Mechanical ventilation in patients with acute ischaemic stroke: from pathophysiology to clinical practice
Most patients with ischaemic stroke are managed on the ward or in specialty stroke units, but a significant number requires higher-acuity care and, consequently, admission to the intensive care unit. Mechanical ventilation is frequently performed in these patients due to swallowing dysfunction and airway or respiratory system compromise. Experimental studies have focused on stroke-induced immunosuppression and brain-lung crosstalk, leading to increased pulmonary damage and inflammation, as well as reduced alveolar macrophage phagocytic capability, which may increase the risk of infection. Pulmonary complications, such as respiratory failure, pneumonia, pleural effusions, acute respiratory distress syndrome, lung oedema, and pulmonary embolism from venous thromboembolism, are common and found to be among the major causes of death in this group of patients. Furthermore, over the past two decades, tracheostomy use has increased among stroke patients, who can have unique indications for this procedure—depending on the location and type of stroke—when compared to the general population. However, the optimal mechanical ventilator strategy remains unclear in this population. Although a high tidal volume (VT) strategy has been used for many years, the latest evidence suggests that a protective ventilatory strategy (VT = 6–8 mL/kg predicted body weight, positive end-expiratory pressure and rescue recruitment manoeuvres) may also have a role in brain-damaged patients, including those with stroke. The aim of this narrative review is to explore the pathophysiology of brain-lung interactions after acute ischaemic stroke and the management of mechanical ventilation in these patients.
KeywordsStroke Brain injury Mechanical ventilation Brain-lung crosstalk Intensive care unit
Acute respiratory distress syndrome
Cerebral blood flow
Intensive care unit
Acute ischaemic stroke
Traumatic brain injury
Predicted body weight
Mean arterial pressure
Central nervous system
Positive end-expiratory pressure
Glasgow Coma Scale
Partial pressure of arterial oxygen
Optic nerve sheath diameter
Partial pressure of carbon dioxide
Brain tissue oxygen tension
Percutaneous dilatational tracheostomy
Jugular venous saturation
European Stroke Organisation
American Stroke Association
National Institute for Health and Care Excellence
Cerebral metabolic rate for oxygen
Heated high-flow nasal cannula
Positive end-expiration pressure
Cerebral perfusion pressure
Respiratory system compliance
Inspired oxygen fraction
Acute ischaemic stroke (AIS) is one of the major causes of morbidity and mortality worldwide  and one of the leading causes for admission to neurological intensive care units (NICUs) . Over the last decades, the incidence of stroke has been increasing, and despite an overall decrease in mortality, it is still the leading cause of severe disability in the adult population . Approximately 80% of all strokes are ischaemic; other major types include intracerebral (ICH) and intraventricular (IVH) haemorrhage, cerebral venous and sinus thrombosis, and subarachnoid haemorrhage (SAH) secondary to aneurysm leak or rupture . The location of the stroke is probably the most relevant factor related to the need for mechanical ventilation (MV), rather than the particular type of cerebrovascular pathology. In this context, impairment of the brain areas that regulate the level of consciousness (thalami, the limbic system, the reticular formation in the brainstem), breathing (respiratory centres in the cortex, pons, and medulla), and swallowing (medulla and brainstem connections) increases the risk of respiratory failure .
Pulmonary complications—such as respiratory failure, pneumonia, pleural effusion, acute respiratory distress syndrome (ARDS), pulmonary oedema, and pulmonary embolism from venous thromboembolism—may occur in this group of patients and are associated with a high risk of mortality [5, 6]. In particular, stroke-associated pneumonia (SAP) is described as an independent risk factor for unfavourable outcome and death [7, 8]. Since the most frequent extra-cerebral complication of neurological ICU patients is respiratory failure , the development of new mechanical ventilation strategies may potentially improve their outcome . So far, few studies have addressed the best respiratory management of patients with AIS. The aim of this manuscript is to review and describe the pathophysiology underlying the development of pulmonary complications and respiratory failure after AIS and the different ventilator strategies in this population, focusing on the risk related to oxygen (O2) therapy and the application of protective lung ventilation. For this purpose, we performed a literature search of four electronic databases (PubMED, Scopus, ScienceDirect, Web of Science), using the following terms: “mechanical ventilation” and “stroke”. Titles and abstracts were retrieved and independently assessed for eligibility by two authors (CR, GB). Disagreements were resolved by discussion and consensus agreement and, if required, input from a third author (DB).
