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Indian J Pediatr

DOI 10.1007/s12098-014-1559-4


Guest Editor: Bhim S. Pandhi

Acute Respiratory Distress in Children: Croup and Acute Asthma

B. S. Sharma & Dhananjay S. Shekhawat & Prity Sharma &
Chetan Meena & Hari Mohan

Received: 24 March 2014 / Accepted: 12 August 2014

# Dr. K C Chaudhuri Foundation 2014

Abstract Acute respiratory distress is one of the most common reason for emergency visits in children under 5 y of age.
An accurate understanding of the epidemiology of these diseases, identification of risk factors and etiology is critical for
successful treatment and prevention of related mortality. The
cause of acute respiratory distress varies in etiology, and hence
is amenable to different treatment modalities. Depending on
the predominant symptoms and signs, a child presenting to the
clinician can be divided into six groups, viz., stridor; cough,
fever and difficulty in breathing or fast breathing; wheezing;
mediastinal shift with severe respiratory distress; slow or
irregular breathing in absence of any pulmonary sign; and
respiratory distress with cardiac findings. A detailed history
followed by a thorough clinical examination and laboratory
evaluation assisted by imaging modalities if indicated, helps
to establish the exact cause of respiratory distress in the child.
Early recognition and prompt institution of appropriate management or referral can significantly improve the outcome of
this illness. This article offers clinicians a brief update on the
general management guidelines of respiratory distress in pediatric patients. Specific treatment depends on the exact cause,
however croup and acute severe asthma have been discussed
in this article.

Keywords Acute respiratory distress in children . Croup

syndrome . Acute severe asthma

B. S. Sharma (*) : D. S. Shekhawat : C. Meena : H. Mohan

Department of Pediatric Medicine, S.M.S. Medical College, Jaipur,
Rajasthan 302004, India
P. Sharma
Department of Pediatric Medicine, Fortis Escorts Hospital, Jaipur,
Rajasthan, India

Acute Respiratory Distress in Children

Any child with respiratory distress has a potential to progress
to respiratory failure. It includes:
1. Altered breathing pattern (fast, slow, feeble or
2. Forced breathing pattern or obstructed breathing
3. Chest wall in drawing
Signs of respiratory failure include respiratory distress and
cyanosis along with central nervous system (CNS) and /or
cardiovascular signs of hypoxemia.
CNS signs of hypoxemia: Restlessness, obtunded sensorium, somnolence, seizures and coma.
Cardiovascular signs of hypoxemia: Marked tachycardia,
bradycardia, hypotension and cardiac arrest.
Causes of Respiratory Distress in Children

Central nervous system disturbances (altered central regulation of respiration)

Neuromuscular problems (paralysis or weakness of respiratory muscles)
Interference with air entry
Obstruction in the upper airways
Acute laryngitis
Foreign body aspiration
Obstruction of the lower airways
Bronchial asthma

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Compression of lungs
Large pleural effusion

Differential Diagnosis
Depending on the predominant symptoms and signs, a child
presenting to the clinician can be divided into following 6

Interference with alveolar gas exchange

1. Stridor
Failure of alveolar ventilation


Cardiovascular problems
Decreased tissue oxygen supply/ Increased oxygen
Congestive heart failure (CHF)
Severe anemia

Diagnostic Evaluation
A. History

Acute, recurrent or chronic and nature of progression

Associated symptoms: cough, fever, rash, chest pain
Preceding events: foreign body inhalation, trauma,
accident, exposure to chemical or environmental
Family history: exposure to infections, tuberculosis,

B. Physical examination

Assess stability of airways and ventilation

i. Respiratory rate, rhythm, depth and work of

ii. Color, level of activity and playfulness
iii. Chest movements and indrawing of chest wall
iv. Abnormal sounds, stridor, wheezing and grunting
& Tracheal position
& Auscultation: air entry, type of breath sounds, adventitious sounds (rhonchi, crepts etc.)
& Assessment of other symptoms
C. Diagnostic workup

