Acute and Critical Care

Ho Cheol Kim

5 Articles

Development of Acute Respiratory Failure on Initiation of Anti-Tuberculosis Medication in Patients with Pulmonary Tuberculosis: Clinical and Radiologic Features of 8 Patients and Literature Review: 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; Korean J Crit Care Med. 2013;28(2):108-114.; DOI: https://doi.org/10.4266/kjccm.2013.28.2.108

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Abstract PDF: 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 Clinical Significance of Weight Change in Mechanical Ventilated, Critically Ill Patients of ICU: Young Sun Seo, You Eun Kim, Seung Jun Lee, Yu Ji Cho, Yi Yeong Jeong, Ho Cheol Kim, Jong Deok Lee, Young Sil Hwang; Korean J Crit Care Med. 2011;26(3):139-144.; DOI: https://doi.org/10.4266/kjccm.2011.26.3.139

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Abstract PDF: BACKGROUND
Critically ill patients may show significant weight change in their course of disease during ICU stay. However, what weight changes occur and their effects on patient outcome have not yet been reported to our knowledge. Therefore, we evaluated weight change in critically ill patients in the medical ICU and the effect this may have on clinical outcome.
METHODS
We measured body weight in patients admitted to the medical ICU daily and evaluated their clinical characteristics and outcome.
RESULTS
Thirty-eight patients (M:F = 30:8, mean age = 65.7 +/- 12.5) were enrolled. Thirteen patients (34.2%) showed weight gain and the mean change was 12.8 +/- 4.2%. In contrast, 25 patients (65.8%) showed weight loss and the mean change was 6.3 +/- 6.9%. Patients who showed weight change over 5% or 10% were 26 (68.4%), and 12 (31.6%), respectively, and their mortality rates were 61.5% and 75%, respectively, showing no statistical significance (p > 0.05). However, when the degree of weight change was stratified with < 5%, 5-10% and > 10%, it was associated with death (p = 0.002). Factors like ICU stay, day of mechanical ventilation, initial APACHE II and SOFA score, body mass index (BMI) and serum albumin were not associated with more than 5% change of weight. BMI at admission was only associated with > 10% change of weight (p < 0.05).
CONCLUSIONS
The majority of critically ill patients showed a significant weight change during their ICU stay and these patients may have a tendency to have worse clinical outcome.

Mechanisms of Muscle Wasting in Patients with Sepsis: Gi Dong Lee, Ho Cheol Kim; Korean J Crit Care Med. 2010;25(1):9-15.; DOI: https://doi.org/10.4266/kjccm.2010.25.1.9

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Abstract PDF

Muscle wasting is commonly seen in patients with sepsis as a consequence of the catabolic response in skeletal muscle. Muscle wasting can occur in cases that have an imbalance between degradation and synthesis of muscle proteins. Although decrements in the synthesis of muscle proteins may contribute to sepsis-induced muscle wasting, it has been recognized that increments in its degradation play a more essential role in muscle wasting. Muscle wasting in sepsis patients has some significant clinical consequences such as reduced ambulation and exercise tolerance, and an increased risk for pulmonary and thromboembolic complications. Several mechanisms have been proposed for sepsis-induced muscle wasting. Increased proteolysis via the ubiquitin-proteasome pathway and the calpains system is one of the principal mechanisms of muscle wasting induced by sepsis. Calpains are activated by calcium, which increases in patients with sepsis. The activation of the calpains system disrupts the sarcomere of the myofibrils, resulting in the release of myofilaments that are subsequently ubiquitinated and degraded by the 26S proteasome complex. Recent studies have suggested that transcriptional factors such as NF-kappaB and FoxO, and the apoptosis and autophagy-lysosome pathways may also be involved in sepsis-induced muscle wasting. This review briefly summarizes the contribution of these mechanisms of muscle wasting in patients with sepsis and the possible therapeutic agents to treat it.

