Case reportAdult respiratory distress syndrome or congestive heart failure in severe burn: A role for brain natriuretic peptide
Introduction
In patients with extensive burns several causes may underlie hypoxic respiratory failure and bilateral infiltrates on the chest X-ray in the first week afterburn: cardiogenic pulmonary edema as a result of congestive heart failure, pneumonia and/or adult respiratory distress syndrome (ARDS). In particular, it is a challenge to differentiate between ARDS and cardiogenic pulmonary edema in these patients because on the one hand the incidence of ARDS in burn shock appears higher than anticipated, whereas on the other hand there is an increased risk for cardiogenic pulmonary edema to develop as intensive fluid resuscitation is mandatory, while myocardial function is depressed as noted by Baxter et al. [1]. Since these two diagnoses have very different treatment options, it is important to be able to differentiate between them as soon as possible.
ARDS is a syndrome characterized by stiff lungs, hypoxia and bilateral infiltrates on a chest X-ray [2]. Within the spectrum of ARDS burns and inhalation injury are infrequent causes. However, within patients with thermal and/or inhalation injury the incidence of ARDS is underestimated. A retrospective study showed that the incidence of ARDS that necessitated mechanical ventilation after severe burns may be as high as 53.6% [3]. A recent prospective study showed the incidence of ARDS in mechanically ventilated burn patients (mean TBSA: 31%, median 26%) to be 40% [4].
Natriuretic peptides are a family of peptides of which atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are produced in cardiomyocytes and secreted in the ventricles as a response to increases in intracardiac volume and pressure [5], [6]. Plasma levels of BNP are a sensitive indicator of left ventricle dysfunction [7] and are significantly elevated in patients with heart failure [8], [9]. BNP levels depend on many other factors. Renal failure increases levels of BNP [10], and BNP is also elevated in patients with severe sepsis or septic shock, regardless of cardiac function [11]. In mechanically ventilated patients positive end expiratory pressure (PEEP) decreases the levels of plasma BNP [12].
One thus might expect plasma BNP to be high in patients with hypoxia due to cardiogenic pulmonary edema as a result of congestive heart failure and low in patients with hypoxia due to ARDS.
The clinical usefulness of plasma BNP in a patient with extensive burns and inhalation injury is illustrated by the following case.
Section snippets
Case report
A 58-year-old male was admitted with severe burns (TBSA 60.5%, 29% partial and 31.5% full thickness burns of legs, buttocks and back) and inhalation trauma. He was intubated and under sedation with midazolam and analgesia with fentanyl. His vital signs were: blood pressure 85/60 mmHg, heart rate 60/min, oxygen saturation 98.4% and body temperature 38.6 °C. Intensive fluid resuscitation was provided according to our local protocol (first period (0–8 h postburn): 1.5 ml NaCl 0.9% × kg × TBSA and 100 ml
Discussion
This patient shows the dilemma of the adult patient with extensive burns and inhalation injury. After several days ventilation becomes difficult with bilateral infiltrates on the chest X-ray. Differential diagnostic considerations are ARDS, cardiogenic pulmonary edema or pneumonia. In particular ARDS and cardiogenic pulmonary edema are difficult to differentiate, which however is clinically important because of the different treatment modalities.
According to the American-European consensus our
Conclusion
In patients with inhalation injury and severe burns use of BNP in the differential diagnosis between ARDS and congestive heart failure seems helpful. Low plasma BNP levels may exclude cardiogenic pulmonary edema in this population and justify the infusion of extra fluids.
Conflict of interest statement
None declared.
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