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38 Cards in this Set
- Front
- Back
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15Q:
Acrocyanosis |
-Cyanosis of the HANDS, FEET and sometimes lips
-Caused by increased tone of peripheral arterioles, usually in response to chilling -Does not usually warrant concern -MUST BE DIFFERENTIATED FROM CENTRAL CYANOSIS |
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15Q:
What consequences does newborn skin have? |
-Increased permeability to topical agents
-Greater tendency to blister -Increased photosensitivity -Decreased response to thermal stress |
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15Q:
How does newborn skin differ from adults? |
-Thinner
-Weaker intercellular attachments -Fewer melanocytes -Fewer sweat and sebaceous glands -Less terminal hair -Greater skin surface to body -volume ratio |
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15Q:
Preterm infants have: |
-Even thinner skin
-Fewer cell attachments -No eccrine glands -Persistent lanugo |
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15Q:
Lanugo |
-Very thin and short body hair
-Resembles peach fuzz -Appears at approximately 20-22 weeks gestation -Begins to thin at 30 weeks gestation |
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15Q:
Baby Dry Skin |
normal. babies molt in the first days of life. it flakes off and new skin comes in.
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15Q:
Cutis Marmorata |
-Netlike, reddish-blue mottling of the skin
-Occurs symmetrically over trunk and extremities -Normal response to chilling -Caused by variable vascular constriction and dilation -Usually transient – resolves with rewarming -Can be a sign of sepsis |
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15Q:
Ichthyosis |
-Also known as a collodion baby
-May be transmitted as autosomal dominant (vulgaris or lamellar) or sex-linked -May be born with parchment-like collodion membrane that distorts the face and extremities -May have difficulty with feeding, respiration, infection, temperature instability and water loss -Treatment is supportive -Membrane usually resolves into scales over time |
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15Q:
Sucking Blisters |
-Superficial bullae
-Present on upper limbs at birth -Result from vigorous sucking on the affected part in-utero |
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15Q:
Miliaria |
Caused by sweat gland obstruction and sweat retention, usually from “over -bundling”
Two types: Miliaria Crystallina – clear vesicles over the head, neck and upper trunk Miliaria Rubra (prickly heat) – erythematous papulopustular eruption at sites of occlusion or flexural areas |
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15Q:
Milia |
-TINY WHITISH-YELLOW PAPULES containing keratin
-Usually present on cheeks, forehead, nose and chin -Persistent but may spontaneously resolve |
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15Q:
Neonatal Acne |
-Resembles teenage acne with COMEDONES, PAPULES, and PUSTULES
-Follows typical distribution pattern of acne -Secondary to the stimulation of sebaceous glands by maternal or endogenous androgens -May be treated with topicals but spontaneously resolves |
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15Q:
Erythema Toxicum Neonatorum |
-Benign and self-limited
-Occurs in 50% of all newborns -Lesions usually appear 24 hours after birth -Intense erythema with a central, 2mm papule or pustule (“fleabite”) -May be several hundred lesions (spares palms and soles) -Smear of pustular contents reveals numerous EOSINOPHILS -Spontaneously fades in 5 to 7 days |
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15Q:
Transient Neonatal Pustular Melanosis |
-Benign and self-limited
-Usually presents at birth and occur on any body part -1-2mm vesiculopustules or ruptured pustules -Disappears in 24 to 48 hours leaving PIGMENTED MACULES WITH A SCALE -Stain of the pustule reveals numerous NEUTROPHILS -Hyperpigmented macules completely resolve in 3 weeks to 3 months |
