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At least 667 records · Page 37Linked to original sources
PubMed1999

Vitrectomy for traction macular edema.

PURPOSE: Traction macular edema may develop through contraction of macular epiretinal membranes (ERM), or due to persistent vitreomacular traction during the evolution of vitreomacular traction syndrome (VMS). The purpose of this retrospective study was to determine the effect of vitreous surgery and the release of the vitreomacular traction or the removal of epiretinal membranes, on the evolution of traction induced macular edema. MATERIAL AND METHODS: Fourteen eyes from 14 patients presenting with idiopathic or secondary epiretinal membranes, and 11 eyes from 10 patients presenting with vitreomacular traction syndrome, underwent vitrectomy for reduced vision and cystoid macular edema, identified by slit-lamp examination and fluorescein angiography. No coexistent ocular conditions that might have caused macular traction were present. History, preoperative eye examination, operative findings, postoperative course and final examination as well as pre- and postoperative fluorescein angiography were reviewed. RESULTS: In the ERM group, cystoid macular edema disappeared in all cases during the postoperative period and the mean visual acuity (VA) at the end of the follow-up (0.48 +/- 0.23) significantly increased compared to the preoperative one (0.29 +/- 0.2) (p=0.004). In the group of patients suffering from VMS, the posterior vitreous traction on the macula was released and macular edema disappeared in all cases but one. The mean v.a. at the end of the follow-up (0.42 +/- 0.24) significantly increased compared to the preoperative one (0.18 +/- 0.1) (p=0.01). Complications included intraoperative small petechias and postoperative progressive nuclear sclerosis, retinal detachment and retinal pigment epitheliopathy. CONCLUSIONS: Cystoid macular edema may develop secondary to vitreomacular traction syndrome or epiretinal membrane contraction. Vitrectomy is effective in releasing macular traction which, in turn, may induce a decrease of the macular edema with improvement of visual acuity.

Aged↗
PubMed2006

In vivo monitoring of cutaneous edema using spectral imaging in the visible and near infrared.

Tissue inflammation is often accompanied by local interstitial fluid accumulation expressed as edema. Edema can be the manifestation of infection, lymphatic blockage, wound healing, or even cancer, and is typically graded visually. Here we demonstrate that the edema reaction can be objectively quantitated in vivo by the use of spectral imaging. To this end we applied the method on a histamine-induced cutaneous edema model. Apparent concentrations of oxy-hemoglobin, deoxy-hemoglobin, and water were calculated for each pixel of a spectral image stack. These values were used to construct concentration maps for each of these molecules as well as an intensity map of an optical tissue-scattering parameter. The oxy-hemoglobin and the tissue water maps are two-dimensional quantitative representations of the skin areas involved in erythema and edema, respectively. These maps demonstrated characteristics of the wheal-and-flare reaction and their gray-level intensities were dependent on the applied histamine dose. We conclude that spectral imaging can be a valuable noninvasive tool in the study of edema pathology and can be used to monitor the edema reaction in vivo or follow the efficacy of treatments in a clinical setting.

Adult↗
PubMed2003

Risk factors for pulmonary edema in triplet pregnancies.

OBJECTIVE: 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. STUDY DESIGN: 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. RESULTS: 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). CONCLUSIONS: 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.

Adult↗
PubMed1995

Ornithine decarboxylase activity and edema formation in cerebral ischemia of conscious gerbils.

General anesthetic agents often affect the biochemical and physiologic changes triggered by cerebral ischemia. This study examined the regional activities of ornithine decarboxylase (ODC) in gerbils subjected to 5 min of bilateral carotid occlusion without anesthesia. At 2, 4, and 6 h of reperfusion, significant ODC activity was observed in both the cortex and the hippocampus. Pretreatment with alpha-difluoromethylornithine (DFMO) significantly blocked the ODC activity at 2, 4, and 6 h. Significant edema formation was found at 2, 4, and 6 h. At 2 h, edema formation was unaffected by administration of DFMO. However, DFMO treatment reduced later edema formation at 4 and 6 h. These results demonstrate that ODC activity and edema formation are delayed in gerbils after the induction of transient ischemia even with the removal of anesthetic agents and their potentially protective effects. These findings suggest that ODC activity and its induction of delayed cerebral edema are specific to cerebral ischemia and not to an anesthetic effect. DFMO treatment reduced both the ODC activity and edema formation, indicating a role for polyamines in postischemic edema formation.

