Recombinant human thrombomodulin for pneumonia-induced severe ARDS complicated by DIC in children: a preliminary study.

PURPOSE: Recombinant human soluble thrombomodulin (rTM) has been used to treat disseminated intravascular coagulation (DIC). Recent studies have shown the efficacy of rTM through its anti-inflammatory effects for treatment of adults with acute respiratory distress syndrome (ARDS). However, the safety and efficacy of rTM in children with severe ARDS complicated by DIC have not been reported. In this preliminary study, we reported the feasibility of using rTM for the treatment of pneumonia-induced severe ARDS complicated by DIC in children. METHODS: Six children (age: median 10 months old) with pneumonia-induced severe ARDS complicated by DIC were enrolled in this preliminary study. rTM (380 U/kg) was administered for a maximum of 6 days, in addition to conventional therapies after diagnosis of severe ARDS complicated by DIC. After administration of rTM, we measured changes in the plasma TM concentration and evaluated the clinical course, status of DIC and ARDS, and other laboratory findings, including levels of cytokines, chemokines, and biomarkers. RESULTS: In all six children, the plasma concentration of TM increased and DIC scores decreased after administration of rTM. Four of the six children recovered from the severe ARDS complicated by DIC after treatment, and were discharged from the hospital with no complications. In survived children, levels of soluble receptors for advanced glycation end products, interleukin-6, interleukin-8 and monocyte chemotactic protein-1 decreased after administration of rTM compared to those before rTM. CONCLUSIONS: The rTM administration is feasible as an adjunctive therapeutic strategy for children over 2 months with pneumonia-induced severe ARDS complicated by DIC.

Tuberculous pneumonia-induced severe ARDS complicated with DIC in a female child: a case of successful treatment.

BACKGROUND: Tuberculous (TB) pneumonia can induce acute respiratory distress syndrome (ARDS). Although TB pneumonia is one of the causes of disease and death among children worldwide, the literature on TB pneumonia-induced ARDS is limited. We report herein on the successful treatment of a two-year-old female child with TB pneumonia-induced severe ARDS complicated with disseminated intravascular coagulation (DIC). CASE PRESENTATION: A two-year-old Vietnamese female child with sustained fever and cough for 20 days was transferred to our hospital. She had severe dyspnea and a chest X-ray showed bilateral infiltration without findings of heart failure. After tracheal intubation, her oxygenation index (OI) and PaO2/FiO2 (PF) ratio were 29 and 60 mmHg, respectively. Mycobacterium tuberculosis was detected by real-time polymerase chain reaction (rPCR) assay of tracheal lavage fluid. She was diagnosed as having severe ARDS that developed from TB pneumonia. Anti-tuberculous therapy and cardiopulmonary support were started. However, her respiratory condition deteriorated despite treatment with high-frequency oscillating ventilation (HFO), vasopressor support, and 1 g/kg of immunoglobulin. On the third day after admission, her International Society on Thrombosis and Hemostasis DIC score had increased to 5. Recombinant human soluble thrombomodulin (rTM) was administered to treat the DIC. After the administration of rTM was completed, OI gradually decreased, after which the mechanical ventilation mode was changed from HFO to synchronized intermittent mandatory ventilation. The DIC score also gradually decreased. Plasma levels of soluble receptor for advanced glycan end products (sRAGE) and high mobility group box 1 (HMGB-1), which are reported to be associated with ARDS severity, also decreased. In addition, inflammatory biomarkers, including interferon-gamma (IFN-γ) and interleukin-6 (IL-6), decreased after the administration of rTM. Although severe ARDS (P/F ratio ≦ 100 mmHg) continued for 19 days, the patient's OI and P/F ratio improved gradually, and she was extubated on the 27th day after admission. The severe ARDS with DIC was successfully treated, and she was discharged from hospital on day 33 post-admission. CONCLUSIONS: We successfully treated a female child suffering from TB pneumonia-induced severe ARDS complicated with DIC using multimodal interventions. (338/350).

