Pitfalls in Pediatric Airway Management
Authors: Ronald M. Perkin, MD, Professor of Pediatrics and Emergency Medicine; Director of Pediatric Critical Care, Inpatient Respiratory Services and Sleep Disorders Center, Loma Linda University Children’s Hospital, Loma Linda, CA; Daved van Stralen, MD, Medical Director, Program in Emergency Medical Care, Department of Cardiopulmonary Sciences, School of Allied Health Professionals; Assistant Director, Pediatric Inservice Care Unit, Loma Linda University Children’s Hospital, Loma Linda, CA.
Peer Reviewer: Marshall S. Salkin, MD, JD, FACEP, FCLM, Attending Physician, Emergency Department, Northwest Community Hospital, Arlington Heights, IL.
The management of pediatric airway emergencies is generally accepted as one of the greatest anxiety provoking settings for pediatric health care providers. Early last year, Perkin and van Stralen provided an expert review of pediatric airway emergencies.1 In this very practical article, they review the most common potential pitfalls and mistakes in the management of pediatric airways. Often the learning process involves gleaning educational insights from our mistakes or therapeutic misadventures. Ideally, the didactic process allows us to learn from the mistakes of others. The editors recognize that we commonly emphasize techniques for performing procedures or managing conditions, but less frequently we review specific pitfalls. In this issue, important insights from this perspective are provided.
The Editor
An open airway and adequate gas exchange are central goals of emergency management. Along with the recognition and treatment of shock, they form the familiar mnemonic "ABC" (airway, breathing, and circulation) that summarizes the basic priorities of oxygen delivery to tissues and, therefore, the required early management principles in acute illness and injury.
Successful cellular respiration depends on the maintenance of several factors, including adequate alveolar ventilation with an oxygen-containing mixture; a functioning gas-exchange surface (airways, capillaries, and alveolar membrane); the capacity to transport oxygen to the tissues (sufficient levels of hemoglobin and cardiac output); and intact tissue respiration, specifically the mitochondrial cytochrome oxidase system.3 Since impairment of any of these factors of cellular respiration can result in end-organ hypoxia, all are clinically important in critically ill patients. Most of these factors can be assessed directly. Others, such as tissue respiration, must be assessed indirectly as end-organ function.
The etiology of cardiopulmonary arrest in pediatric patients is most commonly a primary respiratory disorder. The majority of deaths in children (especially < 1 year of age) involve respiratory diseases likely to result in prehospital evaluation and transport, emergency department evaluation, and, eventually, admission to an intensive care unit. These diseases include infection, poisonings, trauma, submersion or suffocation, and sudden infant death syndrome. Airway obstruction, aspiration, and apnea are among the major hazards to respiratory function in critically ill or injured patients. It is essential that all emergency health care professionals be able to perform skilled oxygenation and ventilation of these children.1,2 When approaching a critically ill child, numerous "pitfalls" in managing the airway and providing oxygenation and ventilation may occur.
Establishing the Severity and Significance of Respiratory Distress in a Child. The child’s limited capability of respiratory compensation makes the early recognition of any respiratory embarrassment essential. Ideally, respiratory failure should be anticipated rather than recognized so that the appropriate measures can be taken before gas exchange is severely altered.1,3 Early intervention will prevent the effects of hypoxemia and hypercarbia on the central nervous and circulatory systems of the patient.
Early recognition of impending respiratory failure is based mainly on clinical findings. While traditional textbook resources stress the blood gas evaluation and place less emphasis on the clinical examination, a good history coupled with a thorough physical examination will almost always give a diagnosis of respiratory failure and its cause.
Observation is the most useful assessment tool. Observational scoring systems such as asthma and croup scores are well-known assessment tools that have been clinically validated.4-6 The elements of these tools can be simplified even further into five parameters of assessment. (See Table 1.)
The physical examination in children with respiratory distress begins with a general overview assessment of the patient’s condition and vital signs. Often, this distinguishes the more critical illnesses in children from self-limiting, mild conditions. The child’s posture, color, and mental status are observed, and a quick assessment of the adequacy of ventilation is made. This assessment includes evaluation of the presence and vigor of the respiratory effort, respiratory rate, extent of the chest excursions, and existence of signs of airway obstruction.
The physical examination process cannot disturb the patient’s mechanisms of respiratory compensation and allows the child to maintain his or her position of comfort. This includes leaving a child with his or her parent to prevent agitation induced by the separation and increased work of breathing leading to respiratory failure. Fortunately, much of the physical examination can be done without touching the child (the first 4 of the 5-point respiratory examination). This gives minimal patient disturbance and allows ease of reassessment.
The signs and symptoms of hypoxemia and hypercapnia are not specific and may be difficult to detect by physical examination.7 (See Table 2.) If severe enough, hypoxemia and hypercapnia impair the function of the central nervous system (CNS). Confusion, lethargy, or even combativeness are thus common signs of respiratory failure and are due to brain hypoxia. Lethargy or coma are also associated with extreme hypercapnia. Similarly, tachycardia is a frequent early response to hypoxemia or hypercapnia.
The child with hypoxemia, evaluated by cyanosis or pulse oximeter, that does not respond to supplemental oxygen or basic airway interventions may benefit from manual ventilation and endotracheal intubation. If the child remains refractory to such measures, then one must evaluate for cyanotic congenital heart disease.
Respiratory rate and rhythm are other examination components to use for assessing the infant or child’s respiratory status. Young infants tend to rely more on respiratory rate than older children, who are able to increase tidal volume. Importantly, a normal respiratory rate in a child with other respiratory distress signs may indicate fatigue and impending respiratory failure. Concurrently, a decreasing respiratory rate, with other signs of respiratory distress, is a sign of impending respiratory failure.
Signs of increased work of breathing include the use of accessory muscles, retractions, nasal flaring, tachycardia, and increased rate and depth or respiratory effort. Cyanosis, dysphagia or drooling, wheezing, rales, stridor, or altered level of consciousness support the diagnosis of respiratory distress or impending failure. Head bobbing (an up-and-down movement of the head) with each breath is a sign of severe distress suggestive of respiratory failure.
Auscultation is an extremely important parameter in the assessment of respiratory distress. Tidal volume estimates can be made visually by noting chest expansion and by auscultation.1,3 Respiratory sounds such as wheeze, stridor, and grunting are also noted and indications of airway obstruction are documented. Upper airway obstruction worsens on inspiration, and stridor is generally produced, which worsens with agitation. Lower airway obstruction worsens on expiration, and wheeze is generally produced, which is more pronounced on forced expiration. As air flow decreases with worsening obstruction, wheezing may disappear and is a worrisome finding. Concurrently, the inspiratory time to expiratory time ratio should be evaluated.
