Variation of Cognitive Function During a Short Stay at Hypobaric Hypoxia Chamber (Altitude: 3842 M).

OBJECTIVE: To observe the effects of a fast-acute ascent to high altitude on brain cognitive function and transcranial doppler parameters in order to understand the physiological countermeasures of hypoxia. METHODS: 17 high-altitude-naïve male subjects (mean age was 26.3 ± 8.1 years) participated in the study. We measured Critical Flicker Fusion Frequency (CFFF), blood oxygen saturation, Psychology Experiment Building (PEBL) including three tests (Modified Math Processing Task, Perceptual Vigilance Task, and Time Estimation Task), as well as Cerebral Blood Flow index (CBFi), mean cerebral artery Systolic and diastolic velocities, Cerebral Pulsatility index (CPi), and heart Rate. All were measured at sea level, at least 1 h after arrival at the hypobaric hypoxia equivalent of 3842 m and 1 h after return to sea level. RESULTS: Under acute exposure to hypobaric hypoxic conditions, significant decrease in CFFF [42.1 ± 1 vs. 43.5 ± 1.7 Hz at sea level (asl), p < 0.01], CBFi (611 ± 51 vs. 665 ± 71 asl, p < 0.01) and blood oxygen saturation (83 ± 4% vs. 98 ± 1% asl, p < 0.001) as compared to pre-ascent values were observed. Physiological countermeasures to hypoxia could be involved as there was no significant change in neuropsychometric tests, Systolic and Diastolic velocities and CPi. A significant increase in Heart Rate (81 ± 15 bpm vs. 66 ± 15 bpm asl, p < 0.001) was observed. All parameters returned to their basal values 1 h after regaining sea level. CONCLUSION: Hypoxia results in a decrease in CFFF, CBFi and oxygen saturation and in an increase in heart rate. As it decreased, Cerebral Blood Flow index does not seem to be the physiological measurement of choice to hypoxia explaining the maintenance of cognitive performance after acute exposure to hypobaric hypoxia and requires further investigation. Cerebral oxygen delivery and extraction could be one of the underlying mechanisms.

Tracheal damage.

Tracheal damage. Blunt/penetrating trauma and inhalation injuries to the trachea can result in acute airway compromise, with life-threatening implications. Early assessment, identification, and prompt and appropriate management are of paramount importance in order to reduce patient morbidity and mortality. Signs and symptoms of these injuries are specific and sometimes subtle, and their seriousness may be obscured by other injuries. Diagnosis can therefore be challenging, requiring a high index of suspicion. Indeed, diagnosis and treatment are often delayed, resulting in attempted surgical repair months or even years after injury. Laryngoscopy, flexible and/or rigid bronchoscopy and computed tomography of the chest are the procedures of choice for a definitive diagnosis. Airway control and appropriate ventilation represent the key aspects of emergency management. Definitive treatment depends on the site and the extent of injury. Surgery, involving primary repair with direct suture or resection and end-to-end anastomosis, is the treatment of choice for patients suffering from tracheal injuries. A conservative approach must be considered for the paediatric population and selected patients with mainly iatrogenic damage. We present a review of the incidence, mechanisms of injury, clinical presentations, diagnosis, initial airway management, anaesthetic considerations and definitive treatment in the case of tracheal damage from blunt/penetrating trauma and inhalation injuries.