MRI is often performed as an adjunct to ultrasound or as a first-line cross-sectional modality in an attempt to replace CT. In some cases the initial diagnosis is known, and MRI serves as a tool to better delineate and quantify the extent of pathology. However, in many situations MRI may prove to be more advantageous than other imaging modalities. Tables 5–2, 5–3, and 5–4 summarize the emergent indications for MRI and the pathology it can elucidate.
Table 5–2Indications for MRI in the Emergency Setting |Favorite Table|Download (.pdf) Table 5–2 Indications for MRI in the Emergency Setting
|As a First Line of Cross-Sectional Imaging ||As a Second-Line Alternative Imaging Modality |
|Contraindication to ionizing radiation (e.g., acute abdominal pain in pregnancy and children) ||Problem-solving tool when other imaging findings are unequivocal |
|Contraindication to iodinated contrast (e.g., allergy, impaired renal function) ||Situations requiring repeated examinations |
Table 5–3Advantages of MRI Over Other Imaging Modalities |Favorite Table|Download (.pdf) Table 5–3 Advantages of MRI Over Other Imaging Modalities
Acute Liver Conditions
Detection of candidal abscesses (better than CT)
Imaging of complications of abscesses
Assessing treatment response
Aging of thrombus in infarcts
Choledocholithiasis (most sensitive modality)
Evaluation of the obstructed biliary system
Contracted gallbladder with chronic cholecystitis, where visualization on USG/CT may be difficult
Detection of impacted calculi in cystic duct or neck of gallbladder
Detection of ductal anatomical variants
Exact localization of ductal disruption
Better depiction of early chronic and hemorrhagic pancreatitis
May be helpful in evaluating the nature of intraperitoneal fluid collections
Inherent contrast of calculus against the backdrop of hyperintense urine in ureter generates intravenous urography-like images without the use of contrast
Superior contrast resolution far supersedes CT
Table 5–4Common Emergent Clinical Applications of MRI |Favorite Table|Download (.pdf) Table 5–4 Common Emergent Clinical Applications of MRI
Acute hepatic infections:
Acute hepatic vascular conditions:
– Hepatic infarcts
– Portal vein thrombosis
– Budd-Chiari syndrome
Focal mass lesions with hemorrhage
|Gallbladder and Biliary System |
|Pancreatitis and its complications |
|Acute Peritoneal and Omental Disease |
|Genitourinary Tract |
The imaging approach to liver lesions focuses on lesion morphology and enhancement characteristics.
About 80% of liver abscesses are secondary to biliary/hematogenous/direct spread from adjacent organs/trauma, and only 20% are cryptogenic.6 Abscesses may present as either microabscesses (<2 cm), macroabscesses (>2 cm), or in a miliary pattern. The miliary pattern is usually due to staphylococcal infection or a cluster of microabscesses that appear to coalesce focally. They appear as focal, peripherally enhancing lesions that are hypointense on T1- and hyperintense on T2-weighted sequences (Figure 5–2). The abscess wall is often imperceptible on unenhanced scans, but the peripheral enhancement persists on delayed venous phases. The nonspecific finding of perilesional edema with or without transient arterial perilesional enhancement may be present, which manifests as a wedge-shaped area surrounding the abscess.
T1-weighted post-contrast axial image showing subtle peripheral enhancement and multiple internal septae in this pyogenic liver abscess (arrow).
Amebic liver abscesses may appear more heterogeneous on T2 and show 1 to 3 layers of concentric rim enhancement.7 MRI ensures a detailed evaluation of the complications such as rupture of abscess into the peritoneum/pleura. Amebic empyema is seen as hyperintense fluid in pleural cavity on both T1- and T2-weighted images (WI). Decrease in perilesional edema and formation of concentric rings in the abscess wall are indications of treatment response.
MRI has been found to be superior to CT in the evaluation of fungal abscesses.8 Fungal abscesses are usually seen in the immunocompromised and appear as microabscesses less than 1 cm in diameter that do not enhance in the early stage of disease. Peripheral enhancement occurs only in the subacute phase. Abscesses show restricted diffusion, appearing bright on diffusion-weighted sequences and hypointense on apparent diffusion coefficient (ADC). ADC is the quantitative estimation of magnitude of diffusion of water molecules within tissues. ADC values can be measured by drawing regions of interest (ROIs) on the tissue under consideration on an ADC image.
