[Acute respiratory distress due to tracheostomy tube migration]. / Détresse respiratoire aiguë par migration d'une canule de trachéotomie.

Tracheostomy cannula care is of paramount importance in the daily management of tracheotomized patients. While some complications are commonplace, specific events can occur, often according to type of cannula. We herein report the case of a 71-year-old patient; following a lengthy stay in the intensive care unit, she had received a Safe T-Tube cannula designed to provide support in a stenotic trachea. At home, while suctioning her tracheal secretions, she suddenly experienced respiratory distress requiring a rapid intervention. On arrival, no seeable cannula was found, either in the tracheostomy or in the patient's immediate surroundings. Following her transfer to intensive care, a new cannula was inserted into the tracheostomy opening, enabling mechanical ventilation to begin and achieving rapid relief of dyspnea and improvement of the patient's overall condition. Bronchial fibroscopy was then performed, during which the Safe T-Tube cannula was found folded on itself in a supra-carinal intra-tracheal position. It was extracted and replaced by a cannula of the same model, which was sewn to the skin. Although rare and usually limited to flexible cannulas, this complication is potentially fatal. Generally speaking, when cannula obstruction is suspected, bronchial endoscopy in an intensive care setting is a vital necessity. It is not only the cornerstone of the diagnosis, but also of paramount importance in treatment taking into full account the mechanism of obstruction.

Norepinephrine exerts an inotropic effect during the early phase of human septic shock.

BACKGROUND: We conducted this study to investigate whether norepinephrine increases cardiac contractility when administered during the early phase of septic shock. METHODS: We studied 38 patients with septic shock who had been resuscitated for <3 h and whose mean arterial pressure (MAP) remained <65 mm Hg. Echocardiographic variables were obtained before (T0) and after either initiation or an increase in the dose of a norepinephrine infusion to increase MAP to ≥ 65 mm Hg (T1). We collected left ventricular ejection fraction (LVEF), velocity-time integral of the left ventricular outflow tract (VTI), tissue Doppler imaging of mean systolic velocity of the lateral tricuspid annulus (Sa) and of the lateral mitral annulus (Sm), and tricuspid annular plane systolic excursion (TAPSE). RESULTS: There were significant (P<0.05) increases from T0 to T1 in MAP [mean (sd): from 56 (7) to 80 (9) mm Hg], LVEF [from 49 (13) to 56 (13)%], VTI [from 18 (5) to 20 (6) cm], Sm [from 10.8 (5.1) to 12.1 (5.0) cm s-1], TAPSE [from 1.8 (0.5) to 2.0 (0.5) cm], and Sa [from 13.0 (5.6) to 15.1 (6.4) cm s-1]. In the subgroup of 15 patients with LVEF ≤45%, significant increases in VTI [from 16 (8) to 18 (7) cm] and in LVEF [from 36 (7) to 44 (10)%] were observed. CONCLUSIONS: Norepinephrine administration during early resuscitation in patients with septic shock increased the cardiac systolic function despite the presumed increase in left ventricular afterload secondary to the increased arterial pressure. Whether such an effect persists over time remains to be evaluated. CLINICAL TRIAL REGISTRATION: NCT02750683.

Iatrogenic peritonitis following an incident during ablation of a pedicle screw.

Immediate complications can arise due to faulty implantation of material during fusion procedures, but none have been reported in connection with ablation of material in the spine. We report a case of intraperitoneal migration of a pedicle screw during attempted removal. It crossed the psoas muscle and perforated a small-intestine loop, triggering hemorrhagic shock and peritonitis by perforation. We analyze the causes and mechanisms underlying this exceptional case of migration, with a view to sharing preventive measures. Initial extra-pedicular screw positioning and the pressure exerted to remove it were responsible for this serious incident.

Efficacy and safety of a new coverlet device on skin microclimate management: a pilot study in critical care patients.

