Management of traumatic brain injury and acute respiratory distress syndrome

Abstract

Introduction:

Up to 20% of patients with traumatic brain injury (TBI) develop acute respiratory distress syndrome (ARDS), which is associated with increased odds of mortality. Guideline-based treatment for ARDS includes “lung protective” ventilation strategies, some of which are in opposition to “brain protective” strategies used for ventilation with patients with TBI. We conducted a scoping review of ventilation management strategies with clinical outcomes among patients with TBI and ARDS.

Methods:

We searched three databases (MEDLINE, Embase, Web of Science) using a systematic search strategy. We included any studies of patients with TBI and ARDS with ventilation strategies including PEEP, oxygenation, prone positioning, recruitment maneuvers, pulmonary vasodilators (e.g., nitric oxide), high frequency oscillatory ventilation (HFOV), and extracorporeal membrane oxygenation (ECMO). All clinical outcomes were included. Extracted data included details about sample (age, gender), study design, inclusion/exclusion criteria, intervention details, and outcomes.

Results:

The search returned 10,514 articles, 35 of which met final inclusion criteria. Interventions studied included ECMO (n = 13 articles), HFOV (n = 4), PEEP interventions (n = 3), prone positioning (n = 3), vasodilators (n = 4), and other lung recruitment maneuvers (n = 9). No randomized controlled trials were identified; studies were mostly case reports (n = 18/35, 51%) and series (n = 7/35, 20%), with some cohort studies (n = 5/35, 14%) and non-randomized experimental trials (n = 5/35, 14%), all at single institutions. Outcomes included physiologic changes (e.g., change in cerebrodynamics or hemodynamics with intervention) and clinical outcomes such as mortality, complications, or neurologic recovery. Five studies (14%) included pediatric patients.

Discussion:

In this scoping review of ventilatory strategies for patients with concurrent TBI and ARDS, we found variation in heterogeneity of study design, interventions, and outcomes. Studies were mostly case report/series and observational studies, seriously limiting our ability to draw conclusions about effectiveness of interventions. Targeted areas of further research are discussed.

Keywords

Extracorporeal membrane oxygenation high-frequency oscillatory ventilation nitric oxide positive end-expiratory pressure ventilation

Introduction

Traumatic brain injury (TBI) is a significant cause of morbidity and mortality globally.¹ TBI is defined as an external force to the brain—termed the primary injury—which is thought to lead to catecholamine surges, systemic inflammation, and hemodynamic instability leading to downstream consequences, termed the secondary injury.² When treating TBI, focus is primarily given to preventing and treating this secondary injury.

Multi-organ dysfunction following TBI is independently linked to higher mortality rates and—in cases of severe TBI—two-thirds of patient deaths involve extracranial organ dysfunction.^3,4 Pulmonary dysfunction following TBI comes in many forms, the most severe of which is acute respiratory distress syndrome (ARDS). A previous study using over 38,000 patients from the National Trauma Databank suggests about 8% of patients with isolated, severe TBI will develop ARDS,⁵ though other estimates have been higher than 20%.^6,7 Further, patients with TBI and ARDS have increased odds of mortality and, among those who survive their hospitalization, poorer neurological outcomes compared to TBI patients without ARDS.^7,8

The mainstay of treatment for ARDS involves mechanical ventilation strategies that are “lung protective.”^2,9 These strategies include limiting tidal volumes and inspiratory pressures, prone positioning, higher positive end-expiratory pressure (PEEP) values, and recruitment maneuvers (Table 1). These strategies are directed as promoting lung recruitment, avoiding atelectotrauma, and minimizing oxygen toxicity to lungs. Additionally, allowing for higher levels of CO₂ (permissive hypercapnia) in patients with ARDS is often tolerated to reduce tidal volume and alveolar stretch.¹⁰ In contrast, in TBI, a high normal PaCO₂ target can promote vasoconstriction and thereby help reduce intracerebral blood volume. ARDS-based strategies such as hypercapnia can cause cerebral vasodilation, intracranial hypertension, and subsequent increase in intracranial pressure, which is typically at odds with goals of TBI therapy.¹¹ Frequently used TBI ventilation strategies (“brain protective”) include goals of normocapnia and normotension with the goals of avoiding hypoxia and maintaining good cerebral perfusion pressure (CPP).¹¹ Tight CO₂ and CPP control can mean greater tidal volumes and other ventilation strategies that strain the lungs, as opposed to lung protective ventilation.¹⁰ Other conflicting strategies include sedation (which is recommended early in ARDS, but can impede an accurate neurological exam in TBI) and fluid balance (conservative fluid resuscitation in ARDS, indeterminant data in TBI).^11,12

Table 1.

Guideline based care for mechanical ventilation in isolated acute respiratory distress syndrome or traumatic brain injury.

ATS/ESICM, SCCM guidelines for mechanical ventilation of adults with ARDS		Brain Trauma Foundation guidelines for management of severe TBI (4^th Edition)
Recommendation	Strength of evidence	Recommendation	Strength of evidence
Limit tidal volumes (4-8 ml/kg PBW) and limit inspiratory pressures (plateau pressure <30 cm H₂O)	Strong recommendation	Prophylactic hyperventilation with a PaCO2 of 25 mm Hg or lower is not recommended.	Level IIB
Recommend prone positioning (>12 hours per day)	Strong recommendation	Hyperventilation recommended to reduce elevated ICP, but should be avoided in the first 24	Weak (Not supported under Edition 4 evidence criteria)
Recommend against routine use of HFOV	Strong recommendation	Jugular venous oxygen saturation and brain tissue O2 partial pressure are recommended for monitoring if hyperventilation is used.	Weak (Not supported under Edition 4 evidence criteria)
Recommend higher PEEP compared to lower PEEP	Conditional recommendation for moderate/severe ARDS only
Recommend recruitment maneuvers	Conditional recommendation for moderate/severe ARDS
Insufficient evidence for ECMO.	No recommendation

Abbreviations. ATS = American Thoracic Society; ESICM = European Society of Intensive Care Medicine; SCCM = Society of Critical Care Medicine; ARDS = acute respiratory distress syndrome; TBI = traumatic brain injury. PBW = predicted body weight; HFOV = high-frequency oscillatory ventilation.

Given the conflicting treatment recommendations for “lung protective” versus “brain protective” management strategies, patients with TBI who subsequently develop ARDS are challenging to manage safely and effectively. While several management strategies have been proposed, these strategies are limited to expert opinion and reviews without systematic search strategies.^11
–14 These strategies are based comparing existing TBI and ARDS guidelines and trials—such as the ARDS Network trial and extrapolating for patients who have both TBI and ARDS.^11
–15

The purpose of a scoping review is to systematically synthesize knowledge on a topic and identify gaps in the literature, particularly in areas where evidence is still emerging and there is insufficient data to conduct a systematic review or meta-analysis.¹⁶ While systematic reviews aim to answer one question with clear clinical implications, a scoping review can help to identify the type of evidence available in an area of practice, but are limited in their ability to summarize information statistically (compared to a meta-analysis).¹⁶ We set out to characterize the evidence on caring for patients with TBI and ARDS. Given there is not robust research on this population, we conducted a scoping review of ventilation management strategies with clinical outcomes among patients with concurrent TBI and ARDS. The aim of this review is to describe published evidence for ventilatory management of these patients and highlight gaps in the existing literature. To our knowledge, there has not been a scoping review on this topic.

Methods

We documented our review according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses standards (PRISMA) guidelines (Appendix 1).¹⁷

Search strategy and data sources

A medical librarian with expertise in scoping reviews (S.K.) composed a search utilizing subject headings and keywords to represent the concepts of traumatic brain injury and adult respiratory distress syndrome (For search terms, see Appendix 2). The search was peer-reviewed by an additional medical librarian using a modified PRESS checklist.¹⁸ The databases, MEDLINE via PubMed, Embase via Elsevier, and the Web of Science Core Collection via Clarivate, were searched from inception to November 7, 2022. When possible, non-human studies and conference abstracts were removed.

