Irreversible electroporation

  • Irreversible electroporation (IRE or NTIRE for non-thermal irreversible electroporation) is a soft tissue ablation technique using ultra short but strong electrical fields to create permanent and hence lethal nanopores in the cell membrane, to disrupt the cellular homeostasis.
  • The resulting cell death results from apoptosis and not necrosis as in all other thermal or radiation based ablation techniques.
  • The main use of IRE lies in tumor ablation in regions where precision and conservation of the extracellular matrix, blood flow and nerves are of importance. The technique is in an experimental stage and has not been approved for use outside of clinical trials.
  • Utilizing ultra short pulsed but very strong electrical fields, micropores and nanopores are induced in the phospholipid bilayers which form the outer cell membranes.
  • A number of electrodes, in form of long needles, are placed around the target volume. The point of penetration for the electrodes is chosen according to anatomical conditions. Imaging is essential to the placement and can be achieved by ultrasound, magnetic resonance imaging or tomography. The needles are then connected to the IRE-generator, which then proceeds to sequentially build up a potential difference between two electrodes. The geometry of the IRE-treatment field is calculated in real time and can be influenced by the user. Depending on treatment-field and number of electrodes used, the ablation takes between 1 to 10 minutes of time. In general muscle-relaxants are administered, since even under general anaesthetics, strong muscle-contractions are induced by excitation of the motor end-plate.
  • One specific device for the IRE procedure is the so-called The NanoKnife system manufactured by AngioDynamics which has received premarket notification from the FDA.

  • Scope of applications:
    • Prostate: Using IRE, the urethra, bladder, rectum and neurovascular bundle can potentially be included in the treatment field without taking (permanent) damage. This would potentially give IRE superiority both for focal therapy and whole gland treatments compared to all other available methods.
    • Liver, kidney, and pancreas: Several inoperable tumors of the liver and the kidney can be treated using IRE. This is due to tissue selectivity regarding blood vessels and epithelial type tissue.
    • Other organs: the feasibility of IRE for breast cancer and other heterogeneous tissue organs have been reported.

    MRI of the brachial plexus

    Normal anatomy :

    The brachial plexus is formed by the ventral roots of C5 to T1 nerve roots. These unite to form three trunks. The trunks split into three anterior and three posterior divisions. These unite to form the three cords that further divide into five peripheral nerves. The roots and trunks are supraclavicular in location while divisions are retroclavicular and the cords are infraclavicular.

    Imaging technique :

    • The T1-weighted images delineate the anatomy of nerves, muscles, and vessels as they are outlined by fat.
    • The T2-weighted images reveal the signal abnormalities within the brachial plexus.
    • Short-tau inversion recovery (STIR) images provide uniform and reliable fat suppression over curved surfaces and large field of view. The scan protocol consists of coronal STIR and T1-weighted images with large field of view (FOV), including both brachial plexi for comparison followed by sagittal T1-and T2-weighted images with small FOV for high spatial resolution.
    • Intravenous Gadolinium is administered in patients with tumors or mass lesions. Gadolinium is not administered in patients with traumatic brachial plexopathy. In patients with traumatic brachial plexus injury, in addition to the previously described protocol, sagittal T2-weighted images are obtained through the cervical spine followed by axial T2-weighted images from C4 to T2 levels. In addition, a 3D gradient echo (GRE) sequence with thin slices is obtained to look for the nerve root avulsion.
    • In patients suspected with thoracic outlet syndrome, in addition to coronal STIR and coronal T1-weighted images, sagittal T1-weighted images are obtained through the symptomatic side extending from midline to the axilla with arm in hyper-abducted position. These are compared with similar sagittal T1-weighted images obtained with arm in neutral position by the side of body.