Hypothiocyanous Acid Suppresses PolyI:C-Induced Antiviral Responses by Modulating IRF3 Phosphorylation in Human Airway Epithelial Cells.

Pattern recognition receptors recognize RNA viruses and trigger type I and III interferon (IFN) production and apoptosis to limit viral replication and spread. Some innate immune cells produce oxidants in response to viral infection to protect against invasion. Recent studies have demonstrated the virucidal activity of hypothiocyanous acid (HOSCN), an oxidant generated by the peroxidase-catalyzed reaction of thiocyanate with hydrogen peroxide. However, the effects of HOSCN on host antiviral responses are still unknown. In this study, we aimed to clarify the role of HOSCN in host antiviral responses against RNA viruses in airway epithelial cells using polyinosinic-polycytidylic acid (polyI:C), a mimic of viral RNA. Our results show that HOSCN repressed antiviral responses in NCI-H292 human airway epithelial cells. HOSCN decreased polyI:C-induced apoptosis and the expression levels of IFNB1, IFNL1, IFNL2 and IFNL3 mRNAs. In addition, the induction of other interferon regulatory factor 3 (IRF3)-dependent genes was also suppressed by HOSCN. Further analyses focused on IRF3 revealed that HOSCN inhibited the phosphorylation of IRF3 at Ser386 and Ser396 as well as its dimerization and nuclear translocation by inhibiting the phosphorylation of TANK-binding kinase 1 (TBK1). Furthermore, HOSCN led to the phosphorylation of IRF3 at residues other than Ser386 and Ser396, implying that HOSCN may cause a conformational change in IRF3 to impair its function. Collectively, these results suggest that HOSCN plays a novel signaling role in the antiviral response, acting as a negative regulator of apoptotic and TBK1-IRF3 signaling pathways and limiting IRF3-dependent gene expression.

Adenovirus Type 7 Pneumonia in Children Who Died from Measles-Associated Pneumonia, Hanoi, Vietnam, 2014.

During a 2014 measles outbreak in Vietnam, postmortem pathologic examination of hospitalized children who died showed that adenovirus type 7 pneumonia was a contributory cause of death in children with measles-associated immune suppression. Adenovirus type 7 pneumonia should be recognized as a major cause of secondary infection after measles.

Avian influenza.

Highly pathogenic avian influenza A (H5N1) came to the attention of the international sci- entific community for the first time in 1997 at Hong Kong. The current global spread of hu- man infection by this subtype started in 2003. Since then, many clinical case reports on H5N1 have been reported. In 2013, China WHO reported new avian influenza virus H7N9 infected to human. After 2013 season, H7N9 infection occurred seasonally in mainly China and total number of patients reached nearly one thousand in 2016 season. Clinically, acute respiratory distress syndrome (ARDS) associated with avian influenza vi- rus infection is more severe than usual, which mortality rate reaches nearly 60%. A patholog- ical study of post-mortem biopsied lung tissues revealed that H5N1 infected alveolar epithe- lial cells and caused primary viral pneumonia, which subsequently developed into ARDS.

Effect of invariant natural killer T cells with IL-5 and activated IL-6 receptor in ventilator-associated lung injury in mice.

