Emerg Radiol (2014) 21:99–113 DOI 10.1007/s10140-013-1183-z
ASER ANNUAL MEETING CASES OF THE DAY
25th Anniversary ASER Annual Meeting October 9–12, 2013 Cases-of-the-Day Andrew Gelbman, DO, PhD Chairman
Published online: 11 January 2014 # Am Soc Emergency Radiol 2014
The “Case-of-the-Day” program is an activity consisting of various unknown interesting examinations encountered in the practice of emergency radiology, presented to challenge ASER annual meeting attendees. Some of these cases are classic examples of a condition, while others are less typical; however, all of the diagnoses can be made using the provided clinical information and accompanying images.
During the ASER Annual Meeting new cases were displayed every morning and the correct answers were displayed the following morning and presented in General Session. Radiologists submitted their best answers daily in a provided box and Gustav Blomquist, MD was awarded with the most correct responses. We gratefully acknowledge the following “Case-of-the-Day” presenters: Edward Hyunsun Ahn, MD Neil Amin, MD Aaron Heinrich Baer, MD Vika Bandari-Bhalla, MD Chitra Chandrasekhar, MD Rebecca Chang, BS Adam Cole, MD Jay Ezra Haggerty, MD Brian Hamm, MD Douglas Kitchin, MD Girish Kumar, MD Brett Mollard, MD Scott Steenburg, MD Adam Stibbe, MD
100 Wednesday, October 9 Case-of-the-Day #1 Brian Hamm, MD Creighton University Medical Center Omaha, Nebraska History: A 72 y/o woman presented to her primary care physician complaining of several weeks of worsening left hip pain. She reported the pain was worse with physical activity involving use of her legs and was partially relieved by over-the-counter pain medication. She had never experienced pain like this before and reported no history of trauma. There was no significant radiation of the pain and she maintained full range of motion. She had no relevant past medical history and her only medications were those she had been taking for many years for high blood pressure, hyperlipidemia and osteoporosis. Physical examination failed to reveal any significant finding. An x-ray was ordered (Fig. 1) followed by an MRI (Fig. 2). What is the diagnosis?
Fig. 1 AP view of the left hip
Fig. 2 Coronal STIR MR image of the left hip Diagnosis: Bisphosphonate related insufficiency fracture
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Discussion The imaging findings are consistent with bisphosphonate related insufficiency fracture. This type of fracture has relatively recently become more widely accepted as a potential complication of long-term bisphosphonate use and consistently demonstrates a characteristic pattern of imaging findings. Focal cortical thickening with a beaked appearance is demonstrated in the lateral subtrochanteric region of the femur with surrounding high signal noted on the corresponding fluid-sensitive MRI sequence. The plain film features, along with a history of long-term bisphosphonate use and pain are diagnostic even without the accompanying MRI [1, 2]. The mechanism behind the development of this rare drugrelated complication is thought to relate to the osteoclast inhibition caused by the bisphosphonates. Areas of high stress, such as the subtrochanteric lateral cortex of the femur, normally undergo osseous turnover to maintain structural integrity. With inhibited osteoclasts in the setting of stress this remodeling process is disrupted resulting in abnormal osseous architecture manifesting as a thickened, beaked area of cortex which can progress to a completed fracture if not treated . The incidence of this type of fracture is poorly understood. Because the diagnosis is rare, many cases are missed completely at imaging or misdiagnosed as a more traditional fracture, especially those which have progressed to completion. Hence, precise estimates as to the incidence of this disease process are not available. However, there is enough data to imply the risk of this complication is still exceeded by the proven benefit of bisphosphonates in preventing osteoporosis related fractures . The treatment for bisphosphonate related insufficiency fractures is varied. Some still opt to treat conservatively with protected, minimal weight bearing and withdrawal of the bisphosphonate. Others opt for a more interventional approach using internal fixation. There is some suggestion that specific MRI features, such as presence of a discernible fracture line through the area of abnormal cortex can help determine which cases would be better treated with surgery. In all cases, imaging the opposite extremity is recommended as the process is often bilateral . Bisphosphonate related insufficiency fracture is a rare complication of bisphosphonate use and appropriate diagnosis is very important to determine treatment. This diagnosis is often first suggesting by the radiologist noticing characteristic findings on a plain film. More awareness in the radiology community can help prevent unnecessary progression to complete fractures. References 1. Venkatanarasimha N, Miles G, Suresh P. Subtrochanteric femoral insufficiency fractures related to the use of long-term bisphosphonates: A pictorial review. Emergency Radiology. 2010; 17(6):511–5. 2. Mohan PC, Howe TS, Koh JSB, Png MA. Radiographic features of multifocal endosteal thickening of the femur in patients on long-term bisphosphonate therapy. Eur Radiol. 2013; 23(1):222–7. 3. Saleh A, Hegde VV, Potty AG, Lane JM. Bisphosphonate therapy and atypical fractures. Orthop Clin North Am. 2013; 44(2):137. 4. Shane E. Evolving data about subtrochanteric fractures and bisphosphonates. N Engl J Med. 2010; 362(19):1825–7.
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Wednesday, October 9 Case-of-the-Day #2 Edward Ahn, MD, Karen Lee, MD, Robin Levenson, MD Beth Israel Deaconess Medical Center Boston, Massachusetts
Diagnosis: Isolated left fallopian tube torsion with fallopian tube cyst.
History: Nineteen-year-old nulligravida female with no significant past medical history presents to the emergency department with 2 days of severe intermittent left lower quadrant pain. Urine HCG was negative. Ultrasound in the emergency department was obtained (Figs. 1 and 2). The left ovary had normal arterial and venous vascular waveforms.
