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Paediatric Respiratory Reviews 14 (2013) 6469

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Paediatric Respiratory Reviews

Mini-Symposium: Paediatric Respiratory Emergencies

Acute respiratory failure in children

rg Hammer Ju
Medical Director, Division of Intensive Care and Pulmonology, University Childrens Hospital Basel (UKBB), Spitalstrasse 33, 4031 Basel, Switzerland

EDUCATIONAL AIMS  To review the physiology behind respiratory failure in children,  to provide guidance on how to assess the child with acute respiratory distress,  to emphasise that correct interpretation of clinical signs allows the physician to pinpoint the cause to a distinct part of the respiratory system without the use of sophisticated medical examinations,  to emphasise the importance of recognising acute respiratory failure early in its course,  to provide some guidance on how to assess the urgency and correct timing of more invasive interventions in children with impending respiratory failure,  to discuss some basic and general management issues of respiratory failure in children and  to emphasise that invasive airway management in critically ill children should be performed by an expert with experience in paediatric critical airway management.



Keywords: Respiratory physiology Infants Work of breathing Cardio-respiratory arrest

Acute respiratory failure is the most common medical emergency in children. One aim of this review is to discuss the physiologic peculiarities that explain the increased vulnerability of infants and children to any pathology affecting the respiratory tract. The other aim is to highlight the importance of history taking and correct physical examination for early recognition of an impending catastrophic progression of respiratory failure. Under most circumstances, correct physical examination alone allows one to pinpoint the cause to a particular part of the respiratory system and to make the appropriate decisions for a proactive and life-saving management of the critically ill child. 2013 Elsevier Ltd. All rights reserved.

INTRODUCTION Paediatric respiratory emergencies are among the most common reasons for hospital admission and result in a signicant number of deaths, particularly in children under 1 year of age. Acute respiratory infections account for about 20% of all deaths in children under the age of 5 years worldwide.1 Acute respiratory failure can be looked at as a derangement in physiology with the potential to result in signicant morbidity and mortality without prompt and appropriate intervention. It is mostly the result of progressive or acute and sudden deterioration of respiratory and circulatory function during the course of various diseases. One frequent avoidable factor associated with child death is the failure to recognise serious illness in children who are previously well. This failure most often occurs at the point of rst contact between the sick child and the health-care service and

includes the failure to understand the importance of the history or the failure to examine the child and interpret the physical signs correctly.2 Early recognition, anticipatory supportive intervention and institution of therapy may interrupt the pathophysiologic process leading to cardiopulmonary arrest. Hence, the objectives of this article are a) to review the denition of respiratory failure, b) to describe the peculiarities of the paediatric respiratory system rendering children more vulnerable to respiratory failure and c) to pinpoint the clinical signs of respiratory failure and to emphasise a problem-based rather than a diagnosis-based approach to initiate life-saving interventions. DEFINITION OF RESPIRATORY FAILURE Respiratory failure can be dened as the inability to provide O2 along with removal of CO2 at a rate that matches the bodys metabolic demand. Respiratory failure can be formally divided into oxygenation and ventilation failure, which occur together as

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J. Hammer / Paediatric Respiratory Reviews 14 (2013) 6469


Intrinsic lung disease

Airway disease

Inadequate respiratory eort



Table 2 Physiologic reasons for the increased susceptibility for respiratory compromise of infants in comparison to adults (from Ref3). Cause Physiologic or anatomic basis " O2 consumption Immaturity of control of breathing

Laboured or decreased respiratory funcon

Increased work of breathing and tachypnoea or shallow breathing and inadequate respiratory rate, tachycardia

Compensated shock
Preferred vital organ perfusion Tachycardia, tachypnoea, prolonged capillary rell, normal systolic blood pressure

Metabolism " Risk for apnoea " Resistance to breathing " Upper airway resistance "

Respiratory failure Cardiopulmonary failure Cardiopulmonary arrest

Uncompensated shock

Figure 1. Pathway of deterioration in critical illness.

