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. 2026 Oct 13;22(4):250340. doi: 10.1183/20734735.0340-2025

Mechanical ventilation in acute brain injury

Luca Ratibondi 1, Virginia Newcombe 1,2, Romit J Samanta 1,2,3,✉
PMCID: PMC13659421  PMID: 42871854

Abstract

Acute brain injury (ABI) includes traumatic brain injury, subarachnoid and intracerebral haemorrhage, ischaemic stroke and global hypoxic–ischaemic injury, and patients often require admission to intensive care. Although pathologically heterogeneous, they share common mechanisms of primary injury followed by secondary brain injury. Systemic derangements such as hypoxaemia, dysregulated carbon dioxide tension and elevated intracranial pressure (ICP) may exacerbate secondary injury and should be avoided. Patients with ABI often require invasive mechanical ventilation (IMV), and of these up to 19–22% may develop acute respiratory distress syndrome.

Lung-protective ventilation (LPV) strategies using low tidal volumes and moderate positive end-expiratory pressure to minimise ventilator-induced lung injury are established practices in patients requiring IMV. However, strict application of LPV principles may conflict with neuro-protective goals, particularly carbon dioxide control to optimise cerebral blood flow and avoid rises in ICP.

This review examines the physiological tension between lung and brain protection, focusing on neuro–respiratory interactions and brain–lung crosstalk. We synthesise the evidence on ventilatory strategies in the context of patients with ABI, discuss the implications for neurological and pulmonary outcomes, and highlight the need for an integrated, individualised approach to ventilation in these patients.

Shareable abstract

It is important to understand ventilation strategies in patients with acute brain injury, especially when balancing both lung-protective and neuro-protective goals https://bit.ly/3Se55sC

Educational aims

  • To describe the pathophysiological interactions between the brain and lung in ABI.

  • To understand LPV strategies in patients with ABI, with particular emphasis on driving pressure, plateau pressure, and their neurological implications.

  • To recall the importance of control of arterial carbon dioxide tension in ABI and the evidence-based, recommended targets for normocapnia.

  • To apply an individualised, physiology-guided approach to ventilatory management in patients with concurrent ABI and acute respiratory distress syndrome by incorporating multimodal intracranial monitoring, thus allowing titration of competing physiological strategies.

  • To recognise possible determinants of weaning success and the role of tracheostomy in patients with ABI and how these differ from the general intensive care unit population requiring IMV.

Introduction

Acute brain injury (ABI) represents a major cause of admission to intensive care units (ICUs) worldwide and encompasses a heterogeneous group of conditions including traumatic brain injury (TBI), subarachnoid haemorrhage, intracerebral haemorrhage, ischaemic stroke and global hypoxic–ischaemic injury. These conditions share common pathophysiological mechanisms of primary injury followed by secondary brain injury, which can be exacerbated by systemic factors including hypoxaemia, hypercapnia, hypocapnia and elevated intracranial pressure (ICP).

A substantial proportion of these patients require invasive mechanical ventilation (IMV) to maintain adequate oxygenation, control carbon dioxide tensions and facilitate neuro-protective interventions. Reported rates vary widely across studies (between 20% and 60% or higher), depending on injury type, severity and study population [1, 2]. Furthermore, patients with ABI have an increased risk of developing acute respiratory distress syndrome (ARDS), which affects 19–22% [3].

The general management of patients requiring IMV has gradually evolved towards the concept of lung-protective ventilation (LPV). Low tidal volumes and moderate positive end-expiratory pressure (PEEP) are widely established as the standard of care [4]. These strategies may, however, be deleterious for the injured brain as the strict application of LPV principles may compromise key tenets of neuro-protection: permissive hypercapnia versus arterial carbon dioxide tension (PaCO2) control with normo- or mild hypocapnia for ICP control.

This review synthesises the conflict between these two physiological priorities while considering recent evidence on ventilatory strategies in ABI and how these may influence patient outcomes.

Neuro–respiratory physiology

Ventilation is regulated by integrated brainstem networks that process chemical and neural inputs, including peripheral and central chemoceptor signalling, as well as cortical influences. These control mechanisms facilitate rapid adaptation to metabolic and environmental changes. Following brain injury, this integration may be disrupted, leading to alterations in respiratory drive and breathing patterns. If these changes are not recognised, they may cause secondary brain injury.

Unlike other organs, the brain is extremely sensitive to even small variations in oxygen and carbon dioxide tensions, which significantly modify cerebral blood flow (CBF) and ICP. Acute neurological injury is frequently associated with intense sympathetic activation that directly affects lung permeability, surfactant function and pulmonary haemodynamics. This complex bidirectional brain–lung interaction, often referred to as “brain–lung crosstalk”, explains why conditions such as neurogenic pulmonary oedema and ARDS are common in neurocritical patients, and emphasises the importance of careful and considered ventilatory strategies in patients with ABI.

