Park, In-Il;Kim, Ick-Keun;Koo, Hyun-Cheol;Han, Jae-Pil;Kim, Young-Mook;Lee, Myung-Goo;Jung, Ki-Suck
Tuberculosis and Respiratory Diseases
/
v.61
no.1
/
pp.13-19
/
2006
Background: Acinetobacter baumannii has emerged as an important nosocomial pathogen worldwide. The incidence of these infections has recently begun to increase. The mortality rate associated with these infections is high (bacteremia; 52%, pneumonia: 23%~73%) and multidrug resistance has been reported. For the effective control of multidrug-resistant Acinetobacter baumannii(MDR-AB), the impact of these organisms in clinical practice should be determined. This study compared the clinical characteristics, mortality and morbidity of Acinetobacter nosocomial pneumonia between MDR strain and non-MDR strain. Methods: From Jan. 1, 2002 to Nov. 1. 2004, 47 adult patients with Acinetobacter nosocomial pneumonia in Chuncheon Sacred Heart Hospital were recruited and analyzed retrospectively. MDR-AB was defined as showing in vitro resistance to all commercially available antibiotics against A. baumannii. Results: There were 47 patients with Acinetobacter nosocomial pneumonia. MDR-AB and non MDR-AB was the cause of the pneumonia in 17 and 30 patients, respectively. Mean age of the former was $69{\pm}11$ years old and the latter was $70{\pm}13$ years old. The mean APCHE II score, ICU days and mortality were not different between the two groups ($16.1{\pm}5.4$ vs. $14.9{\pm}4.8$, P=0.43, $25.1{\pm}13.6$ vs. $39.1{\pm}31.0$, P=0.2, 58.8% vs. 40%, P=0.21). Conclusion: There are no significant differences in mortality and morbidity between MDR and non-MDR Acinetobacter baumannii. The mortality of the two groups is surprisingly high, therefore proper infection control practices are essential.
Koh, Won-Jung;Kwon, O Jung;Yu, Chang-Min;Jeon, Kyeongman;Kim, Kyung Chan;Lee, Byoung-Hoon;Hwang, Jung Hye;Kang, Eun Hae;Suh, Gee Young;Chung, Man Pyo;Kim, Hojoong
Tuberculosis and Respiratory Diseases
/
v.56
no.3
/
pp.248-260
/
2004
Background : As an effective regimen for isoniazid (INH)-resistant pulmonary tuberculosis, several treatment regimens have been recommended by many experts. In Korea, a standard regimen has not been established for INH-resistant tuberculosis, and the treatment by individual physicians has been performed on an empirical bases. The purpose of the present study was to retrospectively describe the treatment characteristics and evaluate the treatment outcomes of patients with INH-resistant tuberculosis. Materials and Methods : Sixty of 69 patients reported to have INH-resistant tuberculosis from 1994 to 2001 were retrospectively analyzed. Exclusion criteria included: death from other causes, with the exceptions of tuberculosis and incomplete treatment, including a patient's transfer-out. Results : A previous tuberculosis history was found in 28 (46.7%) patients. The sputum smear for acid-fast bacilli was positive in 44 (73.3%) patients, and 30 (50.0%) had cavitary disease. Streptomycin resistance coexisted in 25.0% of isolates. INH was to be prescribed continuously, even after INH resistance was reported, in 86.0% of patients. The treatment regimens were diverse between the patients according to drug regimen composition and treatment duration. The most frequent prescribed regimen included rifampin, ethambutol and pyrazinamide, with and without INH, for the full 12-month term of treatment. Treatment failure occurred in 13 (21.7%) patients. Cavitary disease (p=0.005) and a treatment regimen with second-line drugs, excluding rifampin (p=0.015), were associated with treatment failure. One patient experienced a relapse. Conclusions : Standardized treatment guidelines will be needed in Korea to improve the treatment efficacy for INH-resistant tuberculosis.
