Risk Factors For Pulmonary Edema Research Articles

Height below 154 cm is a risk factor for pulmonary edema in twin pregnancy: An observational study.

In recent years, twin pregnancies have become increasingly common. The aim of our study was to analyze the exposure to risk factors for postpartum pulmonary edema in twin pregnancies. We get all our data from the "DATADRYAD" database, which is available directly. We used a variety of statistical methods, including multivariate logistic regression analysis and smoothed curve fitting. The aim was to critically assess the relationship between height and the occurrence of postpartum pulmonary edema in pregnant women with twin pregnancies. Among pregnant women whose height was <154 cm, the risk of postpartum development of pulmonary edema gradually decreased with increasing height (OR = 0.65, P = .0104). There was no relationship between maternal height and postpartum development of pulmonary edema among pregnant women with height higher than 154 cm (P = .9142). Pregnant women who were taller than 154 cm had a 76% lower risk of developing pulmonary edema postpartum compared to pregnant women whose height was lower than 154 cm (P = .0005). Our study suggests that pregnant women with twin pregnancies whose height is <154 cm are more likely to suffer from postpartum pulmonary edema. Therefore, healthcare professionals and caregivers should pay closer attention to twin pregnancies with heights below 154 cm, be alert to the occurrence of pulmonary edema, and take preventive and therapeutic measures as early as possible. This will help prevent the development of pulmonary edema.

Risk Factors and Risk for Severe Maternal Morbidity in Severe Preeclampsia Complicated by Pulmonary Edema: A Case-Control Study.

The objective of this study is to examine risk factors and adverse outcomes related to preeclampsia with severe features complicated by pulmonary edema. This is a nested case-control study of all patients with preeclampsia with severe features who delivered in a tertiary, urban, academic medical center over a 1-year period. The primary exposure was pulmonary edema and the primary outcome was a composite of severe maternal morbidity (SMM), defined according to the Centers for Disease Control and Prevention and based on International Classification of Diseases, 10th revision, Clinical Modification codes. Secondary outcomes included postpartum length of stay, maternal intensive care unit admission, 30-day readmission, and discharge on antihypertensive medication. A multivariable logistic regression model adjusting for clinical characteristics related to the primary outcome was used to determine adjusted odds ratios (aOR) as measures of effect. Of 340 patients with severe preeclampsia, there were seven cases of pulmonary edema (2.1%). Pulmonary edema was associated with lower parity, autoimmune disease, earlier gestational age at diagnosis of preeclampsia and at delivery, and cesarean section. Patients with pulmonary edema demonstrated increased odds of SMM (aOR: 10.11, 95% confidence interval [CI]: 2.13-47.90), extended postpartum length of stay (aOR: 32.56, 95% CI: 3.95-268.45), and intensive care unit admission (aOR: 102.85, 95% CI: 7.43-1422.92) compared with those without pulmonary edema. Pulmonary edema is associated with adverse maternal outcomes among patients with severe preeclampsia, and is more likely to affect patients who are nulliparous, have an autoimmune disease, and are diagnosed preterm. · Pulmonary edema increases odds of severe maternal morbidity in preeclamptics.. · Pulmonary edema prolongs postpartum and intensive care unit stay in preeclamptics.. · Risk factors for pulmonary edema include nulliparity and autoimmune disease.. · Earlier diagnosis of severe preeclampsia increases risk of pulmonary edema..

Betamethasone use and risk factors for pulmonary edema during the perinatal period: a single-center retrospective cohort study in Japan

BackgroundA few studies have reported that maternal administration of antenatal corticosteroids increased the risk of pulmonary edema (PE). However, despite the increasing usage rate of betamethasone as antenatal corticosteroid, maternal administration of betamethasone as a risk factor for PE has not been well studied. This study aimed to evaluate how maternal backgrounds and complications, tocolytic agents, and betamethasone affect the incidence of PE during the perinatal period and determine the risk factor for PE.MethodsThis was a single-center retrospective cohort study in Kurashiki, Japan. The study subjects were patients who had been admitted to our hospital for perinatal management including pregnancy, delivery and puerperium between 2017 and 2020. The primary outcome measure was defined as the incidence of PE during hospitalization. First, in all study subjects, Cox proportional hazards model was used to determine the risk factor for PE during the perinatal period. Next, using propensity score matching, we divided the patients into the betamethasone and betamethasone-free groups and examined the association between betamethasone use and the incidence of PE with Cox proportional hazards model.ResultsDuring the study period, 4919 cases were hospitalized, and there were 16 PE cases (0.3%). In all analyzed subjects, the occurrence of PE was significantly associated with preeclampsia (hazard ratio 16.8, 95% confidence intervals (CI) 5.39–52.7, P < 0.001) and the combined use of the tocolytic agents such as ritodrine hydrochloride and magnesium sulfate, and betamethasone (hazard ratio 11.3, 95% CI 2.66–48.1, P = 0.001). In contrast, after propensity score matching, no statistically significant difference was found between the betamethasone and betamethasone-free groups in the incidence of PE (hazard ratio 3.19, 95% CI 0.67–15.3, P = 0.145).ConclusionsA combined use of tocolytic agents and antenatal corticosteroids such as betamethasone may be an independent risk factor for PE during the perinatal period. On the other hand, betamethasone use alone may not be associated with the incidence of PE. When tocolytic agents and betamethasone are administrated to pregnant women, it is important to pay attention to the appearance of maternal respiratory symptoms.

