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PubMed1997

Evidence for a hydrostatic mechanism in human neurogenic pulmonary edema.

STUDY OBJECTIVES: To identify the relative contribution of hydrostatic and permeability mechanisms to the development of human neurogenic pulmonary edema. DESIGN: Retrospective review of patients with neurogenic pulmonary edema who had pulmonary edema fluid analysis. SETTING: University hospital ICU. PATIENTS: Twelve patients with neurogenic pulmonary edema in whom the associated neurologic condition was subarachnoid hemorrhage (n = 8, 67%), postcraniotomy (n = 2), and stroke (n = 2). MEASUREMENTS: Protein concentration was measured from pulmonary edema fluid and plasma samples obtained shortly after the onset of clinical pulmonary edema. RESULTS: The mechanism of pulmonary edema was classified according to the initial alveolar edema fluid to plasma protein concentration ratio. A hydrostatic mechanism (ratio < or = 0.65) was observed in seven patients, none of whom had cardiac failure or intravascular volume overload. Five patients had evidence for increased permeability (ratio > 0.70). Patients with a hydrostatic mechanism had better initial oxygenation (mean +/- SD PaO2/FIO2 [fraction of inspired oxygen] = 233 +/- 132) compared with patients with increased permeability (PaO2/FIo2 = 80 +/- 42), and oxygenation improved more rapidly in the hydrostatic patients. Overall mortality (58%) was high, but it was related to unresolved neurologic deficits, not to respiratory failure. CONCLUSION: Many of our patients had a hydrostatic mechanism for neurogenic pulmonary edema. This is a novel observation in humans since prior clinical case reports have emphasized increased permeability as the usual mechanism for neurogenic pulmonary edema. These findings are consistent with pulmonary venoconstriction or transient elevation in left-sided cardiovascular pressures as contributing causes to the development of human neurogenic pulmonary edema.

Adult↗
PubMed1999

Fatal postoperative pulmonary edema: pathogenesis and literature review.

STUDY OBJECTIVES: Pulmonary edema is a known postoperative complication, but the clinical manifestations and danger levels for fluid administration are not known. We studied (1) 13 postoperative patients (11 adult, 2 pediatric) who developed fatal pulmonary edema, and (2) one contemporaneous year of inpatient operations at two university teaching hospitals to determine the clinical manifestations, causes, epidemiology, and guidelines for fluid administration. DESIGN: Retrospective analysis of 13 patients with fatal postoperative pulmonary edema and one contemporaneous year of major inpatient surgery. PATIENTS AND METHODS: Thirteen patients had net fluid retention of at least 67 mL/kg in the initial 24 postoperative hours and developed pulmonary edema. Ten were generally healthy while three had serious associated medical conditions. MEASUREMENTS AND RESULTS: There was no measurement, laboratory value, or clinical finding predictive of impending pulmonary edema. The most common clinical manifestation following the onset of pulmonary edema was cardiorespiratory arrest (n = 8). Patients had metabolic acidosis (pH = 7.15 +/- .33), hypoxia (PO2 = 45 +/- 18 mm Hg), and normal electrolytes. The diagnosis of pulmonary edema was established by chest radiograph and confirmed by autopsy and pulmonary artery pressure (21 +/- 4 mm Hg). The mean net fluid retention was 7.0 +/- 4.5 L (90 +/- 36 mL/kg/d) and exceeded 67 mL/kg/d in all patients. Autopsy revealed pulmonary edema with no other cause of death. Among 8,195 major operations, 7.6% developed pulmonary edema with a mortality of 11.9%. Extrapolation to the 8.2 million annual major surgeries in the United States yields a projection of 8,000 to 74,000 deaths. CONCLUSIONS: Pulmonary edema can occur within the initial 36 postoperative hours when net fluid retention exceeds 67 mL/kg/d. There are no known predictive warning signs and cardiorespiratory arrest is the most frequent clinical presentation. The monitoring systems currently in use neither detect nor predict impending pulmonary edema, and as yet, there are no known panic values for excessive fluid administration or retention.

Adult↗
PubMed2003

Edema after intracerebral hemorrhage: correlations with coagulation parameters and treatment.

