Simru Tugrul

Effects of sustained inflation and postinflation positive end- expiratory pressure in acute respiratory distress syndrome: Focusing on pulmonary and extrapulmonary forms*

ObjectiveTo investigate whether the response to sustained inflation and postinflation positive end-expiratory pressure varies between acute respiratory distress syndrome with pulmonary (ARDSp) and extrapulmonary origin (ARDSexp). DesignProspective clinical study. SettingMultidisciplinary intensive care unit in a university hospital. PatientsA total of 11 patients with ARDSp and 13 patients with ARDSexp. InterventionsA 7 ml/kg tidal volume, 12–15 breaths/min respiratory rate, and an inspiratory/expiratory ratio of 1:2 was used during baseline ventilation. Positive end-expiratory pressure levels were set according to the decision of the primary physician. Sustained inflation was performed by 45 cm H2O continuous positive airway pressure for 30 secs. Postinflation positive end-expiratory pressure was titrated decrementally, starting from a level of 20 cm H2O to keep the peripheral oxygen saturation between 92% and 95%. Fio2 was decreased, and baseline tidal volume, respiratory rate, inspiratory/expiratory ratio were maintained unchanged throughout the study period. Measurements and Main ResultsBlood gas, airway pressure, and hemodynamic measurements were performed at the following time points: at baseline and at 15 mins, 1 hr, 4 hrs, and 6 hrs after sustained inflation. After sustained inflation, the Pao2/Fio2 ratio improved in all of the patients both in ARDSp and ARDSexp. However, the Pao2/Fio2 ratio increased to >200 in four ARDSp patients (36%) and in seven ARDSexp patients (54%). In two of those ARDSp patients, the Pao2/Fio2 ratio was found to be <200, whereas none of the ARDSexp patients revealed Pao2/Fio2 ratios of <200 at the 6-hr measurement. Postinflation positive end-expiratory pressure levels were set at 16.7 ± 2.3 cm H2O in ARDSexp and 15.6 ± 2.5 cm H2O in ARDSp. The change in Pao2/Fio2 ratios was found statistically significant in patients with ARDSexp (p = .0001) and with ARDSp (p = .008). Respiratory system compliance increased in ARDSexp patients (p = .02), whereas the change in ARDSp was not statistically significant. ConclusionsSustained inflation followed by high levels of postinflation positive end-expiratory pressure provided an increase in respiratory system compliance in ARDSexp; however, arterial oxygenation improved in both ARDS forms.

Risk Factors for Mortality of Nosocomial Bacteraemia in Intensive Care Units

Objective: The aim of this study was to follow critically ill patients prospectively in intensive care units (ICUs) to determine risk factors for mortality and outcome associated with nosocomial bacteraemia (NB). Subjects and Methods: A case-control study of 176 patients was conducted to identify the risk factors for mortality of NB in ICU patients. The study was performed in emergency, surgical and general surgical ICUs with 23 beds during a 15-month period. A total of 1,450 patients were admitted to the ICUs during the study period. The USA Center for Disease Control and Prevention definitions were used to diagnose nosocomial infections. Nosocomial bacteraemia was defined as the isolation of one or more organisms from blood cultures taken at least 48 h after admission, which were not related to a problem present on admission. An assessment of whether the isolated organisms represented true bacteraemia rather than contamination was made by clinical or laboratory evidence of infection. Results: A total of 214 bacteraemia episodes were found in the 176 patients (64 female, 112 male; 51.3 ± 21.3 years old), 90 of whom died and 86 survived. The bacteraemia rate was 12.1%. The most common etiological agents of bacteraemia were Klebsiella pneumoniae: 46 (21.5%), methicillin-resistant Staphylococcus aureus: 46 (21.5%), Pseudomonas aeruginosa: 32 (14.9%), and Escherichia coli: 20 (9.3%). Multivariate analysis showed that the requirement of mechanical ventilation for more than 7 days (p < 0.001), total parenteral nutrition (p = 0.034), inotropic drug (p < 0.001), and increased creatinine level (p = 0.034) were independent risk factors for mortality of NB in ICUs. Conclusions: Nosocomial infections caused by Gram-negative bacteria continue to be one of the major sources of morbidity and mortality.

