal conditions only a few of these very thin septa will be seen.

There are two lymphatic systems: a central network, that runs along the bronchovascular bundle towards the centre of the lobule and a peripheral network, that is located within the interlobular septa and along the pleural linings.

Centrilobular area is the central part of the secondary lobule. It is usually the site of diseases, that enter the lung through the airways (i.e. hypersensitivity pneumonitis, respiratory bronchiolitis, centrilobular emphysema).

Perilymphatic area is the peripheral part of the secondary lobule.It is usually the site of diseases,  that are located in the lymphatics of in the interlobular septa (i.e. sarcoid, lymphangitic carcinomatosis, pulmonary edema).

These diseases are also usually located in the central network of lymphatics that surround the bronchovascular bundle (8).

CT, How It Works:

The CT Scanner generations:

First and second generation:

Known as the rotate-translate type, it is a single X-ray source with either one (first) or a bank of up to 30 (second) detectors. Both move around the patient in 1° increments. Data was collected through a 180° rotation.

Third generation:

The rotate-rotate type are found in most modern scanners. A large number of small detectors arranged in an arc covering a complete patient cross section allows continous data collection through a full 360° rotation. This permits scan times of less than 0.4s.

Fourth generation:

Detectors are arranged in a stationary ring around the patient and the tube rotates. The outer part of the fan beam is always outside the patient and can be used to measure unattenuated radiation and self-calibrate. It requires vastly increased number of detectors which is prohibitively expensive.

Fifth generation:

This is also known as an electron beam scanner. It has electrons focused on and swept round a high voltage target ring to produce X-rays. It has no mechanical parts, thus, rapid scan times are possible (9).

Configuration of a typical CT scanner

The rotational axis is the Z-axis and X-ray beam is collimated as a wide fan shape big enough to cover the patient. In cross section, it has a narrow width parallel to the Z-axis. For a single slice scanner, this width defines the slice thickness.

Behind the patient is an arc of 500–1000 detectors. The radius of the arc is equal to the focal distance, thus each detector is the same distance from the source.

The patient lies on a couch that can be moved longitudinally through the gantry aperture. The gantry is normally perpendicular to the couch but can be tilted up to 30°. It’s mainly used for head scanning so the scan plane can be made parallel to the skull base. Simple third generation scanner.

The CT X-ray tube

Tubes for CT scanners have to be capable of producing prolonged exposure times at high mA.

They usually have two focal spot sizes, the smallest being ~ 0.6mm. It typically operates at 120 kV but the range is between 80 – 140kV. It also has heat capacities in excess of 4MJ.

Filtration

CT algorithms rely on the X-ray beam being monoenergetic, which, of course, it isn’t. To approximate a monoenergetic beam more closely, the X-ray beam is deliberately hardened by adding filtration. This is usually 0.5mm of copper (equivalent to 8mm of aluminium). It produces a mean energy of ~ 70 keV from
120 kV.

Since the patient cross-section is commonly elliptical, X-rays at the periphery tend to pass through less tissue. To compensate for this difference in attenuation across the field of view, some CT scanners have a bow tie filter after the X-ray tube.

This is a filter that is thin in the center and thick at the edges to artificially harden the beam at the edge.

Collimation

A collimator is mounted on the X-ray tube with the beam collimated to a fixed width (usually 50cm).

In the case of single slice scanners, collimation also defines the slice thickness (0.5 – 20mm).

Single slice scanners also have a post-patient collimator that is mounted in front of the detectors and used to reduce scatter reaching the detectors when the slice thickness is less than the detector width.

It is not needed for multi-slice scanners as the full width of the detectors in each row is used to form theimage and shielding from scatter would also shield from direct radiation.

Detector requirements

The detector must be small to allow good spatial resolution (single slice scanners have 600– 900 in an arc).

It should have high detection efficiency for X-rays in the CT energy range. Also, it should work within a fast response time (with negligible afterglow).

Wide dynamic range is very important as wide range of X-ray intensities (e.g. from zero attenuation when the beam passes to the side of the patient to very high attenuation in a lateral projection of a heavy patient).It should be have a stable and noise-free response.

Types of detectors

Older single slice scanners used ionisation chambers that were filled with high atomic number gases (xenon or krypton) at high pressure (20 atm).

Incident X-rays ionise the gas and produce a charge at the collection electrode. As it’s only 60% efficient, it’s not suitable for use in multislice scanners.

All new scanners use solid state detectors which consist of a scintillant (e.g. bismuth germinate) and embedded photodiode to detect output. It has a very high detection efficiency (98%) (10).

CT Chest Technique

High-resolution CT is a sampling examination of the lung, in which thin sections are taken at staggered intervals, revealing both the pattern and the distribution of abnormality, so that a differential diagnosis—or sometimes a single diagnosis—can be rendered. (11)

For patients with Iinterstitial Lung Disease , the identification of the smallest possible structures of the lung parenchyma and the depiction of their abnormalities is of paramount importance for any imaging approach.

Therefore, CT protocols have to utilize thin collimation and high-spatial-frequency reconstruction algorithms to achieve an optimal spatial resolution and consequently, facilitate an optimal assessment of interstitial and airspace disease.

For decades, patients with ILD have traditionally been investigated with HRCT (Mayo et al. 1987). This technique consists of a “step-and-shoot” approach, in which 0.5- to 1-mm collimation scans are obtained at 10- to 20-mm intervals, a small FOV, and a high radiation dose per section.

It provides excellent image quality, free of partial volume and projection artifacts, and combines high sensitivity in the detection of ILD with high accuracy in establishing the correct diagnosis.

This “classic” HRCT technique still plays a decisive role in the noninvasive investigation of patients with pulmonary disease of a diffuse distribution pattern (Hansell 2001).

With the advent of MDCT, volumetric high-resolution imaging has enriched the diagnostic armamentarium of the radiologist. New-generation MDCT scanners allow fast single-breath-hold scanning, volumetric data acquisition with thinly collimated scans, and high-spatial-frequency reconstruction when scanning the entire lung.

They, thus, combine the advantages of “traditional” HRCT and modern spiral scanning techniques.

Volumetric protocols enable the radiologist to detect those abnormalities that might have been missed during the classic HRCT step-and-shoot approach. Moreover, volumetric isotropic data sets permit the reconstruction of high-quality multiplanar images, which help to appreciate better the distribution of disease, for example, to identify a cephalocaudal gradient of disease severity in certain disorders.

Finally, continuous data acquisition allows the generation of MIP images, which are helpful in the detection of micronodular disease and centrilobular abnormalities.

There are also some trade-offs with volumetric HRCT scanning. The radiation dose is 5 to 10 times higher, and the image quality is discretely lower in comparison to classic sequential HRCT.

This image quality reduction is most apparent in the depiction of small septa and of ground-glass opacities, and its clinical significance has yet to be determined. In order to achieve the best possible balance between diagnostic accuracy, exploitation of the advantages of volumetric CT and radiation dose,
the following options exist:

1. Sequential HRCT protocol:

This protocol utilizes high milliampere-second and kilovolt peak values to obtain the best possible image quality.

Thin collimation (1 mm) scans are obtained at 10- or 20- mm intervals. Therefore, the overall radiation dose is a 5th to a 10th in comparison to the standard or high-resolution volumetric protocols.

This protocol may be regarded as “imaging biopsy” in diffuse lung disease, as it detects disease, allows the specification of disease distribution, and helps in establishing a differential diagnosis with high accuracy and confidence levels. It is the protocol of choice in patients with proven ILD, and in those cases that require imaging follow-up during or after therapy.

Because the classic HRCT leaves 9- to 19-mm broad gaps between the scanned sections unexamined, it should not be utilized as sole protocol in patients with suspicion of focal lung disease, in diffuse interstitial disorders where there is an increased risk associated with focal or even malignant abnormalities (such as dermatomyositis/ polymyositis), or in entities with a distinct propensity to involve extrapulmonary sites in the mediastinum, the chest wall, the diaphragm, and the abdomen.

In such instances, a combination .with a standard volumetric protocol (Table 26.1) is highly recommended.

Another caveat is the assessment of patients with suspected air trapping at supine scans.In these cases, it is advisable to perform single slice step-and-shoot scans in prone positions instead of a continuous volumetric examination in order to reduce radiation burden.

2. Volumetric HRCT protocol:

This protocol combines thin collimation with volumetric scanning and high milliampere-second and kilovolt peak values. During scanning, the dose modulation is off.

The result is a high quality contiguous data set, which allows for high-resolution multiplanar and three-dimensional reconstructions with superb image quality.

The latter is similar to that of sequential HRCT scanning, although it does not match it in every detail.

The major disadvantage of this protocol is the radiation dose, which is approximately 10 times higher than that of conventional HRCT.

It is recommended to use this protocol in ILD patients only when high-quality three-dimensional reconstructions are necessary, for example, for generating a data set for CT bronchoscopy.

3. Volumetric standard CT protocol:

Here, the milliampere-second and kilovolt peak values are reduced in comparison to the sequential or volumetric high-resolution protocol, and dose modulation is switched on.

The result is a substantial reduction in dose in comparison to the volumetric high-resolution protocol.

Nevertheless, thin collimation and high-spatial-resolution reconstruction guarantee very good image quality, and volumetric data acquisition a continuous morphologic assessment of the lung investigated, respectively.

This protocol is best used in combination with the classic sequential HRCT protocol in ILD patients.

It provides a volumetric data set and the best high-resolution images, with a reasonable radiation dose that reaches roughly 50% of the dose resulting from the volumetric high resolution protocol.

It is advisable to utilize this combination protocol in all patients with ILD who are imaged for their first time, in cases where the chest radiogram indicates diffuse and focal disease, and in those who are at risk to develop focal disorders on top of a diffuse lung disease process.

4. Volumetric low-dose CT protocols:

In patients with ILD, the low-dose high-resolution CT technique with a reduction of the milliampere-second values to approximately 40 mAs is in our view a valuable alternative to the standard volumetric protocol when combined with the sequential HRCT technique.