OBJECT: Development of edema is known to contribute to poor outcome after spontaneous intracerebral hemorrhage (ICH). Recent research has identified thrombin as a key mediator in the development of edema in animal models; however, little has been published correlating the coagulation cascade and edema in humans. METHODS: In this retrospective clinical study of 80 patients with spontaneous supratentorial ICH, the authors sought to identify factors associated with edema development and outcome, including lesion imaging parameters, anticoagulant use, international normalized ratio and platelet count on hospital admission, and treatment with mannitol and steroid medications. A multivariate model was used to identify edema volume, use of mannitol, elevated blood glucose, and the presence of intraventricular hemorrhage as predictors of poor outcome at the time patients were discharged from the hospital. The authors developed a quadratic model for predicting edema volume against time by using a random coefficients model, and found that edema peaks between Days 5 and 6 after onset of ICH. The volume of the hemorrhage and the platelet count correlated significantly with edema volume within the first 24 hours post-ICH in the multiple regression analysis (p < 0.0001, r2 = 0.75). Edema growth during the first 5 days post-ICH also correlated with the platelet count, with an increasing platelet count associated with an increasing growth of edema (p = 0.0013). CONCLUSIONS: The authors propose that factors released from activated platelets at the site of hemorrhage, for example vascular endothelial growth factor, may interact with thrombin to increase vascular permeability and contribute to the development of edema.

Adrenal Cortex Hormones↗
PubMedDate not supplied

Gallbladder edema in Dengue hemorrhagic fever and its association with haematocrit levels and type of infections.

AIM: To determine gallbladder edema with type of Dengue infection and hematocrit level. METHODS: A retrospective study was performed on 225 cases of DHF admitted from January to December 1997 to determine the association between the type of Dengue infection, hemoconcentration and the presence or absence of gallbladder edema. Primary or secondary types of Dengue infection consider to determine the severity and degree of plasma leakage in dengue hemorrhagic fever. The Chi square and Spearman 's tests were performed to establish association between variables. RESULTS: out of 225 cases of DHE 129 cases were found with the following dengue serology test results: 92 IgM positive and 37 negative. Abdominal ultrasound was performed in 57 cases, revealing gallbladder edema in 17 cases and none in 40 cases. The 57 cases were classified as primary dengue cases (positive IgMA), secondary dengue(positive IgM and IgG), or seronegative (negative IgM). Primary dengue was found in 5 cases with gallbladder edema and 15 cases without (25%). In the secondary dengue group,10 cases were found with gallbladder edema and 8 cases without (55.5%), while in the non-Dengue group, there were 2 cases with gallbladder edema and 17 cases without (10.5%). There was association between the development of gallbladder edema and the type of dengue infection(p=0.010). Gallbladder edema was more common in secondary Dengue (55%). There was a tendency for gallbladder edema in patients with higher increases in hematocrit. CONCLUSION: It conclude that gallbladder edema is more common in cases of secondary dengue and that there is a tendency for gallbladder edema with higher increase of hematocrit.

Edema↗
PubMed1990

[Plasma atrial natriuretic peptide (ANP) levels in Parkinson's disease--with special reference to foot edema].

Edema in Parkinson's disease has been considered to be caused by autonomic nervous system dysfunctions, however little is still known about the exact pathophysiological mechanism involved. In this study, we focused on plasma atrial natriuretic peptide (ANP) levels in Parkinson's disease to elucidate the relationship between foot edema and plasma ANP levels. Thirty four cases of Parkinson's disease were studied. Plasma ANP levels were measured using the radioimmunoassay method. The incidence of foot edema in Parkinson's disease was approximately 30% of the cases studied, with a tendency to be more common in patients in the Yahr stages II and III groups. Predilection sites of the edema were observed from the pretibial to dorsal pedis of both lower thighs, especially on the side most severely affected by the disease. Onset of the edema was difficult to clarify because almost all of the patients with foot edema did not notice the edema by themselves. There was no clear relationship between edema and L-DOPA treatment of Parkinson's disease. For treatment of the edema, oral administration of Furosemide was effective in many cases, however the efficacy tended to gradually decrease. Plasma ANP levels in each age group of the Parkinson's disease cases were statistically high when compared to the values of the age-matched normal volunteers. Plasma ANP levels in the patients with foot edema were also significantly high when compared with the edema-free patients (p less than 0.001), however no relationships were found between plasma ANP levels, age and duration of the illness. It is known that plasma ANP is a cardiac hormone with fluid volume-reducing and vasodilating functions.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

Corneal edema recovery dynamics in the rabbit. A useful model?

