Various studies and detailed guidelines have been reported or updated for decades since the first use of ECMO. However, the survival rate after ECPR for cardiac arrest remains low. The average survival rates for IHCA and OHCA range from 15–17 to 8–10%, respectively [6]. Therefore, numerous reports have recommended indications, inclusion or exclusion criteria, or careful patient selection for favorable outcomes. However, cardiac arrest patients, specifically those with OHCA who are in emergency situations, have a lack of medical information, which makes it difficult to standardize or determine the application of ECPR.

Our patient’s initial electrocardiogram was a shockable rhythm. After ECMO support, the patient’s cardiac rhythm recovered to a normal sinus rhythm. He was just a usually encountering cardiac arrest patient. An OHCA patient is requiring ECPR for refractory ventricular fibrillation. However, 3 h after ECMO support, an unexpected unexperienced complex complication, ACS, developed.

ACS may lead to lethal outcomes if untreated. Our patient was categorized as having secondary ACS due to iatrogenic massive fluid resuscitation to maintain adequate blood flow of ECMO support under life-threatening cardiac arrest. In patients undergoing ECMO support, large-volume fluid administration is frequently required [7, 8]. In our experience, usually 5 to 10 L of volume resuscitation is required in the first 24 h to maintain adequate blood flow for the ECMO support. And initial excessive volume resuscitation in the first 3 to 6 h helps stabilizing the hemodynamic situation of the ECMO support [9]. Patients typically undergo systemic inflammatory response of the ECMO treatment itself which induces pathologic vasodilation and fluid loss to the interstitial compartment, resulting in reduced vascular volume [8]. In addition, massive volume resuscitation, increased capillary permeability secondary to ischemia/reperfusion injury, and/or decreased oncotic pressures can lead to a rapid increase in IAP and eventual ACS [10].

Considering the patient’s lethal status, it was difficult to reach a consensus on the management even through a multidisciplinary team approach. It is known that if IAP aggravates, central venous pressure is increased, and cardiac output is decreased, leading to further ischemic injury and organ malperfusion, a vicious cycle of volume refractory hypoperfusion or hypotension, despite ECMO support. On the other hand, open surgical management, such as decompressive laparotomy, might be too aggressive for the patient since he had disseminated intravascular coagulation and multi-organ failure [7, 10]. Reports have shown poor prognosis with only one successful case report [2, 3, 5].

Our patient underwent decompressive laparotomy 24 h after ACS diagnosis. Rhabdomyolysis-related laboratory rapidly increased, and IAP showed no sign of decrease. The patient could have died from ACS before recovering from cardiogenic shock. Decompressive laparotomy was performed at the bedside of the intensive care unit, which was simpler than expected. Contrary to our expectations, no laparotomy-related bleeding was observed. Once the abdominal wall was opened, the ACS was released, and the patient waited for recovery on ECMO support.

Another educational aspect of this patient was the ECMO support of a critical illness patient suffering severe systemic inflammatory response. ECMO treatment itself and/or multi-organ failure conditions could induce systemic inflammatory response and also could be associated with profound myocardial depression [8, 11]. Our patient initially received VA ECMO for cardiogenic shock caused by refractory ventricular fibrillation. When right leg ischemia became an issue, we converted VA ECMO to VV ECMO instead of changing the VA ECMO cannulation site from the right to the left common femoral artery. At that time, we underestimated the patient’s systemic inflammatory status and only considered the patient’s volume status and lung condition, because the patient’s heart rhythm was stable, and heart function was nearly normal. But actually, the patient was suffering severe systemic inflammation in a critically ill state. We should have waited and supported the cardiac output for the patient to endure or recover from systemic inflammatory status and/or multi-organ failure.