Nurses play a crucial role in providing high-quality care in intensive care units (ICU). Previous studies have shown an association between nurse staffing levels and outcome of critically ill patients. Increasing nurse staffing levels in ICU has been recommended to improve the outcome of critically ill patients. However, nursing staff shortages associated with decreased budgets may prevent adequate nurse-to-patient ratios although there lies increasing needs for critical care. Several studies have suggested that higher nurse staffing level is associated with favorable patient outcome, including mortality, length of stay, and infections, but some of studies did not find an association between nurse staffing and patient outcome. Although there are some controversies in the associations between nurse staffing levels and patient outcome, it is difficult to apply such effect as compared with other developed countries in North American and Europe as the nurse-to-patient ratio in Korea's ICU is relatively low. By studying the nurse staffing effects for patient outcome from the Korea ICU, it is found that higher nurse staffing level is associated with improved patient mortality. This finding may suggest that a shortage of nursing staff is currently a serious issue for caring of critically ill patients in Korea.
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BACKGROUND Hypothermia is known to suppress inflammation in various experimental and clinical settings. We wanted to investigate how the suppressed inflammation by hypothermia is affected during rewarming. METHODS Mice were being assigned to normothermia (37degrees C) or hypothermia (32degrees C). After 30 minutes at the assigned temperature, lipopolysaccharide was administered intratracheally. The mice were then randomly grouped and subjected to 4 hours of normothermia (N), 24 hours of normothermia (NN), 4 hours of hypothermia (H), or 4 hours of hypothermia followed by normothermia for the next 20 hours (HN). In another experiment, other HN mice were treated with varying doses of anti-TNF-alpha or anti-IL-1beta antibodies (0, 6.25, 12.5, 25, and 50 microg/250 microl) immediately prior to rewarming. RESULTS The neutrophil counts of BAL fluid (x104/ml) were 23.0 +/- 13.1 in the N, 6.4 +/- 3.1 in the H (p = 0.002 vs N), 20.4 +/- 10.2 in the NN, and 49.7 +/- 21.0 in the HN (p = 0.005 vs H; p < 0.001 vs NN). Myeloperoxidase activity of the lung (unit/microg) was 6.7 +/- 2.9, 7.9 +/- 1.9, 17.8 +/- 4.0 (p < 0.001 vs N), and 12.9 +/- 5.9 (p = 0.034 vs H, p = 0.028 vs NN), respectively. Compared with control HN, total WBC and neutrophil counts of mice treated with anti-TNF-alpha antibody or anti-IL-1beta antibody prior to rewarming were lower at all tested doses. The combination of both anti-TNF-alpha or anti-IL-1beta antibodies was not increasingly reducing the neutrophilic sequestration. CONCLUSIONS Rewarming from induced hypothermia resulted in augmentation of neutrophilic sequestration of endotoxin-injured lung. Treatment with antibodies against TNF-alpha or IL-1beta prevented this rebound of neutrophilic infiltration.
BACKGROUND Selenium is an essential trace-element with antioxidant and immunological function. We studied the relationship between blood selenium concentrations, systemic inflammatory response syndrome (SIRS) and organ dysfunctions in critically ill children. METHODS This was a retrospective, observational study of the blood selenium concentrations of critically ill children at the time of a pediatric intensive care unit admission. RESULTS A total of 62 patients with a median age of 18 (5-180) months were included in this study. The mean of blood selenium concentration (microg/dl) was 8.49 +/- 2.42.
