How do you determine whether this patient should be intubated? Are there physical signs that would help in this evaluation? Chest X-ray? Arterial blood gas? Would steroids be of any help in decreasing airway edema?

What toxic products of combustion would you be concerned about? How can you evaluate the clinical significance? What will you do? Would prophylactic antibiotics be of any help in this case? Why? What are the important considerations for the management of carbon monoxide poisoning?

What are your initial considerations in volume resuscitation? What formula would you use to calculate volume replacement? Is there a need to modify this formula in this case? Is it likely that this hemodynamic picture will change? Over what period of time will change occur? Why is this patient hyperdynamic?

Because the child was burned in an enclosed environment, sustained facial burns, and is tachypneic, he probably has thermal injury to the airways and alveoli from inhalation of smoke, noxious gases, and heated air. This child’s trachea should be intubated prophylactically in anticipation of rapid swelling of the upper airways and respiratory tract. With time, edema and secretions/blood in the airway can make laryngeal access difficult or impossible.

Clinically, a facial burn, difficult breathing, and tachypnea are indicators of probable thermal inhalation injury. The chest X-ray may not be very helpful in the early stages of the pulmonary thermal injury. Arterial blood gas analysis may show lactic acidosis. It is not useful in diagnosing carbon monoxide poisoning because it measures dissolved oxygen and thus overestimates the oxygen saturation of hemoglobin. Unless the analyzer is specifically measuring carbon monoxide (CO), it will estimate the saturation based on the PaO₂. Similarly, the pulse oximeter overestimates the oxygen saturation because it cannot differentiate oxyhemoglobin from carboxyhemoglobin. Saturations will generally read in the 88–90 % range even if the true saturation is much lower. Carbon monoxide poisoning is suspected in burn victims when symptoms of headache, dizziness, restlessness, and confusion are present. A co-oximeter or a handheld breath analyzer can be used to confirm the diagnosis of carbon monoxide poisoning. Steroids have not been shown to be helpful with the massive inflammatory process of burns.

Carbon monoxide gas is of most concern because it is colorless and odorless and is produced in large quantities during incomplete combustion of carbon or carbon products and fuels. The clinical significance is that carbon monoxide poisoning can produce severe hypoxemia and long-term neurological impairment. Carbon monoxide gas has 200–250 times the affinity of oxygen for binding with hemoglobin. Carboxyhemoglobin shifts the oxyhemoglobin dissociation curve to the left. As a result, oxygen delivery is seriously compromised. The primary treatment of carbon monoxide toxicity is administration of 100 % oxygen by a non-rebreathing system. Elimination of carboxyhemoglobin is dependent on alveolar oxygen pressure rather than alveolar ventilation. The idea is to provide a huge amount of oxygen so that it can compete with CO for binding sites on Hb. In severe cases (carboxyhemoglobin >30 %), oxygen can be provided via positive pressure ventilation or (preferably) in a hyperbaric chamber. The carboxyhemoglobin half-life can be reduced from 4 h in room air to 90 min with the administration of 100 % inspired oxygen. Prophylactic antibiotics can be helpful to treat opportunistic infection but should not be given indiscriminately. They are not part of the primary treatment for this problem.

Large volume resuscitation is necessary initially and can be guided by the Parkland formula [crystalloid 4mL/kg × percent burn × wt(kg)] or the Brooke formula [crystalloid 0.5 mL/kg + colloid 1.5mL/kg × percent burn × wt(kg)]. “Moderate” and “major” burn criteria require less of a total body surface area burn in the very young and very old when compared to normal adults. In addition, the percentage of body surface area for the head and trunk areas is different for infants and toddlers vs. adults. These formulae are useful guides to the replacement of massive fluid loss, but the overall requirement is determined by clinical monitoring of the patient’s mental status, hemodynamic parameters, acid-base balance, and urine output. Nevertheless, these formulae may underestimate fluid requirement in infants under 10 kg. Some burn centers use hypertonic saline or colloids particularly in the very young and elderly to minimize the potential of edema. To date the controlled trials have not demonstrated a difference in outcome or mortality among the different types of solutions. Usually, the fluid losses from inflamed surfaces continue for days and weeks depending on the extent and severity of the burns. The hyperdynamic circulation is due to a massive surge of catecholamines and corticosteroids, 10–50 times that of a normal patient. Injury-induced cytokines and endotoxins released into the circulation further perturb the hemodynamics of these patients. Elevated metabolic rates also compensate for the large amounts of heat and water lost through disrupted tissues.