Kliegman: Nelson Textbook of Pediatrics, 18th ed.

Copyright 2007 Saunders, An Imprint of Elsevier Chapter 394 Aspiration Syndromes John L. Colombo The spectrum of aspiration spans from an asymptomatic condition to acute life-threatening events, such as occurs with massive aspiration of gastric contents or hydrocarbon products. Other chapters discuss mechanical obstruction of large or intermediate-sized airways (as occurs with foreign bodies; see Chapter 384 ) and infectious complications of aspiration and recurrent microaspiration (see Chapter 395 ), such as may occur with gastroesophageal reflux (see Chapter 320.1 ) or dysphagia (see Chapter 303 ). Occult aspiration of nasopharyngeal secretions into the lower respiratory tract is a normal event in healthy people, usually without apparent clinical significance. GASTRIC CONTENTS. Large volume aspiration of gastric contents usually occurs after vomiting; it is an infrequent complication of general anesthesia, gastroenteritis, and an altered level of consciousness. Pathophysiologic consequences can vary, depending primarily on the pH and volume of the aspirate and the amount of particulate material. Increased clinical severity is noted with volumes greater than approximately 0.8 mL/kg and/or pH < 2.5. Hypoxemia, hemorrhagic pneumonitis, atelectasis, intravascular fluid shifts, and pulmonary edema all occur rapidly after massive aspiration. These occur earlier, become more severe, and last longer with acid aspiration. Most clinical changes are present within minutes to 12 hr after the aspiration event. In the next 2448 hr, there is a marked increase in lung parenchymal neutrophil infiltrations, mucosal sloughing and alveolar consolidation that often correlates with increasing infiltrates on chest radiographs. These changes tend to occur significantly later and are more prolonged after aspiration of particulate material. Infection usually does not have a role in initial lung injury after aspiration of gastric contents; aspiration may impair pulmonary defenses, predisposing the patient to secondary bacterial pneumonia. In the patient who has shown clinical improvement but then develops clinical worsening, especially with fever and leukocytes, secondary bacterial pneumonia should be suspected. Treatment. If a patient has had large volume or highly toxic substance aspiration and already has an artificial airway in place, it is important to perform immediate suctioning of the airway. When immediate suctioning cannot be performed, later suctioning or bronchoscopy is usually of limited therapeutic value. An exception to this is if significant particulate aspiration is suspected. Attempts at acid neutralization are not warranted because acid is rapidly neutralized by the respiratory epithelium. Patients suspected of large volume or toxic aspiration should be observed, have oxygenation measured by oximetry or blood gas analysis, and have a chest radiograph taken, even if asymptomatic. If the chest radiograph and oxygen saturation are normal, and the patient remains asymptomatic, home observation, after a period of observation in the hospital or office, is adequate. No treatment is indicated at that time, but the caregivers should be instructed to bring the child back in for medical attention should respiratory symptoms or fever develop. For those patients who present with or develop abnormal findings during observation, oxygen therapy is given to correct hypoxemia. Endotracheal intubation and mechanical ventilation are often necessary for more severe cases. Bronchodilators may be tried, although they are usually of limited benefit. Animal studies indicate that treatment with corticosteroids does not appear to have any benefit, unless given nearly simultaneously with the aspiration event; their use may increase the risk of secondary infection. Prophylactic antibiotics are not indicated, although in the patient with very limited reserve, early antibiotic coverage may be appropriate. If used, antibiotics should be used that cover for anaerobic microbes. If the aspiration event occurs in a hospitalized or chronically ill patient, coverage of Pseudomonas and enteric gram-negative organisms should also be considered. A mortality rate of 5% is seen if 3 or fewer lobes are involved. Unless complications develop, such as infection or barotrauma, most patients will recover in 23 wk, although prolonged lung damage may persist, with scarring and bronchiolitis obliterans.

