Remote ischemic postconditioning (RIPostC) is the application of a transient and brief ischemic stimulus to a distant site from the organ or texture that is afterward exposed to injury ischemia[8] and has been found to reduce IRI in various animal models.
This might be
leg wraps (9 posts to May 2013)
leg compressions (19 posts to September 2015)
If so, then your hospital and doctors are extremely incompetent for not having protocols on this in place already.
Cerebral protection by remote ischemic post-conditioning in patients with ischemic stroke: A systematic review and meta-analysis of randomized controlled trials
Meng Lu
Yujiao Wang
Xin Yin1, 
Yuanyuan Li- 1Department of Nursing, The First Bethune Hospital of Jilin University, Changchun, China
- 2Department of Neurology, The First Bethune Hospital of Jilin University, Changchun, China
Background: There is evidence that remote limb ischemic postconditioning (RIPostC) can reduce ischemia-reperfusion injury (IRI) and improve the prognosis of patients with ischemic stroke. However, so far, only few relevant clinical studies have been conducted. Therefore, we carried out a meta-analysis of eligible randomized controlled trials to compare the RIPostC group with a control group (no intervention or sham surgery) in patients with ischemic stroke.
Methods: Four English-language publication databases, PubMed, Cochrane, Embase, and Web of Science, were systematically searched up to March 2022. The data were analyzed using Review Manager fixed-effects and random-effects models.
Results: A total of 12 studies were included, and 11 of those were analyzed quantitatively. Compared to controls, The RIPostC group showed significantly reduced NIHHS scores in patients with ischemic stroke, (MD: −1.09, 95% confidence interval [CI]: −1.60, −0.57, P < 0.0001) and improved patients' Montreal Cognitive Assessment (MoCA) scores, (MD: 1.89, 95% CI: 0.78, 3.00, P = 0.0009), Our results showed that RIPostC is safe, (RR = 0.81, 95%CI: 0.61, 1.08, P = 0.15).
Conclusion: Our meta-analysis showed that RIPostC is safe and effective and has a positive cerebral protective effect in patients with ischemic stroke, which is safe and effective, and future large-sample, multicenter trials are needed to validate the cerebral protective effect of RIPostC.
Background
Ischemic stroke is a highly morbid and disabling disease. About two-thirds of patients are left with sequelae including functional impairment of varying degrees (1). Early revascularization therapy such as intravenous thrombolysis and mechanical thrombectomy is an effective treatment for ischemic stroke, but this treatment has a strict time window beyond which the probability of adverse effects will increase, the salvage rate for ischemic penumbra will greatly reduce, and the risk of bleeding will outweigh the therapeutic benefit (2). In recent years, several studies have aimed to explore new neuroprotective strategies. However, few have been successfully translated from basic research to clinical application.
The phenomenon of ischemic preconditioning was first identified in the heart. Ischemic preconditioning provides hope to the study of neuroprotective measures. In 1986, the American scholar Murry performed four ischemia-reperfusion sessions on the anterior descending branch before preparing an infarct model and found that it could lead to a reduction in infarct size (3). In several subsequent studies, it has been confirmed that ischemic preconditioning can reduce myocardial infarct size and coronary vascular injury and improve the clinical prognosis of patients with myocardial infarction (4, 5). Kitagawa et al. showed that ischemic preconditioning of the gerbil brain prior to ischemia had a protective effect on the post-ischemic brain and reduced neuronal death in the C1 region of the hippocampus (6). However, ischemic preconditioning requires intervention before the onset of an ischemic event, which is difficult to achieve in clinical practice because we may not be able to anticipate sudden events.
In 2006, Zhao et al. (7) first found that ischemic post-conditioning attenuated ischemia-reperfusion injury (IRI) after cerebral reperfusion in a rat model of permanent middle cerebral artery occlusion and transient bilateral carotid artery occlusion. Similar to ischemic preconditioning, ischemic post-conditioning is an endogenous mechanism that stimulates endogenous protective mechanisms in the body to reduce IRI to critical vital organs through repeated, transient, non-lethal ischemic treatment of the body. Vinten-Johansen et al. found that post-treatment not only produced similar results to pretreatment, but that post-conditioning reduced infarct size, attenuated vascular dysfunction, and reduced neutrophil accumulation after prolonged reperfusion (8–10). Several studies have confirmed this finding (11–13). Studies have shown that ischemic post-conditioning can inhibit free radical production and initiation of apoptosis during ischemic reperfusion and increase superoxide dismutase and catalase activities in brain tissue (7, 14). Reactive oxygen and nitrogen (ROS/RNS) also play an important role in the mechanism of action of ischemic post-conditioning (15). Although the protective mechanisms are not yet fully elucidated, the protective effect of ischemic post-conditioning on the brain has been confirmed in several studies.
RIPostC is safer than local post-conditioning. RIPostC refers to ischemic post-treatment of non-life-critical organs such as skeletal muscles of the arms and legs to mediate the body's endogenous protective mechanisms, and is a complex, systemic phenomenon (16). RIPostC was first used 30 years ago in patients who suffered a heart attack (17, 18), and it can exert a protective effect on the myocardium through a complex signal transduction including neuronal and humoral (19). Similarly, RIPostC not only protects the myocardium from ischemic injury, but also has a similar protective effect on the brain (20). However, most of these studies have focused on animal models and have achieved ischemic post-conditioning by intermittent occlusion of the carotid and cerebral arteries, which is ethically not possible in humans, as it is associated with high risk. Several clinical studies have investigated the protective effect of post-treatment of RIPostC in patients with ischemic cerebrovascular disease, but the number of available studies is small and the sample size of individual studies is very limited to draw definitive conclusions. Therefore, a systematic evaluation in conjunction with published randomized controlled trials (RCTs) is needed to assess whether RIPostC improves the prognosis and reduces the degree of neurological deficits in patients with ischemic cerebrovascular disease.
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