It allows for the assessment of the pulmonary parenchyma in slim individuals, visualization of focal abnormalities in the lung parenchyma, and analysis of major airways disorders.

The combination with the classic HRCT approach fosters almost the same advantages as those described for the combination of the standard volumetric protocol with classic HRCT. When using this protocol, one has to keep in mind that the somewhat reduced image quality may limit the diagnostic accuracy when scanning
the parenchyma, the mediastinum, chest wall, and upper abdomen in obese patients (12).

Analysis of Different Pattern of Lung Pathologies On HRCT

I) RETICULAR PATTERN:

The main finding consists of thin interlacing linear opacities creating a more-or-less tight mesh.

This finding is produced by a thickening of the structures of the lobular interstitium, and often of the central interstitium as well.

It’s caused by thickened interlobular or intralobular septa or honeycomb (fibrotic) destruction.

It always represents significant interstitial lung disease (ILD). It may be due to a variety of causes (fluid accumulation, amyloid deposits, cellular infiltration, fibrosis) and the pattern may vary accordingly.

The distribution of the lesions and other associated signs are often useful for diagnosis (13) .

A) Smooth:

Centrally, the alteration is characterized by a uniform thickening of the bronchial walls and an increase in the diameter of the adjacent vessels . Peripherally, the thickening of the interstitium appears as an exaggeration of the interstitial borders and by a fine reticulation crossing them (14).

In the centrilobular region the arteriole is more prominent and the bronchiolar walls, normally not evident in CT, are visible.

Interstitial thickening may be caused by edema, organic substances or cellular infiltration.

The lobular architecture is preserved, only is more recognizable than in the normal lung, at times with an exaggerated appearance

From pattern to disease:

1.Lymphangitic Carcinomatosis: its distribution is often unilateral and patchy . it’s associated with well defined nodules , hilar & mediastinal adenopathy and unilateral pleural effusion.

2.Pulmonary Edema, interstitial: its distribution is Bilateral and diffuse. It’s more prominent at Middle and lower zones and Peribronchovascular areas . it’s gravity dependent . it’s associated with Acinar-sized, ill-defined nodules, patchy ground-glass and consolidations, cardiomegaly and bilateral pleural effusion.

3.Amyloidosis, interstitial: it’s distribution is Bilateral, patchy more prominent in Peripheral and Basal areas.It’s associated with Calcified micronodules, consolidations, mediastinal adenopathies, tracheal thickening. (15)

B) Nodular:

Thickening of the central and/or peripheral interstitium with associated micronodules (►)If the interstitium is thickened simply because of a focal accumulation of cells or substance and the architecture of the lobule is preserved.

Beaded appearance

If the interstitium is thickened because of fibrosis and the nodular elements are due to focal fibrosis, the architecture of the lobule may be distorted.

Dotlike opacities

From pattern to disease:

1. Lymphangitic Carcinomatosis: as described above.
2. Amyloidosis, interstitial: as described above.
3. Asbestosis, Early: Its distribution is Bilateral, diffuse or patchy. It’s more prominent in Peripheral, dorsal and Basal areas. It’s associated with Subpleural dotlike opacities, irregular intralobular reticulation, subpleural lines, parenchymal bands, and pleural plaques.

C) Irregular:

The interstitium presents various degrees of thickening along the lobular margins and peribronchovascular bundles . The interstitial structures show an irregular course with a zigzag conformation which distorts their architecture and renders it increasingly unrecognizable. (16)

This pattern is characteristic of the fibrosing diseases, as fibrosis accounts for the distortion of the lobular anatomy. An irregularly thickened intralobular network is often seen together with the loss of the separation between lobules.

The pattern is also accompanied by traction bronchiectasis and bronchiectasis, with vessels and bronchi following an irregular, corkscrew-like path.

From pattern to disease:

1. Sarcoidosis, fibrosing: Its distribution is Bilateral and Patchy. It’s more prominent in the central region, especially Dorsal and Upper zones. It’s associated with Parahilar conglomerations with traction bronchiectasis, perilymphatic nodules,and hilar-mediastinal adenopathies.

2. Hypersensitivity Pneumonitis (HP), chronic: Its distribution is Bilateral and Patchy. It’s more prominent at Subpleural, but also in peribronchovascular
regions. It’s associated with interface sign, traction bronchiectasis, ground-glass and ill-defined centrilobular nodules, mosaic oligemia with air-trapping.

3. Drug Toxicity: Its distribution is Bilateral and Patchy. It’s associated with ground-glass, consolidations with air-bronchogram,
and possible honeycombing.

4. Collagen vascular diseases, early Its distribution is Bilateral and Diffuse. It’s more prominent in Peripheral, Sub-Pleural and Dorsal and Basal
regions. It’s associated with ground-glass and consolidations with traction bronchiectasis, which are specific signs of each disease.

5. Non-Specific Interstitial Pneumonia (NSIP): its distribution is Bilateral, Uniform, and Patchy . It’s more prominent in Peripheral, Dorsal, and Basal regions.
It’s associated with ground-glass and consolidations with bronchiolectasis, bronchial walls thickening, and rare honeycombing.

6. Usual Interstitial Pneumonia (UIP), early: Its distribution is Bilateral, and Patchy in normal parenchyma. It’s typically Sub-Pleural, especially Dorsal, and
in Basal regions, but, also, periperhal up to Upper regions. It’s associated with Subpleural dotlike opacities, irregular intralobular reticular pattern, subpleural lines, parenchymal bands, and pleural plaque.

7. Asbestosis, early: as described above.

II) NODULAR PATTERN

The main alteration consists of small rounded opacities (micronodules if the diameter is less than 3 mm, macronodules if between 3 mm and 1 cm) which tend to be localized in definite positions within the secondary lobule and in relation to the pleural surface.

The nodular pattern may be due to a variety of granulomatous diseases arising directly in the lung or arriving via the bloodstream down to small vessels where they develop concentrically, or via the bronchi,for example, when a reaction to an inhaled substance develops in a small bronchus and the adjacent area.

A) Centrilobular

The nodules tend to be centered at a certain distance from the pleural surface and at times, also from the interlobular septa . As a consequence, they are separated from the lobular margins, the costal margins and the fissures by a transparent rim.

Centrilobular distribution is more typical of diseases in which the elementary lesions originate from or near the peripheral bronchioles When the adjacent
peribronchiolar airspaces are involved, the nodules tend to present low density and ill defined borders (nodular ground-glass).

These are related to endobronchial and small airway disease.the most peripheral nodules are > 5mm from the pleural surface .a ‘tree in-bud’ appearance suggests endobronchial disease.(17)

From pattern to disease:

1. Respiratory Bronchiolitis-Interstitial Lung Disease (RB-ILD):
Its distribution is Bilateral and Patchy with Uniform distributions more prominent at upper and middle zones. It’s associated with Patchy ground-glass, centrilobular emphysema, bronchial wall thickening, and intralobular reticular pattern (rare).

2. Langerhans’ Cell Histiocytosis (LCH), early:
Its distribution is Bilateral and diffuse with Uniform distribution. It’s more prominent at upper and middle zones. It’s associated with well-defined, high density nodules, possibly cavitated, sparing the costophrenic angles and air-trapping.

3. Lymphocytic Interstitial Pneumonia LIP:
Its distribution is Diffuse and Uniform, with more predominance at the middle and lower zones. It’s associated with dense, well-defined, perilymphatic nodules, ground-glass, nodular reticulation, and thinwalled cysts.

4. Hypersensitivity Pneumonitis (HP), subacute:
Its distribution is Diffuse and Uniform, with more predominance at the middle and lower zones. It’s associated with Patchy ground-glass, at times mixed with areas of lobular air-trapping (head-cheese pattern).

B) Random

These nodules are of a good density with sharp borders mainly because they are confined to the interstitium. Their distribution is reasonably uniform in the secondary lobule and the parenchyma.

At times they can be seen in contact with the extremities of the vascular structures, from which they appear to originate (feeding vessel sign). They have a hematogenous origin.

However, they can also be found near the pleural surface ( not the rule). In short, their spatial distribution appears uniform.

Here we need to define a “ground glass Opacity” term: It used to describe Increased hazy opacity within the lung, not associated with obscured underlying vessels. This finding reflects the relative reduction of the quantity of air in the alveoli, either due to partial filling of the air spaces or thickening of the septa (intralobular interstitium) (18).

From pattern to disease:

1. Silicosis:
Its distribution is Bilateral with some right-sided prevalence. It has a tendency to predominate posteriorly
and has prevalence in the middle and upper zones. It’s associated with Pseudoplaques, “egg-shell”
mediastinal adenopathy, larger opacities and conglomerated parahilar masses.

2. T.B, Miliary:
Its distribution is Bilateral, Symmetrical and Uniform. It’s associated with Diffuse or localized ground-glass Opacity and mediastinal adenopathies with central hypodensities.

3. Metastases:
Its distribution is Bilateral and often Symmetrical. While it’s possible to be subpleural, it’s more prominent in basal regions. It’s associated with nodules of different size, possibily cavitated or calcified, shows a feeding vessel sign, and has mediastinal adenopathies.

C) Perilymphatic

First we need to describe “Peri-lymphatic” as a Term used to describe the distribution of nodules which tend to be concentrated in the perilobular and subpleural interstitium (although they may have an intralobular location) and therefore located along the costal margins and major fissures.(19)

These nodules tend to be prevalent in the perilobular and subpleural interstitium and are, therefore, profuse along the costal margins and the fissures.

They are more common in diseases which spread along the lymphatics, and may therefore be found within the lobule, but also along the vessels and bronchi (beaded appearance).

The nodules have well-defined margins as well as high and uniform opacity.The spatial arrangement of the lesions tends to be patchy, interspersed with areas of normal parenchyma.

