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- Intracranial Metastatic Melanoma
76 yo M acute right side weakness • Xray of the Week Figure 1. What is the diagnosis? Figure 2. A. T1 weighted image. Note the hyperintense nodules and masses with surrounding edema (red arrows). There is mass effect with narrowing of the left lateral ventricle and third ventricle, as well as rightward midline shift. B. T1 weighted image with contrast. Hyperintense nodules and masses with surrounding edema which also demonstrate contrast enhancement (yellow arrows) and large hemorrhagic lesion in left frontal lobe (green arrow) with hematocrit level compatible with hemorrhage. C. FLAIR image showing large hemorrhagic lesion in left frontal lobe with hematocrit level (green arrow). Discussion: Epidemiology Melanoma is the third most common source of brain metastasis overall, following lung and breast cancer. However, it carries the highest relative propensity among all primary systemic malignancies to metastasize to the central nervous system (CNS) [1,2]. Approximately 20% of patients with advanced metastatic melanoma will demonstrate intracranial involvement at the time of their initial diagnosis. Furthermore, as systemic disease progresses, greater than 50% of patients will eventually develop brain metastases [1,2]. The incidence of diagnosed brain metastases has grown in recent years, largely reflecting both improved neuroimaging techniques and prolonged patient survival due to advances in systemic therapies [2]. Clinical Findings Patients with intracranial metastatic melanoma frequently present with clinical symptoms indicative of elevated intracranial pressure, focal cortical irritation, or mass effect. Common presenting symptoms include persistent headaches, new-onset seizures, cognitive decline, or acute focal neurological deficits. In this case, a 76-year-old male presented with acute right-sided weakness. Melanoma brain metastases are characterized by profound tumor neovascularization and a direct tendency to invade regional blood vessels, making them highly susceptible to spontaneous hemorrhage. Consequently, many patients present acutely following a sudden intralesional hemorrhagic event, mimicking the presentation of a stroke. Pathology Malignant melanoma is an aggressive neoplasm of melanocytes, which are specialized pigment-producing cells derived from the neural crest [1]. Based on their histopathologic melanin content, intracranial melanoma metastases can be broadly classified as either melanotic (containing greater than 10% melanin-containing cells) or amelanotic (containing fewer than 10% melanin-containing cells) [3]. The unique magnetic resonance (MR) signal characteristics of melanoma are driven largely by melanin and the presence of intralesional hemorrhage [3,4]. Melanin pigment possesses stable free radicals, such as semiquinones, which exert strong paramagnetic effects. These free radicals interact with surrounding protons to alter relaxation times. In addition, melanin acts as a natural chelating agent, binding paramagnetic metal ions such as iron, copper, and zinc [3-6]. The collective result of these paramagnetic interactions is a pronounced, intrinsic shortening of both T1 and T2 relaxation times [3-6]. Radiographic Features Magnetic resonance imaging (MRI) is the gold standard diagnostic modality for the initial evaluation and longitudinal follow-up of suspected intracranial metastatic disease. Most primary and metastatic intracranial tumors exhibit low signal intensity on T1-weighted images. However, melanotic melanoma uniquely demonstrates intrinsic high signal intensity on T1-weighted sequences and relative low signal intensity on T2-weighted sequences when compared to the normal cerebral cortex [3,5]. This distinctive signature is due to the aforementioned paramagnetic effects of melanin. Conversely, amelanotic melanoma lacks sufficient melanin to inherently shorten the T1 relaxation time. In the absence of hemorrhage, amelanotic lesions behave much like typical brain metastases, demonstrating T1 isointensity or hypointensity and T2 hyperintensity [3]. However, neuroimaging interpretation is frequently complicated by the high incidence of intratumoral hemorrhage [4,5]. As seen in the provided case, the presence of subacute hemorrhage results in the accumulation of methemoglobin. Because methemoglobin is also strongly paramagnetic, it inherently shortens T1 relaxation times, producing prominent T1 hyperintensity regardless of the underlying melanin concentration [4-7]. Thus, a purely amelanotic metastasis may still appear diffusely T1 hyperintense if there has been a recent bleed. In the provided case images, there are multiple intra-axial nodules and masses demonstrating intrinsic T1 hyperintensity with abundant surrounding vasogenic edema. Following the administration of gadolinium-based contrast, these lesions exhibit robust enhancement, which can present in a nodular, ring-like, or heterogeneous pattern (Figs. 1-2 ). A prominent, large mass in the left frontal lobe demonstrates a hematocrit fluid-fluid level on the FLAIR and contrast-enhanced images, which is a hallmark radiologic sign of intralesional hemorrhage. The resultant mass effect causes narrowing of the left lateral and third ventricles alongside a rightward midline shift (Figs. 1-2 ). On non-contrast computed tomography (CT), melanoma metastases are often hyperdense relative to the adjacent cortex. This hyperattenuation can be attributed to high cellularity, dense melanin content, or the presence of acute blood products. Susceptibility-weighted imaging (SWI) or T2* gradient-echo sequences are exquisitely sensitive for melanoma, typically revealing profound signal dropout or blooming artifact due to the dense concentration of paramagnetic melanin and blood degradation products [4]. Treatment and Prognosis Historically, the prognosis for patients with intracranial metastatic melanoma was exceptionally grim, with a median overall survival of less than six months [2]. However, the treatment paradigm has shifted radically in the modern era with the advent of targeted therapies (such as BRAF and MEK inhibitors for patients harboring BRAF V600 mutations) and immune checkpoint inhibitors (such as anti-PD-1 and anti-CTLA-4 antibodies) [2]. Current management requires a tailored, multidisciplinary approach. For patients presenting with large, highly symptomatic lesions causing significant mass effect or impending herniation (such as the large hemorrhagic left frontal mass seen in this patient), prompt surgical resection is often pursued to relieve intracranial pressure and stabilize the patient [7-10]. For patients with a limited number of smaller, asymptomatic metastases, stereotactic radiosurgery (SRS) has largely replaced whole-brain radiation therapy (WBRT). SRS offers excellent local control while limiting radiation-induced neurocognitive decline. The integration of localized SRS with modern systemic immunotherapy has synergistically improved outcomes, leading to durable intracranial responses and extending overall survival from months to several years for many patients [2]. Conclusion Intracranial metastatic melanoma is a clinically devastating manifestation of advanced disease that frequently presents with spontaneous intralesional hemorrhage. The distinctive radiologic signature of these lesions—specifically, intrinsic T1 hyperintensity and T2 hypointensity—is driven by the potent paramagnetic properties of melanin or concurrent subacute hemorrhage. Familiarity with these characteristic imaging features and their pathophysiological basis is essential for radiologists to accurately narrow the differential diagnosis and optimally guide multidisciplinary neuro-oncologic management.. References: Patnana M, et al. Multimethod Imaging, Staging, and Spectrum of Manifestations of Metastatic Melanoma. Clinical Radiology, vol. 66, no. 3, Mar. 2011, pp. 224–36. doi:10.1016/j.crad.2010.10.014 PubMed: https://pubmed.ncbi.nlm.nih.gov/21295201/ Vosoughi Elham, et al. Survival and Clinical Outcomes of Patients with Melanoma Brain Metastasis in the Era of Checkpoint Inhibitors and Targeted Therapies. BMC Cancer, vol. 18, no. 1, Apr. 2018, p. 490. BioMed Central, doi:10.1186/s12885-018-4374-x PubMed: https://pubmed.ncbi.nlm.nih.gov/29703180/ Isiklar I, et al. Intracranial Metastatic Melanoma: Correlation between MR Imaging Characteristics and Melanin Content. American Journal of Roentgenology, vol. 165, no. 6, Dec. 1995, pp. 1503–12. doi:10.2214/ajr.165.6.7484597 PubMed: https://pubmed.ncbi.nlm.nih.gov/7484597/ Cakirer S, et al. Spontaneously T1-Hyperintense Lesions of the Brain on MRI: A Pictorial Review. Current Problems in Diagnostic Radiology, vol. 32, no. 5, Oct. 2003, pp. 194–217. doi:10.1016/s0363-0188(03)00026-4 PubMed: https://pubmed.ncbi.nlm.nih.gov/12963867/ Zimny A, et al. Intracranial Lesions with High Signal Intensity on T1-Weighted MR Images – Review of Pathologies. Polish Journal of Radiology, vol. 78, no. 4, 2013, pp. 36–46. PubMed: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3908506/ Ma, Mian, et al. Neurocutaneous Melanosis in an Adult Patient with Intracranial Primary Malignant Melanoma: Case Report and Review of the Literature. World Neurosurgery, vol. 114, June 2018, pp. 76–83. ScienceDirect. doi:10.1016/j.wneu.2018.02.007 Goulart CR, et al. Cerebral Melanoma Metastases: A Critical Review on Diagnostic Methods and Therapeutic Options. ISRN Surgery, vol. 2011, 2011. doi:10.5402/2011/276908 Ma YF, et al. Intracranial Malignant Melanoma: A Report of 7 Cases. Oncology Letters, vol. 10, no. 4, Oct. 2015, pp. 2171–75. PubMed Central, doi:10.3892/ol.2015.3537 Goyal S, et al. The Clinical Management of Multiple Melanoma Brain Metastases: A Systematic Review. JAMA Oncology, vol. 1, no. 5, Aug. 2015, pp. 668–76. doi:10.1001/jamaoncol.2015.1206 Ginat DT, Meyers SP. Intracranial Lesions with High Signal Intensity on T1-weighted MR Images: Differential Diagnosis. RadioGraphics. 2012;32(2):499-516. doi:10.1148/rg.322105761. PubMed: https://pubmed.ncbi.nlm.nih.gov/22411945/ Updated: 08/25/2024: Amara Ahmed is a Radiology Resident at The University of Florida. https://residency.xray.ufl.edu/residents/class-of-2028/ She did her medical school at the Florida State University College of Medicine. She serves on the executive board of the American Medical Women’s Association and Humanities and Medicine. She is also an editor of HEAL: Humanism Evolving through Arts and Literature, a creative arts journal at the medical school. Prior to attending medical school, she graduated summa cum laude from the Honors Medical Scholars program at Florida State University where she completed her undergraduate studies in exercise physiology, biology, and chemistry. In her free time, she enjoys reading, writing, and spending time with family and friends. Follow Amara Ahmed on Twitter @Amara_S98 All posts by Amara Ahmed Kevin M. Rice, MD is the president of Global Radiology CME Dr. Rice is a radiologist with Renaissance Imaging Medical Associates and is currently the Vice Chief of Staff at Valley Presbyterian Hospital in Los Angeles, California. Dr. Rice has made several media appearances as part of his ongoing commitment to public education. Dr. Rice's passion for state of the art radiology and teaching includes acting as a guest lecturer at UCLA. In 2015, Dr. Rice and Natalie Rice founded Global Radiology CME to provide innovative radiology education at exciting international destinations, with the world's foremost authorities in their field. In 2016, Dr. Rice was nominated and became a semifinalist for a "Minnie" Award for the Most Effective Radiology Educator. Follow Dr. Rice on Twitter @KevinRiceMD All posts by Kevin M. Rice, MD
- Emphysematous Pyelonephritis