Background : The therapeutic effects of surfactant on acute lung injury derive not only from its recruiting action on collapsed alveoli but also from its anti-inflammatory effects. Pro-apoptotic action on alveolar neutrophils represents one of the important anti-inflammatory mechanisms of surfactant. In the present study, we evaluated the effects of sufactant on the apoptosis of human peripheral and rat alveolar neutrophils. Methods : In the (Ed- the article is not definitely needed but it helps to separate the two prepositions 'in') in vitro study, human neutrophils were collected from healthy volunteers. An equal number of neutrophils ($1{\times}10^6$) (Ed-confirm) was treated with LPS (10, 100, 1000ng/ml), surfactant (10, 100, $1000{\mu}g/ml$), or a combination of LPS (1000ng/ml) and surfactant (10, 100, $1000{\mu}g/ml$). After incubation for 24 hours, the apoptosis of neutrophils was evaluated by Annexin V method. In the in vivo study, induction of acute lung injury in SD rats by intra-tracheal instillation of LPS (5mg/kg) was followed by intra-tracheal administration of either surfactant (30mg/kg) or normal saline (5ml/kg). Tenty-four hours after LPS instillation, alveolar neutrophils were collected and the apoptotic rate was evaluated by Annexin V method. In addition, changes of the respiratory mechanics of rats (respiratory rate, tidal volume, and airway resistance) were evaluated with one chamber body plethysmography before, and 23 hours after, LPS instillation. Results : in the in vitro study, LPS treatment decreased the apoptosis of human peripheral blood neutrophils (control: $47.4{\pm}5.0%$, LPS 10ng/ml; $30.6{\pm}10.8%$, LPS 100ng/ml; $27.5{\pm}9.5%$, LPS 1000ng/ml; $24.4{\pm}7.7%$). The combination of low to moderate doses of surfactant with LPS promoted apoptosis (LPS 1000ng/ml + Surf $10{\mu}g/ml$; $36.6{\pm}11.3%$, LPS 1000ng/ml +Surf $100{\mu}g/ml$; $41.3{\pm}11.2%$). The high dose of surfactant ($1000{\mu}g/ml$) decreased apoptosis ($24.4{\pm}7.7%$) and augmented the anti-apoptotic effect of LPS (LPS 1000ng/ml + Surf $1000P{\mu}g/ml$; $19.8{\pm}5.4%$). In the in vivo study, the apoptotic rate of alveolar neutrophils of surfactant-treated rats was higher than that of normal saline-treated rats ($6.03{\pm}3.36%$ vs. $2.95{\pm}0.58%$). The airway resistance (represented by Penh) of surfactant-treated rats was lower than that of normal saline-treated rats at 23 hours after LPS injury ($2.64{\pm}0.69$ vs. $4.51{\pm}2.24$, p<0.05). Conclusion : Surfactant promotes the apoptosis of human peripheral blood and rat alveolar neutrophils. Pro-apoptotic action on neutrophils represents one of the important anti-inflammatory mechanisms of surfactant.
Background: Extubation is recommended to be performed at minimum pressure support (PSmin) during the pressure support ventilation (PSV). In field, physicians sometimes perform additional 1 hr T-piece trial to the patient at PSmin to reduce re-intubation risk. Although it provides confirmation of patient's breathing reserve, weaning could be delayed due to increased airway resistance by endotracheal tube. Methods: To investigate the effect of additional 1 hr T-piece trial on weaning outcome, a prospective study was done in consecutive 44 patients who had received mechanical ventilation more than 3 days. Respiratory mechanics, hemodymic, and gas exchange measurements were done and the level of PSmin was calculated using the equation (PSmin=peak inspiratory flow rate $\times$ total ventilatory system resistance) at the 15cm $H_2O$ of pressure support. At PSmin, the patients were randomized into intervention (additional 1 hr T-piece trial) and control (extubation at PSmin). The measurements were repeated at PSmm, during weaning process (in cases of intervention), and after extubation. The weaning success was defined as spontaneous breathing more than 48hr after extubation. In intervention group, failure to continue weaning process was also considered as weaning failure. Results: Thirty-six patients with 42 times weaning trial were satisfied to the protocol. Mean PSmin level was 7.6 (${\pm}1.9$)cm $H_2O$. There were no differences in total ventilation times (TVT), APACHE III score, nutritional indices, and respiratory mechanics at PSmin between 2 groups. The weaning success rate and re-intubation rate were not different between intervention group (55% and 18% in each) and control group (70% and 20% in each) at first weaning trial. Work of breathing, pressure time product, and tidal volume were aggravated during 1 hr T-piece trial compared to those of PSmin in intervention group ($10.4{\pm}1.25$ and $1.66{\pm}1.08$ J/L in work of breathing) ($191{\pm}232$ and $287{\pm}217$cm $H_2O$ s/m in pressure time product) ($0.33{\pm}0.09$ and $0.29{\pm}0.09$ L in tidal volume) (P<0.05 in each). As in whole, TVT, and tidal volume at PSmin were significantly different between the patients with weaning success ($246{\pm}195$ hr, $0.43{\pm}0.11$ L) and the those with weaning failure ($407{\pm}248$ hr, $0.35{\pm}0.10$L) (P<0.05 in each). Conclusion : There were no advantage to weaning outcome by addition of 1 hr T-piece trial compared to prompt extubation to the patient at PS min.
