Ec Boerma

Sublingual microcirculatory flow is impaired by the vasopressin-analogue terlipressin in a patient with catecholamine-resistant septic shock

For many decades arterial blood pressure regulation has been an important issue in the treatment of septic shock. The pathogenesis of this persistent hypotension is complex and multifactorial, but inability of vascular smooth muscle to contract in the presence of vasoconstrictive agents seems to be a key factor. Many mechanisms have been proposed to account for this failure, including nitric oxide (NO) overproduction and vasopressin deficiency ( 1 ). However, improvement of outcome due to intervention in these mechanisms fails to be reported despite the restoration of blood pressure.

Filter Run Time in CVVH: Pre- versus Post-Dilution and Nadroparin versus Regional Heparin-Protamine Anticoagulation

Background/Aims: To study the effect of different modes of continuous veno-venous haemofiltration (CVVH) on filter run time (FRT). Methods: We studied, in two consecutive prospective, randomised and crossover studies, 16 and 15 patients with acute renal failure during critical illness. Study A compared pre- versus post-dilution, and study B compared regional anticoagulation with heparin (pre-filter) and protamine (post-filter) (HP) versus nadroparin (NP) pre-filter. All CVVH sessions were standardised. Analyses were by Wilcoxon rank sum tests. Results: Study A: During pre-dilution the median FRT was 45.7 vs. 16.1 h in post-dilution CVVH (p = 0.005). The median creatinine clearance during pre-dilution was 33 vs. 45 ml/min in post-dilution (p = 0.001). Study B: During NP, median FRT was 39.5 vs. 12.3 h during HP CVVH (p = 0.045). Conclusions: Pre-dilution CVVH results in the greatest FRT but a lower plasma creatinine clearance compared to post-dilution. Regional anticoagulation with heparin-protamine resulted in a significantly shorter FRT compared to systemic NP anticoagulation.

Hypertonic fluid administration in patients with septic shock: a prospective randomized controlled pilot study.

ABSTRACT We assessed the short-term effects of hypertonic fluid versus isotonic fluid administration in patients with septic shock. This was a double-blind, prospective randomized controlled trial in a 15-bed intensive care unit. Twenty-four patients with septic shock were randomized to receive 250 mL 7.2% NaCl/6% hydroxyethyl starch (HT group) or 500 mL 6% hydroxyethyl starch (IT group). Hemodynamic measurements included mean arterial blood pressure (MAP), central venous pressure, stroke volume index, stroke volume variation, intrathoracic blood volume index, gastric tonometry, and sublingual microcirculatory flow as assessed by sidestream dark field imaging. Systolic tissue Doppler imaging velocities of the medial mitral annulus were measured using echocardiography to assess left ventricular contractility. Log transformation of the ratio MAP divided by the norepinephrine infusion rate (log MAP/NE) quantified the combined effect on both parameters. Compared with the IT group, hypertonic solution treatment resulted in an improvement in log MAP/NE (P = 0.008), as well as an increase in systolic tissue Doppler imaging velocities (P = 0.03) and stroke volume index (P = 0.017). No differences between the groups were found for preload parameters (central venous pressure, stroke volume variation, intrathoracic blood volume index) or for afterload parameters (systemic vascular resistance index, MAP). Hypertonic solution treatment decreased the need for ongoing fluid resuscitation (P = 0.046). No differences between groups were observed regarding tonometry or the sublingual microvascular variables. In patients with septic shock, hypertonic fluid administration did not promote gastrointestinal mucosal perfusion or sublingual microcirculatory blood flow in comparison to isotonic fluid. Independent of changes in preload or afterload, hypertonic fluid administration improved the cardiac contractility and vascular tone compared with isotonic fluid. The need for ongoing fluid resuscitation was also reduced.

A before-after study of multi-resistance and cost of selective decontamination of the digestive tract

Abstract.Background:We compared standard antibiotic use with an antibiotic policy based on selective decontamination of the digestive tract (SDD) for cost and microbiology.Patients and Methods:A 2-year before-after observational study was performed in an 11-bed, mixed medical and surgical intensive care unit (ICU). We included all consecutive patients admitted to the ICU 1 year before and 1 year after institution of SDD (patients admitted within the 2-month SDD run-in period were excluded from analysis). In the year before SDD, 513 patients were treated in the ICU (mean APACHE II 19.5), compared to 529 in the year with SDD (mean APACHE II 19.4).Results:The duration of mechanical ventilation was shorter in the SDD-treated patients (median 3, interquartile range [IQR] 2–7 days vs median 4 days, IQR 2–10, p = 0.03). The total of ICU variable costs, microbiological costs and antibiotic costs were equal in both episodes: €1,171 versus €1,168 per patient). Aerobic gram-negative bacilli (AGNB) and multiresistant AGNB were found less frequently in SDD-treated patients, RR 0.37 (95% CI 0.33–0.42) and RR 0.28 (95% CI 0.19–0.42). Multi-resistant AGNB in tracheal secretions and urine more than 72 hours after admission were completely absent in SDD-treated patients.Conclusion:The overall cost per patient treated during an antibiotic policy including SDD was equal to a policy supporting standard antibiotic care. In addition, duration of ventilation decreased and a trend was shown towards a decreased length of ICU and hospital stay. Less frequently, cultures from organ sites containing AGNB were found during SDD and the number of multi-resistant strains was significantly reduced at organ sites, in particular trachea and urine. Fewer patients were colonized with multi-resistant AGNB but these numbers did not reach statistical significance.

