• Journal of Korean Academy of Nursing
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• v.42 no.5
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• pp.719-729
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• 2012

Purpose: This study was done to examine relationships between nurse staffing level and postsurgical patient outcomes using inpatient database from the National Health Insurance. Methods: Records of 111,491 patients who received one of 12 types of surgery between January and December, 2009 were identified and analyzed in this study. Nurse staffing level was measured using adjusted nurse staffing grades from 0 to 7. Patient outcomes were defined as in-hospital mortality, or pneumonia, sepsis, or urinary tract infection after surgery. Logistic regression analyses estimated by Generalized Estimation Model, were used to analyze the association between nurse staffing level and patient outcomes. Results: An inverse relationship was found between nurse staffing and patient mortality. Compared with patients who were cared for in hospitals with the highest nurse staffing (Grades 0-1), increases in the odds of dying were found in those with Grades 6-7 [OR (odds ratio)=2.99, 95% CI (confidence interval)=1.94-4.60], those with Grades 4-5 (OR=1.78, 95% CI=1.24-2.57) and those with Grades 2-3 (OR=1.57, 95% CI=1.25-1.98). Lower nurse staffing level was also associated with higher number of cases in pneumonia and sepsis. Conclusion: Policies for providing adequate nurse staffing is required to enhance quality of care and lead to better perioperative patient outcomes.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.25 no.4
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• pp.375-378
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• 1999

Incidence and mortality rate of maxillofacial infection is relatively low in the era of antibiotics. Despite the use of antibiotics, delayed treatment, underlying systemic diseases, drug-resistant microorganisms may result in life-threatening situations. The deep neck infection developed from odontogenic infection may result in sepsis, mediastinitis, aspiration pneumonia, asphyxia. Sepsis is the most dangerous complication which can quickly result in a number of lethal situations. The treatment of sepsis includes awareness of such complication, use of sensitive antibiotics, removal of infection source, and hemodynamic, respiratory and metabolic support. We experienced a patient who died of sepsis, which developed from odontogenic infection. The initial diagnosis was a buccal space cellulitis. However, in spite of medical and surgical treatment, this progressed to Ludwig's angina and then deep neck infection and finally sepsis. On the 10th hospital day, the patient died of multiorgan failure caused by sepsis.

• Biomolecules & Therapeutics
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• v.24 no.4
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• pp.387-394
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• 2016

Sepsis, a serious clinical problem, is characterized by a systemic inflammatory response to infection and leads to organ failure. Toll-like receptor (TLR) signaling is intimately implicated in hyper-inflammatory responses and tissue injury during sepsis. Histone deacetylase (HDAC) inhibitors have been reported to exhibit anti-inflammatory properties. The aim of this study was to investigate the hepatoprotective mechanisms of trichostatin A (TSA), a HDAC inhibitor, associated with TLR signaling pathway during sepsis. The anti-inflammatory properties of TSA were assayed in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. Polymicrobial sepsis was induced in mice by cecal ligation and puncture (CLP), a clinically relevant model of sepsis. The mice were intraperitoneally received TSA (1, 2 or 5 mg/kg) 30 min before CLP. The serum and liver samples were collected 6 and 24-h after CLP. TSA inhibited the increased production of tumor necrosis factor (TNF)-${\alpha}$ and interleukin (IL)-6 in LPS-stimulated RAW264.7 cells. TSA improved sepsis-induced mortality, attenuated liver injury and decreased serum TNF-${\alpha}$ and IL-6 levels. CLP increased the levels of TLR4, TLR2 and myeloid differentiation primary response protein 88 (MyD88) protein expression and association of MyD88 with TLR4 and TLR2, which were attenuated by TSA. CLP increased nuclear translocation of nuclear factor kappa B and decreased cytosolic inhibitor of kappa B ($I{\kappa}B$) protein expression, which were attenuated by TSA. Moreover, CLP decreased acetylation of $I{\kappa}B$ kinase (IKK) and increased association of IKK with $I{\kappa}B$ and TSA attenuated these alterations. Our findings suggest that TSA attenuates liver injury by inhibiting TLR-mediated inflammatory response during sepsis.

