Risk factors for neonatal death and stillbirth (weak predictive value):- African American race- Advanced maternal age- History of fetal demise- Maternal infertility- History of small for gestational age infant- Small for gestational age infant- Obesity- Paternal age- Poverty and poor quality of careSo in this case the risk factor is the parental unemployment

An important predictor of the foetal well-being is the evaluation of amniotic fluid volumes, commonly done using ultrasonography. Amniotic fluid index (AFI) is calculated by measuring the largest vertical diameter of the fluid pocket in all four quadrants of the uterine cavity and then added together. Oligohydramnios or decreased amniotic fluid volume can be defined as an AFI less than 5cm and occurs in about 4-5% of the pregnancies. It is associated with a number of foetal abnormalities and complications. Foetal abnormalities that lead to oligohydramnios include: premature rupture of membranes, intrauterine growth retardation, and congenital foetal abnormalities among others. A single umbilical artery is an anatomical defect of the umbilical cord, which leads to IUGR, uteroplacental insufficiency and may be associated with multiple congenital abnormalities as well, which all ultimately lead to the development of oligohydramnios. Foetal hydrops, developmental dysplasia of the hip and, macrosomia lead to polyhydramnios. Cleft palate is not associated with any of them.

Alpha-fetoprotein (AFP) is a plasma protein produced by the embryonic yolk sac and the fetal liver. AFP levels in serum, amniotic fluid, and urine functions as a screening test for congenital disabilities, chromosomal abnormalities, as well as some other adult occurring tumours and pathologies.Pregnant maternal serum AFP levels are elevated in:- Neural tube defects (e.g., spina bifida, anencephaly)- Omphalocele- Gastroschisis- posterior urethral valves- nephrosis- GI obstruction- teratomas

Polycythaemia is described as an abnormal increase in the red cell mass. As this influences hyper-viscosity, a peripheral venous sample of blood haematocrit can be used to determine the packed cell volume. Polycythaemia is present if the venous haematocrit is >65% or <22g/dl if converted into a haemoglobin value. Though it is the method of choice for screening, capillary blood samples obtained though heel pricks in new-born may be as much as 15% higher than venous samples and thus high values must be confirmed with a venous sample.

Benign neonatal sleep myoclonus (BNSM) is a disorder commonly mistaken for seizures during the new-born period. It is characterized by myoclonic lightninglike jerks of the extremities that exclusively occur during sleep| it is not correlated with epilepsy.Causes of neonatal seizures:Hypoxic-ischemic encephalopathy: Hypoxic-ischemic encephalopathy disrupts the ATP-dependent sodium-potassium pump and appears to cause excessive depolarization.Intracranial haemorrhage: occurs more frequently in premature than in term infants. Subarachnoid haemorrhage is more common in term infants. This type of haemorrhage occurs frequently and is not clinically significant. Typically, infants with subarachnoid haemorrhage appear remarkably well. Metabolic disturbances include hypoglycaemia, hypocalcaemia, and hypomagnesemia. Less frequent metabolic disorders, such as inborn errors of metabolism, are seen more commonly in infants who are older than 72 hours. Typically, they may be seen after the infant starts feeding.Intracranial infections (which should be ruled out vigorously) that are important causes of neonatal seizures include meningitis, encephalitis (including herpes encephalitis), toxoplasmosis, and cytomegalovirus (CMV) infections. The common bacterial pathogens include Escherichia coli and Streptococcus pneumoniae.Cerebral malformationsBenign neonatal seizures