Background: Minimal pressure support(PSmin) is a level of pressure support which offset the imposed work of breathing(WOBimp) developed by endotracheal tube and ventilator circuits in pressure support ventilation While the lower applied level of pressure support compared to PSmin could induce respiratory muscle fatigue, the higher level than PSmin could keep respiratory muscle rest resulting in prolongation of weaning period during weaning from mechanical ventilation PSmin has been usually applied in the level of 5~10 cm$H_2O$, but the accurate level of PSmin is difficult to be determinated in individual cases. PSmin is known to be calculated by using the equation of "PSmin = peak inspiratory flow rate during spontaneus ventilation$\times$total ventilatory system resistance", but correlation of calculated PSmin and measured PSmin has not been known. The objects of this study were firstly to assess whether customarily applied pressure support level of 5~10 cm$H_2O$ would be appropriate to offset the imposed work of breathing among the patients under weaning process, and secondly to estimate the correlation between the measured PSmin and calculated PSmin. Method : 1) Measurement of PSmin : Intratracheal pressure changes were measured through Hi-Lo jet tracheal tube (8mm in diameter, Mallinckroft, USA) by using pulmonary monitor(CP-100 pulmonary monitor, Bicore, USA), and then pressure support level of mechanical ventilator were increased until WOBimp was reached to 0.01 J/L or less. Measured PSmin was defined as the lowest pressure to make WOBimp 0.01 J/L or less. 2) Calculation of PSmin : Peak airway pressure(Ppeak), plateau airway pressure(Pplat) and mean inspiratory flow rate of the subjects were measured on volume control mode of mechanical ventilation after sedation. Spontaneous peak inspiratory flow rates were measured on CPAP mode(O cm$H_2O$). Thereafter PSmin was calculated by using the equation "PSmin = peak inspiratory flow rate$\times$R, R = (Ppeak-Pplat)/mean inspiratory flow rate during volume control mode on mechanical ventilation". Results: Sixteen patients who were considered as the candidate for weaning from mechanical ventilation were included in the study. Mean age was 64(${\pm}14$) years, and the mean of total ventilation times was 9(${\pm}4$) days. All patients except one were males. The measured PSmin of the subjects ranged 4.0~12.5cm$H_2O$ in 14 patients. The mean level of PSmin was 7.6(${\pm}2.5\;cmH_2O$) in measured PSmin, 8.6 (${\pm}3.25\;cmH_2O$) in calculated PSmin Correlation between the measured PSmin and the calculated PSmin is significantly high(n=9, r=0.88, p=0.002). The calculated PSmin show a tendancy to be higher than the corresponding measured PSmin in 8 out of 9 subjects(p=0.09). The ratio of measured PSmin/calculated PSmin was 0.81(${\pm}0.05$). Conclusion: Minimal pressure support levels were different in individual cases in the range from 4 to 12.5 cm$H_2O$. Because the equation-driven calculated PSmin showed a good correlation with measured PSmin, the application of equation-driven PSmin would be then appropriate compared with conventional application of 5~10 cm$H_2O$ in patients under difficult weaning process with pressure support ventilation.
