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Introduction: Neurogenic pulmonary edema (NPE) is a life-threatening condition caused by various significant central nervous system injuries. It is characterized by an abrupt increase in fluids within the alveoli and interstitium of the lungs. The mechanism underlying NPE remains unclear. Few pathophysiological causes-including neurocardiac factors, neurohemodynamic factors, blast theory, and pulmonary venule adrenergic hypersensitivity-have been proposed. Case report: We report the case of a patient with NPE associated with subarachnoid hemorrhage (SAH) and stress-hemoconcentration. Adrenergic responses have been reported to play a crucial role in both NPE and stress-hemoconcentration. We believe that SAH induces an adrenergic surge, which causes a cascade of reactions and leads to both NPE and stress-hemoconcentration. Conclusion: Central nervous system (CNS) injuries are crucial and common causes of adrenergic stimulation; therefore, any subtle signs indicating CNS injuries should be carefully investigated. The distress of NPE may mask the initial symptoms of CNS injuries. If the patient is intubated and under mechanical ventilation to treat NPE, the inciting neurological injury may be overlooked and result in a delayed diagnosis. [ABSTRACT FROM AUTHOR]

Introduction: Nowadays, Valproic acid (VPA) is widely used for the treatment of seizures, mood disorder, schizophrenia, and migraine prophylaxis. With its extended use, the incidence of acute VPA poisoning is increasing. Though most patients with VPA overdose may recover with supportive care, delayed toxicity may result in the underestimation of the severity. Case Report: We reported on a case of VPA and benzodiazepine overdoses with two-phase alternations of mental states, and the peak serum VPA level developed 22 h post-ingestion. The patient underwent an emergency tracheal intubation and artificial ventilation for the presence of acute respiratory failure and coma. After two courses of hemodialysis, he recovered to clear consciousness and spontaneous respiration. Conclusion: Toxidromes of VPA poisoning can develop late after acute poisoning. Accordingly, we suggest that all intoxicated patients should undergo prolonged observation until the serum VPA level has decreased and the toxidromes have disappeared. Activated charcoal, carnitine, naloxone, and hemodialysis/hemoperfusion are potential regimens to decrease absorption, to reverse the toxidromes, and to enhance elimination for patients with VPA poisoning. [ABSTRACT FROM AUTHOR]

Introduction: Severe accidental hypothermia in trauma patients is rarely encountered in tropical areas. However, unnoticed hypothermia may lead to deleterious consequences and even sudden death. Case report: We report the case of a middle-aged patient who sustained hemorrhagic shock secondary to a traffic accident-induced severe intraabdominal injury, followed by prolonged exposure to a cold and wet environment. Thereafter, the patient was sedated and paralyzed and was administered large infusion volumes of fluid and blood components. In the emergency department, profound hypothermia could not be detected using an infrared forehead thermometer. Subsequently, the patient had a sudden cardiac arrest during the emergency surgery. Conclusion: This case report highlights that even in a tropical city, fatal severe hypothermia may occur in severe trauma patients. Therefore, to avoid accidental hypothermia, emergency physicians and trauma surgeons should use invasive temperature monitoring, and aggressive rewarming should be performed for correcting hypothermia in severe trauma patients. [ABSTRACT FROM AUTHOR]