The imaging features of hepatitis are nonspecific. Hepatomegaly with diffuse heterogeneous enhancement of the liver and periportal edema may be the only imaging manifestations (Figure 5–3). Periportal edema is visualized as high signal intensity paralleling along the portal vein on T2 fat-saturation images.9 Imaging findings of a decrease in periportal edema can be indicative of clinical recovery.10 Associated findings include marked gallbladder wall edema without any distension, which helps to differentiate hepatitis from cholecystitis.
T2-weighted axial image showing bright periportal edema (red arrow) in a patient with acute hepatitis. The blue arrow indicates the portal vein, which appears black.
Acute Hepatic Vascular Conditions
Hepatic infarcts are typically seen as non-enhancing wedge-shaped areas of low signal on T1 and high signal intensity on T2-weighted images. With infarcts secondary to portal vein thrombosis, there may be a transient increase in enhancement of the affected segment due to a compensatory increase in hepatic arterial flow, which becomes homogeneous on delayed phases.11
Imaging of thrombus is feasible on MRI, which has important clinical implications with respect to prognostication of anticoagulant therapy.12 Acute/subacute thrombus appears hyperintense on T2, with enhancement of the wall of the portal vein probably related to inflammation.
In Budd-Chiari syndrome, associated findings of primary pathology, such as hepatic venous or inferior vena caval narrowing, occlusion, or thrombus, may be seen (Figure 5–4). The secondary features include intrahepatic collaterals, seen as comma-shaped enhancing, intraparenchymal vessels.13 The liver itself may show peripheral areas of heterogeneous high signal on T2 and hypointense signal on T1-weighted images. The caudate lobe is typically spared due to its independent venous drainage.14
Post-contrast T1-weighted image showing complete occlusion of the right hepatic vein (arrow) along with perfusion abnormality* in a patient with Budd-Chiari syndrome.
Regenerative nodules may at times pose a diagnostic difficulty on imaging modalities other than MRI. However, on MRI they are easily recognizable: bright on T1-weighted images and enhancing strongly after IV bolus administration of gadolinium contrast. The nodules are predominantly isointense or hypointense relative to the liver on T2-weighted images. This allows for differentiation of these nodules from hepatocellular carcinoma, which is usually hypointense in relation to the liver on T1-weighted images and hyperintense on T2-weighted images.15
Hepatic Hemorrhagic Mass Lesions
Hepatocellular carcinoma and hepatic adenomas are the two most common liver masses that may present with non-traumatic acute hemorrhage.16 Large, peripherally located lesions, devoid of overlying normal hepatic parenchyma, are more likely to rupture and bleed.17 Giant hemangiomas more than 4 cm in size may also bleed. The presence of high signal on T1-weighted image in a T2 heterogeneous mass on MRI is suggestive of hemorrhage.
MRI not only helps in the diagnosis of the bleeding tumor, but also in characterizing the underlying tumor, which in turn can influence treatment. Please refer to the Chapter 17 for further details on characterization of liver masses.
Gallbladder and Biliary System
Calculi in the gallbladder (GB) usually appear as hypointense foci and create symptoms when they become impacted at the GB neck or cystic duct. MRI has been found to be superior to ultrasonography (USG) in the detection of calculi impacted in the cystic duct.18 The signal intensity of the calculi depends on its constituents—lipid or calcium—and water content; however, in all cases they appear as filling defects on heavily T2-weighted sequences19 (Figure 5–5).
T2-weighted axial image showing multiple signal voids (arrow) in the gallbladder, consistent with cholelithiasis.