In general, for patients requiring IMV, it is well established that high tidal volumes (>10 mL·kg−1 ideal body weight (IBW)) and elevated plateau pressures (>15 cmH2O) are associated with increased mortality. This is known as ventilator-induced lung injury (VILI), the mechanism of which is due to a combination of volutrauma, barotrauma and biotrauma. In patients with ABI, VILI may contribute to systemic inflammation via release of inflammatory mediators from injured lung tissue. Both animal models and observational studies in humans have demonstrated that systemic inflammatory processes can exacerbate neuroinflammation and are associated with unfavourable neurological outcomes.

Carbon dioxide and cerebral blood flow

The CBF is tightly coupled to PaCO2. Even small fluctuations can result in large changes in CBF, making carbon dioxide a potent regulator [5]. The effect is due to a rapid and predictable action on the cerebral vascular tone, primarily mediated by pH-dependent effects on cerebral arteriolar smooth muscle cells (figure 1).

FIGURE 1.

FIGURE 1

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Effect of arterial carbon dioxide tension (PaCO2) on cerebral arterioles and mechanisms of vasodilatation. Hypercapnia results in cerebral vasodilatation, and increased cerebral blood flow and cerebral blood volume. The mechanisms include: 1) chemical effects on smooth muscle cells (lower pH, increased bicarbonate (HCO3−) and H+, leading to K+ flux); 2) nitric oxide (NO) release and endothelial relaxation; and 3) astroctye/neurohormonal mechanisms (NBCe1 (Na+/HCO3−) co-transporters in astrocyte foot processes). The physiological effect is a 3–4% increase in cerebral blood flow per 1 mmHg increase in PaCO2, which may increase intracranial pressure (ICP). Hypocapnia results in cerebral vasoconstriction, and reduction in cerebral blood flow and cerebral blood volume. This lowers ICP, but at the expense of cerebral oxygen delivery [6].

In the context of patients with ABI, these effects can be magnified by a reduction of intracranial compliance and impaired autoregulation [7, 8]. The potency of carbon dioxide reactivity forms the physiological basis for using hyperventilation to reduce ICP in patients with intracranial hypertension. However, excessive hypocapnia can compromise cerebral perfusion and oxygen delivery, potentially compounding ischaemic injury [6, 9]. As a result, the relationship between PaCO2 and clinical outcomes appears to be U-shaped, with both severe hypocapnia and hypercapnia associated with unfavourable patient outcomes [10, 11]. Contemporary guidelines discourage the routine use of prophylactic hyperventilation and advocate targeting normocapnia in neurocritical patients [12].

Oxygenation and cerebral metabolism

Neurons are strictly dependent on oxidative metabolism and tolerate hypoxaemia poorly, as anaerobic glycolysis cannot meet their energy demands. Adequate oxygen delivery is therefore essential for ensuring neuronal survival. Hypoxaemia is unequivocally associated with poor neurological outcomes across all subtypes of ABI and should be aggressively avoided.

Hyperoxia is also likely to be harmful [13]. Excessive arterial oxygen tension (PaO2) has been linked to increased oxidative stress, mitochondrial dysfunction and exacerbation of secondary brain injury, particularly following ischaemic stroke. Observational studies in TBI, subarachnoid haemorrhage and post-cardiac arrest populations have demonstrated a U-shaped relationship between PaO2 and outcome, with both hypoxaemia and marked hyperoxaemia associated with increased mortality [11, 14]. Although definitive thresholds remain uncertain, current consensus guidelines advocate targeting PaO2 in the range of 80–120 mmHg (11 kPa–16 kPa) [12].

The role of PEEP and physiological “trade-offs”

PEEP during IMV is intended to maintain alveolar recruitment, improve oxygenation and reduce atelectasis. In the general critical care population, LPV strategies that incorporate low tidal volumes and moderate levels of PEEP are well established and the expected standard of care. However, the application of PEEP in patients with ABI poses challenges due to its effect on the balance between brain physiology, respiratory mechanics and haemodynamics.

From a haemodynamic perspective, PEEP raises intrathoracic pressure and lung volumes, which reduces right ventricular (RV) preload, increases RV afterload and slightly reduces RV stroke volume. There is also a reduction in left ventricular (LV) transmural pressure and LV afterload, and a potential increase in LV stroke volume. These effects are also dependent on other physiological characteristics, e.g. chest wall and lung elastance [15].

