Related Video – How to Treat Conscious Choking Adults

If the patient becomes unresponsive, the provider should immediately activate the emergency response system. The rescuer should lay the child down in a supine position and assess the child. If there is no breathing or if the child only gasps, CPR should be initiated. No pulse check is necessary at this point. 

When it is time to deliver rescue breaths, the rescuer should check the mouth and remove any foreign object. If there is no object, CPR resumes. Blind finger sweeps tend to push the foreign body further into the airway and should not be attempted. 

After 2 minutes of CPR, a sole rescuer should leave the child to activate the emergency response system or call for help. High-quality CPR should be quickly resumed once the provider returns to the child.

Related Video – CPR Techniques – Treating an Unconscious Choking Child

Related Video – CPR Techniques – Treating an Unconscious Choking Infant

Managing Lower Airway Obstruction

The lower airways involve the main bronchi and bronchioles in the thoracic cavity. Bronchoconstriction can trap air in the alveoli and make it difficult to expel it during the expiratory phase. Oxygenation and correction of hypercarbia are fundamental to the management of a pediatric patient with respiratory distress or failure that involves the lower airway.

When bag-mask ventilation is required in a pediatric patient with respiratory distress secondary to lower airway obstruction, the provider should use a slow rate. A slow respiratory rate gives more time for expiration, allowing more air to be expelled from the alveoli. If ventilations are given too quickly, complications such as volutrauma or pneumothorax may occur. 

If a pneumothorax develops, there will be a decrease in preload. The resulting lung collapse leads to severe hypoxemia and obstructive shock. Severe air trapping also causes poor oxygenation and decreased venous return to the heart.

Collapsed Lung X-Ray

Bronchiolitis

Hydration, oral and nasal suctioning, and supplementary oxygen to maintain SpO₂ > 94% are supportive interventions for bronchiolitis management. Bronchodilators (nebulized albuterol and epinephrine) and corticosteroids are not routinely recommended. Nebulized medications may aggravate symptoms in some patients. Infants with a history of wheezing or a family history of asthma may benefit from a bronchodilator trial. Nebulized therapy should be discontinued after a trial if there is no significant improvement.²⁵

Asthma²⁶

Asthma is diagnosed as mild, moderate, or severe. Each category has criteria based on breathlessness, ability to talk, level of consciousness, age, the use of accessory muscles for breathing, grading of wheezes, heart rate, and oxygen saturation.

Guide To Assessing Asthma Severity

Guide to assessing asthma severity.

Pulsus paradoxus may be present in moderate asthma and is almost certainly detectable in severe asthma. Peak expiratory flow rate (PEFR) measurements are useful if the child’s baseline values are known. PEFR may also be helpful in evaluating response to therapy. PEFR measurements may fatigue a child in moderate to severe distress or worsen bronchospasm. 

Treatment for the child with mild to moderate asthma includes: 

• Humidified oxygen via a nasal cannula or oxygen mask, titrated for oxygen saturation of at least 94%
• Albuterol via metered-dose inhaler or nebulizer solution 
• Oral corticosteroids

Treatment for the child with moderate to severe asthma includes:

• Humidified oxygen via a nasal cannula or oxygen mask, titrated for oxygen saturation of at least 94% 
• Albuterol via metered-dose inhaler or nebulizer solution
• Continuous albuterol via nebulization if not improving with intermittent albuterol treatments 
• Ipratropium bromide via nebulization
• IV access 
• Oral or IV corticosteroids
• Magnesium sulfate IV (BP and HR should be closely monitored)
• High flow nasal cannula or noninvasive positive pressure
• Chest X-ray
• Blood gas analysis

Treatment for the child with severe asthma who presents with severe respiratory distress or imminent respiratory failure should include all the above interventions as well as:

• Oxygen supplementation at high concentrations via a nonrebreather mask
• Continuous albuterol nebulization 
• Terbutaline administered subcutaneously or via IV infusion 
• Noninvasive ventilation if the child is alert and cooperative
• Intubation with a cuffed ET tube if the child progresses to respiratory failure

Endotracheal intubation may cause respiratory and circulatory complications. Children in status asthmaticus are very difficult to ventilate with positive pressure ventilation and are at high risk for iatrogenic injury such as pneumothorax. Providers should aggressively treat the child with all other interventions and avoid endotracheal intubation whenever possible.

Managing Lung Tissue Disease

Many clinical conditions can cause lung tissue disease, and this section will present the management of the most common conditions, such as pneumonia, cardiogenic pulmonary edema, ARDS, traumatic pulmonary contusion, and allergic, vascular, and inflammatory insults.

Acute Respiratory Distress Syndrome Lung X-Ray

The general treatment of lung tissue disease includes the initial management of respiratory distress or failure and oxygen supplementation as required. Humidified high-flow nasal cannula oxygen therapy or positive pressure oxygen administration via continuous positive airway pressure (CPAP) noninvasive ventilation, or mechanical ventilation may be beneficial.