The need for immediate artificial airway should be evaluated. Urgent need for intervention is signaled by decreased respiratory effort and breath sounds, decreased mental status, and cyanosis. Frequent assessment is necessary to identify slow deterioration. Impending failure is best identified when the physical examination at a given point in time is interpreted in relation to previous examinations. When the trend is appreciated, specific and aggressive interventions are instituted to interrupt the progression to respiratory failure.
Misinterpretation of the Signs and Symptoms of Pediatric Respiratory Distress/ Failure. Overt respiratory dysfunction such as apnea or inadequate ventilation is easily recognized. However, covert system dysfunction is more difficult to identify but occurs during periods when interventions are more successful. Missing covert signs leads caregivers to believe that children suddenly deteriorate. A quieting child with decreasing respiratory rate or decreasing wheezing, symptoms that change incrementally with time, may herald a lessening of the child’s ability to compensate. Decompensation may then occur cataclysmically.
Much emphasis has been placed on definitions of respiratory failure vs. distress rather than on level of physiological dysfunction or identification of covert compensated states. Vital signs, visual signs, and auscultation help identify covert signs of respiratory dysfunction.
Medical education has placed an emphasis on diagnosis before prescribing therapy. In emergency situations, therapies may come concurrent with or precede the diagnosis.8 Emphasis on diagnosis early in the course of an emergency may generate pressure to conform findings to the previously made diagnosis while ignoring signs of deterioration or other diagnoses.
Vital Signs. Abnormalities in vital signs do not earmark a particular diagnosis but will help to confirm the severity of the process. Tachycardia, unless from primary heart disease, usually occurs as a secondary process, frequently from fever or other demand for increasing cardiac output. Bradycardia is usually seen late in respiratory diseases when hypoxemia, acidosis, and myocardial depression are present.
One must differentiate normal from abnormal respiratory rates and rhythms. (See Table 3.) These are age-specific and must be viewed as such to interpret the severity of your patient’s condition.9,10 However, one study demonstrated that "normal" respiratory rates for children in ED settings cover a wide range, and, consequently, the identification of "abnormal" is more difficult.11
A high respiratory rate is used as one of the most important signs of illness in infants. This is because respiratory tract infections are one of the major causes of morbidity and mortality in the first year of life. Increasing the respiratory rate is the primary method of increasing minute ventilation in infants. However, not every rapidly breathing infant has respiratory tract infections. Non-pulmonary causes of tachypnea include hypovolemia, hyperviscosity syndromes, hyperglycemia, heart failure, exertion, adverse effects of drugs, metabolic acidosis, pain, fever, and anxiety. On the other hand, a normal respiratory rate in the presence of injury or disease is not normal.
A slower than normal respiratory rate, bradypnea, should be considered an ominous sign. Causes of bradypnea include hypothermia, CNS injury, neuromuscular disease, severe shock, hypoxemia in some infants, CNS depression by drugs, and some metabolic disorders.
Apnea, or the absence of respirations, may be caused by a number of factors and must be aggressively identified and treated. (See Table 4.) Apnea longer than 20 seconds is always abnormal. However, any short respiratory pause associated with bradycardia, cyanosis, or pallor must always be investigated.
When parents complain that their child has apnea, the health care provider’s first response obviously must be to check the child’s respiratory status. Once established that the respirations are adequate, every effort should be made to obtain precise history from the first-hand observer. The history should include the following details: 1) where and when the event occurred; 2) duration of event; 3) whether the patient was awake or asleep; 4) associated color changes; 5) presence or absence of respiratory efforts, emesis, choking, cough, stridor, or wheeze; 6) associated movements, posture, or changes in muscle tone; 7) degree of intervention or resuscitation required; 8) relationship to last feeding and position; 9) intercurrent illnesses or fever; and 10) underlying medical conditions.
Visual Signs. Increased effort of the respiratory muscles results in distortions of the chest wall, particularly at the level of the costal insertions of the diaphragm (subcostal retractions) and the intercostal spaces (intercostal retractions). These distortions are particularly noticeable in infants owing to the high compliance of their chest wall. As failure progresses and more compensation becomes necessary, incorporation of accessory muscles to the breathing effort and the greater amplitude of the contractions of the regular respiratory muscles give an impression of air hunger, as if the patient’s attention were solely concentrated on breathing.
The position that the child assumes can often help one to identify the cause of respiratory distress. Children with airway obstruction at the level of the pharynx or above (epiglottitis, adenotonsillar hypertrophy) will usually hyperextend their necks and lean forward in an effort to straighten their upper airway and maximize air entry. This type of posturing does not help to relieve the obstruction at the tracheal or bronchial level.
All patients should be allowed to choose their position of comfort (for example, in the parent’s arms or lap, leaning forward, or supine). Forcing a patient into a different position may worsen respiratory distress and even precipitate respiratory arrest. Abruptly placing a child in respiratory distress onto a stretcher or even having them lie down when they are reasonably comfortable can cause the child to deteriorate. Hence, a conscious decision regarding proper positioning must be made early in a child’s evaluation.
Drooling and dysphagia are hallmarks of infectious causes of supraglottic upper airway obstruction such as epiglottitis, retropharyngeal abscess, or tonsillitis.4 Pain caused by the inflammatory nature of these diseases prevents children from swallowing their secretions.
Cyanosis occurs in diseases involving different organ systems. Hemoglobin desaturation is responsible for the blue discoloration of the skin, lips, mucous membranes, and nail beds. Central cyanosis (blueness of the tongue and mucous membranes), as opposed to peripheral cyanosis, is always a manifestation of hypoxemia. Except for the relatively uncommon causes of methemoglobinemia, sulfhemoglobinemia, and some hemoglobinopathies, central cyanosis is always accompanied by a low arterial pO2. As a result of hypoxemia, an excess amount of hemoglobin is not saturated with oxygen, and this unsaturated hemoglobin is said to be reduced. As a reminder, it is the quantity of reduced hemoglobin (RHB) per deciliter of capillary blood, not the relative lack of oxygenated hemoglobin, that accounts for the bluish color of cyanosis.12
There is a wide range of hemoglobin saturation values (SaO2) at which cyanosis is detectable. Such variability in detection is explained by the numerous factors involved, including hemoglobin content, skin color and perfusion, lighting, and interobserver variation. Nonetheless, all other factors being equal, the greater the hemoglobin content the more readily will cyanosis appear as SaO2 falls; conversely, the lower the hemoglobin content the more SaO2 has to fall before cyanosis becomes manifest. Thus, patients with a significant degree of anemia may not manifest cyanosis in the presence of significant hypoxemia.