    Traumatic injuries to brachial plexus :
    • The common causes of brachial plexus injuries are road traffic accidents and birth palsy.
    • Brachial plexus injuries can be divided into pre- and post-ganglionic lesions.
    • The pre-ganglionic lesions are avulsion of the nerve roots at their origin while post-ganglionic lesions may be lesions in continuity or nerve ruptures.
    • The patient may have a combination of both pre- and postganglionic lesions.
    • It is important to differentiate between pre and postganglionic lesions to determine the prognosis and plan further management.
    • Pseudomeningoceles are formed due to extra-vasation of CSF through tear of the peri-neural sheath. These are seen on T2-weighted images as fluid-intensity lesions at the site of nerve root avulsion. However, presence of a pseudomeningocele is not always seen in nerve root avulsion and vice versa.
    • Brachial plexus injuries may be associated with injuries to the subclavian artery due to their anatomical proximity to each other. Also post-traumatic pseudoaneurysm of subclavian artery may present with delayed brachial plexus paralysis due to compression of the brachial plexus.
    Non-traumatic Brachial Plexus Pathologies :

    1.Radiation fibrosis :
    • Patients undergoing radiation therapy in axillary region, most commonly for breast carcinoma, may present with brachial plexopathy after several months to years.
    • Radiation fibrosis is seen as diffuse thickening of the brachial plexus and iso- or hypointensity on T1- and T2-weighted images.
    • The absence of a focal mass differentiates it from metastatic disease.
    • Moreover, metastases appear hypointense on T1-weighted images and hyperintense on T2-weighted images.
    2.Brachial plexus neuritis :
    • Acute brachial plexitis presents with severe shoulder and upper arm pain lasting for few days to weeks followed by upper arm weakness.
    • Idiopathic brachial neuritis is of unknown cause but an immune-mediated inflammatory reaction following viral infection, vaccination, surgery, pregnancy, etc., has been proposed as etiology.
    • Bilateral brachial plexus neuritis in postpartum period.
    • Brachial plexitis is seen on MRI as focal or diffuse hyperintense signal in brachial plexus.
    3.Brachial plexus tumors :
    • Nerve sheath tumors (schwannoma and neurofibroma) are seen as ovoid lesions isointense to muscle on T1-weighted images and hyperintense on T2-weighted images with ‘target’ sign.
    • These reveal intense enhancement on administration of gadolinium contrast. Most common benign tumors that involve brachial plexus are lipomas and aggressive fibromatosis.
    • Metastatic breast carcinoma , superior sulcus tumors (non-small-cell lung carcinoma arising from lung apex), and lymphoma involve the brachial plexus frequently.
    4.Thoracic outlet syndrome :
    • It is dynamically induced compression of neural and/or arterial structures crossing the cervico-thoraco-brachial junction.
    • MRI plays an important role in demonstrating neurovascular compression, localizing it and identifying the structure causing the compression.
    • The three spaces that are evaluated on sagittal T1-weighted images are the inter-scalene triangle, costo-clavicular, and retro-pectoralis minor spaces with arm in neutral as well as hyperabducted position to look for compression of the neurovascular structures. The costo-clavicular space is the most common site of compression followed by inter-scalene triangle.
    • The lesions causing compression may be bony abnormalities (cervical rib, long transverse process of C7 vertebra, callus or osteochondroma of clavicle or first rib) or soft tissue pathologies (fibrous band, hypertrophy of scalenus anterior muscle, scalenus minimus muscle, and fibrous scarring).
    • Bilateral hypoplastic first ribs fused to second ribs can also cause thoracic outlet syndrome.
    • Contrast-enhanced MR angiography may be performed with the arm in elevated position to demonstrate narrowing of subclavian artery.

    Imaging of constrictive pericarditis

    General considerations:
    o Defined by thickening of pericardium (>4mm) impeding diastolic filling.
    o Thickened pericardium may calcify (50%).
    o Calcified pericardium almost always implies constriction, but not always.
    o About 50% of calcified pericardiums are visible on conventional radiography.
    o Calcification of the pericardium is most likely inflammatory in nature.

     Can be seen with a variety of infections, trauma, and neoplasms.
     Most common causes include:
     Viral pericarditis (most common).
     Tuberculous pericarditis.
     Uremic pericarditis.
     Post-cardiac surgery.
    o Calcification most commonly occurs along the inferior diaphragmatic surface of the pericardium surrounding the ventricles.
     Thin, egg-shell like calcification is more often associated with viral infection or uremia.
     Calcification from old TB is often thick, confluent, and irregular in appearance, especially when compared with myocardial calcification.