Meconium aspiration syndrome (MAS) refers to breathing problems that a new-born baby may have when: – There are no other causes, and- The baby has passed meconium (stool) into the amniotic fluid during labour or deliveryThe most recent guidelines are as follows:- If the baby is vigorous (defined as having a normal respiratory effort and normal muscle tone), the baby may stay with the mother to receive the initial steps of new-born care. A bulb syringe can be used to gently clear secretions from the nose and mouth.- If the baby is not vigorous (defined as having a depressed respiratory effort or poor muscle tone), place the baby on a radiant warmer, clear the secretions with a bulb syringe, and proceed with the normal steps of new-born resuscitation (i.e., warming, repositioning the head, drying, and stimulating). If, after these initial steps are taken, the baby is still not breathing or the heart rate is below 100 beats per minute (bpm), administer positive pressure ventilation.Resuscitation should follow the same principles for infants with meconium-stained fluid as for those with clear fluidContinued care in the neonatal intensive care unit (NICU):Maintain an optimal thermal environment to minimize oxygen consumption.Minimal handling is essential because these infants are easily agitated. Agitation can increase pulmonary hypertension and right-to-left shunting, leading to additional hypoxia and acidosis. Sedation may be necessary to reduce agitation.An umbilical artery catheter should be inserted to monitor blood pH and blood gases without agitating the infant.Continue respiratory care includes oxygen therapy via hood or positive pressure, and it is crucial in maintaining adequate arterial oxygenation. Mechanical ventilation is required by approximately 30% of infants with MAS. Make concerted efforts to minimize the mean airway pressure and to use as short an inspiratory time as possible. Oxygen saturations should be maintained at 90-95%.Surfactant therapy is commonly used to replace displaced or inactivated surfactant and as a detergent to remove meconium. Although surfactant use does not appear to affect mortality rates, it may reduce the severity of disease, progression to extracorporeal membrane oxygenation (ECMO) utilization, and decrease the length of hospital stay.

Neonatal hypoglycaemia is a common yet serious condition characterized by blood sugar levels less than 2.2mmol/L during the first 3 days of life and less than 2.5mmol/L later on. There are multiple aetiologies and various risk factors that lead to hypoglycaemia in new-borns like prematurity, sepsis, inborn errors of metabolism, and maternal diabetes- induced hyperinsulinism in the new-born. Among the inborn errors of metabolism, fatty acid oxidation defects can lead to persistent hypoglycaemia in new-borns. One such defect is the medium- chain acyl CoA dehydrogenase deficiency, which is the enzyme needed for the breakdown of medium- chain fatty acids.

The baby is not clearing CO2 normally despite normal oxygenation so we should increase the delta P. Higher delta P will increase tidal volume and hence CO2 removal.After initial resuscitation and stabilization, the following should be the ventilator settings used:Rate: 30-40/minutePeak inspiratory pressure (PIP) – determined by adequate chest wall movement.An infant weighing less than 1500 grams: 16-28 cm H2O.An infant weighing greater than 1500 grams: 20-30 cm H2O. Positive end expiratory pressure (PEEP): 4 cm of H2O OR 5-6 cm if FiO2 > 0.90.FiO2: 0.4 to 1.0, depending on the clinical situation.Inspiratory time: 0.3-0.5 sec.After 15 to 30 minutes, check arterial blood gases and pH.If the PaO2 or the O2 saturation is below accepted standards, the FiO2 can be raised to a maximum of 1.0. If the PaO2 or O2 saturation is still inadequate, the mean airway pressure can be raised by increasing either the PIP, PEEP, inspiratory time or the rate, leaving inspiratory time constant.If the PaCO2 is elevated, the rate or peak inspiratory pressure can be raised.

The perinatal mortality rate is defined as the number of perinatal deaths per 1000 total births. Perinatal death includes the death of a live-born neonate within 7-days of life (early neonatal death) and the death of a fetus ≥ 22 weeks of gestation (stillbirth). Hence, the perinatal mortality rate is calculated by dividing the number of still births+ the number of early neonatal deaths by 1000 births.

The baby most likely has umbilical granuloma – granulation tissue may persist at the base of the umbilicus after cord separation| the tissue is composed of fibroblasts and capillaries and can grow to more than 1 cm.Medical therapy is indicated only when an infection is present.Silver nitrate application to umbilical granulomas is usually successful. One or more applications may be needed. Care must be taken to avoid contact with the skin. Silver nitrate can cause painful burns. Small umbilical granulomas with a narrow base may be safely excised in the office setting. Large granulomas and those growing in response to an umbilical fistula or sinus do not resolve with silver nitrate and must be surgically excised in the operating room setting.

