Clinical PhenomenonSECTION 1

The etiology is probably multifactorial. There is congenital deficiency or absence of the depressor anguli oris muscle.

Depressor anguli oris muscle draws the corner of mouth downward and everts the lower lip. While it can be an isolated phenomenon, coexisting major anomalies are seen in 10% with cardiovascular system and head and neck anomalies being the most common. Skeletal, genitourinary, gastrointestinal, central nervous system anomalies occur less frequently.

To rule out associated anomalies, e.g. brainstem evoked response audiometry (BERA) for hearing, 2D echo for cardiac defect, etc. should be performed.

Facial palsy is characterized by asymmetrical forehead wrinkling, inability to close eye and loss of nasolabial fold depth on the affected side.

No definitive treatment; parental assurance; treat comorbid conditions, if any.

This is a benign condition and mainly a cosmetic problem. It does not interfere with feeding or speech and improvement is seen within a month. It eventually disappears in the great majority of cases (as the muscle does not contribute significantly to facial expression in childhood/adulthood). Follow-up is required if coexisting anomalies exist.

Acrocyanosis is a functional peripheral vascular disorder often due to vasospasm of small cutaneous arteries, and arterioles along with compensatory dilatation in the capillary and postcapillary venules causing bluish discoloration. Usually, it is seen due to exposure to cold environment and physiologically during first hour of birth in both term and preterm.

The condition is seen in delivery room immediately after birth and is transient and self-limiting. It may be seen in newborns with hypothermia. SpO₂ is normal and above 95%. Pulse rate, volume and rhythm are normal.

Central cyanosis, vaso-occlusive disease.

None.

Re-assurance and ensuring normothermia.

A benign phenomenon.

Neonatal breast enlargement is a normal response to falling levels of maternal estrogen at the end of pregnancy, which trigger the release of prolactin from the newborn's pituitary.

The condition is seen in both males, female and is self-limiting. At times, there may be milky discharge. It can persist for two months though palpable breast buds can persist into childhood.

Mastitis (local inflammation), breast abscess (local inflammation with pus discharge or accumulation).

None.

No treatment is necessary unless the area becomes red or tender. No massage or manipulation of the breast tissue should be carried out. Parents need to be reassured.

Benign condition.

Repeated buffeting of the fetal skull against the maternal pelvis during a prolonged or difficult labor and mechanical trauma caused by use of forceps in delivery have been implicated in rupture of vessels that traverse from skull to periosteum.

The swelling appears after birth. If isolated sign, the infant may be asymptomatic. It is known to exacerbate neonatal jaundice. Common associated complications are skull fracture and intracranial hemorrhage.

Radiographs help in identifying the underlying skull fractures that can be seen in 5.4% of cephalhematomas. Magnetic resonance imaging (MRI) and/or computed tomography (CT) scan if suspect intracranial hemorrhage.

Differentiated from caput succedaneum and subgaleal bleed by its sharp periosteal limitations to one bone, the absence of overlying discoloration, the later initial appearance of the swelling, and the longer time before resolution.

Therapy is not indicated for the uncomplicated cephalhematoma. Significant hyperbilirubinemia may result, necessitating phototherapy. Routine incision or aspiration of a cephalhematoma is contraindicated because of the risk for introducing infection.

Most cephalhematomas are resorbed within 2 weeks to 3 months, depending on their size.

Chest indrawing is a sign of breathing difficulty and a marker of hypoxia. It is due to increased use of the chest muscles for breathing. In a normal breath, when an infant breaths in, the whole chest wall (upper and lower) and the abdomen moves out. With chest indrawing, the lower chest wall goes in while the upper chest and abdomen move out.

It is a sign of increased work of breathing and is associated with hypoxia. It manifests as subcostal or intercostal indrawing. There may be audible sounds like grunt or stridor. It suggests moderate to severe lung disease and is a “danger sign”. It is best detected in a quiet infant.

Lung disease cardiac disease (history s/o heart disease, viz cyanosis, murmur, congestive cardiac failure, cardiomegaly or abnormal heart sound).

X-ray chest; further tests based on clinical suspicion.

Supportive care, oxygen, antibiotics and specific treatment of the underlying cause.

While prognosis depends on the diagnosis, it is generally good with prompt recognition and intervention.