The value of 5 g/dL RHB ± 1 g/dL in the capillaries is the quantity at which cyanosis should be detectable in the majority of patients.12 At this level of capillary RHB, cyanosis should be detectable when SaO2 is between 73% (hemoglobin, 12 g/dL) and 78% (hemoglobin, 15 g/dL). In some patients, cyanosis may be detectable at higher levels of oxygenation.
Supplemental oxygen should be administered to all cyanotic patients until the etiology and the duration of the cyanosis is established. Nevertheless, although this is rarely seen in the pediatric age group, patients with chronic lung disease should receive oxygen carefully because they may rely on hypoxic drive for ventilation. Reliance on hypoxic drive for ventilation may also occur in children with chronic upper airway obstruction or in children with neuromuscular disease.13
Pulse oximetry often allows rapid identification of declining SaO2 long before it is clinically apparent. Shock, carboxyhemoglobin, and fingernail polish may decrease the effective use of oximetry.14-16 Additionally, pulse oximetry is inaccurate in anemia, sickle cell disease, and in the presence of ambient light sources (e.g., sunlight, warming lights, phototherapy, or bright fluorescent bulbs).14-16 It should also be recognized that oximetry provides very little indication of ventilation or acid-base balance. While not widely applied for assessing respiratory emergencies in ED settings, noninvasive capnometry has a potential role in monitoring ventilation or end-tidal CO2.17
Pulse oximetry has also been shown to have significant predictive value for identification of high-risk children in respiratory distress. Pulse oximetry has demonstrated benefit in prehospital care and in the ED.14 Maneker et al demonstrated that clinical evaluation in a pediatric emergency department does not screen adequately for hypoxemia and should be supplemented by routine pulse oximetry in all patients with respiratory symptoms.15 In that study, clinical assessment had a sensitivity of 33%, specificity of 86%, negative predictive value of 85%, and a positive predictive value of 35%.15
Auscultation. Auscultation of the chest provides information about the entry and distribution of gas in the lungs. Breath sounds will often be decreased in intensity if gas exchange is poor. However, the small size of the infant’s chest facilitates the transmission of tracheal sounds to the thoracic surface, limiting the ability to judge the volume of gas that actually enters the lung periphery. Gross asymmetries between the two lungs are always abnormal and may indicate accumulations of gas or liquid in the pleural space. The absence of these asymmetries, however, does not rule out such accumulations in the infant or small child because breath sounds can be easily transmitted from the trachea or the contralateral side. In addition, crackles and rales suggest the presence of liquid or atelectasis in the peripheral air spaces.
Listen to breath sounds not only during quiet but also during crying, deep breathing (for stridor, rales), forced expiration (for wheezing), after coughing (for changes in wheezing or rales), and after nasal suctioning (to eliminate transmitted sounds from upper airway obstruction). Comparison of sounds heard by the stethoscope at the cheek, neck, and chest helps identify transmitted upper airway sounds compared to breath sounds.
Normal respiratory efforts are usually not accompanied by externally audible sounds. Grunting on exhalation is commonly noted during respiratory distress and is caused by an early closure of the glottis during exhalation with active chest wall contraction.18,19 Grunting increases expiratory airway pressure, preventing airway collapse. It is seen in diseases with diminished lung compliance (e.g., pulmonary edema, pneumonia, overcirculated lungs from a ventricular septal defect), and it also may occur as a result of pain. Nonrespiratory disorders such as intraabdominal problems (peritonitis, appendicitis) may present with grunting respirations. Grunting is an ominous sign and should never be ignored.
Stridor, a harsh, crowing sound, usually occurs during inspiration and is usually produced by obstruction to airflow in the extrathoracic or upper airway.4 In few pediatric conditions are the benefits of optimal management and the risks of inappropriate action so clear as they are in acute upper airway obstruction. Infants and small children are uniquely susceptible to these disorders as a consequence of several anatomic and physiologic factors. Severity of obstruction and rapidity of progression vary depending upon cause and time of presentation; precipitous decompensation to complete obstruction and/or respiratory failure is an ever-present possibility.
Wheezing refers to continuous musical breath sounds, usually high-pitched or whistling, that may at times be audible to the unaided ear. Wheezing is produced by high-velocity airflow passing through critically narrowed airways; as such, its presence signifies partial obstruction of passages either of the upper or, more commonly, of the lower airways. Wheezing is either inspiratory or expiratory, characteristic of upper or lower airway obstruction, respectively. The intrathoracic airways (lower trachea, bronchi, and bronchioles) dilate during inspiration and narrow during expiration. Thus, lower airway obstruction is maximal during expiration, and wheezing is accentuated in this phase of respiration. The converse is true for obstruction of the extrathoracic airways (larynx and upper trachea). In either case, as the airway obstruction becomes increasingly severe, wheezing may not be heard.
A variety of pathological processes are responsible for the airway obstruction that occurs in children with wheezing.21,22 Regardless of the etiology, the airway narrowing is the result of one or more of several mechanisms: 1) extrinsic airway compression (mediastinal mass, lymph nodes, vascular ring); 2) intraluminal airway obstruction (foreign body, secretions, cellular debris); or 3) intrinsic airway narrowing (mucosal edema, bronchospasm, stenosis, or bronchomalacia). The most common causes of wheezing are asthma, foreign body inhalation, pneumonia, or bronchiolitis.
Choking or gagging is typically associated with foreign body aspiration or abnormalities of deglutition with aspiration of pharyngeal material. Recurrent vomiting, with or without these symptoms, may indicate gastroesophageal reflux with aspiration of gastric contents. Chronic aspirations syndromes are frequently encountered in children with neuromuscular disease, cleft palate, or developmental delay.
Performance of Overzealous or Unnecessary Examinations. Major errors in evaluating severity of respiratory failure include underestimation of distress and overzealous examinations that agitate the child. Children are emotionally labile, and actions that lead to increased fear or pain will also lead to more vigorous respiratory effort. Increased airflow rates increase resistance in turbulent airflow regions of the lung. Consequently, the child’s response to heightened pain or fear can result in respiratory failure or arrest.
