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A BIMONTHLY PAEDIATRICS C.M.E.

NEWSLETTER
EDIT OR : DR. SANW AR AGRA WAL M.D., EKT A INSTITUTE OF CHILD HEAL TH, EDITOR SANWAR AGRAW EKTA HEALTH, SHANTI NAGAR, RAIPUR (C.G.) : 2424745, 2424426-28

MECONIUM ASPIRATION SYNDROME


Dr. N.C. Mathur Consultant Pediatrician Neonatology & Intensive Care Aditya Hospital, Hyderabad Meconium is the green tangent bowel content of an infant, which is usually passed within 48 hours after delivery. Although it seems impossible, this substance of tarry consistency is sterile and composed of swallowed amiotic fluid,salts,mucus,bile and other cellular debris.(1) In and of itself meconium is harmless; however, if the in-utero infant passes meconium into the amniotic fluid, it may cause serios airway obstruction, air trapping, and enhanced growth of bacteria. Thus it becomes a life-threatening entity that must be dealt with immediately. INCIDENCE Meconium staining of the amniotic fluid at the time of delivery occurs in 8% to 15% of all babies delivered, with approximately 5% of this infants acquiring meconium aspiration syndrome (MAS). Western literature suggests approximately 30% of the infants in whom MAS develops will require mechanical ventilation, at least 11% will experience pneumothorax, and greater than 4% will die. (2) Since meconium passage into the amniotic fluid requires strong peristaisis and anai sphinter tone, which is not common in preterm infants, MAS rarely occurs in infants of less than 36 weeks gestational age. (3) The longer a pregnancy is allowed to continue past 42 weeks, the greater the chances are of the passage of meconium. ETIOLOGY AND PATHOPHYSIOLOGY Fetal passage of meconium has long been accepted as a sign of intrauterine stress of hypoxia. theoretically, the infants becomes hypoxic in utero (possibly because of cord or fetal head compression or prolonged labor), which exhausts oxygen reserves, causing a vagal response, relaxed anal sphincter tone, and passage of meconium into the amniotic fluid. The normal intrauterine activity of the neonate involved the movement of small amounts (1 to 5 ml) of amniotic fluid into and out of the upper airways. The potential of aspiration is always present, but chances are increased with hypoxia or stress because of great respiratory effort and possible gasping respiration in utero. Even more damaging is the aspiration that occurs after delivery of the chest when expansion allows the fluid or meconium, or both, to be dispersed even farther into the infants lungs. (4) After delivery, the normal pulmonary mechanisms are hindered and the clinical picture varies drastically. The amount and viscosity or dilution of the meconium present may significantly affect the degree of obstruction that occurs. If the infant has a large amount of very thick meconium in the airways at the time of delivery, complete obstruction with subsequent alveolar and collapse will result. The more typical picture, however, is that of smaller amounts of meconium within amniotic fluid, causing a ball value effect because of partial obstruction during expiration, causing hyperinflation and greatly predisposing the infant to air leaks, inflammation of the airways and secretion production (a normal body response to a foreign substance within the lungs) also occurs, and a chemical pneumonitis often develops. (5,6) Meconium also hinders surfactant, which may lead yo atelectasis and decreased pulmonary compliance. (7) It has been suggested that intrauterine hypoxia not only stimulates the passage of meconium but also causes restructuring of the pulmonary vascular bed. The profound hypoxia may result in pulmonary vasoconstriction, which may be the reason that many infants with MAS quickly develop PPHN. (8) The figure summarizes the pathophysiologic events that occurs with the passage of meconium and MAS. CLINICAL PRESENTATION The infant with MAS is usually a term or a posterm baby who has been delivered through meconium stained fluid (often resembling pea soup) and has already experienced significant intrauterine stress or hypoxia. The history may include prolonged labour, breech delivery, and abnormal cardiac tracings if fetal monitors are used. On completion of delivery, the physical examination often reveals a mature infant with yellowish skin, nails and cord, as well as peeling skin and long finger nails, the sign of post maturity. The umbinical cord may lack or have very little Whartons Jelly. Depending on the extent of stress or hypoxia, the infant is depressed at birth with low Apgar scores; however, some infants have 1-minute scores of 5 or more. The infant quickly exhibits signs of respirations, grunting, retractions, nasal flaring and tachypnea. The respiratory distress is often related to the viscosity of the meconium, with a thicker meconium causing more respiratory symptoms. (4) (8). Auscultation of the chest reveals rales as well as areas of significantly diminished aeration, with the anteroposterior diameter of the chest often increased. The infant may or may not appear to need immediate intervention, depending on the severity of the aspiration and the degree of hypoxia. ABG analysis indicates hypoxemina in infants with mild MAS having a normal pO2 and normal or decreased PaCO2 resulting form the increased respiratory effort. The baby with moderate to severe MAS has increasing hypoxemia and