OBJECTIVE: To test the effect of a new coverlet device, allowing air circulation at the body/underlying surface interface, on skin microclimate management. METHOD: This prospective observational pilot study took place in a 15-bed university-affiliated intensive care unit. Overall, 34 mechanically ventilated patients were included. Skin humidity and temperature were monitored before and after the implementation of the tested device at the occiput, scapulas, buttocks and sacrum. Humidity and temperature were evaluated through surface skin impedance and an infra-red thermometer, respectively. Health professionals were asked to evaluate the device. RESULTS: After implementation of the coverlet device, there was a rapid, sustained and significant decrease in skin humidity at all sites ranging from 6 % to 15 %, excluding the occiput. Skin temperature also significantly decreased from 1 % at both scapulas, but not at the other studied body sites. No side effects were observed. Health professionals reported that the device was easy and quick to install. Although they did not report a subjective improvement in skin moisture or temperature, they considered the device to be efficient. CONCLUSION: Although limited by its design, this pilot study suggests a good efficacy of the studied device on skin microclimate management. Further data are warranted to test the clinical implications of our findings.

[Mycoplasma-related pneumonia: a rare cause of acute respiratory distress syndrome (ARDS) and of potential antibiotic resistance]. / 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 Down's 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.

Prognostic factors of acute heart failure in patients with pulmonary arterial hypertension.

Acute right ventricular failure in the setting of pulmonary arterial hypertension (PAH) often requires hospitalisation in intensive care units (ICU) to manage the subsequent low cardiac output and its consequences. There are very few data on these acute events. We recorded demographic, clinical and biological data and therapy in consecutive patients suffering from acute right heart failure requiring catecholamine treatment in the ICU of the French referral centre for pulmonary hypertension. These variables were analysed according to the survival status in ICU. 46 patients were included, the mean age was 50.3 yrs. ICU mortality was 41%. We found no difference in terms of demographics, clinical data, last haemodynamic measurements at admission. Systemic arterial pressure was significantly lower in the subgroup of patients whose clinical course was fatal. Plasma brain natriuretic peptide (BNP), C-reactive protein (CRP), serum sodium and creatinine at admission correlated with survival. Demonstration of an infection during the ICU stay was associated with a worse prognosis. These preliminary results underline the importance of some simple clinical and biological parameters in the prognostic evaluation of acute heart failure in the setting of PAH. Whether these parameters can guide therapy needs to be further investigated.

Pulmonary arterial hypertension associated with fenfluramine exposure: report of 109 cases.

The aim of the present study was to describe a large cohort of fenfluramine-associated pulmonary arterial hypertension (fen-PAH) and its possible prognostic markers. The records of all patients with a diagnosis of fen-PAH evaluated at the present authors' centre from 1986-2004 were retrospectively studied. Baseline clinical and haemodynamic data were collected, as well as survival times. The median duration of fenfluramine exposure was 6 months, with a median of 4.5 yrs between exposure and onset of symptoms. Nine (22.5%) out of 40 patients evaluated resulted positive for the presence of germline bone morphogenetic protein receptor (BMPR) type 2 mutations. In these patients, the duration of exposure to fenfluramine was significantly lower than in patients without mutation. The median survival was 6.4 yrs, without significant difference between fen-PAH and a control group of idiopathic and familial pulmonary arterial hypertension patients referred to the present authors' centre during the same time frame and treated identically. Duration of fenfluramine exposure showed no relation to survival, while cardiac index was the only independent predictor of multivariate analysis. Fenfluramine-associated pulmonary arterial hypertension shares clinical, functional, haemodynamic and genetic features with idiopathic pulmonary arterial hypertension, as well as overall survival rates. Therefore, the present authors conclude that fenfluramine exposure characterises a potent trigger for pulmonary arterial hypertension without influencing its clinical course.

[Postembolic pulmonary hypertension]. / Hypertension pulmonaire postembolique.

