The spectrum of acute heart failure after venlafaxine overdose.

OBJECTIVE: Venlafaxine is a bicyclic antidepressant that may be associated with severe cardiotoxicity following large overdose. The purpose of this short case series is to present different patterns of venlafaxine-related cardiotoxicity and to discuss the potential mechanisms. CASE SERIES: Between January 2010 and July 2011, four patients were admitted to an ICU with acute left ventricular failure following large venlafaxine overdoses. The age of the four female patients ranged from 35 to 65 years. None of them had no history of cardiovascular disease. The amount of venlafaxine ingested by history ranged from 3150 to 13500 mg (extended-release preparation in two cases). The peak serum venlafaxine concentration was between 2153.3 and 9950 ng/ml. Three patients died and one recovered rapidly. The initial ECG revealed only mild abnormalities in two cases. In two patients, at least one ECG recording demonstrated a widening of QRS interval. In three patients, echocardiography disclosed a left ejection fraction of 15%-18%. Two patients presented a severe serotonin syndrome, with major rhabdomyolysis. Seizures were noted in two cases, including one patient with status epilepticus. Three patients were mechanically ventilated. The causes of death were refractory hypoxemia, malignant arrhythmias, and cardiogenic shock, respectively. DISCUSSION: Severe and diffuse left ventricular dysfunction may be observed after large venlafaxine overdoses and this is not always associated with severe cardiac conduction function abnormalities. The mechanisms underlying venlafaxine-related cardiac failure with preserved normal cardiac conduction are discussed. A possible explanation may be a catecholamine-induced myocardial damage in relationship with the inhibition of norepinephrine (and dopamine) reuptake.

Early multi-system organ failure associated with acute pancreatitis: a plea for a conservative therapeutic strategy.

The mortality of severe acute pancreatitis still ranges between 10 and 20%. Nowadays, infected pancreatic necrosis is the leading cause of death. Despite advances in intensive care therapy, however, early and worsening multi-system organ failure remains a source of substantial morbidity and still accounts for 20 to 50% of the deaths. In recent years, the systemic inflammatory response syndrome and the relevant cascades of inflammatory mediators have been implicated as the key factor in the emergence of remote tissue damage. Early multi-system organ failure that supervenes in the first week is typically associated with a sterile necrotizing process. There are no pathophysiological, clinical or economical data to support the practice of debridement of sterile necrosis to prevent or to control early multi-system organ failure. This issue has never been addressed in a controlled study. Besides intensive care support, non-surgical therapeutic modalities including urgent endoscopic sphincterotomy for impacted stones, antibiotic prophylaxis for the prevention of pancreatic infection and early jejunal nutrition have been specifically developed hopefully to attenuate multiple organ failure, to obviate the need of surgical drainage and to improve survival. Fine needle aspiration of necrotic areas must be incorporated in any conservative therapeutic strategy in order to identify and not to jeopardize those with infected necrosis that remains an absolute indication for drainage. A specific treatment of acute pancreatitis is still lacking, so far. However, there is ample experimental and pathophysiological evidence in favour of immunomodulatory therapy in severe acute pancreatitis. The administration of one or several antagonists of inflammatory mediators possibly combined with a protease inhibitor may at last provide the opportunity to interfere with the two major determinants of prognosis: the severity of multiple organ failure and the extent of necrotic areas that creates the culture medium for bacterial superinfection. These benefits remain to be substantiated in a controlled study, however.

Lenercept (p55 tumor necrosis factor receptor fusion protein) in severe sepsis and early septic shock: a randomized, double-blind, placebo-controlled, multicenter phase III trial with 1,342 patients.

