Exploring the need for chest physiotherapy following an acute brain injury in patients receiving neuroprotective measures: A retrospective observational study
Issue Name: Phys Resp Care Volume 1 (1)
Issue Date: 30 July 2026
Article Location: p12-20
Mark Price Claire Bradley
DOI: https://doi.org/10.56792/NHCG4242
Lead Author: Mark Price markprice3@nhs.net
Introduction
Acute brain injury (ABI), including traumatic brain injury (TBI), acute ischemic stroke, subarachnoid haemorrhage and intracerebral haemorrhage, is a leading cause of disability and mortality worldwide.1 Over 350,000 people are admitted to hospital within the United Kingdom (U.K.) each year with ABI,2 contributing to long term physical and cognitive impairment. These patients require considerable input from initial injury to rehabilitation and placement.3
Following primary brain injury, a cascade of changes lead to inflammation, vascular dysregulation, cerebral oedema and ischemia, causing secondary brain injury and worsening neurological outcome.4,5 Secondary brain injury can be divided into intracranial causes, such as further bleeding and cerebral oedema, or extracranial origins such as hypoxia and hypoperfusion.1 The initial management of ABI focuses on implementing neuroprotective measures to achieve intracranial homeostasis and minimise ischaemia, further injury and permanent cell death.1 Intracranial homeostasis is dependent on autoregulation of cerebral blood flow (CBF) to maintain an optimal cerebral perfusion pressure (CPP).5 CPP is determined by the relationship between mean arterial blood pressure (MAP) and intracranial pressure (ICP). Any factor increasing ICP or reducing MAP will impair CPP, resulting in hypoxia and further brain injury. Hypoxia and hypercapnia increase ICP by causing vasodilation, resulting in increased CBF and subsequent increased ICP.6 The most potent vasodilatory determinant of CBF is the partial pressure of carbon dioxide (PaCO2), where an increase of 1Kpa in PaCO2 can increase CBF by 25% to 30%.7 Healthy brain tissue autoregulates changes in CBF to maintain ICP and CPP. The ability to autoregulate CBF is lost in acute brain injury. CBF and ICP then become directly proportional to each other with loss of equilibrium resulting in worse outcomes.6 Following traumatic brain injury (TBI), it was found 20%-40% of patients were hypoxic on admission, with a further 20% developing hypoxia within the first week of intubation.8 The combination of hypoxia and hypotension are strongly associated with mortality and poor neurological outcome.9 Timely access to specialised respiratory physiotherapy may be beneficial in patients with an ABI and impaired gas exchange to optimise lung function, reduce the development of respiratory failure and prevent secondary brain damage due to a ventilatory driven increase in ICP.10
There is no one consensus algorithm when attempting to treat raised ICP. The faculty of intensive care medicine (FICM) have produced guidance based on current evidence for neuroprotective management of patients with ABI11 which include deep sedation, mandatory ventilation, temperature control, and 30 degree head up positioning to facilitate cerebrospinal fluid (CSF) drainage with the aim to control ICP between 5-15mmHg.12
These neuroprotective measures can however negatively impact the respiratory system. Deep sedation, prolonged recumbence and immobility lead to impaired secretion clearance, ventilation perfusion (V/Q) mismatch and reduced cough reflex, predisposing patients to mucous plugging, ventilator associated pneumonia (VAP) and respiratory failure.13,14 VAP is estimated to occur in 9-27% of all mechanically ventilated patients,15 typically within the first five days of ventilation. Patients mechanically ventilated following a TBI are reported to have a higher prevalence of VAP, with 20-40% of patients experiencing respiratory complications by day five of admission16 and longer stays in ICU and hospital. This increased incidence of VAP however is not associated with an increase in mortality.16
Whilst physiotherapy is commonly applied to treat secretion retention in mechanically ventilated patients in an attempt to break the self-sustaining cycle or secretion accumulation and risk of VAP,17 interventions such as manual techniques, ventilator hyperinflation (VHI) and manual hyperinflation (MHI) have been shown to transiently raise ICP18 and therefore often applied with caution in patients with an ABI. To date there is limited literature reviewing patients receiving neuroprotective measures, the need for chest physiotherapy and subsequent development of respiratory failure. Additionally, there is no evidence identifying the most effective airway clearance strategies to clear secretions and optimise gas exchange in this patient group.
Aims
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To explore the incidence of respiratory failure in patients receiving neuroprotective management following ABI compared to non neuroprotected ventilated patients.
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To explore the need for physiotherapy airway clearance interventions for patients receiving neuroprotective management following ABI compared to non neuroprotected ventilated patients.
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To review the physiotherapy interventions used to aid secretion clearance in patients receiving neuroprotective management following ABI compared to non neuroprotected ventilated patients.
Method
A service evaluation was undertaken to explore the need for chest physiotherapy following ABI in patients receiving neuroprotective measures. The NHS Health Research Authority decision making tool19 was utilised, and ethical approval was deemed not required. Local governance approval was obtained prior to commencement of this retrospective observational study and the service evaluation registered locally on the Trusts inPhase system.
