Table of contents :

See also pregnancy and diseases of pregnancy

See also hereditary diseases

preimplantation genetic diagnosis

prenatal screenings

An estimated 1 billion children from the total of 2.2 billion in the world are living in poverty. 33% (640 million) children do not have adequate shelter, 500 million had no access to sanitation, and 400 million do not have access to safe water. Furthermore, 90 million children are severely deprived of food and 270 million have no access to healthcare services. Statistics show that poverty is not exclusive to developing countries. The proportion of children living in low income households has increased over the past decade in 11 of the 15 developed countries for which comparable data are available. Extreme poverty is considered one of the central causes of conflict, along with poor governance. 55 of 59 armed conflicts that took place between 1990 and 2003 occured within, rather than between, countries. Children account for nearly half of the 3.6 million people killed in these conflicts. Conflict also had a catastrophic impact on overall health. In a typical 5 year war, the mortality of children under the age of 5 years increased by 13%. The impact of HIV/AIDS on children is seen most dramatically in the number of orphans to AIDS—now totalling 15 million worldwide. In addition, AIDS is now the single largest killer of people aged 15-49 in the developing world

Neonatology : the art and science of diagnosis and treatment of disorders of the newborn infant

• witch's milk / hexenmilch : milk secreted in the breast of the newborn child
• retraction of anterior chest is common in newborns
• caput succedaneum : edema occurring in and under the fetal scalp during labor in vertex presentation, due to accumulation of interstitial fluid (and sometimes even blood) due to pressure gradient between atmorsperic pressure in subcutaneous interstitium of the presented head and subcutaneous capillaries (which are influenced by endouterine pressure)
• cephalohematoma : hematoma between the inner table of skull and periosteum due to rupture of capillaries, developing gradually within 2-3 days since delivery in 2% of newborns, and spontaneously healing within 2-4 weeks. Massive hematomas may cause neonatal anemia and, at resorption, transient jaundice
• birth age
• preterm infant : an infant born at any time before the 37th completed week (259 days) of gestation.
• high-grade preterm infant : an infant born at any time before the 31st completed week of gestation, when Botallo's ductus arteriosus is still patent and blood is shifted from aorta into pulmonary artery (reverse flow) => persistent fetal circulation (PFC) / persistent pulmonary hypertension in the newborn (PPHN) / primary neonatal pulmonary hypertension : pulmonary hypertension in the postnatal period secondary to right-to-left shunting of the blood through the foramen ovale and Botallo's ductus arteriosus. An NO-deficient state characterized by pulmonary vasoconstriction, right-to-left shunt pathophysiology and systemic hypoxemia^ref => pulmonary edema => impaired gas diffusion

During fetal life, pulmonary blood flow is low, with < 10% of the combined cardiac output directed to the lungs. In fetal life, high pulmonary vascular resistance (PVR) is maintained by hypoxia. Following birth, PVR falls and pulmonary blood flow increases dramatically as the lungs assume the function of gas exchange. These changes are stimulated by the combination of rhythmic ventilation of the lung and increase in alveolar oxygen tension. Each of these stimuli by itself will decrease PVR and increase pulmonary blood flow, but the largest effects are seen when the two events occur simultaneously. In some newborns, the normal decrease in pulmonary vascular tone does not occur, resulting in persistent pulmonary hypertension of the newborn (PPHN). This syndrome results in substantial morbidity and mortality in otherwise healthy term newborns.Pathophysiology: PPHN is failure of the normal circulatory transition that follows birth. It is a syndrome characterized by marked pulmonary hypertension that causes hypoxemia and right-to-left extrapulmonary shunting of blood. With inadequate pulmonary perfusion, neonates develop refractory hypoxemia, respiratory distress, and acidosis.
Epidemiology : prevalence = 2-6 in 1,000 live births, a frequent complicating factor in the term or near-term newborn with parenchymal lung disease, such as meconium aspiration syndrome (MAS) or pneumonia.
Aetiology :
• the most commonly encountered scenario is acute pulmonary vasoconstriction from acute perinatal events such as the following:
• alveolar hypoxia secondary to parenchymal lung disease
• hypoventilation resulting from asphyxia or other neurologic conditions
• hypothermia
• hypoglycemia
• pneumonia
• idiopathic, black lung or clear lung PPHN, in which the newborn presents with a normal chest radiograph finding, may be a possible cause. It is believed to result from an abnormally remodeled pulmonary arterial vasculature that develops in utero in response to prolonged fetal stress, hypoxia, and/or pulmonary hypertension. Excessive and peripheral muscularization of pulmonary arterioles can be seen in these cases.
• other possible causes include the following:
• hypoplasia of the pulmonary vascular bed associated with congenital diaphragmatic hernia (CDH)
• oligohydramnios sequence
• congenital cystic adenomatoid malformation (CCAM)
Pathogenesis :
Symptoms & signs : cyanosis and tachypnea, a loud single S₂ or a harsh systolic murmur secondary to tricuspid regurgitation
Therapy :
• high-frequency mechanical ventilation
• central venous catheter (CVC) placement
• arterial catheter placement
• exogenous surfactant administration
• ECMO
• inhalational nitric oxide (iNO) is indicated for newborns with an oxygenation index of > 25 : it has been shown in 2 large randomized trials to reduce the need for ECMO support by approximately 40%. Contraindications to iNO include congenital heart disease characterized by left ventricular outflow tract obstruction (eg, interrupted aortic arch, critical aortic stenosis, hypoplastic left heart syndrome) and severe left ventricular dysfunction. The appropriate starting dose is 20 ppm. Higher doses have not been shown to be more effective and have been associated with side effects including methemoglobinemia and increased levels of nitrogen dioxide. Appropriate lung recruitment and expansion is essential to achieve the best response. If a newborn has severe parenchymal lung disease and PPHN, strategies such as high frequency mechanical ventilation may be required. Most newborns require iNO for fewer than 5 days. In general, the dose can be weaned to 5 ppm after 6-24 hours of therapy. The dose is then weaned slowly and discontinued when FiO₂ < 0.6 and the iNO dose is 1 ppm. Abrupt discontinuation should be avoided as it may cause abrupt rebound pulmonary hypertension. Use of iNO needs to be performed carefully in centers that do not have immediate availability of ECMO support. Because iNO cannot be abruptly discontinued, transport on iNO is generally needed if a subsequent referral for ECMO is necessary. This capability should be determined before initiation of treatment. The use of iNO with high frequency ventilation creates particular problems for transport, and this should be considered before combining these therapies in a non-ECMO center. The use of iNO has not been demonstrated to reduce need for ECMO in newborns with congenital heart disease. In these newborns, iNO should be used in non-ECMO centers cautiously and acute stabilization, followed by immediate transfer to a center that can provide ECMO.
Prognosis : introduction of ECMO reduced mortality from 40% (and prevalence of major neurologic handicap was 15-60%) to 30%. If all available therapies are used, the mortality rate is currently < 20-25% and the prevalence of major neurologic handicap for surviving newborns is approximately 15-20%.
Epidemiology : 7-8% of all births; 5% of preterm infants are VLBW
Aetiology :
• extrinsic :
• psychic or physical trauma
• surgery
• intoxications (lead, fetal alcohol syndrome)
• maternal causes
• preceding pregnancy : pelvic or uterine malformations, genital hypoevolutism, dismetabolic disorders, chronic infections, congenital heart diseases or acquired cardiopathies, relapsing prematurity
• occuring during pregnancy : preeclampsia, retroplacental hematoma, placenta previa, acute infectious diseases, PROM, abortion (as in some countries, including Italy, voluntary abortion doesn't spare the assisting physicians from doing the best for newborn's survival, many survive delivery starting from wk 22 and day 6 (most malformations can be seen echographically only after pregnancy wk 20))
• fetal causes : malformations, erythroblastosis fetalis or neonatorum / hemolytic disease of the newborn (HDN), position anomalies, multiple pregnancy
Special assistance requirements : in highly specialized centres, > 90% of newborns weighing > 800 g and 40-50% of newborns weighing 500-800 g survives
• heating (tendence to cooling due to :
• poor thermogenesis (poor brown fatty tissue and muscle movements)
• high thermodispersion
• nutrition and growth => accentuation of the physiological weight loss up to 10-25% due to
• particular nutritional requirements, as growth has rhythms faster than for the term newborn
• up to wk 33-34 suction and swallowing functions are immature and prevent direct breast lactation => orogastric gavage with fortified (protein up to 2.5-3 g/kg, minerals and vitamins) maternal or artificial milk, minimal enteral feeding (MEF) to activate peristalsis and gastrointestinal hormone incretion, slowly and at low doses to prevent necrotizing enterocolitis (NEC)
Complications :
• more severe deficiency of vitamin-K-dependent coagulation factors due to deficiency of bacterial symbiontic intestinal microflora (bowels are sterile in the first 2-3 days of life), worse when the pregnant has diarrhea or introduces competing drugs (antihemorrhagic prophylaxis with vitamin K is mandatory for all newborns) => hemorrhages in the first 2-3 days of extrauterine life
• hyperbilirubinemia => more common and more prolonged physiologic jaundice
• apnea neonatorum is common in newborn with gestational age < 30 wk
• anemia (NRBC) and late anemia (iron deficiency anemia at mo. 4-5 of extrauterine life)
• systemic arterial hypotension
• respiratory distress syndrome (RDS) due to surfactant deficiency
• bronchopulmonary dysplasia (BPD)
• infections
• patent ductus arteriosus (PDA) : prophylaxis for newborns with gestational age < 25 wk
• retinopathy of prematurity (ROP)
• the EPICure project (sponsored by the London-based charity BLISS) was the first study to follow the health of severely premature British and Irish babies (born after fewer than 26 weeks in the womb) that were born between March and December in 1995 into early childhood^ref :
• 75% die before age 6
• 25% make it to childhood. And even those that do survive have just a 20% chance of being free of disability by the time they are 6 years old.
• 54% of the kids have a satisfactory quality of life
• 20% of the group had no disability at all
• 34% had only mild problems such as poor eyesight
• 46% are more likely to suffer from a wide range of disabilities, including severe cerebral palsy, learning difficulties, below-average intelligence and problems with vision or hearing.
• 72% have impaired intelligence, compared with 14% of term classmates.
• 24% have cerebral palsy
• 4% have severe cerebral palsy
Decisions about whether to save the lives of severely premature babies should continue to be made on a case-by-case basis. The current British approach contrasts with the policy adopted in the Netherlands, in which no effort is made to save babies born before 25 weeks. But an ability to explain clearly to parents what might happen to their child further down the line will be valuable. Despite their low survival rates, particularly at 22 and 23 weeks, the effort going into keeping these babies alive is well worth it
• term infant : an infant born anytime from the beginning of the 38th week (260 days) to the end of the 41st week (287 days) of gestation (90% of infants)
• post-term (or postmature) infant : an infant born at any time after the beginning of the 42nd week (288 days) of gestation
• infant maturity : maturity of surfactant and respiratory centres, fetal blood circulation, suction reflexes, digestive, and other functions
• immature infant : one not physiologically fully developed (and usually weighing < 2500 grams at birth)
• premature infant : one usually born after the 20th completed week and before full term, and arbitrarily defined as an infant weighing 500 to 2499 grams (2.2 to 5.5 lbs.) at birth, having poor to good chance of survival, depending on the weight. In countries where adults are smaller than in the USA, the upper limit may be lower. Other criteria such as crown-heel length (< 47 cm) and occipitofrontal diameter (< 11.5 cm) have also been used.
• mature infant : one weighing > 2500 grams (5.5 pounds), usually at or near full term, physiologically fully developed, and having an optimum chance of survival.
• dysmature, postmature or post-term infant : an infant with dysmaturity syndrome
• dysmaturity or postmaturity syndrome / placental dysfunction syndrome
• birth weight
• during gestation
• large for gestational age (LGA) / macrosomic or hypersomic infant
• adequate for gestational age (AGA) / normosomic infant
• small for gestational age (SGA) / hyposomic infant : a condition where infants are born after 37 weeks of pregnancy (gestation), and therefore have sufficient time to grow and mature, but are nonetheless small in terms of weight. SGA infants are often < 10th percentile of the weight distribution at any given gestational age. Some SGA infants are simply smaller than average, while others are growth retarded. SGA and preterm infants (infants who are born small because they were born before 37 weeks completed gestation) are separate outcomes but are often grouped together in epidemiological studies and measured as low birth weight infants
• at birth
• high birth weight (HBW) : P > 4.5 kg
• normal birth weight (NBW) : 2.5 < P < 4.5 kg
• low birth weight (LBW) : P < 2.5 kg. > 90% of the 25 million low-birth-weight babies born each year are born in developing countries. Statistical analysis shows that poor maternal diet is the key factor in small birth size. In combination with low birth weight, fetal and infant origins of diseases are of particular importance. This aspect has been explored in several studies, which support the main hypothesis and concept of the thrifty phenotype. In addition, new evidence has emerged that nutritional programming during intrauterine life may affect the development of the immune system of the fetus. Although this finding has emerged in a unique context, which combines a natural situation with long-term demographic records, other evidences support the strong interdependence of nutrition and immune system functioning. Such discovery may be of importance to any growth-retarded fetus and may have implications that extend beyond the classic infectious diseases to cancers, autoimmune disorders, and other morbidities^ref.
• heavier low birth weight (HLBW) : 2.0 < P < 2.5 Kg
• lower low birth weight (LLBW) : < 2.0 Kg
• moderately low birth weight (MLBW) infant / macropremies : 1.5 < P < 2.5 kg

very low birth weight (VLBW) (1.4% of infants)) : 800 or 1,000 < P < 1,500 g. 65% of VLBW infants have at least one infection during their hospitalization after birth. Compared with uninfected infants, infected infants are significantly more likely to have adverse neurodevelopmental outcomes at follow-up, including cerebral palsy, low scores in mental development and psychomotor development on the Bayley Scales of Infant Development II test, or vision impairment. Neonatal infection also is associated with impaired head growth, which is known to be a predictor of poor neurodevelopmental outcome.
• extremely low birth weight (ELBW) : P < 800 or 1,000 g. Rumaisa (her name means "white as milk"), the world's smallest surviving baby with a birth weight of just over 240 grams, has been unveiled to the world 3 months after her birth at Loyola University Medical Center in Maywood, Illinois. She and her twin sister Hiba, also tiny at just under 570 grams, were born by Caesarian section on 19 Sep 2004. Doctors ordered the early delivery because the babies' mother Mahajabeen Shaik, originally from Hyderabad and now living in Chicago, was suffering from pre-eclampsia. Without intervention, both the mother and babies' health would have been in danger. The twins' good health is remarkable considering that were born after just 25 weeks and 6 days in the womb. 25 weeks is pretty close to the limit at which a baby can be born and still have a chance of making it. Most babies born later than 25 weeks can be saved by careful resuscitation and ventilation. For those who have to be delivered earlier, the decision on whether to try and save them depends on the baby's condition. It's phenomenally expensive - hundreds of thousands of dollars - , but if the baby survives in good condition they have 70 years of healthy life ahead of them. Before about 23 weeks the baby's airways are so underdeveloped that it is almost impossible to get them to breathe even with a ventilator. In this situation 99% of babies won't survive given our current technology. But for those babies, like Rumaisa and Hiba, who stand a good chance, all of the effort and expense is worthwhile Although not completely in the clear yet - Muraskas puts the chances of her showing signs of handicap such as cerebral palsy over the coming year or so at about 5% - ultrasound scans seem to show that her brain is perfectly healthy.