Selection criteria

The population of interest was patients of any age with TBI and ARDS, with plans to stratify the data by pediatric and adult populations. We included any study where the authors identified the patients having ARDS and collected their chosen definition when stated (Berlin criteria for ARDS; 1994 American European Consensus Conference definition), intentionally casting a wide net for inclusion.^19,20 Similarly, we recorded reported TBI severity when included (e.g., Glasgow Coma Scale (GCS)).²¹ There was no required severity of TBI for inclusion in the study.

Interventions of interest included ventilation strategies, PEEP, oxygenation, prone positioning, recruitment maneuvers, pulmonary vasodilators (e.g., nitric oxide), high frequency oscillatory ventilation (HFOV), and extracorporeal membrane oxygenation (ECMO). These interventions were generated through a preliminary literature review and expert opinion from our team. There was no comparison group specified or required.

We included any clinical outcomes including oxygenation, intracranial pressure (ICP) or cerebral perfusion pressure (CPP), mortality, and functional recovery. Any article type could be included so long as it presented original data (e.g., reviews excluded). Given the paucity of research in this area, we elected to include case reports and case series. Exclusion criteria included animal studies, non-English articles, and articles where we could not obtain the full text. Articles that included patients with brain injury (both traumatic and non-traumatic) were included only if they reported data for the subgroup with TBI separately. Articles looking at risk factors for developing ARDS after TBI were excluded.

All results were compiled in EndNote and imported into Covidence to remove duplicate and conduct screening. Each reference was screened at the title/abstract and the full-text level by two, independent screeners (M.K.H., S.L., A.L.S., A.M.B., H.J.H., or E.O.). Conflicts were resolved by a third member of the team with neurocritical care expertise (J.K. or K.C.).

Data extraction

For the included articles, two members of the research team independently extracted information from each article using the Covidence extraction form, with discussion to reach consensus for conflicts. Data collected included age of patients (adults or pediatrics; descriptive statistics of age of sample), country where study was conducted, study design (case report, case series, cohort study, case control, non-randomized experimental study, etc.), site information (single versus multi-institutional site), gender of sample, inclusion/exclusion criteria, total number of participants, definition of TBI (e.g., Glasgow Coma Scale ⩽ 8²¹), definition of ARDS (2012 Berlin definition¹⁹ or American-European Consensus Conference²⁰), other characteristics of sample (e.g., Injury Severity Score), intervention, primary and secondary outcomes and associated results, and comparison group if present (Appendix 2). This list of extraction variables was generated iteratively by the research team. Adults were considered those greater than 14 years-old, consistent with the trauma literature. The data extraction form was built in Covidence by the research team and downloaded as an Excel file after consensus was reached. We also reviewed the references of included articles for studies that may be missing from our search.

Approach to summarizing data

Article were summarized in tables. As there were multiple study types included in this review, there was no meta-analysis conducted. Due to the scarcity of studies with pediatric patients only, they were included in the final summary tables with the adult patients.

Results

Study selection

Our search identified 10,514 articles, 94 of which were screened at the full-text level, and a final 31 of which met final inclusion criteria (Figure 1). Articles that included patients with ARDS and multiple types of brain injury (e.g., TBI, subarachnoid hemorrhage, hemorrhagic stroke) and did not stratify their data by brain injury type were excluded.^10,22
–26 We also excluded a case report of a patient with TBI, ARDS, and acute kidney injury as the intervention described was related to using citrate anticoagulation for dialysis, and not a ventilation strategy.²⁷ We reviewed the references of the 31 included articles and identified 4 additional studies to include, bringing the final sample to 35 studies.^28
–31

Figure 1.

PRISMA article inclusion flowchart.

Study characteristics

Of the 35 articles, interventions studied included ECMO (n = 13 articles), HFOV (n = 4), PEEP interventions (n = 3), prone positioning (n = 3), vasodilators (n = 4, one of which also looked at prone positioning), and other lung recruitment maneuvers (n = 9) (Table 2). All studies included were reports from single institutions and most focused on adults; five articles included pediatric patients.^32
–35

Table 2.

Data extracted from 35 studies looking at clinical outcomes for patients with ARDS and TBI with ventilatory interventions.