Routine blood investigations: CBC, septic profile,

blood culture
Imaging studies (X-ray, USG, as indicated)

a. Acute laryngotracheitis (Viral croup): Usually a younger child presenting with a viral prodrome of fever,
cough, coryza, suddenly develops a barking cough
and respiratory distress with stridor. Diagnosis in most
cases can be established on clinical grounds and routine X-ray of neck is not recommended.
b. Bacterial tracheitis: It should be suspected when a
clinical picture similar to that of viral croup is complicated by high grade fever, toxicity and copious
purulent tracheal secretions.
c. Foreign body in the larynx or trachea: An acute episode of coughing, choking or gagging followed by
stridor in infants and toddlers while eating nuts or
playing with small objects is typical. However in 1/
3rd patients below 3 y of age, such a history may not
be available. Unequal breath sounds on clinical examination combined with asymmetrical lung aeration
on chest X-ray usually establishes the diagnosis. In
absence of these findings with a strong suspicion of
foreign body, a CT chest is recommended. Diagnostic
bronchoscopy may be indicated in exceptional cases.
d. Diphtheria: Gradual onset with mild sore throat and
moderate fever is usually present. A grayish membrane
forms over the tonsils which may extend to affect the
larynx. The patient presents with harsh cough, hoarse
voice, stridor, neck swelling and increased difficulty in
breathing. The child may be severely toxic and death
may occur due to laryngeal obstruction and an emergency tracheostomy is required in certain cases.
e. Acute epiglottitis: It is a rare cause of stridor in India.
Usually occurs in children between 2 and 7 y of age
and very rarely below 2 y of age. Characteristically,
there is high grade fever of sudden onset, rapidly
progressing rattling or snoring, stridor, toxic appearance, muffled voice, difficulty in swallowing. The
child assumes a characteristic airway protective posture, i.e., sitting and leaning forward with protrusion
of jaw and open mouth with drooling of saliva. X-ray
lateral view of neck may be helpful. It shows a grossly
distended hypopharynx, swollen epiglottis and
aryepiglottic folds, and a normal subglottic airway.
f. Retro-pharyngeal abscess: High-grade fever, sore
throat, inspiratory stridor and difficulty in swallowing.
Neck is generally hyper-extended, so as to achieve
maximum airway. Lateral X-ray of the neck is

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diagnostic. It shows airway narrowing, and widening

of retro-pharyngeal space.
g. Acute severe tonsillitis superimposed on tonsillar and
adenoid hypertrophy is an important cause of severe
upper airway obstruction.
2. Cough, fever and difficulty in breathing or fast breathing
a. Pneumonia: Cough, fever and difficulty in breathing
in the absence of signs of airway obstruction are
suggestive of pneumonia. Presence of grunting, chest
wall indrawing, and inability to feed normally are
signs of severe disease.
3. Wheezing
a. Bronchiolitis: Should be considered in any child less
than 2 y of age with first episode of wheezing and
respiratory distress. There is usually a history of coryza 23 d preceding the onset of irritating cough,
wheezing and respiratory distress. The chest may
appear barrel shaped. Auscultation reveals reduced
air entry, bilateral fine crepitations and sibilant
b. Acute asthma is one of the most common causes of
wheezing in children. Family history of allergy, history of severe attacks in past, intractable cough, expiratory wheeze and multiple adventitious sounds on
auscultation are characteristic. Attacks are frequently
precipitated by exposure to allergens, infections, exercise, and sometimes by emotional disturbance.
c. Bronchitis and pneumonia may be associated with
wheezing and can be confused with the first attack
of asthma. This is secondary to airway edema and
mucus production. A clinical picture consistent with
infection and a chest X-ray are helpful for its differentiation from asthma.
d. Foreign body aspiration: There is usually a sudden
onset with cough, choking and onset of stridor and
wheezing. Stridor may occur initially but once the
foreign body slips below carina, stridor disappears
and wheezing predominates.
4. Mediastinal shift
a. Pleural effusion / Empyema
b. Atelectasis
c. Pneumothorax
These conditions can be diagnosed on the basis of
a meticulous clinical examination, chest X-ray, and
pleural tap / bronchoscopy, if needed.
5. Bradypnea and/or irregular breathing
In the absence of history or physical findings suggestive of primary respiratory illness, bradypnea and/or irregular breathing is most likely to be due to depression of
central nervous system.

