Mechanical Ventilation in the Burn Patient

Abstract

Among the most difficult to treat are severely burned, patients. We examined the conditions of these patients individually and the organ involvement. It is impossible to manage them because they are dealing with multi-organ dysfunction, which affects all system homeostasis. This chapter focuses on the respiratory system, specifically the mechanical ventilation strategies to improve the outcome in the onset of acute respiratory distress syndrome (ARDS) and inhalation injury in severely burned patients, beginning with initial airway management and progressing to new ventilation strategies and modes to assist health providers in choosing what is best for their patients.

1. Introduction

Making the decision to act before ARDS develops is one of the most difficult challenges in the management of severely burned patients. The Abbreviated Burn Severity Index (ABSI) and the modern modified ABSI are two predictors of the development of ARDS in burn patients [1, 2]. We can improve the survival rate and the number of ventilator-free days for burn patients by acting quickly in the airway and ventilator management.

With the development of lung-protective ventilation and the Berlin Criteria for the diagnosis and classification of ARDS, mechanical ventilation management has improved dramatically in recent years [3], and we now rely on new ventilation methods with promising results when it comes to improving ARDS outcomes.

This chapter will focus on the mechanisms of how ARDS develops in severely burned patients, from the chemical foundation to the physical and macroscopic injuries a burned airway must endure.

2. Initial airway management

Airway assessment and cervical spine immobilization are the first steps in the management of severely burn patients, as they are in severe trauma. Burns to the upper and lower airways, as well as inhalation injury (II), pose a higher risk of airway obstruction. Therefore, early recognition of the signs and symptoms indicating the need for advanced airway management is critical.

According to the current trend in difficult airway management, it is preferable to have a team to minimize the complication rate in critical scenarios. Anesthesiologists, trauma surgeons, and head and neck surgeons are typically part of this team.

Burn patients have a difficult airway due to airway edema, the need for cervical protection, and the friability of the airway mucosa (Figure 1). Thus, it is recommended that the intubation be performed by an airway expert to avoid the need for a surgical airway and further complications [4].

Figure 1.

Manuel Araiza managing a severely burned patient airway, in May 2022; notice the neck burns and the airway positioning to stabilize cervical spine, which are included in the difficult airways characteristics.

According to Advanced Trauma Life Support, the following are indications for early intubation:

• Signs of airway obstruction

• Total body surface area burns of >40%

• Deep facial burns or burns inside the mouth

• Edema or risk for edema

• Difficulty swallowing

• Signs of respiratory compromise

• Low level of consciousness, impairment of the airway protective reflexes, and

• Management of unqualified personnel

Rapid sequence intubation (RSI) is the technique of choice for advanced airway management in severely burned patients to minimize the risk of regurgitation and optimize oxygen delivery. Rocuronium and suxamethonium are two neuromuscular blockers used in RSI. Suxamethonium increases the risk of hyperkalemia, bradycardia, high intracranial pressure, high intraocular pressure, and fasciculations [5], so its use in advanced airway management in burn patients should be limited.

3. Carbon monoxide and hydrogen cyanide toxicity

3.1 Carbon monoxide toxicity

Incomplete combustion produces carbon monoxide (CO) as a by-product. It is very common to find exposure to this chemical when inhalation injury is present, as it is odorless and tasteless. The main problem with CO poisoning is the wide range of symptoms it can cause: from a mild headache to seizures and death. Therefore, in all severely burned patients, we should always suspect and assess for CO poisoning.

CO inhibits the release of oxygen into peripheral tissues, resulting in tissue hypoxia. However, the molecular mechanisms are more complex.

The binding of CO to intracellular proteins such as cytochromes, myoglobin, and guanylyl cyclase disrupts cell homeostasis, interferes with oxidative metabolism, promotes the formation of reactive oxygen species, and causes oxidative stress and cell apoptosis [6].

Assessing for CO poisoning using the carboxyhemoglobin (COHb) measurement can provide insight into the severity of the intoxication, but COHb levels do not always correlate with the degree of poisoning [6]. It has been classically stated that COHb levels of 15–40% can cause moderate symptoms, and levels of >40% can cause severe symptoms and death from CO toxicity [4].

