A case of fulminant perimyocarditis leading to extensive ECMO treatment and spinal injury resulting in paraplegia

Abstract

Key Clinical MessagePerimyocarditis has varying disease manifestations and prognosis. It may rapidly deteriorate into a life‐threatening state requiring advanced intensive care including veno‐arterial extra‐corporeal membrane oxygenation, which may be lifesaving. Close follow‐up is warranted to detect both short‐term and long‐term complications.

Spinal cord infarction after withdrawal of veno-arterial extracorporeal membrane oxygenation for cardiogenic shock: A case report

“…Moreover, after spinal cord infarction onset, it is considered important to maintain a mean blood pressure of 90 mm Hg and increase spinal cord perfusion pressure, [12] but these measures were either not possible or not described in the reported cases (Table 1). [8,9,[12][13][14][15][16] Similarly, Figure 2. Blood pressure trend and events.…”

“…Moreover, after spinal cord infarction onset, it is considered important to maintain a mean blood pressure of 90 mm Hg and increase spinal cord perfusion pressure, [12] but these measures were either not possible or not described in the reported cases (Table 1). [8,9,12–16] Similarly, we did not actively raise blood pressure so as to protect the heart after the myocardial infarction. Notably, patients with VA-ECMO often have hypocardiac function; therefore, maintaining an average blood pressure of 90 mm Hg may be difficult.…”

Spinal cord infarction during venoarterial-extracorporeal membrane oxygenation support

“…Coronary angiography and intra-aortic balloon pump (IABP) may cause SCI [3][4][5], as well as venoarterial-extracorporeal membrane oxygenation (VA-ECMO). This latter condition has only been reported as small case series; one patient with refractory cardiac arrest due to myopericarditis [6], and a short case series of three patients with a combination of VA-ECMO and IABP [7]. These SCI were documented by MRI after circulatory support withdrawal, and multifactorial origin was retained by the authors to explain the pathophysiological process that led to ischemia (hypoperfusion, vasoconstriction, thromboembolism of Adamkiewicz artery, etc.…).…”