90 yo F with UTI. Diagnosis? • Xray of the Week Figure 1. Non-contrast CT abdomen & pelvis of a 90-year-old female. Figure 2. Figure 1: Non-contrast CT abdomen & pelvis of a 90-year-old female with a UTI demonstrating emphysematous pyelonephritis and a renal stone within the renal pelvis. A. Coronal non-contrast CT of abdomen & pelvis showing gas (green arrow) and renal stone (red) within the renal pelvis. B. Axial non-contrast CT of abdomen & pelvis showing gas (green arrow) and renal stone (red arrow) within the renal pelvis. C. Axial non-contrast CT of abdomen & pelvis showing gas within the bladder (orange arrow). Discussion: Emphysematous pyelonephritis (EPN) is a necrotizing infection that leads to gas formation within the renal parenchyma, collecting system, and/or perinephric areas. It is commonly seen in patients with uncontrolled diabetes, urinary tract obstruction or urinary stones, or immunocompromised state. Female patients have an increased risk of developing EPN due to higher incidence of UTIs caused by Escherichia coli, Klebsiella pneumonia, and Proteus mirabilis [1]. Like pyelonephritis, patients with EPN often present with fever, abdominal or flank pain, and costovertebral angle tenderness. Urinalysis may show pyuria, leukocytosis, nitrites, hematuria, WBC casts; however, imaging is required to confirm the diagnosis [2,3,4]. CT abdomen and pelvis is the gold standard for confirming EPN [5]. Radiographic Features Diagnostic imaging is mandatory for confirming EPN and dictating patient management. Computed Tomography (CT): Non-contrast CT is the gold standard imaging modality. It accurately confirms the presence of gas, delineates its anatomic extent, and identifies any underlying urolithiasis or obstruction [4, 5]. Infected kidneys typically appear enlarged, heterogeneous, and are embedded with characteristic low-attenuation areas of gas within the parenchyma, the collecting system, or extrarenal spaces [3]. Ultrasound: Findings include an enlarged kidney containing highly echogenic foci associated with posterior "dirty" acoustic shadowing or ring-down artifact, indicating gas bubbles. However, ultrasound can be limited by overlying bowel gas, and intraparenchymal gas may be easily mistaken for staghorn calculi [5]. Plain Radiographs: An abdominal radiograph may reveal mottled, streaky, or crescentic radiolucent gas overlying the renal fossa. However, this is an insensitive method, visible in only about 30% of cases [5]. The most comprehensive classification system used to categorize EPN is developed by Huang and Tseng (Table 1) and best correlates with management [4]. Classification of Emphysematous Pyelonephritis Class 1: Gas accumulation in the renal pelvis Class 2: Gas accumulation in the renal parenchyma Class 3A: Gas extension into the perinephric space Class 3B: Gas extension into the pararenal space Class 4: Gas in solitary or bilateral kidneys Table 1: Classification of Emphysematous Pyelonephritis. [4] It is likely that the 90-year-old female patient shown in Figure 1 had a complication of EPN due to a UTI and a renal stone causing an obstruction at the renal pelvis. The urinary organisms thrive in an immunocompromised host and lead to a rapid progression from a UTI to EPN [4]. Bacteria within the urinary tract can ferment glucose and albumin and produce H2 and CO2 gas seen in Figure 1 (green and orange arrows) [6]. This case is classified as Class 1 EPN because the gas accumulation is restricted to the renal pelvis and complicated by a renal stone. This can be managed with antibiotics, percutaneous catheter drainage (PCD), fluid, electrolyte, and glucose control (Fig. 4) [4,9]. Figure 4. The flowchart for management of emphysematous pyelonephritis (EPN) according to the clinicoradiological classification. Asterisk indicates the presence of 2 or more of the following risk factors: thrombocytopenia, acute renal failure, disturbance of consciousness, and shock. KUB indicates kidneys, ureter, and bladder (plain abdominal radiograph); CT, computed tomography; and PCD, percutaneous catheter drainage. From: Emphysematous Pyelonephritis: Clinicoradiological Classification, Management, Prognosis, and Pathogenesis Arch Intern Med. 2000;160(6):797-805. doi:10.1001/archinte.160.6.797 Copyright © 2000 American Medical Association. All rights reserved. Date of download: 7/25/2021 EPN is a life-threatening condition that warrants an immediate treatment. Most common cause of death in EPN is caused by urosepsis and has a mortality rate of 19-75% [7, 8,9]. In severe cases or patients who do not respond to PCD, treatment with nephrectomy can lead to clinical and radiological improvement (Fig. 4) [4]. References: Ubee SS, McGlynn L, Fordham M. Emphysematous pyelonephritis. BJU Int. 2011;107(9):1474-1478. doi:10.1111/j.1464-410X.2010.09660.x Kuo CY, Lin CY, Chen TC, et al. Clinical features and prognostic factors of emphysematous urinary tract infection. J Microbiol Immunol Infect. 2009;42(5):393-400. https://pubmed.ncbi.nlm.nih.gov/20182668/ Wan YL, Lee TY, Bullard MJ, Tsai CC. Acute gas-producing bacterial renal infection: correlation between imaging findings and clinical outcome. Radiology. 1996;198(2):433-438. doi:10.1148/radiology.198.2.8596845 Huang JJ, Tseng CC. Emphysematous pyelonephritis: clinicoradiological classification, management, prognosis, and pathogenesis. Arch Intern Med. 2000;160(6):797-805. doi:10.1001/archinte.160.6.797 Craig WD, Wagner BJ, Travis MD. Pyelonephritis: Radiologic-Pathologic Review. RadioGraphics. 2008; 28:255-276. https://doi.org/10.1148/rg.281075171 Dhingra KR. A Case of Complicated Urinary Tract Infection: Klebsiella pneumoniae Emphysematous Cystitis Presenting as Abdominal Pain in the Emergency Department. West J Emerg Med. 2008;9(3):171-173. https://pubmed.ncbi.nlm.nih.gov/19561737/ Huang JJ, Chen KW, Ruaan MK. Mixed acid fermentation of glucose as a mechanism of emphysematous urinary tract infection. J Urol. 1991;146(1):148-151. doi:10.1016/s0022-5347(17)37736-4 Michaeli J, Mogle P, Perlberg S, Heiman S, Caine M. Emphysematous pyelonephritis. J Urol. 1984;131(2):203-208. doi:10.1016/s0022-5347(17)50309-2 Sherchan R, Hamill R. Emphysematous Pyelonephritis. In: StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing; 2024. Available at: https://pubmed.ncbi.nlm.nih.gov/38261674/ Mounica Chidurala is a medical student at Marian University College of Osteopathic Medicine in Indianapolis, IN. Prior to medical school, she graduated from Oklahoma State University with a Bachelor of Science degree in Chemical Engineering, minor in Chemistry, and an Honors College Degree. She also obtained her Master of Science degree in Chemical Engineering from the University of Oklahoma where she defended her master’s thesis in biofuels and heterogeneous catalysis. She is excited to pursue a career in Diagnostic Radiology with interests in Interventional Radiology or Nuclear Medicine. She is passionate about research and innovation in medicine and hopes to teach/mentor students in the future. UPDATE: June 2023 Mounica Chidurala is a Radiology Resident at Indiana University School of Medicine. Follow Mounica Chidurala on Twitter @mchidurala227 and Linkedin All posts by Mounica Chidurala Kevin M. Rice, MD is the president of Global Radiology CME Dr. Rice is a radiologist with Renaissance Imaging Medical Associates and is currently the Vice Chief of Staff at Valley Presbyterian Hospital in Los Angeles, California. Dr. Rice has made several media appearances as part of his ongoing commitment to public education. Dr. Rice's passion for state of the art radiology and teaching includes acting as a guest lecturer at UCLA. In 2015, Dr. Rice and Natalie Rice founded Global Radiology CME to provide innovative radiology education at exciting international destinations, with the world's foremost authorities in their field. In 2016, Dr. Rice was nominated and became a semifinalist for a "Minnie" Award for the Most Effective Radiology Educator. Follow Dr. Rice on Twitter @KevinRiceMD and Linkedin All posts by Kevin M. Rice, MD
- Anterior Shoulder Dislocation and Hill-Sachs Defect
Trauma. Left shoulder pain. Diagnosis? • Radiology Case of the Week Figure 1. Left shoulder radiographs. Frontal (A) and scapular Y view (B). Trauma. Left shoulder pain. Diagnosis? Eponym? Figure 2. Left shoulder radiographs. Frontal (A) and scapular Y view (B). Anterior dislocation with the humeral head anterior to the glenoid (yellow arrows). Also note the fracture of the superolateral humeral head (red arrows) indicating a Hill-Sachs defect. Figure 3. Left shoulder frontal radiograph. Anterior dislocation has been reduced so the humeral head is now within the glenoid (yellow arrows). Also note the impaction fracture of the superolateral humeral head (red arrows) indicating a Hill-Sachs Defect. Epidemiology A Hill-Sachs defect is an impaction fracture of the posterolateral humeral head, first described by Hill and Sachs in 1940 [1]. It is very common after anterior glenohumeral dislocation: it is present in about 7 in 10 patients after a first dislocation and in more than 8 in 10 after recurrent dislocation [2,3]. In published series, most patients are young men [4]. Clinical Findings The presence of the Hill-Sachs defect indicates that a complete anterior glenohumeral dislocation has occurred, even if the joint has since been reduced [4,5]. A large humeral head defect can engage the anterior glenoid rim, causing apprehension, popping or catching, and recurrent instability [6]. Pathology During anterior dislocation, the posterolateral humeral head is driven against the anteroinferior glenoid rim, producing a compression (impaction) fracture of the articular surface and underlying subchondral bone. The larger the humeral head defect, and the greater the associated glenoid bone loss, the more likely the defect is to engage the glenoid rim and cause recurrent dislocation [7,8]. Radiographic Features Radiographs are the first-line study. The lesion appears as a groove-like impaction defect of the superolateral humeral head and is best seen on the AP view in internal rotation. The Stryker notch view demonstrated the defect in 25 of 27 shoulders in one study, compared with 7 of 27 on a standard frontal view, so additional views are recommended when the lesion is suspected. CT best defines the size of the defect. In this case, Figure 2 shows anterior dislocation of the humeral head, which is displaced from the glenoid fossa and the defect of the superolateral humeral head. Post-reduction images (Fig. 3) often show the Hill-Sachs defect to better advantage. Treatment and Prognosis Management depends on the size of the humeral head defect and whether it engages the glenoid rim. Engaging Hill-Sachs lesions are an important cause of failure of arthroscopic Bankart repair and should be identified preoperatively, Rowe recommended surgical management of severe lesions [5,6]. One option is remplissage, in which the infraspinatus tendon and posterior capsule are fixed into the defect. Because prevalence rises with recurrent dislocation, early stabilization after a first dislocation has been suggested when the lesion is present. Conclusion A Hill-Sachs lesion is an impaction fracture of the posterolateral humeral head that marks a previous anterior glenohumeral dislocation. It is common, especially after recurrent dislocation. Radiographs usually demonstrate it, CT defines its size, and large engaging lesions may require surgical treatment. References: Ors A, Colak T, Buyukmurat N, Erdemir C, Kibar B. Relationship between Hill-Sachs lesions and morphometry of glenoid, acromion and coracoid process. North Clin Istanb. 2025;12(6):667-673. Published 2025 Dec 10. DOI: 10.14744/nci.2025.51447 Calandra JJ, Baker CL, Uribe J. The incidence of Hill-Sachs lesions in initial anterior shoulder dislocations. Arthroscopy. 1989;5(4):254-257. DOI: 10.1016/0749-8063(89)90138-2 Rutgers C, Verweij LPE, Priester-Vink S, van Deurzen DFP, Maas M, van den Bekerom MPJ. Recurrence in traumatic anterior shoulder dislocations increases the prevalence of Hill-Sachs and Bankart lesions: a systematic review and meta-analysis. Knee Surg Sports Traumatol Arthrosc. 