History

Obstetric history should include a review of maternal medications and infections such as varicella or herpes simplex viruses during the pregnancy. Initial multiple pregnancy with death of a co-twin or any placental anomalies should be determined. Because some forms of aplasia cutis congenita (ACC) are inherited, a thorough family history is also important.

Physical Examination

The diagnosis of aplasia cutis congenita (ACC) is made on the basis of physical findings indicative of an in utero disruption of skin development. Most lesions occur on the scalp lateral to the midline, but they may also occur on the face, trunk, or limbs, sometimes symmetrically.

The lesions are noninflammatory and well-demarcated. The appearance of the lesions varies, depending on when they occur during intrauterine development. Lesions that form early in gestation may heal before delivery and appear as an atrophic, membranous, parchmentlike or fibrotic alopecic scar, whereas less mature defects may present as an ulceration of variable depth. With only the epidermis and the upper dermis involved, minimal alopecic scarring may result, but deeper defects may extend through the dermis, subcutaneous tissue, and rarely periosteum, skull, or dura. Distorted hair growth around a scalp lesion, known as the hair collar sign, is commonly seen with membranous aplasia cutis and is a marker for underlying defects such as encephaloceles, meningoceles, and heterotopic brain tissue.

This area of healed aplasia cutis congenita is located in an area of nevus flammeus. Note the collarette of coarser hair at the margin of the defect.

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Extensive aplasia cutis congenita on the scalp, extending down to the skull.

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A rare bullous variant of aplasia cutis congenita, manifesting as a tense yellow vesicle or cyst on the scalp, has been reported. However, it is usually seen after the bullae have absorbed, leaving a flat scar. Some authors thus equate the terms "bullous" and "membranous."

A complete physical examination should be performed to search for associated physical anomalies or recognizable malformation syndromes. Particular attention should be given to limb and digit defects.

Bilateral involvement of the lower extremities in aplasia cutis congenita associated with fetus papyraceous.

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Complications

Major complications of aplasia cutis congenita (ACC) are rare but include hemorrhage, secondary local infection, meningitis, or sagittal sinus thrombosis.

Larger lesions associated with underlying bony defects may result in death secondary to central nervous system infection or hemorrhage from the sagittal sinus.

Differential Diagnoses

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Media Gallery

Aplasia cutis congenita on the scalp (most common location) shortly after birth.
Triplet areas of aplasia cutis congenita are common in infants with trisomy 13.
This area of healed aplasia cutis congenita is located in an area of nevus flammeus. Note the collarette of coarser hair at the margin of the defect.
Extensive aplasia cutis congenita on the scalp, extending down to the skull.
Bilateral involvement of the lower extremities in aplasia cutis congenita associated with fetus papyraceous.

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Author

Chris G Adigun, MD, FAAD Director and Physician, Dermatology and Laser Center of Chapel Hill; Senior Medical Advisor, Klara

Chris G Adigun, MD, FAAD is a member of the following medical societies: American Academy of Dermatology, American Society for Dermatologic Surgery, Council for Nail Disorders, North Carolina Dermatology Association, North Carolina Medical Society

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Sciton; OrthoDermatologics; Lumenis; PhotonMD; Galderma<br/>Received income in an amount equal to or greater than $250 from: Sciton.

Coauthor(s)

Megan E Freeze MD Candidate, The Brody School of Medicine at East Carolina University

Megan E Freeze is a member of the following medical societies: American Medical Student Association/Foundation

Disclosure: Nothing to disclose.

Specialty Editor Board

Michael J Wells, MD, FAAD Dermatologic/Mohs Surgeon, The Surgery Center at Plano Dermatology

Michael J Wells, MD, FAAD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Texas Medical Association

Disclosure: Nothing to disclose.

Van Perry, MD Assistant Professor, Department of Medicine, Division of Dermatology, University of Texas School of Medicine at San Antonio

Van Perry, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Received income in an amount equal to or greater than $250 from: Elsevier; WebMD<br/>Served as a speaker for various universities, dermatology societies, and dermatology departments.

Additional Contributors

Joy Wan, MD, MSCE Assistant Professor, Johns Hopkins University School of Medicine

Joy Wan, MD, MSCE is a member of the following medical societies: American Academy of Dermatology, Society for Pediatric Dermatology

Disclosure: Received research grant from: Pfizer .

Acknowledgements

Mark A Crowe, MD Assistant Clinical Instructor, Department of Medicine, Division of Dermatology, University of Washington School of Medicine

Mark A Crowe, MD is a member of the following medical societies: American Academy of Dermatology and North American Clinical Dermatologic Society

Disclosure: Nothing to disclose.