OBJECTIVE: Phase III study to confirm a trend observed in a previous phase II study showing that a single dose of lenercept, human recombinant p55 tumor necrosis factor receptor-immunoglobulin G1 (TNFR55-IgG1) fusion protein, decreased mortality in patients with severe sepsis or early septic shock. DESIGN: Multicenter, double-blind, phase III, placebo-controlled, randomized study. SETTING: A total of 108 community and university-affiliated hospitals in the United States (60), Canada (6) and Europe (42). PATIENTS: A total of 1,342 patients were recruited who fulfilled the entry criteria within the 12-hr period preceding the study drug administration. INTERVENTION: After randomization, an intravenous dose of 0.125 mg/kg lenercept or placebo was given. The patient was monitored for up to 28 days, during which standard diagnostic, supportive, and therapeutic care was provided. MEASUREMENTS AND MAIN RESULTS: The primary outcome measure was 28-day all-cause mortality. Baseline characteristics were as follows: a total of 1,342 patients were randomized; 662 received lenercept and 680 received placebo. The mean age was 60.5 yrs (range, 17-96 yrs); 39% were female; 65% had medical admissions, 8% had scheduled surgical admissions, and 27% had unscheduled surgical admissions; 73% had severe sepsis without shock, and 27% had severe sepsis with early septic shock. Lenercept and placebo groups were similar at baseline with respect to demographic characteristics, simplified acute physiology score II-predicted mortality, profiles of clinical site of infection and microbiological documentation, number of dysfunctioning organs, and interleukin-6 (IL-6) plasma concentration. Lenercept pharmacokinetics were similar in severe sepsis and early septic shock patients. Tumor necrosis factor was bound in a stable manner to lenercept as reflected by the accumulation of total serum tumor necrosis factor alpha concentrations. There were 369 deaths, 177 on lenercept (27% mortality) and 192 on placebo (28% mortality). A one-sided Cochran-Armitage test, stratified by geographic region and baseline, predicted 28-day all-cause mortality (simplified acute physiology score II), gave a p value of .141 (one-sided). Lenercept treatment had no effect on incidence or resolution of organ dysfunctions. There was no evidence that lenercept was detrimental in the overall population. CONCLUSION: Lenercept had no significant effect on mortality in the study population.

Prospective evaluation of short-term, high-volume isovolemic hemofiltration on the hemodynamic course and outcome in patients with intractable circulatory failure resulting from septic shock.

OBJECTIVE: To evaluate the effects of short-term, high-volume hemofiltration (STHVH) on hemodynamic and metabolic status and 28-day survival in patients with refractory septic shock. DESIGN: Prospective, interventional. SETTING: Intensive care unit (ICU), tertiary institution. PATIENTS: Twenty patients with intractable cardiocirculatory failure complicating septic shock, who had failed to respond to conventional therapy. INTERVENTIONS: STHVH, followed by conventional continuous venovenous hemofiltration. STHVH consisted of a 4-hr period during which 35 L of ultrafiltrate is removed and neutral fluid balance is maintained. Subsequent conventional continuous venovenous hemofiltration continued for at least 4 days. MEASUREMENTS AND MAIN RESULTS: Cardiac index, systemic vascular resistance, pulmonary vascular resistance, oxygen delivery, mixed venous oxygen saturation, arterial pH, and lactate were measured serially. Fluid and inotropic support were managed by protocol. Therapeutic endpoints were as follows during STHVH: a) by 2 hrs, a > or =50% increase in cardiac index; b) by 2 hrs, a > or =25% increase in mixed venous saturation; c) by 4 hrs, an increase in arterial pH to >7.3; d) by 4 hrs, a > or =50% reduction in epinephrine dose. Patients who attained all four goals (11 of 20) were considered hemodynamic "responders"; patients who did not (9 of 20) were considered hemodynamic "nonresponders." There were no differences in baseline hemodynamic, metabolic, and Acute Physiology and Chronic Health Evaluation and Simplified Acute Physiology Scores between responders and nonresponders. Survival to 28 days was better among responders (9 of 11 patients) than among nonresponders (0 of 9). Factors associated with survival were hemodynamic-metabolic response status, time interval from ICU admission to initiation of STHVH, and body weight. CONCLUSIONS: These data suggest that STHVH may be of major therapeutic value in the treatment of intractable cardiocirculatory failure complicating septic shock. Early initiation of therapy and adequate dose may improve hemodynamic and metabolic responses and 28-day survival.

Chylous ascites: diagnosis, causes and treatment.