hypercarbia. A combination of respiratory and metabolic acidosis eventually develops, as the infant is unable to overcome the obstructive and inflammatory processes. This progresses to the point of respiratory faiture and severe hypoxemia, which alerts the physician to the probability of PPHN. (10). The radiographic appearance varies according to the severity of the disease and complications. The typical chest film shows patchy areas of atelectasis due to obstruction, as well as hyperexpansion from air trapping. The radiograph of the infant with severe MAS may reveal total bilateral opacity with only large bronchi distinguishable. Pulmonary air leaks, including PIE, pneumothorax and pneumomediastinum, may also be found. The chest radiograph of the infant with MAS is similar to tht of an infant with pneumonia, especially when a bacterial infection develops. (11). DIAGNOSIS Although the majority of infants are normal, MAS is suspected whenever there is meconium staining of the amniotic fluid. The diagnosis of MAS is generally made whenever meconium is found below the vocal cords and the infant has clinical signs of respiratory distress, including hypoxemia and a characteristic chest radiographic pattern. TREATMENT SUCTIONING Although no prevention has been found for MAS, prompt intervention in the delivery room can make a drastic diffrence in the outcome. To prevent aspiration into the lungs, pharyngeal suction should be performed when the infants head is delivered and before delivery of the thorax ( before the first breath has been taken ). A bulb syringe may be used; however, an 8 or 10 French flexible suction catheter may be more effective in removing thick meconium. Infants born through thick meconium should be intubated and endotracheal suctioning performed in conjuction with ventilation and oxygenation. Saline lavarge has been used to dilute the meconium. Infants with satisfactory Apgar scores and those born with thin meconium may need only oropharyngeal suctioning. All infants born with meconiumstained amniotic fluid should be closely monitored. (12) There is considerable debate concerning universal verses selective intratracheal suctioning. The American Academy of Pediatrics. (13) recommends intubation of all infants born through moderately thick or thick consistency meconium stained amniotic fluid. MECHANICAL VENTILATION: Inspite of early intervantion with thorough suctioning, some infants will still develop MAS (14). The baby who presents with meconium-stained amniotic fluid and progresses to a state of worsening raspiratory distress and hypoxemia should be intubated and mechanically ventilated. This infant is a management challenge. Sedation and paralysis are often required for effective ventilation. HIGH FREQUENCY VENTILATION HFV has been used in MAS in the hope that the lower pressures and higher frequencies will prove advantageous. (16) Benefits may include less barotraumas, increased mobilization of secretions, maintenance of respiratory alkalosis, and fewer chronic changes. Oxygenation is not necessarily improved with

