JSTC
Journal of Surgery and Trauma Care, Vol. 1 No. 1 (2019) p. 1-3
Journal of Surgery and Trauma Care
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*Corresponding author: [email protected] 2019 FAZ Publishing. All right reserved.
High Risk Chief Complaints: A Misdiagnosis of Acute Aortic Dissection
Hanizah Ngadiron1, Fadzlon Mohd Yatim2
1Faculty of Medicine and Allied Health, Universiti Sains Islam Malaysia (USIM), MALAYSIA
2Department of Anaesthesiology, Universiti Kebangsaan Malaysia Medical Centre (UKMMC), MALAYSIA
Received 01 November 2018;
Accepted 10 January 2019;
Available online 19 February 2019
1. Introduction
Acute aortic dissection (AAD) is the most common catastrophic event that involves the aorta, presenting to the emergency room much more often than a ruptured abdominal aorta. It has been estimated that more than 2000 new cases of aortic dissection occur per year in United States (1). Despite this concern, the frequency and consequences of initial misdiagnosis remain poorly understood. Without a quick and effective diagnosis 75% of patients with ascending aortic dissection can be expected to die within 2 weeks, with a mortality of 1% to 3% per hour in the first 48 hours. In contrast with rapid diagnosis and definitive therapy, 30 days survival rates as high as 90% have been reported (1).
2. Case report
We received a 52-year-old, Malay lady, presented to our emergency department around 1920 hours, 8th of May 2011.
She was referred from private practitioner to rule out acute coronary syndrome after experience 2 episodes of retrosternal chest pain with documented low blood pressure. On further questioning, she started to develop a new onset of retrosternal chest pain at 1600 hours that day associated with profuse sweating. The pain radiated to the back and epigastric region but no radiation to the neck or jaw. She also had vomiting.
Similar pain occurred at 1630 hours made her seek immediate medical attention.
In the emergency department, her vitals were stable, and she was more concerned with the epigastric pain. She was triaged to yellow zone with initial diagnosis of acute gastritis as her electrocardiograph (ECG) was normal (Figure 1), She is
a chronic smoker with no past medical or surgical history. She was given intravenous antacid and analgesia and observed for deterioration. Routine bloods including cardiac enzymes were sent.
After 2 hours of observation, we noted her blood pressure was increasing in trend with systolic blood pressure achieved 230mmHg. She was then given 12.5 mg of captopril stat dose.
At around 1100 hours, she complained again of the similar pain with profuse sweating. She looked pale and her blood pressure was dropping tremendously with systolic blood pressure of 60 mmHg. Repeated ECG also showed no new ischaemic cardiac changes. Blood investigations results reviewed were also normal. She was immediately pushed to resuscitation zone to do the necessity.
Aspirin 300mg per oral was given in view of suspicious acute coronary syndrome. Initial bedside transthoracic echocardiography by emergency medical officer revealed a heart with good contractility but with low volume. Minimal pericardial effusion seen without tamponade effect. Portable Chest radiograph (CXR) was done and revealed a widened mediastinum of 10 cm (Figure 2). Acute aortic dissection was suspected. After managed to bring up her systolic blood pressure around 90 to 100 mmHg, patient was sent for Computed Tomography Angiography (CT) of thorax. Result came back as acute ascending aortic dissection, Stanford A (figure 3). Patient was then referred to cardiothoracic team for further management.
Formal bedside transthoracic echocardiography by cardiologist revealed concentric left ventricular failure, good Abstract: Among high risk chest pain includes acute myocardial infarction, acute dissecting thoracic aortic aneurysm and esophageal rupture. Due to almost similar presentation, it is difficult to differentiate one from the others. More worrisome if we misdiagnosis it with other less threatening conditions such as angina pectoris or acute gastritis. This case regarding a middle age lady who presented with epigastric pain and treated as acute gastritis, whereby turn out to be acute aortic dissecting (AAD). We discuss further regarding the presentation and mode of modalities available to diagnose AAD.
Keywords: Aortic, dissection, AAD
Ngadiron, H. et alJournal of Surgery and Trauma Care, Vol. 1 No. 1 (2019) p. 1-3
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left ventricular function with ejection fraction of 84%, normal chamber sizes, presence of 3 aortic valve cusps with slight calcification, mild aortic regurgitation, no aortic stenosis or global pericardial effusion causing tamponade. Patient was sent to Operation Theater soon after that for surgical repair. It was a successful operation, however complicated with hospital acquired pneumonia. Patient was discharged home safely after a month hospitalization.
Fig 1. – A normal ECG despite symptoms similar to myocardial infarction
Fig 2. – Widened mediastinum of 10cm seen on the chest x- ray
Fig 3. – Acute ascending dissection, Stanford B seen on the CT scan thorax
3. Discussion
Aortic dissection occurs when a tear in the inner wall of the aorta causes blood to flow between the layers of the wall of the aorta and force the layers apart. Aortic dissection is a medical emergency and can quickly lead to death, even with optimal treatment. If the dissection tears the aorta completely open (through all three layers), massive and rapid blood loss occurs
The diagnosis of AAD is unfortunately often a difficult one to make. Symptoms from aortic disease include back pain, chest pain and abdominal pain, all of which can closely resemble symptoms of other emergent problems, such as pulmonary embolism, myocardial infarction and mesenteric ischemia (2). Risk factors for development of AAD are hypertension, male gender, cocaine use, advanced age, pregnancy, connective tissue diseases, smoker, presence of a bicuspid aortic valve or previous aortic valve replacement, Turner syndrome, weightlifting and ecstasy use. There are few, if any, historical features and physical examination findings which when used in isolation, allow the clinician to positively identify those patients with AAD.