Under normal circumstances, in patients receiving IMV, the improvements in ventilatory parameters following administration of moderate PEEP reduce pulmonary vascular resistance due to improved ventilation/perfusion matching, which leads to higher PaO2 and improved carbon dioxide clearance. This offsets the initial impairment in RV function and, when coupled with favourable LV function, can support an improved cardiovascular profile and cardiac output in patients requiring IMV. Normal cardiac output and normotension improve CBF and substrate delivery to the brain.

PEEP and ICP

At a simple level, the effect of PEEP on intrathoracic pressure increases ICP. As PEEP values tend to be in the region of mean systemic filling pressure (∼8 mmHg), which determines venous return, there is a reduction in cerebral venous flow that can increase cerebral blood volume and ICP.

However, the interaction of PEEP with ICP is not a simple or linear mechanism as it depends on additional factors. Several studies have evaluated this relationship [7, 15, 16], reporting baseline ICP, intracranial compliance, lung elastance, recruitability and magnitude of PEEP change as major determinants of ICP variations. In addition, the haemodynamic response to PEEP is critical, as changes in cerebral perfusion pressure (CPP) reflect the balance between ICP and mean arterial pressure (MAP). Physiological studies suggest that moderate increases in PEEP do not necessarily reduce CPP when MAP is preserved, and that reductions in CPP are often driven by PEEP-associated decreases in MAP rather than clinically significant rises in ICP alone.

Recent evidence suggests that moderate PEEP (∼12 cmH2O) results in statistically significant but clinically modest increases in ICP (∼1 mmHg) but without affecting CPP in most patients [8, 16]. Patients with lower baseline ICP may be more susceptible to ICP increases with PEEP elevation, while those with already elevated ICP demonstrate minimal response. This variability probably reflects differences in pressure transmission to the intrathoracic and venous compartments; patients with reduced respiratory system or chest wall compliance, higher central venous pressure, or impaired intracranial compliance may be more prone to ICP elevation during PEEP titration [17].

The natural trade-off when ventilating patients without PEEP is promotion of alveolar de-recruitment and atelectrauma, VILI and systemic inflammation. The resulting hypoxaemia and PaCO2 instability will then have deleterious effects on ICP and cause reduction in CPP [12].

PEEP and brain tissue oxygenation

The effect of PEEP on brain tissue oxygenation (PbtO2) is the result of a double mechanism. As described, PEEP can improve blood oxygenation but can also increase cerebral blood volume. A single-centre retrospective cohort study in 2023 evaluated the effect of PEEP by measuring PbtO2 responsiveness (increase in PbtO2 >20% from baseline) after PEEP increase from 6 to 10 cmH2O. The net effect was a statistically significant PbtO2 increase without ICP increase, suggesting that PEEP may be particularly beneficial in patients with cerebral hypoxia, potentially improving PbtO2 without necessarily increasing ICP [18].

General ventilatory management in patients with ABI

The goal of IMV in patients with ABI is to support gas exchange while minimising adverse effects on cerebral physiology. Unlike in general critical care, where lung protection is often the dominant concern, ventilatory strategies in ABI must balance pulmonary and cerebral priorities, optimising ICP control, preserving cerebral perfusion, supporting autoregulation, and balancing sedation requirements with the need for ongoing neurological assessment, which are of paramount importance in this specific population. Deep sedation and neuromuscular blockade may be required during the acute phase to control ventilation, prevent cough and reduce cerebral metabolic demand, particularly in the presence of refractory intracranial hypertension. These strategies must be weighed against the loss of neurological monitoring by clinical assessment, and risk of unrecognised neurological deterioration, so their duration should be minimised. Furthermore, agitation and delirium, which are common in patients with ABI, pose specific challenges in terms of sedation titration and changes in respiratory effort, for example during tachypnoeic episodes [19].

Ventilator modes and settings

In patients with ABI, the mode of ventilation should be selected to achieve normocapnia, minimisation of patient–ventilator asynchrony and tolerance with minimal sedative requirements, as well as to prevent excessive respiratory effort by the patient and reduce the risk of VILI. In the early phase of ABI, controlled ventilation modes may be required in patients with intracranial hypertension, as deep sedation with neuromuscular blockade is used to manage ICP and ensure precise PaCO2 control.

The evidence basis in general ICU patients does not support a specific ventilation mode for all patients, as most randomised clinical trials have not found any difference between pressure- or volume-controlled models in terms of oxygenation targets or mortality. Institutional practice, the clinical scenario and respiratory mechanics often determine choice of mode.

Volume-controlled ventilation (VCV) modes are widely used, as fixed and predictable minute ventilation facilitates lower variation in PaCO2. Pressure-controlled ventilation (PCV) requires closer monitoring and interventions to ensure consistent minute ventilation, as sudden changes in lung compliance or airway resistance (e.g. secretions or coughing) will reduce delivered tidal volumes and may lead to unpredictable and sudden changes in PaCO2.

