- Department of Neurosurgery, Maastricht University Medical Center, Maastricht,
- Department of ENT, Maastricht University Medical Center, Maastricht,
- Department of ENT, Radboud University Medical Center, Nijmegen, Netherlands.
Yasin Temel, Department of Neurosurgery, Maastricht University Medical Center, Maastricht, Netherlands.
DOI:10.25259/SNI_277_2022Copyright: © 2022 Surgical Neurology International This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-Share Alike 4.0 License, which allows others to remix, transform, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.
How to cite this article: Pawan Kishore Ravindran1, Dirk Kunst2,3, Jerome Waterval2, Koos Hovinga1, Yasin Temel1. A rare complication after vestibular schwannoma surgery: Neurogenic pulmonary edema. 30-Sep-2022;13:441
How to cite this URL: Pawan Kishore Ravindran1, Dirk Kunst2,3, Jerome Waterval2, Koos Hovinga1, Yasin Temel1. A rare complication after vestibular schwannoma surgery: Neurogenic pulmonary edema. 30-Sep-2022;13:441. Available from: https://surgicalneurologyint.com/surgicalint-articles/11909/
Background: In our center, large vestibular schwannoma (VS) is typically managed by a planned partial resection through the translabyrinthine route. Here, we report on a rare complication of VS surgery and severe neurogenic pulmonary edema.
Case Description: A 33-year-old male was referred to our skull-base center with a large VS. A planned partial resection was performed. The surgery was without complications and the patient showed good recovery without facial nerve dysfunction. In the evening of the 2nd day after surgery, the patient showed rapid neurological deterioration, accompanied by cardiac arrest. After the patient was resuscitated, a computed tomography (CT) was made, which showed generalized (infra- and supratentorial) brain edema and hematoma in the resection cavity. Despite rapid removal of the hematoma, there was no change in the neurological situation. The next CT scan showed a further increase of brain edema and the patient died eventually. Autopsy revealed generalized lung edema, brain edema, and Hashimoto’s thyroiditis. The pathologist diagnosed neurogenic lung edema.
Conclusion: Neurogenic lung edema can occur on the 2nd day after surgery and induce rapid deterioration of the patient with massive brain edema.
Keywords: Hashimoto’s thyroiditis, Hematoma, Large vestibular schwannoma, Neurogenic pulmonary edema
A 33-year-old patient was referred to our skull-base center because of a large vestibular schwannoma (VS) (diameter of 4.4 cm,
Here, our patient developed an unusually rapid deterioration in the 2nd day after VS surgery with cardiac arrest. CT imaging showed hematoma in the resection cavity and generalized edema. The time course of a typical hemorrhage after a posterior fossa surgery is different. This occurs in the 1st h after surgery and is characterized by neurological deterioration without hemodynamic instability. However, in our case, the neurological and hemodynamic deterioration occurred relatively late, was very fast, and had a catastrophic clinical course. Rapid evacuation of the hematoma in the resection cavity had no effect at all.
The Berlin definition defines neurogenic pulmonary edema (NPE) as a type of acute respiratory distress syndrome, defined by marked, acute-onset, and extravascular accumulation of pulmonary interstitial fluid.[
What distinguishes NPE from other pulmonary edemas (PE) is that there are two basic mechanisms of PE development at play: (1) increased intravascular and interstitial pressure and (2) an increased permeability of the pulmonary capillaries.[
Certain CNS centers are involved in the regulation of sympathetic innervation and are able to change hemodynamic functions.[
Local edema is a common pathological consequence following surgery. Edema occurs as a result of endothelial cell damage, abnormal tight junctions, and disrupted transcellular transport. The damaged cells and blood vessels activate a plethora of cellular mechanisms, which worsen the injury.[
The present understanding suggests that the elevated intracranial pressure plays a key role in the development of NPE.[
The patient’s autopsy report also revealed an underlying HT which, we believe, may have further exacerbated the PE.[
Another possible etiology of the PE could have a cardiogenic origin despite the “non-cardiogenic” label given to NPE.[
The hematoma in the resection cavity and the HT probably have triggered CNS mechanisms to cause NPE in our case.
The authors certify that they have obtained all appropriate patient consent.
There are no conflicts of interest.
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