Animals↗
PubMed2000

Pulmonary edema in patients after liver transplantation.

The aim of this study is to determine the incidence of radiological pulmonary edema in elective liver transplant recipients and its relationship to perioperative factors and postoperative course. We reviewed 102 chest radiographs from 34 patients who had undergone orthotopic liver transplantation (OLT). Films were assessed by 2 trained radiologists for evidence of pulmonary edema using a standardized system. Clinical and outcome data from the 34 patients were also recorded. There was a high incidence (47%) of postoperative radiological pulmonary edema that was associated with deterioration in gaseous exchange, elevated pulmonary artery pressure, and increased duration of ventilator dependence and intensive care stay. Eighteen percent of the patients developed edema immediately after surgery, which was associated with greater pulmonary artery pressure and transfusion requirements during surgery. An additional 29% developed edema during the next 16 to 20 hours, but there was no association with fluid replacement. We conclude that pulmonary edema is common after OLT and will influence postoperative recovery in a substantial proportion of transplant recipients. Excess perioperative fluid replacement is unlikely to be the sole mechanism of edema in these patients.

Female↗
PubMed1998

Heterogeneity of myocardial edema in isolated pig hearts after perfusion with different types of cardioprotective solutions.

The extent and distribution of myocardial edema induced by perfusion with cardioprotective solutions is of great interest. Domestic pig hearts (n = 12) were perfused in situ after aortic cross clamping either with Bretschneider's cardioplegic solution (HTK, 4 degrees C, n = 3), with a heparinized Krebs-Henseleit solution containing 30 mmol/L 2,3 Butanedionemonoxime (BDM, 4 degrees C, n = 3) or with heparinized pig blood (HPB, 24 degrees C, n = 3). After a three-hours storage period, magnetic resonance tomography (MRI) was carried out. The acquired T1-weighted data were used for the subsequent three-dimensional reconstruction based on the "Heidelberg ray-tracing technique". The small myocardial tissue blocks (n = 216) were excised from these hearts for dry weight measurements for 9 preselected regions in duplicate including ventricular papillary muscle, ventricular free wall, ventricular septum, apex, and atrial tissue. In control hearts (n = 3), dry weight was measured immediately after explantation (no MRI). The results of dry-weight measurements and three dimensional visualization were compared. Dry-weight measurements revealed that considerable myocardial edema is induced by any of the experimental procedures. The effects were most pronounced after BDM perfusion. Regardless how the edema was induced, there were significant differences of the water content within the heart: the water content in the heads of the papillary muscles and in the interventricular septum was always smaller than that of the free left- and right-ventricular walls. The heterogeneity of myocardial edema and its spatial distribution pattern could be qualitatively visualized. The experimental data (biophysical data and 3D visualization) clearly show a heterogeneity of myocardial edema induced by different types of cardioprotective solutions. As the presence of myocardial edema represents one of the crucial events in the pathophysiology of myocardial dysfunction occurring during myocardial infarction, ischemia, heart transplantation, and extracorporeal circulation, the present study represents an interesting contribution towards intravital detection and distribution of myocardial edema.

Animals↗
PubMed1991

Prevention of high-altitude pulmonary edema by nifedipine.

BACKGROUND: Exaggerated pulmonary-artery pressure due to hypoxic vasoconstriction is considered an important pathogenetic factor in high-altitude pulmonary edema. We previously found that nifedipine lowered pulmonary-artery pressure and improved exercise performance, gas exchange, and the radiographic manifestations of disease in patients with high-altitude pulmonary edema. We therefore hypothesized that the prophylactic administration of nifedipine would prevent its recurrence. METHODS: Twenty-one mountaineers (1 woman and 20 men) with a history of radiographically documented high-altitude pulmonary edema were randomly assigned to receive either 20 mg of a slow-release preparation of nifedipine (n = 10) or placebo (n = 11) every 8 hours while ascending rapidly (within 22 hours) from a low altitude to 4559 m and during the following three days at this altitude. Both the subjects and the investigators were blinded to the assigned treatment. The diagnosis of pulmonary edema was based on chest radiography. Pulmonary-artery pressure was measured by Doppler echocardiography and the difference between alveolar and arterial oxygen pressure was measured in simultaneously sampled arterial blood and end-expiratory air. RESULTS: Seven of the 11 subjects who received placebo but only 1 of the 10 subjects who received nifedipine had pulmonary edema at 4559 m (P = 0.01). As compared with the subjects who received placebo, those who received nifedipine had a significantly lower mean (+/- SD) systolic pulmonary-artery pressure (41 +/- 8 vs. 53 +/- 16 mm Hg, P = 0.01), alveolar-arterial pressure gradient (6.6 +/- 3.8 vs. 11.8 +/- 4.4 mm Hg, P less than 0.001), and symptom score of acute mountain sickness (2.0 +/- 0.7 vs. 3.9 +/- 1.9, P less than 0.01) at 4559 m. CONCLUSIONS: The prophylactic administration of nifedipine is effective in lowering pulmonary-artery pressure and preventing high-altitude pulmonary edema in susceptible subjects. These findings support the concept that high pulmonary-artery pressure has an important role in the development of high-altitude pulmonary edema.