Prevention. Prevention of aspiration should always be the goal when airway manipulation is necessary for intubation or other invasive procedures. Feeding with enteral tubes passed beyond the pylorus and elevating the head of the bed in mechanically ventilated patients have been shown to reduce the incidence of aspiration complications in the intensive care unit. HYDROCARBON ASPIRATION. The most dangerous consequence of acute hydrocarbon ingestion is usually aspiration and resulting pneumonitis (see Chapter 58 ). Although significant pneumonitis occurs in <2% of all hydrocarbon ingestions, there are an estimated 20 deaths annually from hydrocarbon aspiration in both children and adults. Some of these deaths represent suicides. Hydrocarbons with lower surface tensions (gasoline, turpentine, naphthalene) have more potential for aspiration toxicity than heavier mineral or fuel oils. Ingestion of >30 mL (approximate volume of an adult swallow) of hydrocarbon is associated with an increased risk of severe pneumonitis. Clinical findings of chest retractions, grunting, cough, and fever may occur as soon as 30 min after aspiration, or may be delayed for several hr. Lung radiograph changes usually occur within 28 hr, peaking in 4872 hr. Pneumatoceles and pleural effusions may occur. Patients presenting with cough, shortness of breath, or hypoxemia are at high risk for pneumonitis. Persistent pulmonary function abnormalities can be present many years after hydrocarbon aspiration. Other organ systems, especially the liver, central nervous system, and heart, may suffer serious injury. Cardiac dysrhythmias may occur and be exacerbated by hypoxia and acid-base or electrolyte disturbances. Treatment. Gastric emptying is nearly always contraindicated because the risk of aspiration is greater than any systemic toxicity. Treatment is generally supportive with oxygen, fluids, and ventilatory support as necessary. The child who has no symptoms and a normal chest radiograph should be observed for 68 hr to ensure safe discharge. Certain hydrocarbons have more inherent systemic toxicity. The pneumonic CHAMP refers collectively to these: camphor, halogenated carbons, aromatic hydrocarbons, and those associated with metals and pesticides. Patients who ingest these compounds in volumes >30 mL, such as might occur with intentional overdose, may benefit from gastric emptying. This is still a high-risk procedure that can result in further aspiration. If a cuffed endotracheal tube can be placed without inducing vomiting, this should be considered, especially in the presence of altered mental status. Treatment of each case should be considered individually, with guidance from a poison control center. Other substances that are particularly toxic and cause significant lung injury when aspirated or inhaled include baby powder, chlorine, shellac, beryllium, and mercury vapors. Repeated exposure to low concentration of these agents can lead to chronic lung disease, such as intersitial pneumonitis and granuloma formation. Corticosteroids may help reduce fibrosis development and improve pulmonary function, although the evidence is limited.

Kliegman: Nelson Textbook of Pediatrics, 18th ed. Copyright 2007 Saunders, An Imprint of Elsevier 101.6 Aspiration of Foreign Material (Fetal Aspiration Syndrome, Aspiration Pneumonia) During prolonged labor and difficult deliveries, infants often initiate vigorous respiratory movements in utero because of interference with the supply of oxygen through the placenta. Under such circumstances, the infant may aspirate amniotic fluid containing vernix caseosa, epithelial cells, meconium, blood, or material from the birth canal, which may block the smallest airways and interfere with alveolar exchange of oxygen and carbon dioxide. Pathogenic bacteria may accompany the aspirated material, and pneumonia may ensue, but even in noninfected cases, respiratory distress accompanied by roentgenographic evidence of aspiration is seen ( Fig. 101-6 ). Postnatal pulmonary aspiration may also occur in newborn infants as a result of tracheoesophageal fistula, esophageal and duodenal obstruction, gastroesophageal reflux, improper feeding practices, and administration of depressant medicines.

To avoid aspiration of gastric contents, the stomach should be aspirated using a soft catheter just before surgery or other major procedures that require anesthesia or conscious sedation. If aspiration is sudden and overwhelming, immediate laryngoscopy and suctioning under direct visualization may prevent the aspirated material from reaching the lungs. The treatment of aspiration pneumonia is symptomatic and may include respiratory support and systemic antibiotics (see Chapters 109.8 and 394 ). Gradual improvement generally occurs over 34 days.