Mechanical ventilation (MV) is well known to potentially cause ventilator-associated lung injury (VALI). It has also been reported recently that activation of invariant natural killer T (iNKT) cells is involved in the onset/progression of airway inflammation. We analyzed the roles of inflammatory cells, including iNKT cells, and cytokines/chemokines in a mouse model of VALI. C57BL/6 and Vα14(+)NKT cell-deficient (Jα18KO) female mice were subjected to MV for 5 hours. The MV induced lung injury in the mice, with severe histological abnormalities, elevation in the percentages of neutrophils in the bronchoalveolar lavage fluid (BALF), and increase in the number of iNKT cells in the lung. Jα18KO mice subjected to MV for 5 hours also showed lung injury, with decrease of the PaO2/FiO2 ratio (P/F ratio) and elevation of the levels of total protein, IL-5, IL-6, IL-12p40, and keratinocyte-derived cytokine (KC) in the BALF. Intranasal administration of anti-IL-5 monoclonal antibody (mAb) or anti-IL-6 receptor (IL-6R) mAb into the Jα18KO mice prior to the start of MV resulted in significant improvement in the blood oxygenation. In addition, the anti-IL-5 mAb administration was associated with a decrease in the levels of IL-5, IL-9, and IL-6R in the BALF, and anti-IL-6R mAb administration suppressed the mRNA expressions of IL-5, IL-6, IL-6R, and KC. These results suggest that iNKT cells may play a role in attenuating the inflammatory caused by ventilation through IL-5 and IL-6R.

Efficacy of intranasal desmopressin for the treatment of nocturnal polyuria in the elderly females.

Older adults often complain of nocturia as one of the most bothersome symptoms of lower urinary tract incontinence. Nocturia places such patients at risk of falling down and insomnia and increases the care burden. The causes of nocturia include various factors, such as neuropathic bladder, prostate hyperplasia and pelvic floor muscle weakness. It has also been reported that nocturia is caused by an increased renal blood flow while lying down and the loss of diurnal variation in vasopressin. The intranasal administration of desmopressin at night may improve nocturia. We experienced a case of severe nocturia that could not be controlled with fluid restriction, urethral catheterization before sleep or anticholinergic drugs. Due to frequent urination during the night, the patient was unable to sleep well and required frequent nursing care. Following the administration of nasal desmopressin before sleep, the number of episodes of nocturia considerably improved. In addition, no adverse events, such as hyponatremia, were observed with desmopressin use. Physicians should therefore consider using desmopressin in cases with treatment-resistant nocturia.

Vibrio fluvialis Bacteremia in an Immunocompetent Patient with Acute Cholangitis.

Vibrio fluvialis is a bacterium that can be found in both seawater and freshwater, and it is responsible for causing gastroenteritis and cholangitis. V. fluvialis bacteremia has rarely been reported. We report a case of V. fluvialis bacteremia due to cholangitis in an immunocompetent adult who was exposed to seawater regularly as a sushi chef. The increased risk of V. fluvialis entry into the body resulting from frequent consumption of raw fish and regular exposure to seawater, bile outflow impairment caused by transient inflammation of the bile duct, and the presence of multiple bile acid resistance-related genes in V. fluvialis may lead to the development of acute cholangitis and subsequent bacteremia in immunocompetent patients.

Pathological study of archival lung tissues from five fatal cases of avian H5N1 influenza in Vietnam.

Highly pathogenic avian H5N1 influenza virus (H5N1) infection in humans causes acute respiratory distress syndrome, leading to multiple organ failure. Five fatal cases of H5N1 infection in Vietnam were analyzed pathologically to reveal virus distribution, and local proinflammatory cytokine and chemokine expression profiles in formalin-fixed, paraffin-embedded lung tissues. Our main histopathological findings showed diffuse alveolar damage in the lungs. The infiltration of myeloperoxidase-positive and/or CD68 (clone KP-1)-positive neutrophils and monocytes/macrophages was remarkable in the alveolar septa and alveolar spaces. Immunohistochemistry revealed that H5N1 mainly infected alveolar epithelial cells and monocytes/macrophages in lungs. H5N1 replication was confirmed by detecting H5N1 mRNA in epithelial cells using in situ hybridization. Quantitation of H5N1 RNA using quantitative reverse transcription PCR assays revealed that the level of H5N1 RNA was increased in cases during early phases of the disease. We quantified the expression of tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, IL-8, regulated on activation normal T-cell expressed and secreted (commonly known as RANTES), and interferon-gamma-inducible protein of 10 kDa (IP-10) in formalin-fixed, paraffin-embedded lung sections. Their expression levels correlated with H5N1 RNA copy numbers detected in the same lung region. Double immunofluorescence staining revealed that TNF-α, IL-6, IL-8 and IP-10 were expressed in epithelial cells and/or monocytes/macrophages. In particular, IL-6 was also expressed in endothelial cells. The dissemination of H5N1 beyond respiratory organs was not confirmed in two cases examined in this study.

