Paeds Vivas · fetal-neonatal-and-perinatal
Neonatal skin disorders and birthmarks — viva
Branching viva on the classification, red flags and management of neonatal skin disorders and birthmarks.
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Target exams
Examiner brief
This viva takes the candidate through a series of neonatal skin findings, probing whether they can classify a lesion, name the red flags that change management, give the correct propranolol dose and monitoring, and counsel a family. [4]
Branch 1 — The proliferating facial plaque
Examiner. A 7-week-old girl has a rapidly growing bright-red lobulated plaque on the right cheek, first noticed at two weeks. Describe your assessment. [4]
Model answer. An infantile haemangioma in its proliferative phase — absent at birth, growing rapidly, classic superficial "strawberry" morphology. Measure and photograph it, count all cutaneous lesions, examine the periocular and beard areas for visual-axis and airway risk, and look for any segmental pattern. [4]
Examiner (escalation). The lesion is in fact a large segmental plaque over 5 cm covering the cheek. What syndrome must you screen for, and how? [8]
Model answer. PHACE syndrome — posterior fossa brain malformation, segmental Haemangioma, Arterial cerebrovascular anomaly, Cardiac coarctation and Eye anomaly. The work-up is brain MRI/MRA, echocardiogram and aortic-arch imaging, and ophthalmology. [8]
Examiner (corner). The mother asks whether propranolol is safe. Give the dose, the duration, and the single most important counselling point. [5]
Model answer. Oral propranolol in divided doses titrated to the standard weight-based target, continued through proliferation to roughly 12 to 18 months, weaned rather than stopped abruptly. The most important counselling point is the risk of silent hypoglycaemia: propranolol masks the adrenergic warning signs, so during any intercurrent illness with poor feeding the parents should hold the dose, encourage feeds, and seek review. [5]
Branch 2 — The non-blanching forehead stain
Examiner. A newborn has a dark-red, non-blanching stain over the forehead and upper eyelid. What is it, and what is the differential? [1]
Model answer. A port-wine stain (capillary malformation) in the V1 dermatome, present at birth, distinguished from a salmon patch (naevus simplex), which blanches and fades, and from an early haemangioma, which will proliferate. [1]
Examiner (escalation). Why does the site matter? [9]
Model answer. Because a port-wine stain in the V1 dermatome carries the highest risk of Sturge–Weber syndrome — leptomeningeal angiomatosis on the same side, with seizures, glaucoma, stroke-like episodes and developmental risk, caused by a postzygotic GNAQ mutation. [9]
Examiner (corner). Give me the surveillance plan. [9]
Model answer. Gadolinium-enhanced brain MRI in early infancy, ophthalmology review for glaucoma, referral for pulsed-dye laser, and developmental and seizure surveillance. A normal early MRI does not eliminate later risk. [9]
Branch 3 — The giant pigmented plaque
Examiner. A newborn has a large dark-brown hairy plaque over the back with satellite lesions. What is it and what are the long-term risks? [13]
Model answer. A giant congenital melanocytic naevus — projected adult size over 20 cm, with satellites. The long-term risks are neurocutaneous melanocytosis and a lifetime melanoma risk, managed in a multidisciplinary team with baseline brain and spine MRI, neurological surveillance, lifelong dermatological surveillance, and an individualised decision about excision or watchful waiting. [13]
Branch 4 — The benign majority
Examiner (trap). A 2-day-old well term infant has a migratory erythematous pustular rash sparing the palms and soles. A Wright stain shows eosinophils. What is your management? [4]
Model answer. This is erythma toxicum neonatorum — a benign self-limiting condition needing only reassurance. Ordering tests, prescribing antibiotics or applying topical agents would be unnecessary and harmful. [4]
Examiner summary
A passing candidate classifies by natural history and distribution, names the four syndromic distributions, gives the propranolol dose and the silent-hypoglycaemia counselling unprompted, and distinguishes the benign majority without over-investigating. [4]
References
- [1]Mulliken JB, Glowacki J Hemangiomas and vascular malformations in infants and children: a classification based on endothelial characteristics. Plastic and Reconstructive Surgery, 1982.PMID 7063565
- [4]Darrow DH, Greene AK, Mancini AJ, Nopper AJ (AAP) Diagnosis and management of infantile hemangioma. Pediatrics, 2015.PMID 26416931
- [5]Drolet BA, Frommelt PC, Chamlin SL, et al Initiation and use of propranolol for infantile hemangioma: report of a consensus conference. Pediatrics, 2013.PMID 23266923
- [8]Metry DW, Haggstrom AN, Drolet BA, et al Consensus statement on diagnostic criteria for PHACE syndrome. Pediatrics, 2009.PMID 19858157
- [9]Shirley MD, Tang H, Gallione CJ, et al Sturge-Weber syndrome and port-wine stains caused by somatic mutation in GNAQ. New England Journal of Medicine, 2013.PMID 23656586
- [13]Krengel S, Scope A, Dusza SW, et al New recommendations for the categorization of cutaneous features of congenital melanocytic nevi. Journal of the American Academy of Dermatology, 2013.PMID 22982004