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Vascular Malformation and Hemangiomatosis Syndromes: Spectrum of Imaging Manifestations

¹ Department of Radiology, University of Michigan Health System, 1500 E Medical Center Dr., Ann Arbor, MI, 48109.
² Mallinckrodt Institute of Radiology, Washington University, St. Louis, MO.

Received January 27, 2007; accepted after revision October 7, 2007.

 
Address correspondence to K. M. Elsayes (kelsayes{at}med.umich.edu).

Abstract

Top Abstract Introduction Hemangiomas, Vascular... Blue Rubber Bleb Nevus... Proteus Syndrome Klippel-Trenaunay Syndrome and... Kasabach-Merritt Syndrome Conclusion References

 
OBJECTIVE. The purpose of this review is to describe the role of imaging and associated findings in the diagnosis of blue rubber bleb nevus syndrome, Proteus syndrome, Klippel-Trénaunay syndrome, and Kasabach-Merritt syndrome.

CONCLUSION. Blue rubber bleb nevus, Proteus, Klippel-Trénaunay, and Kasabach-Merritt syndromes are a diverse group of vascular malformation and hemangiomatosis syndromes. Both cutaneous and visceral vascular lesions are associated with these disorders. Accurate diagnosis of these syndromes is important because they can be associated with serious complications, including life-threatening hemorrhage.

Keywords: hemangioma • hemangiomatosis • imaging • vascular malformation

Introduction

Top Abstract Introduction Hemangiomas, Vascular... Blue Rubber Bleb Nevus... Proteus Syndrome Klippel-Trenaunay Syndrome and... Kasabach-Merritt Syndrome Conclusion References

 
Vascular malformation and hemangiomatosis syndromes, although rare, are a diverse group of disease entities that have characteristic imaging findings. The syndromes discussed—blue rubber bleb nevus syndrome, Proteus syndrome, Klippel-Trénaunay syndrome, and Kasabach-Merritt syndrome—are characterized by distinctive cutaneous and visceral vascular lesions. Vascular lesions of the skin have traditionally been recognized as a clue to the possible existence of these syndromes and potential for associated visceral vascular malformations and hemangiomas. The presence of a vascular malformation or hemangiomatosis syndrome often can be confirmed with a combination of clinical expertise and radiologic evaluation. The diagnosis of these conditions is important because they can be associated with numerous complications, including significant bleeding diatheses. We review the radiologic evaluation of various vascular malformation and hemangiomatosis syndromes, including the roles of specific imaging techniques and pertinent imaging findings.

Hemangiomas, Vascular Malformations, and Arteriovenous Malformations

Top Abstract Introduction Hemangiomas, Vascular... Blue Rubber Bleb Nevus... Proteus Syndrome Klippel-Trenaunay Syndrome and... Kasabach-Merritt Syndrome Conclusion References

 
Hemangiomas are benign neoplasms characterized by abnormal proliferation of blood vessels. These lesions arise from mesenchymal tissue. Histologically, hemangiomas are composed of multiple vascular channels lined with a single layer of endothelium and are supported by a fibrous connective tissue scaffold. Such lesions frequently proliferate early in life before regressing in size [1].

Vascular malformations are somewhat similar to hemangiomas in that they are composed of abnormal vascular channels lined with a single layer of dysplastic endothelium. These lesions, however, do not regress the way hemangiomas do. Vascular malformations are present at birth because they are congenital, although they may not become clinically evident until later in life. These malformations are named after the vascular element they most closely resemble: capillary, venous, and lymphatic malformations [1].

Hemangiomas and vascular malformations are not infrequent in the general population, and they are most commonly limited in extent. These lesions can, however, become quite large (for example, involving an entire extremity) and numerous (for example, affecting multiple organ systems). The term hemangiomatosis may be applied in the setting of very large or numerous hemangiomas. Large cutaneous hemangiomas and vascular malformations can have both superficial and deep components [1]. Hemangiomas and vascular malformations can involve numerous solid organs, including the liver, spleen, gastrointestinal tract, brain, and lungs.