The effects of airway pressure and inspiratory time on bacterial translocation.

BACKGROUND: Mechanical ventilation with high peak inspiratory pressure (PIP) induces lung injury and bacterial translocation from the lung into the systemic circulation. We investigated the effects of increased inspiratory time on translocation of intratracheally inoculated bacteria during mechanical ventilation with and without extrinsic positive end-expiratory pressure (PEEP). METHODS: Rats were ventilated in pressure-controlled mode with 14 cm H2O PIP, 0 cm H2O PEEP, I:E ratio 1/2, and Fio2 1.0. Subsequently, 0.5 mL of 105 cfu/mL Pseudomonas aeruginosa was inoculated through tracheostomy and rats were randomly assigned to six groups; two low-pressure groups (LP)1/2, 14 cm H2O PIP, 0 cm H2O PEEP, I:E = 1/2, and LP2/1 14 cm H2O PIP, 0 cm H2O PEEP, I:E = 2/1; two high-pressure groups (HP)1/2, 30 cm H2O PIP, 0 cm H2O PEEP, I:E = 1/2, and HP2/1, 30 cm H2O PIP, 0 cm H2O PEEP, I:E = 2/1; two HP PEEP groups (HPP)1/2, 30 cm H2O PIP, 10 cm H2O PEEP, I:E = 1/2, and HPP2/1, 30 cm H2O PIP, 10 cm H2O PEEP, I:E = 2/1. Blood cultures were obtained every 30 min. The rats were killed and their lungs were processed. RESULTS: When compared with baseline values, Pao2 decreased in the LP1/2, LP2/1, HP1/2, and HP2/1 groups at the last time point, but the decline in Pao2 reached statistical significance in only the HP1/2 group. The bacterial translocation rate was greater in group HPP2/1 than group HPP1/2 (P = 0.01). CONCLUSIONS: We found that high PIP, with or without prolonged inspiratory time, increased the rate of bacterial dissemination. PEEP prevented bacterial translocation in the high PIP group. However, the protective effect of PEEP was lost when inspiratory time was prolonged.

Case report of severe metabolic alkalosis: life-compatible new level.

Metabolic alkalosis is the most common acid-base disturbance observed in hospitalized patients, accounting for 50% of all acid-base disorders.1 Severe metabolic alkalosis (blood pH 7.55) is a serious medical problem. Mortality rates have been reported as 45% in patients with an arterial blood pH of 7.55 and 80% when the pH was greater than 7.65.1 And, it has been noted in textbooks and practically accepted by the clinicians that the pH value greater than 7.80 is more than the range of clinically viable pH values.2–5 The most common causes of metabolic alkalosis are the use of diuretics and the external loss of gastrointestinal system secretions. The physical signs of metabolic alkalosis are not specific and depend on severity of the decrement in pH. Because metabolic alkalosis decreases ionized calcium concentration, signs of hypocalcemia (e.g., tetany, Chvostek sign, and Trousseau sign), change in mental status, or seizures may be present. Physical examination is helpful to establish the cause of metabolic alkalosis. Important aspects of the physical examination include the evaluation of volume status. Because hypokalemia is usually present, the patient may experience weakness, myalgia, and polyuria. Hypoventilation develops because of inhibition of the respiratory center in the medulla. We presented probably the first report illustrating a surviving case who had severe metabolic alkalosis with a pH of 7.87 induced by gastrointestinal system losses.

