Dmitry I. Levikov

Distributive shock in combination with acute respiratory distress syndrome (ARDS) is an extremely serious condition in terms of the complexity of pathogenesis mechanisms, timely differential diagnosis, high-cost treatment, and is accompanied by high mortality. The simultaneous development of such disorders of vital functions leads to severe acute cardiovascular and acute hypoxemic respiratory failure, in which traditional, standard and documented treatment approaches often prove ineffective. The article will present current data on the features of cardiopulmonary interaction in normal and acute renal failure in combination with severe acute respiratory failure and ARDS, the significant role of right ventricular pulmonary-arterial conjugation and the mutual influence of pathological lung mechanics and impaired vascular regulation. Various cardiac hemodynamic disorders in pulmonary, extrapulmonary, and mixed ARDS phenotypes will be considered, as well as their effect on transpulmonary pressure, venous return, and right ventricular afterload. It will be shown that advanced monitoring methods such as esophageal manometry, echocardiography, and pulmonary artery catheterization are necessary tools for timely detection and phenotyping of respiratory circulatory disorders for personalized selection of respiratory support parameters, cardiohemodynamic correction methods, and adjuvant therapeutic technologies such as pronation and extracorporeal support. The integration of these theoretical data and clinical practice will improve the safety and clinical effectiveness of multicomponent treatment to reduce mortality in this cohort of high-risk patients.

The objective was to investigate the nephroprotective effects of dalargin, a synthetic analog of leu-enkephalin, in a rat model of renal ischemia–reperfusion injury, and to evaluate its impact on the expression and phosphorylation of glycogen synthase kinase-3β (GSK-3β). Materials and methods . Acute kidney injury (AKI) was induced in Wistar rats by 60-minute warm renal ischemia combined with contralateral nephrectomy. Dalargin was administered intraperitoneally at doses of 1, 5, and 10 μg/kg. Serum creatinine and urea levels were measured. GSK-3β expression and phosphorylation were assessed by immunoblotting. Morphological changes in renal tissue were evaluated histologically. Results . Dalargin administration resulted in a dose-dependent attenuation of AKI severity, most pronounced at a dose of 10 μg/kg. This effect was associated with a statistically significant improvement in renal function parameters, increased levels of phosphorylated GSK-3β (pGSK-3β), and reduced histological signs of tubular necrosis. In the lowest-dose group (1 μg/kg), a trend toward worsened functional parameters was observed, possibly related to a survivor selection effect. Conclusion . The findings demonstrate a marked dose-dependent nephroprotective effect of dalargin in renal ischemia–reperfusion injury, associated with inhibition of GSK-3β activity. These results support further investigation of dalargin as a component of organ-protective strategies in critical care settings.

Arterial hypotension and shock of unknown origin are common reasons for intensive care unit admissions and are characterized by significant pharmacoeconomic costs and high mortality. The effectiveness of treatment for patients with shock is determined by the timely and accurate identification of the underlying causes and the implementation of personalized therapy. Differential diagnosis of shock is often possible through the analysis of clinical, laboratory, and non-invasive instrumental data. Echocardiography is now an indispensable tool for urgent and routine assessment of the cardiovascular system, providing rapid information on the anatomy, physiology, and causes of cardiovascular failure. The use of high-quality ultrasonography methods, based solely on 2D visualization, significantly expands diagnostic capabilities. However, accurate diagnosis requires the use of more advanced, semi- quantitative or quantitative ultrasonography methods to identify the underlying mechanisms of shock pathogenesis, allowing the clinician to implement personalized treatment for this patient population.

Postcardiotomy cardiogenic shock is a life-threatening complication after coronary artery bypass grafting (CABG), especially in patients with severely impaired left ventricular systolic function. Management remains challenging, and criteria for repeated levosimendan administration in this setting are not well defined. We report the case of a 74-year-old man with ischemic cardiomyopathy and severely reduced preoperative left ventricular ejection fraction who underwent preoperative levosimendan optimization followed by off-pump CABG. Despite initial improvement, the patient developed postcardiotomy cardiogenic shock in the early postoperative period with progressive hypoperfusion, lactate elevation, worsening ventricular dysfunction, and a low cardiac index confirmed by Swan-Ganz catheterization. Intra-aortic balloon pump support was initiated in the early postoperative period, and norepinephrine was the only vasoactive agent used before repeated levosimendan administration. Because of persistent low-output physiology, invasive hemodynamic findings, and a previously favorable response to levosimendan, repeated levosimendan infusion was administered. Subsequent reassessment showed improvement in cardiac index, filling pressures, vascular resistance, ventricular function, and biochemical markers of hypoperfusion and organ dysfunction. This case illustrates that repeated levosimendan administration, guided by invasive hemodynamic assessment, was associated with hemodynamic improvement in postcardiotomy cardiogenic shock after CABG. These findings are hypothesis-generating and should be interpreted with caution. Further prospective studies are required to define patient selection criteria, optimal timing, and the role of repeated levosimendan administration in this setting.

This report describes two clinical cases involving prolonged inhalation sedation using the AnaConDa device in the ICU. Both patients achieved and maintained adequate sedation levels throughout the treatment period. No significant adverse cardiovascular effects were observed.

