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PubMed2004

Insulin edema in the twenty-first century: review of the existing literature.

Generalized insulin edema, although rare, is a well-recognized complication of insulin therapy. It is mainly appreciated in patients with newly diagnosed or poorly controlled diabetes mellitus after starting intensive insulin therapy. Although the condition is self-limiting, progression to overt cardiac failure and development of pleural effusion have been reported. With current trends toward intensive insulin therapy, clinicians should be aware of the existence of the insulin edema syndrome, and its occurrence should be documented and differentiated from other causes of edema. In this article, we present a recent case that illustrates the clinical features of insulin edema. Specifically, a young male with newly diagnosed type 1 diabetes mellitus developed significant, reversible peripheral edema after starting insulin therapy. A detailed case description is accompanied by the only known published photographs of insulin edema. The overall purpose of this article is to review the scanty existing medical literature surrounding the topic of insulin edema and to raise awareness about its continued occurrence.

Adult↗
PubMed2006

Subchondral bone marrow edema in patients with degeneration of the articular cartilage of the knee joint.

PURPOSE: To retrospectively determine at magnetic resonance (MR) imaging the prevalence of subchondral bone marrow edema beneath arthroscopically proved articular cartilage defects. MATERIALS AND METHODS: The study was performed in compliance with HIPAA regulations, and a waiver of informed consent was obtained from the institutional review board before the study was performed. The study consisted of 132 patients (70 men, 62 women; average age, 53 years) with articular cartilage defects of the knee joint who underwent MR imaging of the knee and subsequent arthroscopic knee surgery. At the time of arthroscopy, each articular cartilage lesion was graded by using the Noyes classification system. MR examinations were retrospectively reviewed to determine the size, depth, and location of subchondral bone marrow edema without knowledge of the arthroscopic findings. Pairwise Fisher exact tests and two-sample t tests were used to correlate MR imaging findings of subchondral bone marrow edema with the arthroscopic grade of articular cartilage degeneration. RESULTS: Subchondral bone marrow edema was seen beneath 105 (19%) of 554 articular cartilage defects identified at arthroscopy. It was not observed beneath any of the six grade 1 cartilage defects but was observed beneath eight (4.9%) of 163 grade 2A defects, 40 (14.4%) of 278 grade 2B defects, 54 (55.1%) of 98 grade 3A defects, and three (33.3%) of nine grade 3B defects. Subchondral bone marrow edema was also seen beneath four (1.4%) of 238 articular surfaces that appeared normal at arthroscopy. The mean depth and cross-sectional area of subchondral bone marrow edema increased with increasing grade of the articular cartilage lesion. CONCLUSION: Higher grades of articular cartilage defects are associated with higher prevalence and greater depth and cross-sectional area of subchondral bone marrow edema.

Adult↗
PubMed1993

Negative-pressure pulmonary edema after endotracheal intubation.

A review of complications occurring in conjunction with general anesthesia identified eight patients with laryngospasm-induced negative-pressure pulmonary edema after endotracheal intubation. Six male and two female patients (mean age, 31.9 years) developed pulmonary edema immediately or up to 25 minutes after extubation. Radiographs obtained 15-165 minutes after symptoms developed revealed alveolar edema and predominating interstitial edema in four patients each. Seven of eight had bilateral centralized patterns, and one had unilateral pulmonary edema. The mean vascular pedicle width was 67 mm +/- 12, a value 40% higher than the normal mean of 48 mm. The mean cardiothoracic ratio was 0.54 +/- .07 (normal mean, 0.53). There were no radiologic abnormalities of the trachea. Negative-pressure pulmonary edema should be suspected in young patients with findings of bilateral centralized pulmonary edema, a wide vascular pedicle, and a normal cardiothoracic ratio in the immediate postoperative period.

Adult↗
PubMed1996

Early-stage breast cancer: arm edema after wide excision and breast irradiation.

PURPOSE: To determine the incidence of arm edema in women with early-stage breast cancer after breast-conserving surgery and irradiation. MATERIALS AND METHODS: Women aged 29-83 years (mean, 55.9 years) treated with breast-conserving surgery and irradiation (n = 183) underwent a series of measurements of the circumference of each arm. Patient and treatment factors were analyzed for predictive value. RESULTS: Arm edema developed in 35.0% (n = 64), and clinically significant edema developed in 17.5% (n = 32) of patients. Dissections that yielded 16 or more nodes led to a 44% actuarial incidence of edema and a 29% actuarial incidence of clinically significant edema. Clinically significant arm changes occurred in 19 of the 87 (22%) women older than 55 years and in 13 of the 96 (14%) women younger than 55 years (P = .002). Chemotherapy, breast radiation dose, and use of tamoxifen had no effect on development of edema. CONCLUSION: Axillary dissection producing more than 15 nodes and age older than 55 years are predictive of arm edema.