Pressure-regulated volume control (PRVC) is a dual-control or “adaptive” ventilatory mode that combines the advantages of VCV, guaranteeing a set tidal volume, with characteristics of PCV in terms of limiting inspiratory pressures and using a decelerating flow pattern. Due to a set tidal volume, PRVC should guarantee a better PaCO2 control. A randomised crossover trial in TBI patients compared PRVC with PCV and found that while mean ICP and PaCO2 were similar, PRVC was associated with less variation in both variables [20].

Assisted modes (e.g. pressure-supported or volume-supported) may be considered as neurological and respiratory stability is achieved, as these modalities facilitate weaning and reduction in sedation dose. The bedside management of assisted ventilation is complex and effort indices (e.g. airway occlusion pressure during the first 0.1 s (P0.1), maximum negative occlusion pressure (Pocc) and pressure muscle index (PMI)) can help to guide titration of ventilatory support. Assisted modalities are not free from VILI or patient self-inflicted lung injury. Accurate estimation of respiratory effort can help to titrate ventilatory support, preventing excessive lung stress, ventilator-induced diaphragmatic dysfunction and the deleterious effects of both over- and under-assistance.

LPV in ABI

LPV strategies refer to a global approach aimed at minimising VILI. They include low tidal volume ventilation (6–8 mL·kg−1 IBW), limitation of plateau pressure (<30 cmH2O) and driving pressure (<15 cmH2O), and appropriate application of PEEP. Together, these approaches have transformed the management of ARDS in ventilated patients. These measures have consistently demonstrated improved outcome in patients with ARDS, including reduced mortality and fewer days spent receiving mechanical ventilation. However, their role in brain injury patients remains contentious (figure 2) [4].

FIGURE 2.

FIGURE 2

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Trade-offs between lung- and neuro-protective priorities in patients with acute brain injury (ABI) and lung injury. Neuromonitoring can help physicians to individualise therapy and safely balance these competing pathophysiological processes. ARDS: acute respiratory distress syndrome; PEEP: positive end-expiratory pressure; IBW: ideal body weight; ICP: intracranial pressure; MAP: mean arterial pressure; VILI: ventilator-induced lung injury; ECMO: extracorporeal membrane oxygenation; PaO2: arterial oxygen tension; PaCO2: arterial carbon dioxide tension.

The recently published VENTIBRAIN international multicentre observational study demonstrated that lung-protective strategies are widely applied worldwide in patients with ABI, but with high variation in compliance with different aspects of LPV, especially with respect to driving pressure and plateau pressure across different centres [11].

LPV in ABI without ARDS

PROLABI was a randomised controlled trial that investigated the effects of lung-protective mechanical ventilation using low tidal volumes and moderate PEEP, compared with traditional ventilation strategies, on the outcomes of 190 patients with severe ABI without ARDS [21]. The primary outcome was a composite of death, ventilator dependency, and ARDS at day 28. Patients randomised to the LPV strategy were more likely to suffer worse outcomes (61.5% versus 45.3%; p=0.025), but the study was terminated early due to funding loss resulting in severe underpowering (190 versus 524 planned) and risk of type 2 errors. The conclusion was that in patients with ABI but without ARDS, an LPV strategy did not reduce mortality. These findings were, in part, consistent with the VENTIBRAIN study, which found that mortality was associated with higher ventilatory pressures (plateau pressure and peak pressure) and driving pressures but lower tidal volumes [11].

The Brain Vent study, a single-centre randomised crossover trial, evaluated the role of a low tidal volume ventilation (6 mL·kg−1 IBW) with low PEEP (5 cmH2O) or high PEEP (12 cmH2O) in 27 patients with ABI without pre-existing lung injury [8]. The study found that most patients tolerated low tidal volume ventilation regardless of the level of PEEP applied, with only moderate ICP increase (2.2 mmHg). However, six of the 27 patients (22%) reached the safety threshold of ICP >22 mmHg, requiring intervention interruption. Interestingly, in this cohort, cerebral oxygenation and cerebral autoregulation were not significantly affected by changes in PEEP.

Asehnoune et al. [22] found in their meta-analysis that protective ventilation was not associated with reduced mortality in patients with ABI, although it did improve oxygenation (PaO2/inspiratory oxygen fraction (FIO2) ratio) over the first 5 days. The lack of mortality benefit may reflect limitations of observational studies, heterogeneity in populations and protocols, or the possibility that LPV prevents complications without directly reducing mortality in this specific population, which may be attributable to non-pulmonary factors. One should also consider the role of reverse causation in this population: patients with normal respiratory compliance can achieve better PaCO2 control without encroaching on harmful plateau, peak or driving pressure thresholds, whereas those with poor compliance are at risk of both pulmonary complications from VILI and neurological complications from poor PaCO2 control.