With the development of clinical pathophysiology, the basic concepts of maintaining fluid homeostasis of the body in normal and critical conditions were revised, and the negative effects of infusion therapy at all stages of its use were studied. Therefore, in the intensive care of shock, the main clinical questions are: when to start fluid therapy, when to stop active fluid therapy, when to start fluid removal from the body, and when to stop fluid de-resuscitation. Thus, in order to implement the principle of personalized treatment, it is important to determine not only the ‘tolerance’ of infusion therapy, but also the ‘sensitivity’ to the infusion of a particular patient – the ability to maintain hemodynamics without the risk of fluid overload. Evaluation of routine clinical, instrumental and laboratory indicators of the state of macro- and microcirculation does not provide an opportunity to accurately answer these questions. Modern sonographic methods for monitoring central and peripheral cardiohemodynamics, ‘venous excess’ using Doppler and extended focus echocardiography allow us to assess the ‘tolerance of infusion therapy’. The implementation of this new direction will increase the efficiency and safety of infusion therapy and improve the outcomes of the critically ill patients’ treatment.

This article presents the Moscow Botkin Hospital experience of using combination of general and superficial cervical plexus regional anesthesia during carotid endarterectomy performed in patients in the acute period of atherothrombotic genesis ischemic stroke. The result of reliable antinociceptive protection of the body from the activation of the sympatho-adrenal system against the background of surgical manipulations was the prevention of episodes of critical hypertension and ensuring normalization of systemic hemodynamics. By reducing the need for opioids, patients’ awakening is accelerated, and their time in the operating room is minimized. In addition, the time of necessary observation in the intensive care unit and the need for anesthesia at the immediate postoperative period, is also reduced. The above factors, as well as a multidisciplinary approach to the patient, allowed not only to provide reliable prevention of recurrent vascular incidents in the acute period of ischemic stroke, but also to improve the neurological outcomes.

Infusion therapy is an important component of many diseases treatment – and one of the main methods of intensive care for intensive care patients. Active infusion therapy using different infusion media, large volumes and high rates of intravenous fluid is especially relevant in critical patients, the most severe of which remains patients with septic shock. For more than two centuries of clinical use, infusion therapy has gone through a long evolutionary path and has become more effective and safer. However, like any drug, infusion therapy (in general and specific infusion media) has a number of side effects, especially when used excessively. Therefore, in recent years, the use of infusion therapy is considered as the appointment of any drug, taking into account indications, contraindications, methods of administration, dosing, duration, deescalation. This made it possible to identify the main stages of infusion therapy of critical conditions and shock: intensive infusion therapy (rapid administration of a large fluid volume), optimization of infusion therapy (reduction of the rate and volume of infusion), stabilization of the patient and minimization of infusion, de-resuscitation – removal of excess fluid from the body. With the development of clinical pathophysiology, the basic concepts of maintaining fluid homeostasis of the body in normal and critical conditions were revised, and the negative effects of infusion therapy at all stages of its use were studied. Therefore, in the intensive care of shock, the main clinical questions are: when to start fluid therapy, when to stop active fluid therapy, when to start fluid removal from the body, and when to stop fluid de-resuscitation. Thus, in order to implement the principle of personalized treatment, it is important to determine not only the «tolerance» of infusion therapy, but also the «sensitivity» to the infusion of a particular patient – the ability to maintain hemodynamics without the risk of fluid overload. Evaluation of routine clinical, instrumental and laboratory indicators of the state of macro- and microcirculation does not provide an opportunity to accurately answer these questions. Modern sonographic methods for monitoring central and peripheral cardiohemodynamics, ‘venous excess’ using Doppler and extended focus echocardiography allow us to assess the ‘tolerance of infusion therapy’. The implementation of this new direction will increase the efficiency and safety of infusion therapy and improve the outcomes of the critically ill patients’ treatment.

Primary hyperparathyroidism (PHPT) is the leading cause of hypercalcemia. Total serum calcium level >3.5 mmol/L is associated with a high risk of a hypercalcemic crisis, manifesting with nausea, vomiting, dehydration, myalgia’s, abdominal pain, acute pancreatitis, acute kidney injury (AKI), cardiac rhythm disorders and disturbances of consciousness. We report here a case of PHPT, manifested with hypercalcemic crisis during pregnancy. A 30-year-old woman in the first trimester of pregnancy admitted complaining on loss of appetite, nausea, vomiting, lower abdomen pain, weakness, and leg pain during the last 10 days. She had a history of two uncomplicated pregnancies, and two episodes of renal colic, her kidney function was normal 2 weeks prior to admission. Work-up showed hypochloremia, hypokalemia, hyponatremia, total serum calcium was 5.34 mmol/L, and serum creatinine 226 µmol/L, and she underwent urgent hemodialysis (HD). Her parathyroid hormone (PTH) was 948 pg/mL, and imaging revealed missed miscarriage 9-10 weeks, soft tissue mass 30x20x33mm near the lower pole of the left lobe of the thyroid gland, small stones in renal calices, and polysegmental pneumonia. She received antibiotics, calcimimetics, and every-day hemodiafiltration (HDF), and underwent vacuum aspiration of uterine cavity and surgical removal of the parathyroidoma. Her PTH shortly returned to the reference level, and serum creatinine dropped to 140 µmol/L after kidney replacement therapy (KRT) secession. Pathology confirmed the diagnosis of parathyroid adenoma. PHPT should be included in the diagnostic algorithm of AKI in pregnancy along with vomiting of pregnant, sepsis, pre-eclampsia and other causes. Successful management of PHPT complications in pregnancy demands multidisciplinary team.