Electronic clinical notes were reviewed retrospectively for all patients admitted to six critical care units within a large London teaching hospital from May 2021 to September 2023. The hospital was both a major trauma and neurosurgical centre.
Patients receiving standard neuroprotective measures following primary admission with an ABI were included in the review. Standard neuroprotective management within our organisation include 30 degree head up positioning, sedation to a target RASS of -4, PO2 >10Kpa, PCO2 <5Kpa, and normothermia. Patients with a pre-existing lung condition were excluded due to potential underlying need for airway clearance strategies at baseline.
The following baseline data were extracted: gender, age, ICP on admission (if bolt inserted), sedation duration, admission fraction of inspired oxygen (FiO2), Richmond Agitation Sedation Score (RASS) and need for neuromuscular blocking agents (NMBA). The same data set was collected for a randomly selected comparison group not receiving neuroprotection across the units during the same period.
All patients were screened and treated as per the local critical care physiotherapy service specification (available on request from the author). Requirement for chest physiotherapy was determined based on handover from the multidisciplinary team and subsequent assessment and clinical reasoning of the treating physiotherapist.
Data was collected on the need for chest physiotherapy, day of intervention, type of intervention given and whether the patient developed respiratory failure whilst ventilated and sedated. For this review, chest physiotherapy was defined as any airway clearance techniques provided to the patients by a physiotherapist following a comprehensive assessment that included more than simple positioning and suction. Respiratory failure was defined as either PaO2 < 8KPa (Type 1) or a PaCO2 > 6.0KPa (Type II) on arterial blood gas (ABG). Once patients were no longer receiving sedation, data regarding chest physiotherapy was no longer recorded.
Data was analysed using descriptive statistics, presented as median (range) and absolute numbers as appropriate.
Results
In total, 62 patients were reviewed in the neuroprotective group and 62 patients in the comparison group. There was no difference between groups in terms of gender, however the neuroprotective group were younger (44 (18-84) years vs 56 (17-85) years respectively), had a higher use of NMBA (27 (44%) v 7 (11%)) and a greater mortality rate (14 (23%) v 8 (13%)). Those on neuroprotection had an ICU length of stay (LOS) of 25 (3-65) days comparted to 24 (1-135) days in the comparison group. (Table 1).
Respiratory failure developed in 50% (n=31) of patients receiving neuroprotective measures compared to 16% (n=10) within the comparison group (Figure 1).
Types of respiratory failure were similar between groups. Type I respiratory failure occurred in 48% (n=15) of patients in the neuroprotective group and 50% (n=5) in the comparison group. Type II respiratory failure occurred in 52% (n=16) of the neuroprotective group and 50% (n=5) of the comparison group (Figure 1).
Of the patients receiving neuroprotective measures, 66% (n=41) required airway clearance strategies administered by physiotherapists compared to 40% (n=25) in the comparison group. Patients within the neuroprotection group required a higher frequency of airway clearance interventions than those in the comparison group (7 sessions, (1-37) vs 3 sessions, (1-16) respectively) (Figure 2).
Peaks in need for airway clearance adjuncts within the neuroprotection group were seen on day one (n=12) and four (n=7), with smaller peaks on days seven (n=4) and day nine (n=4) post intubation. Patients within the comparison group exhibited similar trends however with lower frequencies than the neuroprotective group (Figure 3).
Airway clearance techniques utilised by physiotherapists differed between the two groups. Rib springing and mechanical insufflation/exsufflation (MI:E) were used most in the neuroprotective group (35% (n=20) and 30% (n=17) respectively). Whereas ventilator hyperinflation (VHI) followed by rib springs and expiratory vibrations (25% (n=7) and 21% (n=6) respectively) were used most frequently in the comparison group (Figure 4).
Discussion
The initial management of ABI focuses on medical measures to control ICP and optimise CPP to prevent secondary brain injury.5 These measures may inadvertently impair secretion clearance and gas exchange in sedated and ventilated patients with subsequent impacts on intracranial dynamics.13 In our service evaluation, patients receiving neuroprotective measures demonstrated an increased need for chest physiotherapy whilst sedated and ventilated compared to ventilated patients not on neuroprotective measures. Vomiting frequently occurs during the onset of acute head injury due to trauma and inflammation to the brain. When accompanied with a rapid decrease in GCS this increases the risk for aspiration20 and may explain the initial need for chest physiotherapy on day of admission in the neuroprotection group.
Further peaks in chest physiotherapy requirements were observed on day four of ventilation, with smaller peaks identified on days seven and nine post-intubation for the neuroprotection group. The comparison group showed similar trends in the need for airway clearance techniques at days five and eight, however at a lower frequency.