Adult↗
PubMed2000

Flash pulmonary edema: association with hypertension and reoccurrence despite coronary revascularization.

BACKGROUND: The sudden development of acute (flash) pulmonary edema may be an indication for coronary angiography and revascularization. However, the prevalence of coronary artery disease in these patients and the outcome after revascularization are not known. METHODS AND RESULTS: We evaluated 46 patients with an initial presentation of flash pulmonary edema requiring hospitalization and obtained up to 3 years of follow-up in 45 patients. There were 22 men and 24 women, 44 to 84 years of age (67 +/- 10 years, mean +/- SD). Systolic blood pressure on admission was 194 +/- 38 mm Hg. Twenty-four patients required intubation and mechanical ventilation. Left ventricular ejection fraction was >40% in 27 of 46 patients. Thirty-eight patients underwent coronary angiography; 33 had obstructive coronary artery disease. One other patient had regional wall motion abnormalities. Nineteen patients underwent coronary revascularization surgically and 8 percutaneously. Overall, flash pulmonary edema reoccurred in one half of the patients. Of the 19 patients who underwent coronary revascularization, by 6 months there was 1 death and 9 patients had been hospitalized with recurrent pulmonary edema. CONCLUSIONS: Many patients with flash pulmonary edema have preserved systolic left ventricular function and coronary artery disease. Flash pulmonary edema frequently reoccurs in association with marked systolic hypertension, even after coronary revascularization. This suggests that control of hypertension is important and that coronary revascularization may not be adequate to prevent reoccurrence of flash pulmonary edema.

Adult↗
PubMed2001

Minimal intensity diode laser (810 nanometer) photocoagulation (MIP) for diffuse diabetic macular edema (DDME).

BACKGROUND AND OBJECTIVE: To determine the effectiveness of minimal intensity diode laser (810nm) photocoagulation (MIP) for diffuse diabetic macular edema (DDME). METHODS: Patients demonstrating diffuse diabetic macular edema (DDME) were treated with minimal intensity diode 810 laser photocoagulation or modified grid photocoagulation consecutively. Patients were seen and reevaluated at regular follow up visits every 3 to 4 months and retreated if residual diffuse diabetic macular edema was still present. Selected patients were tested with Goldmann visual field, pre and post-treatment. Visual improvement, visual loss, visual field, reduction/elimination of macular edema, and a number of treatments were studied. RESULTS: Reduction/elimination of DDME was observed in approximately 74% of eyes with 24 months follow up. The number of treatments per eye ranged from 1 to 5. The presence of cystoid macular edema, initial poor visual acuity, the presence of coexisting macular ischemia, or a history of systemic hypertension did not effect the outcome. Patients without a history of systemic vascular disease had a better chance of visual stabilization or improvement compared to those patients with a history of systemic vascular disease. Eighty-eight percent of patients had at least stable visual acuity at the last follow up visit. No post-treatment subjective complaints of increased pericentral scotomas were encountered in this group of patients and post-treatment atrophic scarring was substantially reduced, by using minimal intensity diode laser 810 photocoagulation, compared to eyes previously treated with shorter wavelengths and more visible burns. CONCLUSION: Minimal intensity diode laser 810nm modified grid laser photocoagulation for diffuse diabetic macular edema (DDME) is effective in reducing/eliminating DDME, although resolution of edema may be slightly prolonged and may require 1 or 2 additional treatments compared to eyes previously treated with shorter wavelengths and more visible burns. However, this method appears to be advantageous in that it appears to reduce the objective and subjective effect on the pericentral visual field, as well as substantially reducing the post-treatment atrophic scarring seen in patients treated with shorter wavelength lasers and move visible burns.