CO poisoning symptoms are classified into three levels: mild, moderate, and severe. Mild symptoms include headache, nausea, vomiting, dizziness, and blurred vision; moderate symptoms include syncope, dyspnoea, tachycardia, tachypnea, and rhabdomyolysis; and severe symptoms include palpitations, dysrhythmias, respiratory arrest, cardiac arrest, and coma [6].

Oxygen therapy is the first-line treatment for suspected or confirmed carbon monoxide toxicity, and it is administered through a face mask or, if necessary, an endotracheal tube. The half-life of COHb can be reduced to 40–45 minutes when using 100% FiO₂ through continuous positive airway pressure, and it can be reduced to 20 minutes when using 100% high-flow oxygen therapy [5].

3.2 Hydrogen cyanide toxicity

Hydrogen cyanide, like CO, is a by-product of incomplete combustion, but it is derived from synthetic materials. Similar to CO, hydrogen cyanide enters the cell quickly and inhibits oxidative phosphorylation while promoting anaerobic metabolism [4], inducing a state of ‘chemical shock’ as it causes tissue hypoxia.

4. Inhalation injury

One of the most difficult tasks in the management of burn patients is determining whether the patient is at risk of inhalation injury because this will play a significant role in the patient’s outcome, as this is one of the most important risk factors for the development of ARDS and higher mortality.

4.1 Pathophysiology

Major burns, without a doubt, cause a severe inflammatory response due to tissue destruction and fluid dysregulation. Following a severe burn, an acute phase inflammatory response triggers the release of cytokines and chemokines, which corresponds with a hypermetabolic state, consuming proteins, glucose, and fluid requirement [7]. This translates into initial fluid management in the severely burned patient and a distributive shock, which must be managed with a goal in mind.

The human airway is a highly perfused organ. When there is II, it increases 10–15 times as the hypermetabolic response kicks in, followed by edema of the upper and lower airways (depending on the site of injury), increasing resistance, limiting airflow, and forming a fibrin clot and cast [7]. We may experience significant airway obstruction when this happens, resulting in a ventilation-perfusion mismatch, atelectasis, and hypoxia.

As part of the inflammatory response, edema starts to occur in the upper and lower airways within hours of the burn injury. Then, in the hypermetabolic state, the cardiac output further promotes the airway inflammatory response, causing not only airway edema but also increasing the metabolic demand for analgesic and anesthetic drugs, as well as fluid requirements during the resuscitation phase [7].

This airway compromise, combined with the severe inflammatory response and the need for advanced airway management, makes the respiratory system vulnerable to infections, most notably pneumonia.

Edema, debris, and epithelial destruction eventually form airway casts, causing airway obstruction, high resistance, ventilation-perfusion mismatch, and atelectasis and preventing oxygen and tidal volume from reaching the alveoli, making lung unit recruitment difficult and predisposing the patient to pneumonia, barotrauma, high auto-positive end-expiratory pressure (PEEP), increased plateau pressure and, eventually, ARDS. We can prevent or at least minimize these complications and improve the outcome if we can remove these casts as part of the treatment of inhalation injury [7].

Inhalation injury causes bronchospasm through poorly understood mechanisms, although neuropeptides produced in the submucosa due to inflammation are responsive to aerosolized albuterol or epinephrine, suggesting the origin from a smooth muscle spasm [7].

There is a high airway resistance in the setting for mechanical ventilator management, resulting in auto-PEEP, making maintaining a safe peak pressure and an adequate plateau pressure difficult (Figure 2), implying the need for constant recruitment of lung units based on advanced modes of ventilation, as explained later in this chapter.

Figure 2.

Changes in the airway of a severely burned patient with inhalation injury.

4.2 Treatment

The most critical measure is determining whether advanced airway management, cervical spine stabilization, and, if necessary, life support is required in a deteriorating airway.

After assessing for a secure airway and preventing CO toxicity from progressing, one can focus on improving dynamics in inhalation injury. Beta 2 agonists aerosolized bronchodilators relax the smooth muscle in the upper and lower airways, reducing airway resistance and allowing a more laminar flow in and out during every ventilation cycle [7].

N-acetylcysteine is a mucolytic agent that aids in the prevention of airway mucus secretion accumulation. However, it is pungent to the airway and may cause bronchospasm, so it should not be used without a bronchodilator [7].

As debris is caused by fibrin cloths, casts, and damaged cells, aerosolized anti-coagulants such as heparin have been described to improve lung dynamics [7].