the use of either conventional ventilation or HFV. NEWER MODALITIES Since surfactant within the lung may be hindered by the presence of meconium, surfactant replacement thearpy has currently been studied. (17). The surfactant deficiency is not from insufficient quantity but likely as a result of inhibited surfactant function. Intial data suggested improved oxygenation. (18) In subsequent studies there was no difference in mortality, total stay in hospital. Wiswell et al have suggested further trials. (13) Some infants with MAS will progress to the point of developing severe hypoxemia and respiratory failure and may require ECMO. (19). INTRAPARTUM INTERVANTION Some fetuses may be assessed to be at risk for MAS including those with oligohydramnios, abnormal fetal heart rate tracings, and thick meconium-stained amniotic fluid. An intrapartum intervention for these infants is amnioinfusion. It is believed that by infusing fluid into the mothers uterus, the uterine fluid volume may either dilute the meconium or alleviate compression of the cord and prevent gasping. Intial reports indicated that this would improve Apgar scores and prevent MAS, recent reports have not found to be of benefit (13) and have been found to be associated with complications. NEWER MODALITIES Studies had shown that inhaled Nitric Oxide used in MAS infants improved oxygenation and a decreased need for ECMO but there was no significant difference in the outcome. (13) There are several ongoing trials in animals with MAS for liquid ventilation using perfluorochemicals. COMPLICATIONS Complications of MAS are widespread and are dependent on the severity of the disease and the level of treatment necessary for survival. Barotrauma is always a risk with positive pressure ventilation, especially in the infant with MAS in which the ball-valve effect produces air trapping. The infant is at significant risk for air leaks and need to be monitored so that prompt treatment can be instituted. Another serious complication in MAS is increased intracranial pressure. The neonate with unstable vasculature who is already compromised, may be predisposed to a higher incidence of IVH. The rates of severe mental retardation and cerebal palsy, neonatal seizures, chronic seizures are higher in these infants though the mechanisms of these abnormal neurological outcomes are complex. (13). OUTCOME The outcome in infants with MAS has drastically changed over the last 25 years. (20) Passage of meconium was previously associated with imminent fetal mortality. However, with new techniques at delivery aimed at prevention of further aspiration, as well as the careful administration of resuscitative measures. Many more infants survive today and do well. When managed properly, however, the majority of these infants do mature with abnormal neurological development. Survivors of MAS often acquire chronic respiratory disease, including BPD. (20,21) Another common occurence is spontaneous wheezing or exercise-induced bronchospasm, with a large component of obstructive airway disease found years later.

Physiologic Meconium Passage (Particularly if postdates)