Martin: Fanaroff and Martin's Neonatal-Perinatal Medicine, 8th ed., Copyright 2006 Mosby, An Imprint of Elsevier PART 5 Respiratory Disorders in Preterm and Term Infants Martha J. Miller, Avroy A. Fanaroff, and Richard J. Martin The symptoms of respiratory distress, as identified in Part 2, can be caused by a wide diversity of pathophysiologic states during neonatal life. In the differential diagnosis, nonrespiratory etiologies must always be considered. Some examples are thermal instability, circulatory problems, cardiac disease, sepsis, and anemia or polycythemia, all of which are addressed elsewhere. In the preterm infant, respiratory distress syndrome (RDS) frequently dominates the clinical picture, as discussed in Part 3. This section presents an overview of the many other respiratory disorders, both pulmonary and extrapulmonary, that can affect preterm and term infants. MECONIUM ASPIRATION SYNDROME Meconium staining of the amniotic fluid or fetus usually indicates fetal distress. The passage of meconium in utero accompanies 8% to 20% (average, 12%) of all deliveries and is seen predominantly in infants who are small for gestational age (SGA) and postmature, as well as those with cord complications or other factors compromising the in utero placental circulation. Although knowledge of the pathophysiologic stimuli in the fetus that govern the passage of meconium in response to stress is incomplete, this phenomenon is seldom observed before a gestational age of 34 weeks. Meconium aspiration syndrome is believed to occur in about 4% of deliveries complicated by meconium-stained fluid, although the incidence might be declining due to a reduction in the incidence of postmature births. Many infants with meconium-stained amniotic fluid exhibit no signs of depression, although some brief period of asphyxia could have induced the passage of meconium before delivery. Nonetheless, the presence of meconium in the amniotic fluid necessitates careful supervision of labor and close monitoring of fetal well-being. The delivery team must be alerted to the possibility of a depressed fetus, and personnel skilled in newborn resuscitation should be available for the delivery. With appropriate management of the airway, meconium aspiration syndrome and the complications thereof can be substantially reduced. Pathophysiology The quantity of meconium affects the appearance and viscosity of the amniotic fluid, which ranges from a greentinged, lightly meconium-stained fluid to one with a thick, pea-soup consistency. Meconium in the amniotic fluid can stain the umbilical cord, placenta, and fetus. The time from passage of meconium to delivery of the infant can be estimated from the depth of penetration of meconium pigment into the placental membranes with subsequent uptake by placental macrophages. Under normal circumstances, fetal respiration is associated with movement of fluid from the airways out into the amniotic fluid. When the fetus is distressed, gasping may be initiated in utero. Under these circumstances amniotic fluid and particulate matter contained therein can be inhaled into the large airways. The meconium inhaled by the fetus may be present in the trachea or larger bronchi at delivery. Meconium and squames can also be found as far as the alveoli in stillborn infants, and it is widely recognized that meconium aspiration can occur antenatally. After air breathing has commenced, especially if accompanied by gasping respirations, there is a rapid distal migration of meconium within the lung. Thick meconium, fetal tachycardia, and absence of fetal cardiac accelerations on intrapartum monitoring appear to identify the infant at high risk for meconium aspiration syndrome. Predictors of neonatal morbidity from meconium

