| Abstract|| |
Aortic dissection (AD) is a great imitator, and its diagnosis is quite challenging due to its varied presentations and unreliable clinical findings. Based on the literature search we found, this is the first case report of Stanford-A/DeBakey Type 1 AD reported as a triple mimic, namely stroke, acute limb ischemia, and pericarditis. Here, we describe the case of a 46-year-old male who presented to our emergency department with features suggestive of acute pericarditis, cerebrovascular accident, acute limb ischemia, which could have been attributed to athero-thrombo-embolic disease and AD could have been possibly missed. However, point-of-care ultrasound helped us in the diagnosis of this highly lethal condition.
Keywords: Acute limb ischemia, aortic dissection, cerebrovascular accident, Pericarditis, Point of care ultrasound
|How to cite this article:|
Mahalingam S, Rajendran G, Balaraman N, Kumar K, Rajendran A, Nathan B, Ayyan M, Balassoundaram V, Gara M, Kumar P. Stanford - A aortic dissection presenting as a triple mimic and role of point of care ultrasound in deciphering it. J Emerg Trauma Shock 2021;14:187-9
|How to cite this URL:|
Mahalingam S, Rajendran G, Balaraman N, Kumar K, Rajendran A, Nathan B, Ayyan M, Balassoundaram V, Gara M, Kumar P. Stanford - A aortic dissection presenting as a triple mimic and role of point of care ultrasound in deciphering it. J Emerg Trauma Shock [serial online] 2021 [cited 2021 Dec 1];14:187-9. Available from: https://www.onlinejets.org/text.asp?2021/14/3/187/327088
| Introduction|| |
Aortic dissection (AD) is an elusive fatal diagnosis because aortic intimal tear can de-vascularize/hypo-perfuse any organ due to obstruction which causes pulse deficit features and varied presentations such as acute stroke, paraplegia, acute coronary syndrome (ACS), pericarditis, cardiac tamponade, acute abdominal pain, acute limb ischemia, visceral ischemia, mesenteric ischemia, and hence, 25% of cases can be missed. Thus, it is referred to as Great Masquerader. Every hour, delay in the diagnosis can increase mortality by 1%–2%. The International Registry of AD (IRAD) found 27.4%, 58%, and 26% mortality among in-hospital patients, medically, and surgically managed patients. Here, we describe a case of Stanford-A AD that mimicked acute stroke, pericarditis, and acute limb ischemia and the utility of point of care ultrasound (POCUS) in expediting the diagnosis.
| Case Report|| |
A 46-year-old male, diabetic, hypertensive, and chronic smoker came to our emergency department (ED) with complaints of chest pain for 2 days, left-sided weakness, and right lower limb pain for 1 day. Chest pain was diffuse retrosternal crushing type and radiating to back with associated with dyspnoea, palpitation, and sweating.
He was conscious, oriented, and vitals were pulse rate (PR) 85/min, blood pressure (BP) 180/90 mm Hg, respiratory rate 18/min, and spo2 98% on room air. All peripheral pulses were felt except the right lower limb, which was cold with an absent femoral pulse. Examination findings had pericardial rub, normal neurological findings in right-sided limbs, whereas Left-sided limbs had the power of 2/5, hypotonia, areflexia, and an extensor plantar. Electrocardiography (ECG) showed pericarditis changes (1, AVL, V3, V4, V5, V6 showing-ST elevation and PR depression and automatic voltage regulator (AVR) showing-PR elevation and ST depression in AVR leads) and troponin T was negative. Computed tomography (CT)-brain showed right ganglio-capsular infarct. Hence, a provisional diagnosis of acute pericarditis, stroke with acute limb ischemia was made. The patient had excruciating chest pain, not amenable to opioids.
In a setting of athero-thrombo-embolic phenomena like features in acute pericarditis and excruciating chest pain nonamenable to opioids, we guessed some diagnostic fallacy was there. Hence, we did our routine ED POCUS using phased array probe and curvilinear probe which revealed a dissection flap near the aortic root, descending aorta, and aortic arch [Figure 1]a, [Figure 1]b, [Figure 1]c and dissection flap in abdominal aorta [Figure 1d]. Thus, POCUS helped us to clinch the diagnosis, which led us to activate AD protocol.
|Figure 1: Point of care ultrasound showing dissection flap in ascending aorta (a), descending aorta (b) and arch of aorta (c) and abdominal aorta (d). (Yellow arrow: Ascending aorta, White arrow: Descending aorta, Grey arrow: Aortic arch, Blue arrow: Abdominal aorta)|
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The patient was treated with labetalol to achieve a PR <60/min and systolic BP <110 mm Hg. Later, a CT aortogram was done which showed dissection flap from ascending aorta [Figure 2]a extending above into all three major neck vessels namely the right brachiocephalic artery, left common carotid artery, left subclavian artery and even in right common carotid artery [Figure 2]b and [Figure 2]c and extending below up to the right common iliac artery [Figure 2]d which clearly explained the above clinical presentation. The patient was stabilized in the ED and taken over by a vascular surgeon for surgery.