Actuarial Analysis↗
PubMed1999

Contrast medium-induced pulmonary edema is aggravated by silicone contamination in rats.

PURPOSE: To examine the effect of silicone contamination, which occurs in clinical settings during vial preparation with disposable syringes, on contrast medium-induced pulmonary edema in rats. MATERIALS AND METHODS: Ioxaglate, ioversol, and iohexol, silicone-containing physiologic saline solutions, and three silicone-containing contrast media were separately, intravenously injected at 1.5 mL/min in rats. Pulmonary edema was evaluated as changes in the relative lung weight and in the water, sodium, and potassium contents of the lung. RESULTS: Intravenous injection of ioxaglate induced marked pulmonary edema, even with a dose of only 4 g of iodine per kilogram of body weight. In contrast, ioversol and iohexol induced significant pulmonary edema only after the injection of large doses (6 g of iodine per kilogram; P < .05). The injection of 4 microL/mL silicone-containing physiologic saline at a dose of 18.75 mL/kg also produced marked pulmonary edema, whereas doses of 6.25 and 12.5 mL/kg showed no significant influence. The addition of an ineffective dose (12.5 mL of physiologic saline per kilogram of body weight) of silicone in contrast medium substantially aggravated the pulmonary edema induced by the contrast medium alone; this phenomenon was also confirmed with morphologic observation. CONCLUSION: Ionic contrast media are more toxic to the endothelial cells than are nonionic contrast media. Silicone contamination might be one of the causes of pulmonary edema after intravenous injection. However, caution must be exercised in extrapolating these results to humans.

Animals↗
PubMed1990

Changes in microvascular permeability with acceleration of edema in dog lungs.

Elevation of left atrial pressure to 25-40 mmHg causes continuous pulmonary edema formation in dog lungs. However, after 5-120 min, the rate of edema formation often increases (acceleration of edema). Acceleration of edema could be associated with an increase in microvascular membrane permeability because an increase in permeability would cause fluid to filter through the microvascular membrane more rapidly. To test the hypothesis that acceleration is associated with increased permeability, we used the continuous weight-gain technique to estimate the pulmonary microvascular membrane filtration coefficient (Kf) before and after acceleration of edema in 10 dogs. Acceleration occurred 36 +/- 38 (SD) min after elevation of left atrial pressure to 35.2 +/- 5.4 mmHg. Rate of weight gain increased from 0.47 +/- 0.17 g/min before acceleration to 0.88 +/- 0.26 g/min (P less than 0.05) after acceleration of pulmonary edema. Kf was increased from initial values of 0.058 +/- 0.027 to 0.075 +/- 0.029 ml.min-1.mmHg-1 (P less than 0.05) after acceleration. In five additional dogs we cannulated lung lymphatics and determined the lymph to plasma protein concentration ratio (CL/CP) before and after acceleration. CL/CP increased from base-line values of 0.37 +/- 0.07 to 0.44 +/- 0.06 (P less than 0.05) after acceleration. Both the increase in Kf and CL/CP data support the hypothesis that acceleration of edema is due, in part, to a slight increase in microvascular membrane permeability. However, the findings could also have been caused by an increase in interstitial conductance, washout of interstitial proteins, or alveolar flooding.

Animals↗
PubMed1996

Pulmonary interstitial pressure and proteoglycans during development of pulmonary edema.

