Despite the development of modern intensive care and new antimicrobial agents, the mortality of the patients with severe sepsis and septic shock remains high. The poor outcome is considered to be a consequence of an overactive systemic inflammatory response. Sepsis is now defined as systemic inflammatory response syndrome (SIRS) in which there is an identifiable focus of infection. As a consequence of the overactive SIRS response, the function of various organ systems may be compromised, resulting in multiple organ dysfunction syndrome (MODS) and death.
Systemic inflammation is a consequence of activation of the innate immune system. It is characterized by intravascular release of pro-inflammatory cytokines and other vasoactive mediators, and the concurrent activation of the innate immune cells. In addition to the pro-inflammatory reactions, the host's anti-inflammatory mechanisms are also activated and aimed at counteracting the inflammatory response. The balance between pro- and anti-inflammatory reactions is critical for the outcome of the patient. Understanding the mechanisms of acute inflammatory responses in critical ill patients is necessary for the development of urgently needed therapeutics. The aim of this review is to provide a description of the key components and mechanisms involved in the inflammatory response in patients with SIRS and sepsis.
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Muscle wasting is commonly seen in patients with sepsis as a consequence of the catabolic response in skeletal muscle.
Muscle wasting can occur in cases that have an imbalance between degradation and synthesis of muscle proteins.
Although decrements in the synthesis of muscle proteins may contribute to sepsis-induced muscle wasting, it has been recognized that increments in its degradation play a more essential role in muscle wasting. Muscle wasting in sepsis patients has some significant clinical consequences such as reduced ambulation and exercise tolerance, and an increased risk for pulmonary and thromboembolic complications. Several mechanisms have been proposed for sepsis-induced muscle wasting. Increased proteolysis via the ubiquitin-proteasome pathway and the calpains system is one of the principal mechanisms of muscle wasting induced by sepsis. Calpains are activated by calcium, which increases in patients with sepsis. The activation of the calpains system disrupts the sarcomere of the myofibrils, resulting in the release of myofilaments that are subsequently ubiquitinated and degraded by the 26S proteasome complex. Recent studies have suggested that transcriptional factors such as NF-kappaB and FoxO, and the apoptosis and autophagy-lysosome pathways may also be involved in sepsis-induced muscle wasting. This review briefly summarizes the contribution of these mechanisms of muscle wasting in patients with sepsis and the possible therapeutic agents to treat it.
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BACKGROUND Paraquat has been widely used as a non-selective contact herbicide and it may induce damage to many organs.
This study aimed to assess the factors that can predict the prognosis of paraquat poisoning and to determine the effect of hemoperfusion. METHODS We retrospectively reviewed 132 patients who were poisoned with paraquat from January 2005, to December 2008.
The patients were divided into two groups: The first groups included the death and survived groups, and the second groups included the hemoperfusion and non-hemoperfusion groups. We investigated the mortality, the factors that can predictive the prognosis and the effect of hemoperfusion. RESULTS There were 79 males and 53 female (mean age: 56.1 +/- 15.1 years). The significant differences between the death and survival groups were the volume of paraquat ingested, the mental status, GCS (Glasgow coma scale), pH, base deficit, HCO3, serum Cr (creatinine), serum AST (aspartate transaminase), serum glucose, K (kalium), urine sodium dithionite test and hemoperfusion. The significant differences between the hemoperfusion and non-hemoperfusion groups were the mortality and the mean survival time.
Multivariate regression analysis reveled four predictive factors and their's Odd ratio: 1) urine sodium dithionate test = strong 14.256, 2) hemoperfusion 0.493, 3) Cr > 0.95 mg/kg 31.603 and 4) an amount of ingested paraquat > 45 ml 16.945. CONCLUSIONS The predictive factors for mortality were the amount of paraquat ingested > 45 ml, a urine sodium dithionite test = strong and a serum Cr > 0.95 mg/dl.
Hemoperfusion couldn't be used a predictive factor for mortality, but it increased the mean survival time.
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A 65-year-old woman with type 2 diabetes mellitus was found in an unresponsive state and she was admitted to our hospital. She was comatose on arrival. The bedside blood glucose level on admission was 15 mg/dl (normal range, 55-110 mg/dl). After emergency infusion with 50% dextrose, the blood glucose level rapidly normalized to 98 mg/dl, but there was no clinical improvement of her consciousness.
Three days after admission, diffusion-weighted magnetic resonance imaging of the brain revealed bilateral temporal, occipital and frontal lobes lesions with high signal intensity. The patient's neurological condition did not change over the next 15 days. She died of pneumonia on the 30th day of hospitalization. DWI may be useful for detecting and making the differential diagnosis of hypoglycemic coma.
Further, marked differences in the neuroimaging patterns of patients in a hypoglycemic coma are valuable prognostic predictors. We report here on a case of hypoglycemic coma with a poor outcome.
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Methamphetamine (MA) is an extremely addictive central nervous system stimulant. MA abuse has increased during the past three decades in Korea because it is cheap relatively and easily produced. Acute toxicity can occur via nasal insufflation, intravenous administration and ingestion of liquid formulations. The clinical manifestations include hypertension, tachycardia, hyperthermia, an altered mentality and seizure. Severe complications can occur such as pulmonary edema, rhabdomyolysis, disseminated intravascular coagulation and multiple organ dysfunction syndrome. This case report describes a previously healthy 40-year-old woman who presented to an emergency department with complaints of hyperthermia, an altered mentality and vomiting. This patient was diagnosed as acute MA intoxication by urine toxicology screening, and she showed a variety of clinical manifestations and complications.
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