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15Q:
Seborrheic Dermatitis |
-Red, SCALING eruption mainly on HAIR-BARING and INTERTRIGINOUS AREAS
-Nonpruritic -Scalp lesions are known as cradle cap -No definite pathogenesis -Fungi have been implicated -Responds to shampoos with sulfur and salicylic acid -Persistent lesions may require a topical antifungal or topical steroid to clear |
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15Q:
Mongolian Spots (OBJECTIVE) |
-FLAT, GRAY TO BLUISH-BLACK MACULES from the accumulation of melanocytes in the dermis
-Poorly circumscribed -Commonly over the LUMBOSACRAL AREA AND BUTTOCKS -Range from 1 to 10cm -Most common in black and Asian infants -USUALLY FADE BY 7 YEARS -May be confused with child abuse -NO RISK FOR MALIGNANCY |
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15Q:
Congenital Nevi (OBJECTIVE) |
-Group of congenital pigmented lesions in the dermis
-Contains nevus cells from the neural crest which synthesize melanin -Vary in size and area of distribution -Usually FLAT, TAN MACULES OR PAPULES -WELL CIRCUMSCRIBED -May acquire nevi later in life -follow THROUGHOUT LIFE for changes in size, shape, outline, color, because it can become melanoma -small/medium; <20cm -giant;>20cm |
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15Q:
Giant Congenital Nevi |
Giant (greater than 20cm)
-Frequently in the distribution of a dermatome -UNEVENLY PIGMENTED WITH COLORS FROM BROWN TO BLACK -Over 95% have a hairy component -REMOVE AS EARLY AS POSSIBLE (may require skin grafting) -REQUIRES CLOSE OBSERVATION WITH PALPATION OF ENTIRE LESION EVEN AFTER EXCISION -Melanoma may arise deep without visible skin change |
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15Q:
Hemangiomas |
-Most common benign tumor of infancy
-3 times higher risk in females -Composed of proliferating vascular endothelium -May be:Superficial, Deep, Combined -FILL DEEP WITH BLOOD WHEN IN DEPENDENT POSITION |
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15Q:
Superficial Hemangiomas |
-“Strawberry” capillary hemangiomas
-Usually in HEAD AND NECK region -Usually not noticed in the first few days of life and begin as a flat macule -Grow rapidly during first year of life and protrude from the surface of the skin -Over 75% have INVOLUTION BY AGE 6 |
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15Q:
Deep Hemangiomas |
-Most are deep seated capillary hemangiomas with little penetration of the overlying skin
-May appear as BLUISH RED MASSES with less distinct borders than superficial hemangiomas -May be visceral (liver most affected) |
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15Q:
Complications of Hemangiomas |
rare!
BEAD DISTRIBUTION -Airway compromise NEAR THE EYE -Amblyopia, Strabismus, Astigmatism Lumbosacral Tethered cord, Spinal dysraphism, Imperforate anus, Renal anomalies, Sacral anomalies |
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15Q:
Kasabach-Merritt Syndrome (OBJECTIVE) |
A complication of hemangioma
-Rapidly enlarging hemangioma causing -Thrombocytopenia -Microangiopathic hemolytic anemia -Coagulopathy from red blood cell and platelet trapping -Activation of the clotting system within the hemangioma |
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15Q:
Treatment of Hemangiomas |
-OBSERVATION AS MOST HAVE SPONTANEOUS INVOLUTION
-If causing complications (vision or feeding problems or airway compromise), may use: Systemic steroids Interferon Steroid injections Laser therapy Surgical resection |
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15Q:
Salmon Patch (Stork Bite) |
-Represents localized vascular ectasia
-Usually SYSTEMIC WITH LESIONS ON BOTH SIDES OF MIDLINE -Most commonly in the nuchal area, glabella, eyelids, and lower back -Usually fade in first year of life -May become more apparent during crying, breath-holding, or physical exertion |
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15Q:
