Analysis of hypoxic changes in traumatic shock patients

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The purpose of the study was to investigate the dynamics of post-traumatic hypoxia in traumatic shock patients. Thirty multiple-injured (excluding severe head injury) adult patients were studied. From day 1 to day 5 the following tests were performed: PaO2/FiO2 and SaO2 in arterial blood (ABL-2 'Radiometer'), lactate dehydrogenase (LDG) in arterial blood (enzyme assay, FP900), lactate and pyruvate in arterial blood (blood samples from femoral artery). In order to determine lung blood flow and alveolar ventilation, a lung rheogram was performed on 19 patients at the same time [1]. Patients were divided into two groups. In Group 1 patients (n = 10) PaO2/FiO2 <33.3 KPa on day 2, in Group 2 patients (n = 20) PaO2/FiO2 >33.3 KPa on day 2. Details of the PaO2/FiO2, lung blood volume, alveolar ventilation SaO2, lactate/pyruvate and LDG levels will be given for each of the 5 days for both groups. In the first group four patients died on the 3rd-4th day after the injury; in the second group five patients died and only one during the investigation period. In the first group five patients had thoracic damage (multiple broken ribs), in the second group only two patients had that kind of trauma. In conclusion: (1) thoracic damage leads to serious aggravation of post-traumatic hypoxia; (2) LDG is a good indicator of traumatic shock severity; and (3) the most probable cause of prolonged post-traumatic hypoxia is a decrease in LBF and a corresponding increase of ventilation/perfusion inequality.