Table 1 Most common causes of respiratory failure in children. Disorders involving primarily the respiratory tract  Upper airway obstruction (e.g., croup, foreign body aspiration, epiglottitis, tonsillar hypertrophy)  Lower airway obstruction (e.g., bronchiolitis, status asthmaticus, BPD)  Lung disease (e.g., pneumonia, ARDS, pulmonary oedema, near-drowning) Mechanical impairment of ventilation  Neuromuscular disorders/myopathies/infant botulism/Guillain-Barre syndrome  Chest wall trauma and malformations, severe congenital scoliosis  Large pleural effusion, pneumothorax Failure of the central nervous system to control ventilation  Status epilepticus, infection of the central nervous system, intoxication, trauma, apnoea of prematurity Failure to meet oxygen needs of the tissue  Hypovolaemia, septic shock  Cardiac insufciency  Metabolic disorders, intoxication

Nose breathing Large tongue Airway size # Collapsibility " Pharyngeal muscle tone # Compliance of upper airway structures " Airway size # Lower airway resistance " Collapsibility " Airway wall compliance " Elastic recoil # Lung volume # Numbers of alveoli # Lack of collateral ventilation Efciency of respiratory muscles # Efciency of diaphragm # Rib cage compliance " Horizontal insertion of the diaphragm at the rib cage Efciency of intercostal muscles # Horizontal ribs Endurance of respiratory muscles # Respiratory rate " Fatigue-resistant type I muscle bres #

problem in neonatal and paediatric intensive care units (PICUs) (Table 2). The appreciation of the peculiarities of paediatric respiratory physiology is essential for the correct assessment of any ill child.3 Metabolism The basal metabolic rate is about 23 times higher in infants than in adults (7 at birth vs. 34 ml kg1 min1 in the adult). Hence, the normal resting state in infants is already one of high respiratory and cardiovascular activity. This means that infants have less metabolic reserve if O2 consumption needs to be increased during critical illnesses. Control of breathing A considerable amount of maturation of the control of breathing occurs in the last few weeks of gestation and in the rst few days of life, which explains the high prevalence of apnoea in infants born prematurely. The breathing pattern of newborn infants is irregular with substantial breath-to-breath variability and periodic breathing at times, which increases the risk of prolonged, potentially lifethreatening apnoea under certain circumstances. The responses to hypercapnia or hypoxia are decreased and of variable sensitivity, which renders the young infant much more vulnerable to any noxious stimuli and disturbances of the respiratory control mechanisms.4 Upper and lower airways Major increases in the resistance to airow may occur during respiratory disease because of the lack of supportive structures in the infant airway. The larynx, trachea and bronchi are considerably more compliant than in the adult, thus making the infants airway highly susceptible to distending and compressive forces.5 Thus, with any upper-airway obstruction, signicant dynamic inspiratory collapse of the extra-thoracic trachea can occur during forceful inspirations, which further increases the obstruction already present. With lower-airway obstruction, forced expiratory efforts result in increased intra-thoracic pressures. As a result,

respiratory failure progresses. Gas exchange and the resultant blood gas tensions are dependent on four processes: 1) transport of O2 to the alveolus, 2) diffusion of O2 across the alveolarcapillary membrane, 3) transfer of O2 from the lungs to the organs (depends on cardiac output and haemoglobin concentration) and 4) removal of CO2 from the blood into the alveolus with subsequent exhalation. Although respiratory failure may be dened simply in terms of blood gas abnormalities (partial pressure of oxygen in the blood (PaO2) < 60 mmHg, partial pressure of carbon dioxide in the blood (PaCO2) > 55 mmHg and saturation level of oxygen in hemoglobin (SaO2) < 90%), the institution of appropriately aggressive interventions depends on determining the underlying pathophysiology and assessing the clinical evolution and progression over time. Respiratory failure can evolve from intrinsic lung disease, airway disease or inadequate respiratory effort. At the nal stages of the pathway of deterioration in critical illness, it can be difcult for the inexperienced eye to differentiate clearly respiratory failure from cardiovascular failure (Figure 1). The most common causes of respiratory failure in children are listed in Table 1. THE PHYSIOLOGY BEHIND RESPIRATORY FAILURE IN CHILDREN WHY ARE INFANTS MORE VULNERABLE? The considerable differences in respiratory physiology between infants and adults explain why infants and young children have a higher susceptibility to more severe and speedier manifestations of respiratory diseases and why respiratory failure is a common