Female patients who present to the emergency department with pelvic pain and a negative pregnancy test are often referred for a pelvic ultrasound. Amongst the many diagnoses that an ultrasound may potentially reveal, isolated fallopian tube torsion is a rare but important entity for radiologists to exclude. Isolated tubal torsion occurs in approximately 1 in 1,500,000 women but requires emergent surgery.1 Common presenting symptoms are nonspecific and include pelvic pain, nausea, and vomiting.2 An adnexal mass may or may not be appreciated at the time of referral. Fallopian tube torsion tends to occur on the right, similar to ovarian torsion, purportedly because the sigmoid colon occupies the left side of the pelvis and thereby prevents torsion.3 A few common intrinsic risk factors for isolated tubal torsion include pelvic inflammatory disease, tubal neoplasms, and hydrosalpinx. Extrinsic risk factors include adhesions, adnexal venous congestion, and a gravid uterus.4 In our case, a 5 cm fallopian tube cyst was confirmed at surgery, arising from the ampulla. The cyst and hyperemic, edematous fallopian tube were torsed 360°× 3. The diagnosis of isolated tubal torsion can be made preoperatively with an ultrasound demonstrating a dilated fallopian tube, a convoluted cystic and solid structure representing the thickened torsed tube, and a normal ipsilateral ovary.4 The whirl-
Fig. 1 Ultrasound image of the left adnexa shows a heterogeneous solid structure (thick arrow ) and a cystic lesion (thin arrow ) interposed between the left ovary and the uterus
Fig. 2 Swirled appearance of the heterogeneous structure (thick arrow)
102 pool sign, which is the swirling appearance of the torsed tube, is considered relatively specific for isolated fallopian tube torsion in the appropriate clinical context.5 Both CT and ultrasound can demonstrate the nidus for torsion, if one is present, such as a tubal cyst. On contrast enhanced CT, the fallopian tube can appear dilated and nonenhancing if ischemia is present.6 A beaked appearance of the fallopian tube, similar to the beak sign in volvulus or closed loop bowel obstruction, can also be a specific sign in the appropriate clinical context.4 Definitive treatment of isolated fallopian tube torsion is surgical. Delay in surgery can lead to tubal necrosis with irreversible damage to the ipsilateral ovary and potential gangrenous transformation resulting in peritonitis and infection.2,7 The specific operation performed depends on the stage of disease at presentation and the presence of any complications, and can range from simple surgical detorsion to salpingectomy. 8 Isolated fallopian tube torsion is far less common than ovarian torsion but is a surgical emergency that should be considered in female patients with pelvic pain, a swirled pelvic mass, dilated fallopian tube, and normal ipsilateral ovary. Recognizing the characteristic radiologic appearance of isolated fallopian tube torsion is critical in making a timely diagnosis and expediting definitive treatment. References 1. Orazi C, Inserra A, Lucchetti MC, et al. Isolated tubal torsion: a rare cause of pelvic pain at menarche. Pediatr Radiol 2006; 36(12):1316–8. 2. Ferrera PC, Kass LE, Verdile VP. Torsion of the fallopian tube. Am J Emerg Med 1995; 13(3):312–4. 3. Wong SW, Suen SH, Lao T, et al. Isolated fallopian tube torsion: a series of six cases. Acta Obstet Gynecol Scand 2010; 89(10):1354–6. 4. Gross M, Blumstein SL, Chow LC. Isolated fallopian tube torsion: a rare twist on a common theme. AJR 2005; 185(6): 1590–2. 5. Vijayaraghavan SB, Senthil S. Isolated torsion of the fallopian tube: the sonographic whirlpool sign. J Ultrasound Med 2009; 28(5): 657–62. 6. Bondioni MP, McHugh K, Grazioli L. Isolated fallopian tube torsion in an adolescent: CT features. Pediatr Radiol 2002; 32(8):612–3.
7. Ghossain MA, Buy JN, Bazot M, et al. CT in adnexal torsion with emphasis on tubal findings: correlation with US. J Comput Assist Tomogr 1994; 18:619–625 8. Krissi H, Shalev J, Bar-Hava I, et al. Fallopian tube torsion: laparoscopic evaluation and treatment of a rare gynecological entity. J Am Board Fam Pract 2001; 14(4):274–7 Wednesday, October 9 Case-of-the-Day #3 Iftikhar Ahmad, MD and Scott D. Steenburg, MD Department of Radiology and Imaging Sciences Indiana University School of Medicine Indianapolis, Indiana
Emerg Radiol (2014) 21:99–113 History: The patient is a 67 years old female patient who underwent a CTA of the head and neck for evaluation of clinical signs of subclavian steal syndrome. An incidental finding was subsequently identified.
Fig. 1 Axial CT (bone windows ) demonstrates a right malar cosmetic implant (arrow head ) which has fractured and migrated into the maxillary sinus (arrow ). There is an intact left malar cosmetic implant (curved arrow)
Fig. 2 Sagittal CT multi-planar reformatted image (soft tissue windows) demonstrates a migrated right cosmetic malar implant fragment (arrow), causing an expansile reactive cyst (asterisk) in the maxillary sinus. This reactive cyst causes elevation and demineralization of the orbital floor (arrow head) Diagnosis: Reactive cyst related to the migrated fractured cosmetic malar implant.
Discussion Complications related to the malar implants include infection, migration, extrusion, foreign body reaction (as in this case), and heterotopic bone formation (1, 2). Malar implant migration is a rare but serious complication that may cause inadvertent damage to the vital structures such as eye (3). Fluid accumulation around an embedded foreign body within its capsule constituting a cyst has been reported for other reasons (2, 4) but to the best of our knowledge, migration of a fractured malar cosmetic
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implant fragment resulting in a maxillary sinus expansile reactive cyst has not been previously described in the English language medical literature. Facial cosmetic surgery is common in the United States (2), and these patients may undergo imaging unrelated to their cosmetic surgery. Cosmetic facial implants have been used for reconstruction or augmentation of the cheek, forehead, nose, lips and chin (2). A variety of synthetic material may be used (2), and care should be taken in evaluating patients with cosmetic implants as the density of the material may simulate bone on soft tissue windows, and can easily be mistaken for bone fragments. Cosmetic implants are often used in multiple locations simultaneously to achieve facial symmetry which can aid the radiologist in detecting implant fracture and/or migration (2). References 1. Charles S. Imaging of Facial Cosmetic Surgery. In: Daniel G, Westesson P, editors. Atlas of Postsurgical Neuroradiology. SBN: 978-3-642-15827-8 (Print) 978-3-642-15828-5 (Online);DOI10.1007/ 978-3-642-15828-5_1 ed.: Springer Berlin Heidelberg;Per-Lennart A. Westesson; 2012. p. 1–31. 2. Schatz CJ, Ginat DT. Imaging of cosmetic facial implants and grafts. AJNR 2013;34(9):1674–1681. 3. Hatten K, Morales RE, Wolf JS. Intraorbital erosion of a malar implant resulting in mastication-induced vision changes. Ear Nose Throat J 2012;91(11):E23-5. 4. Mladick RA. Alloplastic cheek augmentation. Clin Plast Surg 1991;18(1):29–38. Wednesday, October 9 Case-of-the-Day #4 Adam Cole MD, John Fantauzzi MD Albany Medical Center Albany, New York History: Fifty-five year old female s/p recent right upper lobectomy, presents with fever and dyspnea.