|Figure 2: Computed tomography - Aortogram showing stanford a dissection in ascending aorta (a), extending into major neck vessels (b and c) and right common iliac artery (d). (Red arrow: Ascending aorta, Blue arrow: Right common carotid artery, Green arrow: Right brachiocephalic artery, Blue arrow: Left common carotid artery, Orange arrow: Left subclavian artery, Violet arrow: Right common iliac artery)|
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| Discussion|| |
Among type A Stanford AD patients, <50% has classical tearing, ripping chest pain, and 25% present without chest pain. Clinical features are usually unrevealing but may show marfanoid habitus, new aortic regurgitation murmur, pulse deficit/BP difference. IRAD registry showed that only 50% of patients were initially hypertensive, whereas others were either normotensive/hypotensive. Risk factors for AD are chronic hypertension, age >50 years, connective tissue disorder, family history of dissection, smoking, cocaine use, amphetamine use, blunt trauma, bicuspid aortic valve, and genetic cause. Usually, surgical repair is needed for Standford A and medical treatment for Stanford B AD. In case of mal-perfusion, ongoing progression, inability to control BP and rupture, surgery may be indicated in Stanford B.
Type A Stanford AD can present with neurological manifestation (17%–40%) such as ischemic stroke, transient ischemic attack, hypoxic encephalopathy, spinal cord ischemia, seizure, and syncope due to dissection of aortic arch vessels. 1%–2% of AD cases can present as an ACS due to ostial occlusion of the coronary artery by dissection flap. Thus, thrombolysing AD patients who mimic like a stroke or ACS can lead to deadly hemorrhagic complications (75%) and mortality (71%). AD can mimic spinal cord syndromes due to occlusion of Arteria Radicularis Magna. AD can present like pericarditis due to the seepage of blood into pericardial tissue or space, causing inflammatory pericarditis. AD can also present like acute mesenteric ischemia, acute limb ischemia due to the abdominal aortic branch involvement, whereas gastrointestinal bleeding can be due to aorto-esophageal fistula and aorto-duodenal fistula.
ECG can be normal up to 30% of cases; in 42%, there can be nonspecific ST-T changes, and in few, it can mimic like STEMI, pericarditis. Furthermore, starting anti-platelets, anticoagulants, or thrombolysis could be potentially fatal when the underlying disease is an AD. The classical chest X-ray (CXR) finding of a widened mediastinum is absent in 37% of patients. Left pleural effusion on CXR is an independent predictor of mortality in Type B dissection.
The American College of Emergency Physicians (EPs) recommend CT angiography as one of the gold-standard diagnostic imaging modalities for AD with 98% sensitivity. ADvISED trial proposed using D-dimer for ruling out AD, which still requires external validation before implementation in clinical practice. Gibbons et al. developed an AD-POCUS protocol combining trans-thoracic echocardiography (TTE) with abdominal aorta ultrasound. POCUS signs of Type A Stanford AD which has high sensitivity are dilated aortic root at end-diastole (>3.5 cm), intimal flap, intramural thrombus, pericardial effusions, aortic regurgitation, and Mercedes Benz sign in sub-xiphoid view., A dilated aortic root has a sensitivity and specificity of 77%–91%, and 72%–95% and intimal flap by TTE have 67%–80% sensitivity and 98%–100% specificity. POCUS can show false lumen signs, namely beak sign and cob-web sign in AD. Nazerian et al. demonstrated that POCUS done by EP was 88% sensitive for Type A Stanford-AD. Pare et al. demonstrated a significant reduction in time to diagnose AD (>145 min) when POCUS is performed early. Extending the POCUS evaluation to the carotid arteries and the distal aorta can diagnose an extensive dissection. AD-POCUS protocol should be used with AD detection risk score (ADD-RS) to achieve high negative predictive value and high sensitivity (96%) [Table 1]. Hence, POCUS can rapidly diagnose AD when all possible TTE/abdominal ultrasound views and ADD-RS are incorporated into the diagnostic protocol.
| Conclusion|| |
AD can extend into any branch of the aorta, which can hypo-perfuse or devascularize any organ. Thus, AD can present in an atypical fashion. The three key points that should be kept in mind to suspect and diagnose AD early in any patients are
- “Sudden migratory tearing type chest/abdominal pain with maximal pain at the onset, radiating to back or abdomen, severe in intensity, not amenable to opioids,”
- “Routinely assess all peripheral pulses, four limb BP and pulse deficit features in high-risk patients” and
- “Use AD detection risk scoring and POCUS.”
A high index of clinical suspicion and POCUS can unmask the diagnosis at bedside. As compared to the great phrase “time is brain” in stroke, “time is life” with regards to AD. Hence, every EP should get a good grip on POCUS knowledge to suspect and diagnose AD at the earliest.
Research quality and ethics statement
The authors followed applicable EQUATOR Network (http://www.equator-network.org/) guidelines, notably the CARE guideline, during the conduct of this report.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that his name and initials will not be published and due efforts will be made to conceal his identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2]