Acute cholecystitis may manifest on MRI via one or more of the 6 criteria mentioned in the following, yielding a sensitivity of 88% and specificity of 89%18:
Gallstones impacted in the gallbladder neck or cystic duct
Gallbladder wall thickening (>3 mm)
Gallbladder wall edema
Gallbladder distention (diameter >40 mm)
Fluid around the liver, termed the “C sign” (small amount of fluid between the liver and the right hemi-diaphragm or the abdominal wall, different from pericholecystic fluid)18
Gallbladder wall edema, rather than just thickening, is an important finding of cholecystitis and is better depicted on MRI than USG.18 Another finding is a diffuse or patchy distribution of increased signal intensity of the gallbladder wall on fat-suppressed T2-weighted images, which enhance on post-contrast T1 fat-saturated images.20 Pericholecystic fluid is usually seen as T2 hyperintense fluid around the gallbladder in the fossa. There may also be a transient increase in the adjacent hepatic enhancement on the arterial phase.20
Hemorrhagic cholecystitis may occur in the presence of lupus erythematosus, metachromatic leukodystrophy, hemodialysis, and anticoagulation therapy. Mucosal ulcerations caused by inflammation due to calculi result in bleeding. The hemorrhage may be seen as heterogeneous, high-signal-intensity foci on T1-weighted images.21 Hemorrhage may appear low signal on T2-weighted sequences, causing lack of visualization of the gallbladder or bile ducts on MR cholangiopancreatography (MRCP). A fluid-fluid level may be observed in the lumen of the gallbladder and bile ducts, where hemorrhagic bile appears as a low-signal-intensity area in the lower dependent layer on T2-weighted images, and normal bile appears relatively hyperintense.
MRI findings of gallbladder torsion include a tapered cystic duct at MRCP and high signal intensity in the wall at T1-weighted imaging. Coagulation necrosis with intramural hemorrhage is also seen with T1-weighted imaging.22 Lack of contrast enhancement confirms the diagnosis.
When cholecystitis progresses to gallbladder empyema, heavily weighted T2 images may demonstrate purulent bile that is dependent and has lower signal intensity, along with edema and wall thickening of the gallbladder. Other conventional MRI sequences may fail to distinguish sludge from pus.
Gangrenous cholecystitis occurs when there is ischemic necrosis of the gallbladder wall and is seen in up to 30% of cases of acute cholecystitis.23 It occurs due to an increase in intraluminal pressure subsequent to cystic duct obstruction. There is dilatation of the gallbladder with ulceration, hemorrhage, necrosis, or microabscess in the gallbladder wall, which may result in inhomogeneous signal intensity of the wall.24 Wall ulceration may be seen as a concave hyperintense area on T2 fat-saturation images. A patchy pattern of mucosal enhancement, resulting in an interrupted mucosal ring of the GB indicative of necrosis and inflammation, is diagnostic for gangrenous cholecystitis. Gangrenous cholecystitis may eventually lead to perforation and pericholecystic abscess.
Gallbladder perforation can be classified into 3 types:
Acute free perforation into the peritoneal cavity
Subacute perforation with a pericholecystic abscess (most common)
Chronic perforation with a cholecystoenteric fistula25
The fundus is the most frequent site of perforation because of its relatively poor blood supply. Perforations may occur in up to 10% of cases of acute cholecystitis and are visualized as disruption of the gallbladder wall. A communication with preexisting pericholecystic or intrahepatic abscess may be demonstrable on MRI.26
In cases of cholecystoenteric fistula, air may be seen as a signal flow void within the non-dependent aspect of the GB communicating with duodenum. Other MRI findings may be thick peritoneum and loculated ascites with homogeneous high signal intensity on heavily T2-weighted images and fat-suppressed T2-weighted images.
Emphysematous cholecystitis is a rare form of acute cholecystitis diagnosed via the presence of gas in the gallbladder lumen and a wall with signal void areas.27 Intraluminal gas appears as floating signal void bubbles in the non-dependent portions of the gallbladder, as opposed to gall stones, which are gravity dependent. Heavily T2-weighted images are less affected by the artifact often associated with air and tissue interface, and so the differentiation between a flow void and calculus is best ascertained in these series.28 Other MRI findings of emphysematous cholecystitis are the same as those seen in gangrenous cholecystitis.