The success adds to Loyola University's impressive track record in rescuing tiny babies. The former record-holder, born weighing just 280 grams but now a healthy high-school student, was also delivered at the centre. Perhaps it's no coincidence that Rumaisa is also a girl : success rates for premature boys remain bafflingly poor in comparison.
Aggressive phototherapy did not significantly reduce the rate of death or neurodevelopmental impairment in ELBW. The rate of neurodevelopmental impairment alone was significantly reduced with aggressive phototherapy. This reduction may be offset by an increase in mortality among infants weighing 501 to 750 g at birth^ref.
• in the first days of life there is weight loss, but the weight returns to the birth number within day 5 of extrauterine life
Neonates are born with an excess of TBW, primarily ECF, which needs to be removed. Term neonate bodies are 75% water (40% ECF, 35% ICF), and term neonates usually lose 5-10% of their weight in the first week. Preterm neonates have more water (at 23 weeks’ gestation, 90% water composed of 60% ECF and 30% ICF), and they may lose 5-15% of their weight in the first week. Insensible water loss (IWL) depends on gestational age; the earlier the gestational age of the preterm infant, the greater the IWL. The magnitude of IWL also depends on the postnatal age. Since skin thickens with age, the IWL decreases as neonates age. All other measurable sources of fluid and electrolyte losses need to be considered as well. Sources include stool (eg, diarrhea and ostomy), nasogastric (NG) or orogastric (OG) drainage, and cerebrospinal fluid (CSF), including ventricular drainage. Neonates have a decreased capacity to concentrate or dilute urine in response to changes in intravascular fluid status, and they are at risk for dehydration or fluid overload. The normal maturation of renal function that occurs with increasing gestational and postnatal age also plays a role in determining fluid requirements. A number of conditions can impact neonatal renal function adversely. The presence of several of these can be suspected on the basis of information found in the prenatal and neonatal history.
• Maternal history : a newborn's fluid and electrolyte (FE) status partially reflects the mother's FE status. For example, excessive administration of oxytocin or hypotonic intravenous fluid (IVF) to the mother can cause hyponatremia in the neonate at birth. Placental dysfunction (eg, from hypertension in pregnancy) can affect intrauterine growth adversely. Infants who are growth retarded at birth (<10th percentile for gestational age) tend to grow poorly despite adequate nutrition after birth. Poorly controlled maternal diabetes mellitus may be associated with renal vein thrombosis. This can affect an infant's renal function adversely. Maternal use of ACEI during pregnancy can lead to acute renal failure in infants. Other medications administered to the mother, including indomethacin, furosemide, and aminoglycoside, also may affect renal function in the neonate. Antenatal steroids may increase skin maturation, thereby decreasing IWL and the risk of hyperkalemia
• Newborn history : the presence of polyhydramnios or oligohydramnios can be associated with either congenital nephrotic syndrome or congenital renal dysfunction. Severe in utero hypoxemia or birth asphyxia may lead to acute tubular necrosis. Posterior urethral valves can be suspected when weak urinary stream and dribbling are present. The environment in which an infant is cared for also affects fluid loss. An environment with high ambient humidity decreases IWL, while the use of a radiant warmer or phototherapy may significantly increase an infant's IWL.
• Clinical evaluation
• Weight factors : sudden changes in an infant's weight do not necessarily correlate with changes in intravascular volume. An infant's weight rises significantly for a number of reasons while intravascular volume has decreased. Examples include the long-term use of paralytic agents and peritonitis, both of which can lead to increased interstitial fluid volume and increased body weight but decreased intravascular volume. While growth charts are valuable in following growth parameters and nutritional status over time, they play little role in the daily management of fluid and electrolyte balances.
• skin and mucosa manifestations: Altered skin turgor, a sunken anterior fontanelle (AF), and dry mucous membranes are not sensitive indicators of dehydration in babies. Remembering that premature infants have poorly keratinized skin that leads to a marked elevation in IWL is important.
• cardiovascular signs : tachycardia can result either from too much ECF (as can be seen in congestive heart failure) or from too little ECF (as can be seen in hypovolemia). Although delayed capillary refill occurs in low cardiac output states, it also can be seen in infants with peripheral vasoconstriction resulting from cold stress. Hepatomegaly can occur in neonates with ECF excess, especially in CHF. As a result of an infant’s compensatory mechanisms, blood pressure (BP) readings usually are normal, with mild or moderate hypovolemia. With severe hypovolemia, hypotension is present almost invariably.
• Laboratory evaluation : Depending on the clinical situation and the suspected etiology of fluid and electrolyte derangements, some or all of the following tests may be warranted:
• serum electrolyte, urea nitrogen, creatinine, and plasma osmolarity levels: Keep in mind that over the first 12-24 hours, results of these tests may still reflect maternal values.
• accurate total urine output and total fluid intake
• urine electrolytes and specific gravity: If the infant is being treated with diuretics, such as furosemide, results of these tests are difficult to interpret.
• calculation of the fractional urinary excretion of sodium in relation to creatinine (FENa)
• blood gas analysis: Metabolic acidosis may be a marker of inadequate tissue perfusion.
• fluid and electrolyte (FE) management is a balancing act between intake and output. Primary goals are to maintain the appropriate ECF volume, ECF and ICF osmolality, and ionic concentrations. Allow the initial loss of ECF over the first week, as reflected by weight loss, while maintaining normal intravascular volume and tonicity, as reflected by heart rate, urine output, and electrolyte and pH values. Subsequently, maintain water and electrolytes while supplying requirements for body growth. Individualize the approach rather than relying on a cookbook formula. Total fluid equals maintenance requirements (IWL plus urine plus stool water) plus growth requirements. In the first few days, IWL is the largest component of lost fluids. Later, as the renal solute load increases, the amount of water the kidneys need to excrete this load increases (80-120 cal/kg/d equals 15-20 mOsm/kg/d, which means that 60-80 mL/kg/d is needed to excrete wastes). Stool requirement usually is 5-10 mL/kg/d. As infants add tissue, they also need to add water to maintain normal ECF and ICF volumes. Since weight gain is 70% water, an infant growing 30-40 g/d requires 20-25 mL/kg/d of water. As the skin matures postnatally, the IWL decreases. Elevated body and environmental temperatures increase IWL. Radiant warmers increase IWL by 50%, phototherapy increases IWL by 50%, and the use of a plastic heat shield reduces IWL by 10-30%. Environmental humidification decreases IWL from the skin and respiratory mucosa by up to 30%. Skin breakdown and skin defects (eg, omphalocele) increase IWL proportionally to the area affected.
• electrolyte requirements : For the first 12-24 hours, sodium, potassium, and chloride usually are not required. Later in the first week, needs are 1-2 mEq/kg/d for potassium and 2-4 mEq/kg/d for sodium and chloride. During the active growth period after the first week, needs for potassium increase to 2-3 mEq/kg/d, and for sodium and chloride to 3-5 mEq/kg/d. Some of the smallest preterm infants have sodium requirements as high as 6-8 mEq/kg/d because of the decreased capacity of the kidneys to retain sodium. Fluids and electrolytes in common neonatal conditions
• respiratory distress syndrome (RDS) : infants with RDS need appropriate fluid replacement. Administration of excessive fluid can lead to hyponatremia and volume overload, worsening the pulmonary condition and increasing the risk of developing bronchopulmonary dysplasia (BPD). Inadequate fluid administration leads to hypernatremia and dehydration
• bronchopulmonary dysplasia (BPD) : as a result of an increased work of breathing, infants with BPD have higher energy requirements. Diuretics often are prescribed in these infants, which can lead to electrolyte disturbances.
• patent ductus arteriosus (PDA) : avoiding volume overloading is critical in infants with a PDA, since this often significantly worsens their respiratory status. This is especially important when indomethacin is prescribed to treat PDA, since indomethacin can decrease urine output significantly.
• perinatal asphyxia : infants who have experienced perinatal asphyxia usual have involvement of multiple organ systems. They are prone to acute tubular necrosis and significant oliguria, and the degree of CNS injury may produce the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Restricting fluid intake to minimize the risk of volume overload often is necessary.
Common electrolyte problems
• sodium (Na)
• hyponatremia is defined as a serum sodium level less than 130 mEq/L. Usually, this is not a cause for concern until the serum sodium has dropped to less than 125 mEq/L. Remember that hyponatremia usually results from excessive free water intake. However, especially in the extremely premature infant or infants with increased sodium losses, inadequate sodium intake can contribute to the development of hyponatremia.
• hypernatremia is defined as a serum sodium level greater than 150 mEq/L. Usually, this is not a cause for concern until the serum sodium level has risen to greater than 150-155 mEq/L. Hypernatremia typically is seen in the first few days of life in ELBW micropremies and is most often the result of inadequate free water intake to compensate for very high IWLs. Very rarely, hypernatremia is the result of excessive administration of sodium in either the diet or intravenous fluids. The usual causes of excessive administration of sodium are administration of sodium bicarbonate to infants with pulmonary hypertension or metabolic acidosis in an effort to increase pH levels.
• potassium (K) : remember that most of the potassium in the body is contained in the intracellular compartment; therefore, serum potassium levels often do not indicate total-body potassium stores accurately. Serum potassium levels also depend on blood pH levels, since pH affects the distribution of potassium between ICF and ECF compartments. A handy rule is that each 0.1 unit of pH change results in a 0.3-0.6 mEq/L change in the serum potassium level. The potassium level rises with acidosis, while it drops with alkalosis.
• hypokalemia is defined as a serum potassium level less than 3.5 mEq/L. Unless the patient is receiving digoxin therapy, hypokalemia is rarely cause for concern until the serum potassium level is less than 3.0 mEq/L. Hypokalemia often results from chronic diuretic use and unreplaced electrolyte loss from NG drainage. ECG manifestations of hypokalemia include a flattened T wave, prolongation of the QT interval, or the appearance of U waves. Severe hypokalemia can produce cardiac arrhythmias, ileus, and lethargy. When significant, this condition is treated by slowly replacing potassium either intravenously or orally
• hyperkalemia is defined as a serum potassium level greater than 6 mEq/L, measured in a nonhemolyzed specimen. Hyperkalemia is of far more concern than hypokalemia, especially when serum potassium levels exceed 6.5 mEq/L or if ECG changes have developed. ECG manifestations of hyperkalemia are a progression from peaked T waves, as the earliest sign, to a widened QRS configuration, bradycardia, tachycardia, supraventricular tachycardia (SVT), ventricular tachycardia, and ventricular fibrillation. Causes of hyperkalemia include potassium release from damaged cells following intraventricular hemorrhage (IVH), trauma, and intravenous hemolysis. In addition, severe acidosis and decreased urinary potassium excretion contribute to elevations in serum potassium. Finally, hyperkalemia may be one of the earliest manifestations of congenital adrenal hyperplasia. Management of significant hyperkalemia may include the following:
• all administration of potassium is discontinued.
• calcium gluconate 100-200 mg/kg (1-2 mL/kg of 10% solution) is administered as a slow IV infusion over 5-10 minutes.
• alkalinization is performed, either with hyperventilation or sodium bicarbonate 1-2 mEq/kg IV.
• insulin is administered to assist in driving potassium into the ICF compartment. Insulin must be administered with glucose as a combined infusion to avoid producing hypoglycemia.
• medications are administered to enhance potassium excretion, including furosemide 1 mg/kg IV or sodium polystyrene sulfonate (Kayexalate) 1 g/kg PR (do not use sorbitol-containing products and do not administer orally). Several hours must pass before any effect is observed with either of these medications.
• dialysis or exchange transfusion may be used to assist in more rapidly removing potassium from the body.
• calcium (Ca) : total serum calcium levels in term infants decline from values of 10-11 mg/dL at birth to 7.5-8.5 mg/dL over the first 2-3 days of life. Approximately 50% of the total calcium is in the ionized form and is the only biologically available form of calcium. Ionized calcium values, rather than total values, correlate better with calcium functions, such as cardiac contractility. Therefore, many centers currently rely exclusively on measurements of ionized calcium. Calcium concentrations can be reported either in milligrams per deciliter (mg/dL) or in millimolar units (mmol/L). Conversion between the two methods is accomplished easily by dividing by 4 (eg, 4 mg/dL of ionized calcium equals 1 mmol/L)
• hypercalcemia is rarely observed in neonates and is defined as a total serum calcium concentration higher than 11 mg/dL or an ionized calcium concentration higher than 5 mg/dL (1.25 mmol/L).
• hypocalcemia occurs more commonly and is defined as a total serum calcium concentration less than 7 mg/dL or an ionized calcium concentration less than 4 mg/dL (1 mmol/L).
• early-onset hypocalcemia may occur within the first 3 days in premature infants born to mothers with poorly controlled diabetes or in infants who experienced perinatal asphyxia. If the infant is asymptomatic and has a total serum calcium level higher than 6.5 mg/dL or an ionized calcium level higher than 0.8-0.9 mmol/L, close observation alone is appropriate. Calcium supplementation should be provided if the total serum calcium level is less than 6.5 mg/dL or if the ionized level is less than 0.8-0.9 mmol/L.
• late-onset hypocalcemia develops after the first week of life and usually is associated with conditions with high serum phosphate levels, including hypoparathyroidism, maternal anticonvulsant use, and vitamin D deficiency. Vitamin D deficiency usually resolves with reduction of the renal phosphate load or vitamin D supplementation.
• Common fluid problems
• oliguria is defined as a urine output less than 1 mL/kg/h. Oliguria can be caused by a variety of conditions that can be classified as prerenal, renal, or postrenal problems. Urine output often is less than 1 mL/kg/h during the first 12-18 hours after birth. Most healthy term babies urinate within the first 12 hours; however, a small number of healthy infants may not urinate until 24-36 hours after birth. Persistent oliguria beyond 36 hours should be evaluated in an otherwise healthy infant
• Nutrition principles
• nutrient requirements
• energy, measured as cal/kg/d
• carbohydrates
• water
• minerals and trace elements
• protein
• vitamins
• fat
• energy needs : The exact energy needs of a given neonate depend upon several factors, including postnatal age, weight, gestational age, route of energy intake, growth rate, activity, and thermal environment. Infants who are ill or experiencing stressful situations (sepsis, surgery, BPD) have higher energy requirements. Infants receiving parenteral nutrition need less energy for adequate growth. Since they do not need to absorb the provided nutrients, they have no fecal losses. As a result, 70-90 cal/kg/d with 2.4-2.8 g/kg/d of protein may be adequate for growth. Protein is not an ideal source of energy; rather, it is provided as a building block for new tissue. If adequate nonprotein calories are provided, the nitrogen balance in the infant is positive, and the protein provided is used to build new tissue. Therefore, even if energy intake from protein is included in calculations of total energy intake, not all the protein-derived calories are available for energy expenditure. The ideal energy ratio is to provide 65% of the energy as carbohydrates and 35% as lipids. Providing more than 165-180 cal/kg/d is of no benefit. As an example, the total energy needs of a growing enterally fed premature infant without any acute illness are listed as follows:
• resting expenditure: 50 cal/kg/d
• minimal activity: 4-5 cal/kg/d
• occasional cold stress: 10 cal/kg/d
• fecal loss (10-15% of intake): 15 cal/kg/d
• growth (4.5 cal/g of growth): 45 cal/kg/d
• total required to produce a 10 g/d weight gain: 125 cal/kg/d
• Total parenteral nutrition management :
• the primary goal is to provide energy and nutrients in sufficient quantities to allow normal growth and development. Although the goal is to have growth rates that follow either the intrauterine growth curve for premature infants or the postnatal growth curve for term infants, this is rarely achieved during the acute phase of an infant's illness. When calculating FEN requirements, most practitioners use an infant's birth weight until the infant has regained the birth weight. Thereafter, daily weight is used in calculations. Total parenteral nutrition (TPN) can be started on the first or second day of life in infants who are not likely to achieve total enteral nutrition within the first week of life. Especially in infants who are ill, protein is required to decrease or prevent catabolism, and starting TPN on the first day is important. The goal for TPN is to provide 90-100 kcal/kg/d with 2.5-3 g/kg/d protein.
• Fluid requirement: Calculate the infant's daily fluid (water) requirement. Then, determine the delivery method, either parenteral (IV) or enteral (OG/PO).
• Energy requirement: Calculate the amount of energy required.
• determine the specific amounts and sources of carbohydrates and lipids.
• determine the amount of protein to deliver based on the total number of calories to be provided. Keep in mind that an infant needs an adequate number of nonprotein calories (150-200 kcal/g nitrogen) to have a positive balance of nitrogen. Most practitioners start at 1.5 g/kg/d of protein on the first or second day and increase daily by 0.5-1.0 g/kg/d, as tolerated. Various amino acid preparations are commercially available for use in the neonate (eg, TrophAmine).
• determine the amounts of vitamins and trace elements to deliver.
• carbohydrate : IV dextrose provides most of the energy in TPN. The caloric content of aqueous dextrose is 3.4 kcal/g glucose, which is equal to 34 kcal/100 mL of D10W. As a result of the high osmolarity of concentrated dextrose solutions, the maximum dextrose concentration that can be delivered safely through a peripheral vein is 12.5%. Even with central venous access, a dextrose concentration > 25% usually is not required. A glucose infusion rate expressed in mg glucose/kg/min is the most appropriate way to express glucose administration, since the rate accounts for both the glucose concentration and rate of infusion. VLBW infants demonstrate impaired glucose tolerance. For this reason, ELBW infants start at an infusion rate of 6 mg/kg/min. In VLBW infants, start at 8 mg/kg/min. If the glucose infusion rate is excessive, hyperglycemia develops. If blood glucose levels are > 150-180 mg/dL, glucosuria occurs, producing an osmotic diuresis and dehydration. This can be controlled either by decreasing the glucose infusion rate or by treating the infant with insulin.
