Intensive care medicine
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Intensive care medicine · Jan 1994
Low intramucosal pH is associated with failure to acidify the gastric lumen in response to pentagastrin.
To determine if low gastric intramucosal pH is associated with impaired secretion of gastric acid after pentagastrin stimulation. ⋯ Some critically ill patients with low gastric intramucosal pH appear to have an impaired ability to acidify the gastric lumen in response to pentagastrin.
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Intensive care medicine · Jan 1994
Comparative StudyAdditive effect on gas exchange of inhaled nitric oxide and intravenous almitrine bismesylate in the adult respiratory distress syndrome.
To assess the additive effect of inhaled nitric oxide (NO) and intravenous almitrine bismesylate (ALM) on gas exchange. ⋯ NO + ALM had additive effects on gas exchange while decreasing MPAP in patients with ARDS. The effects of NO alone were small and non significant, except in a subgroup of 7 patients in whom the combination of both therapies had the more pronounced results.
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Intensive care medicine · Jan 1994
Case ReportsRespiratory syncytial virus triggered adult respiratory distress syndrome in infants: a report of two cases.
Two infants with severe respiratory syncytial virus infection which resulted eventually in classical adult respiratory distress syndrome (ARDS) are presented. Both infants had severe apneic spells, necessitating intubation and mechanical ventilation (MV). ⋯ Assessment of respiratory system mechanics (single breath occlusion technique) revealed severe restrictive disease in both cases. The first patient recovered with residual restrictive changes determined during a follow-up 2.5 months later, whereas the second infant died because of ARDS, pulmonary interstitial emphysema and hypoxemic hypoxia.
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Intensive care medicine · Jan 1994
Comparative StudyA new therapy of post-trauma brain oedema based on haemodynamic principles for brain volume regulation.
To evaluate a new therapy of posttraumatic brain oedema, with the main concept that opening of the blood-brain barrier upsets the normal brain volume regulation, inducing oedema formation. This means that transcapillary fluid fluxes will be controlled by hydrostatic capillary and colloid osmotic pressures, rather than by crystalloid osmotic pressure. If so, brain oedema therapy should include reduction of hydrostatic capillary pressure and preservation of normal colloid osmotic pressure. ⋯ The results indicate that the therapy should focus on extracellular rather than intracellular oedema and that ischemia is not the main triggering mechanism behind oedema formation. We suggest that our therapy is superior to conventional therapy by preventing herniation during the healing period of the blood-brain barrier.