The spinal muscular atrophies (SMAs) comprise a group of autosomal recessive disorders characterized by progressive weakness of the lower motor neurons. several types of spinal muscular atrophies have been described based on age when accompanying clinical features appear. The most common types are acute infantile (SMA type I, or Werdnig-Hoffman disease), chronic infantile (SMA type II), chronic juvenile (SMA type III or Kugelberg-Welander disease), and adult-onset (SMA type IV) forms.SMA type I – Acute infantile or Werdnig-Hoffman diseasePatients present before 6 months of age, with 95% of patients having signs and symptoms by 3 months. They have severe, progressive muscle weakness and flaccid or reduced muscle tone (hypotonia). Bulbar dysfunction includes poor suck ability, reduced swallowing, and respiratory failure. Patients have no involvement of the extraocular muscles, and facial weakness is often minimal or absent. They have no evidence of cerebral involvement, and infants appear alert.Reports of impaired fetal movements are observed in 30% of cases, and 60% of infants with SMA type I are floppy babies at birth. Prolonged cyanosis may be noted at delivery. In some instances, the disease can cause fulminant weakness in the first few days of life. Such severe weakness and early bulbar dysfunction are associated with short life expectancy, with a mean survival of 5.9 months. In 95% of cases, infants die from complications of the disease by 18 months.

The origins of the neural tube and the nape of the neck where nuchal translucency measurements are taken are from embryonic ectoderm.The structural development of the head and neck occurs between the third and eighth weeks of gestation. The 5 pairs of branchial arches, corresponding to the primitive vertebrae gill bars, that form on either side of the pharyngeal foregut on day 22 are the embryologic basis of all the differentiated structures of the head and neck. Each arch consists of 3 layers: an outer covering of ectoderm, an inner covering of endoderm, and a middle core of mesenchyme. These arches are separated further into external, ectoderm-lined pharyngeal clefts and internal, endoderm-lined pharyngeal pouchesA population of ectodermal cells adjacent to the neural fold and not included in the overlying surface (somatic) ectoderm gives rise to the formation of the neural crest. These neuroectodermal crest cells are believed to migrate widely throughout the developing embryo in a relatively cell-free enriched extracellular matrix and differentiate into a wide array of cell and tissue types, influenced by the local environment. Most connective and skeletal tissues of the cranium and face ultimately come from the derivatives of neural crest cells.

A preterm with respiratory distress syndrome presents with the condition as a result of immature lungs and inadequate surfactant production. Management of RDS therefore includes surfactant therapy, oxygen administration and mechanical ventilation, as well as measures such maintaining acid base levels and blood haemoglobin in an intensive care unit. Dexamethasone is not shown to be particularly effective when given to a preterm, but can however be used to prevent or decrease RDS severity when given to the mother before delivery.

Time- EventWeek 1: ImplantationWeek 2: Formation of bilaminar diskWeek 3: Formation of primitive streakFormation of notochordGastrulationWeek 4: Limb buds begin to formNeural tube closesHeart begins to beatWeek 10: Genitals are differentiated

Certain CHDs may present with a differential cyanosis, in which the preductal part of the body (upper part of the body) is pinkish but the post ductal part of the body (lower part of the body) is cyanotic, or vice versa (reverse differential cyanosis). The prerequisite for this unique situation is the presence of a right-to-left shunt through the PDA and severe coarctation of the aorta or aortic arch interruption or severe pulmonary hypertension. In patients with severe coarctation of the aorta or interruption of the aortic arch with normally related great arteries, the preductal part of the body is supplied by highly oxygenated pulmonary venous blood via the LA and LV, whereas the post ductal part is supplied by deoxygenated systemic venous blood via the RA, RV, main pulmonary artery (MPA) and the PDA. In the new-born with structurally normal heart, a differential cyanosis may be associated with persistent pulmonary hypertension of the new-born. In the cases of TGA with coarctation of the aorta or aortic arch interruption, the upper body is mostly supplied by systemic venous blood via the RA, RV, and ascending aorta, whereas the lower body is supplied by highly oxygenated pulmonary venous blood via the LA, LV, MPA, and then the PDA. For accurate detection of differential cyanosis, oxygen saturation should be measured in both preductal (right finger) and post ductal (feet) parts of the body.