aspiration, such as a low umbilical artery pH, can serve as a guideline for how vigorously postnatal therapeutic intervention should be pursued. Pulmonary pathophysiology is due to airway obstruction and a ball-valve phenomenon created by the presence of meconium within the airways. Areas of atelectasis develop within the lung, resulting from total small airway obstruction, adjacent to areas of overexpansion from gas trapping in regions with partial obstruction. Air leaks, including pneumomediastinum and pneumothorax, are more likely to occur after aspiration of meconium and cellular debris. Chemical inflammation secondary to aspirated meconium presumably leads to a pneumonitis. In addition, in vitro data have shown a concentration-dependent inhibition of surfactant by meconiumall of which could aggravate atelectasis, hypoventilation, and intrapulmonary shunting secondary to persistent pulmonary hypertension of the newborn (PPHN). Animal models of meconium aspiration syndrome have been used to demonstrate influx of inflammatory cells and protein accompanied by inactivation of endogenous surfactant and a reversible decrease in surfactant protein levels. PPHN can be a major clinical problem in infants with meconium aspiration. The etiology of the increase in pulmonary vascular resistance is somewhat controversial. Hypoxic pulmonary arterial vasoconstriction is most likely a major contributing factor. Murphy and associates applied morphometric techniques to study the pulmonary vascular bed in infants with fatal meconium aspiration In almost all cases there was abnormal muscularization of the smallest intra-acinar arteries that must have developed before birth. Although the pathophysiology of this disorder is incompletely understood, both prenatal and perinatal maladaptation of the pulmonary circulation can contribute to the development of pulmonary hypertension in infants with meconium aspiration syndrome. Clinical Features The infant with meconium aspiration syndrome often exhibits the classic signs of postmaturity with evidence of weight loss, together with nails, skin, and umbilical cord that are heavily stained with a yellowish pigment. These infants often are depressed at birth. In fact, the initial clinical picture can be dominated by neurologic and respiratory depression secondary to the hypoxic insult precipitating the passage of meconium. Respiratory distress with cyanosis, grunting, flaring, retractions, and marked tachypnea soon ensues. Characteristically, the chest acquires an overinflated appearance, and rales can be audible on auscultation. The chest radiograph shows coarse, irregular pulmonary densities with areas of diminished aeration or consolidation. If such infiltrates are a manifestation of retained lung fluid, they would be expected to clear within 24 to 48 hours. Pneumothorax and pneumomediastinum are common in infants with severe meconium aspiration syndrome. Hyperinflation of the chest and flattening of the diaphragm are sometimes noted on the radiograph. Cardiomegaly also might be detected, possibly as a manifestation of the underlying perinatal hypoxia. Arterial blood gases characteristically reveal hypoxemia with evidence of right-to-left shunting. Hyper-ventilation can result in respiratory alkalosis, although infants with severe disease usually have combined respiratory and metabolic acidosis secondary to hypoxia and respiratory failure. One should be alerted to the possible development of PPHN, which frequently accompanies meconium aspiration syndrome and can contribute substantially to morbidity. Management The presence of meconium in the amniotic fluid is not an indication of fetal distress in all infants. Although it is clear that meconium staining of the amniotic fluid can signal fetal hypoxia, if other parameters such as fetal heart rate and pH remain in the normal range, then the outcome is usually favorable. In cases in which thick meconium is detected in the amniotic fluid during labor, the technique of amnioinfusion (injection of normal saline into the amniotic sac) has shown promise in decreasing both morbidity of the infant from meconium aspiration and the frequency of operative delivery. This technique can benefit the fetus by relieving in utero cord compression, which may be the stimulus for passage of meconium by the stressed fetus. The combination of meconium-stained amniotic fluid and ominous fetal heart rate patterns is often associated with significant fetal and neonatal asphyxia with accompanying morbidity, and appropriate interventions should be

instituted. Traditional practice employs a combined obstetric and pediatric approach to reduce the problem of meconium aspiration syndrome. The preventive approach should begin with thorough suctioning of the nose and pharynx by the obstetrician after the head is delivered but before the thorax is delivered and the infant is able to take a breath. Interestingly, a recent multicenter randomized controlled trial concluded that routine intrapartum oropharyngeal and nasopharyngeal suctioning of term-gestation meconium-stained infants does not prevent meconium aspiration syndrome or its complications. These authors believe that consideration should be given to revision of this widely accepted recommendation. Immediately after delivery, one should consider direct visualization of the larynx and endotracheal intubation to remove residual meconium. This approach is imperative if the infant is depressed and there is need for positive pressure ventilation. Endotracheal intubation is often omitted if staining of the amniotic fluid is light and the infant is not depressed. In support of such an approach, Linder and coworkers found no morbidity in a group of meconium-stained infants with Apgar scores greater than 8 at 1 minute who underwent only oropharyngeal suctioning immediately after the infants head had been delivered.Although it is widely accepted that intubation and tracheal suctioning are needed for the depressed infant and possibly in the presence of thick meconium, current data do not support a policy of indiscriminate intubation in vigorous infants, especially with lightly meconium-stained fluid. Box 42-6 Prevention of Meconium Aspiration Syndrome

Resolved Issues Meconium aspiration can develop in utero Careful, thorough suctioning of the oropharynx before the first breath is an important preventive measure Suctioning via endotracheal tube is indicated for depressed infants before initiation of positive pressure ventilation Unresolved Issue The role of meconium thickness in determining management Recommendations All infants with meconium-stained fluid should receive endotracheal suctioning if there is cardiorespiratory depression or need for positive pressure ventilation Endotracheal suctioning is not indicated if meconium is thin, the infant is vigorous at birth, and the oropharynx has been suctioned at delivery Endotracheal suctioning could be considered if: Meconium has a thick, particulate, or pea-soup consistency Oropharyngeal suctioning has not been performed at the perineum Antenatal monitoring shows evidence of fetal distress