INTRODUCTION: Chronic thromboembolic pulmonary hypertension (CTEPH) is a rare disease characterized by the persistence of thromboemboli obstructing the pulmonary arteries as an organized tissue. The consequence is an increase in pulmonary vascular resistance resulting in pulmonary hypertension (PH) and progressive right heart failure. BACKGROUND: It is difficult to recognize the postembolic nature of PH because there is no known history of thromboembolic disease in more than 50% of cases. Diagnosis is based on the presence of mismatched segmental defects in the ventilation-perfusion scanning. When CTEPH is suspected, pulmonary angiography and high-resolution CT scan are required to establish the diagnosis and to assess the operability. Pulmonary angiography is always performed in conjunction with a diagnostic right heart catheterization, which is required to confirm the diagnosis of PH and to determine the degree of hemodynamic impairement. If there is a good correlation between the pulmonary vascular resistance and the anatomical obstruction, pulmonary endarterectomy (PEA) must be proposed. Otherwise, vasodilator and antiproliferative treatments and lung transplantation represent interesting alternatives. VIEWPOINT AND CONCLUSION: PEA remains the treatment of choice for eligible patients. Nevertheless, there is a need to conduct randomized trials to assess the efficacy of novel medical therapies in some situations: (1) in inoperable CTEPH due to distal lesions, (2) before PEA (therapeutic bridge) in patients who are considered "high risk" due to extremely poor hemodynamics, (3) in patients with persistent pulmonary hypertension after surgery.

[Pulmonary arterial hypertension due to tumor emboli]. / Hypertension artérielle pulmonaire postembolique tumorale.

INTRODUCTION: Pulmonary arterial hypertension (PAH) is rare in the presence of malignancy and tumour embolisation is one of several possible pathological mechanisms. CASE REPORTS: We report our experience of 5 clinical cases and undertake a literature revue of the pathophysiological mechanisms and of the possible diagnostic and therapeutic approaches. CONCLUSIONS: Neoplastic PAH due to tumour micro-emboli is rare and the diagnosis difficult to establish. Cytological examination of pulmonary arterial blood could allow early institution of appropriate chemotherapy and lead to an improvement in the grave prognosis of this condition.

[Genetics of pulmonary arterial hypertension: recent data and practical applications]. / Génétique de l'hypertension artérielle pulmonaire: données récentes et applications pratiques.

INTRODUCTION: Pulmonary arterial hypertension (PAHT) is defined as an increase of mean pulmonary artery pressure above 25 mmHg at rest, or 30 mmHg on exercise, due to obliteration of small calibre pulmonary arteries by proliferation of endothelial cells and smooth muscle. Beside idiopathic PAHT and that associated with other conditions, a familial form has been identified. STATE OF THE ART: Family studies have shown an association between mutations of the BMPR2 gene and PAHT phenotypes. The products of this gene appear to be involved in vascular homeostasis and its mutations are the basis of a loss this function and, in consequence, proliferation of pulmonary vascular cells. PERSPECTIVES: Certain characteristics, such as incomplete penetrance and genetic anticipation, lead to a complex relationship between genotype and phenotype and make genetic counselling difficult. Other members of the extended family of TGF-beta receptors are implicated in the development of the Osler-Rendu syndrome, but may also be associated with the development of PAHT. CONCLUSION: Progress in genetics allows better understanding of the pathophysiology of this disease and could lead to new therapeutic possibilities.

[Clinical, haemodynamic and genetic features of familial pulmonary arterial hypertension]. / Caractéristiques cliniques, hémodynamiques et génétiques de l'hypertension artérielle pulmonaire familiale.

INTRODUCTION: Pulmonary arterial hypertension (PAH) is defined by a raised pressure in the pulmonary arterial circulation associated with small vessel narrowing due to proliferation of the endothelium and vascular smooth muscle. Idiopathic PAH should be distinguished from PAH associated with a causal disease. One familial type (familial PAH), gathered from one family, has recently been linked to a mutation of the BMPR 2 (bone morphogenetic protein receptor 2) gene. It seems important to compare the idiopathic form of PAH with these familial forms to confirm that the same diagnostic and therapeutic principles can be applied to familial PAH. MATERIAL AND METHODS: The demographic, clinical, haemodynamic and prognostic data from 34 cases of familial PAH were compared with those of 451 cases of idiopathic PAH. The genetic characteristics of the familial forms were also defined. RESULTS: Familial PAH presented at a younger age than idiopathic PH (31 +/- 15 vs. 45 +/- 18 years p=0.002) without any other demographic difference (sex-ratio 2.09/1 et 1.42/1 p=NS). There was no difference in exercises tolerance (6 minute walking test 341 +/- 98 and 289 +/- 135 metres p=NS), in haemodynamic parameters (mean PAP 65 +/- 12 and 62 +/- 15 mmHg, p=NS), or in prognosis, with the exception of an absence of a vasodilator response in the familial group to nitric oxide challenge. We found the BMPR 2 gene mutation to be quantitatively and qualitatively comparable to previously published data. CONCLUSION: The only difference between these two forms of this illness were of a younger age at presentation and an absent vasodilator response in the familial PAH group. We do not propose that familial PAH should be treated any differently from the idiopathic form. Genetic counselling will need to be developed in line with the progress being made in the understanding of this condition.

