Andrés Esteban

Accuracy of clinical definitions of ventilator-associated pneumonia: comparison with autopsy findings.

METHODSnWe studied patients requiring mechanical ventilation for more than 48 hours who died in the intensive care unit and whose bodies were autopsied. We evaluated 3 clinical definitions of ventilator-associated pneumonia: loose definition, defined as chest radiograph infiltrates and 2 of 3 clinical criteria (leukocytosis, fever, purulent respiratory secretions); rigorous definition, defined as chest radiograph infiltrates and all of the clinical criteria; and a clinical pulmonary infection score higher than 6 points. Sensitivity, specificity, and likelihood ratios were calculated by using pathology pattern as criterion standard.nnnRESULTSnOne hundred forty-two (56%) of the 253 patients included had histological criteria of pneumonia. Patients who met the clinical criteria of ventilator-associated pneumonia were 163 (64%) for the loose definition, 32 (13%) for the rigorous definition, and 109 (43%) for the clinical pulmonary infection score. The operative indexes (sensitivity and specificity) of each definition were as follows: loose definition, 64.8% and 36%; rigorous definition, 91% and 15.5%; and clinical pulmonary infection score higher than 6, 45.8% and 60.4%. The addition of microbiological data to the clinical definitions increased the specificity and decreased the sensitivity but not significantly.nnnCONCLUSIONSnAccuracy of 3 commonly used clinical definitions of ventilator-associated pneumonia was poor taking the autopsy findings as reference standard.

The impact of time to tracheostomy on mechanical ventilation duration, length of stay, and mortality in intensive care unit patients

INTRODUCTIONnThis study examined the potential effects of time to tracheostomy on mechanical ventilation duration, intensive care unit (ICU), and hospital length of stay (LOS), and ICU and hospital mortality.nnnMETHODSnCohort observational study was conducted in a tertiary care medical-surgical ICU based on a prospectively collected ICU database. We included 531 consecutive patients who were admitted between March 1999 and February 2005, and underwent tracheostomy during their ICU stay. The effect of time to tracheostomy on the different outcomes assessed was estimated using multivariate regression analyses (linear or logistic, based on the type of variables). Other independent variables that were included in the analyses included selected admission characteristics.nnnRESULTSnMean +/- SD was 12.0 +/- 7.3 days for time to tracheostomy, and 23.1 +/- 18.9 days for ICU LOS. Time to tracheostomy was associated with an increased duration of mechanical ventilation (beta-coefficient = 1.31 for each day; 95% confidence interval [CI], 1.14-1.48), ICU LOS (beta-coefficient = 1.31 for each day; 95% CI, 1.13-1.48), and hospital LOS (beta-coefficient = 1.80 for each day; 95% CI, 0.65-2.94). On the other hand, time to tracheostomy was not associated with increased ICU or hospital mortality.nnnCONCLUSIONSnTime to tracheostomy was independently associated with increased mechanical ventilation duration, ICU LOS, and hospital LOS, but was not associated with increased mortality. Performing tracheostomy earlier in the course of ICU stay may have an effect on ICU resources and could entail significant cost-savings without adversely affecting patient mortality.

Aging increases the susceptibility to injurious mechanical ventilation

ObjectiveTo test the hypothesis that aging increases the susceptibility to organ dysfunction and systemic inflammation induced by injurious mechanical ventilation.Design and settingExperimental study in an animal model of ventilator-induced lung injury in the animal research laboratory in axa0university hospital.MethodsYoung (3–4u202fmonths old) and old (22–24u202fmonths old) anesthetized Wistar rats were ventilated for 60u202fmin with axa0protective lung strategy (VTu202f=u202f9u202fml/kg and PEEPu202f=u202f5u202fcm H2O, control) or with an injurious strategy (VTu202f=u202f35u202fml/kg and PEEPu202f=u202f0u202fcm H2O, overventilated; nu202f=u202f6 for each group).Measurements and resultsMean arterial pressure and airway pressures (PAW) were monitored. Arterial blood gases and serum AST, ALT, lactate, and IL-6 were measured. Vascular rings from the thoracic aorta were mounted in organ baths for isometric tension recording. We studied relaxations induced by acetylcholine (10u202fnM–10u202fμM) in norepinehrine-precontracted rings, and contractions induced by norepinephrine (1u202fnM–10u202fμM) in resting vessels. Lungs were examined by light microscopy. Injurious ventilation in young rats was associated with hypoxemia, lactic metabolic acidosis, increased serum AST, hypotension, impairment in norepinephrine and acetylcholine-induced vascular responses ex vivo and hyaline membrane formation. The high-VT induced hypotension, increase in mean PAW, AST, and IL-6, and the impairment in acetylcholine-induced responses were significantly more marked in aged than in young rats.ConclusionsElderly rats showed increased susceptibility to injurious mechanical ventilation-induced pulmonary injury, vascular dysfunction, and systemic inflammation.