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Role of IL-15 in Sepsis-Induced Skeletal Muscle Atrophy and Proteolysis
Ho Cheol Kim, Hee-Young Cho, Young-Sool Hah
Tuberculosis and Respiratory Diseases.2012; 73(6): 312. CrossRef

Change of Antibiotics Resistance Pattern of Microorganism Cultured in Tracheal Aspirate in Mechanical Ventilated Patients after Antibiotics Restriction Policy: Jeong Eun Ma, Soo Kyong Kim, Min Kyung Kang, Yi Yeong Jeong, Ho Cheol Kim, Jong Deok Lee, Young Sil Hwang; Korean J Crit Care Med. 2008;23(1):25-29.; DOI: https://doi.org/10.4266/kjccm.2008.23.1.25

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Abstract PDF

BACKGROUND
To reduce production of resistant bacteria by over-use of antibiotics, an antibiotics restriction policy became effective in several hospitals. However, there are different views on its effect. This study aims to examine antibiotic resistance of pathogenic organisms cultured in tracheal aspirates of the patients who need to maintain mechanical ventilation in medical intensive care unit before and after the antibiotics restriction policy.
METHODS
Before and after 2 years from August 2003, when carried out the antibiotics restriction policy in Gyeongsang university hospital, it was retrospectively investigated the antibiotic resistance pattern of bacteria cultured in tracheal aspirates of the patient who is maintained by mechanical ventilation more than 48 hours in the medical intensive care unit. Restricted antibiotics are ceftazidime, piperacillin/tazobactam, imipenem, meropenem, vancomycin, and teicoplanin.
RESULTS
Before the antibiotics restriction policy, (Sep 2001~Aug 2003) and after, (Sep 2003~Aug 2005), there were 306 and 565 patients applied in each case and the total use of antibiotics, except piperacillin/tazobactam, was reduced and that of cefotaxime and ceftriaxone was increased. There was no significant change in antibiotic resistance among Acinetobacter, Pseudomonas, and Enterobacter species.
CONCLUSION
The result of this study shows that the antibiotics restriction policy does not reduce production of antibiotic resistant bacteria in tracheal aspirate in a medical intensive care unit. However, it is considered that long-term observation may be necessary.

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Clinical Characteristics in Patients with Carbapenem-ResistantAcinetobacter baumanniiIsolates from Tracheal Secretions
Jeong Ha Mok, Mi Hyun Kim, Kwangha Lee, Ki Uk Kim, Hye-Kyung Park, Min Ki Lee
Korean Journal of Critical Care Medicine.2013; 28(3): 173. CrossRef
Overview of Antibiotic Use in Korea
Baek-Nam Kim
Infection & Chemotherapy.2012; 44(4): 250. CrossRef

Relationship between Change of RBC Shape and Multi-organ Failure in Sepsis: Ho Cheol Kim, Yoo Ji Cho, Hwi Jong Kim, Jong Deok Lee, Young Sil Hwang, Me Ae Kim; Korean J Crit Care Med. 2005;20(1):63-67.

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Abstract PDF: BACKGROUND
Microcirculatory derangement in sepsis plays a crucial role in the impairment of tissue oxygenation that can lead to multi-organ failure and death. The change of RBC rheology in sepsis has been known to be important factors in microcirculatory derangement. Several studies have demonstrated that RBCs have decreased deformability in sepsis. We investigated the relationship between multi-organ failure and spherical index of RBC estimated by flow cytometer in critically ill patients with or without sepsis compared with the relationship in healthy volunteers.
METHODS
Fourteen non-septic critically ill patients, 18 septic patients and 10 healthy volunteers were evaluated. We obtained peripheral venous blood from each patient and analyzed the change of RBC shape using flow cytometer (Becton Dickinson FACSCalibur) within 90 minute. The change of RBC shape was accessed with spherical index (M2/M1). A decrease in M2/M1 was correlated with the sphericity of the RBC and considered to have a lower capacity to alter their shape when placed in microcirculation. Multi-organ failure was accessed with sequential organ failure assessment (SOFA) score. RESULTS: The M2/M1 ratio of healthy volunteers, non-septic patients and septic patients were 2.25+/-0.08, 2.16+/-0.39 and 2.05+/-0.53, respectively. But, there was no significant difference between each group (p>0.05). And, there was no significant correlation between M2/M1 ratio of septic and non- septic patients and SOFA score (p>0.05, r2= -0.13). CONCLUSIONS: In our study, the spherical index of RBC was not associated with multi-organ failure in sepsis. But, further studies may be needed to evaluate the role of RBC rheology in sepsis.

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