Dominique Prat

Cardiac troponin level is not an independent predictor of mortality in septic patients requiring medical intensive care unit admission

Turley and Gedney claim that the cardiac troponin Ic level is a predictor of adverse outcome [1] and that their results support those of King and colleagues [2]. Unfortunately, King and colleagues were unable to demonstrate a link between the troponin Ic level and mortality when using a multivariate model including the Acute Physiology Age and Chronic Health Evaluation II score. Interpretation of the results of Turley and Gedney therefore requires caution since their results are based only on univariate analysis [1]. We prospectively evaluated the accuracy of cardiac troponin Ic levels to predict inhospital mortality in 118 adults with documented sepsis and no history of cardiac arrest or acute coronary syndrome, and we then compared this accuracy with the performance of the new Simplified Acute Physiology II score. Seventy-five patients (63.6%) were in shock (systolic blood pressure <90 mmHg), while 58 patients (49%) had a cardiac troponin Ic level greater than 0.3 ng/ml (detection limit, 0.15 ng/ml) and 43 patients (36.4%) a level greater than 1 ng/ml. Nonsurvivors were more severely ill (Simplified Acute Physiology II score [mean ± standard deviation], 74.7 ± 25.2 versus 51.5 ± 18.4; P < 0.001), tended to have higher cardiac troponin Ic levels (5.5 ± 10.3 ng/ml versus 3.6 ± 8.9 ng/ml) and tended to be older. Patients with a cardiac troponin Ic level above 0.3 ng/ml had a twofold risk of dying (odds ratio, 2.56; 95% confidence interval, 1.89–5.542), but the predictive abilities for mortality of cardiac troponin Ic were poor according to the area under the curve of the receiver– operating characteristic curve (0.612; 95% confidence interval, 0.504–0.719) – in contrast to the Simplified Acute Physiology II score (0.775; 95% confidence interval, 0.686–0.864). A logistic regression model identified only the Simplified Acute Physiology II score as an independent predictor of death (β = 0.048; odds ratio, 1.049; 95% confidence interval, 1.028–1.075; per point increment, P < 0.001). We confirm that nearly one-half of patients with severe sepsis have an elevated cardiac troponin Ic level within the first 72 hours of the intensive care unit stay [3-7]. Whereas there is convincing evidence that the cardiac troponin Ic level reflects and correlates with myocardial damage in septic patients whatever the mechanism [3-6] and that every elevated troponin level should not be diagnosed or treated as acute coronary syndrome [7], the impact of an elevated troponin level on the outcome remains a matter of debate, even in studies performing multivariate analysis [2,3,5-7]. Although two series found that mortality was dependent on the troponin level [3,5], like other studies [2,6,7] we failed to reach a similar conclusion. In our opinion, the troponin level can be useful to assess the risk of myocardial dysfunction in patients with sepsis but is not an independent marker of mortality.

Pneumopathie à mycoplasme : une cause rare de syndrome de détresse respiratoire aiguë (SDRA) et de résistance potentielle aux antibiotiques

INTRODUCTION Acute respiratory distress syndrome caused by Mycoplasma pneumoniae infection has rarely been described. OBSERVATION We report a case of community-acquired pneumonia occurring in a patient with Downs syndrome. Persisting hypoxemia raised the questions of nosocomial pneumonia, of the occurrence of a fibrosing alveolitis or of the resistance of the strain to macrolides. After a long period of very severe respiratory impairment, the evolution was progressively favourable and the patient was discharged from ICU with full respiratory recovery 43 days after admission. CONCLUSION Acute respiratory distress syndrome caused by M. pneumoniae infection is rare but must be considered when the appropriate clinical and radiological pattern occurs. The question of the susceptibility of the strain to macrolides has to be raised in some circumstances.