2022;30(6):2130-2140. DOI: 10.1007/s00167-021-06847-7 Rozing PM, de Bakker HM, Obermann WR. Radiographic views in recurrent anterior shoulder dislocation. Comparison of six methods for identification of typical lesions. Acta Orthop Scand. 1986;57(4):328-330. DOI: 10.3109/17453678608994403 Rowe CR, Patel D, Southmayd WW. The Bankart procedure: a long-term end-result study. J Bone Joint Surg Am. 1978;60(1):1-16. https://pubmed.ncbi.nlm.nih.gov/624747/ Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677-694. DOI: 10.1053/jars.2000.17715 Yamamoto N, Itoi E, Abe H, et al. Contact between the glenoid and the humeral head in abduction, external rotation, and horizontal extension: a new concept of glenoid track. J Shoulder Elbow Surg. 2007;16(5):649-656. DOI: 10.1016/j.jse.2006.12.012 Di Giacomo G, Itoi E, Burkhart SS. Evolving concept of bipolar bone loss and the Hill Sachs lesion: from "engaging/non-engaging" lesion to "on-track/off-track" lesion. Arthroscopy. 2014;30(1):90-98. DOI: 10.1016/j.arthro.2013.10.004 Umaiza Ihsan, MD is a medical graduate of King Edward Medical University, Pakistan. She completed her internship at Mayo Hospital, Lahore, including a three month rotation in Radiology, which further strengthened her interest in diagnostic imaging. She has gained additional clinical exposure in Radiology through observerships at Mon Health Morgantown and the University of Maryland, Baltimore. She has a strong interest in Radiology, particularly diagnostic imaging and its role in clinical decision making, and is actively interested in clinical research, with experience in systematic reviews and medical research. All posts by Umaiza Ihsan, MD Kevin M. Rice, MD is the president of Global Radiology CME and is a radiologist with Cape Radiology Group. He has held several leadership positions including Board Member and Chief of Staff at Valley Presbyterian Hospital in Los Angeles, California. Dr. Rice has made several media appearances as part of his ongoing commitment to public education. Dr. Rice's passion for state of the art radiology and teaching includes acting as a guest lecturer at UCLA. In 2015, Dr. Rice and Natalie Rice founded Global Radiology CME to provide innovative radiology education at exciting international destinations, with the world's foremost authorities in their field. In 2016, Dr. Rice was nominated and became a semifinalist for a "Minnie" Award for the Most Effective Radiology Educator. He was once again a semifinalist for a "Minnie" for 2021's Most Effective Radiology Educator by AuntMinnie.com. He has continued to teach by mentoring medical students interested in radiology. Everyone who he has mentored has been accepted into top programs across the country including Harvard, UC San Diego, Northwestern, Vanderbilt, and Thomas Jefferson. Follow Dr. Rice on Twitter @KevinRiceMD All posts by Kevin M. Rice, MD
- Gastric Volvulus
Abdominal Pain and Distension • Xray of the Week 2016 • Week #51 An 83 year old female with multiple comorbidities presented to the Emergency Department with abdominal pain, distention, and altered mental status. What is the diagnosis? Figure 1. Sagittal (A) and axial (B) contrast enhanced CT. Figure 2. Sagittal (A) and axial (B) contrast enhanced CT of mesentero-axial gastric volvulus. Massively dilated stomach, herniating into the thoracic cavity via the gastroesophageal hiatus. The stomach descends into the abdominal cavity before herniating back intrathoracically and the duodenum finally descends intraabdominally with the remainder of the GI tract. Green arrow: GE junction Blue arrow: antrum. Discussion: Gastric volvulus is an uncommon cause of abdominal pain and may be a surgical emergency which requires prompt communication with the clinical team and treatment (1,2). The Borchardt triad of intractable retching, sudden epigastric abdominal pain and inability to pass a nasogastric tube (3) is classically described, but patients may also present with more chronic symptoms. Unlike the sigmoid colon and cecum, the stomach is an uncommon site for volvulus. There are two types of volvulus, organo-axial and mesentero-axial, which are differentiated based on the axis of rotation. Organo-axial volvulus represents an 180◦ twist along the cardiapyloric/long axis of the stomach with the greater curvature often displaced superior to the lesser curvature. This type is more common, representing approximately 2/3 of cases (1) of gastric volvulus, and commonly associated with hiatal hernias and traumatic events such as diaphragmatic rupture (4). With less than 180◦ of rotation, patients are usually asymptomatic and this should be termed organo-axial positioning of the stomach rather than volvulus. Although this may predispose to future volvulus, it is unclear if these patients require treatment. Mesentero-axial volvulus is a twist along the short axis of the stomach, along the mesenteric attachment (2). As seen in this case, the antrum presents above the gastroesophageal junction (Figs. 1 and 2). Although less common in the adult population (3), this tends to present with a more acute symptomatology. Due to the higher association with strangulation of the gastric blood supply, this is a surgical emergency. If diagnosed early, treatment may only require surgical repair. However, late diagnosis may result in gastric necrosis, necessitating a gastrectomy (1,3). References: 1. Peterson CM, Anderson JS, Hara AK, Carenza JW, Menias CO. Volvulus of the gastrointestinal tract: appearances at multimodality imaging. RadioGraphics 2009;29(5):1281–1293. 2. Menuck L. Plain film findings of gastric volvulus herniating into the chest. AJR Am J Roentgenol. 1976;126 (6): 1169-74. 3. Guniganti P, Bradenham CH, Raptis C et-al. CT of Gastric Emergencies. Radiographics. 2015;35 (7): 1909-2 4. Lee NK, Kim S, Jeon TY, Kim HS, Kim DH, Seo HI et al. Complications of congenital and developmental abnormalities of the gastrointestinal tract in adolescents and adults: evaluation with multimodality imaging. Radiographics 2010: 30(6):1489–1507. Alexandra (Sasha) Roudenko, MD is originally from Siberia, Russia and grew up in New York City. After graduating magna cum laude from Barnard College - Columbia University as a chemistry major, she was invited to join the prestigious Phi Beta Kappa Society. She then received her MD degree from New York University School of Medicine. Dr. Roudenko is currently a third year radiology resident at Mount Sinai West - St. Luke's and has developed a passion for body imaging. She is particularly interested in body MRI and plans on pursuing the subspecialty throughout her career. In 2016, Dr. Roudenko was awarded a fellowship in the introduction to academic radiology program at ARRS. All posts by Sasha Roudenko, MD Kevin M. Rice, MD is president of Global Radiology CME and serves as the Chair of the Radiology Department of Valley Presbyterian Hospital in Los Angeles, California and is a radiologist with Renaissance Imaging Medical Associates. Dr. Rice's passion for state of the art radiology and teaching includes acting as a guest lecturer at UCLA. Dr. Rice founded Global Radiology CME to provide innovative radiology education at exciting international destinations, with the world's foremost authorities in their field. In 2016, Dr. Rice was nominated and became a semifinalist for a "Minnie" award for the Most Effective Radiology Educator. Follow Dr. Rice on Twitter @KevinRiceMD All posts by Kevin M. Rice, MD Carol L Hilfer, MD is an assistant professor of Radiology at The Mount Sinai Hospital - Mount Sinai St. Luke's and Mount Sinai West
- Ruptured Quadriceps Tendon
Acute Onset Knee Pain • Xray of the Week A 68 year old female presenting with acute onset knee pain following crush injury of knee. What is the diagnosis? Figure 1. Plain radiographs of the knee AP (A), and lateral (B). Figure 2. Plain radiographs of the knee AP (A), and lateral (B). Green arrow demonstrating the avulsion fracture fragment due to the ruptured quadriceps tendon. Figure 3. Sagittal MRI of the knee. T1 weighted image (A) and T2 weighted image (B). Green arrow demonstrating the ruptured quadriceps tendon with discontinuity and retraction. Discussion: The quadriceps muscle group is the primary extension mechanism of the knee and consists of the vastus lateralis, vastus medialis, vastus intermedius, and rectus femoris.[1] The 4 tendons of these muscles insert onto the patella as the quadriceps tendon or sometimes referred to as the quadriceps expansion.The quadriceps tendon is composed of 3 layers:The superficial layer from the rectus femoris, the middle layer composed of the vastus lateralis and medialis, and the deeper layer from the vastus intermedius [1,2]. There is some variability on the anatomic configuration of the layers of the quadriceps tendon.The vastus medialis and vastus lateralis join the superficial and deep layers of the quadriceps tendon in varying proportions as the most common anatomic arrangement [2]. Quadriceps tendon injury may be secondary to repetitive microtrauma, weakening from underlying medical conditions such as gout, diabetes, collagen vascular diseases, chronic renal failure [3,4,5] or from strong deceleration injury. Additional predisposing factors include older age, obesity and steroid use [4]. Traumatic injuries may result in acute partial or complete tears, usually a few centimeters removed from the upper patellar pole [1]. Complete tendon rupture is usually a clinical diagnosis with loss of extensor function [2,4] and MRI is performed more for surgical planning and confirmation of diagnosis whereas in partial tendon ruptures, MRI serves a more critical role in diagnosis [2]. Initial evaluation with acutely injured patients tends to be with radiographs in the emergency department. Associated radiologic findings include suprapatellar mass usually composed of the retracted tendon and associated edema as well as a joint effusion [Figs.1,2] [4]. On lateral radiographs, disruption of the normal quadriceps outline may be identified as well as a soft tissue defect superior to the patella where a corresponding palpable defect may be felt on physical examination [4], similar to our case above [Figs.1,2]. On MRI, partial rupture of the quadriceps tendon usually is manifested by edema and heterogeneity of the quadriceps tendon. With complete rupture of the quadriceps tendon, MRI demonstrates retraction of the torn ends, and surrounding edema, and frequently a joint effusion [Fig.3] [1]. Treatment needs to be prompt and will be determined by degree of injury and rupture. Partial ruptures may be treated conservatively with immobilization, however complete tendon rupture with or without associated patellar fracture need emergent orthopedic evaluation and surgery in order to regain full function and prevent retraction and fibrosis [4]. References: 1. Bencardino JT, Rosenberg ZS, Brown RR, Hassankhani A, Lustrin ES, Beltran J (2000) Traumatic musculotendinous injuries of the knee: diagnosis with MR imaging. Radiographics. 20(suppl1):S103–S120. 2. Zeiss J, Saddemi SR, Ebraheim NA. MR imaging of the quadriceps tendon: normal layered configuration and its importance in cases of tendon rupture. AJR. 1992;159:1031-1034. 3. Kim, Y.H., Shafi, M., Lee, Y.S. et al. Spontaneous and simultaneous rupture of both quadriceps tendons in a patient with chronic renal failure. Knee Surg Sports Traumatol Arthrosc. 2006 Jan;14(1):55-59. 4. Nance EP Jr, Kaye JJ (1982) Injuries of the quadriceps mechanism. Radiology 142:301–307. 5. Bikkina RS, Chaljub G, Singh H, Allen SD. Magnetic resonance imaging of simultaneous bilateral quadriceps tendon rupture in a weightlifter: case report. J Trauma. 2002; 52(3):582-584.5. Alexandra (Sasha) Roudenko, MD is originally from Siberia, Russia and grew up in New York City. After graduating magna cum laude from Barnard College - Columbia University as a chemistry major, she was invited to join the prestigious Phi Beta Kappa Society. She then received her MD degree from New York University School of Medicine. Dr. Roudenko is currently a third year radiology resident at Mount Sinai West - St. Luke's and has developed a passion for body imaging. She is particularly interested in body MRI and plans on pursuing the subspecialty throughout her career. In 2016, Dr. Roudenko was awarded a fellowship in the Introduction to Academic Radiology program at ARRS. All posts by Sasha Roudenko, MD