As the purpose of this chapter, we will go over ventilator strategies to improve mortality in severely burned patients, as well as the considerations we must make when managing a severely burned patient under mechanical ventilation.

4.2.1 Fluid management

The fluid management in the severe burn has been of great concern, mostly because of its nature as part of the burn pathophysiology. Burn Shock has been described as an endpoint to dehydration, structure modification of plasma proteins, vascular leak, causing cellular ischemia, and switching to anaerobic metabolism (shock).

Traditionally, classic Parkland Formula has been used to guide fluid management in the burn patient with a TBSA >20%. Nevertheless, recent studies show it is not always precise in improving resuscitation in this specific population. The modern approach to fluid management in the severely burn patient, is aiming for a goal – directed fluid balance, with a tendency to zero fluid accumulation and adequate fluid resuscitation, maintaining urine output between 0.5 and 1.0 mL/kg/hr., thus avoiding over-resuscitation and all the consequences of detrimental mortality such as abdominal compartment syndrome, pulmonary edema, pleural effusion, myocardial edema, poor wound healing, tissue edema, and all these factors lead to sepsis, ultimately ARDS [8, 9].

4.3 Diagnosis

Bronchoscopy has recently been proposed as the gold standard for inhalation injury due to direct observation of the injured tissue. However, there were limitations to this method, such as cost, a lack of equipment in some centers, and a lack of operator expertise. There is also a limitation for reaching distal airways, which may explain the lack of relationship between higher grades of II and higher mortality reported in some studies [10], making it necessary to complete the assessment with imaging testing, such as computed tomography showing parenchymal changes in the lung compatible with II [11]. Due to its limitations, it is not recommended to use it as a single test to diagnose II.

To summarize, the most appropriate approach for effectively diagnosing inhalation injury would be a comprehensive assessment that includes clinical features, demographics, mechanism of burn injury, imaging, and bronchoscopy.

5. Risk for ARDS

There is a controversial relationship between II and ARDS. Some studies claim there is no correlation, whereas others claim it is strongly related. Both II and pneumonia have been shown to increase the risk of moderate and severe ARDS [3]. The Berlin Criteria is an effective tool for determining the severity of burn-related ARDS with or without inhalation injury [3].

Other studies have found that, among other variables and demographics, II is a major factor in the development of ARDS. Thus, the Abbreviated Burn Severity Index (ABSI), a scoring system designed for patients suffering from starch-based powder burns, was developed with a reliable OR and a very high sensitivity and specificity ranging above 9 points in the scoring system [1].

6. Mechanical ventilation management

Multiple studies show that II is a significant risk factor for a prolonged ICU stay, the need for mechanical ventilation, the development of ARDS, pneumonia, and an increase in mortality [10].

6.1 Lung-protective ventilation

Prior to the development of lung-protective ventilation, the mortality rate in patients requiring mechanical ventilation was increasing. Much has been written about improving the outcome of mechanically ventilated patients and reducing the risk of ARDS and ventilator-induced lung injury (VILI). The modern view of ventilator management emphasizes different goals than those described before the 2000s.

The ARDSnet protocol, which specified low-tidal ventilation and a plateau pressure goal, was a significant breakthrough in mechanical ventilation. Each step in lung-protective ventilation is described in detail here.

6.1.1 Tidal volume

The modern recommendation for preventing VILI when it comes to tidal volume (Vt) in ARDS patients is that it be limited to 4–8 ml/kg PBW [12], which has been shown to improve mortality by 22% and increase ventilator-free days as stated in the ARDSnet trial and confirmed by numerous authors. Also, keep the ventilation goals for Vt in mind at all times.

Modern therapeutic tidal volume goals explain the relationship between excessive strain, higher tidal volume, and volutrauma [13].

When there is a tendency for airway collapse and increased resistance, higher tidal volumes pose a risk for air trapping, auto-PEEP, barotrauma, and volutrauma; lower volumes are preferred in inhalation injury.

6.1.2 Positive end expiratory pressure

Prior to the implementation of lung-protective ventilation, higher PEEP was thought to be detrimental to lung homeostasis. Higher PEEP is now known to be essential for preventing atelectasis not only in patients with ARDS but also in healthy surgical patients [14]. According to numerous guidelines and studies, higher PEEP (>5 cmH₂O) improves mortality in patients with moderate to severe ARDS, as well as the length of stay in the ICU [15].