Capillary refill time is an indirect marker of circulatory stability. Normally, the capillaries refill instantly (<2 seconds) with adequacy of perfusion.

Hypothermia, infection, shock lead to delayed CRT. One-time assessment and relying only on CRT for adequacy of perfusion is usually not conclusive. More the parameters deranged in addition to CRT (e.g. heart rate, pulse volume, central peripheral pulse volume, respiratory rate, skin temperature, core peripheral temperature mismatch, sensorium, blood pressure, urine output, pulse oximetry) more is the possibility of shock.

Hypothermia, sepsis.

Tests are done depending on the cause suspected (e.g. sepsis screen, evaluation for congenital heart defect, etc.).

Treatment is of the underlying cause. Correction of temperature (hypothermia), and early antibiotics, fluid resuscitation and inotropes for shock are indicated.

Prognosis is dependent on the underlying cause. Early recognition and prompt treatment has good outcome.

It is caused by a vascular response to cold and usually resolves with warming. Sometimes, it may be a vasomotor phenomenon.

The lesions appear spontaneously over the legs, arms or the trunk. They are transient and self-limiting. The infant is asymptomatic. There are no signs or symptoms. There are no associated anomalies.

No specific investigations are required. It is a clinical diagnosis.

Physiologic cutis marmorata must be distinguished from cutis marmorata telangiectatica congenita, a vascular malformation in which the lesions do not resolve with warming. Cutis marmorata telangiectatica congenita is associated with extracutaneous findings.

Resolves with warming. No treatment is required.

It is a benign condition.

Cyanosis is a reflection of the absolute concentration of reduced hemoglobin. It is detected when the amount of reduced hemoglobin in the blood exceeds 5 g%. It is not influenced by oxygen saturation or the ratio of reduced hemoglobin to oxyhemoglobin. While oxygenated hemoglobin is bright red, reduced hemoglobin is dark blue or purple in color, and is what produces the dusky or blue color of the skin and mucous membranes.

Cyanosis is a marker of severity of illness and a “red flag” sign prompting urgent evaluation and stabilization. It is best visualized over mucous membranes. Infants with polycythemia may exhibit cyanosis at relatively high arterial saturations, while it is more difficult to discern cyanosis in a severely anemic infant unless the oxygen saturation is extremely low. Peripheral cyanosis, also known as acrocyanosis, is a bluish discoloration of hands and feet caused by peripheral vasoconstriction.

Acrocyanosis, polycythemia, cyanotic heart defect, upper airway malformation (e.g. atresia, stenosis or stricture), severe congenital or acquired lung disease (e.g. pulmonary hypoplasia, respiratory distress syndrome, meconium aspiration syndrome, pneumonia, air-leak syndrome, persistent pulmonary hypertension of the neonate), sepsis, hypoventilation, abnormal hemoglobin (e.g. congenital methemoglobinemia).

Pulse oximeter; further tests depending upon clinical suspicion.

Supportive care—assess, support and maintain airway, breathing and circulation, initiate oxygen and monitor the vitals—temperature, pulse rate, respiration, blood pressure, and oxygen saturation. Treat the underlying cause, viz partial exchange for polycythemia, prostaglandin infusion for critical cyanotic heart defect and definitive surgery, intercostals drain for air leak, etc.

While prognosis depends on the diagnosis, it is generally good with prompt recognition and intervention.

Epstein pearls are superficial epidermal inclusion cysts that contain laminated keratinized material and epithelial cells. This superficial skin developmental variation probably occurs with increasing maturity of the fetus, which could explain lack of this phenomenon in the preterm.

The Epstein pearls occurs most frequently on the tip of the foreskin at the 6 o'clock position. It is also seen at the roof of the palate. It is a transient, self-limiting condition and disappears within a few days.

None.

None.

Assurance to parents.

Benign condition.

Definition varies from country to country. Definition recommended by the WHO for international comparison is a baby born with no signs of life at or after 28 weeks of gestation. At least half of all stillbirths occur 10in the intrapartum period, representing the greatest time of risk. A fresh stillbirth has usually died during labor. Causes of fresh stillbirths include anoxia, birth trauma, instrumentation during delivery and rupture of the uterus. Anoxia may be acute or acute on chronic. Acute anoxia is due to prolonged labor, cord prolapse and cord compression. Chronic hypoxia states include pregnancy-induced hypertension, diabetes, systemic lupus erythematosus and other maternal systemic disease and infection. Premature and intrauterine growth restriction (IUGR) babies are more prone to asphyxia and trauma related deaths. Stillbirth rate is defined as the number of stillbirths per thousand of total births.