Arteriovenous malformations occur when there is an abnormal communication between the high-pressure arterial system and the low-pressure venous system without an intervening capillary bed. The site at which abnormally dilated feeding arteries and veins communicate is called the nidus. Such lesions typically are associated with increased blood flow (hence, they are called high-flow lesions) and may result in steal phenomenon [1].

Blue Rubber Bleb Nevus Syndrome

Top Abstract Introduction Hemangiomas, Vascular... Blue Rubber Bleb Nevus... Proteus Syndrome Klippel-Trenaunay Syndrome and... Kasabach-Merritt Syndrome Conclusion References

 
Blue rubber bleb nevus syndrome (BRBNS) is a rare disorder characterized by multiple distinctive cutaneous and gastrointestinal venous malformations. Gascoyen [2] described the syndrome in 1860. The name of the syndrome is derived from the bluish color of the associated cutaneous lesions and their rubbery consistency at palpation [3]. BRBNS usually is sporadic and generally presents at birth or in early childhood [4]. The typical cutaneous venous malformations associated with this condition may or may not increase in size and number with age. Cutaneous lesions may number from a few to more than 100. These lesions preferentially involve the trunk and upper extremities, can be painful, and can range from a few millimeters to several centimeters in diameter.

Vascular malformations of the gastrointestinal tract associated with BRBNS can manifest as hematemesis, melena, or hematochezia [5–7]. Early diagnosis and management of this entity is particularly important because of the risk of life-threatening gastrointestinal hemorrhage [5]. Consumptive coagulopathy and iron deficiency anemia secondary to occult bleeding episodes also are complications [5, 8]. BRBNS has been associated with the development of certain tumors, including medulloblastoma, chronic lymphocytic leukemia, renal cell carcinoma, and squamous cell carcinoma [4]. Because BRBNS is quite rare, the exact risk of development of each of these neoplasms is unknown.

The most common site of bowel involvement in BRBNS is the small intestine, although lesions can occur anywhere along the gastrointestinal tract from the oral cavity to the anus [4]. Multiple diagnostic techniques may be needed to visualize these gastrointestinal lesions. Such lesions can be evaluated with endoscopy, barium studies, ^99mTc-labeled RBC nuclear scintigraphy, and contrast-enhanced CT. Fluoroscopic barium examinations may reveal multiple polypoid filling defects that represent venous malformations, possibly mimicking a polyposis syndrome. Although endoscopy is more sensitive for small lesions involving the stomach, duodenum, and colon, barium studies, such as small-bowel follow-through and enteroclysis examinations, are typically needed to evaluate the small bowel. The vascular nature of these lesions cannot be differentiated from other types of polyps solely on the basis of the findings at barium studies. Vascular malformations of the rectosigmoid colon are uncommon and can occur in association with BRBNS (Fig. 1A, 1B, 1C).

View larger version (129K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1A —32-year-old woman with blue rubber bleb nevus syndrome. Axial STIR MR image (TR/TE, 5,500/80; inversion time, 165 milliseconds; slice thickness, 4 mm) shows circumferential rectal wall and perirectal heterogeneous predominantly high signal intensity.

View larger version (117K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1B —32-year-old woman with blue rubber bleb nevus syndrome. Axial unenhanced (B) and contrast-enhanced (C) T1-weighted gradient-recalled echo (225/3.4; flip angle, 70°; slice thickness, 4 mm) delayed venous phase MR images show abnormal circumferential rectal wall and perirectal soft-tissue enhancement pathologically proved to represent large venous malformation.

View larger version (152K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1C —32-year-old woman with blue rubber bleb nevus syndrome. Axial unenhanced (B) and contrast-enhanced (C) T1-weighted gradient-recalled echo (225/3.4; flip angle, 70°; slice thickness, 4 mm) delayed venous phase MR images show abnormal circumferential rectal wall and perirectal soft-tissue enhancement pathologically proved to represent large venous malformation.