J. Hammer / Paediatric Respiratory Reviews 14 (2013) 6469


Shortness of breath

Work of breathing

Crying Forced respiraons Minute venlaon O2 consumpon

Airway collapse Retracons

Figure 2. Viscious cycle of anxiety in airway obstruction in paediatric patients.

dynamic expiratory collapse will cause further limitation of expiratory ow (e.g., worsening of upper- and lower-airway obstruction in the crying child). Understanding this phenomenon of dynamic airway collapse is particularly important in treating agitated children with upper- or lower-airway obstruction (Figure 2). It is important to remain calm, to radiate professional competence and to protect the child as much as possible from noxious or fear-provoking stimuli even under circumstances where one has to progress to more invasive interventions. The airways of a child are relatively large in comparison with those of an adult. However, in absolute terms they are small, and minor changes in the radius of the airway create a much larger increase in resistance to airow in the child than in the adult, as the total resistance increases by the fourth power of any reduction in radius. Chest wall and respiratory muscles Because of its shape, high compliance and deformability, the contribution of the rib cage to tidal breathing is limited in newborn and infants. The highly compliant ribs are horizontally placed and the intercostal muscles are poorly developed, so that the buckethandle motion upon which thoracic respiration depends is eliminated. Contraction of the diaphragm during inspiration will tend to move the lower rib cage inwards, because the diaphragm inserts almost horizontally. The intercostal muscles and the diaphragm are antagonists at the costal margin and the balance of control over the costal margin depends on the arch of the

diaphragm. If the diaphragm is at (e.g., observed with pulmonary hyperination), it wastes energy by constricting the costal margin an essentially forced expiratory act instead of exerting its force by drawing air into the thorax with inspiration. This paradoxical inward motion of the costal margin with inspiration is called the Hoover sign and is a common symptom in children with marked peripheral airway obstruction and hyperination6 (Figure 3). The highly compliant chest wall is easily distorted, so that under conditions of respiratory impairment much energy is wasted by sucking in ribs rather than fresh air. This paradoxical inward movement of the chest wall during inspiration is a common sign of almost any disorder causing respiratory distress in infants but is most pronounced in upper-airway obstruction. The balance between the chest and the lung recoil pressure determines the static resting volume of the lung. The infant reaches equilibrium at a relatively lower lung volume than the adult as a result of the high chest wall compliance. Breathing at tidal volumes overlapping closing volumes would result in airway closure and areas of ventilationperfusion mismatch. Infants are constantly defending their functional residual capacity by actively elevating the end-expiratory lung volume above the elastic equilibrium volume. The main mechanisms involved are incomplete relaxation of the diaphragm during exhalation, high respiratory rate and laryngeal breaking during exhalation.7 In addition, the diaphragm of the young infant is histochemically poorly equipped to sustain high workloads. Maturational changes occur, with increased mass and a progressive increase in the fatigue-resistant type I muscle bres, to approach adult values within the rst year of life.8 Lung parenchyma The area of gas exchange per body surface area is reduced in infants, mainly because of incomplete alveolarisation that carries on into later childhood. The elastic tissue in the septae of the alveoli surrounding the conducting airways provides the elastic recoil that enables the airways to remain open. Early in life there are few relatively large alveoli that provide little support for the airways, which are thus able to collapse easily. Hence, peripheral airway collapse contributes notably to the airway obstruction observed in infants with bronchiolitis or pulmonary oedema. Alveolar addition continues throughout childhood by septal division, providing more elastic recoil and a decreased tendency

Figure 3. The Hoover sign consists in the paradoxical inspiratory indrawing of the costal margin. The intercostal muscles and the diaphragm are antagonists at the costal margin which moves very little during quiet breathing (left panel). Pulmonary hyperination results in a attened diaphragm which exerts direct traction on the lateral rib margin (right panel).