This approach has been confirmed by Wiswell and associates in a multicenter, prospective, randomized clinical trial of vigorous infants with meconium-stained fluid of any consistency.[415] Infants received either routine intubation and suctioning or expectant management that comprised routine delivery room care with intubation only if it was

considered clinically indicated. There was no difference between groups in the occurrence of meconium aspiration syndrome or other respiratory disorders, both of which were in the 3% to 4% range. Reported complications of intubation were mild and transient; however, routine intubation offered no advantage in these apparently vigorous meconium-stained neonates. Subsequent management of meconium aspiration syndrome consists of supportive respiratory therapy. Little can currently be done to enhance the mechanisms by which meconium is phagocytosed and removed from distal portions of the respiratory tract. Bacterial sepsis might have precipitated the passage and subsequent aspiration of meconium; therefore, management could include the use of antibiotics. Indeed, bacterial pneumonia is indistinguishable radiographically from meconium aspiration syndrome. Hydrocortisone is of no benefit in the management of this syndrome. Ventilatory assistance is indicated when adequate levels of partial pressure of arterial oxygen (Pao2) cannot be maintained in a high fraction of inspired oxygen (Fio2). Specific details of respiratory management are considered in Part 4 of this chapter. Pao2 should be maintained at the upper recommended levels, that is, 80 to 90 mm Hg, to minimize hypoxic pulmonary vasoconstriction. Assisted ventilation is indicated for impending respiratory failure and might be required for a prolonged period. Infants struggling against the ventilator can benefit from sedation and, rarely, paralysis with pancuronium, and oxygenation can dramatically improve in response to this therapy. Significant morbidity and even mortality can occur in infants who require assisted ventilation. There is no consensus on the optimal ventilator strategy for these patients, and high-frequency ventilation is an option. In the face of intractable hypoxemia, nitric oxide can be considered for pulmonary vasodilation. Because meconium can inhibit surfactant function, there is a role for exogenous surfactant therapy in meconium aspiration syndrome. Although meconium appears to potently inhibit all available surfactant preparations, some, such as surfactant protein (SP)-A containing natural surfactant, appear more resistant to inactivation. A multicenter study of surfactant use in term infants with severe respiratory failure, 50% of whom had a primary diagnosis of meconium aspiration syndrome, demonstrated that surfactant versus placebo therapy significantly decreased the need for extracorporeal membrane oxygenation (ECMO). Bronchoalveolar lavage with dilute surfactant is also under investigationIn infants who do not respond to conventional pulmonary management, inhalation of nitric oxide and ECMO can be lifesaving (see Part 8 of this chapter). The ultimate prognosis can depend not so much on the pulmonary disease as on the accompanying asphyxial insult. No specific long-term deficits in pulmonary function have been attributed to this disorder, although BPD can result from prolonged assisted ventilation. OTHER ASPIRATION SYNDROMES At the time of delivery the neonate can aspirate clear amniotic fluid or fluid mixed with purulent material or blood. It remains unclear whether infants can aspirate a sufficient volume of clear amniotic fluid to interfere with normal ventilation or whether such infants simply exhibit delayed resorption of lung fluid. In deliveries in which the amniotic fluid is purulent, the risk of bacterial pneumonia necessitates appropriate antibiotic therapy after evaluation is made for sepsis. Aspiration of either fetal or maternal blood requires no specific therapy and can resolve rapidly, although massive blood aspiration can masquerade as pulmonary hemorrhage and lead to a clinical picture similar to meconium aspiration. Squamous debris associated with amniotic fluid aspiration can persist in the lung for some days. Unless the material is assumed to be infected, therapy should be merely supportive. Aspiration after regurgitation is most likely to be seen in preterm infants, those with disorders of swallowing, and infants with esophageal atresia and tracheoesophageal fistula. Small preterm infants are at greatest risk when fed excessive volumes per gavage. These infants might initially present with airway obstruction or apnea and subsequently develop respiratory distress, with pulmonary infiltrates visible on radiographs. The severity of disease varies, and it can be indistinguishable from an inflammatory pneumonitis. Aspiration syndromes associated with disorders of the swallowing mechanisms may be suspected from the perinatal history (asphyxia), feeding history (cyanosis, excessive drooling, poor suck), and physical examination. The precise cause, however, might not be readily apparent, and these infants require extensive neurologic evaluation. Neonates