6. Associated finding of congestive cardiac failure

The presence of significant auscultatory findings on
examination of heart in association of congestive cardiac
failure indicates underlying heart disease. In children with
congenital heart defects with a left to right shunt, there is
an increased incidence of recurrent respiratory tract infections. In these patients, the respiratory distress might arise
either from CHF or a respiratory infection. Chest X-ray,
echocardiography and ECG may be helpful in establishing the exact diagnosis.

General Management
1. General supportive measures
a. Positioning of the child: Allow the child to assume a
position of maximum comfort and allay the anxiety.
b. Minimize handling in procedures: If the diagnosis is
established, there is no urgency to agitate the child for
blood sampling.
c. Ensure adequacy of circulation, maintenance of temperature and hydration.
2. Oxygen should be administered when the child is
cyanosed or have stridor, wheeze, tachypnea with intercostal retractions. Humidified oxygen is administered to
prevent the drying up of epithelium of the respiratory
passages and ciliary dysfunction. Oxygen should be administered without agitating the child.
3. Children with severe respiratory distress, cyanosis (due to
respiratory cause) and impending respiratory failure
should be referred immediately after initial stabilization
to a higher center for further treatment.
4. Specific management depends on the etiology. The detailed discussion of each condition is beyond the scope of
this article; however the authors will discuss here the management of croup and acute asthma.

Croup Syndrome
Croup syndrome is most common cause of stridor in children,
and primarily affects children between 3 mo and 5 y of age,
with the peak in the 2nd year of life. The term croup syndrome refers to a group of diseases that vary in anatomic
involvement and etiologic agents and includes:

Spasmodic croup
Bacterial tracheitis

Indian J Pediatr

(without stridor or significant
chest wall indrawing at rest)

Give oral dexamethasone 0.6 mg/kg

Educate parents
Anticipated course of illness
Signs of respiratory distress
When to seek medical

(stridor and chest wall indrawing
at rest without agitation)

Minimize intervention
Place child on parents lap
Provide position of comfort

(stridor at rest and indrawing of
the sternum associated with
agitation or lethargy)

Minimize intervention (as for

moderate croup)
Provide blow-by oxygen
(optional unless cyanosis is

Give oral dexamethasone 0.6 mg/kg

May discharge home without

further observation

Sustained improvement as
evidenced by no longer
Chest wall indrawing
Stridor at rest
Educate parents (as for mild
Discharge home

Persistent mild symptoms

No recurrences of:
Chest wall indrawing
Stridor at rest
Provide education (as for mild

Discharge Home
Fig. 1 Treatment algorithm of croup

Nebulize with epinephrine

No or minimal improvement

Nebulize with epinephrine

Nebulize epinephrine
Racemic epinephrine 2.25%
(0.5 ml in 2.5 ml saline)
L-epinephrine 1:1000 (5 ml)
Give oral dexamethasone (0.6
mg/kg): may repeat once
If vomiting / too distressed to
take oral medication, consider
administering budesonide (2
mg) nebulized with

Good response to nebulized


Poor response to nebulized


Observe for 2 h

Repeat nebulized epinephrine

Recurrence of severe respiratory

Repeat nebulized epinephrine
If good response continue to

Poor response to nebulized


Shift to pediatric ICU for

further management

Indian J Pediatr

Acute viral infection is the most common cause of croup,

but bacterial and atypical agents have also been identified
[1, 2].


