PURPOSE: For patients with acute respiratory failure due to lung edema or atelectasis, Surplus lung water that is not removed during an initial stay in the Intensive Care Unit (ICU) may be related to early ICU readmission. Therefore, we performed a retrospective study of patient management during the first ICU stay for such patients. MATERIALS AND METHODS: Of 1,835 patients who were admitted to the ICU in the 36 months from January, 2003 to December, 2005, 141 were patients readmitted, and the reason for readmission was lung edema or atelectasis in 21 patients. For these 21 patients, correlations were investigated between body weight gain at the time of initial ICU discharge (weight upon discharge from the ICU ÷ weight when entering the ICU) and the time to ICU readmission, between body weight gain and the P/F ratio at ICU readmission, between the R/E ratio (the period using a respirator (R) ÷ the length of the ICU stay after extubation (E)) and the time to ICU readmission, between the R/E ratio and body weight gain, and between body weight gain until extubation and the time to extubation. RESULTS: A negative linear relationship was found between body weight gain at the time of initial ICU discharge and the time to ICU readmission, and between body weight gain at the time of ICU discharge and the P/F ratio at ICU readmission. If body weight had increased by more than 10% at ICU discharge or the P/F ratio was below 150, readmission to the ICU within three days was likely. Patients with a large R/E ratio, a large body weight gain, and a worsening P/F ratio immediately after ICU discharge were likely to be readmitted soon to the ICU. Loss of body weight during the period of respirator support led to early extubation, since a positive correlation was found between the time to extubation and body weight gain. CONCLUSION: Fluid management failure during the first ICU stay might cause ICU readmission for patients who had lung edema or atelectasis. Therefore, a key to the prevention of ICU readmission is to ensure complete recovery from lung failure before the initial ICU discharge. Strict water management is crucial based on body weight measurement and removal of excess lung water is essential. In addition, an apparent improvement in respiratory state may be due to respiratory support, and such an improvement should be viewed cautiously. Loss of weight at the refilling stage of transfusion prevents ICU readmission and may decrease the length of the ICU stay.
Humans ; Intensive Care Units/*statistics & numerical data ; Patient Readmission/*statistics & numerical data ; Pulmonary Atelectasis/physiopathology/*therapy ; Pulmonary Edema/physiopathology/*therapy ; Retrospective Studies ; Time Factors ; Weight Gain

Atelectasis can impair arterial oxygenation and decrease lung compliance. However, the effects of atelectasis on endotoxemic lungs during ventilation have not been well studied. We hypothesized that ventilation at low volumes below functional residual capacity (FRC) would accentuate lung injury in lipopolysaccharide (LPS)-pretreated rats. LPS-pretreated rats were ventilated with room air at 85 breaths/min for 2 hr at a tidal volume of 10 mL/kg with or without thoracotomy. Positive end-expiratory pressure (PEEP) was applied to restore FRC in the thoracotomy group. While LPS or thoracotomy alone did not cause significant injury, the combination of endotoxemia and thoracotomy caused significant hypoxemia and hypercapnia. The injury was observed along with a marked accumulation of inflammatory cells in the interstitium of the lungs, predominantly comprising neutrophils and mononuclear cells. Immunohistochemistry showed increased inducible nitric oxide synthase (iNOS) expression in mononuclear cells accumulated in the interstitium in the injury group. Pretreatment with PEEP or an iNOS inhibitor (1400 W) attenuated hypoxemia, hypercapnia, and the accumulation of inflammatory cells in the lung. In conclusion, the data suggest that atelectasis induced by thoracotomy causes lung injury during mechanical ventilation in endotoxemic rats through iNOS expression.
Animals ; Blood Pressure ; Carbon Dioxide/blood ; Cardiac Output ; Combined Modality Therapy ; Endotoxemia/*complications/immunology/pathology ; Functional Residual Capacity ; Immunohistochemistry ; Leukocytes, Mononuclear/pathology ; Lipopolysaccharides/pharmacology ; Lung/enzymology/pathology/physiopathology ; Lung Compliance ; Lung Volume Measurements ; Male ; Neutrophils/pathology ; Nitric Oxide Synthase Type II/metabolism ; Oxygen/blood ; Positive-Pressure Respiration/*adverse effects ; Pulmonary Atelectasis/*etiology/pathology/*therapy ; Rats ; Rats, Sprague-Dawley ; Thoracotomy/*adverse effects