Life-threatening hemophagocytic syndrome triggered by disseminated toxoplasmosis in a young patient with previously unknown AIDS.

Hemophagocytic syndrome is a rare life-threatening disorder that can be triggered by various conditions such as HIV infection and opportunistic agents. We report a case of disseminated toxoplasmosis complicated with severe hemophagocytic syndrome and revealing an unknown acquired immunodeficiency syndrome. The patient presented with multiple organ failure in intensive care unit. Once diagnosed, he benefitted from etoposide infusion, administration of specific anti-toxoplasmosis treatments and secondary antiretroviral therapy. He was alive at intensive care unit discharge and returned home with little sequalae. This case illustrates both the importance of rapid investigations of hemophagocytic syndrome etiologies in HIV positive patients and the necessity to prompt etoposide and specific treatments in order to improve potentially dramatic outcomes.

[Amniotic fluid embolism: report of the successful outcome of a case with inaugural cardiac arrest and early DIVC complicated by hemoperitoneum of iatrogen origin and bleeding of an hepatic adenoma]. / Embolie amniotique: à propos de l'issue favorable d'un cas avec arrêt cardiaque inaugural et CIVD précoce compliquée d'un hémopéritoine d'origine iatrogène et d'un saignement sur un adénome hépatique.

Amniotic fluid embolism is a relatively rare clinical entity and with difficult medical recognition. However, it is the second leading cause of maternal mortality. We report here the case of a 32-year-old patient who underwent elective caesarean section complicated by an amniotic fluid embolism with cardiac arrest. The presence of a major disseminated intravascular coagulation favored the occurrence of a retroperitoneal hematoma of iatrogenic origin on attempt of femoral venous catheterization and that of hemoperitoneum on bleeding of an hepatic adenoma. The diagnostic of amniotic fluid embolism was confirmed by the presence of amniotic cells in the bronchoalveolar lavage. The patient survived without sequelae.

High flow nasal oxygen in acute respiratory failure.

Use of high flow nasal cannula oxygen (HFNC) is increasingly popular in adult ICUs for patients with acute hypoxemic respiratory failure. This is the result of the successful long-term use of HFNC in the neonatal field and recent clinical data in adults indicating beneficial effects of HFNC over conventional facemask oxygen therapy. HFNC rapidly alleviates symptoms of respiratory distress and improves oxygenation by several mechanisms, including deadspace washout, reduction in oxygen dilution and in inspiratory nasopharyngeal resistance, a moderate positive airway pressure effect that may generate alveolar recruitment and an overall greater tolerance and comfort with the interface and the heated and humidified inspired gases. Indications of HFNC are broad, encompassing most if not all causes of acute hypoxemic respiratory failure. HFNC can also provide oxygen during invasive procedures, and be used to prevent or treat post-extubation respiratory failure. HFNC may also alleviate respiratory distress in patients at a palliative stage. Although observational studies suggest that HFNC might reduce the need for intubation in acute hypoxemic respiratory failure; such a reduction has not yet been demonstrated. Beyond this potential additional effect on outcome, the evidence already published argues in favor of the large use of HFNC as first line therapy for acute respiratory failure.

Ventilator-induced lung injury.

During mechanical ventilation, high end-inspiratory lung volume (whether it be because of large tidal volume (VT) and/or high levels of positive end-expiratory pressure) results in a permeability type pulmonary oedema, called ventilator-induced lung injury (VILI). Previous injury sensitises lung to mechanical ventilation. This experimental concept has recently received a resounding clinical illustration after a 22% reduction of mortality was observed in acute respiratory distress syndrome patients whose VT had been reduced. In addition, it has been suggested that repetitive opening and closing of distal units at low lung volume could induce lung injury but this notion has been challenged both conceptually and clinically after the negative results of the Acute Respiratory Distress Syndrome clinical Network Assessment of Low tidal Volume and Elevated end-expiratory volume to Obviate Lung Injury (ARDSNet ALVEOLI) study. Experimentally and clinically, involvement of inflammatory cytokines in VILI has not been unequivocally demonstrated. Cellular response to mechanical stretch has been increasingly investigated, both on the epithelial and the endothelial side. Lipid membrane trafficking has been thought to be a means by which cells respond to stress failure. Alterations in the respiratory system pressure/volume curve during ventilator-induced lung injury that include decrease in compliance and position of the upper inflection point are due to distal obstruction of airways that reduce aerated lung volume. Information from this curve could help avoid potentially harmful excessive tidal volume reduction.

Production of inflammatory cytokines in ventilator-induced lung injury: a reappraisal.

We investigated the production of proinflammatory cytokines by the lung during high mechanical stretch in vivo. To do this, we subjected rats to high-volume (42 ml/kg tidal volume [VT]) ventilation for 2 h. The animals developed severe pulmonary edema and alveolar flooding, with a high protein concentration in bronchoalveolar lavage fluid (BALF). The animals' BALF contained no tumor necrosis factor (TNF)-alpha, negligible amounts of interleukin (IL)-1beta, and less than 300 pg/ml of the chemokine macrophage inflammatory protein (MIP)-2, an amount similar to that found in rats ventilated with 7 ml/kg VT. Systemic cytokine levels were below the detection threshold. Because isolated lungs have been shown to produce high levels of proinflammatory cytokines when ventilated with a similarly high VT for the same duration (Tremblay, et al. J Clin Invest 1997;99:944-952), we reconsidered this specific issue. We ventilated isolated, unperfused rat lungs for 2 h with 7 ml/kg or 42 ml/kg VT, or maintained them in a statically inflated state. Negligible amounts of TNF-alpha were found in the BALF whatever the ventilatory condition applied. The BALF IL-1beta concentration was slightly elevated and higher in lungs ventilated with 42 ml/kg VT than in those ventilated with 7 ml/kg VT or in statically inflated lungs (p < 0.05). The BALF MIP-2 concentration was moderately elevated in all isolated lungs (200 to 300 pg/ml), and was slightly higher (p < 0.05) in lungs ventilated with 42 ml/kg VT. After lipopolysaccharide (LPS) challenge, high levels of TNF-alpha, IL-1beta, and MIP-2 were found in the animals' plasma before the lungs were removed. Negligible amounts of TNF-alpha and IL-1beta were retrieved from the BALF of statically inflated lungs. The concentrations of TNF-alpha and IL-1beta were higher in the BALF of ventilated lungs (p < 0.001). The TNF-alpha level did not differ with the magnitude of VT, whereas the level of IL-1beta was significantly higher in BALF of lungs ventilated with 42 ml/kg VT (p < 0.01). The MIP-2 concentrations were similar for the two ventilatory conditions. These results suggest that ventilation that severely injures lungs does not lead to the release of significant amounts of TNF-alpha or IL-1beta by the lung in the absence of LPS challenge but may increase lung MIP-2 production.