Case of the Month

History: A previously healthy young adult presented to the emergency department with fever and altered mentation. Physical exam revealed receptive aphasia, extremity weakness, and right facial droop. Lab work was unremarkable. Cross-sectional imaging of the brain was ordered. 

Findings: 

Non-contrast brain CT revealed rounded areas of hypoattenuation in the left frontal lobe (blue arrows).  Follow-up brain MRI with contrast revealed rim enhancing lesions of varying sizes in the right frontal and parietal lobes with associated diffusion restriction. There is a peripherally enhancing subdural fluid collection overlying the right frontal convexity (red arrows). Confluent T2 and FLAIR hyperintense signal surrounds the enhancing lesions. Mass effect results in rightward midline shift.  

Diagnosis: Intracranial abscesses with subdural empyema. 

Hospital Course: The patient underwent left frontoparietal craniectomy and washout with neurosurgery. The subdural empyema was evacuated and the larger abscesses located peripherally in the brain were drained. The smaller abscesses deeper in the brain were not suitable for operative intervention given their sensitive location. Post-operatively the patient’s aphasia and extremity weakness improved. Surgical cultures grew Fusobacterium necrophorum, an anaerobic gram-negative rod. Infectious disease recommended treatment with IV penicillin and oral metronidazole until there was clinical and imaging evidence of resolution. Follow up imaging three months later revealed resolution of the abscesses with no evidence of recurrent infection and the antibiotics were discontinued. The patient subsequently underwent cranioplasty with plastic surgery to restore the left craniectomy defect. 

Discussion: Intracranial infection can result from bacteria, viruses, fungi, parasites, and rarely prions. Transmission can occur via direct local spread from head trauma, paranasal sinusitis, or hematogenous spread in the setting of septicemia. Presenting symptoms include headache, mental status change, fever, and seizures. White blood cell count can be normal, as it was is in this case. MRI with contrast is the gold standard to diagnose complications of intracranial infection such as intracranial abscesses, empyema, ventriculitis, and sinus venous thrombosis. Treatment typically involves antibiotic administration with the need for surgical intervention determined by the presence of the complications described above.    

History: A young adult presented to the emergency department with several days of abdominal pain. History was notable for a congenital intracranial malformation treated with a lumboperitoneal shunt. Physical exam revealed right abdominal tenderness to palpation. Lab work was notable for leukocytosis of 22,000.  

Findings: 

A CT of the abdomen and pelvis with IV contrast was obtained, demonstrating dilatation of the distal appendix to 15 mm (blue arrow) with extensive fat stranding in the right hemiabdomen. The intraperitoneal component of the lumboperitoneal shunt is seen traversing through the inflamed abdomen with a peripherally enhancing fluid collection encasing a portion of the catheter (green arrow). No obvious abnormality is seen regarding the intraspinal portion of the catheter. Small bowel loops in the right hemiabdomen demonstrate reactive wall thickening (yellow arrow), and several prominent reactive mesenteric lymph nodes are also seen. 

Diagnosis: Perforated acute appendicitis complicated by an abscess encasing the peritoneal catheter.  

Hospital Course: The patient was taken urgently to the operative room for combined surgery with neurosurgery and general surgery. Purulence was noted within the abdomen during laparoscopy and the intraperitoneal portion of the lumboperitoneal shunt was explanted. The appendix appeared inflamed and thus laparoscopic appendectomy was performed. The appendix was sent for surgical pathology, which confirmed the diagnosis of perforated appendicitis. The patient had an unremarkable post-operative course and was discharged home with a short course of oral antibiotics. The lumboperitoneal shunt catheter had been turned off for several years prior to presentation and no revision or replacement was needed per the evaluation of neurosurgery.  

Discussion: Acute appendicitis is inflammation of the appendix secondary to obstruction of its lumen resulting in bacterial proliferation. It most commonly occurs between the ages of 10 and 40. Perforation is a feared complication of appendicitis as it can result in abscess formation and peritonitis. Appendectomy is the gold standard for treatment in the United States. Severe cases of appendicitis may necessitate conversion to ileocecectomy or right hemicolectomy based on the intra-operative findings. Appendiceal malignancy can mimic the imaging and intra-operative appearance of acute appendicitis, requiring pathologic confirmation of the diagnosis after appendectomy.  

History: A 50-year-old female presented to the Emergency Department with right lower quadrant pain. A contrast-enhanced CT of the abdomen and pelvis was performed, revealing suspicious findings in the lumbar spine, which prompted further evaluation with contrast-enhanced MRI of the lumbar spine.

Findings: 

Shown above, sagittal post-contrast CT of the abdomen and pelvis in bone window demonstrates cortical erosions of the inferior endplate of the L2 vertebral body and the superior endplate of the L3 vertebral body (yellow arrows). Soft tissue window on the same study highlights associated prevertebral heterogeneous soft tissue at this level; soft tissue also extends into the ventral epidural space at the L2-3 level (red arrows).

Heterogeneous STIR hyperintense signal is present in the L2-3 disc space and extends to the inferior endplate of the L2 vertebral body and the superior endplate of the L3 vertebral body (green arrows). Comparison between T1 and T1 postcontrast fat saturated images demonstrates associated heterogeneous enhancement in these regions (green arrows). STIR hyperintensity and enhancement extends along the ventral epidural space at the L2-3 level consistent with an epidural phlegmon (purple arrows).

No abnormal cord signal is identified in the distal cord or conus. The above findings are superimposed upon multilevel degenerative changes which altogether result in up to severe spinal canal stenosis at the L2-3 level. 

Diagnosis: Discitis-Osteomyelitis

Teaching Points:

Discitis-osteomyelitis is the infection of vertebrae and associated intervertebral discs. Risk factors include immunocompromised state, IV drug use, and diabetes. In adults, it often occurs through hematogenous bacterial seeding of vertebral bodies, which are particularly susceptible due to their slow arterial inflow. Infection then readily spreads to adjacent avascular discs. Patients present with back or neck pain as well as fevers, although inconsistently.

Changes from discitis-osteomyelitis are often not apparent on plain radiographs up until six weeks. Contrast-enhanced MRI is the modality of choice in diagnosis, in part because it delineates extent of spinal canal involvement. T1-weighted images demonstrate low signal intensity involving the affected vertebral endplates and bodies, while T2-weighted images demonstrate corresponding high signal intensity. Fluid signal is identified in the intervertebral disc. Post-contrast imaging demonstrates homogeneous, patchy, or peripheral enhancement in the affected disc and diffuse enhancement in the affected bone marrow. Associated paravertebral and epidural phlegmon or abscess are characterized by heterogenous signal intensity on T1 and T2-weighted sequences, typically hypointense signal on T1-weighted images and hyperintense signal on T2-weighted images. Post-contrast imaging demonstrates diffuse/rim-like enhancement in the paravertebral and epidural soft tissues.

The utility of CT in the diagnosis of discitis-osteomyelitis is limited. CT may not reveal early destructive vertebral endplate changes and cannot reliably demonstrate extent of spinal canal involvement. However, it may help demonstrate associated adjacent soft tissue masses and abscesses, as in the above case.

Important differential considerations include degenerative endplate disease and neuropathic joint changes. Unlike discitis-osteomyelitis, degenerative changes do not show high signal intensity of the disc on T2-weighted images; there is also no soft tissue involvement. There may be associated vacuum phenomenon. Neuropathic joint changes may include joint debris, spondylolisthesis, lower signal intensity of disc/marrow on T2-weighted images, paraspinal masses related to inadequately healed fractures, and vacuum phenomenon.

Most patients with discitis-osteomyelitis are treated with six weeks of systemic antimicrobials, while others require surgery due to factors such as cord compression or inadequate response to antibiotics. Follow-up MRI is generally not indicated, as imaging findings can lag behind clinical improvement by 4-6 weeks.  

References:

An HS, Seldomridge JA. Spinal Infections. Clinical Orthopaedics & Related Research. 2006;444:27-33. doi:https://doi.org/10.1097/01.blo.0000203452.36522.97

Babic M, Simpfendorfer CS. Infections of the Spine. Infectious Disease Clinics of North America. 2017;31(2):279-297. doi:https://doi.org/10.1016/j.idc.2017.01.003

Hong SH, Choi JY, Lee JW, Kim NR, Choi JA, Kang HS. MR Imaging Assessment of the Spine: Infection or an Imitation? RadioGraphics. 2009;29(2):599-612. doi:https://doi.org/10.1148/rg.292085137

History: A 65-year-old female presented to her primary care office with hypercalcemia and elevated parathyroid hormone. A nuclear medicine parathyroid scan was ordered for further evaluation.

Findings:

The institutional protocol for nuclear medicine parathyroid scan was followed. As seen below on the pinhole images acquired at 30 minutes, there is physiologic uptake of the radiopharmaceutical in the thyroid gland with a focal area of marked uptake in the inferior left neck (red arrow).

On the 3 hour delayed images, there is washout of the radiotracer from the thyroid gland with a persistent focal area of marked radiotracer uptake in the inferior left neck (red arrow). This corresponds to a nodule posterior to the inferior left thyroid lobe on the fused axial SPECT/CT (red arrow) and CT images (red circle) acquired at 30 minutes.

Diagnosis: Parathyroid Adenoma

Teaching Points:

Most cases of primary hyperparathyroidism are due to parathyroid adenomas, or tumors of the parathyroid gland. The initial diagnosis of primary hyperparathyroidism is made upon laboratory evaluation. However, imaging is crucial in determining surgical management.

A commonly used technique for diagnosing parathyroid adenomas is Tc-99m sestamibi parathyroid scintigraphy. For this exam, the patient is injected with Tc-99m-labeled sestamibi radiotracer. Planar images of the neck/mediastinum are acquired 10-30 minutes after injection followed by another set of planar images 90-180 minutes after injection. Radiotracer is initially taken up by both the thyroid gland and parathyroid glands. However, it washes out of most parathyroid adenomas slower than normal thyroid/parathyroid tissue. As in the case above, 10-30 minute images demonstrate a focus of discrete uptake. This focuso of uptake progressively increases on 90-180 minute images. Some institutional protocols also include SPECT or SPECT/CT imaging to help localize lesions.

Another nuclear medicine technique utilizes both Tc-99m sestamibi and an additional radiotracer that accumulates only in the thyroid gland, such as iodine-123 (I-123) or Tc-99m pertechnetate. I-123/Tc-99m pertechnetate images define the thyroid gland, which can then be subtracted from the Tc-99m sestamibi images to determine areas of abnormal parathyroid activity.

Other important techniques that are used to diagnose parathyroid adenomas include ultrasound and 4D-CT, beyond the scope of this discussion.

Nuclear medicine scans prove particularly useful in identifying ectopically located parathyroid adenomas in the neck/mediastinum. They are also generally operator independent. Without concomitant CT, however, these exams are quite limited in providing anatomic data. An important consideration in interpretation is that some adenomas do not follow the typical washout characteristics described above. Furthermore, various other pathologies can result in false positives, including thyroid nodules/carcinomas, other cancers, and Graves’ disease.

Imaging helps identify the presence/absence of parathyroid adenomas. Generally, parathyroid adenomas are amenable to minimally invasive thyroidectomy, unlike multiglandular or non-localizing disease, which may call for bilateral neck exploration. Minimally invasive thyroidectomy is associated with lower morbidity and complications than bilateral neck exploration.

References:

Bunch PM, Kelly HR. Preoperative Imaging Techniques in Primary Hyperparathyroidism. JAMA Otolaryngology–Head & Neck Surgery. 2018;144(10):929. doi:https://doi.org/10.1001/jamaoto.2018.1671

Zarei A, Karthik S, Chowdhury FU, Patel CN, Scarsbrook AF, Vaidyanathan S. Multimodality imaging in primary hyperparathyroidism. Clinical Radiology. 2022;77(6):e401-e416. doi:https://doi.org/10.1016/j.crad.2022.02.018

History: A 70-year-old female presented to the urologist for hematuria. A triphasic CT was performed for further evaluation. An incidental finding was made on this examination.

Findings:

Sequential axial images of the lower abdomen progressing from superiorly to inferiorly (left to right in the top row) and sequential coronal images of the right lower quadrant progressing anteriorly to posteriorly (left to right in the bottom row) demonstrate dilatation of the appendix to 1.2 cm at its base with gradual tapering to normal caliber at the appendiceal tip (yellow arrows). The proximal appendix is filled with fluid density material. There is no periappendiceal fat stranding or appendiceal hyperenhancement to suggest appendicitis. Findings raise suspicion for an appendiceal mucocele, with  appendiceal neoplasm not excluded. The patient was referred for surgical consultation, prompting laparoscopic appendectomy with partial cecectomy. Final pathology was consistent with a low-grade appendiceal mucinous neoplasm (LAMN).

Diagnosis:  Appendiceal mucocele/mucinous appendiceal neoplasm

Teaching Points:

The specific histologic diagnosis in the above case, low-grade appendiceal mucinous neoplasm (LAMN), belongs to the broad pathologic category of appendiceal mucoceles, which comprises both benign and malignant entities. “Mucocele” refers to an appendix that is filled with mucus. Non-neoplastic etiologies of mucoceles include mucosal hyperplasia and retention cysts. Neoplastic etiologies include mucinous adenoma, low-grade appendiceal mucinous neoplasm (LAMN), and mucinous adenocarcinoma. The non-neoplastic etiologies have no potential for metastasis or pseudomyxoma peritonei. Amongst the neoplastic etiologies, mucinous adenoma is typically benign. Meanwhile, LAMN and mucinous adenocarcinoma have the potential to cause pseudomyxoma peritonei as well as hematogenous/nodal metastases. Approximately half of all patients with appendiceal mucoceles are asymptomatic, while the remainder may have a variety of nonspecific presentations. The larger group of epithelial appendiceal neoplasms (including both mucinous and non-mucinous subtypes) are found in the 5^th-7^th decades of life.

