Vol 47, No 3 (2019)

The world prevalence of chronic kidney disease (CKD) stages 1 to 5 ranges from 11.7 to 15.1%. Incidence of fractures in patients with CKD stage 5 is 5-fold higher than that in the general population, which is related to mineral metabolism disorders, secondary hyperparathyroidism, and osteoporosis. By damaging multiple organs and systems, CKD triggers a whole pathological cascade. There are hematopoietic abnormalities, cell lineages, direct toxic effect on blood cell elements, with simultaneously increased risk of bleeding and a high and extremely high risk of thrombi formation and thromboembolic complications. Calcium and phosphorus metabolism disorders lead to calcification and mineralization of vasculature, myocardium and heart valves; progressive renal dysfunction affects the course of heart and vessel diseases, aggravating their clinical manifestations. Cardiovascular disorders become the main cause of death of such patients, and the development of pulmonary hypertension is associated with increased morbidity and mortality. At the same time, protein and energy deficiencies do occur, with disturbance of the acid-base balance, water and electrolyte balance; uremic toxins exert unhealthy effects on the gastrointestinal tract. Various extra-renal pathologies, specific pharmacokinetics, regimen and frequency of renal replacement therapy needed to maintain an adequate volume status make it necessary to thoroughly prepare the patients for surgery and define special requirement to perioperative management in arthroplasty. Currently, there are no guidelines on the perioperative management of this patient category. In this review article we consider specifics and particulars of preoperative, intraoperative and postoperative management of the end stage CKD patients during knee and hip replacement arthroplasties.

Low cardiac output syndrome is one of the most common and serious complications in cardiac surgery and is associated with increased morbidity and mortality. Several prognostic features have been recognized, including preoperative, intraoperative risk factors and laboratory predictors. The pathophysiologic mechanisms of low cardiac output syndrome are not limited by ventricular systolic dysfunction only, diastolic dysfunction and valvular abnormalities also contribute to low cardiac output syndrome development. There is a broad spectrum of monitoring techniques during cardiac surgery, all of them are different in their invasiveness and reliability. Goal-directed hemodynamic therapy should be based on the most informative and accurate monitoring methods and its goal is to optimize the balance between oxygen delivery and consumption. Treatment of low cardiac output syndrome is intended to increase tissue oxygen delivery and prevent organ dysfunction providing adequate hemodynamic support. The first line of low cardiac output syndrome therapy, to be initiated as soon as the volume status is optimized, is the use of inotropes, vasopressors and vasodilators to improve contractility, preload and afterload. In the most severe cases the need of mechanical support might take place, including intra-aortic balloon pump, ventricular assist devices and extracorporeal membrane oxygenation.

Background: The search for methods for protection against delivery and labor pains has led to resumption of studies of non-invasive, safe and effective labor analgesia and inhalational anesthesia that could be used both separately and in combination with other methods. Recent research has demonstrated the highest efficacy of sevoflurane for analgesia of spontaneous delivery.

Aim: To develop an optimized and effective method of inhalational analgesia with sevoflurane for spontaneous delivery.

Materials and methods: We have performed a prospective study of the efficacy of inhalational sevoflurane for analgesia of spontaneous delivery. Thirty three obstetric patients were given sevoflurane-oxygen mixture according to a specially designed technique. The pain intensity was assessed with a visual analogous scale (VAS), sedation level, with Ramsay scale and Richmond Agitation-Sedation Scale (RASS).

Results: The mean duration of inhalational anesthesia was 92.1±28 minutes [60–180']. There were no refusals and no switching to another type of analgesia. After induction of analgesia with Funding sevoflurane, there was a significant decrease of pain intensity by VAS by 34.9% from the baseline level (p = 0.00003); the pain was assessed as “moderate”. This trend was maintained throughout the whole exposure period.

Conclusion: The results obtained confirm the possibility to use the proposed method of inhalational analgesia with sevoflurane to ensure effective analgesia in obstetric patients during delivery and labor.

Background: Fixed pulmonary hypertension (PH) in heart transplant candidates is a risk factor for right ventricular failure in the postoperative period and early mortality. Patients with fixed PH are not included in the waiting list. Thus, the correct assessment of the pulmonary circulation before the operation affects both clinical management and prognosis. Aim: To reduce the risk of incorrect patient non-inclusion to the waiting list by reduction of false negative test results for PH reversibility.