A complete workup for maternal conditions leading to chronic fetal hypoxia states and strict intrapartum fetal monitoring by non-stress test and cardiotocography are necessary. Histopathological examination of the placenta and autopsy of the baby can help at times.

The condition is not compatible with life. There are no signs of life—absent respiration, heart rate and movements to stimuli.

Sometimes live births with poor Apgar scores and severe fetal and prolonged acidosis may be confused with fresh stillbirths.

A prompt delivery by cesarean section or assisted vaginal delivery, if the cervix is fully dilated, will save the baby. Once the fetal death is expected, vaginal delivery is preferred.

Prognosis depends on the etiology of the stillbirth. A sound antenatal workup and good intrapartum fetal monitoring may decrease the incidence of fresh stillbirths in future pregnancies.

One of the commonest causes of large for gestational age infant is maternal diabetes. Uncontrolled maternal diabetes, leads to fetal hyperglycemia stimulating the beta cells of pancreas resulting in fetal hyperinsulinemia. Because insulin is an anabolic hormone, the fetal hyperinsulinemia stimulates protein, lipid and glycogen synthesis causing increased fetal body fat, excessive adipose deposition, visceral organ hypertrophy, and acceleration of body mass accretion to cause macrosomia.

The infant appears large and is asymptomatic. Problems in delivery room include asphyxia, birth trauma, respiratory distress and congenital anomalies (cardiomyopathy, caudal regression syndrome, anencephaly, hydrocephalus, spina bifida). These are prone to hypothermia, hypoglycemia, jaundice, hypocalcemia and polycythemia. Respiratory distress may be due to transient tachypnea, surfactant deficiency, asphyxia, birth injury, hypoglycemia, air leak syndrome, meconium aspiration or underlying heart defects.

Familial, constitutional, hydrops fetalis or genetic syndromes (e.g. Beckwith-Wiedemann syndrome, Simpson-Golabi-Behmel syndrome, Perlman syndrome, Sotos syndrome, Weaver syndrome, Costello syndrome).

Screening for blood sugar, hematocrit, serum calcium, serum bilirubin and birth injury. Further tests are done based on clinical suspicion.

Supervised feeding is initiated in the first hour of life to prevent hypoglycemia. All infant of diabetic mother are screened for hypoglycemia at birth, 30-min, 1-hour, 2-hour, 4-hour, 8-hour, 12-hour, 24-hour, 36-hour, 48-hour or when symptomatic by Dextrostix. Value less than 40 mg/dL identifies hypoglycemia and specific management based on glucose infusion rate is initiated. Anticipation and management of poor feeding, birth asphyxia, respiratory distress, polycythemia, jaundice, birth injury, hypocalcemia and hypomagnesemia is warranted.

Adverse outcomes are likely with prolonged or severe hypoglycemia and moderate to severe asphyxia requiring close neurodevelopmental follow-up. LGA (large-for-gestational-age) neonates continue to grow longer and heavier, and longitudinal data from developed countries convincingly associates macrosomia with long-term metabolic complications.

Growth restriction is reported in 3–10% of all pregnancies and in 20% of stillborn neonates. Maternal infections (malaria) and undernutrition are the major factors for growth restriction. Nearly one-third of intrauterine growth restrictions (IUGRs) are due to genetic causes, and two-thirds are related to the fetal environment. There is a strong link between IUGR, chromosomal abnormalities, and congenital malformations. IUGR occurs 10 times more frequently in twin pregnancies than in single gestations. Fetal growth that is less than normal for the population and for the expected growth of a specific neonate as documented on ultrasound. The term applies to the events in utero that cause fetal growth to be less than desired.

Neonates with IUGR can be described as symmetrical or asymmetrical. If symmetrical growth restriction is present, the growth problems are proportional (less 13weight, length and head circumference). In asymmetric IUGR, weight and height are affected but head is spared.