[A case of large tracheoesophageal fistula after repair of the right discending aortic arch].

A 77-year-old woman with right aortic arch was diagnosed as aortic dissection (De Bakey IIIb) and hospitalized for conservative treatment. But, her respiratory condition deteriorated due to tracheal stenosis with aortic dissection. Surgical graft replacement of the descending aorta was performed to release tracheal stenosis. Six days after surgery, tracheoesophageal fistula (TEF) was noticed. The size of the fistula was 3 cm in diameter, located 3cm to the oral side from the carina and 23 cm from the incisors. Nineteen days after surgery, an esophageal stent was placed leading to temporary improvement of the respiratory status, but it aggravated again. Unfortunately, she died due to ventricular fibrillation 26 days after surgery. The case is extremely rare with dissection of the right aortic arch. Such a case is considered to be a high risk of TEF, and it is necessary to perform early preventive measures.

Contribution of neutrophil-derived myeloperoxidase in the early phase of fulminant acute respiratory distress syndrome induced by influenza virus infection.

Because the pathogenesis of acute respiratory distress syndrome (ARDS) induced by influenza virus infection remains unknown, we can only improve on existing therapeutic interventions. To approach the subject, we investigated immunological etiology focused on cytokines and an acute lung damage factor in influenza-induced ARDS by using a PR-8 (A/H1N1)-infected mouse model. The infected mouse showed fulminant severe pneumonia with leukocyte infiltration, claudin alteration on tight junctions, and formation of hyaline membranes. In addition to interferon (IFN)-α, plenty of keratinocyte-derived chemokines (KC), macrophage inflammatory protein 2 (MIP-2), regulated on activation normal T-cell expressed and secreted (RANTES), and monocyte chemotactic protein 1 (MCP-1) were significantly released into bronchoalveolar lavage fluid (BALF) of the model. We focused on neutrophil myeloperoxidase (MPO) as a potent tissue damage factor and examined its contribution in influenza pneumonia by using mice genetically lacking in MPO. The absence of MPO reduced inflammatory damage with suppression of leakage of total BALF proteins associated with alteration of claudins in the lung. MPO(-/-) mice also suppressed viral load in the lung. The present study suggests that MPO-mediated OCl(-) generation affects claudin molecules and leads to protein leakage and viral spread as a damage factor in influenza-induced ARDS.

The risk of fatal bleeding complications in jugular catheterization in patients with coagulopathy: A retrospective analysis of death cases in closed claims and the Medical Accident Investigating System in Japan.

BACKGROUND: To prevent recurrence of medical accidents, the Medical Accident Investigating System was implemented in October 2015 by the Japan Medical Safety Research Organization (Medsafe Japan) to target deaths from medical care that were unforeseen by the administrator. Medsafe Japan analyzed the 10 cases of central venous catheterization-related deaths reported in the system and published recommendations in March 2017. However, the particular emphasis for the prevention of central venous catheterization-related deaths is unclear. METHODS: This study aimed to identify the recommendation points that should be emphasized to prevent recurrence of central venous catheterization-related deaths. We assessed central venous catheterization in 8530 closed-claim cases between January 2002 and December 2016 covered by the medical insurer Sompo-Japan. Moreover, we compared central venous catheterization-related death in closed-claim cases with death in reported cases. RESULTS: The background, error type, anatomic insertion site, and fatal complication data were evaluated for 37 closed-claim cases, of which 12 (32.4%) were death cases. Of the 12 closed-claim cases and 10 reported cases, 9 (75.0%) closed-claim cases and 9 (90.0%) reported cases were related to vascular access. Among these, 5 closed-claim cases (41.7%) and 7 reported cases (77.8%) were related to internal jugular vein catheterization (p = 0.28). Coagulopathy was observed in 3 (60.0%) of 5 closed-claim cases and 6 (85.7%) of 7 reported cases. CONCLUSIONS: The risk of internal jugular catheterization in patients with coagulopathy must be carefully considered.

