Annals of Burns and Fire Disasters - vol. XVII - n. 1 - March 2004

EARLY AND LATE COMPLICATIONS OF INHALATION INJURY

Valová M.¹, Königová R.¹, BrozŠ L.¹, Vajtr D.²

Third Medical Faculty, Charles University, Faculty Hospital Královské Vinohrady, Prague, Czech Republic
¹ Clinic of Burn Medicine
² Institute of Forensic Medicine

SUMMARY. Severe inhalation injury causes a substantial deterioration in the prognosis and increases the general mortality of patients with extensive burns. Recently, in particular because of the development of the invasive monitoring of patients and the effective treatment of acute burn shock, we encounter with increasing frequency patients who survive the acute stage, including complications such as acute respiratory distress syndrome, and reach the stage of late complications. The latter include tracheo-oesophageal fistulas that develop on the basis of pressure ulcers and chondromalacia, usually at the site of the balloon of the tracheostomic cannula, and the overproduction of fibrous tissue in the area of the airways that leads to the development of stenosis, pulmonary fibrosis, and bronchiectasis. Frequently, different early and late complications combine.

Introduction

The diagnosis of inhalation injury is based on the mechanism of injury (explosion, intoxication...), location of the thermic affection (in the area of the face, around the neck), and the patient’s symptoms, which may lead to securing the patient with orotracheal intubation. This is followed by a laryngoscopic examination, bronchoscopy, a lung X-ray, and bronchoalveolar lavage, and the patient is kept under complete laboratory, haemodynamic, and ventilatory monitoring. In the diagnosis of late post-inhalation changes, we carry out in particular bronchoscopy, HRCT or spiral CT, and spirometry. The monitoring of enzymatic cellular pulmonary activity, cytology, and levels of albumin, surfactant, and procollagen III in bronchoalveolar lavage could be a good marker of acute respiratory distress syndrome (ARDS) or activity of fibroproliferation.

Bronchoscopy is performed in our patients immediately after admission and later on, within the monitoring of the dynamics of changes. The early symptoms of inhalation injury include the presence of soot particles, oedema and mucosal hyperaemia, erosion, and desquamation of the epithelium with soot eschars. Other changes are already a combination of the post-inhalation, inflammatory, and reparative changes. Signs may be seen of pseudo-membranous or necrotic inflammation with granulation tissue, ulceration, and even perforation.

Within the volume resuscitation and during the invasive monitoring of haemodynamics, volume replacement increases by 50-80% in inhalation trauma, and extravascular lung water elevates to 20 ml/kg in disturbances of alveolo-epithelial clearance, which leads to the development of alveolar pulmonary oedema on the noncardial basis. The acute complications of inhalation trauma that develop within about 72 h post-trauma include acute lung injury, ventilator-associated or ventilator-induced lung injury, ARDS, and non-oedematous ARDS. Among the subacute complications we include the development of pneumonia and possibly ventilator-associated pneumonia. The late complications include the development of chronic obstructive bronchopulmonary disease, bronchiectasis, stenosis, fistulae, pulmonary fibrosis, and cor pulmonale. The definition of acute lung injury or ARDS is founded on a rapid progression of the symptoms according to the lung X-ray, showing bilateral, diffuse, non-homogeneous infiltrates and excluding the cardial part (pulmonary capillary wedge pressure under 18 torrs; PaO2/FiO2 under 300 torrs and, in cases of ARDS, under 200 torrs).

The standard therapeutic procedures comprise - in addition to complete care of the airways (including the application of mucolytics, bronchodilators, inhalants, rehabilitation of breathing, and even use of the pronation position) - total therapy of septic patients (with elimination therapy and the application of antibiotics according to sensitivity), the use of conventional ventilation regimes (tidal volume 5-7 ml/kg, positive end-expiratory pressure 10-15, minimal FiO2, fractional concentration of oxygen in inspired gas), pressure controlled ventilation, inversed-ratio ventilation, and peak inspiratory pressure under 35 cm H2O, using permissive hypercapnia and permissive hypoxia. In our burns centre we apply, among unconventional regimes, inhalation of NO and high-frequency oscillation in paediatric patients. The possibility of using surfactant or inhalation vasoactive prostaglandins goes beyond the scope of our experience. The application of corticoids is still a controversial question.