    Radiographic features:

     Plain chest radiographs may show pericardial calcification in as many as 50% of CP patients.
     The cardiac silhouette should be small in a patient with uncomplicated CP.
     CP can also coexist with cardiomyopathy, and a large heart does not exclude the disease. Other, less reliable plain radiographic findings include an abnormal cardiac contour, such as straightening of the right atrial border and, more rarely, straightening of the right and left cardiac borders, with obliteration of the normal curves, on frontal images. On fluoroscopy, diminished cardiac pulsation may be seen.
     The absence of calcification does not exclude the disease, and further testing should include an extensive workup in the echocardiography laboratory, with an assessment of the Doppler velocities across the mitral and tricuspid valves during inspiration and expiration.
    Computed Tomography:
     The pericardium should be diffusely thicker than 3 mm; however, many patients do not present with this finding, and the diagnosis of CP should not be discarded if thickening is not present. The size of all 4 heart chambers should be within the normal range; however, CP can coexist with other diseases, and global or focal dilatation of the cardiac chambers does not exclude CP.
     The inflow veins to the right atrium, including the SVC, inferior vena cava (IVC), and hepatic veins, should be dilated. This finding is necessary but not sufficient to make the diagnosis of CP because it commonly occurs in the setting of congestive heart failure brought on by a variety of causes. Most often, when the hepatic veins and IVC are dilated for reasons other than CP, dilatation of 1 or all of the cardiac chambers is present and caused by systolic dysfunction or valve disease. If significant cirrhosis has already occurred, the hepatic veins may not be dilated.
     In CP, there should be poor opacification of liver parenchyma due to congestion and there should be no contrast enhancement in the portal vein.
     NB: Dilated veins can be caused by right-sided heart failure. Liver cirrhosis can mimic the CT findings of CP.
    Magnetic Resonance Imaging:
     Diffuse thickening of the pericardium greater than 3 mm can be observed on multiplanar MRIs.
     ECG-triggered MRI is sensitive to constrictive disease of the pericardium because the fibrous layers are bordered by fat, which produces a distinct MRI signal. MRI can be used to measure pericardial thickness; the ideal views for measuring pericardial thickness are oriented perpendicular to the long axis of the left ventricle. MRI can also be used to measure chamber sizes at successive 50-msec delays after the R wave and to determine whether or not a filling plateau is present.
     Like echocardiography and/or Doppler imaging, velocity-encoded (VENC) MRI can be used to assess volumetric flow and regurgitant flow to the pulmonary veins and the hepatic vein. MRI can demonstrate focal abnormalities and can cover the heart to determine whether the disease encapsulates its entirety.
     MRI dynamically shows a reversed curvature of the interventricular septum clearly.
     Fast imaging can be performed during deep respiration to establish whether filling is concordant or discordant. CP restriction creates discordance with reduced left ventricular filling, which corresponds to increased right ventricular filling.
     Liver sonograms show dilated hepatic veins and abnormal pulse Doppler waveforms in the portal and hepatic veins due to outflow obstruction.
     Abdominal ultrasonographic findings are nonspecific and must be confirmed with echocardiography and cardiac catheterization results.
     Cardiac echograms show normal contraction and systolic function. Special procedures, including an assessment of Doppler velocities across the mitral and tricuspid valves during inspiration and expiration, are needed to demonstrate ventricular interdependence.
     Budd-Chiari syndrome, cirrhosis, and right-sided heart failure can mimic some of the findings of CP at liver ultrasonography.
    Nuclear Imaging:
     Gated nuclear ventriculography may show rapid ventricular filling in CP. Reportedly, these findings can be used to differentiate CP from restrictive cardiomyopathy.