Key role of regulated upon activation normal T-cell expressed and secreted, nonstructural protein1 and myeloperoxidase in cytokine storm induced by influenza virus PR-8 (A/H1N1) infection in A549 bronchial epithelial cells.

Influenza virus infection causes severe respiratory disease such as that due to avian influenza (H5N1). Influenza A viruses proliferate in human epithelial cells, which produce inflammatory cytokines/chemokines as a "cytokine storm" attenuated with the viral nonstructural protein 1 (NS1). Cytokine/chemokine production in A549 epithelial cells infected with influenza A/H1N1 virus (PR-8) or nonstructural protein 1 (NS1) plasmid was examined in vitro. Because tumor necrosis factor-α (TNF-α) and regulated upon activation normal T-cell expressed and secreted (RANTES) are predominantly produced from cells infected with PR-8 virus, the effects of mRNA knockdown of these cytokines were investigated. Small interfering (si)TNF-α down-regulated RANTES expression and secretion of RANTES, interleukin (IL)-8, and monocyte chemotactic protein-1 (MCP-1). In addition, siRANTES suppressed interferon (IFN)-γ expression and secretion of RANTES, IL-8, and MCP-1, suggesting that TNF-α stimulates production of RANTES, IL-8, MCP-1, and IFN-γ, and RANTES also increased IL-8, MCP-1, and IFN-γ. Furthermore, administration of TNF-α promoted increased secretion of RANTES, IL-8, and MCP-1. Administration of RANTES enhanced IL-6, IL-8, and MCP-1 production without PR-8 infection. These results strongly suggest that, as an initial step, TNF-α regulates RANTES production, followed by increase of IL-6, IL-8, and MCP-1 and IFNs concentrations. At a later stage, cells transfected with viral NS1 plasmid showed production of a large amount of IL-8 and MCP-1 in the presence of the H(2)O(2)-myeloperoxidse (MPO) system, suggesting that NS1 of PR-8 may induce a "cytokine storm" from epithelial cells in the presence of an H(2)O(2)-MPO system.

Clinical factors associated with severity in hospitalized children infected with avian influenza (H5N1).

OBJECTIVE: The World Health organization received reports of 478 laboratory-confirmed cases of influenza A (H5N1) from 15 countries between November 2003 and February 2010. More than 50% of these cases involved patients <20 years of age. Determining an association between the clinical factors at the time of hospital admission and prognosis may be useful for timely and adequate consultation and treatment. It has been difficult to obtain these clinical factors adjusted with other confounding factors, such as age and sex, as published studies of H5N1 virus infection usually reported only a few cases. So, we performed a pooled analysis of the reported cases. METHODS: Five case reports (36 patients <18 years of age) of H5N1 infection from four countries published between 2004 and 2009 were assessed based on available individual clinical data. Using the pooled data for all patients, we investigated the associations between patients' prognosis and available laboratory findings, such as white blood cell (WBC) counts, platelet (PLT) counts, and serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) by adjusting for age and/or sex. RESULTS: The linear regression analysis revealed that mortality was negatively associated with WBC and PLT counts adjusted with age and sex. Increased log AST tended to be associated with a poor prognosis (p = 0.054), but there was no significant association between survival and log ALT level. CONCLUSIONS: Both decreased WBC and PLT counts can be considered to be common predictors of poor prognosis in H5N1 influenza patients <18 years of age. Further studies are needed for clarification.

Histone deacetylase modulates the proinflammatory and -fibrotic changes in tubulointerstitial injury.