Diagnosis: Right middle lobe torsion
Discussion: Lobar torsion involves rotation of the bronchovascular pedicle generally 180° with resultant airway obstruction, venous congestion, ischemia, and possible infarction. If infarction develops subsequent gangrenous infection, sepsis, and shock may ensue. Lobar torsion is a rare disease process which complicates approximately 0.1 % of pulmonary resections, typically right upper lobectomy (70 %), less often left upper lobectomy (15 %). The median presentation time is 10 days after resection. Other less frequent etiologies are blunt trauma, complicated pneumonia, or spontaneous torsion of an accessory lobe. The signs and symptoms are nonspecific and include dyspnea, fever, tachycardia, and hypotension. Differentiation from mucoid impaction and lobar pneumonia is critical as the treatment therapies are vastly different. If unrecognized lobar torsion carries a high mortality rate, reported as high as 20 % as opposed to 2 % if promptly diagnosed. Definitive treatment is surgical fixation or excision of the involved lobe. This process may be prevented by pneumopexy of the remaining lobes at the time of initial resection, especially in instances where the fissure is well developed. The chest radiograph demonstrates a wedge shaped opacity in the right upper-mid lung zone with reorientation and bulging of the major fissure which extends below the level of the hilum. There is volume loss on the right with mediastinal shift and tracheal deviation. The costophrenic sulci are blunted. Additional radiographic findings may include volume increase with mediastinal shift to the contralateral side as the torsed lobe becomes edematous. The CT image demonstrates consolidation of the right middle lobe with bulging of the major fissure. There is faint smooth interlobular septal thickening and ground glass attenuation within the middle lobe secondary to venous obstruction. The bronchus is obliterated with bilateral pleural effusions. Other distinguishing findings may include smooth tapering of the lobar pulmonary artery with lack of contrast enhancement of the affected lobe. In equivocal cases, bronchoscopy may be helpful for further evaluation.
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Lobar torsion although rare, should be considered in a symptomatic patient in the postoperative period with radiograph findings which resemble atelectasis or pneumonia. Prompt diagnosis is necessary to prevent significant morbidity and mortality and is best attained utilizing pertinent clinical history as well as aggressive radiologic evaluation. References 1. Cable DG et al: Lobar torsion after pulmonary resection: presentation and outcome. J Thorac Cardiovasc Surg. 122(6):1091–3, 2001 2. Kim EA et al: Radiographic and CT findings in complications following pulmonary resection. Radiographics. 22(1):67– 86, 2002 3. Nguyen JC et al: Bilateral whole-lung torsion after bilateral lung transplantation. J Thorac Imaging. 26(1):W17-9, 2011 4. Felson B: Lung torsion: radiographic findings in nine cases. Radiology. 162(3):631–8. 1987 5. Moser ES et al: Lung torsion: case report and literature review. Radiology. 162(3):639–43, 1987
Fig. 2 Axial T2 (a) and Sagittal STIR (b) weighted images demonstrating increased central spinal cord intensity consistent with central spinal cord ischemia Diagnosis: Aortic transection (Fig. 1) with associated hypoperfusion induced central spinal cord ischemia (Fig. 2).
Thursday, October 10 Case-of-the-Day #1 Authors: Adam Stibbe, MD and Andrew Gelbman, DO, PhD Department of Diagnostic Radiology Creighton University Omaha, Nebraska History: This 23-year-old male was involved in a high speed motor vehicle collision with chief complaint of severe chest pain on arrival. Vital signs were stable, however, he had decreased lower extremity pulses and strength. He was urgently transferred to the CT scanner where he was found to have a traumatic thoracic aortic transection (Fig. 1). He was then emergently transferred to the OR where he underwent a thoracic endovascular aortic repair (TEVAR). Upon extubation on post-op day 1 he was unable to move his lower extremities. At this time, an MRI of the cervical, thoracic and lumbar spine was performed (Fig. 2).
Fig. 1 CECT demonstrating aortic transection of the distal aortic arch
Discussion: What happened to our patient is quite rare. Patients are in motor vehicle collisions on a daily basis, but the majority with an aortic transection never make it to the hospital (3). Although, with recent advances, the number of patients with traumatic aortic injury surviving until hospitalization is increasing (2). These patients are often treated with TEVAR; formerly these patients were treated with open repair. With the increased use of TEVAR there has been a significant decrease in the number of peri-operative morbidities such as paraplegia and stroke (5). Our patient had lower extremity weakness on arrival which was significantly worse after surgery. His symptoms and imaging findings are consistent with extensive spinal cord hypo-perfusion (4). The spinal cord is supplied by 1 anterior and 2 posterior spinal arteries which extend longitudinally along the spinal cord. The anterior spinal artery (ASA) receives supply from the radicular arteries. The most notable supporting segmental artery is the artery of Adamkiewicz which joins the anterior spinal artery between T9-T12 and helps supply the cord down to the conus medullaris (4). In the thoracolumbar spinal cord there is a greater proportion of gray matter, with higher metabolic demands, thus resulting in an increased risk of hypo-perfusion induced ischemia (1). Aortic transection is a devastating injury with a high risk of morbidity and death. Our patient survived his aortic transection (Fig. 1), yet he experienced a significant associated morbidity with hypo-perfusion induced central cord ischemia (Fig. 2). References 1. Boll DT, Bulow H, Blackham KA, Aschoff AJ, Schmitz BL. MDCT angiography of the spinal vasculature and the artery of adamkiewicz. AJR Am J Roentgenol. 2006 Oct; 187(4):1054–60. 2. Davies MG, Younes HK, Harris PW, Masud F, Croft BA, Reardon MJ, et al. Outcomes before and after initiation of an acute aortic treatment center. J Vasc Surg. 2010 Dec; 52(6):1478–85. 3. Hiller RJ, Mikocka-Walus AA, Cameron PA. Aortic transection: Demographics, treatment and outcomes in Victoria, Australia. Emerg Med J. 2010 May; 27(5):368–71. 4. Novy J, Carruzzo A, Maeder P, Bogousslavsky J. Spinal cord ischemia: Clinical and imaging patterns, pathogenesis, and outcomes in 27 patients. Arch Neurol. 2006 Aug; 63(8):1113–20. 5. Tang GL, Tehrani HY, Usman A, Katariya K, Otero C, Perez E, et al. Reduced mortality, paraplegia, and stroke with stent graft repair of blunt aortic transections: A modern meta-analysis. J Vasc Surg. 2008 Mar; 47(3):671–5.