Cicatrix↗
PubMed1990

Brain edema following an experimental missile wound to the brain.

Brain edema occurs after brain injury and may be life threatening. The occurrence and type of brain edema, its magnitude, and time course have never been ascertained following a missile wound to the brain. We therefore measured the development of brain edema in a series of cats in which a right cerebral hemisphere wound was made with a 2.0 mm, 31.7 mg steel sphere with a velocity of 240-300 m/s (0.9-1.4 J). The entire brain was surveyed for postwounding brain edema by determining the wet weight minus dry weight. Brain edema was seen to develop only in the white matter about the missile wound track in the injured cerebral hemisphere. There, brain water rose from 66 to 73%; white matter sodium also increased significantly from approximately 150 mEq/kg dry weight to 254 mEq/kg dry weight. Potassium levels remained essentially unchanged. This vasogenic edema was relatively mild, peaked at 24-48 h after wounding, and resolved spontaneously within a week without specific treatment. We infer that brain edema following an uncomplicated cerebral missile wound in the human brain is also mild, self-limited, and may resolve spontaneously without special treatment.

Animals↗
PubMed1990

Early polymorphonuclear leukocyte accumulation correlates with the development of posttraumatic cerebral edema in rats.

To evaluate the role of polymorphonuclear leukocytes (PMNs) in the development of posttraumatic cerebral edema, we quantitatively assessed the time course and magnitude of PMN accumulation and its relationship to cerebral edema formation after cerebral trauma in 78 rats. 111In-labeled PMN accumulation was measured in 26 rats in the first 8 h after right hemispheric percussive cerebral trauma or a sham control condition. 51Cr-labeled erythrocyte accumulation was measured simultaneously in 22 rats to assess the contribution of expansion of blood volume to early posttraumatic PMN accumulation. Edema formation [right-left (R-L) hemispheric difference in percent brain water], R-L hemispheric labeled-PMN accumulation, and blood volume index-adjusted PMN accumulation were measured between 0-2 h and 4-8 h posttrauma. PMN accumulation was elevated markedly in the first 2 h posttrauma compared with values in sham controls (13.45 +/- 2.53 vs -0.03 +/- 0.31, p less than 0.01) but not when adjusted for blood volume index (BVI), suggesting that PMN accumulation in the first 2 h posttrauma was due to expansion of blood volume. Between 4 and 8 h posttrauma, however, both total (2.56 +/- 0.82 vs -0.29 +/- 0.52) and BVI-adjusted (8.78 +/- 3.97 vs -0.48 +/- 0.79) PMN accumulation were elevated (p less than 0.05) compared with sham. Brain edema and total PMN accumulation were significantly correlated at both 2 h and 8 h posttrauma (r2 = 0.77, p less than 0.001, and r2 = 0.69, p less than 0.002, respectively), but a significant correlation between edema and BVI-adjusted PMN accumulation was observed only at 8 h posttrauma (r2 = 0.96, p less than 0.001). These data show that PMN accumulation after traumatic brain injury occurs with an initial phase explained by an increase in blood volume in the first 2 h posttrauma followed by a subsequent acute inflammatory phase. The significant correlation between PMN accumulation and the development of cerebral edema is the first quantitative relationship demonstrated between PMN accumulation and a relevant pathophysiological variable. A causal role for PMNs in the genesis of posttraumatic cerebral edema has yet to be proved.

Animals↗
PubMed1995

Effect of hypoxia or hyperbaric oxygen on cerebral edema following moderate fluid percussion or cortical impact injury in rats.