Causative factors for growth restriction should be investigated antenatally.

Small-for-gestational-age (SGA) are infants with birth weight less than 2 SD below the mean or less than 10th percentile of a population-specific birth weight versus a gestational age plot.

There are no effective therapies to reverse fetal growth restriction. Antenatal management is individualized and aimed at determining the ideal time and mode of 14delivery. Postnatal management involves supportive care, anticipating problems and specific treatment of the problem.

There is increased morbidity and mortality among premature IUGR neonates compared to term IUGR. Neurodevelopmental problems (e.g. cerebral palsy, learning deficits, short attention span, hyperactivity, learning difficulties and behavioral problems) are seen 5–10 times more often in IUGR neonates than AGA (appropriate for gestational age) neonates; the outcome depends on the severity and symmetry of the restriction. According to Barker's hypothesis, the SGA babies are more prone to develop diseases with the onset of adult age (diabetes, hypertension, ischemic heart disease, obesity and hypercholesterolemia).

Hyperbilirubinemia may result from an increase of unconjugated (indirect) or conjugated (direct) bilirubin. Hyperbilirubinemia is the result of an imbalance between bilirubin production and its elimination. In majority, early neonatal jaundice is due to rise in unconjugated (indirect) bilirubin. The etiological basis for progressive hyperbilirubinemia is usually multifactorial. Bilirubin is a potential neurotoxin causing bilirubin encephalopathy in some cases. Color of urine (dark colored staining the cloth) and stools (chalky white) suggests direct jaundice.

Jaundice appears first on the face and then the trunk. Association of pallor and organomegaly is a feature of hemolysis. Mother blood group, peripheral smear and Coombs tests help to differentiate hemolytic from nonhemolytic causes. The infant's gestational age, birth weight, risk factors, aggravating factors, timing of onset of jaundice and rate of rise of bilirubin decide the management. Severe jaundice may affect the brain and the newborn may present with decreased activity, decreased tone, shrill cry, hypertonia, opisthotonus, neck retraction and seizures.

Total and direct serum bilirubin, mother-infant blood group.

Not all jaundice newborns need treatment. The decision making in jaundice management is based on gestation of baby, weight of baby, well or ill clinical status, age of onset (in hours) and type and severity of jaundice. Phototherapy is the standard treatment. Exchange transfusion is reserved for infants in whom bilirubin rises rapidly or fails to drop despite intensive phototherapy and for infants who show signs of acute bilirubin encephalopathy. The American Academy of Pediatrics guidelines (2005) are used for initiation of phototherapy and exchange transfusion.

Prognosis is excellent for uncomplicated newborn jaundice. Prognosis is guarded if jaundice is very high and/or baby shows signs of acute bilirubin encephalopathy.

The common causes for large for gestational age (LGA) are familial, constitutional, infant of diabetic mother (IDM) and as a component of syndrome (Beckwith-Wiedemann syndrome, etc.). At times, the cause is idiopathic. The underlying problem in IDM is hyperinsulinemic state in utero due to poor diabetic control in mother leading to fetal hyperglycemia and excessive growth.

Familial, constitutional, transposition of great vessels, syndromic (Beckwith-Wiedemann syndrome).

Large for gestation age infants have weight excessive for the gestation. The infant has a normal head size. The infants appear plethoric, chubby and have excessive thick skin folds. Hypoglycemia, hypocalcemia, hyperbilirubinemia, polycythemia are the common metabolic disturbances. Cardiac, gastrointestinal and neurologic malformations are seen with IDM but not with LGA infants.

Check the diabetic status in mother if not already done (fasting, postprandial glucose and glycosylated hemoglobin), blood sugar and serum calcium monitoring is essential.

Need supervised early breastfeeding. Continuous monitoring for glucose is needed for first 48 hours.

Prognosis is good in isolated LGA infants. With comorbid features, it depends on degree and severity of hypoglycemia.

The common causes of macrocephaly include familial, constitutional, hydrocephalus (increase in CSF volume due to obstruction, inflammation or infection), congenital infections (toxoplasmosis), megalencephaly (increase in brain volume as in Alexander's disease, Canavan's disease), cranial hyperostosis (bone overgrowth) and genetic disorders (e.g. neurofibromatosis, tuberous sclerosis). At times, it may arise as a sequelae to intraventricular hemorrhage, arachnoid cyst or subdural effusion. The associated complications and long-term morbidities include raised intracranial pressure, developmental delay, seizures and cognitive impairment.

