Pulmonary complications after traumatic injuries of the brain and spinal cord are common and can significantly worsen patient outcomes. These include neurogenic pulmonary edema, pneumonia, acute respiratory distress syndrome, and thromboembolic disease. Early recognition and treatment of these conditions is essential to optimize care for neurotrauma patients. This article reviews the pathophysiology and treatment of lung injuries and other pulmonary diseases in this patient population.
Key points
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Acute lung injury is an independent risk factor for poor outcome after traumatic brain injury.
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In acute respiratory distress syndrome, lung protective measures are essential, particularly the avoidance of barotrauma. Other maneuvers, including patient proning, should be considered if necessary.
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Pneumonia may be present at the time of injury or can develop at any point during the patient’s hospitalization.
| ALI | acute lung injury |
| ARDS | acute respiratory distress syndrome |
| CNS | central nervous system |
| CPP | cerebral perfusion pressure |
| ECMO | extracorporeal membrane oxygenation |
| GCS | glasgow coma scale |
| ICP | intracranial pressure |
| NPE | neurogenic pulmonary edema |
| PbtO2 | oxygen partial pressure |
| PE | pulmonary embolism |
| PEEP | positive end-expiratory pressure |
| PF | ratio of partial pressure of oxygen to fraction of inspired oxygen concentration |
| SCIs | spinal cord injuries |
| TBI | traumatic brain injury |
| V T | tidal volumes |
| VAP | ventilation-associated pneumonia |
| VTE | venous thromboembolic disease |
Introduction
Traumatic injury is a growing epidemic, particularly impacting low-income and middle-income countries. Approximately 4.4 million people die from trauma-related incidents annually World Health Organization (WHO), accounting for 8% of all deaths. Traumatic brain injury (TBI) alone afflicts nearly 5.5 million people worldwide annually, with TBI accounting for one-third to half of all deaths—a disproportionate percentage of traumatic fatalities. These traumatic injuries place a significant burden on healthcare systems with prolonged hospitalizations and, for survivors, subsequent need for rehabilitation and aid. The economic costs associated with TBI are also extremely high. The annual economic cost of TBI in the United States is estimated to be approximately $48.3 billion, with a lifetime cost to the patient ranging from $85,000 to $4 million related to hospitalization, rehabilitation, unemployment, and future loss of productivity.
Those with more severe TBI have significantly longer hospitalizations and are less likely to be discharged home. Similarly, those with severe TBI (Glasgow Coma Scale [GCS] ≤ 8) have a 2.47 times higher rate of inpatient mortality compared to those with moderate TBI (GCS 9–12). Pulmonary complications related to severe TBI resulting from lung injuries, immobility, and prolonged mechanical ventilation—may adversely impact length of stay and outcomes. The risk of poorer outcomes is statistically increased in patients with concurrent TBI and acute lung injury (ALI) compared to those with TBI alone.
Spinal cord injuries (SCIs) afflict nearly 1 million patients per year globally, with 90% of these injuries a direct result of trauma, and place a disproportionate cost burden on the healthcare system, with an estimated annual cost of $1.7 billion in the United States. The leading cause of mortality among SCI patients is pulmonary complications. Although the level and degree of completeness of SCI are key determinants of outcome, the number of respiratory complications during initial hospitalization has a high predictive value with respect to the length and cost of stay. It follows that the risk of respiratory failure is directly related to the level of SCI, with higher levels and more complete injury posing a greater threat. High cervical injuries can affect the neurons of the phrenic nerve, causing dysfunction of the diaphragm. Lower injuries can also cause respiratory compromise by affecting the innervation of accessory respiratory muscles.
We review and highlight the unique challenges that exist in treating concomitant lung pathology in the setting of TBIs and SCIs. There is inherent clinical difficulty in treating concurrent brain/spinal cord and lung pathology, since there exists a dichotomy in treatment targets: what is safe and beneficial for the lung may be detrimental to the brain and spinal cord and vice versa. Therefore, intensivists must understand the best practices of pulmonary management in the setting of TBI and SCI.