Appendiceal mucoceles are often found on CT. CT typically demonstrates a hypoattenuating tubular structure in the expected region of the appendix, as in the above case. There is usually an enhancing wall of variable thickness. Calcifications are variably present. Surrounding inflammatory changes or abscesses are not seen, excluding appendicitis as a differential diagnosis. MRI typically demonstrates a T2 hyperintense, T1 hypointense mass near the appendix. While both CT and MRI can demonstrate pseudomyxoma peritonei, MRI has better detection by means of diffusion weighted sequences and delayed gadolinium-enhanced T1 fat-saturation. In general, the imaging features cannot predict the risk of malignancy.

Imaging can sometimes reveal an inverted configuration of a mucocele extending into the cecum. Mucoceles infrequently cause small bowel obstructions related to rupture or extrusion of mucin amongst other etiologies. Even more rarely, they can result in intussusception.  A potential complication of appendiceal mucoceles is pseudomyxoma peritonei, in which mucin fills the peritoneum and coats the serosa of the organs. This has variable imaging features, including mucinous ascites, peritoneal deposits/implants, and omental caking.

The treatment of appendiceal mucoceles is surgical resection. The surgical approach depends on the tumor, node, and metastasis (TNM) staging. Importantly, this staging system is distinct from that of colorectal adenocarcinoma.

References:

Leonards LM, Pahwa A, Patel MK, Petersen J, Nguyen MJ, Jude CM. Neoplasms of the Appendix: Pictorial Review with Clinical and Pathologic Correlation. RadioGraphics. 2017;37(4):1059-1083. doi:10.1148/rg.2017160150

Van Hooser A, Williams TR, Myers DT. Mucinous appendiceal neoplasms: pathologic classification, clinical implications, imaging spectrum and mimics. Abdominal Radiology. 2018;43(11):2913-2922. doi:10.1007/s00261-018-1561-9

History: A 30-year-old female presented to the primary care physician for headache. Noncontrast CT of the brain was obtained to assess for acute intracranial pathology. CT findings prompted evaluation with an MRI of the brain.

Findings:

Axial non-contrast CT demonstrates a focal area of hyperattenuation in the left corona radiata without significant associated mass effect, findings which raise concern for a small parenchymal hematoma versus cavernous malformation. MRI with and without contrast is thus obtained for further evaluation. Subsequent MRI demonstrates a popcorn-like lesion with mixed T1 and T2 intensity, T2 hypointense hemosiderin rim, and associated gradient susceptibility on SWI centered in the left frontal lobe in the corona radiata, corresponding to the hyperattenuating lesion on CT. FLAIR imaging does not demonstrate any associated edema. There is no finding to suggest recent hemorrhage. On the post-contrast MP-RAGE sequence, there are radially oriented vessels along the anterior aspect of the lesion with associated abnormality on SWI (white arrows).

Diagnosis: Cavernous malformation with developmental venous anomaly

Teaching Points: A cavernous malformation, also known as a cavernoma, is a slow-flow vascular malformation that occurs in the central nervous system. Cavernous malformations are made up of multiple endothelial-lined “caverns.” There is no normal intervening brain tissue. While some patients are asymptomatic, others present with intracranial hemorrhage, headache, seizures, or focal neurological deficits. In about one third of cases, cavernous malformations are associated with developmental venous anomalies (DVA), which are the most common type of intracranial vascular malformation. DVAs drain normal brain parenchyma and are comprised of multiple venules that coalesce into a venous trunk that often ultimately drains into a dural sinus.

Cavernomas are challenging to identify on CT. They are also angiographically occult lesions, although catheter angiography may sometimes identify associated abnormal venous flow. Overall, MRI is the best modality in diagnosing cavernomas. A combination of histopathology and MRI categorize cavernomas into four different types. Type 2 cavernomas are the most common. These lesions have a “popcorn” appearance with heterogeneous T1 and T2 signal and a T2 hypointense rim. The internal signal characteristics are related to different ages of internal thrombosis and loculated hemorrhagic products. The T2 hypointense rim is related to peripheral deposition of hemosiderin after it has been cleared from the center of the lesion. With the exception of hemorrhagic lesions, cavernomas typically do not cause significant mass effect. Surrounding vasogenic edema is usually related to hemorrhage.

T2*-weighted gradient recall echo (GRE) and susceptibility weighted imaging (SWI) are important in diagnosis because they not only delineate the cavernoma but also potentially an associated DVA, as in the above case. DVA’s are characterized by a classic “medusa-head” appearance caused by a dominant transcortical venous flow void and multiple associated collecting veins. Contrast-enhanced MRI can also be useful in identifying a DVA associated with a cavernoma, as in the above case. 

In most cases of cavernous malformation, there is a single, isolated cavernoma. However, a small number of patients have an inherited genetic disease known as hereditary/familial cerebral cavernous malformations, characterized by multiple cavernomas.

Solitary cavernomas are sometimes surgically resected if they cause seizures or focal neurological deficits, while management of multiple lesions in hereditary cases is more controversial.

References:

Batra S, Lin D, Recinos PF, Zhang J, Rigamonti D. Cavernous malformations: natural history, diagnosis and treatment. Nature Reviews Neurology. 2009;5(12):659-670. doi:10.1038/nrneurol.2009.177

Das K, Rangari K, Singh S, Bhaisora K, Jaiswal A, Behari S. Coexistent cerebral cavernous malformation and developmental venous anomaly: Does an aggressive natural history always call for surgical intervention? Asian Journal of Neurosurgery. 2019;14(1):318. doi:10.4103/ajns.ajns_196_18

Flemming KD, Kumar S, Brown RD, Lanzino G. Predictors of Initial Presentation with Hemorrhage in Patients with Cavernous Malformations. World Neurosurgery. 2020;133:e767-e773. doi:10.1016/j.wneu.2019.09.161

Kearns KN, Chen CJ, Yagmurlu K, et al. Hemorrhage Risk of Untreated Isolated Cerebral Cavernous Malformations. World Neurosurgery. 2019;131:e557-e561. doi:10.1016/j.wneu.2019.07.222

Vilanova JC, Barceló J, Smirniotopoulos JG, et al. Hemangioma from Head to Toe: MR Imaging with Pathologic Correlation. RadioGraphics. 2004;24(2):367-385. doi:10.1148/rg.242035079

Zafar A, Quadri SA, Farooqui M, et al. Familial Cerebral Cavernous Malformations. Stroke. 2019;50(5):1294-1301. doi:10.1161/strokeaha.118.022314

History: A 12-year-old male presented to his primary care office with right leg pain for a few weeks. Further workup was performed, including radiographs of the right femur followed by an MRI of the pelvis.

Findings:

AP radiograph of the right femur shows mild sclerosis of the medial proximal femur with a subtle central lucent nidus (yellow arrow). No acute fracture is identified.

Axial and coronal T1 weighted images of the pelvis demonstrate a targetoid nidus with central T1 hypointensity compatible with calcification centered in the medial proximal right femur (green arrows). There is moderate cortical thickening surrounding the lesion. There is no evidence for fracture.

Coronal STIR images of the pelvis show extensive edema within the bone marrow surrounding the nidus extending from the proximal metaphysis to the proximal diaphysis of the right femur (teal arrow). 

Diagnosis: Osteoid osteoma

Teaching Points: Osteoid osteomas are benign skeletal lesions characterized by a nidus of osteoid tissue associated with cortical thickening, marrow edema, and sclerosis. They have a predilection for males ranging from 7 to 25 years of age. Classically, patients complain of nighttime pain that is relieved by NSAIDS/aspirin. Symptoms often occur over weeks to years before patients present to a clinician.

One of the classification schemes for osteoid osteomas divides lesions into the following categories: subperiosteal, intracortical, endosteal, and intramedullary. Osteoid osteomas can occur in almost any bone, although they are most commonly found in the long bones (particularly femur and tibia).

On radiographs, osteoid osteomas are characterized by a round/oval nidus measuring less than 2 cm that demonstrates varying degrees of calcification. There may be associated cortical thickening and sclerosis. The sensitivity of radiographs largely depends on the location of the lesion. For example, cortical lesions will often have a radiolucent nidus with surrounding sclerosis, whereas intramedullary lesions demonstrate almost no sclerosis.   

CT is excellent for identifying the nidus when radiographs are not revealing. It also appears to be superior to MRI in identifying the nidus. On CT, there is a low attenuation round/oval nidus that sometimes has high attenuation internally related to mineralization. Varying degrees of sclerosis are associated with the nidus.

On MRI, there is low/intermediate signal intensity on T1 weighted images and low to high signal intensity on T2 weighted images corresponding to different degrees of mineralization in the nidus. Sometimes, this may result in a target-like appearance. There is associated marrow edema. Effusions may be seen in the joints and soft tissues.

Important differential considerations for osteoid osteoma include stress fractures, intracortical abscess, osteoblastoma, and compensatory hypertrophy of the contralateral pedicle with unilateral spondylolysis, amongst others.

Some patients and clinicians may prefer conservative, noninterventional management for osteoid osteomas. Interventional management options include en bloc surgical resection of the osteoid osteoma nidus and image guided approaches including cryoablation, radiofrequency ablation, trephine excision, or laser thermocoagulation.

References:

Chai JW, Hong SH, Choi JY, et al. Radiologic Diagnosis of Osteoid Osteoma: From Simple to Challenging Findings. RadioGraphics. 2010;30(3):737-749. doi:10.1148/rg.303095120

Greenspan A. Benign bone-forming lesions: osteoma, osteoid osteoma, and osteoblastoma. Skeletal Radiology. 1993;22(7). doi:10.1007/bf00209095

Noordin S, Allana S, Hilal K, et al. Osteoid osteoma: Contemporary management. Orthopedic Reviews. 2018;10(3). doi:10.4081/or.2018.7496

Radcliffe SN, Walsh HJ, Carty H. Osteoid osteoma: the difficult diagnosis. European Journal of Radiology. 1998;28(1):67-79. doi:10.1016/s0720-048x(97)00071-5

History: An 80-year-old male presented to the Emergency Department with abdominal pain. A contrast-enhanced CT of the abdomen and pelvis was obtained for further evaluation.

Findings: 

Axial and coronal CT images of the abdomen/pelvis in soft tissue window demonstrate colonic diverticulosis with marked bowel wall thickening and perifascial thickening and surrounding fat stranding (yellow arrows). No definite intramural abscess is seen. There is no drainable fluid collection.

Sagittal CT image of the abdomen/pelvis in lung window demonstrates foci of free air in portions of the abdomen (red arrow).

Diagnosis: Acute perforated diverticulitis

Teaching Points: Diverticulitis refers to the acute inflammation of colon diverticula. Colonic diverticula likely form due to degeneration of the colonic mucosa and local increases in pressure, most commonly in the sigmoid colon. Eighty percent of patients develop diverticulosis by the age of 80; diverticulitis affects 10-25% of patients with diverticulosis. It is believed that diverticulosis progresses to diverticulitis in the context of fecal stasis when a fecalith becomes lodged within a diverticular neck. Diverticulitis can be complicated by perforation, peritonitis, abscess formation, and fistulae amongst other issues. Patients with diverticulitis typically present with left-sided abdominal pain, low grade fevers, and alterations of bowel movements.

Given the nonspecific nature of presenting symptoms, imaging plays an important role in confirming the diagnosis of diverticulitis. CT is highly sensitive and specific in diagnosis. It also demonstrates the extent of disease, ultimately guiding management. Previously, barium enema was used for diagnostic purposes but has been overwhelmingly replaced by CT. Ultrasound, while highly sensitive and specific, depends largely on sonographer expertise and is typically pursued when there is a contraindication to CT. MRI, while also highly sensitive and specific, has not been thoroughly studied and is not widely used.

Findings consistent with diverticulitis on CT include colonic wall thickening along with pericolic fat stranding and hyperemia. Eventually, there is associated thickening of retroperitoneal/peritoneal folds. Phlegmons can be identified as small enhancing masses near the site of inflammation. Abscesses are usually characterized by thick, hyperdense walls with internal hypodensity.

Perforation can be diagnosed when there are foci of extraluminal gas, best demonstrated on lung or bone windows, or in the presence of extraluminal contrast.  During supine CT exams, free air is typically identified in nondependent portions of the abdomen. Sometimes, focal bowel wall discontinuity can be identified to suggest perforation.

The major differential consideration for colonic diverticulitis is perforated colon cancer. Colon cancer may be differentiated from diverticulitis by the presence of eccentric wall thickening and associated lymphadenopathy. However, colonoscopy should be performed in cases of uncomplicated diverticulitis when there are concerning CT features or in accordance with national screening guidelines. Colonoscopy should be performed in all cases of complicated diverticulitis.

Uncomplicated diverticulitis can typically be managed on an outpatient basis. For complicated cases, many patients can be managed nonoperatively with bowel rest and IV antibiotics with some abscesses benefiting from percutaneous drainage. For those patients who do not respond to nonoperative management, the typical course includes a Hartmann procedure or primary anastomosis with or without diversion.

References: You H, Sweeny A, Cooper ML, Von Papen M, Innes J. The management of diverticulitis: a review of the guidelines. Medical Journal of Australia. 2019;211(9):421-427. doi:10.5694/mja2.5027610. 

Sessa B, Galluzzo M, Ianniello S, Pinto A, Trinci M, Miele V. Acute Perforated Diverticulitis: Assessment With Multidetector Computed Tomography. Seminars in Ultrasound, CT and MRI. 2016;37(1):37-48. doi:10.1053/j.sult.2015.10.003

Shin D, Rahimi H, Haroon S, et al. Imaging of Gastrointestinal Tract Perforation. Radiologic Clinics of North America. 2020;58(1):19-44. doi:10.1016/j.rcl.2019.08.004

History: A 60-year-old female presented to the Emergency Department with an ongoing headache for a few days. A non-contrast CT of the head was obtained for further evaluation. 