Port-Wine Stain |
-Nevus Flammeus or Port-Wine Nevus
-Present at birth and remain through life -Consist of mature dilated dermal capillaries and represent a permanent defect -Macular, sharply circumscribed, pink to purple, unilateral -Usually present in HEAD and NECK region |
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15Q:
Sturge-Weber Syndrome (OBJECTIVE) |
-Port-wine stain over the ophthalmic branch of the trigeminal nerve
-Intracranial calcifications -Seizure disorder -Hemiparesis -Glaucoma -Mental retardation **know all these things |
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15Q:
Klippel-Trénaunay-Weber Syndrome (OBJECTIVE) |
-Port-wine stain on an extremity associated with LOCAL OVERGROWTH OF SOFT TISSUE AND BONE
-Usually involves a LOWER LIMB -Enlargement may be gradual -Must monitor for LEG-LENGTH DISCREPANCIES |
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15Q:
TORCH Infections (OBJECTIVE) |
-congenital infections of the fetus
Toxoplasmosis Other (syphilis) Rubella Cytomegalovirus Herpes |
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15Q:
Congenital Toxoplasmosis |
-Caused by fetal infection with Toxoplasma gondii
-SILENT INFECTION IN PREGNANT WOMEN -Transmitted to fetus through the blood -Classic constellation of: -HYDROCEPHALUS -CHORIORETINITIS -INTRACEREBRAL CALCIFICATIONS -Many infants will have microcephaly risk of severe neurodevelopmental sequelae |
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15Q:
Congenital Syphilis |
-Caused by transplacental transmission
-MAJORITY ASYMPTOMATIC AT BIRTH BUT MANIFEST SYMPTOMS IF UNTREATED -Clinical manifestations divided into early (< 2 years) and late (> 2 years) |
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15Q:
Early Congenital Syphilis |
-Large round or oval maculopapular or papulosquamous lesions anywhere, including PALMS AND SOLES
-PERIORAL FISSURES AND SCARRING (Rhagades) -LYMPHADENOPATHY, hepatosplenomegaly (HSM) -RHINITIS (snuffles) -Anemia and jaundice -OSTEOCHONDRITIS (horizontal radiopaque bands in bone metaphases) |
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15Q:
Late Congenital Syphilis |
HUTCHINSON TEETH
upper central incisors are small, barrel shaped, and notched in the center MULBERRY MOLARS Multiple peripheral cusps and a central cusp -8th NERVE DEAFNESS -SABRE SKIN --Anterior tibia hypertrophy resulting in a bowed appearance -SADDLE NOSE DEFORMITY |
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15Q:
Congenital Rubella |
CLASSIC TRIAD
-Cataracts, Deafness, Heart malformations -BLUEBERRY MUFFIN RASH --Dermal erythropoiesis -Large spectrum of other findings including growth retardation, microcephaly, HSM |
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15Q:
Congenital Cytomegalovirus (CMV) |
Majority asymptomatic at birth
May develop long term sequela over time such as sensorineural hearing loss Symptomatic infants may have: --HSM and hepatitis --IUGR --Periventricular calcifications --Rubella-like rash (blueberry muffin) --Chorioretinitis --Microcephaly --Thrombocytopenia |
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15Q:
Neonatal Herpes |
MAD SERIOUS
Caused by either HSV Type 1 or 2 Mother may have NEVER HAD LESIONS May manifest as: -Disseminated disease -Cutaneous disease -Encephalitic disease Skin lesions -VESICLE WITH ERYTHEMATOUS HALO around the base |
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15Q:
Clinical manifestations of neonatal herpes |
Disseminated
-4th or 8th day of life, Herpetic lesions on skin or mucus membranes, RESPIRATORY DISTRESS, HEPATITIS, DIC, shock, CNS involvement (lethargy, FOCAL SEIZURES) Cutaneous 3rd week of life, Localized mucocutaneous lesions, Most will progress to systemic involvement if untreated Encephalitic 2nd to 4th week of life, Isolated CNS involvement, FOCAL SEIZURES, BLOODY LUMBAR PUNCTURE |
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Skin System
Lecture 15 Neonatal Dermatology |
Skin System
Lecture 15 Neonatal Dermatology |
