Abstract
BACKGROUND: Blunt pulmonary contusions are associated with severe chest injuries and are independently associated with worse outcomes. Previous preclinical studies suggest that contusion progression precipitates poor pulmonary function; however, there are few current clinical data to corroborate this hypothesis. We examined pulmonary dynamics and oxygenation in subjects with pulmonary contusions to evaluate for impaired respiratory function.
METHODS: A chest injury database was reviewed for pulmonary contusions over 5 years at an urban trauma center. This database was expanded to capture mechanical ventilation parameters for the first 7 days on all patients with pulmonary contusion and who were intubated. Daily :, oxygenation indexes (OI), and dynamic compliances were calculated. Pulmonary contusions were stratified by severity. The Fisher exact and chi square tests were performed on categorical variables, and Mann-Whitney U-tests were performed on continuous variables. Significance was assessed at a level of 0.05.
RESULTS: A total of 1,176 patients presented with pulmonary contusions, of whom, 301 subjects (25.6%) required intubation and had available invasive mechanical ventilation data. Of these, 144 (47.8%) had mild-moderate pulmonary contusion and 157 (52.2%) had severe pulmonary contusion. Overall injury severity score was high, with a median injury severity score of 29 (interquartile range, 22–38). The median duration of mechanical ventilation for mild-moderate pulmonary contusion was 7 d versus 10 d for severe pulmonary contusion (P = .048). All the subjects displayed moderate hypoxemia, which worsened until day 4–5 after intubation. Severe pulmonary contusion was associated with significantly worse early hypoxia on day 1 and day 2 versus mild-moderate pulmonary contusion. Severe pulmonary contusion also had a higher oxygenation index than mild-moderate pulmonary contusion. This trend persisted after adjustment for other factors, including transfusion and fluid administration.
CONCLUSIONS: Pulmonary contusions played an important role in the course of subjects who were acutely injured and required mechanical ventilation. Contusions were associated with hypoxemia not fully characterized by : , and severe contusions had durable elevations in the oxygenation index despite confounders.
Introduction
Blunt pulmonary contusions are pulmonary parenchymal injuries commonly encountered in patients with blunt chest injury. The incidence of pulmonary contusion in adult chest- injured populations can range from 5.2% to 50%.1,2 Previous investigation in animal models demonstrated that pulmonary contusions evolve after alveolar capillary disruption, with resultant interstitial fluid accumulation.3 This fluid disrupts gas exchange due to ventilation-perfusion mismatch, increased intrapulmonary shunting, and decreased compliance. Traditional crystalloid based resuscitative strategies demonstrate an early contusion expansion or progression.3 Historically, observational studies in humans have shown associations among poor respiratory function, ARDS, morbidity, and mortality in the setting of pulmonary contusions.4-6
Evidence over the past decade suggests that pulmonary contusions may have less of a clinical effect than previously assumed,7-9 but these studies do not stratify pulmonary contusions by severity. We recently demonstrated strong positive associations between moderate-to-severe pulmonary contusion with the duration of mechanical ventilation, ICU length of stay, and hospital length of stay.10 Moreover, moderate-to-severe pulmonary contusions were independently associated with a risk of respiratory failure.10 The previous findings suggest that the pathophysiology of pulmonary contusions precipitates worse outcomes, for example, by changing alveolar gas diffusion or by affecting respiratory dynamics. To date, there is a paucity of direct clinical data to give evidence for or against pulmonary physiology derangements other than hypoxia in the setting of pulmonary contusion. Patients with respiratory failure who require invasive mechanical ventilation may benefit from a more complete understanding of the consequence of pulmonary contusion on respiratory function. By building on our previous work, we hypothesized that severe pulmonary contusion may be associated with worse oxygenation and compromised pulmonary dynamics.
Quick Look
Current Knowledge
Pulmonary contusions are common in thoracic trauma. Previous studies in animal models showed contusions progress and are associated with gas exchange abnormalities. The trend toward lung-protective ventilation and decreased crystalloid resuscitation may have improved the clinical impact of contusions over the past several decades; however, severe contusions continue to be associated with worse outcomes.
What This Paper Contributes to Our Knowledge
In subjects who were injured and required invasive mechanical ventilation, pulmonary contusions were associated with a prolonged hypoxemia and lower oxygenation index. These oxygenation changes appear to be associated with PEEP and peak inspiratory pressure changes, after adjusting for confounders, including the volume of intravenous fluid administered.
