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Pictorial CME
32 (
2
); 157-159
doi:
10.25259/VJIM_5_2022

A Case of Intracranial Aneurysm Masquerading as Space-Occupying Lesion

Associate Professor, Department General Medicine, Government Medical College, Nagpur, Maharashtra, India
Junior Resident, Department General Medicine, Government Medical College, Nagpur, Maharashtra, India
Corresponding author: Nandita Bagchi, Department General Medicine, Government Medical College, Nagpur, Maharashtra, India. nanditabagchi95@gmail.com
Licence
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: Khandait V, Bagchi N. A case of intracranial aneurysm masquerading as space-occupying lesion. Vidarbha J Intern Med 2022;32:157-9.

Abstract

Cerebral or intracranial aneurysms result from abnormal focal dilation of an artery in the brain due to weakening of the blood vessel wall. They occur at the bifurcations of large to medium sized intracranial arteries. Approximately 80% aneurysms occur in the anterior circulation and about 20% have multiple aneurysm sites. Familial aneurysms rupture at a smaller size and younger age than sporadic cases. We present a case of cerebral artery aneurysm in a 49-year-old female patient. The patient was admitted as a case of the intracranial space-occupying lesion with complaints of headache subsequently found to have an internal carotid artery aneurysm.

Keywords

Aneurysm
Space occupying lesion
Headache

INTRODUCTION

Approximately 86.5% of all intracranial aneurysms arise on the anterior (carotid) circulation. Common locations include the anterior communicating artery (30%), the internal carotid artery (ICA) at the posterior communicating artery origin (25%), and the MCA bifurcation (20%). Giant aneurysm (GIA’s) are defined as aneurysm measuring more than 2.5 cm in diameter, occurrence has been reported approximately 5-13% of all intracranial aneurysms. They constitute a special group which do not usually cause subarachnoid haemorrhage (SAH). Instead, they are commonly detected as slow growing, space occupying mass lesion. This particular aneurysm may be confused with other cerebral mass lesions, such as pituitary adenoma.

CASE REPORT

A 49-year-old female patient came with complaints of persistent global headache for 3 days with multiple episodes of vomiting for the past 1 day. On examination, the patient was afebrile, conscious, oriented to time, place, and person; pulse 72/min regular, BP 150/80 mmHg, SpO2 98% on room air, heart sounds were normal and breath sounds were normal. On neurological examination of GCS E4V5M6, reflexes were normal, plantar bilateral flexor response and pupils normal-sized reactive to light with no focal neurological deficit. Contrast-enhanced CT brain showed a well-defined homogenous hyperdense mass in the sella turcica extending superiorly in the suprasellar cistern with likely differentials of Pituitary macroadenoma and Meningioma. Contrast MRI of the Brain with Angiography revealed a large left supraclinoid internal carotid artery aneurysm (1.7 × 1.3 × 1.3 cm) involving the origin of the left anterior and middle cerebral artery with minimal subarachnoid haemorrhage in the left sylvian and temporoparietal cortical sulci suggestive of a leaking aneurysm. Digital subtraction angiography was done and revealed a contrast-filled multilobulated outpouching arising from the left supraclinoid ICA proximal to the origin of the left MCA. Successful coiling was done under radiographic guidance and the patient was monitored for 3 days post-procedure. She was then, discharged in a vitally stable condition [Figures 1 and 2].

Figure 1:: DSA Large supraclinoid ICA aneurysm.
Figure 2:: DSA - post coiling of the aneurysm.

DISCUSSION

Saccular aneurysms are thin-walled protrusions from intracranial arteries composed of very thin or absent tunica media and an absent or fragmented internal elastic lamina. They occur at the bifurcations of large to medium-sized intracranial arteries. Approximately 80% of aneurysms occur in the anterior circulation and about 20% have multiple aneurysm sites.[1] Giant aneurysms those >2.cm in diameter occur at the same sites as small and account for 5% of cases. There is a female preponderance ranging from 34 to 61% higher risks of aneurysms.

Laboratory Data
Investigation 7/09/21
Hb-Haemoglobin 10.5
TLC- Total leukocyte count 7300
Platelets 1.32×105
Total protein 6.5
Total bilirubin 0.68
ALP-Alkaline phosphatase 124
AST-Aspartate aminotransferase 23
ALT-Alanine aminotransferase 40
Urea 17
Creatinine 0.8
Sodium 134
Potassium 4.2
Triglycerides 89
Total cholesterol 127
HDL-High density cholesterol 34
LDL-Low density cholesterol 100

Risks factors for aneurysm formation

  • Hypertension

  • Cigarette smoking

  • Alcohol consumption

  • Hereditary syndromes associated – Connective tissue disorders such as Ehlers–Danlos, autosomal dominant polycystic kidney disease, glucocorticoid remediable aldosteronism, and moyamoya disease

  • Coarctation of aorta

  • Oestrogen deficiency.

SCREENING

Screening should be considered in

  1. First-degree relatives of patients with cerebral aneurysms when two or more family members have been affected

  2. Patients with heritable disorders associated with the presence of intracranial aneurysms – ADPKD, GRA, Ehler–Danlos and pseudoxanthoma elasticum.[2]

Familial aneurysms rupture at a smaller size and younger age than sporadic and multiple numbers is also common. They do not demonstrate the phenomenon of anticipation.

CHOICE OF SCREENING TEST

  1. MR Angiography – can identify 3–5 mm or larger aneurysms. 95% sensitivity

  2. CT angiography identifies small unruptured aneurysms with high accuracy. For detecting <3 mm diameter, sensitivity was lower than MRI.

PRESENTATION

  • Excruciating headache (‘worst headache of my life) followed by the sudden loss of consciousness due to rupture, leading to subarachnoid haemorrhage[3]

  • Nausea and vomiting

  • Neurological deficits.

Unruptured aneurysms may be asymptomatic or may present with a mass effect on cranial nerves or brain parenchyma.

  • Third cranial nerve palsy with focal pain above or behind the eye may occur with expanding aneurysm at the junction of the posterior communicating artery and internal carotid artery

  • Sixth nerve palsy – aneurysm in the cavernous sinus

  • Visual field defects occur in expanding supraclinoid carotid or anterior cerebral artery aneurysm.

MANAGEMENT

  • Surgical management (Surgical Clipping) – the clip is placed across the neck of the aneurysm. Depends on the anatomical location, and size of the neck of the aneurysm. Potential benefits of the early surgery are within 24 to 72 h of haemorrhage with the management of vasospasm.[4]

    Risks – new or worsened neurological deficit due to temporary arterial occlusion, intraoperative haemorrhage.

  • Endovascular therapy (Coil embolism) – Platinum coils are inserted into the lumen of the aneurysm.

    Risks – Thromboembolism and intraprocedural aneurysmal rupture.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

  1. , , , , , . Harrison's Principles of Internal Medicine (20th ed). McGraw-Hill Education; . p. 2084-6.
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  2. , , , , , , et al. Guidelines for management of aneurysmal subarachnoid haemorrahge. Stroke. 2009;40:191395.
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  3. , , , , . Cognitive outcome after aneurysm rupture: Relationship to aneurysm site and perioperative complications. Neurology. 1995;45:875-82.
    [CrossRef] [PubMed] [Google Scholar]
  4. , , , . Prevalence and risk of rupture of intracranial aneurysms a systematic review. Stroke. 1998;29:251-6.
    [CrossRef] [PubMed] [Google Scholar]
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