Role of angiotensin-converting enzyme as prognostic marker in thoracic trauma: A prospective observational study.

BACKGROUND: Chest injuries, accounting for 25% of all trauma-related deaths, are one of the main causes of death in young adults. Our priority is the early identification of life-threatening injuries both immediate and delayed. The role of various biomarkers, such as Clara cell protein 16, von Willebrand factor, interleukin-6, tumor necrosis factor, and angiopoietin, has been studied in trauma-related acute respiratory distress syndrome (ARDS). Serum angiotensin-converting enzyme (ACE) levels have been studied in non-trauma-related ARDS. The aim of this prospective observational study was to evaluate the role of ACE levels as a prognostic marker in thoracic trauma. METHODS: A prospective observational study was conducted to evaluate serum ACE levels in thoracic trauma patients and to explore its prognostic potential with regard to clinical outcome. A total of 48 thoracic trauma patients were included in the study. RESULTS: The mean ACE level in the study population was 66.54+-11.18. A strong positive correlation was found among serum ACE levels and Thoracic Trauma Severity Score (TTSS). CONCLUSION: Our study demonstrates that serum ACE levels are increased in thoracic trauma patients with higher levels, indicating the severe nature of trauma in concordance with increased TTSS scores.

The Role of Cystathionine-γ-Lyase In Blunt Chest Trauma in Cigarette Smoke Exposed Mice.

Pretraumatic cigarette smoke (CS) exposure aggravates posttraumatic acute lung injury (ALI). Cystathionine-γ-lyase (CSE) protects against ALI and CS exposure-induced chronic obstructive lung disease (COPD). Therefore, we tested the hypothesis whether genetic CSE knockout (CSE) would aggravate posttraumatic ALI after CS exposure. After 3 to 4 weeks of CS exposure, anesthetized wild-type (WT) and CSE mice underwent blunt chest trauma, surgical instrumentation and 4 h of lung-protective mechanical ventilation. We measured hemodynamics, lung mechanics, gas exchange, metabolism, and acid-base status together with blood and tissue cytokine and chemokine levels, tissue expression of mediator proteins, parameters of oxidative and nitrosative stress, and histology. CSE mice without CS exposure showed higher cytokine and chemokine levels, and this was further enhanced by CS exposure, particularly in males. CS exposure in WT mice aggravated posttraumatic alveolar membrane thickening, dystelectasis, and inflammatory cell accumulation, which was associated with higher thoracopulmonary compliance. Pretraumatic CS exposure in CSE mice produced a similar response, except for less alveolar membrane thickening, most likely due to lung hyperinflation. CS-exposed WT mice showed the most pronounced metabolic acidosis, while CS exposure in CSE mice resulted in the lowest blood glucose levels. Urinary output and anesthesia rate were highest in male CS-exposed CSE animals. In conclusion, in murine acute-on-chronic pulmonary disease, CSE knockout aggravated posttraumatic inflammation, which was further worsened upon pretraumatic CS exposure, and this effect was particularly pronounced in males. Hence, maintaining CSE expression is critically important for stress adaptation during ALI and CS-induced COPD, most likely in a gender-dependent manner.

Creatinine-kinase-MB determination in non-cardiac trauma: its difference with cardiac infarction and its restricted use in trauma situations.

