Aoritc Dissection

Clinical History

A patient with known hypertension presented to the accdent and emergency department complaining about acute onset of severe central chest pain radiating to his back. He was tachycardiac and hypotensive and the CXR was given (it can be compared with the old CXR).

Imaging Findings

A 62 year old male patient who had a background history of hypertension, well controlled on antihypertensive medication, presented to accident and emergency department during early hours of night, with a complaint of sudden onset of sharp central chest pain radiating to his back. On arrival he was tachycardiac (HR 110), and hypotensive (BP on left arm 68mmHg systolic, on right arm 79mmHg systolic). The ECG showed widespread ischaemic changes (T-wave inversions in leads I, II and aVL, and ST depressions in leads V2 to V6). Despite vigorous fluid resuscitation his BP remained low. His urgent portable chest radiography showed a significantly widened mediastinum, which was new as compared to his old CXR. An urgent CT scan of the thorax was arranged. Unfortunately, the patient collapsed and suffered a cardiac arrest before the CT scan and did not survive despite vigorous resuscitation. Post mortem examination confirmed the cause of death as massive dissecting aneurysm.

Discussion

Aortic dissection is the most common potentially fatal aortic disease. When left untreated, about 35% of patients die within the first 24 hours, 50% within 48 hours. The 2-week mortality rate approaches 75% in patients with undiagnosed ascending aortic dissection [2]. According to Stanford classification, there are 2 types of dissection: Type A involves the ascending aorta, Type B does not. The pathophysiology involves the formation and propagation of a subintimal hematoma which leads to a 'tear' in intimal layer. This produces a false lumen or double-barreled aorta, which can reduce blood flow to major arteries arising from aorta.

Arterial hypertension seems clearly to be a factor in the genesis of aortic dissection. Hypertension can be found in 80% of patients [3, 4]. It is also linked with connective tissue disorders, congenital aortic stenosis or bicuspid aortic valve, and with some heritable diseases like Marfan's syndrome, Ehlers-Danlos syndrome, Familial aortic dissections, Adult polycystic kidney disease, Noonan syndrome, Osteogenesis imperfecta and Metabolic disorders (e.g. homocystinuria, familial hypercholesterolemia). Syphilis and crack cocaine use may cause may precipitate dissection.
Sudden excuriating pain, presumably attributable to the progress of medial cleavage, announces the onset of dissection in 90 percent of instances. Patients may describe the pain as cutting, ripping or tearing, but such classical description cannot always be elicited. A sudden neurological episode accompanies the onset of most instances of 'painless' aortic dissection. Syncope is the most frequent neurologic event and a particularly ominous sign. It seems always to reflect external rupture, almost always of the ascending aorta into the pericardial space [2, 3, 4].
None of the physical examination are diagnostic. The murmur of aortic regurgitation can be heard in about half of all patients with acute type A dissection. Loss or diminution of an arterial pulse may also be detected in half. 20 percent of patients with dissection present with hypotension, and it requires immediate consideration of operative treatment, since external rupture almost always is responsible [3, 4].
As far as diagnostic studies are concerned, chest films provide information of much value. The aortic shadow is abnormal in 80 to 90 percent of cases, but may be abnormal in many instances in patients who do not have dissection. For confirmation of the diagnosis, either CT with contrast or trans-oesophageal echocardiography may be employed with confidence. Both have high sensitivity and specifcity [5, 6].
Sudden life-threatening complications, such as severe hypertension, cardiac tamponade, massive haemorrhage, severe aortic regurgitation, or ischaemic injury to myocardium, CNS and kidneys, threaten the patient with aortic dissection. Optimal management requires close surveillance of vascular pressures, urine flow, mental status and neurological signs in an intensive care unit. Aggressive antihypertensive treatment lessens the stress on the aortic wall and thus likelihood of progression of dissection. Operative treatment represents the most effective long-term remedy. The patients who are hypotensvie on admission warrants urgent surgery. Surgery should be considered in all patients, if there is no contraindication, though timing of surgery may vary [2, 3, 4, 7, 8].

Differential Diagnosis List

Final Diagnosis

Aortic Dissection

URL:	https://eurorad.org/case/6953
DOI:	10.1594/EURORAD/CASE.6953
ISSN:	1563-4086