Findings: 

Coronal non-contrast CT of the head (shown above) demonstrates hyperdensity and expansion of the right transverse sinus with additional hyperdensity in the posterior half of the straight sinus and posterior third of the superior sagittal sinus (blue arrows). The left transverse sinus is comparatively lower in density (purple arrow). Additional areas of hyperdensity and expansion are noted in the torcula, right sigmoid sinus, and right jugular bulb (not shown). These findings are consistent with dural venous sinus thrombosis in the areas of hyperattenuation. A focal curvilinear hyperdensity along the right tentorial leaflet is suspicious for subdural hemorrhage or a thrombosed vein (green arrow). CT venogram was obtained to further investigate these findings.

Coronal and sagittal images from the CT venogram (shown below) demonstrate complete lack of opacification of the right transverse sinus, posterior half of the straight sinus, and posterior third of the superior sagittal sinus with partial filling defect in the mid third of the superior sagittal sinus. The left transverse sinus opacifies with contrast (orange arrow). Additional areas of complete non-opacification are noted in the torcula, right sigmoid sinus, right jugular bulb with partial filling defect in the right upper jugular vein (not shown).

The filling defects on the CT venogram correspond to areas of hyperdensity on the non-contrast exam, consistent with occlusive thrombosis of the right transverse sinus, sigmoid sinus, jugular bulb, torcula, posterior half of the straight sinus, and posterior third of the superior sagittal sinus with subocclusive thrombus in the mid third of the superior sagittal sinus and right upper jugular vein. Associated thrombosis is noted in a superficial vein along the right tentorial leaflet, corresponding to the curvilinear hyperdensity in this location on the non-contrast exam (yellow arrow).

Diagnosis: Dural venous sinus thrombosis

Teaching Points: Dural venous sinus thrombosis refers to the thrombotic occlusion of the intracranial dural sinuses. The dural venous sinuses are vascular structures located between the periosteal and meningeal layers of the dura and receive blood from throughout the brain. Risk factors for dural venous sinus thrombosis include pregnancy, oral contraceptives, mastoiditis or similar conditions, inherited prothrombotic states,  malignancy, and myeloproliferative disorders amongst others. Patient presentation is typically delayed from onset of symptoms. Most commonly, patients present with acute headache.  

Initial evaluation at the time of presentation usually includes non-contrast enhanced CT of the brain. On non-contrast enhanced CT, acute thrombosis is signaled by increased attenuation within the sinuses. As clot retracts, the concentration of red blood cells and hemoglobin increases, resulting in higher attenuation of the thrombus, usually around 60-90 Hounsfield Units. Elevated hemoglobin levels and polycythemia vera have been found to cause false positive results on non-contrast enhanced CT due to the intrinsic high attenuation of blood in these cases.

CT venography can be used to further evaluate for dural venous sinus thrombosis. During this procedure, contrast is injected and images are acquired after a fixed delay at which contrast is expected to opacify the relevant vessels. Any filling defects are suggestive of thrombosis.  

Conventional MRI can be used to evaluate dural venous sinus thrombosis and demonstrates different appearances on T1-weighted imaging and T2-weighted/FLAIR imaging based on the characteristics of hemoglobin degradation. Gradient echo and susceptibility weighted sequences demonstrate blooming artifact during certain stages of thrombus evolution. MR venography is also useful in evaluating dural venous sinus thrombosis and can be performed with or without contrast.

Possible long-term complication of dural venous sinus thrombosis include dural arteriovenous fistulas and idiopathic intracranial hypertension. Treatment of this entity revolves around the initiation of anticoagulation.

References:

Buyck PJ ., De Keyzer F, Vanneste D, Wilms G, Thijs V, Demaerel P. CT Density Measurement and H:H Ratio Are Useful in Diagnosing Acute Cerebral Venous Sinus Thrombosis. American Journal of Neuroradiology. 2013;34(8):1568-1572. doi:10.3174/ajnr.a3469

Ghoneim A, Straiton J, Pollard C, Macdonald K, Jampana R. Imaging of cerebral venous thrombosis. Clinical Radiology. 2020;75(4):254-264. doi:10.1016/j.crad.2019.12.009

History: A 70-year-old female presented to the Emergency Department with left lower quadrant abdominal pain and several episodes of emesis. A CT of the abdomen and pelvis was ordered for further evaluation.

Findings:

Axial and coronal images of the abdomen/pelvis demonstrate numerous loops of mildly dilated small bowel with fecalization of the small bowel contents (red arrows). There is a spigelian hernia in the left lower abdominal wall (yellow arrows). A transition point is identified in the distal ileum within the spigelian hernia (yellow arrows). The bowel loop entering the spigelian hernia is mildly dilated, the loop within the hernia is normal in caliber, while the exiting loop is collapsed. There is nonspecific thickening of the terminal ileum distal to the obstruction. A small amount of fluid is noted in the spigelian hernia sac, and there is a moderate amount of edema adjacent to the dilated loops of bowel.  

Diagnosis: Small Bowel Obstruction Due to Spigelian Hernia

Teaching points: A spigelian hernia is a type of anterior abdominal wall hernia that occurs through the spigelian fascia, which is an aponeurosis between the rectus abdominis muscle and the semilunar line. Spigelian hernias often occur at or below the arcuate line, as there is no posterior rectus sheath at that level. They are also known as lateral ventral hernias.

Overall, spigelian hernias are rare, comprising 1-2% of all abdominal wall hernias. Most often, spigelian hernias are acquired, although children may present with congenital spigelian hernias. Risk factors for acquired spigelian hernias include but are not limited to morbid obesity, multiple pregnancies, COPD, and rapid weight loss. Spigelian hernias are usually small and high risk for strangulation.

Diagnosis of spigelian hernias can be quite challenging. Patients may present with nonspecific pain when they have a reducible hernia. Others present with a complication of the hernia, such as small bowel obstruction. Physical exam is usually not reliable in the diagnosis. The diagnosis is typically made on CT, which also allows physicians to determine the contents, location, and possible complications of the hernia.

On CT, a spigelian hernia is diagnosed when there is a fascial defect in the appropriate location, as described above. The hernia may contain fat, omentum, small bowel, and/or large bowel. Small bowel obstruction, when present, is diagnosed based on the presence of dilated proximal bowel and collapsed distal bowel with an intervening transition point.  

Because of the high risk for strangulation, spigelian hernias are treated surgically. Open and laparoscopic techniques are used, with laparoscopic techniques demonstrating improved morbidity compared to open techniques.  

References:

Harrison LA, Keesling CA, Martin NL, Lee KR, Wetzel LH. Abdominal wall hernias: review of herniography and correlation with cross-sectional imaging. RadioGraphics. 1995;15(2):315-332. doi:10.1148/radiographics.15.2.7761638

Martin M, Paquette B, Badet N, Sheppard F, Aubry S, Delabrousse E. Spigelian hernia: CT findings and clinical relevance. Abdominal Imaging. 2012;38(2):260-264. doi:10.1007/s00261-012-9889-z

Mustaffa N, Leong R, Katelaris P. Gastrointestinal: Spigelian hernia; an uncommon cause of longstanding intermittent abdominal pain. Journal of Gastroenterology and Hepatology. 2012;28(1):202-202. doi:10.1111/jgh.12027

Salameh JR. Primary and Unusual Abdominal Wall Hernias. Surgical Clinics of North America. 2008;88(1):45-60. doi:10.1016/j.suc.2007.10.004

History: A 35-year-old female presented to the Emergency Department with right lower quadrant pain for 1 day. CT of the abdomen and pelvis was ordered due to concern for appendicitis. 

Findings:

The coronal CT image of the abdomen and pelvis shows a large 9.0 cm simple-appearing right adnexal cyst.

Axial and coronal CT images of the abdomen and pelvis show a dilated, tubular, fluid-filled structure along the periphery of the right ovary with a beaked appearance, most consistent with a dilated fallopian tube. There is associated thickening and enhancement of the fallopian tube wall. The right ovary itself is slightly enlarged.  

Diagnosis:  Fallopian Tube Torsion

Teaching Points:

Fallopian tube torsion is a type of adnexal torsion and usually occurs in the setting of coexisting ovarian torsion, although isolated tubal torsion can occur.  Twisting of the ovary and/or fallopian tube around its vascular pedicle (in the suspensory ligament) results in vascular compromise and potentially ovarian infarction.  Initially, the ovarian vein and lymphatics are affected and result in engorgement and enlargement of the ovary.  Eventually, if not treated quickly, the ovarian artery becomes compressed and results in ischemia/infarction.  Complications of isolated fallopian tube torsion include fallopian tube necrosis or gangrenous transformation.  Risk factors for tubal torsion include ovarian or paraovarian masses (especially if greater than 5 cm), adhesions, tubal ligation, pelvic inflammatory disease, and hydro/hematosalpinx. Interestingly, tubal torsion usually occurs on the right. Most patients present with severe acute abdominal pain and vomiting.

On CT, the typical findings suggestive of tubal torsion include an adnexal mass (such as the large adnexal cyst in our case shown above), and a dilated fallopian tube measuring greater than 15 mm in diameter, and associated thickening and enhancement of the fallopian tube wall. Often, the dilated fallopian tube takes on a “beaked” appearance where it tapers toward either end, similar to that seen in closed-loop bowel obstruction.  Occasionally, there may also be intraluminal hyperdense material compatible with hemorrhage, not seen in our case. Secondary signs include free pelvic fluid, adjacent fat stranding, and thickening of the broad ligament.  On ultrasound, there will be similar findings including a dilated fallopian tube with a thick, echogenic wall and internal debris. Twisting of the vascular pedicle is a specific finding though is not always seen.

If associated with ovarian torsion, as is usually the case, the ovary will be significantly enlarged. Due to the increase in size, the ovary does not have enough space in its usual location within the pelvis and migrates superiorly and anteriorly toward the midline, often positioned in front of the uterus.  The uterus has then deviated toward the side of the affected ovary. It is important to remember that normal arterial waveforms within the ovary do not exclude the possibility of torsion, since arterial perfusion is maintained until late in the course of torsion.

Differential considerations based on the imaging appearance of a dilated fluid-filled structure include hydrosalpinx, hematosalpinx, and pyosalpinx.  Early tubo-ovarian abscesses could also have a similar appearance.

Treatment is surgical detorsion. In addition, cystectomy is performed for benign lesions and salpingo-oopherectomy is often performed if there is concern for malignancy. 

References:

1. Dawood MT, et al. Adnexal Torsion: Review of Radiologic Appearances. Radiographics. 2021; 41(2).
2. Gross M, et al. Isolated Fallopian Tube Torsion: A Rare Twist on a Common Theme. American Journal of Roentgenology. 2005; 185(6).
3. Lourenco A, et al. Ovarian and tubal torsion: imaging findings on the US, CT, and MRI. Emergency Radiology. 2014; 21(2).   

History: A 50-year-old woman presented to the Emergency Department complaining of memory loss and “mental fog” since waking up that morning.  Brain MRI was performed for further evaluation.

Findings:

Axial diffusion-weighted MR image of the brain demonstrates a punctate focus of diffusion restriction in the right hippocampus.  There was a corresponding low-intensity signal on ADC images (not shown).

The remainder of the brain was unremarkable.  No significant FLAIR signal hyperintensity was seen to suggest a background of microvascular ischemic disease.

Diagnosis:  Transient Global Amnesia

Teaching Points:

Transient global amnesia is a rare clinical syndrome in which a patient experiences anterograde and partial retrograde short-term memory loss over a time period of less than 24 hours.  Symptoms are transient and usually completely resolve within a few hours, and there are no other associated neurological symptoms. Long-term memory is usually preserved.  The exact cause is unknown, but precipitating factors can include emotional/physical stress or pain.

Imaging is often performed to exclude other causes of amnesia, acute stroke, and structural abnormalities.  On imaging, brain CT will usually be normal. MRI can show punctate regions of diffusion restriction in the hippocampus cornu ammonis 1 (CA1), located along the lateral edge of the hippocampus abutting the temporal horn.  It can be unilateral or bilateral.

A differential consideration is a posterior circulation acute infarct.  However, in cases of posterior circulation infarct that involve the hippocampus, the area of diffusion restriction is usually larger and associated with additional areas of restricted diffusion in the occipital lobe, thalamus, or corpus callosum.

No treatment is required for transient global amnesia.  Outpatient follow-up is the standard management.

References:

1. Vella S, Grech R. Highlighting the classical MRI findings in transient global amnesia.  British Journal of Radiology Case Reports. 2020; 6(2).
2. Jain TP, et al. Transient global amnesia: Diffusion MRI findings. Indian Journal of Radiology and Imaging. 2018; 28(1).

Szabo K, et al. Diffusion-weighted MRI in transient global amnesia and its diagnostic implications. Neurology. 2020: 95(2).

History: A 40-year-old woman presented to the Emergency Department with chronic right hip pain.

A coronal T1 image of the hips shows mild lateral uncovering of the right femoral head. Note the well-formed left femoral head seated within a well-formed left acetabulum.

A coronal T1 image of the hips shows a shallow right acetabulum.

Coronal oblique T2 fat-sat image of the right hip shows hypertrophy of the right acetabular labrum and prominence of the right pulvinar fat.

Coronal T1 image of the hips shows abnormal concavity along with the lateral right femoral head likely related to chronic altered biomechanics of the joint.

Coronal T1 image of the hips and sagittal T2 fat-sat image of the right hip shows moderate right hip osteoarthritis with superior joint space narrowing, superior acetabular subchondral cyst formation, full-thickness cartilage loss over the anterosuperior and superolateral femoral head, and femoral head osteophyte formation.