• fat : at least 3% of the total energy should be supplied as essential fatty acids (EFA). This can be accomplished by providing Intralipid^® 0.5 g/kg/d 3 times per week. Parenteral fat usually is provided as a 20% lipid emulsion made from soybeans (eg, Intralipid^® : soya bean oil + egg yolk phospholipids + glycerol). Intralipid^® is a concentrated source of energy with a caloric density of 2 kcal/mL (for 20% Intralipid^®). Most practitioners start with 0.5-1.5 g/kg/d on the first day and increase steadily to 3-3.5 g/kg/d. Limiting Intralipid^® infusions in infants with sepsis and severe lung disease is generally recommended. Neonates with hyperbilirubinemia who are on phototherapy often have Intralipid^® intake restricted to < 2 g/kg/d (especially if bilirubin levels are rising while on phototherapy) because some evidence exists that high lipid-emulsion intake may decrease bilirubin binding (Spear, 1985). Many practitioners monitor triglyceride levels and adjust infusion rates to maintain triglyceride levels of less than 150 mg/dL.
• Protein : term infants need 1.8-2.2 g/kg/d along with adequate nonprotein energy for growth. Preterm VLBW infants need 3-3.5 g/kg/d along with adequate nonprotein energy for growth. Usually, providing more than 4 g/kg/d of protein is not advisable. Infants under stress or who have cholestasis usually are limited to 2.5 g/kg/d of protein because it has been observed that the severity of TPN-induced cholestasis may depend on the duration of TPN and the amount of amino acids infused (Sankaran, 1985; Yip, 1990). Protein supplementation should be started early, as soon as FE requirements have stabilized. Very high protein intake, at greater than 5-6 g/kg/d, may be dangerous. Maintain a nonprotein-to-protein calorie ratio of at least 25-30:1. The current role of supplements, such as additional glutamine, inositol, and carnitine, is under investigation. Although a physiologic rationale exists for their use, they have not yet been shown to be of benefit in large randomized controlled trials; however, to date, small clinical trials are promising.
• minerals (other than sodium, potassium, chloride)
• calcium and phosphorus (Ca and P): Once protein intake has been started, calcium and phosphorous should be added to the TPN. Take care to ensure that solubility is not exceeded. If this happens, calcium and phosphorous may precipitate spontaneously.
• magnesium (Mg): Supplemental magnesium should be added to TPN once protein has been added.
• vitamins and trace elements
• vitamins A, D, E, and K are fat soluble.
• vtamins B-1, B-2, B-6, B-12, C, biotin, niacin, pantothenate, and folic acid are water soluble.
Vitamin supplementation should be started as soon as protein is added to the TPN. The addition of a commercially available neonatal vitamin preparation provides appropriate quantities of all vitamins, except possibly vitamin A. Evidence exists that therapeutic doses of vitamin A (5000 IU administered IM 3 times/wk) may reduce the incidence of chronic lung disease and other long-term adverse outcomes in ELBW infants.
The trace elements zinc, copper, selenium, chromium, manganese, molybdenum, and iodine also should be added to TPN once protein is started. This can be easily accomplished by the addition of a commercially available solution containing trace elements.
• Enteral nutrition management
• energy : with enteral nutrition, human milk and standard infant formulas (20 cal/oz) provide 67 cal/100 mL. In general, human milk is the preferred source of enteral nutrition because of its trophic and immunologic properties. Evidence is substantial that necrotizing enterocolitis (NEC) is lower in preterm infants fed with breast milk. Higher caloric densities include 22 cal/oz and 24 cal/oz formulas. Formulas with caloric densities higher than 24 cal/oz should be used with caution, as they often have a very high renal solute load and can lead to dehydration.
• carbohydrate : lactose is the carbohydrate source in human milk and in most standard formulas given to term infants. Lactose provides 40-45% of the energy. In preterm infant formulas, lactose provides 50% of the carbohydrates and glucose polymers provide 50%. This is because of the lower intestinal lactase levels and relatively higher intestinal glycosidase levels in premature infants. The use of glucose polymers (rather than monosaccharides or disaccharides) also helps maintain a lower osmolality. Soy and lactose-free formulas use sucrose, maltodextrins, and glucose polymers as the carbohydrate sources.
• fat : with enteral nutrition, approximately 50% of the energy is derived from fat. If more than 60% of the energy is derived from fat, risk of ketosis is increased. Medium-chain triglycerides can be absorbed without pancreatic lipase or bile salt emulsification. As a result, preterm infant formulas have a higher percentage of fat supplied as medium-chain triglycerides.
• protein : protein requirements of 1.8-2.2 g/kg/d are readily provided to term infants by human milk and standard infant formulas. Preterm infant formulas have a higher protein content to allow delivery of the necessary 3-3.5 g/kg/d.
• minerals, vitamins, and trace elements : calcium, phosphorous, and magnesium. During the third trimester, accretion rates for calcium (120-150 mg/kg/d) and phosphorous (75-85 mg/kg/d) are higher than rates that can be provided in premature infants receiving human milk. As a result, a human milk fortifier is essential, and premature infants fed human milk must receive supplementation to minimize the risk of osteopenia of prematurity. Premature infant formulas have a much higher concentration of these minerals, which helps approximate the third trimester accretion rates in infants receiving these formulas. Human milk and term and premature infant formulas all provide amounts of magnesium adequate to meeting an infant’s nutritional requirements if the infant is receiving at least 100 cal/kg/d.
• iron : to minimize the risk of iron deficiency anemia, all formula-fed term infants should receive iron fortified formulas. Breastfed term infants should receive supplemental iron beginning at age several months. Premature infants should be started on supplemental iron once they are receiving full enteral feedings regardless of whether they are fed human milk or premature infant formula.
• vitamins and trace elements : Full-term infants fed standard infant formula do not routinely require vitamin supplements, since adequate quantities of all of the vitamins are present in the formula. Full-term infants fed human milk should receive supplemental vitamin D to minimize the risk of osteopenia and rickets. Premature infants fed human milk without human milk fortifier should be started on a multivitamin supplement as soon as they are receiving full enteral nutrition. Premature infants receiving human milk with human milk fortifier or standard premature infant formulas should not routinely require additional vitamin supplements.
• special formulas : a number of special infant formulas are available to meet the very specific dietary needs of small groups of patients who cannot be maintained on standard term or premature infant formulas. These formulas include soy-based formulas, elemental formulas, and formulas with unique protein, fat, and carbohydrate content. As a result of the low calcium and phosphorous contents of soy-based formulas, they are not appropriate for premature infants. Specialty formulas are available for infants with galactosemia, phenylketonuria, short-bowel syndrome, and protein allergy, as well as many other conditions.
Enteral feeding methods :
• premature infants in the NICU usually are fed by OG or NG tube until they are sufficiently mature to coordinate sucking, swallowing, and breathing. Then, the transition is made gradually to feeding by mouth (PO) at the breast or bottle. Staff at many NICUs encourage nonnutritive sucking, which may facilitate the tube-to-oral (bottle/breast) feeding transition.
• initiation and advancement of feedings: Variation between NICUs and, sometimes, between neonatologists at a single unit is marked regarding when feedings are commonly initiated. Currently, some evidence exists that trophic or minimal enteral feedings are safe and well tolerated. In this technique, small volumes are fed to infants for a few days without significant increments. Many neonatologists start feedings within the first week of life and advance the feedings at a rate dependent on gestational age, degree of illness, and other clinical factors. Although some retrospective studies suggested that a rapid increase in feedings may predispose infants to necrotizing enterocolitis (NEC), prospective studies have not confirmed this. In general, most neonatologists advance feedings over a period ranging from 5-15 days in ELBW infants and over 4-10 days in neonates weighing 1000-1500 g.
• OG feedings: conventionally, infants receive intermittent bolus gavage feedings over 10-20 minutes (by gravity) every 2-3 hours. Feedings also may be administered continuously using an infusion pump. Currently, no evidence strongly indicates that one method of feeding is superior to the other.
• transpyloric feedings initially were believed to reduce the risk of gastroesophageal reflux. However, studies have shown a high rate of complications using the transpyloric route, with no additional benefits; hence, it is not often used unless feeding intolerance using NG or OG tubes is marked (Macdonald, 1992).
• fortification: Infants on breast milk commonly are fed fortified breast milk, which increases energy and mineral intake. That infants fed fortified breast milk have improved short-term growth and bone mineral content has been documented; however, evidence of long-term benefit is insufficient. At present, whether breast milk feeding (with or without fortification) improves long-term neurodevelopment compared to preterm formula is controversial.
• supplementation with long-chain polyunsaturated fatty acids (LCPUFAs), such as docosahexaenoic acid (DHA) and arachidonic acid (AA), has been recommended for preterm infants on physiologic grounds. Although visual maturation may possibly be somewhat accelerated, no long-term benefits have been demonstrated yet.
• feedings at discharge: premature infants usually are fed either breast milk or formula (22 cal/oz or 20 cal/oz). Some evidence exists that 22-cal/oz formula may lead to slightly better nutritional outcomes, probably because of its higher energy, calcium, and phosphate content
• nutrition in newborn
• calorie requirement : daily calories required for a normal growth
• energy quotient : calorie requirement / body weight [kg]
• first trimester of extrauterine life : 100-100 cal/kg
• adulthood : 40-45 cal/kg
• sources :
• carbohydrates : 50-60% (10-11 g/kg/day in the breastfed vs. 7 g/kg/day in adults) : poor hepatic glycogen storages, despite predominance of anaerobic glycolysis => physiological hypoglycemia (40-60 mg/dl), eventually leading to acidosis (increased lipid catabolism) when glycemia < 30 mg/dl
• proteins : 10-15% (1.5-2 g/kg/day in the breastfed vs. 1 g/kg/day in adults), expecially animal proteins (milk and derivatives, fish, eggs, and meat)
• fats : 20-30% (4-6 g/kg/day in the breastfed vs. 1 g/kg/dat in adults), 50% from animal sources, 50% from vegetal sources
• consumption is so divided :
• basal metabolism : 50%
• muscular activity : 20%
• growth : 18%
• dynamic action of nutrients : 7%
• losses : 5%
• water : 150 ml every 100 calories, i.e. multiply calorie requirement for 1.5 = 150 g/kg/day in the breastfed
• first meal : 5-10 ml D5W solution
• since second-third meal (or then if lactation is not ready : artificial milk could cause allergy to cow milk proteins) : breastfeeding, which also improves the psychological relationship between mother and child :
• in the first month : 6 meals/day (every 3 hours)
• first days : colostrum
• first weeks : transition milk
• then : definitive milk
• since month 2 to 4 : 5 meals/day (every 4 hours with nocturnal pause)
• since month 4 : 4 meals
Contraindications to breastfeeding :
• maternal causes :
• hypogalactia or agalactia
• athelia
• acute or chronic wasting disease
• tuberculosis
• conditions of psychological tension with unconscious refuse of the child
• assumption of drugs potentially dangerous to the child
• painful rhagades to the nipple, mastitis, and galactophoritis are not absolute contraindications
• child-related causes :
• cheilo- or palatoschisis
• macroglossia
• fast exhaustion of suction and swallowing reflexes (expecially in premature newborns)
• nasal airways obstruction
• severe stomatitis
Artificial milks :
• unpasteurized fresh milk : it is not recommende for childhood nutrtion as it forms gross rennet flakes in stomach which are slowly digested and it is easily contaminated by pathogenic microorganisms
• pasteurized milk : pasteurization destroys pathogenic bacteria and modifies casein to produce smaller rennet flakes in stomach, less resistant to enzyme digestion. Raw milk is heated at 63°C for 30 minutes or at 72°C for 15 minutes and then rapidly cooled : the tolerable threshold for nonpathogenic bacteria is < 50,000 bacteria/ml. Milk has to be boiled when used for breastfed nutrition : when left in freezer for > 48 hrs its bacterial content increases significatively
• homogeneized milk : homogenization is a process leading to fragmentation of fat particles in smaller particles, which remains in suspension. The main advantage is the formation of smaller and less resistant rennet flakes
• vaporized milk : it has many advantages including the worldwide availability and the long conservation if the pack remains closed, even out of freezer. The aggregates of casein forming in stomach are softer and smaller than those in boiled whole milk and lactoalbumin seems to be less allergizing than that from fresh milk
• processed milk are obtained from cow milk and are marketed as powders or concentrated fluids that have to be diluted with milk in a 1:1 ratio. Composition is very similar to that of maternal milk. They are all fortified with vitamin D, other vitamins and iron. Furthermore, special formulas for preterm newborns are available. Milks containing hydrolyzed casein or seroproteins are useful in breastfed with malabsorption or allergy to milk proteins. Special formulas obtained eliminating some amino acids are useful for breastfed and babies with inborn errors of metabolism but cost much.
• powdered whole milk contains 3.5% of lipids, is not well preserved once exposed to air
• powdered skimmed milk should not be used in babies aged < 2 yrs; both skimmed (fats < 0.5%) and partially skimmed (fats < 1.5%) are available for feeding of babies with fat intolerance. They all contain no vitamin D fortification
• fermented and acidified milks are obtained by adding acid to cow milk formulas previously boiled and cooled or fermented by adding lactic acid-producing microorganisms. These milks require less hydrochloride acid to be digested in stomach as casein forms smaller rennet flakes. Currently they are poorly used in baby feeding as they could cause metabolic acidosis
• goat milk : in USA use is limited to treatment of cow milk allergies. It contains less sodium, more potassium and chloride and more linoleic and arachidonic acid than cow milk. Its fats and proteins are more easily digested. Babies exclusively fed with goat milk are at higher risk for megaloblastic anemia due to vitamin B12 deficiency. Goat is also more susceptible to brucellosis and milk shoud be boiled before use. Goat milk is marketed in powdered or vaporized formulas
• wean : to discontinue the breast feeding of an infant, with substitution of other feeding habits; the transition at month 4-6 from exclusively milky diet to diet including nutrients intended to offer the breastfed higher quantities of iron (meat) more easily absorbed than in milk or other minerals and vitamins (e.g. in fruit and vegetables) absent in milk. The introduction of new nutrients should be gradual to allow identification of eventual untolerated ones. The second milky meal is first replaced by a cereal soup (first gluten-free, ie. containing maize, rice, and tapioca) prepared into vegetal broth with addition of liophilized meat, 1 spoon of maize oil and cheese. Around month 6 this meal can be administered also at evening (fourth meal) eventually varying the kind of cerals (gluten can be introduced as pasta), and fish and egg can replace meat.
• at month 4-5 : 5 meals of which 4 with milk and 1 with broth with rice cream, liophilized meat, maize oil and Parmesan cheese
• at month 5-6 : 4 meals of which 2 with milk and 2 with broth with pasta, meat or fish, maize oil, Parmesan cheese and grated fruit (apple, banana) at end of meal
• at month 11-12 : intruduction of pasta, rice, meat or fish, whole cow milk with biscuits
• after 1 year : nutrition similar to that of adulthood, excluding spicy foods, spices, fried foods, raw meats, sausages, coffee, wine, and alcohol, and limitig sweeties trying to replace them with fruit. The baby should be trained to a breakfast consisting of yoghurt or milk (200-250 ml), 2 other complete main meals including a first and second dish, fruit, vegetables and a small tea consisting of milk or yoghurt or fruit. Bread, whole cereals rich in fibers, legumes and fish should be offered 3-4 times a week
• after 2 years nutrition should be free and personalized according to preferences of baby with a right proportion of carbohydrates, lipids and proteins. The need for sweeties is genetically determinated, so it will be very difficult to forbid sweeties to a baby asking for them, while the need for salt is a cultural topic (ie. it is possible to train a baby toward a salt-poor diet, then useful in following years to prevent systemic arterial hypertension. One of the most important meal is breakfast : a rich meal at the morning improves school performances and feeling of well-being, decreasing the sense of hunger, and may be useful to prevent obesity. During daytime calories should be so distributed :
• breakfast : 25%
• lunch : 35-40%
• tea : 10-15%
• dinner : 25-30%
• each year 4 million babies < 1 month old die out of the 130,000 which are delivered, and 75% of them die in the first week of life from infections, premature birth, or problems during the birth itself. Despite the tragedy equates 1 Asian tsunami striking the world every 2 weeks, our responses are very different to these 2 tragedies : we must see the same response to the invisible tragedy that is happening today. 16 basic, inexpensive treatments, such as encouraging mothers to breast-feed and providing antibiotics for sick babies, could prevent the deaths of 3 million babies every year. The United Nations' 191 member countries have set the ambitious goal of reducing mother and child deaths by 66% by 2015. But most research on preventing infant deaths focuses on expensive medical technologies to save those who die in rich countries - only 1% of the total. About 66% of infant deaths occur in 10 countries: Afghanistan, Bangladesh, China, the Democratic Republic of Congo, Ethiopia, India, Nigeria, Pakistan, Indonesia and the United Republic of Tanzania^{ref1, ref2, ref3}.
• 500,000 babies die every year from tetanus infections. But these deaths could be prevented if their mothers received tetanus vaccinations, which only cost 20 US cents per shot. And most premature babies simply need extra warmth, feeding and prompt treatment of infections, which requires proper training of midwives, mothers-to-be and their families
• it is estimated that breast-feeding could prevent 1.3 million deaths worldwide each year. Save the Children programme has trained midwives in Bolivia to encourage mothers to hold and breast-feed their babies as soon as they are born. Traditionally, midwives there have advised mothers to feed babies tea made from anise or cocoa instead of breast milk
• other cheap interventions promoted by Save the Children include clean delivery kits, which contain soap, a clean razor blade and piece of string for cutting and tying the umbilical cord, and a plastic sheet to place on the ground under the baby. These measures aim to prevent babies from catching infections in the crucial minutes during and just after birth. Some countries, such as Sri Lanka, Vietnam, Indonesia and Honduras, have begun to reduce infant deaths using inexpensive methods like these. Countries could fully address the problem by spending just 90 cents more per person than they do now
Web resources :
• UN Millennium Goals
• Save the Children programme

