Respiratory excursion can be markedly impaired by a burn to the chest wall. The process is most evident with a circumferential third degree burn. The loss of elasticity in the chest wall due to the burn tissue will markedly increase the work of breathing required to maintain functional residual capacity and an adequate tidal volume. As more subeschar edema develops, compressing the chest wall, the end-expiratory intrathoracic volume begins to decrease. Edema from a second degree burn is also sufficient to alter lung mechanics. The loose aureolar tissue in the axilla and lateral chest wall will sequester large amounts of edema fluid, leading to a very heavy tense chest wall. Full thickness burns produce a more severe limitation because tissue expansion is markedly impaired and intrathoracic volume becomes compressed. The result is a significant V/Q mismatch, atelectasis, and hypoventilation. Maximum respiratory effort is frequently required just to maintain adequate gas exchange. Any process that compromises the necessary increase in inspiratory force and muscle activity, such as hypoxia, hypovolemia, pain, or sedation, will accentuate the severity of lung dysfunction.

DEEP CHEST WALL BURN

Symptoms may not be clearly evident until edema formation peaks at about 10 to 12 hours. The first clinical evidence of the chest wall restrictive defected is often labored breathing followed by a rapid respiratory deterioration, particularly in the patient who is not receiving ventilator support. Clearance of secretions can be impaired due to the inability to generate a hyperinflation. In the combined chest burn and inhalation injury, it is very difficult to distinguish the degree of impairment in total lung compliance due to the increased airway edema and bronchospasm compared with that due to the impaired chest wall. The increasing airway pressure required to expand the stiff chest wall will lead to extension of the burn into fat.

Click to Enlarge the Image

Full Thickness chest burn impairing respiratory excursion

Click to Enlarge the Image


Chest Wall escharotomy Mid-axillary lines to normal tissue then connected across the middle

In the presence of carbon monoxide.

The concerns with smoke inhalation are an immediate problem of airway patency and an additional major problem of pulmonary toilet. A tube less than 7mm in an adult is too small for adequate suctioning and thick secretions will compromise ventilation at a time when it is not safe to change the tube due to face, neck, and airway edema.

A chest wall burn, generalized edema, inhalation injury, use of narcotics, all decrease functional residual capacity and all are common in the burn patient. PEEP applied early can help avoid atelectasis and airway collapse. Begin with 5 cm H₂O and increase up to 10 cm H₂O, if needed.

Hypovolemia will not protect the inhalation-injured lung and will only augment the V/Q mismatch because less of the lung is perfused, especially if PEEP is required.

Underestimation of the Effect of Chest Wall Stiffness on Lung Function:

Underestimation of the increased work of breathing created by a rigid chest wall even with normal lung parenchyma leads to fatigue, airway collapse, and secondary infection. This process is particularly prone to occur in the early postanesthesia period.

Causes of Hypoxia