Endobronchial stenting on VV-ECMO in a 6-month-old girl with right lung agenesis and severe stenosis of the left main bronchus.

INTRODUCTION: Lung agenesis is a rare disorder with a variable, but potentially very bad clinical course. It necessitates complex clinical management, especially in life-threatening situations. CASE REPORT: We describe a case of a 6-month-old girl with right lung agenesis who required venovenous extracorporeal membrane oxygenation (VV-ECMO) due to pneumonia complicated by exacerbated previously diagnosed left main bronchus stenosis. The stenosis was resolved by endobronchial intervention and X-ray-guided stent insertion, which enabled weaning from ECMO and was aimed at preventing such a life-threatening respiratory failure in the future. Unfortunately, even with the functional stent, the baby died 2 months post-procedure due to unresolvable bronchial spasms. DISCUSSION: Despite high endobronchial stenting-related mortality in children, in cases where no effective pharmacological or surgical alternatives exist, stenting may be safely performed during VV-ECMO support and be a viable option to overcome critical respiratory failure caused by bronchial stenosis.

Ionized Magnesium and Regional Citrate Anticoagulation for Continuous Renal Replacement Therapy.

BACKGROUND: The regional citrate anticoagulation (RCA) induces changes in total (Catot) and ionized (Ca2+) calcium. As of now, we do not have much information about parallel changes of total (Mgtot) and ionized (Mg2+) magnesium. METHODS: The authors compared changes of Mg2+ and Mgtot with changes of Ca2+ and Catot in 32 critically ill patients on 4% trisodium citrate (4% TSC) with calcium-free fluids. RESULTS: The median continuous venovenous hemodiafiltration balance of Mgtot was -0.91 (-1.18 to -0.53) mmol/h compared to the median balance of Catot 0.86 (0.08-1.55) mmol/h. Postfilter Mg2+ decreased by 68.3% (70.8-65.6) in parallel (r = 0.41, p = 0.03) to decrease of postfilter Ca2+ (by 70.2% (73.0-66.1)) and was significantly related to the postfilter Ca2+ (r = 0.50, p < 0.001). The decrease of prefilter to postfilter Ca2+ correlated to a dosage of 4% TSC per blood flow (r = 0.37, p = 0.04). CONCLUSIONS: The loss of Mgtot during RCA is not covered by magnesium concentration in ordinary dialysis/substitution fluid and may lead to the depletion of total body magnesium. The postfilter Mg2+ is significantly related to the postfilter Ca2+. Video Journal Club "Cappuccino with Claudio Ronco" at http://www.karger.com/?doi = 440972.

The effects of a novel calcium-free lactate buffered dialysis and substitution fluid for regional citrate anticoagulation--prospective feasibility study.

BACKGROUND: Testing metabolic effects of a novel calcium-free, magnesium, phosphate and lactate containing solution (Lactocitrate) in combination with citrate anticoagulation. METHODS: Patients on CRRT (2,000 ml/h, blood flow (Qb) 100 ml/min, trisodium citrate (4% TSC)) with arterial lactate <3 mmol/l were included. At start, bicarbonate-buffered fluid was changed to Lactocitrate and the substitution of magnesium and phosphorus ceased. At 9 h the Qb was increased to 150 ml/min. At 18 h the CRRT dosage was increased to 3,000 ml/h. RESULTS: In 22 CVVHDF patients and another 23 on CVVH the pH, aHCO3 and Na (all p > 0.05) showed no significant changes regardless of the increased dosage of 4% TSC at 9 h (p < 0.001). Mgtot and phosphorus stabilised within normal range. Arterial lactate increased to 1.9 (1.6-2.6) mmol/l at 3,000 ml/h, p < 0.001). Citrate- and lactate-related energetic gains were up to 74 (61-86) kJ/h. CONCLUSIONS: The fluid performed well within ordinary CRRT dosage and Qb up to 150 ml/min. Lactate levels mildly increased and no magnesium and phosphorus replenishments were necessary.

Bioenergetic gain of citrate anticoagulated continuous hemodiafiltration--a comparison between 2 citrate modalities and unfractionated heparin.

PURPOSE: To determine bioenergetic gain of 2 different citrate anticoagulated continuous hemodiafiltration (CVVHDF) modalities and a heparin modality. MATERIALS AND METHODS: We compared the bio-energetic gain of citrate, glucose and lactate between 29 patients receiving 2.2% acid-citrate-dextrose with calcium-containing lactate-buffered solutions (ACD/Ca(plus)/lactate), 34 on 4% trisodium citrate with calcium-free low-bicarbonate buffered fluids (TSC/Ca(min)/bicarbonate), and 18 on heparin with lactate buffering (Hep/lactate). RESULTS: While delivered CVVHDF dose was about 2000 mL/h, total bioenergetic gain was 262 kJ/h (IQR 230-284) with ACD/Ca(plus)/lactate, 20 kJ/h (8-25) with TSC/Ca(min)/bicarbonate (P < .01) and 60 kJ/h (52-76) with Hep/lactate. Median patient delivery of citrate was 31.2 mmol/h (25-34.7) in ACD/Ca(plus)/lactate versus 14.8 mmol/h (12.4-19.1) in TSC/Ca(min)/bicarbonate groups (P < .01). Median delivery of glucose was 36.8 mmol/h (29.9-43) in ACD/Ca(plus)/lactate, and of lactate 52.5 mmol/h (49.2-59.1) in ACD/Ca(plus)/lactate and 56.1 mmol/h (49.6-64.2) in Hep/lactate groups. The higher energy delivery with ACD/Ca(plus)/lactate was partially due to the higher blood flow used in this modality and the calcium-containing dialysate. CONCLUSIONS: The bioenergetic gain of CVVHDF comes from glucose (in ACD), lactate and citrate. The amount substantially differs between modalities despite a similar CVVHDF dose and is unacceptably high when using ACD with calcium-containing lactate-buffered solutions and a higher blood flow. When calculating nutritional needs, we should account for the energy delivered by CVVHDF.