In the 1980s and 1990s numerous studies focused on the application of steroids in the acute stage of ARDS, but the conclusions were mostly negative. It was found that patients subjected to this treatment had a statistically higher mortality from infectious complications; an accumulation was also found of collagen, as well as overproduction of TNF-·, IL 1-‚ beta, IL 6, and IL 8. In 1998 Meduri1,2 presented in JAMA the results of a multicentric, prospective, and random study in which he applied corticoids in the fibroproliferative stage, i.e. between the 7th and the 15th day after the development of ARDS, at a dosage of 2 mg/kg/day of methylprednisolone. The patients involved in this study were those with a lung injury score of over 2.5 who had survived the acute stage of ARDS; their ventilatory parameters did not however substantially improve because of an uncontrolled infection. The aim of the corticotherapy was to modulate the macrophages and fibroblasts, prevent collagen deposition in the lungs, and decrease neutrophilia and the levels of albumin and procollagen III in bronchoalveolar lavage. The results were controversial, and we must therefore await the conclusions of other studies.

Case report

In July 2001 a 34-yr-old female patient (Fig. 1) was admitted to our department suffering from extensive deep burns in the head, face, neck, trunk, back, arms, hands, and right lower extremity in 22% BSA, including burns of the airways. The mechanism of the injury was the intentional pouring of petrol over the patient, who was then set on fire.

Within the framework of primary treatment, the patient was intubated and taken to our burns centre by emergency aircraft service under analgosedation. From the onset of hospitalization the patient had artificial pulmonary ventilation with a regime of manually controlled ventilation requiring the use of distension ventilation regimes with a high fraction of inspired oxygen. Bronchoscopy confirmed signs of inhalation trauma with reddening and oedema of the mucosa at some sites with fibrin and foci of necrotic epithelium in the trachea and main bronchi. Complications manifested by hyperpyrexia started on the 12th day of hospitalization. Lung X-rays showed (Fig. 2) showed that ARDS had developed, combined with noncardiac and cardiac pulmonary oedema. A tracheotomy was performed and pulmonary distension ventilation was used again. The patient was gradually colonized with sp. methicillin-resistant Staphylococcus, Enterobacter, Pseudomonas, Citrobacter, Klebsiella, and Candida. The cultivated flora was polymicrobial and multiresistant, and it was thus difficult to differentiate the colonizing and the true pathogenic flora. The antibiotic combination was applied according to sensitivity. Correlated with the clinical condition, there developed secondary hyperaldosteronism, with a hyperosmolar state. Our pneumologist recommended steroids, on account of suspected alveolitis on the 12th day of hospitalization (150 mg/day methylprednisolone), for two weeks. During administration of corticoids, there was no accentuation of the septic symptoms. X-ray findings of bilateral diffuse infiltrates in the median and lower fields, with bilateral fluidothorax and dilated cardiac shadow, slowly receded (Fig. 3). Practically all the burned areas were converted into full-thickness skin loss, excised, and then autografted. The course of surgical operations was modified in relation to pulmonary findings. From day 50 the patient was breathing spontaneously through a tracheostomic cannula. On day 56 the tracheostomic cannula and nasogastric tube were removed. However, within 24 h, dyspnoea and dysphagia developed. Bronchoscopy revealed a tracheo-oesophageal fistula and subglottic stenosis of the trachea with severe phlegmonous tracheitis. The patient was transferred to a specialized department for intrathoracic surgery for a complete examination, during which the above diagnoses were confirmed. The patient died on the 60th day post-injury in a state of asphyxia as a fatal consequence of inhalation injury (Fig. 4). When an attempt was made to insert a tracheal stent, desaturation developed as well as protracted hypoxia, which made re-intubation very difficult.

In conclusion it may be said that in this patient various serious complications of inhalation injury led to the fatal outcome. To start with, there was the early complication of ARDS with severe alveolitis, and subsequently bilateral bronchopneumonia, due to which the aetiological agents were translocated - endogenous microbes as well as opportunistic nosocomial multiresistant bacteria from the intensive care unit, which in this respect is very exposed. The severe septic condition led to multi-organ dysfunction affecting the cardiorespiratory and hepatorenal systems. Subsequent healing with excessive fibroproduction led to the development of subglottic tracheal stenosis and pulmonary fibrosis, which after a longer time interval was to lead to severe pulmonary hypertension and cor pulmonale.