In anesthetized adult rabbits, pulmonary perivascular interstitial pressure (P(ip)), measured by micropuncture technique with intact pleural space, averaged -10.5 +/- 1.9 (SD) cmH2O in control conditions, with a wet-to-dry lung weight ratio (W/D) of 4.8 +/- 0.2. Saline infusion (120 ml i.v. over 120 min) induced interstitial edema, increasing P(ip) to 3.62 +/- 1.6 cmH2O with no significant increase in W/D (5.13 +/- 0.1). For intravenous saline infusion exceeding 140 ml, P(ip) decreased to about atmospheric pressure with development of severe edema that was characterized by an increase of W/D ( > 7) with no further change in P(ip). In a separate set of animals, pulmonary interstitial proteoglycans (PGs) were investigated after sequential extraction of the tissue with 0.4 and 4 M guanidinium chloride (GuHCl) under control conditions and with interstitial (100 ml saline load in 100 min) and severe edema ( > 200 ml total infusion). The extractability of PGs increased constantly with increasing W/D. PG content in total extracts was evaluated by determination of hexuronate content which was 195.4 +/- 1.5 micrograms/g dry tissue in control lungs, 217.9 +/- 1.6 in interstitial edema, and 316.4 +/- 2.7 in severe edema. Moreover, edema development was coupled with an increase in efficiency of PG extraction with 0.4 M GuHCl. These findings suggested a weakening of PG interactions with other components of the extracellular matrix (ECM). Electrophoretic and gel-filtration analyses showed that the relative content of PG populations of large molecular size decreased constantly in 0.4 M GuHCl extract with increasing water loading. We propose relating the inflection of P(ip) in the transition from interstitial to severe edema to PG breakdown, which might greatly affect ECM structural organization, including collagen spreading and/or rupture of epithelial layer.

Animals↗
PubMed1976

Lung lymph and free interstitial fluid protein composition in sheep with edema.

In 10 anesthetized sheep with mild or moderate pulmonary edema we determined whether the protein composition of lung lymph is representative of free interstitial fluid. We measured protein concentration and albumin fraction in 1-mul samples of plasma, lung lymph, and free interstitial fluid. We also measured lung lymph flow. In five sheep with edema caused by increased pulmonary microvascular pressure, the average (+/- 1 SE) plasma protein concentration was 6.0 +/- 0.4 g/100 ml, lung lymph 3.4 +/- 0.2, and interstitial fluid 3.1 +/- 0.3. Lymph flow increased from an average base-line value of 9.4 ml/h to 43.4 ml/h during edema. Average albumin fractions in lymph and interstitial fluid were 0.56 +/- 0.02 and 0.50 +/- 0.01, respectively, compared with 0.44 +/- 0.01 for plasma. In five sheep with increased-permeability edema, average plasma protein concentration was 5.7 +/- 0.3 g/100 ml, lung lymph 4.1 +/- 0.4, and interstitial fluid 4.6 +/- 0.4. Base-line lymph flow was 11.0 ml/h and increased to 27.8 ml/h during edema. Average albumin fractions in lymph and interstitial fluid were 0.53 +/- 0.01 and 0.50 +/- 0.02, respectively, compared with 0.43 +/- 0.01 for plasma. We conclude in both high-pressure and altered-permeability edema, the protein composition of lung lymph collected from the major lung efferent lymphatic is representative of the free interstitial edema fluid.

Albumins↗
PubMed1980

Effects of pulmonary edema on regional pulmonary perfusion in the intact dog lung.

Regional pulmonary blood flow was determined in dogs during varying degrees of pulmonary edema induced by infusing 179.2-659.4 ml/kg normal saline over 2-3 h. Pulmonary hemodynamics and regional blood flows were measured during the base-line period and at 30 min postinfusion. The degree of pulmonary edema was determined by the final extravascular lung water-to-bloodless dry lung weight ratio (W/D). In dogs developing gross alveolar edema (W/D of 10.70 +/- 0.88 vs. 3.10 +/- 0.30 in controls), the blood flow was shifted to either upper or dependent lung regions. The shift to the upper regions was associated with an increased (P < 0.05) pulmonary arterial pressure (Ppa), whereas the shift to the dependent lung was not associated with a significant change in Ppa. Breathing 100% O2 did not prevent these shifts, suggesting that they were not due to localized hypoxic pulmonary vasoconstriction. The flow distribution patterns were also not related to regional differences in edema. In contrast to the changes during fulminant edema, blood flow distribution did not change after moderate levels of pulmonary edema (W/D of 6.03 0.69), suggesting that gross alveolar flooding is required for a redistribution of pulmonary blood flow. Flow redistribution to the upper lung during airway flooding may be due to increase in Ppa, whereas the increased flow in the dependent lung during the same degree of edema may be due to "bulging" of alveolar vessels into the air spaces, secondary to a decrease in surface activity.

Animals↗
PubMed1987

Effect of regional alveolar hypoxia on permeability pulmonary edema formation in dogs.