• the achievement of biological and sexual maturation
• the development of personal identity
• the development of intimate sexual relationships with an appropriate peer
• establishment of independence and autonomy in the context of the sociocultural environment

	biological	psychological	social
early adolescence	early puberty (girls: breast bud and pubic hair development, start of growth spurt; boys: testicular enlargement, start of genital growth)	concrete thinking but early moral concepts; progression of sexual identity development (sexual orientation); possible homosexual peer interest; reassessment of body image	emotional separation from parents; start of strong peer identification; early exploratory behaviours (smoking, violence)
mid-adolescence	girls: mid-late puberty and end of growth spurt; menarche; development of female body shape with fat deposition Boys: mid-puberty, spermarche and nocturnal emissions; voice breaks; start of growth spurt	abstract thinking, but self still seen as "bullet proof"; growing verbal abilities; identification of law with morality; start of fervent ideology (religious, political)	emotional separation from parents; strong peer identification; increased health risk (smoking, alcohol, etc); heterosexual peer interest; early vocational plans
late adolescence	boys: end of puberty; continued increase in muscle bulk and body hair	complex abstract thinking; identification of difference between law and morality; increased impulse control; further development of personal identify; further development or rejection of religious and political ideology	development of social autonomy; intimate relationships; development of vocational capability and financial independence

• challenging authority
• seeking spiritual paths (organised or cult religions)
• taking risks
• getting a job
• experimenting with drugs, alcohol, and sex
• changing schools and educational environment
• challenging the moral and social structure of society
• developing relationships
• demanding rights
• understanding sexuality
• taking responsibility for self and others
• renegotiating rules at home

• European training in effective adolescent care and health (EuTEACH)
• Society for Adolescent Medicine (SAM)

Pediatric infections

• viruses
• measles virus ("first disease")
• mumps virus
• rubella virus ("third disease")
• HHV-3 / VZV
• HHV-6 ("sixth disease" / roseola (infantum) / exanthem or exanthema subitum / rose rash of infants)
• adenoviruses
• enteroviruses
• polioviruses
• coxsackieviruses ("fourth disease" / Filatov-Dukes' disease / scarlatinella : it probably represented misdiagnosed cases of rubella or scarlet fever, rather than a distinct illness)
• influenzavirus
• parainfluenzavirus
• rhinoviruses
• astrovirus
• calicivirus
• HHV-1 / HSV-1
• HHV-2 / HSV-2
• HHV-4 / EBV
• HHV-5 / CMV
• HHV-7
• HHV-8
• parvovirus B₁₉ ("fifth" disease of the infant / erythema infectiosum / epidemic megaloerythema / "slapped cheek" syndrome)
• human respiratory syncytial virus (RSV)
• human metapneumovirus
• human coronavirus NL63
• HBV
• HCV
• HIV-1
• rotavirus
• bacteria
• Streptococcus pyogenes ("second disease" / scarlet fever)
• Haemophilus influenzae
• Bordetella pertussis
• Corynebacterium diphteriae
• Listeria monocytogenes
• Leptospira interrogans
• minor salmonellosis (no antibacterials are required after age 3 months : they prolong symptoms and increase number of healthy carriers)
• Mycoplasma pneumoniae (after age 5)
• Bartonella henselae
• protozoa
• Toxoplasma gondii
• fungi
• Candida albicans
• neonatal sepsis / sepsis neonatorum
• localizations :
• lymphadenitis
• meningitis : adynamia, negative meningeal irritation signs, Lesage sign
• Enterovirus spp. (+ cutaneous rash) (75-90% of viral meningitis : expecially in babies < age 1, no after age 40)
• Streptococcus pneumoniae (pneumococcal meningitis represents 0÷5 % of all meningitides in newborns < 1 month age, 10÷20 % total meningitis in babies with 1 month < age < 15 years, 30÷50 % after age 15; + cutaneous rash. Up to 50% the cases are secondary to other infections, such as pneumonia, bacterial endocarditis, cranial wounds, otitis, mastoiditis or infectious (paranasal) sinusitis, and reinfection may occur. The incidence is increased in asplenic or immunocompromised patients, such as those with sickle cell anemia (SCA) or lymphocytic leukemia. Mortality = 30%)
• Staphylococcus aureus (5% total meningitis in newborns < 1 month age, 1÷2 % total meningitis in babies with 1 month < age < 15 years, 5÷15 % in adults > 15 years and elderlies; + cutaneous rash, also under nails)
• Neisseria meningitidis (meningococcal meningitis / epidemic cerebrospinal meningitis / cerebrospinal fever represents 0÷1 % total meningitis in newborns < 1 month age, 40÷60 % total meningitis in babies with 1 month < age < 15 years (expecially in babies 6 months < age < 2.5 yrs.), 1÷3 % in adults > 15 years, elderlies and immunocompromised ; + cutaneous rash. Mortality = 7%)
• Listeria monocytogenes (2÷10 % total meningitis in newborns < 1 month age, 1÷2 % total meningitis in babies with 1 month < age < 15 years, 5 % in adults > 15 years, elderlies and immunocompromised)
Therapy : antibacterial therapy using ceftriaxone + vancomycin (linezolid for VRSA; VRE, PRSP, and MRSA)
• resistance :
• penicillins (40%)
• macrolides (28%)
• tetracyclines (20%
• cotrimoxazole (35%)
• sensitivity :
• amoxicillin, clindamycin and fluoroquinolones (90%)
• vancomycin (100%)
Prevention : anti-S.pneumoniae vaccine
• osteomyelitis
• acute pharyngitis