Large head should be seen in relation to other body parts. It large head associated with large body and organomegaly, one should consider Sotos syndrome. Large head with short limbs is characteristic of chondrodysplasia.

The various causes of hydrocephalus and megalencephaly are mentioned in etiopathogenesis, familial and constitutional large heads.

An optimal measurement of the OFC and plotting the same on an appropriate growth chart for confirmation of macrocephaly. Serial measurement (weekly) to monitor the progress/regression of the head size, which may give a clue to the etiology and severity. Neuroimaging including serial cranial ultrasounds and MRI if required.

There is no specific treatment for macrocephaly. Medical care for children with macrocephaly focuses on management of specific symptoms such as developmental delays and mental retardation and treatment of the primary diagnosis responsible for the macrocephaly.

For children with benign familial macrocephaly, the prognosis is excellent. In others, it is dependent upon the underlying cause.

Congenital hypothyroidism is the most common cause of macroglossia. It may be due to an isolated anomaly (vascular—lymphatic malformation) or as an association with Beckwith-Wiedemann syndrome. Abnormal deposition of mucopolysaccharides as in mucopolysaccharidosis (MPS) may also cause macroglossia.

Large tongue may be an isolated phenomenon or part of multisystem disorder. There is spectrum of manifestations from being asymptomatic to feeding, inability to close mouth or apnea depending upon the severity of lesion.

Physical examination and family history help to identify underlying etiology. Chromosomal analysis, radiographs of spine and limbs, thyroid profile and thyroid scan, ultrasound of abdomen for visceromegaly, and urine glycosaminoglycan as indicated.

Beckwith-Wiedemann syndrome, isolated macroglossia, lingual lymphatic anomaly, hypothyroidism, MPS, transient neonatal diabetes, congenital isolated macroglossia (autosomal dominant), tongue hemangioma.

Treatment of underlying condition.

The prognosis depends on the underlying cause.

This pigmented lesions result from delayed disappearance of dermal melanocytes. This is the most often encountered pigmented lesion in a newborn.

It is seen commonly in lumbosacral area but may be found on leg, back and shoulder. Pigmentation is macular and gray-blue, lacks a sharp border, and might cover an area 10 cm or larger in diameter.

Not required.

Congenital pigmented melanocytic nevi, Café au lait spots.

No treatment is required.

Most of these lesions gradually disappear during the first few years of life, but aberrant lesions in unusual sites are more likely to persist.

Natal teeth most often develop on the lower gum, where the central incisor teeth will appear. They have little root structure. Histologic investigation reveals a failure of root formation despite eruption, a large vascular pulp, irregular genesis of dentin and a failure of cementum formation.

It may be firmly fixed or loose, putting the infant at risk for aspiration. Usually, it is asymptomatic but may cause breast discomfort to the mother while feeding. They are different from neonatal teeth, which emerge through gingiva during the first 30 days after birth. Natal teeth are usually not well-formed, but they may cause irritation and injury to the infant's tongue when nursing. Natal teeth may also be uncomfortable for a nursing mother. It may rarely be associated with Ellis-van Creveld syndrome, Hallermann-Streiff syndrome, Pierre Robin syndrome, Pachyonychia congenita and Sotos syndrome.

Neonatal tooth, supernumerary teeth, cysts of the dental lamina, Bohn's nodules.

None; X-ray tooth if surgery planned or diagnosis is doubtful.

When well implanted, the teeth should be left in the arch. Teeth removal is indicated only when they interfere with feeding or when they are highly mobile, with the risk of aspiration. Smoothing of the incisal edge (to prevent potential discomfort during breastfeeding and ulcerations in the floor of the mouth) is also an option.

Good.

Transition from fetal to systemic circulation takes place at the time of birth leading to establishment of spontaneous respiration and cry. In 90% of newborns, this stress is well taken but in few, this may lead to distress and need for resuscitation. A normal newborn needs no intervention.

A normal newborn is very active in the few hours of life. Color is pink, breathing is regular, skin is covered with vernix, umbilical cord is moist and peeling of skin may be seen in post-term infants. Temperature maintenance, feeding and infection control are the main concerns in this newborn.