[Pulmonary hypertension: from genetics to treatments]. / Hypertension artérielle pulmonaire: de la génétique aux traitements.

Pulmonary hypertertension (PHT) is a rare disease defined by increased resistance of the pulmonary arteries inevitably leading to right heart failure if specific treatment is not given. This disease can occur sporadically (idiopathic or primary PHT), within a familial context (familial PHT, BMPR2 gene mutation), or occur as a complication of other diseases (connective tissue disease, congenital cardiomyopathy, human immunodeficiency virus infection, portal hypertension, use of anorexigenic agents). The incidence of primary PHT is 2 million cases per year, probably an underestimation due to the low specificity of clinical signs, predominantly exercise-induced dyspnea. Recent therapeutic advances (prostacyclin and endothelin receptor antagonists administered in continuous infusion) have improved the prognosis of this orphan disease. Inhaled iloprost and type 5 phosphodiesterase inhibitors should be evaluated for this indication. Lung transplantation is reserved for patients unresponsive to medical treatment.

Prevention of hepatopulmonary syndrome and hyperdynamic state by pentoxifylline in cirrhotic rats.

Inhibition of tumour necrosis factor-alpha (TNF-alpha), levels of which are increased in the blood of cirrhotic rats, prevents hyperdynamic circulatory state, mainly by decreasing the vascular overproduction of nitric oxide. Hepatopulmonary syndrome, which is characterised by intrapulmonary vascular dilatation and increased alveolar to arterial oxygen tension difference (PA-a,O2), is mainly related to pulmonary over-production of NO by macrophages accumulated in lung vessels. Since TNF-alpha is a potent activator of macrophagic inducible nitric oxide synthase (NOS), the aim of this study was to investigate whether TNF-alpha inhibition prevented hepatopulmonary syndrome and hyperdynamic circulatory state in rats with cirrhosis. TNF-alpha was inhibited by 5 weeks of pentoxifylline (10 mg x kg body weigh(-1) x day(-1)) in rats with cirrhosis induced by common bile duct ligation. Cardiac output, pulmonary and systemic vascular resistance, PA-a,O2 and cerebral uptake of intravenous technetium-99m-labelled albumin macroaggregates (which reflects intrapulmonary vascular dilatation) were similar in sham- and pentoxifylline-treated cirrhotic rats. Blood TNF-alpha concentrations and pulmonary intravascular macrophage sequestration, as assessed by morphometric analysis and radioactive colloid uptake, were decreased with pentoxifylline. Pentoxifylline also prevented increases in aorta and lung NOS activities and inducible NOS expression. Thus pentoxifylline prevents development of hyperdynamic circulatory state and hepatopulmonary syndrome, probably by inhibiting the effects of tumour necrosis factor-alpha on vascular nitric oxide synthase and intravascular macrophages. These results support an important role for tumour necrosis factor-alpha in the genesis of hepatopulmonary syndrome.

[Pulmonary hypertension and obesity]. / Hypertension artérielle pulmonaire et obésité

Obesity is a morbid condition with hemodynamic consequences affecting the systemic and pulmonary circulations leading to a risk of pulmonary hypertension. Data in the literature do not argue in favor of a direct relationship between pulmonary hypertension and obesity. These two conditions appear to be two distinct entities, the different co-morbidities observed in obesity favoring pulmonary hypertension. Certain co-morbidities, for instance use of anorexic agents, exhibit a clear relationship with pulmonary hypertension. There is also a possible relationship with left ventricular failure, hypoxemia, and other respiratory disorders (including obstructive sleep apnea), hypothyroidism, and thomboembolism.