Technetium-99m-labeled RBC nuclear scintigraphy can be used to localize the site of active bleeding in patients with gastrointestinal hemorrhage. This technique can be particularly important when the findings at endoscopic evaluation are normal. Vascular lesions arising from sites other than the gastrointestinal tract (e.g., viscera, musculoskeletal system) also can be depicted with this imaging technique.

Although it frequently may not show tiny vascular lesions in the small and large bowel, contrast-enhanced CT can be helpful in evaluating certain complications related to this syndrome. Complications related to BRBNS that may be detectable with CT include intestinal intussusception, volvulus, infarction, and, in rare instances, active gastrointestinal bleeding [4, 9]. In addition, CT may reveal phleboliths within bowel-related lesions, suggesting a vascular cause, and may depict vascular lesions within other solid organs.

MRI is particularly useful for visualizing vascular lesions of the musculoskeletal system that may be associated with BRBNS. Such lesions can typically be successfully characterized with MRI. The cutaneous venous malformations that occur in this syndrome vary in depth and may or may not involve underlying muscle, bone, and joint spaces (Fig. 2A, 2B). Venous malformations involving the extremities can be complicated by osseous bowing deformities, pathologic fractures, and overgrowth. MRI is also valuable in the examination of vascular lesions within solid organs, such as the liver and spleen. Solid organ venous malformations associated with this syndrome are typically well-defined, hypointense to isointense in relation to normal adjacent parenchyma on T1-weighted images, and hyperintense in relation to normal adjacent parenchyma on T2-weighted images. These lesions typically become homogeneously enhanced after IV administration of contrast material. They can also, however, exhibit peripheral enhancement with subsequent delayed centripetal fill-in not unlike that of hemangiomas (Fig. 3). The venous malformations associated with BRBNS are low-flow lesions and therefore lack the flow voids that may be seen in high-flow arteriovenous malformations [1, 4].

View larger version (63K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 2A —12-year-old girl with blue rubber bleb nevus syndrome. Coronal STIR (TR/TE, 4,000/26; inversion time, 165 milliseconds; slice thickness, 5 mm) (A) and contrast-enhanced fat-saturated T1-weighted spoiled gradient-recalled echo (255/3.3; flip angle, 90°; slice thickness, 5 mm) (B) delayed venous phase MR images show large venous malformation involving subcutaneous tissue and underlying musculature of left lower extremity.

View larger version (61K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 2B —12-year-old girl with blue rubber bleb nevus syndrome. Coronal STIR (TR/TE, 4,000/26; inversion time, 165 milliseconds; slice thickness, 5 mm) (A) and contrast-enhanced fat-saturated T1-weighted spoiled gradient-recalled echo (255/3.3; flip angle, 90°; slice thickness, 5 mm) (B) delayed venous phase MR images show large venous malformation involving subcutaneous tissue and underlying musculature of left lower extremity.

View larger version (128K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 3 —39-year-old man with blue rubber bleb nevus syndrome. Axial contrast-enhanced portal venous phase fat-saturated T1-weighted spoiled gradient-recalled echo MR image (TR/TE, 4.2/2.0; flip angle, 12°; slice thickness, 4 mm) shows multiple peripherally enhanced hemangioma-like lesions within liver (long arrows), spleen (short arrows), and spine (arrowheads).

Proteus Syndrome

Top Abstract Introduction Hemangiomas, Vascular... Blue Rubber Bleb Nevus... Proteus Syndrome Klippel-Trenaunay Syndrome and... Kasabach-Merritt Syndrome Conclusion References

 
Proteus syndrome is a rare congenital condition described by Cohen and Hayden [10] in 1979. Wiedemann et al. [11] named this condition in 1983 after Proteus, the Greek god of the sea, who was able to change the shape of his body to avoid capture. The name Proteus syndrome thus refers to the condition's protean nature, particularly the unpredictable asymmetric partial gigantism and hemihypertrophy typically associated with this syndrome. Although the cause of Proteus syndrome is not definitely known, there is evidence to suggest that it occurs after mutation of a somatic dominant gene that is typically lethal, except in the setting of mosaicism [12]. Patients with Proteus syndrome may appear healthy at birth, and consequently the condition may not be diagnosed until early adulthood. Proteus syndrome is responsible for a variety of malformations and overgrowths involving multiple tissue types. Asymmetric overgrowth can involve the skin and skeleton and numerous other soft-tissue elements (e.g., vascular, fat, muscle, viscera) [13]. This overgrowth may manifest itself as hemihypertrophy and partial gigantism, and it typically results in disfiguring deformities of the skull, hands, and feet.

