Abstract Number: Esoc2026a920 Inorganic Compounds' Inhalation and Hypoxic Ischaemic Encephalopathy

Abstract Background and aims Inhalation of inorganic toxic substances may rapidly lead to severe respiratory failure and hypoxic ischaemic encephalopathy, because of mechanical airway obstruction and inflammatory oedema. Methods A 50-year-old overweight, chronic smoker male, born after troubled delivery, affected with atopy, but no significant other comorbidities, arrived at the emergency department by ambulance for severe dyspnoea and hypoxemia after accidental inhalation of inorganic toxic material (cement, carbon). Results Imaging showed massive supraglottic oedema and early interstitial changes. Because of failure of conventional intubation approach, flexible endotracheal tube and rotational technique were successfully used. Sequential bronchoscopies revealed and allowed removal of multiple fragments, restoring complete airway patency. On day seven, neurological signs were evident: dysarthria, dysphonia, bilateral reduction of visual field, left ptosis, right deviation of protruding tongue, hyposthenia, deep and superficial hypoesthesia. Magnetic Resonance Imaging showed signs of posterior reversible encephalopathy syndrome (PRES) and hypointense in T1, hyperintense in T2/FLAIR lacunar ischaemias, more evident in left mesencephalon and right medulla oblongata. PRES fully remitted with steroids. The patient was transferred to rehabilitation unit. He recovered in one and half months’ time and was discharged in good physical health condition. Conclusions Outcomes of hypoxic ischaemic encephalopathy may be devastating. Literature supports algorithmic approaches to airway emergencies and emphasizes the role of bronchoscopy. Early recognition, innovative airway techniques avoid procedure-related complications and tracheal injury. Multidisciplinary intensive care are pivotal for successful management of anaphylaxis reaction and/or non-IgE mediated activation of mastcells by environmental toxicants, and management of cerebral ischaemic damage. Conflict of interest Name of author: nothing to disclose