This narrative review focuses on the information specific to stroke patients that do not have brain trauma or intracranial pressure issues, including the concern over the need for tracheostomy as an intervention to prevent aspiration pneumonia rather than for primarily pulmonary issues. We also aimed to highlight the different needs of specific subsets of stroke victims that distinct profiles of neurological impairment—such as decreased level of consciousness, cranial nerve deficits, and central swallow concerns—in order to provide a good roadmap to guide the generalist intensivist.
The pathophysiology of stroke and the risk of pulmonary complications
The concept of brain-organ crosstalk has been widely investigated [9, 10]. Severe brain-damaged patients are commonly unable to protect their airway and therefore are often admitted to the NICU for mechanical ventilation. Prolonged MV is associated with increased risk of developing ventilator-associated lung injury, ARDS, pneumonia, and neurogenic pulmonary oedema . Moreover, ARDS has detrimental effects on the brain, acting synergistically with intracranial hypertension to cause hippocampal damage. A study on rats revealed that focal ischaemic stroke alters the respiratory pattern, induces oedema and inflammation, and decreases the phagocytic capability of alveolar macrophages . Remarkably, all of these changes occurred within 24 h after the induction of cerebral ischaemia, which is in agreement with the rapid onset of respiratory failure in stroke patients .
The mechanism of lung damage after brain injury is described through a “double-hit model”: the catecholamine storm and the systemic production of inflammatory mediators (first hit) create a systemic inflammatory environment which increases pulmonary vascular hydrostatic pressure and activates biological mechanisms that make the lung more susceptible to mechanical and non-mechanical insults (second hit), including mechanical ventilation . On the other hand, lung injury can damage the brain through a complex interaction between the autonomic, neuro-inflammatory, neuroendocrine, and immunologic pathways . Fries et al.  compared pigs with hypoxaemia induced by a lavage model of acute lung injury versus pigs with the same degree of hypoxaemia induced by a reduction in the fraction of inspired oxygen (FiO2). Brain damage was greater in the first group, suggesting that acute lung injury per se leads to neuro-pathologic changes regardless of the occurrence of hypoxaemia. The lungs can communicate with the brain through the autonomic and sympathetic nervous system, leading to a neuro-inflammatory process which triggers the activation of the cytokine and complement cascades , thus contributing to the development of brain oedema and apoptotic cell death.
Immunological response after stroke
Aspiration pneumonia is one of the major causes of respiratory failure after stroke and can be related to a decreased level of consciousness, with impaired swallowing and dysphagia . However, the incidence of pneumonia in stroke patients is higher when compared to other groups of patients who suffer from dysphagia or compromised level of consciousness, thus suggesting that other mechanisms are involved, such as immune activation and alteration in lung injury pathogenesis . PREDICT, a prospective observational multicentre study, confirmed that both dysphagia and stroke-induced immunodepression syndrome are independent risk factors for aspiration pneumonia . The incidence of SAP ranges between 3.9 and 56.6%, with a higher incidence in the ICU compared to stroke units or wards . Several studies have developed clinical scores to predict SAP with the aim of improving risk stratification in patients with acute stroke [21, 22], but their use in the clinical setting is uncommon. In current practice, biomarkers such as C-reactive protein, stroke severity, dysphagia, and the Centres for Disease Control and Prevention criteria  are more frequently used. The most widely recognised measure when acute stroke patients are admitted is nil by mouth status until a swallowing assessment can be completed . Early mobilisation is recommended as it decreases the risk of SAP, while the benefit of antibiotic use in the acute phase remains unproven .