Materials and methods: Fourteen heart transplant candidates were included in this retrospective cohort single center study. Fixed PH with pulmonary vascular resistance (PVR) exceeding 3.5 Wood's units was found in all these patients using right heart catheterization and pulmonary vasoreactivity tests. Initially, these patients had not been put into the waiting list. Pulmonary catheterization was performed in the intensive care unit with a Swan-Ganz catheter and pre-pulmonary thermodilution technique. To perform pulmonary vasoreactivity tests, inhaled iloprost (n = 12) or nitric oxide (n = 2) were used. Subsequently all patients received levosimendan infusion at a dose of 12.5 (0.05–0.2) mg/kg/min, with repeated pulmonary artery catheterization and pulmonary vasoreactivity tests at 72 hours after the infusion. Pulmonary vasoreactivity tests results allowed 13 patients to be included into the waiting list. Heart transplantation was performed in 8 recipients, with postoperative assessment of their hemodynamic and clinical parameters. Data are presented as median [25th percentile; 75th percentile].

Results: After the levosimendan infusion, there was a decrease in the pulmonary artery mean pressure from 45 [36; 47] to 29.5 [23; 37] mm Hg (p < 0.01), and in PVR from 6.9 [4.9; 8.9] to 3.6 [2.9; 5.9] Wood's units (p <0.01). In 7 patients, PVR decreased to less than 3.5 Wood's units: the rest of the patients underwent pulmonary vasoreactivity tests. As a result, 13 of 14 patients showed reversible PH and were included into the waiting list. By the date of the manuscript submission, heart transplantation has been performed in 8 patients. Their PVR 6 hours after surgery was 2.2 [2; 3.1] Wood's units; there were no cases of fixed PH and right heart failure. There was a single death associated to a hemorrhagic stroke at day 6 after heart transplantation. The sensitivity of pre-operative pulmonary vasoreactivity tests with the use of levosimendan was 87.5%.

Conclusion: Levosimendan infusion may increase the sensitivity of the pulmonary vasoreactivity tests before patients' inclusion into the waiting list for heart transplantation.

Background: Neutrophil activation is a  mandatory stage and a  sensitive marker of systemic inflammatory response. The development of this condition is associated with subsequent multiple organ failure which is the main indication for the patients stay in the intensive care unit. The search for drugs that could prevent the development of systemic inflammatory response and reduce mortality remains an urgent task of anesthesiology/resuscitation.

Aim: To study the anti-inflammatory effect of dalargin, a synthetic analogue of lei-enkephalin, on human neutrophils in vitro.

Materials and methods: The study was performed on blood neutrophils isolated from 5 healthy donors. A proportion of neutrophils were activated by 10 mkM formil-Met-Leu-Pro (fMLP) and 100 ng/mL lipopolysaccharide (LPS) with subsequent assessment of their activity by fluorescent antibodies to the degranulation markers CD11b and CD66b. Thereafter intact and activated neutrophils were treated with dalargin solution at concentrations of 50 and 100 mcg/mL.

Results: Dalargin at 100 mcg/mL reduced the expression of CD11b molecules on the surface of intact neutrophils by 5.5-fold (p=0.008). On the contrary, LPS at a  dose of 100  ng/mL increased the expression of the same molecules by 46% (p=0.08). The addition of dalargin at 50 mcg/mL to LPS-activated neutrophils reduced the expression of CD11b molecules (p=0.016). The addition of dalargin at 50  mcg/mL to fMLP-activated neutrophils significantly (p=0.008) reduced the expression of CD11b molecules and reversed their expression virtually to the level of the control. The addition of dalargin at 100  mcg/mL to neutrophils activated by fMLP at 10 mkM reduced the expression of CD11b on their surface to a level below the control by 23% (p=0.08).

Conclusion: Dalargin at the studied concentrations has an anti-inflammatory effect on both intact and pre-activated bacterial components of neutrophils, thus inhibiting the process of activation and degranulation in a dose-dependent manner.