with tracheostomies or gastrostomies are at risk for aspiration. Infants with recurrent aspiration, particularly those with disorders of the swallowing mechanism, present complex management problems. NEONATAL PNEUMONIA The lungs represent a common site for the establishment of sepsis in the neonate. Such infection, whether bacterial or viral in origin, can be acquired before or at the time of birth, or in the early postnatal period. Because bacterial pneumonia carries a substantial mortality in the neonate, an extremely high index of suspicion of infection must be maintained for all infants, preterm and term alike, in whom signs of respiratory distress are observed. Etiology Congenital bacterial pneumonia may be acquired by the fetus via transplacental passage of organisms, although ascending infection from the genital tract before or during labor appears to predominate. It follows that prolonged rupture of membranes is a major predisposing factor, although it is possible that bacteria such as group B streptococci could gain access to the fetus by ascent through intact membranes. Because bacterial colonization of the infant always occurs during vaginal delivery, neonatal pneumonia may well develop in the absence of prolonged rupture of membranes or any maternal symptoms. If the mother has chorioamnionitis, gasping during delivery as a result of fetal asphyxia could predispose the infant to aspirate contaminated amniotic fluid. After the infant is admitted to the neonatal nursery, the risk of acquiring bacterial pneumonia is largely influenced by the rate of nosocomial infection within the hospital environment. Group B streptococci are the major pathogens producing neonatal pneumonia. The organism is characteristically acquired from the maternal genital tract during labor or delivery, and overt group B streptococcal sepsis develops in approximately 1% of infants colonized in this way. This represents an overall infection rate of approximately 1 to 4 per 1000 live births in the absence of large-scale intrapartum prophylaxis with antibiotics. Weisman and associates documented that approximately one third of the infants with group B streptococcal bacteremia are preterm, and the mortality rate is considerably higher in these infants. In 1992, the Committee on Infectious Diseases and Committee on Fetus and Newborn of the American Academy of Pediatrics provided guidelines for prevention of early-onset group B streptococcal disease through intrapartum chemoprophylaxis of maternal group B streptococcal carriers. These guidelines were revised in 1997, and intrapartum chemoprophylaxis with penicillin of mothers who are group B streptococcal positive is recommended. This program has met with success, for there has been a 65% decrease in the incidence of early-onset group B streptococcal sepsis from 1.7 per 1000 births in 1993 to 0.6 per 1000 in 1998. The adoption of chemoprophylaxis for group B streptococcus could alter the spectrum of bacteria that colonize the cervicovaginal area and thus potentially could alter the spectrum of bacterial lung disease in the newborn. Other bacteria that should be considered when pneumonia is acquired in utero or in the immediate perinatal period include Escherichia coli, Klebsiella spp, group D streptococci, Listeria monocytogenes, and pneumococci acquired via transmission from the mother. When neonatal pneumonia develops several days or even weeks after birth, in addition to these organisms, infections from Staphylococcus and Pseudomonas organisms and fungi should be considered. Although infection with Chlamydia trachomatis does appear to be acquired during parturition, pneumonia caused by this organism typically has a gradual onset of respiratory symptoms beyond 3 weeks of postnatal life. Ureaplasma urealyticum is a known cause of maternal chorioamnionitis. This organism has been isolated from the upper and lower respiratory tract of infants with acute respiratory failure or CLD and can contribute to the etiology of these disorders. Viral pneumonia can be acquired by the fetus from transplacental passage of organisms, as may be the case in the congenital intrauterine infections (TORCH syndrome: toxoplasmosis, rubella, cytomegalovirus, herpes simplex virus. Viruses probably also account for a substantial number of postnatally acquired pneumonias. Viral pneumonia is not usually recognized as such in the neonate, although epidemics resulting from respiratory syncytial virus infection and adenovirus have been associated with significant morbidity and mortality. Recent development of a direct fluorescent assay for detecting adenovirus infections could allow rapid diagnosis and appropriate institution of therapy. Bacterial, viral, and fungal pneumonias of later onset are a cause of considerable morbidity in NICUs, and the risk of a subsequent fatal outcome is small but inversely proportional to birthweight.

