Acute ischemic stroke what is hidden behind?

Abstract

Acute aortic dissection (AAD) is a rare and potentially fatal disease. The classic presentation is sudden and severe pain in the chest, back, or abdomen, described as tearing or ripping pain radiating to the interscapular region. Cerebral ischemic complications occur in 18–30% of aortic dissections and patients may present to the emergency department (ED) with isolated focal neurology and no chest pain. In AAD patients, presenting with stroke and subsequently thrombolized, a 71% mortality rate has been reported in patients receiving recombinant tissue plasminogen activator (r-TPA). We present a case of a 58-year-old male patient that presented to ED with sudden onset of headache and left-sided hemiparesis, computed tomography (CT) demonstrated an ischemic stroke of the right middle cerebral artery. When the question of whether to start r-TPA or mechanical thrombectomy was discussed, a cardiac point-of-care ultrasound was performed in ED and showed a type A aortic dissection; immediately a CT aortic angiogram was performed and confirmed the diagnosis. The patient was taken to theater and had a favorable outcome.

<Learning objective: Acute aortic dissection (AAD) may present as acute ischemic stroke with no chest pain. In patients with acute ischemic stroke with an unclear etiology point-of-care ultrasound (POCUS), cardiac, and aortic ultrasound are important rapidly to diagnose AAD and avoid the deleterious effect of thrombolysis. This case supports the feasibility of emergency physicians performing POCUS assessments for AAD.>

Introduction

Acute aortic dissection (AAD) is one of the most dramatic cardiovascular emergencies, and should be recognized and treated urgently. AAD is uncommon with a frequency of 2–4 per 100,000 person-years; however it is a life-threatening pathology with a mortality rate of 1.2% per hour in the first 48 h. Classic AAD has been described as severe or ‘worst ever’ (90%), abrupt (84–90%), sharp or tearing (64%), retrosternal or interscapular pain (50%), migrating (16%), down the back (46%) and maximal at onset [1]. However, not all cases of AAD present with the classic symptoms and establishing the diagnosis may be difficult when the classic pattern of pain is absent [2]. AAD was not diagnosed in the initial presentation in 15–43% of cases [3]. There have been reports of several cases of AAD presenting with non-pain related symptoms, especially neurological and cardiovascular. Although AAD is an infrequent cause of ischemic stroke, neurological manifestations are common [4], [5].

Case report

A 58-year-old male patient presented to the emergency department (ED) with a 24-h history of global headache that had become worse in the previous 4 h. He arrived by himself at the ED and in the triage room had an episode of decreased alertness with a Glasgow scale of 13 points (E4V3M6) accompanied by motor hemiparesis of the left arm and face. No further specific symptoms including chest pain, nausea, vomiting, vertigo, dyspnoea were noted prior to the episode. His medical history was unremarkable, no risk factors were identified. On physical examination, he was able to obey the commands, however he was confused and using innapropiate words. His cardiovascular and respiratory examinations were unremarkable, and there was no specific abnormal finding. His peripheral pulses were symmetric and normal. Observations included blood pressure = 145/77 mmHg, pulse rate = 76/min, respiration rate = 16/min. On neurology examination the patient had a left-sided hemiparesia with muscle power of 3/5 in left arm acompained by central facial weakness. Blood analysis on arrival showed total white cell count 13.7 × 10⁶/μL, red blood cell (RBC) count 4.18 × 10⁶/μL, hemoglobin estimation 136.00 g/L, hematocrit 0.41%, platelet count 177.00 × 10⁹/μL, serum alkaline phosphatase 44.00 IU/L, serum albumin 41.00 g/L, serum calcium 2.25 mmol/L, plasma glucose level 8.0 mmol/L, serum alanine aminotransferase (ALT) level 19.00 IU/L, serum sodium 137.00 mmol/L, serum potassium 4.5 mmol/L, serum urea level 5.3 mmol/L, serum creatinine 118.00 μmol/L.

Ischemic stroke was initially suspected and the stroke team was activated. The time between the activation of the stroke team and the beginning of symptoms was approximately 20 min as the onset time was in the triage room in ED. Immediately the patient went into the resuscitation room and computed tomography (CT) scan of the brain was requested (Fig. 1) showing thrombus in the right middle cerebral artery and signs of acute ischemic infarction. While discussing the case with the interventional radiology service for a possible mechanical thrombectomy, a cardiac point-of-care ultrasound (POCUS) was performed due to the age of the patient in order to rule out a primary cardiac source as the cause of the stroke. We used a FUJIFILM SonoSite’s Edge^® II POCUS system using a 5–1 MHz phased array probe for cardiac images and a 13–6 MHz linear probe for vascular (carotid) images. Surprisingly, there was a dilated aorta with pericardial effusion and evidence of the characteristic image of the dissection “flap” (Fig. 2). CT of the thoracic aorta and CT angiogram of the circle of Willis and carotid were requested on suspicion of AAD causing a thrombotic stroke. The CT scan (Fig. 3) confirmed the findings and the patient was immediately taken to the cardiovascular surgery service where there was an urgent operation. A hemicraniectomy was performed to treat brain swelling and mass effect secondary to the middle cerebral artery (MCA) territory infarction. After 20 days in the intensive care unit, the patient’s condition improved with a residual left side hemiplegia and he remained in hospital for physiotherapy in recovery phase.

