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PubMed1984

Associations of subjective udder edema scores and descriptive trait codes for udder types.

Edema severity was scored by herd personnel in six North Carolina Holstein herds from 1 (none) to 5 (extremely severe). Cows (2612) were scored at calving and 1 and 2 wk postpartum. Total score was calculated as the sum of these three scores. Official Holstein-Friesian classification descriptive udder trait codes were available on a subset of the cows. All statistical analyses were within lactation and included adjustments for herd-year and age as well as classifier and stage of lactation where appropriate. Correlations between corresponding edema scores for first and second lactations were .18, .18, .19, and .20 for scores at calving, 1 wk, 2 wk, and for total score. Stepwise regression procedures showed that udder support codes were associated with a larger amount of variation of edema scores than for any other single mammary trait code. Fore and rear udder codes also were associated with significant variation of edema scores in some analyses. Prediction models showed edema was a significant predictor of subsequent udder support codes, although udder trait codes were not significant predictors of subsequent edema severity. It appeared that severe edema may be one of the causes of pendulous udders.

Animals↗
PubMed1992

Evaluation of a system for rating edema in dairy cattle.

Our objective was to evaluate a subjective edema rating system to quantitate edema severity. Edema was evaluated with 20 nulliparous Holstein heifers from 3 wk before their expected calving date until 3 wk postpartum. Severity of udder edema was evaluated independently daily by five people throughout the 68-d experiment; a 10-point rating system (0 = no edema, 10 = severe edema) was used. One of the people developing the scoring system served as the official scorer. The accuracy of the rating system, defined as the closeness of test evaluator scores to official scores, was highest for scores 2 to 8. The precision of the system, identified by the standard error of the mean, was similar for each score in the rating system. The largest disagreement between official and test evaluator scores was evident postpartum. The large number of defined points in this rating system and the similarity between official and test scores in this study indicate the usefulness of this tool to evaluate precisely the severity of edema in dairy cattle.

Animals↗
PubMed1992

Influence of calcium chloride fed prepartum on severity of edema and lactational performance of dairy heifers.

Twenty Holstein heifers in a completely randomized design were used to evaluate the effects of prepartum dietary CaCl2 on the development and regression of edema and on subsequent lactational performance. Heifers were assigned to diets containing either 2.17% limestone or 1.5% CaCl2 (DM basis) at 3 wk before expected calving date. Except for the Ca sources, diets were identical. Test diets were only fed prepartum; at calving, all heifers were offered a lactation diet for 3 wk. Severity of edema was evaluated independently by five people daily throughout the experiment; a 10-point rating system was utilized to quantify the severity of edema. Calcium chloride reduced the severity of edema, although this response was most evident during the 1st wk that this salt was fed. The beneficial effects of CaCl2 on edema prepartum disappeared postpartum, when CaCl2 was removed from the diet. Indeed, edema was higher for heifers fed CaCl2 than for those fed limestone at 2 wk postpartum. Calcium chloride reduced DMI prepartum, but, following parturition, a compensatory increase in feed intake occurred. Postpartum daily DMI averaged 1.3 kg higher for heifers fed CaCl2 than for those fed the limestone diet prepartum. Milk yield and composition were somewhat lower for heifers fed CaCl2, although this response was most evident at 1 wk postpartum. Feeding CaCl2 prepartum to prevent milk fever also may reduce the severity of udder edema prepartum and increase feed intake during early lactation.

Animals↗
PubMed1984

Acute responses to experimental blunt head trauma. Topography of cerebral cortical edema.

Anesthetized cats subjected to impact followed by acceleration and rotation of the skull were sacrificed at 15 minutes or 6 hours after injury and were selected for study if unilateral cerebral contusion was present. Widespread areas of cerebral cortex were examined bilaterally for edema, using measurement of tissue density with an organic gradient, and for breakdown of the blood-brain barrier to plasma protein tagged with Evans blue dye. At both times tested, a halo of vasogenic edema (Evans blue stain plus decreased density) was present in the cortex surrounding areas of contusion. At 15 minutes after injury, animals with deep contusions also had a slight decrease in density without Evans blue staining, interpreted as cytotoxic edema, in some gyri neighboring the contusion. At 6 hours, cytotoxic edema was not evident, but some animals had vasogenic edema in the gyri adjoining the contusion. Most gyri contralateral to contused areas had neither Evans blue staining nor changes in tissue density. These findings suggest that, with the present head-injury model, acute changes in tissue density and vascular permeability occur in the cerebral cortex of hemispheres with contusion. These responses are related topographically to contusion sites, and change over the two times studied. The authors conclude that events in addition to spread of fluid from areas of contusion contribute to the edema of head injury, and that more than one form of edema can follow mechanical trauma to the brain.

