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The large majority of patients with acute respiratory failure present diffuse pulmonary opacities resulting from pulmonary embolism, intra-alveolar hemorrhage, or a classical cause of ARDS. In a small number of patients however, these opacities correspond to diffuse interstitial pneumonia. This should be suspected in light of the context, the time of formation, and the unusual respiratory and/or extrarespiratory signs. If there is a clinical doubt, thoracic scan and bronchoalveolar lavage should be performed together with infectious and immunology tests. Treatment depends on the cause and/or the type of lesion.

Functional imaging studies in normal humans have shown that the supplementary motor area (SMA) and the primary motor cortex (PMC) are coactivated during various breathing tasks. It is not known whether a direct pathway from the SMA to the diaphragm exists, and if so what properties it has. Using transcranial magnetic stimulation (TMS) a site at the vertex, representing the diaphragm primary motor cortex, has been identified. TMS mapping revealed a second area 3 cm anterior to the vertex overlying the SMA, which had a rapidly conducting pathway to the diaphragm (mean latency 16.7 +/- 2.4 ms). In comparison to the vertex, the anterior position was characterized by a higher diaphragm motor threshold, a greater proportional increase in motor-evoked potential (MEP) amplitude with voluntary facilitation and a shorter silent period. Stimulus-response curves did not differ significantly between the vertex and anterior positions. Using paired TMS, we also compared intracortical inhibition/facilitation (ICI/ICF) curves. In comparison to the vertex, the MEP elicited from the anterior position was not inhibited at short interstimulus intervals (1-5 ms) and was more facilitated at long interstimulus intervals (9-20 ms). The patterns of response were identical for the costal and crural diaphragms. We conclude that the two coil positions represent discrete areas that are likely to be the PMC and SMA, with the latter wielding a more excitatory effect on the diaphragm.

This review describes current knowledge on the mechanisms that underlie glucocorticoid insufficiency in sepsis and the molecular action of glucocorticoids. In patients with severe sepsis, numerous factors predispose to glucocorticoid insufficiency, including drugs, coagulation disorders and inflammatory mediators. These factors may compromise the hypothalamic-pituitary axis (i.e. secondary adrenal insufficiency) or the adrenal glands (i.e. primary adrenal failure), or may impair glucocorticoid access to target cells (i.e. peripheral tissue resistance). Irreversible anatomical damages to the hypothalamus, pituitary, or adrenal glands rarely occur. Conversely, transient functional impairment in hormone synthesis may be a common complication of severe sepsis. Glucocorticoids interact with a specific cytosolic glucocorticoid receptor, which undergoes conformational changes, sheds heat shock proteins and translocates to the nucleus. Glucocorticoids may also interact with membrane binding sites at the surface of the cells. The molecular action of glucocorticoids results in genomic and nongenomic effects. Direct and indirect transcriptional and post-transcriptional effects related to the cytosolic glucocorticoid receptor account for the genomic effects. Nongenomic effects are probably subsequent to cytosolic interaction between the glucocorticoid receptor and proteins, or to interaction between glucocorticoids and specific membrane binding sites.

The extended survival of patients with Duchenne muscular dystrophy (DMD) achieved by the introduction of mechanical ventilation is raising new quality-of-life issues. We evaluated passive range of wrist extension, key pinch strength, and power wheelchair driving in 84 patients. The 47 drivers with restricted driving abilities were older than the 37 unrestricted drivers (27.2+/-5.0 y vs. 22.8+/-3.8 y) and had worse upper limb performance. By multiple logistic regression, only key pinch was significant ( R(2) = 0.224, P = 0.02. Eighteen restricted drivers were reassessed after having swapped a conventional joystick for another control system (mini-joystick, isometric mini-joystick, finger joystick, or pad) and having moved the position of the tested control system so that the patient could use it with different fingers, his chin or his mouth. All of them regained the ability to drive unrestricted. Adults with DMD gradually lose their ability to drive with a conventional joystick but can regain unrestricted driving with alternative control systems.

The use of glucocorticoids (corticotherapy) in severe sepsis is one of the main controversial issues in critical care medicine. These agents were commonly used to treat sepsis until the end of the 1980s, when several randomized trials casted serious doubt on any benefit from high-dose glucocorticoids. Later, important progress in our understanding of the role played by the hypothalamic-pituitary-adrenal axis in the response to sepsis, and of the mechanisms of action of glucocorticoids led us to reconsider their use in septic shock. The present review summarizes the basics of the physiological response of the hypothalamic-pituitary-adrenal axis to stress, including regulation of glucocorticoid synthesis, the cellular mechanisms of action of glucocorticoids, and how they influence metabolism, cardiovascular homeostasis and the immune system. The concepts of adrenal insufficiency and peripheral glucocorticoid resistance are developed, and the main experimental and clinical data that support the use of low-dose glucocorticoids in septic shock are discussed. Finally, we propose a decision tree for diagnosis of adrenal insufficiency and institution of cortisol replacement therapy.