The platelet count (r = -0.378) and PaCO2 (r = -0.403) showed negative correlations with blood selenium concentration, while PaO2/FiO2 (r = 0.359) and PaO2 (r = 0.355) showed positive correlations (p < 0.05, for all variables). Blood selenium concentrations were significantly lower in patients with SIRS than in those patients without SIRS (8.08 +/- 2.42 vs. 9.45 +/- 2.02, p = 0.011). Patients with severe sepsis and septic shock had showed significantly lower blood selenium concentrations than those without SIRS (7.03 +/- 2.73 vs. 9.45 +/- 2.02, p = 0.042). Patients with PaO2/FiO2 < or = 300 had lower blood selenium concentrations than those with PaO2/FiO2 > 300 (7.90 +/- 2.43 vs. 9.54 +/- 2.17, p = 0.018). Blood selenium concentrations were significantly lower in patient with PaO2/FiO2 < or = 200 than in those with PaO2/FiO2 > 300 (7.64 +/- 2.76 vs. 9.54 +/- 2.17, p = 0.018). CONCLUSIONS Patients with systemic inflammatory response syndrome or respiratory dysfunction showed significantly low blood selenium concentrations.
BACKGROUND Thrombocytopenia has been shown to be a useful predictor of mortality in adult intensive care units (ICUs).
The aim of this study is to assess whether the level of platelet count at ICU admission and the changes in platelet counts can predict mortality in the pediatric ICU (PICU). METHODS Platelet counts were checked daily for at least 4 days in a total of 303 children who were admitted to the ICU. We compared the initial platelet counts and changes in platelet counts between survivors and non-survivors. A multivariable logistic regression model, a receiver operating characteristic curve and a linear mixed model were used. RESULTS The initial platelet count was significantly lower in non-survivors when compared to survivors. Multivariate analysis demonstrated that platelet count <120 x 10(9)/L (Odds ratio, 4.913; 95% confidence interval 2.451-9.851; p < 0.0001) was an independent predictor of mortality. In the case of children with thrombocytopenia (<120 x 10(9)/L) at admission to the ICU, the platelet counts increased serially in survivors, whereas non-survivors maintained their decreased platelet counts. In the case of children without thrombocytopenia, the platelet counts decreased most on day 3 in non-survivors. CONCLUSIONS At admission to the ICU, thrombocytopenia defined as a platelet count <120 x 10(9)/L can be a useful predictor of mortality in children. In children who had initial thrombocytopenia, the serial increase of platelet counts can be related to increased survival, whereas in children who did not have initial thrombocytopenia, more than a 10% decrease of platelet counts on day 3 can be related to mortality.
BACKGROUND Patients with decompensated liver cirrhosis usually resulted in admission to the intensive care unit (ICU) during hospitalization. When admitted to the ICU, the mortality was high. The aim of this study is to identify multiple prognostic factors for mortality and to analyze the significance of prognostic survival model with each scoring system in patients with decompensated liver cirrhosis who was admitted to the ICU. METHODS From January 2008 to December 2008, 60 consecutive patients with decompensated liver cirrhosis were admitted in the ICU and retrospectively reviewed. Prognostic models used were Child-Turcotte-Pugh (CTP), model for end-stage liver disease (MELD), model for end-stage liver disease with incorporation of serum sodium (MELD-Na), acute physiology and chronic health evaluation (APACHE) II, and sequential organ failure assessment (SOFA). The predictive prognosis was analyzed using the area under the receiver's operating characteristics curve (AUC). RESULTS The median follow up period was 20 months, and ICU mortality was 17% (n = 10). A total of 24 patients (40%) died during the study period. The average survival of five prognostic models was related with the severity of the disease. All of the five systems showed significant differences in the cumulative survival rate, according to the scores on admission, and the MELD-Na had the highest AUC (0.924). Multivariate analysis showed that bilirubin and albumin were significantly related to mortality. CONCLUSIONS The CPT, MELD, MELD-Na, APACHE II, and SOFA may predict the prognosis of patients with decompensated liver cirrhosis. The MELD-Na could be a better prognostic predictor than other scoring systems.