Related Video – One Quick Question: How Does CPAP Work?

Infectious Pneumonia

Infectious pneumonia can be due to a viral, bacterial, or fungal infection causing inflammation of the alveoli. Diagnostic procedures such as complete blood count, blood culture and sensitivity studies, viral studies, sputum Gram stain, arterial blood gas, and chest X-ray help clinicians determine the etiology and provide the appropriate treatments. 

Appropriate treatment is determined once the provider identifies the offending agent. For bacterial infections, the child should be treated with the most suitable antibiotic based on culture and sensitivity results if available. If there are signs of bronchoconstriction, albuterol via metered-dose inhaler or nebulization should be ordered. In severe cases, noninvasive positive-pressure ventilation may be an option if tolerated. If the patient develops severe respiratory distress or respiratory failure, the team should be prepared for endotracheal intubation.

Chemical Pneumonitis

Aspirating or inhaling toxic vapors, gases, or liquids can cause chemical pneumonitis. Chemical pneumonitis may lead to noncardiogenic pulmonary edema, airway swelling, and gas diffusion impairment at the alveolar-capillary interface. 

After performing the initial steps of managing respiratory distress or failure, treatment of the child with chemical pneumonitis may include:

• Supplementary oxygen
• Nebulized bronchodilators to treat wheezing 
• CPAP or noninvasive ventilation
• Endotracheal intubation if the patient exhibits signs of severe upper airway edema and obstruction with concomitant respiratory distress or failure

Children with severe chemical pneumonitis may require specialized forms of ventilation, such as high-frequency oscillatory ventilation or extracorporeal cardiopulmonary resuscitation (ECMO) The child should be transported to a facility skilled in such interventions.

Aspiration Pneumonitis

Aspiration of stomach acid or oral secretions can cause inflammation and edema to lung tissues. The bacteria from undigested stomach contents can cause pneumonia. Fever is a typical sign of pneumonitis following an aspiration event. 

A chest X-ray and complete blood count aid in the diagnosis of aspiration pneumonia. Treatment includes antibiotics and oxygen as needed. In severe cases, CPAP, noninvasive ventilation, or intubation with mechanical ventilation may be required if the patient progresses to respiratory distress or failure.

Cardiogenic Pulmonary Edema

Pulmonary edema is the extravasation of fluid from capillaries into the interstitial space. Cardiac conditions that cause blood to backflow may increase pressure in the pulmonary arteries and pulmonary veins, causing cardiac pulmonary edema. 

In children, congenital heart diseases, myocarditis, cardiomyopathies, and cardiac-depressant drugs (beta-adrenergic blockers, tricyclic antidepressants, calcium channel blockers, and chemotherapeutic agents) can cause a depressed cardiac ejection fraction due to poor myocardial function.

To treat the child with pulmonary edema, the team must provide invasive or noninvasive ventilatory support with positive end-expiratory pressure (PEEP) Intubation and invasive ventilation are likely needed for the patient with persistent hypoxemia despite high levels of supplementary oxygen and noninvasive positive end-expiratory pressure. 

Using PEEP during mechanical ventilation helps reduce the need for a high oxygen concentration as it helps keep the alveoli patent while fluid is in the interstitium. The typical starting setting for PEEP is 5 cm H₂O, and it can be adjusted upwards until the oxygen saturation is 94% and above. However, excessive PEEP can cause lung hyperinflation and affect the venous return to the heart. In this case, cardiac output and oxygen delivery are compromised. 

Medical interventions include the use of diuretics to reduce left atrial pressure, inotropic infusions, and afterload reducing agents to restore cardiac function. The clinician also seeks help from an expert pediatric cardiologist for the management of these patients.

In pulmonary edema, there is a buildup of fluid in the lungs.

Acute Respiratory Distress Syndrome (ARDS)

ARDS is a form of noncardiogenic pulmonary edema following infectious pneumonia, aspiration pneumonia, or a systemic illness such as sepsis or pancreatitis. ARDS can also be triggered by trauma. 

These medical conditions cause injury to the alveoli and pulmonary capillaries. The body’s compensatory mechanism for repairing the damage is to recruit inflammatory mediators. As a result, oxygen diffusion into the blood, and to a lesser degree, carbon dioxide diffusion from the blood to the alveoli, are inefficient. 

Treatment depends on the diagnosis and usually addresses bacteremia, shock, and respiratory failure.

ARDS is characterized as: 

• an acute onset of symptoms within 7 days after the precipitating event or agent 
• a PaO₂/FiO₂ ratio of 300 or less 
• an oxygen index of 4 or higher 
• formation of new infiltrates on a chest X-ray indicative of parenchymal disease 
• no evidence of cardiogenic causes of pulmonary edema

The complexity of this condition necessitates expert consultation. 