Sagittal T2 fat-sat image of the right hip shows degeneration and tearing of the anterosuperior acetabular labrum.

Diagnosis: Sequelae of Developmental Dysplasia of the Hip (DDH) with right acetabular dysplasia and moderate right hip osteoarthritis

Teaching Points:

This case shows the long-term sequelae of developmental dysplasia of the hip (DDH), a diagnosis most often made in newborns. If diagnosed early, many of these long-term manifestations can be prevented by placing the patient in a Pavlik harness. However, in this case, the patient went undiagnosed and developed early-onset osteoarthritis.

DDH most often occurs in females and is frequently associated with oligohydramnios and abnormal in utero positioning. Additional risk factors include firstborn babies, breech presentations, and family history. Clinically, these babies present with positive Ortolani tests and/or Barlow maneuvers.

Ultrasound is the initial imaging test of choice in newborns, and DDH will show an alpha angle <60 degrees (angle from the acetabular roof to the vertical cortex of the ilium).

In adolescents and adults, DDH eventually leads to acetabular dysplasia or a shallow acetabulum that leads to hip instability due to insufficient coverage of the femoral head, as seen in our case above. Acetabular dysplasia eventually leads to early-onset osteoarthritis, chondral and labral damage, subchondral fractures, and hip instability/subluxation.

Treatment options for adolescents and adults with acetabular dysplasia include the Salter periacetabular osteotomy to reorient the acetabulum in order to provide increased coverage for the femoral head and the

Pemberton acetabuloplasty to change the morphology of the acetabulum. In severe cases, total hip arthroplasty may be indicated.

References:

1. Okano K, et al. Relationship between developmental dislocation of the hip in infant and acetabular dysplasia at skeletal maturity. Medicine. 2015; 94(1): 268.

2. Beltran LS, et al. Imaging Evaluation of Developmental Hip Dysplasia in the Young Adult. Musculoskeletal Imaging. 2012; 200: 1077-1088.

3. Manaster, BJ. Adult Chronic Hip Pain: Radiographic Evaluation. Radiographics. 2000; 20(1): S3-S25.

History: A 45-year-old male presents to the Neurologist with a chief complaint of gradual and progressive bilateral hearing loss.

Findings: 

Bilateral axial CT temporal bone images show demineralization/lucency of the fissula ante fenestrae on both the right and the left.   This finding is classic for fenestral otosclerosis.

Bilateral axial CT temporal bone images show demineralization/lucency of the bone surrounding the cochlea, which is nearly circumferential in involvement.  This finding is classic for retrofenestral otosclerosis.

Diagnosis:  Bilateral fenestral and retrofenestral otosclerosis

Teaching Points:

Otosclerosis is one of the most common causes of hearing loss in adults.  It is primary osteodystrophy of the otic capsule and is often known as otospongiosis rather than otosclerosis because the main imaging feature is bony lucency. There are actually two phases of the disease, with the early/active phase being the lucent phase where osteocytes absorb the bone in the otic capsule, and the late/inactive phase being the sclerotic phase where osteoblasts form irregular foci of new bone.

Otosclerosis is most common in females and usually presents in the 40s-50s with gradual, slowly progressive hearing loss.  The hearing loss is usually conductive but can be sensorineural or mixed. It is often bilateral.

There are two types of otosclerosis: fenestral and retrofenestral.  Fenestral is the most common type (80% of cases) and involves the fissula ante fenestram, just anterior to the oval window near the stapes footplate.  Retrofenestral otosclerosis is less common and is usually seen with fenestral otosclerosis, when present.  The two are a continuum rather than distinct entities.  In retrofenestral otosclerosis, the round window niche or bone surrounding the cochlea is involved.  Most cases are imaged in the early/active otospongiotic phase and the dominant imaging finding is demineralization/lucent bone.  The normal bone within the otic capsule should be very dense, and otosclerosis will appear lucent when compared to the remainder of the bone, as seen in the above case.  In the late/inactive otosclerotic phase, the affected bone actually increases in density and the otic capsule can appear abnormally thickened.

Treatment usually involves a stapedectomy with stapes prosthesis in fenestral otosclerosis, since the stapes can become fixated due to bony overgrowth.

References:

1. Lee TC, Aviv RI, et al. CT Grading of Otosclerosis. American Journal of Neuroradiology. 2009; 30(7): 1435-1439.
2. Juliano AF, Ginat DT, et al. Imaging Review of the Temporal Bone: Part II: Traumatic, Postoperative, and Noninflammatory Nonneoplastic Conditions. Radiology. 2015; 276(3): 655-672.
3. Niyazov D, et al. Fenestration surgery for otosclerosis. American Journal of Neuroradiology. 2000; 21(9): 1670-1672.

History: A 30-year-old male presents to the Emergency Department after cardiac arrest.

Findings: 

Axial image from CT coronary angiogram demonstrates a malignant course of the right coronary artery, which has an aberrant origin from the left coronary cusp.  From the left coronary cusp, it passes at an acute angle to the right between the pulmonary trunk and ascending aorta.  The origin is slit-like and the proximal RCA is narrowed between the ascending aorta and pulmonary trunk.

A curved multiplanar reformatted view of the right coronary artery again demonstrates the slit-like origin of the RCA from the left coronary cusp and significant narrowing of the vessel between the pulmonary trunk and ascending aorta.

Note that the remainder of the RCA distal to its interarterial course is widely patent and otherwise normal in appearance.

Curved multiplanar reformatted views of the left anterior descending artery and left circumflex artery show widely patent vessels without significant stenosis.

Diagnosis:  Malignant Interarterial Course of the Right Coronary Artery

Teaching Points:

When the right coronary artery arises from the left coronary cusp and passes between the pulmonary trunk and ascending aorta, it is termed a “malignant course” because of a potential risk of cardiac ischemia.  When arising from the left cusp, the RCA can take an interarterial/intramural course where a portion of the coronary artery actually travels within the wall of the ascending aorta, an interarterial/extramural course (shown above) in which the coronary artery travels in the space between the pulmonary trunk and ascending aorta, or an interatrial course.  The interatrial/intramural course is associated with the highest risk of sudden cardiac death.  The presence of an intramural segment can be inferred by an elliptical cross-section of the artery.

Anomalous coronary arteries are actually the second most common cause of sudden cardiac death after hypertrophic cardiomyopathy.  The exact etiology of cardiac ischemia/myocardial infarction in the setting of a malignant course of the RCA is debated, with some believing it is due to extrinsic compression of the coronary artery and others postulating that the acute angle and slit-like origin of the RCA as it makes its sharp turn to the right actually causes the ischemia.

Imaging is best with coronary CT angiography, but can also be performed with MR angiography or echocardiography.

Surgical treatment is often (but not always) required for scenarios that involve an anomalous left main coronary artery coursing between the great arteries, documented coronary ischemia due to compression between the great arteries, an intramural course, or an anomalous origin of the right coronary artery between the great arteries with evidence of ischemia.  Surgical options include coronary artery reimplantation, CABG, or unroofing.

References:

1. Agarwal P, Dennie C, et al. Anomalous Coronary Arteries That Need Intervention: Review of Pre- and Postoperative Imaging Appearances. Radiographics. 2017; 37(3): 740-756.
2. Satija B, Sanyal K, et al. Malignant anomalous right coronary artery detected by multidetector-row computed tomography coronary angiography. J Cardiovasc Dis Res. 2012; 3(1): 40-42.
3. Lim J, Beale A, et al. Anomalous origination of a coronary artery from the opposite sinus. Nat Rev Cardiol. 2011; 8(12): 706-719.

History: 17-year-old male presents with chest pain, dyspnea, and generalized weakness. He was noted to be profoundly hypotensive and was resuscitated. Subsequently, the patient endorsed generalized weakness/numbness, worst in the lower extremities, and the inability to urinate.

Findings: 

Sagittal T2 weighted MRI images through the cervical spine demonstrate abnormal high T2 signal originating at the C6-C7 spinal cord level. Axial imaging through the same level demonstrates a high T2 signal in the distribution of the anterior horns bilaterally.

Sagittal ADC and DWI images through the cervical and thoracic spine demonstrate extensive restricted diffusion.

Axial T2 imaging through the conus at L2 demonstrates abnormal high T2 signal.

Diagnosis: Spinal cord infarct

Teaching Points: Spinal cord ischemia is a rare cause of myelopathy although the exact incidence is poorly defined. Etiologies vary from atherosclerotic disease, aortic surgery, systemic hypotension, spinal trauma, embolic states, and vasculitides. Spinal cord infarction most commonly occurs in the thoracolumbar spine. Symptoms are determined based on the arterial distribution: the anterior spinal artery (ASA), posterior spinal artery (PSA), or both may be involved. The ASA is more commonly affected; symptoms typically include bilateral extremity weakness, back pain, areflexia, and loss of pain and temperature sensation below the level of the infarct. PSA infarcts usually present with loss of vibration and proprioception below the level of insult due to involvement of the dorsal columns.

Whole spine MRI is the modality of choice for diagnosis, which will demonstrate hyperintense T2 signal within the cord. Classically, this is described as an “owl eye” or “snake eye” pattern, which refers to bilateral involvement of the anterior horns. There may be slight spinal cord expansion in the early phase and mild atrophy in the chronic phase. If severe, T1 hyperintensity within the ischemic cord may represent hemorrhagic conversion. The infarcted spinal cord will restrict diffusion on ADC/DWI imaging. Enhancement is typically absent in the acute stage but may be present in the subacute setting, often 1-2 weeks after the initial insult.

The primary differential diagnosis for spinal cord infarct includes transverse myelitis which also presents with imaging findings of linear T2 hyperintensity within the anterior portion of the cervical spinal cord. Diagnosis of transverse myelitis requires pleocytosis within the cerebrospinal fluid OR postcontrast enhancement between 4 hours and 21 days of symptom onset in a non-vascular distribution, which help differentiate this diagnosis from SCI.

Clinical management is dependent upon the etiology of SCI. In cases of systemic hypotension (such as with aortic surgery), mean arterial blood pressure must be kept above 90 mm Hg with the aid of volume resuscitation and pressors. SCI resulting from spinal cord compression secondary to a lesion or collection should be urgently resected or drained, respectively.

References:

Transverse Myelitis Consortium Working Group. Proposed diagnostic criteria and nosology of acute transverse myelitis. Neurology. 2002 Aug 27;59(4):499-505. doi: 10.1212/wnl.59.4.499. PMID: 12236201.

Nance JR, Golomb MR. Ischemic spinal cord infarction in children without vertebral fracture. Pediatr Neurol. 2007 Apr;36(4):209-16. doi: 10.1016/j.pediatrneurol.2007.01.006. PMID: 17437902; PMCID: PMC2001276.

Rubin MN, Rabinstein AA. Vascular diseases of the spinal cord. Neurol Clin. 2013 Feb;31(1):153-81. doi: 10.1016/j.ncl.2012.09.004. PMID: 23186899.

Yadav N, Pendharkar H, Kulkarni GB. Spinal Cord Infarction: Clinical and Radiological Features. J Stroke Cerebrovasc Dis. 2018 Oct;27(10):2810-2821. doi: 10.1016/j.jstrokecerebrovasdis.2018.06.008. Epub 2018 Aug 6. PMID: 30093205.

History:  A 45-year-old male presented to the Emergency Department with hip pain.

Findings: 

An AP radiograph of the pelvis and hips demonstrates a lucent lesion within the superior acetabulum with thickening of the trabecula. The hip joint spaces are moderately narrowed superiorly.

Coronal CT images of the lesion demonstrate a lesion with thickened trabecula on bone windows (top image) and foci of intralesional fat (bottom image; shown as the very dark spots within the lesion).  There is no significant cortical thickening or osseous expansion, and the ends of the bones are not involved.

Axial CT images of the calvarium in a separate patient demonstrate a similar-appearing lucent lesion with trabecular thickening.  The cortex is not thickened.  On soft tissue windows (bottom image), the very dark spot pointed out by the arrow represents a tiny focus of intralesional fat.

Sagittal and axial CT images of the lumbar spine in a separate patient demonstrate a lucent lesion in the L4 vertebral body with trabecular thickening.  On sagittal imaging, the thickened, longitudinal trabecula is described as the “corduroy sign” (1^st and 3^rd images).  On axial images, the thickened trabecular takes on the appearance of the “polka dot sign” (2^nd image).   Once again, there is no cortical thickening.  On soft tissue windows (3^rd image), intralesional fat is again seen.

Diagnosis:  Intraosseous Hemangiomas in Various Locations

Teaching Points:

Intraosseous hemangiomas are slow-growing vascular malformations.  They are benign lesions although in rare instances can be locally aggressive. They are most often seen in the spine and calvarium.

Intraosseous hemangiomas share common imaging features regardless of their location in the body. On radiographs and CT, the hallmark finding is thickened trabecular markings. This is described as the “corduroy sign” on coronal and sagittal images and the “polka dot sign” on axial images. Intralesional fat is also a classic feature, so it is important to look on soft tissue windows for foci of fat-density within the lesion.  On MRI, in-and-out of phase imaging can be helpful to look for intralesional fat.  Intraosseous hemangiomas often show some degree of post-contrast enhancement.

While these are usually an easy diagnosis to make in the spine due their classic appearance and prevalence, they can be a source of confusion when seen in unusual locations such as the superior acetabulum in the 1^st patient shown above.  The main differential diagnosis is Paget’s disease given the common imaging feature of trabecular thickening.  However, Paget’s disease should demonstrate additional classic imaging features including 1) trabecular thickening, 2) cortical thickening, 3) osseous expansion, and 4) begins at the end of a bone rather than within the center of the bone.  Using these 4 criteria in the case of our 1^st patient shown above, the lucent lesion in the acetabulum does not demonstrate cortical thickening or osseous expansion and is located within the center of the bone rather than beginning at the end of the bone.  Therefore, the imaging features favor intraosseous hemangioma rather than Paget’s disease.  Think about intraosseous hemangiomas whenever you see trabecular thickening without these additional features of Paget’s disease!