Chylous ascites is a rare form of ascites and generally associated with a poor outcome since it is often secondary to neoplasms. Its true incidence is not well established in the general medico-surgical population. Any source of lymph vessels obstruction or leakage can potentially cause chylous effusions in the peritoneal or retroperitoneal cavities. Any type of cancer and lymph node involvement may be associated with this uncommon type of ascites. Traumatic, and mainly surgical, vessels leakage is the second most common source of chylous effusions. Other even more rare underlying conditions have been described as leading to chyloperitoneum. Large fluid volume losses together with proteins, and lymphocytes can induce additional morbidity in a previously debilitated population or severely ill patients. This includes organ dysfunction related to volume and electrolytes losses, but mainly secondary infections due to impaired immunity by antibodies and lymphocytes depletion. Even if a vast majority of chylous effusions shall heal spontaneously, early and full treatment has to be initiated in order to reduce morbidity and mortality associated with this condition. Adapted oral diet is to be introduced to reduce lymph flow. Low lipid, high medium-chain triglycerides alimentation is the first measure to implement. Total parenteral nutrition is to be reserved to failures of oral diet. In addition, paracentesis is indicated to improve patient comfort, reduce intra-adbominal pressure and secondary renal dysfunction. Somatostatin analogues have been demonstrated to be effective in reducing lymphorragia and may be proposed prior to consider the surgical approach. Direct lymph vessels ligation can be indicated for large lymph vessels leakage demonstrated by radiologic techniques and when medical treatment has failed. Peritoneo-venous shunt becomes a less common technique in refractory chylous effusion because of its high morbidity. Herein, the other causes of chylous effusions are reviewed as the diagnostic procedures. A treatment algorythm is proposed.

Ascites fluid in severe acute pancreatitis: from pathophysiology to therapy.

Several pathophysiological mechanisms are involved in the development of the inflammatory necrotizing process that takes place in the retroperitoneal area during the early phase of acute pancreatitis. They include premature intraglandular activation of pancreatic proenzymes (zymogens) and in particular trypsin, early microcirculatory impairment with subsequent ischaemia/reperfusion and overstimulation of immune effector cells. Although intra-acinar or interstitial activation of trypsinogen is most probably the trigger of acute pancreatitis, in recent years much emphasis has been put on the role of leukocytes. Based on numerous experimental and human data several pro-inflammatory mediators including cytokines, arachidonic acid derivatives, activated oxygen species and proteases are released locally by overactivated neutrophils and monocytes/macrophages among other cells. They are now believed to play a central role in the development of pancreatic necrosis and, once they gain access to the systemic circulation, in the emergence of early multisystem organ failure. However the sequential and relative contribution of each of these 3 pathophysiological mechanisms remain controversial and the precise identification of the mediators incriminated in local and remote tissue injury is still awaited. Severe acute pancreatitis still carries a mortality of 20% to 30%. With advances in intensive care management 80% of the deaths occur somewhat late in the attack due to infected pancreatic necrosis. Nevertheless early remote organ failures still remain a lifethreatening condition for most of these patients. A peritoneal exudate rich in activated lipolytic and proteolytic enzymes, vasoactive substances and several other pro-inflammatory mediators collect in over 60% of the patients with severe acute pancreatitis. On the basis of favourable animal experiments early percutaneous or surgical peritoneal lavage with or without the addition of antiproteases has been carried out in human acute pancreatitis. The rationale behind this procedure was the washout of potential toxic mediators from the peritoneal cavity before they gain access to the systemic circulation. Contrary to animal and uncontrolled human data no prospective randomized study could ever demonstrated a significant effect of peritoneal lavage neither in the prevention and control of remote organ failures or in early mortality and ultimate survival after severe acute pancreatitis in humans. Differences between experimentally-induced pancreatitis, difference in the timing of the initiation of lavage and a type II error in controlled human studies may account for the discrepancy in the outcome between these studies. Anyway, this disparity should raise the question as whether the peritoneal cavity acts simply as a reservoir or as a route of transfer of toxic mediators to the systemic circulation. Although data are scarce, conflicting and limited to animal experiments and to a few molecules, peripancreatic veins and lymphatics seem to be the major routes of transfer whereas transperitoneal absorption is trivial. Nevertheless early peritoneal aspiration of ascitic fluid in acute pancreatitis and measurement of trypsinogen activation peptides may be used as a means of severity assessment and identification of pancreatic necrosis. This implies that even if not taking part actively in the emergence of remote organ failures ascitic fluid may reflect the peripancreatic necrotizing process. So careful comparative analysis of peritoneal exudate, plasma and lymph with regards to putative mediators of local and remote injury may provide essential pathophysiological clues. At the time of trials of antimediator therapy early in the attack this kind of insight is essential.

Skin signs in the diagnosis of thallium poisoning.