Prolonged recumbence, immobility and sedation can result in atelectasis and impaired secretion clearance, increasing the risk of mucous plugging, VAP and respiratory failure.13 VAP occurs 48 hours after intubation with an estimated prevalence of 9-27% for all mechanically ventilated patients15 increasing to 36% for patients with a TBI.16 Occurrence peaks within the first 5 days of ventilation15 which may account for observed peaks in chest physiotherapy requirements at days 4, 7 and 9 in our data.
Chest physiotherapy interventions were more frequently applied in patient’s receiving neuroprotective measures compared to those receiving standard critical care management. These findings may be explained by the underlying pathophysiology of acute brain injury and timescales of VAP, but additionally compounded by the need for deep sedation, suppression of the cough reflex and immobility to optimally manage intracranial dynamics and minimise the risk of secondary brain injury. Of interest, more patients in the neuroprotective group received NMBA during their initial management period than in the comparison group (44%, n=27 vs 11%, n=7). This may have impacted the ability to clear secretions with routine suction alone due to the absence of a cough reflex.
The development of respiratory failure was higher in the neuroprotection group but an equal occurrence of Type I and Type II respiratory failure were noted across groups. Airway clearance techniques in ventilated patients aim to increase lung volumes whilst augmenting expiratory airflow bias.17 Whilst the evidence supports the use of VHI, MI:E and manual techniques to assist with secretion removal and increase lung volumes,17 there are limited studies specifically relating to the effects of chest physiotherapy on patients with ABI. Ferreira et. al,18 completed systematic review evaluating the impact of chest physiotherapy on ICP of patients admitted to ICU following ABI, concluding manual techniques transiently increased ICP in some patients but was not associated with short term haemodynamic, respiratory or CPP changes. There is little direct evidence relating to the impact of VHI and MI:E on patients with raised ICP, however lung recruitment manoeuvres have been found to negatively impact cerebral haemodynamics in patients with acute brain injury due to an increase in intrathoracic pressure, impairing venous return and cerebral drainage.21
Despite limited evidence relating to secretion clearance in patients with ABI, different treatment modalities appeared to be favoured for patients receiving neuroprotection to those receiving standard critical care management. Our data showed when patients receiving neuroprotective measures required chest physiotherapy, the most commonly used techniques were MI:E followed by rib springing. Whilst the clinical reasoning of the treating therapists was not explored in this study, it may be reasonable to consider that rib springing was chosen as a favourable treatment for patients with a raised ICP as a method of increasing lung volumes without increasing intrathoracic pressure. An increase in intrathoracic pressure may reduce venous return and subsequently increase ICP if maintained for a prolonged period.21 It is possible MI:E was favoured in patients managed with neuroprotective measures due to deep sedation levels (RASS -5) and more frequent utilisation of NMBA resulting in an absence of the cough reflex to aid secretion clearance. The physiological principle of exsufflation pressures during MI:E augments expiratory airflow bias in the absence of a cough reflex promoting movement of secretions from distal to proximal airways, aiding clearance. The negative intrathoracic pressure applied during exsufflation may also facilitate (CSF) drainage within this patient group.22
Patients in the comparison group requiring chest physiotherapy were treated preferentially with VHI, followed by rib springing and expiratory vibrations. VHI is a common physiotherapy airway clearance technique but may have more significant effects on blood pressure and venous return due to increases in intrathoracic pressure. Whilst potentially problematic in patients with a raised ICP, a transient reduction in venous return and MAP may not impact as greatly on the clinical reasoning process when ICP management is not of concern. Whilst our observations didn’t consider therapist’s rationale for clinical reasoning, given the paucity of data it is plausible therapists’ preference and level of experience may account for these findings.
Limitations
This retrospective analysis did not examine specific airway clearance techniques impact on ICP, the rationale for therapist choices, standardising how these techniques were delivered to the patient, or additional risk factors such as additional trauma injuries or pre-existing lung conditions. Treating therapists were not blinded to the application of neuroprotective measures which may have introduced an element of bias when assessing and treating.
Conclusions
Our service evaluation found patients receiving neuroprotective management following ABI have a higher prevalence of respiratory failure and increased need for physiotherapy airway clearance strategies whilst sedated and ventilated than patients not receiving neuroprotective management measures. This is driven by both the underlying pathophysiology of the injury and the subsequent neuroprotective measures employed to reduce the risk of secondary brain injury. These findings highlight the importance of timely physiotherapy to optimise secretion clearance and reduce pulmonary complications to limit secondary brain injury. It appears the selection of treatment techniques differed between those receiving neuroprotection and those not. There is currently no evidence supporting favourable airway clearance strategies for patients with raised ICP. A larger data set is required to further examine these trends with regards to treatment selection and patient outcome.
Declaration of interest
The authors have no conflicts of interest.
Funding
Funding was not required for the completion of this work.
Ethical and R&D Approval
The NHS Health Research Authority decision making tool14 was utilised and ethical approval was deemed not required for completion of this service evaluation.
