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G. Falk, MD

Co-Director, University of Nevada, Reno School of Medicine

Ductal closure is delayed in infants with pulmonary hypertension and respiratory failure as a consequence of acidosis or persistence of low oxygen tensions; in such circumstances, prostaglandin E2 levels remain high. The increased pulmonary blood flow is associated with a decrease in pulmonary compliance. The typical ductal murmur is systolic (in about 75% of cases), but it can be continuous and is best heard at the upper-left sternal edge. As the pulmonary vascular resistance falls, the left-to-right shunt through the ductus increases and the peripheral pulses become bounding. This reflects the widened pulse pressure due to blood being shunted from the high-pressure systemic circulation into the lower pressure pulmonary circulation. The left-to-right shunt means higher blood flow in the lungs, resulting in the infant being tachypneic, and crackles heard at the lung bases. The diagnosis can be confirmed by echocardiography; echocardiographic signs of a ductal shunt precede the development of overt clinical signs by on average 3 days. Echocardiographic examination is also important to exclude other congenital heart abnormalities. This is less likely in infants born between 23 and 25 weeks of gestation; such infants are also more likely to be refractory to treatment. Diuretics are frequently given, but theoretically furosemide might promote ductal patency via its effect on renal prostaglandin synthesis; administration of furosemide before each dose of indomethacin is not recommended because it can result in significant increases in serum creatinine and hyponatremia and no increase in urine output. These results, however, have not been confirmed in a study that has included infants routinely exposed to antenatal corticosteroids and postnatal surfactant. Indomethacin is a nonselective cyclooxygenase inhibitor, reducing the synthesis of prostaglandin E. Ductal closure is achieved with indomethacin treatment in 48 hours in approximately 70% of infants. Administration by infusion rather than bolus is associated with less alteration in cerebral, renal, and mesenteric circulation, but the clinical meaning of such an effect remains uncertain. Like indomethacin, ibuprofen also inhibits both isoforms of the cyclooxygenase inhibitor, but it appears to have less impact on urine output. The risk of treatment failure is increased by sepsis and more common in very immature infants. This can occur when the pulmonary capillary pressure is greater than the plasma oncotic pressure or there is disruption of the barriers between the vascular space and the lung interstitium. In addition, cardiac arrhythmias, particularly tachyarrhythmias, can result in an acute onset of heart failure and pulmonary edema. Fluid accumulates if the lymphatic system is overloaded, and thus pulmonary edema also occurs if there are abnormalities of the pulmonary lymphatic drainage. Initially, any excess fluid builds up in the interstitium; however as the fluid accumulates it disrupts the alveolar membrane, and fluid fills the alveoli. The infant with pulmonary edema is tachycardic, pale, and sweaty and has poor volume peripheral pulses with reduced cardiac output. The chest radiograph demonstrates perihilar shadowing obscuring the vascular structures. Cardiac causes of pulmonary edema can be diagnosed from the echocardiogram or electrocardiogram. Chest radiograph of an infant with patent ductus arte- Fluid input should be restricted and fluid overload avoided. Diuretic treatment is given to reduce the circulating volume and the clinical manifestations of pulmonary edema, but it may critically lower the cardiac output. Pulmonary hemorrhage is a severe form of lung edema with leakage of red cells and is better named hemorrhagic pulmonary edema. In most cases, the amount of blood lost is small because the hematocrit of the lung effluent is less than 10%. Infants who suffer a massive pulmonary hemorrhage deteriorate suddenly with copious bloody secretions appearing from the airway.