Physiologically, PEEP reduces stress by acting as a buffer to the constant opening and closing of the alveoli, eliminating the need to reach the opening threshold in each respiratory cycle [16]. Of course, there are exceptions to the rule, such as in patients with a fibrotic lung pattern, in which the non-recruitable areas predominate, as higher PEEP is associated with higher mortality [16].

However, higher PEEP (>5 cmH₂O) is an important part of lung-protective ventilation because it has been shown to improve oxygenation and alveolar recruitment, improve mortality and reduce stress to the alveolar unit [12, 13].

Airway resistance and a proclivity for airway collapse in severely burned patients increase the risk of air trapping and, as a result, auto-PEEP and increased effort to ventilate distal lung units. Therefore we can use higher PEEP in severe ARDS for severely burned patients with inhalation injury, so we can avoid or at least minimize air trapping while using lower tidal volumes and respiratory rates.

6.1.3 Plateau pressure

Peak pressure (Ppeak) and plateau pressure (Pplat) differ significantly. Peak pressure is the representation of the pressure in the airway as a unit, without differentiating between small alveolar units and larger airway components. Pplat, in contrast, is the pressure where gas exchange occurs in the lung and the alveoli. Therein lies the importance of maintaining an optimal Pplat while ventilating our patients.

Several studies have set the higher point of Pplat in 30 cmH₂O, or close to 28 cmH₂O, as high Pplat represents increased strain and mortality [12].

As previously stated, the severely burned patient tends to generate high pressure in the lung due to increased resistance in the airway, decreasing compliance. The Pplat must be given special attention to prevent barotrauma in the stiff chest wall and narrow airways of the ventilated, severely burned patients.

6.1.4 Driving pressure

The formula for driving pressure (DP) is plateau pressure minus PEEP, which represents the difference in alveolar pressure at the end of the inspiration (Pplat) and pressure at the end of expiration (PEEP) or, in other words, the changes in alveolar pressure between each cycle of ventilation.

A DP of <15 cmH₂O is expected to minimize lung stress and prevent VILI [12].

DP is one of the best modern predictors of VILI in any type of patient under mechanical ventilation. This influence is explained either by elastance or tidal volume (stress and strain). However, we should always keep its components (Pplat and PEEP) in mind when guiding lung-protective ventilation. As such, the DP could be in a safe range but not them [13].

The burn patient’s low lung compliance and stiff chest wall made achieving lower DP values in lung-protective ventilation the most difficult. Most severely burned patients will need to be intubated immediately after the injury and before a chest escharotomy can be performed, so we may have to adjust our parameters as low as possible to truly minimize lung damage and avoid VILI.

6.1.5 FiO₂

FiO₂ should be titrated in any ventilated patient to achieve oxygen and CO₂ goals, but in the case of a burn patient, we must consider the risk of carbon dioxide poisoning, which is a very common acute complication.

Diagnosis and management of carbon dioxide are very important, as they could pose very serious complications. With carboxyhemoglobin half-life and our patients’ clinical evidence in mind, we can choose between hyperbaric oxygen therapy (HBOT) and 100% O₂ [6].

Once the carboxyhemoglobin levels have been determined to be safe, we can begin titrating FiO₂ for therapeutic targets such as arterial PO₂ 55–88 mmHg, SatO₂ 88–95%, and a PCO₂ of ≤50 mmHg for a pH between 7.30 and 7.40 [17].

6.1.6 Mechanical power

Mechanical power is a novel concept that aims to bring together all of the factors that contribute to VILI [18]. Its components are respiratory system elastance, a dynamic measure that represents variations in airway pressure as volume changes in the lung with each cycle; airway resistance, which, as mentioned earlier, is high in the burned airway; and PEEP.

Mechanical power represents the energy applied to the lung on a molecular level, and forcing the lung to receive high energy and stress, damaging elastin to a molecular level, increases the risk for ventilator-induced complications [16].

Lowering the mechanical power may be essential to the new lung-protective ventilation strategies, especially in the high resistance, stiff, burned lung developing ARDS, where compliance is unstable and minor changes in the volume represent deteriorating lung pressure.

All these recommendations are summarized in Table 1.