Open-eye and closed-eye recovery from contact lens-induced corneal edema was measured on the right eyes of 10 New Zealand White rabbits using ultrasound pachometry. Edema was produced by either 2 hours of eye closure (Patch Test) or 2 hours wearing of a thick hydrogel contact lens over the closed eye (Lens Test). The measured corneal edema recovery data were analyzed by both linear-regression analysis and nonlinear-regression analysis based on a previously published exponential open-eye edema recovery model. Linear-regression analysis revealed that the initial rabbit open-eye edema recovery rate of 36.3 +/- 11.9 (standard deviation) micron/hr was not significantly different (P greater than 0.25) from the initial young human open-eye edema recovery rate of 35.6 +/- 3.4 micron/hr. Similarly, the initial rabbit closed-eye edema recovery rate of 14.3 +/- 5.4 micron/hr was found to be not significantly different (P greater than 0.25) from the initial young human closed-eye edema recovery rate of 15.0 +/- 2.2 microns/hr. Corneal edema recovery indices derived using nonlinear-regression analysis also had a strong similarity between rabbit and human corneal edema recovery rates. For example, the calculated percent recovery per hour (PRPH) for rabbit open-eye corneal edema recovery of 41.4 +/- 11.3%/hr agreed well with the reported human open-eye PRPH of 34.2-58.9%/hr. The rabbit closed-eye PRPH of 25.6 +/- 10.7%/hr was also found to lie between the calculated human closed-eye PRPH values of 19.9-30.2%/hr.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

[Effects of photocoagulation on diabetic macular edema].

Retrospective analysis of clinical cases observed for three years with respect to the appearance of the fundus and visual acuity was conducted to evaluate the effect of photocoagulation therapy on macular edema in relation to whither diabetic retinopathy was accompanied by, focal or cystoid, macular edema. In addition to glycemic control, focal and direct treatment of responsible lesions was found effective for focal macular edema in simple diabetic retinopathy. Concerning all types of retinopathy, the prognosis of focal macular edema was significantly favorable to that of cystoid macular edema. Blood sugar control also influenced the prognosis of focal edema. The changes of retinopathy were closely associated with the prognosis of focal macular edema in preproliferative and proliferative retinopathy. Disseminated photocoagulation and panretinal photocoagulation showed no difference as to the results of indirect treatment of focal macular edema in preproliferative retinopathy. Macular alterations other than macular edema occurred in a higher proportion of cases of proliferative retinopathy than in simple or preproliferative retinopathy. This accounted for low visual recovery in the former group in comparison to simple retinopathy. It was concluded that the direct treatment of the involved lesions is effective for focal macular edema in simple retinopathy and that extensive photocoagulation in preproliferative and proliferative retinopathy indirectly has a favorable influence on focal edema by means of amelioration of retinopathy.

Adult↗
PubMed1983

Enhancement of carrageenan and dextran-induced edemas by 2,3,7,8-tetrachlorodibenzo-p-dioxin and related compounds.

Paw edema formation after the subplantar injection of carrageenan was enhanced in rats treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). The enhanced carrageenan response could be detected as early as 4.5 hr after TCDD; however, the magnitude of enhancement was greatest when rats were challenged with carrageenan 5 days after TCDD. In the latter case, the ED50 of TCDD in enhancing the carrageenan response was 6 micrograms/kg. TCDD also enhanced dextran-induced paw edema, which follows a time course different from that of carrageenan-induced edema and is produced by a different mechanism. The enhancement of carrageenan and dextran paw edemas was due to an increase in the edema-producing potency of the irritants and not to a change in their maximum effect. The ability of other 3-methylcholanthene-type inducers to enhance carrageenan-induced paw edema and the inability of phenobarbital-type inducers to cause the response suggest that the TCDD binding protein might be involved in edema enhancement. TCDD also enhanced carrageenan-induced pleural edema; however, the number and type of leukocytes recovered in the pleural exudate was not affected. TCDD did not alter granuloma formation produced by the subcutaneous implantation of cotton pellets, indicating that enhancement by TCDD was peculiar to edema formation and not to inflammation in general. It is suggested that TCDD may enhance carrageenan and dextran edemas by increasing the availability of mediators involved in each type of edema formation and/or by increasing the responsiveness of the vasculature to mediators.