In summary, in patients with ABI without ARDS, LPV using low tidal volumes is feasible but has not shown a consistent benefit on mortality or neurological outcomes in randomised evidence. While PROLABI was negative, physiological and observational data suggest that higher plateau pressure, driving pressure and possibly mechanical power (as a surrogate of the total energy delivered during ventilation) are associated with worse outcomes. Low tidal volume ventilation can be applied in most patients but may increase ICP in a subset. Taken together, current evidence supports an individualised brain–lung-protective strategy, avoiding excessive ventilatory stress while closely monitoring intracranial dynamics, rather than routine application of strict LPV protocols.

Optimising PEEP in ABI

As already described, the role of PEEP in brain-injured patients is complex and has a U-shaped relationship with mortality. Recent evidence suggests that moderate PEEP could be safely applied in patients with ABI with only modest increases in ICP, especially in patients with reduced lung compliance (e.g. with ARDS), with likely improvements in PbtO2 for selected patients [18]. High PEEP strategies should be used cautiously and ideally only in patients with invasive ICP and multimodal cerebral monitoring [23].

Strategies to individualise and identify the “best PEEP” has been a debated for decades. A recent review identified 22 methods for PEEP selection, but consensus remains lacking. Chen et al. [24] found that an individualised PEEP approach that minimised driving pressure in 111 TBI patients undergoing emergency surgery significantly improved post-operative pulmonary outcomes, with lower lung ultrasound scores (2.50 versus 5.25 in the zero-PEEP group), and was associated with lower brain injury biomarker levels (neuron-specific enolase (NSE) and high mobility group box 1 protein (HMGB1)) on post-operative days 1 and 3.

Carbon dioxide control: the evidence basis

Traditional practice has long advocated for prophylactic hyperventilation to reduce ICP, but accumulating evidence suggests that routine hyperventilation may be harmful, while targeted mild hyperventilation for intracranial hypertension may be beneficial when used judiciously with appropriate monitoring [9].

It is widely established that normocapnia is associated with a reduction in mortality in TBI patients [25]. Despite this, the CENTER-TBI study demonstrated that ventilation management varied considerably between centres and this was likely to be influenced by intracranial dynamics: patients with monitored ICP and intracranial hypertension had lower PaCO2 [26]. A secondary analysis of the ENIO study demonstrated a U-shaped relationship between PaCO2 and in-hospital mortality, with threshold PaCO2 values of <31 and >45 mmHg [10].

The 2020 European Society of Intensive Care Medicine (ESICM) consensus on mechanical ventilation in ABI patients recommended maintaining normocapnia (PaCO2 35–45 mmHg), allowing short-term hyperventilation only as a temporary therapeutic option in patients with ABI who have brain herniation [12].

Recruitment manoeuvres

Recruitment manoeuvres are transient increases in airway pressure designed to open collapsed alveoli and improve oxygenation during mechanical ventilation, but their application in patients with ABI is controversial due to potential adverse effects on cerebral haemodynamics. In mixed ABI cohorts, traditional volume recruitment manoeuvres with sustained high inspiratory pressures (up to 60 cmH2O) significantly elevate ICP, reduce MAP and CPP, impair cerebral autoregulation, impact RV function and worsen jugular venous oxygen saturation, with only marginal and transient improvements in systemic oxygenation, leading some original authors to caution against routine use in brain-injured patients. Recent ESICM guidelines on ventilation in ARDS patients recommend against routine use of high-pressure recruitment manoeuvres, with stronger evidence for avoidance of prolonged ones (>1 min) [27]. Emerging expert consensus suggests that while recruitment manoeuvres may be considered in select cases of severe hypoxaemia, high-pressure recruitment manoeuvres (PEEP ≥20 cmH2O) should generally be avoided in patients at risk for intracranial hypertension, and that careful titration of PEEP with ICP monitoring is essential in ABI populations [28].

Fluid management

Fluid management in patients with ABI requires balancing pulmonary and cerebral priorities. While in ARDS a fluid-restrictive strategy is usually advocated as likely to be beneficial for lung protection, its application in the presence of concurrent ABI must be approached with caution. In the TBI population, maintaining adequate CPP can be challenging considering the fragile equilibrium required to maintain cerebral perfusion in cases of impaired autoregulation. We use algorithm-guided autoregulation monitoring to ensure euvolaemia, with optimised and individualised CPP targets. The aim is to maintain adequate CPP in the autoregulatory range while avoiding hyperaemia, which may exacerbate cerebral oedema and lung injury from excessive fluid administration. In the context of aneurysmal subarachnoid haemorrhage, euvolaemia is essential to reduce the risk of delayed cerebral ischaemia and is recommended by current consensus guidelines for the management of these patients [29].

