Aeromedical transport is challenging not only because of limitations of equipment, unfamiliar surroundings, and challenging environmental conditions, but also due to difficulty in developing methodologies for research and data collection. To our knowledge, neurological changes at the oxygen tensions of a pressurized cabin have not been systematically studied. Here we report a case of intracranial hemorrhage during aeromedical transport and review the body’s cardiovascular and respiratory adaptation to decreased ambient oxygen tension. Previous experience with high altitude cerebral edema serves as guidance for mitigating the effects of vasogenic edema in patients at risk of neurological events who travel by air. Review of this case and relevant altitude-related physiological changes may be grounds for more conservative recommendations on aeromedical transport after an acute neurological event.
During air travel, passengers are exposed to unique conditions such as rapid ascent and descent that can trigger significant physiological changes. In addition, the cabins of commercial aircraft are only partially pressured to 552–632 mmHg or the equivalent terrestrial altitudes of 1,500–2,500 m (5,000–8,000 feet) above sea level. While studies in high-altitude medicine have shown that all individuals experience some degree of hypoxia, cerebral edema, and increased cerebral blood flow, the neurological effects that accompany these changes are otherwise poorly understood. In this study, we report a case of acute subarachnoid hemorrhage from a ruptured cerebral aneurysm associated with travel on commercial aircraft. We then review relevant cases of neurological incidents with possible air travel-related etiology and discuss the physiological factors that may have contributed to the patient’s acute subarachnoid hemorrhage. In the future, this report may serve as reference for more detailed and conservative medical guidelines and recommendations regarding air travel.
Acute subdural hematoma (SDH) resulting from head trauma is a potentially life-threatening condition that requires expedient diagnosis and intervention to ensure optimal patient outcomes. Rapidly expanding or large hematomas, elevated intracranial pressure, and associated complications of brain herniation are associated with high mortality rates and poor recovery of neurological function. However, smaller bleeds (clot thickness <10 mm) or hematomas occurring in infrequent locations, such as the tentorium cerebelli, may be difficult to recognize and patients may present with unusual or subtle signs and symptoms, including isolated cranial nerve palsies. Knowledge of neuroanatomy supported by modern neuroimaging can greatly aid in recognition and diagnosis of such lesions. In this report, we present a case of isolated oculomotor nerve palsy resulting from compressive tentorial SDH following blunt head trauma, review the literature concerning similar cases, and make recommendations regarding the diagnosis of SDH in patients presenting with isolated cranial nerve palsies.
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