There are numerous complications associated with tuberculum sellae meningioma (TSM) surgery documented in the literature. These range from cerebrospinal fluid (CSF) leaks and visual complications to vascular events that may occur during surgery.[ 1 ] Bleeding occurs and is expected in anatomically proximal locations to the surgical corridor. However, one rare but devastating location is the posterior fossa, which surprisingly only complicates transcranial surgeries and not endoscopic approaches for supratentorial pathologies.[ 5 ] Such bleeding manifests as subdural hematomas in the posterior fossa or intracerebellar hemorrhages on the superior surface of the cerebellum. In one case, we had to place a ventriculoperitoneal shunt to prevent hydrocephalus secondary to the hemorrhage in the posterior fossa, a location that was not directly manipulated during surgery [ Figure 1 ]. While most other complications are successfully managed medically, this event, with unknown etiology, can result in patient death.

Figure 1:

The left panel (a-d) depicts a 67-year-old man with a history of visual disturbances and vertigo, who was diagnosed with a tuberculum sellae meningioma with no history of hypertension, coagulopathy, or other possible risk factors. (a and b) preoperative axial and coronal magnetic resonance imaging sections of the tumor, highlighting its compression of the cavernous sinus. The patient experienced difficulty with breathing and became unconscious during the postoperative period in the intensive care unit. (c and d) postoperative imaging revealing a complication of posterior fossa (cerebellar) hemorrhage. Unfortunately, his condition deteriorated, and he expired before further work could be done. The right panel (e-h) features a 59-year-old male with a history of tinnitus who was also diagnosed with a tuberculum sellae meningioma. This tumor exhibited a similar growth pattern to the previous case, directly impacting the cavernous sinus, as seen in the sagittal and coronal sections. Following surgery, the patient’s condition deteriorated, and brain imaging indicated posterior fossa bleeding that followed a similar pattern to that observed in the other case (g and h). His medical condition remained stable. A ventriculoperitoneal shunt was placed to prevent hydrocephalus and was followed up. No further intervention was required, and the bleeding was resolved.

While the etiology remains unknown, the bleeding behavior provides important clues. The distribution and the pattern of bleeding, spreading horizontally along the cerebellar folia and fissures [ Figure 1 ], do not follow intraparenchymal hemorrhages that occur secondary to arterial incidents, which are more common in patients with coagulopathy or hypertension.[ 4 ] This raises the suspicion that such bleeding originates from venous sources in the subarachnoid space.

Many hypotheses have been previously suggested to address this unique observation. This kind of complication is classically attributed to head position. Furthermore, it is claimed that gravitational retraction of the cerebellum and its bridging veins may lead to superficial bleeding on the cerebellum.[ 2 ] In this situation, rupture of veins as they course through the subarachnoid space of a cerebellar fissure or where they enter the cerebellar parenchyma, owing to a loss of CSF, may have been the mechanism behind the hemorrhage. CSF loss through the craniotomy and lumbar drain, as well as possible suction drainage of CSF through the epidural drain from a small dural leak after surgery, might have contributed to the development of the hemorrhages. This has been hypothesized to be the case, especially in supratentorial surgeries for aneurysms where a large amount of CSF is drained to relax the brain.[ 4 ] Furthermore, intracranial hypotension stemming from loss of CSF can result in downward displacement of the cerebellum and brainstem. This downward displacement relative to the tentorium may put tension on the veins extending from the cerebellar surface to the tentorial and straight sinuses, which could lead to venous occlusion/injury caused by rapid shifting of the brain consequent to CSF loss, which has also been suggested as another possible mechanism. However, this is challenged in open surgeries for TSM, where CSF drainage is not necessarily used. Moreover, this type of posterior fossa hemorrhage has not been reported as a complication of intracranial hypotension resulting from lumbar puncture.

Others have also suggested that turning and extending the head could occlude the jugular vein on the side toward which the head is turned, resulting in elevated venous pressure, especially if it is the dominant jugular vein being compressed or catheterization was performed.[ 3 ] However, this may not be the leading factor in our cases, as the dominant jugular vein was on the bending side of the neck, the neck was mildly rotated, and no history of venous manipulation or catheterization was present.

In our opinion, the above-suggested hypotheses lack a thorough pathophysiological explanation of posterior fossa hemorrhages with a unique bleeding pattern. In our view, the proposed hypotheses inadequately explain the specific pathophysiological mechanisms underlying the unique bleeding patterns observed in posterior fossa hemorrhages. To illustrate, while surgeries for other pathologies (e.g., clinoid meningiomas, craniopharyngiomas, pituitary adenomas) may utilize similar surgical corridors and techniques to access deeper brain regions, this particular hemorrhagic complication is not typically encountered. For example, craniopharyngioma resections, often involving more extensive interventions, head positioning, prolonged operative times, and greater CSF leakage, are performed on a larger patient cohort. Yet, we have not observed this complication in our experience.

In our vision, in the case of TSMs, due to their shape and location, the tumor compresses the medial part of the cavernous sinus [ Figure 1 ]. Upon tumor removal, this compression is alleviated, which may lead to recirculation of blood flow with a lower resistance through the cavernous sinus into the superior petrosal sinus and Dandy vein (also known as the superior petrosal vein). This venous hyperemia and elevated pressure on the superior surface of the cerebellum could potentially result in intracerebral hemorrhage in the vermis and along both superior surfaces of the cerebellum, which are anatomically correlated with areas of theoretical venous hyperemia. Consequently, subdural hematomas may occur due to the rupture of small veins, explaining the subdural complications associated with open surgeries for TSM. One limitation that hinders us from making an assured hypothesis is the rarity of this complicating event and the number of patients who are enrolled in our center. Larger multicenter studies with a great number of pooled samples could better dismantle the condition.

In summary, we make an opinion that CSF hypotension or cerebellar vessel traction, as well as jugular vein nicking during surgery, may not be the main factors leading to venous accidents. We hypothesize that the shape and location of TSMs compress the medial part of the cavernous sinus and hinder the physiologic venous circulation. The removal of these tumors may open up and alter blood flow through the cavernous sinus to the superior petrosal sinus and Dandy vein, occasionally leading to subdural complications due to rupture of small veins.

Author’s contributions:

GS: Conceptualization, EM: Writing-original draft, AJ: Resources.

Financial support and sponsorship:

This has been added by the journal since they waived publication fees for us, therefore they know the correct spellings and Carolyn R. Ausman Educational Foundation.

Disclaimer

The views and opinions expressed in this article are those of the authors and do not necessarily reflect the official policy or position of the Journal or its management. The information contained in this article should not be considered to be medical advice; patients should consult their own physicians for advice as to their specific medical needs.

References

1. Chi JH, McDermott MW. Tuberculum sellae meningiomas. Neurosurg Focus. 2003. 14: e6

2. König A, Laas RH, Herrmann HD. Cerebellar haemorrhage as a complication after supratentorial craniotomy. Acta Neurochir. 1987. 88: 104-8

3. Papanastassiou V, Kerr R, Adams C. Contralateral cerebellar hemorrhagic infarction after pterional craniotomy: Report of five cases and review of the literature. Neurosurgery. 1996. 39: 841-52

4. Van Calenbergh F, Goffin J, Plets C. Cerebellar hemorrhage complicating supratentorial craniotomy: Report of two cases. Surg Neurol. 1993. 40: 336-8

5. Yang C, Fan Y, Shen Z, Wang R, Bao X. Transsphenoidal versus transcranial approach for treatment of tuberculum sellae meningiomas: A systematic review and meta-analysis of comparative studies. Sci Rep. 2019. 9: 4882