As mentioned previously during assessment, all children are continually observed but with minimal interference. Children with relatively compensated respiratory disease should not be separated from their parents. Doing most of the examination from a distance minimizes disturbance and enables more reliable observation by avoiding the increases in heart rate, respiratory rate, and retractions produced by crying. The parent is asked to remove the child’s shirt, and the following are rapidly assessed from a few feet away: general appearance, color, respiratory rate, audible sounds, retractions and use of accessory muscles, drooling, and state of consciousness. Thereafter, the patient can be approached slowly in order to check the pulse and auscultate the chest. If these efforts provoke anxiety in the child, they should be abandoned, as pulse will be unreliable and auscultatory findings altered.
As noted in Pitfall #1, the level of respiratory dysfunction or impending respiratory arrest can be identified by physical examination. Obtaining blood for an ABG inflicts pain and alters the evaluation. In some cases, this leads to deterioration that necessitates intervention. It is also difficult to interpret blood gas values from an agitated patient, since such values fail to reflect baseline status.
Failure to Constantly Reassess the Patient’s Condition and Response to Therapy: Deterioration is a Process not an Event. The recognition and management of impending respiratory failure may prevent progression to failure and its serious consequences, including cardiopulmonary arrest. However, impending respiratory failure is not always readily apparent from a single examination; it is as much a trend as a static condition. Therefore, it is best identified when the physical examination at a given time is interpreted in relation to previous examinations and the patient’s history. When the trend is appreciated, specific interventions are frequently able to interrupt the progression to respiratory failure.
Children uncommonly deteriorate rapidly from a state of normal physical examination. More likely, the child is in a covert state of compensated system dysfunction with a gradual but progressive deterioration in respiratory function. Frequent documented examinations with the above five-point respiratory examination will bring to caregiver’s attention the child with subtle but clear deterioration.
Inadequate Knowledge of Important Anatomic and Physiologic Differences in the Pediatric Airway. The human infant is not a miniature child or adult. While this seems self-evident, many of the anatomic and physiologic mechanisms that underlie the differences among the infant, child, and adult are still poorly understood. Table 6 reviews many of the differences between the pediatric and adult airway.1
Delivery of respiratory care to patients in the pediatric age group presents several unique problems that relate to size, physical and intellectual maturation, and diseases specific to neonates, infants, and children. These problems create therapeutic difficulties that necessitate additional equipment and precautions.
Failure to Recognize an Abnormal or Difficult Airway. Maintenance of a patent airway to allow adequate gas exchange is fundamental to the management of the critically ill patient. Most often this involves endotracheal intubation via direct laryngoscopy. Expert performance of endotracheal intubation can be life-saving, while inability to perform this technique adequately can be life-threatening. Identification of potential problems, pre-intubation anatomic evaluation, equipment and drug preparation, and anticipation of potential complications will allow for a high success rate. Furthermore, physicians must have a logical, safe, alternate plan for airway management when faced with a patient who is difficult to intubate or who cannot be ventilated.
If time allows, a pre-intervention history and physical examination will identify most patients who will be difficult to intubate. The American Society of Anesthesiologists risk classification system will identify patients at highest risk for adverse outcome from administration of general anesthetics, paralysis, and endotracheal intubation. (See Table 6.)
Direct examination of the airway can identify patients who will be at greatest risk for difficult intubation and inability to ventilate. A few simple measurements can be useful and include the mental-hyoid distance and the upper-lower incisor distance. The upper-lower incisor distance with open mouth should be assessed in infants and children. A quick look into the posterior pharynx (without any instruments) will reveal either evidence of a difficult airway (a large tongue, blood, swelling, or secretions) or an easier airway with visible faucial pillars, soft palate, and uvula. While a short neck, small mandible, large tongue, obesity, high arched palate, scoliosis, and limited mandible or cervical spine mobility account for a significant number of difficult airway cases,23-25 some patients who appear normal to conventional examination may still present an unanticipated airway problem. (See Table 7 and 8.)
Prior to endotracheal intubation, clinicians must have a plan of action for dealing with difficult or failed attempts at intubation. Always prepare rescue equipment in advance whether or not difficulties are anticipated. If patients have anatomic obstruction (e.g., epiglottitis, fractured larynx) or maxillofacial trauma, equipment and personnel (e.g., surgeon) should be readied in case surgical airway techniques are necessary. All EDs should have a difficult airway cart prepared with a variety of airway rescue devices. (See Table 9.)
A mental checklist should be completed prior to any intubation. Ideally, clinicians should prepare all equipment, medications, and the patient before any interventions take place.
• Perform brief airway examination and assessment of anesthesiology risk;
• Elevate the bed so that the nose of the patient is at the intubator’s sternum;
• Apply a cardiac monitor and pulse oximeter to the patient;
• Ready and test two wall suction devices in case one fails;
• Prepare two endotracheal tubes (one that is 0.5-1.0 sizes smaller) with balloons that are functioning properly;
• Identify personnel for in-line cervical immobilization, cricoid pressure, and medication administration;
• Ensure that two functioning IV lines are in place;
• Prepare medications and estimate drug dosages (e.g., using a Broselow tape);
• Premedicate with atropine for bradycardia if less than 5 years of age, lidocaine for head injury, and consider a defasciculating agent;
• Pre-oxygenate for at least 3-5 minutes so that apnea can be tolerated for a prolonged period of time; and
• Administer drugs for intubation (e.g., sedating and paralyzing agents).
To successfully intubate a patient, certain conditions must be fulfilled.23,24 The axes of the mouth, pharynx, and larynx all need to be aligned. This involves placing patients in the sniffing position: flexion of the neck at the lower cervical spine and extension of the head at the atlanto-occipital joint (if trauma is not suspected). The ability to open the mouth (intact hinge action at the temporomandibular joint) is essential to permit the introduction of the laryngoscope and endotracheal tube.
Despite adequate preparation, clinicians occasionally may still be unable to intubate a patient successfully. If clinicians are unable to visualize the vocal cords or epiglottitis, and cannot successfully intubate the trachea on a first attempt, specific techniques will increase the success rates for future attempts. Always recheck the position of the head and position of the head and neck (sniffing position if no trauma). Ventilate so that the patient is again preoxygenated. A smaller styletted tube and possibly a different laryngoscope blade (a straight blade or a longer laryngoscope blade) will allow for successful vocal cord visualization during a second attempt. Application of posterior and cephalad pressure to the thyroid cartilage (by the person applying cricoid pressure) will often bring the airway into view. Additionally, application of lateral and posterior pressure to the cheek will move the lips out of the way allowing for better visualization of the hypopharynx. If the above maneuvers are unsuccessful, clinicians must move rapidly to alternate airway techniques. (See Table 9.) If all attempts are unsuccessful, then a skilled anesthesiologist should be consulted, or more invasive techniques to secure the airway will have to be performed.23-25
Limitation or Misapplication of Oxygen Administration. Of the two gas exchange aberrations (hypoxemia, hypercapnia) that occur during respiratory failure, hypoxemia is by far the most dangerous to the patient. Usually it is also the easiest to correct.
