Hepatic congestion and metabolic acidosis caused by aortic dissection with massive pericardial effusion

Acute aortic syndrome (AAS) is a cardiovascular emergency characterized by damage to the structural integrity of the aortic wall, which can affect any segment of the aorta. Particularly, Stanford A aortic dissection carries an extremely high mortality rate once it occurs.1 Currently, emergency surgical intervention is the preferred treatment strategy for AAS. However, patients who are unable to undergo surgical treatment for various reasons must receive conservative medical management. Although international guidelines provide non-surgical treatment options for AAS, detailed protocols are limited, especially for cases of aortic dissection rupture into the pericardium, leading to significant pericardial effusion. Typically, the primary cause of death in patients with aortic dissection is the dissection rupturing into the thoracic or abdominal cavity and causing massive hemorrhage. However, for patients with aortic dissection complicated by pericardial effusion who receive conservative medical treatment, refractory acidosis and systemic metabolic disturbances could be the underlying causes of mortality.

Rupture of aortic dissection into the pericardium prevents massive hemorrhage and delays sudden death to some extent, creating an opportunity for surgical intervention. However, if timely surgical treatment were not performed, sudden massive pericardial effusion could lead to cardiac tamponade. Particularly when intrapericardial thrombosis occurs, these complications would exacerbates systemic venous congestion, resulting in liver congestion, rapid elevation of transaminases, a sharp reduction in left ventricular output, inadequate renal perfusion, oliguria or anuria, and, ultimately, refractory metabolic acidosis along with circulatory and respiratory failure. Certainly, aortic dissection rupturing into the pericardium does not immediately reach the severe stage of systemic venous congestion. How to stratify the risk for patients with aortic dissection complicated by pericardial effusion and strive for earlier surgical intervention is a critical issue that requires in-depth consideration by vascular surgeons. Here, we report a case of death caused by hepatic congestion and metabolic acidosis after aortic dissection with massive pericardial effusion.

A 65-year-old male experienced chest pain 9 h ago without any apparent inducement and relieved after resting, which did not attract his attention. Subsequently, he experienced a brief episode of loss of consciousness and recovered consciousness after about 1 min without any limb movement or language impairment, and urinary or fecal incontinence. Then, he was taken to the emergency department of our hospital. The patient had a 10-year history of hypertension, with a highest recorded blood pressure of 200/100 mmHg. He did not regularly take antihypertensive medication, and the control of his blood pressure was unclear. On admission, his blood pressure was 129/79 mmHg. The patient appeared anxious and dyspneic, with coarse breath sounds in both lungs and had no obvious dry or wet rales. Heart sounds were dull, with a heart rate of 115 beats per minute and a regular rhythm. No significant murmurs were heard in any valve areas, and there was no obvious edema in the lower limbs.