We studied the effects of regional alveolar hypoxia on permeability pulmonary edema formation. Anesthetized dogs had a bronchial divider placed so that the left lower lobe (LLL) could be ventilated with a hypoxic gas mixture (HGM) while the right lung was continuously ventilated with 100% O2. Bilateral permeability edema was induced with 0.05 ml/kg oleic acid and after 4 h of LLL ventilation with an HGM (n = 9) LLL gross weight was 161 +/- 13 (SE) g compared with 204 +/- 13 (SE) g (P less than 0.05) in the right lower lobe (RLL). Bloodless lobar water and dry weight were also significantly lower in the LLL as compared with the RLL of the study animals. In seven control animals in which the LLL fractional inspired concentration of O2 (FIO2) was 1.0 during permeability edema, there were no differences in gravimetric variables between LLL and RLL. In eight additional animals, pulmonary capillary pressure (Pc), measured by simultaneous occlusion of left pulmonary artery and vein, was not significantly different between LLL FIO2 of 1.0 and 0.05 either before or after pulmonary edema. We conclude that, in the presence of permeability pulmonary edema, regional alveolar hypoxia causes reduction in edema formation. The decreased edema formation during alveolar hypoxia is not due to a reduction in Pc.

Animals↗
PubMed1988

Synthetic smoke with acrolein but not HCl produces pulmonary edema.

The chemical toxins in smoke and not the heat are responsible for the pulmonary edema of smoke inhalation. We developed a synthetic smoke composed of carbon particles (mean diameter of 4.3 microns) to which toxins known to be in smoke, such as HCl or acrolein, could be added one at a time. We delivered synthetic smoke to dogs for 10 min and monitored extravascular lung water (EVLW) accumulation thereafter with a double-indicator thermodilution technique. Final EVLW correlated highly with gravimetric values (r = 0.93, P less than 0.01). HCl in concentrations of 0.1-6 N when added to heated carbon (120 degrees C) and cooled to 39 degrees C produced airway damage but no pulmonary edema. Acrolein, in contrast, produced airway damage but also pulmonary edema, whereas capillary wedge pressures remained stable. Low-dose acrolein smoke (less than 200 ppm) produced edema in two of five animals with a 2- to 4-h delay. Intermediate-dose acrolein smoke (200-300 ppm) always produced edema at an average of 147 +/- 57 min after smoke, whereas high-dose acrolein (greater than 300 ppm) produced edema at 65 +/- 16 min after smoke. Thus acrolein but not HCl, when presented as a synthetic smoke, produced a delayed-onset, noncardiogenic, and peribronchiolar edema in a roughly dose-dependent fashion.

Acrolein↗
PubMed1988

Effect of tidal volume and PEEP on rate of edema formation in in situ perfused canine lobes.

The effects of raising tidal volume and positive end-expiratory pressure (PEEP) on rate of edema formation were studied in in situ canine left upper lobe preparations. Edema was induced by increasing blood flow to the left upper lobe (4-8 times normal). In the same animal, at equivalent flows and microvascular hydrostatic pressures, rate of edema formation observed with larger tidal volumes was significantly higher than that observed with smaller tidal volumes (0.73 +/- 0.29 vs. 0.58 +/- 0.30, P less than 0.001). Edema was also induced under static conditions (i.e., flow = 0) over a wide range of vascular pressures. Rate of edema formation was plotted against pressure and the best-fit linear regression was obtained. The slopes (g.min-1.mmHg-1.100 g-1) of the regression lines were significantly higher with larger tidal volumes compared with smaller tidal volumes [0.106 +/- 0.010 (SE) vs. 0.081 +/- 0.009, P less than 0.01]. The pressure intercepts were not different (16.1 +/- 1.6 vs. 15.7 +/- 1.8). When mean airway pressures were increased to levels equivalent to those obtained with larger tidal volumes, but by raising end-expiratory pressures, rate of edema formation dropped to levels below base line. We conclude that increasing the amplitude of cyclic changes in lung volume increases edema formation through mechanisms that are independent of changes in operating (i.e., mean) lung volume.

Animals↗
PubMed1992

Expiratory muscle activity during pulmonary edema in the anesthetized dog.

The present study evaluated the reflex response of the expiratory muscles to pulmonary congestion and edema. The electromyograms of two thoracic and four abdominal expiratory muscles were recorded in 12 anesthetized dogs. Pulmonary edema was induced by rapid saline infusion in six dogs and injection of oleic acid into the pulmonary circulation in the remaining six dogs. Both forms of pulmonary edema reduced pulmonary compliance, interfered with gas exchange, and induced a rapid and shallow breathing pattern. The electrical activity of all abdominal muscles was suppressed during both forms of pulmonary edema. In contrast, the electromyogram activity of the thoracic expiratory muscles was not significantly affected by pulmonary edema. Acute pulmonary arterial hypertension produced in two dogs by inflating a balloon in the left atrium had no effect on ventilation or expiratory muscle electrical activity. In two vagotomized dogs, pulmonary edema did not inhibit the expiratory muscles. We conclude that pulmonary edema suppresses abdominal but not thoracic expiratory muscle activity by vagal reflex pathway(s). Extravasation of fluid into the lung appears to be more important than an increase in pulmonary vascular pressure in eliciting this response.