First author (year)	Study design	Location of study	Population	Number of participants (gender)	Inclusion criteria	Intervention	Outcomes
Extracorporeal membrane oxygenation (ECMO)
Parker 2021	Retrospective cohort	United States	Adults	13 (11 M, 2 F)	TBI: Intracranial blood on CT following traumaARDS: Berlin 2012Other: –	VV-ECMO6/13 patients received systemic A/C	5/13 (38%) patients survived to hospital discharge. No patient had worsening intracranial bleeding. Of the six patients who received systemic A/C while on ECMO, two (33%) had bleeding complications (extracranial).
Bosarge 2016	Case series	United States	Adults	4 (–)	TBI: –ARDS: Berlin 2012 definition (severe only)Other: –	VV-ECMO, VA-ECMO (vs conventional ventilation)Systemic A/C given to most patients (exact number not specified)	Case 1 who received ECMO: VV, no complications, survivedCase 2 who received ECMO: VV and VA bleeding and upper extremity thrombus, survivedCase 3 who received conventional ventilation: died of hypoxiaCase 4 who received conventional ventilation: died of multiorgan failure
Biscotti 2015	Case series	United States	Adults	2 (2 M)	Case 1: GCS = 14 (at presentation), PaO2/FiO2 = 42.Case 2: GCS = 3 (at presentation), PaO2/FiO2 = 30.	VV-ECMO with low dose A/CCase 1 indication: hypercapnia resulting in increased ICP and hypoxemiaCase 2 indication: failed conventional therapy for ARDS. Also employed cooling to 33 C and paralytics.	Case 1: Full neurologic recovery. Decannulated on ECMO day 13.Case 2: Full neurologic recovery. Decannulated on ECMO day 6.
Muellenbach 2012	Case series	Germany	Adults	3	Case 1: GCS = 4, PaO2/FiO2 = 58 mm HgCase 2: GCS = 3, PaO2/FiO2 = 40 mm HgCase 3: GCS = 6, PaO2/FiO2 < 40 mm Hg	VV-ECMO without heparin due to contraindications	Case 1: 5/8 ECMO days without heparin due to open abdomen. Decannulated day 8 of ECMO.Case 2: Day 1 of ECMO without heparin due to intracranial injury, then started. Decannulated day 3. Returned to school after 6 months.Case 3: 2/3 ECMO days without heparin due to surgery. Decannulated day 3. IVC thrombi which resolved with 5 days high dose heparin.
Bruzek 2014	Case report	United States	Adults (age 25)	1 (1 M)	GCS 7T, ARDS	VV-ECMO with systemic A/C	Immediate oxygen saturation improvement from 70 to 90%ICP low and managed with paralytics, cooling, sedation.Decannulation after 7 days with CT head without evidence of hemorrhageMild cognitive deficits at 6 months, but good physical recovery
Anton-Martin 2018	Case report	United States	Pediatrics (age 8)	1 (1 F)	GCS 12, ARDS	VV-ECMO with systemic A/C with conservative anticoagulation goals	Severe bleeding on ECMO day 3 around chest tube site, transfused with aminocaproic acid for 3 days. On day 7, an intraventricular and intraparenchymal hemorrhage was found with 12 mm midline shift necessitating hyperosmolar therapy, sedation, heparin reversal, and bedside decompressive craniectomy.Returned to school 10 months after injury.
Zhou 2015	Case report	China	Adult (age 31)	1 (1 M)	Cerebral contusion, PaO2/FiO2<40 mmHg, PaO2 = 40 mmHg	VA-ECMO with systemic A/C for 9 hours including intraoperatively during exploratory thoracotomy	PaO2 70-80 mmHg after initiation. Blood products, mannitol, Lasix, and sodium bicarbonate required for hemodynamic stability (details not provided). ECMO continued 4 hours post-operatively.No evidence of worsening intracranial hemorrhage post-ECMO.Full neurologic recovery several months later.
Stoll 2014	Case report	Germany	Adults (age 18)	1 (1 M)	Traumatic intracranial hemorrhage, ARDS	VV-ECMO without systemic A/C. Heparin coated cannula used.	Developed posttraumatic systemic inflammatory response syndrome and required continuous renal replacement therapy which resolved after 72 hours.Low-dose heparin started later (day not stated).Weaned on ECMO day 7.
Messing 2014	Case report	United States	Adults (age 18)	1 (1 M)	Traumatic subdural and subarachnoid hemorrhage with diffuse axonal injury, ARDS	VV-ECMO with heparin-bonded circuit. Systemic A/C started on ECMO day 5	Multiple thrombi in ECMO machinery (before starting systemic A/C). No progression of intracranial hemorrhage.
McKinlay 2008	Case report	United Kingdom	Adults (age 20)	1 (1 M)	GCS 8, ARDS	VA-ECMO (Novalung).No A/C (circuit or systemic).	Reduction of PaCO2 from 8.8 kPa prior to 5.2 kPa after ECMO placement; ICP reduction from 26 to 14 mmHg.Decannulated on day 5, followed by tracheostomy for 2 weeks and discharge just over 3 weeks after hospitalization.
Martindale 2017	Case report	United Kingdom	Adults (age 21)	1 (1 M)	GCS 7, ARDS	VV-ECMO.No A/C (circuit or systemic).	Decrease in PaCO2 from 6.44 to 5.06 kPa. Decrease in ICP from 26 to 7 mmHg. Decrease in peak airway pressure from 36 to 30 cm H20 and tidal volume from 10 to 6 mL/kg.Neurologic recovery with return to work 4 months post-injury.
Leloup 2011	Case report	France	Adult (age 27)	1 (1 M)	Traumatic cerebral hemorrhage, ARDS	VV-ECMO. A/C use not stated. Second oxygenator added.	Compared to one oxygenator for ECMO, a second oxygenator decreased PaCO2. Oxygen delivery unchanged.ECMO weaned on day 7. Discharged home.
Yen 2008	Case report	Taiwan	Adult (age 21)	1 (1 M)	GCS 12, epidural hematoma requiring decompressive hemicraniectomy, cardiopulmonary failure	VA-ECMO. Only circuit heparin used.	Required 49 h of VA-ECMO followed by 48 h of inhaled nitric oxide. Required continuous renal replacement therapy for 2 weeks (shock-related renal failure)Full neurologic recovery by discharge.
High frequency oscillatory ventilation (HFOV)
Vrettou 2013	Non-randomized experimental study	Greece	Adults	13 (9 M, 4 F)	TBI: GCS < 8ARDS: PaO2/FiO2<100 mm Hg within 72 hoursOther: anesthetized, requiring hyperosmolar therapy, mechanical ventilation	12-hours HFOV with tracheal gas insufflation then 12-hours conventional mechanical ventilation. Discontinued if PaO2/FiO2 > 100 mm Hg for > 12 h	PaO2/FiO2 increased significantly by 130-163% during HFOV with tracheal gas insufflation and remained elevated after by 73% (p < 0.01).Improvements in PaCO2 (41 prior to 38 mm Hg after), ICP (20 prior to 17 mm Hg after) 4 hours after, and CPP 4 hours after (72 prior to 77 mm Hg after) (p < 0.05). Plateau pressure (30 prior versus 28 cm H₂O after) and respiratory compliance (38 prior versus 45 mL/cmH₂O after) improved after TGI (p < 0.01). Systemic hemodynamics did not significantly change.
David 2005	Retrospective cohort		Adults	5 (5 M)	TBI: –ARDS: –Other: ICP monitoring; failed pressure-controlled ventilation	HFOV with mean airway pressure set 5 cm H2O than airway pressure measured using pressure-controlled ventilation	No adverse events (mucous obstruction, pneumothorax, tracheal injury).HFOV did not need to be terminated for change in cerebrodynamics (decreased CPP, increased ICP, worsening PaO2).Descriptively report of 11/390 (3%) hourly datasets indicating increased ICP (> 25 mm Hg), 66/390 (17%) showed decreased CPP (<70 mm Hg), 8/390 (2%) showed PaCO2 perturbations. 4/5 (80%) patients had increased PaO2/FiO2 (descriptively).
Sherr 2007	Case series	United States	Adults	5 (2 F, 3 M)	TBI: GCS range at time of intubation: 4-7ARDS: –Other: –	HVOF after failure of conventional management	All 5 cases (100%) transitioned from HFOV back to conventional mechanical ventilation. No clinically significant changes in ICP, CPP, or BP with transition. Increased PaO2 improvement in all; PaCO2 increased in some. PbrO2 improvement in 3 with intracranial monitoring.Two deaths (hemodynamic collapse; withdrawal of care due to prognosis); one complete return to baseline after rehab; one near complete return to baseline with some residual memory deficits; one still in rehab with tracheostomy.
Lo 2008	Case series	United Kingdom	Pediatrics	2 (2 M)	TBI: GCS 3 (both cases)ARDS: –	HVOF with persistent hypercapnia despite conventional mechanical ventilation	Improved PaCO2 (lowered) in both cases. Improved PaO2 in one, unchanged in second. Reduced in ICP for both cases.One death (fungal sepsis 1 month after injury) and one survival with residual cognitive, behavioral, and motor deficits.
Positive end expiratory pressure (PEEP) interventions
Zhang 2011	Non-randomized experimental study	China	Adults	9 (3 F, 6 M)	TBI: ICH or GCS < 8ARDS: lung injury (not defined)Other: mechanical ventilation; ICP monitor	Gradually increasing PEEP up to 21 cm H2O when PaO2/FiO2 < 150	Significantly increased PaO2/FiO2 after (245 mm Hg) recruitment maneuver compared to before (128 mm Hg, p < 0.01).PEEP positively correlated with CVP (R = 0.85, p < 0.01), ICP (R = .64, p < 0.05). Negatively correlated with CPP (R = −0.58, p < 0.05). No sig relationship to MAP (R = −0.05).
