Acute Type A aortic dissection is a time-critical cardiovascular emergency with a broad clinical spectrum. Although sudden severe chest or back pain is the classical presentation, neurological or malperfusion symptoms may be the initial manifestation and can lead clinicians toward alternative diagnoses. We report the case of an 82-year-old man, a known case of hypertension, who presented to the Emergency Department with sudden-onset bilateral lower-limb numbness after a sequence of stretching, walking, generalized discomfort and subsequent rest. On arrival he was profoundly hypotensive with a blood pressure of 70/40 mmHg, while remaining conscious with a Glasgow Coma Scale score of 15/15. Initial management included cautious intravenous fluid resuscitation and noradrenaline support, with spinal pathology considered because of the presenting neurological symptoms. Approximately 20 minutes after arrival, he developed chest pain associated with back pain. Serial electrocardiograms demonstrated evolving abnormalities, including sinus bradycardia with T-wave changes followed by lateral ST-segment changes. High-sensitivity troponin was initially negative and echocardiography did not demonstrate an obvious intimal flap or pericardial effusion. As the clinical picture evolved, urgent coronary angiography was undertaken, where Type A aortic dissection with left main coronary artery involvement was identified. Left main coronary intervention was performed and cardiothoracic surgical opinion was obtained. The patient subsequently developed cardiac arrest and could not be resuscitated. This case emphasizes that acute aortic dissection may initially masquerade as a neurological emergency and highlights the importance of integrating age, risk factors, unexplained shock, evolving symptoms and serial investigations rather than relying on the presence or absence of classical chest pain.
Acute aortic dissection; Stanford Type A; neurological presentation; bilateral lower-limb numbness; hypotension; coronary malperfusion; left main coronary artery; emergency medicine.
Acute aortic dissection results from disruption of the aortic intima with propagation of blood through the media, creating a false lumen. Stanford Type A dissection involves the ascending aorta and carries a high risk of fatal complications including cardiac tamponade, acute aortic regurgitation, coronary malperfusion, myocardial ischemia, cerebral or spinal malperfusion and circulatory collapse.
The classical presentation is abrupt severe chest pain, often radiating to the back. However, presentation can be highly variable. Neurological symptoms, syncope, hypotension, limb ischemia and myocardial ischemia may dominate the initial clinical picture. In such situations, failure to recognize the underlying vascular pathology can result in diagnostic delay.
We present an elderly hypertensive patient whose initial manifestation was sudden bilateral lower-limb numbness with profound hypotension, followed shortly by chest and back pain and evolving electrocardiographic abnormalities, ultimately revealing Type A aortic dissection with coronary involvement.
An 82-year-old male, a known case of hypertension, presented to the Emergency Department at approximately 9:00 AM. According to the history subsequently correlated with the patient’s attender, he had been apparently well while performing yoga/stretching exercises. Following the stretches, he went for a walk around the house. During the walk, he experienced a generalized discomfort and subsequently went to bed. After going to bed, he developed numbness involving both lower limbs and became unable to walk. He was taken to the Emergency Department, and en route he developed low back pain extending from the mid-thoracic region to the lumbar region, associated with the lower-limb numbness. Importantly, the lower-limb numbness did not develop immediately after the yoga/stretching exercises. The chronology of events was clarified and correlated with the history provided by the attender. There was no reported preceding trauma.
The absence of initial chest pain made the presentation predominantly neurological at the time of arrival. There was no reported preceding trauma.
A cautious intravenous fluid bolus of 250 mL was administered. Intravenous paracetamol was given and, in view of persistent hypotension, noradrenaline infusion was initiated. The spine team was involved because of the acute bilateral lower-limb neurological symptoms and the possibility of an acute spinal pathology.
At this stage, the combination of sudden neurological symptoms and profound shock remained unexplained. The patient’s advanced age and history of hypertension represented important vascular risk factors.
At approximately 9:20 AM, the patient developed new-onset chest pain associated with back pain. Four-limb blood pressure assessment did not demonstrate a significant difference and no obvious pulse deficit was noted. High-sensitivity troponin was initially negative. Cardiology consultation was obtained.
ECG 1 – 09:01 AM: Initial ECG
Figure 1. Initial ECG recorded at approximately 09:01 AM. Sinus rhythm at approximately 78/min with low-voltage QRS complexes in the limb leads; no definite acute ischemic pattern is evident on this tracing.
ECG 2 – 09:20 AM: ECG during development of chest/back pain
Figure 2. ECG recorded at approximately 09:20 AM after development of chest and back pain. Sinus bradycardia with frequent premature ventricular complexes/bigeminal pattern and repolarization abnormalities.
Echocardiography during cardiology review: Normal left ventricular systolic function (LVEF approximately 60%); dilated aortic root measuring 42 mm; trace pericardial effusion; pulmonary artery pressure within the normal upper limit. No obvious intimal flap was visualised on the available echocardiographic assessment.
An echocardiographic assessment did not demonstrate an obvious intimal flap and only trace pericardial effusion was noted. Given the evolving clinical picture, a triple-rule-out CT was planned to evaluate for acute coronary syndrome, acute aortic syndrome and pulmonary embolism.
While the evaluation was ongoing, the patient became increasingly restless and complained of worsening chest pain. Morphine 2 mg IV stat was administered for analgesia. A subsequent ECG demonstrated further repolarization abnormalities with ST-segment changes in the lateral leads. In view of ongoing chest pain and evolving ECG changes, the decision was made to transfer the patient urgently to the cardiac catheterization laboratory.
