Cerebrospinal fluid (CSF) shunting into the pleural space can cause complications such as long-standing pleural effusions and trapped lung. These complications can be difficult to manage due to the propensity of effusions to recur, and the irreversible nature of trapped lung. This report describes the case of a woman with a pleural CSF shunt who developed chronic pleural effusions and trapped lung over two years, following a 24-year period without any respiratory shunt complications. Management options for this patient included thoracentesis, lung decortication, insertion of an indwelling pleural catheter, and shunt revision. Advocating for pleural shunt revision when symptomatic or increasingly large pleural effusions occur may prevent the development of trapped lung.

Introduction: Doxorubicin (DOX) is an anthracycline that is used for a wide range of malignant conditions. However its off-target effect causes cardiotoxicity. Dexrazoxane (DEX) is the only clinically approved cardioprotective agent against anthracycline toxicity. Its activity has been attributed to its iron-chelating effects. The aim of this project was to assess the protective effect of DEX against DOXinduced toxicity in an HL-1 cardiomyocyte model, and to investigate an early stage marker involved in cellular damage by DOX. Methods: HL-1 cardiomyocytes were cultured for the purpose of bioactivity studies. The half maximal inhibitory concentration (IC-50) of DOX was established. Then the ability of DEX to recover damaged cells was assessed using measures of cell viability. A variety of DEX concentrations with HL-1 s were studied in vitro. Finally, an early stage marker involved in cellular damage by DOX was examined. An assay kit was used for the study of dsDNA breaks through the detection of γ-H2AX -a phosphorylated histone historically proven as a highly specific and sensitive molecular marker for dsDNA damage detection. Results: The IC-50 of DOX was 3 μM. When DEX was combined, there was an additional toxic effect on HL-1 s. The inhibitory effect of DEX on cell viability ceased at 10 μM. The γ-H2AX assay showed decreased dsDNA breaks in cells treated with DEX compared with those treated with DOX alone. The dsDNA breaks were increased in cells treated with DOX alone compared with control (cells alone) (P < 0.05), and dsDNA breaks were increased in cells treated with DOX alone versus those treated with combined DOX and DEX (P < 0.05). Discussion: DEX was found to abolish the DNA damage signal γ-H2AX caused by DOX in HL-1 s as demonstrated in the γ-H2AX assay, suggesting an alternative mechanism of cardioprotective action of DEX.