Given the benignity of these lesions, intraosseous hemangiomas require no treatment in the vast majority of cases.  

References:

1. Rigopoulou A, Saifuddin A. Intraosseous hemangioma of the appendicular skeleton: imaging features of 15 cases, and a review of the literature. Skeletal Radiology. 2012; 41: 1525-1536.
2. Kaleem Z, Kyriakos M, et al. Solitary skeletal hemangioma of the extremities. Skeletal Radiology. 2000; 29(9): 502-513.
3. Theodorou D, Theodorou S, et al. Imaging of Paget Disease of Bone and Its Musculoskeletal Complications: Review. American Journal of Roentgenology. 2011; 196: S64-S75.

History: A 55-year-old female presented to the Emergency Department with a chief complaint of a palpable lesion in her posterior right thigh.

Findings:

Pelvis and bilateral hip radiographs demonstrate the smooth, homogenous expansion of the bones with endosteal scalloping and cortical thinning.  The internal matrix of the bones has a “ground-glass” appearance. 

MRI of the right femur demonstrates two well-circumscribed T2/STIR hyperintense masses, the larger of which corresponded to the patient’s palpable area of concern.  The largest is located in the inferior gluteus maximus muscle and the smaller is located in the vastus intermedius muscle.

In addition, the visualized femur and pelvic bones demonstrate heterogeneous T2/STIR hyperintensity, enhancement, and osseous expansion.

Post-contrast images demonstrate heterogenous internal septal enhancement of the intramuscular masses.

Diagnosis: Mazabraud Syndrome

Teaching Points:

Mazabraud Syndrome is a rare condition characterized by fibrous dysplasia and intramuscular myxomas. It is predominantly seen in middle-aged females.  Patients may be asymptomatic or could present with palpable masses or pathologic fractures.

Fibrous dysplasia is caused by a defect in osteoblastic maturation, which results in bone being replaced by fibrous stroma and immature bone.  It primarily affects younger patients (~30 years old) as opposed to Paget’s disease which affects older populations.  It is usually an isolated finding but can be associated with syndromes such as Mazabraud syndrome or McCune-Albright syndrome.  Fibrous dysplasia is most often monostotic (affecting only one bone) and less often polyostotic (affecting multiple bones).  The most common sites involved are the ribs and proximal femur. On radiographs and CT, the bones will demonstrate an internal ground-glass matrix with osseous expansion, endosteal scalloping, and cortical thinning.  There may be fusiform enlargement of the ribs or a shepherd crook deformity of the femoral neck. Treatment is most often conservative as patients are usually asymptomatic, although surgery may be required due to pathologic fractures, pain, or compression of adjacent structures due to osseous expansion.  Malignant transformation to osteosarcoma, fibrosarcoma, or malignant fibrohistiocytoma can occur in rare cases, usually in the polyostotic form.

Intramuscular myxomas are benign tumors that affect skeletal muscle.  They most often occur in the quadriceps, hip adductors, and gluteus muscles.  In the setting of Mazabraud Syndrome, they tend to occur in the areas most affected by fibrous dysplasia (typically the pelvis and lower extremities).  On imaging, they are well-circumscribed ovoid lesions that are very T2 hyperintense with variable enhancement patterns (peripheral/internal/heterogenous).  Treatment is most often conservative given the benign nature of these tumors. 

References:

1. McLaughlin A, Stalley P, et al. Correlative Imaging in an Atypical Case of Mazabraud Syndrome.  American Journal of Roentgenology.  2007; 189: W353-356.
2. Gaumetou E, Tomeno B, et al. Mazabraud’s syndrome: A case with multiple myxomas.  Orthopaedics and Traumatology: Surgery and Research. 2012; 98(4): 455-460.
3. Munksgaard P, Salkus G, et al. Mazabraud’s syndrome: case report and literature review.  Acta Radiol Short Rep. 2013; 2(4).
4. Kushchayeva Y, Kushchayev S, et al. Fibrous dysplasia for radiologists: beyond ground glass bone matrix. Insights into Imaging. 2018; 9: 1035-1056.

History: A 30-year-old male presented to the Emergency Department with right lower quadrant pain.

Coronal and axial CT images of the abdomen and pelvis demonstrated a 3 x 2 cm blind-ending pouch in the right lower quadrant arising from the distal ileum that does not fill with oral contrast.  There is mild surrounding fat stranding.  A normal, non-dilated, air-filled appendix was visualized separately from this structure.

Diagnosis:  Meckel’s Diverticulitis

Teaching Points:

Meckel’s diverticulitis is inflammation of a Meckel’s diverticulum.  It is a clinical mimic of acute appendicitis as it often presents in young patients with right lower quadrant pain.  It is important to keep this entity in your mind as a possible source of right lower quadrant pain when you visualize a normal-appearing appendix.  In addition to pain, patients can present with painless rectal bleeding.

A Meckel’s diverticulum is a remnant of the omphalomesenteric-vitelline duct.  It follows the “rule of 2’s” meaning that it occurs in 2% of the population, is located within 2 feet of the ileocecal valve, measures approximately 2 inches long, has 2 types of ectopic tissue (gastric and pancreatic), and most often presents within the first 2 years of life.

It is most often diagnosed via ultrasound or CT.  Ultrasound will demonstrate an incompressible, blind-ending, hypoechoic tubular structure with irregular margins, very similar in appearance to an appendix.  CT will similarly demonstrate a fluid-filled, blind-ending pouch arising from the distal ileum with surrounding inflammatory changes, wall thickening, and mural hyperenhancement.  A non-enhancing wall is suggestive of gangrenous Meckel’s diverticulitis.  Identification of a normal appendix is necessary to distinguish from acute appendicitis, which has very similar imaging features.   A nuclear medicine pertechnetate study can also be obtained to identify the ectopic gastric mucosa, which is often present in bleeding diverticula.

In addition to Meckel’s diverticulitis, other complications of a Meckel’s diverticulum include GI bleed, small bowel obstruction, intussusception, or perforation.

References:

1. Elsayes K, et al. Imaging Manifestations of Meckel’s Diverticulum. American Journal of Roentgenology. 2007; 189(1): 81-88.
2. Milam R, et al. Meckel Diverticulitis. Radiology. 2017; 283(1).
3. Kotha V, et al. Radiologist’s perspective for the Meckel’s diverticulum and its complications. Br J Radiol. 2014; 87(1037).

History: A 30-year-old female with a history of trichotillomania and trichophagia presented to the Emergency Department with abdominal pain, abdominal distention, and vomiting.

Findings:

Coronal and axial images of the abdomen demonstrate marked distention of the stomach and proximal duodenum secondary to complex mass-like, well-circumscribed collections of intraluminal debris. The “masses” are mottled in appearance with internal foci of air. There is associated wall thickening of the involved stomach and duodenum.

Post-operative images of the abdomen demonstrate soft tissue-stranding in the left upper quadrant with apparent discontinuity of the greater curvature of the stomach near the gastric cardia with a large, complex fluid collection compatible with abscess extending from the stomach into the splenic parenchyma.  An additional, smaller abscess is seen more medially with the posterior spleen.

Diagnosis: Gastric and Duodenal Bezoars Causing Gastric Outlet Obstruction

Teaching Points:

A trichobezoar is an intraluminal mass within the gastrointestinal tract formed from ingested hair.  Hair is resistant to digestion and accumulates over time to form a hairball, which can result in gastric outlet obstruction or small bowel obstruction (Rapunzel syndrome).  Bezoars do not usually pass or resolve spontaneously, so treatment most often requires endoscopic removal, and if not performed in time can result in bowel perforation.  

There are multiple types of bezoars, depending on the main component of the mass.  While trichobezoars are composed of hair, phytobezoars are composed of indigestible food materials such as vegetable fibers or poorly digested fruit (classically persimmons), pharmacobezoars are composed of undigested medications tablets, and lactobezoars are composed of undigested milk curds.

CT is the imaging modality of choice for diagnosis, which will demonstrate dilatation of the stomach or small bowel loops depending on the level of obstruction.  The bezoar will appear as a focal, well-circumscribed, round or oval, mottled mass within the lumen of the bowel.  The mottled appearance is secondary to air trapped within the mass. The wall of the stomach should be able to be delineated separately from the wall of the mass in order to distinguish a bezoar from a large amount of retained gastric contents.

Most bezoars occur in patients with a history of gastric surgery or altered gastric motility. However, trichobezoars are found almost exclusively in younger females with trichophagia.

References:

1. Ripollés T, García-aguayo J, Martínez MJ et-al. Gastrointestinal bezoars: sonographic and CT characteristics. AJR Am J Roentgenol. 2001;177 (1): 65-9.
2. Altintoprak F, et al. CT Findings of Patients with Small Bowel Obstruction due to Bezoar: A Descriptive Study. The Scientific World Journal. 2013.
3. Verstandig AG, et al. Small bowel phytobezoars: detection with radiography. Radiology. 1989.

History: A 40-year-old woman presented to the Emergency Department with one week of abdominal pain, nausea, and vomiting.  Labs were notable for elevated lipase.

Finding:

Axial and coronal images from the contrast-enhanced CT of the abdomen and pelvis demonstrated a lobulated focus of soft tissue posterior to the duodenal-jejunal junction.  It has the appearance of pancreatic tissue with interdigitating fat and measures approximately 2.5 cm in diameter. There is associated inflammation with surrounding fat stranding and adjacent lymph nodes.

Additional images of the same patient demonstrate that there is normal-appearing pancreatic tissue in the expected location without associated inflammation.

A follow-up CT after treatment of acute pancreatitis demonstrates a persistent soft tissue mass posterior to the duodenal-jejunal junction with a resolution of the adjacent fat stranding.  Note that this ectopic pancreatic tissue could easily be mistaken for an enlarged lymph node, bowel, or tumor when there is no surrounding fat stranding. 

Diagnosis:  Heterotopic pancreas with acute pancreatitis

Teaching Points:

Ectopic/heterotopic pancreatic tissue is defined as pancreatic tissue in the submucosal, muscularis, or subserosal layers of the luminal GI tract.  It lacks any ductal or vascular connection with the main pancreatic gland.  The most common locations for ectopic pancreas include the proximal duodenum, proximal jejunum, and gastric antrum.  Less common sites include the ileum, esophagus, and Meckel’s diverticulum. The cause of the ectopic pancreas is unknown, but it is embryological/developmental in etiology and is thought to be related to deposits of pancreatic tissue being “dropped” into the developing GI tract.

It is most commonly asymptomatic but can demonstrate any pathology that can be seen in the normal pancreas including pancreatitis or pancreatic tumors.  Most lesions are solitary and measure less than 3 cm.

There are multiple histologic subtypes of ectopic pancreatic tissue.  Type 1 heterotopic tissue contains acini, ducts, and islet cells similar to normal pancreatic tissue.  Type 2 contains only acini and ducts and Type 3 contains only ducts.

On fluoroscopic barium studies, ectopic pancreatic tissue has the appearance of an extramucosal intramural lesion with a broad base and smooth surface, and often contains a central barium-filled pit or umbilication.

On CT, the characteristic location, endoluminal growth pattern, microlobulated borders, and prominent enhancement of the overlying mucosa help to differentiate the ectopic pancreas from other tumors. 

On MRI, the heterotopic pancreatic tissue will have similar signal characteristics as the main pancreatic gland with a characteristic high intrinsic T1 signal.

References:

1. Resvani M, et al. Heterotopic Pancreas: Histopathologic Features, Imaging Findings, and Complications. 2017; 37(2).
2. Kim JY, et al. Ectopic Pancreas: CT Findings with Emphasis on Differentiation from Small Gastrointestinal Stromal Tumor and Leiomyoma. Radiology. 2009; 252(1).

Subramanian M, et al. Clinics in diagnostic imaging: duodenal ectopic pancreas.  Singapore Medical Journal. 2014; 55(12): 629-634.

History: 70-year-old male with a history of cardiac amyloidosis who presented to the Emergency Department with shortness of breath.

Findings:

The PA chest radiograph demonstrates an enlarged cardiac silhouette. The cardiothoracic ratio is a measurement obtained on PA chest radiographs and is defined as the ratio of maximal horizontal cardiac diameter (top line) to maximal horizontal thoracic diameter measured from inner rib to inner rib (bottom line). When this ratio measures greater than 0.5, the cardiac silhouette is considered enlarged. This could be related to cardiomegaly or pericardial effusion.  Prominent epicardial fat pads can also sometimes lead to this ratio measuring enlarged when there is no true pathology involving the heart or pericardium.

The lateral chest radiograph of the same patient demonstrates the “Oreo Cookie” sign.  This sign describes two vertical linear lucent lines (yellow arrows) separated by an opaque line (green arrow) on the lateral chest x-ray.  The most anterior lucent line (directly posterior to the sternum) represents paracardial fat and the most posterior lucent line represents epicardial fat.  In between these two fat layers is the opaque line (green arrow), which represents pericardial fluid.  When this sign is seen on a chest x-ray, it is highly suggestive of pericardial effusion. 

A sagittal view from a PET/CT on the same patient confirms the presence of pericardial effusion. The two yellow arrows in the picture correspond to the two vertical lucent lines on the chest radiograph and are seen to represent paracardial fat and epicardial fat. The green arrow shows the moderate-sized pericardial effusion between the two fat layers, which corresponds to the opaque vertical line on the chest radiograph.

A sagittal view from a cardiac MRI in the same patient shows similar findings, again confirming the presence of pericardial effusion as suggested on the chest radiograph.