Handgrip Strength Predicts Difficult Weaning But Not Extubation Failure in Mechanically Ventilated Subjects

BACKGROUND: Muscle weakness, defined by the Medical Research Council scale, has been associated with delay in mechanical ventilation weaning. In this study, we evaluated handgrip strength as a prediction tool in weaning outcome. METHODS: This was a 1-y prospective study in 2 ICUs in 2 university hospitals. Adult patients who were on mechanical ventilation for at least 48 h and eligible for mechanical ventilation weaning were screened for inclusion. Handgrip strength was evaluated using a handheld dynamometer before each spontaneous breathing trial (SBT). Attending physicians were unaware of handgrip strength and decided on extubation according to guidelines. RESULTS: Eighty-four subjects were included (median age 66 [53–79] y, with a median Simplified Acute Physiology Score II of 49 [37–63]). At the first evaluation, median handgrip strength was significantly associated with weaning outcome as defined by international guidelines: simple (20 [12–26] kg), difficult (12 [6–21] kg), or prolonged (6 [3–11] kg) weaning (P = .008). Time to liberation from mechanical ventilation and ICU stay were significantly longer for subjects classified as having muscle weakness according to the handgrip strength-derived definition (P = .02 and P = .03, respectively). In multivariate analysis, known history of COPD (odds ratio [OR] 5.48, 95% CI 1.44–20.86, P = .01), sex (OR 6.16, 95% CI 1.64–23.16, P = .007), and handgrip strength at the first SBT (OR 0.89, 95% CI 0.85–0.97, P = .004) were significantly associated with difficult or prolonged weaning. Extubation failure, as defined by re-intubation or unscheduled noninvasive ventilation within 48 h after extubation, occurred 14 times after 92 attempts, leading to an extubation failure rate of 15%. No association was found between handgrip strength and extubation outcome. CONCLUSIONS: Muscle weakness, assessed by handgrip strength, is associated with difficult or prolonged mechanical ventilation weaning and ICU stay, but not with extubation outcome.

Cas cliniquePneumopathie à mycoplasme : une cause rare de syndrome de détresse respiratoire aiguë (SDRA) et de résistance potentielle aux antibiotiquesMycoplasma-related pneumonia: A rare cause of acute respiratory distress syndrome (ARDS) and of potential antibiotic resistance

INTRODUCTION Acute respiratory distress syndrome caused by Mycoplasma pneumoniae infection has rarely been described. OBSERVATION We report a case of community-acquired pneumonia occurring in a patient with Downs syndrome. Persisting hypoxemia raised the questions of nosocomial pneumonia, of the occurrence of a fibrosing alveolitis or of the resistance of the strain to macrolides. After a long period of very severe respiratory impairment, the evolution was progressively favourable and the patient was discharged from ICU with full respiratory recovery 43 days after admission. CONCLUSION Acute respiratory distress syndrome caused by M. pneumoniae infection is rare but must be considered when the appropriate clinical and radiological pattern occurs. The question of the susceptibility of the strain to macrolides has to be raised in some circumstances.

Renal Replacement Therapy in Patients with Severe Precapillary Pulmonary Hypertension with Acute Right Heart Failure

Background: Renal replacement therapy has been suggested as a therapeutic option in the setting of acute right ventricular failure in patients with severe precapillary pulmonary hypertension. However, there are few data supporting this strategy. Objectives: To describe the clinical course and the prognosis of pulmonary hypertensive patients undergoing renal replacement therapy in the setting of acute right heart failure. Methods: This was a single-center retrospective study over an 11-year period. Data were collected from all patients with chronic precapillary pulmonary hypertension requiring catecholamine infusions for clinical worsening and acute kidney injury that necessitated renal replacement therapy. Results: Fourteen patients were included. At admission, patients had a blood urea of 28.2 mmol/l (22.3-41.2), a creatinine level of 496 µmol/l (304-590), and a mean urine output in the 24 h preceding hospitalization of 200 ml (0-650). Sixty-eight renal replacement therapy sessions were performed, 36 of which were continuous and 32 of which were intermittent. Systemic hypotension occurred in 16/32 intermittent and 16/36 continuous sessions (p = 0.9). Two patients died during a continuous session. The intensive care unit-related, 1-, and 3-month mortality was 46.7, 66.7, and 73.3%, respectively. Conclusion: Renal replacement therapy is feasible in the setting of acute right ventricular failure in patients with severe precapillary pulmonary hypertension but is associated with a poor prognosis. The best modality and timing in this population remain to be defined.

Carboplatin: a new cause of severe type B lactic acidosis secondary to mitochondrial DNA damage.