Fluid management is further complicated by electrolyte and body water derangement, which are common in ABI (e.g. cerebral salt wasting syndrome or diabetes insipidus). Positive fluid balance has also been associated with worse outcomes in critically ill patients [30]. In this context, the 2018 ESICM consensus underlines the importance of multimodal monitoring and goal-directed therapy to optimise the fluid status [31].

Concurrent ARDS and ABI: rescue strategies

The co-occurrence of ARDS and ABI presents one of the most challenging scenarios in critical care, as optimal management strategies for each condition oppose each other. Up to 20% of severe TBI patients develop ARDS, with even higher incidence in the post-cardiac arrest population [32, 33]. ARDS in an ABI population is associated with increased odds of mortality, but there is a paucity of randomised controlled trial-based evidence for these patients [3].

LPV in ARDS with ABI

Rachel et al. [34] conducted a multicentre retrospective study of LPV in 301 patients with severe TBI complicated by ARDS. The LPV group were ventilated with a tidal volume of <8 mL·kg−1 IBW and PEEP >5 cmH2O. 28-day mortality correlated with lower Glasgow Coma Scale (GCS) score and more severe ARDS, higher tidal volume and lower PEEP, with an important reduction in mortality in patients who received LPV (78.6% versus 31.4%).

Prone positioning

Prone positioning improves recruitment of dependent lung regions and oxygenation. The PROSEVA trial demonstrated a mortality benefit for patients with PaO2/FIO2 ratio <150 mmHg who were positioned prone for ≥16 h·day−1 [35]. Unfortunately, there is little high-quality evidence on the role and safety of prone positioning patients with ABI [12, 36]. Lying prone causes neck vein distension and abdominal compression and restricts head elevation, all of which contribute to increased ICP. A few observational studies and case reports have reported this, although, by and large, the CPP was mostly preserved, alongside an improved oxygenation in these patients [37]. In parallel to a mean increase in ICP across the available literature, CPP is generally maintained as MAP often increases during proning, but some data show a mild CPP decrease often associated with raised ICP episodes. Bernon et al. [38] reported that an ICP >17.5 mmHg before proning identified patients who developed intracranial hypertension. These drawbacks are usually outweighed by beneficial effects in terms of oxygenation and concurrent PbtO2 increase. Indeed, available data, even if from small cohorts, indicate that PbtO2 tends to increase with prone positioning, in parallel to an increase in PaO2 and PaO2/FIO2 ratio [39, 40].

If prone positioning is considered in patients with TBI, head positioning, decompressive craniectomy flaps, ICP wires and external ventricular drain catheters must all be taken into account to avoid complications [41]. Head and neck position should be optimised to minimise the impact on jugular drainage, and pads should be placed under shoulders and pelvis to reduce intra-abdominal pressure as much as possible. Presence of other, extracranial injuries (e.g. spinal injury, external fixators, cervical collars, abdominal surgery) must also be considered as they may preclude safe prone positioning. For patients where the “head-up” (reverse Trendelenburg) prone position is used, because of the issues described, higher doses of vasoactives and intravenous fluids may be required to maintain CPP.

Additional rescue strategies

Given that there is a paucity of good evidence for use of pulmonary vasodilators (inhaled prostaglandin I2) or high frequency oscillatory ventilation (HFOV) outside of research settings, in the general adult population with ARDS these therapies are not recommended in ABI patients [12].

Extracorporeal membrane oxygenation (ECMO) is widely used for patients with refractory severe ARDS but requires systemic anticoagulation. In the context of ABI there are immediate concerns related to secondary haemorrhage, expansion of intracranial haematoma or unresolved extracranial haemorrhage (which is common in trauma patients). The evidence for its use in ABI populations is limited to single-centre case series and registry data, which report similar mortality rates to the non-ABI ARDS population [42]. However, one has to consider the risks of selection and reporting biases when interpreting the results from these studies.

Weaning considerations

In general ICU populations, weaning from mechanical ventilation is based on daily, protocolised assessments of readiness to wean, combining sedation minimisation with evaluation of spontaneous respiratory capacity. The “wake up and breathe” strategy uses spontaneous breathing trials, consisting of periods of pressure support ventilation or T-piece, with or without PEEP [43].

The neurocritical patient

Patients with ABI have decreased levels of consciousness, impaired airway reflexes, dysphagia and altered central respiratory drive, which pose significant challenges to liberation from mechanical ventilation. Several studies in neurocritical populations have consistently shown that traditional predictors of weaning success like the rapid shallow breathing index (RSBI) may be unreliable in neurological patients, as these patients are rarely included in large studies [44]. Recently, the VISAGE (VIsual pursuit, Swallowing, Age, Glasgow for Extubation) score has been validated in the neurocritical population and shown to improve risk stratification for extubation failure by integrating neurological and airway-protective variables rather than relying solely on respiratory indices [45].

