Increased microvascular water permeability in patients with septic shock, assessed with venous congestion plethysmography (VCP)

Christ, F.; Gamble, J.; Gartside, I B; Kox, W. J.

doi:10.1007/s001340050509

Cited by 54 publications

(51 citation statements)

References 26 publications

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“…The significantly higher blood flow in the affected arm does not oppose this hypothesis since in CRPS-I an inhomogeneous perfusion may well exist in the affected limb similar to the changes seen in sepsis, where areas with the high flow are close to no-flow areas, thus causing functional shunting. The highest P vi values so far were found in patients suffering from sepsis and septic shock and correlated with patient outcome [34, 45], hence we would not rule out the possibility that the increased P vi values found in the affected limb reflect impaired microvascular perfusion despite a high arterial blood flow into the limb.…”

Section: Discussionmentioning

confidence: 99%

Assessment of the Peripheral Microcirculation Using Computer-Assisted Venous Congestion Plethysmography in Post-Traumatic Complex Regional Pain Syndrome Type I

Schürmann¹,

Zaspel²,

Gradl³

et al. 2001

J Vasc Res

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In complex regional pain syndrome type I (CRPS-I), edema of the affected limb is a common finding. Therefore, the changes in macro- and microcirculatory parameters were investigated to elucidate the underlying pathophysiology. Twenty-four patients with post-traumatic CRPS-I and 25 gender- and age-matched healthy subjects were examined by means of an advanced computer-assisted venous congestion strain-gauge plethysmograph. The recording of the volume response of the forearm to a stepwise inflation of an occlusion cuff placed at the upper arm enabled the calculation of the arterial blood flow into the arm (Q_a), the vascular compliance (C), the peripheral venous pressure (P_v), the isovolumetric venous pressure (P_vi; = hydrostatic pressure needed to achieve net fluid filtration) and the capillary filtration capacity (CFC) – an index of microvascular permeability. The study revealed no difference in any of the parameters between the right and left hand of healthy subjects. In CRPS-I patients, however Q_a, P_v, P_vi and CFC were significantly (p < 0.01/0.001) elevated in the affected arm (Q_a 11.2 ± 7.0 ml min^–1 100 ml^–1, P_v 20.2 ± 8.1 mm Hg, P_vi 24.7 ± 4.2 mm Hg, CFC 0.0058 ± 0.0015 ml min^–1 100 ml^–1 mm Hg^–1) compared to the unaffected arm (Q_a 4.2 ± 2.4 ml min^–1 100 ml^–1, P_v 10.0 ± 5.1 mm Hg, P_vi 13.2 ± 3.7 mm Hg, CFC 0.0038 ± 0.0005 ml min^–1 100 ml^–1 mm Hg^–1) and the values obtained in healthy controls (Q_a 5.1 ± 1.3 ml min^–1 100 ml^–1, P_v 10.4 ± 4.3 mm Hg, P_vi 15.7 ± 3.3 mm Hg, CFC 0.0048 ± 0.0012 ml min^–1 100 ml^–1 mm Hg^–1). Whereas the values in the unaffected arm of CRPS-I patients revealed no difference in Q_a, P_v and P_vi but a lower CFC (p < 0.01) compared to those from healthy controls. These results suggest profound changes in both macro- and microvascular perfusion in the affected arm of CRPS-I patients. The high CFC contributes to the edema formation, and combined with the elevated P_vi, they are in agreement with the hypothesis of an inflammatory origin of CRPS.

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Section: Discussionmentioning

confidence: 99%

Assessment of the Peripheral Microcirculation Using Computer-Assisted Venous Congestion Plethysmography in Post-Traumatic Complex Regional Pain Syndrome Type I

Schürmann¹,

Zaspel²,

Gradl³

et al. 2001

J Vasc Res

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“…Lipopolysaccharides also induce an increase in paracellular permeability along with a selectively-elevated filtration capacity. 11 In addition, the shedding of apoptotic endothelial cells in the bloodstream of septic patients occurs in a rate-dependent relationship with outcome/mortality 12,13 and represents another per-missive factor to permeability, as observed in capillary leak syndromes. 14 Epithelial dysfunction, although a less popular concept in sepsis, can nevertheless be involved, either as a very impermeable barrier, in the course of pro-inflammatory, pro-coagulatory and hyperpermeable phenotype as well, [15][16][17] or behave altogether differentially from the endothelium.…”

Section: Fluid Distribution To Endothelial/epithelial Cells In Sepsismentioning

confidence: 99%

Review article: Organ per fusion/permeabilityrelated effects of norepinephrine and vasopressin in sepsis