Clinical Features

A. Supportive Care

Initial prodromal phase lasting 1248 h is associated with

rhinorrhea, pharyngitis, low-grade fever, with or without
cough, following which there is gradual development of the
triad of barking cough, hoarseness, and inspiratory stridor.
Fever may or may not be present.
Child may develop more severe obstruction with inspiratory stridor at rest, increased heart rate, respiratory rate, nasal
flaring, chest wall retractions, progressive hypoxia and cyanosis. Symptoms may worsen at night, with agitation and on
crying. Mild illness lasts for 37 d, but in the severe form it
can last upto 2 wk.
Spasmodic croup tends to occur at evening or night in
young children between 3 mo and 3 y of age. The child
awakens with a characteristic barking cough, stridor and
respiratory distress and is usually afebrile. Symptoms
usually subside within several hours. Less severe attacks
without severe respiratory distress may occur for the next
two or three successive nights. Spasmodic croup represents an allergic reaction to viral antigens rather than a
direct infection.
The diagnosis of croup is made on clinical grounds. Radiography is not routinely indicated.

Management of Croup (Fig. 1)


Assess severity of airway obstruction and NOT the stridor.

Worsening obstruction may lead to soft stridor.
Repeated clinical assessment is the key.

Children with pre-existing upper airway narrowing such

as sub-glottic stenosis and those having Downs syndrome
are at higher risk of severe croup.


Child should be calm and comfortable. Agitation may

worsen airway obstruction.
Do not examine the throat with a tongue depressor.

B. Oxygen
Blow-by (administration of oxygen through a plastic
hose with the end opening held near the childs nose and
mouth) oxygenation is often the most beneficial way of
administering oxygen and should be reserved for children
having moderate to severe croup. Current evidence does
not support the role of humidified air in management of
croup [3].
C. Pharmacological Management

1. Adrenaline [4, 5]
Mechanism of action: Constriction of capillary
arterioles resulting in consequent decrease in laryngeal mucosal edema.
Duration of action: 2 h
Efficacy: Racemic and L-epinephrine are equally
efficacious (Racemic form not available in India)
Indications: Moderate to severe stridor at rest, the
possible need for intubation, respiratory distress, and
Dose: 0.5 ml/kg/dose of 1:1,000 Lepinephrine in 2.5 ml of normal saline
via nebulizer
Frequency: Repeat every 2 hourly if
needed. Where possible, nebulisation
should be driven by oxygen
Maximum dose: 5 ml

Table 1 Pulmonary score index


Add Score

Respiratory rate

>6 y

< 30
03 Mild
46 Moderate
>6 Severe


Wheezing present*

Accessory muscles usage

Terminal expiration with stethoscope
Entire expiration with stethoscope
During inspiration and expiration without stethoscope
*If wheezing is absent (due to minimal air flow), score >3

No apparent activity
Questionable increase
Increase apparent
Maximal activity

Indian J Pediatr


As its activity diminishes, symptoms of croup can reappear

Use cautiously in patients with congenital heart disease
such as Tetralogy of Fallot, or ventricular outlet

2. Corticosteroids: [612]
Corticosteroids decrease edema of the laryngeal
mucosa via their anti-inflammatory action.

MILD (PS 0-3)

SA 2 agonist
MDI + spacer mask 4-6
puffs q20 min x 3

4-6 h

Not sustained
for 4-6 h or
risk factors,
start first dose
rescue steroid
1 mg/kg/d


SA 2 agonist neb q20 mins x 3
SA 2 agonist MDI + spacer 2
puffs q2-3 mins till 6 puffs x 3
If inhalation therapy is not
Adrenaline 0.01 ml/kg sc q20
min x 3
Or Terbutaline 0.01 ml/kg s.c.
one dose
Commence /continue rescue
Observe hourly for 3-4 h
SA 2 agonist neb q1 hour p.r.n.

