Hemorrhagic stroke due to cerebellar arteriovenous malformation managed in a Medium-Complexity Public Hospital: a case report

CASE REPORT

MELATI, Maria Eduarda Gonzales ^[1], SCHUSTER, Andrei Leonardo ^[2], GRECO, Maria Antonia Schluter ^[3], SCOZZIERO, Fábio Estrada ^[4], PAGLIARIN, Nicole Brunello ^[5]

MELATI, Maria Eduarda Gonzales et al. Hemorrhagic stroke due to cerebellar arteriovenous malformation managed in a Medium-Complexity Public Hospital: a case report. Revista Científica Multidisciplinar Núcleo do Conhecimento. Year 10, Ed. 09, Vol. 02, pp. 146-153. September 2025. ISSN:2448-0959. Access link: https://www.nucleodoconhecimento.com.br/health/hemorrhagic-stroke, DOI: 10.32749/nucleodoconhecimento.com.br/health/hemorrhagic-stroke

ABSTRACT

Cerebellar Arteriovenous Malformations (CMAVs) are rare but clinically significant vascular anomalies with a high risk of hemorrhage. We report a case of a 51-year-old hypertensive male who presented with a thunderclap headache and cerebellar hemorrhage due to an arteriovenous cerebellar malformation. Initial CT revealed two intraparenchymal hemorrhages in the left cerebellar hemisphere with mild mass effect. Angio tomography and MRI confirmed the vascular anomaly. The patient underwent neurocritical care with blood pressure control and showed partial neurological recovery, with residual gait ataxia, horizontal nystagmus, and a positive Romberg sign. This case underscores the importance of considering CMAVs in spontaneous cerebellar hemorrhages. Even in medium-complexity public hospitals, timely neurocritical care and diagnostic imaging can stabilize patients, allowing for appropriate referral to specialized care.

Keywords: Hemorrhagic stroke, Cerebellar arteriovenous malformation, Public hospital, Neurosurgery.

1. INTRODUCTION

Arteriovenous Malformations (AVMs) are vascular anomalies defined by direct connections between arteries and veins without an intervening capillary bed. While they can occur systemically, intracranial AVMs are relatively rare, with an estimated annual incidence of 1.12–1.34 per 100,000 individuals. Cerebellar AVMs (CMAVs) represent 7–15% of these lesions and are associated with a higher risk of rupture and more severe clinical presentations due to the confined anatomy of the posterior fossa. In a large series involving 1,311 AVM cases, 8.6% involved the posterior fossa, predominantly affecting males (63.1%) with a mean age of 38.6 years. Hemorrhage was the initial presentation in 78.9% of cases [1]. Microsurgical resection remains the gold standard, though preoperative embolization and stereotactic radiosurgery are commonly used adjuncts or alternatives depending on AVM architecture and location[3]. Preoperative embolization is used to reduce AVM flow, facilitating safer surgical resection by minimizing intraoperative bleeding. Embolization may serve as definitive therapy, especially for inoperable AVMs or to alleviate venous hypertension [5–7]. Stereotactic radiosurgery induces progressive vascular occlusion via radiation-triggered endothelial injury. [3].

2. CASE PRESENTATION

A 51-year-old Brazilian male with systemic arterial hypertension, managed with Losartan 50 mg twice a day, and a remote history of tobacco exposure (2 pack-years, ceased over 40 years ago), presented to a medium-complexity public hospital in the city of Gravataí, located in the state of Rio Grande do Sul (Brazil) with a sudden, severe occipital headache reaching maximal intensity in under one minute — clinically consistent with a thunderclap headache. Accompanying symptoms included blurred vision, bilateral lower limb weakness, nausea, and vomiting. Neurological examination revealed mild dysmetria and horizontal nystagmus.

Initial non-contrast cranial Computed Tomography (CT) revealed two hyperdense intraparenchymal lesions in the left cerebellar hemisphere (2.7 cm and 2.6 cm), surrounded by mild vasogenic edema and causing early compression of the fourth ventricle without hydrocephalus.

Figure 1: Non-contrast CT scan of the skull performed on arrival as an emergency, showing two hemorrhagic formations in the left cerebellar hemisphere, the largest measuring 2.7 cm and the other 2.6 cm, lobes with mild adjacent vasogenic edema that obliterate the cerebellar sulci and compress the fourth ventricle discreetly. Ventricular system with usual morphology, topography and dimensions. Centered median structures. Absence of subdural pathological collections

Immediate management included neurocritical monitoring (head of bed kept elevated, with systolic blood pressure controlled below 140 mmHg, along with strict temperature and capillary blood glucose monitoring, intravenous antihypertensives, and serial neurological examinations). It was discussed with neurosurgery, and conservative management was chosen. The following day, the patient continues to present with nausea, vomiting, headache, and diplopia. In objective evaluation the patient was off sedated, alert and oriented, with good general status and mucosae preserved. Stable vital signs, except for blood pressure at 143/88 mmHg. On sodium nitroprusside at 15 mL/h. Peak inspiratory flow rate preserved. Right-sided diplopia and nystagmus observed. Speech and strength preserved in all four limbs, with no evident focal neurological deficits. Oral antihypertensives (enalapril, hydralazine, hydrochlorothiazide, and amlodipine) were initiated with plan to discontinue sodium nitroprusside and subsequent non-contrast CT imaging confirmed lesion stability (no signs of herniation or active rebleeding). By the end of the second day antihypertensive doses were increased at maximum dosage, along with clonidine every 8 hours. Serial neurological examinations were performed, with persistence of nystagmus and dysmetria. The patient reported headache that improved with dipyrone.  On the sixth day of hospitalization in the intensive care unit: no dense focal motor signs, mean arterial pressure 106, cleared for transfer to the general ward.

