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. 2019 Mar 31;32(1):37–42.

ARDS among cutaneous burn patients combined with inhalation injury: early onset and bad outcome

NN Lam 1,∗, TD Hung 1
PMCID: PMC6588331  PMID: 31285733

Summary

Our aims are to determine the clinical and preclinical characteristics and outcome of ARDS among burn patients with inhalation injury. A retrospective study was conducted on 66 selected patients with ARDS, treated in the ICU of the National Burns Hospital from 11/2013 to 10/2016. The patients were divided into two groups and matched by age and burn extent: the study group consisted of 33 patients with inhalation injury and the control group 33 patients without inhalation injury. Outcome measures included blood gas criteria and oxygenation state at ARDS onset, mechanical ventilation duration, length of stay in the ICU and in the hospital, ventilation-free time and mortality rate until 28 days postburn. Results showed that ARDS onset was earlier in the study group (5.9 ±.7 vs. 9.2 ± .9 days postburn respectively; p < 0.01) and blood oxygenation disorder was more severe (PaO2/FiO2: 117.8 ± 6.1 vs. 125.9 ± 6.5 respectively; p < .01). There was no significant difference between the two groups (p > .05) regarding incidence of complications, ventilation time, ventilation-free duration, and length of stay in the ICU and in the hospital. Mortality rate until 28 days post burn was significantly higher among the study group (69.7% vs. 54.6% respectively; p < .001). In addition, time from admission and from ARDS onset to death was shorter in the study group (P < .05). In conclusion, compared to cutaneous burn-induced ARDS, ARDS in patients with inhalation injury has earlier onset, causes more severe oxygenation disorder and has a higher mortality rate.

Keywords: acute respiratory distress syndrome, inhalation injury, cutaneous burn

Introduction

Acute respiratory distress syndrome (ARDS) is a severe complication in the intensive care unit (ICU) resulting in almost 75 000 deaths per year in the United States. Universally, it is estimated that ARDS develops in 10% of patients in the ICU.1 Current review indicated that no pharmacologic treatments were significantly effective, and that the main management for ARDS is still lung-protective ventilation strategy.2

ARDS is also one of the leading complications among severe burn patients with or without inhalation inury.3,4,5 ARDS among cutaneous burn patients is due to inflammatory response in the acute phase of burn or sepsis phase postburn.6,7 Meanwhile, the pathological mechanism of ARDS in patients with inhalation injury is considered as a disorder of bronchial circulation, impact of Nitric Oxide and obstruction of the respiratory tract.8 Previous study indicated that inhalation injury is an independent risk factor for the development of ARDS but severity ofinhalation injury assessed by score did not contribute to the development of ARDS.9 Manifestation and outcome of burn patients with smoke-induced ARDS may be different to that of cutaneous burninduced ARDS patients. This study compared characteristics and outcomes of ARDS among burn patients with and without inhalation injury, treated at the National Burns Hospital of Vietnam.

Materials and methods

A retrospective study was conducted on 330 adult burn patients admitted within 48h post burns to the Burn ICU in the National Burns Hospital from 11/2013 to 10/2016, with burn extent ≥ 20% total body surface area (TBSA). Inhalation injury was diagnosed if patients had the following symptoms: history of a closed space fire, facial burns with singed nasal hair, carbonaceous sputum, hoarseness, stridor or laboured breathing. Bronchoscopy was performed within 48h from admission to confirm the diagnosis.10,11,12,13 Diagnosis of ARDS was based on the Berlin definition and protective ventilation strategy with low tidal volume of 6ml/kg of ideal body weight was applied for all ARDS patients, as recommended by the ARDS network.14,15,16 Out of 330 admitted patients, 86 developed ARDS. Thirty-three of these patients were diagnosed with inhalation injury and were selected as the study group. The control group included 33 ARDS patients without inhalation injury who matched the study group by age (± 5 years), burn surface area (± 5%) total body surface area (TBSA) and full thickness burn area (± 5%) TBSA (Fig. 1).

