600001 May 2020

STUDY OF SPECTRUM OF DERMATOLOGICAL MANIFESTATIONS IN NEONATES

This dissertation is submitted to

THE TAMILNADU DR.M.G.R. MEDICAL UNIVERSITY

In partial fulfillment of the requirement of the award for the degree of M.D DEGREE IN DERMATOLOGY, VENEREOLOGY AND LEPROSY BRANCH XX

GOVERNMENT STANLEY MEDICAL COLLEGE CHENNAI – 600001 MAY 2020

DECLARATION BY THE CANDIDATE

I, Dr. STACY ANN MARBANIANG solemnly declare that the dissertation titled “STUDY OF SPECTRUM OF DERMATOLOGICAL MANIFESTATIONS IN NEONATES” is a bonafide work done by me at the Department of Dermatology, Venereology and Leprosy, Government Stanley Medical College and Hospital during 2017 – 2020 under the guidance of my guide, Prof. Dr. V. ANANDAN, M.D (Dermatology) and under the supervision of my HOD, Prof. Dr. PARIMALAM KUMAR, M.D,D.D.,Dip.,N.B., MNAMS.,FIAD.,FRCP.

The dissertation is submitted to THE TAMILNADU DR.M.G.R. MEDICAL

UNIVERSITY towards the partial fulfillment of requirement for the award of

M.D Degree in DERMATOLOGY, VENEREOLGY and LEPROSY (BRANCH XX)

Place:

Date: Signature of the candidate:

CERTIFICATE BY THE INSTITUTE

Certified that this dissertation entitled “STUDY OF SPECTRUM OF DERMATOLOGICAL MANIFESTATIONS IN NEONATES” is a bonafide work done by Dr. STACY ANN MARBANIANG, post graduate student of the Department of Dermatology, Venereology, Leprosy, Government Stanley Medical College and Hospital, Chennai – 600001 during the academic year 2017 – 2020 for the partial fulfillment of university rules and regulation for the award of M.D Degree in DERMATOLOGY, VENEREOLOGYAND LEPROSY (BRANCH XX). This work has not been submitted previously for the award of any degree.

Dr. PARIMALAM KUMAR Dr. R. SHANTHI MALAR M.D., D.D., Dip.N.B., MNAMS.,FIAD.,FRCP., MD, DA Professor and Head of Department Dean, Department of Dermatology Govt. Stanley Medical College, Govt. Stanley Medical College Chennai-600 001. Chennai-600 001

Dr. V. ANANDAN, M.D (Dermatology )(GUIDE) Professor, Department of Dermatology, Govt. Stanley Medical College, Chennai-600 001.

CERTIFICATE BY THE HEAD OF THE DEPARTMENT

Certified that this dissertation entitled “STUDY OF SPECTRUM OF

DERMATOLOGICAL MANIFESTATIONS IN NEONATES” is a bonafide work done by Dr. STACY ANN MARBANIANG, post graduate student of the

Department of Dermatology, Venereology, Leprosy, Government Stanley Medical

College and Hospital, Chennai – 600001 during the academic year 2017 – 2020 for the partial fulfillment of university rules and regulation for the award of M.D Degree in

DERMATOLOGY, VENEREOLOGY AND LEPROSY (BRANCH XX). This work has not been submitted previously for the award of any degree.

Dr. PARIMALAM KUMAR, M.D.,D.D.,Dip.N.B.,MNAMS.,FIAD.,FRCP., Professor and Head of Department, Department of Dermatology, Govt. Stanley Medical College, Chennai-600 001

CERTIFICATE BY GUIDE

Certified that this dissertation entitled “STUDY OF SPECTRUM OF

DERMATOLOGICAL MANIFESTATIONS IN NEONATES” is a bonafide work done by Dr. STACY ANN MARBANIANG , post graduate student of the Department of Dermatology, Venereology, Leprosy, Government Stanley Medical

College and Hospital, Chennai – 600001 during the academic year 2017 – 2020 for the partial fulfillment of university rules and regulation for the award of M.D Degree in

DERMATOLOGY, VENEREOLOGY AND LEPROSY (BRANCH XX). This work has not been submitted previously for the award of any degree.

Dr. V. ANANDAN, M.D (Dermatology), Professor, Department of Dermatology, Govt. Stanley Medical College, Chennai-600 001.

ACKNOWLEDGEMENT

It is with immense pleasure and gratitude that I thank Dr. SHANTHI MALAR. M.D., D.A., Dean, GOVERNMENT STANLEY MEDICAL COLLEGE for bestowing me the permission and privilege of presenting this study and for enabling me to avail the institutional facilities.

I am gratefully indebted to Prof. Dr. PARIMALAM KUMAR, M.D., D.D., Dip.N.B., MNAMS., FIAD.,FRCP., Professor and Head of Department of Dermatology and Leprosy for her invaluable guidance and motivation. I would like to express my sincere and heartfelt thanks to Prof. Dr. V. ANANDAN M.D., (Dermatology), for his guidance and encouragement.

I express my deep sense of gratitude to Dr. N. SARAVANAN

Professor and Head of Department of Venereology, Dr. ARUN KUMAR, M.D., former professor, Department of Venereology, for their constant support and motivation.

I am grateful to Dr. P. SARADHA, M.D DVL.,Associate Professor of Venereology for her support and inspiration.

Words will not suffice the gratitude I owe to my beloved co-guide Dr. MANI SURYA KUMAR, M.D (DVL)., Assistant professor, Department of Dermatology, for his guidance and endless patience in moulding of the study.

All our Assistant professors, Department of Dermatology,

Dr. SOWMIYA, M.D (DVL), Dr NITHYAGAYATHRI DEVI M.D(DVL),

Dr. MOHANASUDARI, M.D(DVL). Dr.V.SENTHILKUMAR D.V,DNB(Derm)., Dr.SARASWATHI,M.D(DVL), Dr.N.S.JAYANTHIM.D(DVL), Dr. ANBULAKSHMI.J DDVL., are thanked for their enthusiasm in motivating me with their efforts to materialize this study.

I am inclined to thank Dr. KAYALVIZHI, M.D(DVL), Dr. SARAN KUMAR,

M.D (DVL), Dr. SYED IQBAL, M.D (DVL), Assistant professors, Department of

Venereology for their help and suggestions.

I would like to take this opportunity to thank Professor DR. KALAIVANI , Medical Superintendent RSRM , Chennai for allowing me to conduct my study in her Department. .I would also like to express my gratitude to Professor DR. P. RAVICHANDRAN Head of Department of Paediatrics and Professor DR. MANIMEGALAI incharge of NICU for allowing me to conduct the study in their Department.

I also express my thankfulness to my batch mates and my beloved juniors for having helped me in constructing this study.

I duly acknowledge the paramedical staffs and my colleagues for their help and favours.

I also wholeheartedly thank my parents and my family members who constantly made me aware of the values of this noble profession.

A sincere thanks to all my patients for their cooperation & participation in this study.

Last but not least I thank the Almighty God, whose blessings are always with me.

CONTENTS

S.NO. TITLE PAGE NO.

1. INTRODUCTION 1

2. REVIEW OF LITERATURE 2-37

3. AIMS AND OBJECTIVES 38

4. MATERIALS AND METHODS 39-42

5. RESULTS 43--54

6. DISCUSSION 55-61

7. CLINICAL PHOTOGRAPHS 62-73

8. SUMMARY 74-77

9. CONCLUSION 78-80

10. BIBLIOGRAPHY

ANNEXURE

PROFORMA

PATIENT CONSENT FORM

ETHICAL COMMITTEE APPROVAL

PLAGIARISM APPROVAL

KEY TO MASTERCHART

MASTER CHART

STUDY OF SPECTRUM OF DERMATOLOGICAL MANIFESTATIONS IN NEONATES

INTRODUCTION INTRODUCTION

Neonatal period is defined by the World Health Organisation (WHO) as the period of less than 28 days after birth. Hence Neonatal Dermatology includes the spectrum of cutaneous manifestations occurring during these first four weeks of life.

Skin changes are common in neonates and often cause anxiety and serious concern to the parents. Although most are benign and self-limited some may require further work- up in order to rule out a serious condition . Many factors may influence the pattern of dermatoses in newborns like environmental ,maternal , regional and racial factors

.Therefore a thorough understanding of the physiologic characteristics and peculiarities of neonatal skin is important.

Neonatal dermatoses can be classified as :

1) Transient benign skin disorders

2) Developmental abnormalities

3) Acquired skin disorders.

4) Iatrogenic and traumatic disorders.

There are very few published literature on neonatal dermatoses in our country.

REVIEW OF LITERATURE

DEVELOPMENT OF SKIN

The skin arises by the juxtaposition of two major embryological elements: the prospective epidermis that originates from a surface area of the early gastrula, and the prospective mesoderm that comes into contact with the inner surface of the epidermis during gastrulation.

The mesoderm provides the dermis and is also essential for inducing differentiation of the epidermal structures, such as the hair follicle. The melanocytes are derived from the neural crest.

After gastrulation a single-layered neuroectoderm lies on the surface of the embryo. Depending upon the molecular signal it receives this layer will go on to form the nervous system or the skin epithelium .

