Acute respiratory distress syndrome, the critical care paradigm : what we learned and what we forgot

In the last several years, we definitely learned that the acute respiratory distress syndrome lung is small, nonhomogeneous, and that mechanical ventilation in this baby lung may cause physical damage as well as inflammatory reaction. The clinical benefit of the gentle lung treatment, based on a decrease of global/regional stress and strain into the lung, has been finally proved. However, we forgot the importance of lung perfusion and its distribution in this syndrome and, besides a low tidal volume, we still do not know how to handle the other variables of mechanical ventilation. Measurements of variables as transpulmonary pressure and end expiratory lung volume, for a rational setting of mechanical ventilation, should be introduced in routine clinical practice

A complication of amiodarone infusion

A 76-year-old man underwent an emergency laparotoray for a ruptured abdominal aortic ancurysm After a few days he presented ischemia of the left side of the colon and subsequently atrial fibrillation developed that was treated with Amiodarone. After an intravascular loading dose of 300 mg, he received a maintenance dose of 600 mg daily through a central line access. After 28 days of intravascular drug therapy, a chest X-ray showed a high attenuation homogeneous image in the right part of the mediastinum. A contrast enhanced thoracic and abdominal computed tomography scan showed: a high attenuation intravascular mass in the superior vena cava around the catheter. The catheter was substituted but the intravascular mass remained. The Amiodarone was then given by mouth. The mass spontaneously decreased its size and after three months completely disappeared Due to high iodine content, any deposition of Amiodarone can be detected by a radiological study as a high attenuation image. After reviewing all the drugs infused through the catheter, we did not find any other drugs that contain iodine or other material that could justify the chest X-ray image. We hypothesized that this intravascular mass was due to a deposition of the Amiodarone during the infusion in the central lin

Heat stress : characteristics, pathophysiology and avoidable mistakes

In August 2003 an exceptional heatwave was recorded in Europe. The authors would like to describe 6 patients for which the intensivist was called as a consultant. All patients had a skin temperature >40 degrees C, central nervous system impairment, severe hyponatremia [124.7 mEq/l+/-5.6 (range 117-130)] and severe metabolic acidosis [BE -6.28 mEq/l+/-3.55 (range -9.5-0), HCO3- 17.75 mEq/l+/-3.25 (range 13.4-21.9)]. All patients had decreased platelet count and coagulation abnormalities. Two patients were hypertensive, 4 hypotensive. The heat stress due to the hot environment is characterized by systemic inflammatory response (as in severe sepsis) and hemodynamic impairment (as in hypovolemic shock). The association between hypovolemia and altered microcirculation leads to cell energy failure with metabolic lactic acidosis. The energy failure may induce structural irreversible damage of mitochondria. It is possible to differentiate, during energy failure, the irreversible or reversible condition by volume loading and vasoactive drugs challenge tests. In fact, if the hemodynamic correction is associated with normalization of SvO2 with disappearance of metabolic acidosis, this suggests hemodynamic impairment with intact mitochondrial function. In contrast, if the hemodynamic improvement with normalization of SvO2 is associated and acidosis persists, this suggests irreversible structural mitochondrial damage. The threshold between reversibility and irreversibility is likely time dependent, as suggested by biochemical consideration and by 2 large randomized studies on hemodynamic treatment. The comparative analysis of these 2 studies suggests that the time of intervention may lead to significant differences in mortality. In these patients time is essential