Soft-tissue abnormalities associated with Proteus syndrome include vascular malformations (Figs. 4A and 5B), lipomas and fatty hypertrophy (Figs. 4B and 5A), regional fatty atrophy, hyperpigmentation, and nevi. Abdominal solid organs may be abnormally enlarged and exhibit splenomegaly and nephromegaly. Skeletal abnormalities, such as macrodactyly, exostosis, progressive scoliosis, and limb-length discrepancy, are frequent and striking findings [14]. The highly variable manifestations of Proteus syndrome frequently lead to initial misdiagnosis. Severe neurofibromatosis type 1, Klippel-Trénaunay syndrome, hemihyperplasia–multiple lipomatosis syndrome, Maffucci syndrome, and Ollier disease can be confused with Proteus syndrome. To help minimize such errors, specific diagnostic criteria have been developed for Proteus syndrome (Appendix 1) [14, 15]. Consistent application of these diagnostic criteria allows reliable clinical diagnosis.

View larger version (125K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 4A —23-year-old man with Proteus syndrome. Axial contrast-enhanced portal venous phase CT scan through upper abdomen reveals multiple low-attenuation splenic lesions thought to represent vascular malformation.

View larger version (139K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 5B —10-year-old boy with Proteus syndrome. Axial contrast-enhanced T1-weighted FLAIR venous phase image (2,055/21; slice thickness, 4 mm) through level of midthoracic spine reveals enhanced large right paraspinous presumed vascular malformation (arrows).

View larger version (126K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 4B —23-year-old man with Proteus syndrome. Axial CT scan through lower abdomen shows marked soft-tissue asymmetry, including asymmetric prominence of right gluteus and iliopsoas muscles (long arrows) (compared with opposite side) and increased fatty tissue within left lower quadrant of abdomen and left lateral body wall (short arrows).

View larger version (129K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 5A —10-year-old boy with Proteus syndrome. Axial T1-weighted FLAIR MR image (TR/TE, 2,036/21; slice thickness, 5 mm) through lower abdomen shows large well-circumscribed mass of high signal intensity in left anterior abdominal wall consistent with lipoma (arrows).

View larger version (150K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 6A —5-year-old boy with Proteus syndrome and megalencephaly. (Courtesy of Parmar H, University of Michigan Health System, Ann Arbor, MI) Axial T2-weighted fast spin-echo MR image (TR/TE, 3,200/102; slice thickness, 6 mm) through level of upper cervical spine and maxilla shows extensive right facial soft-tissue hypertrophy (asterisks).

View larger version (127K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 6B —5-year-old boy with Proteus syndrome and megalencephaly. (Courtesy of Parmar H, University of Michigan Health System, Ann Arbor, MI) Axial T2-weighted fast spin-echo MR image (3,200/102; slice thickness, 6 mm) through level of cerebral hemispheres reveals enlargement of right cerebrum with associated abnormal cortical sulcation and gyration (arrowheads).

Top Abstract Introduction Hemangiomas, Vascular... Blue Rubber Bleb Nevus... Proteus Syndrome Klippel-Trenaunay Syndrome and... Kasabach-Merritt Syndrome Conclusion References

