DYSFUNCTION OF VARIOUS ORGAN SYSTEMS INDUCED BY SEPSIS WITH UNDERLYING SEVERE MYELOMIC DISEASES AND PROSTATE CANCER (CASE REPORT).

A 65-year-old male patient, unconscious, was admitted into the clinic by the Ambulance. From the patient's medical history it was revealed that several hours before the admission in the clinic the following symptoms were present: shortness of breath, fever, hypotonia, consciousness inhibition, because of which emergency brigade was called and was brought by the Emergency Brigade. The history is loaded by chronic pathologies: myeloma disease, prostate cancer, ciliary arrhythmia, heart failure; received several courses of polichemotherapy, last ten days has been treated for pneumonia with antibiotics of ceftriaxone group in outpatient setting. It is also noteworthy that for the last three months dysfunction of musculoskeletal system with muscle weakness, restricted motion has been present. Clinically there was present dysfunction syndrome of several organs: disorder of function of several organs that required emergency intervention, recovery chance was very low, correlation with morbidity in PIRO was high. By investigation it is known, that as SIRS aggravates, and turns into septic shock, lethal index increases, especially when the underlying severe diseases are present. On basis of certain data we can conclude that the severity of the disease may have some compatibility with results, although it is alteration of further clinical status of initial stage that has the closest compatibility with results. Sepsis toward MODS experiences progress with lethal results. Mortality rate in the patients with acute respiratory deficiency increases from 50% to 80%. In most patients with sepsis syndrome, who have 3 or more organs damaged, lethality is more than 90%. In this certain case organ systems that are mostly involved in the process during the sepsis, are respiratory, blood, renal and cardiovascular systems, were all involved , in the mentioned case a reasonable symptomatic and pathognomic treatment and the appropriate measures led to the recovery of the above mentioned patient. Sepsis syndrome is developed when the balance between the substances that contribute to the inflammation and anti-inflammatory substances is violated. By the mentioned case there is sepsis - induced polyorganic insufficiency with underlying severe somatic pathological condition, with violation of hemodynamics. Clinically the insufficiency of all the organic systems developed at the background of cardio-respiratory-cerebral insufficiency, with functional insufficiency of all the organ systems and violation of buffer system. With reasonable pathognomic and symptomatic treatment eradication of vicious circle was possible. The patient was discharged from the clinic with positive clinic-laboratory recovery. The condition is stable. Neurological status -contact, adequate, with high capacity to work, and with an achievement of 2 year remission.

Vasoplegia in septic shock (review).

Vasoplegia is considered as a key factor responsible for the death of patients with septic shock, due to persistent and irreversible hypotension. The latter associated with vascular hyporeactivity to vasoconstrictors is a significant independent prognostic factor of mortality in severe sepsis. Loss of control of the vascular tone occurs through the complex, multifactorial mechanism and implicates deeply disrupted balance between vasoconstrictors and vasodilators. The aim of this review is to discuss in detail the recent suggested alternative mechanisms of vasoplegia in severe sepsis: Overproduction of nitric oxide (NO) by activation of inducible form of nitric oxide synthase (iNOS); up-regulation of prostacyclin (PG12); vasopressin deficiency; significantly elevated levels of circulating endothelin; increased concentrations of vasodilator peptides such as adrenomedulin (AM) and calcitonin gene-related peptide (CGRP); oxidative stress inducing endothelial dysfunction and vascular hyporeactivity to vasoconstrictors; inactivation of catecholamines by oxidation; over-activation of ATP-sensitive potassium channels (KATP channels) during septic shock and their involvement in vascular dysfunction. The review also discusses some therapeutic approaches based on pathogenetic mechanisms of severe sepsis and their efficacy in treatment of patients with septic shock. The loss of vascular tone control occurs through the complex, multifactorial mechanism and implicates deeply disrupted balance between vasoconstrictors and vasodilators in the pathogenesis of septic shock. Overproduction of nitric oxide (NO) by the inducible form of nitric oxide synthase (iNOS); up-regulation of prostacyclin (PG12); vasopressin deficiency; elevated levels of circulating endothelin; increased concentrations of vasodilator peptides such as adrenomedulin (AM) and calcitonin gene-related peptide (CGRP); oxidative stress inducing endothelial dysfunction and vascular hyporeactivity to vasoconstrictors; inactivation of catecholamines by oxidation; over-activation of ATP-sensitive potassium channels (KATP channels) and their involvement in vascular dysfunction - all these factors combined together lead to steady refractory shock with the lethal outcome in patients.

Myocardial dysfunction during septic shock (review).

Patients with septic shock frequently develop myocardial dysfunction evidenced by severely depressed ejection fraction with ventricular dilatation, as measured by an increase in mean systolic and end diastolic ventricular volumes. The pathophysiology of myocardial dysfunction is complex and involves a multitude of factors. The current review describes individual contributing factors and mechanisms such as upregulation of proinflammatory cytokines (IL-1, TNFα, IL-2, IL-6, IFN-γ), reduced myocardial responsiveness to ß-adrenergic stimulation, elevated circulating endothelin levels, Impaired calcium uptake and release from calcium sarcoplasmic reticulum storage, and decreased calcium channel sensitivity, overexpression of inducible NOS and increased production of Nitric oxide. We also discuss possible reasons for apparently detrimental effect of NO inhibition on cardiovascular function in large clinical trials with sepsis patients.