From pattern to disease

1. Sarcoidosis, granulomatous:
Its distribution is Bilateral and Patchy. It’s more prominent at Perihilar regions, mainly Dorsal and subpleura.
It has middle and upper zone predominance. It’s associated with Bronchovascular nodules, pseudoplaques,
hilar and mediastinal adenopathies, micronodular ground-glass, and lobular air-trapping.
2. Lymphocytic Interstitial Pneumonia LIP: as described before.

III) ALVEOLAR PATTERN

The main finding consists of opacities resulting from alveolar filling their density varies in proportion to the extent of this filling, from partial (ground-glass) to complete (consolidation) Involvement of the small airways may either take the form of luminal narrowing (indirect signs of which are hypodensities of the distal
parenchyma due to regional oligemia), or filling by various materials (in which case they become ectatic and their opacity can stand out against the surrounding lung parenchyma)(20)

A) Mixed-density, acute

This pattern is recognizable by the presence of the two characteristic findings of the alveolar diseases, ground-glass and consolidation , combined in varying proportions. The ground-glass may be accompanied by a reticular pattern (crazy paving).

The simultaneous findings of bronchial involvement (bronchial wall thickening, bronchiectasis) and ill-defined centrilobular nodules due to alveolar filling is not
uncommon.

The acute form usually presents with bilateral and often extensive consolidations which may change in appearance, location, and size within hours or days.

From pattern to disease

1. Pneumocystis Carinii Pneumonia (PCP):
Its distributions is Bilateral, Symmetrical, and Patchy or Diffuse. It’s often parahilar and more prominent in the middle and upper zones. It’s associated with Walled cysts, crazy paving, hazy micronodules, mediastinal adenopathies, and pleural effusion.

2. Diffuse Alveolar Hemorrhage (DAH) in Wegener’s granulomatosis:
Its distribution is Bilateral and Diffuse or Patchy. It’s more prominent Parahilar or diffuse, and not peripheral.
It shows hazy, centrilobular nodules, crazy paving, large cavitating nodules and mediastinal findings.

3. Acute Interstitial Pneumonia (AIP):
Its distribution is Bilateral, Symmetrical, and Diffuse or Patchy. It’s usually peripheral and gravity dependent.
It’s associated with reticular pattern, parenchymal distortion, traction bronchiectasis, and sporadic honeycombing.

4. Hypersensitivity Pneumonitis (HP), acute:
Its distribution is Bilateral and Patchy, occasionally uniform, but most often basal. It’s associated with Hazy centrilobular nodules, mediastinal adenopathies and mosaic oligemia with air-trapping.

5. Adult Respiratory Distress Syndrome (ARDS):
Its distribution is Bilateral, Symmetrical, and Patchy. The prevalence is in the dependent lung. It is more extensive at the lung bases. It’s associated with Asymmetrical and less gravity-dependent if pulmonary ARDS.

6. Pulmonary Edema (PE), alveolar:
Its distribution is Bilateral, Symmetrical, and Diffuse or Patchy. Its subpleural and gravity dependent. It has Basal prevalence and is associated with redistribution of pulmonary perfusion, smooth reticular pattern,pleural effusion, and cardiomegaly.

B) Mixed-density, chronic:

This pattern is recognizable by the presence of the two characteristic findings of the alveolar diseases, groundglass and consolidation combined in varying proportions.

The ground-glass may be accompanied by a reticular pattern (crazy paving). The simultaneous finding of bronchial involvement bronchial wall thickening, bronchiectasis) and ill-defined centrilobular nodules due to alveolar filling is not uncommon.

The chronic form usually presents with consolidations often localized and patchy which progress slowly, even over weeks or months.

Here we need to describe the term “Crazy Paving”: it used to described Scattered or diffuse groundglass attenuation with superimposed interlobular septal thickening and intra lobular lines. (21)

From pattern to disease:

1. Chronic Eosinophilic Pneumonia (CEP):
Its distribution is Bilateral and Patchy with more prominence at peripheral and subpleural regions and middle and upper zones. It’s associated with Ill-defined nodules, mediastinal adenopathies and rarely pleural effusion.

2. Mucosa-Associated Lymphatic Tissue lymphoma(MALToma):
Its distribution is Bilateral or Unilateral, Diffuse or Patchy, with more prominence in the peribronchial area. It’s associated with Bronchi stretched and thinned within the consolidations; centrilobular nodules, small or large masses, and halo sign.

3. Pulmonary Alveolar Proteinosis (PAP):
Its distribution is Bilateral, Diffuse or Patchy. It’s associated with predominant ground-glass, extensive crazy paving, and sharp interfaces with the healthy parenchyma.

4. BronchioloAlveolar Carcinoma (BAC):
Its distribution is Uni- or Bilateral, Asymmetrical, or Patchy. It’s often peripheral and subpleural as well as basal. It’s associated with possible pseudocavitations, nodules and hazy ground glass, crazy paving, adenopathies, and pleural effusion.

5. Desquamative Interstitial Pneumonia (DIP):
Its distribution is Bilateral, Symmetrical, and Patchy. It’s subpleural but also diffuse prevalently basal.
It’s assocuated with ground-glass predominant, limited parenchymal distortion with traction bronchiolectasis, and microcysts.

6. Cryptogenic Organizing Pneumonia (OP):
Its distribution is Bilateral and Patchy. It’s peripheral but also peribronchial basal. It’s associated with air bronchogram and bronchiolectasis within the opacities, centrilobular nodules with ill-defined margins, and macronodules or masses.
N.B. The Term (Air Brochogram) used to described Visualization of patent bronchial structures within areas of parenchymal consolidation.(22)

7. Drug toxicity:
Its distribution is Bilateral, Symmetrical, and Patchy. It’s peripheral basal and associated with Amiodarone, which has hyperdense consolidations (compared to the muscles), reticular pattern and micronodules, with pleural thickening.

C) Mosaic oligemia with air-trapping

This term used to describe Areas of low parenchymal density in which the vessels are reduced in size and number. The extent of oligemia may be lobular or segmental, while the distribution is typically patchy Mosaic perfusion (23)

The main characteristics of this pattern are areas of patchy hyperlucency , often with lobular distribution, associated with vessels reduced in number and diameter. This pattern is a typical expression of small airway obstruction. The oligemia is due to hypoxic vasoconstriction secondary to alveolar hypoventilation.

The surrounding normal parenchyma appears “relatively” hyperdense partially because of hyperperfusion (pseudo-ground-glass). While oligemia from vascular obstruction (e.g. in patients with chronic pulmonary thromboembolism) does not change during expiration, hypoxic oligemia accentuates (air-trapping) Mosaic perfusion.

From pattern to disease

1.Constrictive Bronchiolitis (CB):
Its distribution is Bilateral, Asymmetrical, and Patchy. It’s associated with direct signs of airway disease (bronchiectasis) and shows pseudo-ground-glass in the normally ventilated areas.

D) Tree-in-bud

This term used to describe Thin branching opacities which terminate with small nodular opacities, usually visible in the lung periphery.

his finding is particularly common in diseases with endobronchial spread of infection.

Its appearance is due to the presence of dilated adjacent bronchioles and air spaces filled with material such as pus, mucous or fluid. (24)

it’s identified by the presence of thin branching opacities in the peripheral lung, which terminate with small nodular opacities of different density.

The branching opacities (the tree) reflect the presence of dilated bronchioles filled with material other than air, whereas the nodular opacities (the buds) are due to clusters of partially or completely filled alveoli, usually with poorly-defined margins (centrilobular nodules).

The tree-in-bud sign is typical of diseases with bronchogenic spread.

From pattern to disease:

1. Infections, endobronchial:
Its distribution is Uni- or Bilateral, and Patchy. It’s variable often in relation to the bronchi. It’s associated with Atypical mycobacteriosis, bronchial wall thickening, bronchiectasis, cavitation, and possibly cavitated consolidations.

IV) CYSTIC PATTERN

The main finding consists of small areas of absolute hyperlucency (cysts) – black holes which, more-or-less, extensively occupy the lung parenchyma. They may or may not be delimited by walls.

Cyst formation may result from bronchial and bronchiolar enlargement due to wall distention, traction, increased endoluminal pressure, or a focal hyperinflation of the air spaces with rupture of the walls.(25)

A) Clusters of grapes

The cysts are arranged in grape-like clusters, often around a stem (the bronchovascular pedicle).
Usually, these lesions have thick walls; their diameter may not be uniform air-fluid levels or inclusions inside the cysts are common.

The fluid may be of varying nature: mucus, pus or blood. An intracystic mass is often due to a mycetoma, more rarely neoplastic; however, only a mycetoma moves when the patient’s position is changed!

At times the cysts may be completely full of material and assume a pseudo-nodular appearance.

From pattern to disease:

1. Bronchiectasis, Cystic, and Cystic Fibrosis (CF):
Its distribution is Uni- or Bilateral, and Patchy. It’s central or peripheral with more prominence at middle and upper zones. It’s associated with air-fluid levels, tubular or varicose bronchiectasis and tree-in-bud, and oligemia with air-trapping.

B) String of pearls

The cysts are arranged in a single layer in the subpleural region and resemble a string of pearls.

Usually, these lesions have thin walls (comparable to the thickness of a fissure), which are interlobula septa at times thickened by minimal fibrosis.

If the diameter of the cysts is greater than 1 cm, the term bulla is used , it tend to have thicker walls owing to a greater quantity of fibrosis

From pattern to disease:

1. Emphysema,Paraseptal:
Its distribution is Uni- or Bilateral, and Patchy. It’s peripheral and subpleural with more prominence at middle and upper zones. It’s associated with Centrilobular emphysema as well as spontaneous pneumothorax.

C) Honeycombing:

This term used to describe Small thick-walled cystic spaces arranged in several concentric layers.
Honeycombing is the radiological hallmark of end-stage lung disease, and therefore traction bronchiectasis and bronchiolectasis as well as interface signs are often present. (26)

This pattern refers to thick-walled, rounded cysts arranged in several layers .

In the affected regions, the pulmonary architecture is distorted and traction bronchiectasis and bronchiolectasis are often present Honeycombing is the expression of the end phase of a number of fibrotic diseases (end-stage lung).