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Thursday, October 10 Case-of-the-Day #2 Rebecca Chang, BS Winthrop-University Hospital Mineola, New York
Definitive treatment for Bouveret’s syndrome is an enterolithotomy or a gastrotomy, with or without fistula repair and cholecystectomy. Up to 42 % of patients undergoing surgical treatment have failed previous attempts at nonsurgical management. Repair of the fistula continues to be controversial, as with other forms of gallstone ileus, since spontaneous closure of the tract has been documented after the removal of the obstructing stone. In addition, inflammatory processes make repair difficult, prolonging surgery time for patients who may already be poor surgical candidates. However without fistula repair, the patient may be at risk for recurrent disease.
History: Ninety-five-year-old woman presented with nausea, vomiting, and a mildly elevated serum lipase level. Non-contrast CT was performed.
Diagnosis: Bouveret’s Syndrome
Discussion: Gallstone ileus is an uncommon complication of cholelithiasis, where a small bowel obstruction is created from stone impaction at some point in the bowel. Rarely, obstruction at the level of the gastric outlet—called Bouveret’s syndrome—can occur. This syndrome is named after the French internist Leon Bouveret, who first described the death of two patients from complications of outlet obstruction secondary to gallstones in 1896. This more proximal site of obstruction is what distinguishes it as a specific form of gallstone ileus. Bouveret’s syndrome is usually caused by a single stone of at least 2.5 cm in diameter. The size of the stone is an important pathophysiologic factor, and as a general rule, the larger the stone, the more proximal the obstruction will be. Larger stones are also thought to cause mucosal irritation, leading to sustained muscle contraction, exaggerating stone impaction. This disease is diagnosed most commonly in elderly women, with an average age of 74 years. These elderly patients often have multiple comorbidities, making treatment difficult and morbidity and mortality high. The clinical presentation of patients with Bouveret’s syndrome is often non-specific. Patients may have nausea and vomiting, abdominal pain, anorexia, constipation, melena, and early satiety. Physical examination may reveal signs of dehydration, abdominal tenderness and distention, and fever. Evidence of biliary disease may not be apparent clinically, creating delays in diagnosis. CT is the imaging examination of choice, and is diagnostic in approximately 65 % of cases, with Rigler’s triad commonly identified, as with the more typical forms of gallstone ileus. Additional findings include pericholecystic inflammatory changes that extend to the duodenum, an obstructing mass, gas in the gallbladder, a thickened gallbladder wall, and a contracted gallbladder. The differential diagnosis includes complicated xanthogranulomatous cholecystitis and gallbladder carcinoma with a fistula. If oral contrast can be tolerated, CT may reveal a filling defect, and the fistulous tract may be identified. If tract enhancement is not directly visualized, contrast in the gallbladder also supports the diagnosis of a cholecystoenteric fistula. Endoscopic extraction with or without lithotripsy is a potential initial non-surgical treatment, especially for patients with multiple comorbidities. However, these procedures are shown to be technically challenging, with reported success rates of less than 10 %.
References 1. Brennan GB, Rosenberg, RD, Arora S. Bouveret syndrome. RadioGraphics 2004; 24:1171–1175. 2. Cappell MS, Davis M. Characterization of Bouveret’s syndrome: a comprehensive review of 128 cases. Am J Gasteroenterol 2006; 101:2139–2146. 3. Doycheva I, et al. Bouveret’s syndrome: case report and review of literature. Gastroenterol Res Pract 2007; vol. 2009, Article ID 914951, 4 pgs, 2009. doi:10.1155/2009/914951. 4. Koulaouzidis A, Moschos J. Bouveret’s syndrome: narrative review. Ann Hepatol 2007; 6:89–91. 5. Rehman A, et al. Bouveret’s syndrome. J Coll Phys Surg Pakistan 2008; 18:435–437. 6. Shinil KS, et al. Bouveret syndrome [published online ahead of print June 18 2013]. J Gastrointest Surg. http://www.ncbi.nlm.nih.gov/ pubmed/23775095. Accessed June 2013. 7. Zachary PE, et al. Bouveret syndrome: gallstone ileus of the duodenum. Surg Laparosc Endosc Percut Techn 2012; 22:301–303. Thursday, October 10 Case-of-the-Day #3 Iftikhar Ahmad, MD and Scott D. Steenburg, MD Department of Radiology and Imaging Sciences Indiana University School of Medicine Indianapolis, Indiana
History: Eight years old patient on chemotherapy presents with headache and altered mental status.
Fig. 1 Axial CT demonstrates Soft tissue density in the left retroantral fat pad (straight arrow) compared to normal retroantral fat on the right (arrow head) and the sinus disease
Emerg Radiol (2014) 21:99–113 5. Fatterpekar G, Mukherji S, Arbealez A, Maheshwari S, Castillo M. Fungal diseases of the paranasal sinuses. Semin Ultrasound CT MR 1999; 20(6):391–401. 6. McNab AA. Invasive fungal sinusitis: ophthalmic emergency. Clin Exp Ophthalmol 2013; 41(6):521. Thursday, October 10 Case-of-the-Day #4 Aaron H. Baer, MD; Suzanne T. Chong, MD, MS; Ursula S. Knoepp, MD; Hemant A. Parmar, MD University of Michigan Medical Center Ann Arbor, Michigan
Fig. 2 Coronal T1 post contrast images demonstrates thick enhancement of the cavernous sinuses (straight arrows) and intraluminal carotid cavernous enhancement (arrow head), consistent with angioinvasive fungal disease related thrombosis. There was absent left petrous carotid flow void on axial T2 image (not shown) consistent with thrombosis Diagnosis: Angioinvasive fungal sinusitis (path proven Aspergillus). Discussion: Aspergillus species are responsible for up to 80 % of sinonasal and central nervous system infections in the neutropenic immunocompromised patient (1). Invasive fungal sinusitis may present with painless necrosis of the nasal septum, sinusitis, and rapid orbital and intracranial spread leading to rapid death. The fungus invades the mucosa, submucosa, blood vessels, and bony walls of the nasal cavity and paranasal sinuses with subsequent intracranial and hematogenous dissemination (1, 2). Obliteration of the retroantral fat on head/face CT is a subtle but sensitive sign of the invasive sinusitis and should be included in the routine face and sinus CT search pattern, particularly in patients at risk for invasive sinus disease (3). In invasive fungal disease, frank bone erosion may be subtle (as in this case) or may be absent (4). MR imaging remains superior in evaluating intracranial and intraorbital extension as well as in the evaluation of complications, which can include cerebritis, abscess formation, meningitis, cavernous sinus thrombosis, osteomyelitis, mycotic aneurysm formation and stroke (5, 6). Our patient underwent aggressive anti-fungal therapy and did not develop a stroke, likely a result of robust collateral supply.