Development of the epidermis starts at the third week of life . Initially a basal layer of cuboidal cells overlying the mesoderm or future dermis is seen. By the fifth week, a secondary layer of squamous, non-keratinizing, cuboidal cells, known as periderm or epitrichium, develops atop the basal layer. This periderm eventually sloughs

3 off to become a component of a waxy substance called vernix caseosa which serves to protect the fetus from bacterial and environmental insults.

ANATOMY

Vernix caseosa-

It is a greasy, yellow-white substance which is found to coat the skin of a newborn and persists for the first several days of postnatal life. Vernix means “ to varnish” and “caseous” means cheesy nature. Vernix consists of water (81%), lipid (9%), and proteins (10%). Cholesterol esters , wax esters, ceramides ,squalene, cholesterol, triglycerides, free fatty acids are the major lipid composition.1

The development of vernix caseosa proceeds in a cephalocaudal manner and is the result of an orderly progression of epithelial maturation.2

At birth, vernix may cover the entire skin surface or only confined to body folds. It may be absent in very low birth weight and premature infants. Hence they lack the protective function of vernix caseosa.

The functions of vernix includes formation of an epidermal barrier in utero to facilitate epidermal growth underneath it , minimises friction of fetal parts during delivery, antimicrobial cover against the bacteriologically rich environment of the mother's genital tract3 .

It also prevents loss of fluids and electrolytes or TEWL (Trans Epidermal Water

Loss). In addition it also has anti-oxidant 4 ,moisteurising 5, temperature regulation and wound healing properties. 6

The colour of the vernix at birth may reflect intra-uterine problems . For example, it appears golden yellow in hemolytic disease of newborn .Human skin consists of three layers: epidermis, dermis, and subcutaneous fat.

Epidermis-

The epidermis is the outermost compartment of the skin which arises from surface ectoderm and at about the third week of fetal life. The various layers of the epidermis (from above downwards) are the stratum corneum, stratum granulosum , stratum spinosum, and stratum corneum respectively. In certain areas like the palms and soles, the stratum lucidum is present between the granular and corneal layers.

Individual cells of the epidermis are called keratinocytes .

Stratum corneum-

It is composed of 20-25 layers of flattened, nonnucleated keratinized cells

(corneocytes) arranged in an overlapping fashion. Langerhan cells may be seen in this layer.

Stratum granulosum-

It comprises of 2-5 layers of darkly stained keratinocytes which contain keratohyaline granules.7 Lamellar bodies (Odland bodies, membranecoating granules) are found in this layer.8

Stratum spinosum –

Consists of 8-10 layers of polyhedral keratinocytes with numerous tiny, spiny projections on the surface. These projections are composed of desmosomes, which form communication junctions between adjacent cells . 9

Stratum basale –

Single layer of cuboidal or columnar cells which contribute to the dermoepidermal junction. In addition, melanocytes and the merkel cells are two other cells found in the basal layer.

The epidermis forms projections into the papillary dermis called rete ridges which lie interspersed between the dermal papillae.

Dermo-epidermal junction -

The dermoepidermal junction (DEJ) forms an extensive interface between the epidermis and dermis. It can be divided into several layers which includes the basal keratinocyte, an electron-lucent lamina lucida; an electron-dense lamina densa; and the

6 sublamina densa region. Hemidesmosomes anchor the basal keratinocytes to the underlying structures. Intermediate filaments ( composed of keratin 14,5) in the basal keratinocytes are inserted into the hemidesmosomes . 10 Major constituents of the DEJ include bullous pemphigoid (BP) antigens, alpha 6 beta 4 integrin, laminin-5, type IV collagen, and type VII collagen.11

Dermis-

The dermis is divided into superficial (papillary) and deep (reticular) components, which are anatomically divided by a thin plexus of blood vessels. Collagen is the major constituent accounting for approximately 75% of the dry weight of the skin. 12 Types I and III collagen are the major collagens found in human dermis, and smaller amounts of types IV (a primary component of the basement membrane as noted above), V, VI, and

VII are also present.13

Elastic fibers are located in the papillary and reticular dermis. They consist of two components: elastin and elastic fiber-associated microfibrillar component. They play an important role in the structure and function of skin, providing elasticity and resilience.13

In the papillary dermis elastic fibres are of two types , namely the elaunin fibers, lying parallel to the DEJ, and oxytalan fibers, which connect the elaunin fibers to the

DEJ. 14

The ground substance embedding the fibrous and cellular components in this dermis are mostly composed of glycosaminoglycans(GAG) and proteoglycans (PG).

Chondroitin sulfate, dermatan sulfate, heparin sulfate, chondroitin 6-sulfate, and hyaluronic acid are the major GAG and PG.12

Other structures found within the dermis include the cutaneous appendages i.e the pilosebaceous units, eccrine and apocrine sweat glands, nerves, blood vessels, and lymphatics.

Fibroblasts, monocytes, macrophages, dendrocytes ,mast cells, lymphocytes, leukocytes, pericytes and Schwann cells are also present.

Subcutaneous Fat-

The individual cells in this layer are called adipocytes.Groups of adipocytes form lobules which are separated by fibrous septa. Neural and vascular structures are found in the fibrous septa.

PHYSIOLOGY OF THE NEW BORN SKIN

Skin is a dynamic organ and plays an important role for the survival of the newborn outside the mother’s womb. It’s proper structure and functioning depends on the gestational age.

Skin maturation usually begins immediately after birth in full-term newborns whereas this process may begin at 2-3 weeks after birth for a preterm infant.15 . Skin performs a variety of function which includes Physical barrier against pathogens and environmental factors like UV radiation, regulation of body temperature and sensory perception.

Various biophysical skin parameters are present which allow the study of skin in a non-invasive manner. These parameters include transepidermal water loss, hydration, and skin acidity which are affected in skin diseases.16

Transepidermal Water Loss

Transepidermal water loss (TEWL) is defined as the amount of water loss through the epidermis through evaporation. It is dependent on multiple factors, including skin temperature, skin blood flow, local hemodynamics, degree of activity and stratum corneum lipid content.19

TEWL is measured by electrical skin impedance, where lower impedance indicates higher skin hydration.

There is a relationship between TEWL and gestational age. In term neonates, the

TEWL ranges from 4-8g/m2/h. In premature infants TEWL is inversely proportional to gestational age being as high as 100g/m2/h in an immature infant 24-26 weeks gestation.18

TEWL plays an important role in the heat exchange between the infant and its environment.

Preterm infants loose more heat through evaporation . This excess loss is a result of immature barrier function , thinner epidermal layers , increased blood flow to the skin and a high ratio of total body surface area to volume. These factors lead to increased insensible water loss. 18

Skin pH

Fully mature stratum corneum is characterised by an acidic pH that is essential for epidermal barrier maturation and defense against infection.This acidic mantle is formed an maintained by sebum and sweat secretions like lactic acid, amino acids and amino acid derivatives like urocanic acid and pyrrolidone carboxylic acid, fatty acids.

At birth the surface skin pH is neutral or alkaline ranging from 6.2-7.5pH, in both term and preterm infants. Average pH on the first day was found to be 6.2.This pH declines rapidly in the first week, and thereafter slowly till the fourth week of life, when a range of 5.0-5.5 is reached similar to that of adults.20

Skin Hydration

Maintenance of skin hydration is essential for proper skin functioning like barrier function and percutaneous absorption.

At birth there is a decrease in hydration of the skin and it appears rough and dry.

In the months that follow, the skin hydration improves which may be attributed to the maturation of sweat gland function 21

Percutaneous respiration

Percutaneous respiration is <2 % of total respiration in adults and term infants whereas in preterms it is 6-11 times higher , then normalize by 2-3 weeks after birth.

Percutaneous absorption

Skin permeability is inversely proportional to gestational age. Percutaneous absorption is higher in neonates because of high body surface area to weight ratio .

Application of topical substances like antiseptics, alcohol dressings, salicylates, urea have all been associated with neonatal toxicity .17

Thermoregulation

In first few days of life , premature infants are unable to sweat in response to heat.

After the second week of life they are able to sweat however they require a higher thermal stimulus and produce a low sweat output.

Immaturity of the sweat gland function in neonates does not appear to have any clinical implications , even in conditions where there is absence of sweating like anhidrotic ectodermal dysplasia, hyperpyrexia occurs only until late infancy or early childhood.17

Heat transfer from the newborn to the environment occurs through four basic mechanisms. These include radiation, conduction, convection and evaporation, which can create an unstable thermal environment for the newborn. In the extremely low birth weight (ELBW) infants the major form of heat loss is through evaporation .22 This may be reduced by occlusive wrapping of the infant.

CARE OF THE NEWBORN SKIN

The anatomy and physiology of newborn skin is different from that of adults. Due to the immature skin barrier and a high ratio of body surface area to weight, there is increased risk of excessive transepidermal water loss (TEWL) accompanied by thermodysregulation, water and electrolyte imbalance, increased percutaneous absorption and cutaneous infections.