Effect of Intra- and Post-Operative Fluid and Blood Volume on Postoperative Pulmonary Edema in Patients with Intraoperative Massive Bleeding

In patients with intraoperative massive bleeding, the effects of fluid and blood volume on postoperative pulmonary edema are uncertain. Patients with intraoperative massive bleeding who had undergone a non-cardiac surgery in five hospitals were enrolled in this study. We evaluated the association of postoperative pulmonary edema risk and intra- and post-operatively administered fluid and blood volumes in patients with intraoperative massive bleeding. In total, 2090 patients were included in the postoperative pulmonary edema analysis, and 300 patients developed pulmonary edema within 72 h of the surgery. The postoperative pulmonary edema with hypoxemia analysis included 1660 patients, and the condition occurred in 161 patients. An increase in the amount of red blood cells transfused per hour after surgery increased the risk of pulmonary edema (hazard ratio: 1.03; 95% confidence interval: 1.01–1.05; p = 0.013) and the risk of pulmonary edema with hypoxemia (hazard ratio: 1.04; 95% confidence interval: 1.01–1.07; p = 0.024). An increase in the red blood cells transfused per hour after surgery increased the risk of developing pulmonary edema. This increase can be considered as a risk factor for pulmonary edema.

Combined use of cardiopulmonary ultrasound in the diagnosis of pulmonary edema in patients with heart failure: a retrospective analysis.

Heart failure (HF) is generally complicated with pulmonary edema (PE), the early diagnosis and treatment is essential. We aimed to evaluate the effects of combined use of cardiopulmonary ultrasound in the diagnosis of PE in HF patients, to provide reference for the management of HF. HF patients treated in our hospital from January 1, 2019 to June 30, 2020 were included. All patients underwent echocardiography and lung ultrasonography, and analyzed the characteristics of patients and related detected results. Logistic regression analyses were conducted to identify the potential risk factors. And the receiver operating characteristic (ROC) curve was conducted to compare the predictive value of factors. A total of 183 HF patients were included, the incidence of PE in HF patients was 62.84%. Logistic regression analyses indicated that NT-proBNP (OR 2.24, 95% CI: 1.28-5.04), LAVI (OR 2.03, 95% CI: 1.02-4.45), E/e' (OR 1.57, 95% CI: 0.13-2.28), SPAP (OR 1.35, 95% CI: 0.02-2.84) were the independent risk factors for PE in patients with HF (all P<0.05). The AUC of NT-proBNP, LAVI, E/e' and SPAP were 0.705, 0.668, 0.674 and 0.691 respectively. NT-proBNP ≥8,842.37 ng/L, LAVI ≥42.14 mL/m2, E/e' ≥19.20, SPAP ≥38.16 mmHg were the independent risk factors for PE in patients with HF (all P<0.05). Combined use of cardiopulmonary ultrasound is beneficial to the early diagnosis of PE in patients with HF, and early interventions are needed for those patients with risk factors.

Risk factors of pulmonary edema in women with preeclampsia from south India: a case-control study.