Immediately administer 100% oxygen to all dyspneic, cyanotic, or bradycardic pediatric patients.25 Finger pulse oximetry will quickly establish if adequate arterial oxygenation can be achieved.
Although there are few contradictions to oxygen properly used, there are important precautions in its administration. As in any aged patient, oxygen should be considered a drug that has proper doses and routes of administration for maximum benefit, minimum toxicity, and reasonable cost-effectiveness.
In general, therapeutic manipulation to maintain a PaO2 of 60 mmHg ensures adequate relief from hypoxemia. Little additional benefit is gained from further increases because of the functional characteristics of hemoglobin, that is, 90% saturation is achieved with a PaO2 of 60 mmHg. This relationship assumes the presence of normally functioning hemoglobin; in settings such as carbon monoxide poisoning, even supranormal PaO2 may be associated with a reduction in available hemoglobin and a resultant lower oxygen content.
Although oxygen administration will rarely be detrimental to the pediatric patient, the means by which oxygen is administered may so agitate the child that respiratory distress and hypoxemia is worsened rather than improved. Therefore, while oxygen should be offered to any pediatric patient, the method of administration must be adjusted if it produces marked agitation.
As part of the decision to administer oxygen, the health care professional must determine if passive oxygen administration (such as with mask or cannulas) is adequate or if positive-pressure ventilation is required. Positive-pressure ventilation is needed if there is apnea, sustained high work of breathing, altered mental status, or persistent cyanosis despite a brief trial of high-concentration oxygen administration. Positive-pressure or assisted ventilation should be initiated.
Failure to Maintain an Open and Protected Airway. Airway management in children is a difficult task. The anatomic and physiologic factors outlined previously must be kept in mind when approaching the patient. Remember that the single most common cause of respiratory deterioration in infants and children is an inadequate airway.
Airway management in children is not simple. The first consideration in airway management is head position. If the patient is obtunded or otherwise unable to maintain a position of comfort, then the patient is placed in the sniffing position in order to minimize upper airway obstruction from soft tissues.2,3 It must again be emphasized that, if able, patients should be allowed to choose their position of comfort.
Specific techniques for maintaining an airway such as positioning the child into a sniffing position, jaw thrust or chin lift maneuvers, insertion of an oral airway, or a nasopharyngeal airway are reviewed elsewhere27-32 and will not be included in this discussion.
Inability to Provide Assisted Ventilation. It is sometimes technically difficult to assist respiration efficiently with a bag-valve device and mask; nevertheless, this is a mandatory skill for all emergency health care providers.
The use of the bag-valve device and mask has several advantages: it provides an immediate means of ventilatory support, it conveys a sense of compliance of the patient’s lungs to the rescuer, it can be used with spontaneously breathing patients, and it can deliver an oxygen-enriched mixture to the patient.
Typically, the bag-valve device is available in three sizes: adult (capable of storing between 1000 mL to 1600 mL of gas), child (500-700 mL of gas), and infant (150-240 mL of gas). A recent study showed that standardized adult and pediatric bag-valve devices provide equally effective ventilation in an infant mannequin lung model.2,33 Also, the use of larger resuscitation bags did not result in excessive ventilation.
Small-volume (infant), self-inflating bag devices do not deliver an adequate tidal volume to the infant with poorly compliant lungs. The small bag volumes also limit the duration of inspiration, which needs to be prolonged when the lungs are atelectatic. Thus, child-size and adult-size self-inflating bags may be used for the entire range of infants and children.2,34
While its use has gained widespread acceptance in all care settings, the bag-valve mask device has also been characterized as cumbersome and difficult to use. The most frequent problem with the bag-valve mask device is the inability to provide adequate ventilatory volumes to a patient who is not endotracheally intubated. This most commonly results from the difficulty of providing a leak-proof seal to the face while maintaining an open airway. It also occurs when the bag is not squeezed sufficiently enough to force an adequate amount of air into the patient’s lungs.
The following points are offered as a review of effective ventilation techniques.
1. While acceptable in some situations, a bag-valve mask device used in emergency situations should not contain a "pop-off" valve. The pressures required for ventilation in many emergency situations may exceed the pop-off limit, and delivered tidal volume will be insufficient.2,35
2. Mask fit is much more important than resuscitation bag size to ensure adequate ventilation.36
3. The chin of the patient should be held forward in a sniffing position.
4. The most advantageous position for ventilating will be slightly different for each patient. Therefore, the head should be moved into various positions by flexion, extension, and lateral rotation until the best airway is obtained.
5. It may be helpful to insert an oral or nasal airway.
6. The mask used for assisted ventilation should be of an appropriate size for each patient. The upper end of the mask should fit over the bridge of the nose and be well below the eyes. The lower end should be on or directly above the mandible.
7. Place the finger of the left hand just under the mandible to support it in an anterior position (pull the face into the mask). Position the mandible with the left hand; place the mask on the bridge of the nose with the right hand, and encircle the mask with the thumb and forefinger of the left hand. Hold tightly. Do not apply pressure to the soft parts of the chin, or the tongue may be pushed into the posterior pharynx and obstruct the airway further. Apply pressure to the mask primarily with the thumb and forefinger of the left hand. Squeeze the ventilating bag with the right hand, using a smooth compression. Once ventilatory assistance is begun, continual assessment is necessary for determining whether an adequate amount of air is being delivered with the bag-valve device. Chest rise must be visualized with each delivered ventilation. If there is no chest movement, there is no ventilation.
8. To effectively use the bag-valve device with the mask attached, the rescuer must be positioned at the top of the patient’s head. Otherwise it will be nearly impossible to maintain an effective seal between the mask and the patient’s face and keep the airway open at the same time.