The clinical relevance of these considerations is reflected by the prolonged duration of mechanical ventilation frequently observed in patients with ABI. The mean length of mechanical ventilation in the PEEP-PIC study was 16.5 days, indicating that many patients with ABI require often extended ventilatory support [16]. Beyond disease severity, adherence to structured ventilation, weaning and extubation protocols has been identified as an independent factor associated with shorter duration of mechanical ventilation in critically ill patients, including those with neurological injury. Furthermore, extubation failure rates are consistently higher than in general ICU populations.

Across the larger studies, failure rates generally range from 20% to 30%, while observational cohorts report rates as high as 38%, with up to 32% of patients ultimately requiring tracheostomy [46]. The recent ENIO study (in 2022), the largest international prospective multicentre study focused on extubation in neurocritical care patients, reported a 28-day extubation failure rate of 21.2% [47]. Patients who failed extubation were less likely to have TBI, were older, and had a lower baseline GCS score [47]. Predictors for extubation failure vary across studies, but a recent meta-analysis shows that older age, prolonged mechanical ventilation and impaired airway-protective mechanisms (cough and swallow) are the most consistent [48]. In addition, the high incidence of delirium (up to 70%) further complicates the weaning process due to impaired co-operation, respiratory control and tolerance of spontaneous breathing [19].

Observational studies of patients with stroke, TBI or subarachnoid haemorrhage have demonstrated that delayed extubation based solely on impaired consciousness may unnecessarily prolong mechanical ventilation without reducing the risk of reintubation. In contrast, premature extubation in patients with marginal airway protection exposes them to high reintubation rates, which are independently associated with worse neurological and overall outcomes [49]. These findings have supported a paradigm shift towards early but cautious extubation, guided by structured neurological and airway assessments rather than rigid consciousness thresholds. Extubation readiness in neurocritical patients should be evaluated even in the presence of reduced GCS scores, challenging traditional dogma that equates impaired consciousness with extubation failure.

A recent systematic review and meta-analysis found that older age and duration of invasive ventilation were associated with a higher risk of extubation failure in ABI, while cough and intact swallowing lowered the risk. Importantly, GCS score was not associated with extubation failure [48]. Successful weaning in patients with ABI is also likely to be influenced by systemic factors like systemic inflammation and organ function.

Collectively, these findings reinforce the concept that optimal weaning and extubation in ABI require a quantitative, multimodal assessment integrating respiratory mechanics, airway protection, neurological trajectory and systemic physiology, rather than extrapolation from general ICU weaning paradigms.

In the post-extubation phase, noninvasive respiratory support methods such as high-flow nasal oxygen (HFNO) and noninvasive ventilation (NIV) have been proposed to mitigate post-extubation respiratory failure and reduce reintubation in selected critically ill patients. While systematic meta-analyses in general ICU populations suggest that both HFNO and NIV can reduce reintubation compared with conventional oxygen therapy in high-risk patients, these results are not specific to ABI populations. In a large prospective multicentre cohort of brain-injured patients undergoing weaning, prophylactic use of HFNO or NIV after extubation was not associated with a significant reduction in reintubation rates compared with conventional oxygen therapy [50].

Tracheostomy

Tracheostomy plays a central role in the management of ABI patients with prolonged ventilatory dependence. Approximately 15% of intubated ICU patients require mechanical ventilation beyond 7 days, and 4.6% remain ventilator-dependent at 60 days, with prolonged mechanical ventilation associated with poor functional outcomes. For patients with ABI, tracheostomy may facilitate weaning by reducing sedation requirements, improving comfort, enabling earlier mobilisation, allowing more accurate neurological assessment and expediting discharge to non-hospital locations. Percutaneous tracheostomy can be safely performed at the bedside and has been associated with shorter ventilation duration and ICU length of stay, although a consistent mortality benefit has not been demonstrated. Observational data in patients with TBI suggest that earlier tracheostomy (within 7 days) may be associated with shorter ICU stay and a trend towards improved neurological outcomes, although confounding factors are likely to play an important role in this causal relationship [51]. Conversely, evidence from a randomised clinical trial in severe stroke patients (SETPOINT2), and meta-analyses, have failed to demonstrate a clear survival advantage or improved functional outcome at 6 months for early tracheostomy compared with a standard approach, emphasising that timing should be guided by individualised assessment rather than fixed temporal thresholds [52].

These findings collectively support the concept of individualised ventilatory management guided by baseline patient characteristics and multimodal monitoring, rather than one-size-fits-all protocols.