Prediction of extubation success and safe extubation are important in stroke patients. A prospective observational study  that focused on extubation readiness in stroke patients showed that patients who failed in swallowing tests were those who later experienced extubation failure. The reintubation rate was 24.1%, and the main determinant of reintubation (in half of these patients) was dysphagia, followed by respiratory complications . Prolonged endotracheal intubation is a major cause of swallowing dysfunction, and the determination of extubation readiness is challenging in this population. The criteria used in the general population for the prediction of extubation failure are based on airway parameters and lung mechanics, whereas in stroke patients, neurological status has a prominent role in the development of dysphagia and is a leading contributor to poor outcome . The prevalence of post-extubation dysphagia ranges from 12 to 69% in the general ICU population, reaching 93% in neurological patients . The main causes of post-extubation dysphagia are cerebrovascular disease due to damage to the central swallowing network, pharyngo-laryngeal lesions, neuropathies, and myopathies, as well as sedation and mucosal damage . Although several techniques have been developed to diagnose dysphagia, only videofluoroscopy has been considered the goal standard for swallowing dysfunction. An interventional study using fiberoptic endoscopy and including general ICU patients within 48 h from extubation found that post-extubation dysphagia could be diagnosed in 50% of patients, and the overall incidence of aspiration events was 56%, of which 25% were silent . This technique demonstrated its utility in the diagnosis of post-extubation dysphagia in 69.3% of patients . In summary, current evidence agrees on the utility and feasibility of bedside fiberoptic endoscopic swallowing study for assessment of post-extubation dysphagia in patients at risk for aspiration and swallowing dysfunction.
Due to the high incidence of respiratory complications in stroke patients, optimal ventilator management is mandatory . The main goal of MV should be to maintain appropriate oxygen levels and tight control of carbon dioxide tension (PaCO2), without inducing ventilator-associated lung damage.
Studies evaluating the use of oxygen therapy in acute ischaemic stroke patients
Rønning et al. 1999 
To test the hypothesis that breathing 100% O2 for the first 24 h after an AS would not reduce mortality, impairment, or disability
555 (66/555 ICH)
O2 therapy (100% atm, 3 L/min for 24 h [n = 292]) versus controls (no additional O2)
Supplemental O2 should not routinely be given to non-hypoxic stroke victims with minor or moderate strokes.
Ali et al. 2005 
To assess the effects of different doses and routes of O2 administration on SatO2 in patients with stroke
21 (15 AIS; 6 ICH)
-Room air for 30 min; − 2-3 L/min of O2 (nasal cannula)
-FiO2 0.24 (VM)
-FiO2 0.3535% (VM)
There was a dose-response relationship between the amount of O2 given and the resultant changes in SatO2.
Singhal et al. 2005 
To investigate the effects of high-flow oxygen (HFO) in AIS
HFO (humidified O2 at 45 L/min via facemask for 8 h [n = 9]) versus controls (room air or nasal O2 1–3 L/min to maintain SaO2 95% [n = 7])
HFO is associated with a transient improvement of clinical deficits and MRI abnormalities in select patients with AIS.
Chiu et al. 2006 
To investigate the feasibility of eubaric hyperoxia therapy by VM in a group of patients who experienced a severe AIS
O2 therapy (FiO2 0.4via VM [n = 17]) versus controls (nasal cannula [n = 29])
By using VM therapy with a FiO2 of 0.4, there might be less mortality and comorbidities in treated patients who experienced a severe AIS.
Singhal et al. 2007 
To investigate the metabolic effects of normobaric oxygen (NBO) on AIS brain tissues using MRSI and diffusion-perfusion MRI
NBO (45 L/min O2 via face mask for 8 h [n = 4]) versus controls (room air [n = 2])
NBO improves aerobic metabolism and preserves neuronal integrity in AIS brain.