Methods
We performed a retrospective review, over a 5-year period between January 2014 and December 2018 at a single urban level I trauma center, of patients who had sustained blunt chest-wall injury. All adult patients (age > 15 y) with bony chest-wall injuries were screened for pulmonary contusions as documented on computed tomography imaging from a prospectively maintained institutional injury database. Subjects were included in this study cohort if they had pulmonary contusions and required intubation and invasive mechanical ventilation for at least 24 h during the initial admission after injury. Patients were excluded for death or discharge within 48 h if invasive mechanical ventilation was started > 48 h after injury or if there were incomplete respiratory or radiographic data. A portion of this database has previously been used11,12; however, the current dataset was expanded to include respiratory dynamics and oxyg-enation information. Data gathering and analysis was conducted as per University of Cincinnati Institutional Review Board (IRB) approval (IRB 2017–2673).
Data on blood gas measurements and respiratory data were collected for up to 7 d of invasive mechanical ventilation. Dynamic respiratory data collected included breathing frequency, tidal volume (), peak inspiratory pressure, mean airway pressure (), PEEP, , and . Arterial oxygen to inspired oxygen ratio is calculated as /. Oxygenation index (OI) is calculated as the ( × × 100)/. Dynamic compliance is /peak inspiratory pressure – PEEP). Pulmonary contusions were stratified by severity by using the Blunt Pulmonary Contusion 18 score.2,13 This score assigns a value of 0–3 based on contusion density in each of the upper middle and lower lung zones seen on computed tomography of both the left and right lungs for a composite score of 0–18. Severe pulmonary contusion was defined as a Blunt Pulmonary Contusion 18 score ≥ 4.2,10,13
Intravenous fluids administered over the first 5 d of hospitalization were recorded. These were defined as crystalloid fluids, including parenteral medications, electrolyte replacement solutions, and parenteral nutrition. Blood products transfused, including red blood cells and fresh frozen plasma, were similarly recorded over the same time period. Platelets, cryoprecipitate, and other blood fractions, which represent a small amount of volume and overall use, were excluded. Daily liquid output volumes were recorded in milliliters and included urine, liquid feces, drain outputs, blood loss, and dialyzed volume removed. Volume status was analyzed as a daily net volume subtracting intake crystalloid from outputs. Data collection and analysis was conducted as per University of Cincinnati IRB approval (IRB 2017–2673).
Data were analyzed by using descriptive statistics and univariate analysis. All analyses were conducted by using SAS 9.4 (SAS Institute, Cary, North Carolina). Non-normally distributed continuous data were evaluated according to medians with interquartile ranges (IQR), and discrete data are presented as mean with percentage. Univariate statistics were evaluated by using Fisher exact tests and chi-square analysis for categorical variables. Continuous variables were evaluated by using non-parametric Mann-Whitney U-tests. A multivariable logistical regression analysis was performed to evaluate for confounding factors of significant respiratory physiology findings. Significance was determined by a P value of < .05.
Results
Over the course of 5 years, 3,836 patients presented with blunt chest-wall injuries, of whom 1,176 (30.6%) had concomitant pulmonary contusion. Of these patients, 301 (25.6%) subjects required intubation and invasive mechanical ventilation and had complete records available for review over the first 2 d after injury (Fig. 1). The overall severity of injury was high (median [IQR] injury severity score 29 [22–38]), hospital and ICU lengths of stay were long (16 d and 12 d, respectively), with 46 deaths (15.3%) within 30 d of hospital admission. When stratified by pulmonary contusion severity, 144 subjects (47.8%) had mild-moderate pulmonary contusion and 157 (52.2%) had severe pulmonary contusion. The baseline subject characteristics between mild-moderate pulmonary contusion and severe pulmonary contusion groups were well matched, and only age was significantly different (Table 1).
By contrast, the injury characteristics of the severe pulmonary contusion group revealed significantly worse chest-wall injuries and more frequent occurrence of hemothorax and pneumothorax as well as the need for tube thoracostomy placement compared with the mild-moderate pulmonary contusion group (Table 1). There was no difference between the subjects with severe brain injury (defined as a head abbreviated injury score > 3) between the pulmonary contusion groups. The median (IQR) duration of invasive mechanical ventilation for mild-moderate pulmonary contusion was 7 (3–14.25) d versus 10 (4–18) d for severe pulmonary contusion (P = .048). The mild-moderate pulmonary contusion group had a lower rate of pneumonia then did the severe pulmonary contusion group (16.6% vs 32.5% respectively; P = .002). During the study period, a chest reconstruction program was initiated, and 12 subjects with contusions and mechanical respiration underwent rib plating, 1 with mild-moderate pulmonary contusion and 11 with severe pulmonary contusion (P =.003).
