The risk of misdiagnosis in acute thoracic aortic dissection: a review of current guidelines.

Acute aortic syndrome and in particular aortic dissection (AAD) persists as a cause of significant morbidity and mortality despite improvements in surgical management. This clinical review aims to explore the risks of misdiagnosis, outcomes associated with misdiagnosis and evaluate current diagnostic methods for reducing its incidence.Due to the nature of the pathology, misdiagnosing the condition and delaying management can dramatically worsen patient outcomes. Several diagnostic challenges exist, including low prevalence, rapidly propagating pathology, non-discrete symptomatology, non-specific signs, analogy with other acute conditions and lack of management infrastructure. A similarity to acute coronary syndromes is a specific concern and risks patient maltreatment. AAD with malperfusion syndromes are both a cause of misdiagnosis and marker of disease complication, requiring specifically tailored management plans from the emergency setting.Despite improvements in diagnostic measures, including imaging modalities and biomarkers, misdiagnosis of AAD remains commonplace and current guidelines are relatively limited in preventing its occurrence. This paper recommends the early use of AAD risk scoring, focused echocardiography and most importantly, fast-tracking patients to cross-sectional imaging where the suspicion of AAD is high. This has the potential to improve the diagnostic process for AAD and limit the risk of misdiagnosis. However, our understanding remains limited by the lack of large patient datasets and an adequately audited processes of emergency department practice.

Diagnosis and management of acute Type-A aortic dissection in emergency departments: Results of a UK national survey.

BACKGROUND: Type A-aortic dissection (TAAD) is a life-threatening diagnosis made in the emergency department (ED). Many presentations mimic acute coronary syndrome (ACS) and over a third of TAAD patients present with raised cardiac enzymes, many of whom have ACS-like changes on the electrocardiogram. The aim of this study was to assess the current practice in diagnosis and management of TAAD. METHODS: Between April and October 2018, a structured survey was distributed to ED Consultants across the UK. Questions surrounded: i) simulated clinical scenarios which mimicked ACS in the early stages (where TAAD could simultaneously be the diagnosis); and ii) ED infrastructure for TAAD management. RESULTS: Responses were received from 175 ED consultants across 70 hospital Trusts. In the context of chest pain and ST elevation, 97% of ED consultants considered this sufficient to diagnose ACS, and over half (54%) agreed with committing to treatment (including the use of thrombolysis) prior to further investigation. Early committers to ACS treatment were statistically less likely to ever order a CT scan or d-dimer (OR 0.31, 95% CI 0.12-0.83, p = 0.02). In total, 32% of consultants reported they would ever request a CT chest in the context of chest pain and elevated troponin. The lack of an AD algorithm was the strongest predictor of clinicians avoiding the use of more definitive investigations for TAAD (OR 0.31, 95% CI 0.01-0.64, p = 0.05). CONCLUSIONS: In TAAD patients presenting with chest pain and elevated cardiac enzymes there is a high probability of ACS treatment being commenced and a significant risk of failing to request the necessary imaging to diagnose TAAD.