Removal of the vernix caseosa

Immediately after delivery, the vernix caseosa is usually wiped off the baby with a clean towel. However, it is not necessary to remove it as it serves many important functions like thermoregulation, prevention of water loss, bacterial protection, and wound healing. 23

Care of the cord

Nothing should be applied to the cord after delivery. The use of antiseptics may prevent bacterial colonization but it runs the risk of exposure to sensitizing agents and may lead to delayed cord separation. 24

Washing and bathing

The skin can be washed with luke warm water not exceeding 37 C. Soaps and cleansers are best avoided in the first few weeks of life.Bathing of preterm babies should not be initated until atleast 32weeks of life. They should be bathed every 4days. In term infants with normal birth weight for gestational weight , bathing can be initiated when vitals are stable for atleast 2-6 hours after birth . For atleast 2 times a week. In a lowbirth weight baby washing should be delayed till the cord falls off.Post term babies can be bathed when the vitals are stable.

After bathing , the baby should be toweled dry from head to toe and wraped with a warm cloth .25

Care of the nails

Fingernails should be trimmed to prevent self-inflicted excoriation.

Care of the scalp and ears

Shampoo helps to remove scales and crust from the scalp (cradle cap). Application of animal oil or mineral oil can l limit the spread of seborrheic dermatitis. Ears are cleaned with cotton swabs soaked in boiled water . Special care should be taken not to hurt auditory canals26

Care of the napkin area

The diaper area is more prone to colonization by microorganisms due to large moisture content and occlusion. Here the skin also comes in contact with strong alkalinizing agents like urine and feces which damages the skin. The mother is advised to change the napkins frequently atleast 4-5 times a day. Soft cotton wool can be used to wipe with warm water from front to back. 25

Role of massage and emollients

Gentle massage given by the mother increases the bondage between her and the baby. It helps in the physiological and psychological development of the babies and creases parental stress 27 .

Mineral oils best used for massaging as it is an effective emollients that can soften and smoothe the skin. It spreads easily and has a long lasting tactile effect.28

An emollient in as agent that softens and smoothens the skin. They are also referred to as

“moisturizers” and “lubricants”. They are essentially composed of lipids which may be animal or vegetable derived, or obtained from mineral oils or alternatively, may be synthetic in origin33. Coconut oil , sunflower oil and olive oil massage has been associated with rapid weight gain in neonates .

SKIN CARE IN PRETERM INFANT

After birth, the preterm skin may take 2- 8 weeks to attain maturity. Measures to allow retention of heat, fluid and electrolyte balance, prevention of infection and rapid epithelial maturation should be provided.

Disinfection: Hand washing by staff and parents is important . Chlorhexidine, alcohol or povidone iodine based solutions can be used

The incubator: Regular change of infants’ posture reduces the risk of skin erosions and bed sores.

Reduction of water loss: Water loss can be reduced by humidification of the surrounding air, use of plastic bubble blanket, heat shields or topical application of paraffin.

Emollients: They decrease fragility, improve wound care and help to protect the infants.

Vegetable oil, lanolin and petrolatum based ointments reduce scaling and fissure and enhance cutaneous hydration.41

TRANSIENT AND PHYSIOLOGICAL CUTANEOUS CONDITIONS IN

NEONATES

A variety of skin conditions seen during the neonatal period are considered physiological and completely resolve. To differentiate between benign and pathological skin lesions in newborn is important as the latter needs to be thoroughly investigated and treated.29

VERNIX CASEOSA

Vernix caseosa is a whitish, greasy film which covers the skin surface composing of sebaceous gland secretions, desquamated skin cells and shed lanugo hair. It dries up after birth and comes off easily.It is usually not seen in preterm infants. This plays an important role of skin hydration and barrier against infection. 30

The colour of the vernix may indicate intrauterine problems such as golden yellow colour in post mature babies and haemolytic disease of the newborn31 . In case of fetal distress it may be stained with the colour of bile pigments from the meconeum.

PERIPHERAL CYANOSIS (Acrocyanosis)

It is the bluish discolouration of the palms , soles and lips of the infant usually seen during the first 48 hours of life and improves on warming and is associated with increased tone of the peripheral arterioles.31

ERYTHEMA NEONATORUM

Also known as Rubor , it is the generalised erythema or hyperaemia of the skin that occurs a few hours after birth and fades within a few days. It occurs as a result of reflex vasodilatation of cutaneous capillaries following decreased sympathetic tone.

CUTIS MARMORATA

It is the reticulate, mottled, blanchable, bluish pattern of the skin which occurs on exposure to cold due to the constriction of capillaries and venules. It usually disappears on rewarming.It should be distinguished from cutis marmorata telengiectasia congenital which ia a vascular formation. Here the mottling is fixed and may persist for years .

Persistence of the mottling may also be associated with Down syndrome, trisomy 18, hypothyroidism, and Cornelia de Lange syndrome 32

HARLEQUIN PHENOMENON

This phenomenon occurs during the first week of life and seen seen in around 15

% of infants.

When the infant is lying on its side the upper half of the body appears pale while the lower half shows deepred discolouration.This colour change may last from 30 seconds to 20 minutes and may reverse on turning the baby to the other side . It is thought to be a result of immaturity of the hypothalamic centres that control the sympathetic peripheral vascular tone.

It is occasionally reported with prematurity, low birth weight, hypoxia, systemic use of prostaglandin E1and intracranial injury .34 Persistence beyond the fourth week should arise suspicion of cardiovascular abnormalities.

PHYSIOLOGICAL DESQUAMATION

It is a very common physiological change that can be seen in upto 75% of normal neonates .35 It is mostly localised to the hands and feet but can involve the trunk and face as well. It is more severe in post-mature infants .

The differential diagnosis of this condition includes ichthyosis and hypohidrotic ectodermal dysplasia. Other inherited conditions like Refsum’s disease, Rud’s syndrome, neutral lipid storage disease, essential fatty acid deficiency, amino acid deficiencies, and congenital infections can also present as desquamation at birth .The rare familial peeling

syndrome is characterised by superficial sheet like skin peeling and pruritus and occasionally by erythema or vesiculation.36

SUCKLING BLISTERS

These are tense fluid filled lesions present at birth on fingertips, lips or forearms.

They may be single or multiple and occur as a result of vigorous sucking in utero33

The blisters may rupture leaving behind erosions. After birth, infants who are vigorous suckers may develop calluses or pads on the lips following blistering.

They are differentiated from other serious disorders like herpes simplex by their solitary, asymmetric nature and characteristic location . No treatment is required. 36

Histopathology of the blisters shows hyperkeratosis with intracellular oedema.

Intracellular oedema occurs due to passive diffusion of fluid into the cell, mostly saliva.The hyperkeratosis is regarded as an adaptive phenomenon to friction during sucking37

NEONATAL OCCIPITAL ALOPECIA

The hair development on the fetal scalp begins at 9~12 weeks of gestation and the whole scalp is covered with anagen hair by 18~20 weeks of gestation38

By the fifth month of life , scalp hair starts shedding synchronously. The regrown hair starts entering telogen phase at 12 weeks prior to term from front to back in a wave form. Therefore the telogen phase of occipital area coincides with term and at birth it is visible as occipital alopecia . Neonatal occipital alopecia may also be a result of localized pressure owing to the neonate’s sleeping position.

In some neonates , rarely there may be hair loss in the form of diffuse alopecia or telogen effluvium32

SEBACEOUS HYPERPLASIA

Sebaceous gland hyperplasia is a physiological event in the newborn, reflecting the influence of maternal androgens. 40 They appear as multiple, smooth , pinpoint yellowish follicular papules occurring in groups on the sebaceous areas like nose, cheeks and upper lip and rarely on the trunk, genitlia and limbs .41 There is no surrounding erythema. Although more common in term neonates it may be seen in premature infants

42 They are differentiated from milia which are more solitary and whitish .

MILIA

Milia are 1- to 2-mm pearly white or yellow papules caused by retention of keratin within the dermis. They commonly occur on the forehead, cheeks, nose, and chin, rarely on the upper trunk, limbs, penis, or mucous membranes.43 They are discrete , smooth and whitish in colour. They disappear spontaneously within the first month of life, although they may persist into the second or third month44

Milia arising from infundibula of vellus hairs are called primary milia. While secondary milia may arise from a variety of epithelial structures like hair follicles, sweat ducts, sebaceous ducts, or epidermis usually following trauma .45

Milia may be associated with certain genodermatoses like Bazex-Dupre-Christol syndrome, Brooke-Spiegler syndrome , Orofaciodigital syndrome type 1 ,Hereditary vitamin Dedependent rickets , Pachyonychia congenita type II , Basal cell nevus syndrome , KID syndrome, Epidermolysis bullosa, Hereditary porphyrias. 46

BOHN`S NODULE AND THE EPSTEIN `S PEARLS

Epstein’s pearls and Bohn’s nodules are oral mucosal microcysts located in the palate and alveolar ridges respectively. They are seen in nearly 60% to 85% of newborn infants. Japanese are most commonly affected (up to 92%), followed by Caucasians and

African-Americans47

They appear as smooth, asymptomatic yellow to gray-white papules of size 1-

2mm occuring singly or in clusters. These are also keratinized cysts which occur from the epithelium entrapped along the line of fusion. It is believed that fragments of dental lamina that remains within the alveolar ridge mucosa after tooth formation proliferate to form these small keratinized cysts. They usually disappear within weeks 48

LANUGO

Lanugo hairs are fine, unmedullated vellus hairs which are most prominent in preterm infants. They are shed and replaced by vellus hairs during the first few months of life. Lanugo hairs are increased and widespread in congenital hypertrichosis lanuginosa, congenital lipodystrophy, leprechaunism, Cornelia de Lange syndrome andmucopolysaccharidoses32

STERILE TRANSIENT NEONATAL PAPULOPUSTULAR ERUPTIONS

ERYTHEMA TOXICUM NEONATORUM

Erythema toxicum neonatorum or Toxic Erythema of the newborn was termed in

1912 by Dr. Karl Leiner, an Austrian pediatrician. It is a benign, self-limited, transient, evanescent eruption that affects around 48% to 72% of neonates49. It was propsed by

Leiner to be due to a toxic gastrointestinal effect.

