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    A rare case of fatal venous and cerebral air embolism
    (Turkish Assoc Trauma Emergency Surgery, 2019) Petekkaya, Semih; Celbis, Osman; Oner, Bedirhan Sezer; Turan, Omer; Yener, Zeynep
    A venous air embolism can occur as a result of circumstances that include blunt head or chest trauma, thoracentesis, arterial catheterization, neurosurgery, cardiac surgery, and Caisson disease. The formation of a venous air embolism requires an air source, interaction between the air source and the vessel, and a pressure gradient supporting air migration into the vessel. Air enters through the impaired venous structure and travels to the right side of the heart and the pulmonary arteries, and depending on the amount of air, may occasionally be fatal. This report is the description of the case of a 3-year-old child who developed a fatal venous and cerebral embolism during neurosurgery for the treatment of skull fractures with epidural and subdural bleeding due to blunt head and chest trauma resulting from a television falling on her. The pathophysiology of death and notes regarding the medico-legal autopsy procedure in such cases are discussed. Meticulous autopsy techniques must be used to determine the presence of an air embolism in cases of blunt trauma, especially in patients with blunt trauma to the head who die during neurosurgery, and possible future malpractice claims should be kept in mind.
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    Acute and subacute cardiovascular effects of synthetic cannabinoid JWH-018 in rat
    (Springer, 2025) Ozhan, Onural; Ermis, Necip; Celbis, Osman; Samdanci, Emine; Petekkaya, Semih; Oruc, Mucahit; Soylu, Ozcan
    PurposeThis study investigates the cardiovascular effects of the synthetic cannabinoid naphthalene-1-yl-(1-pentylindole-3-yl)methanone (JWH-018) in rats. The research aims to evaluate the pharmacologic, cardiologic, biochemical, and histopathological effects of acute and subacute administration at low and high doses. The primary research question is how JWH-018 impacts heart function, blood pressure, ECG patterns, and cardiac tissue integrity.MethodsWistar albino rats were divided into five groups: control, acute low-dose (ALD, 0.5 mg/kg), acute high-dose (AHD, 5 mg/kg), subacute low-dose (SALD, 0.5 mg/kg for 14 days), and subacute high-dose (SAHD, 5 mg/kg for 14 days). Cardiovascular effects were assessed using echocardiography, hemodynamic and ECG analysis, histopathology, biochemical markers, and LC-MS/MS quantification of JWH-018 and its metabolites in heart tissue.ResultsAcute high-dose JWH-018 caused bradycardia and hypotension, while subacute high-dose increased heart rate but continued to lower blood pressure. JWH-018 induced cardiac arrhythmias, conduction blocks, and ischemic ECG changes, with prolonged QT intervals in subacute high-dose rats. Histopathological findings revealed myocardial infarction-like features, including contraction bands and ischemic damage, particularly in subacute groups. Elevated pro-BNP and triglycerides indicated cardiac stress and metabolic effects. JWH-018 and its metabolites were detected in heart tissue, primarily in high-dose groups.ConclusionsJWH-018 has significant cardiovascular risks, causing heart rate dysregulation, hypotension, arrhythmias, and ischemic damage. These effects depend on dose and duration. The study highlights the potential dangers of synthetic cannabinoids, emphasizing that they should not be considered safe alternatives to natural cannabis.