    MRI findings of tuberculosis of the hip joint

    1. The infection may originate in the synovium, the proximal femur (epiphysis, metaphysis, femoral neck, or trochanteric apophysis), the acetabulum, or the gluteal/ iliopsoas bursae.
    2. Cold abscesses may be palpable in the femoral triangle, the ischiorectal fossa, or the thigh. Sinuses may occur in any of these locations.
    3. The radiographic findings vary considerably depending on the primary location and degree of involvement.
    4. A lesion in the acetabular roof (“wandering acetabulum”) may result in subluxation, and clinically there will be limb shortening without positioning. True pathologic dislocation may occur as well, which will be associated with both limb shortening and positioning.
    5. Protrusio may be associated with lesions in the acetabular floor.
    6. Coxa magna may be confused with Perthes' disease in pediatric patients.
    7. Significant joint space narrowing without an osseous focus (“atrophic”) may be difficult to differentiate from rheumatoid arthritis.
    8. Destruction on both sides of the joint may result in irregularity of the femoral head and incongruity (“mortar and pestle”).
    9. Disease passes into 4 stages:
    (A) Stage of synovitis:
    - X-RAY – soft tissue swelling , haziness of articular margins & rarefaction
    - USG – soft tissue swelling
    - MRI – synovial effusion
    (B) Stage of early arthritis:
    - X-RAY – osteopenia , erosion of articular margins , ↓ joint space.
    - MRI  synovial effusion , edema , minimal bone destruction
    (C) Stage of advanced arthritis:
    - X-RAY  further decrease in joint space.
    (D) Advanced arthritis with subluxation / dislocation :
    - X-RAY Furhter destruction of acetabulum , head , capsule and ligaments. Head – upwards and posteriorly. Wandering / migrating acetabulum. Mortle & pestle appearance. Reduced joint space.

    Osteoporosis and osteomalacia by radiographic imaging

    Osteoporosis radiographic manifestations:

    1. The vertebral bodies may develop a biconcave shape or compression fractures.
    2. In tubular bones the trabecular bone loss may cause the metaphyses to appear radiolucent.
    3. Pathological fractures may occur at multiple sites.
    4. Schmorls nodes.
    5. Acute and insufficiency fractures.
    6. MR imaging:
    (A) In transient osteoporosis of the hip manifested as decreased signal intensity on T1-weighted sequences and increased signal intensity on T2-weighted sequences.
    (B) The patient commonly has associated joint effusions in the affected hip.
    (C) Chemical shift fat suppression and STIR imaging techniques can be effective in the detection of transient bone marrow oedema.

    Osteomalacia radiographic manifestations:

    1. Loosers zones (cortical fractures on the compression side of the bone) or Milkmans pseudofractures are strongly suggestive but not diagnostic of osteomalacia. i.e. linear lucencies oriented perpendicular to the cortical margin.
    2. Decreased bone density (Osteopenia).
    3. Coarsening of the trabecular pattern and cortical striations.
    4. Cortical thinning.
    5. MRI : insufficiency fractures seen as a hypointense lines or fissures on T1- and T2-weighted and STIR MR images.

    Normal ultrasonographic anatomy of the liver

  • Hepatic US is performed with standard curvilinear and high-resolution linear probes.
  • The curvilinear probe (2–6 MHz) allows acoustic penetration of deeper parenchyma while a high-resolution probe (7–12 MHz) may be used to depict greater surface detail.
  • Optimization of the gain, time-gain compensation, and tissue harmonics by an experienced sonologist, and second-look sonography by informed radiologists are requisites for achieving diagnostic examinations.
  • Normal liver parenchyma has a homogeneous echotexture, the assessment is subjective but the liver should not appear granular or coarsened if speckle reduction and compound imaging parameters are optimized.
  • Hepatic echogenicity is subjectively compared with that of adjacent solid viscera such as the kidneys and spleen; normal hepatic echogenicity is marginally higher than that of the kidney but less than that of the spleen.
  • The spleen provides a more reliable comparison because numerous intrinsic kidney diseases can alter their echogenicity.
  • Normal hepatic vessels have smooth walls and anechoic lumens.
  • Intrahepatic arteries are difficult to resolve on gray scale alone, but parallel the portal veins.
  • Normal spectral Doppler interrogation shows a low-resistance waveform with continuously hepatopetal diastolic flow.
  • Normal portal veins have thin echogenic walls and monophasic waveforms with mild respiratory variation. 
  • Alterations of portal mural echogenicity should be considered abnormal.
  • Normal hepatic veins and the inferior vena cava (IVC) lack discernible walls.
  • The normal hepatic venous waveform is triphasic, owing to 2 hepatofugal peaks and 1 hepatopetal peak reflecting primarily right atrial pressure.
  • The normal common bile duct measures up to 6 mm in normal individuals, but radiology dogma suggest that the diameter of the duct can increase with age.
  • The central intrahepatic ducts should normally measure 3 mm or less.
  • The diameter of the common bile duct may vary following cholecystectomy.
  • The normal perihepatic spaces should contain a variable amount of homogeneous fat; any ascites, fluid collection, or soft-tissue lesion should be considered abnormal.