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Published on: April 7, 2021
Protein C depletion early after trauma increases the risk of ventilator-associated pneumonia
Mitchell J Cohen1, Natasha Bir, Pamela Rahn
1Department of Surgery, University of California, San Francisco, California, USA. mcohen@sfghsurg.ucsf.edu
Insights
Low plasma protein C (PC) levels in trauma patients are linked to ventilator-associated pneumonia (VAP). Persistent low PC levels within 24 hours after injury indicate increased VAP risk.
Area of Science:
- Critical care medicine
- Trauma surgery
- Infectious disease
Background:
- Mechanically ventilated trauma patients face a high risk of ventilator-associated pneumonia (VAP).
- Reduced plasma protein C (PC) levels post-trauma are associated with coagulopathy and mortality.
- Tissue injury and shock increase VAP susceptibility in trauma patients.
Purpose of the Study:
- To investigate the association between early plasma protein C (PC) levels and the development of VAP in trauma patients.
- To test the hypothesis that low PC levels increase VAP susceptibility.
Main Methods:
- Studied 59 intubated trauma patients admitted to the critical care unit.
- Measured serial blood samples for coagulation factors, including protein C (PC).
- Diagnosed VAP using bacterial presence in bronchial lavage, chest X-ray infiltrates, and clinical signs (fever/elevated WBC).
Main Results:
- Patients who developed VAP had longer ventilator, hospital, and ICU days, and higher mortality.
- While PC levels decreased initially in all patients, those who acquired VAP had significantly lower PC levels at 12 and 24 hours post-injury.
- Lower soluble endothelial PC receptor (sEPCR) levels at 24 hours were observed in VAP patients.
Conclusions:
- Persistently low plasma PC levels within 24 hours post-trauma are associated with increased VAP risk.
- The protein C pathway's activation and potential consumption by inflammatory mediators may play a role in VAP development.
- Further research is needed to determine if PC influences the host response to nosocomial lung infections.
Introduction:
Mechanically ventilated trauma patients have a high risk for the development of ventilator-associated pneumonia (VAP). We have recently reported that reduced plasma protein C (PC) levels early after trauma/shock are associated with coagulopathy and mortality. Furthermore, trauma patients with tissue injury and shock are at higher risk for the development of VAP.
Objective:
We hypothesized that low PC levels early after trauma are associated with an increased susceptibility to VAP in trauma patients.
Methods:
Fifty-nine acutely injured, intubated trauma patients were admitted to the critical care unit. Serial blood samples were drawn and coagulation factors were measured. VAP was diagnosed by presence of bacteria on bronchial alveolar lavage specimen, bilateral infiltrates on chest roentgenogram, and fever or elevated white blood cell count.
Results:
There were no differences in demographic or injury characteristics between patients who developed VAP and those who did not. As expected, patients who developed VAP had more ventilator days, hospital days, intensive care unit days, and greater mortality (all p < 0.05). Patients in both groups had lower mean PC levels at 6 hours compared with baseline. Noninfected patients' PC subsequently returned to near baseline levels, whereas those patients who eventually acquired VAP had significantly lower PC levels at both 12 and 24 hours (12 hours: 79 vs. 96%, p = 0.05; 24 hours: 75 vs. 97% p = 0.02). Soluble endothelial PC receptor (sEPCR) levels were also lower at 24 hours (82 vs. 99% in the noninfected group, p = 0.04).
Discussion:
The activation of PC pathway early after trauma may protect the vascular endothelium by both its anticoagulant and cytoprotective effects. However, trauma patients who later developed VAP have significantly lower plasma levels of PC within 24 hours after injury, suggesting a possible consumption of this vitamin K-dependent protein and an inhibition of its activation by inflammatory mediators. EPCR is involved in the activation of PC and is also a mediator of its cytoprotective effects.
Conclusion:
Critically ill trauma patients have an early activation of the PC pathway, associated with a rapid decrease in the plasma levels of this protein and increase in EPCR. Plasma levels of PC return to normal levels within 24 hours in most patients. However, patients who go on to acquire VAP have persistently low plasma levels of PC in the immediate period after trauma. Whether PC could play a mechanistic role in the host response against nosocomial lung infection warrants further study.
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