None.

Screening for metabolic disorder and hearing prior to discharge is desirable.

Delayed cord clamping, early skin to skin contact, early and exclusive breastfeeding, assessment for risk factors, a thorough head to toe examination with special concern for congenital anomalies, assessment of weight, administration of vitamin K, parental assurance and counseling for hygiene, feeding, danger signs and vaccination prior to discharge.

Good.

Meconium is the black green stool, the newborn passes in the first few days of birth. As the newborn accepts milk feeds, the stool color changes to green and then to yellow. Transitional stool represents the change from meconium to the normal yellow, seedy stools that characterize infants feeding on milk only.

The newborn stool normally shows variations in color, frequency and consistency, which varies with postnatal age. A well infant with weight gain is an assuring sign irrespective of the stool frequency. The stool pattern evolves over the first few days of life. After birth, a baby's first bowel movements are black and tarry called meconium, which last for couple of days. After few days, meconium is replaced with green-brown and then yellow-brown bowel stools. By about 5 days after birth, breastfed babies usually have seedy, loose bowel movements that are yellow to yellowish green or tan in color. The frequency of bowel movements varies widely from one baby to another.

None.

Transitional stools, infective diarrhea.

Assurance; continuation of exclusive breastfeeding.

Benign condition.

Vitellointestinal duct (VID), is an embryonic communication between the intraembryonic gut and yolk sac which is usually obliterated by the 7th week of intrauterine life. In about 2% of humans, this duct persists and gives rise to a group of anomalies—Meckel's diverticulum, vitelline cord, enteric cyst, umbilical sinus, enteric fistula or hemorrhagic umbilical mass.

Presents as an umbilical nodule or polyp, bleeding from intestinal mucosa and intestinal small bowel prolapsed. There may be discharge from the umbilicus and the umbilicus is mostly moist. It may be associated with umbilical hernia, intestinal atresias, cardiac malformation, cleft lip and palate, and exomphalos.

Ultrasound examination of the abdomen for intra-abdominal collections/other congenital anomalies and water soluble 24contrast injecting through the opening to show the dye in the intestine.

Antibiotics, primary closure of the VID if the patient arrives early without any complications. Where the defect is large, resection of the loop of intestine near the patent duct followed by primary anastomosis is the procedure of choice.

Delayed diagnosis may lead to peritonitis or intestinal perforation.

There is fullness of dorsum of feet in preterm infant. There is no associated fullness over any other site of the body. The infant is not ill and the edema is transient, occurred on day 2 or 3 of age in the lower limbs (Figs 1.22A and B).

Typically, subcutaneous fluid collects on the dorsum of the feet and hands. It may occur in isolation or may be associated with generalized edema. The exact mechanisms remain unknown. About 30% of babies with Turner's syndrome have congenital lymphedema. Preterm infants may develop physiological edema due to immature kidneys and circulatory instability. Localized chronic cold injury may cause pitting edema with erythema of hands and feet. Capillary leak as in chikungunya fever may also cause pedal edema.

Venous edema is typically pitting, dependent and bilateral. Lymphatic edema is non-pitting. Mechanical obstruction by amniotic bands may cause local edema. The systemic signs depend on the underlying cause.

Sclerema, subcutaneous fat necrosis, edema of prematurity, Milroy's disease, localized cold injury, chikungunya fever.

For suspected edema of prematurity, no tests are required. Additional tests may be done depending on the cause.

Treatment is directed to the underlying cause.

The condition is transient in preterm babies and resolves spontaneously. Peripheral lymphedema seen in neonates with Turner's syndrome usually resolves within a year. Residual lymphedema of the dorsum of the fingers may persist, along with swelling of the lower extremities, into adulthood.

It is a common minor congenital anomaly of the first branchial arch or second branchial arch. It may appear as a skin tag or dimple. There is a known association with Goldenhar syndrome (oculo-auriculo-vertebral spectrum) and with Wildervanck syndrome.

Skin tag is detected incidentally on routine evaluation. It may be single or multiple, unilateral or bilateral. It may be an isolated defect or part of syndrome. When an isolated defect, there are no signs or symptoms. It may be associated with cleft palate, cleft lip, ocular coloboma, hand or digit anomalies, mandibular hypoplasia or heart defects.