Animals↗
PubMed1995

Intracerebral infusion of thrombin as a cause of brain edema.

Purified thrombin from an exogenous source is a hemostatic agent commonly used in neurosurgical procedures. The toxicity of thrombin in the brain, however, has not been examined. This study was performed to assess the effect of thrombin on brain parenchyma, using the formation of brain edema as an indicator of injury. Ten microliters of test solution was infused stereotactically into the right basal ganglia of rats. The animals were sacrificed 24 hours later, and the extent of brain edema and ion content were measured. Concentrations of human thrombin as low as 1 U/microliter resulted in a significant increase in brain water content. Rats receiving 10 U/microliters had a mortality rate of 33% compared to no mortality in the groups receiving smaller doses. Thrombin-induced brain edema was inhibited by a specific and potent thrombin inhibitor, hirudin. A medical grade of bovine thrombin commonly used in surgery also caused brain edema when injected at a concentration of 2 U/microliters. Edema formation was prevented by another highly specific thrombin inhibitor, N alpha-(2-Naphthalenesulfonylglycyl)-4-DL-phenylalaninepiperidid e (alpha-NAPAP). Thrombin-induced brain edema was accompanied by increases in brain sodium and chloride contents and a decrease in brain potassium content. Changes in brain ions were inhibited by both hirudin and alpha-NAPAP, corresponding to the inhibition of brain water accumulation. This study shows that thrombin causes brain edema when infused into the brain at concentrations as low as 1 U/microliter, an amount within the range of concentrations used for topical hemostasis in neurosurgery.

Animals↗
PubMed1996

Edema from intracerebral hemorrhage: the role of thrombin.

The mechanism by which intracerebral hemorrhage leads to the formation of brain edema is unknown. This study assesses the components of blood to determine if any are toxic to surrounding brain. Various solutions were infused stereotactically into the right basal ganglia of rats. The animals were sacrificed 24 hours later; brain edema and ion contents were measured. Whole blood caused an increase in brain water content and ion changes consistent with brain edema. Concentrated blood cells, serum from clotted blood, and plasma from unclotted blood all failed to provoke edema formation when infused directly into the brain. On the other hand, activation of the coagulation cascade by adding prothrombinase to plasma did produce brain edema. The edema response to whole blood could be prevented by adding a specific thrombin inhibitor, hirudin, to the injected blood. This study indicates that thrombin plays an important role in edema formation from an intracerebral blood clot.

Animals↗
PubMed2001

Attenuation of intracerebral hemorrhage and thrombin-induced brain edema by overexpression of interleukin-1 receptor antagonist.

OBJECT: Adenovirus-mediated overexpression of interleukin-1 receptor antagonist (IL-1ra) attenuates the inflammatory reaction and brain injury that follows focal cerebral ischemia. Recently, an inflammatory reaction after intracerebral hemorrhage (ICH) was identified. In this study the authors examine the hypothesis that overexpression of IL-1ra reduces brain injury (specifically edema formation) after ICH. METHODS: Adenoviruses expressing IL-1ra (Ad.RSVIL-1ra) or LacZ, a control protein (Ad.RSVlacZ), or saline were injected into the left lateral cerebral ventricle in rats. On the 5th day after virus injection, 100 microl of autologous blood or 5 U thrombin was infused into the right basal ganglia. Rats with ICH were killed 24 or 72 hours later for measurement of brain water and ion content. Thrombin-treated rats were killed 24 hours later for edema measurements and an assessment of polymorphonuclear leukocyte (PMNL) infiltration by myeloperoxidase (MPO) assay, as well as histological evaluation. Compared with saline-treated and Ad.RSVlacZ-transduced controls, Ad.RSVIL-1ra-transduced rats had significantly attenuated edema in the ipsilateral basal ganglia 3 days after ICH (81.5 +/- 0.3% compared with 83.4 +/- 0.4% and 83.3 +/- 0.5% in control animals). Thrombin-induced brain edema was also reduced in Ad.RSVIL-1ra-treated rats (81.3 +/- 0.4% compared with 83.2 +/- 0.4% and 82.5 +/- 0.4% in control rats). The reduction in thrombin-induced edema was associated with a reduction in PMNL infiltration into the basal ganglia, as assessed by MPO assay (49% reduction) and histological examination. CONCLUSIONS: Overexpression of IL-1ra by using an adenovirus vector attenuated brain edema formation and thrombin-induced intracerebral inflammation following ICH. The reduction in ICH-induced edema with IL-1ra may result from reduction of thrombin-induced brain inflammation.