Results

Since August 2000 we have been regularly performing bronchoscopic examinations in patients with inhalation trauma. Until August 2003 we admitted to our intensive care unit 136 patients with inhalation injury who were treated with artificial pulmonary ventilation. In 38 patients (27.94%) we diagnosed a severe form of inhalation injury; the other patients were extubated for 7 days without any need for tracheostomy and without late consequential complications. Of the 38 patients with severe inhalatory trauma, 21 died. All had a burn extent of over 40% and were above 60 years of age, or there was a combination with intoxication. In 23 patients (16.91% of the total number) we performed percutaneous tracheostomy on day 8 of orotracheal intubation. Ten patients (7.35%) sequentially underwent surgical solution of the post-inhalation and post-intubation sequelae. Seven of these patients (5.15%) had tracheostomy and three patients (2.20%) did not. Of these 10 patients, two died, six had permanent tracheostomy (defects at the tracheostomy site), and two underwent radical reconstructive operations.

Discussion

In general, it may be said that inhalation injury combined with extensive burns has a 40-100% mortality from early or late complications, usually with the development of a septic state and ventilation pneumonia. It is also important to consider the part played by long-term intubation, i.e. the position of the tracheostomic cannula and the nasogastric and nasojejunal tube, the pressure of large-volume balloons on the background of inflammatory, ischaemic, secondarily infected mucosa, the direct entry into the airways when all natural protective barriers are lacking, and last but not least the manipulation by nursing staff during toilet of the airways. It is important to mention the difficulty of weaning patients from the ventilator in cases with prolonged analgosedation, frequently with extreme psychomotor unrest but inadequate spontaneous respiratory activity. In patients in whom respiratory insufficiency calls for long-term artificial pulmonary ventilation, the indication for tracheostomy remains a very controversial question. There is certainly no doubt concerning early and thus timely tracheostomy under generally acceptable conditions. However, in patients with extensive burns, this procedure is usually implemented against a background of a skin cover damaged by thermal injury; the epithelium of the airways has also already undergone gross macroscopic changes. It is no surprise that during the procedure tracheal rings dissolved by inflammation are denuded.

Conclusions

The above considerations make us select, in each patient, an individual approach in close collaboration with intensive care specialists. However, we evaluate different complications so that the outcome will serve to create a generally valid algorithm (e.g. as regards bronchoscopy classification and the classification and establishment of diagnostic and prognostic criteria of inhalation injury) for the prophylactic administration of antibiotics in inhalation trauma, the carriership of infection (sp. Staphylococcus aureus), the time indicated for tracheostomy and the technique of its implementation, toilet of the airways, the type of tracheostomic cannulas used, microbiological surveillance, and the controversial administration of systemic steroids.

RESUME. Les lésions sévères dues à l’inhalation provoquent une détérioration marquée du pronostic et augmentent la mortalité générale des grands brûlés. Récemment, en particulier à la suite du développement du monitorage invasif des patients et du traitement efficace du choc aigu dû aux brûlures, nous voyons toujours plus fréquemment des patients qui survivent à la phase aiguë, y compris les complications comme le syndrome de détresse respiratoire aiguë, et arrivent jusqu’à la phase des complications tardives. Celles-ci incluent les fistules trachéo-oesophagiennes qui se manifestent à cause des escarres de décubitus et de la chondromalacie, généralement au site du ballon de la canule trachéostomique, et de la surproduction du tissu fibreux dans la zone des voies aériennes, ce qui mène au développement de la sténose, la fibrose pulmonaire et la dilatation des bronches. Fréquemment plusieurs complications précoces et tardives se manifestent ensemble.

Bibliography

1. Meduri G.U.: Procollagen types I and III aminoterminal propeptide levels acute respiratory distress syndrome and in response to methyprednisolone therapy in unresolving ARDS. JAMA, 280: 159-65, 1998.
2. Meduri G.U.: Glucocorticoid treatment of sepsis and acute respiratory distress syndrome. Critical Care Medicine, 26: 630-3, 1998.