In adults, type B lactic acidosis is rare and generally associated with a toxin, particularly metformin or antiretroviral nucleosides analogues. We report a case of lactic acidosis caused by carboplatin in a 50-year-old woman suffering from primary peritoneal carcinoma. She was admitted for severe lactic acidosis (pH 6.77, lactate 19 mmol/L) associated with multiple organ failure (PaO₂/FiO₂ 96, creatinine 231 μmol/L, aspartate aminotransferase > 25,000 UI, factor V 13%) occurring during the sixth carboplatin cycle. In the absence of sepsis, internal bleeding, alcohol poisoning, or other causes of lactic acidosis, the hypothesis of mitochondrial DNA (mtDNA) damage secondary to carboplatin and subsequent mitochondrial dysfunction leading to increase in glycolysis and lactic acidosis was suspected. L-Carnitine therapy associated with aggressive intensive care support led to a progressive improvement (pH 7.29, bicarbonate 24 mmol/L, lactate 7.8 mmol/L), but life support was withdrawn on day 7 because of peritoneal relapse. A respiratory chain dysfunction of enzyme activities encoded by mtDNA and multiple mtDNA deletions were found in muscle and liver tissue. It is generally accepted that carboplatin toxicity results in bone marrow suppression, renal dysfunction, or neurotoxicity and that platinating agents have no direct mitochondrial effect. However, although very unusual, emergency physicians must be aware that carboplatin can cause mitochondrial toxicity and trigger lactic acidosis.

Sophisticated biomarkers for community-acquired pneumonia severity asessment: gadgets or useful tools?

Sir: To assess the severity of community-acquired pneumonia (CAP) emergency department (ED) physicians can use specific, validated prediction rules [1] or various biochemical biomarkers such as cortisol [2], procalcitonin [2, 3], proatrial-natriuretic peptide, and provasopressin [3]. However, because these biomarkers may be expensive [3], and most of them are not immediately available for the practitioner, their usefulness for ED triage remains questionable. Furthermore, there are conflicting data concerning the prognostic value of cortisol [4] and procalcitonin levels [2, 3]. Whereas Christ-Crain and colleagues [2] demonstrated that total cortisol level is the sole biochemical predictor of severity and outcome, Salluh et al. [4] and our group were unable to demonstrate the impact of cortisol levels in severe CAP re-

Valproic acid overdose and continuous venovenous haemodiafiltration

Age 49 ± 19.64 44.7 ± 15.12 0.27 Gender (M/F) 6/14 16/14 0.02∗ Duration of dialysis (months) 63.5 ± 51.43 68.8 ± 59.49 0.40 BMI (kg/m2) 23.51 ± 5.55 24.49 ± 4.73 0.11 Education Primary 20% 20% 0.50 Secondary/tertiary 50% 45% 0.45 Higher education 10% 25% 0.02∗ Uneducated 20% 10% 0.07 History of transplant 0/20 1/40 0.43 Diabetes mellitus 10% 10% 0.50 Marital status Single 30% 20% 0.07 Divorced 0% 15% 0.02∗ Widowed 30% 5% 0.01∗ Married 40% 60% 0.01∗ Employment Employed 0% 20% 0.04∗ Unemployed 100% 80% 0.04∗ Malnutrition–inflammation score (MIS) 9.8 ± 3.25 7.55 ± 4.63 0.06 Serum albumin (g/dl) 3.78 ± 0.47 3.82 ± 0.45 0.40 Haemoglobin (g/dl) 9.18 ± 1.26 9.47 ± 1.78 0.30 Urea reduction ratio (URR) 66.2 ± 7.25 66.65 ± 4.93 0.43 Blood urea (mg/dl) 162.10 ± 38.56 164.18 ± 40.10 0.41 Serum creatinine (mg/dl) 7.30 ± 2.02 8.89 ± 3.15 0.39 Serum calcium (mg/dl) 8.79 ± 0.59 8.71 ± 0.69 0.48 Serum phosphorus (mg/dl) 5.52 ± 1.03 5.44 ± 1.20 0.47 F-36 total scores 58.94 ± 13.09 69.90 ± 9.63 0.01∗ F-36 mental component 59.54 ± 13.70 71.39 ± 9.85 0.01∗ F-36 physical component 58.92 ± 13.57 66.76 ± 11.10 0.06

Atteinte musculaire diaphragmatique et/ou périphérique en réanimation : que la force soit avec nos patients !

