calca-protein--human and Brain-Injuries

We investigated the role of the clinical pulmonary infection score (CPIS), serum levels of procalcitonin (PCT), C-reactive protein (CRP), and serum amyloid A (SAA) in the detection of patients with early ventilator-associated pneumonia (VAP).. Observational study in a university hospital. In 58 patients with severe brain injury receiving mechanical ventilation, CPIS, PCT, CRP and SAA were evaluated at ICU entry and at days 3 to 4 of hospital stay for VAP diagnosis (confirmed by endotracheal aspirate or BAL cultures).. We found the following: (1) PCT at entry was increased in patients who later had early VAP develop (25 patients) compared to no VAP (median, 1.4 ng/mL; 25-75 percentiles, 0.14-0.78; vs median, 0.2 ng/mL; 25-75 percentiles, 0.76-2.4, p<0.001; sensitivity, 76%; and specificity, 75%); (2) CPIS increased at the day of VAP diagnosis, compared to entry (median, 6.6+/-1.1 vs 1.5+/-1.1, p<0.001; sensitivity, 97%; specificity, 100%), while other serum inflammatory markers did not change; and (3) deterioration in oxygenation and changes in tracheal secretions were the main determinants of CPIS changes.. PCT may be a useful marker to predict which patients subsequently have early VAP. The CPIS could help as an early way to detect the patients with early VAP and who need further diagnostic testing.

Topics: Adult; Aged; Biomarkers; Brain Injuries; C-Reactive Protein; Calcitonin; Calcitonin Gene-Related Peptide; Early Diagnosis; Female; Humans; Male; Middle Aged; Pneumonia, Ventilator-Associated; Prognosis; Protein Precursors; Retrospective Studies; Sensitivity and Specificity; Serum Amyloid A Protein; Ventilators, Mechanical

This prospective study evaluated serum procalcitonin (PCT) and C-reactive protein (CRP) as markers for systemic inflammatory response syndrome (SIRS)/sepsis and mortality in patients with traumatic brain injury and subarachnoid haemorrhage. Sixty-two patients were followed for 7 days. Serum PCT and CRP were measured on days 0, 1, 4, 5, 6 and 7. Seventy-seven per cent of patients with traumatic brain injury and 83% with subarachnoid haemorrhage developed SIRS or sepsis (P=0.75). Baseline PCT and CRP were elevated in 35% and 55% of patients respectively (P=0.03). There was a statistically non-significant step-wise increase in serum PCT levels from no SIRS (0.4+/-0.6 ng/ml) to SIRS (3.05+/-9.3 ng/ml) to sepsis (5.5+/-12.5 ng/ml). A similar trend was noted in baseline PCT in patients with mild (0.06+/-0.9 ng/ml), moderate (0.8+/-0.7 ng/ml) and severe head injury (1.2+/-1.9 ng/ml). Such a gradation was not observed with serum CRP There was a non-significant trend towards baseline PCT being a better marker of hospital mortality compared with baseline CRP (ROC-AUC 0.56 vs 0.31 respectively). This is the first prospective study to document the high incidence of SIRS in neurosurgical patients. In our study, serum PCT appeared to correlate with severity of traumatic brain injury and mortality. However, it could not reliably distinguish between SIRS and sepsis in this cohort. This is in part because baseline PCT elevation seemed to correlate with severity of injury. Only a small proportion of patients developed sepsis, thus necessitating a larger sample size to demonstrate the diagnostic usefulness of serum PCT as a marker of sepsis. Further clinical trials with larger sample sizes are required to confirm any potential role of PCT as a sepsis and outcome indicator in patients with head injuries or subarachnoid haemorrhage.

Topics: Adult; APACHE; Biomarkers; Brain Injuries; C-Reactive Protein; Calcitonin; Calcitonin Gene-Related Peptide; Diagnosis, Differential; Female; Hospital Mortality; Humans; Male; Middle Aged; Protein Precursors; Sepsis; Subarachnoid Hemorrhage; Survival Rate; Systemic Inflammatory Response Syndrome

Clinical and experimental evidence suggests that traumatic brain injury (TBI) leads to a systemic immune response. To examine whether TBI causes a release of procalcitonin (PCT) or neopterin (NT) into the circulation, we compared plasmatic mediator levels among multiple injured patients with or without TBI. In total, 98 trauma patients (24 with TBI only, 39 with extracranial injuries excluding TBI, and 35 with combined injuries) and 35 healthy volunteers were studied. Blood was sampled at 15 predefined time points within 132 h after injury and analysed for NT and PCT. Multivariate statistical comparisons were adjusted for different severity of head, thorax, abdomen and extremity injuries, as quantified by the Abbreviated Injury Scale (AIS). PCT was normal 3 h after trauma, but 24 h after extracranial injuries a massive release (median 3 ng/mL) was observed. Significant positive associations between injury severity and posttraumatic PCT levels were found for abdominal and extremity, but not for cranial or thoracic injuries. Only modest changes of marginal statistical significance were detected for NT. The maximum increase per AIS point was 9% (95% confidence intervals [CI]: 3-16%). The effect of TBI on NT release was significant only at 108 h posttrauma with a 5% (95% CI: 1-10%) increase per AIS point. TBI induces a release of PCT and NT into the plasma, but this effect seems to be smaller for intra- than for extracranial injuries, probably due to more extensive surgery for abdominal and extremity injuries.

Topics: Adult; Brain Injuries; Calcitonin; Calcitonin Gene-Related Peptide; Confidence Intervals; Female; Humans; Male; Middle Aged; Multiple Trauma; Multivariate Analysis; Neopterin; Prospective Studies; Protein Precursors; Time Factors