The lung volume characteristically reduces; an early sign of loss of volume is the dislocation of thin structures such as the fissures, whereas in the more advanced phases the bronchovascular bundles and the mediastinum are also displaced.

From pattern to disease:

1. Asbestosis, advanced:
Its distribution is Bilateral, and Patchy. It’s peripheral, subpleural, and basal. we can find it with Traction bronchiectasis and bronchiolectasis, irregular reticular pattern, subpleural lines, and pleural plaques.

2. Collagen vascular diseases, advanced:
Its distribution is Bilateral and Patchy. It’s peripheral, subpleural, and basal. we can find it with Traction bronchiectasis and bronchiolectasis, irregular reticular pattern, and disease-specific signs.

3.Usual Interstitial Pneumonia UIP, advanced:
Its distribution is Bilateral and Patchy. It’s peripheral, subpleural, and basal. we can find it with Traction bronchiectasis and bronchiolectasis,irregular reticular pattern, and mediastinal adenopathies.

D) Random cysts

We can arrange The cysts without obvious aggregations.

Their walls are of variable thickness,and in some diseases they are absent.

The presence of a minute central hyperdensity can indicate the presence of a centrilobular arteriole.

The distribution of the cysts is relatively homogeneous in the affected parenchyma, so their profusion is uniform.

the overall appearance of the diseases presenting with this pattern can be very similar.

The differential diagnosis, therefore, requires a careful assessment of the craniocaudal distribution of the lesions and the involvement of the costophrenic angles.

From pattern to disease:

1. Lymphangioleiomyomatosis (LAM):
Characterized by Thin-walled cysts of variable sizes surrounded by normal lung parenchyma can be seen throughout the lung with interlobular septal thickening.

It may show a dilated thoracic duct.haemorrhages , that we can see as areas of increased attenuation.(27)
.
2. Langerhans’ Cell Histiocytosis (LCH), advanced:
Its distribution is Bilateral, Symmetrical, and Uniformly distributed. It’s more prominent at middle and upper zones, with costophrenic angles spared. It’s associated with thick walls, bizarre coalescent cysts,associated cavitated nodules, and possible pneumothorax.

3. Emphysema,centrilobular:
Its distribution is Bilateral, Symmetrical or Asymmetrical. It’s Uniformly distributed with more prominence at middle and upper zones. It’s assocaited with lack of walls, a visible centrilobular artery, paraseptal emphysema, and saber-sheath trachea.

Conclusion:

Interstitial lung diseases (ILDs) comprises a diverse group of diseases that lead to inflammation and fibrosis of the alveoli, distal airways, and septal interstitium of the lungs.

The ILDs consist of disorders of known cause (e.g., collagen vascular diseases, drug-related diseases) as well as disorders of unknown etiology. The latter include idiopathic interstitial pneumonias (IIPs),sarcoidosis and a group of miscellaneous, rare, but nonetheless interesting, diseases.

In patients with ILD, MDCT enriches the diagnostic armamentarium by allowing volumetric high resolution scanning, i.e.,continuous data acquisition with thin collimation and a high spatial frequency reconstruction algorithm.

CT is a key method in the identification and management of patients with ILD.

It not only improves the detection and characterization of parenchymal abnormalities, but also increases the accuracy of diagnosis.

The spectrum of morphologic characteristics that are indicative of interstitial lung disease is relatively limited and includes four main patttern Reticular (smooth,Nodular,Irregular) ,Nodular (Centrilobular ,Random,perilymphatic) , Alveolar (mixed density acute, mixed density chronic , Mosaic olidemia with air
trapping, Tree in bud) , Cystic (clusters of grapes,string of pearls, honeycombing, random cysts ).

In the correct clinical context, some patterns or combination of patterns, together with the anatomic distribution of the abnormality, i.e., from the lung apex to the base, or peripheral subpleural versus central bronchovascular, can lead the interpreter to a specific diagnosis. However, due to overlap of CT morphology between various entities, complementary lung biopsy is recommended in virtually all ILDS cases.

References:

1. Interstitial Lung Diseases at : Multislice CT, by M.F.Reiser 3rd revised edition 2009; 334-335.

2. Epidemiology, Interstitial (Nonidiopathic) Pulmonary Fibrosis by Eleanor M Summerhill, MD, FACP, FCCP; 9 August 2016 ; available at : http://emedicine.medscape.com/article/301337-overview#a6

3. High resolution CT, History and etymology by Dr Ayush Goel, Radiopaedia.org , available at :https://www. radiopaedia.org/articles/high-resolution-ct

4. Anatomy,Secondary Lobules at: Diffuse Lung Diseases – Clinical Features, Pathology, HRCT by MAFFESSANTI 2004; 5

5. Radiological features , the lungs. Thorax at: Anatomy of Diagnostic Imaging – Stephanie Ryan 2nd ed 2004; 118-119.

6.Weibel ER. Fleischner Lecture. Looking into the lung: what can it tell us? AJR Am J Roentgenol 1979, 133:1021

7.Weibel ER. Structural organization of the pulmonary interstitium. In: The Lung, vol 1, Raven Press, 1991

8. Secondary Lobule HRCT part I : basic interpretation by Robin Smithuis, Otto van Delden and Cornelia Schaefer-Prokop; published at 24-12-2006; available at :
www.radiologyassistant.nl/en/p42d94cd0c326b/lunghrctbasicinterpretation.html

9. Scanners Generations , The CT Scanner at A Radiologist’s Notes on Physics by Dr Garry Pettet MBBS BSc(Hons) FRCR (1st) 2014;133-136.

10. Types of detectors, The CT Scanner at A Radiologist’s Notes on Physics by Dr Garry Pettet MBBS BSc(Hons) FRCR (1st) 2014;133-136.

11. High-Resolution CT of the Lungs by Ella A. Kazerooni , September 2001, Volume 177, Number 3; available at http://www.ajronline.org/doi/full/10.2214/ajr.177.3.1770501.

12. CT technique . Interstitial Lung Diseases at : Multislice CT, by M.F.Reiser 3rd revised edition 2009; 26.2.2.

13., HRCT at: Grainger & Allison’s Diagnostic Radiology Essentials ; Elsevier 2013 ; 1.7 .1.

14. Smooth , Reticular Pattern, at : Diffuse Lung Diseases – Clinical Features, Pathology, HRCT by MAFFESSANTI 2004; 9.

15. Geusens EA. Primary pulmonary amyloidosis as a cause of interlobular septal thickening. AJR Am J Roentgenol 1997.

16. Irregular , Reticular Pattern, at : Diffuse Lung Diseases – Clinical Features, Pathology, HRCT by MAFFESSANTI 2004; 11.

17. Nodular Pattern , interstitial Lung Diseases at Grainger & Allison’s Diagnostic Radiology Essentials. 2013;1.7

18. Remy-Jardin M. Computed tomography assessment of ground-glass opacity: semiology and significance. J Thorac Imaging 1993, 8: 249.

19. Gruden JF. Multinodular disease: anatomic localization at thin-section CT-multireader evaluation of a simple algorithm. Radiology 1999, 210: 711.

20. Alveolar , Reticular Pattern, at : Diffuse Lung Diseases – Clinical Features, Pathology, HRCT by MAFFESSANTI 2004; 16.

21. Rossi SE. “Crazy paving” pattern at thin-section CT of the lungs: radiologic-pathologic overview. Radiographics 2003, 23:1509.

22. Wong JS. Bronchioloalveolar carcinoma and the air bronchogram sign: a new pathologic explanation. J Thorac Imaging 1994, 9: 141

23. Stern EJ. CT mosaic pattern of lung attenuation: etiologies and terminology. J Thorac Imaging 1995, 10: 294.

24. Eisenhuber E. The tree-in-bud sign. Radiology 2002, 222: 771.

25. Cystic Pattern, at : Diffuse Lung Diseases – Clinical Features, Pathology, HRCT by MAFFESSANTI 2004; 21.

26. Akira M. Idiopathic pulmonary fibrosis: progression of honeycombing at thin-section CT. Radiology 1994, 192: 582.

27. Lymphangioleiomyomatosis by Dr Yuranga Weerakkody at radiopaedia.org website avialable at:
https://radiopaedia.org/articles/lymphangioleiomyomatosis-1

MR FAT SATURATION TECHNIQUES




 Fat suppression is a key consideration in MRI imaging. The following techniques result in fat saturation

  • Short Tau Inversion recovery
  • Spectral pre saturation with inversion recovery
  • Chemical shift selective inversion recovery
  • Dixon method

1) Spectral presaturation with inversion recovery Technique

Spectral pre saturation with inversion recovery technique or SPIR technique is a type of crossbred fat suppression technique(1).

That could acquire an image without fat in it (fat suppression), we can do it by selective protons saturation.

The SPIR technique is useful technique it makes significant attenuation of the fat proton sensitivity while preserving the water proton sensitivity (2).

It uses T1 sequence relaxation and fat frequency excitation then applies of 180-degree radio-frequency inversion pulse to induce a flip angle along the longitudinal axis(3).

This inversion should be followed with a 90-degree excitation pulse which nulls signals of the processing fat molecules as they will not exhibit transverse magnetization hence improving differentiation of pathology.

That could work with RF-pulse fat-selective and also with spoiler gradient, they it ‘s together with residual longitudinal fat magnetization nulling through the mechanism of inversion delay.

the frequency of excitation pulse should be higher than RF pulse (4). This can be helpful only in the fat contenting examed region, as signals coming out of other tissues and water remain unaffected.

2) Chemical shift selective inversion recovery

Chemical shift is the most commonly used technique for fat suppression.

In this technique, we use a selective RF pulse at 90 degrees of narrow bandwidth target processing fat molecules,

so we can process them in the transverse plane (5).

After that immediately gradient spoiler is applied causing them to dephase. Over time imaging sequence begins (d) and no fat signal is seen and the water peak is imaged only (6).