Fig. 1a Fig. 1b
Keywords: Retroantral fat pad sign, Invasive fungal sinusitis References 1. Gillespie MB and O’Malley BW. An algorithmic approach to the diagnosis and management of invasive fungal rhinosinusitis in the immunocompromised patient. Otolaryngol Clin North Am 2000; 33(2):323–334. 2. Anselmo-Lima WT, Lopes RP, Valera FC, Demarco RC. Invasive fungal rhinosinusitis in immunocompromised patients. Rhinology. 2004; 42(3):141–144. 3. Aribandi M, McCoy VA, Bazan C,3rd. Imaging features of invasive and noninvasive fungal sinusitis: a review. Radiographics 2007 Sep–Oct; 27(5):1283–1296. 4. Gorovoy IR, Kazanjian M, Kersten RC, Kim HJ, Vagefi MR. Fungal rhinosinusitis and imaging modalities. Saudi J Ophthalmol 2012 Oct; 26(4):419–426.
Fig. 2a Fig. 2b History: This is a case of a 16 year-old female with a history of T-cell acute lymphoblastic leukemia who presented with dysarthria, discoordination, left-sided paresthesias, and left sided weakness. The onset of these symptoms occurred 6 days after the intrathecal administration of
Emerg Radiol (2014) 21:99–113 methotrexate. Diffusion-weighted imaging (DWI) demonstrates signal hyperintensity in the corona radiata bilaterally with corresponding hypointensity on the apparent diffusion coefficient (ADC) maps (Fig. 1). These regions were mildly hyperintense on FLAIR and T2weighted imaging (Fig. 2a), minimally hypointense on T1-weighted imaging, and did not enhance following intravenous contrast administration (Fig. 2b). Diagnosis: The patient was diagnosed with acute methotrexate neurotoxicity. Discussion: Methotrexate-related neurotoxicity is a stroke-like leukoencephalopathy that has been described in acute, subacute, and chronic forms. Acute and subacute forms present in days-to-weeks following intrathecal or high-dose intravenous methotrexate administration and often present as stroke-like symptoms such as aphasia, dysarthria, or hemiplegia. This toxicity is fairly common, with transient paralysis or seizures being reported in up to 10 % of patients receiving intrathecal methotrexate. Classic imaging findings in acute and subacute phases include evidence of relatively symmetric restricted diffusion in the bilateral corona radiata, centrum semiovale, and subcortical white matter. As in this case, there is generally no abnormal contrast enhancement and T2-weighted and FLAIR sequences are often normal or subtly increased in signal intensity. The exact pathophysiology is poorly understood, but it has been postulated that methotrexate is directly toxic to axons by impairing folic acid metabolism, which may explain the characteristic sparing of gray matter. Months later, in the chronic phase, there is resolution of diffusion restriction, with ADC abnormalities normalizing before DWI findings. The affected regions will also become hyperintense on FLAIR sequences. Restriction of diffusion within cerebral white matter is most commonly associated with irreversible cytotoxic injury. There are, however, a few processes in addition to methotrexate neurotoxicity that impede diffusion in the acute setting with complete resolution on subsequent imaging. Common examples of such processes include prolonged seizure activity (especially in the splenium of the corpus callosum), successfully treated thromboembolic disease, and acute exacerbations of leukodystrophies. The primary differential consideration for these findings in the emergency setting is acute ischemia, but the absence of gray matter involvement and distribution outside a typical vascular territory should argue against an ischemic etiology. A history of recent methotrexate administration is obviously critical to making the diagnosis. However, even in the absence of such a history, attention to the unique imaging features of this process can lead to an expedient diagnosis, full reversal of focal neurological deficits, and a favorable outcome for our patients. References 1. Balin J, Parmar H, Kujawski L. Conventional and diffusionweighted MRI findings of methotrexate related sub-acute neurotoxicity. J Neurol Sci. 2008; 269(1–2): 169–71. 2 Rollins N, Winick N, Bash R, et al. Acute methotrexate neurotoxicity: findings on diffusion-weighted imaging and correlation with clinical outcome. AJNR Am J Neuroradiol. 2004; 25(10): 1688–95. 3. Haykin M, Gorman M, van Hoff J, et al. Diffusion-weighted MRI correlates of subacute methotrexate-related neurotoxicity. J Neurooncol. 2006; 76(2): 153–7.
107 Friday, October 11 Case-of-the-Day #1 Brett J. Mollard, MD; Ursula S. Knoepp, MD; Suzanne T. Chong, MD, MS University of Michigan Medical Center Ann Arbor, Michigan History: 31-month-old boy with acute decline in gait following head injury.
Emerg Radiol (2014) 21:99–113 MRI is usually diagnostic, demonstrating abnormal signal in all or almost all cerebral white matter. Over time, MRI demonstrates progressive cystic degeneration of the affected white matter, which is replaced by fluid that is best seen on FLAIR), leaving behind a cobweb of better preserved tissue strands. The cerebellar and brainstem white matter are relatively spared. Cerebral and cerebellar cortices and basal ganglia often have a normal appearance, though lesions may appear in the thalamus and globus pallidus.