MRI is the most sensitive imaging modality for detection of ductal calculi.29 They appear as hypointense foci in the background of high-signal-intensity bile (Figure 5–6). MRCP can detect calculi as small as 2 mm.30 However, small calculi in the periampullary region may be missed due to lack of background contrast from bile. At times, it may be difficult to differentiate whether a polypoidal lesion obstructing the biliary system is a calculus or a tumor. Coronal steady-state coherent imaging may be helpful in these cases. A calculus usually shows extremely low signal on steady-state coherent images, while a malignant tumor typically has intermediate signal intensity.28
Coronal T2-weighted image showing a filling defect in the distal common bile duct (CBD) (arrow), consistent with choledocholithiasis.
Acute cholangitis occurs due to stasis and infection of bile secondary to obstruction and may lead to widespread sepsis by hepaticovenous reflux of bacteria. MR findings include a dilated biliary system with diffusely smooth and symmetrically thickened ductal wall more than 1.5 mm. MRCP also allows characterization of the primary cause of obstruction, which may be ductal calculi in 80% of cases.31 Areas of parenchymal edema in the form of hypointense periportal or less commonly wedge-shaped areas around a duct on T1 and hyperintense on T2-weighted images may be seen. Such areas show transient hepatic arterial enhancement.32 Band-like irregularities of the duct margins have also been reported33 (Figure 5–7).
Heavily T2-weighted MR cholangiopancreatography coronal images showing pruned and irregular right hepatic duct (arrow), a characteristic feature of cholangitis.
Mirizzi syndrome is a form of obstructive jaundice that develops secondary to extrinsic compression of the common bile duct from a stone in the cystic duct or neck of the gallbladder.34 Hence it is vital to trace all the draining ducts of the biliary system for detection of intrinsic or extrinsic abnormalities in search of a transition point that should be evaluated in greater detail.
CT scan is still the mainstay in the evaluation of pancreatitis, and the role of MRI is mainly to follow up on complications in young patients. MRI also finds its role in cases of renal impairment, which often accompanies acute pancreatitis, or to look for a ductal abnormality, which may be a primary cause of pancreatitis.
The pancreas normally shows high signal on T1 as compared to liver, due to the presence of acinar proteins, which decrease the signal. In any event of abnormality, coronal and axial HASTE (half-Fourier acquisition single-shot turbo spin-echo) images help in the identification of choledocholithiasis, and in the evaluation of pancreatic duct and anatomical variants, such as pancreatic divisum, which may be the underlying cause of pancreatitis.
Fat-suppressed T1-weighted images are particularly useful for depicting a focal or diffuse enlargement of the pancreas, resulting in loss of pancreatic lobulations (Figure 5–8). Axial short tau inversion recovery (STIR) images enable detection of pancreatic edema in mild forms of pancreatitis, which may not be seen on T1-weighted images. Pancreatic interlobular septal inflammation and edema may be seen as subtle threadlike hyperintense structures on fat-suppressed T2-weighted images.35 In later stages, there is pancreatic enlargement with heterogeneous low signal on T1 and hyperintense on T2-weighted sequences.
T1-weighted post-contrast axial image showing edematous, heterogeneously enhancing pancreas (arrow) with peripancreatic fat stranding, consistent with acute pancreatitis.
The absence of enhancement of pancreatic parenchyma during arterial, venous, and delayed phases is essential to making a diagnosis of pancreatic necrosis. Pancreatic necrosis usually sets in 2 to 3 days after the initial symptoms of pancreatitis, hence scans may be deferred until then for an accurate assessment. Focal pancreatic necrosis is characterized by patchy non-enhanced areas on contrast-enhanced MR images (Figure 5–9). Diffuse pancreatic necrosis is seen as large, diffuse, non-enhanced zones of the pancreas on enhanced MR images.36 When there is a demonstrable discontinuity in pancreatic parenchyma, it is termed “gland liquefied necrosis.” Dynamic contrast-enhanced T1-weighted images help in the quantification of pancreatic necrosis, which may be seen as areas of non-enhancement. Subtraction scans obtained by subtracting the pre-contrast from the post can help differentiate necrosis from ischemia and normal high-signal pancreas from hemorrhagic pancreatitis. Necrotic areas show complete lack of enhancement and ischemic areas show attenuated enhancement.