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Figure 4. Left panel: Decreased elastic recoil pressure render the bronchi of infants vulnerable to collapse. Right panel: Collateral pathways of ventilation do not appear until 35 years of age.

for airway collapse with increasing age. Collateral pathways of ventilation (intra-alveolar pores of Kohn and bronchoalveolar canals of Lambert) do not appear until 34 years of age, which excludes alveoli beyond obstructed airways to be ventilated by these alternate routes and predisposes the infant to the development of atelectasis.9 Hypoxaemia and hypercapnia occur early and can become profound quickly in infants (Figure 4). CLINICAL EVALUATION OF RESPIRATORY PERFORMANCE The presenting symptoms of respiratory failure are often not specic to a particular respiratory illness, but correct interpretation of clinical signs should allow one to localise the cause to a particular part of the organ systems. Life-threatening upperairway obstruction, lower-airway disease, lung parenchymal disease and non-pulmonary causes of respiratory failure such as cardiovascular disorders mostly manifest with clearly distinguishable symptoms. Therefore, a pathophysiology-based approach with correct interpretation of history and clinical signs is most helpful to assess the severity of respiratory failure. The rst task when evaluating a child with breathing difculties is to determine the urgency of more invasive interventions such as intubation and non-invasive or invasive ventilatory support. This decision is either reached within the rst few minutes of presentation or during close monitoring of disease progression in the ICU. The most useful indicators are vital signs, work of breathing and level of consciousness. The rst step is to evaluate whether the child is breathing spontaneously and able to maintain patency of the upper airways. Partial or complete airway obstruction jeopardises sufcient oxygenation. In this situation, the most important and efcient manoeuvre is to manually open up the upper airway and to ensure its patency. Urgent interventions such as suctioning and performing a jaw-thrust manoeuvre alone or together with bagmask ventilation are needed if this is not the case.10 Airway foreign-body obstruction manoeuvres may also be considered. Airway obstruction during mask ventilation can be avoided by paying close attention to the positioning of the head, by applying jaw thrust and most importantly by keeping the mouth of the child open under the mask.11 Airway foreign-body obstruction manoeuvres (Heimlich manoeuvre, back blows and chest

compression) may only be considered if there is a history or possibility of recent choking and the child is still responsive, but unable to make a sound. Choking occurs in the eld and children with large foreign bodies lodged in the larynx often arrive unconscious or even dead in the emergency room. In this rare situation, bag-mask ventilation together with chest compression is recommended until direct laryngoscopy can be performed by a person with sufcient expertise. Chin lift, an airway-opening manoeuvre commonly taught because of its simplicity, should be used with caution in patients with adeno-tonsillar hypertrophy because it may convert partial into almost complete airway obstruction.12 Oral or nasopharyngeal airway devices such as a Guedel tube may be useful under such circumstances and facilitate bag-mask ventilation. If the child is breathing spontaneously, further steps are to assess respiratory rate, work of breathing, the efciency of respiration and the consequences of respiratory failure on other organ systems. Tachypnoea is commonly the rst manifestation of respiratory distress. Noisy tachypnoea typically occurs in children with respiratory disease and is an indication of increased work of breathing. The character of the noise allows the experienced physician to attribute the problem to a dened part of the respiratory system. By contrast, quiet or effortless tachypnoea mostly occurs in the context of non-pulmonary diseases and reects severe metabolic acidosis such as in shock, diabetic ketoacidosis, inborn errors of metabolism, cardiac insufciency and poisoning. In severe cardiogenic shock, increased work of breathing occurs due to the development of pulmonary oedema. A slow or irregular respiratory rate (bradypnoea) is usually an ominous clinical sign and indicates impending cardio-respiratory arrest. One must be aware that a decrease in respiratory rate from a rapid to a more normal (often shallow) rate may indicate deterioration and fatigue rather than clinical improvement. This is usually accompanied by a decreasing level of consciousness, which, however, can be masked by the use of sedation in the clinical setting. Assessment of the work of breathing is most important to evaluate the respiratory performance of the critically ill child. General signs of increased work of breathing, besides tachypnoea, are chest retractions, thoraco-abdominal asynchrony (which is more pronounced in upper-airway obstruction), nasal aring and the use of accessory muscles (head bobbing). Head bobbing occurs


