Approaches to a child with fast breathing

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11th Apr 2017 Health Reference this

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APPROACH TO A CHILD WITH FAST BREATHING

Fast breathing is the most common presentation in children visiting a hospital emergency. These children have the respiratory rate more than the normal upper limit for that age group; (see table 1), with or without increased work of breathing in the form of chest indrawing, nasal flaring and head nodding. It may also be associated with stridor or wheeze suggestive of upper and lower airway obstruction respectively. There is a need of urgent assessment of airway patency and breathing when a child with fast breathing is first evaluated. Stabilization of vital parameters may require intubation, oronasal suctioning, use of oxygen by hood/nasal prongs, intravenous fluid boluses, correction of hypoglycaemia, nebulization with bronchodilator, intercostal tube drainage, correction of hyperthermia/ hypothermia etc. Such initial treatment coupled with a thorough history, physical examination and relevant investigations, is followed by establishing a provisional diagnosis and instituting appropriate empirical treatment in the emergency ward itself.

Table 1: The upper limits of respiratory rate defined by the WHO

Age group

Respiratory rate cut-off

Young infant (<2 months)

>60/minute

Infant (2 mo-1yr)

>50/minute

Children (1-5yr)

>40/minute

School children (>5yr)

>30/ minute

Etiology of fast breathing:

Fast breathing may not always result from a lung disease. It may be physiological e.g., exercise induced, or pathological due to pulmonary or non-pulmonary causes (table 2)

Table 2: Causes of fast breathing in children

Upper respiratory tract involvement

  • Croup, acute epiglottitis, Ludwig’s angina
  • Retropharyngeal abscess
  • Foreign body aspiration
  • Diphtheria
  • Laryngospasm

Lower respiratory tract involvement

  • Pneumonia,
  • Bronchiolitis
  • Asthma
  • Pleural effusion or empyema and hemothorax
  • Pneumothorax
  • Atelectasis
  • Hypersensitivity pneumonitis

Non pulmonary causes

  • Congestive heart failure due to heart disease or severe anemia
  • CNS infections, cerebral edema, tumor (raised ICT, compression of the brainstem), spinal cord injury, Guillain Barre syndrome
  • Metabolic Acidosis as in Renal failure, Diabetic ketoacidosis, Renal tubular acidosis, etc.
  • Psychogenic Hyperventilation, anxiety, panic attacks

Clinical Features:

A child with fast breathing be may have increased work of breathing (suggested by use of accessory muscles), cyanosis and lethargy or altered sensorium. Alteration in sensorium (in the form of irritability, agitation, lethargy or coma) indicates brain hypoxia and is one of the earliest indicators of impending respiratory failure. While fast breathing is commonly associated with respiratory diseases, it may also occur with fever, crying or metabolic acidosis. However, normal or decreased respiratory rate may be more ominous if it is associated with severe retractions (paradoxical breathing), cyanosis, grunting or altered sensorium. Central cyanosis is a late sign but may not be detected in presence of severe pallor (low Hb) and dark skin colour.

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Stridor is a harsh inspiratory sound that indicates upper airway obstruction. Grunt is a loud noise produced by a forceful expiration against a closed glottis. Grunt and wheeze (a musical sound) are suggestive of lower airway obstruction.

A complete history should reveal the onset, duration, progression of dyspnea, the aggravating and relieving factors as well as the associated symptoms like fever, cough, sore throat, chest pain, choking episodes, accidental ingestion of poisons etc. (table 3)

Table 3: Symptom based diagnostic clues

Fever, cough and rapid breathing

Lower respiratory tract infections like Pneumonia, bronchiolitis and virus associated wheeze

Exercise induced dyspnea

Asthma, CHF, severe anemia

Nocturnal cough, orthopnea and dyspnea

congestive heart failure

Fever, sore throat, stridor

Acute epiglottitis

Severe chest pain with rapid, shallow breathing, decreased air entry

Pneumonia, pneumothorax, pulmonary embolism

Persistent wheezing, recurrent vomiting, failure to thrive

Gastroesophageal reflux disease

Acute respiratory distress after sudden choking, hyperinflated chest

Foreign body inhalation

Fever with altered sensorium, convulsions, fast breathing

Encephalitis involving brain stem

Chest wall retractions, paraplegia

Acute flaccid paralysis

Acute respiratory distress with vomiting, altered sensorium

Poisoning

Anuria, generalized edema, shock, anemia

Acute kidney injury/ chronic kidney disease with metabolic acidosis

Fast breathing, altered sensorium, polyuria, dehydration

Diabetic ketoacidosis

Clinical pearls:

Investigations:

Laboratory investigations help to confirm the diagnosis but the immediate management of a patient should not be delayed pending the reports of the investigations. Use of non-invasive devices such as pulse oximeter and ET CO2 detector (fitted in the ventilator) lessen the need for repeated invasive tests for monitoring of the child. Table 4 shows the relevant investigations to ascertain the cause of respiratory distress in a child.