Padma et al. 2010 
To study the role of NBO in AIS in Indian patients
NBO (10 L/min O2 for 12 h [n = 20]) versus controls (room air/2 L/min O2 via face mask to maintain SaO2 ≥ 95% [n = 20])
NBO did not improve the clinical scores of stroke outcome in Indian patients with AIS.
Roffe et al. 2011 
To report the effects of routine use of O2 supplementation for 72 h on SatO2 and neurological outcomes at 1 week after an AS
AS (clinical diagnosis)
289 (257 AIS, 24 ICH, 8 undetermined)
O2 therapy (O2 via nasal cannula for 72 h [n = 148]) or controls (room air/O2 if clinically indicated [n = 141])
Routine O2 supplementation started within 24 h of hospital admission with AS led to a small, but statistically significant, improvement in neurological recovery at 1 week. The difference in NIHSS improvement may be due to baseline imbalance in stroke severity between the two groups.
Ali et al. 2013 
To report the effects of routine O2 supplementation for 72 h on SatO2 and neurological outcomes at 6 months after AS
AS (clinical diagnosis)
289 (257 AIS, 24 ICH, 8 undetermined)
O2 therapy (O2 via nasal cannula for 72 h [n = 148]) or controls (room air/O2 if clinically indicated [n = 141])
None of the key outcomes differed at 6 months between the groups. Although not statistically significant and generally of small magnitude, the effects were predominantly in favour of the O2 group.
Jeon et al., 2014 
Prospective, observational cohort study
To determine the association between exposure to hyperoxia and the risk of DCI after SAH
Hyperoxia (the highest quartile of an area under the curve of PaO2, until the development of DCI [PaO2 ≥ 173 mmHg])
Exposure to excess O2 after SAH may represent a modifiable factor for morbidity and mortality in this population.
Rincon et al. 2014 
Retrospective multicentre cohort study
To test the hypothesis that hyperoxia was associated with higher in-hospital mortality in ventilated AS patients admitted to the ICU
2894 (554 AIS, 936 SAH, 1404 ICH)
O2 therapy to obtain PaO2 ≥ 300 mmHg
Hyperoxia was an independent predictor of in-hospital death.
Mazdeh et al. 2015 
To evaluate the effects of normobaric hyperoxia on clinical outcomes of patients with severe AS
O2 therapy (VM for 12 h) versus controls (no O2)
NBO therapy in the first 12 h of AS could improve long-time outcome of the patients with either ischaemic or haemorrhagic stroke.
Roffe et al., 2017 
Multicentre single-blind RCT
To assess whether routine prophylactic use of low-dose O2 therapy was more effective than control O2 administration at reducing death and disability at 90 days, and if so, whether O2 given at night only, when hypoxia is most frequent, and O2 administration is least likely to interfere with rehabilitation, was more effective than continuous supplementation
AS (clinical diagnosis)
8003 (6555 AIS, 588 ICH, 294 AS without CT diagnosis, 168 TIA, 292 non-stroke diagnoses, 106 missing data)
Continuous O2 (2–3 L/min via nasal cannula for 72 h [n = 2668]) versus nocturnal O2 (2–3 L/min via nasal cannula for 3 nights [n = 2667]) versus controls (O2 if clinically indicated [n = 2668])
Among non-hypoxic patients with AS, the prophylactic use of low-dose O2 supplementation did not reduce death or disability at 3 months.
Ding et al. 2018 
To analyse the current data of NBO on brain protection as used in the clinical settings
NBO group (… [n = 3207]) versus controls [n = 3159]
The existing trends toward benefits revealed in this meta-analysis help us appreciate the promising value of NBO, although current evidence of NBO on improving clinical outcomes of stroke is insufficient.