Anesthesia↗
PubMed1995

Lung tissue and airway impedances during pulmonary edema in normal range of breathing.

How pulmonary edema affects lung tissue and airway properties is not clear. From measurements of airway pressure and flow, we measured lung elastance (EL) and resistance (RL) in 5 anesthetized-paralyzed open-chested dogs during sinusoidal forcing in the frequency (f) and tidal volume (VT) ranges of normal breathing. RL was divided into its tissue (Rti) and airway (Raw) components from measurements of alveolar pressure through capsules glued to the lung surface. After induction of severe pulmonary edema by injection of oleic acid into the right atrium, forcing was repeated at the same mean airway pressure (Paw) as in control animals (11 cmH2O) and at a higher Paw (14 cmH2O), as would occur in closed-chested dogs during edema (G. M. Barnas, D. Stamenovic, and K. R. Lutchen. J. Appl. Physiol. 73: 1040-1046, 1992). Edema increased EL, and this increase was greater at Paw = 14 cmH2O (P < 0.05). The f dependences of EL and Rti were increased by edema (P < 0.05), and there was a large negative dependence of EL on VT at Paw = 14 cmH2O. Edema increased RL (P < 0.05), but this increase depended on f, VT, and Paw. The increase in RL was due largely to increases in Rti at Paw = 14 cmH2O and to increases in Raw at Paw = 11 cmH2O. We conclude that the functional effects of oleic acid-induced pulmonary edema on RL are due mostly to changes in lung tissue.

Airway Resistance↗
PubMed1998

Effect of cardiogenic and noncardiogenic pulmonary edema on histamine responsiveness in sheep.

We compared the effects of cardiogenic pulmonary edema, brief pulmonary vascular congestion without frank edema, and noncardiogenic pulmonary edema on responsiveness to inhaled histamine in chronically instrumented awake sheep. Histamine responsiveness was measured before and after 1) cardiogenic pulmonary edema induced by raising left atrial pressure to 35 cmH2O (Pla) for 3.5 h by partial obstruction of flow across the mitral valve, 2) brief cardiogenic congestion via Pla for 0.5 h, 3) noncardiogenic pulmonary edema induced by 25 mg/kg intravenous perilla ketone (PK), and 4) 3.5 h of monitoring without Pla or PK (controls). Treatment for 3.5 h with Pla (n = 9) and PK (n = 11) each significantly lessened the histamine dose required to cause a fall to 65% of baseline dynamic lung compliance (ED65Cdyn), i.e., increased responsiveness. Sheep treated for 0.5 h with Pla (n = 7) and controls (n = 5) showed no significant change in ED65Cdyn. Intravenous atropine (0.1 mg/kg) before the second histamine challenge altered neither the reduction of ED65Cdyn in Pla (n = 8) and PK (n = 9) sheep nor the ED65Cdyn level of controls (n = 9). These data imply that the local effects of edema, rather than bronchial vascular hemodynamics, cholinergic reflexes, and permeability changes, are germane to lung hyperresponsiveness during pulmonary edema in sheep.

Aerosols↗
PubMed1999

Radiographic evidence of interstitial pulmonary edema after exercise at altitude.

Pulmonary function abnormalities after exercise are suggestive of pulmonary edema; however, radiographic evidence is lacking. Well-trained cyclists were studied to determine whether there is radiographic evidence of pulmonary edema after endurance exercise (cycling distance 5.3-131.5 km) at altitude. Chest radiographs obtained before exercise were coded for later interpretation. Films obtained after exercise were coded with a different number. A total of 74 sets of posteroanterior and lateral films were analyzed by three radiologists for signs of pulmonary edema. Radiographic changes were graded on a three-point scale. An edema score was calculated by summing the score for each individual radiographic finding for each radiologist and an overall edema score representing the mean scores from all three radiologists. The overall edema score increased from 0.8 +/- 1.2 before exercise to 1.8 +/- 1.6 after exercise (P < 0.01). These results suggest that, after prolonged high-intensity exercise at moderate altitude, there is radiographic evidence of early pulmonary edema in some cyclists.

