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Report by Chad VanderLinden, Senior Resident
Checked by Dr Jeffrey Jones and Dr Michael Brown, Research Director and Director of the Emergency Medicine Residency Program, respectively
Grand Rapids MERC/Michigan State University, Michigan, USA
A short cut review was carried out to establish whether a raised D‐dimer could be used to identify patients with an acute thoracic aortic dissection. Seven papers were found addressing the clinical question. The author, date and country of publication, patient group studied, study type, relevant outcomes, results and study weaknesses of these papers are presented in table 11.. The clinical bottom line is that a D‐dimer value <500 ng/ml makes the diagnosis unlikely but there is still the possibility of a thrombosed false lumen.
In [emergency department patients with chest pain] can [D‐Dimer] [detect acute thoracic aortic dissection]?
A 71‐year‐old woman with a history of hypertension presents to the emergency department with a sudden onset of chest pain radiating to her back. Her ECG shows ischaemic changes and cardiac enzymes are pending. Chest x ray shows a normal appearing mediastinum but clinical suspicion for a thoracic aorta dissection remains. You wonder if a D‐dimer assay has enough negative predictive value to exclude an acute thoracic aortic dissection (ATAD) to allow you to quickly anticoagulate this patient without any further imaging study.
Medline 1950‐ August 2007 using the OVID interface, Cochrane Library (2007) [(exp Aneurysm, Dissecting/or Aneurysm/or aneurysm.mp.) OR (exp Aortic Aneurysm/or exp Aortic Aneurysm, Thoracic/or aortic dissection.mp.)] AND [(exp Fibrin Fibrinogen Degradation Products/or fibrinogen degradation products.mp.) OR (d‐dimer.mp.)] LIMIT to human AND English.
Ninety‐five papers were found of which 88 were irrelevant or of insufficient quality, and seven were relevant and of sufficient quality for inclusion (table 11).
D‐dimers are specific cross‐linked fibrin derivatives that are the product of fibrinolytic degradation. They are considered the best available marker of coagulation activity and are well studied as a marker in the diagnosis of pulmonary embolism (PE). D‐dimer would theoretically be elevated in thoracic aorta dissection due to exposure of the false lumen. Chronic thoracic aorta dissection would theoretically not produce significant elevation in D‐dimer secondary to endothelialisation of the false lumen. The clinical usefulness of a screening laboratory test for ATAD has several advantages. First, it would reduce the number of invasive diagnostic procedures as well as contrast induced nephropathy. Second, the rapid availability of the result would significantly reduce the time necessary to raise suspicion of ATAD. Third, a positive result could prevent patients from getting thrombolytic therapy when the underlying aetiology of the patient's chest pain is ATAD. Finally, if the negative predictive value of D‐dimer is high enough to exclude ATAD in patients with chest pain, anticoagulation could be initiated sooner in chest pain patients because treating physicians would not have to worry as much about ATAD masquerading as an acute coronary syndrome.
Preliminary studies using D‐dimer to exclude clinically suspected ATAD show promise. Clearly, the sensitivity of D‐dimer for ATAD falls when a thrombosed false lumen is present. Large prospective validation studies need to be done before D‐dimer can be used to dictate clinical decision making in emergency department patients suspected of having ATAD.