Pulmonary edema is a potentially life-threatening complication of preeclampsia, but only few studies have looked at possible risk factors. This study assessed the association between various potential risk factors and the development of pulmonary edema. An age-matched case-control design with hospital records from a tertiary care center in south India was used. A total of 55 pregnant women with preeclampsia who developed pulmonary edema were included as cases, who were 4:1 aged-matched as controls with 220 preeclamptic women, and who did not develop pulmonary edema. Multivariate conditional logistic regression was used to produce adjusted odds ratios with 95% confidence intervals for the likelihood to develop pulmonary edema (OR; 95% CI). Nulliparity (3.94; 1.44-10.7), multifetal pregnancy (5.06; 1.59-16.0), mean arterial blood pressure in mmHg (1.08; 1.03-1.13), and mild (3.25; 1.02-1.29) and moderate (4.43; 1.76-11.1) anemia showed increased odds. Multifetal pregnancy in nulliparous women had higher odds (39.5; 6.2-251) compared with those with singleton pregnancies (3.17; 1.13-8.88). While early aggressive blood pressure treatment can reduce the risk of pulmonary edema, the other risk factors are either non-modifiable or relate to disease severity; thus, continuous monitoring would be relevant for early diagnosis and management, especially among nulliparous preeclamptic women with multifetal pregnancies.

370. Risk factors of pulmonary edema among patients with pre-eclampsia : A case control study

Introduction Pulmonary edema (PE), an uncommon event in preeclampsia, is associated with an increased risk of maternal and fetal morbidity and mortality. Patho-physiological changes associated with preeclampsia such as endothelial dysfunction and increased capillary permeability predispose them to PE. Due to the effect of anti-angiogenic mediators which is found to be increased in nulliparous women, the risk of development of PE is increased in these women compared to those with multiparity. We aimed to assesses the association of parity and other risk factors with development of pulmonary edema in preeclamptic women. Methods A matched case control study was conducted using data extracted from the hospital records matched for age during the time period January 2012 and December 2018 in a tertiary care and regional centre in South India. We used matched analysis using conditional logistic regression to assess the association of parity and other risk factors with pulmonary edema. Results PE developed in 2.67% of the preeclamptic women in this time period. More women were nulliparous among those who developed PE compared with the matched controls (76.7% vs. 50.0%, p = 0.032). Bivariate analysis adjusted for age showed nulliparous women to be at higher risk of development of PE (OR 5.0, 95%CI 1.06 23.41, p = 0.041). After adjusting for other variables (BMI, platelet counts, Systolic & diastolic blood pressure, presence of anaemia, serum albumin levels, and presence of help syndrome), analyses revealed matched OR of 5.44 (95% CI 1.36 −21.33) indicating that nulliparous women were at higher risk to develop PE compared with multiparous women). Conclusion Nulliparous preeclamptic women were found to be at increased risk of development of pulmonary edema. Being an uncommon complication, a prospective study, also taking into consideration of the stress on cardiac function, is needed to stratify the risk of PE.

Observational study of potential risk factors of immersion pulmonary edema in healthy divers: exercise intensity is the main contributor

BackgroundThe risk factors of pulmonary edema induced by diving in healthy subjects are not well known. The aim of the present study was to assess the parameters contributing to the increase in extravascular lung water after diving.MethodsThis study was carried out in a professional diving institute. All divers participating in the teaching program from June 2012 to June 2014 were included in the study. Extravascular lung water was assessed using the detection of ultrasound lung comets (ULC) by chest ultrasonography. Clinical parameters and dive profiles were recorded using a questionnaire and a dive computer.ResultsOne-hundred six divers were investigated after 263 dives. They used an open-circuit umbilical supplying compressed gas diving apparatus in 202 cases and a self-contained underwater breathing apparatus in 61 cases. A generalized linear mixed model analysis was performed which demonstrated that the dive induced a significant increase in ULC score (incidence rate ratio: 3.16). It also identified that the predictive variable of increased extravascular lung water after the dive was the exercise intensity at depth (z = 3.99, p < 0.0001). The other parameters studied such as the water temperature, dive profile, hyperoxic exposure, or anthropometric data were not associated with the increase in extravascular lung water after the dive.ConclusionsIn this study, the exercise intensity was the main contributor to the increase in extravascular lung water in healthy divers. To improve the prevention of immersion pulmonary edema, the exercise intensity experienced during the dive should thus be adapted to the aerobic fitness level of the divers.

Predictive Value of Echocardiographic Abnormalities and the Impact of Diastolic Dysfunction on In-hospital Major Cardiovascular Complications after Living Donor Kidney Transplantation.