Roffe et al. 2018 
Multicentre, prospective, randomised, open, blinded-end point trial
(1) To assess whether or not routine low-dose of O2 supplementation in patients with AS improves outcome compared with no O2 and (2) to assess whether or not O2 given at night only, when SatO2 is most likely to be low, is more effective than continuous supplementation
AS (clinical diagnosis)
8003 (6555 AIS, 588 ICH, 168 TIA, 292 non-stroke diagnoses, 106 missing data)
Continuous O2 (2–3 L/min via nasal cannula for 72 h [n = 668]) versus nocturnal O2 (2–3 L/min via nasal cannula for 3 nights [n = 2667]) versus controls (O2 if clinically indicated [n = 2668])
Routine use of low-dose O2 supplementation in stroke patients who are not severely hypoxic is safe but does not improve outcome after AS.
Respiratory management of patients with stroke according to 2018 AHA/ASA guidelines 
Intubation and ventilation are recommended in patients with decreased consciousness, bulbar dysfunction with inability to protect the airway, or intracranial hypertension (level I).
Aim for normoxia and normocapnia (NA).
Continuous monitoring of oxygenation is strongly recommended in patients with AIS in ICU. Supplemental oxygen should be administered if SpO2 > 94% (level I).
Supplemental oxygen is not recommended in non-hypoxic patients (level III).
Hyperbaric oxygen is not recommended, except in case of air embolism (level III).
Causes of intubation in stroke patients
GCS < 9
Hypoxaemia despite supplemental oxygen
Impaired swallowing and gag reflexes
Inability to clear secretions
Seizures or drugs suppressing respiratory drive
Need for intracranial pressure management
Anticipated neurological or cardiopulmonary decline requiring transport or immediate treatment
Hypoxaemia and hyper/hypocapnia should be avoided to decrease the risk of secondary brain injury. PaCO2 is a powerful determinant of cerebral blood flow ; however, not only hypercapnia is dangerous in stroke patients, but also hyperventilation, because cerebral vasoconstriction can cause brain tissue hypoxia and compromise cerebral compliance and blood flow . No consensus is available regarding the optimal respiratory rate and tidal volume (VT) to achieve the PaCO2 target, with higher VT being generally applied in this group of patients . However, after severe brain injury, higher VT is associated with both an increased risk of acute lung injury and acute intracranial hypertension [9, 52]. Similarly, higher driving pressure is associated with a higher risk for ARDS . Moreover, in patients recovered from acute lung injury, the shorter is the inspiratory rise time, the shorter will be the inspiratory work of breathing; also, at 15 cmH2O of pressure support ventilation, the lowest cycling off criteria reduced respiratory rate and increased VT . In critically ill patients requiring MV, protective ventilation with a VT of 6 mL/kg, adequate positive end-expiration pressure (PEEP) levels and limiting plateau pressure to < 30 cmH2O has shown to reduce absolute mortality by 10% . However, clinical trials testing ventilation strategies designed for lung protection frequently excluded brain-injured patients; therefore, ventilator management has been scarcely evaluated in neurocritical settings. Indeed, in critically ill patients with acute brain injury, the use of protective lung ventilation is controversial and might even be contraindicated, as it can increase ICP due to permissive hypercapnia and the use of high airway pressures during recruitment manoeuvres . In a porcine model of acute lung injury, major improvement in cerebral oxygenation was observed in animals ventilated with low VT when compared with high VT . A multicentre trial with 749 brain-injured patients (36% in the pre-intervention group and 46% in the intervention group were stroke patients)  suggested that protective ventilation (VT ≤ 7 mL/kg of ideal PBW and PEEP 6–8 cmH2O) can significantly improve the number of ventilator-free days at day 90, as well as reduce the mortality rate. No specific studies focusing on optimal ventilator settings in patients with stroke are available, and only a minority of patients included in the large trials exploring the role of protective ventilation on outcome had stroke; we recommend keeping Pplat between 18 and 25 cmH2O and minimising respiratory rate to reduce mechanical power. Future studies are needed to better define the optimal VT in stroke patients requiring MV.