Guillain-Barré Syndrome is the leading cause of nontraumatic acute paralysis in industrialized countries. About 30% of patients have respiratory failure requiring intensive care unit (ICU) admission and invasive mechanical ventilation. Progressive weakness of both the inspiratory and the expiratory muscles is the mechanism leading to respiratory failure. Aspiration pneumonia and atelectasis are common consequences of the bulbar muscle weakness and ineffective cough. The classical signs of respiratory distress occur too late to serve as guidelines for management, and measurements of vital capacity and static respiratory pressures are useful to determine the best times for starting and stopping mechanical ventilation. Several factors present at admission and during the ICU stay are known to predict a need for invasive mechanical ventilation. They include rapidly progressive motor weakness, involvement of both the peripheral limb and the axial muscles, ineffective cough, bulbar muscle weakness, and a rapid decrease in vital capacity. Specific treatments (plasma exchange and intravenous immunoglobulins) have decreased both the number of patients requiring ventilation and the duration of ventilation. The need for mechanical ventilation is associated with residual functional impairments, although all patients eventually recover normal respiratory muscle function.

The sniff nasal inspiratory pressure (SNIP) consists in the measurement of pressure through an occluded nostril during sniffs performed through the controlateral nostril. It is an accurate and noninvasive approximation of esophageal pressure swing during sniff maneuvers. However SNIP can underestimate esophageal pressure swing in subjects with nasal obstruction, patients with chronic obstructive pulmonary disease and severe neuromuscular patients. Nevertheless, since SNIP maneuver has predicted normal values, is noninvasive and is easier to perform than maximal inspiratory pressure (MIP) maneuver, it could be considered as the first simple test to use in order to assess inspiratory muscle weakness. In addition, because it is as reproducible as MIP, it can be suitable to follow inspiratory muscle function in chronic neuromuscular patients. Because, of the important limit of agreement between SNIP and MIP, these two methods are not interchangeable but complementary.

Many patients with respiratory failure related to neuromuscular disease receive chronic invasive ventilation through a tracheostomy. Improving quality of life, of which speech is an important component, is a major goal in these patients. We compared the effects on breathing and speech production of assist-control ventilation (ACV) and bilevel positive-pressure ventilation (BPPV) in nine patients with neuromuscular disease. Ventilator-delivered flow was measured using a pneumotachograph, and respiratory rate, inspiratory time, and ventilator-delivered volume were measured on this flow signal. Gas exchange was assessed using oxygen saturation and end-tidal carbon dioxide measurement. Microphone speech recordings were subjected to quantitative analysis. At rest, ventilatory parameters were similar with both modes. Speech induced an increase in inspiratory time during BPPV, with a greater increase in the volume released by the ventilator during speech as compared with ACV (172 +/- 194 versus 26 +/- 31 ml). Consequently, speech duration was longer during inspiration with BPPV. Moreover, BPPV allowed speech production to extend into expiration, and three patients could speak continuously during several respiratory cycles while receiving BPPV. Blood gas exchange was not modified by speech with BPPV or ACV. This study shows that BPPV provides better speech duration than ACV with no detectable short-term deleterious effects.

The present study was conducted to confirm the presence of severe lymphocytic alveolitis and to determine the factors responsible for the very different alveolar CD4 to CD8 T-cell ratios (CD4/ CD8) described in methotrexate-induced pneumonitis (MTX-pneumonitis). Clinical and radiologic findings, as well as bronchoalveolar lavage (BAL) data, including CD4 and CD8 subset analysis, were retrospectively reviewed for patients hospitalized between 1985 and 2000 for MTX-pneumonitis. BAL cell counts from patients with MTX-pneumonitis (cases) were compared with those from patients receiving MTX but who did not have evidence of MTX toxicity (MTX-exposed patients) and those from healthy subjects (control subjects). Nineteen BAL were performed in 14 consecutive cases of MTX-pneumonitis. MTX was given for various underlying diseases. All cases presented a subacute diffuse interstitial pneumonitis that recovered, with MTX discontinuation and/or initiation of adjunctive steroid therapy. At the time of diagnosis, BAL cell counts in MTX-pneumonitis indicated severe lymphocytic alveolitis when compared with MTX-exposed patients and control subjects and moderate neutrophil alveolitis compared with control subjects. The lymphocytic alveolitis resulted from an increase in both CD4 and CD8 lymphocyte cell counts. Nevertheless, alveolar CD4/ CD8 T-cell ratios ranged from 0.4 to 9.6. CD4/CD8 values correlated positively with lymphocyte counts but negatively with time elapsed between last MTX administration and BAL and with steroid cumulative dose received by the patients. Severe lymphocytic alveolitis was confirmed in our series of MTX-pneumonitis. The between-patient variation in CD4/CD8 T-cell ratios may reflect the large range of time intervals between last MTX administration and BAL evaluation and the use of adjunctive steroid therapy.