The newborn can survive at least 20 minutes of complete oxygen deprivation as the neonatal brain can metabolize lactate and ketones. In addition, infants have large glycogen stores in their brain, liver, and myocardium, which can be metabolized anaerobically to produce energy. Growth-retarded infants, who have low glycogen stores, are less able to withstand oxygen deprivation. Birth depression can result in hypoxic ischemic encephalopathy, convulsions, and abnormal neurodevelopmental outcome. Affected infants may also suffer myocardial ischemia and heart failure, pulmonary hemorrhage, and acute tubular necrosis. Respiratory distress is worsened by asphyxia as pulmonary blood flow falls during asphyxia, but after the asphyxia has ceased there is a reactive hyperemia. This is associated with fluid transudation and edema; the protein-rich edema fluid inhibits surfactant function, and any persisting academia inhibits surfactant synthesis. A low Apgar score at 5 minutes is associated with the development of long-term neurologic problems. Delivery Room Resuscitation Approximately 10% of infants require some form of resuscitation, and approximately 2% require intubation and positive pressure ventilation. Routine oropharyngeal suction should not be undertaken as it will inhibit the onset of respiratory effort if applied too vigorously. This is most easily achieved using a round facemask and a T-piece in the inspiratory line, as bag-and-mask systems produce more variable inflation pressures and tend to deflate in less than 1 second. Intubation and ventilation should be undertaken in infants in whom facemask ventilation fails to produce an improvement in oxygen saturation or respiratory efforts within 30 seconds or who have a heart rate that is either below 60 bpm at birth or falls despite basic resuscitation using the same ventilatory settings. Results from randomized trials have highlighted that the onset of spontaneous breathing and crying were significantly delayed in infants being resuscitated with 100% oxygen rather than air and that the use of air significantly reduces mortality and tends to reduce the incidence of severe hypoxic ischemic encephalopathy. External cardiac massage should be commenced in all infants whose heart rate is below 60 bpm and who fail to improve within 30 seconds of onset of adequate ventilatory support. Cardiac massage is best achieved by placing both hands around the chest so that the thumbs are over the lower part of the sternum and the fingertips close to the spine. The sternum is then depressed by one third of the diameter of the chest, approximately 2 cm. A ratio of three compressions to one inflation, with a rate of 120 "events" (that is 90 compressions and 30 inflations) per minute is recommended. If the heart rate fails to improve on commencing external cardiac massage, adrenaline should be given. Naloxone should not be given to the newborns of opiate-addicted mothers, as this will precipitate acute withdrawal symptoms. Group O Rh-negative blood (10 ml/ kg body weight) should be given over 5 to 10 minutes if the infant is hypotensive due to blood loss. It is important, however, to consider any underlying conditions that may make the infant difficult to resuscitate. On one hand, they often have insufficient surfactant in their lungs, which results in low compliance. This indicates that high inflation pressures should be used, yet there is evidence that the use of excess ventilatory tidal volumes (volutrauma) may increase the incidence of chronic lung disease. It is important to maintain normal body temperature during the stabilization of very premature infants; plastic bags or plastic wrapping in combination with overhead radiant heat is more effective than the conventional drying and wrapping approach. The phasic transition from inspiration to expiration is modulated by input from the slowly adapting pulmonary stretch receptors and pontine neurons; suppression of either input prolongs inspiration (apneusis). The rhythm is transmitted to spinal motor neurons and cranial premotor neurons; the latter control the activity of airway muscles. Afferents from the forebrain, hypothalamus, central and peripheral chemoreceptors, muscles, joints, and pain receptors are integrated into the "center. The excitatory neurotransmitter, glutamate, excites receptors involved in generating 360 Respiratory Disorders in the Newborn and transmitting respiratory rhythms to spinal and cranial respiratory neurons. Opioids (endorphins and exogenous drugs) decrease respiration by peripheral and central actions; the latter are due to suppression of recurrent excitation by glutaminergic inputs within the primary respiratory network. Deficiency of glycinergic inhibition in knockout mice results in a slower frequency of breathing. Central and peripheral chemoreceptors modify respiratory activity in response to changes in blood gases.

In this approach, a second set of primers is designed against sequences that were localized internally in the sequences that were amplified in the first round. Discrimination within or between species can be also accomplished by digesting the amplicons with restriction endonucleases. Detection of rhinovirus genetic material by reverse tran- scriptase polymerase chain reaction and its differentiation from enteroviruses. Rhinovirus (lanes 1 to 6) is detected as a single band with approximately 190 base pairs (bp) consisting of two almost identical bands. This easily allows differentiation from a poliovirus isolate (lane 10), whose amplicon remains undigested (~380 bp) and from a coxsackie virus (lane 11), which produces a duplet (~175 and 200 bp, respectively). Each primer pair demands different conditions for optimal target amplification, and therefore increased attention is needed upon development of this technique. Recent developments in this method include semi-quantitation of results with the use of specialized equipment and primers specific for additional viral and bacterial species. Heteroduplex formation between the amplicons may result in differential mobility of the product when run in a gel, and can be used for subtyping viral genomes. Thus, the specificity of the method is tested by the melting curves at which the final amplicon is briefly heated to denature. The continuously measured fluorescence data recorded during this last stage are plotted against the temperature and allow calculation of the melting peak that characterizes a given amplicon under the conditions used. When the melting peak of a particular product coincides with the standard, it is considered specific. Limitations in the number of viruses and viral serotypes are inherent in the real-time approach, especially in the protocols using a labeled probe, because most platforms do not allow the simultaneous use of more than two fluorochromes. In their approach, the specific probes were labeled with different fluorochromes. Molecular methods allowing for simultaneous detection of 7 to 26 different viruses at the same time have been attempted. If the complementary bases are present in the viral sequence, then successful amplification will occur. Using an inkjet oligonucleotide synthesizer, these oligonucleotides are synthesized in situ and placed onto directed locations of a glass wafer. Human and cellular transcripts are also included to normalize against nonspecific hybridization. This material is labeled with cyanin 5 or cyanin 3, which provides red or green coloring, respectively, to allow color visualization of microarray data that are obtained after the arrays are scanned with confocal laser scanners and analyzed with suitable instrumentation and software. This method allows the detection of paramyxoviruses, orthomyxoviruses, AdVs, and picornaviruses from clinical samples. Although it is extremely promising, this technique needs further evaluation, including cost-effectiveness, before being applied in clinical practice. However, false-positive or false-negative findings can be a problem, if certain practical measures in the handling of viral genetic material are not meticulously followed. First, preservation of the sample is of particular importance for the integrity of the viral genomic material. In this case, dilution of the sample or treatment with a suitable agent such as dimethyl sulfoxide may facilitate detection of the virus. If contamination occurs, replacement of the pipettes is required, as well as a review of laboratory and handling practices. Techniques to Diagnose Respiratory Viruses in Clinical Practice Threatening influenza pandemics and mortal epidemics of previously unknown respiratory viruses. Moreover, large epidemiologic studies are required to better define the involvement of these viruses in noninfectious diseases. These studies will help in drug development and the implementation of intervention strategies, even during an outbreak. It is not possible to determine the optimal method for virus detection because many factors vary, depending on the particular conditions and the scope of the analysis (cost-effectiveness, time required, sensitivity, availability of skilled personnel, and laboratory equipment). A combination of methods, rather than a single one, is best used in particular cases because most protocols are not ideal or do not provide enough information. Their commercial availability, ease of performance, and rapidity have made antigenbased methods increasingly popular, especially in small units that lack advanced facilities. However, they can be inferior to cell culture in terms of sensitivity and are of limited value for the detection of some respiratory viruses.