Application of PEEP improves arterial oxygenation. However, in brain-injured patients, caution is warranted because PEEP may worsen or trigger intracranial hypertension [51, 58]. Mascia et al. suggested that ICP increases significantly when PEEP is applied, but only in patients where PEEP induces alveolar hyperinflation with a consequent increase in PaCO2, whereas ICP remains constant when PEEP causes alveolar recruitment with no change in PaCO2 . In an experimental study in both healthy and stroke pigs, high PEEP levels (up to 25 cmH2O) did not impair ICP, cerebral oxygenation, or regional cerebral blood flow . Application of high PEEP (up to 20 cmH20) in patients with haemorrhagic stroke resulted in a significant decrease in mean arterial pressure (MAP) and regional cerebral blood flow, but further analyses showed that changes in regional cerebral blood flow depend on MAP changes as a result of impaired cerebrovascular autoregulation . Georgiadis et al. showed that PEEP can be safe in patients with acute stroke, even after increasing PEEP levels up to 12 mmHg, providing that MAP is maintained . In addition, a recent trial in non-ARDS patients demonstrated the non-inferiority of a low-VT, low-PEEP strategy as compared to high VT . Therefore, PEEP is considered safe if (1) haemodynamic status and euvolaemia are maintained to minimise the effects of PEEP on cerebral perfusion pressure and (2) the value of PEEP is lower than ICP, to avoid a decrease in venous outflow , thus resulting in a beneficial effect on brain oxygenation  while (3) avoiding excessive over-distention and keeping the lung at rest .
Recruitment manoeuvres (RMs) may improve pulmonary gas exchange and respiratory mechanics . However, they may also cause intracranial hypertension by impairing jugular venous outflow and impeding cerebral venous return to the right atrium . In a study by Bein and colleagues of patients with brain injury (6 of 11 were stroke patients) and acute lung injury, volume RMs (which included a 30-s progressive increase in peak pressure up to 60 cmH2O and a sustained pressure at the same level for the next 30 s) led to a deterioration of cerebral oxygenation and, simultaneously, a reduction of MAP and an increase in ICP, with critical reduction of the cerebral perfusion pressure. In 9 brain-injured patients (of whom 6 were stroke patients), a stepwise RM with 3-cmH2O intermittent increments and decrements of PEEP was applied , resulting in a positive correlation between PEEP and ICP and a negative correlation between PEEP and cerebral perfusion pressure (CPP). These data suggest that the effects of PEEP on blood pressure and cerebral perfusion pressure vary greatly in acutely brain-injured patients and that strict MAP and ICP monitoring is of benefit when PEEP is applied. Therefore, RMs could be safely performed when indicated in patients with both stroke and lung injury, especially if setting a PEEP level lower than the ICP and maintaining an effective MAP .
Similarly to RMs, prone positioning has demonstrated to be an efficient technique to improve oxygenation but should be used cautiously in patients with stroke and reduced intracranial compliance, as it can increase intrathoracic pressure and raise ICP . Only one study investigating the effects of the prone position on respiratory failure provided data on cerebral haemodynamic in patients with stroke, with contradictory results . Thus, the benefits and risks of prone positioning in patients with stroke are still unclear. Nekludov et al. found a significant improvement of pulmonary oxygenation, but a rise in ICP in a group of 8 patients with a GCS ≤8 (3 of them with stroke) and pulmonary injury . Thelandersson and colleagues investigated 11 neurological patients (5 of them with stroke) with FiO2 > 0.4 in prone position for only 3 h, and also found an increase in systemic oxygenation, but unlike the previous study, without significant changes in ICP or MAP . Altogether, prone positioning can present challenges in stroke patients because of the risk of developing intracranial hypertension and displacement of neuromonitoring tools. However, it could be taken into consideration in patients with severe, refractory hypoxaemia and under strict multimodal neuromonitoring.