Farand¹,

Hamel

Lauzier

et al. 2006

Can J Anesth/J Can Anesth

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Purpose:One invariable hallmark of severe sepsis is generalized tissue "malperfusion" and hyperpermeability secondary to microcirculatory/capillary leakage. This review focuses on direct and/or indirect influences of norepinephrine, as a standard of care, and vasopressin, as an alternative vasoactive drug, on organ and tissue perfusion/permeability in severe sepsis.Source: English and French language articles and books published between 1966 and 2005 were identified through a computerized Medline search using the terms "sepsis, permeability, norepinephrine and vasopressin". Relevant publications were retrieved and scanned for additional sources. Principal findings:There are few randomized clinical trials comparing different vasopressors in sepsis; most available literature consists of clinical reports, animal experiments and occasional reviews. Based on the best current evidence from these sources, we describe the status of major organ perfusion/ permeability in sepsis (i.e., the lung, the kidney, the heart, the intestine/gut) in the context of sepsis-induced organ dysfunction/failure. Potential and differential therapeutic effects of the vasopressors norepinephrine and arginine-vasopressin, in the setting of sepsis, are identified. Conclusions:In the treatment of sepsis, arginine-vasopressin exhibits organ-specific heterogeneity in vascular responsiveness, compared to norepinephrine. While norepinephrine is a current standard of care in sepsis, arginine-vasopressin shows promise for the treatment of septic shock. Objectif

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“…Patients with SIRS suffer from increased microvascular permeability [3][4][5][6], which may result in hypovolemia, in turn leading to reduced venous return and cardiac output, as well as generalized vasoconstriction due to activation of the baroreceptor reflex [7]. Altogether, these alterations predispose the patient to the development of tissue ischaemia, reperfusion injury and organ failure [8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Effect of blood pressure on plasma volume loss in the rat under increased permeability

2007

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This is an author produced version of a paper published in Intensive care medicine. This paper has been peerreviewed but does not include the final publisher proofcorrections or journal pagination.Citation for the published paper: Dubniks M, Persson J, Grände PO. "Effect of blood pressure on plasma volume loss in the rat under increased permeability" Intensive care medicine, 2007, Vol: 33, Issue: 12, pp. 2192 http://dx.doi.org/10.1007/s00134-007-0756-2Access to the published version may require journal subscription. Published with permission from: Springer Verlag Design: Prospective randomised laboratory study.Subject: Forty-five adult male Sprague-Dawley rats.Interventions: Permeability was increased via an anaphylactic reaction by injection of 0.5 ml dextran 70. One hour later, volume expansion with 15 ml/kg of 5% albumin was given for 15 min.Plasma volume was measured just before and 2.5 hours after the albumin infusion ( 125 I-albumin tracer technique). The study included a control group, a noradrenalin group and a metoprolol/clonidine group (n=10 in each group). The vasoactive treatment started after albumin infusion and continued throughout the experiment. Plasma volume was also measured in a separate group without albumin infusion, to evaluate the effect of noradrenalin-induced increase in blood pressure under hypovolemia (n=9). CVP was measured to estimate the venous pressure effect of noradrenalin (n=6). Results:The remaining increase in plasma volume 2.5 h after infusion of 15 ml/kg of albumin was 11.8 ± 3.6 ml/kg in the control group compared with 0.5 ± 6.3 ml/kg in the noradrenalin group (p < 0.001) and with 12.5 ± 4.9 ml/kg in the metoprolol/clonidine group (ns). The reduction in plasma volume by noradrenalin infusion was much smaller in the group not given albumin, or 3.5 ± 3.0 ml/kg. Conclusion:Noradrenalin infusion increases the loss of plasma volume during a state of increased permeability which, according to the 2-pore theory of transvascular fluid exchange, may be explained by increased hydrostatic capillary pressure. The loss was less pronounced in hypovolemia.3

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Increased microvascular water permeability in patients with septic shock, assessed with venous congestion plethysmography (VCP)

Cited by 54 publications

References 26 publications

Assessment of the Peripheral Microcirculation Using Computer-Assisted Venous Congestion Plethysmography in Post-Traumatic Complex Regional Pain Syndrome Type I

Assessment of the Peripheral Microcirculation Using Computer-Assisted Venous Congestion Plethysmography in Post-Traumatic Complex Regional Pain Syndrome Type I

Review article: Organ per fusion/permeabilityrelated effects of norepinephrine and vasopressin in sepsis

Effect of blood pressure on plasma volume loss in the rat under increased permeability

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