Nemer 2015	Non-randomized experimental study	Brazil	Adults	20 (15 M, 5 F)	TBI: severe (no stated definition, mean GCS = 5.9)ARDS: 2012 Berlin; AECCOther: PbrO2 monitor (Licox)	Increase of PEEP from 5 to 10 to 15 cm H2O for 20 min each	PbrO2 (24 at 5 cm H2O, 26 at 10 cm H2O, 29 at 15 cm H2O, p < 0.0001) and SpO2 (93% at 5 cm H2O, 95% at 10 cm H2O, 96% at 15 cm H2O, p = .0001) increased with each 5 cm H2O increase of PEEP.CPP (92 mm Hg across PEEP increases), ICP (8–9 mm Hg across PEEP increases) did not change significantly with increasing PEEP.
Lou 2012	Case report	China	Adults (age 17)	1 (1 M)	GCS motor score 2, ARDS	Titration of PEEP to 5-15 cm H2O	Increase in peak airway pressure from 20 to 30 cm H2O and CVP from 5 to 12 cm H2O. Increase in ICP from 15 to 18 mmHg. Decrease in cerebral perfusion pressure from 78 to 72 mmHg.Full neurologic recovery.
Prone positioning
Gritti 2013	Case report	Italy	Adult (age 37)	1 (M)	GCS 3, severe ARDS	Nitric oxide and prone positioning intraoperatively during spine stabilization, then postoperatively prone positioning every 8–12 h with continuous NO at 10-20 ppm	Improvement in PaO2 during prone positioning, with one instance of increased ICP resolved with a dose of mannitol.NO weaned at 22 days, ventilator removed at 43 days. GCS 14 after 4 months of rehab.
Ashton-Cleary 2011	Case report	United Kingdom	Adult (age 52)	1 (M)	TBI, ARDS	Prone positioning for 20 h	PaO2/FiO2 ratio increased from 39.6 two hours pre-prone to 58.4 one hour post-prone.ICP increased from 17 two hours pre-prone to 30 one hour post-prone but was transient.Complete neurologic recovery.
Kayani 2015	Case report	United States	Adult (age 23)	1 (1 M)	GCS 7, ARDS	Prone positioning for 2 days	No outcomes reported other than survival and discharge to rehabilitation.Persistent fever required cooling.
Vasodilators (e.g., nitric oxide)
See Gritti 2013
Papadimos 2009	Case report	United States	Adults (age 37)	1 (1 M)	GCS 3, severe ARDS	Inhaled nitric oxide (INO) at 20 ppm	ICP changed from over 50 mm Hg to 15 mm Hg with PaO2 of 86 mm Hg (from 54 mm Hg prior) over 35 min.INO weaned over several days with mechanical ventilation weaned on day 30.Moderate-severe long term cognitive deficits
Khan 2014	Case report	Saudi Arabia	Pediatrics (age 13)	1 (1 M)	GCS 5, severe ARDS	Inhaled nitric oxide (INO) started at 10 ppm and increased to 35 ppm	Decreased PaCO2 and increased PaO2 during the 24 h following INO. Improvement in CPP and ICP and decreasing PEEP and FiO2 requirements.INO weaned on day 7. No neurologic deficits long term.
Vavilala 2001	Case report	United States	Pediatrics (age 10)	1 (1 F)	GCS 4T, ARDS, pulmonary hypertension	Inhaled nitric oxide (INO) started at 5 ppm and increased to 35 ppm	At 10 ppm, pulmonary vascular resistance and mean pulmonary artery pressure decreased with improved cardiac index.With further increase in inhaled concentration, systemic vascular resistance and mean arterial blood pressure (MABP) increased, with sustained increase in MABP despite decreasing concentration INO requiring cessation. MABP returned to baseline 15 min after cessation of INO.
Other lung recruitment maneuvers
Salim 2004	Cohort	United States	Adults	10 (3 F, 7 M)	TBI: GCS < 8ARDS: AECC definitionOther: ventriculostomy drain, CSF drainage	High-frequency percussive ventilation (HFPV) at discretion of physician (typically PF ratio <100 mm Hg for >6 hrs)	PF ratio (pre HFPV 92) increased at 4 h (192, p < 0.01), 16 h (270, p < 0.01); ICP (pre HFPV 31 mm Hg) decreased at 4 h (19 mm Hg, p < 0.01), 16 h (17 mm Hg, p < 0.05); PaCO2 (pre HFPV 38 mm Hg) decreased at 4 hrs (32 mm Hg, p < 0.05), 16 hrs (33 mm Hg, p < 0.05); peak inspiratory pressure (pre HFPV 49 cm H2O) decreased at 16 h (41 cm H2O, p < 0.05).No significantly change in PEEP, mean airway pressure.
Pitoni 2021	Non-randomized experimental study	Italy	Adults	18 (33% female)	TBI: GCS < 9ARDS: 2012 Berlin Definition (PaO2/FiO2 < 100 excluded)Other: intracranial pressure monitoring	Heated humidifiers (HH) with tidal volume titrated to PaCO2 = 30-35 mm Hg. Proceeded and followed with same PaCO2 goal using heat and moisture exchangers	During HH phase, tidal volume reduced by 120 mL [95% CI = 98–144], plateau pressure and driving pressure reduced by 3.7 cm H2O [95% CI = 2.9–4.3], lower airway dead space of -84 mL [95% CI = −79 to −89], and total lung dead space -86 mL [95% CI = −73 to −98].PaCO2, alveolar recruitment, oxygenation, MAP, CPP, ICP, and middle cerebral artery mean flow velocity not significantly different during HH phase.
Oliynyk 2016	Retrospective cohort	Ukraine	–	267 (–)	TBI: severe (not defined)ARDS: Not definedOther: –	BiPAP (5-7 L/kg) (i.e., pressure support) versus forced ventilation volume control	Decreased mortality in BiPAP group (55%, 37/67 died) compared to volume control (69%, 35/51 died, p = 0.01).Among survivors, BiPAP had shorter ventilation time (18 days) than volume control (24 days, p < 0.01).
Munoz-Bendix 2015	Retrospective cohort	Germany	Adults (n=9), Pediatric (n=1)	10 (8 M, 2 F)	TBI: AIS > 3ARDS: Berlin definitionOther: Elevated ICP > 20 mm Hg (measured by EVD)	Pumpless extracorporeal lung assist (pECLA) with systemic heparin	Significant decrease in pCO2 (47 to 40 mm Hg, p = .005), and mean plateau pressure (28 to 25 cm/H2O, p < 0.001).Significant increase in pH (7.42 to 7.46, p = .02), PEEP (12 to 14 cm/H2O, p < 0.001), and ΔP (17 to 12 cm/H2O, p = .01).Unchanged pO2/FiO2 ratio, respiratory rate, and mean ventilation pressure.Decrease in daily CSF drainage (141 to 62 mL) required to maintain normal ICP (<20 mm Hg) (p = 0.037).Complications: one patient developed right heart failure requiring cessation of pECLA and start of vv-ECMO
Martínex-Pérez 2004	Non-randomized experimental study	Spain	Adult	7 (6 M, 1 F)	TBI: GCS < 9ARDS: AECCOther: –	Mid to end tracheal gas insufflation at 8 l/min flow rate for 90 min while maintaining normocapnia (35-40 mmHg) and PaO2>70 mmHgPlaced intracranial monitors (Camino)	Significant decrease in tidal volume (9 to 7 mL/kg, p = 0.018) and driving pressure (18 to 13 cm H2O, p = .018).Significant increase in autoPEEP (0.3 to 3.7 cm H2O, p = .018), total PEEP (9 ti 13 cm H2O, p < 0.05), and PaO2/FiO2 (151 to 164 mm Hg, p = 0.018) during TGI.No change in heart rate, mean systemic arterial pressure, central venous pressure, peak pressure, plateau pressure, ICP, CPP, jugular venous oxygen saturation, and PaCO2.Significant decrease in right cerebral middle artery (CMA) pulsatility index (1.3 to 1.1, p ⩽ 0.05), but not left. Significant increase in left CMA mean velocity (63 to 77 cm/s, p ⩽ 0.05, but not right.
Bein 2005	Case series	Germany	Adult	5 (4 M, 1 F)	TBI: Marshall et al (2000)⁶⁶ CT classification, diffuse injury IV; severe GCSARDS: severe, PaO2/FiO2 < 150 mm HgOther: ICP monitor	Pumpless extracorporeal lung assist with heparin in circuitIndication: hypercapnia	4/5 (80%) survived, 1 (20%) died of multiorgan failure 10 days after pECLA was started.Hypercapnia eliminated after starting in 4/5 (80%) patients. Minute volume of ventilation and intracranial hypertension reduced in 3/5 (60%), with CPP stable. Improved arterial oxygenation in 3/5 (60%).No bleeding complications. One patient (20%) had acute ischemia and ulcer in leg after pECLA cannula removed requiring stent and venous patch.
Levy 1995	Case series	France	Adult	2 (2 M)	TBI: head trauma with increased ICPARDS: Severe (Murray et al 1988 definition⁶⁷)	Tracheal gas insufflation with continuous O2 at 4l/min	Descriptively decreased ICP for both patients within 1 hour of starting TGI (Patient 1: 25 prior to 15 1-h after starting; patient 2: 32 prior to 20 1-h after starting).TGI stopped after 1 week. Patient 1 had a complete recovery; patient 2 was withdrawn from ventilation with major neurologic impairment due to hemorrhagic transformation of cerebral contusion.
Theodore 2019	Case report	United States	Adult (age 19)	1 (1 M)	GCS 3, traumatic subdural hematoma with contusions, ARDS	Esophageal balloon catheter with goal PEEP < 15 cm H2O.	Esophageal catheter guided PEEP improved PaO2 (to 114 mmHg; P/F ratio > 100 mmHg), lowered PaCO2, and lowered ICP (<20 mmHg).Discharged home with mild cognitive deficits after 7 weeks in ICU and 2 mo in rehabilitation.
Reynolds 1999	Case report	United States	Adult (age 16)	1 (1 M)	GCS 6, diffuse alveolar infiltrates, right middle lobe laceration, sustained desaturation despite ventilatory support	VV-pumpless extracorporeal lung assist without systemic A/C	Massive pulmonary hemorrhage requiring thoracotomy with resection of right middle lobe. No evidence of cerebral hemorrhage on CT.Decannulated on day 7. Moderate cognitive defects at time of discharge.