Clinical Course The nonspecific nature of the clinical signs that are characteristic of neonatal sepsis makes a high index of suspicion the key to early diagnosis. In some cases of severe pneumonia the infants could be totally lacking in pulmonary symptoms and manifest only mild or severe neurologic depression. Other alerting features include thermal instability, apneic spells, abdominal distention, or jaundice. Tachypnea, cyanosis, or other signs of respiratory distress should focus attention on the lungs. Chest radiograph findings range from unilateral or bilateral streaky densities, confluent mottled opacified areas, or a diffusely granular appearance with air bronchograms. Thus, it may be impossible to radiographically differentiate bacterial pneumonia from RDS (particularly when caused by group B streptococci). Problems also may be experienced in differentiating severe neonatal pneumonia on radiograph from widespread meconium aspiration or the profound pulmonary venous congestion associated with total anomalous pulmonary venous return. The difficulty in making a definitive diagnosis of neonatal pneumonia by radiograph has led to the widely accepted practice of administering antibiotics to infants with respiratory distress after appropriate cultures have been obtained. White blood cell count with differential, platelet count, or Gram stain and culture of tracheal aspirate are useful adjuncts to diagnosing neonatal sepsis. However, the Gram stain of tracheal aspirates might not differentiate overt pulmonary infection from early colonization. Detection of group B streptococcal antigen in blood or cerebrospinal fluid by latex particle agglutination can facilitate diagnosis of group B streptococcal sepsis. However, false-positive results can occur, particularly in blood and urine, owing to nonspecific substances that cross-react with group B streptococcal antigens or colonization of mucosal surfaces with group B streptococci. A definitive diagnosis of group B streptococcal sepsis must still be established through direct culture of the organism. If congenital intrauterine infection is suspected, appropriate serologic tests should be performed and specific cord blood immunoglobulins can be measured, although not all infants with intrauterine pneumonia have elevated IgM levels. Chlamydial pneumonitis can be diagnosed by culturing nasopharyngeal or tracheobronchial secretions under appropriate laboratory conditions. Treatment almost invariably is instituted before the pathogenic organism is identified and its antibiotic sensitivities are determined. Broad-spectrum coverage, including a penicillin and an aminoglycoside, is the initial line of treatment. For pneumonia of later onset, agents specific for staphylococcal infection should be added. In small premature infants weighing less than 1500 g, infection with Staphylococcus epidermidis is most prevalent and can require the addition of vancomycin to the antibiotic regimen. Once the responsible bacterium has been isolated and antibiotic sensitivities have been identified, the most effective drug or combination of antibiotics should be continued for 10 days or longer, depending on the infants clinical course. The duration of chlamydial pneumonia in the neonate appears to be shortened by a 14-day course of oral erythromycin. Although antibiotics form the mainstay of treatment, good supportive care is essential. This must include careful fluid management, blood gas monitoring, and ventilatory assistance, as indicated. PPHN can complicate the clinical course of neonatal pneumonia. Animal studies have confirmed that intravenous infusion of group B streptococci rapidly increases pulmonary arterial pressure (with accompanying decrease in cardiac output and oxygenation) These effects can be mediated via thromboxane or prostacycline metabolites.[391] Pulmonary vascular injury also can be aggravated by granulocytes trapped at sites of injury in the neonatal lung.

Aspiration Pneumonitides Pediatric Critical Care Medicine 1st edition thn 2006 Aspiration of a variety of substances can induce severe pneumonitis and respiratory failure. Most commonly, aspiration of gastric contents can occur either as a primary event, often in conjunction with gastroesophageal reflux in infants, or as a secondary event in a patient with altered mental status and impairment of protective airway reflexes.

Aspiration of activated charcoal during attempted decontamination of a toxic ingestion can produce an injury greater than the toxicity of the ingested agent being treated, and caution in use is emphasized. Aspiration of hydrocarbons can produce profound chemical pneumonitis, even with relatively small exposure to these agents. Aspiration of fresh or salt water occurs with near-drowning, inducing a pneumonitis that is associated with impairment of surfactant production irrespective of the type of water ingested. A relatively small amount of water ingestion may produce a significant injury, and the process may be a greater result of inflammatory response to produce ARDS, or from ischemia-reperfusion lung injury due to cardiorespiratory arrest in drowning. Treatment of aspiration pneumonitis is supportive and may require significant ventilatory support. Because surfactant impairment may occur in each of these settings, exogenous surfactant therapy has been suggested but is not proven to be specifically effective. Neither prophylactic antibiotics nor corticosteroids are recommended. If evidence of bacterial infection such as fever, purulent tracheal secretions, or leukocytosis develops, antibiotic choice should include coverage of anaerobic organisms.