Fatal compromise (hypoxia, cord compression, and so on) Meconium passage

Meconium stained amniotic fluid

Postpartum aspiration

In utero gasping

Continued compromise

Meconium aspiration

Peripheral airway obstruction

Proximal airway obstruction

Infalmmatory and chemical pneumonitis Acidosis Hypoxemia hypercapnea

Remodelling of pulmonary vasculature

Complete

Partial

Atelectasis

Ball-valve effect

Persistent pulmonary hypertension

V/Q mismatch

Air trapping

Air leaks

FIG. MECHANISM FOR MECONIUM ASPIRATION SYNDROME


References :
1. Goetzman BW: Meconium aspiration. Am J Dis Child 1992; 146: 1282. 2. Wiswell TE, Tuggle JM, Turner BS: Meconium aspiration syndrome: Have we made a difference? Pediatrics 1990; 85:715. 3. Wiswell TE, Bent RC: Meconium staining and the meconium aspiration syndrome. Pediatr Clin North Am 1993; 40:955 4. Rossi EM, Philipson EH, William TG, et al: Meconium aspiration syndrome: Intrapartum and neonatal attributes. Am J Obstet Gynecol 1989; 161: 1106. 5. Tyler DC, Murphy J, Cheney FW: Mechanical and chemical damage to lung tissue caused by meconium aspiration. Pediatrics 1978; 62: 454. 6. Wiswell TE, Foster NH, Slayter MV, et al: Management of a piglet model of the meconium aspiration syndrome with higher frequency or conventional ventilation. Am J Dis Child 1992; 146:1287. 7. Moses D, Holm BA, Spital P et al: Inhibition of pulmonary surfactant by meconium. Am J Obstet Gynecol 1991; 104:758. 8. Perlman EJ, Moore GW, Hutchins GM: The pulmonary vasculature in meconium aspiration Hum Pathol 1989; 20:701. 9. Dooley SL, Pesavento DJ, Depp R, et al: Meconium below the vocal cords at delivery: Correlation with intrapartum events. Am J Obstet Gynecol 1985; 153:767. 10. Mitchell J, Schulman H, Fleischer A, et al: Meconium aspiration and fetal acidosis. Obstet Gynecol 1985; 65:352. 11. Yeh TF, Harris V, Srinivasan G, et al: Roentgenographic findings in infants with meconium aspiration syndrome. JAMA 1979; 242:60. 12. American Academy of Pediatrics and American college of Obstetricians and Gynecologists: Guidelines for Perinatal Care, Evantson, IL 1983, p 69. 13. Wiswell TE, Cleary GM: Meconium-stained amniotic fluid and the Meconium Aspiration Syndrome. An update. Pediatr Clin North Am 45:511, 1998. 14. Davis RO, Philips JB III, Harris BA Jr, et al: Fatal meconium aspiration syndrome despite airway management considered appropriate. Am J Obstet Gynecol 1985; 151:731. 15. Vidyasagar D, Yeh TF, Harris V, et al: Assisted ventilation in infants with meconium aspiration syndrome, Pediatrics 1975; 56:208. 16. Wiswell TE, Davis JM, Merritt TA: Surfactant thearpy and high frequency jet ventilation in the management of a piglet model of the meconium aspiration syndrome. Pediatr Res 1993; 33:350A. 17. Koumbourlis C, Moyoyama EK Mutich RL: Airway reactivity in neonates after extracorporeal membrane oxygenation (ECMO) for meconium aspiration syndrome (MAS). Pediatr Res 1992. 18. Khammash H, Periman M, Wojtulewicz J, et. Al: Surfactant thearpy in full-term neonates with severe respiratory failure. Pediatrics 92:135, 1993. 19. Henleigh P, Loots M: Complications associated with amnioinfusion for meconium. Am J Obstet Gynecol 1991; 1991; 164:317. 20. Swaminathan S, Quinn J Stabile MW, et al: Long term pulmonary sequelae of meconium aspiration syndrome. J Pediatr 1989; 114:356. 21. MacFarlance PI, Heaf DP: Pulmonary function in children after neonatal meconium aspiration syndrome. Arch Dis Child 1988; 63:368.

RETROPHARYNGEAL
Dr. Sanwar Agrawal MD Consultant Pediatrician Ekta Institute of Child Health, Raipur A retropharyngeal abscess is an infection in one of the deep spaces of the neck. An abscess in this location is an immediate life-threatening emergency, with potential for airway compromise and other catastrophic complications. Physicians must be familiar with the diagnosis and treatment of a retropharyngeal abscess. The retropharyngeal space is located immediately posterior to the nasopharynx, oropharynx, hypopharynx, larynx, and trachea. The visceral (i.e., buccopharyngeal) fascia, which surrounds the pharynx, trachea, esophagus, and thyroid, forms the anterior border of the retropharyngeal space. Bounded posteriorly by the alar fascia, the retropharyngeal space is bounded laterally by the carotid sheaths and parapharyngeal spaces. It extends superiorly to the base of the skull and inferiorly to the mediastinum at the level of the tracheal bifurcation Two other potential spaces (i.e., danger space, prevertebral space) also are present. The danger space is formed anteriorly by the alar fascia and posteriorly by the prevertebral fascia. The prevertebral space is bounded anteriorly by the prevertebral fascia and posteriorly by the longus colli muscles of the spine. The danger space extends down the mediastinum to the level of the diaphragm, while the prevertebral space continues to the insertion of the psoas muscles. Some authors consider the danger space as part of the retropharyngeal space, while others consider the danger space to be part of the prevertebral space. Still other authors refer to all 3 deep potential spaces as the retropharyngeal space. Pathophysiology : The retropharyngeal space can become infected in 2 ways. Either infection spreads from a contiguous area or the space is inoculated directly secondary to penetrating trauma. Typically, an upper respiratory infection (URI) causes spread to retropharyngeal lymph nodes, which form chains in the retropharyngeal space on either side of the superior constrictor muscle. Sources of infection can include pharyngitis, tonsillitis, adenitis, otitis, sinusitis, and other infections (i.e., nasal, salivary, dental). Infectious sources (eg, osteomyelitis of the spine) also can spread anteriorly from the prevertebral space. Penetrating trauma is involved prominently in retropharyngeal space infection. Accidental lacerations are not uncommon in children who run and fall down after they have placed an object (eg, toy, stick, frozen popsicle, lollipop, toothbrush) in their mouths. Foreign bodies (eg, fishbones) also have been implicated in penetrating trauma to the retropharyngeal space. Iatrogenic causes of inoculation to this space include instrumentation with laryngoscopy, endotracheal intubation, surgery, endoscopy, feeding tube placement, and dental injections and procedures. Complications of retropharyngeal abscesses are secondary to mass effect, rupture of the abscess, or spread of