Physiological jaundice is the condition in which there is a yellow discolouration of the eyes and the skin of the baby caused by the build up of bilirubin in the blood due to an immature liver. No other symptoms accompany physiological jaundice, thus it will not present with difficulty in feeding. All the other conditions listed can present with feeding problems.

The most probable diagnosis for this patient is Maple syrup urine disease (MSUD).Note:- Healthy new-borns have blood sugars between 3.3 and 5 mmol/L- Neonatal hypoglycaemia is glucose < 2.2 mmol/L if measured in the first 3 days of life.- Neonatal hypoglycaemia is glucose < 2.5 mmol/L after the first 3 days of life.Causes of persistent hypoglycaemia include:- Preterm- IUGR- SGA- Hyperinsulinism due to maternal diabetes- Beckwith-Wiedemann syndrome- Hypoxia at birth- Sepsis- Cardiopulmonary disease- Inborn errors of metabolism- Hepatic enzyme deficiencies- Glycogen storage disease

Bilious (green) gastric aspirate or emesis indicates that the intestines are obstructed below the ampulla of Vater.Gastrointestinal (GI) endoscopy is actually considered an essential diagnostic and therapeutic technique. Upper GI endoscopy in neonatal age allows for exploration of the oesophagus, stomach and duodenum| instead lower GI endoscopy easily reaches the sigmoid-colon junction.

Infants may require tracheal intubation if:- direct tracheal suctioning is required- effective bag-mask ventilation cannot be provided- chest compressions are performed- endotracheal (ET) administration of medications is desired- congenital diaphragmatic hernia is suspected, or – a prolonged need for assisted ventilation exists.

Neonatal hyperbilirubinemia is a common clinical condition and can be categorized as conjugated and unconjugated hyperbilirubinemia. Conjugated hyperbilirubinemia results from obstructive or hepatocellular causes mainly. The causes of conjugated hyperbilirubinemia include inborn errors of metabolism like galactosemia and aminoaciduria, obstruction from choledochal cysts, and biliary atresia. Long term TPN also leads to conjugated hyperbilirubinemia. Spherocytosis is a hereditary condition belonging to the group of haemolytic anaemias, resulting from plasma membrane protein deficiency. This defect of the RBC plasma membrane decreases their life span, making them osmotically fragile and prone to haemolysis. This leads to an increase in the unconjugated bilirubin levels, with a risk of developing kernicterus.

Sepsis can be described as a condition in which there is a dysregulated inflammatory response to an infection. In the case of neonates, sepsis can be life threatening and may present with respiratory distress more than 4 hours after birth, shock, seizures, and multi organ failure. Risk factors that further point to sepsis include prolonged rupture of maternal membranes for more than 24 hours before birth, a history of a maternal fever during labour, or parenteral antibiotic treatment given to the mother for a suspected or confirmed bacterial infection.

Shoulder dystocia occurs when the fetal anterior shoulder impacts against the maternal symphysis following delivery of the vertex. Less commonly, shoulder dystocia results from impaction of the posterior shoulder on the sacral promontory. Risk Factors for Shoulder DystociaMaternalAbnormal pelvic anatomyGestational diabetesPost-dates pregnancyPrevious shoulder dystociaShort statureFetalSuspected macrosomiaLabour relatedAssisted vaginal delivery (forceps or vacuum)Protracted active phase of first-stage labourProtracted second-stage labour

Treatment of depression is an important component of maternal and neonatal health. The use of SSRIs and antidepressants in the first trimester are unlikely to carry any congenital risks. However the use of the antidepressants closer to delivery may result in some respiratory, motor, gastrointestinal and central nervous system problems, with the most concerning of these being persistent pulmonary hypertension of the new-born. Other conditions such as cleft palate, jaundice, neural tube defects or floppy baby syndrome have not been shown to occur with SSRI use.

