eMedicine Specialties > Dermatology > Diseases of the Vessels

Infantile Hemangioma: Differential Diagnoses & Workup

Author: Richard J Antaya, MD, Director of Pediatric Dermatology, Associate Professor, Departments of Dermatology and Pediatrics, Yale University
Contributor Information and Disclosures

Updated: Aug 18, 2009

Differential Diagnoses

Capillary Malformation
Oral Lymphangiomas
Cherry Hemangioma
Pyogenic Granuloma (Lobular Capillary Hemangioma)
Cobb Syndrome
Dabska Tumor
Lipomas

Other Problems to Be Considered

Angiosarcoma
Arteriovenous malformation
Congenital hemangioma (noninvoluting and rapidly involuting)
Infantile fibrosarcoma
Infantile myofibromatosis
Kaposiform hemangioendothelioma
Lymphatic malformation
Teratoma
Venous malformation
Diffuse neonatal hemangiomatosis
Gorham syndrome
Rhabdomyosarcoma
Riley-Smith syndrome
Dermatofibrosarcoma protuberans
Lipoblastoma of infancy

Workup

Laboratory Studies

  • No laboratory studies have been universally accepted for the diagnosis and treatment of infantile hemangiomas; however, reports in the literature have investigated the use of urinary beta-fibroblast growth factor and serum vascular endothelial growth factor (VEGF) as markers of hemangioma proliferation and differentiation.27,28
  • Use of glucose transporter 1 (GLUT-1) stain is helpful for evaluating tissue removed during biopsy or excision.29 Both proliferating and involuting infantile hemangiomas uniformly stain positively for GLUT-1, while other cutaneous vascular neoplasms, malformations, and normal cutaneous vasculature do not, making this stain very sensitive and specific for histologic confirmation of infantile hemangiomas. In addition, red blood cell membranes stain positively for GLUT-1, creating an effective internal control.

Imaging Studies

  • MRI with and without intravenous gadolinium is the imaging modality of choice to delineate the location and extent of both cutaneous and extracutaneous hemangiomas. MRI also helps in differentiating other high-flow vascular lesions (eg, arteriovenous malformations vs proliferating hemangiomas). Involuting hemangiomas have features that resemble low-flow lesions (eg, venous malformations).
  • Ultrasonography is useful in differentiating hemangiomas from other deep dermal or subcutaneous structures, such as cysts or lymph nodes. Ultrasonography is generally limited by its inability to fully evaluate the magnitude and extent of the hemangioma. Dubois et al found that an evaluation exhibiting high vessel density (>5 vessels/cm2) and high peak arterial Doppler shift (exceeding 2 kHz) was both sensitive and specific for infantile hemangiomas compared with other soft tissue masses.30
  • Plain radiography is fairly limited but may be useful for evaluating hemangiomas that impinge on the airway.

Procedures

  • If the diagnosis is in question after a thorough history and physical examination, a skin biopsy can be helpful in distinguishing unusual or atypical hemangiomas from other vascular lesions. Specimens may be evaluated by routine histological examination and special stains as outlined in Histologic Findings.

Histologic Findings

Routine histopathology varies according to the stage of the hemangioma. In early proliferation, hemangiomas are characterized by nonencapsulated masses and dense cords of mitotically active, plump endothelial cells in close association with pericytes. Few, small caliber lumina are present. Special stains reveal well-developed basement membranes around primitive vessels. Mast cells are present in varying numbers in all stages. As the hemangioma proliferates, the vascular lumina enlarge. An increase of apoptotic endothelial cells and a decrease in plump, mitotically active endothelial cells herald the involution phase.

As involution progresses, the endothelial cells continue to mature and assume a flatter appearance. The vascular lumina continue to enlarge until few, mature ectatic vessels remain.31 The proliferating endothelial cell mass may be replaced with fibro-fatty tissue. Varying degrees of epidermal atrophy, scar tissue, and loss of elastic tissue can be seen in late involuting lesions.32

Specimens may be evaluated for tissue-specific immunohistochemical markers such as GLUT-1, merosin, Fc-gamma-RII, and Lewis Y antigens. These markers may aid in differentiating infantile hemangiomas (positive staining for all) from other vascular neoplasms or malformations, such as the congenital hemangiomas (eg, rapidly involuting congenital hemangioma, noninvoluting congenital hemangioma), kaposiform hemangioendothelioma, tufted angioma, or pyogenic granuloma, none of which stains positively for these antigens. These markers are coexpressed by infantile hemangiomas, erythrocyte cell membranes, and placental microvessels.29

More on Infantile Hemangioma

Overview: Infantile Hemangioma
Differential Diagnoses & Workup: Infantile Hemangioma
Treatment & Medication: Infantile Hemangioma
Follow-up: Infantile Hemangioma
Multimedia: Infantile Hemangioma
References
Further Reading

References

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Keywords

infantile hemangiomas, hemangioma of infancy, hemangioma, superficial hemangioma, deep hemangioma, compound hemangioma, strawberry mark, angioma, cavernous hemangioma, capillary hemangioma

Contributor Information and Disclosures

Author

Richard J Antaya, MD, Director of Pediatric Dermatology, Associate Professor, Departments of Dermatology and Pediatrics, Yale University
Richard J Antaya, MD is a member of the following medical societies: American Academy of Dermatology, American Academy of Pediatrics, and Society for Pediatric Dermatology
Disclosure: Nothing to disclose.

Medical Editor

Jean Paul Ortonne, MD, Chair, Department of Dermatology, Professor, Hospital L'Archet, Nice University, France
Jean Paul Ortonne, MD is a member of the following medical societies: American Academy of Dermatology and American Dermatological Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Michael J Wells, MD, Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center
Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Van Perry, MD, Assistant Professor, Department of Medicine, Division of Dermatology, University of Texas Health Science Center
Van Perry, MD is a member of the following medical societies: American Academy of Dermatology and American Society for Laser Medicine and Surgery
Disclosure: Nothing to disclose.

CME Editor

Joel M Gelfand, MD, MSCE, Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania
Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology
Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds None; Genentech Consulting fee Consulting; Centocor Consulting fee Consulting; Centocor Grant/research funds None; Covance Consulting fee Consulting; Shire  Consulting

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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