- Köhler Disease
A 5-year-old male with medial foot pain. Diagnosis? Eponym? • Radiology Case of the Week Figure 1. 5-year-old male with medial foot pain. Diagnosis? Eponym? Figure 2. Radiographs of the foot (A–C) show thinning and mild fragmentation of the navicular (red arrows) with extensive sclerosis throughout and mild overlying soft tissue swelling. Diagnosis: Köhler disease. Epidemiology Köhler disease is a rare, self-limiting osteonecrosis of the tarsal navicular in children. It typically presents between 4 and 7 years of age, although onset as early as 2 years has been described [1,2]. Boys are affected more often than girls, with StatPearls citing a roughly five-fold male predominance [1]. The disease is usually unilateral, and about 25% of cases are reported to be bilateral [1]. Clinical Findings Children present with pain and swelling of the dorsomedial midfoot [3]. Examination may show point tenderness over the navicular, with or without redness, warmth, or swelling. Affected children often have an antalgic limp, bearing weight along the lateral foot [4]. A blood count and inflammatory markers are obtained when infection is suspected. Pathology The cause remains uncertain. The navicular is the last tarsal bone to ossify. As the child grows heavier, it may be compressed between the talus and cuneiforms, compromising its blood supply and causing central ischemia. Delayed ossification may contribute, and the central third of the navicular is a watershed area prone to avascular necrosis. Radiographic Features Plain radiographs are the imaging modality of choice. The navicular may appear thinned (wafer-like), flattened or collapsed, and fragmented, with patchy sclerosis, loss of the normal trabecular pattern, and overlying soft tissue swelling. Fragmentation should not be mistaken for a fracture. CT and MRI are usually unnecessary but may be considered if pain persists or the diagnosis is unclear. If symptoms persist, tarsal coalition should be considered [5,6]. In this patient, the navicular is thinned and mildly fragmented with extensive sclerosis and mild soft tissue swelling, consistent with Köhler disease. Treatment and Prognosis Management is conservative, and surgery is not indicated. A short leg walking cast for 4 to 6 weeks may shorten symptom duration. In one series, symptoms lasted an average of 15 months without casting and less than 3 months with a short leg cast [5]. At an average follow-up of 31.5 years, treatment did not affect the final outcome [6]; in another series, all 12 patients were asymptomatic at an average of 33 years [7]. Radiographic improvement typically occurs 6 to 48 months after symptom onset. Conclusion Köhler disease is a self-limiting osteonecrosis of the tarsal navicular in young children, most often boys, who present with medial midfoot pain, that worsens with weight bearing. Radiographs showing a thin, fragmented, sclerotic navicular establish the diagnosis. Management is conservative, and the prognosis is usually excellent. References: Trammell AP, Davis DD, Scott A. Kohler Disease. In: StatPearls. Treasure Island (FL): StatPearls Publishing; August 7, 2023. https://pubmed.ncbi.nlm.nih.gov/29939608/ Shastri N, Olson L, Fowler M. Kohler's Disease. West J Emerg Med. 2012;13(1):119 120. DOI: 10.5811/westjem.2011.1.6691 Holley KW, Price BJ, McCormick WF Jr, Littlefield ZL, Green BM. Kohler Disease With Concurrent Avascular Necrosis of the Medial Cuneiform: A Report of Two Cases. Cureus. 2025;17(8):e89411. Published 2025 Aug 5. DOI: 10.7759/cureus.89411 Achar S, Yamanaka J. Apophysitis and Osteochondrosis: Common Causes of Pain in Growing Bones. Am Fam Physician. 2019;99(10):610-618. https://pubmed.ncbi.nlm.nih.gov/31083875/ Williams GA, Cowell HR. Köhler's disease of the tarsal navicular. Clin Orthop Relat Res. 1981;(158):53-58. https://pubmed.ncbi.nlm.nih.gov/7273526/ Borges JL, Guille JT, Bowen JR. Köhler's bone disease of the tarsal navicular. J Pediatr Orthop. 1995;15(5):596-598. DOI: 10.1097/01241398-199509000-00009 Shastri N, Olson L, Fowler M. Kohler's Disease. West J Emerg Med. 2012;13(1):119 120. DOI: 10.5811/westjem.2011.1.6691 Umaiza Ihsan, MD is a medical graduate of King Edward Medical University, Pakistan. She completed her internship at Mayo Hospital, Lahore, including a three month rotation in Radiology, which further strengthened her interest in diagnostic imaging. She has gained additional clinical exposure in Radiology through observerships at Mon Health Morgantown and the University of Maryland, Baltimore. She has a strong interest in Radiology, particularly diagnostic imaging and its role in clinical decision making, and is actively interested in clinical research, with experience in systematic reviews and medical research. All posts by Umaiza Ihsan, MD Kevin M. Rice, MD is the president of Global Radiology CME and is a radiologist with Cape Radiology Group. He has held several leadership positions including Board Member and Chief of Staff at Valley Presbyterian Hospital in Los Angeles, California. Dr. Rice has made several media appearances as part of his ongoing commitment to public education. Dr. Rice's passion for state of the art radiology and teaching includes acting as a guest lecturer at UCLA. In 2015, Dr. Rice and Natalie Rice founded Global Radiology CME to provide innovative radiology education at exciting international destinations, with the world's foremost authorities in their field. In 2016, Dr. Rice was nominated and became a semifinalist for a "Minnie" Award for the Most Effective Radiology Educator. He was once again a semifinalist for a "Minnie" for 2021's Most Effective Radiology Educator by AuntMinnie.com. He has continued to teach by mentoring medical students interested in radiology. Everyone who he has mentored has been accepted into top programs across the country including Harvard, UC San Diego, Northwestern, Vanderbilt, and Thomas Jefferson. Follow Dr. Rice on Twitter @KevinRiceMD All posts by Kevin M. Rice, MD
- Leriche Syndrome
An 86-year-old female with chronic back pain and lower extremity pain. Diagnosis? Eponym?• Radiology Case of the Week Figure 1. An 86-year-old female with chronic back pain and lower extremity pain. Diagnosis? Eponym? Figure 2. Sagittal (A) and coronal (B) CT angiography reformats. Patent proximal abdominal aorta (yellow arrows) and the occluded distal aorta (red arrows). Extensive calcification of the plaque indicates that the occlusion is chronic. Note the dilated inferior mesenteric artery with reverse flow (green arrows). Diagnosis: Chronic Leriche syndrome. Figure 3. Axial CT angiography. A. Complete occlusion of the abdominal aorta below the level of the renal arteries (red arrow). B. Distal abdominal aorta is patent (yellow arrow) due to extensive collateral flow from superior mesenteric artery branches and reversed flow in a markedly dilated inferior mesenteric artery (green arrow). Figure 4. Doppler ultrasound of the common femoral arteries. A. Right (RT CFA). B. Left (LT CFA). Note the monophasic waveforms bilaterally indicating aortoiliac atherosclerotic stenotic disease or occlusion. Epidemiology The exact prevalence and incidence of Leriche syndrome are unknown. Leriche and Morel originally described it in young men, but older patients and women have since been reported [1,2]. It results from chronic aortoiliac atherosclerotic disease, so risk factors include age, smoking, hypertension, diabetes, and hyperlipidemia [3]. Clinical Findings The classic triad is claudication, impotence in men, and absent or diminished femoral pulses [3]. Claudication is cramping pain in the buttocks, hips, and thighs that is reproduced by exercise. Reduced or absent femoral pulses are the hallmark finding. Limb-threatening ischemia is not universal, because collateral circulation develops as the disease progresses slowly [3]. An ankle-brachial index below 0.9 is abnormal and is usually the first test. Pathology Leriche syndrome is caused by atherosclerotic plaque within the lumen. Stenosis greater than 50% produces claudication, because oxygen demand during exercise exceeds supply. The plaque can progress to complete occlusion of the distal aorta, and extensive calcification indicates a chronic process. Classification Leriche syndrome is classified by the extent of disease [3]. Type I is confined to the distal abdominal aorta and common iliac arteries. Type II involves mainly the distal abdominal aorta and extends into the common and external iliac arteries. Type III involves the aortoiliac segment and the femoropopliteal vessels. Radiographic Features Duplex ultrasound and CT angiography define the location and degree of disease. Duplex ultrasound is noninvasive and is typically the first imaging test, often after the ankle-brachial index. CT angiography is the imaging modality of choice: it confirms the occlusion, shows plaque calcification, and maps the collateral pathways before treatment [4,5]. MR angiography is an alternative when iodinated contrast is a concern. In this 86-year-old woman with chronic back and lower extremity pain, ultrasound and CT angiography together showed a chronic aortic occlusion with the distal aorta reconstituted by collateral flow (Figs. 1-4). Treatment and Prognosis Management combines risk-factor control with revascularization when needed. Therapy includes supervised walking, smoking cessation, diabetes control, antiplatelet, statin and antihypertensive therapy. Revascularization options are aortobifemoral bypass, thromboendarterectomy, and angioplasty with or without stenting [6]. In fit patients, aortobifemoral bypass has the best long-term patency, about 85% to 90% at five years; endovascular treatment suits patients with multiple comorbidities. Prognosis is poor without treatment but good with modern therapy. Complications include limb ischemia, gangrene, myocardial infarction, and death. Conclusion Leriche syndrome is chronic atherosclerotic occlusion of the distal aorta and may present with nonspecific back and leg pain. Monophasic lower extremity waveforms on Doppler ultrasound should prompt CT angiography, which confirms the occlusion and its collateral pathways and guides treatment. References: Leriche R, Morel A. The Syndrome of Thrombotic Obliteration of the Aortic Bifurcation. Ann Surg. 1948;127(2):193-206. DOI: 10.1097/00000658-194802000-00001 Kita K. Leriche syndrome (Aortoiliac occlusive disease). J Gen Fam Med. 2017;18(5):297-298. Published 2017 Apr 21. DOI: 10.1002/jgf2.63 Brown KN, Gonzalez L. Leriche Syndrome (Archived). In: StatPearls. Treasure Island (FL): StatPearls Publishing; February 13, 2023. https://pubmed.ncbi.nlm.nih.gov/30855836/ Frederick M, Newman J, Kohlwes J. Leriche syndrome. J Gen Intern Med. 2010;25(10):1102-1104. DOI: 10.1007/s11606-010-1412-z Ahmed S, Raman SP, Fishman EK. CT angiography and 3D imaging in aortoiliac occlusive disease: collateral pathways in Leriche syndrome. Abdom Radiol (NY). 2017;42(9):2346-2357. DOI: 10.1007/s00261-017-1137-0 Krankenberg H, Schlüter M, Schwencke C, et al. Endovascular reconstruction of the aortic bifurcation in patients with Leriche syndrome. Clin Res Cardiol. 2009;98(10):657 664. DOI: 10.1007/s00392-009-0052-y Umaiza Ihsan, MD is a medical graduate of King Edward Medical University, Pakistan. She completed her internship at Mayo Hospital, Lahore, including a three month rotation in Radiology, which further strengthened her interest in diagnostic imaging. She has gained additional clinical exposure in Radiology through observerships at Mon Health Morgantown and the University of Maryland, Baltimore. She has a strong interest in Radiology, particularly diagnostic imaging and its role in clinical decision making, and is actively interested in clinical research, with experience in systematic reviews and medical research. All posts by Umaiza Ihsan, MD Kevin M. Rice, MD is the president of Global Radiology CME and is a radiologist with Cape Radiology Group. He has held several leadership positions including Board Member and Chief of Staff at Valley Presbyterian Hospital in Los Angeles, California. Dr. Rice has made several media appearances as part of his ongoing commitment to public education. Dr. Rice's passion for state of the art radiology and teaching includes acting as a guest lecturer at UCLA. In 2015, Dr. Rice and Natalie Rice founded Global Radiology CME to provide innovative radiology education at exciting international destinations, with the world's foremost authorities in their field. In 2016, Dr. Rice was nominated and became a semifinalist for a "Minnie" Award for the Most Effective Radiology Educator. He was once again a semifinalist for a "Minnie" for 2021's Most Effective Radiology Educator by AuntMinnie.com. He has continued to teach by mentoring medical students interested in radiology. Everyone who he has mentored has been accepted into top programs across the country including Harvard, UC San Diego, Northwestern, Vanderbilt, and Thomas Jefferson. Follow Dr. Rice on Twitter @KevinRiceMD All posts by Kevin M. Rice, MD