Conclusion

The management of mechanical ventilation in patients with ABI has evolved substantially over recent years, with updates to guidelines based on large observational studies and a small number of randomised clinical trials. There remains a paucity of large high-quality comparative studies examining different ventilation strategies in the ABI population. Extrapolation from general ICU populations, small observational studies and physiological investigations unfortunately remains the core of the evidence basis.

LPV strategies are probably safe in patients with ABI when key determinants of lung injury (tidal volume, plateau pressure, driving pressure and PEEP) are balanced and individualised according to both respiratory and cerebral physiology. Patients who are difficult to ventilate should have multimodal intracranial monitoring (ICP, PbtO2, microdialysis) to help guide changes to ventilator settings by observing the effects of rescue interventions on brain physiology.

Achieving adequate PaCO2 control remains of paramount importance in ABI, and guidelines continue to recommend normocapnia (35–45 mmHg) as the default strategy, with mild hypocapnia (32–35 mmHg) as temporary rescue therapy for intracranial hypertension management. Both severe hypocapnia and hypercapnia are associated with increased mortality and should be avoided.

The management of patients with concurrent ARDS and ABI remains challenging, due to a lack of high-quality evidence to guide practice. However, recent studies suggest that LPV strategies can be implemented, with careful monitoring and individualised approaches. Future investigations to address the problems will require large, detailed, multicentre studies to ensure sufficient numbers and account for important confounders.

Key points

  • LPV is both safe and feasible in patients with ABI when key parameters associated with VILI (e.g. driving pressure, tidal volume, PEEP) are balanced and individualised, rather than rigidly adhering to PEEP ladders or ultra-low tidal volumes. In difficult-to-ventilate patients, multimodal neuromonitoring (ICP, PbtO2, cerebral microdialysis) can guide ventilator adjustments by directly assessing cerebral physiological responses.

  • Precise PaCO2 control is essential in ABI management. Current guidelines recommend normocapnia (35–45 mmHg) as the default strategy, with mild hypocapnia (32–35 mmHg) reserved for short-term rescue therapy in intracranial hypertension crises. Both hypocapnia and hypercapnia should be avoided as they are associated with increased mortality.

  • Concurrent ARDS and ABI pose significant management challenges and there is limited high-quality evidence. Observational data suggest LPV can be applied safely with careful monitoring and individualised strategies. Definitive guidance will require large multicentre studies while accounting for neurological and respiratory confounders.

  • In patients with ABI, weaning from mechanical ventilation is frequently prolonged and driven by neurological rather than respiratory factors. Extubation readiness should be based on a structured assessment of airway protection, neurological trajectory and systemic factors, using an individualised approach as traditional respiratory indices may be unreliable in these patients.

Self-evaluation questions

  1. Why might LPV strategies be problematic in patients with ABI?

  2. Which ventilatory parameters are the most important when applying LPV in patients with ABI?

  3. What PaCO2 targets are recommended in patients with ABI?

  4. How can multimodal neuromonitoring guide ventilator adjustments in difficult-to-ventilate patients with ABI?

  5. Why is the coexistence of ARDS and ABI particularly challenging to manage?

Suggested answers

  1. Strict adherence to LPV may lead to permissive hypercapnia or higher PEEP, both of which can increase CBF and ICP. Neuro-protective goals prioritise tight PaCO2 control and ICP management, which may be in conflict with LPV strategies.

  2. Driving pressure, plateau pressure, tidal volume and PEEP contribute to LPV. For patients with ABI, a balanced and individualised approach is required as there is no strong evidence supporting the prioritisation of a single parameter.

  3. Normocapnia (35–45 mmHg) is recommended as the default strategy. Mild hypocapnia (32–35 mmHg) may be used temporarily as rescue therapy for intracranial hypertension. Both hypocapnia and hypercapnia should be avoided due to associations with worse outcomes.

  4. Multimodal monitoring incorporating ICP, PbtO2 and cerebral microdialysis allows clinicians to directly observe the cerebral effects of ventilatory changes or rescue therapies, supporting individualised and physiology-guided patient care.

  5. ARDS management prioritises lung protection, while ABI management prioritises cerebral perfusion and ICP control. High-quality evidence to guide the balancing of these competing priorities is limited. Individualised strategies with close neurological and respiratory monitoring can help to inform clinical decisions in this challenging group of patients.

Footnotes

Generative AI was not used for preparation of the text or figures for this article.

Conflict of interest: The authors report no conflicts of interest related to this article.

Support statement: R.J. Samanta is supported by a research grant from the National Institute for Health Research (NIHR) (NIHR304175). V. Newcombe is supported by research grants from the NIHR.

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