Undisclosed Abdominal Aortic Aneurysm as a Risk Factor for Hemorrhage in Tenecteplase Stroke Thrombolysis: A Case Report

Introduction

Acute ischemic stroke (AIS) is a leading cause of mortality and long-term disability worldwide, accounting for most stroke cases [1]. The primary mechanisms include large-artery atherosclerosis, cardioembolism, and small-vessel occlusion, with clinical presentation typically involving sudden neurological deficits, such as unilateral weakness, speech disturbance, or visual impairment. Early diagnosis is achieved by non-contrast-enhanced computed tomography (CT) to exclude intracerebral hemorrhage, followed by vascular imaging when feasible. International guidelines emphasize rapid reperfusion therapy as the cornerstone of management [1].

Tenecteplase (TNK) is a genetically engineered variant of alteplase and is classified as a recombinant tissue plasminogen activator. Compared with alteplase, it has greater fibrin specificity and a longer half-life, allowing administration as a single intravenous (i.v.) bolus [2]. TNK was first approved for acute myocardial infarction and has since been evaluated in AIS, in which randomized controlled trials have demonstrated non-inferior or superior efficacy compared with alteplase [3]. For AIS, the recommended dose is 0.25 mg/kg (maximum 25 mg) given as a single i.v. bolus. The European Stroke Organisation now endorses TNK as an effective alternative to alteplase in eligible patients within the 4.5-h time window [4].

Nonetheless, evidence regarding the safety of TNK in patients with complex vascular anomalies, such as abdominal aortic aneurysm (AAA), remains extremely limited. AAAs are often asymptomatic and can remain undiagnosed until incidentally discovered [5]. Pathophysiological features, such as mural thrombus, chronic inflammation, and vessel wall fragility, can alter bleeding risks under fibrinolytic therapy [6].

In this report, we present the case of a 77-year-old man treated with TNK fibrinolysis for AIS, in whom an incidental AAA complicated by mural thrombus and ulceration was later identified.

Case Report

A 77-year-old man presented to the Emergency Department approximately 4 h after symptom onset, which occurred at 8: 30 a.m., with acute left-sided weakness. Relevant medical history included hypertension, coronary artery disease, and past sigmoid colon carcinoma surgery. The overall sequence of clinical events is summarized in a timeline (Figure 1). On admission, his National Institutes of Health Stroke Scale (NIHSS) score was 12, and a non-contrast-enhanced head CT excluded intracranial hemorrhage (Figure 2). His blood pressure was 128/66 mmHg, without clinical indicators of vascular instability.

At 12: 47 p.m., he received guideline-recommended TNK dosing (total 21.25 mg i.v., 0.25 mg/kg), as he met eligibility criteria for thrombolysis, and TNK is endorsed as an effective alternative to alteplase in AIS [4]. Partial neurological improvement was observed, with the NIHSS decreasing to 10 and muscle strength improving to just below grade 3 on the Medical Research Council scale. Large-vessel occlusion was suspected, and thrombectomy was discussed with the family, who ultimately declined.

Three hours later, at 3: 45 p.m., the patient exhibited diaphoresis, right groin pain, and significant inter-arm blood pressure asymmetry (left arm: 212/102 mmHg, right arm: 134/70 mmHg). An urgent repeat head CT scan showed no evidence of intracranial hemorrhage (Figure 3). Intravenous sodium nitroprusside was promptly administered to control blood pressure. A vascular surgery consultation led to a comprehensive aortic CT angiography at 5: 49 p.m., which revealed an infrarenal AAA with mural thrombus and penetrating ulceration. The maximum aneurysm diameter was 41 mm (Figure 4), increased from 34 mm on imaging performed 5 years earlier.

At 8: 00 p.m., the patient experienced sudden neurological deterioration. A follow-up head CT scan showed new right thalamic and cerebellar hemorrhage (Figure 5). Laboratory test results indicated systemic inflammation and coagulopathy, including a white blood cell count of 24.8×109/L (reference range: 3.5–9.5), D-dimer level of 3.3 mg/L (reference range: <0.5), fibrinogen level of 0.2 g/L (reference range: 1.9–4.0), and international normalized ratio of 1.8 (reference range: 0.8–1.2).

Although TNK reversal strategies were proposed, the family declined further aggressive interventions, including Intensive Care Unit admission and neurosurgical procedures. The patient’s condition deteriorated rapidly, and he died at 10: 03 p.m.

Discussion

This case illustrates that TNK thrombolysis, although effective and convenient for AIS, can pose substantial hemorrhagic risk in patients with unrecognized vascular anomalies, such as AAA. It highlights the need for careful pre-thrombolysis history-taking, attention to subtle clinical warning signs, and individualized risk assessment in elderly patients.

In our patient, the diagnosis of AIS was confirmed by clinical presentation and exclusion of hemorrhage on initial non–contrast-enhanced CT, making thrombolysis appropriately indicated. The fatal intracerebral hemorrhage occurred several hours later, consistent with a complication of treatment. Nevertheless, the patient’s underlying AAA, complicated by mural thrombus and ulceration, created a fragile vascular substrate, as immune and inflammatory mechanisms are known to weaken the aortic wall [7]. This fragility likely increased susceptibility to bleeding, even though TNK has demonstrated a generally favorable safety profile in randomized clinical trials [8–10]. Pharmacologically, TNK provides enhanced fibrin specificity and an extended half-life, allowing rapid and efficient single-bolus administration [11]. However, TNK’s prolonged fibrinolytic activity, while advantageous for clot dissolution, may exacerbate bleeding in structurally compromised vessels. Preclinical studies have also shown that TNK can increase blood–brain barrier permeability via complement activation (C5a/C5aR1), a mechanism potentially relevant to aneurysmal vessel walls [12]. Taken together, these factors highlight how the inflammatory and structural pathology of AAA can render the aortic wall particularly vulnerable under fibrinolytic stress [7].

The clinical course in this case also provides key insights. Early warning signs, such as inter-arm blood pressure asymmetry and groin pain, indicated underlying vascular compromise, suggesting that bilateral blood pressure monitoring should be considered in acute stroke evaluation [13]. Although AAA is not explicitly listed as a contraindication to thrombolysis in current guidelines [4], previous case reports have described hemorrhage complications after fibrinolysis. For example, Mayette et al reported an aortic stent graft leak and aneurysm rupture after alteplase administration in a patient with stroke [6], while Das et al described a rare case of non-aneurysmal subarachnoid hemorrhage following TNK thrombolysis in AIS [14]. Other reports have similarly emphasized the complexity of managing AAA in patients undergoing vascular interventions, such as stent-graft implantation [15]. Collectively, these reports highlight that systemic and intracranial hemorrhagic complications can occur after fibrinolysis, even in the absence of typical risk factors. Compared with these prior reports, our case is unique in demonstrating fatal intracerebral hemorrhage after TNK in the context of an undisclosed AAA, reinforcing the importance of transparency and thorough medical documentation.

Finally, this case underscores the influence of family-centered decision-making on treatment pathways. The refusal of thrombectomy and later aggressive interventions limited therapeutic options and contributed to the fatal outcome. Furthermore, the prior non-disclosure of an existing AAA critically affected treatment decisions, reinforcing the importance of meticulous history review and clear communication between clinicians, patients, and families in acute stroke management.

Conclusions

This case highlights the potential hemorrhagic risk of TNK in patients with AIS and an undisclosed AAA. It emphasizes the importance of thorough vascular history-taking, individualized risk assessment, and clear communication with patients and families before thrombolytic therapy.