Inhalation injury after exposure to indoor fire and smoke: The Brazilian disaster experience.

OBJECTIVE: To describe the pre-hospital, emergency department, and intensive care unit (ICU) care and prognosis of patients with inhalation injury after exposure to indoor fire and smoke. MATERIALS AND METHODS: This is a prospective observational cohort study that includes patients admitted to seven ICUs after a fire disaster. The following data were collected: demographic characteristics; use of fiberoptic bronchoscopy; degree of inhalation injury; percentage of burned body surface area; mechanical ventilation parameters; and subsequent events during ICU stay. Patients were followed to determine the ICU and hospital mortality rates. RESULTS: Within 24h of the incident, 68 patients were admitted to seven ICUs. The patients were young and had no comorbidities. Most patients (n=35; 51.5%) only had an inhalation injury. The mean ventilator-free days for patients with an inhalation injury degree of 0 or I was 12.5±8.1 days. For patients with an inhalation injury degree of II or III, the mean ventilator-free days was 9.4±5.8 days (p=0.12). In terms of the length of ICU stay for patients with degrees 0 or I, and patients with degrees II or III, the median was 7.0 days (5.0-8.0 days) and 12.0 days (8.0-23.0 days) (p<0.001), respectively. In addition, patients with a larger percentage of burned surface areas also had a longer ICU stay; however, no association with ventilator-free days was found. The patients with <10% of burned body surface area showed a mean of 9.2±5.4 ventilator-free days. The mean ventilator-free days for patients who had >10% burned body surface area was 11.9±9.5 (p=0.26). The length of ICU stay for the <10% and >10% burned body surface area patients was 7.0 days (5.0-10.0 days) and 23.0 days (11.5-25.5 days) (p<0.001), respectively. CONCLUSIONS: We conclude that burn patients with inhalation injuries have different courses of disease, which are mainly determined by the percentage of burned body surface area.

Evaluation of Serum Lactate, Central Venous Saturation, and Venous-Arterial Carbon Dioxide Difference in the Prediction of Mortality in Postcardiac Arrest Syndrome.

INTRODUCTION: Tissue hypoperfusion and hypoxia markers predict mortality in critically ill patients. This study evaluates the ability of serum lactate, central venous oxygen saturation (Scvo 2), and venous-arterial carbon dioxide difference (GapCo 2) to predict mortality in patients with postcardiac arrest (post-CA) syndrome. METHODS: A prospective observational study of patients with post-CA in a tertiary teaching hospital. Serial assessments of lactate, lactate clearance (Clac), GapCo 2, and Scvo 2 in the first 72 hours post-CA were analyzed. Adults (≥18 years) patients resuscitated from CA were included. The primary end point was 28-day mortality and secondary end points were 24- and 72-hour mortality. RESULTS: A total of 54 patients were recruited, 33 (61,1%) of 54 were men, with a 28-day mortality of 75.9%. Cardiac arrest occurred in-hospital in 84.6% of survivors and 97.5% of nonsurvivors. Lactate and Clac were significantly associated with mortality at 28 days, yielding an area under the receiver-operating characteristic curve of 0.797 (lactate 6 hours) and 0.717 (Clac 6 hours) with a positive predictive value of 96% for lactate 6 hours (> 2.5 mmol/L) and 89.5% for Clac 6 hours (<50%). Survival analysis confirmed the difference between the groups from the 24th hour post-CA. Considering mortality at 24 hours, lactate, Clac, and Scvo 2 (immediately post-CA, 6 and 18 hours) were different between the groups. In mortality at 72 hours, lactate, Clac, Scvo 2 (48 hours), and GapCo 2 (36 and 48 hours) were associated with mortality. CONCLUSION: In post-CA syndrome, serum lactate and Clac were consistently able to predict mortality.

The role of serum lactate in post-cardiac arrest syndrome

Cardiopulmonary arrest is a medical emergency with significant mortality. The success of resuscitation led to the emergence of post-cardiac arrest syndrome (PCAS), which originates from ischemia-reperfusion injury and its consequent increase in serum lactate. Despite the robust evidence correlating hyperlactatemia as a prognostic marker in critically ill patients, there is insufficient evidence about the role of serum lactate in the outcome of PCAS. Thus, the purpose of this review is to check the current evidence on the role of lactate in predicting mortality in PCAS.