Histone deacetylase (HDAC) regulates gene expression by modifying chromatin structure. Although changes in the expression and activities of HDAC may affect the course of kidney disease, the role of HDAC in tubulointerstitial injury has not been explored. We therefore investigated the alterations in HDAC expression and determined the effects of HDAC inhibition on the tubulointerstitial injury induced by unilateral ureteral obstruction. The induction of HDAC1 and HDAC2, accompanied by a decrease in histone acetylation was observed in kidneys injured by ureteral obstruction. Immunohistochemical analysis revealed that HDAC1 and HDAC2 were induced in renal tubular cells. Treatment with an HDAC inhibitor, trichostatin A (TSA), attenuated macrophage infiltration and fibrotic changes in tubulointerstitial injury induced by ureteral obstruction. The induction of colony-stimulating factor-1 (CSF-1), a chemokine known to be involved in macrophage infiltration in tubulointerstitial injury, was reduced in injured kidneys from mice treated with TSA. TSA, valproate, and the knockdown of HDAC1 or HDAC2 significantly reduced CSF-1 induced by TNF-alpha in renal tubular cells. These results suggest that tubular HDAC1 and HDAC2, induced in response to injury, may contribute to the induction of CSF-1 and the initiation of macrophage infiltration and profibrotic responses. These findings suggest a potential of HDAC inhibition therapy aimed at reducing inflammation and fibrosis in tubulointerstitial injury.

[Trends of HIV patients operated at International Medical Center of Japan].

BACKGROUND: HIV-infected patients are on the increase in Japan, and anti-HIV therapy improved their prognosis. It is expected that the number of operations in HIV patients will increase. METHODS: We surveyed the prevalence of HIV 30,188 patients operated at International Medical Center of Japan, a major, HIV/AIDS hospital, from 2001 to 2007. RESULTS: The number of HIV-positive cases was 389 in 7 years, and the prevalence of HIV seropositivity was 1.3% in total, 1.0% in scheduled, and 2.0% in emergent cases. The prevalence of male (2.0%) was higher than female (0.7%) patients and the prevalence was highest (9.2%) in male patients in their 30's. They were parallel with the HIV occurrence trend of Japan. The prevalence was the highest (2.4%) in the division of general surgery, as well as in obstetric and gynecology. The number of major surgery in HIV patients has been increasing. CONCLUSIONS: We assume that the perioperative management in each hospital has become more important. The annual trend of the number of the operations performed in HIV-positive patients at our hospital did not show annual changes.

Azithromycin, a 15-membered macrolide antibiotic, inhibits influenza A(H1N1)pdm09 virus infection by interfering with virus internalization process.

The pandemic influenza 2009 (A(H1N1)pdm09) virus currently causes seasonal and annual epidemic outbreaks. The widespread use of anti-influenza drugs such as neuraminidase and matrix protein 2 (M2) channel inhibitors has resulted in the emergence of drug-resistant influenza viruses. In this study, we aimed to determine the anti-influenza A(H1N1)pdm09 virus activity of azithromycin, a re-positioned macrolide antibiotic with potential as a new anti-influenza candidate, and to elucidate its underlying mechanisms of action. We performed in vitro and in vivo studies to address this. Our in vitro approaches indicated that progeny virus replication was remarkably inhibited by treating viruses with azithromycin before infection; however, azithromycin administration after infection did not affect this process. We next investigated the steps inhibited by azithromycin during virus invasion. Azithromycin did not affect attachment of viruses onto the cell surface, but blocked internalization into host cells during the early phase of infection. We further demonstrated that azithromycin targeted newly budded progeny virus from the host cells and inactivated their endocytic activity. This unique inhibitory mechanism has not been observed for other anti-influenza drugs, indicating the potential activity of azithromycin before and after influenza virus infection. Considering these in vitro observations, we administered azithromycin intranasally to mice infected with A(H1N1)pdm09 virus. Single intranasal azithromycin treatment successfully reduced viral load in the lungs and relieved hypothermia, which was induced by infection. Our findings indicate the possibility that azithromycin could be an effective macrolide for the treatment of human influenza.

