Although the use of ethanol solution containing >0.5% chlorhexidine gluconate (chlorhexidine alcohol solution, CH-AL) as a skin disinfectant has been recommended in the United States Centers for Disease Control and Prevention Guidelines for the Prevention of Intravascular Catheter-Related Infections in recent years, many institutions in Japan still use 10% povidone iodine. The superiority of CH-AL compared to povidone iodine has been repeatedly demonstrated, but the level of evidence for these studies has not always been high and the prophylactic effects at different CH-AL concentrations remain to be clarified. In order to evaluate the validity of CH-AL, high-quality comparative research is required regarding the relative efficacies of povidone iodine and CH-AL at various concentrations, including 0.5%, for the prevention of catheter-related bloodstream infections and catheter colonization.

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History of beta-blocking agents can be traced back to the isolation of adrenaline and the clarification of sympathetic nerve activities. The first beta-stimulant, isoproterenol, was synthesized in 1948, while the antagonist, propranolol, was synthesized in 1962. The progresses in molecular pharmacology facilitated the synthesis of more subtype-specific beta-blockers. Currently, short and ultra-short acting agents are commonly used for the management of fluctuating heart function, such as paradoxical tachycardia and ischemic heart failure.

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Background: Endotoxin activity assay (EAA) is an ex vivo diagnostic test for endotoxemia and is based on the biological response of the patient's neutrophils. Reportedly, acute kidney injury (AKI) and continuous renal replacement therapy (CRRT) can induce neutrophil activation. The present study examined whether EAA can detect sepsis in AKI treated by CRRT. Methods: AKI patients who needed CRRT in the intensive care unit were prospectively analyzed. EAA was performed at the initiation of CRRT (0 hr) and 24 hrs and 48 hrs after CRRT. Results: Endotoxin activity (EA) values in the sepsis group were significantly higher than those in the non-sepsis group at 0 hr. No significant increase of EA values was observed after CRRT initiation. Conclusion: EAA can detect sepsis without being influenced by AKI and CRRT.

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Neurogenic pulmonary edema is commonly caused by damages to the central nervous system, such as subarachnoid hemorrhage, head injury, and epilepsy, but is rarely caused by cerebral infarction. We report a case of neurogenic pulmonary edema caused by cerebral infarction in a 54-year-old woman who was hospitalized for glaucoma filtration surgery. The operation was performed under general anesthesia, and she was transferred from the operation theater to her room after extubation. She complained of severe dyspnea just after returning to her room and developed cardiopulmonary arrest within a short time. She was successfully resuscitated, but chest radiograph and chest CT showed marked infiltrative shadows over both lung fields, indicating pulmonary edema. We required an extracorporeal membrane oxygenation system to treat severe hypoxia. We did not suspect cardiogenic pulmonary edema because pulmonary artery wedge pressure monitored by the Swan-Ganz catheter was not high and echocardiography showed normal left ventricular wall motion. Head CT showed early signs of cerebral infarction, and we diagnosed the condition of the patient as neurogenic pulmonary edema. Thus, we should consider the possibility of neurogenic pulmonary edema while treating sudden-onset pulmonary edema.

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A 78-year-old man with alcoholic cirrhosis was admitted to our hospital for progressing systemic purpura and impaired consciousness. His first computed tomographic (CT) scan indicated no remarkable changes. Because his left thigh gradually became discolored and purpura progressed every hour, and lactic acidosis and shock state deteriorated, a second CT scan was performed approximately 4 hours later, which showed the inflammatory changes of subcutaneous tissue at the left thigh but considered not in need of surgical intervention. Although he was admitted to the intensive care unit and treated with antibiotics (meropenem, ciprofloxacin, minocycline, linezolid, and clindamycin), he was still in shock state. The vesicle newly appeared on his left thigh and systemic purpura increasingly progressed. A third CT scan (9 hours after arriving at the hospital) indicated massive gas at the fascia and muscle layer of his left thigh, then debridement and vacuum-assisted closure therapy was performed. The deep soft tissue was necrotic, and a large amount of foul-smelling pus was released after incising the fascia. Despite intensive care, he died 28 hours after admission. Extended-spectrum β-lactamase (ESBL)-producing Escherichia coli was detected from the blood and pus, and genetic testing confirmed a single strain possessing a CTX-M-8-like gene. The diagnosis was necrotizing soft-tissue infection (NSTI) at the left thigh caused by ESBL-producing E. coli. We should note that ESBL-producing bacteria can be a causative organism of fatal community-acquired infections such as NSTI.

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There have been many cases of infection caused by influenza A/H1N1pdm09. We encountered a case of hemophagocytosis with co-infections of influenza and group A streptococcus. A 24-year-old man was referred to us with multiple organ dysfunction syndrome due to influenza infection. When he was transferred to the previous hospital, he had high fever and disturbance of consciousness. On admission to our hospital, he showed respiratry and cardiac failure. His heart function was severely decreased, and we initiated mechanical ventilation, percutaneous cardiopulmonary support, and intra-aortic balloon pumping. Clinical findings of neutropenia, thrombocytopenia, and disseminated intravascular coagulation suggested a complication of hemophagocytosis; therefore, we tried immunosuppressive therapy and plasmapheresis. However, group A streptococcal bacteremia also occuered, and the patient expired in approximately 2 days. Necropsy showed histiocytes phagocytosing red blood cells and severe streptococcal invasion. Influenza is a very common disease. However, fatal complications may occur on rare occasions.

