Children with posterior fossa ependymomas most often have slowly evolving signs and/or symptoms of intra-cranial hypertension or cerebellar dysfunction. However, there are rare occasions where the tumor can lead to a severe illness. Hemorrhage into these tumors is not rare and might present as apoplexy [5–7]. The main pathophysiologies of hemorrhage into tumors include structural abnormalities in tumor vessels, tumor invasion into cerebral vessel walls, tumor or brain necrosis, and coagulation defects, either related to systemic cancer or iatrogenically induced .
However, the pathophysiological mechanisms by which air travel could predispose the tumors to bleed are not fully-understood. Decreased barometric pressure, hypoxemia, and local hemostatic abnormalities are well-known physiological changes during air travel.
Commercial airplanes cruising at typical altitudes of 30,000 to 40,000 feet partially pressurize their cabins to the atmospheric pressures found at 5000 to 8000 feet, or 552 to 632 mmHg. Due to the resultant decrease in the partial pressure of oxygen in the inspired air, blood oxygen saturation levels of as low as 85% may be reached . These changes in oxygen levels can cause considerable effects on hemostasis in humans. Infants and young children are particularly susceptible to hypoxemic episodes . Due to this relative hypoxemia, patients who have recently suffered strokes by cerebrovascular accidents are often advised not to fly in order to prevent additional ischemic neuronal loss. Goldberg and Hirschfeld suggest that the relative hypoxemia experienced during the flight may result in differential ischemic changes in tumor tissue, and with an already tenuous blood supply delivered through the thin-walled, non-autoregulating vasculature, tumor necrosis and respective hemorrhage into the necrotic tissue are more likely .
Additionally, local tissue ischemia may be a manifestation of decreased perfusion due to hypovolemia. The most commonly reported in-flight malady is syncope. Venous pooling of blood in the lower extremities as a result of prolonged sitting combined with dehydration from low cabin humidity and poor fluid intake have been reported to contribute to intra-vascular volume depletion. However, cerebral vasculature may be able to compensate for this through normal autoregulatory mechanisms, which are lacking in the tumor vascular structure .
An alternative hypothesis concerns the role of decreased cabin pressure resulting in an increase in tumor venous pressure due to transmission of mildly increased intra-abdominal pressure through the inferior vena cava and cranial dural sinuses. At a cabin pressure of 575 mmHg, gas expands to 132% of its baseline volume at sea level . Expansion of intestinal gas may have brought about a mild elevation of intra-abdominal pressure with consequent venous rupture or thrombosis within the intra-cranial tumor. The increased transmural pressure across tumor blood vessels due to the rapid lowering of intra-cranial pressure has been implicated in tumors that bleed after ventricular shunts or drainage . The decreased atmospheric pressure in the airplane cabin may have caused a similar effect that induces a transmural pressure difference within blood vessels and the surrounding environment, resulting in tumor hemorrhage.
Another mechanism may be related to increased levels of inspired CO2 in commercial flights. Cabin air undergoes a degree of recycling as well as exchange with atmospheric air. This process leads to an increasing inspired fraction of CO2 levels in aircraft cabins during flight. US federal aviation law specifies a CO2 level of less than 0.5% in the cabin air . However, this mild degree of hypercapnia may lead to the well-documented phenomenon of cerebral vasodilation [8, 10] and consequent tumor vessel rupture.
The sudden onset of neurological deficits in our patient, who had previously been well and with a functioning shunt, suggest bleeding in the pre-existing intra-cranial tumor, which was confirmed intra-operatively. The possible mechanisms of bleeding in the highly vascular and potentially hemorrhage-prone tumor in our patient during flight can be more than a coincidence and might be related to fluctuation of cabin CO2, oxygen levels and interior pressure. Therefore, it seems reasonable to assume that these physiological changes pose an additional risk of hemorrhage into brain tumors in decompensated individuals.