H5N1-infected cells in lung with diffuse alveolar damage in exudative phase from a fatal case in Vietnam.

Necropsied lung tissues of three fatal cases with avian influenza A virus (H5N1) infection in Vietnam were analyzed to detect H5N1 virus-infected cells. Formalin-fixed and paraffin-embedded lung tissue sections showed typical histological features of diffuse alveolar damage (DAD) in all cases. Immunohistochemistry for the influenza A virus nucleoprotein antigen revealed positive signals of bronchiolar and alveolar epithelial cells in only one patient, who exhibited DAD with an exudative phase and died on the 6th day after onset. However, no signal was detected in the other two cases of DAD with a proliferative phase. These patients died on day 16 and day 17 after onset, respectively. H5N1 virus antigens were detected predominantly in epithelial cells in terminal bronchioles and in alveoli, i.e., type I and type II alveolar pneumocytes, and in alveolar macrophages. The pathogenesis of exudative DAD caused by H5N1 infection is discussed.

[Current status of HIV/AIDS anesthetic experiences in Japan--questionnaire for anesthesia teaching hospitals].

BACKGROUND: As the number of HIV-infected patients in Japan increases every year, the opportunity for a HIV-positive patient to undergo an operation is also increasing. METHODS: Authors sent questionnaire to 952 anesthesia teaching hospitals, in order to investigate the experience and management of the HIV-positive anesthetic cases. RESULTS: The reply was obtained from 480 teaching hospitals. One hundred and nine hospitals (22.7%) experienced HIV-positive operation, 367 hospitals (76.5%) had no experience. With regard to the number of experienced HIV-positive cases, only one case was the most numerous answer and most of the hospitals had fewer than ten cases. General anesthesia was selected in 74% of cases, regional anesthesia (spinal or/and epidural anesthesia) were selected in 26% of cases. Preoperative HIV examination for almost all scheduled cases were carried out in 24% of the hospitals, but 23% of the hospitals did not carry out the examination at all. Eighteen percent of the hospitals had a severe rule for the management of a HIV-positive case, and 58% of the hospitals had a rule almost the same as for HBV-HCV positive cases. CONCLUSIONS: Almost one fourth of anesthesia teaching hospitals experienced HIV-positive cases. Anesthesiologists should know how to manage HIV-positive surgical patients and be prepared for the cases.

Pathogen screening and prognostic factors in children with severe ARDS of pulmonary origin.

BACKGROUND: Acute respiratory distress syndrome (ARDS) is one of the most lethal diseases encountered in the pediatric intensive care unit (PICU). The etiological pathogens and prognostic factors of severe ARDS of pulmonary origin in children with respiratory virus infections were prospectively investigated. METHODS: Enrolled children fulfilled the following criteria: (1) PICU admission; (2) age of 1 month to 16 years; (3) diagnosis of infectious pneumonia and respiratory virus infection; and (4) development of severe ARDS within 72 h after PICU admission. Pathogens were detected in the blood and tracheal lavage fluid using molecular techniques and a conventional culture system. The serum levels of inflammatory mediators on the day of PICU admission were examined. RESULTS: Fifty-seven patients (32 boys; median age, 9 months) were enrolled. Multiple virus infections, co-infection with bacteria/fungus, and bacteremia/fungemia were observed in 60%, 49%, and 32% of children, respectively. Adenovirus-B, measles virus, and cytomegalovirus were detected predominantly in tracheal lavage fluid. There were no statistically significant differences between non-survivors and survivors regarding the types of pathogen, incidence of multiple virus infection, gender, age, clinical features, and treatment. The serum levels of interferon (IFN)-γ and the IFN-γ/interleukin (IL)-10 ratio were higher in non-survivors. CONCLUSIONS: IFN-γ upregulation as detected on the day of PICU admission was found to be one of the possible prognostic factors affecting a fatal outcome. These results suggest that modulation of inflammatory responses is critical for the clinical management of children with ARDS.