9. Leaks around the mask occur if the breathing bag collapses without inflating the patient’s chest. To prevent leaking, change the mask position or size, or hold it more tightly in place. However, do not press down on the mask and force the mandible backwardthis occludes the airway. To ensure ventilatory effectiveness, attention must be paid to the resistance in the bag with each delivered breath. A great deal of resistance (noted by a bag that is hard to squeeze) is indicative of upper or lower airway obstruction. The most likely culprit is a tongue that has fallen back against the oropharynx. To correct this problem, unless trauma is suspected, further hyperextend the patient’s head by applying more backward pressure on the mandible with the two or three fingers of the right hand. If not already in place, insert an oropharyngeal airway if the patient lacks a gag reflex. Other possible causes include foreign body obstruction, tension pneumothorax, and severe bronchospasm. Note: a bag that compresses extremely easily is indicative of a leak somewhere in the bag system. The best indicator of effective ventilations is the rise and fall of the patient’s chest.
10. If it is necessary to use both hands to hold the mandible forward and hold the mask on the face, a second person can squeeze the bag.
11. With each squeeze of the ventilating bag, the chest should expand and good breath sounds should be audible. The patient’s color should improve, and, if airway obstruction was present, breathing should become noticeably easier.
12. If the head is malpositioned, gastric distension will occur as the bag is squeezed. To correct this, the head should be repositioned. Gastric distention caused during artificial ventilation interferes with ventilation by elevating the diaphragm and decreasing lung volume. This occurs most often in children but is also seen in adults. The incidence of gastric distention is minimized by limiting ventilation volumes and pressures to those that raise the chest, thus avoiding exceeding the esophageal opening pressure. Manual ventilation should be performed with cricoid pressure (Sellick maneuver). The Sellick maneuver, or posterior displacement of the larynx, is produced with steady pressure on the cricoid cartilage. Appropriate application of cricoid pressure prevents gastric gas insufflation during airway management via mask up to 40 cm H2O peak inspiratory pressure in infants and children.37 Gastric distention may have occurred due to previous aerophagia. Attempts at relieving gastric distention by pressure on the abdomen should be avoided because of the high risk of aspirating gastric contents into the lungs during this maneuver. If ventilation is totally ineffective because of gastric distention, then gastric decompression should be attempted. The patient’s entire body is turned to the side before pressure is applied to the epigastrium or, preferably, a nasogastric tube is passed.
13. Take care to allow the patient to completely exhale after each delivered breath. Ventilatory assistance that is too rapid will lead to gas trapping.32 The ventilatory rate described above will give the patient sufficient time to passively exhale. There is no predetermined ventilatory rate.
14. If assisted ventilation is necessary for an extended period of time, an endotracheal tube should be inserted. Good bag-valve-mask ventilation technique is mandatory to keep the child alive while preparations are made for a safe and controlled intubation. This is not a basic life support skill as much as an initial life support skill.
Improper Plan for Intubation. While endotracheal intubation is clearly an emergency procedure, it often can be accomplished after the airway has been controlled and the patient has been adequately ventilated with a bag-valve mask device to ensure oxygenation and removal of carbon dioxide.
The decision to intubate and begin ventilatory assistance is always a clinical one; arterial blood gas values are at best a helpful guide. Frequently, this decision is based on a best guess of what might happen. Early "elective" intubation is often wise, even if progressive CO2 retention occurs without CNS depression, or if hypoxemia is corrected but with high concentrations of supplemental oxygen.
The decision to begin ventilatory assistance is often based on more than one factor. Hypoxemia, respiratory acidosis, and excessive respiratory work often occur together during acute respiratory failure. Likewise, rhonchi, a poor cough reflex, CNS depression, and mild hypercapnia form another frequent combination. Any such combination of indications should lower one’s threshold for initiating airway protection and ventilatory support.
Mechanical ventilatory assistance should be initiated if the work required to maintain adequate gas exchange is greater than that which can be sustained indefinitely, even if gas exchange is still satisfactory. The work of breathing ordinarily requires less than 3% of the body’s total O2 consumption.38 During acute respiratory failure, ventilatory work may increase 10- to 20-fold. Unfortunately, it is difficult to accurately quantify an "excessive" work of breathing.
Tracheal intubation is indicated if the airway cannot be kept clear of secretions or if the lungs cannot be protected from aspiration, even when gas exchange and ventilatory work are normal. Common settings include any state of depressed consciousness, facial or neck trauma, and infections or infiltrative diseases (including malignancy) of the upper airway. Clinical clues include hearing rhonchi over the central airways or performing tracheal suctioning without stimulating an effective cough, especially if depressed consciousness is present.
The recognition and management of impending failure may prevent progression to failure and its serious consequences, including cardiopulmonary arrest. When the trend is appreciated, specific interventions frequently are able to interrupt the progression to respiratory failure.
Bronchodilators for wheezing, racemic epinephrine aerosols for croup, or a nasogastric tube for gastric distension are examples of the specific therapies that may be used in impending failure. When the patient’s condition has progressed or is about to progress to frank respiratory failure, as defined clinically or by arterial blood gases, the only therapeutic modality is oxygenation and assisted ventilation. Implement it without delay; pursuit of other therapeutic modalities can have disastrous consequences.
A plan for intubation helps decrease the chance of hypervigilant behaviors developing when a child deteriorates and needs intubation. Hypervigilance leads to high anxiety during the procedure, rapid attempts to identify alternatives, and potentially inappropriate responses.39
Improper Airway Management in the Non-apneic Patient. Although intubation of the apneic patient is extremely successful in the prehospital and ED setting, intubation of the struggling, "awake" child is difficult, hazardous, and often unsuccessful. Such attempts can adversely affect oxygenation, circulation, and intracranial pressure.
An alternative to orotracheal intubation is the blind nasotracheal intubation route. However, in children, this route is difficult, time-consuming, fraught with complications, and often contraindicated.32 This technique cannot be used in patients requiring a tube less than 5 mm internal diameter as these tubes are not stiff enough, and the angle from the nares to the glottis does not lead to high success.32 Nasotracheal intubation is at least relatively contraindicated in patients with coagulopathy or on anticoagulation therapy, basilar skull fracture with potential involvement of the cribriform plate, nasal obstruction, significant facial trauma, upper airway foreign body, or an upper airway abscess or friable tumor.