Fig. 1.

Computed tomography of the brain; there is a hyperdense right middle cerebral artery, consistent with acute thrombosis.

Fig. 2.

Echocardiogram that shows dilated aortic root (5 cm), intimal flapping in the ascending aorta, and pericardial effusion. Right carotid artery ultrasound shows the intimal flapping.

Fig. 3.

Computed tomography (CT) angiogram carotid: extensive thrombus, secondary to dissection, within the right common carotid, from the level of the inferior margin of the thyroid cartilage, superiorly through the neck, into petrous segment of the carotid. Contrast fills the external carotid artery and branches on the right side.

CT thoracic aorta: type A dissection of the ascending aorta and aortic arch, involving the brachiocephalic artery, extending into the right common carotid artery. The dissection flap lies very close to the origin of the right coronary artery. There is abnormal fluid/hemorrhage within the pericardial space. The dissection flap is not visible below the level of the inferior margin of the left atrium.

Discussion

Thrombolysis is an established therapy for selected patients with ischemic stroke within a narrow time window of 4.5 h from the onset of symptoms. However, sometimes it may be applied without understanding the secondary cause of cerebral infarction due to limited time. AAD is an absolute contraindication for thrombolysis. We report an illustrative case of ischemic stroke as the onset of type A aortic dissection.

Neurological manifestations occur in 17–40% of AAD [5], the most common being ischemic stroke (6–32%) [6], predominantly right hemispheric (69.2–71%), although bilateral cases have been described [7]. This preference has been related to the greater proximity of the right carotid axis with the aortic root and, therefore, with the advance of dissection. Although the cardinal symptom in aortic dissection is pain, one-third of patients starting with ischemic stroke do not present with it. In addition, low level of consciousness or alterations of speech or language may hinder or prevent the recognition of this symptom [5], [7]. All this explains that it is more difficult to diagnose AAD that begins with neurological symptoms and, therefore, it is associated with a higher mortality, 30%, than those who do not, 22.6% [5]. There are several complementary techniques that allow the diagnosis of AAD, but given the infrequent cause of ischemic stroke, screening is not indicated for all patients.

In those cases where AAD is suspected (beginning with typical pain, suggestive exploratory signs such as hypotension, weak and asymmetric pulse, and murmur of aortic regurgitation) [6], [8], it is important to rule out ADD because, although the presence of stroke does not contraindicate surgical treatment [7], type A dissection does not contraindicate intravenous fibrinolysis [8], with 71% mortality in patients receiving r-TPA [7]. In our patient, there were no usual risk factors, no chest pain at any time, and clinical data indicated a primary ischemic stroke. The initial symptom of presentation prior to focal neurology was global headache that could have been the initial symptom of AAD and sudden worsening of the headache that could be explained by hyperacute stroke. In addition, there were no accompanying findings such as abnormal pulse or electrocardiographic results. Initially AAD was not suspected. The role of POCUS continues to expand in all aspects of medicine. POCUS is a useful bedside diagnostic tool that can decrease the time to diagnosis and help determine a patient’s disposition. Aortic-focused transthoracic echocardiography [7] has been proposed as a rapid and non-invasive method to rule out this entity when considering intravenous fibrinolysis. POCUS is becoming increasingly popular in the ED and may be useful to help rule in or out AAD [9]. There are many signs of AAD that can be seen on US including dilated aorta, presence of a flap, pericardial effusions, aortic regurgitation, and Mercedes Benz sign on subxiphiod view [10], [11]. Doppler on the aorta can be used to assess for true and false lumens. As in the reported case in patients with neurological symptoms, the carotid arteries can undergo ultrasound to assess extension of the dissection.

The literature on the topic is scant. A small case series of 5 cases suggested that emergency physicians have a sensitivity of 67% and a specificity of 99–100% for detecting an intimal flap on POCUS; however this is operator dependent and requires further investigation [12]. In a retrospective study of 27 patients with AAD, 14 (52%) had prior POCUS, 11 were confirmed, and 3 supported the diagnosis, suggesting that POCUS is increasingly used in the initial emergency management of patients with AAD, especially in hemodynamically unstable patients and in patients with atypical clinical presentation [13]. Taylor et al. [14] in a retrospective study demonstrated good agreement of POCUS with computed tomography angiogram (CTA) measurements of maximal thoracic aortic diameter and Nazerian et al. [15] in a 140 patient prospective single-center cohort study showed that POCUS performed by emergency physicians is specific for ascending aorta dilation and aneurysm when compared to CTA and appears a reproducible technique.

Stroke is a highly dreaded complication of type A AAD. This case demonstrates how POCUS can help to diagnose and care for patients with stroke and AAD. POCUS is more useful than routine examination of thoracic aorta to be performed during cardiac ultrasound in the emergency department. Extending the evaluation to the carotid arteries and the distal aorta can also help diagnose an extensive dissection. POCUS ultrasound should be used to quickly make a diagnosis, accelerate further imaging and as a rule in a diagnosis, rather than to rule out a diagnosis, but a decision of r-TPA administration should not be made with POCUS alone. It is important to make a diagnosis of type A AAD for thrombolysis, in patients with acute ischemic stroke, combining POCUS with X ray and CT.

Conflict of interest

The authors have no conflict of interests.