Table 4: Laboratory investiagations

Investigation

Suggested diagnosis

Complete blood count with peripheral smear

Leucocytosis/leucopenia, toxic granules, shift to left, anemia/polycythemia, eosinophilia-Pneumonia, sepsis, TPE

CRP, ESR

Raised-pneumonia, bronchiolitis

Blood culture

Sepsis with pneumonia

Kidney function tests

Acute/ chronic kidney disease

Arterial blood gas

Hypoxemia, hypercarbia, acidosis (metabolic/respiratory)-pneumothorax, AKI

Chest X ray, X ray soft tissue neck

Pneumonia, pneumothorax, effusion, foreign body, acute epiglottitis, CHF

Bronchoscopy

Foreign body

Echocardiography

Cardiac disease

24 hr pH monitoring

GERD

Pleural tap

Pneumonia (bacterial, tubercular)

Lumbar puncture/ cranial CT scan

Pleocytosis, raised protein and decreased sugar-Meningoencephalitis/raised ICT

Treatment: The management of a child with fast breathing includes supportive treatment in the form of stabilization of vital parameters i.e. temperature, airway, breathing and circulation followed by definitive treatment by instituting appropriate respiratory support, antibiotics, chest tube drainage, decongestive measures etc. Acute onset of fast breathing, esp following choking, and stridor indicate foreign body, and warrants prompt bronchoscopic search and removal of foreign body.

Algorithmic approach to management of fast breathing:

Conclusion:

It is essential to promptly triage children with impending respiratory failure and quickly institute supportive management, simultaneously searching for the etiology and planning a definitive treatment. The above mentioned approach will improve the outcome of children, especially the under-five ones, in whom respiratory infections contribute to the highest number of mortalities.

Suggested reading:

APPROACH TO A CHILD WITH FAST BREATHING

Fast breathing is the most common presentation in children visiting a hospital emergency. These children have the respiratory rate more than the normal upper limit for that age group; (see table 1), with or without increased work of breathing in the form of chest indrawing, nasal flaring and head nodding. It may also be associated with stridor or wheeze suggestive of upper and lower airway obstruction respectively. There is a need of urgent assessment of airway patency and breathing when a child with fast breathing is first evaluated. Stabilization of vital parameters may require intubation, oronasal suctioning, use of oxygen by hood/nasal prongs, intravenous fluid boluses, correction of hypoglycaemia, nebulization with bronchodilator, intercostal tube drainage, correction of hyperthermia/ hypothermia etc. Such initial treatment coupled with a thorough history, physical examination and relevant investigations, is followed by establishing a provisional diagnosis and instituting appropriate empirical treatment in the emergency ward itself.

Table 1: The upper limits of respiratory rate defined by the WHO

Age group

Respiratory rate cut-off

Young infant (<2 months)

>60/minute

Infant (2 mo-1yr)

>50/minute

Children (1-5yr)

>40/minute

School children (>5yr)

>30/ minute

Etiology of fast breathing:

Fast breathing may not always result from a lung disease. It may be physiological e.g., exercise induced, or pathological due to pulmonary or non-pulmonary causes (table 2)

Table 2: Causes of fast breathing in children

Upper respiratory tract involvement

  • Croup, acute epiglottitis, Ludwig’s angina
  • Retropharyngeal abscess
  • Foreign body aspiration
  • Diphtheria
  • Laryngospasm

Lower respiratory tract involvement

  • Pneumonia,
  • Bronchiolitis
  • Asthma
  • Pleural effusion or empyema and hemothorax
  • Pneumothorax
  • Atelectasis
  • Hypersensitivity pneumonitis

Non pulmonary causes

  • Congestive heart failure due to heart disease or severe anemia
  • CNS infections, cerebral edema, tumor (raised ICT, compression of the brainstem), spinal cord injury, Guillain Barre syndrome
  • Metabolic Acidosis as in Renal failure, Diabetic ketoacidosis, Renal tubular acidosis, etc.
  • Psychogenic Hyperventilation, anxiety, panic attacks

Clinical Features:

A child with fast breathing be may have increased work of breathing (suggested by use of accessory muscles), cyanosis and lethargy or altered sensorium. Alteration in sensorium (in the form of irritability, agitation, lethargy or coma) indicates brain hypoxia and is one of the earliest indicators of impending respiratory failure. While fast breathing is commonly associated with respiratory diseases, it may also occur with fever, crying or metabolic acidosis. However, normal or decreased respiratory rate may be more ominous if it is associated with severe retractions (paradoxical breathing), cyanosis, grunting or altered sensorium. Central cyanosis is a late sign but may not be detected in presence of severe pallor (low Hb) and dark skin colour.

