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==Overview==
==Overview==
On gastrointerstinal MRI, systemic lupus erythematosus (SLE) may be characterized by hepatomegaly, pancreatic parenchymal enlargement, and hypervascularity of mesentery. On cardiac MRI, SLE may be characterized by mitral leaflet thickening, pericardial thickness, and pericardial effusions. On neurologic MRI, SLE may be characterized by white matter lesions, changes in brain vessel blood flow, and Patchy areas of enhancement. On musculoskeletal MRI, SLE may be characterized by intramuscular edema, [[Tenosynovitis|proliferative tenosynovitis]], and [[bone marrow]] edema.


===== Joint and synovial evaluation =====
== Key MRI findings in systemic lupus erythematosus ==
Reveal erosive changes and abnormalities of the soft tissues more often, including:
Most of the SLE complications can be found with other more feasible imaging techniques. So MRI is not indicated primarily in the diagnosis of most complications of SLE, but if done, the following results can be found regarding the organ system involvement:
*
 
===== Neurological evaluation =====
MRI is more sensitive than CT, and may reveal the following abnormalities:
*
 
===== Cardialogical evaluation =====
* Cine cardiac MR imaging as an noninvasive tool for evaluating
** Abnormal flow patterns
** Ventricular dimensions
** Stroke volume
** Regional myocardial function
 
===== Bone evaluation =====
* Avascular necrosis (AVN)
** Lack of enhancement and devascularized areas on gadolinium-enhanced MR imaging 
** Bone marrow edema on MRI with  
** Low-signal-intensity marginal areas on standard spin-echo T1- and T2-weighted images 
** Intermediate to high signal intensity inside bone tissue on T2-weighted images, producing a line of low signal intensity with an adjacent high-signal-intensity line 
** High signal intensity on T2-weighted images due to subchondral fractures that may be accompanied by fluid signal intensity or edema 
** Low signal intensity on T2-weighted images due to collapse of the articular surface 
 