Diagnosis: “Oreo Cookie” Sign of Pericardial Effusion"

Teaching Points:

Pericardial effusions are collections of excess fluid within the pericardial space. There are numerous etiologies for pericardial effusions, including idiopathic, uremia, malignancy, infection, systemic lupus erythematosus, rheumatoid arthritis, post-myocardial infarction (Dressler syndrome), traumatic, and pulmonary arterial hypertension, among many other causes.

In order for pericardial effusions to be visible on the chest radiograph, over 200 mL of fluid must be present.  On the PA view, the cardiac silhouette will be globally enlarged and often takes on a “water bottle” configuration.  The cardiothoracic ratio described above will be greater than 0.5.  The “oreo cookie” sign described above can be seen on the lateral radiograph.

If there are signs suggestive of pericardial effusion on chest radiograph, further evaluation with echocardiography should be recommended.

Symptoms from a pericardial effusion are related to the speed of fluid accumulation rather than the absolute volume.  If the fluid accumulates gradually, the pericardium can stretch and accommodate larger volumes.  However, if the fluid accumulates rapidly, even a small amount of fluid can impair cardiac function and potentially lead to cardiac tamponade. Echocardiography is the most reliable method to assess the hemodynamic impact of the effusion.

Treatment is most often conservative, but if the patient is symptomatic and there is evidence of hemodynamic compromise, then a pericardiocentesis can be performed for drainage.

References:

1. Chiarenza A, et al. Chest imaging using signs, symbols, and naturalistic images: a practical guide for radiologists and non-radiologists. Insights into Imaging. 2019;10(114).
2. Wang ZJ, Reddy GP, et al. CT and MR imaging of pericardial disease. 2003;23: S167-180.
3. Weissman NJ, Adelmann GA. Cardiac imaging secrets.  Elsevier Health Sciences.  (2004) ISBN: 1560535156.

History: A 50-year-old woman presented to the Emergency Room with acute left lower quadrant abdominal pain.

Findings:

Axial, coronal, and sagittal views of the contrast-enhanced CT abdomen and pelvis demonstrate two adjacent ovoid-shaped, fat-density structures located anterior to the descending/proximal sigmoid colon.  These structures demonstrate thin enhancing rims and significant surrounding inflammatory fat stranding.  A central hyperdense “dot” is seen within the center of these structures.

Diagnosis: Epiploic appendagitis

Teaching Points: Epiploic appendagitis is a self-limiting inflammatory process involving an appendix epiploica of the colon.  There are approximately 50-100 appendices epiploicae located along the colon, the majority of which are located in the region of the rectosigmoid colon.  These appendages are peritoneal pouches arising from the serosal surface of the colon and are attached to the colon via a vascular stalk.  Epiploic appendagitis results when there is torsion or spontaneous thrombosis of the venous outflow to one or more of these appendices epiploicae.

Patients with epiploic appendagitis present with acute abdominal pain, which can often mimic diverticulitis or appendicitis.  There is a predilection for middle-aged women and obese patients.

On CT, epiploic appendagitis will appear as a fat-density, ovoid structure adjacent to the colon, most often along the anterior aspect of the sigmoid or descending colon.  They tend to have thin, hyperdense rims and surrounding inflammatory fat stranding.  Sometimes, a “central dot sign” can be seen (as in our case shown above), in which the thrombosed vascular pedicle appears as a punctate hyperdense dot within the fat-density structure.  Epiploic appendages are typically visible on CT only when they are inflamed.  There is usually no significant wall thickening of the adjacent bowel. In its chronic stage, the infarcted epiploic appendage can calcify and detach from the colon wall, forming an intraperitoneal loose body.

Epiploic appendagitis is self-limiting and usually responds well to NSAIDs.  Surgery is not necessary.  Symptoms resolve within 2 weeks for most patients, although CT findings can persist for several months. 

The main differential consideration is an omental infarct. Still, these are more often located adjacent to the cecum or ascending colon and are typically larger (greater than 3 cm, as opposed to epiploic appendagitis, which more often measures 1.5-3 cm).  Omental infarcts also lack the hyperdense rim seen with epiploic appendagitis.

References:

1. Singh AK, et al. Acute Epiploic Appendagitis and Its Mimics. 2005; 25(6): 1521-1534.
2. Nadida D, et al. Acute epiploic appendagitis: radiologic and clinical features in 12 patients.  Int J Surg Case Rep. 2016;28: 219-222.
3. Giambelluca D, et al. CT imaging findings of epiploic appendagitis: an unusual cause of abdominal pain. Insights Imaging.  2019;10:26.

History: 30-year-old male with a history of neuromyelitis optica presented to the Emergency Department with intractable hiccups for 3 weeks, with associated intermittent nausea and vomiting.

Post-contrast axial and sagittal MRI images of the brain shown above demonstrate a 3 mm focus of enhancement in the left dorsal aspect of the medulla in the region of the area postrema.

Post-contrast axial and coronal MRI images through the orbits demonstrate enhancement of the right optic nerve.  Note the normal left optic nerve without enhancement.

Diagnosis:  Neuromyelitis Optica with Area Postrema Syndrome and Optic Neuritis 

Teaching Points:

Neuromyelitis Optica spectrum disorders (NMOSD) are a group of inflammatory, autoimmune, demyelinating diseases. The majority are associated with a pathologic antibody specific for the aquaporin-4 (AQP4) water channel.  In fact, the clinical diagnosis of NMOSD requires a positive AQP4-IgG and 1 core clinical characteristic, or 2 core clinical characteristics without the AQP4 antibody.  Core clinical characteristics of NMOSD include optic neuritis, transverse myelitis, area postrema syndrome, acute brainstem syndrome, and symptomatic narcolepsy.

Brain lesions in NMOSD tend to occur in areas rich in AQP4.  One of these areas is known as the area postrema, as seen in the top 2 pictures shown above.  The area postrema is located in the dorsal tegmentum of the medulla at the floor of the 4^th ventricle and acts as an emetic reflex center and mediates hiccups due to its extensive network of chemo-sensitive neurons and connections with the hypothalamus, brainstem, and bloodstream.  Lesions in the dorsal medulla cause inflammation in this area and loss of AQP4 reactivity and therefore result in attacks of intractable nausea, vomiting, and hiccups lasting longer than 48 hours, known as Area Postrema Syndrome.  It is estimated that 30% of patients with NMOSD will have Area Postrema Syndrome during the course of their illness.  Symptomatic therapies such as antiemetics are typically ineffective, but steroids or plasmapheresis tend to result in rapid cessation of symptoms.

The main imaging feature of area postrema syndrome is an abnormal enhancement of the dorsal medulla in the correct clinical setting. An abnormal FLAIR signal in this region can also be seen.

Additional typical areas of brain involvement in NMOSD at sites of AQP4 include the periependymal surface of the corpus callosum, hypothalamus, periaqueductal area, lateral ventricles, third ventricle, fourth ventricle, and optic chiasm.

More classic symptoms in NMOSD include optic neuritis and transverse myelitis, the other core clinical characteristics which meet the criteria for NMOSD diagnosis.  When area postrema syndrome does occur, it tends to precede involvement of the orbits or spinal cord and therefore can serve as a warning sign for progressive symptoms.  Treatment of area postrema syndrome not only helps relieve symptoms of vomiting and hiccups but can also prevent subsequent episodes of optic neuritis or transverse myelitis. 

Our patient also had optic neuritis, as shown in the bottom 2 pictures. Imaging features of optic neuritis include high T2 signal and abnormal enhancement of the optic nerve.  In NMOSD, optic neuritis tends to occur bilaterally, whereas it is more often unilateral in the case of multiple sclerosis (although our patient shown above only has unilateral involvement). 

References:

1. Shosha E, Dubey D, et al. Area Postrema Syndrome: Frequency, Criteria, and Severity in AQP4-IgG positive NMOSD. 2018;91(17): e1642-1652.
2. Hyun JW, Kwon YN, et al. Value of Area Postrema Syndrome in Differentiating Adults with AQP4 vs. MOG Antibodies. Frontiers in Neurology. 2020;11:396.
3. Chan KH, Vorobeychick G. Area postrema syndrome: a neurological presentation of nausea, vomiting, and hiccups. BMJ Case Reports. 2020; 13: e238588.
4. Dutra BG, et al. Neuromyelitis Optica Spectrum Disorders: Spectrum of MR Imaging Findings and Their Differential Diagnosis. 2018; 38(1): 169-193.

History: A 70-year old male with a history of hypertension and COPD presented to the Emergency Department with acute onset chest pain and shortness of breath. 

Findings:

The initial chest radiograph obtained in the Emergency Department showed hyperinflation of the lungs and flattening of the diaphragms, which can be seen with COPD/emphysema. In addition, a focal opacity in the left retrocardiac region was seen, which appeared to silhouette the contour of the distal descending thoracic aorta. Given the history of acute chest pain, further evaluation with a CT angiogram of the chest was recommended.

Three images from the CT angiogram of the chest demonstrate an irregularly shaped, focal outpouching of the distal descending thoracic aorta. This outpouching is contrast-filled, directed anterolaterally to the left, and measures approximately 2.5 x 2.1 x 1.7 cm. It is associated with an area of calcified atherosclerotic plaque. Soft tissue attenuation areas along the margins of this outpouching that do not fill with contrast likely represent a component of mural thrombus.

Diagnosis: Penetrating Atherosclerotic Ulcer (PAU)

Teaching Points:

A penetrating atherosclerotic ulcer (PAU) describes an atherosclerotic plaque that erodes the internal elastic lamina into the media of the aortic wall. They occur in regions of advanced atherosclerosis.

Patients with PAU present with the classic symptoms of the acute aortic syndrome, most commonly acute tearing chest pain. They tend to occur in the older male population with a history of hypertension, smoking, coronary artery disease, peripheral artery disease, and COPD.

CT angiogram is the test of choice for PAUs. Our case described above is interesting because we can actually detect the focal outpouching of the aorta on the chest radiograph. On CTA, PAUs appear as contrast-filled outpouchings off the wall of the aorta. They most often involve the aortic arch or mid-distal thoracic aorta. They occur in areas of advanced atherosclerosis as evidenced by jagged, irregular aortic walls from atheroma and the presence of intimal calcification.

In general, PAUs can be classified according to the Stanford classification in the same way as aortic dissections. PAUs occurring in the ascending aorta proximal to the left subclavian artery origin (Stanford type A) have a higher risk of rupture and are treated with early surgical intervention. PAUs that do not involve the ascending aorta (Stanford type B) can be managed with antihypertensive medication and imaging follow-up if asymptomatic or with endovascular repair if symptomatic and/or progressing.

PAUs can rupture and lead to intramural hemorrhage, which can subsequently cause a limited intermedial dissection, saccular pseudoaneurysm, or aortic rupture. If associated with intramural hematoma, non-contrast CT will show a high-density hematoma surrounding the PAU. Intramural hematomas associated with PAU have a worse prognosis compared to intramural hematomas in the absence of PAUs. PAUs actually have an even higher incidence of aortic rupture when compared to aortic dissection. PAUs measuring greater than 10mm in depth or 20mm in diameter have a higher rate of progression. Persistent or recurrent pain, as well as new/increased pleural effusions, are also important predictors of disease progression.

It is important to distinguish PAU from irregular atherosclerotic plaque, a very common finding in which atheromatous plaque causes irregular margins of the aortic wall. Still, no contrast material extends beyond the level of the intima.

References:

1. Maddu KK, Shuaib W, et al. Nontraumatic Acute Aortic Emergencies: Part 1, Acute Aortic Syndrome. American Journal of Roentgenology. 2014;202: 656-665.

2. Hayashi H, Matsuoka Y, et al. Penetrating Atherosclerotic Ulcer of the Aorta: Imaging Features and Disease Concept. Radiographics. 2000;20(4): 995-1005.

3. Ganaha F, Miller DC, et al. Prognosis of Aortic Intramural Hematoma With and Without Penetrating Atherosclerotic Ulcer. Circulation. 2002;106(3).

4. Macura KJ, Corl FM, et al. Pathogenesis in Acute Aortic Syndromes: Aortic Dissection, Intramural Hematoma, and Penetrating Atherosclerotic Aortic Ulcer. American Journal of Roentgenology. 2003;181: 309-316.

A pregnant woman in her 30's was noted to have a uterine anomaly during prenatal ultrasound. Patient now presents for MRI after successful delivery for further evaluation of this anomaly.

The above pictures show two widely-spaced uterine corpora and edometrial cavities with separate, non-communicating divergent uterine horns and a large fundal cleft.

The above picture shows two separate cervices.

The above picture shows a partially duplicated vagina superiorly near the two cervices. The normal H-shaped appearance of the vagina is lost.

Diagnosis: Uterine Didelphys

Uterine didelphys is a type of Mullerian duct anomaly secondary to complete failure of ductal fusion. Normally, the Mullerian ducts fuse during the 6th to 11th weeks of gestation to form the uterus, Fallopian tubes, cervix, and upper 2/3 of the vagina. In uterine didelphys, however, the failed fusion resulted in complete duplication of the uterine horns and cervix.

Imaging findings include two widely-spaced uterine bodies and endometrial cavities, each with a single Fallopian tube. The divergent uterine horns are separated by a large fundal cleft. Two separate cervices are always present. In 75% of cases, there is also an upper vaginal septum.

Mullerian duct anomalies are commonly associated with renal anomalies, most commonly in the form of ipsilateral renal agenesis. Ectopia, hypoplasia, fusion, malrotation, and duplication are other renal anomalies that can be seen.

