Background: Detection of risk factors for an air embolism in the left atrium, left ventricle, or systemic circulation (systemic air embolism, SAE) during a percutaneous core needle biopsy (PCNB) of the thorax.Methods: In a retrospective observational study, all PCNBs of the thorax in 610 patients between 2007 and 2009 were analyzed. The SmartStep™ technique (General Electric) was used for the biopsy, with which the examiner can prepare a batch of three 1.25-mm or 2.5-mm collimated slices within a second using a foot switch in the CT room to check the needle position. The image data thus generated and the control CT scans that followed were examined retrospectively for the presence of intravascular air. Intravascular air was defined as two or more adjacent voxels with absorption values of < -200 HU in the left atrium, left ventricle, aorta, or arteries during or after the procedure. The univariate statistical analysis of categorical variables was made using 2 by 2 tables and the Fisher test. The groups were compared using the Mann-Whitney test. Finally, a multivariate logistic regression analysis was used to identify independent risk factors for the occurrence of an SAE.Results: The radiological incidence of an SAE during a PCNB was 3.8% (23/610 patients), whereas the clinically apparent incidence was 0.49%. Two patients developed clinical symptoms consisting of transient hemiplegia or transient amaurosis; one died due to a fatal SAE of the coronary arteries. The mortality was thus 0.16%. The depth of the needle in the lesion (Wald: 6.859), endotracheal anesthesia (Wald: 5.721), location of the lesion above the level of the left atrium (Wald: 5.159), and prone position of the patients (Wald: 4.317) were independent risk factors for the incidence of an SAE (p < 0.05 each). Using explorative criteria, the acute angle of the needle to the tumor surface, and the transition of ventilated lung were independent factors. The frequency of biopsies, needle penetration depth, and tumor location near the diaphragm or in the lower lobe also played a subordinate role, not however, the needle penetration depth through the lung.Conclusion: If possible, the PCNB should be performed under local anesthesia. We recommend avoiding endotracheal anesthesia and prone position. Whenever possible, patients should be positioned on the back in such a way that the tumor is lower than the left atrium. The tip of the needle should be within the tumor during the biopsy procedure.

Circulating serum levels of procalcitonin rise significantly during bacterial infection. Because calcitonin is known to be a monocyte chemoattractant, we investigated whether procalcitonin, a prohormone of calcitonin, also affects leukocyte migration. Prospective, controlled in vitro study. University research laboratories. Forearm venous blood polymorphonuclear neutrophils and monocytes were isolated from healthy human donors. Cell migration was assessed in a blindwell chemotaxis chamber. The distance of migration into filter micropores was measured. To biochemically confirm functional data on cell migration, effects of procalcitonin on cellular levels of cyclic adenosine monophosphate were measured by high-performance liquid chromatography. Both procalcitonin and calcitonin elicited dose-dependent migration of monocytes at concentrations from the femtomolar to the micromolar range. Neutrophils did not migrate toward procalcitonin or calcitonin, nor was their oxygen free radical release affected as measured fluorimetrically. Checkerboard analysis of monocyte locomotion revealed procalcitonin-induced migration as true chemotaxis. Pretreatment of monocytes with procalcitonin or calcitonin rapidly deactivated their migratory response to formyl-Met-Leu-Phe, and both also induced homologous deactivation of migration. Procalcitonin elevated levels of cyclic adenosine monophosphate in monocytes. In vitro procalcitonin is a monocyte chemoattractant that deactivates chemotaxis in the presence of additional inflammatory mediators. Procalcitonin stimulates cyclic adenosine monophosphate production in monocytes, suggesting that its action may be specific and comparable with calcitonin, which exerts similar functions.

To assess the relations between anemia, serum erythropoietin (EPO), iron status, and inflammatory mediators in multiply traumatized patients. Prospective observational study. Intensive care unit. Twenty-three patients suffering from severe trauma (injury severity score ≥30). None. Blood samples were collected within 12 hrs after the accident (day 1) and in the morning on days 2, 4, 6, and 9 to determine blood cell status, serum EPO, tumor necrosis factor-α (TNF-α), soluble tumor necrosis factor-receptor I (sTNF-rI), interleukin-1 receptor antagonist (IL1-ra), interleukin-6 (IL-6), neopterin, and iron status, respectively. Hemoglobin concentration was low at admission (mean, 10.0 g/dL; range, 6.8–12.9 g/dL) and did not increase during the observation time. Serum EPO concentration was 49.8 U/L (mean value) on day 1 and did not show significant increases thereafter. No correlation was found between EPO and hemoglobin concentrations. TNF-α remained within the normal range. sTNF-rI was high at admission and increased further. IL1-ra was above the normal range. IL-6 was very high at admission and did not decrease thereafter. The initial neopterin concentration was normal, but increased until day 9. Serum iron was significantly decreased on day 2 posttrauma and remained low during the study. Serum ferritin increased steadily from day 2, reaching its maximum on day 9. In contrast, concentrations of transferrin were low from admission onward. Multiply traumatized patients exhibit an inadequate EPO response to low hemoglobin concentrations. Thus, anemia in severe trauma is the result of a complex network of bleeding, blunted EPO response to low hemoglobin concentrations, inflammatory mediators, and a hypoferremic state.