BackgroundBevacizumab is used in addition to standard, platinum-based chemotherapy to treat advanced-stage ovarian cancer patients. Thrombosis is a well-documented adverse effect of bevacizumab.ObjectiveThe aim of this study was to identify predictive parameters for thromboembolic events in ovarian cancer patients and to explain how bevacizumab increases the risk of these events.Patients and MethodsFifty-seven FIGO stage III ovarian cancer patients who underwent cytoreductive surgery and chemotherapy were identified and included in this retrospective study. Twenty-six patients were treated with carboplatin and paclitaxel (CP) only (control group), and 31 patients received CP with bevacizumab (study group). The two groups were compared with regard to thrombosis risk factors and laboratory parameters (total leukocytes, platelet count, hemoglobin, APTT, prothrombin time, INR, fibrinogen levels, D-dimer concentration) before treatment, after each course of chemotherapy, and during thromboembolic events.ResultsOnly patients in the group receiving bevacizumab experienced venous thromboembolism (VTE) (p=0.03, χ² test). VTE occurred on average at the 13th cycle of chemotherapy. Patients who experienced VTE had increased BMI before chemotherapy as compared to patients with no thromboembolic event (27.2 vs. 23.3, p=0.005, Mann-Whitney test). D-dimer concentration before treatment was also elevated more in patients affected by VTE (3132.5) than in the non-VTE group (956.43) (p=0.0007, Mann-Whitney test). During the first four administrations of chemotherapy in patients with future VTE, there was a reduction in D-dimer concentration and an extension of APTT. A D-Dimer level higher than 485 ng/mL prior to first chemotherapy indicates for a risk of VTE with 94% sensitivity and 36% specificity.ConclusionsAn elevated D-dimer level and high BMI before chemotherapy are risk factors for VTE in ovarian cancer patients receiving bevacizumab. Bevacizumab possibly increases the risk for VTE.

Despite a failure of intrapartum treatment in the fourth case, we strongly recommend this procedure for deliveries of fetuses with a suspicion of airway obstruction.

IntroductionFormation of a capsule is a natural inflammatory response to a foreign body such as a breast implant. Breast capsular contracture is the most severe complication of implant surgery.AimTo evaluate breast tissues and the periprosthetic reaction with sonoelastography.Material and methodsNineteen patients aged 20-41 underwent breast augmentation with silicone-filled implants. Their 38 breasts were evaluated before surgery, and 7 and 14 days after surgery. Whole breast stiffness was measured by applanation tonometry. Patients underwent shear wave elastography and Young's moduli of breast tissues and the periprosthetic capsule were estimated. During surgery patients underwent standard anaesthesia and were released home 2 days later after removal of drainage. Each day, patients completed the pain visual analogue scale questionnaire separately for left and right breasts.ResultsApplanation tonometry did not correlate with any parameter. In shear wave elastography we observed statistically significant changes in elasticity of all breast tissues with the highest values on day 7 after surgery and decreasing on day 14. The correlations between pain and capsule elasticity in lower quadrants measured were significant between days 4 and 10, whereas correlations of pain with applanation tonometry were insignificant. Glandular tissue elasticity in lower quadrants did not correlate with pain, whereas in upper quadrants there was a significant correlation on days 6-10. Fatty tissue, muscle and thoracic fascia elasticity did not correlate with breast pain. Breast implant volume correlated with pain only shortly after surgery, but did not correlate with any sonoelastographic parameters.ConclusionsBreast pain correlates strongly with periprosthetic stiffness in elastography 4 to 10 days after breast augmentation, suggesting the possible role of an inflammatory reaction.

A serious case of barium intoxication from suicidal ingestion is reported. Oral barium chloride poisoning with hypokalemia, neuromuscular and cardiac toxicity, treated with intravenous potassium supplementation and hemodialysis, was confirmed by the determination of barium concentrations in gastric contents, blood, serum and urine using the inductively coupled plasma mass spectrometry method. Barium concentrations in the analyzed specimens were 20.45 µg/L in serum, 150 µg/L in blood, 10,500 µg/L in urine and 63,500 µg/L in gastric contents. Results were compared with barium levels obtained from a non-intoxicated person.