None for isolated lesions. Presence of associated two or more minor anomalies or one major anomaly warrants renal ultrasound and hearing assessment.

Teratoma.

Assurance; when part of syndrome, treatment is symptomatic; for cosmetic purpose, the skin tag may be removed.

A benign condition for an isolated defect.

Retractions may occur in several areas of the chest and are a sign of increased use of the chest muscles for breathing. Sternal indrawing is a clinical sign of respiratory distress. It is a mechanism to increase the intrathoracic negative pressure.

It is associated with other chest signs like subcostal or intercostal indrawing and audible sounds like grunt or stridor. It may be seen normally in very preterm due to pliable chest wall. It serves as a soft marker sign for hypoxia.

Normal variant in preterm, pectus excavatum, respiratory distress (respiratory or cardiac cause) and sepsis.

History and clinical examination gives a clue to possible etiology. Tests are done depending on the cause.

Treatment is of the underlying cause. Supportive care involves correction of temperature (hypothermia), oxygenation, fluid therapy and antibiotics as indicated.

Prognosis is dependent on the underlying cause. Early recognition and prompt treatment has good outcomes.

It is proposed that in the majority of cases subconjunctival hemorrhage (SCHN) are a consequence of elevated venous pressure in the head and neck produced by compression of the fetal thorax and/or abdomen by uterine contractions. Tight umbilical cord around the neck probably represents an additional mechanism for SCHN. There is breakage of small blood vessels during pressure of delivery.

The condition is asymptomatic. There are no signs or symptoms. It is self-limiting and transient in nature. In a minority of cases, it may also be indicative of child maltreatment. Therefore when SCHN is observed, it warrants a thorough and systematic assessment of the neonate.

None.

Conjunctivitis, battered baby syndrome.

None.

It is a benign condition.

There is a tight piece of skin between the underside of their tongue and the floor of the mouth (Fig. 1.26).

It is a birth defect, the cause of which is not known. It may be familial in some cases. Normally, the tongue is loosely attached to the base of the mouth with a piece of skin called the lingual frenulum. If it is short and tight, it interferes with tongue movement leading to difficulty in feeding.

Tongue-tie leads to inability to protrude the tongue past the edge of the lower gingiva or mandibular incisors. At times, the tongue may appear notched or heart-shaped when stuck out. Opinion varies regarding how frequently ankyloglossia truly causes problems. Babies with tongue-tie are not able to open their mouths wide enough to latch on to their mother's breast properly leading to sore nipples and inadequate breastfeeding and poor weight gain. In infancy, tooth decay and gingivitis may set in.

Bifid tongue, oral ranula, congenital furrowing, lingual thyroid.

None.

No consensus for management of short frenulum. Surgical intervention (frenotomy or frenuloplasty) is done only if the tongue-tie interferes with feeding. Speech difficulty (interfere with the ability to make certain sounds, such as “t,” “d,” “z,” “s,” “th” and “l,” and feeding difficulty of select food items may be seen in older age group and may require intervention.

Asymptomatic tongue-tie may cause no problems, as child gets older.

These are categorized as true cysts and false cyst. True cysts are lined with cells, and generally contain remnants of early embryonic structures. False cysts are fluid-filled sacs that can be related to a swelling of the Wharton's jelly.

They may be isolated clinical phenomenon or associated with underlying malformations (20% cases). The cyst may be single (more common) or multiple. The cysts tend to resolve by the end of the first trimester if detected antenatal.

Pseudocysts, omphalomesenteric duct cysts, vascular disorders, abdominal wall defects, bladder exstrophy and urachal anomalies.

Fetal karyotyping is indicated when other anomalies are found or when the cyst persists into the second trimester.

Treatment of comorbid conditions, if any.

While single cysts in the first trimester are associated with favorable pregnancy outcome, the presence of multiple umbilical cord cysts, their persistence in the second and third trimester and their combination with other ultrasonographic abnormalities, is associated with increased risk of miscarriage, aneuploidy or other structural anomalies.

Umbilical granuloma is not a true congenital abnormality, but represents ongoing inflammation and granulation tissue formation, of an umbilicus that has yet to epithelialized. Bacterial colonization and low-grade infection may play a role in the pathogenesis.

