insuficiencia respiratoria

1. Mini-Symposium: Paediatric Respiratory Emergencies
Acute respiratory failure in children
Jürg Hammer
Medical Director, Division of Intensive Care and Pulmonology, University Children’s Hospital Basel (UKBB), Spitalstrasse 33, 4031 Basel, Switzerland
INTRODUCTION
Paediatric respiratory emergencies are among the most
common reasons for hospital admission and result in a significant
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 significant 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 first
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
definition 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 defined as the inability to provide O2
along with removal of CO2 at a rate that matches the body’s
metabolic demand. Respiratory failure can be formally divided into
oxygenation and ventilation failure, which occur together as
Paediatric Respiratory Reviews 14 (2013) 64–69
A R T I C L E I N F O
Keywords:
Respiratory physiology
Infants
Work of breathing
Cardio-respiratory arrest
S U M M A R Y
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.
ß 2013 Elsevier Ltd. All rights reserved.
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.
E-mail address: juerg.hammer@unibas.ch.
Contents lists available at SciVerse ScienceDirect
Paediatric Respiratory Reviews
1526-0542/$ – see front matter ß 2013 Elsevier Ltd. All rights reserved.
http://dx.doi.org/10.1016/j.prrv.2013.02.001

2. 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 alveolar–capillary 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 defined 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 inter-
ventions 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 final stages of the
pathway of deterioration in critical illness, it can be difficult 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
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 2–3 times higher in infants
than in adults (7 at birth vs. 3–4 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 first 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 breath-
ing at times, which increases the risk of prolonged, potentially life-
threatening 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 airflow 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 infant’s airway
highly susceptible to distending and compressive forces.5
Thus,
with any upper-airway obstruction, significant dynamic inspira-
tory 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,
Intrinsic
lung disease
Airway
disease
Inadequate
respiratory
effort
Cardiogenic Hypovolaemia
Compensated shock
Preferred vital organ perfusion
Tachycardia, tachypnoea, prolonged capillary
refill, normal systolic blood pressure
Laboured or decreased respiratory
funcon
Increased work of breathing and tachypnoea
or shallow breathing and inadequate
respiratory rate, tachycardia
Respiratory failure Uncompensated shock
Cardiopulmonary failure
Cardiopulmonary arrest
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-Barré
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 insufficiency
Metabolic disorders, intoxication
Table 2
Physiologic reasons for the increased susceptibility for respiratory compromise of
infants in comparison to adults (from Ref3
).
Cause Physiologic or anatomic basis
Metabolism O2 consumption
Risk for apnoea Immaturity of control of breathing
Resistance to breathing
Upper airway resistance Nose breathing
Large tongue
Airway size #
Collapsibility
Pharyngeal muscle tone #
Compliance of upper airway structures
Lower airway resistance Airway size #
Collapsibility
Airway wall compliance
Elastic recoil #
Lung volume # Numbers of alveoli #
Lack of collateral ventilation
Efficiency of respiratory muscles # Efficiency of diaphragm #
Rib cage compliance
Horizontal insertion of the diaphragm at
the rib cage
Efficiency of intercostal muscles #
Horizontal ribs
Endurance of respiratory muscles # Respiratory rate
Fatigue-resistant type I muscle fibres #
J. Hammer / Paediatric Respiratory Reviews 14 (2013) 64–69 65

3. dynamic expiratory collapse will cause further limitation of
expiratory flow (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 airflow 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 bucket-
handle 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 flat (e.g., observed with pulmonary
hyperinflation), 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 hyperinflation6
(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 ventilation–perfusion 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 histochemi-
cally poorly equipped to sustain high workloads. Maturational
changes occur, with increased mass and a progressive increase in
the fatigue-resistant type I muscle fibres, to approach adult values
within the first 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
Shortness of breath
Fear
• Crying
• Forced respiraons
• Minute venlaon
• O2 consumpon
Airway collapse
Retracons
Work of breathing
Figure 2. Viscious cycle of anxiety in airway obstruction in paediatric patients.
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 hyperinflation results in a flattened diaphragm which exerts direct traction on the lateral rib
margin (right panel).
J. Hammer / Paediatric Respiratory Reviews 14 (2013) 64–69
66