Parameter	Therapeutic Goal
Tidal Volume	4–8 mL/kg of PBW
PEEP	>5 cmH2O, preferably >10 cmH2O in ARDS
Pplat	≤28 cmH2O
Driving Pressure	≤ 15 cmH2O
Mechanical Power	< 17 J
FiO2	100% while assessing for CO Poisoning, then titrate to achieve the goal of pO2
pH	7.30–7.40
pO2	55–88 mmHg
PCO2	< 50 mmHg
SatO2	88–95%

Table 1.

Goals for the lung protective ventilation in the severely burned.

6.2 Other alternatives in the ventilator management

6.2.1 High-frequency percussive ventilation (HFPV)

High-frequency percussive ventilation is a pneumatically driven, pressure-limited, time-cycled mode of ventilation. It is an advanced ventilation mode with a promising future in managing ARDS, specifically in the management of burn patients.

A series of studies have shown that it reduces the incidence of ventilator-associated pneumonia (VAP), improves gas exchange, and reduces the need for higher peak pressures with lower tidal volumes [19].

HFPV has not been shown to reduce mortality when compared to low-tidal volume. Still, it improves oxygenation and the number of available alveolar units, so it is now used regularly in burn centers in the United States [20].

6.3 Airway pressure release ventilation (APRV)

Stock et al. first described APRV as a mode for continuous positive airway pressure with deliberate release periods, in which it generates a high pressure (P high) for a long period of time (T high), simulating long alveolar recruitment, followed by a release phase in a lower pressure (P low) during the set release period (T low) (Figure 3) [21].

Figure 3.

Mechanically ventilated patient with APRV – TCAV. T high is lower than usual and a T – PEFR of 75%, used as a rescue strategy for a recruitable lung. Courtesy from Pedro González – Noris, MD.

One of the most convenient advantages is the amount of sedation required to maintain this mode. Although in some patients with ARDS, we require a RASS of −3 or −4, this mode requires a RASS of −2, and it is also compatible with prone positioning, which preserves reflexes, favors spontaneous breathing, and reduces the risk for VAP [20, 22]. We could theoretically use this mode in patients with low compliance and poor oxygenation, such as severely burned patients [23].

However, there are some concerns about using this mode, specifically in burn patients. According to some animal studies, the APRV-treated population developed ARDS faster than the conventional ventilation population [20]. In contrast, a retrospective study performed by Foster et al. on burn patients suggests that APRV is a safe ventilation model for these patients [24].

When managing this mode, we must be mindful of some precautions, such as patients with underlying comorbidities who do not tolerate low sedation, commonly neurologically critical patients [21], as well as patients generating auto-PEEP and air trapping [20].

Complementing APRV, time-controlled adaptive ventilation is a method developed to minimize the dynamic alveolar strain by adjusting the delivered breath, focusing on the release phase for the expiratory flow to terminate (EFT) at 75% of the expiratory flow peak (EFP).

The formula E_FP × 75% = E_FT was empirically identified at the bedside as effective at lung stabilization and maintaining open and stable alveoli, resulting in homogeneously ventilated alveoli. This novel ventilation method changes the current approach to mechanical ventilation from arbitrary to personalized and adaptive, but more randomized controlled trials are required [25].

7. Conclusions

The multifactorial causes of ARDS in burn patients are significant. A severely burned patient has an increased inflammatory response after a prolonged hypermetabolic phase that can last longer than usual severe trauma; early management is critical and can dramatically change the outcome.

We must consider ARDS in severely burned patients as a rapidly progressing fibrosis in which we are racing against metabolic, chemical, and physical damage to the respiratory system. If lung-protective ventilation is not achieved in a modern setting, mortality will keep increasing hour by hour.

When it comes to selecting a mode of ventilation for a burn patient, nothing is entirely clear. The outcomes are very similar as long as we achieve the lung-protective ventilation goals. Thus, there is no one-size-fits-all ventilation technique in these situations. We must choose what our patient responds better to and always be aware of complications, how to prevent them and how to solve them.

Acknowledgments

This chapter is made possible in part by the Anesthesiology and the Plastic Surgery team from the Burn Unit of the Traumatology Hospital of Dr. Victorio de la Fuente Narváez in Mexico City for their training on the management of burn patients in critical scenarios.

Thank you to all of the Anesthesia Attending staff and chief of Anesthesia in the Dr. Darío Fernández General Hospital for pushing me to learn more about mechanical ventilation.

Conflict of interest

The authors declare no conflict of interest.

Notes

The figures and tables used in this chapter were photos and diagrams developed by the author and colleagues.