ABSCESS

infection. The most urgent complication involves the abscess expanding against the pharynx or trachea, causing airway compression. Rupture of the abscess can cause aspiration of pus, resulting in asphyxiation or pneumonia. The infection can spread, resulting in inflammation and destruction of adjacent tissues. Spread of the infection to the mediastinum can result in mediastinitis, purulent pericarditis and tamponade, pyopneumothorax, pleuritis, empyema, or bronchial erosion. Spread of the infection laterally can involve the carotid sheath and cause jugular vein thrombosis or carotid artery rupture. Posterior spread of infection can result in osteomyelitis and erosion of the spinal column, causing vertebral subluxation and spinal cord injury. The infection itself can evolve into necrotizing fasciitis, sepsis, and death. Mortality/Morbidity Airway compromise must be identified and addressed first in patients with retropharyngeal abscess; consider consultation with a surgeon specializing in airway management and treatment in an operating room. The abscess can compress the pharynx or trachea, causing suffocation. The abscess also can rupture, causing asphyxiation or aspiration and pneumonia. Positioning the airway correctly and avoiding unnecessary manipulation is essential. Closely monitor patients with airway compromise and do not allow these patients to leave the acute care area until deemed sufficiently stable. Sedation and paralytics can relax airway muscles, leading to complete obstruction. Endotracheal intubation is dangerous unless performed under direct visualization. If direct visualization is not possible secondary to trismus or anatomic distortion, consider fiberoptic intubation or a surgical airway (eg, cricothyroidotomy, tracheotomy). Spread of infection to adjacent structures in the neck can be catastrophic. Carotid artery rupture has a 20-40% mortality rate. Even if the artery is ligated successfully, longterm morbidity secondary to stroke is common. Jugular vein thrombosis had a mortality rate of 60% prior to the use of antibiotics. Identifying this complication is essential. Osteomyelitis and vertebral erosion can cause subluxation and subsequent spinal cord injury. Atlantooccipital separation secondary to erosion of the transverse ligament of the atlas has been reported.These complications are rare in children in the post antibiotic era. Children have a different pathophysiologic disease process than adults. In young children (i.e., preschool, elementary), the abscess starts from a suppurative node that ruptures or a ruptured node. In older children and adults, the disease spreads directly into the fascial planes and is a more deadly disease that must receive immediate surgical treatment. Spread of infection into the chest has significant complications. Mediastinitis has a 40-50% mortality rate secondary to sepsis. Acute necrotizing mediastinitis and purulent pericarditis with tamponade also can be fatal. Mediastinal abscess, bronchial erosion, pyopneumothorax, pleuritis, and empyema have significant morbidity and mortality. Age : Retropharyngeal abscess is almost exclusively a pediatric diagnosis. Most incidents occur in children aged 6 "