Abbreviations. ECMO = Extracorporeal membrane oxygenation. TBI = traumatic brain injury. ARDS = acute respiratory distress syndrome. VV = venous venous. VA = venous arterial. A/C = anticoagulation. GCS = Glasgow Coma Scale. IVC = inferior vena cava. ICP = intracranial pressure. HFOV = high frequency oscillatory ventilation. CPP = Cerebral perfusion pressure. BP = blood pressure. ICH = intracranial hemorrhage. AECC = European Society of Intensive Care Medicine. pECLA = pumpless extracorporeal lung assist. PEEP = positive end expiratory pressure. INO=inhaled nitric oxide. PaCO2 = partial pressure of carbon dioxide in arterial blood. PaO2/FiO2 = partial pressure of oxygen in arterial blood/inspired oxygen concentration. PbrO2 = brain tissue oxygenation. AIS = Abbreviated Injury Scale. EVD = extraventicular drain.

ECMO

We found one retrospective cohort study, three case series, and nine case reports of use of ECMO in patients with TBI and concomitant ARDS.^{31,32,36
–46} Generally articles reported use of venous-venous ECMO (VV-ECMO), though there were four cases using venous-arterial ECMO (VA-ECMO).^31,37,41,43 The retrospective cohort study of 13 adults who received VV-ECMO only reported descriptive outcomes which included survival (38% (5/13) patients survived) and bleeding complications (15% (2/13) patients). In terms of complications for all included ECMO articles, three patients developed thrombi; two of these patients were not given anti-coagulation, and for the third anticoagulation use was not specified.^37,39,42 Three patients developed bleeding complications.^32,36,37 There was one report of a patient who developed posttraumatic systemic inflammatory response after starting VV-ECMO that required continuous renal replacement therapy (CRRT) for 7 days.⁴² Another case also required CRRT for two weeks after VA-ECMO due to shock related renal failure.³¹

HFOV

We found one retrospective cohort study, one non-randomized experimental study, and two case series reporting on use of HFOV in patients with concomitant TBI and ARDS.^35,47
–49 Vrettou et al prospectively collected physiologic data during HFOV and conventional mechanical ventilation and found that PaO2/FiO2 increased significantly during HFOV use, which was sustained after returning to conventional ventilation.⁴⁷ David et al retrospectively reviewed patients who received HFOV and descriptively reported PaO2/FiO2 increased in four of five of the patients, with infrequent occurrences of increased ICP, decreased CPP, and PaCO2 changes that did not require termination of HFOV.⁴⁸ The remainder of the articles reported either no clinically significant changes in ICP or decreased ICP following initiation of HFOV.^35,47,49 Several deaths were reported that were not attributed to HFOV.

PEEP interventions

Two non-randomized experimental studies and one case report described PEEP interventions, all of which involved up titrating PEEP.^50
–52 Both Nemer et al and Zhang et al (non-randomized experimental studies) found that oxygenation improved with increasing PEEP.^50,51 ICP was found to be positively correlated with PEEP in one study,⁵⁰ descriptively increased in a case report,⁵² and not significantly changed with increasing PEEP in the third.⁵¹

Prone positioning

Three case reports described use of prone positioning in patients with TBI and ARDS.^53
–55 Two of the case reports described improved oxygenation with prone positioning, with associated increases in ICP, one of which required treatment with mannitol.^53,54 The third case study did not provide outcomes beyond survival.⁵⁵

Vasodilators

Four case reports described use of inhaled nitric oxide (range of dosing: 5-35 ppm).^30,33,53,56 The cases described by Papadimos et al and Khan et al both descriptively report improvements in ICP and oxygenation following initiation of inhaled nitric oxide, in an adult and pediatric patient respectively.^33,56 Gritti et al mentioned that use of inhaled nitric oxide of lab values without further elaboration (case report was focused on use of prone positioning).⁵³ Vavilala et al describe the use of inhaled nitric oxide in a pediatric patient with TBI, ARDS, and pulmonary hypertension which initially resulted in improvement in pulmonary vascular resistance, mean pulmonary artery pressure, and cardiac index, but increasing the concentration of inhaled nitric oxide resulted in increased systemic vascular resistance and mean arterial blood pressure requiring cessation of therapy, which resolved the hemodynamic disturbances.³⁰

Other lung recruitment maneuvers

Several other articles were included that describe other lung recruitment maneuvers.^{28,29,34,57
–62} Salim et al describe a cohort of 10 patients who received high-frequency percussive ventilation which significantly improved oxygenation status but also increased ICP.⁵⁷ Pitoni et al reported use of heated humidifiers in a non-randomized experimental trial of 18 patients and found heated humidifier use reduced required tidal volume and dead space without increasing ICP.⁵⁸ Oliynyk et al looked at corticosteroid usage for patients with severe TBI, sepsis and ARDS using a retrospective cohort study; however, in addition to comparing those exposed to corticosteroids and those not, they also compared two ventilation strategies: BiPAP (i.e., pressure support) and forced ventilation volume control and descriptively found decreased mortality in patients who received pressure support (in the groups who did not receive corticosteroids).⁵⁹ Three articles reported use of pumpless extracorporeal lung assist (pECLA). Munoz-Bendix et al reported significantly improved hypercapnia, but one of ten patients in the retrospective cohort study developed right heart failure necessitating VV-ECMO; Bein et al also reported improved hypercapnia in four of five patients in their case series, with one patient developing ischemia and an ulcer related to removal of the pECLA cannula, and one death attributed to multiorgan failure.^34,61 Reynolds et al reported a case of VV-pECLA in a 16 year old who survived, but had massive pulmonary hemorrhage necessitating surgery.²⁹ Martínex-Pérez et al prospectively looked at the use of tracheal gas insufflation in seven patients and found a significant increase in PaO2/FiO2 without change in cerebral oxygenation or pressure after initiation.⁶⁰ Levy et al reported two cases of patients with increased ICP which dropped to normal within one hour of starting tracheal gas insufflation.²⁹ Finally, Theodore et al described a case of the use of an esophageal balloon catheter to guide PEEP titration and descriptively found improved oxygenation and decreased ICP.⁶²

Discussion

We conducted a scoping review of clinical outcomes associated with ventilatory strategies (ECMO, HFOV, PEEP interventions, prone positioning, vasodilators, and other lung recruitment maneuvers) of patients with concurrent TBI and ARDS. Overall, there was a very weak evidence base (few studies, mostly limited to cohort studies, and case reports and series) for each of the interventions with varying outcomes and lack of control groups, limiting our ability to compare studies or draw conclusions about effectiveness. Outcomes varied and included both physiologic changes (e.g., change in cerebrodynamics or hemodynamics with intervention) and clinical outcomes such as mortality, complications, or neurologic recovery. Studies were all conducted at single institutions, most were with adult populations, and none were randomized controlled trials.