* Early or subtle insufficiency fractures especially on T2-weighted MR imaging
** In characteristic stress locations insufficiency fractures may appear as areas of high signal intensity due to bone marrow edema
{| class="wikitable"
{| class="wikitable"
!Organ
!
!Disease
!Disease
!MRI
!MRI
!SONO
|-
|-
| rowspan="4" |Gastrointestinal system
| rowspan="3" |Gastrointestinal system
|[[Hepatitis]]
|[[Hepatitis]]
|
|
* nodules ranging around 0.5-4.5 cm in diameter 
* Hepatomegly
** '''T2:''' nonspecific, increased periportal oedema 4
* Nodules that ranging around 0.5-4.5 cm in diameter 
** '''MRCP:''' primary sclerosing cholangitis (PSC) should be excluded
** T2: nonspecific, increased periportal oedema
|
|-
|-
|[[Acute pancreatitis]]
|[[Acute pancreatitis]]
|Contrast-enhanced MR is equivalent to CT in the assessment of pancreatitis.
Abnormalities that may be seen in the pancreas include:
* typical findings
** focal or diffuse parenchymal enlargement
** changes in density because of oedema
** indistinct pancreatic margins owing to inflammation
** surrounding retroperitoneal fat stranding
* liquefactive necrosis of pancreatic parenchyma
** lack of parenchymal enhancement
** often multifocal
* infected necrosis
** difficult to distinguish from aseptic liquefactive necrosis
** the presence of gas is helpful
** FNA helpful
* abscess formation
** circumscribed fluid collection
** little or no necrotic tissues (thus distinguishing it from infected necrosis)
* haemorrhage
** high-attenuation fluid in the retroperitoneum or peripancreatic tissues
|
|
* to identify gallstones as a possible cause
* Contrast-enhanced MR is equivalent to CT in the assessment of pancreatitis
* diagnosis of vascular complications, e.g. thrombosis
** Abnormalities that may be seen in the pancreas include:
* identify areas of necrosis which appear as hypoechoic regions
*** Parenchymal enlargement
*** Surrounding retroperitoneal fat stranding
*** Abscess formation
**** Circumscribed fluid collection
|-
|-
|[[Mesenteric vascular occlusion|Mesenteric vasculitis]]
|[[Mesenteric vascular occlusion|Mesenteric vasculitis]]
|
|
* The '''comb sign''' refers to the hypervascular appearance of the mesentery 
* Comb sign
* This forms linear densities on the mesenteric side of the affected segments of small bowel, which give the appearance of the teeth of a comb. 
** Hypervascular appearance of the mesentery 
|
|-
|-
|[[Acute cholecystitis]]
| rowspan="4" |Cardiac involvement
|MR cholangiopancreatography (MRCP) may show an impacted stone in the gallbladder neck or cystic duct as a rounded filling defect.
|[[Mitral stenosis]]
|
|
* gallbladder wall thickening (>3 mm) and pericholecystic fluid 
* Mitral leaflet thickening
* Positive Murphy sign
* Reduced diastolic opening
* gallbladder distension
* Abnormal valve motion toward the left ventricular outflow tract
*  
|-
|-
| rowspan="5" |Cardiac involvement
|[[Pericarditis|Acute pericarditis]]
|Mitral stenosis
|
* mitral leaflet thickening
* reduced diastolic opening
* abnormal valve motion toward the left ventricular outflow tract
|
|
* The normal pericardial thickness is considered 2 mm while a thickness of over 4 mm suggests a [[pericarditis]]
|-
|-
|Mitral regurgitation
|[[Pericardial effusion]]
|
|
|
|-
* Fluid [[density]] material surrounding the heart
|Acute pericarditis
|The normal pericardial thickness is considered 2 mm while a thickness of over 4 mm suggests a pericarditis 
|
|-
|Pericardial effuson
|Fluid density material is seen surrounding the heart
|Echocardiography is the method of choice to confirm the diagnosis, estimate the volume of fluid and most importantly assess the haemodynamic impact of the effusion
|-
|-
|[[Myocarditis]]
|[[Myocarditis]]
|
|
* regional or global wall motion abnormalities are common, but nonspecific (biventricular wall motion abnormality, however, is the main predictor of death or transplantation)
* Regional or global wall motion abnormalities
* pericardial effusion is reported in ~45% (range 32-57%) of patients with myocarditis
* Pericardial effusion
** regional vasodilatation and increased blood volume due to the inflammation in myocarditis causes early postcontrast enhancement
** Early postcontrast enhancement due to regional vasodilatation and increased blood volume, secondary to the inflammation
|
|-
|-
|
| rowspan="4" |Neurological involvement
|General
|General
|
|
Line 119: Line 62:
* Periventricular hyperintensities
* Periventricular hyperintensities
* Detects clinically silent lesions
* Detects clinically silent lesions
|
|-
|-
| rowspan="2" |Neurological involvement
|[[Stroke]]
|[[Stroke]]
|
|
* the affected parenchyma appears normal on other sequences, although changes in flow will be detected (occlusion on MRA) and the thromboembolism may be detected (e.g. on SWI). Slow or stagnant flow in vessels may also be detected as a loss of normal flow void and high signal 
* Changes in brain vessel blood flow (occlusion on MRA)  
* after 6 hours, high T2 signal will be detected
* No parenchymal changes 
|
* Slow or stagnant flow in vessels as a loss of normal flow void 
* High T2 signal after 6 hours of stoke
|-
|-
|[[Neuropathies]]
|[[Neuropathies]]
|
|
* Optic neuritis:
* [[Optic neuritis]]
** Typically findings are most easily identified in the retrobulbar intra-orbital segment of the optic nerve, which appears swollen, with high T2 signal. High T2 signal persists and may be permanent; chronically the nerve will appear atrophied rather than swollen.  Contrast enhancement of the nerve, best seen with fat-suppressed T1 coronal images, is seen in >90% of patients if scanned within 20 days of visual loss
** Retrobulbar intra-orbital segment of the optic nerve appears swollen
|
*** High T2 signal that may persists and be permanent
** Chronic involvement of optic nerve
*** Atrophied nerve
*** Contrast enhancement of the nerve, best seen with fat-suppressed T1 coronal images
|-
|-
|
|Autoimmune encephalitis
|Autoimmune encephalitis
|mesial temporal lobes and limbic systems, typically manifested by cortical thickening and increased T2/FLAIR signal intensity of these regions. Bilateral involvement is most common (60%), although often asymmetric
Patchy areas of enhancement
|
|
* Mostly in temporal lobes and limbic systems
* Bilateral involvement is most common (60%), although often asymmetric
* [[Cortical area|Cortical]] thickening
* Increased T2/FLAIR signal intensity of affected regions
* Patchy areas of enhancement
|-
|-
| rowspan="4" |Musculoskeletal involvement
|Raynaud phenomen
|
|
|Raynaud phenomen
* Contrast-enhanced MR angiograph
|contrast-enhanced MR angiography may also reveal characteristic narrowing and tapering of digital vessels 
** Characteristic narrowing of digital vessels
|Doppler sonography:
** Tapering of digital vessels
flow volume and vessel size irregularities 
|-
|-
|
|Myositis
|Myositis
|'''Intramuscular oedema''' (increased high T2/STIR signal)
|
|
* Intramuscular edema (increased high T2 signal)
|-
|-
| rowspan="4" |Musculoskeletal involvement
|[[Arthritis]]
|[[Arthritis]]
|
|
* Capsular swelling
* Capsular swelling
* Proliferative tenosynovitis
* [[Tenosynovitis|Proliferative tenosynovitis]]
* Synovial overgrowth
* [[Synovial]] overgrowth
|
|-
|-
|[[Osteonecrosis]] ([[Avascular necrosis]])
|[[Osteonecrosis]] ([[Avascular necrosis]])
|
|
|
* Lack of enhancement and devascularized areas on gadolinium-enhanced MR imaging 
|-
* Bone marrow edema on MRI 
|Subcutaneous nodules
* Low-signal-intensity marginal areas on standard spin-echo T1- and T2-weighted images 
|
* Intermediate to high signal intensity inside bone tissue on T2-weighted images, producing a line of low signal intensity with an adjacent high-signal-intensity line 
|
* High signal intensity on T2-weighted images due to subchondral fractures that may be accompanied by fluid signal intensity or edema 
|-
* Low signal intensity on T2-weighted images due to collapse of the articular surface 
|Osteoporosis
 