Concomitant use of beta-1 adrenoreceptor blocker and norepinephrine in patients with septic shock.

BACKGROUND: Betablockade has been shown to have cardioprotective effects in patients under perioperative stress. Besides animal model of septic shock and a small cohort of septic patients, these benefits have not been studied in septic shock patients who require norepinephrine administration. METHODS: After correction of preload, an esmolol bolus (0.2-0.5 mg/kg) followed by continuous 24 h infusion was administered in septic patients with sinus or supraventricular tachycardia (HR > 120/min). Exclusion criteria were severe LV systolic dysfunction, atrioventricular blockade and norepinephrine infusion at rates over 0.5 mg/kg/min. Monitoring with echocardiography and pulmonary artery catheter before, at 2, 6, 12, 24 h following the start and 6 h after ceasing of the esmolol drip. Patients were maintained normovolemic throughout the study and adjustments of concomitant norepinephrine infusion rates were made as required. RESULTS: Ten septic patients (mean age 54.4 ± 18.7), APACHE II 21.5 ± 6.2, CRP 275 ± 78 mg/l, procalcitonin 14.5 ± 10.1 mg/l, were given esmolol drip of 212.5 ± 63.5 mg/h at start to 272.5 ± 89.5 mg/h at 24 h. Heart rate decreased from mean 142 ± 11/min to 112 ± 9/min (p < 0.001) with parallel insignificant reduction of cardiac index (4.94 ± 0.76 to 4.35 ± 0.72 l/min/m(2)). Stroke volume insignificantly increased from 67.1 ± 16.3 ml to 72.9 ± 15.3 ml. No parallel change of pulmonary artery wedge pressure was observed (15.9 ± 3.2 to 15.0 ± 2.4 mmHg) as well as no significant changes of norepinephrine infusion (0.13 ± 0.17 to 0.17 ± 0.19 mg/kg/min), DO(2), VO(2), OER or arterial lactate. CONCLUSIONS: Saving the heart 30 beats/min did not demonstrate adverse impact on global haemodynamics in rates above 110/min. Using well titratable betablocker seems to be safe and cardioprotective in septic shock patients with high cardiac output.

Local metabolism of glucocorticoids and its role in rat adjuvant arthritis.

11beta-Hydroxysteroid dehydrogenase 1 (11HSD1) regulates local glucocorticoid activity and plays an important role in various diseases. Here, we studied whether arthritis modulates 11HSD1, what is the role of pro-inflammatory cytokines in this process and whether altered local metabolism of glucocorticoids may contribute to the feedback regulation of inflammation. Adjuvant arthritis increased synovial 11HSD1 mRNA and 11-reductase activity but treatments with tumor necrosis factor alpha (TNF-alpha) and interleukin 1beta (IL-1beta) antagonists etanercept and anakinra reduced 11HSD1 upregulation. Treatment with carbenoxolone, an 11HSD inhibitor, increased expression of TNF-alpha, cyclooxygenase 2, and osteopontin mRNA without any changes in the plasma levels of corticosterone. Similar changes were observed when arthritic rats were treated with RU486, an antagonist of GR. This study suggests that arthritis upregulates synovial 11HSD1, this upregulation is controlled by TNF-alpha and IL-1beta and that the increased supply of local corticosterone might contribute to feedback regulation of inflammation.

11beta-hydroxysteroid dehydrogenase 1 and 2 expression in colon from patients with ulcerative colitis.

BACKGROUND AND AIM: 11beta-hydroxysteroid dehydrogenase (11betaHSD) is an enzyme responsible for the interconversion of active 11beta-hydroxysteroids (cortisol) into biologically inactive 11-oxosteroids (cortisone). The isoform 11betaHSD1 operates predominantly as a reductase converting cortisone to cortisol, whereas 11betaHSD2 catalyzes oxidation of cortisol to cortisone. This mechanism of peripheral metabolism of glucocorticoids has been suggested to be involved in increasing the availability of anti- inflammatory glucocorticoids as a response to inflammatory stimuli. The aim of this study therefore was to investigate the impact of inflammatory bowel disease on the expression of colonic 11betaHSD1 and 11betaHSD2. METHODS: Quantitative real-time RT-PCR was used to assess messenger RNA for 11betaHSD1 and 11betaHSD2 in bioptic samples taken from patients with ulcerative colitis and in healthy controls, and in colon of rats with colitis induced by dextran sulfate sodium (DSS). Rat colonic fragments were used for assessment of local metabolism of glucocorticoids. RESULTS: In both human and rat specimens colitis up-regulated the expression of colonic 11betaHSD1 mRNA and down-regulated 11betaHSD2 mRNA. A similar pattern was observed at the level of local metabolism of corticosterone. Oxidation of corticosterone to 11-dehydrocorticosterone was decreased and reduction of 11-dehydrocorticosterone to corticosterone was increased in colonic tissue of rats with DSS-colitis. CONCLUSIONS: Colonic inflammation induces local glucocorticoid activation via 11betaHSD1 and impairs glucocorticoid inactivation via 11betaHSD2. The observed changes indicate a role for local metabolism of glucocorticoids in the control of colonic inflammation.