Higher incidence was observed in term than preterm neonates. 50 It was found to be associated with other factors like first pregnancy,births in the summer or autumn season, milk powder feedings, vaginal delivery, and duration of labor. It is also known as erythema papulatum ,erythema dyspepsicum ,erythema neonatorum allergicum and urticaria neonatorum .51 There is no sexual or racial predilection.

Genetic factor may play a role in the etiology of erythema toxicum as reported by

Carr et al where 34.04 % of babies in the consanguineous group developed erythema toxicum whereas only 21.4% of babies in non-consanguineous group developed it. 52

The classical lesions are papules or pustules , 1 to 3-mm , yellow-white in colour , firm with a surrounding irregular erythematous base . The lesions are seen on the cheeks, forehead, chest, trunk, and extremities and rarely over the skin of the scrotum .49 The

surrounding erythema may have an irregular shape which is described as a “flea-bitten appearance”. Erythema toxicum neonatorum has been described as consisting of 2 variations: erythematopapular and pustular.53

On histopathological examination, eosinophilic pustules are found at the subcorneal or intraepidermal position and related to the orifice of pilosebaceous structures.Macular erythema shows dermal oedema with perivascular infiltrate. 54

The etiology of ETN is unknown. One proposed theory is that it is a graft-versus- host reaction against maternal lymphocytes , but there are insufficient data to support this

. Another proposed theory is, that its is an immune response to colonization of microbes through the hair follicles49. Wright or Giemsa stain shows eosinophils with a few neutrophils.

The differential diagnosis includes sepsis, staphylococcal folliculitis, miliaria rubra, miliaria crystallina, pustular miliaria, congenital candidiasis, acne neonatorum, transient neonatal pustular melanosis (TNPM), infantile acropustulosis, neonatal varicella, and occasionally incontinentia pigmenti .51

No therapy is needed for erythema toxicum except for parental reassurance.

TRANSIENT NEONATAL PUSTULAR MELANOSIS (TNPM)

It is a benign and self-limited disease of unknown etiology that commonly affects full term black infants .TNPM was first reported and described by Ramamurthy et al in

1976 .56

Its incidence among black infants is 4.4% and 0.2 to 0.6 % in white newborns .57

The lesions are usually present at birth.

These are flaccid , superficial pustules of size 1-3 mm diameter with no surrounding erythema distributed over chin, neck, forehead, back, and buttocks and sometimes over the palms and soles . The pustules rupture leaving behind a brown crust with surrounding collarette of scales and finally pigmented macules which may persist upto 3 months.58

Smear from pustules content reveals predominance of neutrophils with occasional eosinophils on Wright stain preparation.59

Biopsy shows subcorneal or intraepidermal vesicles which contain primarily polymorphonuclear leukocytes, some eosinophils, keratinous debris, serous fluid, and fragmented hair shafts. The dermis is usully uninvolved but there may be perivascular inflammatory infiltrates . 56

The differential diagnosis of TNPM includes erythema toxicum neonatorum, infantile acropustulosis, transient cephalic neonatal pustulosis, and eosinophilic pustular

folliculitis of infancy, acne neonatorum, pustular miliaria, congenital self-healing

Langerhans cells hystiocytosis, and incontinentia pigmenti.57

No treatment is needed except parental reassurance.

ACNE NEONATORUM

Acne occurring in newborns at birth or within 4-6 weeks after birth is called neonatal acne or acne neonatorum . It is more common in boys. The incidence of neonatal is approximately 20% of newborns . 60 The exact etiology is unknown. It is believed to be an inflammatory response to the saprophytic yeast Malassezia and not a true acne .61

There is a role of genetic factors, maternal and neonatal androgen resulting in increased productionof β-hydroxysteroids which eventually lead to enlargement in the sebaceous glands, thereby, increasing sebum production.60

Lesions are primarily closed comedones, but open comedones , papules and pustules may be seen. Cysts and nodules are very rare, but may lead to scarring.Lesionsare usually distributed over the cheeks or forehead but may involve the chest, back, or groin .62

Neonatal acne usually resolves spontaneously without scarring. But if they extensive and remain for several months can treat infants with 2.5% benzoyl peroxide lotion. 63

MILIARIA

Miliaria is a condition which results from retention of sweat in eccrine ducts that are occluded by keratin plugs. Retrograde pressure results in rupture of duct and leakage of sweat in to the epidermis and/or dermis. Miliaria are of three types depending on the level of blockage of eccrine sweat duct i.e miliaria crystallina, rubra, and profunda.64

The causes of eccrine duct occlusion are unknown. An accumulation of periodic acid-Schiff (PAS)-positive material has been described as blocking the sweat duct in miliaria. Furthermore, a PAS-positive extracellular polysaccharide substance (EPS) has been identified as a product of some strains of Staphylococcus epidermidis.

Miliaria crystallina, or sudamina,is seen in 4.5% to 9% of neonates with greatest incidence at 2 weeks of age or less. Miliaria rubrais is commonly seen between 1 and 3 weeks of age . Miliaria profunda is rare and most commonly seen in recurrent episodes of miliaria rubra .65

Miliaria crystallina is caused by superficial eccrine duct closure. Lesions are vesicles of size 1-2mm without surrounding erythema, most commonly on the head,

neck, and trunk . They rupture leaving behind desquamation that may persist for days.

Miliaria rubra is caused by a deeper level of sweat gland obstruction. The lesions are small erythematous papules and vesicles.65

Miliaria crystalline and Miliaria rubra are benign conditions which are usually self-limited and resolves spontaneously in response to a cooler, dryer environment.

INFANTILE ACROPUSTULOSIS(IA)

Infantile acropustulosis is a condition of unknown etiology . It is characterized by recurrent crops of 1- to 2-mm pruritic vesiculopustules, which appear predominantly on distal extremities of infants. 66 Episodes of pustular eruptions lasting from 8 to 14 days are followed by longer intervals with no symptom. 67

Although the aetiology is unknown scabies infestation has been frequently noted to precede IA, suggesting a relationship between the two diseases. 68

Biopsy shows intraepidermal pustule, which progresses to a subcorneal pustule which contain neutrophils or eosinophils.69

The lesions usually resolve spontaneously topical corticosteroids have been tried are a safe and effective first-line therapy. 68

In severe cases Dapsone 1–2 mg/k/day can be administered however there is risk of methemoglobinemia and other adverse effects 70

. There is no specific treatment for the condition is mostly symptomatic.

PIGMENTARY CHANES IN NEONATES

PIGMENTARY CHANGES

In certain newborn babies hyperpigmentation of the skin can be seen in the genital areas , over the lower abdomen( linea nigra) , areolar region, over the axilla, pinna and at the fingers . This is believed to result from the influences of maternal and placental hormones. This may persist for a few months and fade. An important differential diagnosis is hyperpigmentation induced by congenital adrenal hyperplasia (CAH).32

.MONGOLIAN SPOTS

Mongolian spots (MS) are congenital birthmarks present at birth or in the first weeks of life , located mostly on the gluteal and lumboscaral region. They are bluish- green to black colour macules or patches ; oval to irregular in shape. These lesions are most prominent at the age of one year and start regressing thereafter.72

Their incidence is around 90% of African Americans, about 80% of Asians, about

70% of Hispanics and fewer than 10% of Caucasians 71

MS can be classified as sacral and extra-sacral; based on the speed of regression, they have been classified into Common type (regress by early childhood), Extensive type

(regress very slowly) and Persistent type(persist into adulthood). Other variants include generalised MS, aberrant MS, superimposed MS, halo-like MS and speckled MS73

The blue color of the lesion is due to Tyndall effect whereby light falling on any medium, the particles of which scatter and reflect light, making the beam visible. Light of longer- wavelength is transmitted more while the shorter-wavelength is more reflected . 72

Histopathological examination shows elongated, spindle shaped, bipolar, wavy or irregular, dendritic cells in the mid-dermis of size 5-10 μm thick and 30-100 μm in length, lying parallel to the skin surface without disturbing the normal architecture of skin.Melanin granules may be found in these dendritic cells on higher magnification which stain positive with Masson-Fontana silver stain. These cells stain positively with

S-100, HMB45, Melan A/MART-1, Tyrosinase, PNL-2 Ag and MIT. 73

Diffuse, multiple, persistent and unusual MS have now been shown to co-exist with inborn errors of metabolism, most commonly GM1 gangliosidosis and mucopolysaccharidosis type I (Hurler’s disease), followed by mucopolysaccharidosis type

II (Hunter’s syndrome), mucolipidosis, Niemann-Pick disease and mannosidosis.72

CAFÉ –AU-LAIT MACULE

Café-Au-Lait macules are round or oval uniformly tan to brown macules and patches with distinct margins and variable border. During the first few years of life they enlarge in size in proportion with the general body growth and then stabilize. They do not regress in adulthood. They can occur in up to 2.5 percent of newborn infant. 87

On histological examination there is increased epidermal melanin without melanocytic proliferation. Ultrastructurally, giant pigment granules

(macromelanosomes) are seen .