Epidemiology : 9 million new cases per year in France
Symptoms & signs : pharyngeal examination has negative predictive value = 97% for GAS, but positive predictive value = 45% only. Viral aetiology should be suspected when associated with rhinitis, laryngitis, cough, diarrhea, conjunctivitis, stomatitis, or ulcer. Bacterial aetiology should be suspected when onset of phayngodynia is sudden, headache, fever, abdominal pain, nausea, vomiting, red throat with exudate (also from adenoviruses and HHV-4 / EBV, petechiae over soft palate, swollen uvula, laterocervical or angulomandibular lymphadenopathy, scarlatiniform rash.
Laboratory examinations : rapid test is positive in 26.6% (which should begin antibacterial therapy) and negative in 73.4% (which should undergo neither pharyngeal swab culture (positive in only 2.4% !) nor antibacterial therapy). The status of healthy carrier doesn't require therapy as the disease is poorly transmissable, unless familiarity for rheumatic fever exists. Pharyngeal swab is not recommended in the first 3 years of life, unless asymptomatic familiars, schoolmates, after adequate therapy, and to prove rare aetiology. Hypocomplementemia and > 4-fold increase in ASLO is used in suspected RF and APSGN, where antibacterials may reduce duration of symptoms, period of transmittability, prevent RF and locoregional suppurations : for this purpose Therapy : amoxicillin (40-50 mg/kg bid for 6 days), cephalosporins (4 days), azithromycin (5 days), or benzathine penicillin (10 days) are used, but intracellular persistance can occur.
• acute otitis media : in fever of unknown origin (FUO), otoscopy is recommended and could show extroflexion and hyperemia of eardrum; otopneumoscope can show hypomobility of eardrum. AOM usually is self-limiting without complications

Therapy : as antibacterials are poorly effective in reducing symptoms, they can be delayed in the first 24-72 hours. When indicated, amoxicillin (40-100 mg/kg/day for S.pneumoniae, H.influenzae, M.catarrhalis and S.pyogenes) +/- clavulanic acid should be administered for 10 days in newborns or severely ill children or for 3-5 days in older children or mild cases; cefuroxime-axetil, cefpodoxime and ceftriaxone for 1-3 days are second-choices. Prevention : anti-influenza vaccine (influenzaviruses cause a transient immunodepression, leading to ciliary paralysis, hyperplasia of secretory epithelium and expression of receptors for bacteria => overinfections and new onset of fever. Antibacterial prophylaxis is not useful during viral infections, but it should be started once bacterial overinfection is established).
• bronchitis : they have almost a viral aetiology and antibacterials should not be administered even in febrile patients
• pneumonia

Epidemiology : 1,000 new cases every 100,000 people per year
Symptoms & signs : pharyngitis, rhinitis, transmissibility among relatives, conscious patient, lack of respiratory distress suggest viral aetiology => no antibacterials
Laboratory examinations : tracheal swab in bronchopneumonia is meaningful only when detects viruses;  CXR only when relapsing
Therapy :
• since month 4 to age 4 years aetiology is mainly viral, S.pneumoniae, M.pneumoniae, H.influenzae => cephalosporins, amoxicillin (80-90 mg/kg/day), axetil cefuroxime or clavamox for 2-3 days => if not improving macrolides for 10-14 days
• after age 5 to 15 years aetiology is viral, S.pneumoniae, M.pneumoniae or C.pneumoniae => macrolides for 2-3 days => if not improving amoxicillin or ceftriaxone
Prognosis : radiological negativization requires
• 2 weeks-2 months for M.pneumoniae and S.aureus
• 1-2 months for S.pneumoniae and C.pneumoniae
• 3-6 months for L.pneumophila and  and Gram-negative enterobacteria
Slow resolution may be due to
• inadequate therapy (choice or dosage of antibacterial, poor compliance)
• development of antimicrobial resistance
• immunodeficiency
• virus/mycobacteria/fungi
• urethrocystitis

Symptoms & signs : anorexia, irritability, pallor, vomiting, diarrhea or constipation; no dysuria, stranguria, pollakiuria (on the contrary of adults);
Laboratory examinations : urinoculture after suprapubic puncture (false positives), nitrites (if retained for > 4 hrs in bladder)
Therapy : p.o. (i.v. only for MDR germs) for 3-7 days
• amoxicillin 50 mg/kg/day in 2 doses
• cotrimoxazole 6 mg/kg/day in 2 doses
• nitrofurantoin 5-7 mg/kg7day in 3-4 doses
• clavamox : 50 mg/kg/day in 2 doses
• cefixime : 8 mg/kg/day in a single dose
• ceftibuten : 9 mg/kg/day in a single dose
Onset of fever suggests cystopyelitis or pyelonephritis, for which i.v. antibacterials are recommended if age < 2 years, sepsis or cachexia (alternative regimens are p.o. or i.v. for 3 days => p.o.)
• ceftriaxone 50-75 mg/kg/day for < 2 days
• ceftazidime 10 mg/kg/day for 2 days
• amikacin (cefoxime, ceftibuten, clavamox) 15 mg/kg/day for 2 days
Prophylaxis :
• after febrile UTI while waiting for voiding cystourethrography
• medical therapy for vesicoureteral reflux (mandatory in males < 1 year and females < 2-3 years)
• relapsing UTI
• malformative uropathy
Regimen :
• continuous : amoxicillin for 15 days
• evening monodose : cotrimoxazole for 2 days
• 1/3 of therapeutic dose :
• nitrofurantoin 1-1.3
• cefixime or ceftibuten for 3 days
• clavamox for 15 day
Therapy : antibacterial therapy should be started in neutropenic patients (< 500/ml), using a 4th generation cephalosporin (ceftriaxone) + aminoglycoside + vancomycin (if signs persist for > 5 days => amphotericin B); p.o. ROA should be preferred (i.r. route gives poor absorption), but i.m. route can be used for children with vomiting and/or diarrhea and i.v. route is recommended in oncological patients. When antibacterials are effective, apyrexia should be achieved within 24-48 hours. Respiratory tract infections are the commonest cause of malpractice in antibacterial administration : despite 90% of them are caused by viruses, antibiotics are prescribed for 50-70% of patients who seek medical care for these conditions (Niederman, 1998). Prescribing antibiotics for conditions for which there is no proven benefit is not a harmless practice; it contributes to the development of antibiotic resistance^ref
• URTI : unusual bacteria in the first 2-3 years of life. In scholar children S.pyogenes is the commonest bacterium, but viral infections are the leading cause
• LRTI : bacteria rarely cause laryngitis, tracheitis, bronchitis and bronchiolitis

Pediatric cardiology : in a consciousless newborn the central pulse is searched at the level of the brachial artery

• congenital heart diseases
• coarctation of the aorta, infantile type
• pediatric hypertension
• harlequin sign : reddening of the lower half of the laterally recumbent body and blanching of the upper half, due to temporary vasomotor disturbance in newborn infants

• developmental disorders
• age specificity of signs (changes in EEG) and natural history of all diseases
Reflexes :
• grasping (up to simultaneous arm and leg suspension
• automatic march after vestibular trigger
• Chateau's postural reaction : absence of labyrinthine righting, as for rabbits without labyrinths
Newborns focus at 40-80 cm, the range useful for activities of daily life
Early sensory capacities :
• hearing : ability to distinguish phonemes
• preference for native language
• vision :
• slighthly blurred, slightly double vision at birth
• color vision at 2 months of age
• ability to distinguish patterned stimuli from plain
• large numbers of endogenously generated motor patterns mainly located in spinal cord and brainstem, modulable by internal and external afferences, highly sensitive adverse conditins for the CNS; already at week 12-15; slow (general movements (GM) and streches in seconds or minutes) or fast.
• neural maturationist theory : macroscopic (weight of encephalon, diameter of skull) and microscopic (cortex layers)
• Griffiths mental development scales (0-7 yrs)
• 0-2 yrs scale (1954) :
• locomotor: 54 item
• personal-social: 58 item
• hearing & language: 56 item
• eye & hand: 54 item
• performance: 54 item
• 2-8 yrs scale (1970) :
• locomotor: 86 item
• personal-social: 86 item
• hearing & speech: 86 item
• hand & eye co-ordination: 86 item
• performance tests: 86 item
• practical reasoning: 86 item

motor milestones	25%	50%	75%	90%
lifts head up	1.3 mo.	2.2 mo.	2.6 mo.	3.2 mo.
walks holding up to furniture
walks well
walks on steps

Gross motor milestones :

skill	age
Rolls over	4-5 months
Sits without support (trunk control)	6-7 months
Pulls to a standing position	9-10 months
Walks independently	12-14 months
Developing spatial confidence	18 months
Can seat self in small chairs	18 months
Runs	18-24 months
Enjoys jumping	24 months
Can walk on tip-toes	24 months
Plays well with large and small balls	24 months
Pedals tricycle	3 years
Climbs/descend sstairs with alternating feet	3.5-4 years
Developing coordinations	4 years
Rides a bicycle without training wheels	6-7 years

Visual tactile or motor milestones :

skill	age
Transfers object from hand to hand	3-5 months
Brings all objects to mouth	6 months
Holds a bottle	6 months
Pincer type grasp	10-12 months
Eye movements fully coordinated but with head movement	12 months
Throws objects to the floor	12-15 months
Eyes team well with little head movement	18 months
Points to objects and pictures when identifying	18 months
Scribbles	18-24 months
Converges eyes easily & accurately to inspect objects	24 months
Copies a circle	3 years
Eyes team well at all distances	3 years
All visual-tacual integrations now developing quickly	3 years
Buttons clothes	3.5 years
Using eyes & hands together productively & with increased skill	4 years
Catchs a ball	4-5 years
Ties shoelaces	5-6 years

Language milestones :

skill	age
Attends to familiar voices	3-4 months
Babbles	5-6 months
"Mama" & "Dada" used	12 months
Recognizes names of familiar objects	13-15 months
Can follow simple commands	15-18 months
Two-word sentences	2 years
Simple sentences (subject, verb and object)	3 years
Can name primary colors	4 years
Vocabulary of 2000-2500 words, counts to "10"	5 years