|
* Early or subtle insufficiency fractures especially on T2-weighted MR imaging
|
** In characteristic stress locations insufficiency fractures may appear as areas of high signal intensity due to bone marrow edema
|}
|}
==Examples of MRI Findings in Systemic Lupus Erythematosus==


==References==
==References==

Revision as of 19:56, 17 July 2017

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

On gastrointerstinal MRI, systemic lupus erythematosus (SLE) may be characterized by hepatomegaly, pancreatic parenchymal enlargement, and hypervascularity of mesentery. On cardiac MRI, SLE may be characterized by mitral leaflet thickening, pericardial thickness, and pericardial effusions. On neurologic MRI, SLE may be characterized by white matter lesions, changes in brain vessel blood flow, and Patchy areas of enhancement. On musculoskeletal MRI, SLE may be characterized by intramuscular edema, proliferative tenosynovitis, and bone marrow edema.

Key MRI findings in systemic lupus erythematosus

Most of the SLE complications can be found with other more feasible imaging techniques. So MRI is not indicated primarily in the diagnosis of most complications of SLE, but if done, the following results can be found regarding the organ system involvement:

Disease MRI
Gastrointestinal system Hepatitis
  • Hepatomegly
  • Nodules that ranging around 0.5-4.5 cm in diameter 
    • T2: nonspecific, increased periportal oedema
Acute pancreatitis
  • Contrast-enhanced MR is equivalent to CT in the assessment of pancreatitis
    • Abnormalities that may be seen in the pancreas include:
      • Parenchymal enlargement
      • Surrounding retroperitoneal fat stranding
      • Abscess formation
        • Circumscribed fluid collection
Mesenteric vasculitis
  • Comb sign
    • Hypervascular appearance of the mesentery 
Cardiac involvement Mitral stenosis
  • Mitral leaflet thickening
  • Reduced diastolic opening
  • Abnormal valve motion toward the left ventricular outflow tract
Acute pericarditis
  • The normal pericardial thickness is considered 2 mm while a thickness of over 4 mm suggests a pericarditis
Pericardial effusion
  • Fluid density material surrounding the heart
Myocarditis
  • Regional or global wall motion abnormalities
  • Pericardial effusion
    • Early postcontrast enhancement due to regional vasodilatation and increased blood volume, secondary to the inflammation
Neurological involvement General
  • Focal neurological defects
  • White matter lesions
  • Periventricular hyperintensities
  • Detects clinically silent lesions
Stroke
  • Changes in brain vessel blood flow (occlusion on MRA)  
  • No parenchymal changes 
  • Slow or stagnant flow in vessels as a loss of normal flow void 
  • High T2 signal after 6 hours of stoke
Neuropathies
  • Optic neuritis
    • Retrobulbar intra-orbital segment of the optic nerve appears swollen
      • High T2 signal that may persists and be permanent
    • Chronic involvement of optic nerve
      • Atrophied nerve
      • Contrast enhancement of the nerve, best seen with fat-suppressed T1 coronal images
Autoimmune encephalitis
  • Mostly in temporal lobes and limbic systems
  • Bilateral involvement is most common (60%), although often asymmetric
  • Cortical thickening
  • Increased T2/FLAIR signal intensity of affected regions
  • Patchy areas of enhancement
Musculoskeletal involvement Raynaud phenomen
  • Contrast-enhanced MR angiograph
    • Characteristic narrowing of digital vessels
    • Tapering of digital vessels
Myositis
  • Intramuscular edema (increased high T2 signal)
Arthritis
Osteonecrosis (Avascular necrosis)
  • Lack of enhancement and devascularized areas on gadolinium-enhanced MR imaging 
  • Bone marrow edema on MRI 
  • Low-signal-intensity marginal areas on standard spin-echo T1- and T2-weighted images 
  • Intermediate to high signal intensity inside bone tissue on T2-weighted images, producing a line of low signal intensity with an adjacent high-signal-intensity line 
  • High signal intensity on T2-weighted images due to subchondral fractures that may be accompanied by fluid signal intensity or edema 
  • Low signal intensity on T2-weighted images due to collapse of the articular surface 
  • Early or subtle insufficiency fractures especially on T2-weighted MR imaging
    • In characteristic stress locations insufficiency fractures may appear as areas of high signal intensity due to bone marrow edema

References

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