The baby needs more oxygen saturation which could be attempted by increasing the mean airway pressureAfter initial resuscitation and stabilization, the following should be the ventilator settings used:Rate: 30-40/minutePeak inspiratory pressure (PIP) – determined by adequate chest wall movement.An infant weighing less than 1500 grams: 16-28 cm H2O.An infant weighing greater than 1500 grams: 20-30 cm H2O. Positive end expiratory pressure (PEEP): 4 cm of H2O OR 5-6 cm if FiO2 > 0.90.FiO2: 0.4 to 1.0, depending on the clinical situation.Inspiratory time: 0.3-0.5 sec.After 15 to 30 minutes, check arterial blood gases and pH.If the PaO2 or the O2 saturation is below accepted standards, the FiO2 can be raised to a maximum of 1.0. If the PaO2 or O2 saturation is still inadequate, the mean airway pressure can be raised by increasing either the PIP, PEEP, inspiratory time or the rate, leaving inspiratory time constant.If the PaCO2 is elevated, the rate or peak inspiratory pressure can be raised.

Pulmonary surfactant is a lipoprotein complex that is responsible for preventing the collapse of alveoli and increasing lung compliance.It is produced in the endoplasmic reticulum and secreted from the lamellar bodies of type 2 pneumocytes.Surfactant is essential for reducing surface tension at the air-water interface in the alveoli, thus preventing the collapse of alveoli during expiration. It is composed of dipalmitoyl phosphatidylcholine (DPPC), which is a phospholipid.In fetal development, production of surfactant begins around 26 weeks of gestation and reaches mature levels by 35 weeks.The deficiency of surfactant can result in neonatal respiratory distress syndrome or hyaline membrane disease, particularly in premature new-born babies.

The embryonic period comprises of the first 8 weeks of pregnancy. It is divided into a preembryonic phase (from the 1st to the 3rd week), in which the three germinal layers arise, and into the embryonic phase proper (from the 4th to 8th week), in which the embryonic organ anlagen arise.

According per the national guidelines, 5 inflation breaths should be given with a gas pressure of 30cmH2O for term babies. Each breath should be given for 2-3 seconds. Pre-term babies should be aerated with a lower pressure of 20-25cmH2O.

In this particular case, the symptoms and signs are suggestive for congenital dislocation of the hip. There are several risk factors present including, a breech delivery, female gender (female:male = 6:1) and oligohydramnios. It is also more common in the left hip than the right.

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common enzyme deficiency in humans.It has a high prevalence in persons of African, Asian, and Mediterranean descent. It is inherited as an X-linked recessive disorder.G6PD deficiency is polymorphic, with more than 300 variantsG6PD deficiency can present as neonatal hyperbilirubinemia. Besides, persons with this disorder can experience episodes of brisk haemolysis after ingesting fava beans or being exposed to certain infections or drugs. Less commonly, they may have chronic haemolysis. However, many individuals with G6PD deficiency are asymptomatic.Most individuals with G6PD deficiency do not need treatment. However, they should be taught to avoid drugs and chemicals that can cause oxidant stress. Infants with prolonged neonatal jaundice as a result of G6PD deficiency should receive phototherapy with a bili light.

Congenital hypothyroidism results from insufficient levels of thyroid hormone in the body since birth, which is either due to dysgenesis of the thyroid gland or dyshormonogenesis. The important features of this disease include coarse facial features (macroglossia, large fontanelles, depressed nasal bridge, hypertelorism, etc.), failure to thrive, cardiomegaly, hypotonia, umbilical hernia, and low core body temperature among many others. Frontal bossing is the usual feature of rickets and acromegaly. Mitral regurgitation is not usually associated with congenital hypothyroidism.