The patient remained stable, awaiting angiotomography and magnetic resonance imaging, which were performed after two weeks of hospitalization due to the high patient demand relative to the hospital’s capacity. Cranial angiotomography revealed a venous developmental anomaly in the left cerebellar hemisphere. Brain MRI with gadolinium confirmed the presence of hemorrhagic foci and ruled out aneurysmal components or midline shift, suggesting a mixed-type AVM.

Figure 2: Head contrast-enhanced MRI with a flair sagittal cut and axial T1 cut, respectively, indicating two areas of intraparenchymal hemorrhage in the left cerebellar hemisphere, each measuring approximately 2.5 cm in the largest axial axis, causing a small mass effect and bulging of the lateral wall of the fourth ventricle

The patient showed progressive clinical improvement during hospitalization. Neurological examination at discharge revealed residual gait ataxia, horizontal nystagmus, and a positive Romberg sign. He remained hemodynamically stable, was ambulatory with assistance, and was discharged on optimized oral antihypertensive therapy. Outpatient referral was made to neurosurgery and interventional neuroradiology at a tertiary center for further evaluation and management of the vascular lesion.

Figure 3: Arterial and venous computed tomography angiography of the intracranial vessels with contrast showing patent internal carotid, middle cerebral, anterior cerebral, vertebral, basilar and posterior cerebral arteries. Circle of Willis with anatomical configuration. There is no evidence of demonstrable aneurysms in the present study. Main dural venous sinuses, superficial cortical veins and internal cerebral veins are patent. Anomaly of venous development in the left cerebellar hemisphere with drainage to a vein in the left lamina of the tentorium. Diagnostic impression: Anomaly of venous development in the left cerebellar hemisphere, accompanied by intraparenchymal bleeding, inferring mixed vascular malformation

3. DISCUSSION

AVMs, particularly those in infratentorial locations, pose diagnostic challenges due to their rarity and nonspecific presentation. According to the American Heart Association/American Stroke Association (AHA/ASA) guidelines [9,10], initial management of AVM-related hemorrhage must prioritize hemodynamic stabilization, blood pressure control, and multidisciplinary evaluation to define the best therapeutic approach [10]. Even in an environment with limited resources like ours, the emergency management of intracerebral hemorrhage recommended by the AHA was carried out (It is important to emphasize that it was primarily managed only as a case of intracerebral hemorrhage, since there was no knowledge of the AVM), focusing on hemodynamic stabilization and reduction of blood pressure, and no therapies were performed that have historically been used to treat patients with intracranial hemorrhage in the emergency setting that appear to confer no benefit, such as prophylactic corticosteroids or continuous hyperosmolar therapy, and the use of platelet transfusions, that outside the context of emergency surgery or severe thrombocytopenia appears to be associated with worse outcomes. Surgical intervention for cerebellar hemorrhage is now also advised for volumes over 15 mL, alongside established triggers like neurological worsening, brainstem compression, and hydrocephalus [9]. Once a brain AVM is identified or suspected by CT or MR, Digital Subtraction Angiography (the reference standard for the diagnosis of brain MAVs) is generally pursued to further characterize the lesion if treatment is being considered because it provides the most detailed and accurate information about angioarchitecture and hemodynamics [10]. In our case, the lack of access to digital subtraction angiography and advanced neuroimaging complicates the diagnostic pathway and after initial stabilization, it was possible to perform the etiological diagnosis, only two weeks after, due to the AngioTC that showed the CMAV. However, it was not possible to assess the need for treatment, since there was no interventional neuroradiology service in the hospital and more appropriate neuroimaging, such as digital subtraction angiography. However, the lesion described likely corresponds to a Spetzler-Martin grade II or III, given its location, moderate size, and uncertain venous drainage, which possibly implies a moderate surgical risk [8].

4. CONCLUSION

This case reinforces the importance of considering cerebellar AVMs in the differential diagnosis of spontaneous posterior fossa hemorrhages. It also demonstrates that, even within the constraints of a medium-complexity hospital, structured neurocritical care and the use of accessible imaging modalities can ensure adequate stabilization, enabling appropriate referral for specialized evaluation, mainly, aiming to avoid new similar events. The educational value of this case extends to clinicians working in emergency and primary care, particularly regarding the early recognition of red flag symptoms such as thunderclap headache and the relevance of stringent blood pressure control in the acute setting.

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^[1] Medical Student at the University of Vale do Rio dos Sinos. ORCID: https://orcid.org/0009-0009-7820- 0292. Currículo Lattes: http://lattes.cnpq.br/2411868620403061.

^[2] General Practitioner. ORCID: https://orcid.org/0000-0001-7275-3819. Currículo Lattes: http://lattes.cnpq.br/5373214785071553.

^[3] Medical Student at the University of Vale do Rio dos Sinos. ORCID: https://orcid.org/ 0009-0007-4098-2183. Currículo Lattes: https://lattes.cnpq.br/9157789098008104.

^[4] Medical Student at the University of Vale do Rio dos Sinos. ORCID: https://orcid.org/0009-0000-7836-526X.

^[5] Medical Student at the University of Vale do Rio dos Sinos. ORCID: https://orcid.org/0000-0002-2306-7289. Currículo Lattes: https://lattes.cnpq.br/3557506744241210.

Material received: June 21, 2025.

Peer-approved material: July 10, 2025.

Edited material approved by authors: September 8, 2025.