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During surgical endarterectomy, carotid cross clamping is needed for arteriotomy and plaque removal. Carotid cross clamping reduces the blood flow to the circle of Willis, and some patients show intolerance to the temporary occlusion of the internal carotid artery (ICA). Aim. This study demonstrates locoregional anesthesias safety in patients with carotid cross clamping intolerance (CCI) and the risk factors that predict this condition. Materials and Methods. All patients who underwent surgical carotid endarterectomy between January 2019 and December 2020 (n=53, 29 were male, age (median with range) 78 (56-90) years) were identified in a retrospective review. The indication for surgical treatment was made for a stenosed ICA of 70-99% or in the case of symptomatic stenosis. Surgical technique. An incision is made at the front edge of the sternocleidomastoid muscle. The common carotid artery (CCA) is identified and isolated from the surrounding tissues with sharp dissection and continued toward the bifurcation. Next, the internal and external carotid arteries can be isolated. Heparin (5000 U) is administrated intravenously, and the systolic arterial pressure is increased and kept over 160 mm Hg. In the next step, the cross clamping tolerance test is performed for 60 s. During clamping, the patient is neurologically meticulously observed. In the case of CCI, the operation proceeds with the insertion of a temporary shunt. The arteriotomy is started in the CCA and continues to the ICA. The plaque is completely removed, and the arteriotomy incision is covered with a patch. Before completing the suture, the clamps are partially removed to flush out the debris using the blood flow. Now, the external and common artery can be released. Finally, the clamp of the ICA can be removed. Results. Eight patients had cross clamping tolerance test intolerance. In all these cases, the surgical procedure was continued with a shunt. The further operation course remained uncomplicated. The in-hospital mortality was nil, and a transient ischemic attack occurred in only one case. Coronary artery disease (CAD) [odds ratio (OR) 12.65, 95% confidence interval (CI) 1.43-112.50], a history of cerebrovascular events [OR 10.50, 95% CI 1.83-60.30], and contralateral stenosis of 70% or more [OR 26.66, 95% CI 2.29-304.37] presented a significant association with the CCI and the need to shunt. The remaining factors showed no significant association with intolerance. Conclusions. Regional anesthesia is a safe method for identifying patients with CCI and safely performing the surgical procedure. Contralateral stenosis of the ICA and a history of cerebrovascular events are significant factors to predict CCI.

The effect of acetyl - tyrosyl-valyl-alanyl-aspartyl - chloromethylketone (ac-YVAD-cmk), an irreversible caspase-1 (IL-1beta converting enzyme, ICE) inhibitor on mortality, leukocyte and platelet counts and cytokine levels was investigated in a double-blind rat model of endotoxaemia. Intravenous (i.v.) bolus administration of lipopolysaccharide (LPS) (25-75 mg kg(-1), n=12 per group) to anaesthetized rats induced a dose dependent increase in mortality over 8 h (LD(50)=48 mg kg(-1)). During this period, animals became leukopenic and thrombocytopenic. Serum levels of IL-beta, IL-6, and TNF-alpha were highly elevated. Pretreatment of rats with ac-YVAD-cmk at a dose of 12.5 micromol kg(-1) significantly reduced mortality from 83 to 33% using Log Rank analysis. However, ac-YVAD-cmk did not modify blood cell counts or cytokine profiles as compared with the LPS-drug vehicle group. These data lay credence to the potential importance of caspase-1-inhibition in modifying the inflammatory response to endotoxin. Further investigations are warranted in understanding the relationship between caspase-1 inhibition, cytokine production and animal survival in different experimental paradigms of sepsis.

Our objective was to investigate the levels of chemokines (MIP1-alpha, MCP-1, and Gro-alpha), Interleukin-18 (IL-18), and Interleukin (IL-6) in bronchoalveolar lavage (BAL) fluid and serum at the onset and ongoing states of sepsis as defined by the American College of Chest Physicians/Society of Critical Care Medicine in septic surgical ICU patients. Our summary background data was to understand the significance of compartmentalized inflammatory mediator production in an immunologically active organ (lung) in comparison with levels in the systemic circulation. The study group consisted of 20 septic patients and 10 non-septic patients on surgical ICU. At the onset of sepsis, both BAL fluid and serum samples were taken and levels of MIP-1alpha, MCP-1, GRO-alpha, IL-18, and IL-6 were measured by ELISA. Furthermore, over a subsequent 8-day period, levels of these mediators were determined in serum. In some experiments, IL-18 mRNA levels were determined in peripheral blood lymphocytes (PBL) of septic and non-septic patients. At the onset of sepsis, MIP-1alpha, MCP-1, GRO-alpha, IL-18, and IL-6 levels were significantly up-regulated in BAL fluid as compared with non-septic controls. In marked contrast, with the exception of IL-18 mRNA and IL-6 peptide, there was no increase in serum levels of inflammatory mediators determined both at the onset and during the ongoing states of sepsis. Based on the present data, monitoring levels of serum chemokines and IL-18 protein as markers of sepsis might be misleading since despite their non-detection in serum, they were highly up-regulated in the lung tissue compartment. These data might underscore the role of MIP-1alpha, MCP-1, GRO-alpha, and IL-18 in the mediation of local tissue damage. Furthermore, these findings raise the notion that mediator measurement in immunologically active organs might serve as pivotal indicators of sepsis prior to the actual fulfillment of specific clinical criteria that defines the patient as being septic.