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because the neck extensor muscles are not strong enough to stabilise the infants head, when the scaleni and sternocleidomastoid muscles are recruited to assist ventilation. Every child with head bobbing in the context of acute respiratory distress should be meticulously assessed and closely monitored. Correct interpretation of the clinical signs usually allows relating the cause of respiratory distress to a particular part of the respiratory system. Inspiratory stridor indicates upper-airway obstruction. Expiratory stridor develops as upper-airway obstruction increases and is an ominous sign of severe obstruction if accompanied by active expiratory muscle activity (e.g., abdominal muscle contraction). Pulsus paradoxus can be palpated or observed on the plethysmographic waveform of the pulse oximeter demonstrating a decrease in pulse pressure during inspiration under these circumstances. Active expiration together with pulsus paradoxus implies severe upper-airway obstruction and warrants close monitoring or even intubation.13 The Croup scoring system proposed by Max Klein is a clinically very useful tool for assessing the severity of upperairway obstruction in children14 (Figure 5). Expiratory wheezing and the presence of the Hoover sign (inward movement of the lower rib cage during inspiration) reect lower-airway obstruction and hyperination. Grunting or groaning and thrusting expirations signify a parenchymal lung problem. Grunting is the result of premature closure of the glottis during expiration to increase intrinsic positive end expiratory pressure (PEEP) and to prevent alveolar collapse. It is commonly observed in children with pulmonary oedema, acute respiratory distress syndrome (ARDS), and severe lobar pneumonia. Assessment of the efciency of respiration is performed by evaluating air entry by auscultation and cyanosis by pulse oximetry. The latter is often referred to as the fth vital sign.15 Children with acute respiratory failure are almost always hypoxaemic. If the human eye is able to detect cyanosis, O2 saturation is commonly below 90%. Lastly, the effect of respiratory failure on other organ systems has to be immediately and continuously assessed in children with acute respiratory failure. Cardiac output is mainly heart-rate dependent in children, because of the limited ability of the paediatric heart to increase stroke volume. Again, bradycardia is a sign of impending cardio-respiratory arrest, as is a falling blood pressure. The same applies to the level of consciousness. Agitation and depressed mental status as a result of hypoxaemia and/or

Figure 6. Arterial O2 and CO2 tensions may be maintained virtually to the point of exhaustion during the course of respiratory failure.

hypercapnia can both be warning signs of impending cardiorespiratory arrest. Any change in alertness has to be considered an ominous sign for a disastrous evolution of respiratory failure. Laboratory and radiographic examinations are important diagnostic tools in the management of children with acute respiratory failure. Nevertheless, serial blood gas analyses should only be regarded as one little piece of the whole puzzle to guide timing for more invasive interventions (Figure 6). A young child will readily tolerate most given stress to the respiratory system. As the disease progresses, minute ventilation may be virtually maintained to the point of exhaustion, at which time hypoxaemia and hypercapnia rapidly progress into cardio-respiratory arrest. The biggest difference in the development of cardio-respiratory failure between young children and adults is not the physiology, but the speed at which cardio-respiratory arrest can occur. Assessment of the need for an articial airway is primarily based on clinical signs general appearance is of most value. Warning signs are worried appearance, restlessness, impression of fatigue, marked retractions, head bobbing and increasing tachycardia. Intubation is performed too late when respiratory efforts decrease (bradypnoea, shallow breathing and decreased stridor) and loss of consciousness and bradycardia occur. MOST COMMON CAUSES OF ACUTE RESPIRATORY FAILURE IN CHILDREN A multitude of conditions can lead to acute respiratory failure. Common respiratory causes include respiratory infections of the upper and lower airways (such as croup, bronchiolitis and pneumonia), asthma and foreign-body aspiration. Rare causes such as malformations of the upper- and lower-respiratory system, plastic bronchitis or pulmonary haemorrhage have to be considered as well. The patient population of a PICU can often be compared to a rare stamp collection and the unusual is often the usual. Non-pulmonary causes need also to be considered, because heart failure, septic shock, inborn errors of metabolism and neurologic disorders (seizures and neuromuscular diseases) may present with breathing disturbances (Table 2). MANAGEMENT OF ACUTE RESPIRATORY FAILURE IN CHILDREN It is not the purpose of this review to discuss in detail the specic management strategies of the many causes of acute respiratory failure. Management depends not only on the specic cause, but also on the severity of respiratory failure. Extensive training and experience are required to acquire the knowledge and skills to stabilise children with critical illness in the emergency room or the PICU. Most important among these is the ability to