A 45-year-old man developed a painful and rapidly progressive sensory-motor polyneuropathy associated with confusion and convulsions. This resulted in hypoventilation and led to respiratory failure and coma. A rapid and diffuse alopecia occurred after 3 weeks in the intensive care unit. Examination of hair roots under polarized light detected dystrophic anagen hairs with dark bands caused by empty spaces in the disorganized cortex. These dark zones were originally reported in patients with thallium poisoning and a toxicological investigation confirmed thallium exposure. The classical systemic symptoms and the various dermatological signs are reviewed, and the origins of contamination and physiopathology discussed.

Severe acute pancreatitis: pathophysiologic mechanisms underlying pancreatic necrosis and remote organ damage.

Despite advances in surgical and intensive care the mortality of severe acute pancreatitis still ranges between 10 and 20%. Fundamentally, the severity of acute pancreatitis, both in term of propensity and intensity of locoregional and remote complications, relies on the development of regional necrosis, the extent of the necrotizing process and the bacterial contamination of these necrotic areas. Intraacinar activation of pancreatic enzymes, overstimulation of inflammatory effector cells and vascular mechanisms are the 3 inter-related factors, acting sequentially to promote the severity of the inflammatory reaction, the ensuing necrosis and the emergence of locoregional complications. Numerous toxic substances, including inflammatory mediators, are released by this inflammatory retroperitoneal necrotizing process, gain access to the systemic circulation and mediate remote organ dysfunctions. Nowadays, pancreatic infection whose occurrence is mainly dependent upon the volume of necrosis and secondary bacterial translocation from the gut, accounts for 80% of the mortality in acute pancreatitis. The understanding of the pathophysiologic mechanisms underlying the inflammatory necrotizing process is critical so that the extent of necrosis can ultimately be limited at an early stage and these patients may be granted a better outcome.

[Prognosis and intensive care of severe acute pancreatitis]. / Pronostic et réanimation des pancréatites aiguës sévères.

Severe acute pancreatitis is morphologically characterized by an extensive and prolonged pancreatic and retroperitoneal inflammation with surimposed patchy or generalized areas of necrosis and hemorraghe in the pancreas and surrounding tissues. Clinical hallmarks include the early development of remote organ dysfunctions, notably cardiorespiratory failure and the late emergence of local complications (hemorraghe, acute pseudocyst and, most importantly, infection). The severity of the attack and the outcome of the patient are critically dependent on the presence and the extent of regional necrosis and are closely related to the casual bacterial contamination of these devitalized areas. The early identification of severe episodes is of therapeutic interest. This prognostic staging is best achieved with a combination of a set of clinical and laboratory data, initial CT findings and single biochemical indicators. Sequential assessment of severity, using biochemical markers and morphological data, is mandatory in order to monitor the fate of regional necrosis. Intensive care treatment includes supportive care of distant organ failures, prophylactic antibiotics and nutritional support.

Significance of pathologic oxygen supply dependency in critically ill patients: comparison between measured and calculated methods.

OBJECTIVE: oxygen supply dependency at normal or high oxygen delivery rate has been increasingly proposed as a hallmark and a risk factor in critical illnesses. We hypothesized that as far as an adequate oxygen delivery is provided, oxygen consumption, when determined by indirect calorimetry, is not dependent on oxygen delivery in critically ill patients whereas calculated oxygen consumption is associated with artefactual correlation of oxygen consumption and delivery. DESIGN: oxygen delivery, oxygen consumption and their relationship were analyzed prospectively. Metabolic data gained from both measured and calculated methods were obtained simultaneously before and after volume loading. SETTING: the study was completed in the intensive care unit as part of the management protocol of the patients. PATIENTS: 32 consecutive patients entered the study and were divided into 3 groups according to a clinical condition known to favour oxygen supply dependency: sepsis syndrome, adult respiratory distress syndrome and acute primary liver failure. INTERVENTION: the rise in oxygen delivery was obtained by colloid infusion (oxygen flux test) performed in hemodynamically and metabolically stable patients. All were mechanically ventilated. No change in therapy was allowed during the test. MEASUREMENTS AND RESULTS: oxygen consumption was simultaneously evaluated by calculation (Fick Principle) and direct measurement using indirect calorimetry. Oxygen delivery was derived from the cardiac output (thermodilution) and arterial content of oxygen. Oxygen supply dependency was considered while observing an increase in oxygen delivery greater than 45 ml/min.m2. Irrespective of patient's clinical diagnosis and outcome, measured oxygen uptake remained unaltered by volume infusion whereas both oxygen delivery and calculated oxygen consumption increased significantly. Arterial lactate level > 2 mmol/l and measured oxygen extraction ratio > 25% failed to identify oxygen supply dependency when measured data were considered. CONCLUSION: analysis of oxygen uptake, when measured by indirect calorimetry, failed to substantiate oxygen supply dependency in the vast majority of the critically ill patients irrespective of diagnosis and outcome. Mathematical coupling of shared variables accounted for the correlation between oxygen delivery and calculated oxygen consumption.