Su Jin Lim, Donghoon Lew, Haa Na Song, You Eun Kim, Seung Jun Lee, Yu Ji Cho, Yi Yeong Jeong, Mi Jung Park, Kyoung Nyeo Jeon, Ho Cheol Kim, Jong Deog Lee, Young Sil Hwang
BACKGROUND Acute respiratory failure can occur paradoxically on initiation of anti-tuberculosis (TB) treatment in patients with pulmonary TB. This study is aimed to analyze the clinical features of anti-TB treatment induced acute respiratory failure. METHODS We reviewed the clinical and radiological characteristics of 8 patients with pulmonary tuberculosis (5 men and 3 women; mean age, 55 +/- 15.5 years) who developed acute respiratory failure following initiation of anti-TB medication and thus required mechanical ventilation (MV) in the intensive care unit (ICU). RESULTS The interval between initiation of anti-TB medication and development of MV-requiring acute respiratory failure was 2-14 days (mean, 4.4 +/- 4.39 days), and the duration of MV was 1-18 days (mean, 7.1 +/- 7.03 days). At admission, body temperature and serum levels of lactate dehydrogenase and C-reactive protein were increased. Serum levels of protein, albumin and creatinine were 5.8 +/- 0.98, 2.3 +/- 0.5 and 1.8 +/- 2.58 mg/ml, respectively.
Radiographs characterized both lung involvements in all patients. Consolidation with the associated nodule was noted in 7 patients, ground glass opacity in 2, and cavitary lesion in 4. Micronodular lesion in the lungs, suggesting miliary tuberculosis lesion, was noted in 1 patient. At ICU admissions, the ranges of the APACHE II and SOFA scores were 17-38 (mean, 28.2 +/- 7.26) and 6-14 (mean, 10.1 +/- 2.74).
The mean lung injury score was 2.8 +/- 0.5. Overall, 6 patients died owing to septic shock and multiorgan failure. CONCLUSIONS On initiation of treatment for pulmonary TB, acute respiratory failure can paradoxically occur in patients with extensive lung parenchymal involvement and high mortality.
The number of organs transplanted worldwide is increasing annually. As a result, there is a shortage of available donor organs. This scarcity has led to the progressive broadening of donor organ criteria. The expanded criteria include infections such as bacterial meningitis. A 55-year old male visited our emergency room with cardiac arrest and recovered after cardiopulmonary resuscitation. The cause of the cardiac arrest was bacterial meningitis caused by Streptococcus pneumoniae. While proper antibiotics were applied, the patient met the clinical criteria for brain death. Prophylactic antibiotics were administered to the recipients, and liver and kidney transplantations were done successfully.
A 9-month-old infant presented with cough, tachypnea, and grunting was admitted. The patient was revealed to have cardiomegaly, high NT-proBNP, and severe left ventricular dilation and dysfunction; she was subsequently diagnosed with acute myocarditis and congestive heart failure.
Intravenous immunoglobulin, inotropics, diuretics, angiotensin converting enzyme inhibitors and beta blocker were used. However, left hemiparesis suddenly developed at 30-day after treatment. Brain MRI showed high signal intensity in the right middle cerebral arterial territory on diffusion weighted brain MRI and in the left parietal lobe with gyral enhancement. Echocardiogram revealed no definite intraventricular thrombus. The patient was started on an antiplatelet agent only without anticoagulant therapy for the treatment of cerebral infarct in respect of the risk to the infant. Four years after the cerebral ischemic stroke (CIS), she showed complete recovery from hemiparesis, with no more CIS. In conclusion, severe ventricular dilatation and dysfunction can lead to thromboembolic events in infants. We should keep in mind that anticoagulant or antiplatelet agents can be used in specific situations.
Thromboembolism in patients receiving extracorporeal membrane oxygenation (ECMO) support is a feared complication. Systemic anticoagulation during ECMO in patients with a massively dilated left ventricle (LV) and decreased LV systolic function is still debated. Hearin, we report a case of a 5-month old infant on ECMO support who had fatal thrombus formation in the massively dilated LV and a consequent thromboembolic event.
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Flexible bronchoscopy is a safe medical procedure, but the incidence rate of major complications is 0.08-0.3%. Here, we report 2 cases of stress induced cardiomyopathy, which developed immediately after flexible bronchoscopy. Stress related cardiomyopathy was confirmed by EKG, echocardiography, and coronary angiogram. The cardiac functions of these patients were fully recovered with conservative treatment. Although, the pathogenesis of stress related cardiomyopathy is not well understood, post-bronchoscopy tachycardia or arrhythmia is thought to be associated with hypoxemia or catecholamine excess. Because the clinical presentation is quite similar to acute myocardial infarction, discrete evaluations are required for appropriate treatment.