The main disadvantage of this technique is that it should be used at a frequency higher than 1 Tesla and are not working at frequencies less than 0.3 Tesla (7) .

and it should acquire a homogeneous field to work, so we cannot get clear images or findings from an inhomogeneous field like field have a metallic device or any area of abnormal anatomy variants (7).

The main advantage of this technique is that it ‘s very helpful in merging with any pulsed sequences of MRI.

FIGURE (a) to (d) show the different Frequencies of fat suppression selective technique.(8)

Factors that affect chemical shift:

There are two parameters that affect the size of the chemical shift, So in the following sentences, we will discuss the impact of changing these parameters.

Chemical shift artifact is that artifact noticed between fat and water protons due to the difference in the magnetic shields.

it is a powerful artifact which we can use to rule out the existence of lesions consisting of fat  (12).

The artifact of Chemical shift makes dark edge between water and fat interference  (13).

There are several parameters that affect the size of chemical shift artifact including; Magnetic field of the used magnet, gradient strength, and the used bandwidth (14).

the first and most important and crucial parameter is magnetic field strength. In McRobbie et al (2007) textbook, doubling the strength of the magnetic field will increases the chemical shift induced (14).

Moreover, decreasing the gradient strength will increase the chemical shift. Finally, the third parameter that would affect the chemical shift is the bandwidth of the used radio-frequency pulse.

Narrower the bandwidth gives a higher chemical shift while increasing the bandwidth will decrease the chemical shift artifact.

 

 

3) Dixon method:

 

The sequence was named after the man who described it, WT Dixon in 1984(9). It ‘s based on imaging of in and out-of-phase.

we acquire 2 images sets,  the first in-phase TE and the other at out-of-phase TE.

These 2 sets, when added to each other, give ‘water-only’ image while if they subtracted from each other gives ‘fat-only’ image (Fig. below).

So this method is very helpful  in high magnetic susceptibility areas, but it may need magnetic field good homogeneity.(10)

four images of Dixon method, the (A) represent in-phase,(B) represent out-of-phase, (C) represent fat-only, and (D) represent water-only images. (11)

Dixon method has special favors and characters rather than other fat suppression techniques, as its fat signal suppression is less affected by artifacts and more uniform.

also, we can use it with other types of sequences and we can merge ir and use it with different MR sequences, for example, T1 . from a single acquisition, it can give images with or without fat suppression.

 

 

MRI GLIOBLASTOMA MULTIFORM (GBM MRI)

GBM MRI

This is a well known medical truth that Glioblastoma is the most malignant tumor of the brain. It has different terms, it may be called Grade IV astrocytoma or malignant astrocytoma or glioblastoma multiforme (GBM), Here we will discuss MRI Glioblastoma.

Glioblastoma In another word is a fast growing malignant astrocytic tumor which has special characters of having necrosis and neovascularity. considering 1ry malignant intracranial neoplasm, GBM is the most common tumor.

Glioblastoma has 2 types: the first type is Primary or could be named de novo. The second type is secondary, as degeneration
from astrocytoma that has a lower grade, and characterized by necrosis and microvascular proliferation.

According to WHO classifications. According to WHO grading, GBM is grade IV (1).

GBM is which is the most malignant astrocytic tumor, makes about 15% to 20% of all intracranial tumors. In adults, GBM is considered the most wide-spreading primary brain neoplasm (2).

It is believed that most glioblastomas arise from an existent astrocytoma or anaplastic astrocytoma, but few could grow as the primary tumor. According to a clinicopathologic study of 241 gliomas with necropsy data, about 7.5% of glioblastomas appear to have a multicentric origin(3).

Age incidence of GBM is markedly increased after the age of 50. its peak incidence appears more prominent in the sixth decade. GBM is very rare to occur in young age especially less than 30 years.Male to Female ratio is 3:2, it has male prominence as all type of glioma.

The same occurs in clinical presentation, a symptom of rapid increase intracranial pressure, after a short period of one month from its beginning. These forms of tumors have the worst prognosis with the median survival of 12 months.

Good prognosis cause includes young age, GBM occurring as a secondary to another lesion, not as a primary tumor, the third one is surgical debulking (4).

 

Pathological Process and clinical presentation of  GBM 


          GBM pathological malignant characters are a reflection in the MR imaging, and unfortunately, MR imaging suffers from som

e of the limitations seen on pathologic examination.

At the MR, we could see the heterogenicity inside the tumors which is the image of the necrosis and hemorrhage and hypercellularity (5). T2-WI would be very helpful to detect these changes, in this sequence cystic necrosis foci and hemorrhage is shown with debris–fluid levels and lower-intensity regions in areas of hypercellularity.

on spin echo, MR imaging, within the tumors linear regions of the signal void are seen, which reflect the effect of angiogenesis that characterizes glioblastomas. it’s very rare to find calcification in these lesions except they arise in lesions which have a low grade.

The bleeding tumor is a character of GBM, but unfortunately not alone, other tumors as oligodendroglioma and ependymoma have this character, so In MR we should be aware to the good differentiation between Intratumoral hemorrhage and Benign hemorrhage this is well described in the table below (Table 1).

The extensive edema (appear more prominent on WM) associated with this tumor makes a significant mass effect. So it’s very important to define tumor margins and differentiate it from surrounding edema.In the real world, what we call edema is very precise to be described as “tumor plus edema“(6).

The is appears on MR imaging more clear than CT, especially with the improvement of the MR contrast resolution imaging. So every radiologist and physician should know that tumor extends beyond the appeared abnormality regions MRI (7).

Patient with glioblastoma Symptoms usually varies with location. They may present with Seizures, focal neurologic deficits which are common to affect a motor area or limb function. Age Peak of glioblastoma range from 45 to 75 years, although it’s rare in young patients it may occur at any age.gliobasltoma has Relentless progression, its survival rate often < 1 year (8).

Intratumoral hemorrhage Benign hemorrhage
Markedly heterogeneous, related to
Mixed stages of blood
Debris–fluid (intracellular–extracellular blood) levels
Edema + tumor + necrosis with blood
Shows expected signal intensities of acute, subacute, or chronic blood, depending on stage of hematoma
Identification of nonhemorrhagic tumor component No abnormal nonhemorrhagic mass
Delayed evolution of blood-breakdown products Follows expected orderly progression
Absent, diminished, or irregular ferritin/hemosiderin Regular complete ferritin/hemosiderin rim
Persistent surrounding high intensity on long–repetition time images (i.e., tumor/edema) and mass effect, even in late stages Complete resolution of edema and mass effect in chronic stages

Table (1): Difference between Mlaginent intratumoral Hge Vs Bening intracranial Hematoma.(9) (Table 11.8)

Figure (1): Glioblastoma multiforme, gross specimen. A brain section from an autopsy specimen shows a nonhomogeneous cut surface with hemorrhage and necrosis. (Courtesy of Dr. N. K. Gonatas, Pennsylvania University Hospital, Philadelphia, Pennsylvania. (10)

MRI sequences of Localize and characterizations of GBM.

MRI is the best imaging choice for localization and characterization of Glioblastoma. Contrast-enhanced MR is most sensitive, Newer techniques help improve diagnosis/biopsy accuracy like MRS, perfusion, hypoxia imaging, DTI.

Glioblastoma appears as thick, irregularly enhancing tumor, has a  necrotic core.The mass could be seen as heterogeneous, hyperintense mass associated with adjacent infiltration of the tumor and vasogenic edema. (11)

With GBM we could expect to see necrosis, hemorrhage, cysts, fluid levels, neovascularity. GBM may appear diffuse infiltrative mass, and appear necrotic and have poor margins, GBM could cross WM and affect the other side of the cerebral hemisphere, If it occurs and affects corpus callosum, it’s so called butterfly tumor.it may include also anterior and posterior commissures. It’s rare to invade meninges and rarely to be multifocal (~5%).(12)

Most common Location of GBM is supratentorial white matter (WM), the frontal, temporal, parietal which are more likely to be invaded by GBM more than occipital lobes.Cerebral hemispheres are more likely than brainstem, which is more probable location than cerebellum.

Basal ganglia and thalamus are less common(13). In children, brain stem and cerebellum are more common. (14)

So, let’s talk a look at MRI sequences used to help localization and characterization of glioblastoma multiform, and how it appears in each sequence.

T1 Weighted Image: GBM appears as irregular isointense, hypointense WM mass. It’s common to see irregular margins and cyst and of course, necrosis is the main sign. Also, GBM could cause subacute hemorrhage.(15)

T2 Weighted Image: GBM appears as heterogeneous, hyper intense mass with adjacent tumor infiltration or vasogenic edema. We expect to see expect to see hemorrhage,  necrosis, cysts, fluid levels, neovascularity. Viable tumor extends far beyond signal changes. (16)

FLAIR: GBM appears as heterogeneous, hyper intense tumor, associated with infiltration and vasogenic edema. (17)

GRE T2-Weighted MRI: there is the probability of artifact that related to products of the blood. (18)

PWI: in this sequence elevated maximum relative cerebral blood volume in comparison with low-grade tumors, also it has elevated permeability in comparison to low-grade tumors. (19)

T1WI C+: on the sequence, the tumor appears as an irregular enhanced tumor with central necrosis .the tumor enhancement could be patchy or nodular or ring shape. (20)

Figure (2): T1-WI GBM appears as hypo intense lesion affecting corpus callosum genu  forming what is called a butterfly tumor (21)

 

 

Figure (3): T2-WI, GBM appears as hyper intense lesion affecting corpus callosum genu  forming what is called a butterfly tumor (22)

 

Figure (4): (GBM MRI) Axial T1WI C+ FS MR in a 60-year-old man with acute onset of seizures shows a heterogeneously enhancing occipital lobe mass with central necrosis and extension across the splenium of the corpus callosum , characteristic of GBM. The frontal and temporal lobes are the most common locations for GBM.(23)

 

 

Figure (5): (GBM MRI)Axial T1 C+ FS MR in the same patient shows a thick enhancing rind of tumor that surrounds the necrotic tumor core, characteristic of GBM. Other lesions including lymphoma and demyelination may also involve the corpus callosum.(24)

Figure (6):(GBM MRI) Axial FLAIR MR in a patient with GBM shows a heterogeneous mass and the typical extensive surrounding signal abnormality that represents a combination of tumor cells and vasogenic edema. Pathologically, tumor cells are found beyond the regions of signal abnormality.(25)

Figure (7):(GBM MRI) MRS in a patient with recurrent GBM shows a classic malignant tumor spectrum with a markedly elevated choline (Cho) , a low NAA at 2.02 ppm, and an inverted lactate peak  at 1.33. (26)

Sequences are used to plan treatment, assess the completeness of treatment and detect a change in the lesion.