Café au lait spots have been found to be associated with the following conditions

Neurofibromatosis -1 , Mc Cune Albright Syndrome, Bloom syndrome, Basal cell nevus syndrome, Chediak Higashi Syndrome, Gaucher disease, Hunter Syndrome, Maffucci

Syndrome, Noonan Syndrome, Watson Syndrome, Wiskott-Aldrich Syndrome, Silver-

Russel Syndrome, Ataxia telangiectasia ,Tuberous Sclerosis, Fanconi anaemia .88

For a diagnosis of neurofibromatosis type 1 in infants, the presence of six or more café au lait spots greater than 0.5 cm in diameter (or greater than 1.5 cm in diameter in adults) is one criteria. 87

CONGENITAL MELANOCYTIC NEVI

Melanocytic nevi are benign proliferations of melanocytic cells arranged in nests in the epidermis, dermis or in other tissue. They are usually seen at birth but some may appear upto the second year of life.

Giant congenital melanocytic nevus (GCMN) is defined as a congenital melanocytic lesion that will reach, at least, 20 cm in adult life.

They are brown to black moles which are present at birth, which are commonly found over the back and the thigh areas.

HYPOPIGMENTED BIRTHMARKS

Nevus depigmentosus is a nonprogressive hypopigmented macule or patch that is present at birth. It is stable in its relative size and distribution throughout life.89

Coupe in 1976 proposed the following criteria for the diagnosis of Nevus depigmentosus 90

1. Leukoderma present at birth or onset early in life

2. No alteration in the distribution of leukoderma throughout life

3. No alteration in texture, or change of sensation in the affected area

4. No hyperpigmented border around the achromic area

Nevus anemicus is a congenital circumscribed round or oval patch of pale or mottled skin. Appearing at birth or in early childhood.91 It is a localized vascular hypersensitivity to catecholamines which produces increased vasoconstriction and skin pallor.

On diascopy, the border between lesion and normal skin disappears because the normal skin becomes blanched. No treatment is required.92

EPIDERMAL NEVI

An epidermal nevus is an abnormal, benign yellowish-brown patch or velvety, granular or warty plaque usually single or multiple having linear or whorled appearance or following blashko lines caused by an overgrowth of skin cells which is seen at birth.

The various subtypes are keratinocyte (verrucous epidermal nevus), sebaceous gland

(nevus sebaceous), pilosebaceous unit (nevus comedonicus), eccrine gland (eccrine nevus), or apocrine gland (apocrine nevus). Malignant degeneration (e.g. basal cell carcinoma or squamous cell carcinoma) of epidermal nevi is rare. Syndromes associated with epidermal nevus include CHILD syndrome (congenital hemidysplasia with ichthy- osiform nevus and limb defect), phakomatosis pigmen-tokeratotica, sebaceous nevus,

Becker's nevus, proteus syndrome and nevus comedonicus syndromes 93

VASCULAR BIRTHMARKS

Vascular anomalies are a group of congenital blood vessel disorders more typically referred to as birthmarks. They may be categorized into vascular tumors and malformations.

Haemangiomas are common tumours of childhood and infancy that enlarge by proliferation of endothelial cells and may involute by progressive cellular death

.Histopathological examination shows proliferation of endothelial cells with or without vascular lumens.94

At five years 50 % of cases, 70% at 7 years and 90 percent of cases at 9 years undergo spontaneous remission 81

Treatment is indicated when there is functional impairment (orbital, oral,

Subglottic) , complications like haemorrhage, congestive heart failure hypoprothrominemia and extremely large lesions.94

Oral and intralesional corticosteroids , Interferon alpha , Pulse dye laser are used.

Recently betablocker agent propranolol have been tried with success. 81

VASCULAR MALFORMATIONS

Vascular anomalies was classified by Mulliken into vascular malformations and vascular tumors. Vascular malformations can be subcategorized according to the type of vessel into capillary malformation (CM), venous malformation (VM), arterial malformation (AM), and lymphatic malformation (LM).95

Salmon patch and Portwine stain are two main subtypes of Capillary malformation.

Salmon patch ( Nevus Simplex) :

They appear as flat, pink, vascular lesion found in the glabellar area, on the upper eyelids or at the nape of the neck(Erythema nuchae, Unna nevus) , occipital are ( Stork bite) in 40 % of newborns.Common in Caucasian babies.

Histologically they comprise of dilated superficial dermal capillaries which represent persistence of the fetal circulation. No treatment is necessary, since 95 % of salmon patches fade, generally within the first year of life91

They may be associated with other signs such as faun tail, pit, bumps, or other lesions that could raise the suspicion of an underlying defect in the spine such as spina bifida or to be syndromic as in Cobb syndrome.95

Port-wine stain( nevus flammeus)

The incidence of Port wine stains is reported to be between 0.1% and 2%.

They are present at birth as pinkish-red to bluish macules of variable size with sharp edges that blanches .

During childhood, the lesion lightens minimally due to skin thickening and changes in pigment. In or following adolescence, the lesion may begin to darken and develop varicosities, nodules or pyogenic granulomas.

When present over the face they may be associated with Sturge–Weber syndrome while lower limb lesions are associated with Klippel–Trenaunay syndrome. 95

Pulsed-dye laser therapy can be used to lighten a nevus flammeus lesion, to reduce the risk of Klippel-Trenaunay-Weber syndrome and to minimize the deformities that can occur with progression of the lesion 96

AIMS AND OBJECTIVES

AIM: To determine the most common spectrum of dermatological manifestations in

Neonates

OBJECTIVES:

1) To study the clinical pattern of dermatological manifestations in neonates.

2) To establish the correlation between various neonatal factors, maternal factors or environmental factors and the occurrence of dermatological manifestations.

MATERIALS AND METHODS

STUDY APPROVAL: Prior to commencement of this study – Thesis and Ethical

Committee of Government Stanley Medical College , Chennai has approved the thesis

protocol.

PLACE OF STUDY:

Department of Dermatology ,Postpartum ward, Neonatal Intensive Care

Unit (NICU)

Government Stanley Medical College, Chennai -1

SAMPLE SIZE, STUDY DESIGN AND DURATION

Minimum of 116 neonates, an observational cross-sectional study was carried out for a period of 1 ½ years.

INCLUSION CRITERIA:

1. Neonates with skin lesions attending the Dermatology Outpatient Department

2. Neonates with skin lesions admitted in the postpartum ward

3. Neonates with skin lesions admitted to Neonatal Intensive Care Unit (NICU)

4. Neonates with consent taken from the mother were included in the study.

EXCLUSION CRITERIA:

1. Neonates with skin lesions whose mothers/ guardians do not give consent for

clinical examination and photograph

2. Neonates without skin lesions

METHODOLOGY OF COLLECTION OF DATA :

All neonates born in OBG ward , those admitted in Neonatal Intensive Care Unit

(NICU) and those attending the Department of Dermatology at Government Stanley

Medical College and Hospital , Chennai with consent being taken from the mother were included in the study. A detailed history was recorded in a proforma including the age of the mother, parity of mother, history of consanguinity, mode of delivery, and history of maternal illness during pregnancy. The sex, birth weight and age at the time of examination was noted in each case. Thorough examination of neonate in daylight with proper description of morphology of skin lesions was recorded. Diagnosis of disorder was based on clinical impression. Photographic records were maintained.

Variables analysed here are

1. Colour of the newborn skin at birth.

2. No. of Pregnancies (Primigravida / Multigravida / Elderly Primi)

3. Mode of Delivery (Vaginal, Forceps / LSCS)

5. Birth weight, age & sex of the new born

6. H/O Consanguinity

RESULTS

SEX –WISE DISTRIBUTION

Table 1 : Distribution according to sex SERIAL NO. SEX CASES % 1 Female 51 44 2 Male 65 56

In this study out of 116 neonates 51 were females and 65 were males.

Distribution according to sex 60

0 FEMALE MALE

Chart 1 shows distribution according to sex

DISTRIBUTION ACCORDING TO GESTATIONAL AGE

Table 2: Distribution according to gestational age SERIAL NO. GESTATIONAL AGE NO. OF CASES % 1 PRETERM 16 14

2 TERM 87 75 3 POSTTERM 13 11

Most of the cutaneous lesions were seen in term neonates (75%).