Fig. 1. Flow diagram of included and excluded patients.

Fig. 1

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Outcome measures included ARDS onset time, blood gas parameters and blood oxygenation state at ARDS onset, duration of mechanical ventilation, length of stay in the ICU and in the hospital, ventilation-free time, complications and mortality rate until 28 days postburn. Data were collected and analyzed using Stata software version 11.0, with p value <.05 regarded as the significant level. This study was approved by the hospital’s committee for human research ethics.

Results

Baseline criteria of patients, including age, burn severity, gender and admission time from burn occurrence were not significantly different between the two groups (Table I). All 66 patients were classified as having moderate to severe ARDS. It is noted that ARDS onset postburn was approximately 3 days earlier in the study group than in the control group (5.9 ± .7 days vs. 9.2 ± .9 days; p < .01).

Table I. Patient characteristics.

Table I

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Clinical and preclinical criteria at ARDS onset are indicated in Table II. Common symptoms were fever > 38.50C, increased heart rate > 130bpm, low SpO2, minor anaemia and leukocytosis. No remarkably different values were recorded between the two groups (p > .05).

Table II. Patient features at ARDS onset.

Table II

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At the time of ARDS diagnosis, data from blood gas analysis (Table III) indicated significantly lower PaO2 in the study group (59.4 ± 3.1 vs. 65.6 ± 3.5 respectively; p < .05). Higher PaCO2 values and lactate levels were also recorded in the study group with p <.05. In addition, blood oxygenation was significantly lower in the study group (PaO2/FiO2: 117.8 ± 6.1 vs. 125.9 ± 6.5 mmHg respectively; p < .01).

Table III. Blood gas parameters and oxygenation state at ARDS onset.

Table III

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Common complications recorded were septic shock and multiple organ failure (MOF), followed by acute renal failure and pneumothorax (Table IV). There was no significant difference between the two groups (p > .05) regarding complication frequency, ventilation time, ventilator-free duration up to the 28th day postburn and length of stay in the ICU and in the hospital. Death rate within 28 days post burn was significantly higher for the study group (69.7% vs. 54.6% respectively; p < .001) and most deaths were due to MOF (data not shown). In addition, time from admission and from ARDS onset until death was shorter in the study group (P < .05).

Table IV. Complications and outcomes in the two groups.

Table IV

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Discussion

Since first described by Ashbaugh et al. in 1967, the definition of ARDS has changed over time. In 1994, a formal definition and classification of ARDS was reported by the American-European Consensus Conference Committee on ARDS (AECC). In 2012, the Berlin definition was introduced with more detail, making clinical diagnosis easier.14,17 Over several decades, despite the great achievements of research and clinical trials, many questions about the pathogenesis and treatment of ARDS remain unanswered.15,18,19,20

Despite advances in fluid resuscitation, hypermetabolic response intervention, early surgical excision, tissue engineering and mechanical ventilation, the mortality rate of burn patients with inhalation injury is still high.8,10 Inhaled smoke causes damage to the airway or lung parenchyma by heat or chemicals that occurs in combination with cutaneous burns or separately. It was reported that there were more than 23,000 cases of inhalation injury annually in the United States.21

Respiratory dysfunction after burns is multifactorial and ARDS and inhalation injury are the most important causes.22,23,24 To date, significant reports on clinical characteristics, risk factors and outcome of ARDS amongst burn patients have been published.3,4,5,25,26