4. for airway collapse with increasing age. Collateral pathways of
ventilation (intra-alveolar pores of Kohn and bronchoalveolar
canals of Lambert) do not appear until 3–4 years of age, which
excludes alveoli beyond obstructed airways to be ventilated by
these alternate routes and predisposes the infant to the develop-
ment 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
specific to a particular respiratory illness, but correct interpreta-
tion of clinical signs should allow one to localise the cause to a
particular part of the organ systems. Life-threatening upper-
airway obstruction, lower-airway disease, lung parenchymal
disease and non-pulmonary causes of respiratory failure such as
cardiovascular disorders mostly manifest with clearly distinguish-
able 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 first task when evaluating a child with breathing difficulties
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 first 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 first 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
sufficient oxygenation. In this situation, the most important and
efficient 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 bag-
mask 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 field 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 sufficient 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 efficiency of respiration and
the consequences of respiratory failure on other organ systems.
‘Tachypnoea’ is commonly the first 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 defined part of the
respiratory system. By contrast, quiet or effortless tachypnoea
mostly occurs in the context of non-pulmonary diseases and reflects
severe metabolic acidosis such as in shock, diabetic ketoacidosis,
inborn errors of metabolism, cardiac insufficiency 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 flaring and
the use of accessory muscles (head bobbing). Head bobbing occurs
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
3–5 years of age.
J. Hammer / Paediatric Respiratory Reviews 14 (2013) 64–69 67

5. because the neck extensor muscles are not strong enough to
stabilise the infant’s head, when the scaleni and sternocleidomas-
toid 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 interpreta-
tion 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 plethysmo-
graphic 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 upper-
airway obstruction in children14
(Figure 5).
Expiratory wheezing and the presence of the Hoover sign
(inward movement of the lower rib cage during inspiration) reflect
lower-airway obstruction and hyperinflation. 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 efficiency of respiration’ is performed by
evaluating air entry by auscultation and cyanosis by pulse
oximetry. The latter is often referred to as the fifth 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
hypercapnia – can both be warning signs of impending cardio-
respiratory 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 artificial 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 con-
sidered 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
specific management strategies of the many causes of acute
respiratory failure. Management depends not only on the specific
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. Klein’s Croup Score.14
Figure 6. Arterial O2 and CO2 tensions may be maintained virtually to the point of
exhaustion during the course of respiratory failure.
J. Hammer / Paediatric Respiratory Reviews 14 (2013) 64–69
68