This study was designed to evaluate the production of cerebral edema [as measured by tissue specific gravity (SpG)] following moderate fluid percussion (FP) and cortical impact (CI) injury in rodents. To determine the effects of a secondary systemic insult, hypoxia (13% oxygen for 30 min) was added to some experimental groups immediately after head injury. To determine the effects of hyperbaric oxygen (HBO) on injured cortical tissue, additional animal groups were exposed to HBO (1.5 atm, for 60 min), beginning 4 h after head trauma. Both injury models produced equal amounts of tissue edema at the site of injury (mean SpG +/- SEM = 1.035 +/- 0.001), when measured 6 h posttrauma. There was no significant edema at the tissue sites immediately adjacent to the trauma sites. The addition of hypoxia to either injury system did not increase edema formation beyond that produced by injury alone. HBO reduced the water content of the trauma site in animals that had received FP, but not in animals receiving CI. We conclude that with the injury parameters used in this protocol, both FP and CI appear to produce focal cerebral edema at the site of trauma. Hypoxia does not worsen edema. HBO appears to reduce edema produced by FP, but not by CI.

Animals↗
PubMed2005

Diffusion-weighted imaging of edema following traumatic brain injury in rats: effects of secondary hypoxia.

Hypoxia and edema are frequent and serious complications of traumatic brain injury (TBI). Therefore, we examined the effects of hypoxia on edema formation after moderate lateral fluid percussion (LFP) injury using NMR diffusion-weighted imaging (DWI). Adult Sprague-Dawley rats were separated into four groups: sham uninjured (S), hypoxia alone (H), trauma alone (T), and trauma and hypoxia (TH). Animals in Groups T and TH received LFP brain injury, with Groups H and TH undergoing 30 min of moderately severe hypoxia (FiO2 = 0.11) immediately after surgery or TBI (respectively). DWIs were obtained at 2, 4, and 24 h and at 1 week post injury, and apparent diffusion coefficient (ADC) maps were constructed. Animals in Groups T and TH showed an early decrease (p < 0.001) in ADC values in the cortex ipsilateral to TBI 4 hr post injury, followed by elevated ADCs 1 week later (p < 0.05). No significant differences in ADC values were seen between T and TH groups in the ipsilateral cortex. In contrast, the ipsilateral hippocampus for Group TH showed only increasing ADC values. This hyperintensity in the ADC map began at 2 h after TBI, was significant by 24 h (p < 0.05), and reached a maximum at 1 week. This hyperintensity was not observed in Group T. Histopathology seen in TBI animals corresponded well with the pathology observed with MRI. Midline shifts reflecting edema were only observed in TBI animals with little difference between normoxic (T) and hypoxic animals (TH). In sum, this study demonstrates that the development and extent of brain edema following TBI can be examined in vivo in rats using DWI technology. TBI resulted in an early decrease in ADC values indicating cytotoxic edema in the cortex that was followed at 1 week by an increase in the ADC that was associated with decreased tissue cellularity. Histopathology corresponded well to the regions of brain injury and edema visualized by T2 and DWI procedures. Overall, the addition of hypoxia to brain injury resulted in a small increase in the magnitude of edema in hippocampus and cortex over that seen with trauma alone.

Animals↗
PubMed2004

Water permeability and TCDD-induced edema in zebrafish early-life stages.

A common response to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure in teleost embryos is blue-sac disease, characterized by pericardial and yolk-sac edema. The cellular and extracellular fluids of freshwater fish are hyperosmotic compared to the surrounding water. In order to be in osmotic balance, freshwater fish must maintain a barrier to minimize water entry and excrete excess water that passes the barrier. We hypothesized that edema observed in TCDD-exposed zebrafish was caused by a failure of a barrier to incoming water. As a test of this hypothesis, we removed the osmotic gradient that drives water entry by increasing the osmolarity of the surrounding water with mannitol. Abolishing the osmotic gradient between the interior body fluids and the water environment of the developing zebrafish significantly reduced both pericardial and yolk-sac edema. When added after edema formation had already started, mannitol only partially reversed pre-existing edema. An alternate hypothesis is that TCDD impairs water excretion, allowing water to accumulate as edema fluid. However, we were unable to demonstrate an alteration in kidney function: expression of early markers for kidney development appeared normal, and we did not observe TCDD-induced changes in kidney filtration. An alteration in the overall shape of the kidney was observed, but this may be a consequence of compression by edema. In conclusion, TCDD exposure may inhibit the function of a permeability barrier to water, which is critical for maintaining osmotic balance in early development.

Aging↗
PubMed1993

Opposing roles of cyclic AMP in the vascular control of edema formation.