Animals↗
PubMed1983

Relationship of pulmonary edema after hemorrhagic shock to intravascular coagulation.

We examined the relationship between hemorrhage-induced alterations in the extravascular lung water content and the degree of intravascular coagulation in nonheparinized dogs. The severity of pulmonary edema was assessed by the extravascular lung water content to bloodless dry lung weight ratio (W/D), and the degree of intravascular coagulation in the lung was assessed by prior injection of 125I-labeled fibrinogen. Pulmonary edema developed in only 4 of 12 dogs (ie, W/D ratio of 4.86 +/- 0.12 ml/gm vs 3.21 +/- 0.056 in controls), while in others the W/D ratio of 3.23 +/- 0.11 was in the normal range. The animals that developed pulmonary edema also had increased 125I-activity in the lungs, while the activity was not increased in dogs that did not develop pulmonary edema. Pulmonary vascular resistance (PVR) increased to the same extent in both groups, while arterial pO2 decreased and venous admixture increased during hemorrhage only in dogs that developed pulmonary edema. Pulmonary blood volume decreased in dogs with pulmonary edema, and the decrease was largely confined to the dependent lung regions. The results suggest the activation of intravascular coagulation and pulmonary thromboembolization in only those dogs developing pulmonary edema. The relationship of intravascular coagulation to edema in these animals suggests that the edema was due to activation of cellular (eg, granulocytes) or humoral factors (eg, fibrin degradation products) associated with intravascular coagulation. However, most dogs subjected to hemorrhage did not have intravascular coagulation in lungs and did not develop pulmonary edema. Thus, differences in activation of intravascular coagulation may explain why pulmonary edema does not commonly occur after hemorrhage.

Animals↗
PubMed1993

Tumor prostaglandin levels correlate with edema around supratentorial meningiomas.

The pathophysiological mechanisms to explain peritumoral edema have not been clarified. Multiple aspects of brain edema secondary to supratentorial meningiomas were prospectively investigated in a group of 29 patients who underwent surgery consecutively. Sixty-nine tumor samples were analyzed for prostanoid levels. Levels of 6-keto-PGF1 alpha, the stable metabolite of prostacycline, were found to correlate well with the extent of edema (r = 0.51, P < 0.01). The ratio, 6-keto-PGF1 alpha x PGE2/TXB2, was found to have the best correlation with edema index (extension/tumor volume) (r = 0.69, P < 0.005). A case of a hemangiopericytic meningioma with the largest edema extent within the study group also exhibited the highest level of 6-keto-PGF1 alpha (2420 pg/mg protein). Steroid treatment (dosage, duration of therapy, and their product) did not correlate with prostaglandin levels. These findings may explain the inconsistent clinical effects of steroids on meningioma-induced edema. Possible explanations for this phenomenon are discussed. Otherwise, histology, pathological features of tumor aggressiveness, or mechanical parameters, such as its volume, location, and insertion site, did not correlate well with edema parameters or with prostaglandin levels. Similarly, tumor water content, imaging parameters in computed tomography and magnetic resonance, and operative findings (including dissection plane, vascularity, and tumor firmness) did not correlate well with edema parameters. Although a direct cause-effect relationship between prostaglandins and peritumoral edema is not conclusively established, the circumstantial evidence of the ability of prostaglandins to induce vasogenic brain edema and the robust association with peritumoral edema is persuasive.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1975

[Pulmonary edemas. Anatomic study].