DWI is the best MRI used to accurate pre-operative diagnosis, and also to monitor treatment effects on lesion and differentiation between true and pseudo progression. As Glioblastoma has Lower measured ADC than low-grade gliomas, and there is variable diffusion restriction in solid portions of the tumor.(27)

Figure (8): Axial MR perfusion in the same patient shows an increased rCBV . in the solid parts of the tumor and a low rCBV in the necrotic center .Perfusion MR is helpful to provide an accurate preoperative diagnosis. In addition, it is often used to help guide a biopsy if the location of the tumor prevents the patient from undergoing a complete resection.(28)

 

 

As ADC maps present a very good service to assess tumor grading and effect of treatment. Histogram analysis based on ADC  maps of contrast enhanced Tumor provide a great assessment True from pseudo progression.

Yet we should also assess biomarkers values, e.x percentile values of cumulative ADC histogram . to the good differentiation between true and pseudo progression of the tumor, we should know that at Histogram, the underlying hypothesis indicates the viable tumor components while the higher one indicates the edema and necrotic tissue. this sequence is very useful with heterogeneous nature of glioblastomas that include mixed parts of the active tumor and necrotic parts.(29)

DWI is useful not just in that, it’s also very helpful to differentiate between radiation affection and tumor recurrence and progression by assessment of ADC value differentiate of the GBM during after therapy examinations. (30)

Figure (9): This sequences of MR images of the patient on therapy. These represent the phenomenon of pseudoprogression. Note the upper images were obtained just after initiation of treatment show restriction of enhancement which indicates regression of tumor while the tumor is still growing as illustrated in lower images. Lower images were obtained 1 month later show the enlarged tumor.(31)

 

Diffusion tensor imaging (DTI): can also be used to improve surgical planning.(32)

Perfusion Weighted Imaging (PWI): this sequence is more accurate in illustration tumor outlines, so is very helpful in radiation and surgical planning.also, it’s helpful in the assessment of patients response to radiotherapy by measuring of rCBV. (33)

Functional MRI:  it’s the sequence used to the good planning of the neurological risks and treatment of the tumors. As fMRI helps in localization of the invasion of the cortical center that is responsible for the vital functions like memory, motor, and language .it can alter a neurosurgical decision to approach the GBM either by surgery or not.(34)

MRI Sequences used to grade GBM condition.

In addition to previously described routine anatomical sequences ( T1W C+ and T2W, etc). theses sequence are helpful in the grading of Glioblastoma.

MR perfusion very clever in assessment of tumor components that have a higher grade especially in guiding stereotactic biopsy and provide a good estimation of grading of tumors.(35)

Figure (10): An Example of MR perfusion of (GBM) (36)

Spectroscopy:
it’s used in combination with MRI, MRS to evaluate Glioblastoma type and grade, as the high-grade GBM has higher Cho/Cr and Cho/NAA ratios and also have lipid and lactate as result of necrosis
(Figure 6). it’s  used to differentiate the tumor when it enhances from other enhancement cause (e.g necrosis ), also it’s used to  differentiating the tumor when it does not enhance from edema and other T2 prolongation causes.(37)

Figure (11): An Example of Spectroscopy of (GBM) (38)

 

Functional MRI
Functional MRI is very helpful in grading the condition of glioblastoma patient condition . as it used to map language function. Language paradigms vary with  Tumor location. Yet till now  no a dependable way to measure memory tasks for neurosurgical planning.  fMRI used also for Motor mapping depending on the location of the tumor.(39)

Figure (12): Example of fMRI image of Glioblastoma (40)

Generally speaking, the integration of several techniques of advanced imaging (such as spectroscopy, perfusion imaging, and functional MRI) is very helpful in grading good assessment of the pathological process of glioblastoma.

 

 

 

Treatment options and outcomes for the patient

The usual course of treatment of glioblastoma include Biopsy, then tumor debulking followed by XRT, chemotherapy (temozolomide). Newer anti-angiogenesis agents, particularly bevacizumab (vascular endothelial growth factor blocker) for recurrent disease, let’s talk about it :

 

Radiation therapy: Studies show that radiation therapy, when combined with surgery, give prolonged survival rate if we compared it to the choice of surgery alone. It increases survival from three to four months to seven to twelve months.(41)

 

Chemotherapy – Antineoplastic agents:  No optimal chemotherapeutic regimen could be defined till now, however many studies say that about more than 25% of patient receive adjuvant chemotherapy have a more prolonged survival benefits.(42)

 

Surgery: Many studies say that surgery (biopsy vs resection) have a very important effect on survival length . in a study proves that high-grade GBM who underwent total resection, get two years survival incidence up to 19%.(43) .

in another patient, when we do a subtotal resection, he only had two-year survival incidence of 0%. When we made an analysis of 28 studies, we found survival advantage of the total over subtotal resection. (14 vs 11 ).(44)

GBM MRI Recurrence Monitoring sequences.

Glioblastoma Recurrence is not uncommon, so monitoring of recurrence is important, several sequences we have discussed in this article can be used to monitor GBM recurrence, as beside usual MRI sequences that show a well appeared classic lesion, there are sequences can see beyond standard images, here we are to discuss some of these.

MRI Perfusion:  it’s very helpful in detection of GBM recurrence and differentiation between it and effects of radiation.  this is done by monitoring  ADC values differences. by capturing fluid-volume changes in intracellular and extracellular parts of enhanced parts after post-therapy imaging. (45)

Proton MRS: it gives important biochemical details about metabolites of the brain, this help in the diagnosis of the disease and help neurologist to understand the disease. 1.5 T brain MRS currently has a number of clinical applications, one of its most important application is the early diagnosis of GBM recurrence.(46)

DWI: on its images, the necrosis appears heterogeneous spotty and marked hypointense, so that in tumor recurrence, the maximal ADC is lower than in necrosis. (47)

 

 

 

 

 

 

 

 

 

References:

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  9. Table 11.8 Intratumoral Hemorrhage Versus Benign Intracranial Hematomas, Adult Brain Tumors by Mahesh V. Jayaraman and Jerrold L. Boxerman, Glioblastoma Multiform, Magnetic Resonance Imaging of the Brain and Spine, by Scot W.Atlas, 5th ed (2016); 460.
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  11. Imaging, Glioblastoma, Astrocytic Tumours, Infiltrating, Neoplasms, Diagnostic Imaging of the Brain by Osborn, 3rd edition 2013; 442.
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  14. Location, General Features, Glioblastoma, Astrocytic Tumours, Infiltrating, Neoplasms, Diagnostic Imaging of the Brain by Osborn, 3rd edition 2013;       443.
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  2. T2WI, MR Findings, Glioblastoma, Astrocytic Tumours, Infiltrating, Neoplasms, Diagnostic Imaging of the Brain by Osborn, 3rd edition 2013; 443.
  3. FLAIR MR, Findings, Glioblastoma, Astrocytic Tumours, Infiltrating, Neoplasms, Diagnostic Imaging of the Brain by Osborn, 3rd edition 2013; 443.
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  9. Right upper image, Glioblastoma, Astrocytic Tumours, Infiltrating, Neoplasms, Diagnostic Imaging of the Brain by Osborn, 3rd edition 2013; 442.
  10. Right lower image, Glioblastoma, Astrocytic Tumours, Infiltrating, Neoplasms, Diagnostic Imaging of the Brain by Osborn, 3rd edition 2013; 442.
  11. Left lower image, Glioblastoma, Astrocytic Tumours, Infiltrating, Neoplasms, Diagnostic Imaging of the Brain by Osborn, 3rd edition 2013; 445.
  12. Right lower image, Glioblastoma, Astrocytic Tumours, Infiltrating, Neoplasms, Diagnostic Imaging of the Brain by Osborn, 3rd edition 2013; 445.
  13. DWI, Research “The basics of diffusion and perfusion imaging in brain tumors” published by By Panagiotis Korfiatis, Ph.D., and Bradley Erickson, MD, Ph.D. at July 2014, available at http://appliedradiology.com/articles/the-basics-of-diffusion-and-perfusion-imaging-in-brain-tumors.
  14. Right middle image, Glioblastoma, Astrocytic Tumours, Infiltrating, Neoplasms, Diagnostic Imaging of the Brain by Osborn, 3rd edition 2013; 445.
  15. DWI, Research “The basics of diffusion and perfusion imaging in brain tumors” published by By Panagiotis Korfiatis, Ph.D., and Bradley Erickson, MD, Ph.D. at July 2014, available at http://appliedradiology.com/articles/the-basics-of-diffusion-and-perfusion-imaging-in-brain-tumors.
  16. DWI, Research “The basics of diffusion and perfusion imaging in brain tumors” published by By Panagiotis Korfiatis, Ph.D., and Bradley Erickson, MD, Ph.D. at July 2014, available at http://appliedradiology.com/articles/the-basics-of-diffusion-and-perfusion-imaging-in-brain-tumors.
  17. Figure (7), Research “The basics of diffusion and perfusion imaging in brain tumors” published by By Panagiotis Korfiatis, Ph.D., and Bradley Erickson, MD, Ph.D. at July 2014 available at http://appliedradiology.com/articles/the-basics-of-diffusion-and-perfusion-imaging-in-brain-tumors.
  18. DTI, MR Findings, Glioblastoma, Astrocytic Tumours, Infiltrating, Neoplasms, Diagnostic Imaging of the Brain by Osborn, 3rd edition 2013; 443.
  19. PWI, MR Perfusion, Research “Advanced MR techniques in brain tumor imaging” published by By Sasan Karimi, MD; Nicole M. Petrovich, BA; Kyung K. Peck, Ph.D.; Bob L. Hou, Ph.D.; Andrei I. Holodny, MD available at: http://appliedradiology.com/articles/advanced-mr-techniques-in-brain-tumor-imaging.
  1. Functional MR, Research “Advanced MR techniques in brain tumor imaging” published by By Sasan Karimi, MD; Nicole M. Petrovich, BA; Kyung K. Peck, Ph.D.; Bob L. Hou, Ph.D.; Andrei I. Holodny, MD available at:http://appliedradiology.com/articles/advanced-mr-techniques-in-brain-tumor-imaging.
  1. MR Perfusion, Research “Advanced MR techniques in brain tumor imaging” published by By Sasan Karimi, MD; Nicole M. Petrovich, BA; Kyung K. Peck, Ph.D.; Bob L. Hou, Ph.D.; Andrei I. Holodny, MD available at:http://appliedradiology.com/articles/advanced-mr-techniques-in-brain-tumor-imaging.
  1. Image (2), Research “Advanced MR techniques in brain tumor imaging” published by By Sasan Karimi, MD; Nicole M. Petrovich, BA; Kyung K. Peck, Ph.D.; Bob L. Hou, Ph.D.; Andrei I. Holodny, MD available at http://appliedradiology.com/articles/advanced-mr-techniques-in-brain-tumor-imaging.
  2. Spectroscopy, Research “Advanced MR techniques in brain tumor imaging” published by By Sasan Karimi, MD; Nicole M. Petrovich, BA; Kyung K. Peck, Ph.D.; Bob L. Hou, Ph.D.; Andrei I. Holodny, MD available at:http://appliedradiology.com/articles/advanced-mr-techniques-in-brain-tumor-imaging.
  1. Image (7), Research “Advanced MR techniques in brain tumor imaging” published by By Sasan Karimi, MD; Nicole M. Petrovich, BA; Kyung K. Peck, Ph.D.; Bob L. Hou, Ph.D.; Andrei I. Holodny, MD available at http://appliedradiology.com/articles/advanced-mr-techniques-in-brain-tumor-imaging.
  2. Functional MR, Research “Advanced MR techniques in brain tumor imaging” published by By Sasan Karimi, MD; Nicole M. Petrovich, BA; Kyung K. Peck, Ph.D.; Bob L. Hou, Ph.D.; Andrei I. Holodny, MD available at:http://appliedradiology.com/articles/advanced-mr-techniques-in-brain-tumor-imaging.
  1. Image (8), Research “Advanced MR techniques in brain tumor imaging” published by By Sasan Karimi, MD; Nicole M. Petrovich, BA; Kyung K. Peck, Ph.D.; Bob L. Hou, Ph.D.; Andrei I. Holodny, MD available at http://appliedradiology.com/articles/advanced-mr-techniques-in-brain-tumor-imaging.
  2. Stupp R, Mason WP, van den Bent MJ, Weller M, Fisher B, Taphoorn MJ. Radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma. N Engl J Med. 352(10):987-96.
  3. Fine HA, Dear KB, Loeffler JS, Black PM, Canellos GP. Meta-analysis of radiation therapy with and without adjuvant chemotherapy for malignant gliomas in adults. Cancer. 71(8):2585-97.
  4. Ammirati M, Vick N, Liao YL, et al. Effect of the extent of surgical resection on survival and quality of life in patients with supratentorial glioblastomas and anaplastic astrocytomas. Neurosurgery. 1987 Aug. 21(2):201-6.
  5. Sanai N, Berger MS. Glioma extent of resection and its impact on patient outcome.Neurosurgery. 2008 Apr. 62(4):753-64; discussion 264-6. [Medline]. Fadul C, Wood J, Thaler H, et al. Morbidity and mortality of craniotomy for excision of supratentorial gliomas. Neurology. 38(9):1374-9.
  6. MR Perfusion, Research “Advanced MR techniques in brain tumor imaging” published by By Sasan Karimi, MD; Nicole M. Petrovich, BA; Kyung K. Peck, Ph.D.; Bob L. Hou, Ph.D.; Andrei I. Holodny, MD available at:http://appliedradiology.com/articles/advanced-mr-techniques-in-brain-tumor-imaging.
  1. Proton MRS in Neuroradiology, 3.0 T MR Spectroscopy, High Field Brain MRI Use in Clinical Practice by U. Salvolini · T. Scarabino (Eds.) 2nd 2017;6.1.1.
  2. Distinguishing Radiation-Induced Necrosis from Tumour Recurrence, Clinical Applications, Diffusion MRI From Quantitative Measurement to In vivo Neuroanatomy by Heidi Johansen-Berg Timothy E.J. Behrens, 2nd Edition 2013;192.

Here we are finish GBM MRI topic.

MRI DUCTAL CARCINOMA IN SITU (DCIS)

Introduction:

Ductal Carcinoma in Situ (DCIS) is the most common non-invasive type of breast cancer nowadays.

It’s more commonly affect women older than 50 years. Yet prevalence age of DCIS is 32.5 per 100,000 women, this rate jumps to 88 per 100,000 women between the ages of 50 and 64 years.35

its imaging management has wide variation and competition between different imaging modalities.

Ultrasound and mammography are very good in the assessment of DCIS. but nowadays after great advancement of MR technology.

MR overcome the drawback of ultrasound and underestimation of the tumor. So, MRI now is the most sensitive and most accurate way of diagnosis of DCIS.

DCIS isn’t life-threatening when well diagnosed and treated, but if not well managed it can develop invasive breast cancer later on.32

Pathology and clinical condition of DCIS:

Ductal Carcinoma in Situ (DCIS) is a clonal proliferation of malignant epithelial cells originating in terminal duct lobar unit without invasion of the basement membrane2.

DCIS can be multi-focal, (it appears > 1 site within 4 – 5 cm). Or Multi-centric(it appears > 1 quadrant separated by 4-5 cm).

Central necrosis dividing DCIS into comedo-carcinoma which have central necrosis and non-comedo-carcinoma which doesn’t have.

DCIS classify intro three grading:

1-Low-grade it refers to low nuclear grade with the absence of necrosis.

It contains monomorphous, small nuclei with or very few mitosis that causes expansion of the duct (3).

It contains No or few Apoptotic bodies, nuclei are usually diploid. (4).

it’s most commonly present as punctate or rounded calcifications, which is not as much as the extent of the lesion, unlike High-grade type. (3)

DCIS has architectural subtypes: Cribriform, Papillary, micropapillary and solid. The first two types are more common with low-grade type. (4)

2-The intermediate type characterized by a focal area of necrosis (not central necrosis), they tend to be noncomedo-carcinoma.

3- Hight grade type has pleomorphic nuclei 2.5-3 times more than the size of red blood cell (>15 microns). They also comedo-carcinoma as they have central necrosis in duct lumens. (4)

Clinical presentation :

Most DCIS patients are Asymptomatic but when there are symptoms, they come with a palpable mass and nipple discharge.

These are more common in Comedo than Non-Comedo type and it’s more to have micro-invasion and lymph node involvement.(5)

MRI sequences of Localize and characterizations of DCIS:

MRI is the most sensitive and accurate investigation of choice for detecting DCIS (up to 92
% sensitivity for DCIS) (6).

A) DYNAMIC CONTRAST ENHANCED (DCE) MRI SEQUENCES;

The Aim of the MRI detects the tumor and its extent, So the thickness of the slice of the scan ≤ 3 mm, the resolution ≤ 1mm, this leads to decrease volume averaging, making the MR able to make 3D images which much better than 2D images in detecting small tumors . 31

Fat suppression is very effective in detecting DCIS as the MR tumor detection depend on subtraction of pre- & post contrast sequences.

At T1WI pre-contrast, the breast emit a fatty bright signal which may lead under- or over assessment of the lesion31. But removing fat signal, then using subtraction images will lead to more accurate detecting enhancing tumors.

DCIS has MR appearance of mass enhancement or clumped ring enhancement (figure 1and 3 and4), as it raises inside milk ducts, so it follows the ductal tracts and it appears in ductal or regional or segmental distribution

1) T1 WI SEQUENCES:

T1-weighted sequences performed both before & after contrast injection. (associated with fat suppression), this lead to increase spatial and temporal resolution and decrease minimizing section thickness as follows:

MR tumor detection depends on subtraction of pre- & post contrast sequences, At T1WI pre-contrast: breast emit a fatty bright signal which may lead under- or over assessment of the lesion31. But removing fat signal, then using subtraction images  more accurate to detect enhancing tumors.

Most often, these sequences are performed in the axial or sagittal plane as fellow: 30
I) T1WI Axial fast spoiled gradient-echo imaging (TE/TR, 4.2/150) as in figure (2).

II) T1 WI Sagittal fast spoiled gradient echo imaging (TE/TR, 4.2/9) as in figure (2).

III) T1 WI Sagittal fat-saturated imaging (TE/TR,3.2/6.6).

IV) Pre-contrast T1 axial 3D with fat suppression, (mask images for
subtraction).

V) Post-contrast T1 axial dynamic multiphase 3D sequence with fat-suppression (6
acquisitions).

2) T2 WI SEQUENCES:

these increase specificity of MR to detection of DICS, as it appears iso to the-intense at noncontrast T2WI32 .T2WI sequences are the best to visualize breast anatomy and skin and it’s sensitive to fluid 31

I) T2WI Sagittal fast spin-echo fat-suppressed imaging (TE/TR, 88/3000) through both
Breasts.