Patients with end-stage renal disease (ESRD) show characteristic abnormalities in cardiac structure and function. We evaluated the influence of these abnormalities on adverse cardiopulmonary outcomes after living donor kidney transplantation in patients with valid preoperative transthoracic echocardiographic evaluation. We then observed any development of major postoperative cardiovascular complications and pulmonary edema until hospital discharge. In-hospital major cardiovascular complications were defined as acute myocardial infarction, ventricular fibrillation/tachycardia, cardiogenic shock, newly-onset atrial fibrillation, clinical pulmonary edema requiring endotracheal intubation or dialysis. Among the 242 ESRD study patients, 9 patients (4%) developed major cardiovascular complications, and 39 patients (16%) developed pulmonary edema. Diabetes, ischemia-reperfusion time, left ventricular end-diastolic diameter (LVEDd), left ventricular mass index (LVMI), right ventricular systolic pressure (RVSP), left atrium volume index (LAVI), and high E/E' ratios were risk factors of major cardiovascular complications, while age, LVEDd, LVMI, LAVI, and high E/E' ratios were risk factors of pulmonary edema. The optimal E/E' cut-off value for predicting major cardiovascular complications was 13.0, showing 77.8% sensitivity and 78.5% specificity. Thus, the patient's E/E' ratio is useful for predicting in-hospital major cardiovascular complications after kidney transplantation. We recommend that goal-directed therapy employing E/E' ratio be enacted in kidney recipients with baseline diastolic dysfunction to avert postoperative morbidity. (http://Clinical Trials.gov number: NCT02322567)

The Pulmonary Edema Preeclampsia Evaluation (PEPE) Study

BackgroundWomen with preeclampsia may develop pulmonary edema, but the reasons for this are largely unknown. MethodsWe performed a case–control study of women with preeclampsia at two major obstetrical centres in Toronto, ON, between 2005 and 2012. Cases (n=28) were women with preeclampsia who had pulmonary edema on a chest CT or plain X-ray during the index delivery hospitalization. Control subjects (n=64) were those with preeclampsia but no diagnosis of pulmonary edema or heart failure in the index hospitalization for delivery. Study variables were abstracted from each woman’s paper chart and electronic medical record. Multivariable logistic regression with backward elimination was used to select a final set of significant predictors. ResultsApproximately one half of the cases of pulmonary edema occurred antepartum. Each 10×109/L reduction in platelet count (OR 1.32; 95% CI 1.06 to 1.65) or 10μmol/ L increase in peak serum uric acid concentration (OR 1.19; 95% CI 1.06 to 1.34) was significantly associated with pulmonary edema, as was receiving magnesium sulphate (OR 10.42; 95% CI 1.39 to 78.22). Multiparity (OR 0.03; 95% CI 0.004 to 0.29) and each 500mL increase in the volume of intravenous crystalloids received (OR 0.60; 95% CI 0.37 to 0.98) were associated with a lower risk of pulmonary edema. ConclusionWe identified several preliminary risk factors for pulmonary edema in women with preeclampsia. Additional work is needed to better understand the role of these and other factors predicting the development of pulmonary edema in women with preeclampsia.

Effect of magnesium sulfate and nifedipine on the risk of developing pulmonary edema in preterm births

To evaluate the risk of developing pulmonary edema in women exposed to nifedipine, magnesium sulfate (MgSO4), or both in a preterm setting. We carried out a retrospective case-control study at a large tertiary care center from 2007 to 2012. Cases of pulmonary edema were age, and gestational age matched to controls at a ratio of 1 case to 4 controls. Logistic regression analysis was used to estimate the effect of nifedipine and/or MgSO4 on the development of pulmonary edema while controlling for predetermined confounding variables. Stepwise logistic regression analysis was used to evaluate additional risk factors of pulmonary edema. A total of 150 charts were reviewed (28 cases and 122 controls). Nifedipine did not increase the odds of developing pulmonary edema [adjusted odds ratio (OR)=1.22 (confidence interval (CI) 0.50, 3.01), P=0.67], whereas exposure to MgSO4, or both MgSO4 and nifedipine, significantly increased the risk of developing pulmonary edema [adjusted OR=3.91 (CI 1.44, 10.65), P=0.008 and adjusted OR=4.75 (CI 1.15, 19.71), P=0.032, respectively]. In the stratified analysis, this association persisted even in nonpreeclamptic women [nifedipine: adjusted OR=0.91 (CI 0.33, 2.52), P=0.852; MgSO4: adjusted OR=3.51 (CI 1.26, 9.76), P=0.016; both: adjusted OR=3.39 (0.76, 15.07), P=0.108]. Other independent risk factors for pulmonary edema were multi-fetal pregnancy, azithromycin, and erythromycin administration. MgSO4 treatment is strongly associated with the development of pulmonary edema when used either as a tocolytic agent or for seizure prophylaxis. In light of the availability of safer alternatives, MgSO4 should be used for tocolysis only in cases whereby the benefits clearly outweigh the risks.