However, few of these mentioned specific aspects of ARDS in the inhalation injury population.22 For cutaneous burn patients, the main pathological mechanism of ARDS is an inflammatory response associated with the burn wound or burn wound infection. In the case of inhalation injury, additionally direct lung injury due to inhaled smoke and fumes is involved. In extensive burns, increased capillary permeability not only occurs locally but also in all the other organs. This process leads to the leakage of fluid into the interstitial space, and the risk of pulmonary edema becomes more serious due to the combination with inhalation inury.27 Experimental studies reported a 10-fold increase in bronchial blood flow within 20 minutes of smoke inhalation, as well as a six-fold increase in pulmonary transvascular fluid flux and a fall in PaO2/FiO2 ≤ 200, but these were delayed until 24 hours. Similar findings have been reported in patients with isolated smoke inhalation or in combination with large cutaneous thermal injury.28,29,30 A study on sheep suggested that NO produced by iNOS plays an important role in the changes in systemic and pulmonary microvascular permeability in combined smoke inhalation/third-degree burn injury.8,31 There are three types of inhalation injury: respiratory tract direct thermal injury, tissue damage due to chemical irritants, and systemic effects of inhaled toxins.9,10,12 Most patients with inhalation injury have burns on the face and neck and may have chest burns, so developing local edema can affect the respiratory tract, edema and obstruction due to exudate, leading to respiratory obstruction during the first 48h.7 Chest burn can lead to decreased lung compliance, increased relative resistance of the respiratory tract and laboured beathing.11 These all lead to impaired gas exchange, pneumonia and ARDS.

Current reports indicate that inhalation injury is an independent risk factor for the development of ARDS amongst burn patients, with early onset and greater severity compared to cutaneous burn-induced ARDS.2,26 Our study indicated an earlier onset of 3 days and more severe blood oxygenation and blood gas parameter disorders in ARDS patients with inhalation injury compared to the control group. In 2005, Liffner et al. investigated incidence, mortality and time of onset of ARDS in relation to extent of burn and inhalation injury in patients who required mechanical ventilation. They found that 70% of ARDS patients had early onset post burn (less than 6 days).9 In 2016, Cartotto et al. reported that ARDS developed in the 1st week after burn in 86% of cases: worsening severity of ARDS related to inhalation injury also led to a longer duration of mechanical ventilation and a reduction in ventilator-free days compared to the non inhalation injury-induced ARDS group.4

Common features of postburn ARDS were a large reduction in blood oxygenation measured by PaO2: FiO2 ratio, pulmonary compliance and increased extra vascular lung water. Mortality rate for ARDS patients is still high, especially in developing countries. 26 The early onset of ARDS, together with organ dysfunction (reduced platelet count, acute kidney injury…) induced by an inflammatory process related to burn wound and inhalation injury, leads to a high mortality rate.22 In our study, the death rate was 61.1%: a significantly higher rate was seen for inhalation injury-induced ARDS (69.7% vs. 54.6%) and time from admission and from ARDS onset until death was shorter in the inhaled smoke-induced ARDS group.

Our understanding of the mechanisms of fire-related inhalation injury that results in the development of ARDS is still limited.23 Several challenges have been encountered when investigating the pathogenesis and the role of smoke toxicants involved in the process of ARDS development. Moreover, it is difficult for researchers to be exposed to large numbers of animals (sheep or dogs) in order to conduct studies on smoke-induced ARDS in a serial manner.12However, new treatment interventions are being investigated, with promising results. For example, in 2017 Yang et al. reported the results of treatment administered to 13 patients with different degrees of ARDS caused by inhalation of white smoke from a burning smoke bomb. Their results showed that application of glucocorticoid early enough and in an uninterrupted manner can significantly reduce ARDS caused by inhalation of white smoke from burning smoke bomb. Sequential application of glucocorticoid and pirfenidone can effectively treat pulmonary fibrosis in the late stage.32

Conclusion

We have shown that ARDS has a significantly earlier onset, causes more severe blood oxygenation disorder, and has a higher mortality rate in cutaneous burn patients with inhalation injury than in those without inhalation injury.

Acknowledgments

Acknowledgement.We are grateful to all the staff of the National Burns Hospital, Hanoi, for helping us to collect data.

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