Distribution according to gestation age

11% 14% PRETERM

TERM

75% POSTTERM

Chart 2 Shows distribution according to gestational age

DISTRIBUTION ACCORDING TO BIRTH WEIGHT

Table 3: Distribution according to the birth weight

SERIAL NO. BIRTH WEIGHT NO OF CASES % 1 AVERAGE BIRTH 83 72 WEIGHT 2 LOW BIRTH 33 28 WEIGHT

In the above table the numbers of cases of average birth weight are 83and the low birth weight cases are 33

Distribution according to the birth weight

AVERAGE BIRTH 28% WEIGHT

LOW BIRTH 72% WEIGHT

Chart 3 shows distribution according to the birth weight

DISTRIBUTION ACCORDING TO THE PARITY

Table 4: Distribution according to the parity

SERIAL NO. PARITY NO. OF CASES % 1 PRIMI 50 43 2 MULTI 66 57

Out of 116 cases 50 were primiparae and 66 were multiparae

Distribution according to the parity

PRIMI 43%

57% MULTI

Chart 4 shows distribution according to the parity

DISTRIBUTION ACCORDING TO THE MODE OF DELIVERY

Table 6: Distribution according to the mode of delivery

SERIAL NO. MODE OF NO. OF CASES % DELIVERY 1 NORMAL VAGINAL 49 42 DELIVERY 2 CAESAREAN 62 54 SECTION 3 OTHERS 5 4

Out of 116 cases studied the mode of delivery of 49 cases were normal vaginal, 62 were caesarean mode of delivery and 5 were others.

Distribution according to the mode of delivery

4% NORMAL VAGINAL DELIVERY 42% CAESAREAN SECTION

54% OTHERS

Chart 5 shows distribution according to the mode of delivery

DISTRIBUTION ACCORDING TO CONSANGUINITY

Table 6: Distribution according to Cansanguinity

SERIAL CONSANGUINITY NO. OF CASES % NO. 1 CONSANGUINEOUS (C) 18 16 2 NON- 98 84 CONSANGUINEOUS(NC)

Out of 116 cases 18 babies born out of consanguineous marriage and 98 were of non- consanguineous marriage

Distribution according to Consanguinity

16% CONSANGUINEOUS

NON- 84% CONSANGUINEOUS

Chart 6 shows distribution according to the Consanguinity

116 neonates with cutaneous manifestations were considered for the study. The observations made from this study are:

Table 7: Distribution of cases according to the percentage

SERIAL DIAGNOSIS NO. OF CASES % NO. 1 Mongolion spot 26 22.4 2 Physiological desquamation 21 18.1 3 Erythema Toxicum Neonatorum 14 12.1 4 Acrocyanosis 9 7.8 5 Seborrheic hyperplasia 7 6.0 6 Hypertrichosis lanugosa 6 5.2 7 Miliaria 6 5.2 8 Milia 5 4.3 9 Café-au-lait macule 2 1.7 10 Vernix caseosa 2 1.7 11 Axillary pigmentation 2 1.7 12 Congenital melanocytic nevus 2 1.7 13 Aplasia cutis congenital 2 1.7

14 Others : INCONTINENTIA PIGMENTI 1 ACROPUSTULOSIS OF INFANCY 1 NEONATAL ALOPECIA 1 INFANTILE HAEMANGIOMA 1 PORT WINE STAIN 1 SALMON PATCH 1 10.3% PIEBALDISM 1 ACESSORY TRAGUS 1 DERMATOPHYTOSIS 1 SCABIES 1 COLLODIAN BABY 1 SUBCUTANEOUS FAT NECROSIS 1

Mongolian spot was the commonest skin manifestation observed in 26 cases followed by

Physiological desquamation seen in 21 cases. ETN was found in 14 cases involving the trunk commonly. Acrocyanosis was seen in 9 cases.

25.0 20.0 15.0 10.0 5.0 0.0

Chart 7 shows distribution of skin lesions according to percentage

Table 8: Distribution of skin lesions according to the age of mother, consanguinity Skin lesions Age of the Mother Consanguinity <20yrs 20-30yrs >30yrs C NC Mongolion spot 4 20 2 1 24 Physiological 1 20 0 3 18 desquamation Erythema Toxicum 2 11 1 6 8 Neonatorum Acrocyanosis 2 6 1 3 6 Seborrheic hyperplasia 1 6 0 4 3 Hypertrichosis 2 4 0 2 4 lanugosa Miliaria 0 5 1 0 6 Milia 0 5 0 3 2 Café-au-lait macule 0 2 0 2 0 Vernix caseosa 0 1 1 0 2 Axillary pigmentation 1 1 0 1 1 Congenital 0 2 0 1 1 melanocytic nevus Aplasia cutis 0 2 0 1 1 congenital

Most of the mothers in the study belong to the age group 20-30 yrs.

Table 9: Distribution of skin lesions according to the mode of delivery and parity Skin lesion Mode of delivery Parity NVD CS Others Primi Multi Mongolion spot 10 14 2 15 11 Physiological 8 12 1 8 13 desquamation Erythema Toxicum 3 10 1 5 9 Neonatorum Acrocyanosis 7 2 0 2 7 Seborrheic hyperplasia 4 3 0 1 6 Hypertrichosis lanugosa 2 4 0 1 5 Miliaria 1 5 0 1 5 Milia 2 2 0 0 5 Café-au-lait macule 0 2 0 0 2 Vernix caseosa 1 1 0 0 2 Axillary pigmentation 0 1 1 0 2 Congenital melanocytic 1 1 0 0 2 nevus Aplasia cutis congenital 2 0 0 0 2

Erythema toxicum neonatorum was more common in neonates born by Caesarean

Section ( 10 cases) than Normal vaginal delivery(3 cases). Acrocyanosis was more common in births born by normal vaginal delivery in 7 out of 9 cases.

DISCUSSION

Cutaneous manifestation in neonates are not uncommon. Their prevalence has been found to be between 57% and 99.3%. In our study, all live neonates born in the

Obstetrics and Gynaecology ward ,neonates admitted in NICU and including those who visited the Dermatology OPD were screened for cutaneous manifestations .

Out of 116 neonates in the study, 56% were males and 44% were females( Chart

1) which correlates well with a study done by Gudurpenu et al. 74 There was a male preponderance in our study as contrast to Zagne et al 75 where more incidence of females was seen. Most of the mothers were in the age group of 20 and 29 years at the time of delivery similar to the findings of Sachdeva et al .76

75% were term babies, 14% were preterm babies and rest 11% were post term babies( Chart 2).In our study 28 % were low birth weight neonates while the rest 78% had a birth weight of 2.5 kg or more ( Chart 3). In a study by Behera et al 7722 % and

78% had low birth weight and adequate birth weight respectively.

43% of the births were primigravida while 57 % were multigravidae ( Chart 4) which correlates well with the finding of Zagne et al 75 42% of the neonates were born by

Normal vaginal delivery, 54 % by caesarean section and the rest 6 % by other modes(

Chart 5).

Sixteen babies were born of consanguineous marriage.

This cross sectional study was done to assess the cutaneous manifestation in newborns .

The discussion of this result have been presented below:

Mongolian spot

Mongolian spot was the most common cutaneous manifestation observed in our study which was noted in 22.4% of neonates( Chart 7)( Figure 1). A similar incidence was found in a study done by Gokdemir et al.78 However this incidence of Mongolian spots in our study was quite low in comparison with other study observed in 60.2% by

Sachdeva et al & 64.5% by Jain et al.79 The lumbosacral region and buttocks were the commonest site . Few lesions were found on the legs, arms and shoulders. The colour varied from light blue to bluish green with a female preponderance. There was no relation to maternal illness or mode of delivery similar to a study by Sachdeva et al.76

Physiological desquamation

It was noted in 18.1 % of the cases (Chart 7)( Figure2) which was identical to a study done by Zagne et al 75 18.2 % .However higher incidence were reported by

Gokdemir et al78 31.29% , 40% by Sachdeva et al.76 and 83% by Baruah et al. 80.

The scales mostly involved the trunk, extremities and ankle. It was more in term and post - term neonates with no sex predilection .

Erythema Toxicum Neonatorum

In this study 12.1 % (Chart 7) ( Figure3) of neonates had erythema toxicum neonatorum. This was comparable to a study by Gokdemir et al 78(13.9%). This incidence was found to be higher as reported by Jain et al 79 in 38%, 34.8% by Baruah et al80 & 27% by Dash et al81 The lesions were most commonly seens over the cheeks, upper trunk, thighs, and arms with sparing of the palms and soles .

There was no sex predilection. But it was more common in term neonates as also reported by Baruah et al. 80 and Dash et al 81. The lesions were more common in neonates born by caesarean section which was similarly observed by Behera et al.77

Acrocyanosis

This was observed in 7.8% (Chart 7) of newborns. Jain et al 79reported it in

10.5% of newborns and Zagne et al 75 in 12.32% This incidence is much lower as observed by Behera et al (3%).77 It was more common in neonates born by vaginal delivery because a lot of pressure is exerted on the fetus inside the birth canal coupled with longer time duration for this mode of delivery , similarly observed by Zagne et al75

Seborrheic hyperplasia

Sebaceous gland hyperplasia was seen in 6% (Chart 7) ( figure8 ) of the cases .

