[Propofol infusion syndrome]. / Le syndrome de perfusion du propofol.

OBJECTIVE: Propofol is commonly used for sedation of children or adult patients in intensive care unit as an alternative to benzodiazepines for the long-term sedation of mechanically ventiled patient. However, the life-threatening complication of propofol-infusion syndrome (PRIS) may in some case occur. The objective of this article is to review the clinical features, physiopathology and management of PRIS. DATA SOURCES: A PubMed database research in English and French languages published until December 2008. Keywords were propofol, propofol infusion syndrome (PRIS), rhabdomyolysis, heart failure, arrhythmias, metabolic acidosis, brain injury, sedation, intensive care. DATA SYNTHESIS: PRIS is a rare and potentially lethal complication, especially if there's no early identification of the syndrome. The physiopathology of PRIS mechanism remains unclear, however a dysfunction of mitochondrial respiratory chain could be involved and potential genetic factor may account. Clinical features consist of arrhythmias, metabolic acidosis, lipemia, rhabdomyolisis, myoglobinuria. PRIS has been described classically in children and adults undergoing a long term infusion with propofol (more than 48 hours) at doses higher than 4 mg/kg per hour. However, it can be observed with lower doses and after shorter duration of sedation. Steroids, vasopressors and low carbohydrate intake act as triggering factors. Early recognition of the syndrome improve patient's outcome. Propofol infusion must be avoided in susceptible patients and another sedative agent should be considered. When using prolonged sedation with propofol, arrhythmia and serum triglyceridemia level should be monitored.

Intrapericardial teratoma in newborn babies.

We report two cases of intra pericardial tumor with pericardial effusion, diagnosed in utero by echocardiography at 21 and 28 weeks of gestation. Both fetuses underwent an intra uterine pericardiocentesis to treat a hydrops fetalis. Surgical resection of the tumor was undertaken immediately after birth and histological description reported cystic teratoma. Both babies had a favorable post operative course.

[Use of oral sildenafil (Viagra) in pulmonary hypertension after cardiac pediatric surgery]. / Intérêt du sildénafil (Viagra) per os en cas d'hypertension artérielle pulmonaire après chirurgie cardiaque pédiatrique.

Pulmonary hypertension remains a major cause of morbidity after cardiac surgery, although inhaled nitric oxide (iNO) was shown to have clinical benefit. Some patients are dependent on iNO, increasing the length of hospital stay. The authors report a case of a girl, nine years old (17 kg), with mitral insufficiency, atrial septal defect and pulmonary hypertension (80% of systemic pressure). Following cardiac surgery, pulmonary hypertension persisted and iNO could not be withdrawn. Sildenafil was administered orally (1,5mg x kg(-1), every 4 h) at the 15th postoperative day and iNO could be withdrawn within 24h with clinical improvement.

Effects of interleukin-10 on monocyte/endothelial cell adhesion and MMP-9/TIMP-1 secretion.

OBJECTIVE: Monocyte adhesion to endothelial cells and subsequent secretion of matrix metalloproteinases (MMPs) by activated macrophages are key events in arteriosclerosis and restenosis. We tested the hypothesis that interleukin-10 (IL-10), a potent anti-inflammatory cytokine, inhibits monocyte-endothelial cell interactions. METHODS: The effect of IL-10 on monocyte/endothelial cell adhesion, as well as on the expression of MMP-9 and the tissue inhibitor of MMP-9, TIMP-1, were first tested in vitro in coculture systems. In addition, we used an ex vivo binding assay to study the inhibitory effect of IL-10 on monocyte adhesion to carotid arteries obtained from either normal, or L-nitro arginine-methyl ester (L-NAME)-treated rats. The effect of IL-10 on the expression of monocyte adhesion molecules (CD18 and CD62-L) was studied by flow cytometry. RESULTS: IL-10 (150 ng/ml) inhibits monocyte adhesion to endothelial cells (by 35%) and to carotid arteries (by 40 and 50%, in normal and L-NAME-treated rats, respectively), via direct modulation of the expression of CD18 and CD62-L. Moreover, IL-10 dose-dependently decreases MMP-9 activity and increases TIMP-1 levels in coculture systems, both at the transcriptional level. CONCLUSIONS: Our results suggest that IL-10 is an important modulator of monocyte-endothelial cell interactions.

Molecular plasticity of vascular wall during N(G)-nitro-L-arginine methyl ester-induced hypertension: modulation of proinflammatory signals.

It has previously been reported that hypertension induced by the chronic blockade of NO production is characterized by a proinflammatory phenotype of the arterial wall associated with a periarterial accumulation of inflammatory cells. In the present study, the cellular and molecular mechanisms involved in the luminal and perivascular accumulation of inflammatory cells were evaluated in the aortas of N(G)-nitro-L-arginine methyl ester (L-NAME)-treated rats. Because the medial layer remains intact, putative markers of the resistance of the vascular wall to cell migration and to oxidative stress were also explored. For this purpose, monocyte adhesion, cytokine expression, superoxide anion production, and nuclear factor-kappa B (NF-kappa B) activation were assessed in the aortas of L-NAME-treated rats. Expressions of tissue inhibitor of metalloproteinases-1 (TIMP-1) and heme oxygenase-1 (HO-1) in the aortic wall were also studied as possible markers of such resistance. Chronic blockade of NO production increased ex vivo monocyte adhesion to the endothelium, increased the production of superoxide anions, and activated the NF-kappa B system. In concert with this modification of the redox state of the vascular wall in L-NAME-treated rats, the expression of proinflammatory cytokines interleukin-6, monocyte chemoattractant protein-1, and macrophage colony-stimulating factor was increased. In parallel, expressions of both TIMP-1 and HO-1 were increased. All these changes were prevented by treatment with an angiotensin-converting enzyme inhibitor (Zofenopril). Hypertension associated with a proinflammatory phenotype of the vascular wall induced by blockade of NO production could be due to an increase in oxidative stress, which, in turn, activates the NF-kappa B system and increases gene expression. In parallel, the arterial wall overexpresses factors such as TIMP-1 and HO-1, which could participate in the resistance to cell migration and oxidative stress.

Tricuspid insufficiency after blunt chest trauma in a nine-year-old child.

The case of a traumatic tricuspid insufficiency in a child, due to an anterior and septal leaflet rupture at the annulus level is reported for the first time. The early diagnosis 2 months after the trauma enabled a rapid and simple tricuspid valvuloplasty by laeflet reinsertion on the annulus associated with annuloplasty with a good result 6 months after the repair.