Impaired Left Ventricular Stroke Volume Reserve During Clinical Dobutamine Stress Predicts Future Episodes of Pulmonary Edema

The purpose of this study was to determine whether dobutamine-induced abnormal stress changes in left ventricular stroke volume (LVSV) and aortic stiffness predict future pulmonary edema. Increased aortic stiffness that decreases LVSV during adrenergic stress may serve as a marker for future pulmonary edema (PE). We measured LVSV, ventriculovascular stiffness (pulse pressure/LVSV(index)), and aortic distensibility at rest and during intravenous dobutamine administration using cardiovascular magnetic resonance. Personnel blinded to dobutamine cardiovascular magnetic resonance followed participants longitudinally over time to identify those admitted to the hospital with PE. Data for 44 participants who had a hospital admission for PE were compared with data for 72 participants of similar age, sex, and resting left ventricular ejection fraction who remained PE free. Expressed as median and interquartile range, participants with and without PE exhibited a decreased stress/rest LVSV ratio (0.9 [range 0.7 to 1.1] vs. 1.0 [range 0.9 to 1.2], respectively; p = 0.002), an increased ventriculovascular stiffness stress/rest ratio (1.4 [range 1.0 to 1.6] vs. 1.0 [range 0.8 to 1.3], respectively; p ≤ 0.001); and a decreased stress-induced measure of aortic distensibility (0.8 mm Hg(-3) [range 0.3 to 1.3 mm Hg(-3)] vs. 1.6 mm Hg(-3) [range 1.2 to 3.2 mm Hg(-3)], respectively; p = 0.002). After accounting for age, sex, left ventricular ejection fraction, risk factors for PE, and the presence of dobutamine-induced ischemia, LVSV reserve and the stress/rest ventriculovascular stiffness ratio still differed (p < 0.008 for both) in those with and without PE. In patients without inducible ischemia during dobutamine stress testing in whom one might otherwise assume a favorable prognosis, the failure to increase LVSV or an increase in ventriculovascular stiffness indicates patients at risk of subsequent PE.

Negative Pressure Pulmonary Edema Following Foramen Magnum Decompression for Chiari Malformation Type I -Case Report-

A 57-year-old obese female presented with vagal and hypoglossal nerve pareses, and magnetic resonance imaging revealed Chiari malformation type I. Standard surgical treatment for Chiari malformation type I was successfully performed. However, immediately after the patient was extubated, she developed signs of upper airway obstruction and chest radiography revealed pulmonary edema. Her ventilation was assisted by maintaining positive end-expiratory pressure at 8 cmH2O. Intravenous furosemide and hydrocortisone were administered. Her respiratory status improved 12 hours later, and she was extubated 3 days after the operation. Postextubational course was uneventful, and the patient was discharged 2 weeks after extubation. The initial neurological deficits had mostly disappeared by 10 months after the operation. This unusual case of negative pressure pulmonary edema indicates that obesity and lower cranial nerve paresis are further risk factors for pulmonary edema as a postextubational complication of surgical treatment.

Risk factors for acute pulmonary edema in preterm delivery

Objective To determine the risk factors for pulmonary edema in women with preterm delivery. Study design This was a case-controlled study of 52 (6.7%) cases with and 722 (93.3%) cases without pulmonary edema in a cohort of women who delivered between 24 and 33 weeks. Univariate and logistic regression analysis were used as indicated. Results Of subjects with pulmonary edema 98% received tocolytics while 94% had antenatal corticosteroid therapy versus 50% and 40% in controls. Significant positive associations of pulmonary edema only on univariate analysis were multiple pregnancy, earlier presenting gestational age, positive maternal cultures, small for gestational age while significant negative associations were indicated by preterm delivery and premature rupture of membranes. Independent predictors of pulmonary edema on logistic regression analysis were spontaneous preterm labor (odds ratio {OR} = 10.9, p = 0.026; 95% CI 1.3, 90), tocolytic therapy (OR = 4.3, p = 0.000; 95% CI 2.3, 8.4) especially magnesium sulfate and nifedipine, antenatal corticosteroid therapy (OR = 2.3, p = 0.002; 95% CI 1.3, 4), chorioamnionitis (OR = 2.7, p = 0.028; 95% CI 1.1, 6.5), blood product transfusion (OR = 2.3, p = 0.038; 95% CI 2.2, 8.4) and tobacco use (OR = 2.5, p = 0.016; 95% CI 1.2, 5.4). Conclusions In mothers delivering prematurely, pulmonary edema is more likely with spontaneous preterm labor, smokers, infections or those receiving blood transfusions. It occurs almost exclusively in patients treated with antenatal corticosteroids and tocolytic medication.