La faiblesse musculaire acquise en réanimation est le résultat d’une atteinte des muscles et/ou des nerfs, en proportion variable, acquise durant le séjour en réanimation [1]. Elle est due à des altérations métaboliques, inflammatoires et énergétiques multiples, qui sont le fruit de la pathologie causale, mais aussi des moyens mis en œuvre pour la traiter [2]. Les muscles respiratoires, dont le principal est le diaphragme, peuvent également souffrir de ces différents facteurs affectant leur performance. Les conséquences démontrées de ces atteintes musculaires sont importantes, avec notamment des difficultés de sevrage de la ventilation mécanique et l’augmentation adjacente en termes de morbimortalité [3,4]. Il n’y a pas à proprement parlé de traitement efficace [5] et la prévention, basée sur une limitation des facteurs de risque, la mobilisation et l’usage le plus précoce possible des muscles respiratoires par des modes ventilatoires assistés, reste l’élément principal de prise en charge. Même si ces deux entités (faiblesse diaphragmatique et musculaire) partagent certains facteurs de risque, la prévalence respective de chacune, voire leur éventuelle coexistence est débattue, et est pourtant probablement un élément majeur dans la prédiction de la difficulté du sevrage de la ventilation mécanique et du succès de l’extubation. Quelques études se sont intéressées à cette coexistence et ses conséquences. Dres et al. ont réalisé une étude prospective monocentrique évaluant la prévalence de chacune de ces atteintes et leur poids respectif dans le succès du sevrage lorsque ces variables étaient mesurées au moment du test de sevrabilité [6]. L’atteinte diaphragmatique était évaluée par la réponse à une stimulation phrénique magnétique et l’échographie diaphragmatique et la force musculaire par le score MRC. Un des premiers enseignements de cette étude est que la faiblesse musculaire périphérique et l’atteinte diaphragmatique étaient retrouvées respectivement chez 34 % et 63 % des patients, et que 21 % d’entre eux présentaient la coexistence des deux. Cette étude soulignait que seule l’atteinte diaphragmatique, et non l’atteinte musculaire périphérique, était associée à l’échec du sevrage, soulignant les possibles différences physiopathologiques. Cette étude présentait toutefois les spécificités suivantes : le nombre de patients inclus (n=76) est important au regard des méthodes de mesure, mais reste néanmoins limité pour la thématique du sevrage de la ventilation mécanique, avec une définition de l’échec de sevrage qui regroupait à la fois les échecs de tests de sevrabilité (79 % des échecs) et les réintubations après extubation (21 % des échecs). De plus, les patients étaient enfin évalués assez précocement après l’initiation de la ventilation invasive (quatre jours en moyenne).

Does a 1-h rest after a successful spontaneous breathing trial really improve extubation outcome?

Initial correspondence from Drs. Cherel, Prat and Sztrymf Dear Editor, We read with great interest the article by Fernandez et al. [1] reporting the positive effect of a 1 h rest after a successful spontaneous breathing trial (SBT) on extubation outcome. Nevertheless, some issues deserve to be reported. First, although the authors highlighted fatigue subsequent to the SBT, it has to be recalled that others also evidenced that work-of-breathing of a T-piece weaning trial was not higher as compared to the postextubation period [2]. Second, the external validity is questionable. The rate of tracheostomized patients was rather high (13% of patients ventilated more than 12 h). The sparse use of prophylactic non-invasive ventilation (NIV) (3.7%), and frequent use of rescue NIV (more than 50% of patients with post-extubation respiratory failure) have to be underlined as well. Third, occurrence of copious secretions, which was one of the most frequent reasons for rescue NIV and reintubation, was more frequent in the control group as compared to the rest group (respectively, 15 vs. 9%, p = 0.06). Last, from a statistical point of view, the authors stated that they realized after concluding the study that 1372 patients (instead of 470) would have been necessary to reach 80% power. Though they admitted that the study was underpowered, they stated that the size of the effect was much larger than expected, leading to a significant difference between groups. We would like to remind the authors that premature discontinuation of a study often leads to overestimating the effect of the tested intervention [3]. Therefore, the observed consequences of reconnection to mechanical ventilation might merely represent the effect of chance.