Unplanned extubation in the ICU: a marker of quality assurance of mechanical ventilation

One of the most frequent complications associated with endotracheal intubation itself in intensive care units is unplanned extubation, which represents a potentially serious complication given that many patients may need reintubation while in poor condition. This scenario may account for an increase in morbidity and even in mortality. To be able to compare the rates of unplanned extubation in clinical practice, unplanned extubation should be expressed as incidence density of days at risk. Also, this complication (unplanned extubation and reintubation rates) may be used as a marker of quality of weaning care in intensive care units.

Lung histopathological findings in fatal pandemic influenza A (H1N1)

OBJECTIVEnTo describe the lung pathological changes in influenza A (H1N1) viral pneumonia. We studied morphological changes, nitro-oxidative stress and the presence of viral proteins in lung tissue.nnnMETHODS AND PATIENTSnLight microscopy was used to examine lung tissue from 6 fatal cases of pandemic influenza A (H1N1) viral pneumonia. Fluorescence for oxidized dihydroethydium, nitrotyrosine, inducible NO synthase (NOS2) and human influenza A nucleoprotein (NP) (for analysis under confocal microscopy) was also studied in lung tissue specimens.nnnRESULTSnAge ranged from 15 to 50 years. Three patients were women, and 5 had preexisting medical conditions. Diffuse alveolar damage (DAD) was present in 5 cases (as evidenced by hyaline membrane formation, alveolo-capillary wall thickening and PMN infiltrates), and interstitial fibrosis in one case. In the fluorescence studies there were signs of oxygen radical generation, increased NOS2 protein and protein nitration in lung tissue samples, regardless of the duration of ICU admission. Viral NP was found in lung tissue samples from three patients. Type I pneumocytes and macrophages harbored viral NP, as evidenced by confocal immunofluorescence microscopy.nnnCONCLUSIONSnLung tissue from patients with pandemic influenza A (H1N1) viral pneumonia shows histological findings consistent with DAD. Prolonged nitro-oxidative stress is present despite antiviral treatment. Viral proteins may remain in lung tissue for prolonged periods of time, lodged in macrophages and type I pneumocytes.

Evidencias de la posición en decúbito prono para el tratamiento del síndrome de distrés respiratorio agudo: una puesta al día

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) have high incidence and mortality rates. Most of the recently introduced treatments have failed to improve the prognosis of patients with ALI or ARDS or to reduce mortality. Several studies have shown improved oxygenation in the prone position during mechanical ventilation in patients with ARDS. However, current evidence strongly suggests that placing ARDS patients in prone position does not improve survival or reduce the duration of mechanical ventilation. Therefore, though in clinical practice this position may improve refractory hypoxemia in patients with ARDS, there is no evidence to support its systematic use.

Severe Acute Respiratory Failure Secondary to Acute Fibrinous and Organizing Pneumonia Requiring Mechanical Ventilation: A Case Report and Literature Review

A 27-year-old woman was admitted to our ICU with acute hypoxemic respiratory failure and criteria for ARDS. Despite an FIO2 of 1.0 and a lung protective strategy, the patient died on day 15 without any improvement. The relatives gave consent for post-mortem analysis. The histopathologic study of the lung showed findings typical of an acute fibrinous and organizing pneumonia. Apropos of this case we performed a PubMed search. We found 13 articles, including a total of 29 patients. Acute fibrinous and organizing pneumonia is an unusual cause of acute lung injury. The diagnostic criterion is histopathologic. There is little information regarding the pathophysiology of this illness. Important questions remain regarding this disease, including predisposing factors and management. Patients who require mechanical ventilation have poor outcomes.

