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  • Title: [The course of extravascular lung water in severely injured patients in intensive care with and without thoracic trauma].
    Author: Mutz N, Neumann M, Hörmann C, Koller W, Putensen C, Putz G, Benzer H.
    Journal: Anaesthesist; 1990 Oct; 39(10):535-9. PubMed ID: 2278374.
    Abstract:
    In patients with multiple injuries, the development of permeability edema can be assumed. However, no uniform shape of this fluid accumulation can be found even in the presence of severe injuries. Based on the first clinical observations, our aim was to search for correlations between the development of extravascular lung water (EVLW) and the individual injury pattern in severely traumatized ICU patients. PATIENTS and METHODS. Our investigations were performed in 48 artificially ventilated ICU patients. According to the prevailing injury pattern patients were divided into three groups: group A: 18 patients (mean age: 32 years, mean Injury Severity Score (ISS) = 29) with isolated thoracic trauma; group B: 10 patients (mean age: 27 years, mean ISS = 42) with severe multiple trauma but without any thoracic injury; group C: 20 patients (mean age: 33 years, mean ISS = 43) with severe multiple trauma and concomitant thoracic trauma. In all patients (group A, B, C), EVLW was determined by means of a double indicator method on a daily basis from the patient's admission to the ICU (day of trauma) until day 10. Additionally, the hemodynamic parameters (heart rate, mean arterial pressure, mean pulmonary arterial pressure, pulmonary capillary wedge pressure and cardiac index) were determined at the same time. RESULTS. As shown in Fig 1, EVLW was slightly elevated on day 1. However, on day 2 EVLW decreased within normal values and remained in that range until the end of the observation period. On day 3 a slight and fleeting increase of EVLW, but within normal range, can be seen. In group B (Fig.2), EVLW can be observed within normal range within a period of 4 days. Starting from day 5 until day 7 a marked increase (p greater than 0.01) in EVLW can be seen. From that maximum point EVLW development reverses slightly until day 10--however, without returning to the normal range. In group C, a marked biphasic pattern can be seen due to EVLW maximum values on post-traumatic days 3 and 7. However, in this group the EVLW was in the pathological range during the whole observation period. No statistically significant differences could be seen, when looking at hemodynamic variables. CONCLUSION. Isolated thoracic trauma will not lead to a marked pathological elevation of EVLW within the lungs. Moreover, EVLW decreases rapidly within a short time period. Based on our results, it seems that severe extrathoracic injuries will intensify microvascular injury in the initial period, as shown in our patients in group C. Increase of EVLW at a later time (day 7), as observed in groups B and C, is possibly the expression of a mediator and activator-induced "septiformal" injury of the microvascular endothelium. This may be caused by the underlying massive peripheral soft-tissue trauma. Specific elevations of EVLW subsequent to the individual injury pattern can indicate that that process has begun and is responsible for the origin of the microvascular injuries.
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