The diagnosis of Klippel-Trénaunay syndrome can be made when any two of the three features are present [22, 23]. Sixty-three percent of patients with Klippel-Trénaunay syndrome have all three components of the triad, and 37% have only two. The lower extremity is the site of involvement in approximately 95% of patients. The port-wine stain, a cutaneous capillary vascular malformation, is present in 98% of patients with this syndrome and is the most common manifestation [22]. This capillary vascular malformation typically does not markedly progress or regress with time (unlike a hemangioma), and it can have both superficial (cutaneous) and deep (muscular and osseous) components. Osseous and soft-tissue limb hypertrophy is the least common finding of the three classic features of Klippel-Trénaunay syndrome [22]. This hypertrophy can affect both extremity length and circumference, and it can be the result of local hyperemia and venous stasis secondary to associated venous abnormalities (Fig. 7). Causes of venous stasis in Klippel-Trénaunay syndrome include valvular insufficiency, venous varicosities, venous malformations, obstructed venous outflow, and abnormal lymphatic drainage. Varicose veins are present in most patients with Klippel-Trénaunay syndrome and can be superficial, deep, or perforating [24, 25].

View larger version (99K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 7 —19-year-old woman with Klippel-Trénaunay syndrome. Axial contrast-enhanced CT scan through midthigh level reveals soft-tissue hypertrophy (arrows) of right thigh, including asymmetrically increased circumference compared with opposite side.

View larger version (142K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 8 —22-year-old man with Klippel-Trénaunay syndrome. Axial contrast-enhanced portal venous phase CT scan through upper abdomen shows multiple low-attenuation splenic lesions (arrows), presumably hemangiomas or vascular malformations.

View larger version (117K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 9A —12-year-old girl with Klippel-Trénaunay syndrome. Axial (A) and coronal (B) contrast-enhanced CT scans of thorax show large avidly enhanced mass (arrows) within posterior mediastinum, including bilateral paraspinous regions, representing pathologically proven hemangioma.

View larger version (169K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 9B —12-year-old girl with Klippel-Trénaunay syndrome. Axial (A) and coronal (B) contrast-enhanced CT scans of thorax show large avidly enhanced mass (arrows) within posterior mediastinum, including bilateral paraspinous regions, representing pathologically proven hemangioma.

View larger version (26K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 10A —29-year-old woman with Klippel-Trénaunay syndrome. Coronal STIR MR image (TR/TE, 4,308/30; inversion time, 165 milliseconds; slice thickness, 5 mm) of left forearm shows extensive venous malformation with both superficial and deep venous components.

View larger version (89K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 10B —29-year-old woman with Klippel-Trénaunay syndrome. Conventional venogram shows findings similar to those in A, including venous varices and aneurysms.

View larger version (167K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 11 —22-year-old woman with Kasabach-Merritt syndrome. Axial STIR MR image (TR/TE, 3,200/55; inversion time, 165 milliseconds; slice thickness, 4 mm) shows presumed hemangiomatosis of spleen and overlying subcutaneous tissue (arrows). Both splenic and body wall lesions are hyperintense on STIR images, as is typical of hemangiomas.

View larger version (125K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 12A —25-year-old man with Kasabach-Merritt syndrome. Coronal T2-weighted single-shot fast spin-echo MR image (TE, 180 milliseconds; slice thickness, 8 mm) shows innumerable hyperintense lesions within spleen.

View larger version (131K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 12B —25-year-old man with Kasabach-Merritt syndrome. Contrast-enhanced axial portal venous phase (B) and delayed phase (C) fat-saturated T1-weighted spoiled gradient-recalled echo MR images (TR/TE, 4.2/2.0; flip angle, 12°; slice thickness, 4 mm) through upper part of abdomen show multiple enhanced presumed hemangiomas (hemangiomatosis) of spleen.

View larger version (133K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 12C —25-year-old man with Kasabach-Merritt syndrome. Contrast-enhanced axial portal venous phase (B) and delayed phase (C) fat-saturated T1-weighted spoiled gradient-recalled echo MR images (TR/TE, 4.2/2.0; flip angle, 12°; slice thickness, 4 mm) through upper part of abdomen show multiple enhanced presumed hemangiomas (hemangiomatosis) of spleen.