Post-contrast delayed images in a patient with focal necrotizing pancreatitis, showing normal enhancement of the pancreatic tail (red arrow). Note the lack of enhancement in the pancreatic body, consistent with pancreatic necrosis (white arrow).
Uncomplicated pseudocysts appear as walled off areas of T1 hypointense and T2 hyperintense fluid collections. Hemorrhagic collections, on the other hand, appear hyperintense on both T1- and T2-weighted images.37 The extent of necrosis can be further quantified to less than 30% (mild), 30% to 50% (moderate), and greater than 50% (severe) of the pancreatic gland.
Pancreatic hemorrhage is a finding associated with severe forms of pancreatitis and occurs in 2% to 5% of patients with acute pancreatitis.35 Hemorrhagic foci appear as spotted or patchy or threadlike girdle-shaped hyperintensities on fat-saturated T1-weighted images.36
Edematous thickening of the pancreatic capsule and subcapsular fluid collections can be accurately depicted on MR fat-suppressed T2-weighted images and in-phase T1-weighted gradient-echo sequence.38 MRI features of peripancreatic fat necrosis are indistinguishable from peripancreatic fat edema. The fat necrosis may be extensive, located in omental and mesenteric areas, as well as the extrapancreatic retroperitoneal fatty tissue in the anterior pararenal space. The tissue necrosis eventually leads to liquefaction and the development of fluid collections. MRI not only helps in the accurate delineation of fluid collections, but also in further characterizing hemorrhagic collections. Over time, these collections may resolve completely or evolve into pseudocysts or pancreatic abscesses.
Complications of Pancreatitis
Pseudocysts are among the most common sequelae of acute necrotizing pancreatitis. They may be classified depending on their location, whether intra- or extrapancreatic, and their internal content into simple or complex. The intraparenchymal pseudocyst may communicate with pancreatic ducts and may be associated with partial pancreatic ductal obstruction, while the extrapancreatic pseudocyst is usually related to the development of peripancreatic fluid collections.
On MRI, pseudocysts are seen as fluid collections with a definite wall. Depending on their content, they may be hypointense on T1 and hyperintense on T2 if simple, or hyperintense on T1 if hemorrhagic (Figure 5–10).
T2-weighted coronal image showing a cystic lesion (arrow) arising from the body of the pancreas in this patient with acute pancreatitis. The lesion is consistent with pancreatic pseudocyst.
Vascular complications after pancreatitis include vasculitis, pseudoaneurysm, thrombosis, and regional portal hypertension. The splenic, gastroduodenal, and pancreaticoduodenal arteries are most often involved.39
Vasculitis manifests as obscure and rough edges of the involved arterial wall that may progress to partial or complete occlusion. The splenic vein is the most common to undergo thrombosis. Loss of flow voids on T2-weighted sequence, recognized by a lack of opacification or a filling defect on the arterial phase of the scan, indicates thrombosis.
A pseudoaneurysm appears as a focal outpouching from the parent vessel. These enhance markedly following contrast administration, with non-enhanced zones reflecting mural thrombus in the pseudoaneurysm (“Yin-Yang” sign).40
Splenic vein thrombosis leads to diversion of flow into collateral circulation, which usually involves gastric short veins around the fundus of the stomach, gastroepiploic veins close to the greater curvature of the stomach, and splenic veins adjacent to the spleen hilum, resulting in pancreatogenic regional portal hypertension.41
HASTE forms the cornerstone of subsecond imaging of the bowel, as it provides excellent contrast between the hypointense bowel wall and hyperintense intraluminal fluid inside and mesenteric fat outside the intestine. Normal wall thickness of small bowel is 2 mm, and thickness of more than 3 mm is considered abnormal.42
MRI findings in mesenteric ischemia may be divided into direct and indirect signs. Direct visualization of embolus is diagnostic. Embolus is usually seen 3- to 10-cm distal to the origin of the superior mesenteric artery (SMA) or distal to the origin of the middle colic artery branch.43 Indirect signs include thickening of the bowel wall with alternating layers of low and high signal in the thickened wall on T2-weighted images.44 There may be a complete non-enhancement of the bowel wall.45 Superior mesenteric vein thrombosis may also be seen.