ECMO (primarily venous-venous) was the most studied intervention with reports of survival and some neurologic recovery following its use, though there was only one cohort study which lacked a control group; the remainder were case series or case reports. Both bleeding and thrombotic-related complications were reported amalgamated across the reports; there was inconsistent use of systemic anticoagulation reported.

Two tentatively promising areas of further investigation were use of HFOV and inhaled nitric oxide. HFOV was studied in four studies with reports for some patients of sustained improvements in PaO2/FiO2 with reports of both improved and unchanged ICP compared to prior to starting HFOV. HFOV—as the name suggests—uses high respiratory rate and low tidal volumes while holding mean airway pressure constant, preventing alveoli from undergoing the expansion/collapse cycle which can cause trauma.⁶³ Evidence is generally equivocal for HFOV use in adult patients with ARDS compared to conventional ventilation. The ATS/ESICM/SCCM guidelines recommend against the routine use of HFOV for patients with ARDS, though they recognize there is inconclusive evidence on HFOV’s role as a rescue therapy (e.g., for those who fail conventional ventilation).^9,64,65 To this point, in our review most studies on HFOV reported its use in patients who failed conventional management. In addition, three case studies reported successful use of nitric oxide to decrease intracranial pressure. Nitric oxide is a known as a vasodilator, but there is also speculation based on animal models that it could provide some anti-inflammatory effects in the acute period.^56,66 While tentatively promising, case studies are one of the lowest levels of the evidence pyramid and use of NO needs further study.

Overall, the studies included in this review are limited by study design, included populations, and outcomes. Most studies were retrospective and prone to selection bias due to study design, especially the case reports and series. Outcomes were often reported descriptively, without statistical tests of comparison which severely limits our ability to draw conclusions about effectiveness or superiority of interventions. Finally, some studies only included patients who failed conventional management most likely due to the experimental nature of the interventions; this limits generalizability to all hospitalized patients with ARDS and TBI. Given the landscape of evidence in this area, it is difficult to make evidence-based recommendations for clinical care of patients with ARDS and TBI, but clinicians can at least be aware this area of practice does not have a robust evidence-base and continues to be guided based on biological and physiological rationale, extrapolated data from other disease states, individual guidelines from ARDS and TBI care, and local practice and culture. Finally, few studies included pediatric patients; little is known about how to best care for pediatric patients with concurrent ARDS and TBI.⁶⁷

There are several limitations to our review process to note. We included all study designs and outcomes in our review, including case studies, as we suspected evidence for each intervention in this population would be limited. While this allowed us to broadly describe the landscape of evidence, it limited our ability to perform any meta-analysis across these study types and outcomes. As a result, our review cannot draw conclusions about the efficacy of studied interventions. We recognize our inability to perform a meta-analysis is a major limitation; a future meta-analysis would be useful to the field as the research surrounding care for TBI and ARDS patients becomes more robust with standardized interventions and outcomes. As included studies were at high risk of bias, particularly case studies and series which fall prey to selection bias, our speculations about promising interventions could tend towards overstating benefits. We also had broad inclusion criteria for the study populations. We did not standardize our definitions of TBI and ARDS, and included populations of all ages, illness severity, and both isolated TBI and polytrauma patients to broadly describe the existing evidence, though this also limited our ability to compare across studies.

In this scoping review of ventilatory strategies for patients with concurrent TBI and ARDS, we found a heterogeneous group of studies with high risk of bias due to study design. The heterogeneity of studies limits our ability to draw conclusions about efficacy of studied interventions which included ECMO, HFOV, PEEP interventions, prone positioning, vasodilators, and other lung recruitment maneuvers. This review highlights the limited data that exists in ventilatory strategies for patients with ARDS and TBI. Future research should focus on robust, prospective studies with patient-centered outcomes (e.g., neurologic and functional recovery) including randomized controlled trials, and may consider looking at subgroups of this heterogeneous patient population of TBI and ARDS (e.g., isolated versus polytrauma, age, severity, comorbidities). Prospective studies with comparison groups could help to establish clear, evidence-based guidelines on caring for patients with ARDS and TBI.

Supplemental Material

sj-docx-1-inc-10.1177_17511437241311398 – Supplemental material for Management of traumatic brain injury and acute respiratory distress syndrome—What evidence exists? A scoping review

Supplemental material, sj-docx-1-inc-10.1177_17511437241311398 for Management of traumatic brain injury and acute respiratory distress syndrome—What evidence exists? A scoping review by Margot Kelly-Hedrick, Sunny Liu, Jordan Hatfield, Alexandria L. Soto, Alyssa M. Bartlett, Helen J. Heo, Ellen O’Callaghan, Evangeline Arulraja, Samantha Kaplan, Tetsu Ohnuma, Vijay Krishnamoorthy, Katherine Colton and Jordan Komisarow in Journal of the Intensive Care Society

Supplemental Material

sj-docx-2-inc-10.1177_17511437241311398 – Supplemental material for Management of traumatic brain injury and acute respiratory distress syndrome—What evidence exists? A scoping review

Supplemental material, sj-docx-2-inc-10.1177_17511437241311398 for Management of traumatic brain injury and acute respiratory distress syndrome—What evidence exists? A scoping review by Margot Kelly-Hedrick, Sunny Liu, Jordan Hatfield, Alexandria L. Soto, Alyssa M. Bartlett, Helen J. Heo, Ellen O’Callaghan, Evangeline Arulraja, Samantha Kaplan, Tetsu Ohnuma, Vijay Krishnamoorthy, Katherine Colton and Jordan Komisarow in Journal of the Intensive Care Society

Footnotes

Acknowledgements

None.

Declaration of conflicting interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: R01NS130832 (Krishnamoorthy)

Prior abstract publication/presentation

None.

ORCID iD

Margot Kelly-Hedrick

Supplemental material

Supplemental material for this article is available online.

References

Dewan

Rattani

Gupta

, et al. Estimating the global incidence of traumatic brain injury. J Neurosurg 2018; 130(4): 1080–1097. DOI: 10.3171/2017.10.JNS17352.

Krishnamoorthy

Komisarow

Laskowitz

, et al. Multiorgan dysfunction after severe traumatic brain injury: epidemiology, mechanisms, and clinical management. Chest 2021; 160(3): 956–964. DOI: 10.1016/j.chest.2021.01.016.

Krishnamoorthy

Temkin

Barber

, et al. Association of early multiple organ dysfunction with clinical and functional outcomes over the year following traumatic brain injury: a transforming research and clinical knowledge in traumatic brain injury study. Crit Care Med 2021; 49(10): 1769–1778. DOI: 10.1097/CCM.0000000000005055.

Kemp

Johnson

Riordan

, et al. How we die: The impact of nonneurologic organ dysfunction after severe traumatic brain injury. Am Surg 2008; 74(9): 866–872.

Komisarow

Chen

Vavilala

, et al. Epidemiology and outcomes of acute respiratory distress syndrome following isolated severe traumatic brain injury. J Intensive Care Med 2022; 37(1): 68–74. DOI: 10.1177/0885066620972001.

Aisiku

Yamal

Doshi

, et al. The incidence of ARDS and associated mortality in severe TBI using the Berlin definition. J Trauma Acute Care Surg 2016; 80(2): 308–312. DOI: 10.1097/TA.0000000000000903.

Fan

Huang

Gedansky

, et al. Prevalence and outcome of acute respiratory distress syndrome in traumatic brain injury: a systematic review and meta-analysis. Lung 2021; 199(6): 603–610. DOI: 10.1007/s00408-021-00491-1.

Holland

Mackersie

Morabito

, et al. The development of acute lung injury is associated with worse neurologic outcome in patients with severe traumatic brain injury. J Trauma Injury Infect Crit Care 2003; 55(1): 106–111. DOI: 10.1097/01.TA.0000071620.27375.BE.