Animals↗
PubMed1976

Blood pressure, edema and proteinuria in pregnancy. 9. Proposal for classification.

The frequency distributions of blood pressures in large populations fail to show two groups, one normotensive and the other hypertensive. In the spectrum of pressures, some people merely have higher levels than others and division of abnormal from normal is artificial and arbitrary, although it is useful for prognosis. The blood pressure of 140/90 as the conventional dividing line does not seem to be appropriate in pregnant women. From the standpoint of fetal prognosis, a level of 125/75 before the thirty-second week and 125/85 thereafter seems more reasonable. Moreover, those levels are close to the 120/80 that Robinson and Brucer specified as the upper limit of normal for all adults and are close to the 130/70 and 120/80 that the eminent British authority, F.J. Browne, used successively in the diagnosis of hypertensive disorders in pregnancy. If the standard of 125/75 were adopted, however, a quarter of all pregnant women would be hypertensive in the second trimester and half in the last month, which are disturbingly high proportions. For the diagnosis of preeclampsia, a rise in blood pressure probably is more significant than an arbitrary level. The usual blood pressure in midpregnancy merely defines the patient's place in the spectrum. Figure 9-1 indicates that in white nulliparas the diastolic pressure rises an average of 10 mm. Hg in the middle of the third trimester. If the mean and median are close together, greater increases would occur in half of the women. The classification of the American Committee on Maternal Welfare and of the Committee on Terminology of the American College of Obstetricians and Gynecologists specify increases of 30 mm. Hg or more in the systolic or 15 mm. Hg or more in the diastolic pressures as criteria of preeclamptic hypertension. pperhaps the rise in diastolic pressure should be set at some greater value. Our analysis of data made thus far cannot decide that issue. The next phase of the study will include analyses in individual women of the times, magnitudes, persistence or transience, and the like of changes in blood pressure, edema, and proteinuria. Such data will afford much more information than can be derived from the preliminary studies reported here. Although edema of the hands and face may be more common in preeclamptic than in normal women, such edema is so common in normal pregnancy as to suggest that it usually is normal. In our data, edema seems to bear no relation to hypertension or proteinuria. The triad of signs -- hypertension, proteinuria, and edema -- is generally accepted as characteristic, though far from specific for preeclampsia. Our data support Hytten's conclusion that edema should by dropped from the triad. There is some indication, however, that some edema is abnormal and that it is associated with an adverse effect when it coincides with proteinuria late in pregnancy.

Adult↗
PubMed1999

[Radiographic diagnosis of cardiogenic pulmonary edema].

Development of pulmonary edema (increased extravascular lung water) is a common and sometimes life-threatening clinical problem in critical-care unit patients. There are three principal causes: cardiac failure, overhydration, and increased pulmonary capillary permeability. Among these, cardiogenic edema consists of left heart failure and overhydration. Determining the specific cause of any given case of pulmonary edema is important and leads to more rapid and definitive treatment. A plain chest film can often explicate the cause of edema with a high degree of accuracy if careful attention is given to certain radiographic features. The principal features useful for correctly determining the cause of edema in a high percentage of cases are the distribution of pulmonary blood flow, distribution of pulmonary edema, and vascular pedicle width. Ancillary features are pulmonary blood volume, bronchial cuffing, septal lines, pleural effusion, and air bronchograms. Cardiac size and shape as well as specific intracardiac calcifications could also help distinguish cardiogenic from noncardiogenic pulmonary edema.

Adult↗
PubMed1998

Pulmonary edema in cerebral malaria patients in Thailand.