The subjects were assessed for cohort dropout by assessing survivorship and the ongoing need for invasive mechanical ventilation per day. Overall, 144 subjects (47.8%) remained on invasive mechanical ventilation for 7 d: 61 subjects (42.4%) in the mild-moderate pulmonary contusion cohort and 83 subjects (52.9%) in the severe pulmonary contusion cohort. During the first 7 d, 25 subjects (8.3%) died: 14 (9.7%) in the mild-moderate pulmonary contusion cohort and 11 (7%) in the severe pulmonary contusion cohort. When comparing the need for mechanical ventilation by severity of contusion, the severe pulmonary contusion group tended to require mechanical ventilation longer than did the mild-moderate pulmonary contusion group. This trend reached significance on postinjury day 5 when 67.5% (n = 106) of the subjects with severe pulmonary contusion remained intubated compared with only 55.6% (n = 80) of those with mild-moderate pulmonary contusion (P = .034) (Fig. 2).
All the subjects displayed moderate hypoxemia that worsened until a nadir by day 4–5 after intubation (median : range of 183–203). Severe pulmonary contusion was associated with significantly worse early hypoxia on day 1 (median : 204 vs 258; P = .002) and day 2 (median : 208 vs 230; P = .02) versus mild-moderate pulmonary contusion. Severe pulmonary contusion also had a higher OI over the entire course of intubation and was significantly higher than mild-moderate pulmonary contusion on days 1, 2, 3, and 5 (Fig. 3). There was a nonsignificant trend toward lower dynamic compliance for severe pulmonary contusions compared with mild-moderate pulmonary contusions in the first 3 days of intubation but without a significant decrease. The constituent variables of OI were individually analyzed for significance. Only and peak inspiratory pressure demonstrated a significant difference between the mild-moderate pulmonary contusion and severe pulmonary contusion cohorts (Fig. 4). Other respiratory variables, such as , PEEP, , and , did not demonstrate significant differences between the mild-moderate pulmonary contusion and severe pulmonary contusion cohorts over the first week.
To evaluate the effects of other factors on OI, a multivariable regression analysis was performed. The subjects in the mild-moderate pulmonary contusion group received a mean ± SD of 3.3 ± 7.6 units of transfusion over the first 5 d of hospitalization compared with 3.5 ± 7.8 units in the severe pulmonary contusion group (P = .68). Over the same period, the average total intravenous fluid administration of the mild-moderate pulmonary contusion versus severe pulmonary contusion groups was 2,877 ± 4,594 versus 2,887 ± 4,592 mL (P = .84). Adjustments for age, body mass index, injury severity score, net fluid balance by day 5, and transfusion requirements in the first 24 h were undertaken. After adjustment, OI remained significantly higher for the severe pulmonary contusion group for every day after the first 24 h. Adjusted OI over time can be seen in Table 2.
Discussion
In this study, we presented one of the largest patient populations to date that demonstrated that severe blunt pulmonary contusions were associated with worse pulmonary function. These severe pulmonary contusions were associated with worse early hypoxemia, which lasted for several days. In addition, more severe contusions were associated with higher mean and peak airway pressures as well as a prolonged increase in OI, which may persist over the course of the first week after injury. Blunt pulmonary contusions are injuries that are well known to evolve over time in the early postinjury period,14,15 but there is a paucity of modern patient-level data about associated oxygenation and respiratory dynamic changes.
Previous work showed relationships between pulmonary contusions and hypoxemia to some degree, but most studies had either small uncontrolled sample sizes or significant confounding. For example, Kishikawa et al16 reported on hypoxia and decreased functional residual capacity in the setting of pulmonary contusion that was suggested to last up to 6 months after the injury, but more than half of the subjects studied had flail chest, which is a well-known independent predictor of respiratory dysfu-nction. Hypoxemia in the setting of pulmonary contusion has previously been observed. For example, Tyburski et al13 noted that rapidly increasing, or progressing, contusions had associated worsening hypoxemia, and Bilello et al17 reported hypoxemia in the setting of pulmonary contusion that required mechanical ventilation seemed to be a predictor for successful ventilator liberation.
