Adrenaline-induced hypokalemia and critical QT prolongation in a patient with refractory anaphylactic shock complicated by myocardial ischemia: a case report.

Ocular ischemic syndrome (OIS) is a visual dysfunction caused by carotid artery stenosis []. OIS occurs more frequently, particularly in cases where collateral circulation between the left and right internal carotid arteries is insufficient []. The disease, which initially presents with ischemic episodes, may progress to retinopathy, neovascularization, and ultimately vision loss [,]. The retina is one of the most oxygen-demanding tissues in the eye; therefore, various ocular vascular disorders can readily lead to retinal ischemia []. Ischemia is defined as a condition resulting from inadequate blood supply to an organ or tissue []. The primary intervention to prevent ischemia-induced tissue damage is restoration of blood flow (reperfusion). However, ischemia followed by reperfusion (I/R) often results in more severe tissue injury. Although multiple mechanisms contribute to I/R injury, excessive production of reactive oxygen species (ROS) is considered the principal pathogenic factor []. During the ischemic period preceding reperfusion, the inability of cells to generate high-energy phosphates leads to depletion of intracellular adenosine triphosphate (ATP) stores []. Reduced ATP levels render tissues more vulnerable to ROS-mediated injury []. This process is accompanied by increased intracellular calcium (Ca), ROS generation, and elevated levels of proinflammatory cytokines, ultimately triggering oxidative and inflammatory damage in retinal tissue []. A recent study also reported that increased oxidative stress and proinflammatory cytokine production play important roles in the pathogenesis of OIS []. Anakinra, whose therapeutic potential was investigated in the present study, is a recombinant human interleukin-1 receptor antagonist (IL-1Ra). IL-1Ra is a naturally occurring anti-inflammatory cytokine that is also present in human breast milk and was the first biological therapy shown to block the pro-inflammatory effects of IL-1 in patients with rheumatoid arthritis [,]. Experimental studies have demonstrated that anakinra protects intestinal tissue against oxidative and inflammatory injury by preventing increases in malondialdehyde (MDA), interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α), while preserving antioxidant defenses []. Previous evidence has also indicated that proinflammatory IL-1β contributes to ATP depletion during shock, and that anakinra may improve survival in hemorrhagic shock by preventing ATP depletion in vital organs []. Furthermore, anakinra has been shown to prevent the decrease in ATP levels induced by proinflammatory cytokines in pancreatic islet cells, whereas the IL-6 antagonist tocilizumab failed to exert a similar effect []. To the best of our knowledge, no previous study has investigated the effects of anakinra in OIS.