Fan

Del Sorbo

Goligher

, et al. An official American thoracic society/European society of intensive care medicine/society of critical care medicine clinical practice guideline: mechanical ventilation in adult patients with acute respiratory distress syndrome. Am J Respir Crit Care Med 2017; 195(9): 1253–1263. DOI: 10.1164/rccm.201703-0548ST.

10.

Mascia

Acute lung injury in patients with severe brain injury: a double hit model. Neurocrit Care 2009; 11(3): 417–426. DOI: 10.1007/s12028-009-9242-8.

11.

Taran

Cho

Stevens

RD.

Mechanical ventilation in patients with traumatic brain injury: Is it so different?

Neurocrit Care 2023; 38(1): 178–191. DOI: 10.1007/s12028-022-01593-1.

12.

Della Torre

Badenes

Corradi

, et al. Acute respiratory distress syndrome in traumatic brain injury: how do we manage it? J Thorac Dis 2017; 9(12): 5368–5381. DOI: 10.21037/jtd.2017.11.03.

13.

Frisvold

Robba

Guérin

What respiratory targets should be recommended in patients with brain injury and respiratory failure?

Intensive Care Med 2019; 45(5): 683–686. DOI: 10.1007/s00134-019-05556-7

14.

Robba

Camporota

Citerio

Acute respiratory distress syndrome complicating traumatic brain injury. Can opposite strategies converge?

Intensive Care Med 2023; 49(5): 583–586. DOI: 10.1007/s00134-023-07043-6.

15.

Brower

Matthay

Morris

, et al. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000; 342(18): 1301–1308. DOI: 10.1056/nejm200005043421801.

16.

Munn

Peters

MDJ

Stern

, et al. Systematic review or scoping review? Guidance for authors when choosing between a systematic or scoping review approach. BMC Med Res Methodol 2018; 18(1): 143. DOI: 10.1186/s12874-018-0611-x.

17.

Tricco

Lillie

Zarin

, et al. PRISMA extension for scoping reviews (PRISMA-ScR): checklist and explanation. Ann Intern Med 2018; 169(7): 467–473. DOI: 10.7326/M18-0850.

18.

McGowan

Sampson

Salzwedel

, et al. PRESS peer review of electronic search strategies: 2015 guideline explanation and elaboration. 2016: 1–79. https://www.cadth.ca/sites/default/files/pdf/CP0015_PRESS_Update_Report_2016.pdf

19.

ARDS Definition Task Force, Ranieri

Rubenfeld

, et al. Acute respiratory distress syndrome: the Berlin Definition. JAMA 2012; 307(23): 2526–2533. DOI: 10.1001/jama.2012.5669.

20.

Bernard

Artigas

Brigham

, et al. The American-European Consensus Conference on ARDS. Definitions, mechanisms, relevant outcomes, and clinical trial coordination. Am J Respir Crit Care Med 1994; 149: 818–824. DOI: 10.1164/ajrccm.149.3.7509706.

21.

Jain

Iverson

LM.

Glasgow Coma Scale. In: StatPearls. StatPearls Publishing; 2022. Accessed January 17, 2023. http://www.ncbi.nlm.nih.gov/books/NBK513298/

22.

Wolf

Plev

Trost

, et al. Open lung ventilation in neurosurgery: an update on brain tissue oxygenation. Acta Neurochir Suppl 2005; 95: 103–105. DOI: 10.1007/3-211-32318-X_22.

23.

Bernon

Mrozek

Dupont

, et al. Can prone positioning be a safe procedure in patients with acute brain injury and moderate-to-severe acute respiratory distress syndrome? Crit Care 2021; 25(1): 30. DOI: 10.1186/s13054-020-03454-9.

24.

Boone

Jinadasa

Mueller

, et al. The effect of positive end-expiratory pressure on intracranial pressure and cerebral hemodynamics. Neurocrit Care 2017; 26(2): 174-181. DOI: 10.1007/s12028-016-0328-9.

25.

Roth

Ferbert

Deinsberger

, et al. Does prone positioning increase intracranial pressure? A retrospective analysis of patients with acute brain injury and acute respiratory failure. Neurocrit Care 2014; 21(2): 186–191. DOI: 10.1007/s12028-014-0004-x.

26.

Wolf

Plev

Trost

, et al. Open lung ventilation in neurosurgery: an update on brain tissue oxygenation. Acta Neurochir Suppl 2005; 95: 103–105. DOI: 10.1007/3-211-32318-x_22.

27.

Medow

Sanghvi

Hofmann

RM.

Use of high-flow continuous renal replacement therapy with citrate anticoagulation to control intracranial pressure by maintaining hypernatremia in a patient with acute brain injury and renal failure. Clin Med Res 2015; 13(2): 89–93. DOI: 10.3121/cmr.2014.1238.

28.

Levy

Bollaert

Nace

, et al. Intracranial hypertension and adult respiratory distress syndrome: usefulness of tracheal gas insufflation. J Trauma 1995; 39(4): 799–801. DOI: 10.1097/00005373-199510000-00039.

29.

Reynolds

Cottingham

McCunn

Habashi

Scalea

TM.

Extracorporeal lung support in a patient with traumatic brain injury: the benefit of heparin-bonded circuitry. Perfusion 1999; 14(6): 489-493. DOI: 10.1177/026765919901400612.

30.

Vavilala

Roberts

Moore

, et al. The influence of inhaled nitric oxide on cerebral blood flow and metabolism in a child with traumatic brain injury. Anesth Analg 2001; 93(2): 351–353. DOI: 10.1097/00000539-200108000-00023.

31.

Yen

Liau

Chen

Chao

Extracorporeal membrane oxygenation resuscitation for traumatic brain injury after decompressive craniotomy. Clin Neurol Neurosurg 2008; 110(3): 295–297. DOI: 10.1016/j.clineuro.2007.10.017.

32.

Anton-Martin

Braga

Megison

, et al. Craniectomy and traumatic brain injury in children on extracorporeal membrane oxygenation support. Pediatr Emerg Care 2018; 34(11): e204–e210. DOI: 10.1097/pec.0000000000000907.

33.

Khan

Azfar

Khurshid

SM.

The role of inhaled nitric oxide beyond ARDS. Indian J Crit Care Med 2014; 18(6): 392–395. DOI: 10.4103/0972-5229.133931.

34.

Munoz-Bendix

Beseoglu

Kram

Extracorporeal decarboxylation in patients with severe traumatic brain injury and ARDS enables effective control of intracranial pressure. Crit Care 2015; 19: 381. DOI: 10.1186/s13054-015-1088-1.

35.

Jones

Freeman

McFadzean

Minns

RA.

The role of high frequency oscillatory ventilation in the management of children with severe traumatic brain injury and concomitant lung pathology. Pediatr Crit Care Med 2008; 9(5): e38–e42. DOI: 10.1097/PCC.0b013e3181731ab7.

36.

Parker

Menaker

Berry

, et al. Single center experience with veno-venous extracorporeal membrane oxygenation in patients with traumatic brain injury. Am Surg 2021; 87(6): 949–953. DOI: 10.1177/0003134820956360.

37.

Bosarge

Raff

McGwin

Jr , et al. Early initiation of extracorporeal membrane oxygenation improves survival in adult trauma patients with severe adult respiratory distress syndrome. J Trauma Acute Care Surg 2016; 81(2): 236–243. DOI: 10.1097/ta.0000000000001068.

38.

Biscotti

Gannon

Abrams

, et al. Extracorporeal membrane oxygenation use in patients with traumatic brain injury. Perfusion 2015; 30(5): 407–409. DOI: 10.1177/0267659114554327.

39.