Other ventilation strategies
There are insufficient studies to evaluate the role and safety of high-frequency oscillatory ventilation (HFOV) in stroke population. Theoretically, the application of higher mean airway pressures could decrease cerebral venous drainage, and the PCO2 clearance could be insufficient; both aspects are unadvisable in severe brain-injured patients. Very few observational studies have evaluated the use of HFOV in adults with acute brain injury, with even fewer focusing on stroke . In a systematic review of the effects of HFOV on cerebral perfusion pressure and intracranial pressure, the authors concluded that, for patients with traumatic brain injury and ARDS, HFOV may improve oxygenation and increase PaCO2. Thus, if HFOV is considered, continuous monitoring of oxygen saturation, MAP, PaCO2, and ICP is paramount .
In case of life-threatening hypoxia refractory to conventional MV, the use of rescue therapies has been encouraged to re-establish adequate levels of oxygenation while minimising ventilator-associated injury. In selected cases, extracorporeal lung support techniques have been considered .
In summary, in stroke patients requiring MV, protective ventilation with close monitoring of neurological and respiratory variables is essential to ensure lung safety and avoid secondary brain injury. Furthermore, monitoring of cerebral oxygenation should be used when possible to allow the clinician to discriminate between normal and critically impaired tissue oxygenation and help refine ventilator settings [9, 55]. In future, non-invasive cerebral monitoring could be implemented to individualise ventilator settings .
Neurological patients experienced prolonged ICU stays and mechanical ventilation, a higher rate of early tracheostomy, and higher incidence of ventilator-associated pneumonia compared to non-neurological patients . Although often necessary and life-saving, MV is time-dependently associated with various complications and may increase morbidity and mortality . Therefore, weaning from mechanical ventilation has been suggested to take place as early as is safely possible. Moreover, there is evidence that neurological patients are especially prone to extubation failure, with high reintubation rates, ranging from 20 to 40% . Prediction of successful extubation is critical, as both delayed and premature extubation increase complication rates need for tracheostomy, duration of ICU stay, and mortality . Unfortunately, classic respiratory predictors for successful extubation in general critical care (such as VT, respiratory rate, negative inspiratory force, forced vital capacity, rapid shallow breathing index, and PaO2/FiO2) are unreliable in brain-injured patients . The level of consciousness at the moment of extubation could be considered a risk factor for extubation failure , but a recent study  showed controversial results. In a meta-analysis  specifically looking for predictors of extubation failure in neurocritical care patients, a low GCS (7–9) was identified as a risk factor, with a nearly fivefold increased risk of reintubation. Other factors included the ability to follow commands, secretion texture, and presence of a gag reflex. In a small retrospective study of middle cerebral artery stroke patients, a composite GCS score of 8 with an eye subscore of 4 was associated with successful extubation . However, GCS alone cannot be considered a predictive factor for extubation success, as it has never been validated in intubated patients whose verbal component is impossible to assess and often arbitrarily scored . More recently, Godet et al.  developed a clinical score to predict extubation failure in the general brain-injured population with a GCS < 12 before tracheal intubation, intubated for neurological reasons, and ventilated for more than 48 h; it includes upper airway functions (e.g. gag reflex, cough, and deglutition) and neurological status (evaluated through the visual subscale of the Coma Recovery Scale-Revised). However, external validation of this score is required, and no data specific to stroke patients are available. Recent data have evaluated new physical features in patients with severe brain injury. In a multicentre study, age < 40 years, visual pursuit, attempts at swallowing, and a GCS > 10 were found to be predictors of successful extubation . On the basis of these items, the VISAGE score was constructed. If three or more items are positive, an extubation success rate of 90% can be expected. Visual pursuit and preserved upper airway reflexes , younger age , negative fluid balance, and the presence of cough have been described as favourable signs of extubation success by other observational studies. Further studies are warranted to confirm the findings of the latest studies on neurological patients in general and stroke in particular.
