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Josef Finsterer
  1. Department of Neurology, Neurology and Neurophysiology Center (NNC), Vienna, Austria

Correspondence Address:
Josef Finsterer, Department of Neurology, Neurology and Neurophysiology Center (NNC), Vienna, Austria.

DOI:10.25259/SNI_691_2024

Copyright: © 2024 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: Finsterer J. Before blaming glucocorticoids for prolonged postoperative hypotension, alternative explanations must be carefully ruled out. Surg Neurol Int 27-Sep-2024;15:352

How to cite this URL: Finsterer J. Before blaming glucocorticoids for prolonged postoperative hypotension, alternative explanations must be carefully ruled out. Surg Neurol Int 27-Sep-2024;15:352. Available from: https://surgicalneurologyint.com/surgicalint-articles/13115/

Date of Submission
14-Aug-2024

Date of Acceptance
08-Sep-2024

Date of Web Publication
27-Sep-2024

Dear Editor,

We read with interest the article by Sharma and Venkatapura on a 9-year-old girl with an extra-axial mass lesion along the vermis who suffered persistent arterial hypotension intraoperatively.[ 3 ] The intraoperative hypotension was attributed to suppression of the hypothalamic-pituitary-adrenal (HPA) axis, as only hydrocortisone was effective.[ 3 ] It was concluded that resistant perioperative hypotension can occur not only with chronic steroid use but also after a single high dose of steroids and that risk factors for HPA suppression after steroid administration include cumulative duration of use, long-acting agents, and parenteral administration.[ 3 ] The study is excellent, but some points should be discussed.

The first point is that left ventricular systolic dysfunction has not been adequately ruled out as a cause of persistent arterial hypotension during surgery. Since surgery and anesthesia are stressful for any patient, it cannot be ruled out that the index patient also reacted with a cardiac stress response in the form of stress cardiomyopathy, also known as Takotsubo syndrome (TTS). Numerous cases of intraoperative TTS have been described in the literature.[ 1 , 4 ] Since TTS can be complicated by systolic dysfunction, heart failure, ventricular arrhythmias, and cardioembolism,[ 2 ] it would have been useful to perform bedside echocardiography to rule out this particular stress reaction.

Second, it was not considered that the mass lesion itself or the intraoperative manipulations were responsible for the persistent intraoperative arterial hypotension. Since manipulations of the brainstem were most likely also performed during the operation,[ 3 ] it cannot be excluded with certainty that a transient pressure lesion or ischemia in the brainstem at the site of the cardiorespiratory or vasoregulatory centers was responsible for the described phenomenon.

The third point is that the anesthetic drugs administered before and during surgery or their delayed metabolization and excretion were responsible for the described symptoms. We should, therefore, know what kind of analgesics, muscle relaxants, sedatives, and anesthetics were used in what dosage for this particular generalized anesthesia.

The fourth point is that there was no mention of whether pituitary hormones were measured pre- or postoperatively and whether any irregularities, particularly with regard to adrenocorticotropic hormone (ACTH), were detected. If dexamethasone were indeed responsible for the arterial hypotension, one would expect low ACTH. It is also conceivable that antidiuretic hormone production was impaired.

The fifth point is that the pathologic diagnosis of the mass lesion was not reported. Knowing the classification of the tumor could explain the blood pressure problem. What was the histopathologic diagnosis? Is it conceivable that the tumor was hormone-producing and, therefore, causing hypotension?

To summarize, this interesting study has limitations that put the results and their interpretation into perspective. Addressing these limitations could strengthen the conclusions and corroborate the study’s message. Before blaming glucocorticoids and consecutive HPA suppression for persistent intraoperative hypotension, all alternative explanations must be thoroughly ruled out.

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. Cakan F, Say MA, Adar A. Intraoperative takotsubo cardiomyopathy: A case report. J Perianesth Nurs. 2024. p. S1089-9472 (23)01103-6

2. Ranieri M, Finsterer J, Bedini G, Parati EA, Bersano A. Takotsubo syndrome: Clinical features, pathogenesis, treatment, and relationship with cerebrovascular diseases. Curr Neurol Neurosci Rep. 2018. 18: 20

3. Sharma P, Venkatapura R. Acute suppression of the hypothalamo-pituitary-adrenal axis from a large singular dose of dexamethasone: A case report on a hypothesis for resistant intraoperative hypotension. Surg Neurol Int. 2024. 15: 230

4. Ved YP, Sharan S, Bandebuche A, Ram SH, Rathod A, Keshan R. Perioperative takotsubo stress cardiomyopathy during endoscopic spinal surgery: A case report. JBJS Case Connect. 2024. 14:

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