- Kommerell Diverticulum
A 58-year-old male, asymptomatic. Identify the indicated structures and state the potential life-threatening complication. • Radiology Case of the Week Figure 1. Name the anatomy and potential life-threatening complication. Figure 2. A. Axial CT of the chest. The right-sided aortic arch lies to the right of the air-filled trachea (orange arrow), with the esophagus (blue arrow) situated immediately posterior to the trachea. An aberrant left subclavian artery (red arrow) arises from a focal, aneurysmal outpouching of the proximal descending aorta, the Kommerell diverticulum (yellow arrow). B. Sagittal CT of the chest. The Kommerell diverticulum (yellow arrow) is seen posterior to the esophagus (blue arrow). The air-filled trachea (orange arrow) is marked. Figure 3. A. Coronal CT of the chest, posterior projection. The right-sided aortic arch gives origin to an aberrant left subclavian artery (red arrow) that arises from the Kommerell diverticulum (yellow arrow). B. Coronal CT of the chest, anterior projection. The right-sided ascending aorta (green arrow) is seen on the right side of the air-filled trachea (orange arrow). The main pulmonary artery (purple arrow) is also well seen. Figure 4. A. Volume-rendered CT, anterior view. The ascending aorta (green arrow) gives rise to the right subclavian artery (white arrow) as its first branch; the right-sided aortic arch continues to the origin of the aberrant left subclavian artery (red arrow) arising from the Kommerell diverticulum (yellow arrow), with the main pulmonary artery (purple arrow) seen anteriorly. B. Volume-rendered CT, posterior view. The Kommerell diverticulum (yellow arrow) is again seen giving rise to the aberrant left subclavian artery (red arrow) from the right-sided aortic arch, which also gives rise to the right subclavian artery (white arrow). Epidemiology Kommerell diverticulum is a rare congenital anomaly of the aortic arch that is associated with an aberrant subclavian artery in the majority of reported cases, with most series describing an association in roughly 60–80% of patients [1]. Because an aberrant right subclavian artery is itself uncommon, occurring in approximately 0.5–2% of the general population, and an aberrant left subclavian artery is markedly rarer still, occurring in only about 0.04–0.4% of the population, Kommerell diverticulum with a right-sided aortic arch and aberrant left subclavian artery, as in the present case, represents one of the least frequently encountered configurations of this anomaly [1]. Clinical Findings Kommerell diverticulum is frequently discovered incidentally when cross-sectional imaging is performed for an unrelated indication, as illustrated by the asymptomatic 58-year-old man described [2]. When symptoms do occur, they most often relate to mechanical compression of the adjacent trachea and esophagus by the diverticulum and its associated vascular ring, presenting as dysphagia and dyspnea [3]. Less commonly, patients may present with chest pain or with embolic phenomena arising from mural thrombus within the diverticulum. The most feared complications, though uncommon, are aortic dissection and frank rupture of the diverticulum. Pathology Embryologically, the Kommerell diverticulum represents the persistent remnant of the dorsal portion of the fourth aortic arch [4]. In the setting of a right-sided arch specifically, it reflects persistence of the right fourth aortic arch together with involution of the left fourth arch, which normally forms the definitive arch in the more common left-arch configuration [5,6]. Histologic examination of resected diverticular tissue has demonstrated cystic medial necrosis within the wall of the diverticulum in a substantial proportion of cases, a finding that likely explains the propensity of this lesion toward dissection and rupture [7] which can be life-threatening. Classification Three principal patterns of aortic arch diverticulum have traditionally been described in the literature: a left-sided aortic arch with an aberrant right subclavian artery, which is the most common configuration; a right-sided aortic arch with an aberrant left subclavian artery, the pattern demonstrated in the present case; and, less commonly, a diverticulum situated at the aortoductal junction. When a right-sided aortic arch is present, further sub-classification follows the Edwards system, in which type I demonstrates mirror-image branching without a retroesophageal component, type II, the pattern seen here, consists of an aberrant left subclavian artery arising from a Kommerell diverticulum, and type III, the rarest variant, consists of an isolated left subclavian artery that communicates instead with the pulmonary artery via a ductal remnant [4]. Radiographic Features The aberrant subclavian artery can be seen to arise from a focal, saccular dilatation of the proximal descending thoracic aorta (Figs. 1-4). The diverticulum itself is conventionally measured in cross-section at the level of the origin of the aberrant subclavian artery, and in a right-sided arch such as this one, the arch and its proximal descending continuation characteristically lie to the right of the trachea rather than to the left (Fig. 1). Careful attention should also be paid to the caliber of the adjacent trachea and esophagus, since both structures may be compressed by the diverticulum and its associated ligamentous or ductal remnants. Treatment and Prognosis Small, asymptomatic diverticula can generally be managed with periodic imaging surveillance alone, since growth tends to be slow, on the order of roughly 1.5 mm per year in reported series. Most studies favor surgical or endovascular repair once the diverticulum orifice exceeds approximately 30 mm, once the adjacent descending aorta exceeds approximately 50 mm, or once the patient becomes symptomatic from airway or esophageal compression [7,8]. In one large surgical series, at least one death from aortic rupture has been reported in a nonoperatively managed patient whose diverticulum measured only 3.4 cm, a reminder that even moderately sized lesions warrant close follow-up. Conclusion Kommerell diverticulum is an uncommon congenital anomaly of the aortic arch that is most often identified incidentally in asymptomatic adults. Because the lesion is closely associated with an aberrant subclavian artery and carries a recognized risk of dissection and rupture, accurate characterization is essential once it is discovered. The three-dimensional reconstructions such as shown in Fig.4 are particularly valuable for delineating the overall arch anatomy and for planning any subsequent operative or endovascular approach [9]. References: Irshad S, Adrejiya P, Abubaker M, Whitaker J. Kommerell's Diverticulum Masquerading in a Right Aortic Arch: A Vascular Surprise. Methodist Debakey Cardiovasc J. 2025;21(1):81-83. Published 2025 Aug 20. DOI: 10.14797/mdcvj.1641 Erben Y, Brownstein AJ, Velasquez CA, Li Y, Rizzo JA, Mojibian H, Tanweer M, Zafar MA, Ziganshin BA, Elefteriades JA. Natural history and management of Kommerell's diverticulum in a single tertiary referral center. J Vasc Surg. 2020;71(6):2004-2011. DOI: 10.1016/j.jvs.2019.08.260. Vinnakota A, Idrees JJ, Rosinski BF, et al. Outcomes of Repair of Kommerell Diverticulum. Ann Thorac Surg. 2019;108(6):1745-1750. DOI: 10.1016/j.athoracsur.2019.04.122 Kanwal D, Khalil S, Attia K, Fam M, Arakkal M. Kommerell's diverticulum with right-sided aortic arch and anomalous origin of neck vessels: Uncommon imaging finding in neonate with cyanosis. BJR Case Rep. 2021;7(4):20200173. Published 2021 Apr 30. DOI: 10.1259/bjrcr.20200173 Summa CH, DeMaioribus CA, Swink D, et al. Hybrid repair of Kommerell's diverticulum with aberrant subclavian artery. J Vasc Surg Cases Innov Tech. 2026;12(2):102129. Published 2026 Jan 5. DOI: 10.1016/j.jvscit.2026.102129 Mubarak MY, Kamarul AT, Noordini MD. Right-sided Aortic Arch with Aberrant Left Subclavian Artery from Kommerell's Diverticulum. Iran J Radiol. 2011;8(2):103-106. https://pmc.ncbi.nlm.nih.gov/articles/PMC3522316/ Tanaka A, Milner R, Ota T. Kommerell's diverticulum in the current era: a comprehensive review. Gen Thorac Cardiovasc Surg. 2015;63(5):245-259. DOI: 10.1007/s11748-015-0521-3 Silva AF, Dos Santos JA. Aortic arch anomaly in an adult patient: a case of right aortic arch with aberrant left subclavian artery and Kommerell's diverticulum. Radiol Bras. 2016;49(4):274-275. DOI: 10.1590/0100-3984.2015.0087 Osawa H, Shinohara D, Orii K, et al. Right Aortic Arch and Kommerell's Diverticulum Repaired without Reconstruction of Aberrant Left Subclavian Artery. Case Rep Vasc Med. 2013;2013:840804. DOI: 10.1155/2013/840804 Umaiza Ihsan, MD is a medical graduate of King Edward Medical University, Pakistan. She completed her internship at Mayo Hospital, Lahore, including a three month rotation in Radiology, which further strengthened her interest in diagnostic imaging. She has gained additional clinical exposure in Radiology through observerships at Mon Health Morgantown and the University of Maryland, Baltimore. She has a strong interest in Radiology, particularly diagnostic imaging and its role in clinical decision making, and is actively interested in clinical research, with experience in systematic reviews and medical research. All posts by Umaiza Ihsan, MD Kevin M. Rice, MD is the president of Global Radiology CME and is a radiologist with Cape Radiology Group. He has held several leadership positions including Board Member and Chief of Staff at Valley Presbyterian Hospital in Los Angeles, California. Dr. Rice has made several media appearances as part of his ongoing commitment to public education. Dr. Rice's passion for state of the art radiology and teaching includes acting as a guest lecturer at UCLA. In 2015, Dr. Rice and Natalie Rice founded Global Radiology CME to provide innovative radiology education at exciting international destinations, with the world's foremost authorities in their field. In 2016, Dr. Rice was nominated and became a semifinalist for a "Minnie" Award for the Most Effective Radiology Educator. He was once again a semifinalist for a "Minnie" for 2021's Most Effective Radiology Educator by AuntMinnie.com. He has continued to teach by mentoring medical students interested in radiology. Everyone who he has mentored has been accepted into top programs across the country including Harvard, UC San Diego, Northwestern, Vanderbilt, and Thomas Jefferson. Follow Dr. Rice on Twitter @KevinRiceMD All posts by Kevin M. Rice, MD