Sources of variability in walking :
• ethnical
• biological
• choices (top-down and bottom-up) : e.g. arms longer than legs => bear-like walking, relaxed ligaments => limb abduction => quadrupedic; kind of furniture (crawling over moquette, over parquet, ...)
Critical (sensitive) periods in postnatal development : regulator genes require environmental inputs.
• experience (e.g. amblyopia for vision)
• hand movement (first 7 months)
• for basic social relationship)
• learning
• brain plasticity (vision, corticospinal tract)
Experience plays a crucial role for the normal development of many perceptual and cognitive functions, such as speech perception. For example, between 6 and 10 months of age, the infant's ability to discriminate among native speech sounds improves, whereas the ability to discriminate among foreign speech sounds declines. Some experience with nonnative languages from 9 months of age facilitates the maintenance of this ability at 12 months. Nelson has suggested that the systems underlying face processing may be similarly sculpted by experience with different kinds of faces. In human infants between 6 and 9 months of age, exposure to nonnative faces, in this case, faces of Barbary macaques (Macaca sylvanus), facilitates the discrimination of monkey faces, an ability that is otherwise lost around 9 months of age^ref.
• pediatric neurology (neuropediatrics)
• nervous system malformations
• anencephalia
• hydrocephalus
• microcephaly
• spina bifida
• children brain tumors
• cerebral palsy
• obstetric brachial plexus palsy
• epilepsy
• kernicterus
• headache
• congenital muscular dystrophies
• congenital deafness
• amblyopia
• ametropias
The mortality from acute neurologic disorders of childhood, such as status epilepticus and stroke, is highest in infants < 1 year of age. Certain forms of newborn brain injury, such as stroke, have an incidence as high as 1 in 4000 live births. > 95% of infants who have a stroke survive to adulthood, and many have residual motor or cognitive disabilities. Stroke and other forms of brain injury have a considerable effect on surviving babies, their families, and society^ref.
• pediatric psychiatry
• developmental disorders
• mental retardation
• learning disorders
• motor skills disorder
• communication disorders
• pervasive developmental disorders
• attention-deficit/hyperactivity disorder (ADHD) and disruptive behavior disorders
• eating disorders
• tic disorders
• increasing numbers of children are being treated for depression. At the end of 2003, over 50 000 children were prescribed antidepressants, and over 170 000 prescriptions a year for antidepressants were issued to people under 18 years old in the United Kingdom. Recent evidence has suggested that selective serotonin reuptake inhibitors are largely ineffective and may be dangerous in this age group^{ref1, ref2}. Older antidepressants have already been shown to have no beneficial effect in people under 18. The medicalisation of children's unhappiness is hindering our ability to respond effectively to this problem. Western society's ideas about childhood and child rearing have changed radically in the past 60 years. The West's attitude to child rearing changed from viewing relations between adults and children primarily in terms of discipline and authority to a focus on permissiveness and individual rights. In addition, whereas the model used before the second world war prepared children for the workplace within a society of scarcity, the post-war model prepared them to become pleasure seeking consumers (along with their parents) within a prosperous new economy. Shifting economic structures also led to profound changes in the organisation of family life. Suburbanisation and the economic demands of successful market economies resulted in greater mobility, less time for family life, and a breakdown of the extended family. Many families (particularly those headed by young women) became isolated from traditional sources of childrearing information. Guides on childrearing took on an unprecedented importance, allowing for a greater change in parenting styles than would have been conceivable in more rooted communities and giving professionals increased ownership of the knowledge base for the task of parenting. The new child centred permissive culture was a godsend to consumer capitalism. Childhood could now be commercialised, and an industry of consumer goods for children developed. As a result, children have gained access to the world of adult information and entertainment. The boundaries between what is considered adulthood and what is considered childhood have become blurred, and this has led to children coming to be viewed as, in effect, miniature adults. One effect of these changing expectations of childhood and parenting is that more childhood behaviours previously considered normal are now seen as problematic, and problematic behaviours are more likely to be medicalised. Just as our concepts of childhood have changed, so have our concepts of childhood problems. It was only in the late 1980s that our understanding of childhood depression began a far reaching transformation. Before this, childhood depression was viewed as very rare, different from adult depression, and not amenable to treatment with antidepressants. A shift in theory, and consequently practice, then took place as influential academics claimed that childhood depression was more common than previously thought (8-20% of children and adolescents), resembled adult depression, and was amenable to treatment with antidepressants (often resulting in antidepressants becoming a first line treatment^ref). Childhood depression has become a popular notion, reflecting the broader cultural changes that have taken place in our view of childhood and its problems. These days we are as likely to use medicalised terminology to describe children's feelings (such as depressed) as we are less pathological descriptions (such as unhappy). According to the current criteria, psychiatric comorbidity in childhood depression is so high that nearly every child can be diagnosed with at least one other psychiatric condition. This raises doubts over the specificity of the construct. Despite awareness of the continuity between normal sadness and clinical depression, the diagnosis assumes that clinical depression exists as a category (rather than on a continuum). It is unclear, however, who decides where the cut-off mark is, and on what basis. Furthermore, the categorical diagnosis bears only a tenuous relation with levels of psychosocial impairment. Many children below the threshold of diagnosis show higher levels of impairment than those above the threshold^ref. Similarly, a diagnosis of childhood depression is only weakly associated with suicide (stronger predictors include history of aggression and use of drugs or alcohol). The biological markers (such as cortisol hypersecretion) that are sometimes found in adults diagnosed with depression do not work with children and adolescents diagnosed as depressed. With regard to genetics, separating environmental from biological factors in the familial clustering has been virtually impossible, particularly as children whose parents have depression are at risk of developing a wide range of psychiatric disorders. Childhood depression has been argued to be a precursor of adulthood depression^ref. However, follow up studies of children deemed to have had "major depressive disorders" have used dubious standards for diagnosing childhood and adult psychiatric disorders, have discovered high rates of comorbidity (in childhood and adulthood), have been unable to differentiate biological factors from continuing social adversity^{ref1, ref2}, and have not taken into account the possible effects of any treatment received (such as continuing morbidity as a result of toxic side effects of drug treatment and the experience of psychosocial adversity and decreased self worth arising from becoming a psychiatric patient). Leading researchers claim that childhood depression resembles adult depression. However, based on symptoms alone, children do not show many of the symptoms said to be common in adult depression (such as loss of weight and appetite, sleep disturbance, and feelings of guilt). Instead more non-specific symptoms such as irritability, running away from home, decline in schoolwork, and headaches are described as indicative of childhood depression. The problem with context deprived notions of childhood problems is that they lead to context deprived, often medicalised, solutions of dubious value that may carry considerable risks. The increase in rates of childhood depression in Western society may reflect a lowering of the threshold for the diagnosis arising from a change in the meaning we give to childhood unhappiness. However, there may also be a genuine increase in the amount of unhappiness experienced by children as a result of growing up in a cultural context that has seen huge changes in child rearing practices, family structures, lifestyles, and education. Changes in Western economies, working practices in competitive global markets, and capitalism's need for never ending growth mean that more parents feel forced to work for longer hours. State support for children and families has been cut (particularly in the 1980s and 1990s), resulting in widespread child poverty. With the increase in the number of divorces and 2 working parents, fathers and mothers are around their children for less of the day, contributing to a generation of "home aloners": children who have largely to raise themselves. Much evidence suggests that children and adolescents in the West experience greater mental health problems as a result of these sociocultural changes. In the second half of the last century, rates of psychosocial problems (such as crime, suicidal behaviour, anxiety, unhappiness, and substance abuse) increased sharply among children and adolescents in Western societies. Understanding the impact of these adverse social changes is likely to be vital in helping us develop appropriate interventions for unhappy children. For example, an increase in family decay (from factors such as divorce rates) is associated with increases in youth violence, substance misuse, and suicide^ref. Context deprived models, such as childhood depression, that conceptualise problems in individualistic terms and therefore lead to individualistic interventions (such as pharmacotherapy and cognitive therapy) push more context rich interventions (such as systemic ones) to the margins. We need a multiperspective approach to both assessment and treatment of unhappy children and their families. Such an approach should normalise emotional responses to adverse life experiences, emphasise more positive approaches (such as building on existing strengths and resilience), and engage more systemic biopsychosocial interventions (including biological factors such as diet, exercise, and cognitive abilities). Medical researchers need to develop a more creative dialogue with researchers from other disciplines (such as sociology) to integrate within-body perspectives with broader ones. Childhood depression as an individualised, context depleted label that offers little explanatory power and can marginalise more helpful, context rich explanations, may first need to be abandoned before more comprehensive theory and practice with regard to children's unhappiness can emerge^ref. However, some are concerned at the underemphasis on possible consequences of depression, such as school failure, social withdrawal, antisocial behaviour, substance misuse, family disharmony, and suicide, which are more than just potential comorbidities. Psychoeducation is an important component of treatment : this includes acknowledging that some life experiences can be more difficult than others, particularly losses; that sleep can be improved by exercise; that mood can be improved by activity scheduling; and that an emphasis on the positive is more likely to help than a focus on the negative. But some cannot see that this is enough; nor do they think that child mental health professionals can in general change the contexts that contribute to adolescent depression, such as schools that pressurise, parents who are too busy, or friends who are unsupportive. Is it enough to refer such young people to psychologists or psychotherapists? The idea that the symptoms of depression in children are different from those in adults is not new. But this does not mean that treatments have to be different. On the contrary, available evidence suggests that those treatments effective for adults are also effective for adolescents^{ref1, ref2}. Despite the debate about suicidal ideation with some antidepressants, a consensus seems to have emerged that fluoxetine is both effective and safe^ref. The danger of abandoning the diagnosis of depressive disorder is that the evidence base for effective psychological and pharmacological treatments may also be disregarded. Just because depression is on a continuum with unhappiness is hardly a reason for not setting a cut-off point for treatment. Applying the same argument to blood pressure could lead to an epidemic of preventable strokes and renal disease. Child psychiatrists who treat adolescents with severe depression know that both psychological therapies and antidepressants work: the more severe the depression, the more likely are the benefits to outweigh the risks^ref.

Pediatric immunology

• lymphadenopathies in children :
• characterizing the disease (never pathognomonic) : e.g.
• regional lymphadenitis / cat-scratch disease (Bartonella henselae)
• lymphomas
• atypical mycobacteria (before age 5)
• not to be ignored (e.g.
• HHV-4 / EBV (bilateral)
• Toxoplasma gondii
• Brucella spp.
• rheumatoid arthritis (RA)
• sarcoidosis
• hypersensitivity to hydantoin
• lymphadenitis due to pyogenic bacteria
• streptococcal pharyngitis
• to be ignored
• measles virus
• HHV-3 / VZV
• aspecific reactive hyperplasia / lymphatism (bilateral : angulomandibular, occipital or inguinal)
• pseudolymphadenopathies :
• cysts of thyroglossal duct (72%), sometimes suppurating
• branchial cysts (acute, painless, on the middle third in front of the sternocleidomastoid muscle)
• fever : between age 1 and 10 yrs, fever lasting > 2-3 weeks may be due to :
• infections
• bacteria
• Bartonella henselae (also distal ileitis)
• Bartonella quintana
• Bartonella bacilliformis
• Borrelia recurrentis
• Borrelia burgdorferi sensu latu
• Coxiella burnetii
• Salmonella typhi
• Treponema pallidum subsp. pallidum
• Mycobacterium tuberculosis
• Plasmodium spp
• Burkholderia pseudomallei
• Leptospira interrogans
• Neisseria meningitidis (chronic meningococcemia)
• Brucella melitensis
• rat-bite fever (Spirillum minus and Streptobacillus moniliformis)
• acute rheumatic fever
• protozoa
• Leishmania donovani
• Babesia spp.
• fungi
• Histoplasma capsulatum
• Coccidioides immitis
• viruses
• LCMV
• dengue virus
• YFV
• Colorado tick fever virus
• non-influenza respiratory viruses
• HHV-4 / EBV
• HHV-5 / CMV
• noninfectious
• Crohn's disease (anemia, nocturnal abdominal pain, no intestinal symptomatology)
• malingering in victims of bullism (exagerated cough disappearing during bedtime)
• hereditary periodic fever syndromes
• periodic fever, aphthous stomatitis, pharyngitis, and adenopathy syndrome (PFAPA syndrome) / Marshall syndrome
• Weber-Christian disease (panniculitis)
• Behcet disease
• SLE
• leukocytoclastic angioitis
• Sweet syndrome
• Castleman's disease
• early onset sarcoidosis
• fever of unknown origin (FUO) : vomiting and diarrhea occur in 50% of extraintestinal infections; the younger the children, the less apparent are symptoms and sign in severe diseases : in the first 3 month of life the clinical examination is not sufficient to identify severe bacterial infection (e.g. there are occult bacteremias and in meningitis lumbar puncture is required as the swellin of fontanelles could be due also to the endocranial hyperhidrosis due to fever)
• in immunocompetent babies
• 0-28 days
• 29-90 days
• 3-36 months
• immunocompetent babies
• newborns < 28 days : meningitis and sepsis
• breastfed < 3 months : severe bacterial infections (10-15%)
• breastfed and babies aged 3 months to 3 years : occult bacteremia in 1.5% (higher likelihhod if T > 39°C and WBC > 150,000/mL)
• hyperpirexia > 40°C
• petechial fever : bacteremia and meningitis (N.meningitidis, H.influenzae b, S.pneumoniae)
If sepsis occurs admit the children to hospital and evaluate past vaccinations : hexavalent vaccination has eradicated occult bacteremias due to Hib and 90% of those due to S.pneumoniae (it also eliminated carrier status)
Negative predictive values for bacterial infections :
• CRP < 40 mg/dl : 95%
• PCT < 9 mg/L : 97%
• WBC < 15,000/ml : 90%
• negative urinary stick : 98%
Therapy : if > 39°C or risk of febrile convulsions => antipyretics (aspirin may cause Reye's syndrome in babies), sponging with water at RT
Febrile convulsions when T > 39°C : generalized tonic-clonic convulsions lasting seconds to a few minute followed by postepileptic sleepiness. If lasting > 15' => toxic or infectious aetiology (viral URT infections, exanthema criticum, and acute otitis media > meningitis)
Epidemiology : 9 months - 5 years (peak between 14 and 18 months : prevalence = 3-4%)
Aetiology : usually positive family history (autosomal dominant trait)
Pathogenesis : febrile seizures are frequent during early childhood, and prolonged (complex) febrile seizures are associated with an increased susceptibility to temporal lobe epilepsy. The pathophysiological consequences of febrile seizures have been extensively studied in rat pups exposed to hyperthermia. The mechanisms that trigger these seizures are unknown, however. A rise in brain pH is known to enhance neuronal excitability. Hyperthermia causes respiratory alkalosis in the immature brain, with a threshold of 0.2–0.3 pH units for seizure induction. Suppressing alkalosis with 5% ambient CO₂ abolished seizures within 20 s. CO₂ also prevented 2 long-term effects of hyperthermic seizures in the hippocampus: the upregulation of the I_h current and the upregulation of CB1 receptor expression. The effects of hyperthermia were closely mimicked by intraperitoneal injection of bicarbonate^ref
Laboratory examinations : no EEG for single convulsion (always nonepileptic tracing), only for atypical convulsion (> 15', more days (50% of babies), focal, at risk for epilepsy on the basis of family history, onset before month 9, atypical, neuropsychological developmental delay : RR= 9)
Therapy : antipyretics; AED prophylaxis is not recommended (0.3 mg/kg p.o. diazepam is the gold-standard for sustained convulsions with few side effects; phenytoin and carbamazepine are uneffective, phenobarbital is effective to prevent relapsing febrile convulsions, but may reduce cognitive functions; sodium valproate is effective but use is unjustified due to side effects)
• childhood vaccinations (Italian laws)
• type I hypersensitivities
• type IV hypersensitivities
• autoimmune diseases
• type I diabetes mellitus => diabetic ketoacidosis
• rheumatic fever
• celiac disease (asymptomatic, low stature)
• inflammatory bowel diseases (IBDs)
• juvenile rheumatoid arthritis (JRA)
• primary sclerosing cholangitis (PSC)
• Kawasaki's disease
• monogenic immune disorders

