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Introduction: Aim of the study is to investigate whether there is a correlation between causes of brain death, blood gas parameters before and after the apnea test and optic nerve sheath diameter (ONSD). Method: The records of 92 patients with brain death diagnosis were retrospectively analyzed for ONSD measurements of the right and left eyes, partial carbon dioxide pressure (pCO2), blood gas parameters before and after the apnea test. Results: Subarachnoidal hemorrhage and intracerebral hemorrhage were the two most common brain death etiology. Mean ONSD for right eye was 6.37±1.03 mm. Mean ONSD for left eye was 6.43±1.02 mm. Only 8 patients had ONSD below 5.00 mm. There was no statistically significant correlation between the percent change of pCO2 and ONSD change (p>0.05). Conclusion: The present study shows that ONSD values are very high regardless of the partial pressure of carbon dioxide in patients with brain death diagnosis. We can suggest that ONSD can find itself a place for evaluating comatose patients for brain death diagnosis.

Aim: COVID-19 can cause clinical pictures ranging from asymptomatic to severe respiratory failure and sudden death. The severity of the disease varies depending on many factors such as comorbidity, vaccination status, as well as demographic characteristics such as age and gender. In this study, it was aimed to investigate the independent risk factors that have an effect on mortality in COVID-19 patients. Materials and Methods: In the study, records of 140 patients with a diagnosis of COVID-19 followed in the intensive care unit between 01.01.2021 and 01.01.2022 were examined. Demographic characteristics such as age and gender, comorbidity, vaccination status and clinical course of the patient were investigated and recorded. Results: In our study, a statistically significant difference was found between mortality and age, and the number of days of total invasive/noninvasive mechanical ventilation support (p=0.01, p=0.25, p

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Morphine is a drug used in chronic pain such as diabetic neuropathy, but the development of tolerance to its antinociceptive effect is an important clinical problem. Recently, it has been stated that morphineinduced neuronal apoptosis can stimulate morphine tolerance. Our aim in this study was to investigate the effects of aspirin on morphine-induced neuronal apoptosis and analgesic tolerance in rats with diabetic neuropathy. After morphine tolerance induction, the antinociceptive effects of aspirin (50 mg/kg) and morphine (5 mg/kg) were evaluated by thermal pain tests at 15 or 30 minute intervals.Streptozotocin (STZ, 65 mg/kg) was injected intraperitoneally to induce diabetic neuropathy. To evaluate apoptosis in dorsal root ganglion (DRG) tissue, ELISA kits were used to measure caspase-3, Bax and Bcl-2 levels. Apoptotic cells were detected histologically by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) method. Study results indicate that prior administration of aspirin to diabetic rats signi cantly increased the antinociceptive e cacy of morphine compared to morphine alone. Thermal pain tests showed that aspirin signi cantly reduced morphine tolerance in rats with diabetic neuropathy. Biochemical analysis revealed that aspirin signi cantly decreased the levels of proapoptotic proteins, caspase-3 and Bax, while increasing the anti-apoptotic Bcl-2 in DRG neurons. Semiquantitative scoring demonstrated that aspirin provided a signi cant reduction in apoptotic cell counts in diabetic rats. In conclusion, these data suggested that aspirin attenuated morphine antinociceptive tolerance through anti-apoptotic activity in diabetic rat DRG neurons. Further studies are needed to elucidate these effects of aspirin on morphine tolerance.