Whatever the etiology of pulmonary edema, i.e. increase in intrapulmonary water, edema passes through three, moreover intricate phases: 1- intracellular edema clearly visible in the type 1 pneumocyte. This intracellular edema appears at the same time as: 2- interstitial edema; that which appears when: 3- numerous vesicules of pinocytosis and separation of the capillary endothelial cells account for it; 4- intra-alveolar edema itself appears later and corresponds to the major clinical phase of pulmonary edema. There is nothing surprising about this as the cellular functions of pneumocytes are impervious as can be shown for example by studies carried out with tracers. This intracellular alveolar edema seems to have two different aspects depending on whether the experimental conditions create an acute or sub-acute pathology. In the acute form, the edema is poor in lipids and in proteins. In the sub-acute of chronic forms, it is on the contrary very rich in them. 5-In the last phase, a veritable desquamation of the pneumocytes then of the endothelial cells is produced which is very frequently lethal. If survival occurs, two sorts of lesions are found: -colonisation of the alveolar surface with type II pneumocytes; - occurrence of possible intersitial fibrosis. The remarkable fact is that such lesions are visible in a more or less identical manner in all cases of pulmonary edema, whether they be hemodynamic or lesional. The morphology does not confirm this physiopathological distinction which is moreover questionable as all pulmonary edema become lesional sooner or later.

Humans↗
PubMed2006

Peripheral edema due to heart disease: diagnosis and outcome.

BACKGROUND: The purpose of this study was to determine whether baseline physical examination and history are useful in identifying patients with cardiac edema as defined by echocardiography, and to compare survival for patients with cardiac and noncardiac causes of edema. HYPOTHESIS: Physical examination and history data can help to identify patients with edema who have significant cardiac disease. METHODS: We reviewed the medical records of 278 consecutive patients undergoing echocardiography for evaluation of peripheral edema. We classified cardiac edema as the presence of any of the following: left ventricular ejection fraction < 45%, systolic pulmonary artery pressure > 45 mmHg, reduced right ventricular function, enlarged right ventricle, and a dilated inferior vena cava. RESULTS: The mean age of the 243 included patients was 67 +/- 12 years and 92% were male. A cardiac cause of edema was found in 56 (23%). Independent predictors of a cardiac cause of edema included chronic obstructive pulmonary disease (COPD, odds ratio [OR] 1.74, 95% confidence interval [CI] 1.14-2.60) and crackles (OR 1.98, 95% CI 1.26-3.10). The specificity for a cardiac cause of edema was high (91% for COPD, 93% for crackles); however, the sensitivity was quite low (27% for COPD, for 24% crackles). Compared with patients without a cardiac cause of edema, those with a cardiac cause had increased mortality (25 vs. 8% at 2 years, p < 0.01), even after adjustment for other characteristics (hazard ratio 1.55, 95% CI 1.08-2.24). CONCLUSIONS: A cardiac cause of edema is difficult to predict based on history and examination and is associated with high mortality.

Aged↗
PubMed1990

Genetically determined transient edema found in the WB/ReJ mouse strain in a teratogenic survey with acetazolamide.

A continuing survey of the genetic variability of different mouse strains to acetazolamide teratogenesis demonstrated the WB/ReJ strain expresses a high frequency of induced subcutaneous edema in day 15 fetuses. In treated WB/ReJ fetuses, the probability of expression of edema is independent of the expression of forelimb ectrodactyly and, with the dosage regime, there is no significant increase in acetazolamide-induced resorption. It was surprising to find a high frequency of spontaneous edema on day 15 in untreated WB/ReJ fetuses. The spontaneous edema is a transient trait with maximum expression (56%) on day 14, and it is resolved by day 17 without apparent consequence to the survival of previously affected fetuses. There is no sex dimorphism in the liability to express the transient edema. Preliminary genetic crosses to investigate the spontaneous edema were made between WB/ReJ and the C57BL/6J strain, which historically had not be observed to express spontaneous edema. A low frequency of spontaneous edema was observed on day 14 in both C57BL/6J and the reciprocal F1 fetuses. The trait is not additive because there is dominance deviation of the BC1 fetuses in the direction of the F1 fetuses. The data were fitted to a threshold model suggesting that the developmental liability to express the difference in transient edema is determined by more than one gene, but the data can be interpreted by a minimum of two loci with duplicate epistasis. The observed differences in frequencies of edema suggest the genetic model can be tested with relatively few test crosses.

Acetazolamide↗
PubMed1994

Regional cerebral blood flow trends in head injured patients with focal contusions and cerebral edema.