The normal appendix is a blind tubular structure with a diameter of less than 7 mm and a wall thickness of less than 2 mm. The classic finding of appendicitis is a fluid-filled, blind-ending lumen of more than 7 mm diameter, devoid of air or oral contrast within its lumen (Figure 5–11). The thickened wall is hypointense on T1 and hyperintense on T2, with hyperintense periappendicial inflammation on T2 fat saturation/STIR sequence.46 An appendicolith may be seen as a T2 hypointense structure within the appendix. On contrast examination, the inflamed appendiceal wall enhances.
T2-weighted axial image through the right iliac fossa of a pregnant patient, showing an enlarged appendix (arrow) measuring 10 mm in diameter. Appendicitis was confirmed at surgery.
MRI finds its role particularly in the detection of appendicitis in pregnancy, when the USG findings are inconclusive. It may also help in detecting subchorionic hematoma and hemorrhagic adnexal cysts on T1-weighted images, both key contributors to the differential diagnosis of pelvic pain in pregnancy. MRI is considered a second-line modality after USG and before CT in the evaluation of appendicitis in the pregnant patient.
CT continues to be the modality of choice for diagnosing diverticulitis. Diverticuli are seen as focal outpouchings from the bowel, with a thickened wall and pericolic fat stranding and fluid being well-demonstrated signs of diverticulitis with STIR images.47 Abscess formation may be seen as pericolonic fluid collections with peripheral rim enhancement. A major disadvantage is detection of small perforations, as small extraluminal pockets of air may be completely missed on MRI.
Primary Epiploic Appendagitis
Primary epiploic appendagitis is a relatively common condition caused by acute inflammation resulting from the torsion or spontaneous venous thrombosis of appendages epiploicae of the colon.48 On MRI, an oval or lanceolate-shaped lesion appears anterior to or anterolateral to the colon, with a central area of fat. There is inflammation of the visceral peritoneum seen as a low intensity rim surrounding the fatty appendage, and it may enhance on post-contrast scan. A hypointense central dot corresponding to the fibrous septa may be seen on T1- and T2-weighted images.49
Acute Peritoneal and Omental Disease
MRI is superior to CT in demonstrating the heterogeneity within fluid collections, which may be seen in peritoneal diseases. MRI can also further characterize the nature of fluid.50 Acute hemorrhagic fluid may be seen as hypointense on T1 and hyperintense on T2. Inherent contrast resolution of MRI allows for easy visualization of a thickened peritoneum, which is a feature of peritonitis.
Calculi, being relatively devoid of protons, are incapable of generating a signal on MRI. Calculi being hypointense are easily seen against a background of high signal intensity of Urine. Heavily weighted T2 images, which accentuate this contrast, form the basis of MRI detection of ureteric obstruction. Thin-slice HASTE are reconstructed using maximum intensity projections, or thick-slab coronal Rapid acquisition with relaxation enhancement (RARE) sequences help in generating urography-like images.51 The calculi are seen as hypointense filling defects in the renal calyses or ureter. A major limitation of MRI lies in its inability to detect small ureteral stones. Meanwhile, in renal calyces the sensitivity of MRI in detection of calculi is only for calculi larger than 1 cm.52
Ureteric dilation, wall thickening, and surrounding edema enhance the likelihood that a ureteric calculus will be detected. In acute obstruction, there may be perirenal hyperintense fluid caused by lymphatic congestion or forniceal rupture. Intraluminal clots, debris, or neoplasms may all mimic stones within the ureter.
Gadolinium-enhanced MR urography involves administration of IV furosemide at 0.1 mg/kg, followed by IV gadolinium, which enables a complete distension of the entire urinary tract.53 In cases of high-grade obstruction, the excretion of contrast into the ureter may be delayed, and hence delayed imaging is required to evaluate the level and cause of the obstruction. Delayed images also help in detecting perirenal fluid due to forniceal rupture.