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If families meet certain income criteria, the government offers tax credits to help pay for insurance. Inability to process the essential amino acid phenylalanine, which accumulates and damages the brain. Can lead to severe mental retardation unless detected soon after birth and treated with a special formula and a low-protein diet, continued indefinitely. Genetic metabolic disorder with mild to severe symptoms, which can lead to mental retardation or death. Lack of an enzyme that converts the amino acid homocysteine into cystathionine, needed for normal brain development. Untreated, leads to mental retardation, eye problems, skeletal abnormalities, and stroke. Treatment consists of a special diet, one or more vitamins (B6 or B12), and other supplements (betaine). Buildup of citrulline and ultimately ammonia, which untreated can lead to seizures, coma, brain damage, and death. Treatment with lowprotein diet, medications to prevent ammonia buildup, and nutritional supplements allows normal development. Buildup of argininosuccinic acid and ultimately ammonia, leading to brain swelling, coma, and sometimes death. Treatment consists of a low-protein diet, frequent meals, medications to prevent ammonia buildup, nutritional supplements, and sometimes liver transplant. Lack of an enzyme that causes the byproducts of the amino acid tyrosine, particularly a very toxic compound (succinylacetone), to build up in the liver. Without early diagnosis and prompt treatment when needed, can lead to brain damage, low muscle tone, cerebral palsy-like symptoms, and death. Inability to process leucine, leading to low blood sugar and accumulation of several organic acids, especially after illness or missed meals. Defect in an enzyme that activates several other enzymes, leading to buildup of lactic acid and other organic acids. Symptoms, including skin rashes and hair loss, usually begin between birth and 15 months. Defect in processing four amino acids, resulting in illness in first week of life. Severity varies, but death during first month and lifelong brain damage are common. Treatment includes low-protein diet, vitamin B12 injections, and nutritional supplements. Can lead to buildup of acids in blood, brain damage, seizures, paralysis, coma, and death. Defect in processing leucine, leading to brain damage, seizures, liver failure, and infant death, or sometimes no symptoms until adulthood. Defect in processing four amino acids leading to illness in newborns, including brain damage, coma, and death. Even with treatment, which includes a low-protein diet and nutritional supplements, some children have development delays, seizures, increased muscle tone, frequent infections, and heart problems. Periodic episodes of acid buildup, often triggered by illness, which can lead to coma, brain damage, and death. Intravenous treatment to regulate blood sugar and blood acid levels can permit normal development. March of Dimes Organic Acid Metabolism Disorders Isovaleric acidemia (<1 in 100,000). Can cause coma, brain damage, or death in infancy, or emerge later in childhood after infectious illness. Early diagnosis and treatment with low-protein diet and nutritional supplements allow most children to develop normally. Inadequate levels of an enzyme that helps break down the amino acids lysine, hydroxylysine, and tryptophan, which are building blocks of protein. Often unrecognized for up 67 Fatty Acid Oxidation Disorders Medium-chain acyl-CoA dehydrogenase deficiency (>1 in 25,000).