Evaluation of oxygen uptake and delivery in critically ill patients: a statistical reappraisal.

OBJECTIVE: The evaluation of oxygen consumption (VO2) and oxygen delivery (DO2) has gained increasing importance in the monitoring of critically ill patients. They can be obtained from either direct measurements or by indirect calculations based on the Fick principle. However the choice between these two approaches remains controversial. The aim of the study was to investigate whether these 2 methods provide similar results, and if not, to define the best one in terms of reproducibility. DESIGN: Oxygen delivery and oxygen consumption were prospectively analyzed in 171 consecutive critically ill patients. Metabolic data were obtained simultaneously. SETTING: The study was completed in the intensive care unit as part of the management of the patients studied. PATIENTS: A first "group" of 279 evaluations was carried out in 73 consecutive critically ill patients. The results were subsequently validated by 423 observations performed in the 98 following patients. INTERVENTIONS: Before and during each evaluation, the patients were kept in stable hemodynamic and metabolic conditions. All were mechanically ventilated. MEASUREMENTS AND RESULTS: VO2 was evaluated by calculation (Fick principle) and direct measurement using indirect calorimetry. Cardiac output was both measured by the thermodilution technique and calculated (Fick principle) and the data were used for the evaluation of the directly measured and indirectly calculated DO2. For both VO2 and DO2 the agreement between direct and indirect evaluations was not satisfactory. Differences as great as 55 ml/min.m2 and 267 ml/min.m2 between simultaneously measured and calculated VO2 and DO2 respectively may be expected. Finally, the indirect calculated methods were less reproducible than the measured ones. These observations resulted mainly from the cumulative effects of the random errors in the metabolic data entering into the calculation of VO2 and DO2. CONCLUSIONS: Our data suggested that the indirect calculation (Fick equation) and the direct measurement (indirect calorimetry, thermodilution) of both VO2 and DO2 did not provide similar results. Direct measurements are more reproducible methods and must be preferred.

[Hypersensitivity interstitial pneumopathy and ulcero-hemorrhagic rectocolitis: role of methotrexate]. / Pneumopathie interstitielle d'hypersensibilité et rectocolite ulcéro-hémorragique: rôle du methotrexate.

The authors report the case of a 46-year-old man with refractory ulcerative colitis treated with methotrexate who was admitted in the hospital for asthenia, fever, cough and dyspnea. Owing to the development of adult respiratory distress syndrome despite broad spectrum antibiotherapy, the patient was transferred to the intensive care unit. A diagnosis of pneumonitis due to methotrexate was made. Patient's condition improved after discontinuation of the drug, mechanical ventilation, and corticosteroids. The increasing use of methotrexate in several gastroenterological diseases warrants further consideration of the potential devastating side effects of this drug, particularly on the lungs. A review of the literature on this topic is provided in the "discussion" section.

[Clinical evaluation, evolution and intensive care treatment of severe acute pancreatitis]. / Evaluation clinique, évolution et traitement aux soins intensifs des pancréatites aiguës sévères.

Severe acute pancreatitis is morphologically characterized by an intense and necrotizing inflammatory process responsible for early remote organ dysfunctions and late regional complications. Retroperitoneal necrosis has to be identified early by several biological markers and abdominal CT study. A better understanding of the pathophysiological mechanisms underlying the natural history of severe acute pancreatitis, progress in intensive care support and the emergence of new conservative or surgical strategies aimed at removing the necrotic areas and their toxic by-products have led to a dramatic reduction in early and overall mortality for the patient with this disease.

Atrial fibrillation in patients with an accessory pathway: importance of the conduction properties of the accessory pathway.

