Pediatric Burns By Bradley J. Phillips

direct injury to the lung parenchyma by inhalation of toxic gases such as chlorine and phosgene was recognized during WWI. This injury featured “pulmonary oedema, rupture of the pulmonary alveoli and concentration of the blood, with increased viscosity and a tendency to thrombosis.” Treatment included oxygen and (for patients with deep cyanosis) venesection of as much as 400 ml of blood.⁸⁶

The potential of indoor fire disasters to cause rapid, early death by asphyxia or inhalation injury was demonstrated by the Cleveland Clinic fire of 1929. This fire, started by ignition of highly flammable X-ray film, claimed 125 lives. Most of the deaths have been attributed to inhalation of carbon monoxide, hydrogen cyanide, and nitrogen oxides.⁸⁷ Those caring for the Cocoanut Grove victims were aware of that earlier experience and noted that the majority of patients arriving at MGH who did not survive to admission had elevated carbon monoxide levels. A sense of the situation can be gleaned from this description: “The first clue to the high incidence of pulmonary burns was afforded by the number who died within the first few minutes after reaching the hospital. They were very cyanotic, comatose or restless, and had severe upper respiratory damage.”⁸⁸ From this description, it appears likely that some patients died with airway obstruction. In the patients surviving to admission, these authors provided a classic description of smoke inhalation injury. Severe upper respiratory and laryngeal edema mandated “radical therapy” in 5 patients, namely endotracheal intubation followed by immediate tracheotomy. Oxygen was provided via tent or transtracheal catheter. Those surviving this initial phase developed diffuse bronchiolitis, bronchial plugging, and alveolar collapse.⁸⁸

Further improvements in the care of patients with inhalation injury required the development of positive-pressure mechanical ventilators. In the course of thoracic trauma research in North Africa during WWII, Brewer, Burbank, and colleagues of the Second Auxiliary Surgical Group (with the support of theater consultant surgeon Colonel Churchill) delivered oxygen via mask along with an intermittent, hand-operated positive airway pressure device to casualties with “wet lung of trauma.”^89,90 Dr Forrest Bird, V. R. Bennett, and J. Emerson built mechanical positive-pressure ventilators towards the end of WWII, all inspired by technology developed during the war to deliver oxygen to pilots flying at high altitudes.⁹¹ The availability of these and similar machines, as well as the Scandinavian polio epidemic of 1952, spurred the creation of intensive care units (ICUs).⁹² At the USAISR and several other centers, burn ICUs were located within the burn unit under the direction of surgeons who ensured continuity of care and clinical research.

Once accurate diagnosis of inhalation injury by bronchoscopy and xenon-133 lung scanning became available, it became apparent that these patients were at increased risk of pneumonia and death.⁹³ Large animal models were developed and the pathophysiology of the injury was defined.⁹⁴ Unlike ARDS as a result of mechanical trauma or alveolar injury due to inhalation of chemical warfare agents, smoke inhalation injury was found to damage the small airways, with resultant ventilation-perfusion mismatch, bronchiolar obstruction, and pneumonia.^95,96 This injury process featured activation of the inflammatory cascade, which in animal models was amenable to modulation by various anti-inflammatory agents. However, the most effective interventions to date are those directly aimed at maintaining small airway patency and avoiding injurious forms of mechanical ventilation. These include use of high-frequency percussive ventilation with the Volumetric Diffusive Respiration (VDR-4®) ventilator developed by Bird and delivery of heparin by nebulization.^97,98

Metabolism and Nutrition

Bradford Cannon described the nutritional management of survivors of the Cocoanut Grove fire: “All patients were given a high protein and high vitamin diet…it was necessary to feed [one patient] by stomach tube with supplemental daily intravenous amogen, glucose, and vitamins.”⁹⁹ But it soon became apparent that survivors of major thermal injury evidenced a hypermetabolic, hypercatabolic state which continued at least until wounds were closed and often resulted in severe loss of lean body mass. Cope and colleagues reported measurements of metabolic rate up to 180% of normal in the early postburn period and recognized a relationship between wound size and metabolic rate.¹⁰⁰ Wilmore and colleagues identified the role of catecholamines as mediators of the postburn hypermetabolic state.¹⁰¹ They further documented that the burn patient is internally warm and not externally cold, and that hypermetabolism is wound-directed, as evidenced by elevated blood flow to the burn wound.^102-104 Consequently, the metabolic needs of the burn patient should be met rather than suppressed.

Earlier (1971), Wilmore et al. demonstrated the feasibility of providing massive amounts of calories by a combination of intravenous and enteral alimentation.¹⁰⁵ Curreri published the first burn-specific formula for estimating caloric requirements: calories/day = 25(wt in kg) + 40(TBSA).¹⁰⁶ However, the provision of adequate calories and nitrogen failed to arrest hypermetabolism and reduced, but did not eliminate, erosion of lean body mass in these patients. Three approaches have recently been taken to address this problem: the use of anabolic steroids such as oxandrolone,²⁹