• pediatric oncology : to retest previous findings that childhood cancers are probably initiated by prenatal exposures to combustion process gases and to volatile organic compounds (VOCs); and to identify specific chemical hazards, birth and death addresses of 22,500 fatal child cancers in Great Britain between 1966 and 1980 were linked with high local atmospheric emissions of different chemical species. Among migrant children, distances from each address to the nearest emissions "hotspot" were compared. Excesses of outward over inward migrations show an increased prenatal or early infancy risk. Maps of emissions of many different substances were published on the internet by the National Atmospheric Emissions Inventory and "hotspots" for 2001 were translated to map coordinates. Child cancer addresses were extracted from an earlier inquiry into the carcinogenic effects of obstetric radiographs; and their postcodes translated to map references. Significant birth proximity relative risks were found within 1.0 km of hotspots for carbon monoxide, PM₁₀ particles, VOCs, nitrogen oxides, benzene, dioxins, 1,3-butadiene, and benz(a)pyrene. Calculated attributable risks showed that most child cancers and leukaemias are probably initiated by such exposures. Reported associations of cancer birth places with sites of industrial combustion, VOCs uses, and associated engine exhausts, are confirmed. Newly identified specific hazards include the known carcinogens 1,3-butadiene, dioxins, and benz(a)pyrene. The mother probably inhales these or related materials and passes them to the fetus across the placenta^ref.
• blood cell tumors (70%)
• malignant fibrous histiocytoma
• acute lymphoblastic leukemia (B-ALL)
• acute myelocytic leukemia (AML)
• AML-M4 / acute myelomonocytic leukemia
• AML-M5 / acute monocytic leukemia
• AML-M7 / acute megakaryocytic leukemia (AMKL)
• transient myeloproliferative disorder (TMD) in babies with Down syndrome
• chronic myeloid leukemia (CML)
• Hodgkin's disease (HD)
• non-Hodgkin's lymphomas (NHL) :
• diffuse large B-cell lymphoma (DLBL / DLBCL) (25%)
• Burkitt's lymphoma (BL) / African lymphoma (30%)
• T-cell acute lymphoblastic leukemia (T-ALL) (40%)
• peripheral T cell non-Hodgkin's lymphoma (5%)
• anaplastic large T/null cell lymphoma
The decade-long investigation United Kingdom Childhood Cancer Study, which compiled information from studies of > 10,000 children, including 1,737 with leukaemia, concludes that infection is a far more important factor. By identifying the exact types of infections involved, one might be able to prevent some cases of leukaemia : exposure to infections very early in life may help to develop children's immune systems and protect them against developing tumours in later years. Their work agrees with previous studies that have shown no connection between power lines and leukaemia. Leukaemia accounts for 33% of all cancers in children under the age of 15, mostly affecting industrialized countries. The disease commonly strikes infants in the first 2-4 years of life, and is treated with aggressive chemotherapy. About 80% of those affected survive the first 5 years following diagnosis. Researchers first proposed a link between childhood leukaemia and viruses such as measles in the 1920s. 5 decades later, researchers discovered that viruses were to blame for the onset of leukaemia in cats and cattle. And one particular virus has been found to be a trigger for a rare form of leukemia that occurs primarily amongst adults in Japan. But it took the UK assessment to convince researchers of a credible link between infection and most types of leukaemia. Infections induce a proliferation of WBCs in bone marrow as part of the normal immune response. In those genetically predisposed to leukaemia, the infection could cause an uncontrolled proliferation of cells, leading to cancer. Exposure to pathogens in the first year of life may help to train a child's immune system to somehow prevent this : the incidence of childhood leukaemia in East Germany before reunification was 33% less than its Western counterpart. This may be in part because every 3-month-old infant in East Germany was sent to playgroups, exposing them to a healthy dose of disease. From a survey of > 9,000 UK children, it concludes that infants who attend group day care twice a week in the first few months of life are half as likely to develop childhood leukaemia. US and Finnish studies have suggested that the Hib vaccine against acute respitory infection helps to protect against childhood leukaemia, but many details about the biological mechanisms remain unknown.
Web resources : Leukemia Research Foundation
• solid tumors (30%)
• childhood brain tumors (CBT) (16% of all childhood malignancies)

Epidemiology : the second most common pediatric malignancy, have an incidence of 21.3 to 24.5 cases per million children (15 years or younger) per year. Every year in the USA, approximately 1500 to 2000 children are affected by one of these tumors. About 50% of pediatric brain tumors are malignant.
• PNS neuroblastoma
• medulloblastomas/PNET (21%)
• high-grade gliomas (HGGs)
• ependymomas (9%)
• germ cell tumors
• brain stem tumors
• chordoma
Nonmalignant CBTs (50% of CBTs) comprise an eclectic group of pathologic entities that have fascinating clinical features. Many of these tumors demonstrate a favorable prognosis :
• low-grade gliomas (LGGs) (19%) (most common class of pediatric brain tumor)
• supratentorial LGGs (35% of all pediatric CNS tumors)
• cerebellar LGGs (10%-20% of all pediatric CNS tumors)
• astrocytomas (52% of all CBTs)
• low grade astrocytomas (such as cerebellar astrocytomaand optic pathway glioma)
• subependymal giant cell astrocytomas
• diffuse intrinsic pontine gliomas
• pilocytic astrocytoma
• fibrillary astrocytoma
Therapy : The optimal treatment of unresectable or recurrent childhood LGGs is undefined. The major goals of therapy for unresectable LGGs are to reverse or arrest the progression of tumor growth and neurologic deficits (e.g., visual loss, diencephalic syndrome, and cranial neuropathies) and to minimize the side effects of treatment. While cranial irradiation may prolong survival, it is also associated with detrimental neurocognitive and endocrine effects when applied to young children. Chemotherapy potentially offers treatment with less neurodevelopmental toxicities to children with progressive, unresectable LGGs. Regimens that have been shown to cause tumor shrinkage and increase progression-free survival have included carboplatin and vincristine and the combination of PCVT. These regimens have significant toxicities that limit their utility. > 10% of children treated with carboplatin and vincristine develop allergic reactions to carboplatin, often requiring cessation of treatment. The PCVT regimen includes carcinogenic agents that preclude its use in patients with neurofibromatosis and place all treated children at risk for the development of secondary leukemias. Additionally, CCNU and procarbazine are cumulatively myelotoxic and produce occasional hepatic and pulmonary toxicities. Temozolomide is a second-generation DNA alkylating agent that has in vitro activity against many chemotherapy-resistant tumors. It has almost 100% oral bioavailability, can cross the blood-brain barrier, demonstrates linear pharmacokinetics, and has minimal, noncumulative myelotoxicity. Pilot studies of temozolomide in adults with high-grade and low-grade glial tumors have shown it to be active, producing objective radiographic responses. The initial studies used a regimen of temozolomide 150 mg/m² per day for 5 days of treatment every 28 days. A subsequent regimen of temozolomide 75 mg/m² per day for 6 to 7 weeks at a time has been piloted in patients with malignant gliomas and has been found to be well tolerated and to provide a greater delivered dose over time. The initial phase I study suggested that the continuous dosing regimen was more efficacious than the 5-day regimen, but this finding was not confirmed in a subsequent phase II study.
Prognosis : LGGs that are completely resected have 5- and 10-year survival rates of nearly 100%. However, complete resections are possible only in approximately 80% of patients with cerebral and cerebellar tumors and 40% of patients with diencephalic tumors. Unfortunately, incomplete resection results in 5- and 10-year survival rates of only 50% and 38%, respectively.
• central neurocytomas
• dysembryoplastic neuroepithelial tumor
• choroid plexus papilloma
• craniopharyngioma
Therapy : about 25% of patients are treated with surgery alone, 40% undergo surgery plus radiation, and 30% are treated with surgery, radiation, and chemotherapy (particularly for nonresectable tumors and in infants, for whom the adverse effects of radiation therapy are severe)
Prognosis : the current 5-year survival rate for all pediatric CNS tumors is 67%, but rates differ considerably among tumor types. Survivors of childhood brain tumors are at substantial risk for increased morbidity and late mortality. 5-year survivors of brain tumors are 13 times more likely to die than healthy age- and sex-matched peers. Disease recurrence remains the single most common cause of late deaths (70%). Neurological, neurocognitive, and endocrine disturbances are the most prevalent disabilities observed among long-term survivors of pediatric brain tumors.
• childhood renal cancers (Wilms' tumor)
• rhabdomyosarcoma (5-15% of all malignant solid childhood cancer)
• osteosarcoma
• Ewing's sarcoma
• testicular cancers
• retinoblastoma
• odontogenic cancers
• rhinopharyngeal cancers
• cardiac rhabdomyoma
• cardiac fibroma
• lung cancers
• pleuropulmonary blastoma (PPB) in infants and young children
• bronchioloalveolar carcinoma (BAC) in older children and adults
• blood vessels cancers
• lymph vessels cancers
• colon cancers
• skin cancers
• endocrine cancers
• adenohypophysis cancers
• thyroid cancers
• parathyroid cancers
• islet cell tumor / nesidioblastoma
• adrenal cortex cancers
• pheochromocytoma
• chemodectoma / nonchromaffin paraganglioma
• pineal gland cancers
• ovarian cancers
Prevention : metaanalyses suggested lower risks associated with having been breast-fed of 9% (95% CI = 2-16%) for acute lymphoblastic leukemia (B-ALL) 24% (3-40%) for Hodgkin's disease (HD) and 41% (22-56%) for neuroblastoma, with little between-study heterogeneity. The estimates for Hodgkin's disease and neuroblastoma, however, were driven by single studies. There was little evidence that breast-feeding was associated with acute nonlymphoblastic leukemia, non-Hodgkin's lymphoma, central nervous system cancers, malignant germ cell tumors, juvenile bone tumors, or other solid cancers^ref.
Prognosis : physical impairment and social life goals among adult long-term survivors of childhood cancer :
• high school or university education is as high as in the general population
• occupation is as high as in the general population
• marriage : patients of both genders were married less than expected
• quality of life (QOL) : patients with leukemia (112 cases), non-Hodgkin's lymphoma (34) or Hodgkin's lymphoma are reported to have the highest QOL. In contrast, patients with tumors of the CNS have the highest frequency of sequelae and the lowest score for health-related QOL. They-also present the lowest educational achievement, the lowest proportion of employment and, among males, the lowest frequency of marriage^ref
• pediatric hematology:
• erythroblastosis fetalis or neonatorum / congenital or hemolytic anemia of newborn / hemolytic disease of the newborn (HDN)
• lymphadenitis
• Langerhans cell histiocytosis (LCH) before age 5
• asplenia
• thymic aplasia
• Kostmann infantile agranulocytosis
• anemia (< 10.5 g/dl). Newborns have higher [2,3-BPG]_plasma than adult
• anemia of inflammation : normocytic, or possibly microcytic, mild to moderate anemia with a normal peripheral blood smear following mild infections with fever, antimeasles vaccination^ref (reversible and unrelated to iron deficiency in most cases), ... : first or second cause of anemia in pediatric patients^{ref1, ref2, ref3, ref4}. In 50% of cases after 9-14 days there is a decrease in sideremia, transferrin saturation, ferritin which comes back to normal within 3 month. IL-1 and TNF-a inhibit Epo incretion^{ref1, ref2}, while activation of macrophages increases clearanc of RBCs^ref.
• iron deficiency anemia : there is a higher requirement during growth (expecially in the first 2 years of life and in adolescence). Breastfeeding satisfies iron requirements for the first 6 months even if the mother is sideropenic. Cow milk impair iron absorptions. Anemia is a late sign of iron deficiency. When the newborn doubles his body mass, iron storages (maternal plasma, colostrum) are exhausted and transferrin saturation decreases => iron deficient erythropoiesis => decreased soluble transferrin receptor (sTfR) marks beginning of tissue sideropenia (inflammation-independent marker).
• sickle cell anemia (SCA)
• thalassemia
• hemorrhages : 33% of children presenting with recurrent epistaxis have a diagnosable coagulopathy
• early onset (0-24 hours)
• localization :
• encephalic hematoma
• subgaleal
• intracranial
• gastrointestinal
• umbilical
• intraabdominal
• aetiology and risk factors :
• drugs assumed by mother during pregnancy (phenobarbital, phenytoin, warfarin, rifampicin, isoniazid)
• inherited coagulopathy
• von Willebrand disease (the commonest)
• Bernard-Soulier syndrome
• fibrinogen deficiency
• factor V deficiency
• factor VII deficit / Alexander's disease
• combined factor V and VII deficiency
• mild factor VIII deficiency / hemophilia A / classical or true hemophilia
• factor IX / PTC deficiency / hemophilia B / Christmas' disease
• factor XI deficit / hemophilia C / Rosenthal's disease
• factor XIII deficiency
• Wiskott-Aldrich syndrome
• prevention and therapy :
• avoid high-risk drugs
• vitamin K administration at birth or to mother before delivery (20 mg)
• classic onset (2-7 days; prevalence = 2%)
• localization :
• gastrointestinal
• nasal, ear, and throat mucosae
• intracranial
• abundant bleeding at site of injections or surgical operations (e.g. circumcision)
• cutaneous and gastrointestinal bleeding
• aetiology and risk factors :
• vitamin K deficiency
• breastfeeding (low vitamin K concentration, expecially when intestinal microflora is not developed or hepatopathies prevent absorption)
• prevention and treatment : vitamin K administration at birth
• late onset (2-6 months; prevalence varies according to disease)
• localization :
• intracranial
• gastrointestinal
• cutaneous
• nasal, ear and throat mucosae
• injection site
• intrathoracic
• aetiology and risk factors
• cholestasis (biliary atresia, cystic fibrosis, hepatitis)
• abetalipoproteinemia
• idiopathic in breastfed Asian babies
• warfarin ingestion
• prevention and therapy : vitamin K administration p.o. or i.v. during cholestatic period
• PAI deficiency
• hemorrhagic disease of the newborn
• chronic hepatopathies
• DIC
• thrombocytopenia
• thrombotic thrombocytopenic purpura (TTP)
• autoimmune or idiopathic thrombocytopenic purpura (ITP)
• neonatal alloimmune thrombocytopenia
• TAR
• splenomegaly
• coagulation inhibitor : SLE (LAC)
• vitamin C deficiency
• malnutrition
• chronic GR agonists
Web resources : Associations : European Society for Pediatric Hematology & Immunology (ESPHI)