This was similar to the findings of S. Gudurpenu et at ( 6.8%)74 . Commonly observed over the cheeks, nose, forehead, and upper lips. This incidence is lower that the observations of Gokdemire et al 78 (48.4%) and 47.78% by Zagne et al 75. It was more commonly observed in term neonates in contrast to the finding of Jain et al .79 No sex predilection as also reported by Zagne et al75

Hypertrichosis lanugosa

Hypertrichosis lanugosa was seen in 5.2% (Chart 7) ( figure 10) of the cases in our study. This is comparable to the incidence of Dash et al in 81 in 7 % and Ferabas et al

84 in 7.8% While Gokdemire et al 78and Nobby et al 82 reported it in 13.9% and 14.6% respectively. Higher incidence was noted in preterm babies which correlates with the findings of Gorur et al 83

Miliaria

The overall frequency of Miliaria in this study is 5.2%( Chart 7). This was similar to the findings of Gorur et al 83 in 3.49% cases. However higher incidence was noted by

Sachdeva et al 76 in 20.6% and Baruah et al 80in 13.2%. Higher incidence was noted among the neonates admitted in the NICU under incubators which could be due to the warm and humid environment. This was a similar observation made by Jain et al 79

Milia

In this study milia was found in 4.3%( Chart 7) of the neonates. This was comparable to the incidence reported by Gudurpenu et al74 in 6.8% . The incidence of

Miliaria shows wide variation from study to study . It was reported as high as 44.2% in a study by Nobby et al 82 and 93.1 % by Baruah et al 80.A higher incidence was observed in term babies and in babies weighing more than 2.5 kg as similarly observed by Gorur et al 83

Café-au-lait macule

CALM was observed in 1.7% % (Chart 7) of neonates which is similar to the study by Nobby et al 82 who reported it in 1.6% of cases. However a higher percentage of CALM (3 %) was seen in a study in by Gorur et al.83 A single case had multiple lesions (< 6) with no other diagnostic features of Neurofibromatosis-1.

Vernix Caseosa

In our study we observed vernix caseosa in 2 cases amounting to 1.7% (Chart 7)( figure 4) . However slightly higher incidence has been reported in 2.9% of cases by

Gorur et al 83 and 4.5% by Gudurpenu et al74. In both cases it was seen over the axillary folds in term neonates.

Axillary Pigmentation

Axillary pigmentation observed in our study amounted to 1.7% (Chart 7)(figure

6). Lower incidence was found by Gudurpenu et al74 in 0.5% cases. Hyperpigmentation of the skin in neonates is common and it is believed to result from the influences of maternal and placental hormones.

Congenital melanocytic nevi

In our study, congenital melanocytic nevus, brown flat was found in 1.7 % (Chart

7). This correlates well with the incidence of a study done by Sadana et al 85 and Dash et al 81 . Single lesions of melanocytic nevus was seen in our cases.

Aplasia cutis

Two cases in our study had aplasia cutis which amounted to 1.7% (Chart 7)( figure

5). The incidence reported by Bose et al 86 was much lower in 0.2% cases. A single atrophic patch was present on the scalp near the vertex with no secondary changes.

CLINICAL PHOTOGRAPHS

Figure 1 shows Mongolion spot

Figure 2 shows Physiological desquamation

Figure 3 shows Erythema Toxicum Neonatorum

Figure 4 shows Vernix caseosa

Figure 5 shows Aplasia cutis congenital

Figure 6 shows Axillary pigmentation

Figure 7 shows Infantile haemangioma

Figure 8 shows Seborrheic hyperplasia

Figure 8 shows Collodian baby

Figure 9 shows Hypertrichosis lanuginose

Figure 10 shows Accessory tragus

SUMMARY

1. In this Observational Study of Spectrum of Dermatological Manifestation in Neonates

116 cases with dermatological findings were considered for this study .

2. Out of these 116 cases, 65 were males and 51 were females.

3. Thorough clinical examination was conducted for all neonates under the study.

4. The number of preterm cases was 16 , whereas the term cases were 87 in number and

13 cases of post term.

5. The average birth weight 2.93 Kg was seen in 83 while low birth weight was observed in 33 cases.

6. Out of the 116 cases 43% and 57% were primiparae and multiparae respectively.

7. The modes of delivery of the cases were 42% of normal vaginal whereas 54% were caesarean and 4 % were delivered by forceps

8. The percentage of consanguineous marriage and non-consanguineous marriage in the parents of neonates were seen as 16% and 84% respectively.

9. The commonest cutaneous manifestations found in our study were that of pigmentary type i.e Mongolian spot amounting to 22.4%of the cases most commonly over the lumbosacral region.

10. The physiological desquamation were the commonest finding of papulosquamous changes that were seen in our study amounting to 18.1% of cases .

11. The next commonest condition was of Erythema toxicum neonatorum amounting to

12.1% of the cases most frequently observed on the trunk .

12. Acrocyanosis amounted to7. 8% of the cases in this study.

13. The nose demonstrated both the cases of Sebaceous gland hyperplasia amounting to

6% of our case study.

14. 5.2% of the cases were hyprertrichosis lanugosa occurring over the shoulder, trunk and limbs.

15. Miliaria accounted for 5.2% of the cases. It was more common in neonates admitted in NICU.

16. Milia was found in 4.3% of the cases and most commonly occurred in neonates with birth weight > 2.5kg

17. Of the solitary lesions of Café au lait macules which were seen in our study; these cases amounted only to 1.7 %.

18. The 1.7% of cases where vernix caseosa seen were prominently observed in the axilla

19. Axillary Hyperpigmentation amounted to 1.7% of the cases.

20. In our study two neonates demonstrated congenital melanocytic nevi amounting to

1.7 % of the cases.

21. Congenital melanocytic nevus was seen in 1.7 % of the cases.

22. Other skin changes included Incontinentita pigmenti, acropustulosis of infancy, neonatal alopecia, infantile hemangioma, port wine stain, salmon patch, piebaldism, accessory tragus, dermatophytosis, scabies , collodian baby, subcutaneous fat necrosis amounting to 10.3% in total

CONCLUSION

 In this Observational Study of Spectrum of Dermatological Manifestation in

Neonates , the most common cutaneous manifestations observed were mostly in

the spectrum of physiological changes like Mongolian spot, Physiological

desquamation, Erythema toxicum neonatorum and Acrocyanosis.

 A few pathological conditions like Incontinentia pigmenti , Piebaldsim were seen.

 The pattern of neonatal dermatoses is influenced by various factors which include

racial , geographical , environmental , maternal and foetal factors.

 For example , in this study acrocyanosis was common in neonates born by normal

vaginal delivery with history of prolonged labour. This may be due to more

pressure impacted on the fetus .

 Although neonatal tinea is rare we have diagnosed a case of tinea corporis in an 8

day old baby who had a positive family history of dermatophytosis.

 Miliaria rubra was common in neonates incubated in NICU . The warm

environment of the NICU may be a contributing factor .

 Appropriate Antenatal Care can prevent many neonatal manifestations

contributed by maternal factors like scabies, dermatophytosis which were

observed in this study.

 Awareness of cutaneous manifestations in neonates helps us to differentiate

between the benign transient lesions from the pathological conditions. So that

timely intervention and necessary followup may be done where needed as well as to give assurance to the anxious parents.

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1999;65:99-103

ANNEXURES

PROFORMA

INFORMANT:

BIRTH WEIGHT:

GESTATIONAL AGE:

DATE OF BIRTH: SEX:

TIME OF BIRTH:

MODE OF DELIVERY:

2. OBSTETRIC HISTORY:

AGE OF THE MOTHER:

GRAVIDA:

PARA:

LIVING:

ABORTION:

ANY CONTRACEPTION USED:

ANY PREVIOUS MEDICATIONS:

3. PAST HISTORY:

H / O Consanguinity / genetic disorders/ consumption of alcohol by mother.

4. FAMILY DISORDER:

Any h /o Atopy.

5. PERSONAL HISTORY OF MOTHER:

Diet (veg/non veg/mix)/ sleep (regular/irregular)/bowel and bladder (normal/abnormal)

Smoking /tobacco /alcohol /others.

6. GENERAL EXAMINATION

Heart rate:

Respiratory rate:

Temperature: febrile/afebrile

Present weight:

7. ANTHROPOMETRIC MEASUREMENTS:

HC: CC: LENGTH:

REFLEXES:

General appearance of the skin, colour:

Icterus /pallor /clubbing /cyanosis /edema /lymphadenopathy.

8. CUTANEOUS EXAMINATION:

8.1 LESIONS

Macules /papules /patches /vesiculopustular /vesicles.

8.2 SITE

Face/neck/trunk/axillae/upperlimb/abdomen/back/groins/genitals/buttocks/lower limbs/palms and soles/nails/scalp.

8.3 PATTERN OF LESIONS

Linear / Arcuate / Annular/ Serpiginous/ Bizzare

Symmetrical/assymetrical/solitary/well demarcated.

8.4 MUCOUS MEMBRANE (Oral cavity/genital):

8.5 PALMS AND SOLES:

8.6 SCALP AND HAIR:

8.7 NAILS- colour and shape

8.8 SYSTEMIC EXAMINATION:

CVS CNS RS P/A

9.BEDSIDE INVESTIGATIONS: DIASCOPY/SCRAPING/WOOD`S LAMP/GRAM`S STAIN

CONSENT FORM

Mr/Mrs/Miss: Age:

Address:

Phone:

Name of the procedure:

I undersigned Mr/Mrs

Have been explained about the above said procedure (questionnaire), being done to investigate the prevalence of dermatological diseases in neonates in my regional language. I am also aware that the study is only an observational study. Thereby no intervention/ possible side effects are expected.

