Transient ischemic attack as the initial symptom of a life-threatening condition

This is an unauthorised machine translation into English made using the DeepL Translate Pro translator. The editors do not guarantee that the content of the article corresponds fully to the original language version.

Dear Editor,

We present the case of a man with a transient ischemic attack (TIA) resulting from an unusual cause, requiring prompt diagnosis and urgent treatment.

In September 2022, a man was brought to the Department of Emergency Medicine (KUM) at our teaching hospital with suspected stroke. The emergency medical services (EMS) reported that the patient was an 86-year-old man found at home with sudden-onset severe right-sided hemiparesis and aphasia. An occlusion of a major cerebral artery was therefore suspected. Upon arrival at the KUM, however, the patient was subjectively completely asymptomatic.

He was a man at high vascular risk with arterial hypertension, dyslipidemia, and atrial fibrillation. He was taking antihypertensives, a statin, and warfarin. He had been fully self-sufficient until then and lived with his wife. He described the episode himself as follows: he went to the bathroom, where he suddenly felt generally unwell and his head spun. He did not know “what happened next.” Notable was the report of low blood pressure (BP) measured by the EMS on-site (90/50 mmHg) with a heart rate of 110 beats per minute.

Upon arrival at the emergency department, his BP was 96/63 mmHg and his heart rate was 130/min. Otherwise, the internal examination was unremarkable, and the objective neurological examination was normal—the neurological symptoms had completely resolved within approximately one hour. Clinically, this was therefore a TIA. The patient reported only mild general weakness and aching in the lower back. A native brain CT and CTA of the cerebral arteries were performed acutely, with normal findings. Arterial hypotension gradually progressed to 70/52 mmHg, and tachycardia increased to 140/min. The patient continued to report only aching in the lower back, but objectively he was pale, sweaty, and visibly in distress. A suspicion of intra-abdominal hemorrhage was raised. An abdominal ultrasound revealed an abdominal aortic aneurysm (AAA) measuring 8 × 8.5 cm with suspected blood leakage (Fig. 1). A CT angiography (CTA) of the abdominal aorta confirmed a fusiform aneurysm of the subrenal portion of the abdominal aorta measuring 4.6 × 4.1 × 9 cm with a covered perforation and an associated retroperitoneal hematoma measuring 11.8 × 11.3 × 25 cm, displacing the right kidney (Fig. 2).

The patient was urgently transported to the operating room. A vascular surgeon performed resection and replacement of the ruptured AAA with an aorto-aortic graft. Circulatory support with catecholamines was already required during the operation. Volume resuscitation was continued postoperatively; two days later, the patient was extubated and weaned from mechanical ventilation. The subsequent postoperative course and recovery were uneventful. Thirteen days after surgery, he was discharged home with normal objective neurological findings and in generally good condition.

An aneurysm is caused by a localized weakening of the blood vessel wall, in this case the abdominal aorta. The causes of aneurysms are not entirely clear, but the most commonly cited cause is atherosclerosis. Risk factors include smoking, being over 65 years of age, and being male. The aneurysm itself develops over years and usually causes no symptoms, sometimes only a feeling of pressure or pulsation in the abdomen. In the event of an aneurysm rupture, symptoms are pronounced, and the condition can rapidly progress to circulatory instability. AAA rupture typically presents as sudden, severe abdominal pain radiating to the groin or lower back. Symptoms of hemorrhagic shock then gradually develop—pallor, tachycardia, arterial hypotension, and impaired consciousness.

Neurological symptoms (syncope or transient focal neurological deficit) are extremely rare in AAA rupture and occur in only a few percent of cases. In our case, the TIA was a consequence of global cerebral hypoperfusion following a sudden drop in blood pressure. This unusual presentation underscores the need to investigate etiologies of stroke other than purely neurological ones, particularly in the presence of arterial hypotension and signs of shock, as performing intravenous thrombolysis (IVT) in a patient with an undiagnosed AAA rupture would have fatal consequences [1]. The diagnosis is established using ultrasound or CT. The causal treatment is urgent surgical repair or endovascular aneurysm repair (EVAR); administration of blood products and comprehensive care for the patient in hemorrhagic shock are essential.

The prevalence of AAA in men over 65 has decreased significantly and currently stands at around 2%, primarily due to a decline in smoking and improvements in preventive care. Despite these advances, mortality from AAA rupture remains very high—roughly half of patients die before reaching the hospital [2,3].

If a patient survives the acute phase of the rupture, they are indicated for open surgery or EVAR. Open surgery is associated with high perioperative mortality, ranging from 35–40%; the extreme surgical risk is linked to the poor condition of patients and frequent complications, such as multiple organ failure or myocardial infarction [4,5]. EVAR reduces perioperative mortality to approximately 24% [6]. In contrast, long-term outcomes favor open surgery.

According to a large population-based study involving more than 32,000 patients, open surgery for unruptured AAA was associated with lower six-year mortality (35.6% vs. 41.2%), a lower risk of late rupture (5.8% vs. 8.3%), and a lower rate of reintervention (11.6% vs. 16.0%) compared to EVAR. The most significant benefits of open surgery become apparent over the longer term, 1–2 years after the procedure, while the risk of early perioperative complications and death is higher with this approach. The conclusions of this large-scale study underscore the necessity of individualized treatment selection and careful follow-up of patients after EVAR due to the higher risk of late complications [7].

Long-term complications of EVAR for AAA were analyzed by Černá et al. in a cohort of 69 patients followed for more than ten years after stent graft implantation, in whom 29 serious complications (42%) occurred on average after 14 years, requiring treatment in 22 cases. The most common complications were stent graft migration, type Ia, Ib, and III endoleaks, endotension, thrombosis of a limb or the entire stent graft, and retroperitoneal abscess. Complications occurred within 1–18 years of implantation, most frequently between the 5th and 10th year. These late complications can also occur in patients without prior symptoms and confirm the necessity of lifelong follow-up after EVAR [8].

Late complications following open surgical treatment of AAA are relatively rare. The most common are anastomotic pseudoaneurysms, occlusion of one of the branches of the vascular prosthesis, and infection of the vascular prosthesis—their incidence is around 2% [9]. These complications may necessitate reoperation or further treatment; therefore, long-term follow-up of patients is recommended even after a successful operation to ensure early detection of any potential late complications.

The case of our patient with a rare cause of TIA—cerebral hypoperfusion resulting from sudden arterial hypotension due to AAA rupture—underscores the necessity of a thorough internal examination of patients with suspected stroke. The primary warning signs that the cause of the symptoms was not purely neurological were worsening arterial hypotension and increasing tachycardia, general weakness, and unusual aching in the lower back. If a neurological deficit had persisted, performing IVT would have been a fatal mistake. In our case, however, rapid diagnosis and subsequent successful surgery led to the patient’s survival, which is rather rare in cases of AAA rupture at this age.

Financial Support

Supported by Charles University (Cooperatio program, NEUR research area) and the Ministry of Health of the Czech Republic (RVO –⁠ FHNK 00179906).

Conflict of Interest

The authors declare that they have no conflict of interest in connection with the subject of this work.