Skincare of Newborn and Common Skin Lesions

Skin Of Newborn

• The skin has two layers, the epidermis and the dermis. The epidermis contains keratinocytes, later stratum corneum, and dermis comprises of collagen, elastin, blood vessels, nerves, and sweat glands etc. Structural development of the epidermis is done by 24 weeks, but the barrier function is not complete until after birth. Maturation typically occurs 2-4 weeks after exposure to extrauterine development.
• Preterm epidermis has fewer stratum corneum layers than term babies and adults. Preterm skin has a translucent ruddy appearance.  Infants born at <30 wk may have less than 2-3 layers of stratum corneum at birth compared to 10-20 in term baby/adult. Maturity improves over 10-14 days after birth.
• Other features of preterm skin (as compared to term skin) are decreased cohesion between the epidermis and dermis, less collagen, and increased transepidermal water loss.

Skincare

• The daily assessment is done by neonatal skin condition score (NCSC). The best score is 3, and the worst is 9. The temperature of any product in contact with the skin should not be more than 41 degrees Celsius or 105 degrees Fahrenheit. Greater than that can lead to burns.  Soap should be mild, non-alkaline, and preservative-free soap. Pectin barriers should be applied to the skin before application of adhesives. Adhesive removers containing hydrocarbons and petroleum distillates should not be used as they can result in toxicity. Routine application of alcohol is not recommended on the umbilical cord as this may delay separation.
• Humidity is required for a baby born less than 32 weeks gestation or 1200 grams of baby weight. It is typically needed for 10-14 days. Start with 60-80% humidity, decrease by 5-10% every 12 hours, and stop after it reaches 30%. Povidone-iodine is not recommended for disinfection as there is a risk of systemic absorption, which can lead to thyroid dysfunction.

Extravasation

• The main treatment is the elevation of limbs. Heat and cold should not be applied as it leads to tissue damage. The best management is active non-intervention. Pharmacological management, if needed, should begin within 12-24 hours. This includes hyaluronidase and phentolamine. Neonates are at high risk of extravasation due to reduced venous muscle tone, low vessel diameter, easily distended subcutaneous tissue, and extra caution is needed while administering Calcium and ionotropic.

Related: Pediatric Dermatology Basics and Transient Phenomena

Common Skin Lesion

• Erythema toxicum is seen in 70% of neonates and is rare in preterms. It starts with the trunk, but the lesions may also be visible on the face and hands. The lesions contain eosinophils, and no treatment is needed.
• Milia is multiple pearly white or pale yellow papules or cysts visible on the forehead, nose, and chin. They are epidermal cysts upto 1mm in diameter and disappear a few weeks after birth. Sebaceous gland hyperplasia is similar to milia, with a smaller and more number of lesions. It is seen in the nose, upper lip, and chin.
• Vascular abnormalities occur in 40% of neonates, including hemangiomas, fading capillary stains, and port wine stains.
• Hemangiomas- They occur in 5% of infants and are more common in preterms. The lesions grow in the first 5 months of life, begin regressing at 12 months, and improve by 3.5 years. The treatment options include topical timolol, intralesional triamcinolone, oral prednisolone, and oral propranolol.
• Fading capillary stains- It is also called stork bites or angel’s kiss. It is the most common vascular lesion in neonates. It is flat, pink, macular lesion on the forehead, upper eyelid, nasolabial area, glabella, and nape of the neck. It mostly resolves by 2 years of age.
• Port wine stain/Capillary malformations- They are pink lesions that can occur in any part of the skin. They are dilated capillaries that do not involute.
• Pigmentation abnormalities- Mongolian spots arise due to increased melanocytes. Cafe au lait spots are flat brown lesions in 10% of neonates. It may be associated with neurofibromatosis if greater than six in number and larger than 4-6 cm. Piealbinism or partial albinism is an autosomal dominant disorder. It may present with white hair forelock typically associated with Waardenburg syndrome.

Nevi

• Junctional Nevi are benign and present at the epidermis and dermis junction. No treatment is required. Compound Nevi are larger than junctional nevi, involving the epidermis and dermis. It needs removal as it can lead to malignant melanoma.
• Giant hairy Nevi involves 20-30% of body surface area. It has a brown-to-black leathery appearance and is also called bathing trunk nevi. It may involve CNS and surgical removal is recommended as it can lead to malignant melanoma. Skin dimples are seen over bony prominences like the hip, knee, and scapula. Some deep sinuses may connect to CNS. MC site of dermal sinus is Pre auricular sinus

Aplasia Cutis

• It is most frequent in the midline of the posterior part of the scalp.  Treatment involves protection from trauma and infection. It may be associated with trisomy 13.

Scaling Disorders

• They include Harlequin ichthyosis, colloidal baby, X-linked ichthyosis, and bulbous ichthyosis.

Vesiculobulbous Eruptions

• Epidermolysis bullosa- It is a congenital genetic blistering disorder and a heterogeneous group of disorders. Three types are EB simplex, EB junctional, and EB dystrophic. EB simplex is the most common type. It is autosomal dominant with a keratin 5 or 14 gene defect and affects intraepidermal bullae
• EBS is further of 3 types- 1.EBS generalized is present at birth/neonatal period. Skin lesions over the hand, knee, elbow, and scalp are present. No oral lesions or nail damage is seen. It improves with age and supportive care. 2. EBS localized is the Weber-Cockayne type, beginning when the child starts to walk. Shoes and trauma and lesions precipitate it may be mild to severe. 3. EBS Dowling-Meara or herpetiformis is a group of blisters similar to HSV. It may involve mucosa and oral lesions. It is associated with hyperhidrosis and hyperkeratosis.
• Junctional EB is an autosomal recessive disorder, and it is life-threatening. It is associated with the laminin defect.
• JEB Herlitz is an autosomal recessive, life-threatening lesion. There are lesions personally, scalp, neck, diaper area, and thorax. There is permanent nail loss or damage and mucosa involvement to some extent. Death due to septicemia. JEB non-Herlitz type is associated with pyloric atresia. The treatment for both is supportive.
• Dystrophic EB is due to a mutation in collagen VII, and subepidermal blisters are seen. Dominant DEB is the most common type, and it is present at birth. There are lesions over acral bony prominences that heal with a scar, nail loss/nail dystrophy is observed, and no/insignificant involvement of mucous membrane involvement.
• Recessive DEB is a severe and generalized type, and it is also called as Hallopeau-Siemens disorder. Extensive erosions and blisters may be seen at birth(mucosa/skin). It may interfere with feeding and can cause mitten hand deformity. It is also associated with esophageal erosions and strictures which is a characteristic feature. Squamous cell carcinoma and infection are the major causes of death.
• Kindler type of EB is a distant type of EB. It has features of both epidermolysis as well as poikiloderma. It is associated with photosensitivity, congenital poikiloderma, and progressive skin atrophy.

Also Read: Key Points And Recommendations In Pediatric Advanced Life Support

Hope you found this blog helpful for your NEET SS pediatrics dermatology preparation. For more informative and interesting posts like these, keep reading PrepLadder’s blogs.