Figure 5. Kleins Croup Score.14

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manage the upper airway, which is the cornerstone of paediatric resuscitations as respiratory failure is the major cause of cardiorespiratory arrest in infants and children. This includes immediate recognition of a potentially difcult airway problem, appropriate medical-intervention strategies and experienced manual skills using appropriate equipment. Because children require resuscitation less frequently than adults, paediatric residents usually have little training opportunities to advance their airway expertise. It is not uncommon for paediatric residents to lack competency and knowledge of advanced life-saving skills such as strategies to improve bag-mask ventilation in difcult situations. It is essential to understand the anatomic and physiologic consequences of simple manoeuvres such as chin lift or jaw thrust and to apply these and use other non-invasive airway devices correctly to assure efcient mask ventilation. Excessive manual ventilation must be avoided because of its detrimental haemodynamic consequences during low ow states such as cardiopulmonary resuscitation.16 It increases intrathoracic pressure and impedes venous return, thereby reducing cardiac output, cerebral blood ow and coronary perfusion. Excessive ventilation also causes air trapping and barotrauma in patients with small-airway obstruction and increases the risk of stomach ination, regurgitation and aspiration. Oxygen should be given to all children with breathing disturbances to maintain an O2 saturation above 9294%. The appropriate device for O2 supplementation depends on the age of the child, the amount of O2 to be given and the local circumstances. Inhaled medications such as adrenaline or salbutamol may be useful to prevent further deterioration of severe upper- or lower-airway obstruction. The biggest mistake in using inhaled adrenaline in severe croup or inhaled salbutamol in acute asthma is under-dosing. Both medications can be safely and repetitively (or continuously) administered as full-strength solutions in critical situations. A winwin situation is already achieved if acute respiratory failure is recognised early in its course and the urgency of more invasive interventions is correctly anticipated. For in-house patients, regular communications among and between physicians and nursing staff facilitate prompt recognition and transfer of potentially worrisome patients to a higher level of care. Many inhospital cardiac arrests are potentially avoidable. Multiple system failures include delays and errors in diagnosis, inadequate interpretation of investigations, incomplete treatment, inexperienced doctors and management in inappropriate clinical settings.17 The aim to respond to acute patient deterioration before a cardiopulmonary arrest occurs with the intention of preventing the arrest from ever occurring is the main reason for the recent development of medical-emergency response teams in hospitals. Emergent endotracheal intubations carry a high risk of morbidity and mortality and should possibly be avoided. Be careful if its late when you intubate.18 Such intubations should be performed by a skilled team familiar with emergency airway management outside the controlled environment of the operating room. Such expertise is usually restricted to paediatric intensivists and anaesthetists. In most situations, the major difculty is not to stick the endotracheal tube down the trachea, but to organise a controlled and non-chaotic setting and to use the most appropriate drugs for sedation, analgesia and paralysis. Many sedatives used for rapid sequence induction may cause hypotension, which, in addition to neuromuscular blockade and positive pressure ventilation, may cause a lifethreatening reduction in cardiac output. For the invasive airway management, new technological aspects in endotracheal tube design have recently changed Paediatric Advanced Life Support (PALS) programme recommendations for emergency tracheal intubations in children, now suggesting the use of cuffed tubes of appropriate size in children.19,20 Algorithms have

recently been proposed to be used in the situation of a difcult intubation or the worst-case scenario: cannot ventilate and cannot intubate. These algorithms advocate the use of bre-optic intubation if mask ventilation is possible and the use of the laryngeal mask airway if mask ventilation is compromised.21,22 Conventional treatment of acute respiratory failure includes positive pressure ventilation with supplemental O2. The management of mechanical ventilation should incorporate the underlying pathophysiology and current concepts for prevention of ventilatorinduced lung injury. Non-invasive ventilation can be used in selected patients to decrease work of breathing or to assist weak respiratory muscles in patients with preserved respiratory drive. If adequate oxygenation cannot be achieved with conventional mechanical ventilation, surfactant instillation, inhaled nitric oxide and highfrequency oscillation may be considered. Extracorporeal membrane oxygenation is the ultimate option and needed in the rare situation where children with a reversible underlying illness fail conventional ventilation strategies. Further details of ICU management of children with respiratory failure are beyond the scope of this review.

