Faculty Opinions recommendation of Recruitment of extravascular fluid by hyperoncotic albumin.

Following a significant thermal or electrical injury, tissues beneath the skin swell through fluid loss into the interstitial space. The increase in extravascular fluid together with the inelastic nature of the overlying burned skin compound to increase pressure within the affected limb. This increase in pressure can compromise the vascular supply distally in an affected limb or increase ventilatory pressures in those with circumferential burns of the chest and abdomen. This chapter will give guidance on when and how to perform escharotomies; however, the final decision is usually based on experience and clinical judgment. Figures illustrate detail markings and techniques for escharotomies and fasciotomies of the upper limb, lower limb, chest and abdomen.

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An extravascular fluid transport system based on structural framework of fibrous connective tissues in human body

Cell Proliferation ◽

10.1111/cpr.12667 ◽

2019 ◽

Vol 52 (5) ◽

Cited By ~ 2

Author(s):

Hongyi Li ◽

Chongqing Yang ◽

Yajun Yin ◽

Fang Wang ◽

Min Chen ◽

...

Keyword(s):

Transport System ◽

Human Body ◽

Fluid Transport ◽

Connective Tissues ◽

Structural Framework ◽

Extravascular Fluid

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Evidence for increased intrathoracic fluid volume in man at high altitude

Journal of Applied Physiology ◽

10.1152/jappl.1979.47.4.670 ◽

1979 ◽

Vol 47 (4) ◽

pp. 670-676 ◽

Cited By ~ 36

Author(s):

J. J. Jaeger ◽

J. T. Sylvester ◽

A. Cymerman ◽

J. J. Berberich ◽

J. C. Denniston ◽

...

Keyword(s):

Pulmonary Edema ◽

High Altitude ◽

Transpulmonary Pressure ◽

Fluid Volume ◽

Pulmonary Mechanics ◽

Volume Curve ◽

Extravascular Fluid ◽

Pressure Volume Curve ◽

Transthoracic Electrical Impedance ◽

Extravascular Fluid Volume

To determine if subclinical pulmonary edema occurs commonly at high altitude, 25 soldiers participated in two consecutive 72-h field exercises, the first at low altitude (200–875 m) and the second at high altitude (3,000–4,300 m). Various aspects of ventilatory function and pulmonary mechanics were measured at 0, 36, and 72 h of each exercise. Based on physical examination and chest radiographs there was no evidence of pulmonary edema at high altitude. There was, however, an immediate and sustained decrease in vital capacity and transthoracic electrical impedance as well as a clockwise rotation of the transpulmonary pressure-volume curve. In contrast, closing capacity and residual volume did not change immediately upon arrival at high altitude but did increase later during the exposure. These observations are consistent with an abrupt increase in thoracic intravascular fluid volume upon arrival at high altitude followed by a more gradual increase in extravascular fluid volume in the peribronchial spaces of dependent lung regions.

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Effect of endotoxin on lung fluid balance in unanesthetized sheep

Journal of Applied Physiology ◽

10.1152/jappl.1984.56.2.489 ◽

1984 ◽

Vol 56 (2) ◽

pp. 489-494 ◽

Cited By ~ 21

Author(s):

J. C. Gabel ◽

T. N. Hansen ◽

R. E. Drake

Keyword(s):

Left Atrial ◽

Capillary Permeability ◽

Dry Weight ◽

Base Line ◽

Lung Fluid ◽

Modified Method ◽

Lung Fluid Balance ◽

Extravascular Fluid ◽

Pulmonary Capillary ◽

Four Levels

We used a gravimetric technique to test for increased pulmonary capillary permeability after Escherichia coli endotoxin infusion in unanesthetized sheep. The sheep were chronically prepared with cannulas placed into the left atrium and pulmonary artery 1–2 wk before the experiments. We estimated pulmonary capillary pressure (Pc) as the average of pulmonary arterial and left atrial pressures, and used the modified method of Pierce to estimate the ratio of extravascular fluid weight (EVF) to blood-free dry weight. In 15 sheep we inflated a left atrial balloon to raise Pc to -10.7, 5, 10, or 15 mmHg above plasma oncotic pressure (IIc) for 3 h, then measured EVF. EVF averaged 4.0 +/- 0.2 (base line), 4.3 +/- 0.1, 4.5 +/- 0.1, and 5.1 +/- 0.5 (SD), respectively, for the four levels of Pc - IIc. We gave seven additional sheep 1 microgram/kg of E. coli endotoxin (0127:B8) and measured EVF after 3 h of stable Pc. Endotoxin increased Pc in each sheep. EVF was higher than control for the endotoxin sheep with Pc - IIc greater than -1. This finding is consistent with an increase in pulmonary capillary permeability caused by endotoxin. However, EVF was not elevated in the endotoxin sheep with Pc - IIc less than 1 mmHg. This shows that the increased permeability was insufficient to cause edema unless Pc was elevated. Thus endotoxin may cause edema by two mechanisms, 1) an increase in capillary permeability, and 2) an increase in Pc.