Pulmonary edema is a serious complication of falciparum malaria that usually occurs in association with cerebral malaria, acute renal failure, high parasitemias, or delayed antimalarial treatment. From 1993 to 1996, 120 adult patients admitted to the intensive care unit of the Bangkok Hospital for Tropical Diseases were enrolled in a prospective study to assess the combination of artesunate and mefloquine for the treatment of cerebral malaria. Twenty-five patients (21%) presented with pulmonary edema and a majority developed complications in other organs as well, especially acute renal failure. In most patients (19 of 25), pulmonary edema was noted on the first day of admission and was associated with higher parasitemias and levels of acidemia, than in patients without pulmonary edema. Ten of the 25 patients diagnosed with pulmonary edema developed signs consistent with adult respiratory distress syndrome (ARDS). The mean central venous pressure when pulmonary edema was diagnosed was markedly lower in ARDS than in non-ARDS patients, supporting the argument that fluid imbalance is not essential for malaria-induced lung injury. Seven of 10 patients with ARDS died, 5 within 24 hours of admission, but there were no deaths in the 15 pulmonary edema patients without ARDS. Early diagnosis and prompt treatment remain important principles to reduce the morbidity and mortality associated with complicated falciparum malaria. This report emphasizes that ARDS, when concurrently occurs, is a poor prognostic clinical indicator in cerebral malaria.

APACHE↗
PubMed1997

Effect of dl-3-n-butylphthalide on brain edema in rats subjected to focal cerebral ischemia.

The present study evaluated the effect of dl-3-n-butylphthalide(NBP), a novel brain protective agent, on brain edema in rats following focal ischemia. Edema was induced by occluding the right middle cerebral artery (MCAO), producing permanent focal ischemia in the right cerebral hemisphere, which developed ipsilateral brain edema reproducibly. Edema was assessed 24 h after MCA occlusion by determining the brain water content from wet and dry weight measurements, and the sodium, potassium concentrations with ion-selective electrodes. In this model, NBP at the dose of 80, 160 and 240 mg/kg p.o. 15 min after MCAO prevented from brain edema in a dose-dependent manner. A significant reduction of sodium content and an increase in potassium level were observed in all drug-treated groups. It showed that NBP strongly attenuated brain water entry, sodium accumulation and potassium loss. Nimodipine treatment (5 mg/kg s.c.) also reduced brain edema (P < 0.05). The results suggest that a strong anti-edema activity of NBP may play an important role to contribute to the treatment of ischemic damage.

Animals↗
PubMed2002

[Vitreous surgery for macular edema in branch retinal vein occlusion].

PURPOSE: To examine the efficacy of vitreous surgery for macular edema in branch retinal vein occlusion (BRVO). PATIENTS AND METHODS: This study included 183 patients (183 eyes) that underwent vitreous surgery for macular edema in BRVO. They were 77 males and 106 females. The average age of the patients was 65 years (range, 35-87 years). The average duration of macular edema was 18 weeks (range, 1-161 weeks). Mean preoperative visual acuity was 0.32 (0.01-1.2). Preoperative visual acuity was less than 0.1 in 27% and more than 0.5 in 26% of the cases. The average follow-up period was 24 months (range, 12-83 months). RESULTS: Macular edema was absorbed in 21% at 1 month, 54% at 3 months, 81% at 6 months, and 95% at 12 months postoperatively. The mean absorption period of macular edema was 4.5 months. Postoperative visual acuity improved to 0.68, which was statistically significant. Postoperative visual acuity was less than 0.1 in 9% of the cases, more than 0.5 in 68%, and more than 0.8 in 47%. CONCLUSION: After vitreous surgery for macular edema in BRVO, macular edema was absorbed rapidly and visual acuity improved. Vitreous surgery may be an effective treatment.

Adult↗
PubMed2003

A correlative study between AQP4 expression and the manifestation of DWI after the acute ischemic brain edema in rats.

OBJECTIVE: To investigate the rule of the aquaporin-4 (AQP4) expression in acute ischemic brain edema, and to study the correlation between AQP4 expression and diffusion-weighted imaging (DWI). METHODS: Thirty-six Wistar rats were divided into 2 groups randomly, control group (n = 12) and operation group (n = 24) in which right middle cerebral artery of each animal had been occluded unilaterally (MCAO) at interval times of: 15 minutes, 30 minutes, 1 hours, 3 hours, 6 hours and 24 hours, respectively. The operation process of the control group was the same as the operation group except for the MCAO. All groups were examined using DWI. The apparent diffusion coefficient (ADC), relative density (rd) and relative area (rs) of the biggest hyperintensity signal layer on DWI were measured. After that the animals were sacrificed and perfused with the mixture solution consisting of TTC. The biggest layers of the ischemic cerebral tissues in each rat corresponding to the DWI were stained with TTC and examined with immunochemistry (DeltaS), in situ hybridization (alpha) and histology. RESULTS: There was no significant change in the control group. In the operation group, a hyperintensity signal was found in the DWI of the right MAC territory at 15 minutes after MCAO. The ADC value decreased quickly within one hour after MCAO, while the AQP4 expression, rd-DWI and rs-DWI increased rapidly during this stage. As time progressed, the ADC value decreased further to (2.1 +/- 0.6) x 10(-4) mm(2)/s at 3 hours, and then began to increase slowly till 24 hours. But the AQP4 expression (DeltaS and alpha) and rd as well as the rs continuously increased slowly between 1 hour and 6 hours after MCAO, followed a peak after 6 hours. The AQP4 expression (alpha) showed a positive relationship with the rs-DWI, they all presented two peaks and a plateau. The corresponding sequential pathologic changes were a gradual increase of intracellular edema (within one hour), then an emergence of vasogenic edema (1-6 hours), and final necrosis and liquefaction (6 - 24 hours). CONCLUSIONS: Upregulated expression of AQP4 may play a significant role in acute ischemic brain edema, especially during the stages of intracellular edema and necrosis, but it has no correlation to vasogenic edema. Certainly, the high expression of AQP4 is perhaps one of the most important reasons of the decrease of ADC and hyperintensity on the DWI in the intracellular edema.