References 1. Van der Knaap S, Pronk JC, Scheper G. Vanishing white matter disease. Lancet Neurol 2006; 5(5):413–423. 2. Schiffmann R, van der Knaap M. Invited article: an MRI-based approach to the diagnosis of white matter disorders. Neurology 2009; 72:750–759. 3. Van der Voorn, J, Pouwels P, Hart A, Serrarens J, Willemsen M, Kremer H, Barkhof F, van der Knaap M. Childhood white matter disorders: quantitative MR imaging and spectroscopy. Radiology 2006; 241(2):510–517. 4. Senol U, Haspolat S, Karaali K, Luleci E. MR imaging of vanishing white matter. AJR 2000; 175:868–828.
Unenhanced CT, 5 years later
Findings: On the initial CT study, there is low attenuation diffusely involving the white matter. This corresponds to hyperintensity on FLAIR, which was also present on T2W (not shown). There were no areas of abnormal enhancement post-contrast (not shown). Five years later, the CT study demonstrates that the white matter has “vanished”, especially in the frontal lobes where the white matter loss extends to the subcortical margin, and replaced with cerebrospinal fluid.
Friday, October 11 Case-of-the-Day #2 Chitra Chandrasekhar, MD University of Texas Health Science Center at Houston Bellaire, Texas History: A 39 year-old male presents to the ER with sudden onset of severe scrotal pain and swelling.
Diagnosis: Vanishing White Matter Disease
Discussion: Vanishing white matter (VWM) disease is one of the most prevalent inherited childhood leukoencephalopathies. Patients present with chronic neurological deterioration dominated by cerebellar ataxia. VWM is unusual due to its apparent sensitivity to febrile infections, minor head trauma, and acute fright, that may cause rapid neurological deterioration and unexplained coma. Oligodendrocytes and astrocytes are predominantly affected. The majority of patients die within a few years following onset.
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109 Conservative management may be indicated in those cases with delayed presentation based on the clinical findings. Other complications of testicular trauma include traumatic epididymitis, traumatic orchitis, phlegmonous funiculitis, or corditis. Extratesticular hematomas and hematoceles may also be present. Avulsion of the testicular vascular pedicle may lead to testicular infarction. Atrophy of the testis can occur remotely with missed infarction. References 1. Bhatt S, Dogra V. Role of US in Testicular and Scrotal Trauma. Radiographics. 2008 Oct; 28(6):1617–29. 2. Deurdulian C et al. US of Acute Scrotal Trauma: Optimal Technique, Imaging Findings, and Management. Radiographics. 2007 Mar-Apr; 27(2):357–369.
Diagnosis: Traumatic right testicular rupture with subcapsular hematomas and ruptured testicular capsule (tunica albuginea). Findings: Longitudinal grey scale images of the right testis show several ill-defined, somewhat rounded, hypoechoic areas along the subcapsular substance of the right testis representing intra-testicular hematomas (arrows image # 1). Discontinuity of the testicular capsule or tunica albuginea (anterior echogenic line) (arrow image #2) represents evidence of intra-testicular rupture.
Friday, October 11 Case-of-the-Day #3 Neil Amin, MD Emory University Hospital - School of Medicine Atlanta, Georgia Case-of-the-Day was presented at the meeting but unavailable for publication. Friday, October 11 Case-of-the-Day #4 Girish Kumar, MD John H. Stroger Jr. Hospital of Cook County Stickney, Illinois History: A 34-year-old patient with no significant past medical history presented to the ER with lower abdominal pain, subjective fever and chills. In the ER, his temperature was 101.2 F. On physical examination, there was suprapubic tenderness on deep palpation, without rebound tenderness. Urinalysis revealed >50 WBCs and 20 RBCs. CT abdomen/ pelvis was performed.
Discussion: Testicular trauma can be blunt or penetrating. Straddling injuries with blunt trauma of the scrotum can also occur. The testicular capsule or the tunica albuginea is normally recognized as a thin echogenic line noted anteriorly on testicular sonograms. The capsular artery of the testis runs along the tunica albuginea. Blunt trauma to the testis may produce subcapsular hematomas as noted in this case. Traumatic rupture of the testis is recognized as rupture of the tunica albuginea or testicular capsule and is considered a surgical emergency. Rupture of the tunica albuginea can be recognized on the sonogram as disruption or discontinuity of the normally appearing thin echogenic line anteriorly that represents the tunica albuginea. Testicular rupture calls for surgical intervention including debridement and closure of the tunica albuginea. Better salvage rates are achieved in cases that are recognized early with emergent surgical intervention.
Diagnosis: CT abdomen and pelvis demonstrated a tubular low attenuation lesion with peripheral enhancement, extending from apex of urinary bladder towards the umbilicus, consistent with Urachal sinus abscess.
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Discussion: Urachus is a midline tubular structure that extends upward from the anterior dome of the bladder towards the umbilicus. It is a vestigial remnant of Cloaca, which is the cephalic extension of the urogenital sinus (a precursor of the fetal bladder), and Allantois, which is a derivative of the yolk sac. The tubular urachus normally involutes before birth, remaining only as a fibrous band “median umbilical ligament”, with no known function. However, persistence of an embryonic urachal remnant can give rise to various clinical problems. Because urachal remnant diseases are uncommon and manifest with nonspecific abdominal or urinary signs and symptoms, definitive presurgical diagnosis is often difficult. Various abnormalities can be confusing unless one is familiar with the basic embryologic anatomy and imaging features of the subumbilical and prevesical region. A patent urachus may present radiologically as:
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2. Urachal Remnant Diseases: Spectrum of CT and US Findings. Jeong-Sik Yu, MD et al, Radiographics. 21(2):451–61, 2001 3. Thali-Schwab CM et al: Computed tomographic appearance of urachal adenocarcinomas: review of 25 cases. Eur Radiol. 15(1):79–84, 2005 4. StatDx Saturday, October 12 Case-of-the-Day #1 Brett J. Mollard, MD; Suzanne T. Chong, MD, MS University of Michigan Medical Center Ann Arbor, Michigan History: Seventy year old male status post motor vehicle collision.