II) T2WI Axial 2D fast spin echo: (TE/TR,3.3/6.8)

3) KUHL ENHANCEMENT CURVES,

These curves represent contrast uptake into breast lesions rate which is variable according to its nature, very helpful when used in association with morphologic features to get a better diagnosis . as shown in figure (6)

I) First curve called persistent curve: show prolonged signal increase along with time.indicate Benign lesions up to 90%. (11)

II) The second curve is called “Plateau” pattern curve start by increase signal then steady of the curve along with time. Probable malignant lesions obsess this curve(11).

III) The third curve is called: “washout” pattern curve, begin with increasing curve then it falls until end of the curve along with time. This curve indicates high possible malignant lesion. (12)(13)
DCIS has many subtypes of pathology and therefore its presence on MR different widely, But most of DCIS have plateau curves, some have washout curve. (6)

Figure (1) RT side: T1WI pre-contrast Sagittal MR image of Lt breast shows an area of enhancement with no abnormality. Lt side: T1WI Sagittal early post-contrast reveals foci of clumped enhancement (arrowhead) with nearby ductal enhancement (arrow) at the 12 o’clock position. Histopathology reveals DCIS.30

 

Figure (2): 2 Rt Image: axial early post-contrast T1WI fat-suppressed 3D fast spoiled gradient-recalled echo images reveals area of ductal & clumped enhancement (arrows) Lt Image: Sagittal delay post-contrast T1WI of the same lesion. Histopathology reveals DCIS 2

 

Figure (3):
Rt Image: T2WI Sagittal; shows high non mass signal intensity in ductal distribution(11)
Left Image: T1WI Sagittal delayed postcontrast; shows high clumped enhancement in ductal distribution. (11)

 

Figure (4): T1WI Axial fat saturation post-contrast reveals homogenous non-mass enhancement that has segmental distribution., pathology revealed comedo-necrosis High-grade DCIS 11)

 

Figure (5): Transverse T1-WI contrast-enhanced GRE subtracted MR images
of Rt breast, with morphologic characteristics suggestive of (DCIS), look at nonmass enhancement (white arrow )34

Figure (6): shows kinetic enhancement curve analysis show three different type of curves. (6)

 

B) DIFFUSED WEIGHTED IMAGING (DWI):

It now has a promising role in breast tumors differential diagnosis .as ADC level has lower value in malignant than benign tumours10.

But unfortunately, DWI-MR has a limited role indefinite diagnosis of DCIS (figure 7) as the nation mass enhancement that characterizes the DCIS can’t be well assessed with small ROI due to diffuse tumor effect and partial volume effect20.

But it ‘s very helpful when combining DWI with other MR sequences.20

Figure (7): Upper Rt Image: Sagittal 3D T1WI CE fat-suppressed reveals Pre-pectoral enhanced spiculated mass in Rt breast.28


Upper Lt Image: Applying of color enhancement kinetics map reveals tumor with kinetic type II in the center (yellow color) and type I in the periphery (blue color).28


Middle Image: Axial DWI isotropic (b: 700 s/mm2) image reveal high signal intensity within
the mass28


Lower Image: Axial ADC color map image (10.3.5) show restriction of diffusion of the mass with an ADC value of 1.21 × 10−3 mm2/s (ROI number 1)28

C) MR ELASTOGRAPHY

used in the breast tumors to differentiate between Malignant and benign tumors, (10).

Malignant tumors have lower elasticity and the less malignant have more elasticity.

so it’s very helpful in differential diagnosis of DCIS and invasive ductal carcinoma as the invasive ductal carcinoma is very stiff 33.

When used with Dynamic contrast-enhanced MRI, it raises its specificity up to 90 % in detection DCIS (14)

MRI sequences used to plan treatment, assess the completeness of treatment and detect a change in the lesion.

MR is the most sensitive module in determining tumor response to treatment and detecting residual lesions after chemotherapy and before surgery.

MRI can overcome other investigations problems at this point (for example, fibrosis mimic residual at ultrasound).

A) CONVENTIONAL MRI SEQUENCES:

by measuring the changing size of a tumor. but it can’t detect early assessment of treatment response.(20)

B) DYNAMIC CONTRAST ENHANCED MRI:

injection of contrast material with concentration 0.1-0.2 ml/kg. 9This includes taking T1WI post-contrast sequences and compare it with pre-contrast T1WI and T2WI, then we take T2WI post-contrast sequence to reach too high specificity(10)

we use the difference in enhancement kinetic curves parameters to measures the early response of DCIS to chemotherapy with 2 weeks early (10).

There is constantly called Transfer constant, Ktrans.10 we can use it predict the response of DCIS to chemotherapy(15).and vascular disruptive agents or antiangiogenic drugs response to treatment when there is change more than 40%, it’s considered a good response.(16)

C) MR-SPECTROSCOPY:

Its idea base on un-paired protons atoms like Hydrogen (1H), we use its properties of nuclear spin in MR field to absorb and emit radiofrequency(10), as Example 1H MRS enough water suppression is obligatory to detect proton resonances within Cells that increase in cancer, such as choline and lipids.

Choline is invisible and not detected in the normal breast at peak at 3.25 ppm indicates No malignancy (17). Recent studies show very good results, as decrease choline signal after 2 cycles of chemotherapy (figure 8), making MRS more sensitive in detected tumor size changing (18) and even more sensitive than DWI in predicting and detecting the pathological response.(19)

Figure (8): an example of MR-S; A) indicate responders and non-responders after chemotherapy cycle by the level of total choline. the responders begin with high choline level, then markedly decrease. B) indicate an example of lesion monitored after 4 cycles of chemotherapy. (9)

D) DIFFUSED WEIGHTED IMAGING (DWI):

ADC is very effective in predicting the early response of DCIS to treatment than the usual measurement of tumor size changing (20). Increase ADC level means good response to treatment (21)(22).

The main drawback of DWI is that the high signal intensity in cases of DCIS doesn’t get accurate differentiation between it and malignant lesions, so it’s advised to use with other sequences as a figure (7). (20)

E) MRI, T2*/BOLD:

this is Blood oxygen level-dependent (BOLD), the whole idea of this sequence is the use of Deoxyhaemoglobin as a contrast agent to detect the degree of hypoxia of tissue.

This revealed that the tumor tissue is less hypoxic than normal breast tissue. (20it can be used to detected tumor response to treatment although it’s less efficient than other sequences. (24)

MRI Sequences used to grade DCIS:

DCIS is graded into three main categories Low Grade, Intermediate grade, and high-grade DCIS. Sequences :

A) DYNAMIC CONTRAST ENHANCED MRI:

this is the most accurate in detecting different grading of DCIS(20), but its limitation is that contra-indicated with a patient having an allergy to the contrast media or any other contrast related problems. (20)

B) T1WI AND T2WI WITHOUT CONTRAST:

in case of contrast contra-indicated cases. it has low accuracy than DCE-MRI but it’s still good and can be used to avoid the contrast problems. (20)

C) DIFFUSED WEIGHTED IMAGING (DWI):

it’s the sequence of choice in grading DCIS as it doesn’t need contrast so we avoid the contrast problems(20), and it’s easy to process and have short acquisition time. although DCE-MR is more accurate, DWI can’t replace it, but it’ superior to it as it overcomes contrast limitation problems (20). DWI also can also diagnosis and grade DCIS even in the dense breast. (20)

Treatment options and outcomes for the patient:

To get away all risks of DCIS treatment we should ensure as much as the possible complete removal of the tumor. and prevent its recurrence (25). But treatment differs variably according to size, grade, patient age, family history; so, it may include surgery and radiotherapy. L.N removal surgery or hormonal therapy.

A-Surgery:

when we talk about surgery we mean to mention two types of surgery according to DCIS size if small DCIS, so conservative breast surgery or lumpectomy is done. If large DCIS, mastectomy is done. Usually, a simple mastectomy is of choice in most cases then we are going to the adjuvant therapy (chemotherapy or radiotherapy) (25).

B-Radiotherapy:

it’s used in associated / after conservative breast surgery. it has an important role in that. (5)

C- Hormonal therapies:

it helps in a reduced rate of local recurrence rates in DCIS patients. It’s standard now for estrogen & most prog receptor-+ve DCIS. (6)

Outcome: 5- year survival of in-situ patients give 100% five-year survival rate, death rate < 0.7%. (6)

MRI Recurrence Monitoring sequences:

MR is not routinely performed in monitoring recurrence of DCIS as it may overestimate the detected lesion, so it’s considered as good negative (as if MR don’t detect lesion recurrence it’s considered negative for recurrence ) but not good positive sequences.

MRI sequences used in monitoring recurrence are as follows :

A) DCE-MR sequences can accurate detection of any new lesion.The sequences include: Un-enhanced and two contrast-enhanced T1WI fat suppression 3D fast spoiled gradient recall sequence 36 Figure (9)

B) DWI-MR sequences: these play a major role in monitoring recurrence as measurements of ADC is very helpful in differentiation between scar tissue and tumor recurrence. Average ADC value of recurrences was statistically lower of scarring (p < 0.001). (26)

Figure (9):37 MR imaging features comparison between
a, b) a 41-year-old woman with recurrence after definitive surgical treatment for DCIS and
(c, d) the matched 45-year-old control subject

MR images in

(a) Subtracted maximum intensity projection shows increased BPE (background parenchymal enhancement), which measured as mean BPE of 86%. The BPE measurement excludes the known DCIS lesion in the ipsilateral breast (arrow).

(b) SER (signal enhancement ratio )map with color overlay shows a peak SER of 1.57 and an FTV (functional tumor volume )of 8.69 cm3 were calculated from kinetics data. Blue indicates persistent delayed enhancement
(SER,0.9); green, plateau enhancement (SER, 0.9–1.1); and red, washout (SER .1.1).

(c) Subtracted maximum intensity projection for the matched control subject shows minimal BPE (arrow), which measured as mean BPE of 71%.

(d) SER map with color overlay shows a peak SER of 1.17 and an FTV of 1.27 cm3 were calculated from kinetics data. 37

 

Conclusion:

MRI Imaging different sequences are the best investigation of choice for detection and characterization of DCIS and detecting its tumor response to treatment, but they are not ideal for monitoring tumor recurrence.

 

 

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