In patients suffering from major burns, outline the possible physiologic derangements and their underlying mechanisms that could contribute to problems of oxygenation and ventilation.
Can affect 4 anatomic areas of the respiratory tract:
Supraglottal, tracheobronchial, and pulmonary parenchymal, and chest/abdominal wall.
Loss of airway patency due to mucosal oedema
Loss of airway reflexes due to coma (e.g. blast Traumatic brain injury, intoxications such as carbon monoxide,)
Bronchospasm resulting from inhaled irritants
Mucosal oedema and endobronchial sloughing causing small airway occlusion, leading to intrapulmonary shunting.
3. Pulmonary Parenchymal
Pulmonary (alveolar) oedema and collapse leading to decreased compliance, and further intrapulmonary shunting.
Loss of tracheobronchial epithelium and airway ciliary clearance contributing to tracheobronchitis and pneumonia.
Barotrauma, ARDS, pleural effusions, Ventilator associated pneumonia, TRALI and tracheobronchitis may all result from Intensive Care resuscitation, and treatments of the above.
Circumferential full thickness burns of the chest and abdomen may cause reduced static compliance resulting in restrictive ventilator defect, made worse by large volumes of oedema with fluid resuscitation and capillary leak.
Toxic inhalation of carbon monoxide (CO) resulting in a left shift of the ODC and oxygen transport capacity (Carboxy Hb) and decreased cellular oxidative processes.
Other toxic gases NH3, HCL – pulmonary oedema,mucosal irritation and ALI CN- poisoning, cellular hypoxia
Increased metabolic requirements may overwhelm a respiratory system already impaired by all the above.
This question asks, "what are the influences of smoke inhalation on respiratory function and gas exchange?" The college has decided to divide their answer anatomically. An equally valid systematic approach could see the candidate divide this issue into ventilation, diffusion, shunting and oxygen transport.
- Decreased respiratory effort due to a decreased level of consciousness
- Poor lung expansion resulting in a restrictive ventilatory defect, due to the presence of circumferential torso burns (or even non-circumferential)
- Poor air entry due to upper/lower airway burns; an obstructive pattern of ventilation
- Decreased lung compliance due to pulmonary thermal injury, ensuing pulmonary oedema and ARDS
- Pulmonary oedema could also be due to the vigorous fluid resuscitation
- ARDS could also be due to the SIRS which results from widespread burns.
- Decreased gas exchange due to increased pulmonary interstitial and alveolar fluid, due to pulmonary thermal injury
- Increased shunt fraction due to collapse of oedematous lungs
- Increased shunt fraction due to airway swelling, obstruction and subsequent atelectasis
- Increased sputum retention and increased risk of pneumonia due to epithelial damage and impaired mucociliary escalator function.
- Decreased oxygen delivery to tissues, due to:
- Metabolic/respiratory acidosis and consequent right shift of oxygen-haemoglobin dissociation curve
- Carbon monoxide poisoning
- Decreased oxygen utilisation due to cyanode poisoning
Enkhbaatar, Perenlei, and Daniel L. Traber. "Pathophysiology of acute lung injury in combined burn and smoke inhalation injury." Clinical Science 107.2 (2004): 137-144.
Whitener, D. R., et al. "Pulmonary function measurements in patients with thermal injury and smoke inhalation." The American review of respiratory disease 122.5 (1980): 731-739.
Crapo, Robert O. "Smoke-inhalation injuries." JAMA 246.15 (1981): 1694-1696.