Urachal fistula (Open channel from bladder to navel through which urine can leak) Urachal sinus (Persistence of only superficial segment of channel opening onto skin surface) Urachal diverticulum (Persistence of only deep segment creating diverticulum off anterosuperior aspect of bladder wall) Urachal cyst (Persistence of intermediary segment, with fibrous attachments to bladder and umbilicus)
Urachal remnant may manifest clinically with stone formation in the urachal diverticulum, urachal abscess or cystitis. These infected remnants are frequently confused with a wide spectrum of midline intra-abdominal or pelvic inflammatory disorders at clinical examination and with malignant tumors at imaging. The route of infection may be lymphatic, hematogenous, or vesical, and a wide variety of gram-positive and gram-negative microorganisms have been cultured from infected urachal remnants. Rarely, spontaneous rupture of an infected cyst into the abdominal cavity leads to localized or generalized peritonitis. Inhomogeneous attenuation with variable contrast enhancement in and around the disease process at CT often makes it difficult to differentiate an infected urachal remnant from urachal carcinoma. In the majority of cases, percutaneous needle biopsy or fluid aspiration is mandatory for diagnosis and therapeutic planning. Total removal of the cyst wall is essential because there is a 30 % reinfection rate. Also, there is increased risk of urachal adenocarcinoma in unresected or incompletely resected urachal remnant. Urachal tumors are typically silent because of their extraperitoneal location; consequently, the majority of patients exhibit local invasion or metastatic disease at presentation. Metastases occur initially in the pelvic lymph nodes, followed by systemic metastases to the lung, brain, liver, and bone (39). Local invasion and systemic metastases result in a 5-year survival ≤15 %. Our patient was treated with antibiotics. Surgery was performed at a later date and the whole sinus tract was removed. Pathologic analysis did not reveal any evidence of neoplasm. Patient was doing very well at his last clinical follow up.
References 1. Yiee JH et al: A diagnostic algorithm for urachal anomalies. J Pediatr Urol. 3(6):500–4, 2007
Findings: CT: The scalp is prominently thickened, with convoluted folds and furrows resembling a cerebriform pattern. Diagnosis: Cutis Veritis Gyrata
Discussion: Cutis verticis gyrate (CVG) is a rare skin disorder with progressive deformity of the scalp, consisting of thick, gyrated skin ridges and folds that mimic the appearance of brain sulci and gyri. Patients eventually seek medical attention for a number of reasons, including underlying associated neuropsychiatric and endocrine disorders, recurrent skin infections, and cosmetic correction of the condition. CGV is categorized into three variations- primary essential, primary non-essential, and secondary. Primary essential CVG is the idiopathic form, occurs more commonly in men, and usually develops during or shortly following puberty. Primary essential CVG has an insidious onset and is asymptomatic in the early stages, resulting in delayed diagnosis. Primary non-essential CVG is often associated with a number of neurological and ophthalmological abnormalities including mental retardation, epilepsy, schizophrenia, cerebral palsy, and cataracts. In secondary CVG, scalp changes may develop at any age and are usually asymmetric. Secondary CVG has been found to occur with certain tumors such as neurofibromas, cerebriform intradermal nevi, and inflammatory conditions. It is also
Emerg Radiol (2014) 21:99–113 associated with systemic diseases such as acromegaly, myxedema, amyloidosis, and pachydermoperiostosis. CVG is occasionally detected incidentally on imaging modalities such as CT and MRI. When identified, 3D volume rendering may be utilized to more accurately characterize the gyriform fold pattern which may have important implications for surgical planning and potentially aid in determining the type of CVG. Given the potential association with various neurologic, ophthalmologic, and systemic diseases, awareness of this rare skin condition may lead to early detection and diagnosis of the associated conditions.
References 1. Sommer A, Gambichler T, Altmeyer P, Kreuter A. A case of cutis verticis gyrata, induced by misuse of anabolic substances? Clin Exp Dermatol 2006; 31(1):134–136. 2. Nguyen N. Cutis verticis gyrata. Dermatology Online Journal 2003; 94(4):32. 3. Diven D, Tanus T, Raimer Sl. Cutis verticis gyrata. Int J Dermatol 1991;30:710 4. Chang GY. Cutis verticis gyrata: Underrecognized neurocutaneous syndrome. Neurology 1996; 47:573. 5. Oh D, Park J, Kang S, Hwang S, Park S. Primary non-essential cutis verticis gyrate revealed with 3-D magnetic resonance imaging. Acta Derm Venereol 2006; 86:458–459.
111 and pericholecystic fat stranding. The inflammatory process extends into the adjacent liver parenchyma
Fig. 2 Coronal contrast-enhanced CT shows markedly enlarged gallbladder with diffuse gallbladder wall thickening, low-attenuation intramural nodules, and cholelithiasis. There are inflammatory changes involving adjacent bowel (not shown). Diagnosis: Xanthogranulomatous Cholecystitis
Saturday, October 12 Case-of-the-Day #2 Jay E. Haggerty, MD; Suzanne T. Chong, MD, MS Division of Emergency Radiology Department of Radiology University of Michigan School of Medicine Ann Arbor, Michigan History: Seventy-one-year-old male presenting with chronic nausea and abdominal discomfort.
Fig. 1 Axial contrast-enhanced CT demonstrates diffuse gallbladder wall thickening with intramural low-attenuation nodules
Discussion: Xanthogranulomatous cholecystitis (XGC) is a rare form of a chronic cholecystitis characterized pathologically by the presence of lipid-laden macrophages expanding and distorting the gallbladder wall, and is associated with fibrosis and inflammatory changes that can extend beyond the gallbladder into adjacent structures (1). Clinically, patients present with symptoms of cholecystitis, although biliary colic is rare (1). Most patients are found to have cholelithiasis, and this is thought to contribute to the development of XGC through chronic inflammation (2). Several studies have examined the sonographic, CT and MRI features of XGC (2–6). The most characteristic sonographic feature of XGC is hypoechoic nodules or bands within the gallbladder wall (3). Other common sonographic findings include cholelithiasis and gallbladder wall thickening. Characteristic CT features include diffuse gallbladder wall thickening, lowattenuation intramural nodules, lumen surface enhancement, and cholelithiasis (4, 5). On MRI, intramural nodules appear hypointense on T1-weighted imaging and hyperintense on T2weighted imaging (4) and may demonstrate post-contrast enhancement (6). In contrast to XCG, acute cholecystitis is characterized on CT by gallbladder wall enhancement and generally less pronounced wall thickening, without low-attenuation nodules or bands within the gallbladder wall. Imaging similarities between XGC and gallbladder carcinoma make distinguishing between the two entities difficult. This distinction is important, however, because gallbladder carcinoma requires curative surgical resection that may include segmental hepatectomy or pancreaticoduodenectomy (3). Gallbladder wall thickening and intramural hypoattenuating nodules or bands are sensitive for XCG but they are non-specific and can be seen in both XGC
112 and gallbladder carcinoma, whereas a continuous mucosal line and cholelithiasis have been shown to have higher specificity for XGC (3). Other features specific for XCG and that can help distinguish it from gallbladder carcinoma include the absence of macroscopic hepatic invasion, intrahepatic biliary dilatation, or metastatic disease. The combination of three or more of these features has been shown to have excellent accuracy in distinguishing XCG from gallbladder cancer (4).