Rapid-sequence intubation (RSI), the use of pharmacologic adjuncts to facilitate endotracheal intubation and to reduce adverse effects of this procedure,40-42 is an organized approach to emergency intubation comprising rapid sedation and muscle relaxation with minimal or no positive-pressure ventilation. In addition, adjunctive pharmacologic agents and techniques are used to minimize complications such as aspiration, hypoxemia, and sympathomimetic-mediated rises in blood and intracranial pressures. Pharmacologic paralysis to facilitate endotracheal intubation maximizes the probability of successful tube placement while minimizing hemodynamic responses and complications. Studies of the safety of RSI in the ED as well as the prehospital care environment have been documented.43,44 Indications for and relative contraindications to RSI have been outlined in previous publications and will not be reviewed here.40,41
The basic process of RSI involves preparation, preoxygenation, sedation, muscle relaxation, intubation, and endotracheal tube stabilization. The risks of attempting intubation without the benefit of sedation and paralysis in the child with compromised cardiorespiratory reserve are substantial. Intubation is likely to be unsuccessful, may result in oral and airway damage, and further exacerbates hypoxia and acidosis. Furthermore, intubation of an awake, struggling patient cannot be justified on humane grounds.
Healthcare providers should also be knowledgeable of dosages, side effects, indications, and contraindications of the medications to be used during intubation.45 Pharmacologic agents are frequently used to facilitate endotracheal intubation. Paralysis using neuromuscular blocking agents allows laryngoscopy and placement of the artificial airway without a struggling or biting patient. In addition, paralysis allows effective control of ventilation. Muscle relaxants are contraindicated if inability to establish an artificial airway and maintain adequate ventilation are anticipated. Among the hazards of using muscle relaxants, the most dramatic is the failure to establish a secure airway and ventilate the lungs following administration of the drug. A good rule of thumb regarding use of these agents is to avoid them whenever upper airway obstruction is suspected or airway anatomy is uncertain.25 It is far better to allow the patient to continue to breathe spontaneously than to risk complete loss of respiratory effort following administration of a muscle relaxant. Remember dyspnea is better than apnea.
Failure to Maintain the Airway after Intubation. The endotracheal tube then needs to be secured with tape so that displacement does not occur with movement. Taping the tube is a two person job and should not be attempted alone. Although there are several methods of effective taping, always be sure that the head and the tube move as a unit and that kinking and angular bends of the tube are not possible. Stabilization to prevent rotation, flexion, or extension of neck is necessary before patient movement. Flexion and extension of the head may displace the tube either into a mainstem bronchus or up into the pharynx, with potential catastrophic consequences.1,46 Always measure and record the depth of the endotracheal tube (ETT) (at incisors). After any patient movement or changes in the clinical status of the patient, confirm that the depth of the ETT has not changed.
Once the ETT is placed and secured, constant cardiopulmonary monitoring is essential. If an intubated child begins to deteriorate, one should consider the following possible complications: 1) displacement of the endotracheal tube into the right mainstem bronchus, pharynx, or esophagus; 2) endotracheal tube obstruction with saliva, mucus, blood, foreign body, or purulent secretions; 3) mechanical failure involving the bag-valve device or the ventilator; and 4) pneumothorax.1
In any child with cardiopulmonary deterioration, first remove the child from the ventilator, assess bilateral breath sounds, and end tidal CO2. Bag the endotracheal tube, and reassess. Check for signs of tension pneumothorax (e.g., JVD, unilateral breath sounds, and hyperresonance) if there is any question about the adequacy of the tube remove and replace it. Once the tube is replaced, reassess the cardiopulmonary status and consider other causes for the deterioration (worsening of underlying condition, bleeding, etc.)
In this article, pitfalls associated with the management of pediatric airways have been reviewed. These pitfalls include inadequately establishing the severity and significance of respiratory distress, misinterpretation of the signs and symptoms of respiratory distress or failure, performance of overzealous or unnecessary examinations, failure to constantly reassess the patient’s condition, lack of knowledge about airway differences, failure to recognize a difficult airway, misapplication of oxygen administration, failure to maintain an open/protected airway, inability to provide assisted ventilation, improper planning for intubation, improper management of the non-apneic patient, and failure to maintain the airway after intubation. Attention to these pitfalls will help prevent therapeutic misadventures in children with respiratory diseases.
References
1. Perkin RM, van Stralen D, Mellick LB. Managing pediatric airway emergencies: Anatomic considerations, alternative airway and ventilation techniques, and current treatment options. Pediatric Emerg Med Rep 1996;1:1-12.
2. Todres ID. Pediatric airway control and ventilation. Ann Emerg Med 1993;22:440-444.
3. Higgins TL, Yared JP. Clinical effects of hypoxemia and tissue hypoxia. Respiratory Care 1993;38:603-615.
4. Rothrock SG, Perkin R. Stridor: A review, update, and current management recommendations. Pediatric Emerg Med Rep 1996;1:29-40.
5. Davis HW, Gartner JC, Glavis AG, et al. Acute upper airway obstruction: Croup and epiglottitis. Pediatr Clin North Amer 1981;28:859.
6. Chantarojanasir T, Nichols DG, Rogers MC. Lower airway disease: Bronchiolitis and asthma. In: Rogers MC (ed). Textbook of Pediatric Intensive Care Baltimore: Williams and Willkins; 1987:199-235.
7. Anas NG. Respiratory Failure. In: Levin DL, Morris FC (eds). Essentials of Pediatric Intensive Care. St. Louis: Quality Medical Publishing, Inc.; 1990:64-72.
8. Mellick LB, van Stralen D, Perkin RM. The role of emergency medicine in a teaching hospital: Decision making in an uncontrolled environment. Am J Emerg Med 1993;11:187.
9. Morley CJ, Thorton AJ, Fowler MA, et al. Respiratory rate and severity of illness in babies under six months old. Arch Disease Child 1990;65:834-837.
10. National Conference on Cardiopulmonary Resuscitation (CPR) and Emergency Cardiac Care (ECC). Pediatric Advanced Life Support. JAMA 1992;268:2262-2275.
11. Hooker EA, Danzl DF, Brueggmeyer M, et al. Respiratory rates in pediatric emergency patients. J Emerg Med 1992;10:407-410.
12. DiMaio AM, Singh J. The infant with cyanosis in the emergency room. Pediatr Clin North Am 1992;39:987-1006.
13. Gay PC, Edmonds LC. Severe hypercapnia after low-flow oxygen therapy in patients with neuromuscular disease and diaphragmatic dysfunction. Mayo Clin Proc 1995;70:327-330.
14. Mower WR, Sachs C, Nicklin EL, et al. Effect of routine emergency department triage pulse oximetry screening on medical management. Chest 1995;108:1297-1302.
15. Maneker AJ, Petrack EM, Krug SE. Contribution of routine pulse oximetry to evaluation and management of patients with respiratory illness in a pediatric emergency department. Ann Emerg Med 1995;25:36-40.