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Comparison of capsular and intra-alveolar fluid pressures in the lung

Journal of Applied Physiology ◽

10.1152/jappl.1982.52.6.1444 ◽

1982 ◽

Vol 52 (6) ◽

pp. 1444-1452 ◽

Cited By ~ 11

Author(s):

J. C. Parker ◽

A. E. Taylor

Keyword(s):

Vertical Gradient ◽

Colloid Osmotic Pressure ◽

Considerable Variability ◽

Tissue Pressure ◽

Capillary Filtration ◽

Filtration Pressure ◽

Extravascular Fluid ◽

Pulmonary Capillary ◽

Negative Pressures ◽

Spontaneously Breathing

The fluid pressures measured in chronically implanted capsules were compared with fluid absorptive pressures in small degassed lung segments. Capsules were implanted, and bronchiolar catheters were placed at different vertical heights in the lungs of spontaneously breathing dogs. Increases in pulmonary capillary filtration pressure were produced by volume infusions of Tyrode's solution and increased left atrial pressure. A vertical gradient in fluid pressures was consistently observed with more negative pressures near the top of the lungs. Capsular fluid pressures averaged -7.82 cmH2O with a gradient of -0.60 cmH2O/cm distance up the lung. The intra-alveolar absorptive pressures averaged -14.4 cmH2O with a gradient of -0.78 cmH2O/cm distance up the lung. The fluid pressures in both the capsules and alveolar segments responded to changes in capillary filtration pressure (capillary hydrostatic pressure minus plasma colloid osmotic pressure). The overall change in these extravascular fluid pressures amounted to approximately 25% of the change in filtration pressure, although considerable variability in individual measurements was obtained. Because they respond to imbalances in Starling capillary forces, both the capsular and intra-alveolar fluid pressures may be considered a function of perimicrovascular tissue pressure in the lung.

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Angiographic features of drug-induced bilateral angle closure and transient myopia with Ciliochoroidal effusion

BMC Ophthalmology ◽

10.1186/s12886-019-1230-y ◽

2019 ◽

Vol 19 (1) ◽

Cited By ~ 3

Author(s):

Yong Koo Kang ◽

Byeong Jae Son ◽

Dong Ho Park ◽

Jae Pil Shin

Keyword(s):

Case Series ◽

Ultrasound Biomicroscopy ◽

Angle Closure ◽

Drug Induced ◽

Idiosyncratic Reaction ◽

Transient Myopia ◽

Extravascular Fluid ◽

Ciliochoroidal Effusion ◽

Myopic Shift ◽

Shallow Anterior Chamber

Abstract Background To report five cases of acute drug-induced angle closure and transient myopia with ciliochoroidal effusion and to analyze angiographic findings of these cases. Methods This study is an observational case series. Five patients with acute drug-induced angle closure and transient myopia with ciliochoroidal effusion were examined by fluorescein angiography, indocyanine green angiography (ICGA) and ultrasound biomicroscopy (UBM). Results Five patients presented with bilateral visual loss and ocular pain after intake of topiramate, methazolamide, phendimetrazine tartrate or mefenamic acid. All patients showed elevated intraocular pressure (IOP) with shallow anterior chamber and myopic shift from − 0.5 to − 17.0 diopters (D). UBM showed ciliochoroidal effusions with diffuse thickening of the ciliary body in all cases. Rapid normalization of IOP and decrease of myopic shift occurred in all patients after discontinuing the suspected drugs. We classified the ICGA findings into 2 major signs (hypofluorescent dark spots, hyperfluorescent pinpoints) and 3 minor signs (diffuse choroidal hyperfluorescence, early hyperfluorescence of choroidal stromal vessel, and leakage and dilated retinal vessels). Conclusions The pathogenesis of acute drug-induced angle closure and transient myopia with ciliochoroidal effusion may be idiosyncratic reaction of uveal tissue to systemic drugs. Accumulation of extravascular fluid in the ciliochoroidal layer had a major role in the pathogenesis. ICGA could be a useful method to examine the pathophysiology of this condition by imaging of the choroidal layer.

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