Adolescent↗
PubMed2000

Vascular hyperpermeability in nephrotic edema.

BACKGROUND/AIM: There is increasing evidence that hypoalbuminemia and the inability of the renal distal tubule to excrete salt are not the only factors responsible for nephrotic edema. We tested the possibility that vascular hyperpermeability also plays a role in the pathophysiology of nephrotic edema in human primary glomerulonephritis. METHODS: We investigated the capillary permeability by means of a standardized test using albumin labelled with technetium (99mTc-albumin) in 20 healthy adults and in 101 nephrotic adult patients comprising 60 patients with idiopathic nephrotic syndrome (INS; minimal-change nephropathy and segmental glomerulosclerosis), 32 with idiopathic membranous nephropathy (IMN) and 9 patients with idiopathic type I membranoproliferative glomerulonephritis (MPGN). The patients and healthy controls were also compared with a group of women (n = 25) with idiopathic cyclic edema, a disease in which an increase in capillary permeability plays a pivotal role. The capillary permeability measured by the Landis isotope test is normal in edematous patients with cardiac and renal impairment unrelated to glomerular disease, cirrhosis, hypothyroidism, lymphatic obstruction and diuretic abuse. As values were not normally distributed, nonparametric analysis of variance was used (Kruskal-Wallis test), and patient groups were compared with healthy controls and with women with idiopathic cyclic edema by means of the two-tailed nonparametric Mann-Whitney test. The effects of high-dose steroids and Ginkgo biloba extract (Tanakan); an agent able to improve capillary permeability) were analyzed by means of the two-tailed nonparametric Wilcoxon test. RESULTS: The capillary permeability was significantly increased (Mann-Whitney test) in each glomerular disease group compared with the healthy controls. 99mTc-albumin extravasation values (%; median and range in parentheses were the following: healthy controls 0 (0-8.4); idiopathic cyclic edema patients 11.5 (8-24), p < 0.001; INS 20 (0-50), p < 0.0001; IMN 12.5 (0-40), p < 0.001, and MPGN 10 (0-40), p < 0.05. An increase in capillary permeability exceeding the upper limit of control values (>8% of 99mTc-albumin extravasation) was observed in 88% of INS, in 53% of IMN and in 44% of MPGN patients. The increase in capillary permeability (%) was greater in idiopathic nephrotic patients than in idiopathic cyclic edema patients (p < 0. 005, Mann-Whitney test) and was markedly reduced in nephrotic patients receiving high-dose steroids (n = 8) [before 25 (8-40); after 0 (0-25), p < 0.005 (Wilcoxon's test)] and high doses of G. biloba extract (n = 16) [before 30 (8-50); after 2.5 (0-20, p < 0. 0005 (Wilcoxon's test)]. CONCLUSIONS: We conclude that capillary permeability is severely altered in most of the nephrotic patients with primary glomerulonephritis. These results strongly suggest that the capillary hyperpermeability plays a role in the pathophysiology of nephrotic edema in primary glomerular disease, especially in INS. We postulate that this widespread abnormality in capillary permeability is related to the release of vascular permeability factor and other cytokines by immune cells.

Adolescent↗
PubMed1975

Pulmonary edema during volume infusion.

The relationship between left ventricular filling pressure and plasma colloid osmotic pressure to pulmonary edema was examined in a group of 37 patients, the majority of whom were hypovolemic. Sixteen patients developed pulmonary edema during fluid infusion. In the 21 patients who did not develop pulmonary edema, the left ventricular filling pressure was slightly elevated but the colloid osmotic pressure was not reduced. The majority of these patients were treated with colloid solutions (group I). In five of the 16 patients who developed pulmonary edema, the left ventricular filling pressure was elevated and there was no reduction in the plasma colloid osmotic pressure. These patients received only colloids (group II). In the other 11 patients who developed pulmonary edema, the left ventricular filling pressure was normal but the plasma colloid osmotic pressure was reduced to 16 +/- 2 torr (group III). The colloid osmotic pressure in this group was significantly less than in the other two groups (P less than 0.01). Most of these patients received large volumes of crystalloid solutions. After administration of furosemide, clearing of pulmonary edema in this group was associated with normalization of the plasma colloid osmotic pressure. Infusion of large volumes of crystalloids in hypovolemic patients can be hazardous, for reduction of the plasma colloid osmotic pressure may predispose to the development of pulmonary edema even when the left ventricular filling pressure remains normal.

Adult↗