Aspiration Pneumonia Current Pediatric Diagnosis and Treatment ed 18th thn 2007 Patients whose anatomic defense mechanisms are impaired are at risk of aspiration pneumonia (Table 182). Acute disease is commonly caused by bacteria present in the mouth (especially gram-negative anaerobes). Chronic aspiration often causes recurrent bouts of acute febrile pneumonia. It may also lead to chronic focal infiltrates, atelectasis, illness resembling asthma or interstitial lung disease, or failure to thrive. Table 182. Risk Factors for Aspiration Pneumonia.

Seizures Depressed sensorium Recurrent gastroesophageal reflux, emesis, or gastrointestinal obstruction Neuromuscular disorders with suck-swallow dysfunction Anatomic abnormalities (laryngeal cleft, tracheoesophageal fistula, vocal cord paralysis) Debilitating illnesses Occult brainstem lesions Near-drowning Nasogastric, endotracheal, or tracheostomy tubes Severe periodontal disease

Clinical Findings Symptoms and Signs

Acute onset of fever, cough, respiratory distress, or hypoxemia in a patient at risk suggests aspiration pneumonia. Chest physical findings, such as rales, rhonchi, or decreased breath sounds, may initially be limited to the lung region into which aspiration occurred. Although any region may be affected, the right sideespecially the right upper lobe in the supine patientis commonly affected. In patients with chronic aspiration, diffuse wheezing may occur. Generalized rales may also be present. Such patients may not develop acute febrile pneumonias. Laboratory Findings and Imaging Chest radiographs may reveal lobar consolidation or atelectasis and focal or generalized alveolar or interstitial infiltrates. In some patients with chronic aspiration, perihilar infiltrates with or without bilateral air trapping may be seen. In severely ill patients with acute febrile illnesses, a bacteriologic diagnosis should be made. In addition to blood cultures, cultures of tracheobronchial secretions and bronchoalveolar lavage specimens may be desirable (see section on Culture of Material from the Respiratory Tract). In patients with chronic aspiration pneumonitis, solid documentation of aspiration as the cause of illness may be elusive. Barium contrast studies may provide evidence of suckswallow dysfunction, laryngeal cleft, occult tracheoesophageal fistula, or gastroesophageal reflux. Overnight or 24-hour esophageal pH probe studies may also help establish the latter. Although radionuclide scans are commonly used, the yield from such studies is disappointingly low. Rigid bronchoscopy in infants or flexible bronchoscopy in older children can be useful in more definitively excluding tracheoesophageal fistula and obtaining bronchoalveolar lavage specimens to search for lipid-laden macrophages, which can suggest chronic aspiration. Differential Diagnosis In the acutely ill patient, bacterial and viral pneumonias should be considered. In the chronically ill patient, the differential diagnosis may include disorders causing recurrent pneumonia (eg, immunodeficiencies, ciliary dysfunction, or foreign body), chronic wheezing, or interstitial lung disorders (see section on Children's Interstitial Lung Disease Syndrome), depending on the presentation. Complications Empyema or lung abscess may result from acute aspiration pneumonia. Chronic aspiration may result in bronchiectasis. Treatment Antimicrobial therapy for acute aspiration pneumonia includes coverage for gram-negative anaerobic organisms. In general, clindamycin is appropriate initial coverage. However, in some hospital-acquired infections, additional coverage for multiply resistant P aeruginosa, streptococci, and other organisms may be required. Treatment of recurrent and chronic aspiration pneumonia may include the following: surgical correction of anatomic abnormalities; improved oral hygiene; improved hydration; and inhaled bronchodilators, chest physical therapy, and suctioning. In patients with compromise of the central nervous system, exclusive feeding by gastrostomy and (in some) tracheostomy may be required to control airway secretions. Gastroesophageal reflux, often requiring surgical correction, is commonly present in such patients.

Prognosis The outlook is directly related to the disorder causing aspiration.