Muellenbach

Kredel

Kunze

, et al. Prolonged heparin-free extracorporeal membrane oxygenation in multiple injured acute respiratory distress syndrome patients with traumatic brain injury. J Trauma Acute Care Surg 2012; 72(5): 1444–1447. DOI: 10.1097/TA.0b013e31824d68e3.

40.

Bruzek

Vega

Mathern

BE.

Extracorporeal membrane oxygenation support as a life-saving measure for acute respiratory distress syndrome after craniectomy. J Neurosurg Anesthesiol 2014; 26(3): 259–260. DOI: 10.1097/ANA.0b013e3182a5d0fd.

41.

Zhou

Liu

Lin

, et al. ECMO support for right main bronchial disruption in multiple trauma patient with brain injury–a case report and literature review. Perfusion 2015; 30(5): 403-406. DOI: 10.1177/0267659114554326.

42.

Stoll

Rademacher

Klak

, et al. Veno-venous extracorporeal membrane oxygenation therapy of a severely injured patient after secondary survey. Am J Emerg Med 2014; 32(10): 1300.e1–1300.e1.2. DOI: 10.1016/j.ajem.2014.03.039.

43.

Messing

Agnihothri

Van Dusen

, et al. Prolonged use of extracorporeal membrane oxygenation as a rescue modality following traumatic brain injury. Asaio J 2014; 60(5): 597-599. DOI: 10.1097/mat.0000000000000103.

44.

McKinlay

Chapman

Elliot

, et al. Pre-emptive Novalung-assisted carbon dioxide removal in a patient with chest, head and abdominal injury. Anaesthesia 2008; 63(7): 767–770. DOI: 10.1111/j.1365-2044.2008.05484.x.

45.

Martindale

McGlone

Chambers

, et al. Management of severe traumatic brain injury and acute respiratory distress syndrome using pumped extracorporeal carbon dioxide removal device. J Intensive Care Soc 2017; 18(1): 66–70. DOI: 10.1177/1751143716676821.

46.

Leloup

Rozé

Calderon

, et al. Use of two oxygenators during extracorporeal membrane oxygenator for a patient with acute respiratory distress syndrome, high-pressure ventilation, hypercapnia, and traumatic brain injury. Br J Anaesth 2011; 107(6): 1014–1015. DOI: 10.1093/bja/aer365.

47.

Vrettou

Zakynthinos

Malachias

, et al. High-frequency oscillation and tracheal gas insufflation in patients with severe acute respiratory distress syndrome and traumatic brain injury: an interventional physiological study. Crit Care 2013; 17(4): R136. DOI: 10.1186/cc12815.

48.

David

Karmrodt

Weiler

, et al. High-frequency oscillatory ventilation in adults with traumatic brain injury and acute respiratory distress syndrome. Acta Anaesthesiol Scand 2005; 49(2): 209-214. DOI: 10.1111/j.1399-6576.2004.00570.x.

49.

Sherr

Defillo

Bergman

, et al. High frequency oscillatory ventilation to support brain tissue oxygen in the setting of acute respiratory distress syndrome and traumatic brain injury. Crit Care Med 2007; 35(12): A287–A287.

50.

Zhang

Yang

Wang

, et al. Impact of positive end-expiratory pressure on cerebral injury patients with hypoxemia. Am J Emerg Med 2011; 29(7): 699–703. DOI: 10.1016/j.ajem.2010.01.042.

51.

Nemer

Caldeira

Santos

, et al. Effects of positive end-expiratory pressure on brain tissue oxygen pressure of severe traumatic brain injury patients with acute respiratory distress syndrome: a pilot study. J Crit Care 2015; 30(6): 1263–1266. DOI: 10.1016/j.jcrc.2015.07.019.

52.

Lou

Xue

Chen

, et al. Is high PEEP ventilation strategy safe for acute respiratory distress syndrome after severe traumatic brain injury? Brain Inj 2012; 26(6): 887–890. DOI: 10.3109/02699052.2012.660514.

53.

Gritti

Lanterna

, et al. The use of inhaled nitric oxide and prone position in an ARDS patient with severe traumatic brain injury during spine stabilization. J Anesth 2013; 27(2): 293–297. DOI: 10.1007/s00540-012-1495-2.

54.

Ashton-Cleary

Duffy

MR.

Prone ventilation for refractory hypoxaemia in a patient with severe chest wall disruption and traumatic brain injury. Br J Anaesth 2011; 107(6): 1009–1010. DOI: 10.1093/bja/aer374.

55.

Kayani

Feldman

JP.

Prone ventilation in a patient with traumatic brain injury, bifrontal craniectomy and intracranial hypertension. Trauma 2015; 17(3): 224–228. DOI: 10.1177/1460408614557857.

56.

Papadimos

Medhkour

Yermal

Successful use of inhaled nitric oxide to decrease intracranial pressure in a patient with severe traumatic brain injury complicated by acute respiratory distress syndrome: a role for an anti-inflammatory mechanism?

Scand J Trauma Resusc Emerg Med 2009; 17: 5. DOI: 10.1186/1757-7241-17-5.

57.

Salim

Miller

Dangleben

, et al. High-frequency percussive ventilation: an alternative mode of ventilation for head-injured patients with adult respiratory distress syndrome. J Trauma 2004; 57(3): 542–546. DOI: 10.1097/01.ta.0000135159.94744.5f.

58.

Pitoni

D’Arrigo

Grieco

, et al. Tidal volume lowering by instrumental dead space reduction in brain-injured ARDS patients: effects on respiratory mechanics, gas exchange, and cerebral hemodynamics. Neurocrit Care 2021; 34(1): 21–30. DOI: 10.1007/s12028-020-00969-5.

59.

Oliynyk

Pereviznyk

Yemiashev

, et al. The effectiveness of corticosteroid usage in complex therapy for severe sepsis and acute respiratory distress syndrome in cases of severe traumatic brain injury. Adv Clin Exp Med 2016; 25(6): 1223–1226. DOI: 10.17219/acem/61013.

60.

Martínez-Pérez

Bernabé

Peña

, et al. Effects of expiratory tracheal gas insufflation in patients with severe head trauma and acute lung injury. Intensive Care Med 2004; 30(11): 2021–2027. DOI: 10.1007/s00134-004-2439-6.

61.

Bein

Scherer

Philipp

, et al. Pumpless extracorporeal lung assist (pECLA) in patients with acute respiratory distress syndrome and severe brain injury. J Trauma 2005; 58(6): 1294–1297. DOI: 10.1097/01.ta.0000173275.06947.5c.

62.

Theodore

Mahanes

Leite

Oesophageal pressure-guided management of severe acute respiratory distress syndrome in a patient with intractable intracranial hypertension. BMJ Case Rep 2019; 12(11). DOI: 10.1136/bcr-2019-230723.

63.

Meyers

Rodrigues

Ari

High-frequency oscillatory ventilation: a narrative review. Can J Respir Ther 2019; 55: 40–46. DOI: 10.29390/cjrt-2019-004.

64.

Young

Lamb

Shah

, et al. High-frequency oscillation for acute respiratory distress syndrome. N Engl J Med 2013; 368(9): 806–813. DOI: 10.1056/NEJMoa1215716.

65.

Ferguson

Cook

Guyatt

, et al. High-frequency oscillation in early acute respiratory distress syndrome. N Engl J Med 2013; 368(9): 795–805. DOI: 10.1056/NEJMoa1215554.

66.

Chen

Hedenstierna

Nitric oxide up-regulates the glucocorticoid receptor and blunts the inflammatory reaction in porcine endotoxin sepsis. Crit Care Med 2007; 35(1): 26–32. DOI: 10.1097/01.CCM.0000250319.91575.BB.

67.

Tasker

RC.

Traumatic brain injury and pediatric acute respiratory distress syndrome: moving the field forward. Pediatr Crit Care Med 2020; 21(2): 198–199. DOI: 10.1097/PCC.0000000000002181.

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