A Case of Giant Cell Arteritis Presenting As Catastrophic Posterior Circulation Stroke: A Diagnostic Dilemma
Joshua Wong1, Siang Chan1, Ashit Shetty1
1Stroke Service, Nottingham University Hospitals NHS Trust, Nottingham, GBR.
Insights
Giant cell arteritis (GCA), a rare vasculitis, can cause serious complications like stroke and vision loss. Early corticosteroid treatment is crucial for improving outcomes in patients with GCA.
Area of Science:
- Rheumatology
- Neurology
- Cardiology
Background:
- Giant cell arteritis (GCA) is an immune-mediated vasculitis primarily affecting the elderly.
- Prompt diagnosis and treatment with corticosteroids are essential to prevent severe complications.
Observation:
- A 75-year-old woman with GCA presented with jaw claudication and headache, later developing vision loss, confusion, and multiple arterial thrombi.
- Imaging revealed bilateral vertebral artery thrombus and left anterior descending artery thrombus, alongside a left ventricular thrombus.
Findings:
- The patient experienced stroke, bilateral visual loss, and cardiac arrest, highlighting the severe thromboembolic potential of GCA.
- A complex interplay of vasculitis, atherosclerosis, and cardiac emboli likely contributed to the clinical events.
Implications:
- This case underscores the importance of high clinical suspicion for GCA complications, including stroke and visual impairment.
- Utilizing advanced imaging like ultrasonography, echocardiography, and contrast-enhanced body scans is vital for diagnosing GCA and its thromboembolic sequelae.
Abstract:
Giant cell arteritis (GCA) is an immune-mediated systemic vasculitis usually seen in the older population. We describe a case of a 75-year-old woman who presented with jaw claudication and temporal headache. A colour duplex ultrasonography and later biopsy of the temporal arteries confirmed GCA and she was commenced on oral steroids. She was subsequently readmitted with a new worsening vision of both eyes and confusion. Her brain images revealed acute bilateral vertebral artery thrombus with haemorrhagic transformation. She was loaded on intravenous steroids. The next day she developed vomiting, bilateral visual loss and a cardiac arrest from ventricular fibrillation. Following the return of spontaneous circulation, she was taken to the cardiac catheterisation laboratory for a coronary angiogram, which showed diffuse thrombus at the apical left anterior descending artery. A bedside echocardiogram revealed a sizable left ventricular thrombus. She was managed with heparin and antiplatelet therapy. This case presented a complex diagnostic dilemma to the medical team as vasculitis, atherosclerosis, and cardiac emboli could have contributed to her stroke and visual loss. This patient also had some vascular risk factors for occlusive cerebrovascular disease, potentially suggesting a clinical event with multiple aetiologies. Stroke and visual loss are rare but serious complications of GCA, which require a high index of suspicion and early treatment with corticosteroids to improve prognosis. Although a temporal artery biopsy remains to be the definitive diagnostic modality for GCA, the use of radiological investigations in the diagnosis of GCA is increasingly common. A non-invasive colour duplex ultrasonography of the temporary arteries could be used to assess GCA in highly suspected patients. Echocardiograms and contrast-enhanced body imaging should be performed in patients with suspected or established GCA to assess for secondary thromboembolic and vascular complications.