Eight agents that increase the intracellular concentration of cyclic AMP were tested for their effect on edema formation. The specificity of the agents for vascular smooth muscle or the endothelium was determined by measuring vasodilation with a laser Doppler flow probe and cAMP production by endothelial cells and vascular smooth muscle cells in culture. The agents were injected intradermally in anesthetized rabbit skin and the local accumulation of 125I-labeled albumin in response to intradermal bradykinin was measured. Iloprost, prostaglandin E1, prostaglandin E2, pituitary adenylate cyclase activating polypeptide (PACAP), and vasoactive intestinal polypeptide (VIP) potentiated bradykinin-induced edema. These same agents also increased blood flow and vascular smooth muscle cAMP concentrations, but did not increase endothelial cell cAMP production. Albuterol suppressed edema formation, did not cause vasodilation, but did increase endothelial cell cAMP concentrations. The phosphodiesterase inhibitor rolipram did not cause vasodilation, but suppressed edema and potentiated the cAMP response to albuterol in cultured endothelial cells. L-Isoproterenol affected both cell types. At a lower concentration L-isoproterenol was a potent stimulus to endothelial cell cAMP production and inhibited edema formation; a higher dose had additional effects on vascular smooth muscle and significantly increased blood flow. These findings support the hypothesis that increasing intracellular cAMP concentrations in vascular smooth muscle promotes edema via increased blood flow. In contrast, increasing cAMP concentrations in endothelium may suppress edema by enhancing the permeability barrier.

Albuterol↗
PubMed1979

The significance of mammary skin edema in noninflammatory breast cancer.

Mammary skin edema has been quantitated in 205 cases of T1, T2 and T3 breast cancer by mammographic measurement, and its prognostic significance assessed. Edema was present in 70% of patients and the incidence was directly related to tumor size. Edema was seen on occasions in all quadrants of the breast, but the inner and lower quadrants were the most frequent sites of edema irrespective of the site of tumor. Histology showed the skin thickening located in the reticular dermis; the papillary dermis and epidermis showed no change. It was shown that neither dermal lymphatic involvement nor lymphatic obstruction by regional node involvement was of primary etiological significance. Skin edema correlates with prognosis since there is an increased likelihood of both systemic and local recurrence if skin edema exceeds 0.5 mm. Further investigation and longer follow-up is necessary to show whether skin edema represents a parameter which carries prognostic significance independent of the more usual clinical indications.

Breast Diseases↗
PubMed2001

Pulmonary edema: new insight on pathogenesis and treatment.

Pulmonary edema is one of the most serious and life-threatening situations in emergency medicine. Lately it has become apparent that in most cases pulmonary edema is not caused by fluid accumulation but rather fluid redistribution that is directed into the lungs because of heart failure. Based on a series of recently published studies, we propose that often the pathogenesis of pulmonary edema is related to a combination of marked increase in systemic vascular resistance superimposed on insufficient systolic and diastolic myocardial functional reserve. This resistance results in increased left ventricular diastolic pressure causing increased pulmonary venous pressure, which yields a fluid shift from the intravascular compartment into the pulmonary interstitium and alveoli, inducing the syndrome of pulmonary edema. Therefore, the emphasis in treating pulmonary edema has shifted from diuretics (ie, furosemide) to vasodilators (ie, high-dose nitrates) combined with noninvasive positive airway pressure ventilation and rarely inotropes. New classes of drugs that are currently being investigated for treating decompensated heart failure such as natriuretic peptides, calcium promoters, and endothelin antagonist are also being assessed for treating pulmonary edema. This review will explore this new hypothesis put forward to explain the pathogenesis of pulmonary edema and the evolving management strategies.

Humans↗
PubMed1987

Radiographic differentiation between different etiologies of pulmonary edema.

We compared the plain chest radiographs of critically ill patients who had different types of pulmonary edema and evaluated the radiographs according to a standardized score sheet of findings. We included 94 total cases of pulmonary edema: 49 with cardiogenic, 33 with permeability, and 12 with renal/overhydration pulmonary edema. Patients with cardiogenic edema had enlarged hearts, vascular engorgement, septal lines, and absence of air bronchograms significantly more often than patients with permeability pulmonary edema. Renal/overhydration patients had enlarged hearts significantly more often than patients with permeability edema. There were no other statistically significant differences. Heart size and presence or absence of septal lines could have been used to distinguish cardiogenic and permeability edema in 83% of cases.

Capillary Permeability↗