Local heat generation during screw insertion into diaphyseal bone: a biomechanical study on different conditions (e.g. screw type, material, mode of insertion)

Background The implantation of screws is a standard procedure in musculoskeletal surgery. Heat can induce thermal osteonecrosis, damage the bone and lead to secondary problems like implant loosening and secondary fractures. The aim of this study was to investigate whether screw insertion generates temperatures that can cause osteonecrosis. Methods We measured the temperature of twenty human femur diaphysis in a total of 120 measurements, while screws of different material (stainless steel and titanium alloy) and different design (locking and cortex screw) were inserted in three different screwing modes (manual vs. machine screwing at full and reduced rotational speed) with 6 thermocouples (3 cis and 3 trans cortex). Each was placed at a depth of 2 mm with a distance of 1.5 mm from the outer surface of the screw. Results The screw design (cortical > locking), the site of measurement (trans-cortex > cis-cortex) and the type of screw insertion (hand insertion > machine insertion) have an influence on the increase in bone temperature. The screw material (steel > titanium), the site of measurement (trans-cortex > cis-cortex) and the type of screw insertion (machine insertion > hand insertion) have an influence on the time needed to cool below critical temperature values. The combination of the two parameters (maximum temperature and cooling time), which is particularly critical for osteonecrosis, is found only at the trans-cortex. Conclusion Inserting a screw hast the potential to increase the temperature of the surrounding bone tissue above critical values and therefore can induce osteonecrosis. The trans-cortex is the critical area for the development of temperatures above the osteonecrosis threshold, making effective cooling by irrigation difficult. It would be conceivable to cool the borehole with cold saline solution before inserting the screw or to cool the screw in cold saline solution. If possible, insertion by hand should be considered.

Cold Saline Perfusion before Ischemia-Reperfusion Is Harmful to the Kidney and Is Associated with the Loss of Ezrin, a Cytoskeletal Protein, in Rats

Background: Organ protection for transplantation is perfusion with ice-cold preservation solutions, although saline is also used in animal experiments and living donor transplantations. However, ice-cold perfusion can contribute to initial graft injury. Our aim was to test if cytoskeletal damage of parenchymal cells is caused by saline itself or by the ice-cold solution. Methods: F344 rat kidneys were flushed with cold (4 °C) saline, ischemic and sham kidneys were not perfused. In a separate set, F344 kidneys were flushed with saline or preservation solution at 4 or 15 °C. Ischemia time was 30 min. Results: Renal injury was significantly more severe following cold ischemia (CI) than after ischemia-reperfusion without flushing (ischemia/reperfusion (I/R)). Functional and morphologic damage was accompanied by severe loss of ezrin from glomerular and tubular epithelial cells after CI. Moreover, saline caused serious injury independently from its temperature, while the perfusion solution was more beneficial, especially at 4 °C. Conclusions: Flushing the kidney with ice-cold saline can cause more severe injury than ischemia-reperfusion at body temperature even during a short (30 min) ischemia. Saline perfusion can prolong recovery from ischemia in kidney transplantation, which can be prevented by using preservation solutions.

Intra-arterial neuroprotective therapy as an adjunct to endovascular intervention in acute ischemic stroke: A review of the literature and future directions

Mechanical thrombectomy for acute ischemic stroke due to large vessel occlusion has been shown to significantly improve outcomes. However, despite efficient rates of recanalization (60–90%), the rates of functional independence remain suboptimal (14–58%), most likely due to pathways of cell death in the brain that have already committed despite successful reperfusion. Pharmacologic neuroprotection provides a potential means of preventing this inevitable damage through targeting excitotoxicity, reactive oxygen species, cellular apoptosis, and inflammation. Numerous clinical trials using various neuroprotective agents have failed, but the majority of these trials did not include endovascular reperfusion, and thus the drugs were not reaching the therapeutic target. Intra-arterial delivery of neuroprotective agents via the guide catheter already in place for mechanical thrombectomy could provide a way to deliver high doses directly to the affected territory while limiting systemic exposure. Agents that have shown promise via the intra-arterial route in preclinical as well as some clinical models include magnesium sulfate, verapamil, cold saline, stem cells, and various combined approaches. Targeted hypothermia, achieved with intra-carotid infusion of cold saline, may provide an effective means of achieving hypothermia of the ischemic tissue while avoiding the systemic effects that have limited its use previously. Combination therapy of targeted hypothermia and a cocktail of drugs that provide anti-excitotoxic, anti-oxidant, anti-apopototic, and anti-inflammatory effects may provide an ideal approach that deserves further study in clinical trials.