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Dexmedetomidine (DEX) is a highly selective α2 receptor agonist that is widely used as a sedative drug in intensive care units (ICUs). We experienced two cases in which hyperthermia developed under long-term administration of DEX. Propofol and DEX were started as sedative drugs during artificial respiration immediately after entry to the ICU. Body temperature rose to around 39°C during administration of DEX and the high temperature continued for several days. We searched for the cause of the high temperature, with a particular focus on infection, but we were unable to identify the heat source. The general condition of each patient was stable despite the high temperature, and the temperature lowered in several hours when DEX administration was suspended after extubation. In case 2, body temperature rose again after re-administration of DEX, and thus we suspected that drug-induced fever was the probable cause of the high temperature. These cases indicate that a high body temperature may be a problem in long-term administration of DEX. We suggest that caution regarding non-infectious drug-induced fever is required in use of DEX.

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We describe two cases in which abnormal findings from brain CT and MRI were seen in patients with extreme hypoglycemia and hyperglycemia. In case 1, an 82-year-old male suffering from diabetes mellitus experienced right hemiparesis. Brain CT and MRI were taken immediately as cerebral infarction was suspected. Brain CT showed the disappearance of fissures in the left occipital and parietal lobe, indicating cerebral edema. Diffusion weighted imaging (DWI) revealed areas of high intensity signal in the left cerebral cortices and subcortices, which was consistent with his right hemiparesis. Simultaneous blood glucose test revealed extreme hypoglycemia (11 mg/dl) and his right hemiparesis partially recovered after the administration of glucose. The cerebral edema which was initially shown on brain CT also improved 5 days later. In case 2, a 54-year-old male was admitted by an ambulance due to convulsions and diabetic ketoacidosis (blood glucose: 1,087 mg/dl). Brain CT taken before admitted to the ICU showed a high density region in the left putamen. He was treated with the administration of insulin and his convulsion disappeared. Three days later, blood glucose normalized, and he was discharged from the ICU. On T1-weighted MRI which was taken 2 days after the admission, a high intensity region was seen in the left putamen. This finding on brain CT partially disappeared at the 10th hospital day. In these 2 cases, hypoglycemia and hyperglycemia supposedly caused the abnormal findings on brain CT and MRI. The differentiation between the abnormal findings caused by extreme blood glucose value and cerebral infarction or hemorrhage should be carefully considered.

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Background: The acid-base balance may alter in postoperative critically ill patients. This retrospective observational study was conducted to determine the degree and cause of acid-base derangements using Stewart-approach. Methods: Sixty post-esophagectomy patients who required intensive care for at least 7 days were included in this study. We measured all relevant variables for acid-base analysis according to the Stewart-approach from postoperative day (POD) 1 to POD 6. The study was approved by the local institutional ethics committee. Results: After admission to the ICU, patients developed metabolic alkalosis with mild elevated carbon dioxide (P<0.01). This change was mostly secondary to an increase in strong ion difference apparent (SIDa) (delta SIDa: +5.3 mmol/l, P<0.01) due to decrease in chloride levels (Cl) (delta Cl: -3.9 mmol/l, P<0.01). Conclusions: Most of the post-esophagectomy patients developed metabolic alkalosis, which was mainly secondary to an increase in strong ion difference due to decreased chloride. The Stewart-approach is a useful tool for acid-base analysis.

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To investigate the current status of premedical intensive care education in Japan, the National Public University Hospital Conference Intensive Care Division conducted a survey in November 2010. A questionnaire was sent to 53 institutes, and responses were received from 48 of them. ICUs that were attached to an emergency department accounted for one-third of all the ICUs. The median number of beds was 11 in the ICUs that were attached to an emergency department and 10 in those that were not. The median number of full-time ICU physicians was 8 in the ICUs that were attached to an emergency department and 3.5 in those that were not. More than half units have lecture hours less than 5 hours. The reported numbers of lecture hours and practice hours have wide ranges among the institutes. Further investigation including private university hospitals is warranted.

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Objective: We simulated the effect of using absorptive material to reduce the noise level in one of the noisiest part of a hospital, the pediatric ICU (PICU). Methods: Using GEONOISE^® (Nittobo Acoustic Engineering Co., Ltd.), software to estimate the noise level, we compared measured and simulated values of noise in the PICU of Osaka Medical Center and Research Institute for Maternal and Child Health. We also made simulation to evaluate if noise could be reduced by architectural modifications. Results: Estimates from simulation indicated that the noise level could be reduced by approximately 5.9 A-weighted decibels (dBA) if the ceiling and walls in the PICU would be replaced with absorptive material. Conclusions: Replacing the ceiling and wall materials with noise absorbing ones may be an effective method of noise reduction.

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[in Japanese]

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[in Japanese]

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[in Japanese]

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