Jeong, Jeong Ihm;Jung, Bock Hyun;Kim, Mi Hye;Lim, Jae Min;Ha, Dong Cheon;Cho, Sung-Won;Rhui, Dae Sik
Tuberculosis and Respiratory Diseases
/
v.67
no.4
/
pp.325-330
/
2009
Background: Pulmonary tuberculosis (TB) is still common disease among the elderly patients in Korea where the overall incidence of TB is decreasing. Adverse drug reactions (ADR) associated with anti-TB drugs occurs frequently. Especially the aged tends to have more frequent ADRs than younger ones. These ADRs can cause significant morbidity, compromise therapeutic effects of drugs and even induce drug resistance. Therefore we evaluated the effect of ADRs on the first-line anti-TB drugs in elderly patients with active pulmonary TB. Methods: We retrospectively reviewed the charts and radiological findings of the patients with 65 and older who were bacteriologically confirmed as active TB and treated with standard anti-TB drugs for at least 6 months. Major ADR was defined with temporary or continuous stop of any first-line drugs intake. Results: An ADR was noted in 54% of all patients. The incidence of major ADR was 32% in all elderly patients. Dermatologic ADR (9%) was the most common among the major ADRs. GI trouble (8%), arthralgia (6%), visual change (6%), hepatotoxicity (4%), and fever (1%) were also noted. The drugs responsible for major ADR were ethambutol (62%), pyrazinamide (35%), rifampin (18%) and isoniazid (9%). Major ADRs were associated with higher ESR level at the initiation of anti-TB drugs. Conclusion: First-line anti-TB drugs in elderly patients frequently caused the major ADRs. Therefore the elderly patients receiving anti-TB drugs should be closely monitored and better tolerable therapy should be considered as part of a TB research agenda.
Studies of cardiopulmonary function and acid-base balance were performed on 29 dogs during control period, during oligemic hypotension and following return of blood to the animals. Intravenous morphine and local anesthesia were used. Fifteen of the 29 animals survived the complete experiment. The 14 animals that failed to survive the experimental period died between 15 to 90 minutes after the onset of bleeding. The results were as follows. 1. The heart rate increased after the onset of bleeding and failed to return to control level following reinfusion. Stroke volume decreased markedly after bleeding and failed to recover after return of blood from the reservoir. Cardiac output also decreased during oligemic hypotension and was maintained at this level after re-infusion. Total peripheral resistance decreased significantly immediately after bleeding, however it increased soon over the pre-bleeding level. Central venous pressure decreased after the onset of bleeding and remained at lower level for the rest of the experimental period. Arterial blood pressure, clown to 40-45 mmHg by acute hemorrhage, was elevated near to control level. Left ventricular work decreased tremendously during oligemic hypotension and failed to return to control level with the re-infusion of blood. Hematocrit value showed no significant decrease after bleeding and increased after re-infusion. Hemoglobin decreased after the onset of bleeding and recovered to control value after re-infusion. 2. The respiratory rate fell rapidly after bleeding from 124 to 29 and remained at this lower level for the remainder of the experiment. The tidal volume increased after bleeding and was maintained at this level for the remainder of the experiment. The respiratory minute volume showed no significant changes throughout the experimental period. Oxygen consumption fell lightly in all animals during oligemic hypotension and returned to normal levels following re-infusion. Arterial oxygen content and arterial oxygen saturation decreased following bleeding and the values returned to normal levels after the return of blood from the reservoir The arterio-venous oxygen difference increased after the onset of bleeding. It failed to return to normal values following re-infusion. Arterial $Pco_2$ decreased in all animals after the beginning of the bleeding. Partial pressure of $Co_2$ continued to fall until re-infusion, after which the values returned toward normal. Animals became acidotic. The pH fell to lower level following bleeding. Lactic acid and lactate: pyruvate ratio also increased during same period. Arterial pH and lactic acid failed to return to control value and lactate: pyruvate ratio increased more after re-infusion. Sodium bicarbonate decreased after bleeding and returned to control value following re-infusion.
We r viewed a policy of primary surgical closure of large ventricular septal defects in small infants. Sixty-three infants met criteria for inclusion in the study, and were divided into two groups based on age: group 1 infants aged less than 5 months(n = 31), and group 2 infants aged 5 months or more(n = 32). Both groups had similar variation in ventricular septal defect location(paramembranous versus muscular), and showed no significant difference in left to right shunt and in ratio of systemic and pulmonary vascualr resistance. Three early deaths(9.7%) occurred in group 1, but no death(0%) in group 2. The causes of death were preoperative cardiac arrest and cerebral injury followed by postoperative respiratory insufficiency in two patients, and preoperative tracheomalacia followed by laryngeal edema and respiratory arrest in one Two patients in group 1 showed postoperative low cardiac output syndrome(6.5% in group 1 versus 0% in group 2). There was no late death during the follow-up per od in both groups. No surviving patients had postoperative patch leakage, or required a second operation. These results indicate that primary surgical closure of large ventricular septal defects, if logical perioperative care is accompanied, can be saefly performed in small infants aged less than 5 months with low postoperative mortality or morbidity rates.