Cardiac injuries can be life threatening. The possibility of late complications urges the practitioner to search for any evidence of cardiac trauma. But the diagnosis of cardiac injury remains difficult. Electrocardiography and cardiac enzyme determination are most widely used, because they are readily available. Many studies advocate creatine-kinase-MB (CK-MB) isoenzyme levels as a sensitive test for cardiac contusion. Others have discarded CK-MB testing as useless in trauma situations. An elevated CK-MB value in haemodynamically stable patients may confuse the individual practitioner. To better clarify its role we investigated the course of CK/CK-MB release after trauma, with no or only a very small chance of cardiac injury and compared it with patients with severe chest trauma having cardiac complications. A total of 25 trauma patients with only skeletal muscle injury were studied. Blood samples were taken during the first 4 days after trauma. These results were compared with those of a group of 91 consecutive patients with severe chest injury, including 10 with cardiac complications. Initial results in skeletal trauma patients were indicative of cardiac injury (CK > 5% of total CK and at least 20 U/l) in 10 patients. These findings were identical to those found in patients with severe chest injury having cardiac complications. CK/CK-MB tests are frequently positive after trauma without cardiac injury, even when selective criteria are used. The time each isoenzyme is released from muscle tissue after trauma greatly influences the outcome of the test. As this release does not occur at the same moment for each isoenzyme, the test result is very much time-dependent. As a result of these findings CK-MB testing tends to cause more confusion than clarification in trauma situations. We therefore eliminated CK-MB testing from our trauma protocol as a screening investigation for cardiac injury.

[Diagnostic value of CK-MB isoenzyme determinations in children with craniocerebral injuries and polytrauma]. / Diagnostischer Wert von CK-MB-Isoenzym-Bestimmungen bei Kindern mit Schädelhirntrauma und Polytrauma.

Total creatine kinase (CK) and its myocardial isoenzyme (CK-MB) were determined in 71 children with isolated acute head injury (N = 30), with head injury and polytrauma but without chesttrauma (N = 11) and with head injury and polytrauma including chest trauma (N = 30) on the second and third day after injury. Electrocardiograms were recorded in 56/71 children on each of the first three days in hospital. Elevations of CK-MB isoenzyme over 6% respectively over 10% of total CK are found as frequently in children with head injury without chest trauma as in children with head trauma and chest trauma. In addition there is no significant correlation between the level of the CK-MB and the incidence of ECG features characteristically associated with heart contusion. This study shows that the determination of CK-MB cannot be used as a criterion for diagnosing heart contusion in children with head injury. The finding of CK-MB in the serum of 53% children with isolated head injury exceeding 6% of total CK, and in the serum of 33% children exceeding 10% of total CK strongly suggests myocardial damage to be a frequent complication of cerebral damage with consecutive extreme sympathetic stimulation.

The postmortem determination of CK isozymes in the pericardial fluid in various causes of death.

The authors have studied the CK isozyme pattern in the pericardial fluid of 100 cadavers autopsied in the Anatomic Forensic Institute of Granada. The samples were classified into several groups according to the cause of death: --Multiple trauma with thoracic contusion --Pneumonia and pulmonary embolism --Mechanical asphyxia --Cranio-cerebral trauma --Acute haemorrhage --Myocardial infarction --Others. The results showed that the CK isozyme pattern of pericardial fluid provides useful postmortem information of cardiac "status", adding to the diagnostic potential of CK isozymes.

Hyperamylasemia in critically injured patients.

We found that in traumatic shock patients without pancreatic injury, hyperamylasemia occurs in high frequency [49 of 61 (80%)]. Isoenzyme studies of 19 of these patients revealed 18 of them (94%) to have the salivary type of hyperamylasemia. Further, based on the results of the present study, the salivary gland as the organ of origin and the permeability of its cell membranes are suggested as the mechanism for traumatic hyperamylasemia.

CPK-MB isoenzume determinations in blunt chest trauma.

To identify the most sensitive screening test for cardiac contusions, a series of 35 patients with blunt chest trauma was evaluated with serial electrocardiograms (ECGs)- creatine phosphokinase isoenzymes, and serum enzymes (serum glutamic-oxaloacetic transaminase, lactic dehydrogenase, and creatine phosphokinase). Twenty of the 35 patients had diagnoses of cardiac contusions by ECG. Three with contusions developed complications. Although isoenzyme elevation was present in most patients sustaining blunt chest trauma, no complications of the injury were seen in patients with elevated enzymes and normal ECGs. The ease of obtaining ECGs and their reliability in identifying patients who will have complications make it the best screening procedure for the diagnosis of cardiac contusions.