Pediatric Acute Respiratory Distress Syndrome Clinical Presentation

Updated: Nov 23, 2016
  • Author: Prashant Purohit, MD; Chief Editor: Timothy E Corden, MD  more...
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Presentation

Physical Examination

The onset of ARDS can be as rapid as few hours, but it can have a gradual onset with evolution of clinical features over 1 to 5 days. The evolution of clinical signs depends on the type, acuity, and severity of the initial insult. As lungs undergo changes during the first exudative stage of the disease, tachypnea is typically noted as the initial physical finding. Respiratory distress, agitation and hypoxemia could be other initial clinical features at this stage. Crackles may be audible throughout the lung fields, signifying pulmonary edema coinciding with infiltrates on chest radiographs. Concomitant fever may reflect the underlying process causing ARDS (eg, pneumonia, sepsis) or may reflect massive cytokine release. Although these are non-specific features and can be seen with any other respiratory or even systemic illness. Hypoxemia might be evident by high oxygen requirement, higher CPAP or PEEP and elevated alveolar-arterial (A-a) oxygen gradient. A-a gradient can be calculated from the equation as mentioned below for the sea level assuming 100% humidification at the alveolar level. Link the equation.

A-a gradient = PAO2 – PaO2 = {FiO<sub>2</sub> (Patm – PH<sub>2</sub>O) – PaCO<sub>2</sub>/0.8} – PaO2

                     = {0.6 (760-46) – 40/0.8} – 85

                     = {428.4 – 50} – 85

                     = 293.4 

This is for the patient that was discussed earlier for other calculations, who was on mechanical ventilation with FiO2 0.6, PaO2 of 85, SPO2 of 98% and PCO2 of 40 mm Hg.

Reduction in lung compliance and functional residual capacity is noticed with the development of pulmonary edema. Hypoxemia results from intrapulmonary shunting and ventilation-perfusion mismatch. At this stage, utilization of high PEEP will help in oxygenation by alveolar recruitment. Certain areas of lung still would have maintained normal lung compliance and remain at risk of air leak syndromes from high PEEP. After the initiation of fibro proliferation, lung compliance is further reduced. Benefit of PEEP on oxygenation is less remarkable at this stage. In fact, difficulty in achieving adequate ventilation might be experienced at this stage with resultant hypercarbia and respiratory acidosis. The requirement of mechanical ventilation might be as long as few weeks with overall clinical recovery in months. Pediatric patients have exhibited reduced lung function, broncho reactivity, muscle wasting and weakness for a prolonged period of time after survival from ARDS. [45]

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Complications

Several complications are associated with ARDS, though many of these are due to the precipitating conditions that lead to ARDS. Acute complications include air-leak syndromes, ventilator-induced lung infection (VILI), and multiple organ dysfunction syndrome (MODS), although definitive evidence linking this syndrome to ARDS or ventilator use remains controversial.

Numerous pulmonary complications may result from ARDS. The most common are the air-leak syndromes, particularly pneumothorax but also pneumomediastinum, pneumopericardium, pneumoperitoneum, and subcutaneous emphysema. Features of a pneumothorax include decreased air entry on the side of the air leak, an increased percussion note on the same side, and tracheal deviation away from the affected side in a tension pneumothorax. Heart sounds may be muffled, and signs of decreased cardiac output may be observed with a tension pneumothorax. Clinicians must also maintain a high index of suspicion for tension pneumothoraces as a cause for acute onset of decreased cardiac output.

VILI is an entity receiving attention with the publication of landmark trials suggesting that a “kinder, gentler” form of mechanical ventilation improves outcomes in ARDS. VILI most likely has several causes, including excessive lung stretching due to high tidal volumes, repetitive opening and closing of alveoli leading to shear stress, oxygen toxicity, and cytokine release.

ARDS patients may also be compromised from a cardiovascular standpoint. Patients with sepsis, trauma, or other multisystem insults may lose their ability to tolerate higher airway pressures often required to maintain adequate oxygenation. Higher airway pressures lead to a higher net intrathoracic pressure, which results in decreased preload and cardiac output. Moreover, hypoxia, hypercarbia, and acidosis may elevate pulmonary artery pressures, increasing right ventricular afterload and leading to increased right ventricular work. Right ventricular dilatation can develop and then result in leftward movement of the intraventricular septum and cause left ventricular outflow tract obstruction.

Gastrointestinal complications commonly observed in the critically ill population include stress ulcers, liver failure, pancreatitis, and pancreatic insufficiency, leading to glucose intolerance.

Renal failure may result from the primary illness or may occur secondarily as a result of poor cardiac output, acute tubular necrosis, and MODS.

Secondary or nosocomial pneumonia is not uncommon in critically ill children. In addition to Staphylococcus aureus, other organisms more typically isolated include Pseudomonas species, Acinetobacter baumanniiStenotrophomonas maltophiliaEscherichia coli, and Candida species. Bacteremia from indwelling vascular catheters and skin ulcerations may also occur. Risk of urinary tract infection increases with prolonged indwelling Foley catheters.

Critical illness polyneuropathy and myopathy (CIPNM) is seen in a subset of patients of unclear etiology. Many factors have been identified to have an increased association with CIPNM, such as sepsis, systemic inflammatory response syndrome, MODS, and prolonged mechanical ventilation. Use of muscle relaxants, especially in conjunction with steroids, appears to have a particularly high association with CIPNM. Initial reports describe CIPNM with concomitant use of nondepolarizing muscle relaxants and corticosteroids. However, case reports of weakness with cisatracurium and corticosteroids have also been described. Clinically, patients develop profound or flaccid weakness that is often prolonged. This may complicate the mechanical ventilator weaning process and may also require inpatient rehabilitation care upon discharge from the hospital. [46, 47]

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