Risk factors for pulmonary edema in triplet pregnancies.

Multiple gestations are known to be at increased risk for pulmonary edema. Our objective was to characterize this morbidity in a cohort of triplet pregnancies. Charts from triplet pregnancies managed by the Georgetown University Hospital Maternal-Fetal Medicine service were abstracted for demographic information and complications. Cases who developed pulmonary edema were compared with those who did not using Fisher exact test, chi(2) and Student's t-test with p <0.05 considered significant. Of 66 triplet pregnancies with complete records, 15 (22.7%) were complicated by pulmonary edema. Patients developing this condition were more likely to be receiving magnesium sulfate therapy than those who did not [14/15 (93.3%) vs 32/51 (62.7%) p=0.049]. There was no difference between patients developing pulmonary edema and those who did not in terms of maternal age (mean+/-SD: 34.5+/-6.8 vs 34+/-4.3 years, p=0.8) or gestational age at delivery (33.3+/-2.3 vs 32.8+/-3.5 weeks, p=0.6), but the former group had smaller babies than the latter (1739+/- 369 vs 1891+/-538 g, p=0.04). Among the patients treated with magnesium sulfate, those who developed the more severe form of pulmonary edema were more likely than those who did not to have been treated for pre-eclampsia than preterm labor (6/10 (60%) vs 7/33 (21.2%), p=0.04). Pulmonary edema is a common complication of triplet pregnancy. Patients receiving magnesium sulfate, having pre-eclampsia or fetal growth restriction are at increased risk for pulmonary edema, particularly in its worst clinical presentation.

Pulmonary Edema After Resection of a Fourth Ventricle Tumor: Possible Evidence for a Medulla-Mediated Mechanism

A well-recognized fact is that some patients may have development of pulmonary edema in association with disorders of the central nervous system. The origin of this phenomenon, known as neurogenic pulmonary edema, is unclear but may result, in part, from select pulmonary venoconstriction modulated by autonomic outflow from the medulla oblongata. We describe a 21-year-old man who had development of pulmonary edema in association with surgical resection of a brain tumor that was close to the medulla. Other than the possibility of medullary dysfunction, which could have occurred after surgical manipulation, no other risk factor for pulmonary edema was identified. Of note, the patient's blood pressure remained normal throughout the perioperative period, and no fluid overload or primary cardiac dysfunction was evident. This case supports the theory that the medulla is an important anatomic site of origin for neurogenic pulmonary edema and that alterations in medullary function can induce pulmonary edema in humans, independent of systemic hypertension.

Peripartum colloid osmotic pressure changes: Effects of controlled fluid management

A prospective, fluid-controlled study of serially measured colloid osmotic pressure changes in the peripartum period was undertaken. Seventeen patients with uncomplicated pregnancies undergoing elective cesarean section at term were administered a predelivery bolus of 15 ml/kg of lactated Ringer's solution prior to operation. Maintenance crystalloid fluids were infused at 125 to 150 ml/hr both intraoperatively and post partum without the addition of blood or other colloid solutions. Serial colloid osmotic pressure measurements were obtained before hydration, after hydration, after delivery, and at 6 and 24 hours post partum. The results demonstrated a 15.9% decline in colloid osmotic pressure immediately following the hydration bolus (20.7 ± 1.5 to 17.4 ± 1.8 mm Hg) (p < 0.01). A further decline in colloid osmotic pressure to 16.6 ± 1.7 mm Hg occurred after delivery and represented an overall 22% decrease from the baseline value (p < 0.05). The lowest mean colloid osmotic pressure value occurred at 6 hours post partum (16.1 ± 1.1 mm Hg). These data support previous observations that colloid osmotic pressure is uniformly lowered in the immediate postpartum period with peak reductions identified at 6 hours following delivery. In addition, intravenous crystalloid administration during the peripartum interval can substantially influence this decline in colloid osmotic pressure. Although no clinical evidence of cardiopulmonary compromise was observed in this set of normal gravid women, these data may be useful in the management of the parturient patient with established risk factors for pulmonary edema where alterations in the pulmonary capillary wedge pressure-colloid osmotic pressure gradient have been shown to correlate with the development of this complication.