# Late Intracerebral Hemorrhage After Successful Endovascular Closure of a Carotid-Cavernous Fistula: A Case Report and Updated Review

**Authors:** Karol Uscamaita, Marta García Pla, Mikel Terceño, Adrià Arboix, Yolanda Silva

PMC · DOI: 10.3390/reports8040234 · Reports - Clinical Practice and Surgical Cases · 2025-11-13

## TL;DR

A 48-year-old woman developed a rare brain bleed 12 days after a successful treatment for a carotid-cavernous fistula, highlighting the need for long-term monitoring and understanding of molecular mechanisms.

## Contribution

This case report identifies delayed intracerebral hemorrhage after CCF closure and explores molecular mechanisms like NPPB and ICA1L variants.

## Key findings

- ICH occurred 12 days after CCF closure, later than the typical 48-hour window.
- Molecular mechanisms like NPPB, oxidative stress, and ICA1L variants may contribute to delayed ICH.
- Hemodynamic monitoring is crucial in patients with vascular comorbidities post-treatment.

## Abstract

Background and Clinical Significance: Intracerebral hemorrhage (ICH) is a very rare complication following endovascular closure of direct carotid-cavernous fistulas (CCFs). When reported, ICH typically appears within the first 48 h after CCF closure. We performed an extensive literature review, starting from the case of a 48-year-old patient presenting with an intracerebral hemorrhage after CCF closure. Case Presentation: A 48-year-old woman with arterial hypertension developed an intracerebral hemorrhage in the right frontal lobe 12 days after successful closure of a traumatic CCF. The patient exhibited acute neurological deterioration in a previously hypoperfused territory. A narrative review identifies the classical molecular theory of hemodynamic dysregulation, known as Normal Perfusion Pressure Breakthrough (NPPB), as the principal pathophysiological mechanism. Other mechanisms such as oxidative stress, microglial activation, blood–brain barrier disruption, metalloproteinase expression, and possible genetic alterations such as ICA1L variants are also implicated. Conclusions: This case underscores the importance of considering molecular mechanisms in the pathophysiology of delayed post-endovascular treatment of ICH, as well as the need for hemodynamic monitoring and follow-up in patients with vascular comorbidities.

## Linked entities

- **Genes:** ICA1L (islet cell autoantigen 1 like) [NCBI Gene 130026]
- **Diseases:** intracerebral hemorrhage (MONDO:0013792)

## Full-text entities

- **Genes:** ICA1L (islet cell autoantigen 1 like) [NCBI Gene 130026] {aka ALS2CR14, ALS2CR15}
- **Diseases:** neurological deterioration (MESH:D009422), CCF (MESH:D003025), CCFs (MESH:D020216), Fistula (MESH:D005402), ICH (MESH:D002543), arterial hypertension (MESH:D000081029)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

61 references — full list in the complete paper: https://tomesphere.com/paper/PMC12643439/full.md

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Source: https://tomesphere.com/paper/PMC12643439