A proinflammatory state is detectable in obese children and is accompanied by functional and morphological vascular changes.

BACKGROUND: Obesity is generally accepted as a risk factor for premature atherosclerosis. Subclinical inflammation as quantified by blood levels of C-reactive protein (CRP) contributes to the development and progression of atherosclerosis. We hypothesized that inflammation in obese children is related to functional and early morphological vascular changes. METHODS AND RESULTS: Blood levels of high sensitivity (hs) CRP, hsIL-6, the soluble intercellular adhesion molecule1 (ICAM-1), vascular cell adhesion molecule (VCAM)-1, and E-selectin were measured in 145 severely obese (body mass index [BMI], 32.2+/-5.8 kg/m2) and 54 lean (BMI, 18.9+/-3.2 kg/m2) children 12+/-4 years old. Flow-mediated dilation (FMD) of the brachial artery and carotid intima-media thickness (IMT) measured by high-resolution ultrasound as markers of early vascular changes were assessed in 92 (77 obese and 15 lean) and 59 (50 obese and 9 lean) children, respectively. Obese children had significantly higher levels of hsCRP, hsIL-6, and E-selectin than healthy controls (4.1+/-4.8 versus 0.9+/-1.5 mg/L, P<0.001 for hsCRP; 1.99+/-1.30 versus 1.42+/-1.01 pg/mL, P=0.05 for hsIL-6; and 78+/-38 versus 59+/-29 ng/mL, P=0.01 for E-selectin). There were no differences in the levels of ICAM-1 and VCAM-1 between groups. Obese children had lower peak FMD response (7.70+/-6.14 versus 11.06+/-3.07%, P=0.006) and increased IMT (0.37+/-0.04 versus 0.34+/-0.03 mm, P=0.03) compared with controls. Morbidly obese children (n=14, BMI 44.1+/-3.9 kg/m2) had highest levels of hsCRP (8.7+/-0.7 mg/L), hsIL-6 (3.32+/-1.1 pg/mL), and E-selectin (83+/-40 ng/mL). CONCLUSIONS: A proinflammatory state is detectable in obese children, which is accompanied by impaired vascular endothelial function and early structural changes of arteries, even in young subjects at risk. It remains to be determined whether high hsCRP in obese children predicts cardiovascular events.

Severe accidental hypothermia with or without hemodynamic instability: rewarming without the use of extracorporeal circulation.

BACKGROUND: The optimal rewarming technique for patients in deep accidental hypothermia with core temperatures below 28 degrees C is not established. Several authors believe that extracorporeal rewarming is essential, especially for patients with hemodynamic instability. Others believe that invasive rewarming ought to be reserved for patients in cardiac arrest. We describe our experience with a strictly conservative technique without the use of invasive rewarming devices in patients with severe accidental hypothermia and a sustained perfusion rhythm. METHODS: A cohort study extending from 1991 to 2000, including all patients received at the emergency department of the University Hospital of Vienna with severe hypothermia, a core temperature of maximum 28 degrees C and no preclinical cardiac arrest. RESULTS: 36 patients with deep hypothermia were included in the study. Their core temperatures ranged from 20.2 degrees C to 28 degrees C; the median temperature was 25.75 degrees C (25th and 75th percentile, 24.2/27.3). Fourteen patients were intoxicated and their multimorbidity was high. All of 19 patients with stable hemodynamics and 14 of 17 patients with unstable hemodynamics were successfully rewarmed to normothermia with warmed infusions, inhalation rewarming and forced air rewarming. The rewarming process took 9.5 hours (8/10.5) and required a volume load of 4820 ml (2735/5770). The rewarming rate was 1.09 degrees C per hour (0.94/1.25). Although 92% of the patients were successfully rewarmed to normothermia, in-hospital mortality was 42%, but was largely related to comorbidity. DISCUSSION: A conservative approach is highly successful in achieving normothermia in patients with deep hypothermia with or without stable hemodynamics. In-hospital mortality of severe accidental hypothermia in urban conditions is high; comorbidity might play a major role. The influence of the rewarming strategy on late in-hospital mortality remains unclear.