The maximum breathing capacity (MBC) and the maximum mid-expiratory flow rate (MMF) are widely used in evaluation of the ventilatory function, among various parameters of pulmonary function. The MBC volume is the amount of gas which can be exchanged per unit time during maximal voluntary hyperventilation. Performance of this test, unlike that of single breath maneuvers, is affected by the integrity of the respiratory bellows as a whole including such factors are respiratory muscle blood supply, fatigue, and progressive trapping of air. Because of this, the MBC and its relation to ventilatory requirement correlates more closely with subjective dyspnea than does any other test. The MMF is the average flow rate during expiration of the middle 50% of the vital capacity. The MMF is a measurement of a fast vital capacity related to the time required for the maneuver and the MMF relates much better to other dynamic tests of ventilatory function and to dyspnea than total vital capacity, because the MMF reflects the effective volume, or gas per unit of time. Therefore, it is important to have a prediction formula with one can compute the normal value for the subject and the compare with the measured value. However, the formulas for prediction of both MBC and MMF of the Korean children and adolescents are not yet available in the present. Hence, present investigation was attempt to derive the formulas for prediction of both MBC and MMF of the Korean children and adolescents. MBC and MMF were measured in 1,037 healthy Korean children and adolescents (1,035 male and 1,002 female) whose ages ranged from 8 to 18 years. A spirometer (9L, Collins) was used for the measurement of MBC and MMF. Both MBC and MMF were measured 3times in a standing position and the highest values were used. For measurement, the $CO_2$ absorber and sadd valve were removed from the spirometer in order to reduce the resistance in the breathing circuit and the subject was asked to breathe as fast and deeply as possible for 12 seconds in MBC and to exhale completely as fast as possible after maximum inspiration for MMF. During the measurement, investigator stood by the subject to give a constant encouragement. All the measured values were subsequently converted to values at BTPS. The formulas for MBC and MMF were derived by a manner similar to those for Baldwin et al (1949) and Im (1965) as function of age and BSA or age and height. The prediction formulas for MBC (L/min, BTPS) and MMF (L/min, BTPS) of the Korean children and adolescents as derived in this investigation are as follows: For male, MBC=[41.70+{$2.69{\times}Age(years)$}]${\times}BSA$$(m^{2})$ MBC=[0.083+{$0.045{\times}Age(years)$}]${\times}Ht$ (cm) For female, MBC=[45.53+{$1.55{\times}Age(years)$}]${\times}BSA$$(m^2)$ MBC=[0.189+{$0.029{\times}Age(years)$}]${\times}Ht$ (cm) For male, MMF= [0.544+{$0.066{\times}Age(years)$}]${\times}Ht$ (cm) For female, MMF=[0.416+{$0.064{\times}Age(years)$}]${\times}Ht$ (cm)
Background : Outbreaks of multidrug-resistant tuberculosis(MDR-TB) are caused by the low rate of treatment response due to limitation in number of available drugs and high rates of adverse drug side-effects. This study analysed the risk factors for MDR-TB patients, who did not respond to treatment, with an aim to improve the rate of treatment response. Methods : Retrospective study of 111 MDR-TB patients at National Mokpo Tuberculosis Hospital from Jan. 1996 to Dec. 1998 was made. The patients were separated into two groups ; group I comprised of patients who were treated successfully and group II comprised of those were not treated successfully. In order to analyze the risk factors for treatment failure, differences between the two groups were compared and the confidence limit regarding the results were tested using an independent t-test. chi-square test and a Fisher's exact test. Results : The treatment failure rate of MDR-TB patients was 32% (36 patients), and treatment success rate 68%(75 patients). This study found no significant difference between two groups in terms of age, sex, family history, extent of the disease on the chest X-ray, the number of sensitive drugs in the treatment regimen, and the number of sensitive bactericidal drugs in the treatment regimen (p>0.05). However, a past history of pulmonary tuberculosis, cavitary lesions on the chest X-ray, the number of treatments, the number of resistant drugs and the number of drugs used showed a significant difference(p<0.05). Conclusion : The rate of treatment failure in MDR-TB was increased by a past history of pulmonary tuberculosis, cavitary lesions on the chest X-ray, the number of treatments, the number of resistant drugs and the number of drugs used. For improving the treatment response of MDR-TB, every effort should be made to reduce the drug resistance caused by failure of the first treatment.
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