It is a granular polyp-like structure protrudes from the umbilicus. No contents are seen and there is no inflammation. The infant is asymptomatic. The lesion may ulcerate or bleed occasionally in case of friction.

None.

The common treatment is putting common salt over couple of days. Cauterization with 75% silver nitrate/copper sulfate, usually repeated 2–3 times may be considered. Rarely, if persistent, they need surgical removal.

Excellent; no residue.

It occurs due to fall in level of sex hormones after birth when the baby is removed from placenta.

Spontaneous vaginal bleed may occur episodically during first few weeks of life. There are no associated signs or systemic manifestations, and the infant is otherwise well. The condition is benign and resolves on its own.

None.

Disseminated intravascular coagulation (sick, multiple bleeding sites).

Assurance to the parents. Bleeding is mild and lasts for few days to week. Local hygiene of genitals is advised.

It is a self-limiting condition.

There is a white, creamy, substance covering over the entire skin surface at birth (Fig. 1.30).

Vernix caseosa is laid down in the last trimester of pregnancy over the fetal skin produced in part by fetal sebaceous glands consisting of sebaceous gland secretions, lanugo, and desquamated epithelial cells. It consists of water (81%), lipid (9%) and proteins (10%). It facilitates extrauterine adaptation of skin in the first postnatal week. It facilitates passage through the birth canal, serves as a barrier to water loss, helps maintain temperature serves as moisturizer and anti-oxidant, and provides innate immunity. Absence of vernix caseosa is associated with the presence of physiological scaling of the newborn. Vernix caseosa peritonitis due to spillage of vernix has been reported as a complication in post cesarean mothers.

This white creamy layer is present on the body at birth. This natural biofilm covering may at times be only confined to body folds. The closer to term the infant, the less the vernix; post-term infants have very little vernix. Preterm infants with less than 28 weeks of gestation lack the protective mantle of vernix. The coating progresses in cephalocaudal manner.

None.

None.

It is recommended to leave vernix intact on skin surface after birth. Removal of vernix is not necessary for hygienic reasons.

Emerging research suggests that vernix applied to burnt adult skin may enhance wound healing.

There are rhythmic, wave-like muscular contractions over the abdomen (Figs 1.31A to C).

Peristalsis is normal mechanism for propulsion of food across the alimentary canal. Visible peristalsis occurs as a result of mechanical block in the alimentary canal signifying surgical emergency. Peristalsis waves temporarily increase in frequency and strength due to contraction of intestine to force the content past the obstruction. As a consequence, the wave of peristalsis become visible. The peristalsis wave may vanish suddenly due to increase in peristalsis overcoming the obstruction and the gastrointestinal tract become atonic.

It appears episodic in nature. It is usually visible on stooping at the sides of the patient and inspecting the abdominal contour while the patient in supine position, immediately post-feed and in quiet condition. Pyloric obstruction is characterized by visible waves of peristalsis, which roll form left to right or from swollen epigastrium. Small and large bowel obstruction may also present with peristalsis waves visible in the upper abdomen in the early stages of bowel obstruction. It is associated with irritability, vomiting, dehydration, weight loss, acidotic breathing, hyperactive bowel sounds and distended abdomen. 34Visible peristalsis waves may also occur with normal stomach and those who are malnourished.

Pyloric stenosis, small bowel obstruction, large bowel obstruction, obstructed gastric outlet.

Abdominal X-ray and barium studies.

Nil by mouth, correction of hydration, electrolyte and acid-base imbalance, with surgical exploration once bowel obstruction is confirmed.

Detection in early stage has good outcomes. Late diagnosis may result in necrosis or gangrene of bowel requiring significant resection and anastomoses.

Lanugo is fine, soft downy hair found on the body of the newborn baby.

It is the first hair to be produced by the fetal hair follicles at about 24–25 weeks gestation and shed around 7 or 8 months of gestation. In some newborns, it may be present at birth and disappears within a few days or weeks. It is replaced by mature hair at about 33 to 36 weeks of gestational age. Lanugo functions as an anchor to hold the vernix caseosa on the skin. These hairs are transient and self-resolving.

None.

None.

Reassurance.

Benign phenomenon.