ARDS is managed by monitoring the heart rate and rhythm, blood pressure, respiratory rate, pulse oximetry, and end-tidal carbon dioxide. The clinician should order an arterial blood gas, a central venous blood gas, and a complete blood count to determine the oxygenation and ventilation status of the patient. The patient likely requires ventilatory support, particularly when there is a worsening of clinical and radiographic findings and persistent hypoxemia despite the delivery of high concentrations of oxygen.

The patient’s hypoxemia must be corrected to prevent the progression of respiratory distress or failure to cardiac arrest. PEEP can be increased to augment oxygen saturation. A lung-protective ventilator strategy should be used during mechanical ventilation. Tidal volumes should be limited to 5–8 mL/kg, and inspiratory plateau pressures should be kept at ≤ 28 cm H₂O.²⁷

Managing Disordered Control of Breathing

Disordered control of breathing is usually due to neurologic disorders secondary to increased intracranial pressure (ICP), neuromuscular diseases, CNS infections, traumatic brain injuries, brain tumors, and hydrocephalus. Some conditions and medical interventions can induce disordered control of breathing, such as deep sedation, drug overdose, hyperammonemia, metabolic conditions, and seizures. Clinical findings of increased ICP include unequal pupils not responding to light, disordered breathing, apnea, bradycardia, hypertension, and decerebrate and decorticate positions.

For trauma patients, a patent airway is maintained by positioning the patient and performing the jaw thrust maneuver. Aside from maintaining a patent airway, this maneuver also supports the patient’s spine in case there is spinal involvement from trauma. If there is poor perfusion secondary to poor end-organ function, the provider can administer 20 mL/kg isotonic crystalloid solution or blood products.

Pharmacologic therapy to decrease ICP includes osmotic agents and hypertonic saline solution. After establishing an airway, the team must address the patient’s anxiety and give pain medications to prevent further agitation. Fever should be aggressively treated in these patients to lessen metabolic demands.

The provider must ensure the child receives adequate oxygenation and ventilation. Brief periods of hyperventilation may prevent uncal herniation when there are sudden ICP increases.  

Aggressive prophylactic hyperventilation to a PaCO₂ of < 30 mm Hg is to be avoided, though. Hyperventilation decreases cardiac output because it hinders the venous return of blood into the heart. Excessive hyperventilation also causes cerebral vasoconstriction, inhibiting blood perfusion and potentially causing cerebral ischemia. Mild hyperventilation is only indicated in the first 48 hours after the injury for acute signs of cerebral herniation. These patients must be monitored for cerebral ischemia.

Increased Intracranial Pressure

Increased ICP disrupts the breathing centers of the brain. Certain conditions such as subarachnoid hemorrhage, tumor growth, meningitis, encephalitis, intracranial abscess, subdural hematoma, and epidural hematoma can cause increased ICP. Patients will present with an irregular respiratory rate and respiratory pattern. 

Patients can present with the Cushing triad, which includes a change in respirations, bradycardia, and widening pulse pressure. The triad may herald imminent uncal herniation, which is fatal. The team must seek expert consultation from a neurosurgeon. Specific management depends on the etiology.

Cushing Triad

Neuromuscular Disease

Chronic progressive neuromuscular disease is potentially fatal when the muscles for respiration are affected. Preliminary symptoms include ineffective coughing and difficulty removing secretions. Due to the damaged muscles, certain complications arise, such as atelectasis, aspiration pneumonitis, pneumonia, restrictive lung disease, and, eventually, respiratory failure. If the patient has an advanced neuromuscular disorder, they may require long-term noninvasive ventilation support. 

Succinylcholine, a drug commonly used for intubation, should not be administered to a child with neuromuscular disease. This medication may trigger a life-threatening condition such as hyperkalemia or malignant hyperthermia. Antibiotics in the aminoglycoside family are also known to cause neuromuscular blockade and should be avoided in a child with a neuromuscular disorder.

Drug Overdose and Poisoning

CNS depression from narcotic use or prescription drug overdose may eventually lead to respiratory distress or failure. Sometimes, these drugs cause the temporary loss of function of respiratory muscles and loss of consciousness, leading to upper airway obstruction by the tongue. 

After performing the initial management of respiratory distress and failure, the team seeks expert consultation with a toxicologist. If the child has vomited, the team may need to suction the gastric contents to prevent aspiration. If the offending agent is identified and has an antidote, the provider administers the antidote as recommended. For example, a child with an opioid overdose requires the antidote naloxone. Standard BLS and PALS measures are never delayed while waiting on an antidote.

After the initial treatment, other diagnostic assessment tools to guide the next interventions for the patient include an arterial blood gas, ECG, chest X-ray, electrolytes, blood glucose, serum osmolality, and drug screening tests.

When responding to a child with a suspected opioid overdose and resultant respiratory arrest, rescue breathing should be administered until spontaneous breathing begins. The child in respiratory arrest should receive intranasal or intramuscular naloxone. However, standard PALS measures (CPR) should be the priority for the child in suspected cardiac arrest.