Focal contusions following head injury may be associated with focal or diffuse cerebral edema. Early global hyperemia and perifocal hyperemia may play a role in cerebral edema, although causal relationships have yet to be clearly been defined. We studied 27 patients with head injury (admission GCS 3-12) resulting in focal contusions (without evidence of subarachnoid, intraventricular or intraparenchymal hemorrhage by CT). Patients were studied with ICP monitors, head CTs, and intravenous 133Xenon regional cerebral perfusion studies serially over several days post injury. Low cortical blood flow and a low mean CBF15 flow were evident on the day of the injury. Additionally, F1 analysis indicated significantly (p < 0.05) greater cortical blood flow in the surrounding brain (mean 60 cc/100 g/min) compared to the contusion area (mean 43 cc/100 g/min) on the day of trauma. Mean regional CBF remained below normal in the contused areas (CBF15 < 35 cc/100 g/min), however the cortical flow increased in the first few days post-injury (peak F1 = 95 cc/100 g/min on day 3) then decreased to sub-normal levels. The mean CBF in the surrounding brain was low on the day of injury (CBF15 = 29 cc/100 g/min), although higher than the contused area, and increased to a peak of 45 cc/1009/min on day 3 posttrauma. Cortical flow in the surrounding brain, however, exhibited a different trend. The mean F1 was low on the day of trauma and significantly higher one day after trauma (mean 105 cc/100 g/min). Only 15 of the 27 patients with focal contusions had evidence of cerebral edema. Eleven of these exhibited focal edema and 4 exhibited diffuse edema. Focal edema developed over the first few days posttrauma as seen in followup CT, whereas patients with diffuse edema exhibited edema on the admission CT. Initial oligemia in the contused areas was associated with a subsequent hyperemic rim about the contusion. Focal hyperemia was associated with focal edema in 41% of the patients, whereas diffuse edema appeared to be independent of the hyperemic response in contusions.

Adolescent↗
PubMed2002

Alterations in diffusion and perfusion in the pathogenesis of peritumoral brain edema in meningiomas.

Magnetic resonance perfusion and diffusion studies were undertaken to clarify the significance of ischemia in the pathogenesis of peritumoral brain edema in patients with meningiomas. Included in this study were 26 patients with 27 meningiomas and 5 gliomas. Perfusion-weighted imaging (PWI) was performed using a gradient-echo, echo-planar-imaging (EPI) sequence for calculation of the relative regional cerebral blood volume (rrCBV) and the relative regional cerebral blood flow index (rrCBFi). Furthermore, multi-slice spin-echo EPI sequences were applied in order to obtain anisotropic and isotropic diffusion-weighted imaging (DWI). Apparent diffusion coefficient (ADC) values were then calculated for peritumoral brain parenchyma from tumors, with and without edema, using various diffusion sensitivities. Meningiomas without edema demonstrated a minimal increase of perfusion parameters in the peritumoral brain tissue. In contrast, cases with brain edema had highly significant ( p<0.0005) lower rrCBV and rrCBFi. The edema index (EI) correlated strongly with the rrCBV. A fitting procedure resulted into the following mathematical relation: EI=0.1/rrCBV(2). The DWI showed a significantly larger ADC value within areas of brain edema, compared with the normal white matter (0.74 x 10(-3) vs 1.55 x 10(-3) mm(2)/s; p<0.0001). Increases in EI correlated with increases in ADC values. In 31% of the meningiomas associated with edema, areas with increased signal, probable ischemia, demonstrated significantly lower ADC values, in comparison with the rest of the edematous areas. These areas were confined to tissue immediately adjacent to the tumor. In general, the decrease in rrCBV in brain edema represents a consequence from, rather than a cause of, vasogenic edema. Ischemic alterations can be regarded as secondary, facultative phenomena in the pathogenesis of meningioma-related brain edema.

Adult↗
PubMed2003

Spontaneous remission of edema and regranulation of goblet cells in rat tracheae after capsaicin-induced acute inflammation.