Whole lung lavage (WLL) is a challenging procedure; because lavage fluid may perturb the respiratory and hemodynamic systems. We observed severe airway obstruction and flattening arterial pressure wave during WLL for treatment of pulmonary alveolar proteinosis. The aim of this case report is to discuss the anesthetic requirement in order to prevent bronchospasm during WLL. Furthermore, we discuss the potential of lavage fluid to cause airway obstruction and decrease cardiac outflow through the mass effect.
A 16-year-old male patient presented with left side chest pain. The initial chest radiograph showed tension pneumohtorax on the left side. Air was evacuated by closed thoracostomy. About 72 hours later, during administration of general anesthesia for thoracoscopic bullectomy, unilateral pulmonary edema affecting the contralateral lung developed without definite infiltration in the left lung. The operation was suspended and the patient was admitted to the intensive care unit. A close observation of the patient and conservative therapy were enough to manage this pulmonary edema. This is a very rare manifestation of reexpansion pulmonary edema that is unpredictable and could be fatal.
The clinical course is described in this article.
Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion-related mortalities. Each type of blood product is likely to cause TRALI. Patients with TRALI present with dyspnea/respiratory distress and fever. The symptoms, signs and chest radiological findings in TRALI are similar to transfusion associated circulatory overload.
Therefore, it is difficult to distinguish such from circulatory overloads. We report a case of TRALI in a 49-year-old woman after stored packed red blood cell transfusion. The patient developed hypoxemia and pulmonary edema after packed red blood cell transfusion during postoperative period. The patient completely recovered after an oxygen support for 3 days.
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A Case Report of Transfusion-Related Acute Lung Injury Induced in the Patient with HLA Antibody after Fresh Frozen Plasma Transfusion Ki Sul Chang, Dae Won Jun, Youngil Kim, Hyunwoo Oh, Min Koo Kang, Junghoon Lee, Intae Moon The Korean Journal of Blood Transfusion.2015; 26(3): 309. CrossRef
Endotracheal tube cuff volume and pressure require constant monitoring to prevent tracheal injury. Acquired tracheoesophageal fistula is common from complications of mechanical ventilation as a result of pressured necrosis of the tracheoesophageal wall by endotracheal tube cuff. It still represents a life-threatening condition, especially when the diagnosis is being delayed. We present our modest experience through an acquired TEF patient who had an excessively enlarged cuff diameter on chest radiogram in order to consider the potential of using radiological-measured cuff diameter as a simple technique for predicting tracheal damages. Although the cuff pressure was monitored with a manometer by the medical team, it was possible that the tube cuff was excessively enlarged. Proper procedures for preventing the tracheal damage by cuffs include the following: monitoring of endotracheal cuff pressure and volume, observation of cuff size on the chest radiogram, and being mindful and attentive for possibilities of misjudgements by manometer or medical teams.
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The Morphometric Study of Main Bronchus in Korean Cadaver Ik Sung Kim, Chang Ho Song Korean Journal of Physical Anthropology.2017; 30(1): 7. CrossRef
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Paraganglioma is a tumor originating from the extra-adrenal chromaffin cells, and functional paraganglioma causes paroxysmal hypertension, headache and tachycardia, due to excess excretion of catecholamine. However, rarely, ARDS, acute myocardial infarction, heart failure, arrhythmia, and pulmonary edema are also seen in patients with paraganglioma and clinical manifestations are depending on the patient's intravascular volume status. Seventy one-years-old male was presented with hypotension and pulmonary edema after intravenous midazolam injection during colonoscopy under conscious sedation. The patient was initially suspected with anaphylactic shock, due to midazolam injection. However, later, he was diagnosed with paraganglioma, and blood pressure was successfully controlled with alpha adrenergic blockade. We suggest that when we encounter heart failure, pulmonary edema and shock of unknown origin, pheochromocytoma must be taken into consideration.