• Advances in pediatric surgery
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• v.6 no.1
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• pp.10-18
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• 2000

Multisystem organ failure resulting from gram negative bacterial sepsis is associated with high morbidity and mortality in surgical neonates. There are differences in the clinical characteristics of organ failure in neonates and adults. The purpose of this study is to identify the differences and determine the order of organ failure between baby rats and adult rats after induction of gram negative sepsis. Fifty baby rats less than 30-day-old and another 50 adult rats more than 2-month-old were divided into control group (G1) and experimental group (G2). The G1 consisted of 10 baby- and 10 adult-rats, and the G2 consisted of 40 babies and 40 adults. E. coli ($10^8/mL$ per 100g of body weight) were injected into the peritoneal cavity in G2 and same amount of saline was injected in G 1. Blood samples were obtained before injection, 24 hour, 48 hour, 72 hour and after death. WEC, platelet, $PaO_2$, $PaCO_2$, total bilirubin, BUN, creatinine, albumin and abdominal wall thickness were measured to evaluate the sequence of organ failure. The mortality was 55.0 % in G2-babies and 32.5 % in G2-adults. In baby rats, microvascular, hematologic and renal failure appeared within 24 hours after injection and pulmonary failure followed. Pulmonary, renal and liver failure developed within 24-48 hours in adult rats; however, microvascular failure did not appear until they were moribund. Thrombocytopenia, hypoalbuminemia, increased BUN and generalized edema was the earlist sign of sepsis in baby rats.

• Tuberculosis and Respiratory Diseases
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• v.83 no.3
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• pp.248-254
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• 2020

Background: Although few studies have reported improved clinical outcomes with the administration of vitamin B1 and C in critically ill patients with septic shock or severe pneumonia, its clinical impact on patients with sepsis-related acute respiratory distress syndrome (ARDS) remains unclear. The purpose of this study was to evaluate the association with vitamin B and C supplementation and clinical outcomes in patients with ARDS. Methods: Patients with ARDS requiring invasive mechanical ventilation, admitted to the medical intensive care unit (ICU) were included in this study. Clinical outcomes were compared between patients administered with vitamin B1 (200 mg/day) and C (2 g/day) June 2018-May 2019 (the supplementation group) and those who did not receive vitamin B1 and C administration June 2017-May 2018 (the control group). Results: Seventy-nine patients were included. Thirty-three patients received vitamin B1 and C whereas 46 patients did not. Steroid administration was more frequent in patients receiving vitamin B1 and C supplementation than in those without it. There were no significant differences in the mortality between the patients who received vitamin B1 and C and those who did not. There were not significant differences in ventilator and ICU-free days between each of the 21 matched patients. Conclusion: Vitamin B1 and C supplementation was not associated with reduced mortality rates, and ventilator and ICU-free days in patients with sepsis-related ARDS requiring invasive mechanical ventilation.

• Journal of Microbiology and Biotechnology
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• v.27 no.4
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• pp.838-843
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• 2017

Sepsis is a major health problem worldwide, with an extremely high rate of morbidity and mortality, partly due to delayed diagnosis during early disease. Currently, sepsis diagnosis requires bacterial culturing of blood samples over several days, whereas PCR-based molecular diagnosis methods are faster but lack sensitivity. The use of biosensors containing nucleic acid aptamers that bind targets with high affinity and specificity could accelerate sepsis diagnosis. Previously, we used the systematic evolution of ligands by exponential enrichment technique to develop the aptamers Antibac1 and Antibac2, targeting the ubiquitous bacterial peptidoglycan. Here, we show that these aptamers bind to four gram-positive and seven gram-negative bacterial sepsis agents with high binding efficiency. Thus, these aptamers could be used in combination as biological recognition elements in the development of biosensors that are an alternative to rapid bacteria detection, since they could provide culture and amplification-free tests for rapid clinical sepsis diagnosis.

• Molecules and Cells
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• v.40 no.12
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• pp.935-944
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• 2017

More than 50% of sepsis cases are associated with pneumonia. Sepsis is caused by infiltration of bacteria into the blood via inflammation, which is triggered by the release of cell wall components following lysis. However, the regulatory mechanism of lysis during infection is not well defined. Mice were infected with Streptococcus pneumoniae D39 wild-type (WT) and lipase mutant (${\Delta}lipA$) intranasally (pneumonia model) or intraperitoneally (sepsis model), and survival rate and pneumococcal colonization were determined. LipA and autolysin (LytA) levels were determined by qPCR and western blotting. S. pneumoniae Spd_1447 in the D39 (type 2) strain was identified as a lipase (LipA). In the sepsis model, but not in the pneumonia model, mice infected with the ${\Delta}lipA$ displayed higher mortality rates than did the D39 WT-infected mice. Treatment of pneumococci with serum induced LipA expression at both the mRNA and protein levels. In the presence of serum, the ${\Delta}lipA$ displayed faster lysis rates and higher LytA expression than the WT, both in vitro and in vivo. These results indicate that a pneumococcal lipase (LipA) represses autolysis via inhibition of LytA in a sepsis model.

