Commentary: Early malperfusion syndrome—a new concept

Abstract

More and more cardiac surgeons are realizing the gravity of visceral malperfusion in acute type A aortic dissection (ATAAD) and choose to treat the visceral malperfusion first when a patient has already developed malperfusion syndrome (MPS). [1][2][3] The difference between malperfusion and MPS is similar to the difference between bacteremia and sepsis, or between HIVand AIDS. End-organ malperfusion is inadequate blood flow to the end organs, which can be diagnosed by clinical exam (peripheral pulses) and computed tomography angiography. MPS is the consequence of prolonged malperfusion, including cell, tissue, and organ necrosis, dysfunction, and failure, which can be clinically diagnosed based on symptoms (eg, abdominal pain), physical exam (eg, peritoneal signs), and laboratory tests (eg, serum lactate, arterial blood gases). Just like sepsis, MPS is a process of development of end-organ damage. In the early stage, because of ischemia, patients start to have cell death, tissue death, and organ dysfunction, but no organ death and failure. For example, patients with superior mesenteric artery (SMA) malperfusion can have abdominal pain, mildly elevated lactate, and mild metabolic acidosis but no bloody stools, peritoneal signs, or transmural necrosis of intestine, as in the case described by Ni and colleagues. 2 We can define this stage of malperfusion syndrome as early-stage MPS, which also includes mildly increased liver enzymes, bilirubin, creatinine, and myoglobin in early MPS due to celiac artery, renal artery, and extremity malperfusion. If the malperfusion is not resolved, patients will continue to develop extensive organ

Treating lower extremity malperfusion syndrome in acute type A aortic dissection with endovascular revascularization followed by delayed aortic repair

“…The difference between malperfusion and MPS is similar to the difference of "bacteremia and sepsis (septic syndrome) or "HIV and AIDS." 14 For ATAAD patients with LE malperfusion, we all are in agreement that those patients should be treated with emergency open aortic repair. However, for ATAAD patients with LE-MPS (necrosis and dysfunction of LE), same as mesenteric MPS, the optimal management remains controversial.…”

“…MPS frequently is complicated with multiorgan failure and metabolic acidosis. The difference between malperfusion and MPS is similar to the difference of “bacteremia and sepsis (septic syndrome) or “HIV and AIDS.” 14 Malperfusion of the LE was not an indication for emergency endovascular fenestration/stenting and delayed open aortic repair, such as loss of femoral artery pulse but with normal function of the LE. However, MPS was an indication for emergency endovascular fenestration/stenting, such as loss of femoral pulse with LE motor or sensory deficit, elevated CK or serum lactate level, and radiographic evidence of dynamic or static obstruction of iliac or femoral arteries.…”

Progression of distal aorta after endovascular fenestration/stenting in acute type A aortic dissection with malperfusion syndrome

“… 5 , 6 MPS was characterized by tissue necrosis and end-organ dysfunction/failure due to insufficient blood flow to end organs and dissection-related aortic branch vessel obstruction. 5 , 9 …”