Vaginal septa may cause obstruction from one uterine horn and can result in subsequent hematometrocolpos (appearing on MRI as a markedly distended unilateral uterine horn with high T1 signal related to blood). In addition, vaginal septa can lead to retrograde menstrual flow and result in endometriosis, infection, and pelvic adhesions. In the absence of an obstructing vaginal septum, most patients with uterine didelphys are asymptomatic.

Successful pregnancy is possible in the setting of uterine didelphys, but remains relatively high risk in relation to the normal population. It most commonly occurs unilaterally. Breech presentation is common due to the reduced uterine volume. In addition, the nonpregnant uterus may block the pelvic inlet. For these reasons, cesarean sections are common in these patients.

Differential diagnosis includes bicornuate uterus and separate uterus. In a bicornuate uterus, only the uterine horns are separated and there is communication between them. In a separate uterus, a midline uterine septum is seen.

References

1) Behr SC, Courtier JL, Qayyum A. Imaging of Mullerian duct anomalies. Radiographics. 2012;32:233-50.

2) Dykes TM, et al. Imaging of Congenital Uterine Anomalies: Review and Self-Assessment Module. American Journal of Roentgenology. 2007; 189:S1-S10.

3) Felker EA. Uterus Didelphys and Pregnancy. Journal of Diagnostic Medical Sonograph. 2004; 20:131-133.

An older male with multiple comorbidities presented with nonspecific shortness of breath, found to be in florid heart failure. COVID-19 testing returned positive. Here’s what we are seeing on imaging throughout the admission.

Prior comparison CXR: clear, without significant evidence of underlying lung disease on radiographs. 

Admission CXR: Patchy bilateral airspace opacities with mild consolidation in the right lower lobe. 

CXR 2 days later: florid progression of disease with extensive patchy airspace opacities throughout both lungs. Denser areas of consolidation are also seen more pronounced in the lower lobes. 

CT Chest (same day as above): Progressive ground-glass opacities with dense consolidation in the bilateral lower lobes, suspicious for pneumonia including atypical etiologies such as coronavirus. No pleural effusions.

Follow-up CT Chest (almost 2 weeks after above exam): Progression of extensive ground-glass opacities throughout the lungs with a slight peripheral predominance, as well as progressive dense consolidation of the lower lobes. No pleural effusions.

Clinical Bullet Points

•  Nonspecific clinical presentation delays or precludes diagnosis in many cases.
•  Clinical diagnosis is by RT-PCR, with a known significant false negative rate. New rapid testing is being developed with goals of higher sensitivity.
•  Complications include ARDS, acute cardiac injury, secondary infection (bacterial pneumonia), sepsis, AKI, multiorgan failure.

Imaging Bullet Points:

•  Here’s a summary of what the Fleischner Society consensus published 7 April 2020:
  •  Imaging is not indicated in patients with suspected COVID-19 and mild clinical symptoms
  •  Imaging is indicated in a COVID-19 patient with worsening respiratory symptoms
  •  In the setting of resource limitations, imaging is indicated for medical triage of patients with suspected COVID-19 presenting with moderate-severe clinical features and high pretest probability.
•  Key Imaging features: findings of atypical pneumonia or organizing pneumonia in the setting of clinical suspicion for COVID-19:
  •  Plain Radiograph: airspace opacities (consolidation or ground-glass opacities); bilateral, peripheral, lower lung predominant; pleural effusion is rare.
    •  May be normal in early disease
    •  Findings are most extensive 10-12 days after symptom onset
  •  Chest CT: 
    •  Ground-glass opacities (GGOs) - bilateral, peripheral/subpleural
    •  Crazy paving (GGOs with interlobular septal thickening)
    •  Air space consolidation
    •  Bronchovascular thickening
    •  Traction bronchiectasis
  •  Many asymptomatic patients may have CT abnormalities.

Take home point: Peripheral distribution, predominantly ground-glass opacities without pleural effusions should raise suspicion for COVID-19 in the appropriate clinical setting

This week, we have a younger gentleman with multiple comorbidities. On the supplied image we see hyperenhancement of the liver - specifically in segment IV as well as multiple abnormal collateral vessels throughout the abdominal wall.

Hot quadrate sign refers to a focal area of increased enhancement in the medial segment of the left hepatic lobe (segment IV). This finding is classically due to obstruction of the superior vena cava with portosystemic venous shunting between the SVC and left portal vein (via the internal thoracic and paraumbilical veins). This is contrasted with the Budd-Chiari syndrome which causes hypervascularity of the caudate lobe due to differential venous outflow.

Key point: Identifying the abnormal enhancement in this specific location as well as the collaterals suggests pathology elsewhere (in the SVC).

A middle-aged man came in with hand pain and swelling.

There is nodular soft tissue swelling of several fingers and mild osteoarthritis (joint space narrowing and osteophytosis) of several joins in a distal distribution, favoring DIPs. There are few erosions which are characterized as juxtaarticular erosions, meaning the lucencies are not actually along the join but outside of the synovial covering of the joint space. (See the small arrows.) A few areas of mineralization are seen in the soft tissues as well.

A notable negative is that the MCPs are essentially unaffected.

Diagnosis: Gouty arthritis.

Key takeaways: This case is an example of a bunch of gouty tophi around the joints. The swelling around the joins is classic due to the urate crystal deposits around the joint. These can calcify (see the mineralization around the radial side of the second MCP on the left hand). The urate deposits cause an inflammatory reaction that can result in bone resorption and lytic foci in the juxtaarticular bone. This is not within the synovial joint, hence why we're not seeing joint space destruction.

A middle-aged woman with a palpable abnormality. She noted her skin has been red and tender on her left breast.

Findings: The first image shows the initial evaluation demonstrating a mass in the outer left breast with mild skin thickening. Remaining images are a follow-up diagnostic mammogram workup months after.

This case shows a large irregular mass in the upper-outer left breast (2 o'clock position), with remarkable skin thickening throughout the left breast. There's a trabecular thickening and slightly increased density of the left breast overall.

If you look closely, there's a small calcification associated with the mass as well as a biopsy clip -- a finding that should should raise the radiologist's suspcions for cancer. Other findings include multiple enlarged left axiliar nodes in the LMO projection. US shows a large irregular hypoechoic mass without shadowing.

Diagnosis: Inflammatory breast cancer - a clear case for BIRADS 5.

Inflammatory breast cancer is a diagnosis that requires both tissue biopsy and clinical evidence of inflammatory disease. It is a common occurrence for a middle-aged woman to come in having developed a hot, swollen breast very rapidly, sometimes showing the peau d'orange appearance clinically. This appearance is due to tumor invasion of the skin lymphatics so tissue sparing surgeries are generally not performed. Up to 30% of these cancers are metastatic at presentation. Inflammatory breast cancer itself is considered stage IIIb at presentation due to skin invasion so immediate action is required.

An important distinction: DDX is mastitis clinically. Mastitis is usually related to breast feeding so the patient can be younger. This should be resolved with therapy. Inflammatory breast cancer can also be associated with pregnancy, which is something to look out for.

A 50 year-old female presented to the hospital with shortness of breath. She had a history of breast cancer. A chest X-ray was ordered. 

A PA view of the chest demonstrates the classic findings of left lower lobe atelectasis. The retrocardiac sail sign describes a triangular opacity in the posteromedial aspect of the left lung (shown with the yellow arrow). The flat waist sign describes flattening of the left heart border as is also shown in this example. There is also slight inferior displacement of the left hilum. On this example, the hila are approximately level with eachother whereas the left hilum is normally slightly superior to the right hilum. 

A repeat chest radiograph the following day demonstrates persistent left lower lobe atelectasis with suggestion of an abnormal density within the left mainstem bronchus. CT was recommended for further evaluation. 

The CT showed a 2.6m mass in the left hilar region that completely obstructs the left lower lobe bronchus and results in complete collapse of the left lower lobe. Bronchoscopic biopsy was recommended for further evaluation. 

Diagnosis: The left hilar mass resulting in obstruction of the left lower lobe bronchus. Differential includes primary lung or bronchogenic malignancy, as well as metastasis. Bronchoscopic biopsy in this case confirmed a primary squamous cell carcinoma. 

This case shows typical findings for left lower lobe atelectasis on chest X-ray. It is important to be aware of the radiographic appearance of all types of lobar atelectasis. 

It is also a good example of the satisfaction of search phenomenon. On the second X-ray, it would be easy to call this persistent left lower lobe atelectasis. However, you should always look further for the cause of the lobar collapse as seen in this instance. 

The differential for an endobronchial lesion is broad. In children, central obstruction is most often due to a mucus plug or foreign body. In young adults, a low-grade endobronchial tumor such as carcinoid or adenoma enters the differential. After age 40, bronchogenic carcinoma is a common cause. 

A 30 year-old female presented with epigastric pain and nausea after eating. An epigastric bruit was noted on the physical exam. Ultrasound was ordered to look for abdominal aortic aneurysm.

Findings show, during expiration there is narrowing of the origin of the celiac artery with a fish-hook configuration. 

With inspiration, the celiac artery assumes a more vertical orientation with decreased narrowing at its origin. 

A side-by-sie view demonstrates the difference in orientation of the celiac artery during expiration and inspiration. 

During expiration, there is elevation of the peak systolic velocity of the celiac artery to 297 cm/ sec. There is also focal aliasing at the origin of the celiac artery, indicative of turublent high-velocity flow. 

During inspiration, there is normalization of the peak systolic velocity to 171 cm/ sec and resolution of the focal aliasing at the origin of the celiac artery.

Diagnosis: Median arcuate ligament syndrome

Median arcuate ligament syndrome, also known as celiac artery compression syndrome, is a condition in which the proximal part of the celiac trunk is compressed by the median arcuate ligament of the diaphragm during expiration. This ligament is a fibrous arch that connects the diaphragmatic crura on either side of the aortic hiatus. 

During inspiration, the celiac artery descends in the abdomen and the artery assumes a more vertical orientation, relieving the compression. For this reason, the symptoms associated with MALS are also relieved during standing as the celiac artery descends further in the abdominal cavity on standing. 

On ultrasound, this can be diagnosed when there is narrowing at the origin of the celiac artery (often with a fish-hook orientation) and a peak systolic velocity in the compressed segment of the celiac artery >200 cm/ sec during expiration. There should also be a >3:1 ratio of peak systolic velocity in the celiac artery during expiration compared to the peak systolic velocity in the abdominal aorta immediately below the diaphragm. Normalization of the velocity on inspiration and standing is classic. 

CT is the more common method to diagnose this condition. On CT, you will see proximal celiac stenosis with the classic fish-hook configuration. You may also see post-stenoic dilation and prominent collaterals as seen int he example below obtained from Dr. Mahmoud Yacout Alabd on Radiopaedia.org. 

This is often treated surgically with laparoscopic division of the median arcuate ligament. 

A 70 year-old male reported dysphagia and sensation of food getting stuck at the level of the suprasternal notch. A fluoroscopic esophagram was ordered for further evaluation. 

Frontal and lateral views show a mild posterior and lateral impression on the upper thoracic esophagus at the level of the aortic arch. Note that there is also laryngeal penetration and a small amount of tracheal aspiration in the second picture due to the patient's difficulty swallowing. 

There is also a cricopharyngeal bar at the C5-C6 level causing greater than 50% impression on the posterior cervical esophagus. 

Subsequent CT of the chest demonstrates an aberrant right subclavian artery which courses posterior to the esophagus and causes posterior compression on the esophagus. Note the calcific atherosclerosis at the origin of the aberrant right subclavian artery. 

Diagnosis: Dysphagia lusoria and cricopharyngeal bar

Dysphagia lusoria is impairment in swallowing due to an aberrant right subclavian artery. Fluoroscopy will show an indentation in the posterior wall of the esophagus at the level of the aortic arch. Cross-sectional imaging is necessary to confirm the presence of the aberrant vessel. It is important to note that most patients with an aberrant right subclavian artery do not have symptoms. As in this case, the presence of atherosclerosis or aneurysm in the aberrant artery will often lead to worse symptoms. 

A cricopharyngeal bar will appear on lateral fluoroscopic images as a smooth posterior indentation of the cervical esophagus at the C5-C6 level - which is the level of the cricopharyngeus muscle. It can be idiopathic or related to cricopharyngeus muscle spasm or hypertrophy. It is usually an incidental finding. However, some patients complain of dysphagia. It can result in a Zenker diverticulum so be sure to look for that as well. 

This week, an older gentleman reported progressive shortness of breath. 

What we are seeing in the CXR is the Golden S-sign or S-sign of Golden. Here, the right upper lobe collapse is related to a mass in the hilum. As the right upper lobe collapses, it pulls the minor fissure upwards and the hilar mass impresses on the fissure downwards resulting in the S-shape. 

This is one of the signs residents learn about but don't often see. This, like many radiologic signs, were really important in the days before CT. Radiologists at that time were amazing at plain film interpretation. 

In this case, we have an image of a quick scan through the CT showing the mass and the right upper lung bronchus that's almost collapsed. The presenting X-ray a few months after the CT shows a complete collapse. The other image is the prior X-ray before the right upper lung collapse. 

A man in his 60s with a history of right inguinal hernia repair within the past year is now presenting with several weeks of right testicular pain. 

The echotexture of the right testicle is heterogeneous when compared to the normal homogenous echotexture of the left testicle. The hypoechoic (dark) regions within the testicle represent areas of necrosis. Note also the large complex hydrocele surrounding the necrotic right testicle with multiple septations, which is reactive in the setting of testicular torsion.

Doppler images of the right testicle demonstrate no evidence of arterial or venous blood flow. Absence of blood flow within the testicle is a sign of complete torsion. 

Compare the absent arterial and venous waveforms of the right testicle shown above to this normal arterial waveform in the left testicle. Note the arterial waveforms with sharp systolic upstrokes -- a normal finding.

The cine clip shown above shows the classic "whirlpool sign" of twisting of the right spermatic cord including the vascular pedicle. 