• Proceedings of the Korean Society of Applied Pharmacology
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• 2003.11a
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• pp.77-77
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• 2003

Sepsis remains common surgical problems with high morbidity and mortality despite improvement in the management for septic patient. Although hepatocellular dysfunction occurs during sepsis, the mechanism responsible for this remains unclear. In sepsis, a state of severe oxidative stress is encountered, with host endogenous antioxidant defenses overcome. Therefore, the aim of this study was to determine the effect of a-tocopherol (AT) vasoregulatory gene expression during polymicrobial sepsis. Rats were subjected to polymicrobial sepsis by cecal ligation and puncture (CLP). AT (15 mg/kg) was intraperitonealy injected for 3 days prior to CLP. Blood samples were taken 24 h after CLP for measurement of the extent of hepatocellular damage. Liver samples were taken for RT-PCR analysis of mRNA for genes of interest: endothelin-l (ET-l), its receptors $ET_{A}$ and $ET_{B}$, nitric oxide synthases (iNOS and eNOS), cyclooxygenase-2 (COX -2), heme oxygenase-l (HO-l), and tumor necrosis factor-$\alpha$ (TNF-$\alpha$). The activities of serum alanine aminotransferase and lipid peroxidation level were significantly increased; an increase which was prevented by AT pretreatment. CLP significantly increased the mRNA levels of ET-1 and $ET_{B}$; an increase that was prevented by AT pretreatment. However, the level of $ET_{A}$ mRNA significantly decreased after CLP; a decrease that was not prevented by AT pretreatment. There were significant increases in the mRNA expression of iNOS, HO-l and COX -2 in CLP groups. This increase was prevented by AT pretreatment. The expression of eNOS and TNF-$\alpha$ mRNA significantly increased in CLP, which was not prevented by AT pretreatment. Our findings suggest that there was an imbalanced vasoregulatory gene expression in sepsis, and AT ameliorates this change through its free radical scavenging activity.

• Journal of Chest Surgery
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• v.23 no.5
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• pp.1040-1046
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• 1990

Despite the improved diagnostic and treatment modalities recently introduced for a variety of esophageal disorders, a perforation or leak from the esophagus remains a sources of morbidity and mortality regardless of the cause of leak. After the perforation of esophagus, the contamination of mediastinum and pleural cavity with food, bacteria and corrosive gastric juice leads to sepsis and cardiopulmonary dysfunction. The early diagnosis and early treatment are very important, and the delayed treatment leads to high risk of morbidity and mortality. We experienced one case of esophageal perforation, after forced vomiting in 48 years old male patient. We used omentum on the treatment of ruptured esophagus, and it was successfully managed.

• Proceedings of the Korean Society of Applied Pharmacology
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• 2001.11a
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• pp.109-109
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• 2001

The present study was done to investigate the relationship between Kupffer cells and alteration of cytochrome P-450 (CYP)-dependent drug metabolizing enzyme activities during polymicrobial sepsis. Male rats were subjected to polymicrobial sepsis by cecal ligation and puncture (CLP) followed by fluid resuscitation. The gadolinium chloride (GdC1$_3$, 10 mg/kg), blocker of Kupffer cells, was pretreated intravenously at 48 h and 24 h prior to the induction of CLP. All assay parameters were determined at 24 h after CLP or sham operation. In CLP-treated rats, the mortality rate of animals increased to 50% and serum alanine (ALT) and aspartate aminotransferase (AST) levels also significantly elevated. However, this increase was not suppressed by GdC1$_3$ pretreatment. Microsomal lipid peroxidation markedly increased after CLP operation. This increase was significantly attenuated by pretreatment. Total cytochrome P-450 content and NADPH-cytochrome P-450 reductase activity were not changed after CLP operation, but GdC1$_3$pretreatment reduced total cytochrome P-450 content, The hepatic microsomal CYP 1A1, 1A2, 2Bl and 2El activities in CLP-induced rats were also not significantly different from sham-operated rats. However, GdC1$_3$pretreatment showed a moderate increase in CYP1A1 and 1A2 activities. Our findings suggest that Kupffer cells may be partly responsible for producing hepatocellular dysfunction during sepsis.