16 Voter KZ, McBride JT. Diagnostic tests of lung function. Pediatr Rev 1996;17:53-63.
17. Abramo TJ, Wiebe RA, Scott SM et al. Noninvasive capnometry in a pediatric population with respiratory emergencies. Pediatr Emerg Care 1996;12:252-254.
18. Poole SR, Chetham M, Anderson M. Grunting respirations in infants and children. Pediatr Emerg Care 1995;11:158-161.
19. Singer JI, Losek JD. Grunting respirations: Chest or abdominal pathology? Pediatric Emerg Care 1992;8:354-358.
20. Santamaria JP, Schafermeyer R. Stridor: A review. Pediatric Emerg Care 1992;8:229-234.
21. Shapiro GG. Childhood asthma. Pediatr Rev 1992;13:403-412.
22. Nickerson BG. Approach to the wheezing infant. Pediatr Annals 1986;15:99-104.
23. Schwartz DE, Wiener-Kronish JP. Management of the difficult airway. Clin Chest Med 1991;12:483-495.
24. Einarsson O, Rochester CL, Rosenbaum S. Airway management in respiratory emergencies. Clin Chest Med 1994;15:13-34.
25. Tobias JD. Airway management for pediatric emergencies. Pediatr Annals 1996;25:317-328.
26. Stewart CE. Management of the difficult airway: Advanced intubation techniques. Emerg Med Rep 1992;13:53-62.
27. Inaba AS, Seward PN. An approach to pediatric trauma. Emerg Med Clin North Am 1991;9:523-548.
28. Schafermeyer R. Pediatric trauma. Emerg Med Clin North Am 1993; 11:187-205.
29. Hastings RH, Kelly SD. Neurologic deterioration associated with airway management in a cervical spine-injured patient. Anesthesiology 1993;78:580-582.
30. Mellick LB, Dierking BH. One size doesn’t fit all: Choosing pediatric equipment-part II. J Emerg Med Serv 1991;17:35-46.
31. Coleman DL, Cohen NH. Airway management of the nonintubated patient. J Intensive Care Med 1987;2:354-362.
32. Barkin RM. Pediatric airway management. Emerg Med Clin North Am 1988;6:687-692.
33. Kanter RK. Evaluation of mask-bag ventilation in resuscitation of infants. Am J Dis Child 1987;141:761-763.
34. Finer NN, Barrington KJ, Al-Fadley F, et al. Limitations of self-inflating resuscitations. Pediatrics 1986;77:417-420.
35. Kain ZN, Berde CB, Benjamin PL, et al. Performance of pediatric resuscitation bags assessed with an infant lung simulator. Anesth Analg 1993;77:261-264.
36. Terndrup TE, Kanter RK, Cherry RA. A comparison of infant ventilation methods performed by prehospital personnel. Ann Emerg Med 1989;18:607-611.
37. Moynihan RJ, Brock-Utne JG, Archer JH, et al. The effect of cricoid pressure on preventing gastric insufflation in infants and children. Anesthesiology 1993;78:652-656.
38. Schuster DP. A physiologic approach to initiating, maintaining, and withdrawing mechanical ventilatory support during acute respiratory failure. Am J Med 1990;88:268-277.
39. Janis IL. Coping patterns among patients with life-threatening diseases. Issues Ment Health Nursing 1985;7:461-476.
40. Gerardi MJ, Sacchetti AD, Cantor RM, et al. Rapid-sequence intubation of the pediatric patient. Ann Emerg Med 1996;28:55-74.
41. Yamamoto LG. Rapid sequence anesthesia induction and advanced airway management in pediatric patients. Emerg Med Clin North Am 1991;9:611-638.
42. Walker LA. Using rapid sequence induction to facilitate tracheal intubation. Emerg Med Rep 1993;14:125-132.
43. Gnauck K, Lungo JB, Scalzo A, et al. Emergency intubation of the pediatric medical patient: Use of anesthetic agents in the emergency department. Ann Emerg Med 1994;23:1242-1247.
44. Brownstein D, Shugerman R, Cummings P, et al. Prehospital endotracheal intubation of children by paramedics. Ann Emerg Med 1996;28:34-39.
45. Schoenfeld PS, Baker MD. Management of cardiopulmonary and trauma resuscitation in the pediatric emergency department. Pediatrics 1993;91:726-729.
46. Conrardy PA, Goodman LR, Lainge F, et al. Alteration of endotracheal tube position. Crit Care Med 1976;4:8-12.
Physician CME Questions
12. When using a bag-valve mask, providers must pay special attention to:
A. maintaining a specific ventilatory rate.
B pressing down on the mask in order to prevent leaking of the delivered volume.
C. volume of air moved with each squeeze of the bag as assessed by chest movement and auscultation.
D. the supplemental oxygen flow rate.
13. The use of pharmacologic adjuncts to facilitate endotracheal intubation:
A. is contraindicated in pediatric patients less than 1 year of age.
B. requires a prolonged period of bag-valve mask ventilation.
C. cannot be done safely outside of the intensive care unit or operating room.
D. maximizes the probability of successful tube placement while minimizing complications.
14. A grunting sound on expiration:
A. is an ominous sign and should never be ignored.
B. specifically reflects an intrathoracic problem.
C. can be a normal finding in infants.
D. decreases expiratory airway pressure.
15. Delcining oxygen saturation is most rapidly and most correctly identified by:
A. tongue and mucosal cyanosis.
B. perioral cyanosis.
C. pulse oximetry.
D. blood gas analysis.
16. The decision to intubate the child’s trachea is based on:
A. arterial blood gas values.
B. pulse oximetry.
C. clinical evaluation.
D. radiologic findings.
E. a good history.
17. A normal respiratory rate and the presence of injury or disease:
A. is a sign of compensation.
B. maintains ventilation.
C. is a sign of adequate oxygenation.
D. indicates absence of obstruction.
E. is not normal.
18. Overzealous or unnecessary examinations are not recommended because they:
A. can offend parents.
B. can result in respiratory failure.
C. needlessly increase cost of care.
D. provide too much information.
19. A 4-month-old infant with an one-day history of cold symptoms develops labored breathing. On arrival, the infant is sleepy but easily arousable, has mild intercostal retractions, and a respiratory rate of 56. She is pale, but not cyanotic. Auscultation reveals good air movement but coarse rales. Peripheral pulses are strong. The proper approach to this child is:
A. begin airway clearing maneuvers.
B. offer oxygen, position child appropriately, monitor, and continuously evaluate.
C. prepare to intubate.
D. initiate bag-mask ventilatory support.
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