Prone Position for the Treatment of Acute Respiratory Distress Syndrome: A Review of Current Literature

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) have high incidence and mortality rates. Most of the recently introduced treatments have failed to improve the prognosis of patients with ALI or ARDS or to reduce mortality. Several studies have shown improved oxygenation in the prone position during mechanical ventilation in patients with ARDS. However, current evidence strongly suggests that placing ARDS patients in prone position does not improve survival or reduce the duration of mechanical ventilation. Therefore, though in clinical practice this position may improve refractory hypoxemia in patients with ARDS, there is no evidence to support its systematic use.

Influence of mechanical ventilation and sepsis on redox balance in diaphragm, myocardium, limb muscles, and lungs

Mechanical ventilation (MV), using high tidal volumes (V(T)), causes lung (ventilator-induced lung injury [VILI]) and distant organ injury. Additionally, sepsis is characterized by increased oxidative stress. We tested whether MV is associated with enhanced oxidative stress in sepsis, the commonest underlying condition in clinical acute lung injury. Protein carbonylation and nitration, antioxidants, and inflammation (immunoblotting) were evaluated in diaphragm, gastrocnemius, soleus, myocardium, and lungs of nonseptic and septic (cecal ligation and puncture 24 hours before MV) rats undergoing MV (n = 7 per group) for 150 minutes using 3 different strategies (low V(T) [V(T) = 9 mL/kg], moderate V(T) [V(T) = 15 mL/kg], and high V(T) [V(T) = 25 mL/kg]) and in nonventilated control animals. Compared with nonventilated control animals, in septic and nonseptic rodents (1) diaphragms, limb muscles, and myocardium of high-V(T) rats exhibited a decrease in protein oxidation and nitration levels, (2) antioxidant levels followed a specific fiber-type distribution in slow- and fast-twitch muscles, (3) tumor necrosis factor α (TNF-α) levels were higher in respiratory and limb muscles, whereas no differences were observed in myocardium, and (4) in lungs, protein oxidation was increased, antioxidants were rather decreased, and TNF-α remained unmodified. In this model of VILI, oxidative stress does not occur in distant organs or skeletal muscles of rodents after several hours of MV with moderate-to-high V(T), whereas protein oxidation levels were increased in the lungs of the animals. Inflammatory events were moderately expressed in skeletal muscles and lungs of the MV rats. Concomitant sepsis did not strongly affect the MV-induced effects on muscles, myocardium, or lungs in the rodents.

Kidney histopathological findings in fatal pandemic 2009 influenza A (H1N1)

Dear Editor, A new pandemic was originated by a novel influenza A (H1N1) virus [1– 3]. Severe cases were characterized by acute respiratory distress syndrome (ARDS), shock, and acute kidney injury (AKI) [3]. Lung histopathological changes in fatal cases showed signs of diffuse alveolar damage, necrotizing bronchiolitis, and occasional alveolar hemorrhage [2]. However, histopathological changes in organs other than the lungs are not known. Here we report kidney histopathological findings and describe for the first time the specific kidney cell type targeted by pandemic 2009 influenza A (H1N1) virus infection. With the approval of our Ethics Committee and with closest relative informed consent, renal biopsies from four patients who died in the intensive care unit (ICU) with diagnosis of confirmed influenza A (H1N1) virus infection were studied by microscopy after hematoxylin and eosin (HE), Masson’s or periodic acid-Schiff (PAS) staining. Cell nuclei were revealed by staining with 4’,6-diamidino-2-phenylindole (DAPI). Localization of viral antigen and specific kidney cells was carried out by double immunofluorescence (IF) labeling [4] using antibodies (Santa Cruz) specific for either: (1) aquaporin 1, a marker of proximal tubular cells; (2) CD10, a marker of proximal tubular cells; (3) cytokeratin 7, a marker of distal tubular cells; or (4) CD34, a marker of endothelial cells, and a rabbit antiserum specific for influenza nucleoprotein (NP). This antibody was generated by immunization of rabbits with purified recombinant NP and validated by IF, Western blotting, and immunoprecipitation of control and influenzainfected human cells [5]. This antibody is cross-reactive with several influenza A virus subtypes (data not shown). Secondary antibodies were fluorescein isothiocyanate (FITC)labeled goat anti-mouse immunoglobulin G (IgG) (Santa Cruz) and Alexa 546-conjugated goat anti-rabbit IgG. Sections were studied under confocal microscopy (Leica SP5), and single optical sections are presented. Only cases 3 and 4 were diagnosed with AKI. Cases 3 and 4 had focal changes consistent with acute tubular necrosis (ATN) in the distal tubules (epithelial cell swelling, individual cell necrosis, and shedding of