Acute Disease↗
PubMed1992

[Clinical characteristics of pulmonary edema in patients with unstable angina].

To elucidate the clinical characteristics of pulmonary edema in unstable angina, 120 patients with unstable angina who admitted to the hospital within 6 hours after the onset of chest pain were studied. The criteria for the diagnosis of pulmonary edema included interstitial pulmonary edema and diffuse alveolar edema. Pulmonary edema was present in 24 patients. In these patients, the duration of chest pain was relatively longer, and the incidences of diabetes mellitus, emergency coronary revascularization and multiple-vessel coronary artery disease were higher than in those without pulmonary edema. In addition, in-hospital mortality rate in patients with pulmonary edema was higher than in those without it (21 vs 1%, p < 0.001), which is probably due to a large area of myocardial ischemia. For these patients, therefore, early diagnosis and appropriate therapy to save viable segments of the myocardium are mandatory.

Aged↗
PubMed2004

[Neuroprotective effect of monoamine oxidase monoclonal antibody against vasogenic brain edema in rats].

OBJECTIVE: To observe the therapeutic effect of monoamine oxidase (MAO) monoclonal antibody (mAb) for vasogenic brain edema (VBE) in rats. METHODS: A total of 75 Wistar rats were randomized into non-edema, non-treated edema, saline-treated edema, mannitol-treated edema and MAO mAb-treated groups. Rat models of VBE were established by intraperitoneal injection of phenylephrine in the latter 4 groups. Brain water content in the gray and white matter was measured respectively with a moisture analyzer, and the permeability of the blood-brain barrier (BBB) determined by Evan's blue (EB) extravasation method. RESULTS: MAO mAb administration significantly reduced the brain water content in the gray and white matter as well as the permeability of BBB (P<0.01), Which was especially effective for the white matter, producing results comparable with those of the non-edema group (P>0.05). MAO mAb markedly alleviated brain edema, with better dehydrating effect on the white matter than mannitol (P<0.01), which reduced the water content of the brain gray and white matter undiscriminatingly and showed poor effect on the permeability of BBB. CONCLUSION: The pathogenesis of BBB permeability changes in VBE is related to the activity of monoamine oxidase, and MAO mAb has selective therapeutic effect on VBE, which is especially obvious on brain white matter.

Animals↗
PubMed1992

[Pathophysiology, prevention and therapy of altitude pulmonary edema].

Alveolar hypoxia and resulting tissue hypoxia initiates the pathophysiological sequence of high altitude pulmonary edema (HAPE). Very rapid ascent to high altitude without prior acclimatization results in HAPE, even in subjects with excellent tolerance to high altitude. Upon acute altitude exposure, HAPE-susceptible individuals react with increased secretion of norepinephrine, epinephrine, renin, angiotensin, aldosterone and atrial natriuretic peptide. In response to exercise at high altitude, subjects developing acute mountain sickness and HAPE secrete more aldosterone and antidiuretic hormone than subjects who remain well. This results in sodium and water retention, reduction of urine output, increase in body weight and development of peripheral edemas. The hypoxic pulmonary vascular response is enhanced in HAPE-susceptible subjects, thus favouring the development of severe pulmonary hypertension on exposure to high altitude. It has been postulated that uneven pulmonary vasoconstriction enhances filtration pressure in non-vasoconstricted lung areas, leading to interstitial and alveolar edema. The high protein content of the edema fluid in HAPE characterizes this edema as a permeability edema. The prophylactic administration of nifedipine prevents the exaggerated pulmonary hypertension of HAPE-susceptible subjects upon rapid ascent to 4559 m and thus prevents HAPE in most cases. This finding illustrates the crucial role of hypoxic pulmonary hypertension in the development of HAPE. The causal treatment of HAPE is descent, evacuation and administration of oxygen. Treatment of HAPE patients with nifedipine results in a reduction of pulmonary artery pressure, clinical improvement, increased oxygenation, decrease of the alveolar arterial oxygen gradient and progressive clearing of pulmonary edema on chest x-ray. Thus nifedipine offers a pharmacological tool for the treatment of HAPE.