ECG 3 – 10:19 AM: Evolving ischemic/repolarization abnormalities
Figure 3. ECG recorded at approximately 10:19 AM demonstrating evolving diffuse repolarization abnormalities, including ST-segment depression and T-wave flattening/inversion in multiple leads.
During coronary angiography, a Stanford Type A aortic dissection was identified with involvement of the left main coronary artery resulting in significant coronary compromise. Left main coronary artery PCI was performed because of the critical coronary involvement. Cardiothoracic surgical opinion was obtained for definitive management of the Type A aortic dissection.
Despite aggressive multidisciplinary management, the patient’s condition deteriorated and he subsequently developed cardiac arrest. Advanced Cardiac Life Support (ACLS) was initiated and resuscitative efforts were continued according to standard protocol. Return of spontaneous circulation could not be achieved and the patient was declared deceased.
The defining feature of this case was the initial neurological presentation. The patient did not initially present with chest pain; instead, sudden bilateral lower-limb numbness was the dominant complaint. This can direct emergency clinicians toward primary neurological or spinal pathology. However, acute aortic dissection can produce neurological manifestations through spinal cord ischemia, branch-vessel malperfusion or systemic hypoperfusion.
The simultaneous presence of profound hypotension should increase concern for a systemic vascular or cardiac cause. In an elderly patient with hypertension, sudden neurological symptoms associated with unexplained shock should therefore prompt consideration of acute aortic syndrome alongside neurological differentials.
In neurological and other high-stakes emergency presentations, the sequence and timing of symptoms can be as important as the symptoms themselves. In this case, the initial history could easily have been interpreted as numbness occurring immediately after yoga or stretching. A more detailed history, however, established a different chronology: the patient completed the stretches, walked around the house, developed generalized discomfort, went to bed, and only subsequently developed bilateral lower-limb numbness with inability to walk. While being transported to the Emergency Department, he then developed back pain extending from the mid-thoracic region to the lumbar region. This evolution provided an important clue to the underlying pathology and helped place the neurological symptoms in the context of a potentially vascular emergency.
History obtained directly from the patient may be incomplete, particularly when the patient is distressed, in pain, hypotensive, confused, or focused on the most prominent symptom. Correlating the history with an attender or witness can clarify the exact sequence of events, identify preceding symptoms, establish the true onset time, and distinguish an apparent trigger from the actual onset of neurological deficit. In neurological presentations, this
distinction is particularly important because the diagnostic pathway and time-sensitive interventions depend heavily on accurate symptom chronology. A careful reconstruction of the timeline should therefore be considered an essential component of emergency assessment, especially when the initial presentation does not fit a single anatomical or diagnostic pattern.
Why the diagnosis is difficult
The absence of a pulse deficit does not exclude aortic dissection. Similarly, an initially negative high-sensitivity troponin does not rule out acute aortic pathology, and a nondiagnostic echocardiographic study cannot reliably exclude an acute Type A dissection when clinical suspicion remains significant.
In this case, the diagnosis became increasingly apparent as the clinical picture evolved from neurological symptoms and shock to severe chest/back pain and dynamic ECG changes. This emphasizes the importance of serial reassessment rather than anchoring on the initial working diagnosis.
Coronary artery involvement is a recognized and potentially fatal complication of Type A dissection. Extension of the dissection into or compression of a coronary ostium can result in myocardial ischemia, ECG changes, cardiogenic shock and cardiac arrest.
The left main coronary artery involvement in this patient created a clinical picture that could mimic primary acute coronary syndrome. The evolving ECG changes and chest pain therefore required urgent coronary assessment, while the underlying aortic pathology simultaneously required cardiothoracic surgical management.
Emergency department diagnoses are dynamic. A patient may initially present with one organ-system manifestation and subsequently develop features that reveal a unifying diagnosis. In this case, serial assessment of symptoms, haemodynamics and ECG findings was critical. The transition from isolated neurological symptoms to chest/back pain and evolving electrocardiographic abnormalities represented a major change in diagnostic probability.
This case illustrates the diagnostic challenge posed by an atypical presentation of Stanford Type A aortic dissection. The initial manifestation of sudden bilateral lower-limb numbness in an elderly hypertensive patient with profound hypotension preceded the more classical development of chest and back pain. The subsequent evolution of ECG abnormalities and left main coronary involvement demonstrated the rapidly progressive nature of the disease.
For emergency physicians, the key message is that acute aortic dissection should not be excluded simply because the initial presentation is neurological or because classical signs such as pulse discrepancy are absent. When sudden neurological symptoms are accompanied by unexplained shock in a high-risk patient, acute aortic syndrome must remain in the differential diagnosis. A high index of suspicion, serial reassessment and timely definitive imaging are central to early recognition.
“When symptoms mislead, chronology guides.”
Patient identifiers have been omitted from the manuscript. The ECGs included in this educational case presentation are reproduced for academic discussion.
Dr Ashok, Kauvery Hospital, Chennai.
Dr Srikumar, Senior Consultant Cardiologist Kauvery Hospital, Chennai.
Dr. Ramya Kamakshi, 2nd Year MEM Trainee Kauvery Hospital, Chennai.
