Drowning in freshwater kills many people around the world. Complications are multiple and sometimes impossible to treat. Fluid and electrolyte resuscitation is difficult because of all the physiological, biophysical and biochemical changes that decrease the rate of survival. Extreme lung injury and cardiovascular disorders are responsible for tissue hypoxia, increased production of inflammation markers, biosynthesis of reactive oxygen species and finally, multiple organ damage. Hypothermia, frequently associated with drowning, provides multiple benefits to this type of patients. Various studies have developed the idea that hypothermia protects the brain from biochemical mediators, thereby preventing neuronal cell destruction. In this case report we present the biological parameters and evolution of a patient drowned in freshwater, and also the benefits of hypothermia to the clinical picture.
Traumatic Brain Injury (TBI) is one of the leading causes of death among critically ill patients from the Intensive Care Units (ICU). After primary traumatic injuries, secondary complications occur, which are responsible for the progressive degradation of the clinical status in this type of patients. These include severe inflammation, biochemical and physiological imbalances and disruption of the cellular functionality. The redox cellular potential is determined by the oxidant/antioxidant ratio. Redox potential is disturbed in case of TBI leading to oxidative stress (OS). A series of agression factors that accumulate after primary traumatic injuries lead to secondary lesions represented by brain ischemia and hypoxia, inflammatory and metabolic factors, coagulopathy, microvascular damage, neurotransmitter accumulation, blood-brain barrier disruption, excitotoxic damage, blood-spinal cord barrier damage, and mitochondrial dysfunctions. A cascade of pathophysiological events lead to accelerated production of free radicals (FR) that further sustain the OS. To minimize the OS and restore normal oxidant/antioxidant ratio, a series of antioxidant substances is recommended to be administrated (vitamin C, vitamin E, resveratrol, N-acetylcysteine). In this paper we present the biochemical and pathophysiological mechanism of action of FR in patients with TBI and the antioxidant therapy available.
The management of the critically ill polytrauma patient is complex due to the multiple complications and biochemical and physiopathological imbalances. This happened due to the direct traumatic injury, or due to the post-traumatic events. One of the most complex physiopathology associated to the multiple traumas is represented by microvascular damage, subsequently responsible for a series of complications induced through the imbalance of the redox status, severe molecular damage, reduction of the oxygen delivery to the cell and tissues, cell and mitochondrial dead, augmentation of the inflammatory response and finally the installation of multiple organ dysfunction syndrome in this type of patients. A gold goal in the intensive care units is represented by the evaluation and intense monitoring of the molecular and physiopathological dysfunctions of the critically ill patients. Recently, it was intensely researched the use of microRNAs as biomarkers for the specific physiopathological dysfunctions. In this paper we wish to present a series of microRNAs that can serve as biomarkers for the evaluation of microvascular damage, as well as for the evaluation of other specific physiopathology for the critically ill polytrauma patient.
Increased levels of homocysteine (HCYS) represent a risk factor for a series of physiopathological conditions: mental retardation, cardiovascular and neurodegenerative diseases, Parkinson's and Alzheimer's disease, depression, osteoporosis, endothelial dysfunction and inhibition of cell proliferation. This paper aims to present the pathophysiological implications of HCYS and the correlation of hyperhomocysteinemia (H-HCYS) with critical condition in the intensive care unit (ICU). Hypovitaminosis B and folate deficiency is directly involved in the inhibition of HCYS metabolism and the accumulation of HCYS in the plasma and tissues. Critically ill patients are more prone to H-HCYS due to hypermetabolism and accelerated synthesis produced by reactive oxygen species (ROS). In conclusion it can be affirmed that the determination and monitoring of HCYS plasma levels may be of interest in optimizing the therapy for critically ill patients. Moreover, by controlling HCYS levels, and implicitly the essential cofactors that intervene in the specific biochemical pathways, such as vitamin B6, vitamin B12 and folic acid can provide a diversified and personalized treatment for each patient.
Background: Numerous studies discuss the protective effects of halogenated anesthetics on myocyte injury induced by the ischemia-reperfusion syndrome of the heart. This mechanism is known as pharmacological preconditioning.
Aim of the study: The objective of this study was to identify the effects of two volatile anesthetics frequently used in current clinical practice, Isoflurane and Sevoflurane, on the in situ heart. The study was performed on laboratory animals with induced brain death.
Material and methods: The animals were divided into 3 groups, the control group (n = 8), IZO-PRE group (n = 8) and SEVO-PRE group (n = 8), on which the experimental protocol established for this study was applied. From a molecular point of view, the expressions of protein kinase C-epsilon (PKCε) and of glycogen synthase kinase – 3 beta (GSK-3β) were investigated.
Results: Following the statistical analysis, we observed a significant reduction in the size of the infarcted area in the IZO-PRE group compared to the control group (p <0.0001). Regarding the SEVO-PRE group, no reduction was observed (p >0.05). The expression of GSK-3β is more pronounced in case of the SEVO-PRE group, at 5 minutes after reperfusion, and the effect disappears after 15 minutes. The expression of PKCε as a total form of the enzyme, occurs at 5 minutes after reperfusion in the SEVO-PRE group and late in the IZO-PRE group (after 15 minutes).
Conclusions: Both anesthetics that were applied showed a cardioprotective effect. Isoflurane provided a better structural and morphological protection, but Sevoflurane resulted in a more effective protection in terms of functionality, significantly reducing the incidence of extremely severe life-threatening arrhythmias.
A patient with multiple traumas is usually found in severe haemorrhagic shock. In 40% of the cases, the patient with multiple traumas and haemorrhagic shock cannot recover due to secondary injuries and complications associated with the shock. In this paper we present the case of a male patient 30 years old, who suffered a car accident. The patient is admitted in our hospital with haemorrhagic shock due to femur fracture, acute cranial-cerebral trauma and severe thoracic trauma with bleeding scalp wound, associated with lethal triad of trauma. The clinical and biological parameters demand massive transfusion with packed red blood cells (PRBCs), fresh frozen plasma (FFP), cryoprecipitate (CRY) and colloidal solution (CO) sustained with vassopresor for the haemodynamic stabilisation. During his stay in the ICU, the patient benefits from anti-oxidative therapy with Vitamin C, Vitamin E and Vitamin B1. After 14 days the clinical state of the patient improves and he is transferred in Polytrauma Department.