Diagnosis: Testicular Torsion with Necrosis

This is a classic case of complete testicular torsion with necrosis. This occurs when the spermatic cord and vascular pedicle twist and cut off blood supply to the testicle. Initially, the twisting is less than 360 degrees and only obstructs the venous outflow (incomplete torsion). Over time, as the twisting becomes greater than 360 degrees, the arterial inflow is also obstructed (complete torsion) and the testicular necrosis occurs. 

These patients usually present with acute testicular pain. Early diagnosis is important so that the testicle can be salvaged before testicular necrosis or infarction occurs. The time between onset of pain and detorsion is directly related to testicular salvage with nearly 100% salvage if the detorsion occurs within six hours. Only 20% salvage is expected if there is a delay of 12-24 hours. Treatment involves orchiectomy in order to prevent subsequent infection of the necrosed testicle. 

A review of the typical ultrasound findings, many of which are shown above: 

• Twisting of the spermatic cord or "whirlpool sign" (the most sensitive and specific finding)
• Absence of blood flow in complete torsion; elevated resistive indices or to-and-fro flow in incomplete torsion
• Homogenous texture early on before necrosis occurs; heterogeneous echotexture with areas of necrosis in late presentations
• Reactive hydrocele
• Reactive thickening of scrotal skin

A male in his 60s presents to the Emergency Department with acute onset of slurred speech. Stroke code was activated.

Findings show a large, mixed attenuation subdural hematoma overlying the left frontoparietal cerebral convexity with hyperdense (bright) components with acute blood products.

The large subdural collection results in significant effect with effacement/ flattening of the underlying cerebral gyri and 1.4 cm of left-to-right midline shift at the level of the septum pellucidum. The coronal image above nicely demonstrates subfalcine herniation and the axial image demonstrates mild effacement of the left aspect of the suprasellar cistern, indicative of developing uncal herniation.

There is also effacement of the atrium of the left lateral ventricle (shown on the left) and asymmetric dilatation of the temporal horn of the left lateral ventricle (shown on the right). These findings are related to ventricular trapping from mass effect by the large subdural collection.

Due to the significant mass effect and developing herniation, the patient underwent emergent craniotomy for decompression. On the left, you can see the postsurgical changes including a subdural drain that was left in place for drainage of the large hematoma. On the right, you can see the significantly decreased mass effect after surgery including decreased midline shift and decreased effacement of the atrium of the left lateral ventricle.

Diagnosis: Subdural hematoma requiring emergent decompressive craniotomy

Subdural hematomas are collections of blood located between the dura and arachnoid mater. They occur from tearing of the bridging cortical veins as they cross the subdural space before draining into a dural venous sinus. They are often crescent-shaped and are not limited by cranial sutures, which is why the subdural collection in this case extends across nearly the entirety of the left cerebral convexity.

This is in opposition to epidural hematomas, which are often secondary to tearing of the middle meningal artery in the presence of a skull fracture. They appear lens-shaped and are limited by cranial sutures.

On CT, the appearance of the subdural hematoma changes with time. In the first hour (hyperacute stage), the collection often has a swirling appearance due to mixing of clot and ongoing unclotted blood. In the acute stage, they key imaging feature is hyperdense (bright) blood as seen in our case here. In rare cases, acute SDH can appear isodense to the brain due to anticoagulation/ coagulopathy or severe anemia. In the subacute phase (3-21 days), the collection becomes isodense to the underlying cortex. In the chronic phase (beyond 3 weeks), the collection becomes hypodense (dark) relative to the cortex. An acute-on-chronic SDH will often appear with a hematocrit level, with a hyperdense component layering posteriorly.

Treatment depends on the degree of mass effect. Small subdural collections are often managed with serial CT scans to exclude enlargement. Symptomatic cases with a large amount of mass effect, as seen in our case, require surgery to evacuate the collection.

A patient presented at the hospital after experiencing a few hours of left-sided weakness following trauma. 

The initial non-contrast CT was mostly unremarkable without any bleed or big infarct visible on CT. What can be seen adjacent to the suprasellar cistern is a hyperdense curvilinear structure in the region where one would normally expect the M1 segment of the right MCA. Typically, these vessels can be visualized on a few slices on noncontrast CT but the appearance here is far more dense. 

This finding should raise suspicions for an obstructing thrombus in the vessel - the so-called "hyperdense MCA sign." Oftentimes, clinicians reviewing imaging will think they see a dense MCA but it's usually just an artifact. If the appearance is for hyperdense MCA - if the clinical picture fits and if the patient is within the window for treatment - vascular imaging is a must. 

Here, we got a CTA which shows complete occlusion of the distal M1 segment of the right MCA in the same region as the hyperdense MCA. This finding confirms our suspicion that the patient was taken for mechanical thrombectomy. 

Also shown was complete occlusion of the internal carotid artery on the same side due to a bad acute dissection. 

The following MRI shows a large right MCA territory infarct with increased signal on DWI and corresponding low ADC signal (diffusion-restriction). A tiny infarct in the left frontal lobe suggests this is all related to showering emboli from the ICA dissection. 

Follow-up vascular imaging post-thrombectomy shows reconstitution of the right ICA AND MCA. 

The hyperdense MCA sign is the earliest visible sign of MCA infarction - seen within 90 minutes after the event. The sensitivity is very low, however, at 30%, the absence of this sign doesn't rule out pathology. 

The finding is, as it sounds, just hyperdensity of the MCA relative to the other side and basilar artery. Be careful not to overcall this on just thick axial slices as there can be asymmetry. Use thin-section CT and multiplanar reformats to confirm in addition to vascular imaging. 

References:

Chayhan GB, Shroff MM. Twenty classic signs in neuroradiology: A pictoral essay. Indian J Radiol Imaging. 19 (2): 135-45. doi: 10.4103/0971-3026.50835

Tomsick T, Brott W, Broderick J, Haley EC, Spilker J, Khoury J. Prognostic value of the hyperdense middle cerebral artery sign and stroke scale score before ultraearly thrombolytic therapy. (1996) AJNR. American journal of neuroradiology. 17 (1): 79-85. 

A female in her 40s presented at the Emergency Department with acute-on-chronic abdominal pain and diarrhea. CT abdomen and pelvis was ordered. 

The pictures above show a long segment of markedly thickened, inflamed bowel most prominently involving the mid-distal and terminal ileum. There is associated mucosal hyperenhancement of the thickened bowel loops. Some of the involved bowel loops show mural stratification with low attenuation of the thickened wall relating to submucosal edema juxtaposed with mucosal hyperenhancement. 

Multiple strictures with areas of focal luminal narrowing and interposing regions of relative dilation are seen throughout the involved bowel segments, representing sites of fibrosis from prior bouts of active inflammation. 

The picture above shows a pseudosacculation or pseudodiverticulum, which is a broad outpouching of normal bowel wall along the anti-mesenteric side, secondary to retraction / scarring of the opposite bowel wall from chronic ulcers. 

The involved bowel segments demonstrate intramural fat deposition, shown as thin, hypodense (fat density) layers within the bowel wall. This is known as "fat halo" sign. 

In addition to the bowel findings described above, this patient also has engorgement of the vasa recta ("comb sign") and mesenteric hyperemia. 

The picture above shows fibrofatty proliferation of the mesenteric fat ("creeping fat") along the mesenteric border of the involved bowel segments. 

Diagnosis: Active Crohn-related bowel inflammation

Teaching points:

Crohn disease is an idiopathic chronic granulomatous inflammatory bowel disease. It is most common in young adults, and often presents wtih abdominal pain and diarrhea. 

Characteristic features include:

• Discontinuous involvement of the entire gastrointestinal tract from mouth to anus ("skip lesions")
• Usually involves the small bowel, and almost always involves the terminal ileum
• When involving the stomach, it favors the gastric antrum
• When involving the colon, it favors the right side / ascending colon and often spares the rectosigmoid colon
• Forms strictures secondary to chronic fibrotic change (marked narrowing at the terminal ileum / ileocecal valve, often termed "string sign")
• Transmural inflammation with linear longitudinal and circumferential ulcers extending deep into bowel wall lead to formation of fistulae
• Mesenteric abscess formation
• Perianal abscesses and fistulae
• Increased risk of small bowel and colonic adenocarcinoma and lymphoma, preferentially involving the distal and terminal ileum

Many of the most standard CT findings are shown above. CT findings indicative of active Crohn inflammation include:

• Bowel wall thickening
• Mucosal hyperenhancement
• Mural stratification: juxtaposition of mucosal hyperenhancement with hypodense submucosal edema in the thickened bowel wall
• Engorgement of the vasa recta ("comb sign") and mesenteric hyperemia

CT findings of chronic Crohn disease include:

• Intramural fat deposition: This is a nonspecific finding. In patients with acute symptoms and preferential involvement of the terminal ileum, it may be related to Crohn disease. If preferentially involving the duodenum and proximal jejunum, it may relate to celiac disease. However, in a patient without a history of inflammatory bowel disease, it is most often related to obesity. 
• Strictures representing sites of fibrosis from prior bouts of active inflammation. These strictures can lead to true bowel obstructions.
• Fibrofatty proliferation of mesenteric fat along mesenteric border of involved bowel segments ("creeping fat")
• Pseudosacculation / pseudodiverticulum on anti-mesenteric border of bowel wall secondary to scarring of opposite bowel wall from chronic ulcers
• Abscesses and fistulae

Extraintestinal features of Crohn disease include: gallstones, hepatic abscesses, pancreatitis, sacroiliitis, erythema nodosum, uveitis, oxalate renal stones, and many more. 

Treatment includes medical management with steroids and immunomodulating agents. Surgery is often necessary in cases with strictures, bowel obstructions, fistulae, and perianal disease. 

References:

1. Raman SP, Horton KM, Fishman EK. Computed tomography of Crohn's disease: The role of three dimensional technique. World J Radiol, 2013; 5(5):193-201. doi:10.4329/wir.v5.i5.193
2. Furukawa A, Saotome T, Yamasaki M et al. Cross-sectional imaging in Crohn disease. Radiographics 2004;24(3):689-702.
3. Gore RM, Balthazar EJ, Ghahremani GG et al. CT features of ulcerative colitis and Crohn's disease. AJR Am J Roengenol. 1996;167 (1):3-15.
4. Lee SS, Kim AY, Yang SK et al. Crohn disease of the small bowel: comparison of CT enterography, MR enterography, and small-bowel follow-through as diagnostic techniques. Radiology. 2009;251 (3): 751-61.

A man in his 60s presented at the Emergency Department with right upper quadrant pain and leukocytosis. Right upper quadrant ultrasound was obtained followed by a CT abdomen and pelvis. 

The green arrows point to echogenic foci within the gallbladder lumen with associated posterior acoustic shadowing compatible with cholelithiasis. The yellow arrows point to a markedly thickened and edematous gallbladder wall with associated gallbladder wall hyperemia (increased flow on color Doppler images). In addition, there is pericholecystic fluid and the patient reported severe abdominal pain from pressure of the ultrasound probe over the gallbladder (positive sonic Murphy sign). 

The ultrasound study also shows a focus of gallbladder wall discontinuity with a complex fluid collection between the gallbladder and liver. CT was recommended for further evaluation.

CT redemonstrates a markedly thickened gallbladder wall with pericholecystic free fluid and surrounding fat stranding (green arrows). There is focal discontinuity of the gallbladder wall with a complex fluid collection in the subhepatic space between the liver and gallbladder (yellow arrows).

Diagnosis: Acute cholecystitis with type 2 gallbladder perforation and subhepatic abscess formation

Gallbladder perforation is a severe complication of acute cholecystitis that occurs in less than 5% of cases but increase morbidity and mortality. It tends to occur in elderly patients or patients with underlying chronic medical conditions. It presents with right upper quadrant pain. 

Acute cholecystitis is most often caused by a gallstone obstructing the cystic duct, which leads to retention of secretions within the gallbladder and resultant gallbladder distention. Eventually, the intraluminal pressure exceeds the arterial perfusion pressure and obstructs venous drainage causing ischemia / necrosis of the gallbladder wall with subsequent perforation. The gallbladder fundus is the most common site of perforation as it receives the terminal blood supply. Perforation can also occur in the setting of trauma. 

Perforation can occur between two days to several weeks after the onset of acute cholecystitis. There are four types of perforation according to the Neimeier classification:

• Type 1: Acute free perforation of the gallbladder with generalized peritonitis
• Type 2: Subacute perforation of the gallbladder with localized pericholecystic abscess and phlegmon (the most common type)
• Type 3: Chronic perforation of the gallbladder with choecystoenteric fistula formation
• Type 4: Perforation into the biliary tree with cholecystobiliary fistula formation

Additional complications include intraperitoneal free air, bile leak, hepatic abscess (via direct extension or hematogenous dissemination), and small bowel obstruction among others. 

Treatment includes cholecystectomy and abscess drainage with or without preceding percutaneous cholecystostomy tube placement to relieve the infection and inflammation prior to surgery. Additional procedures such as fistula repair may be necessary. 

References: 

1. Anderson BB, Nazem A. Perforations of the gallbladder and cholecystobiliary fistulae: a review of management and a new classification. J Natl Med Assoc. 1987; 79(4): 393-9.
2. Derici H, Kara C, Bozdag AD et-al. Diagnosis and treatment of gallbladder perforation. World J. Gastroenterol. 2006;12 (48): 7832-6.
3. Patel NB, Aytekin O, Thomas S. Multidetector CT of emergent biliary pathologic conditions. Radiographics. 2013;33:1867-88.
4. Madrazo BL, Francis I, Hricak H, Sandler MA, Hudak S, Gitschlag K. Sonographic findings in perforation of gallbladder. AJR Am J Roentgenol 1982;139(3):491-496.