Top Abstract Introduction Hemangiomas, Vascular... Blue Rubber Bleb Nevus... Proteus Syndrome Klippel-Trenaunay Syndrome and... Kasabach-Merritt Syndrome Conclusion References

Kasabach-Merritt syndrome can be found in the setting of a large hepatic or splenic vascular lesion, most commonly called a hemangioma (Figs. 11, 12A, 12B, 12C, 13A, 13B, 13C, 13D) [33, 34]. Some authors, however, have indicated that such lesions are not classic hemangiomas but are tufted angiomas or kaposiform hemangioendotheliomas [35]. This syndrome can occur in infancy as a complication of a large hemangioma or other vascular lesion usually involving the skin, although deeper lesions may be seen (Fig. 14A, 14B, 14C). In rare instances, a condition called diffuse neonatal hemangiomatosis occurs that is characterized by widespread hemangiomas of the skin and viscera. This condition can be complicated by Kasabach-Merritt syndrome, congestive heart failure, and gastrointestinal bleeding. Other vascular lesions associated with Kasabach-Merritt syndrome include angiosarcoma and arteriovenous malformations.

View larger version (90K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 13A —64-year-old man with giant hepatic cavernous hemangioma and consumptive coagulopathy (elevated international normalized ratio and D-dimer levels) suggesting Kasabach-Merritt-like syndrome. Abdominal radiograph shows large upper abdominal mass (arrows) displacing bowel loops into pelvis.

View larger version (109K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 13B —64-year-old man with giant hepatic cavernous hemangioma and consumptive coagulopathy (elevated international normalized ratio and D-dimer levels) suggesting Kasabach-Merritt-like syndrome. Contrast-enhanced coronal fat-saturated T1-weighted spoiled gradient-recalled echo portal venous phase MR image (TR/TE, 4.0/2.0; flip angle, 12°, slice thickness, 3 mm) (B) and 99mTc-labeled RBC nuclear scintigraphic image (C) confirm presence of extremely large hepatic cavernous hemangioma. Arrowhead (C) denotes central filling defect consistent with central scar or thrombus.

View larger version (156K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 13C —64-year-old man with giant hepatic cavernous hemangioma and consumptive coagulopathy (elevated international normalized ratio and D-dimer levels) suggesting Kasabach-Merritt-like syndrome. Contrast-enhanced coronal fat-saturated T1-weighted spoiled gradient-recalled echo portal venous phase MR image (TR/TE, 4.0/2.0; flip angle, 12°, slice thickness, 3 mm) (B) and 99mTc-labeled RBC nuclear scintigraphic image (C) confirm presence of extremely large hepatic cavernous hemangioma. Arrowhead (C) denotes central filling defect consistent with central scar or thrombus.

View larger version (124K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 13D —64-year-old man with giant hepatic cavernous hemangioma and consumptive coagulopathy (elevated international normalized ratio and D-dimer levels) suggesting Kasabach-Merritt-like syndrome. Conventional angiogram after selective celiac artery injection and before transcatheter embolization of lesion confirms presence of giant cavernous hemangioma.

View larger version (108K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 14A —2-month-old boy with Kasabach-Merritt syndrome. Axial contrast-enhanced portal venous phase MR images through levels of midright kidney (A) and iliac fossae (B) reveal large enhanced retroperitoneal mass (arrows) extending from left renal hilum to left midthigh.

View larger version (107K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 14B —2-month-old boy with Kasabach-Merritt syndrome. Axial contrast-enhanced portal venous phase MR images through levels of midright kidney (A) and iliac fossae (B) reveal large enhanced retroperitoneal mass (arrows) extending from left renal hilum to left midthigh.

View larger version (101K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 14C —2-month-old boy with Kasabach-Merritt syndrome. STIR MR image (TR/TE, 4,000/24; inversion time, 165 milliseconds; section thickness, 5 mm) shows hyperintense mass (arrows) that represents pathologically proven hemangioendothelioma.

Top Abstract Introduction Hemangiomas, Vascular... Blue Rubber Bleb Nevus... Proteus Syndrome Klippel-Trenaunay Syndrome and... Kasabach-Merritt Syndrome Conclusion References

References

Top Abstract Introduction Hemangiomas, Vascular... Blue Rubber Bleb Nevus... Proteus Syndrome Klippel-Trenaunay Syndrome and... Kasabach-Merritt Syndrome Conclusion References

 

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