There is a literature that suggests that physicians can improve their diagnosis accuracy by specifically asking about the quality of the patient's pain, the radiation of the pain and the intensity of the onset. In one retrospective study, only 42% of patients who were found to have AAD were asked all 3 of these questions. When all 3 questions were asked, the clinician's initial impression of AAD was correct in 91% of cases (2, 3).
Other combinations of findings, such as the presence of sudden onset of pain that is tearing or ripping in quality, blood pressure or pulse differentials and mediastinal widening on CXR, have been found to have positive LR of 66%. It is disappointing that the presence of these 3 factors was found in only 27% of patient with AAD.
The importance of accurate, rapid diagnosis and intervention for AAD is underscored by its clinical and epidemiologic overlap with acute coronary syndrome and by
Journal of Surgery and Trauma Care, Vol. 1 No. 1 (2019) p. 1-3
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the risks of inappropriate treatment with anti-thrombotic therapy. In another retrospective study done to measure the frequency of and inappropriate treatment of misdiagnosis of AAD, misdiagnosis occurred in 39%. Acute coronary syndrome was the most common misdiagnosis, resulting in inappropriate treatment with anti-thrombotic agents. Exposure to this was associated with higher rates of major bleeding and mortality (4). Other complications of antithrombotic agents that can occur are pericardial and pleural effusion due to bleeding.
For most emergency patients with chest pain, CXR and ECG are part of the initial diagnostic evaluation. Unfortunately, the sensitivity of both tests is limited. Perhaps the greatest use of ECG is to distinguish ST segment elevation myocardial infarction from AAD. However, the conditions are known to coexist, if the dissection extends proximally to include the coronary ostia, most commonly affecting the right coronary artery causing proximal coronary artery occlusion.
Several imaging modalities, including conventional angiography, ultrasonography (USG), CT and magnetic resonance imaging (MRI), have been used to diagnose AAD.
In many institutions, CT is the diagnostic test of choice due to its easy accessibility, rapid data acquisition, high sensitivity and ability to simultaneously exclude other morbid causes of chest pain. Transesophageal echocardiography (TEE) although more portable, but requires esophageal intubation, may lead to an increase in blood pressure and subsequently increase risk of rupture (4). There is also a case report regarding use of transthoracic echocardiography (TTE) to diagnose AAD where they clearly demonstrated a dissection flap superior to the sinuses of Valsalva and severe aortic insufficiency. Although CT and TEE are typically the initial test of choice, but TTE can rapidly confirm the suspected diagnosis of AAD, especially when the patient too unstable to undergo CT. This modality has higher sensitivity and specificity for diagnosis of type A AAD (5). MRI should be reserved for the subacute or chronic evaluation of equivocal cases or to image complex true versus false lumen anatomy in the arch or other branch of vessel (4).
Laboratory testing played only a minor role in diagnosis of AAD. A blood D-dimer level less than 500 ng/mL may be able to rule out the diagnosis of aortic dissection alleviating the need for further imaging.
For emergency management we need to stabilize patient as stable as possible so that chances of getting patient to Operation Theater as soon as possible. Our aim systolic blood pressure is between 100-120 mmHg. If the patient is hypertensive, this can be reduced by giving beta blocker infusion, preferably beta blocker, such as labetolol for the first line of treatment. Calcium channel blockers can be used in the treatment of aortic dissection, particularly if there is a contraindication to the use of beta blockers. If the individual has refractory hypertension (persistent hypertension on the maximum doses of three different classes of antihypertensive agents), involvement of the renal arteries in the aortic dissection plane should be considered. For hypotensive, consider transfusing blood products early to prevent coagulopathy.
For type A dissection, definitive treatment is operative intervention, compared with type B which can successfully be treated with medical therapy alone. This is to prevent the expected sequelae of rupture with cardiac tamponade, acute
aortic regurgitation as consequences of loss of commissural suspension or myocardial infarction secondary to coronary artery involvement (4).
4. Conclusion
Unfortunately, misdiagnosis always occurs with incomplete history and physical examination. With a history of typical pain, pulse or blood pressure differentials and mediastinal or aortic widening on chest radiography, always suspected high probability of acute aortic dissection.
References
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Schussler. Acute Ascending Aortic Dissection Diagnosed with Transthoracic Echocardiography. J of the American Society of Echocardiogarphy. 2009;
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4. Mark S. Hansen, Gustavo J. Nogareda, Stuart J.
Hutchison. Frequency of and inappropriate treatment of misdiagnosis of acute aortic dissection.
American J of Cardiology. 2006; 10:854-856 5. Marc R. Moon. Approach tonthentreatment of aortic
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