To investigate how the electrophysiologic properties of the accessory pathway affect the occurrence of atrial fibrillation in the Wolff-Parkinson-White syndrome, programmed stimulation data of 57 patients with overt pre-excitation and 33 patients with a concealed accessory pathway with documented circus movement tachycardia were reviewed. Atrial fibrillation had occurred spontaneously in 31 (54%) of the 57 patients with the Wolff-Parkinson-White syndrome and in 1 (3%) of the 33 with a concealed accessory pathway (p less than 0.001). Sustained atrial fibrillation was induced in 23 of 31 patients with the Wolff-Parkinson-White syndrome and spontaneous atrial fibrillation (Group A), in 7 of 26 patients with the Wolff-Parkinson-White syndrome without spontaneous atrial fibrillation (Group B) and in 5 of 33 patients with a concealed accessory pathway (Group C). The anterograde effective refractory period of the accessory pathway was shorter in Group A than in Group B (252 versus 297 ms, p less than 0.001). There were no differences among groups in PA interval, right to left atrium conduction time, cycle length of tachycardia and atrial and retrograde accessory pathway effective refractory period. Atrial fibrillation is more frequent in patients with the Wolff-Parkinson-White syndrome than in those with a concealed accessory pathway. Patients with overt pre-excitation and atrial fibrillation have a shorter anterograde accessory pathway refractory period. It seems therefore that the anterograde rather than the retrograde conduction properties of the accessory pathway are the critical determinants of atrial fibrillation in the Wolff-Parkinson-White syndrome.

[Respiratory complications in severe acute pancreatitis]. / Les complications respiratoires de la pancréatite aiguë sévère.

The two basic mechanisms underlying most of the pleuropulmonary complications of severe acute pancreatitis include pulmonary atelectasis and alveolar flooding. Like in any abdominal catastrophe, pleural effusion and limited diaphragmatic excursion due to pain and intestinal atony are the main factors responsible for alveolar collapse and secondary infection. Physical therapy and needle pleural evacuation are the cornerstones of management. Owing to its pathophysiologic mechanisms adult respiratory distress syndrome is peculiar to acute pancreatitis. Alveolar capillary membrane injury is related to pancreatic necrosis, to its regional extent and to the subsequent over-amplification of the inflammatory reaction. Diversion of those potential mediators of the syndrome either surgically or by thoracic duct drainage is essential in order to improve survival in these patients.

Scintigraphy with Indium-labelled leukocytes in acute pancreatitis.

The authors assessed the clinical and prognostic value of abdominal (ASCI) and pulmonary (PSCI) scintiscans with 111Indium-labelled leukocytes in the early phase of acute pancreatitis. A grading scale was constructed for both ASCI (scored 0 to 3) and PSCI (scored 0 to 2) according to the intensity of isotope fixation versus adjacent structures. Results were compared in accordance to the presence or absence of a Ranson's score greater than or equal to 3, the presence or absence of respiratory failure and of late pancreatic complications. ASCI showed an important lack of specificity making its use uninteresting. PSCI revealed a very significant correlation with evaluation by Ranson's score and appears to have a high sensitivity and specificity to evaluate the patients who will develop ARDS or risk of ARDS. This demonstrates the pathophysiological role of leukocytes in the early phase of severe acute pancreatitis. The test might also be a reliable test for the assessment of therapeutic efficiency in acute pancreatitis.

Primary infection of ascitic fluid with Clostridium difficile.

A case of a primary infection of ascitic fluid with a toxigenic strain of Clostridium difficile is described. The strain belonged to the serogroup H which is often implicated in pseudomembranous colitis. Nevertheless, our patient did not have any sign of colitis or diarrhoea before the ascitic infection. She was successfully treated by the intravenous administration of metronidazole but relapsed a few weeks later. A similar strain of serogroup H was again isolated.

Adult respiratory distress syndrome and miliary tuberculosis.

Miliary tuberculosis presenting as fatal adult respiratory distress syndrome is reported in a 69-year-old man. Idiopathic thrombocytopenic purpura led to splenectomy 2 years before admission and was currently treated with corticosteroids. Moderate dyspnea, a dry cough and weight loss were presenting clinical features, preceding respiratory failure by only a few days. In these patients with atypical symptoms early diagnosis and prompt antituberculous chemotherapy are life-saving. The diagnosis of miliary tuberculosis should be systematically considered in ARDS of unknown origin.