6. manage the upper airway, which is the cornerstone of paediatric
resuscitations as respiratory failure is the major cause of cardio-
respiratory arrest in infants and children. This includes immediate
recognition of a potentially difficult 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
residentstolackcompetency andknowledgeof advanced life-saving
skills such as strategies to improve bag-mask ventilation in difficult
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 efficient mask ventilation. Excessive manual
ventilation must be avoided because of its detrimental haemody-
namic consequences during low flow states such as cardiopulmon-
ary resuscitation.16
It increases intrathoracic pressure and impedes
venous return, thereby reducing cardiac output, cerebral blood flow
and coronary perfusion. Excessive ventilation also causes air
trapping and barotrauma in patients with small-airway obstruction
and increases the risk of stomach inflation, regurgitation and
aspiration.
Oxygen should be given to all children with breathing
disturbances to maintain an O2 saturation above 92–94%. The
appropriatedeviceforO2 supplementationdependsonthe ageof 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 win–win 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 in-
hospital cardiac arrests are potentially avoidable. Multiple system
failures include delays and errors in diagnosis, inadequate
interpretation of investigations, incomplete treatment, inexper-
ienced doctors and management in inappropriate clinical set-
tings.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 it’s 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 difficulty 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 life-
threatening 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 difficult
intubation or the worst-case scenario: cannot ventilate and cannot
intubate.Thesealgorithmsadvocatetheuseoffibre-opticintubation
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 manage-
ment of mechanical ventilation should incorporate the underlying
pathophysiology and current concepts for prevention of ventilator-
induced 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 high-
frequency 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.
References
1. Mathers CD, Boerma T, Ma Fat D. Global and regional causes of death. Br Med
Bull 2009;92:7–32.
2. Pearson GA, Ward-Platt M, Harnden A, Kelly D. Why children die: avoidable
factors associated with child deaths. Arch Dis Child 2011;96:927–31.
3. Hammer J, Eber E. The peculiarities of infant respiratory physiology. in: Ham-
mer J, Eber E, (eds.), Paediatric Pulmonary Function Testing. Basel, Switzerland:
Karger AG; Prog Respir Res 2005: Vol 33, pp. 2–7.
4. Cohen G, Katz-Salamon M. Development of chemoreceptor responses in infants.
Respir Physiol Neurobiol 2005;149:233–42.
5. Deoras KS, Wolfson MR, Searls RL, Hilfer SR, Shaffer TH. Developmental changes
in tracheal structure. Pediatr Res 1991;30:170–5.
6. Klein M. Hoover sign and peripheral airways obstruction. J Pediatr 1992;120:
495–6.
7. Kosch PC, Stark AR. Dynamic maintenance of end-expiratory lung volume in
full-term infants. J Appl Physiol 1984;57:1126–33.
8. Keens TG, Bryan AC, Levison H, Ianuzzo CD. Developmental pattern of muscle
fiber types in human ventilatory muscles. J Appl Physiol 1978;44:909–13.
9. Boyden EA. Notes on the development of the lung in infancy and early child-
hood. Am J Anat 1967;121:749–61.
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;138:826–30.
11. Holm-Knudsen RJ, Rasmussen LS. Paediatric airway management: basic
aspects. Acta Anaesthesiol Scand 2009;53:1–9.
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;
17:1239–43.
13. Argent AC, Newth CJ, Klein M. The mechanics of breathing in children with
acute severe croup. Intensive Care Med 2008;34:324–32.
14. Klein M. Croup, epiglottitis and the febrile dysphagia syndrome. S Afr J Cont Med
Educ 1986;4:45–51.
15. Mower WR, Sachs C, Nicklin EL, Baraff LJ. Pulse oximetry as a fifth pediatric vital
sign. Pediatrics 1997;99:681–6.
16. Aufderheide TP, Sigurdsson G, Pirrallo RG, Yannopoulos D, McKnite S, von Briesen
C, Sparks CW, Conrad CJ, Provo TA, Lurie KG. Hyperventilation-induced hypoten-
sion during cardiopulmonary resuscitation. Circulation 2004;109:1960–5.
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;54:115–23.
18. Carroll CL, Spinella PC, Corsi JM, Stoltz P, Zucker AR. Emergent endotracheal
intubations in children: be careful if it’s late when you intubate. Pediatr Crit Care
Med: 11:343–348.
19. Newth CJ, Rachman B, Patel N, Hammer J. The use of cuffed versus uncuffed
endotracheal tubes in pediatric intensive care. J Pediatr 2004;144:333–7.
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 Guide-
lines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.
Circulation: 122(18 Suppl 3) S876–908.
21. Frei FJ ET, Jonmarker C, Werner O, Robert Sümpelmann R. Offenhalten der
Atemwege. in: Frei FJ ET, Jonmarker C, Werner O, Robert Sümpelmann R, (Eds),
Kinderanästhesie. Heidelberg Springer Medizin Verlag 2009, 131–152.
22. Weiss M, Engelhardt T. Proposal for the management of the unexpected difficult
pediatric airway. Paediatr Anaesth: 20:454–464.
J. Hammer / Paediatric Respiratory Reviews 14 (2013) 64–69 69