months to 6 years, with a mean age of 3-4 years. Other deep neck abscesses (eg, parapharyngeal, peritonsillar) are observed more frequently in adults and older children. In children, retropharyngeal abscess usually is caused by an infection that spreads to the retropharyngeal lymph nodes, with subsequent cellulitis and abscess formation. Due to repeated infection throughout childhood, fibrosis and atrophy start in these nodes when the individual is aged 4 years. By the time the child is aged 6 years, fibrosis and atrophy have regressed completely. History : Patients with retropharyngeal abscess present with constitutional complaints such as fever, chills, malaise, decreased appetite, and irritability. Patients may complain of sore throat, difficulty swallowing (dysphagia), pain on swallowing (odynophagia), jaw stiffness (trismus), or neck stiffness (torticollis). Patients also may complain of muffled voice, the sensation of a lump in the throat, and/or pain in the back and shoulders upon swallowing. Difficulty breathing is an ominous complaint that signifies impending airway obstruction. Patient history is not always straightforward. One study identified the following symptoms in patients: fever (74%); sore throat (47%); dysphagia (38%); trismus (36%); decreased appetite (22%); voice change (18%); odynophagia (17%); neck pain (15%); irritability (11%); and difficulty breathing (8%). The course of pharyngeal abscess can be insidious. Sometimes a URI can precede symptoms by weeks. Many patients do not recall (or parents are not aware of) incidences of penetrating trauma. Maintain a high index of suspicion, especially in patients with URIs that do not appear to resolve in a normal course or with conventional therapy. Physical : Most patients with retropharyngeal abscess are febrile. Some appear toxic and irritable. Cervical lymphadenopathy, usually unilateral, is the most common physical finding in these patients. Patients may have decreased or painful range of motion of their necks or jaws. A neck mass or tenderness may be appreciated. These patients may present with a muffled hot potato voice (i.e., dysphonia) or with a voice that sounds like a duck quack (i.e., cri du canard). Upon inspection of the oral cavity (usually with a tongue blade), the physician may be able to appreciate a mass in the posterior pharyngeal wall. As many as 30% of patients have this mass, according to 1 study. This is not midline, due to the presence of the raphe in the retropharyngeal space caused by the superior constrictor

muscle; midline masses are usually in the prevertebral space. While this mass has been described as fluctuant to palpation, deferring this part of the examination probably is best; at least use extreme caution, especially in a combative child. This maneuver has led to abscess rupture and subsequent aspiration. Tracheal rock sign elicits pain while gently moving the larynx and trachea from side to side. Patients in respiratory distress or those who present with stridor or drooling have potential airway compromise.

These patients prefer to lie supine with their necks extended, maximizing their airway patency.
Sitting up or flexing their necks worsens their respiratory distress. Jugular vein thrombophlebitis may manifest as tender induration at the anterior sternocleidomastoid border, vocal cord paralysis, or sepsis of an unknown source. Sentinel bleeding from the ear, nose, or mouth can herald carotid artery rupture. Ecchymosis may be detected in the lateral neck. Pathogens : Bacteria are often polymicrobial, with gram-positive organisms and anaerobes predominating, but gram-negative bacteria also have been isolated. The source is usually oropharyngeal flora. The most common cause is group A beta-hemolytic streptococci. Other nonhemolytic streptococci can be present. Staphylococcus aureus is also fairly common, especially secondary to osteomyelitis. The most common anaerobes are Bacteroides species. Other causative agents include Haemophilus parainfluenzae and Veillonella, Peptostreptococcus, Fusobacterium, and Eikenella species. The incidence of beta-lactamase production is high. One study noted 22% beta-lactam resistance. Suspect mycobacterium tuberculosis and coccidiosis in patients who may be predisposed, especially if they are not responding to more conventional therapy. Lab Studies : Lab findings are nonspecific. WBC counts can be elevated, with a mean level of 17,000. One study recorded ranges of 4,000-45,000. A Gram stain can help direct early empiric antibiotic therapy. If an incision and drainage is performed, sending a piece of the abscess wall to pathology helps increase the yield of culture and sensitivity testing. Imaging Studies : A lateral soft tissue neck x-ray is helpful in making the diagnosis of a retropharyngeal abscess. Obtain the film during #

inspiration with the neck held in normal extension. An abscess occupies the soft tissue space, which can be observed between the radiolucent airway (i.e., pharynx, trachea) and the spine. Widening of these soft tissues is pathologic until proven otherwise. Measuring at the level of C2, the distance from the anterior surface of the vertebrae to the posterior border of the airway should be 7 mm or less, regardless of the patients age. At C6, this distance should be 14 mm or less in children younger than 15 years. A distance of 22 mm is considered normal in an adult. A simpler (but less precise) rule is that the soft tissue plain should be less than one half the width of the corresponding vertebral body.