Aldosterone↗
PubMed2004

Blood pressure destabilization and edema among 8538 users of celecoxib, rofecoxib, and nonselective nonsteroidal antiinflammatory drugs (NSAID) and nonusers of NSAID receiving ordinary clinical care.

OBJECTIVE: To investigate the relationship between nonselective nonsteroidal antiinflammatory drugs (NS NSAID), rofecoxib, celecoxib, and risk of edema and blood pressure destabilization in patients with rheumatoid arthritis (RA) and osteoarthritis (OA) receiving ordinary clinic care. METHODS: Patients participating in a longterm outcome study reported drug use, as well as the presence of edema and blood pressure increases occurring during the previous 6 months. To measure pure drug effect, analyses were restricted to 8538 patients who exclusively used a NS NSAID, rofecoxib, or celecoxib, and compared to nonusers of NS NSAID, rofecoxib, or celecoxib. We evaluated blood pressure destabilization using patient-reported increases in blood pressure and/or difficulty in controlling blood pressure. RESULTS: Compared with nonusers, after adjusting for age, sex, presence of RA, and history of heart disease and hypertension, patients using rofecoxib, but not celecoxib or NS NSAID, had an increased rate of edema (23.3% vs 18.0%), while the rates for celecoxib and NS NSAID were 17.5% and 18.2%, respectively. The adjusted risk of edema was significantly increased for rofecoxib compared to celecoxib (OR 1.33, 95% CI 1.08-1.64). For blood pressure increases, among patients who did not report having hypertension, no significant increase was noted for NS NSAID and celecoxib compared with nonusers. However a significant increased risk of blood pressure increase was seen for rofecoxib (OR 2.08, 95% CI 1.41-3.06). Among patients who reported having hypertension, patients taking rofecoxib had a significant increased risk of blood pressure increase compared to nonusers (OR 1.55, 95% CI 1.23-1.96), while the risks of blood pressure increase for users of celecoxib and NS NSAID were not significantly different than among nonusers. After controlling for age, sex, RA, and new starts on NSAID, the risk of blood pressure increase was significantly higher for users of rofecoxib than celecoxib (OR 1.21, 95% CI 1.03-1.61) among patients with hypertension, and numerically higher for nonhypertensives (OR 1.42, 95% CI 0.96-2.22). The increased risk for hypertension and edema of rofecoxib compared to celecoxib users was further confirmed by analysis of specific reported side effects during 2 separate 6-month periods (July 1 to December 31, 1999, and January 1 to June 30, 2000). During these 2 periods, rofecoxib-treated patients were 2.16 to 3.82 times more likely to report edema or blood pressure increase side effects compared to celecoxib-treated patients. CONCLUSION: Rofecoxib, but not celecoxib and NS NSAID, is associated with an increased risk of edema and blood pressure increase compared to nonusers of NSAID.

Adult↗
PubMed2004

[Two cases of negative pressure pulmonary edema after induction of anesthesia and extubation].

Two cases of negative pressure pulmonary edema are described. In one case, tracheal intubation was not successful and airway obstruction occurred after induction of anesthesia. Spontaneous breathing was restored by reversal of neuromuscular blocking action, but airway obstruction persisted. Urgent tracheostomy was therefore performed. A chest x-ray and clinical features indicated pulmonary edema immediately after tracheostomy. Treatment with mechanical ventilation and positive end-expiratory pressure improved pulmonary edema. In the other case, airway obstruction occurred after extubation. Removal of secretion in the oral cavity and assisted ventilation improved airway obstruction, but pulmonary edema was found by chest x-ray. Forced diuresis using furosemide and oxygen inhalation resulted in the improvement of pulmonary edema. Fortunatetly, in both cases, significant complications associated with pulmonary edema did not occur. Care should be taken of the risk of pulmonary edema when the airway was obstructed after induction of anesthesia or extubation under spontaneous breathing.

Adult↗