However, significant factors intuitively associated with hypoxemia traditionally have not been controlled for in much of the literature.18 In recognizing this, we attempted to control for this multifactorial confounding of pulmonary function in trauma by accounting for age, obesity, a wide variability of other associated injuries, blood product transfusion, and crystalloid fluid administration. Even with regular use of lung-protective ventilation, crystalloid fluid restrictive treatment strategies, and transfusion-guided trauma resuscitation, each of which is significantly different when compared with just 15 years ago, it is notable that severe pulmonary contusion continues to remain an independent clinically important entity.
We previously demonstrated that the presence or absence of pulmonary contusion is a very coarse assessment of injury. We identified that more severe pulmonary contusions are associated with and may portend worse outcomes (a longer duration of invasive mechanical ventilation, ICU stays, and hospital lengths of stay as well as readmissions).10 As pulmonary contusion severity worsens, it would be useful to be able to demonstrate what interventions may be able to ameliorate or curb these poor outcomes. We structured this study to evaluate pulmonary function in the setting of the most-severe pulmonary contusions, such as those patients being exposed to positive-pressure ventilation. Our hope is that the identification of functional derangements, such as high peak inspiratory pressure and , could lead to novel rescue or treatment strategies to improve pulmonary function. Examples of such therapies may include the early use of pressure volume curves to titrate PEEP, mechanical ventilation mode selection to mitigate compliance changes, or development of a pulmonary contusion bundle in which fluids are minimized below a certain threshold or OI is trended.
An interesting phenomenon in our early data showed a trend toward increased OI in both the mild-moderate and severe contusion groups starting on day 3, which may coincide with resuscitation fluid mobilization. It is possible that this residual evidence of the traditional contusion blossoming effect,3,15 and further study into in situ contusion physiology may improve the understanding of the consequences of modern resuscitation fluid management. Our findings are at the intersection of patient management and highly granular data. Emerging technologies, for example, machine learning, may offer assistive technology to be able to find the needle in the proverbial haystack of patient data in real time. Identification of early predictors of poor outcomes from pulmonary contusions may help to steer patients away from adverse events. The ability to better predict the clinical course of pulmonary contusions may assist clinicians to decide the timing of critical interventions such as operations like chest-wall reconstruction. Unfortunately, our study encompassed a time period both before and during the introduction of a chest reconstruction program, and conclusions cannot be drawn from subjects who had rib plating and were included here.
Our study was not without limitations. First, this was a retrospective review from prospectively maintained institutional databases that track chest-wall injuries and mechanical ventilation parameters for the subjects who were intubated. Significant confounding information and treatment intentions may not be captured in the electronic medical record. Second, we were unable to use static lung compliance as a measure due to the infrequency with which it is obtained in our clinical practice. Our hope was that OI, as a method to account for nonelastic resistance and dynamic compliance to portray the changes in peak inspiratory pressure and PEEP utilization, serves as a reasonable surrogate for analysis. Third, due to the heterogenous nature of injury patterns, we were unable to account for effects of other injuries that may affect oxygenation (eg, more detailed information about head injuries and infectious complications) without significantly reducing the size of our sample. Fourth, there is room for improvement in the assessment of contusion severity because the skew of the Blunt Pulmonary Contusion 18 score may not adequately graduate clinically important contusions. However, as a clinical assessment tool, it remains the best bedside-usable one available for contusions. Also, restricting our subjects of study to patients who were intubated excluded many other patients who may have had severe contusion but had a more indolent course. Moreover, in the subjects with polytrauma, the reason for intubation and subsequent extubation within the first 7 days may not be solely due to primary pulmonary reasons.
Conclusions
Pulmonary contusions factored significantly in the course of subjects who were critically injured and required invasive mechanical ventilation. Contusions were associated with poor oxygenation not fully characterized by : and more severe contusions showed a longer impairment of OI than : over the first week of intubation. Severe contusions seem to independently correlate with worse OI even after adjustment for factors such as crystalloid fluid administration. Further prospective study may also demonstrate changes in dynamic compliance as well.
ACKNOWLEDGMENTS
The authors thank Lauren Andreasson, Timothy Pritts, John Shin, and Devon Wakefield for their assistance and insight with this study.
Footnotes
- Correspondence: Christopher F Janowak MD, Department of Surgery, University of Cincinnati, 231 Albert Sabin Way, ML 0558, Cincinnati, OH 45267. E-mail: christopher.janowak{at}uc.edu
↵† Deceased.
A version of this article was presented by Drs Zingg and Janowak at the Chest Wall Injury Summit, held April 22, 2021, in Denver, Colorado.
The authors have disclosed no conflicts of interest.
Authors have disclosed no conflicts of interest.
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