Renal enlargement with a heterogeneous appearance, with multiple cortical areas of high signal intensity showing striations following contrast administration, are typical imaging findings in acute pyelonephritis (Figure 5–12). Non-enhancing wedge-shaped cortical defects representing infarcts, or areas with peripheral enhancement suggestive of abscesses, may be seen as complications of pyelonephritis. There may be associated segmental vein thrombosis, seen as absence of usual flow void. Perirenal edema may be seen in the form of a hyperintense area on T2-weighted images.
T2-weighted axial image showing patchy areas of T2 hyperintensity (arrows) scattered throughout the kidneys in this patient with pyelonephritis.
Pyelonephritis frequently accompanies an obstructed collecting system. MRI can help differentiate between hydronephrosis and pyonephrosis on the basis of diffusion-weighted imaging (DWI). Pus in the collecting system is markedly hyperintense on DWI and hypointense on ADC, as opposed to hypointense on DWI in hydronephrotic kidneys.54
Loss of corticomedullary differentiation, which is easily visualized on unenhanced T1-weighted images in the normal kidney, is indicative of renal failure.55
Renal Artery Thrombosis/Infarct
Loss of signal flow void in renal vessels on routine T1- and T2-weighted images, or non-visualization of arteries on contrast MR angiography, is indicative of thrombosis. Renal infarcts can demonstrate different signal intensities on T1- and T2-weighted images, depending on the duration of the vascular insult.
Ultrasound forms the first option in the evaluation of pelvic organs; however, in cases of obesity or in an event of non-visualization of the ovary on USG, and in the characterization of pelvic masses, MRI is preferred. The diagnostic findings in torsion are ovarian enlargement and stromal edema (Figure 5–13). There may be thickening of the twisted fallopian tube, smooth non-enhancing thickening of the wall of the cystic ovarian mass with hemorrhage within, ascites/hemoperitoneum, and uterine deviation to the side of torsion. Hemorrhage within the ovary or tube may also be seen. An ovarian mass like a dermoid may be commonly associated with torsion.56
T2-weighted coronal image in a young woman who presented with left pelvic pain showing enlarged left ovary (arrow). Note the normal-appearing right ovary. Acute onset of pain supplemented with imaging pointed toward a diagnosis of adnexal torsion, which was confirmed at surgery.
Pelvic Inflammatory Disease
MRI is the investigation of choice in the detection of adnexal and parametrial edema, which is a feature of pelvic inflammatory disease. Other than these subtle features, gross pathology such as a tubo-ovarian abscess may be seen as a fluid collection with a thick enhancing wall involving the fallopian tube and ovary (Figure 5–14). Hydrosalpinx manifests as an adjacent fluid-filled tubular structure, which represents an inflamed fallopian tube.
T1-weighted axial post-contrast image showing a peripherally enhancing abscess (arrow) in the left adnexa of an adult woman, consistent with pelvic inflammatory disease.
Red Degeneration of Fibroid
Red degeneration is a type of hemorrhagic infarction of leiomyomas that may occur during pregnancy. In pregnancy, USG is the modality of choice for evaluation of fibroids; however, MRI may prove more beneficial in the identification of peripheral hemorrhage, seen as high signal on T1- and T2-weighted images, and edema, which is hypointense on T1 and hyperintense on T2 sequences. In red degeneration an unusual signal intensity pattern at MR imaging is peripheral or diffuse high signal intensity on T1-weighted images and variable signal intensity with or without a low-signal-intensity rim on T2-weighted images.57 The high signal intensity on T1-weighted images is due to the proteinaceous content of the blood.
Endometriosis is ectopic implantation of endometrial mucosa, which tends to bleed cyclically. MRI is the imaging study of choice for the detection of these ectopic mucosal deposits in the ovaries, cul-de-sac, posterior uterine wall, uterosacral ligaments, anterior uterine wall, and bladder dome. They may appear hyperintense on T1-weighted images due to blood and blood degradation products (Figure 5–15). On T2-weighted images, hypointense signal may be produced within the endometriotic cyst due to high concentrations of protein and iron resulting from recurrent hemorrhage.
T1-weighted post-contrast axial image showing enhancing foci of endometriosis (arrows) in a 34-year-old woman who presented with cyclical pelvic pain.