Sustained 4-6 h
Reduce SA 2 agonist q4-6 h

Pulmonary score < 3
Slept well at night
Feeding well

Continue treatment with inhaled SA 2 agonist MDI + spacer
mask q4-6 h till symptoms
Continue course of rescue steroid for 3-7 d (tapering not
Review adherence, trigger elimination, preventer drug use
Review/initiate long term strategy
Plan follow up visit within 7-14 d

Dexamethasone: Most commonly used

Dose: 0.15 to 0.6 mg/kg orally (preferred),
Frequency: Once
Duration of action: 24 to 72 h
Nebulized Budesonide
Efficacy equals to dexamethasone. Consider
in children with emesis or severe respiratory

SEVERE (PS > 6)/Red flag signs

Oxygen + I.V. fluids
May switch to IV steroid
Continue SA 2 agonist neb q1h/
Start Ipratropium neb q30 mins x 3 and
then q6 h for 24 h
Observe over 1-2 h

If no response on above therapy:

IV magnesium sulfate 25-50 mg/kg + 50
ml NS infusion over 30 mins stat (max 2g)
IV aminophylline 5 mg/kg bolus followed
by IV infusion 0.8-1 mg/kg/h
Terbutaline infusion if no response: 2-10
mcg/kg loading dose followed by infusion
of 0.1-0.4 mcg/kg/min

No response/ill sustained response

Continue intensified ward plan
Blood gas studies
Possible intubation and mechanical
ventilation with Ketamine and
Midazolam/Fentanyl IV infusion
Paralysis with Vecuronium, if required

Response sustained 4-6 h

Follow the principle Last in-First out

Fig. 2 Management of acute severe asthma. PS Pulmonary score; SA Short acting; MDI Metered dose inhaler; NS Normal saline

Indian J Pediatr

Dose: 1 mg/kg and prescribe a second dose
for the next evening.
In patients with severe distress or near respiratory
failure, the simultaneous administration of
budesonide and epinephrine is logical and may be
more effective than epinephrine alone.
3. Antibiotics
Antibiotics are not indicated in viral croup.
Antibiotics are reserved for patients who have
evidence of laryngotracheobronchitis or
laryngotracheobronchopneumonitis, which have a
bacterial disease component.
4. Analgesics and anti-pyretics
Acetaminophen, may be given if the child has a fever.
5. Antitussive and decongestants not indicated.
D. Endotracheal intubation may be required only for a
brief period until laryngeal edema resolves for patients who have severe croup that does not respond
to the previously cited therapies.

Criteria for Discharge


No stridor at rest
Normal pulse oximetry
Normal color
Normal level of consciousness


Arterial blood gases: rate of rise of PaCO2 >5 mm Hg/h,

PaCO2 >40 mm Hg, PaO2 <60 mm Hg, metabolic acidosis
(Base excess >710)
SpO2 on room air <92%

List of various causes of acute respiratory distress as illustrated
in the article will guide us in arriving to a precise diagnosis. A
thorough history, good clinical examination and judicious use of
laboratory investigations and imaging can pinpoint the cause of
respiratory distress in majority of situations. In addition to the
general principles of ABC, the treatment directed towards specific cause can be rewarding in most of the situations. Applying
the protocols of management of acute asthma and croup mentioned in the article can make the approach simple for the
treating physician in the ER.

Contributions BSS: Conceptualised the article and scrutinised and

finalised the contents; DS: Collected the material from different sources
and helped in writing the manuscript; PS: Searched the different references and finally shaped the manuscript; CM: Helped in typing the
manuscript; HM: Helped in collection and compilation of data. BSS will
act as guarantor for this paper.
Conflict of Interest None.
Source of Funding None.

Acute Severe Asthma
Pulmonary Score Index (Table 1) [13, 14]
It is applied to assess the severity of acute asthma and
management planning as per the protocol summarized in
Fig. 2. Time should not be wasted in applying the pulmonary
score in case of severe asthma having red flag signs.

Red Flag Signs

If any of these signs are present, urgent PICU admission and
management is required.

Altered sensorium
Poor pulse volume
Cyanosis (with 60 % oxygen)
Excessive use of accessory muscles or state of exhaustion
Excessive diaphoresis
Silent chest on auscultation

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