Stridor is a harsh inspiratory sound that indicates upper airway obstruction. Grunt is a loud noise produced by a forceful expiration against a closed glottis. Grunt and wheeze (a musical sound) are suggestive of lower airway obstruction.

A complete history should reveal the onset, duration, progression of dyspnea, the aggravating and relieving factors as well as the associated symptoms like fever, cough, sore throat, chest pain, choking episodes, accidental ingestion of poisons etc. (table 3)

Table 3: Symptom based diagnostic clues

Fever, cough and rapid breathing

Lower respiratory tract infections like Pneumonia, bronchiolitis and virus associated wheeze

Exercise induced dyspnea

Asthma, CHF, severe anemia

Nocturnal cough, orthopnea and dyspnea

congestive heart failure

Fever, sore throat, stridor

Acute epiglottitis

Severe chest pain with rapid, shallow breathing, decreased air entry

Pneumonia, pneumothorax, pulmonary embolism

Persistent wheezing, recurrent vomiting, failure to thrive

Gastroesophageal reflux disease

Acute respiratory distress after sudden choking, hyperinflated chest

Foreign body inhalation

Fever with altered sensorium, convulsions, fast breathing

Encephalitis involving brain stem

Chest wall retractions, paraplegia

Acute flaccid paralysis

Acute respiratory distress with vomiting, altered sensorium

Poisoning

Anuria, generalized edema, shock, anemia

Acute kidney injury/ chronic kidney disease with metabolic acidosis

Fast breathing, altered sensorium, polyuria, dehydration

Diabetic ketoacidosis

Clinical pearls:

Investigations:

Laboratory investigations help to confirm the diagnosis but the immediate management of a patient should not be delayed pending the reports of the investigations. Use of non-invasive devices such as pulse oximeter and ET CO2 detector (fitted in the ventilator) lessen the need for repeated invasive tests for monitoring of the child. Table 4 shows the relevant investigations to ascertain the cause of respiratory distress in a child.

Table 4: Laboratory investiagations

Investigation

Suggested diagnosis

Complete blood count with peripheral smear

Leucocytosis/leucopenia, toxic granules, shift to left, anemia/polycythemia, eosinophilia-Pneumonia, sepsis, TPE

CRP, ESR

Raised-pneumonia, bronchiolitis

Blood culture

Sepsis with pneumonia

Kidney function tests

Acute/ chronic kidney disease

Arterial blood gas

Hypoxemia, hypercarbia, acidosis (metabolic/respiratory)-pneumothorax, AKI

Chest X ray, X ray soft tissue neck

Pneumonia, pneumothorax, effusion, foreign body, acute epiglottitis, CHF

Bronchoscopy

Foreign body

Echocardiography

Cardiac disease

24 hr pH monitoring

GERD

Pleural tap

Pneumonia (bacterial, tubercular)

Lumbar puncture/ cranial CT scan

Pleocytosis, raised protein and decreased sugar-Meningoencephalitis/raised ICT

Treatment: The management of a child with fast breathing includes supportive treatment in the form of stabilization of vital parameters i.e. temperature, airway, breathing and circulation followed by definitive treatment by instituting appropriate respiratory support, antibiotics, chest tube drainage, decongestive measures etc. Acute onset of fast breathing, esp following choking, and stridor indicate foreign body, and warrants prompt bronchoscopic search and removal of foreign body.

Algorithmic approach to management of fast breathing:

Conclusion:

It is essential to promptly triage children with impending respiratory failure and quickly institute supportive management, simultaneously searching for the etiology and planning a definitive treatment. The above mentioned approach will improve the outcome of children, especially the under-five ones, in whom respiratory infections contribute to the highest number of mortalities.

Suggested reading:

  1. Kilham H, Gillis J, Benjamin B. Severe upper airway obstruction. Pediatr Clin North Am 1987; 34: 1–14.
  2. Mathew JL, Singhi SC. Approach to a child with breathing difficulty. Indian J Pediatr 2011 Sep;78(9):1118-26.
  3. Fallot A. Respiratory distress. Pediatr Ann. 2005;34:885–91.
  4. Singh V, Tiwari S. Respiratory problems. In: Gupta P,editor. Textbook of Pediatrics, editition 1. India: CBS publishers;2013, pp 335-368.

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