I have been explained that this study will be conducted by Dr. Stacy Ann Marbaniang.

I further state that I have carefully read and understood all the information provided in this form and with full conscious mind I hereby give my consent for the said procedure.

Signature /thumb impression of the parent/guardian:

Name and relationship if signed by other than parent:

Witness

Name: Signature:

KEY TO MASTER CHART

BW- Birth weight

M- Male

F- Female T-term

P- preterm

C- Consanguinity

NC- Non – consanguinity

MOD- mode of delivery

MS- Mongolian spots

SD- Superficial desquamation

ETN- Erythema toxicum neonatorum

AC- Acrocyanosis

SGH- Sebaceous gland hyperplasia

HL- Hypertrichosis lanugosa

MR-Miliaria

ML-Milia

CALM- Café au lait macules

VC- Vernix Caseosa

AP-Axillary pigmentation

CMN- Congenital melanocytic nevi

ACC- Aplasia cutis congenital MISC- miscellaneous

Age of mother Term/pre/ Serial no. Name B/o Sex parity MOD BW C/NC VC ML MS PD ETN HL AC CALM CMN SH MR AP ACC MISC in years Postterm 1 VAIJAYALAKSHMI 32 T F Primi NVD 2.7 C + 2 KALPANA 29 postterm M P2 CS 3.8 NC + 3 SUGANYA 30 T F P1 NVD 2.73 NC + 4 PRIYADARSHINI 27 T F P1 CS 3.7 NC + 5 SIVARNJINI 17 P F primi NVD 2.15 NC + 6 VIDHYA 24 T M primi CS 3.02 NC + 7 VIJI 21 T F primi NVD 2.65 NC + 8 DIVYA 24 T F primi NVD 3.2 NC + 9 JANANI 22 P M P1 NVD 2.95 NC + 10 BHUVANESHWARI 22 T M P2 NVD 2.8 NC + 11 SUMATHY 25 T M primi CS 2.6 C + 12 ABINA 18 P M P1 CS 2.338 NC + 13 KAVITHA 20 P F P3 others 3.025 NC + 14MEGALA 19 T F primi CS 1.38 NC + 15 SANGEETHA 23 T F P2 CS 2.195 NC + 16 UMA 30 T M primi NVD 2.7 NC + 17 GOWRI 23 T F primi CS 3.1 NC + 18 NITHYA 21 T F P1 others 2.8 NC + 19 VIJAYA 27 T F P3 CS 2.85 NC + 20 SAJEETA 25 T M P2 NVD 2.75 NC + 21 MEGALA 19 P M primi CS 2.25 NC + 22 CHITRA 26 T M P1 CS 5.02 NC + 23 LAKSHMI 18 T F P2 NVD 2.582 C + 24 DEVI 26 T F primi NVD 2.2 NC + 25 JANAKI 27 post term M primi CS 2.9 NC + 26MEGALA 22 T M P1 CS 2.1 NC + 27 ANITHA 23 T M P1 CS 3 C + 28 DEVI 25 P M primi NVD 2.3 NC + 29 MITHRA 21 T M P1 CS 2.2 NC + 30 KAVITHA 23 P M primi CS 2.65 NC + 31SOUMYA 24 T M P1 others 2.9 C + 32 JAYA 18 T M primi NVD 2.2 NC + 33 PADMAVATHY 27 P F P4 NVD 3.4 NC + 34 SAJEETHA 22 T F P1 CS 2.33 NC + 35 PREMA 22 T M primi NVD 2.4 NC + 36 KAYAL 31 postterm M P2 CS 2.9 C + 37 SUJATA 18 T F primi CS 3.4 NC + 38 SARANYA 20 T M primi CS 2.38 NC + 39 BHARATHI 25 T M P2 CS 2.6 C + 40 CHITRA 24 T F P2 CS 2.8 NC + 41 VIJAYLAKSHMI 19 T M P3 NVD 3 NC + 42RAMYA 27 T F primi CS 2.3 NC + 43 PARVEEN 26 P F P2 CS 2.8 NC + 44 RINI 26 T M primi others 2.8 NC + 45 PUSHPA 30 T M primi NVD 2.1 NC + 46 SAKTHI 23 postterm M P1 CS 2.8 NC + 47 TAMIL SELVI 21 T M P1 NVD 2.7 C + 48 VALARMATHI 29 T M primi CS 2.1 NC + 49 LATHA 30 T F P1 CS 3.3 NC + 50 SUMITHA 31 T M P1 NVD 2.9 NC + 51 RUBINI 27 T M primi CS 3.2 NC + 52 MEENAKSHI 25 T F P1 NVD 2.9 NC + 53 SANDHIYA 22 T F P1 NVD 2.45 NC + 54 CHELLAMAL 25 postterm F primi CS 2.7 NC + 55 ANNALAKSHMI 24 postterm M primi CS 2.9 NC + 56 KRITIKA 21 T M primi CS 2.5 NC + 57 MAHALAKSHMI 30 P F primi NVD 2.35 NC + 58 RAZIA 32 T F P2 CS 2.6 NC + 59 LAKSHMI 24 T M primi CS 2.7 C + 60 KANNYAMAL 18 T M P1 CS 2.8 NC + 61 CHITRA 23 T M P3 NVD 2.37 NC + 62 LAKSHMI 25 T F P2 NVD 3 NC + 63 AARTHI 28 T F primi CS 2.32 NC + 64 VALARMATHY 30 T M P1 CS 3.2 NC + 65 SHANTHI 19 T M P1 NVD 2.8 NC + 66 ARCHANA 23 T M primi CS 1.7 C + 67 BHARATHI 21 P F P1 NVD 2.59 NC + 68 GIRIJA 22 T M primi CS 3.2 NC + 69 SHANTHI 34 T M P2 CS 2.9 NC + 70PUSHPA 30 T F primi CS 3.6 NC + 71 TEJASHRI 27 postterm F P2 NVD 3 NC + 72 JAYANTHY 20 T M P1 NVD 2.6 NC + 73 VASANTHA 26 T M primi NVD 2.6 NC + 74ROSE 25 P F P2 CS 2.5 NC + 75 JAYA 21 T M P1 NVD 3.12 NC + 76LAKSHMI 19 T M P2 CS 3.2 C + 77 DEVI 32 T F primi CS 2.8 NC + 78 MARIAMMAL 22 T F P1 CS 2.9 NC + 79LATHA 21 T M P3 CS 2.2 NC + 80 VANAJA 21 P M P4 CS 3 NC + 81 SAKILA 27 postterm M primi CS 3 NC + 82 ANUSHIYA 26 T M P2 CS 3.4 C + 83 ARUNA 33 T F P1 CS 2.7 NC + 84 MIRIAM BEE 20 T F P1 NVD 2.7 NC + 85 MARY 25 T M primi others 2.9 NC + 86 DEVI 31 T M P1 NVD 2.5 C + 87 SARASWATHY 29 postterm F primi NVD 2.9 NC + 88 PREMA 24 T M primi CS 1.87 NC + 89 NANDINI 24 postterm F P1 CS 3.1 NC + 90 DIVYA 27 T F P1 NVD 2.9 NC + 91 VIJAYLAKSHMI 22 T F P2 CS 2.87 NC + 92 ANBU 25 T M primi CS 2.1 C + 93 NITHYA 17 P F primi CS 2.38 NC + 94 VIJI 27 T F primi CS 3.112 NC + 95 GIRIJA 31 T M P1 NVD 2.95 NC + 96 RANI 20 T M primi NVD 2.2 NC + 97 SUGIRTHA 23 T M P1 CS 2.68 NC + 98 FATHIMA 28 postterm M primi CS 3.5 C + 99 CHRISTY 25 P F P1 CS 2.5 NC + 100 RAJESHWARI 26 T F P2 NVD 2.87 NC + 101 SIVARNJINI 27 T F primi NVD 2.2 NC + 102 PAVAI 21 T M primi CS 2.3 C + 103 FATHIMA 28 T F P3 NVD 2.6 NC + 104 PUJA 25 T F primi CS 2.8 NC + 105 RAMYA 30 T F P3 NVD 2.8 NC + 106 ANUSHIYA 29 T M P2 CS 3.1 NC + 107 FATHIMA 29 postterm M P1 CS 3.02 NC + 108 UMA 19 T M primi CS 2.2 NC + 109 RANI 21 T F P1 NVD 2.9 NC + 110 DIVYA 21 T F P1 NVD 2.875 C + 111 THASLIMA 23 T M primi CS 1.98 NC + 112 PARVEEN 26 T M P2 NVD 2.7 NC + 113ESTER 22 P F primi CS 2.1 C + 114 VIJI 24 T M P2 NVD 2.7 NC + 115 GOKILA 30 postterm M P2 NVD 3 NC + 116 LAKSHMI 18 T M primi NVD 2.43 NC +