Emerg Radiol (2014) 21:99–113 obstructing mass, thought to be a colon cancer based on its firm nature. A CT was obtained for further evaluation.
References 1. Houston JP, Collins MC, Cameron I, et al. Xanthogranulomatous cholecystitis. Br J Surg 1994; 81:1030–1032. 2. Parra JA, Acinas O, Bueno J, et al. Xanthogranulomatous cholecystitis: Clinical, sonographic, and CT findings in 26 patients. AJR 2000; 174:979–983. 3. Uchiyama K, Ozawa S, Ueno M, et al. Xanthogranulomatous cholecystitis: The use of preoperative CT findings to differentiate it from gallbladder carcinoma. J Hepatobiliary Pancreat Surg 2009; 16:333– 338. 4. Goshima S, Chang S, Wang JH, et al. Xanthogranulomatous cholecystitis: Diagnostic performance of CT to differentiate from gallbladder carcinoma. European Journal of Radiology 2010 ; 74:79–83. 5. Zhao F, Lu PX, Yan SX, et al. CT and MR features of xanthogranulomatous cholecystitis: An analysis of consecutive 49 cases. European Journal of Radiology 2013; 82:1391–1397. 6 . S h e t t y G S , A b b e y P, P r a b h u S M , e t a l . Xanthogranulomatous cholecystitis: Sonographic and CT features and differentiation from gallbladder carcinoma: a pictorial essay. Jpn J Radiology 2012; 30:480–485. Saturday, October 12 Case-of-the-Day #3 Vika Bandari-Bhalla, MD Albany Medical Center Albany, New York Case-of-the-Day was presented at the meeting but unavailable for publication. Saturday, October 12 Case-of-the-Day #4 Douglas Kitchin, MD University of Wisconsin Madison, Wisconsin History: Fifty-eight year old man who presented with a 3 month history of waxing and waning abdominal pain. A colonoscopy was attempted as the initial diagnostic evaluation, but the colonoscope could not be passed through the transverse colon due to an
Diagnosis: This patient has a colocolonic intussusception secondary to a large submucosal lipoma. Note the large fatty mass as the lead point with telescoping of the transverse colon into the splenic flexure. The patient underwent partial colectomy which confirmed the intussusception and pathologically confirmed the diagnosis.
Discussion: Adult bowel intussusception is a different disease process than in children and has been associated with a lead point mass in up to 93 % of cases in the surgical literature (1). However, the majority of series evaluating adult intussusception are surgical series in symptomatic patients. The percentage of adult intussusception identified at imaging associated with a lead
Emerg Radiol (2014) 21:99–113 point mass is likely lower given the commonly seen transient small bowel intussusception. Enteric intussusception is more common than colonic by a ratio of 3:1 and a preoperative diagnosis is made with variable success (32–66 %) (1, 2). Classically, cases of adult intussusception have been managed surgically, although a more recent surgical study by Rea at al. suggests that intussusception identified on imaging can sometimes be monitored. Most of the cases which were successfully monitored in their series were enteroenteric intussusception without a lead point mass. The presence of a lead point mass or evidence of bowel obstruction were associated with a higher rate of operative intervention (1, 3). Colocolonic intussusception is a well-known presentation of colonic lipomas (4–8). Colonic lipomas are often asymptomatic, but 75 % of those greater than 4 cm in size become symptomatic (9, 10). Presenting symptoms can be vague and intermittent, as in our patient. Identification of the lead point mass is important as it can alter therapy, making operative intervention more likely. Management of incidentally found asymptomatic colonic lipomas can include observation (particularly for lesions less than 2 cm), endoscopic resection, or partial colectomy (11).
References 1. Azar T, Berger DL. Adult intussusception. Annals of surgery. 1997;226(2):134–8. 2. Wang N, Cui XY, Liu Y, et al. Adult intussusception: a retrospective review of 41 cases. World journal of gastroenterology : WJG. 2009;15(26):3303–8. 3. Rea JD, Lockhart ME, Yarbrough DE, Leeth RR, Bledsoe SE, Clements RH. Approach to management of intussusception in adults: a new paradigm in the computed tomography era. The American surgeon. 2007;73(11):1098–105.
113 4. Ongom PA, Wabinga H, Lukande RL. A ‘giant’ intraluminal lipoma presenting with intussusception in an adult: a case report. Journal of medical case reports. 2012;6(1):370. 5. Laleman W, Bisschops R, Vermeire S. Electronic clinical challenges and images in GI. Colocolonic intussusception of pediculated lipoma. Gastroenterology. 2009;136(1):e5–6. 6. Fatima H, Gregory A, Matthews D. Colocolonic intussusception secondary to an intraluminal lipoma. Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association. 2007;5(9):e38. 7. Abou-Nukta F, Gutweiler J, Khaw J, Yavorek G. Giant lipoma causing a colo-colonic intussusception. The American surgeon. 2006;72(1):83–4. 8. Triantopoulou C, Vassilaki A, Filippou D, Velonakis S, Dervenis C, Koulentianos E. Adult ileocolic intussusception secondary to a submucosal cecal lipoma. Abdominal imaging. 2004;29(4):426–8. 9. Rogy MA, Mirza D, Berlakovich G, Winkelbauer F, Rauhs R. Submucous large-bowel lipomas-presentation and management. An 18year study. The European journal of surgery = Acta chirurgica. 1991;157(1):51–5. 10. Bahadursingh AM, Robbins PL, Longo WE. Giant submucosal sigmoid colon lipoma. American journal of surgery. 2003;186(1):81–2. 11. Nallamothu G, Adler DG. Large colonic lipomas. Gastroenterology & hepatology. 2011;7(7):490–2.
Conflict of Interest All Case-of-the-Day presenters indicated having no conflict of interest regarding to their participation in this continuing medical education activity.