Safety of citrate based hemofiltration in critically ill patients at high risk for bleeding: a comparison with nadroparin.

Purpose To study the incidence and severity of bleeding in high risk critically ill patients during high volume, citrate based continuous veno-venous hemofiltration (CVVH). Design A prospective 1-year observational cohort study comparing citrate based CVVH with nadroparin based CVVH. Procedures Critically ill patients with multiple organ dysfunction and in need of CVVH were observed for bleeding complications during their CVVH sessions. Pre-defined criteria determined that patients were treated with citrate based CVVH in case of active bleeding or increased risk for bleeding. Otherwise nadroparin was used as anticoagulant. Statistical and Outcome Methods The incidence of bleeding complications, the number of transfused blood cell concentrates and the filter-run-time were recorded. Analyses were made by non-parametric tests. Main Findings Fifty-five patients received 272 CVVH sessions. In the citrate group 14.8% experienced a bleeding complication compared to 25% in the nadroparin group (p=0.04). The number of transfused red blood cell concentrates was not different between groups. The nadroparin group had a longer filter run time (median 31.5 hours versus 22.5 hours, p=0.0001). Conclusions In high risk critically ill patients citrate based anticoagulation for CVVH is safe in terms of bleeding complications and transfusion requirements.

0020. Microcirculatory perfusion and vascular reactivity are altered in post cardiac arrest patients, irrespective of target temperature management to 33° vs 36° (substudy TTM)

After cardiopulmonary resuscitation (CPR), following an out of hospital cardiac arrest (OHCA) hemodynamic failure is common, due to a combination of heart failure and ischemia reperfusion injury. Comatose post-cardiac arrest patients are treated on the intensive care unit (ICU) with mild therapeutic hypothermia (33°), nowadays referred to as target temperature management (TTM) for an assumed neuroprotective effect.

The role of the microcirculation in the etiology of ischemic skin and mouth lesions during vasopressin therapy

Sir, We would like to express our appreciation for the valuable and complementary comments on our case reported by Dr Dünser and coworkers, and for the opportunity to discuss the two important issues raised by their letter(1), namely the pathogenesis of ischemic skin and mouth lesions during arginine—vasopressin (AVP) therapy and the timing of AVP therapy during sepsis in relation to volume status and inotropic/vasopressor support. In their discussion of the first issue, the authors highlight a retrospective analysis performed in their group (2) concerning the etiology of ischemic skin and mouth ulcerations during the use of AVP in patients with catecholamine-resistant vasodilatory shock, with a remarkably high reported incidence of 30.2%. Although, in a multiple regression analysis, the presence of septic shock and a history of peripheral arterial occlusive disease were identified as independent risk factors for the development of such ischemic lesions during AVP treatment, this must not distract from the fact that the magnitude of this incidence is unprecedented for any form of vasopressor therapy during septic shock in humans. Moreover, in our case report, all circumstances were kept unaltered during terlipressin therapy; a 60% decrease in perfused vessels was observed with orthogonal polarization spectral (OPS) imaging within a time frame of 20 min after injection of the drug, thus making influencing factors other than the vasopressin analog used unlikely. The second issue touches an equally important and complex matter: were fluid resuscitation and inotropic/vasopressor support adequate at the start of AVP therapy? We agree that the lack of invasive cardiac output and mixed-venous saturation measurements is a limitation of our study. However, to date, no macrohemodynamic parameters have been reported to discriminate between survival and non-survival, whereas a decrease in microcirculatory flow is associated with non-survival (3). Spronk et al. (4) reported a startling decrease in microcirculatory flow in the sublingual region, despite aggressive fluid resuscitation and inotropic support according to international sepsis guidelines. The fact that, in our patient, there was no such decrease in microcirculatory flow, together with signs of adequate peripheral perfusion (central-to-toe temperature difference), in the presence of considerable doses of norepinephrine suggests the absence of marked hypovolemia. In conclusion, we agree that the cause of microcirculatory alterations during sepsis is multifactorial, and that generalized conclusions about the effect of vasopressin on the microcirculation should be made with restraint. Concomitant diseases, volume status and timing are paramount in this respect. The only way to establish the net result of all of these influencing factors is to directly monitor their impact on the microcirculation. OPS imaging, as shown in our study, provides a noninvasive and clinically applicable tool to do so.