1. Mathers CD, Boerma T, Ma Fat D. Global and regional causes of death. Br Med Bull 2009;92:732. 2. Pearson GA, Ward-Platt M, Harnden A, Kelly D. Why children die: avoidable factors associated with child deaths. Arch Dis Child 2011;96:92731. 3. Hammer J, Eber E. The peculiarities of infant respiratory physiology. in: Hammer J, Eber E, (eds.), Paediatric Pulmonary Function Testing. Basel, Switzerland: Karger AG; Prog Respir Res 2005: Vol 33, pp. 27. 4. Cohen G, Katz-Salamon M. Development of chemoreceptor responses in infants. Respir Physiol Neurobiol 2005;149:23342. 5. Deoras KS, Wolfson MR, Searls RL, Hilfer SR, Shaffer TH. Developmental changes in tracheal structure. Pediatr Res 1991;30:1705. 6. Klein M. Hoover sign and peripheral airways obstruction. J Pediatr 1992;120: 4956. 7. Kosch PC, Stark AR. Dynamic maintenance of end-expiratory lung volume in full-term infants. J Appl Physiol 1984;57:112633. 8. Keens TG, Bryan AC, Levison H, Ianuzzo CD. Developmental pattern of muscle ber types in human ventilatory muscles. J Appl Physiol 1978;44:90913. 9. Boyden EA. Notes on the development of the lung in infancy and early childhood. Am J Anat 1967;121:74961. 10. Hammer J, Reber A, Trachsel D, Frei FJ. Effect of jaw-thrust and continuous positive airway pressure on tidal breathing in deeply sedated infants. J Pediatr 2001;138:82630. 11. Holm-Knudsen RJ, Rasmussen LS. Paediatric airway management: basic aspects. Acta Anaesthesiol Scand 2009;53:19. 12. Reber A, Bobbia SA, Hammer J, Frei FJ. Effect of airway opening manoeuvres on thoraco-abdominal asynchrony in anaesthetized children. Eur Respir J 2001; 17:123943. 13. Argent AC, Newth CJ, Klein M. The mechanics of breathing in children with acute severe croup. Intensive Care Med 2008;34:32432. 14. Klein M. Croup, epiglottitis and the febrile dysphagia syndrome. S Afr J Cont Med Educ 1986;4:4551. 15. Mower WR, Sachs C, Nicklin EL, Baraff LJ. Pulse oximetry as a fth pediatric vital sign. Pediatrics 1997;99:6816. 16. Aufderheide TP, Sigurdsson G, Pirrallo RG, Yannopoulos D, McKnite S, von Briesen C, Sparks CW, Conrad CJ, Provo TA, Lurie KG. Hyperventilation-induced hypotension during cardiopulmonary resuscitation. Circulation 2004;109:19605. 17. Hodgetts TJ, Kenward G, Vlackonikolis I, Payne S, Castle N, Crouch R, Ineson N, Shaikh L. Incidence, location and reasons for avoidable in-hospital cardiac arrest in a district general hospital. Resuscitation 2002;54:11523. 18. Carroll CL, Spinella PC, Corsi JM, Stoltz P, Zucker AR. Emergent endotracheal intubations in children: be careful if its late when you intubate. Pediatr Crit Care Med: 11:343348. 19. Newth CJ, Rachman B, Patel N, Hammer J. The use of cuffed versus uncuffed endotracheal tubes in pediatric intensive care. J Pediatr 2004;144:3337. 20. Kleinman ME, Chameides L, Schexnayder SM, Samson RA, Hazinski MF, Atkins DL, Berg MD, de Caen AR, Fink EL, Freid EB, Hickey RW, Marino BS, Nadkarni VM, Proctor LT, Qureshi FA, Sartorelli K, Topjian A, van der Jagt EW, Zaritsky AL. Part 14: pediatric advanced life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation: 122(18 Suppl 3) S876908. mpelmann R. Offenhalten der 21. Frei FJ ET, Jonmarker C, Werner O, Robert Su mpelmann R, (Eds), Atemwege. in: Frei FJ ET, Jonmarker C, Werner O, Robert Su sthesie. Heidelberg Springer Medizin Verlag 2009, 131152. Kinderana 22. Weiss M, Engelhardt T. Proposal for the management of the unexpected difcult pediatric airway. Paediatr Anaesth: 20:454464.