- Cystic Hygroma
A 23-Year-Old female at First-Trimester Ultrasound. Diagnosis? • Radiology Case of the Week Figure 1. Transabdominal first-trimester pelvic ultrasound. 23-year-old patient presenting with vaginal bleeding: Diagnosis? Figure 2. A. Magnified sagittal ultrasound of the cystic structure shows a thin, complete outer wall (red arrow) and an internal septation (yellow arrow) crossing the cyst; ultrasound calipers measure 1.6 x 1.2 cm. Fetal pole (green arrow) is seen with the cystic structure (red arrows) immediately dorsal to it, at the craniocervical junction (blue arrow). B. Calipers placed across the dorsal nuchal region measure an additional, smaller 0.5 cm focus, in keeping with a markedly thickened/septated nuchal translucency. Note the midline septum representing the nuchal ligament (white arrow). Epidemiology Fetal cystic hygroma is identified in approximately 1 in 285 pregnancies undergoing first trimester nuchal translucency screening, with an estimated overall prenatal prevalence of 0.2-3%. It is far less common as a postnatal diagnosis, with an incidence at birth of only about 1 in 6000, since most affected pregnancies end in miscarriage, intrauterine fetal death, or elective termination (1). A chromosomal abnormality is identified in roughly half of prenatally detected cases overall, most commonly monosomy X (Turner syndrome), trisomy 21, trisomy 18, and triploidy (2,3). Clinical Manifestations Cystic hygroma is usually an incidental finding on first- or early second-trimester sonography, typically identified as a markedly increased and septated nuchal translucency. Severe lymphatic obstruction may progress to nonimmune hydrops fetalis, with generalized skin edema, pleural or pericardial effusion, and ascites, a combination associated with a markedly worse outcome. If it persists after birth, it can present as a soft, compressible, transilluminant neck mass (1). Pathology Cystic hygroma is a macrocystic lymphatic malformation resulting from failure of the paired jugular lymphatic sacs to establish normal communication with the internal jugular veins and the remainder of the venous system during the fifth to ninth week of gestation. The resulting obstruction causes progressive dilation of the sequestered sacs, producing thin-walled, multiloculated cystic spaces filled with proteinaceous lymphatic fluid within the posterior soft tissues of the fetal neck. Histologically, the cyst walls are lined by a single layer of flattened endothelium with scant surrounding stroma (1). Classification Cystic hygromas are classified sonographically as septated or nonseptated, a distinction with direct prognostic importance. The nonseptated form is a simple, markedly thickened nuchal translucency without an internal dividing line. The septated form, as in this case, shows a midline septum representing the nuchal ligament, flanked by paired symmetric cystic spaces. This distinction carries prognostic weight: in one comparative series, septated lesions had a 72% aneuploidy rate, a 40% rate of hydrops, and only a 12% livebirth rate, compared with 5.7%, under 2%, and 94%, respectively, for nonseptated lesions (3). Pathologically, lymphatic malformations are further categorized by cyst size as macrocystic (individual cysts greater than 2 cm), microcystic (less than 2 cm), or mixed. Radiographic Features On prenatal ultrasound, cystic hygroma appears as a thin-walled, anechoic to hypoechoic cystic structure in the soft tissues dorsal to the fetal craniocervical junction, frequently traversed by one or more internal septa (Figures 1-2) (4). Caliper measurements are used to document lesion size and to distinguish it from a simple increased nuchal translucency. Color Doppler characteristically shows no internal flow. Postnatally, MRI is the modality of choice for defining the full extent and its relationship to adjacent neurovascular structures before surgical planning. Treatment and Prognosis Once identified, cystic hygroma warrants karyotype, microarray testing (chorionic villus sampling or amniocentesis), a detailed fetal anatomic and cardiac survey, and serial sonographic surveillance for hydrops. Prognosis is governed chiefly by septation status, karyotype, and the presence of hydrops (5,6); pregnancies reaching the second trimester without these adverse features generally do well. Postnatally, a persistent or isolated lymphatic malformation is managed with intralesional sclerotherapy as first-line treatment, with surgery reserved for lesions that fail sclerotherapy, recur, or threaten the airway; an ex utero intrapartum treatment (EXIT) procedure may be needed when a large lesion is expected to obstruct the airway at delivery (7). Conclusion Fetal cystic hygroma is an important early sonographic marker of aneuploidy and adverse pregnancy outcome. Its recognition should prompt genetic counseling, karyotype testing, and close sonographic follow-up. References: Rangel V, Having K. Cystic Hygroma. J Diagn Med Sonogr. 2008;24(4):218-222. DOI: https://doi.org/10.1177/8756479308319969 Malone FD, Ball RH, Nyberg DA, et al. First-trimester septated cystic hygroma: prevalence, natural history, and pediatric outcome. Obstet Gynecol. 2005;106(2):288-294. DOI: 10.1097/01.AOG.0000173318.54978.1f Bronshtein M, Bar-Hava I, Blumenfeld I, Bejar J, Toder V, Blumenfeld Z. The difference between septated and nonseptated nuchal cystic hygroma in the early second trimester. Obstet Gynecol. 1993;81(5 ( Pt 1)):683-687. https://pubmed.ncbi.nlm.nih.gov/8469454/ Sepúlveda WH, Ciuffardi I. Early sonographic diagnosis of fetal cystic hygroma colli. J Perinat Med. 1992;20(2):149-152. DOI: 10.1515/jpme.1992.20.2.149 Chen HY, Zheng JQ, Zhang HP. A case report of Turner syndrome associated with fetal nuchal cystic hygroma and bilateral syndactyly of the hands and feet. Ital J Pediatr. 2019;45(1):85. Published 2019 Jul 18. DOI: 10.1186/s13052-019-0680-4 Rosati P, Guariglia L. Transvaginal ultrasound detection of septated and non-septated cystic hygroma in early pregnancy. Fetal Diagn Ther. 1997;12(3):132-135. DOI: 10.1159/000264452 Gowda M, Godipelli L, Gangadhar L, Jindal B, Deodar K, Yadav M. Management of isolated fetal lymphangiomas following prenatal diagnosis: case series. J Fetal Med. 2021;8(1):39-43. DOI: https://doi.org/10.1007/s40556-021-00288-5 Umaiza Ihsan, MD is a medical graduate of King Edward Medical University, Pakistan. She completed her internship at Mayo Hospital, Lahore, including a three- month rotation in Radiology, which further strengthened her interest in diagnostic imaging. She has gained additional clinical exposure in Radiology through observerships at Mon Health Morgantown and the University of Maryland, Baltimore. She has a strong interest in Radiology, particularly diagnostic imaging and its role in clinical decision making, and is actively interested in clinical research, with experience in systematic reviews and medical research. All posts by Umaiza Ihsan, MD Kevin M. Rice, MD is the president of Global Radiology CME and is a radiologist with Cape Radiology Group. He has held several leadership positions including Board Member and Chief of Staff at Valley Presbyterian Hospital in Los Angeles, California. Dr. Rice has made several media appearances as part of his ongoing commitment to public education. Dr. Rice's passion for state of the art radiology and teaching includes acting as a guest lecturer at UCLA. In 2015, Dr. Rice and Natalie Rice founded Global Radiology CME to provide innovative radiology education at exciting international destinations, with the world's foremost authorities in their field. In 2016, Dr. Rice was nominated and became a semifinalist for a "Minnie" Award for the Most Effective Radiology Educator. He was once again a semifinalist for a "Minnie" for 2021's Most Effective Radiology Educator by AuntMinnie.com. He has continued to teach by mentoring medical students interested in radiology. Everyone who he has mentored has been accepted into top programs across the country including Harvard, UC San Diego, Northwestern, Vanderbilt, and Thomas Jefferson. Follow Dr. Rice on Twitter @KevinRiceMD All posts by Kevin M. Rice, MD
- Os Odontoideum
Adolescent with Chronic Neck Pain and Suboccipital Discomfort: Diagnosis? • Xray of the Week Figure 1. CT images of the cervical spine (A) sagittal view and (B) coronal view. What is the important finding on this CT scan? Figure 2. A. Sagittal CT shows a small, round, well-corticated ossicle (yellow arrow) representing the os odontoideum separated from the underlying body of C2 (green arrow). Note the smooth, radiolucent gap between the body of C2 and the os odontoideum (red arrow). Also note the thickening and abnormal rounding of the anterior arch of C1 (blue arrow). B. Coronal CT section again demonstrates the well-corticated ossicle representing the os odontoideum (yellow arrow) positioned symmetrically between the lateral masses of C1 (blue arrows) and separated from the underlying body of C2 (green arrow). C. Axial CT through the ring of C1 shows the os odontoideum (yellow arrow) situated just posterior to the anterior arch of C1 (blue arrow). Note the thickening and abnormal rounding of the anterior arch of C1 (blue arrow). Feature Os Odontoideum Chronic Fracture Dens (Nonunion) Ossicle Margins Smooth, distinct, and completely well-corticated. Often irregular, sclerotic, but lack a uniform smooth outer cortex of an independent ossicle. Gap / Interface Wide, smooth, radiolucent gap with corticated margins on both opposing surfaces. Jagged or sharply angulated lucent cleft matching the original fracture line (typically Type II base). Morphology of Dens Hypoplastic, foreshortened, or round/oval ossicle located superiorly. Normal height/shape of the residual dens base, matching the displaced fragment size. C1 (Atlas) Remodeling Frequently shows hypertrophy and rounding of the anterior arch. Anterior arch of C1 is usually normal in morphology unless secondary degenerative changes exist. Location of Gap Typically well above the superior articulating facets of C2. Typically at the base of the dens (classic Type II location). Clinical Context May be an unrecognized childhood injury or congenital variant; highly prone to atlantoaxial instability. Known prior acute trauma history with documented failure of bony union. Table 1. Differentiating Os odontoideum from a chronic nonunited Type 2 dens fracture on a CT scan relies on margin characteristics, gap appearance, and associated bony remodeling as summarized here. Epidemiology Os odontoideum is a rare anomaly of the craniocervical junction. Its true prevalence and incidence are unknown, since most cases are discovered incidentally or only after symptoms develop; reported prevalence on adult imaging series is well under 1%. Diagnosis spans a wide age range, from early childhood through late adulthood, although many patients present within the first three decades of life. An increased frequency has been reported in patients with Down syndrome, spondyloepiphyseal dysplasia, Morquio syndrome, and other skeletal dysplasias, supporting a multifactorial rather than a single unifying etiology (1,2). Clinical Findings Many cases are asymptomatic and are identified incidentally on imaging obtained for unrelated indications. When symptomatic, neck pain is the most common complaint, followed by mechanical or intermittent neurologic symptoms related to atlantoaxial instability, including myelopathy, transient quadriparesis after minor trauma, and vertebrobasilar symptoms such as vertigo or syncope from vertebral artery compromise. Because an unstable ossicle may be tolerated for years before a seemingly trivial injury precipitates catastrophic cord compression, even an incidentally detected os odontoideum warrants further clinical and radiographic evaluation (3,4). Pathology The etiology of os odontoideum remains debated. The congenital theory attributes the anomaly to failure of fusion between the odontoid process and the body of the axis at the subdental synchondrosis. Growing evidence instead favors an acquired origin: an unrecognized fracture through the odontoid synchondrosis before ossification is complete (roughly before 5-6 years of age), with subsequent avascular remodeling of the separated fragment into a smooth, independently corticated ossicle (5). Both mechanisms likely contribute in different patients. Because the transverse atlantal ligament inserts on the mobile ossicle rather than on a fixed dens, it is rendered ineffective at restraining atlantoaxial translation. Classification Os odontoideum is divided into two types based on the position of the ossicle relative to the atlas and clivus. In the orthotopic type, the more common pattern, the ossicle lies in the normal anatomic position of the odontoid tip and moves together with the anterior arch of C1. In the dystopic type, the ossicle is displaced, most often superiorly, and may fuse to the basion/clivus, moving with the occiput rather than the atlas; this pattern is more frequently associated with instability and neurologic injury (6). Radiographic Features CT best depicts the bony morphology of os odontoideum and is the modality of choice for surgical planning. The ossicle appears round-to-oval, roughly half the size of a normal dens, with a smooth and completely corticated margin. It is separated from the hypoplastic dens/axis body by a wide, smooth, radiolucent gap located above the level of the superior articular facets of C2 (Figures 1-2). Compensatory hypertrophy and rounding of the anterior arch of C1 is a recognized associated finding. Dynamic flexion-extension radiographs or CT, together with MRI, are used to quantify atlantoaxial instability and to assess for cord compression or signal change (6,7). Differentiating os odontoideum from a chronic nonunited (Type II) dens fracture on CT relies on margin characteristics, gap appearance, and associated bony remodeling (Table 1). Treatment and Prognosis Management depends on symptoms and the degree of instability rather than on the mere presence of the ossicle. Asymptomatic patients without instability on flexion-extension imaging can be managed with observation and serial radiographic surveillance. Operative posterior C1-C2 fusion is favored for patients with neurologic deficits, myelopathy, or significant instability, given the risk of delayed neurologic deterioration, which has been documented even after a period of apparent clinical stability (7). Fusion rates and symptomatic improvement after surgery are high, although the timing of surgery in asymptomatic patients remains controversial. Conclusion Os odontoideum is an important, often incidental, cause of atlantoaxial instability that must be reliably distinguished from a chronic ununited dens fracture, as the two entities carry different implications for surveillance and treatment. Recognizing the smooth, corticated ossicle, the wide suprafacetal gap, and the hypertrophied anterior arch of C1 on CT allows a confident diagnosis and appropriate management, helping to avert neurologic catastrophe. References: Fielding JW, Hensinger RN, Hawkins RJ. Os Odontoideum. J Bone Joint Surg Am. 1980;62(3):376-383. https://pubmed.ncbi.nlm.nih.gov/7364809/ Sankar WN, Wills BP, Dormans JP, Drummond DS. Os odontoideum revisited: the case for a multifactorial etiology. Spine (Phila Pa 1976). 2006;31(9):979-984. DOI: 10.1097/01.brs.0000214935.70868.1c Fagan AB, Askin GN, Earwaker JW. The jigsaw sign. A reliable indicator of congenital aetiology in os odontoideum. Eur Spine J. 2004;13(4):295-300. DOI: 10.1007/s00586-004-0732-2 Klimo P Jr, Kan P, Rao G, Apfelbaum R, Brockmeyer D. Os odontoideum: presentation, diagnosis, and treatment in a series of 78 patients. J Neurosurg Spine. 2008;9(4):332-342. DOI: 10.3171/SPI.2008.9.10.332 Cho S, Shlobin NA, Dahdaleh NS. Os odontoideum: A comprehensive review. J Craniovertebr Junction Spine. 2022;13(3):256-264.DOI: 10.4103/jcvjs.jcvjs_71_22 Nelson C, Mujahed T, Tedford NJ. Adolescent male with neck pain. J Am Coll Emerg Physicians Open. 2024;5(3):e13222. Published 2024 Jun 16.DOI: 10.1002/emp2.13222 Menezes AH. Os odontoideum: database analysis of 260 patients regarding etiology, associated abnormalities, and literature review. Front Surg. 2023;10:1291056. Published 2023 Dec 5. DOI: 10.3389/fsurg.2023.12910561 Umaiza Ihsan, MD is a medical graduate of King Edward Medical University, Pakistan. She completed her internship at Mayo Hospital, Lahore, including a three month rotation in Radiology, which further strengthened her interest in diagnostic imaging. She has gained additional clinical exposure in Radiology through observerships at Mon Health Morgantown and the University of Maryland, Baltimore. She has a strong interest in Radiology, particularly diagnostic imaging and its role in clinical decision making, and is actively interested in clinical research, with experience in systematic reviews and medical research. All posts by Umaiza Ihsan, MD Kevin M. Rice, MD is the president of Global Radiology CME and is a radiologist with Cape Radiology Group. He has held several leadership positions including Board Member and Chief of Staff at Valley Presbyterian Hospital in Los Angeles, California. Dr. Rice has made several media appearances as part of his ongoing commitment to public education. Dr. Rice's passion for state of the art radiology and teaching includes acting as a guest lecturer at UCLA. In 2015, Dr. Rice and Natalie Rice founded Global Radiology CME to provide innovative radiology education at exciting international destinations, with the world's foremost authorities in their field. In 2016, Dr. Rice was nominated and became a semifinalist for a "Minnie" Award for the Most Effective Radiology Educator. He was once again a semifinalist for a "Minnie" for 2021's Most Effective Radiology Educator by AuntMinnie.com. He has continued to teach by mentoring medical students interested in radiology. Everyone who he has mentored has been accepted into top programs across the country including Harvard, UC San Diego, Northwestern, Vanderbilt, and Thomas Jefferson. Follow Dr. Rice on Twitter @KevinRiceMD All posts by Kevin M. Rice, MD
- Type 1 Dens Fracture
Trauma due to motor vehicle collision. Diagnosis? • Xray of the Week Figure 1. CT images of the cervical spine (A) sagittal view and (B) coronal view. What is the important finding on this CT scan? Figure 2. CT scan of a Type I dens fracture. Red arrows point to the fracture line at the tip of the dens. Figure 3. Anderson and D’Alonzo dens fracture classification system. Diagram by Neal Joshi. Type I is an oblique avulsion fracture involving the upper tip of the dens, usually at the alar ligament insertion, and is generally considered stable when isolated. Type II occurs at the junction of the dens and the body of C2 and has a greater risk of displacement and nonunion. Type III extends from the base of the dens into the body of C2 and generally has better healing potential because the fracture extends into cancellous bone. Introduction: The odontoid process, or dens, is a superior projection of C2 that articulates with the anterior arch of C1 and functions as the pivot for atlantoaxial rotation. The alar ligaments arise from the upper dens and attach to the medial aspects of the occipital condyles, contributing to stability of the craniocervical junction (1,2). The Anderson and D'Alonzo classification is the most widely used system for classifying odontoid fractures according to the location of the fracture (3,4) (Fig. 3). Type I fracture is usually stable, however, an apparent Type I avulsion fracture may be associated with injury to the alar or other craniocervical ligaments; therefore, the surrounding ligamentous structures and craniocervical alignment should be assessed (5). Epidemiology Odontoid fractures are among the most common fractures of the upper cervical spine, particularly in older adults. Type I odontoid fractures are rare, representing approximately 2–3% of odontoid fractures. In a prospective study from the Swedish Fracture Register, 30 of 1,154 odontoid fractures were classified as Type I, compared with 583 Type II and 541 Type III fractures. Odontoid fractures in older adults are commonly associated with low-energy falls, whereas higher-energy mechanisms such as motor vehicle collisions are more frequent in younger patients (6,7). Clinical Manifestation Patients with Type I dens fractures typically present with upper cervical or posterior neck pain and tenderness following trauma. Pain may be aggravated by cervical movement and may be associated with restricted range of motion. Neurological deficits are uncommon but may occur in the presence of associated cervical or craniocervical injuries. Because Type I fractures are uncommon and may be associated with ligamentous injury, careful clinical and radiologic assessment for craniocervical instability is important (3). Radiographic Features Plain radiographs, including lateral and open-mouth odontoid views, may demonstrate a small avulsion fragment at the tip of the dens; however, a negative examination does not exclude fracture. When clinical suspicion persists, thin-section CT with sagittal and coronal reformations is the preferred imaging modality, allowing accurate assessment of fracture location, displacement, and atlantoaxial and craniocervical alignment (Fig. 1). In this patient, CT performed following a motor vehicle collision demonstrated a type I dens fracture (Fig. 2). Associated fractures of C1 and C2 should also be carefully evaluated (5). CT is also useful in distinguishing a type I odontoid fracture from os odontoideum. MRI may be useful when there is concern for associated ligamentous injury or craniocervical instability and can provide additional evaluation of the spinal cord. Treatment and Prognosis Isolated, nondisplaced Type I dens fractures are generally considered stable and are treated conservatively with external immobilization, most commonly with a rigid cervical collar. Current recommendations support immobilization with a hard collar for approximately 6–8 weeks, with clinical and radiographic follow-up to confirm stability and healing; duration may be extended based on follow-up imaging (8). Surgical treatment is rarely required for an isolated Type I fracture. However, operative stabilization may be considered when there is significant displacement, craniocervical instability, or associated ligamentous injury. The prognosis of an isolated Type I fracture is generally favorable with appropriate immobilization. In elderly patients specifically, rigid immobilization methods such as halo-vest bracing carry an increased mortality risk and should be weighed carefully against a rigid collar alternative when isolated Type I injuries are stable (9). Conclusion Type I dens fractures are rare avulsion injuries involving the superior tip of the odontoid process, usually at the site of alar ligament attachment. Although generally stable when isolated, they require careful evaluation for associated ligamentous injury and craniocervical instability. CT is the imaging modality of choice for defining the fracture and assessing alignment, while MRI may provide additional evaluation of ligamentous and neural structures. Recognition of this uncommon fracture pattern is important for appropriate management and favorable outcome. References: Clark CR, White AA 3rd. Fractures of the dens. A multicenter study. J Bone Joint Surg Am. 1985;67(9):1340-1348. https://pubmed.ncbi.nlm.nih.gov/4077905/ O'Brien WT Sr, Shen P, Lee P. The Dens: Normal Development, Developmental Variants and Anomalies, and Traumatic Injuries. J Clin Imaging Sci. 2015;5:38. Published 2015 Jun 30. DOI: 10.4103/2156-7514.159565 Anderson LD, D'Alonzo RT. Fractures of the odontoid process of the axis. J Bone Joint Surg Am. 1974;56(8):1663-1674. https://pubmed.ncbi.nlm.nih.gov/4434035/ Nouri A, Da Broi M, May A, et al. Odontoid Fractures: A Review of the Current State of the Art. J Clin Med. 2024;13(20):6270. Published 2024 Oct 21. DOI: 10.3390/jcm13206270 Jain N, Verma R, Garga UC, Baruah BP, Jain SK, Bhaskar SN. CT and MR imaging of odontoid abnormalities: A pictorial review. Indian J Radiol Imaging. 