Previous studies have investigated the short-term effect of capsaicin on edema formation and goblet-cell secretion in the trachea. The present study sought to investigate the long-term effect of a high dose of capsaicin (90 micro g/ml/kg), administered intravenously, on changes in the formation of endothelial gaps among venular endothelial cells, mucosal tissue edema and the secretory activity of goblet cells, including the number and size of goblet cells, and the mucus score and secretory ratio of goblet-cell mucus secretion in the trachea of rats. The tracheal whole mounts with silver staining, those stained with chloroacetate esterase reagent and Alcian blue and tracheal tissue sections stained with Alcian blue and periodic acid-Schiff reagent were used for evaluation. Formation of endothelial gaps occurred a few min after administration of capsaicin, and gaps almost closed within 12 min after capsaicin injection. Five min after capsaicin, the leaky blood vessels were numerous and the subepithelial edema ratio (% of length of edema along the inner circumference of tracheal cross section) was found to be 57.8+/-3.0% ( n=6). The number of Alcian blue-positive goblet cells (1,090+/-220 per mm(2) of mucosal surface) was reduced to half the number of goblet cells in the vehicle-treated rats (2,200+/-230). The mucus score of goblet cell secretion was not changed. The secretory ratio was greatly increased. One day after capsaicin, the edema ratio remained large and the number of Alcian blue-positive goblet cells was also small. The mucus score was also not changed. The secretory ratio was still large. On day 3, the edema ratio remained large, but the number of Alcian blue-positive goblet cells was increased to the level of the controls. The mucus score and secretory ratio returned to the control level. On day 5, the edema ratio was greatly decreased, but it was still significantly larger than that of the controls. The mucus score and secretory ratio remained at the baseline level. Seven days after capsaicin, the edema ratio was similar to the controls. The number of goblet cells was even larger than controls. It is concluded that capsaicin-induced acute inflammation in the rat trachea involves formation of endothelial gaps, extensive plasma extravasation and edema formation, and depletion of goblet-cell secretory granules. Spontaneous gradual remission of edema was accompanied by regranulation of goblet cells with gradual mucogenesis for several days.

Acute Disease↗
PubMed1991

Comparison of angiographic findings and demographic variables in patients with coronary artery disease presenting with acute pulmonary edema versus those presenting with chest pain.

One hundred nineteen patients admitted to the coronary care unit with pulmonary edema were retrospectively reviewed to identify the demographic characteristics and underlying cardiac disorders of this population. The patients with pulmonary edema were compared with 119 patients admitted to the coronary care unit with chest pain. Cardiac catheterization in 71 patients with pulmonary edema and 93 with chest pain showed left main and 3-vessel coronary artery diseases to be equally common in both groups, although anginal pain was infrequent in patients with pulmonary edema (n = 28, 24%). Left ventricular function was reduced in the patients with pulmonary edema compared with those with chest pain (mean ejection fraction 42 vs 59%; p less than 0.001). More patients with pulmonary edema were black, and had diabetes and preexisting hypertension than those with chest pain. The results of cardiac catheterization were the same for black and white patients with pulmonary edema. In conclusion, patients with pulmonary edema have a high incidence of cardiac disease, and pulmonary edema may be 1 manifestation of silent myocardial ischemia. Important demographic differences exist between patients admitted with pulmonary edema and those who present with chest pain.

Adult↗
PubMed2004

Optical coherence tomography and confocal scanning laser tomography for assessment of macular edema.

PURPOSE: To compare optical coherence tomography (OCT) and confocal scanning laser tomography (cSLT) for quantitative retinal thickness mapping of the macula and their ability to detect macular edema. DESIGN: Prospective, comparative, clinical observational study. METHODS: The study population of 138 eyes (97 patients) was divided into a study group consisting of 45 (32.6%) eyes with macular edema and a control group consisting of 93 (67.4%) eyes without macular edema. All patients underwent OCT and cSLT of the macula. Retinal thickness measurements obtained by OCT were compared with signal width and edema index, determined by cSLT. RESULTS: The OCT measurements and cSLT edema index were significantly (P <.001) correlated with each other. Correlation coefficients decreased (P <.001) with increasing diameter of the measurement circle. In the macular edema group, correlation coefficients were significantly (P <.001) higher than in the control group. To separate the study and control groups, receiver operator characteristic curves covered a larger area for OCT measurements than for cSLT measurements. Retinal thickness measurements and edema index correlate with visual acuity (correlation coefficient r = -.653 for OCT, r = -.608 for cSLT; P <.001). CONCLUSIONS: Macular edema can be quantitatively mapped by OCT and cSLT. The retinal thickness and edema index measurements correlate with visual acuity. The fast and standard examination modes of OCT give similar measurements. Both OCT and cSLT can differentiate between eyes with and without macular edema, with OCT showing a higher predictive value.

Aged↗