compressed. A CT scan can be used to determine the presence of an abscess and help distinguish it from cellulitis (an abscess has a central area of lucency). The study also can assist in determining the location of the abscess, extent of abscess spread, and presence of any complications. CT scan provides much information not readily determined by plain film. Depending on the study, CT scan can be more than 90% sensitive. The false-positive rate (1125%) is better than that of x-ray. The false-negative rate is 1015%. Overall accuracy is 75% in most large studies (i.e., those with >30 subjects). The disadvantage of CT scan is that it is not located in a monitored setting. Ensure that patients with impending airway compromise are stabilized prior to leaving the acute care area. A portable plain film may have to suffice. Also, younger children may not tolerate a CT scan without sedation. Such medications can cause airway muscle relaxation with ensuing occlusion. MRI produces images superior to the other studies, but this is usually unnecessary and rarely used, unless a concern is present that the abscess has spread to the CNS. Additionally, this study requires a protracted period of time when the patient is in an unmonitored setting. Children usually require sedation for this test, which is also dangerous in any patient with a potentially unstable airway. Ultrasound is an imaging modality that is gaining popularity. It is safer than CT scan, since it is portable and does not use radiation. Ultrasound is also less traumatic to children, requiring less frequent use of sedation. In experienced hands, ultrasound can help determine the presence and location of an abscess and can allow the clinician to distinguish an abscess from cellulitis with some accuracy. Further studies are needed to explore the practical use of ultrasound. Procedures : Needle aspiration of a suspected abscess can be performed. Aspiration can help determine the presence of an abscess and help distinguish it from cellulitis. It can be diagnostic and therapeutic. An intraoral route usually is indicated, except when an abscess is isolated lateral to the carotid sheath. In this case, an external approach can be used. CT scan or ultrasound can help guide the aspiration. With an abscess involving multiple spaces, perform needle aspiration with an open external approach. Needle aspiration never should be performed outside the operating room suite. Definitive airway management must be imminently available throughout the procedure. Medical Care : Determining airway stability remains a top priority. Allow patients to remain in a position of comfort, which is usually supine with their necks extended. Neck flexion or forcing a child to sit up can occlude the airway. Sometimes positioning is all that is necessary to maintain airway patency. Administer supplemental oxygen as needed. Provide a definitive airway only under direct visualization. If $

A plain film also may demonstrate gas or a foreign body (eg, fishbone) in the retropharyngeal space. The normal spinal lordosis may be reversed. With a childs head extended, the width of the soft tissue is no more than a vertebral body width in an average child. Obtaining the film with the head extended is important. Lateral plain film is not very sensitive or specific. One study demonstrated a 33% false-negative rate. False-positive rates are also high. Poor neck extension or an expiratory view can produce a false-positive result. A few authors have suggested that plain films are an unnecessary diagnostic step. A plain film of the chest is necessary to exclude mediastinal or pulmonary complications. CT scanning is currently the imaging modality of choice. Obtain a study with intravenous contrast to help demarcate the lesion and determine if vascular involvement is present. Inform the radiologist of the purpose of the study in advance, because a standard CT scan of the neck may not use thin enough slices (3-5 mm) and may not scan through the entire extent of the retropharyngeal space (the base of the skull to T2). An abscess is found in the deep spaces of the neck. It is an area of low attenuation, surrounded by an enhanced ring. Gas sometimes is present within the abscess cavity. The nearby soft tissue is edematous, and fat planes may be obliterated. Neighboring structures, including the airway, can be