Lung injury
The brain and the lungs do not exist in isolation but are intimately connected. It is not unexpected that injury to one vital organ may lead to secondary and subsequent complications in another. Patients with TBI or SCI are at increased risk of pulmonary complications such as neurogenic pulmonary edema (NPE), ventilation-associated pneumonia (VAP), acute respiratory distress syndrome (ARDS), and pulmonary embolism (PE). The 2 leading hypotheses of mechanisms of injury include: (1) systemic catecholamine release with activation of the sympathetic nervous system leading to a blast injury and (2) a second hit phenomenon due to superimposed infections, surgeries, and mechanical ventilation that contribute to further injury ( Fig. 1 ).
Factors that may promote pulmonary function may be deleterious to brain function and outcome. Our understanding of the treatment of lung pathologies is isolated from our understanding of the treatment of TBI because the majority of major ALI studies excluded TBI patients precisely due to this divergence in optimal targets. Therefore, the level of evidence to support specific pulmonary management in TBI patients is poor. We aim to explain the key considerations in managing cranial and spinal pathologies and highlight strategies for treatment in pulmonary disorders, with specific regard for the neuro population.
Mechanical ventilation is the mainstay of pulmonary management. Intubation with mechanical ventilation is recommended for airway protection in patients with severe TBI. Ventilator settings can be adjusted to optimize ventilation and oxygenation while minimizing potential complications. These parameters, including tidal volume, respiratory rate, and positive end-expiratory pressure (PEEP), need to be carefully monitored and tailored to each patient’s specific condition to ensure adequate gas exchange and prevent further pulmonary or cerebral injury. Adjustments to these settings can significantly impact the patient’s overall stability and recovery, making precise management essential in the care of patients with severe TBI ( Box 1 , Table 1 ).
Expected Interventions:
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Admission to ICU
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Endotracheal intubation and mechanical ventilation
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Serial evaluations of neurologic status and pupillary reactivity
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Elevate head of bed (HOB) 30° to 45°
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Analgesia to manage signs of pain (not ICP directed)
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Sedation to prevent agitation, ventilator asynchrony, etc. (not ICP directed)
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Temperature management to prevent fever
Measure core temperature
Treat core temperature above 38°C
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Consider antiseizure medications for 1w only (in the absence of an indication to continue)
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Maintain CPP initially ≥60 mm Hg
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Maintain Hb greater than 7 g/dL
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Avoid hyponatremia
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Optimize venous return from head (eg, keeping head midline, ensure cervical collars are not too tight)
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Arterial line continuous blood pressure monitoring
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Maintain SpO 2 ≥94%
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Recommended interventions:
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Insertion of central line
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End-tidal CO 2 monitoring
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| Variable | Targets from Patients without Brain Injury a | Potential Caveats for Patients with Brain Injury |
|---|---|---|
| V t | Maintain V t at 4–8 mL/kg PBW | Low V t may result in hypercapnea Hypercapnea may be poorly tolerated (ie, can increase ICP) in patients with baseline low-intracranial compliance |
| P plat | Maintain P plat at <30 cm H 2 O | P plat is often achieved by reduction of V t with the consequent potential for hypercapnea |
| PEEP | Higher PEEP (variably defined) advised in moderate to severe ARDS Maintain PEEP of at least 5 cm H 2 O | Potential for increasing ICP in supine position when PEEP exceeds ICP Potential for reduction of cardiac output and MAP, with consequent CPP reduction |
| ΔP | No specific target advised but strong observational data suggest increasing mortality with each additional 1 cm H 2 O ΔP > 15 cm H 2 O | ΔP reduction often achieved by reducing Vt with potential for hypercapnea ΔP reduction may also be achieved by increasing PEEP, with potential PEEP-related hemodynamic perturbations |
| Prone position | Initiate if P/F ≤150 | May increase ICP and decrease CPP Intracranial perturbations likely more severe in patients with worse brain injury |
| Sedation | Goal-directed titration in hyperacute phase to ensure ventilator-patient synchrony | Compromise neurologic examination Tissue accumulation with prolonged infusion Risk of propofol infusion syndrome with propofol |
| NMBA | Consider short courses only if unable to achieve LPV with appropriate sedation titration | No direct evidence for patients with TBI Compromise neurologic examination |
| Veno-venous ECMO | Consider for patients with very severe ARDS refractory to other measures, including prone positioning | Multiple neurologic complications, including seizure, ischemic stroke, and intracranial hemorrhage Longer circuit runs may require anticoagulation and increase risk of intracranial hemorrhage Current data limited to case reports and case series |
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