2016;26(1):108-119. DOI: 10.4103/0971-3026.178358 Baranto D, Steinke J, Blixt S, et al. The epidemiology of odontoid fractures: a study from the Swedish fracture register. Eur Spine J. 2024;33(8):3034-3042. DOI: 10.1007/s00586-024-08406-3 Hashem M, Surur S, Hamad AS. Clinical and Radiological Outcomes of Halo Vest Application for Type II and III Odontoid Fractures. Int J Gen Med. 2024;17:457-469. Published 2024 Feb 5. DOI: 10.2147/IJGM.S440126 Gonschorek O, Vordemvenne T, Blattert T, Katscher S, Schnake KJ; Spine Section of the German Society for Orthopaedics and Trauma. Treatment of Odontoid Fractures: Recommendations of the Spine Section of the German Society for Orthopaedics and Trauma (DGOU). Global Spine J. 2018;8(2 Suppl):12S-17S. DOI: 10.1177/2192568218768227 Tashjian RZ, Majercik S, Biffl WL, Palumbo MA, Cioffi WG. Halo-vest immobilization increases early morbidity and mortality in elderly odontoid fractures. J Trauma. 2006;60(1):199-203. DOI: 10.1097/01.ta.0000197426.72261.17 Umaiza Ihsan, MD is a medical graduate of King Edward Medical University, Pakistan. She completed her internship at Mayo Hospital, Lahore, including a three- month rotation in Radiology, which further strengthened her interest in diagnostic imaging. She has gained additional clinical exposure in Radiology through observerships at Mon Health Morgantown and the University of Maryland, Baltimore. She has a strong interest in Radiology, particularly diagnostic imaging and its role in clinical decision making, and is actively interested in clinical research, with experience in systematic reviews and medical research. All posts by Umaiza Ihsan, MD Kevin M. Rice, MD is the president of Global Radiology CME and is a radiologist with Cape Radiology Group. He has held several leadership positions including Board Member and Chief of Staff at Valley Presbyterian Hospital in Los Angeles, California. Dr. Rice has made several media appearances as part of his ongoing commitment to public education. Dr. Rice's passion for state of the art radiology and teaching includes acting as a guest lecturer at UCLA. In 2015, Dr. Rice and Natalie Rice founded Global Radiology CME to provide innovative radiology education at exciting international destinations, with the world's foremost authorities in their field. In 2016, Dr. Rice was nominated and became a semifinalist for a "Minnie" Award for the Most Effective Radiology Educator. He was once again a semifinalist for a "Minnie" for 2021's Most Effective Radiology Educator by AuntMinnie.com. He has continued to teach by mentoring medical students interested in radiology. Everyone who he has mentored has been accepted into top programs across the country including Harvard, UC San Diego, Northwestern, Vanderbilt, and Thomas Jefferson. Follow Dr. Rice on Twitter @KevinRiceMD All posts by Kevin M. Rice, MD
- Traumatic Diaphragmatic Rupture
A 30-year-old female, after a motor vehicle collision, presented with chest pain, abdominal pain, shortness of breath, and rib fractures. Diagnosis? • Xray of the Week Figure 1. Coronal and axial CT Scan. Diagnosis? Figure 2. CT scan of traumatic left hemi-diaphragmatic rupture. (A) Coronal CT images demonstrate abdominal viscera herniating into the left hemithorax (yellow arrow pointing to colon), consistent with traumatic disruption of the left hemidiaphragm. (B) Axial CT image also demonstrates abdominal organs including spleen (red arrow) in the chest. Figure 3. Prior CT examination. Coronal CT image obtained one year earlier demonstrates the pre-trauma thoracoabdominal anatomy in the same patient without the left-sided intrathoracic visceral herniation seen on the current examination. Normal left hemidiaphragm (yellow arrow). Epidemiology Traumatic diaphragmatic rupture is uncommon, occurring in approximately 0.5% of all trauma patients and around 1–2% of patients with blunt trauma [1]. Motor vehicle collisions are a major cause of blunt diaphragmatic rupture. Left-sided injuries predominate, accounting for approximately 65–80% of cases, while right-sided and bilateral ruptures are less frequent. Diaphragmatic rupture commonly occurs in the setting of high-energy thoracoabdominal trauma and is frequently accompanied by other traumatic injuries [1,2]. Clinical Findings Clinical presentation of traumatic diaphragmatic rupture is variable and may be obscured by associated thoracic or abdominal injuries. Patients may present with chest or abdominal pain, dyspnea, tachypnea, or respiratory distress. Physical examination may demonstrate decreased breath sounds or, when abdominal viscera have herniated into the thorax, bowel sounds within the chest. Some injuries may initially be clinically occult, contributing to delayed diagnosis [1,2]. In this case, the 30-year-old woman presented following a motor vehicle collision with chest pain, abdominal pain, and shortness of breath; associated rib fractures were also documented. Pathology Traumatic diaphragmatic rupture results from disruption of the musculotendinous diaphragm following blunt or penetrating thoracoabdominal trauma. In blunt trauma, sudden elevation of intra-abdominal pressure and shearing forces can produce diaphragmatic tears, which commonly involve the posterolateral diaphragm [2]. The resulting defect may permit abdominal viscera to herniate into the thoracic cavity because of the pressure gradient between the abdomen and chest. If unrecognized, progressive herniation may lead to incarceration or strangulation of herniated viscera. Classification Traumatic diaphragmatic injuries are graded according to the American Association for the Surgery of Trauma (AAST) Organ Injury Scale. Grade I represents diaphragmatic contusion; Grade II, a laceration <2 cm; Grade III, a laceration 2–10 cm; Grade IV, a laceration >10 cm with tissue loss <25 cm²; and Grade V, a laceration with tissue loss >25 cm². Bilateral injuries are advanced by one grade up to Grade III [3]. This classification describes the anatomical severity of diaphragmatic injury. Radiographic Features Chest radiography may demonstrate an elevated or irregular hemidiaphragm, intrathoracic abdominal viscera, abnormal diaphragmatic contour, or associated pleural and pulmonary abnormalities; however, findings may be subtle or nonspecific [4]. Multidetector CT is the principal imaging modality for evaluating suspected traumatic diaphragmatic injury [5]. Direct CT findings include focal diaphragmatic discontinuity and the dangling diaphragm sign, representing inward curling of the torn diaphragmatic edge [6]. Indirect findings include intrathoracic herniation of abdominal viscera, the collar sign from waist-like constriction of herniated viscera at the defect, and the dependent viscera sign, in which herniated abdominal organs lie against the posterior thoracic wall [7]. Coronal and sagittal multiplanar reformations may facilitate identification of diaphragmatic defects and visceral herniation. Associated thoracoabdominal injuries, including rib fractures, may also be identified. Treatment and Prognosis Traumatic diaphragmatic rupture requires surgical repair once the patient's condition permits. Herniated abdominal viscera are reduced and the diaphragmatic defect is usually closed primarily with sutures; mesh may be required for larger defects that cannot be closed without tension [8]. The operative approach may be abdominal, thoracic, or minimally invasive depending on clinical stability, associated injuries, and timing of presentation [1,8]. Prognosis is largely determined by the severity of associated traumatic injuries rather than the diaphragmatic defect itself. Delayed or missed diagnosis may result in visceral incarceration, strangulation, or respiratory compromise [8]. Conclusion Traumatic diaphragmatic rupture is an uncommon but important complication of thoracoabdominal trauma that may be difficult to recognize clinically. Awareness of characteristic imaging findings, particularly on multidetector CT, is essential for prompt diagnosis and appropriate management, helping to reduce complications associated with delayed or missed injury. References Furák J, Athanassiadi K. Diaphragm and transdiaphragmatic injuries. J Thorac Dis. 2019;11(Suppl 2):S152-S157. doi:https://doi.org/10.21037/jtd.2018.10.76 Petrone P, Asensio JA, Marini CP. Diaphragmatic injuries and post-traumatic diaphragmatic hernias. Curr Probl Surg. 2017;54(1):11-32. doi:https://doi.org/10.1067/j.cpsurg.2016.11.001 Moore EE, Malangoni MA, Cogbill TH, et al. Organ injury scaling IV: thoracic vascular, lung, cardiac, and diaphragm. J Trauma. 1994;36(3):299-300. doi:https://doi.org/10.1097/00005373-199403000-00002 Desir A, Ghaye B. CT of blunt diaphragmatic rupture. Radiographics. 2012;32(2):477-498. doi:https://doi.org/10.1148/rg.322115082 Nchimi A, Szapiro D, Ghaye B, et al. Helical CT of blunt diaphragmatic rupture. AJR Am J Roentgenol. 2005;184(1):24-30. doi:https://doi.org/10.2214/ajr.184.1.01840024 Desser TS, Edwards B, Hunt S, Rosenberg J, Purtill MA, Jeffrey RB. The dangling diaphragm sign: sensitivity and comparison with existing CT signs of blunt traumatic diaphragmatic rupture. Emerg Radiol. 2010;17(1):37-44. doi:https://doi.org/10.1007/s10140-009-0819-5 Bergin D, Ennis R, Keogh C, Fenlon HM, Murray JG. The “dependent viscera” sign in CT diagnosis of blunt traumatic diaphragmatic rupture. AJR Am J Roentgenol. 2001;177(5):1137-1140. doi:https://doi.org/10.2214/ajr.177.5.1771137 Giuffrida M, Perrone G, Abu-Zidan F, et al. Management of complicated diaphragmatic hernia in the acute setting: a WSES position paper. World J Emerg Surg. 2023;18(1):43. doi:https://doi.org/10.1186/s13017-023-00510-x Umaiza Ihsan, MD, is a medical graduate of King Edward Medical University, Pakistan. She completed her internship at Mayo Hospital, Lahore, including a three- month rotation in Radiology, which further strengthened her interest in diagnostic imaging. She has gained additional clinical exposure in Radiology through observerships at Mon Health Morgantown and the University of Maryland, Baltimore. She has a strong interest in Radiology, particularly diagnostic imaging and its role in clinical decision-making, and is actively interested in clinical research, with experience in systematic reviews and medical research. All posts by Umaiza Ihsan, MD Kevin M. Rice, MD is the president of Global Radiology CME and is a radiologist with Cape Radiology Group. He has held several leadership positions including Board Member and Chief of Staff at Valley Presbyterian Hospital in Los Angeles, California. Dr. Rice has made several media appearances as part of his ongoing commitment to public education. Dr. Rice's passion for state of the art radiology and teaching includes acting as a guest lecturer at UCLA. In 2015, Dr. Rice and Natalie Rice founded Global Radiology CME to provide innovative radiology education at exciting international destinations, with the world's foremost authorities in their field. In 2016, Dr. Rice was nominated and became a semifinalist for a "Minnie" Award for the Most Effective Radiology Educator. He was once again a semifinalist for a "Minnie" for 2021's Most Effective Radiology Educator by AuntMinnie.com. He has continued to teach by mentoring medical students interested in radiology. Everyone who he has mentored has been accepted into top programs across the country including Harvard, UC San Diego, Northwestern, Vanderbilt, and Thomas Jefferson. Follow Dr. Rice on Twitter @KevinRiceMD All posts by Kevin M. Rice, MD