Up to 45% of patients admitted to the ICU for stroke require tracheostomy (TT)  versus 10–15% in the general ICU population . Recognised advantages of tracheostomy compared with prolonged oro-tracheal intubation are a reduction of pharyngeal and laryngeal lesions, a better oral hygiene and nursing care, and higher patient comfort . Predictors that may suggest the decision to perform a tracheostomy in stroke patients have been described in few studies [82, 83]. Different types of stroke are associated with the need for tracheostomy, including large hemispheric stroke, basilar thrombosis, brainstem infarction, and space-occupying cerebellar stroke . Indeed, the location and extension of brain damage and its secondary effects (including cerebral oedema and secondary ischaemia) may influence the need for MV support. In particular, the compromise of the brain regions which regulate breathing (respiratory centres in the pons, or medulla), level of consciousness (reticular formation, thalami), and swallowing (medulla and brainstem) may lead to respiratory failure and need for tracheostomy . There are two main clinical scenarios in which mechanical ventilation and tracheostomy are usually considered after stroke. The first is in patients with such an extensive stroke that ICU admission and MV are required. In these, long-term ventilation and prolonged insufficient airway protection if extubation fails or is deemed infeasible are the main indications for tracheostomy [82, 83]. The second scenario is in patients with stroke of only moderate overall severity, but which affects the swallowing centres of the brain (such as infarcts of the brainstem or the medulla oblongata), causing dysphagia. In this case, the decision to perform a tracheostomy can be related to severe dysphagia posing a risk of aspiration .
In a retrospective study by Szeder et al.  on patients with intracranial haemorrhage, features associated with the need for TT were GCS < 9 at day 3 as well as radiological findings such as hydrocephalus, midline shift, and intraventricular haemorrhage. Schonenberger et al.  proposed the stroke-related early tracheotomy (SET) score to screen patients for prolonged intubation and need for TT by combining neurological parameters (e.g. dysphagia and GCS < 10), neuroimaging features (e.g. brainstem lesion, hydrocephalus, intracranial haemorrhage volume > 25 mL), general organ function, and surgical procedures. Furthermore, Steidl et al. conducted a two-centre, prospective observational study on both ischaemic and haemorrhagic stroke patients to evaluate the extubation rate over tracheostomy. Overall, 47% of patients were tracheostomised without any extubation attempt, whereas 53% were primarily extubated. Among patients primarily tracheotomised, most had haemorrhagic stroke, higher National Institute of Health Stroke Scale, and lower Glasgow Coma scores on admission. Additionally, they received more neurosurgical treatments as compared to those extubated . As can be deduced by the literature, the optimal timing of TT in stroke patients is still unclear. Potential benefits of early TT (such as ventilation duration and length of stay, ventilator weaning, airway safety, rate of pneumonia, outcome, and mortality) have yet to be proven . McCann et al. demonstrated a reduced length of stay in patients undergoing earlier (within 1 week) tracheostomy and percutaneous endoscopic gastrostomy (PEG) placement in patients with haemorrhagic stroke . A recent meta-analysis by McCredie et al. evaluated the effect of early versus late TT or prolonged endotracheal intubation in acute brain-injured patients. Ten trials met the selection criteria. Early TT reduced long-term mortality and duration of mechanical ventilation, but insufficient trials were available to perform subgroups analysis; thus, the study refers to the general neuro-ICU population, and no specific data are reported about stroke patients . Overall, as procedural risk is low and early tracheostomy does not seem to affect the clinical course of the ventilated stroke patient, it is suggested that ventilation needs be assessed after the first week of intensive care and tracheostomy considered if an extubation attempt failed or is judged not to be feasible .
Recommendations and conclusions
CR, GB, and DB wrote the manuscript. CR, PP, and GB designed the review. CR, GB, DB, PRMR, and PP revised the manuscript. All authors read and approved the final manuscript.
Ethics approval and consent to participate
Consent for publication
The authors declare that they have no competing interests.
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