• associations
• Children's Oncology Group (COG) is a National Cancer Institute-supported clinical trials cooperative group devoted exclusively to childhood and adolescent cancer research.
• National Childhood Cancer Foundation (NCCF)
• Association of Pediatric Oncology Nurses (APON)
• Cancer Source Kids
• Candlelighters Childhood Cancer Foundation
• Candlelighters Childhood Cancer Foundation Canada
• Children Hospice International
• Off Treatment for Acute Lymphoblastic Leukemia
• journals
• Journal of Pediatric Hematology/Oncology
• International Journal of Pediatric Hematology/Oncology

• dysodontiasis
• prepubertal periodontitis
• juvenile periodontitis
• caries
• congenital epulis
• acute pharyngitis
• tonsillitis
• congenital malformations of the esophagus
• congenital diaphragmatic hernia (CDH)
• Caroli's disease
• congenital malformations of the small bowel
• infantile hypertrophic pyloric stenosis (IHPS)
• meconium ileus
• intussusception
• congenital megacolon
• juvenile or retention polyps
• juvenile intestinal polyposis
• imperforate anus
• neonatal jaundice => kernicterus. Neonatal bilirubin production is about 6-8 mg/kg/24h (vs. 3-4 mg/kg/24 hrs in adulthood). Newborns eliminate more bilirubin monoglucuronide than adults. In the fetus, hydrophobic BMG and BDG, have to be deconjugated by tissue b-glucuronidases to allow transplacental transit. After birth, intestinal and colostrum glucuronidases contribute to enterohepatic recirculation and eventually to hyperbilirubinemia
• prehepatic jaundice
• icterus praecox
• resorption of cephalohematoma
• icterus gravis neonatorum / erythroleukoblastosis
• eryhroblastosis fetalis
• hereditary spherocytosis
• hepatic icterus
• physiologic jaundice
• breast milk jaundice
• epidemic jaundice / hepatitis A
• homologous serum jaundice / human serum jaundice / hepatitis B
• Dubin-Johnson syndrome
• Crigler-Najjar syndrome
• Gilbert syndrome
• Rotor's syndrome
• Lucey-Driscoll syndrome
• posthepatic icterus : cholestatic jaundice

Epidemiology : 1 case every 2,500 newborns
Aetiology :
• extrahepatic (5%) :
• choledocholithiasis
• biliary perforation
• stenosis
• congenital dilatation
• mixed (50%) :
• biliary atresia
• primary sclerosing cholangitis (PSC) with neonatal onset
• intrahepatic (45%)
• infections
• fetopathies
• perinatal bacterial infections
• postnatal urinary tract infections
• Alagille syndrome
• cystic fibrosis (CF)
• a₁ antitrypsin deficiency
• alteration of the bile acid metabolism
• mitochondrial diseases
• peroxisomal diseases
• Niemann-Pick disease type 2 (NPD2)
• Gaucher disease
• transient neonatal cholestasis is due to immaturity of bile secretion and leads to hypoxia/ischemia, bacteremia, and delayed enteral feeding within 7 days
Symptoms & signs : hyperbilirubinemia doesn't causes pruritus in the first 3 months of life as cutaneous receptors are not mature yet
• diarrhea
• meconiorrhea

• North American Society for Paediatric Gastroenterology, Hepatology and Nutrition (NASPGHAN / NASPGAN)
• European Society for Paediatric Gastroenterology and Nutrition (ESPGAN)
• Società Italiana di GastroEnterologia Pediatrica (SIGEP)

Pediatric gynaecology

• vulvovaginitis

Pediatric andrology

• cryptorchidism
• varicocele
• hypospadias
• epispadia
• gynecomastia

Pediatric endocrinology

• infantile hypothyroidism
• Hashimoto's thyroiditis
• rickets
• congenital adrenal hyperplasia (CAH)
• type I diabetes mellitus => diabetic ketoacidosis
• obesity
• delayed puberty
• precocios puberty
• short stature
• primary hyperlipidemias / familial hyperlipoproteinemias

• pyeloureteral joint stenosis
• vesicoureteral reflux
• enuresis
• autosomal recessive PKD

Pediatric urology

• vesical exstrophy
• epispadia
• hypospadias
• phymosis
• hematuria
• proteinuria

Pediatric pneumology

• acute rhinitis
• sinusitis
• laryngotracheobronchitis
• cystic fibrosis
• infant respiratory distress syndrome (IRDS)
• hyalinous membrane disease (HMD) / surfactant deficiency syndrome
• meconium aspiration syndrome (MAS)
• congenital atelectasis
• pneumonia
• congenital pulmonary airway malformation (CPAM)
• pulmonary hypoplasia
• pulmonary or bronchopulmonary sequestration (BPS)
• congenital cystic adenomatoid malformation (CCAM)
• bronchial or bronchogenic cyst

Pediatric dermatology

• erythema toxicum neonatorum
• Gianotti-Crosti syndrome
• Sweet syndrome
• measles virus
• mumps virus
• rubella virus
• HHV-3 / VZV

Pediatric orthopedics

• craniostenosis
• congenital torticollis
• scoliosis and kyphosis
• congenital hip luxation
• clubfoot
• fibromatosis colli : a firm, fusiform, fibrous mass in the midportion of the sternocleidomastoid muscle, usually occurring between 2 weeks and 2 months of age, and commonly disappearing in 4-8 months; in some instances, torticollis may develop. It is believed by some to be a small hematoma due to injury to the muscle at birth.

Pediatric surgery

• neonatal surgery :
• esophageal atresia
• diaphragmatic herniation
• prepyloric web
• pyloric web
• gastroschisis
• prune belly syndrome
• inguinal hernia
• epigastric hernia
• duodenal atresia
• annular pancreas
• jejunoileal atresia
• biliary atresia
• congenital diaphragmatic hernia (CDH)
• colonic atresia
• anorectal malformations
• omphalocele
• meconium ileus
• intestinal malrotation
• general pediatric surgery
• acute abdomen
• in newborn
• without sepsis : intestinal occlusions
• esophageal atresia
• duodenal atresia
• jejunoileal atresia
• colonic atresia
• intestinal malrotation
• volvolus
• Ladd's syndrome +/- volvolus
• internal hernia, expecially mesocolic hernia
Onset :
• 30% within 1 week
• 50% within 1 month
Symptoms & signs : biliary or bloody vomiting, abdominal distension
Complications : intestinal ischemia (superior mesenteric artery) => peritonitis, melena, RDS
Laboratory examinations :
• direct abdomen X-rays shows volvulus neonatorum, double boil (as in duodenal atresia, but less dilated)
• opaque enema : zig-zag configuration or duodenum and jejunum
Therapy : derotation + resection of Ladd's bands => second look after 24-48 hours if necrotic endings, nonphysiological repositioning
• innervation defects : Hirschprung's disease
• biliary ileum
• meconium ileus
• infantile hypertrophic pyloric stenosis (IHPS)
• with sepsis
• meconium peritonitis
• necrotizing enterocolitis (NEC) (pneumoperitoneum with intestinal pneumatosis)
• gastrointestinal perforation (pneumoperitoneum without intestinal pneumatosis)
• spontaneous
• secondary to atresias
Symptoms & signs : abdominal distension (half abdomen if superior duodenal occlusion, whole abdomen if ileal or colonic occlusion), no expulsion of meconium, persistent vomiting (duodenal occlusions if within 1 hr since meal; ileal or colonic occlusions within 24 hrs since meal; biliary vomiting in subvaterian occlusions (light green, gelly, poor), nonbiliary vomiting in supravaterian occlusions (normal meconium))
Laboratory examinations :
• prenatal echographic suspect diagnosis with polyhydramnios
• anal inspection to exclude anorectal malformations
• digital rectal exploration (DRE) to detect meconium plug, rectovesical or rectovaginal fistulas
• direct anteroposterior or laterolateral abdomen X-rays in orthostasis to assess shape, number and location of hydroaereal levels : the distinction between small and large bowel is difficult in premature newborns due to incomplete intestinal rotation. Opaque rounded images suggest volvolus, while dilated loop with fecal shadows and small extraintestinal (grouped or isolated) calcifications due to in utero meconium peritonitis with healed intrauterine perforation. Physiologically after delivery you can see air in
• stomach after the first vagitus
• small bowel after 1 hour
• right colon and caecum after 4 hours
• sigma and rectum after 9 hours
• in infant
• requiring surgical treatment :
• with sepsis :
• acute appendicitis (after age 4)
• primary peritonitis
• without sepsis :
• intestinal invagination (usually at age 6-10 months, at transition from milky to solid diet)
• acute intestinal constipation (faecalomas)
• Meckel's diverticulum
• internal hernia or external hernia
• adhesion- or malrotation mediated intestinal occlusions
• ovarian torsion
• meconium ileus
• Chilaiditi's syndrome
• ventriculoperitoneal shunt
• requiring medical treatment :
• acute nonspecific abdominal pain (ANSAP)
• urinary tract infections (UTI)
• mesenteric lymphadenitis
• gastroenteritis
• Yersinia enterocolitis
• hemolytic-uremic syndrome (HUS)
• acute leukemia
• right basal pneumonia
• acute pancreatitis
• acute cholecystitis
• inflammatory bowel diseases (IBDs)
• pseudomembranous colitis
Symptoms & signs : pain, vomiting, gastrointestinal bleeding, abdominal distension, palpable mass
Timing :
• isolated (acute appendicitis) => general conditions and hydratation status
• relapsing acute abdomen : acute pancreatitis, adhesions
• chronic abdominal pain
• childhood renal cancers or adrenal mass
• choledocus cyst
• hepatic and splenic lesions
• inguinal and umbilical hernias
• cervical diseases (thyroid, cysts of thyroglossal duct, branchial cysts, adenopathies, ...)
• pediatric oncological surgery
• thyroid cancers
• testicular cancers
• liver cancer
• ovarian cancers
• childhood renal cancers
• adrenal cancers
• childhood brain tumors
• rhabdomyosarcoma
• teratoma
• pediatric uro-andrological surgery
• hydrocele
• cryptorchidism
• varicocele
• hypospadias
• epispadia
• phymosis
• pyeloureteral joint stenosis
• vesicoureteral reflux
• megaureter
• ureterocele
• pediatric mini-invasive surgery
• nonpalpable testis diagnosis
• mullerian rests diagnosis and treatment
• intersexual statuses diagnosis and treatment
• ovarian cysts diagnosis and treatment
• appendicectomy
• cholecystectomy
• GERD therapy
• colon, renal, adrenal, and splenic diseases

• American Pediatric Surgery Association (APSA)
• British Association of Pediatric Surgeons (BAPS)
• European Pediatric Surgeons' Association (EUPSA)
• World Federation of Associations of Pediatric Surgeons (WOFAPS)

• perinatal diseases (24.2%) : 25% would be preventable. Very low birth weight (VLBW) infants (0.63%) represent 40% of deaths in the first month of life. Increasing the number of neonatologists and intensive care beds would improve survival rates. The average recovery duration for natural and caesarean delivery is 3 and 4 days, respectively (in USA uncomplicated delivery is rembursated by the health ensurance and this has led to day hospital deliveries). The countries were caesarean delivery is most used are USA (due to ensurance reasons) > Brazil > Italy. In USA a law against early postpartum discharge improved newborn follow-up, adverse events and health maintenance organization (HMO) expenditures^ref. Both social (e.g. immigrants) and cultural factors (e.g. religions) impair service access.
• immaturity (34.4%)
• asphyxia (28%)
• malformations (22%)
• other (15%)
• accidents/trauma (11.1%)
• respiratory apparatus (3.5%)
• neurological diseases (3.3%)
• other (3.3%)
• sudden infant death syndrome (SIDS)

first year	1-4 years	5-14 years	15-24 years	1-14 years
perinatal causes : IUGR/LBW neonatal respiratory diseases newborn affected by maternal complications of pregnancy newborn affected by placental, umbilical cord and adnexal diseases perinatal infections intrauterine hypoxia/neonatal hypoxia congenital anomalies suddent infant death syndrome (SIDS) accidents and similar events (respiratory) infections	traumas congenital anomalies malignant neoplasms homicides and legal intervention cardiopathies respiratory infections	traumas  malignant neoplasms homicides and legal interventions congenital anomalies cardiopathies suicide	traumas homicide malignant neoplasms cardiopathies	malformations (3%) accidents (10%) neurological diseases (2.2%) neoplasms (4.7%) others (7.1%)

Web resources :

• Associations (see also Italian associations) :
• American Academy of Pediatrics (AAP)
• American Pediatric Society & Society for Pediatric Research (APS-SPR)
• Union of National European Paediatric Societies and Associations (UNEPSA)
• Society for Pediatric Pathology (SPP)
• Pediatric Oncall
• The Hospital for Sick Children

Copyright © 2001-2014 Daniele Focosi. All rights reserved  |  Terms of use  | Legal notices
About this site  |  Site map  |  Acknowledgements |  Current link partners
 Abbreviations and acronyms  |  Medical terminology  |  Add a link  |  Translate   |  Softwares |  Cite this page!

---

---

SearchEntrezNCBI Web Site-------------PubMedGeneLocusLinkTaxonomyProteinNucleotideStructureGenomeBooksCancerChromosomesConserved Domains3D DomainsGEO ProfilesGEO DatasetsHomoloGeneJournalsMeSHNLM CatalogOMIMPMCPopSetPubChem BioAssayPubChem CompoundPubChem SubstanceSNPUniGeneUniSTS for

Search AboutAltaVistaAsk JeevesDictionaryDirectHitExciteFindWhatGoogleGoogle GroupsHotBotLookSmartLycosMetacrawlerMetaLocateNorthern LightOpen DirectorySnapThesaurusWebcrawlerYahoo for

Search Medical Dictionary  for