The effects of IgM-enriched immunoglobulin preparations in patients with severe sepsis: another point of view – authors' response

Thank you for the opportunity to respond to the letter by Karatzas et al. [1] commenting on our recent paper concerning the effects of IgM-enriched immunoglobulin preparations in severe sepsis [2]. It was mentioned in the letter that the study protocol of Karatzas et al. regarding the design and inclusion criteria (except the age) was similar to our study design. It seems that there is another important difference between two studies, which is the subgroup analysis. Because of the limited number of patients included in our study, it was not intended to focus on the role of immunotherapy in reducing the mortality rate of severe sepsis patients. Mortality rate analyses in the subgroups of patients with different admission Acute Physiology and Chronic Health Evaluation II (APACHE II) scores were therefore not performed in our study. As Karatzas et al. noted, the APACHE II scores of our patients were lower than those found in their preliminary data analysis. This is an important difference indicating that the patient populations of their study and our study are far beyond similarity. Neurological evaluation in APACHE II scoring is based on the Glasgow coma scale (GCS) and is usually complicated by the frequent use of sedative agents in critically ill patients. It is often not clear whether to assume GCS in the absence of sedative drugs or to consider the actual GCS of the patient. Certainly this computation might be very confusing and prone to errors in data collection. In our clinical practice, we generally assume the mental state of the patients in the absence of sedative drugs while calculating the GCS. This might be the reason for relatively low levels of APACHE II scores in our study population. We agree with Karatzas et al. that the interpretation of data could be more relevant by homogenising the patients according to some clinical characteristics, especially in larger studies investigating the beneficial effects of immunotherapy in septic patients. Our study, which is the initial step of a new series of clinical investigations on this subject, was performed in a small group of patients with severe sepsis. We mentioned in our paper that recruiting this number of patients could confirm a change in severity and mortality of sepsis with the administration of IgM-enriched immunoglobulin preparations. As we pointed out in our paper, we think that in addition to investigating subgroups of septic patients, further studies should focus on laboratory and clinical measures to identify patients who might benefit from specific immunomodulatory therapies.

Recruitment Maneuver Does not Increase the Risk of Ventilator Induced Lung Injury

BACKGROUND Mechanical ventilation (MV) may induce lung injury. AIMS To assess and evaluate the role of different mechanical ventilation strategies on ventilator-induced lung injury (VILI) in comparison to a strategy which includes recruitment manoeuvre (RM). STUDY DESIGN Randomized animal experiment. METHODS Thirty male Sprague-Dawley rats were anaesthetised, tracheostomised and divided into 5 groups randomly according to driving pressures; these were mechanically ventilated with following peak alveolar opening (Pao) and positive end-expiratory pressures (PEEP) for 1 hour: Group 15-0: 15 cmH2O Pao and 0 cmH2O PEEP; Group 30-10: 30 cmH2O Pao and 10 cmH2O PEEP; Group 30-5: 30 cmH2O Pao and 5 cmH2O PEEP; Group 30-5&RM: 30 cmH2O Pao and 5 cmH2O PEEP with additional 45 cmH2O CPAP for 30 seconds in every 15 minutes; Group 45-0: 45 cmH2O Pao and 0 cmH2O PEEP Before rats were sacrificed, blood samples were obtained for the evaluation of cytokine and chemokine levels; then, the lungs were subsequently processed for morphologic evaluation. RESULTS Oxygenation results were similar in all groups; however, the groups were lined as follows according to the increasing severity of morphometric evaluation parameters: Group 15-0: (0±0.009) < Group 30-10: (0±0.14) < Group 30-5&RM: (1±0.12) < Group 30-5: (1±0.16) < Group 45-0: (2±0.16). Besides, inflammatory responses were the lowest in 30-5&RM group compared to all other groups. TNF-α, IL-1β, IL-6, MCP-1 levels were significantly different between group 30-5&RM and group 15-0 vs. group 45-0 in each group. CONCLUSION RM with low PEEP reduces the risk of ventilator-induced lung injury with a lower release of systemic inflammatory mediators in response to mechanical ventilation.