this is not possible due to trismus or distorted anatomy, abort the attempt. Excessive manipulation or blind oral or nasotracheal intubation can cause abscess rupture with catastrophic consequences. Sedatives and paralytics can cause relaxation of airway muscles with subsequent complete occlusion. Broad-spectrum coverage is indicated. Given the increasing frequency of resistant bacteria, treatment may be initiated alone or in combination with cefoxitin or a betalactamaseresistant penicillin, such as ticarcillin/clavulanate, piperacillin/tazobactam, or ampicillin/sulbactam. Patients with cellulitis can be treated with parenteral antibiotics alone. Closely observe these patients for development of an abscess. Some authors advocate the use of antibiotics alone for small abscesses. These patients need to be monitored closely for improvement. A CT scan may be helpful in distinguishing cellulitis from an early abscess. Surgical Care : Surgical airway control may be necessary in patients whose airways are difficult to visualize or are obstructed completely. Depending on the age of the patient and the experience of the physician, perform needle cricothyroidostomy or cricothyroidotomy only if the child cannot be transported to the operating room safely or quickly enough to secure the airway there. Alternatively, a qualified surgeon can perform a tracheotomy. Needle aspiration of an abscess can be performed both to assist in diagnosis and to treat an abscess.

Infection can spread either laterally or posteriorly to adjacent structures in the neck, or it can progress inferiorly to the mediastinum. Infection can spread laterally to the carotid sheath, where it can cause vascular complications. Jugular vein thrombosis manifests as tenderness over the anterior border of the sternocleidomastoid, vocal cord paralysis, or sepsis without an obvious source. Aggressive antimicrobial therapy is indicated. Carotid artery rupture, which presents as ecchymosis in the neck, usually is heralded by a sentinel bleed from the nose, mouth, or ear. Immediate surgical repair usually requires ligation, which can lead to stroke. Infection also can spread posteriorly, affecting the cervical spine. Osteomyelitis requires long-term antibiotics. Erosion of the ligaments can cause subluxation and subsequent spinal cord injuries. Destruction of the transverse ligament of the atlas has been known to cause atlantooccipital dislocation. Inferior spread of infection can cause several lifethreatening complications. A chest x-ray is indicated in the initial workup. Inflammation in the mediastinum can cause mediastinitis, purulent pericarditis, pericardial tamponade, bronchial erosion, and mediastinal abscess. Spread to the adjacent pleura can cause pleuritis, pyopneumothorax, or empyema. In addition to antibiotics, drainage of pus via pericardiocentesis, pericardial window, chest tube thoracostomy, or open thoracotomy may be necessary. The infection also can evolve into overwhelming sepsis or necrotizing fasciitis in the neck or mediastinum. Bibliography : Choi SS, Vezina LG, Grundfast KM: Relative incidence and alternative approaches for surgical drainage of different types of deep neck abscesses in children. Arch Otolaryngol Head Neck Surg 1997 Dec; 123(12): 1271-5 Marra S, Hotaling AJ: Deep neck infections. Am J Otolaryngol 1996 Sep-Oct; 17(5): 287-98 Nicklaus PJ, Kelley PE: Management of deep neck infection. Pediatr Clin North Am 1996 Dec; 43(6): 1277-96. Ungkanont K, Yellon RF, Weissman JL, et al: Head and neck space infections in infants and children. Otolaryngol Head Neck Surg 1995 Mar; 112(3): 375-82.

A small retropharyngeal abscess can be aspirated with an 18-gauge needle by the intraoral route. Larger abscesses require incision and drainage using either an intraoral or transcervical approach or both, depending on the location of the carotid sheath in relationship to the abscess. Completely evacuate pus from the abscess. Send a specimen to the lab for Gram stain, culture, and sensitivity. Abscesses in the parapharyngeal space isolated lateral to the carotid sheath can be aspirated by an external approach.

Complications : Complications of retropharyngeal abscess occur from mass effect, rupture, or spread. The mass of the abscess in the retropharyngeal space can compress the airway, which lies immediately anterior to it. Because this is the most immediately life-threatening complication of retropharyngeal abscess, address this complication first. Secure the airways of patients in respiratory distress, or in those with stridor or drooling. Abscess rupture can lead to asphyxiation or aspiration pneumonia. The abscess can rupture spontaneously, or it can be ruptured iatrogenically during vigorous physical examination or attempted intubation. Obtain a chest x-ray to assess for pneumonia. Abscess rupture requires aggressive airway management, including suctioning and broad-spectrum antimicrobial therapy.

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