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PubMed1982

Edema formation in the newborn lung.

Pulmonary edema is an important cause of respiratory distress in newborn infants. It occurs with severe perinatal asphyxia, heart failure, hyaline membrane disease, persistent patency of the ductus arteriosus, pneumonitis from group B beta-hemolytic streptococcus, and chronic lung disease (bronchopulmonary dysplasia). Neonatal pulmonary edema often develops from increased pressure in the microcirculation of the lungs. This may occur in conjunction with sustained hypoxia; left ventricular failure associated with congenital heart disease or myocardial dysfunction; following excessive intravascular infusions of blood, colloid, fat, or electrolyte solution and in conditions that increase pulmonary blood flow. Low intravascular protein osmotic pressure from hypoproteinemia may predispose infants to pulmonary edema. Hypoproteinemia is common in infants who are born prematurely. Large intravascular infusions of protein-free fluid further decrease the concentration of protein in plasma and thereby facilitate edema formation. Lymphatic obstruction by air (pulmonary interstitial emphysema of fibrosis (chronic lung disease) also may contribute to the development of edema. Bacteremia, endotoxemia, and prolonged oxygen-breathing injure the pulmonary microvascular endothelium and cause protein-rich fluid to accumulate in the lungs. Epithelial protein leaks may develop when the transpulmonary pressure needed to inflate the lungs increases because of high surface tension at the air-liquid interface. Fibrin clots from in some of the air spaces, which in combination with atelectasis and edema constitute the pathologic features of hyaline membrane disease. The risk of neonatal pulmonary edema can be reduced by several therapeutic measures designed to lessen fluid filtration pressure, increase plasma protein osmotic pressure, and prevent or reduce the severity of lung injury.

Animals↗
PubMedDate not supplied

Patterns of edema in tumors vs. infarcts: visualization of white matter pathways.

The computed tomographic (CT) scans of 339 patients with recent nonhemorrhagic cerebral infarct and 155 patients with supratentorial tumors were reviewed to evaluate the appearance of cerebral edema. White matter pathway edema characterized the CT pattern in 106 (68%) of the 155 tumor cases. In these 106 cases, there were 143 tumors, with edema in the arcuate white matter (73%), the external capsule (33%), the internal capsule (12%) and the corpus callosum (14%). In contrast, only four of the 339 cases of infarct had edema in the white matter pathways. In addition, 260 (77%) of the infarct cases had edema in both gray and white matter and 98% had at least gray matter involvement, while only two of the tumor cases had any gray matter edema. White matter pathway involvement with respect to tumor site is useful in differentiating tumor and infarct edema.

Brain Neoplasms↗
PubMed1981

[Neurogenic pulmonary edema following severe head injury--case report (author's transl)].

A case of severe head injury associated with fulminant pulmonary edema considered as neurogenic which developed within short time after the injury was presented. A five-year-old boy who had no previous history of cardiopulmonary disease was struck on his right frontal region by car accident at 15.30 PM on July 5 of 1979. Immediately after the impact he lost his consciousness and subsequently transferred to a local hospital where bilateral dilated pupil and flaccid paralysis of the limbs were noted. On transmission of the patient to Omuta City Hospital 30 minutes after the injury, massive foamy fluid was discharged from the tracheal tube. On admission, he was comatous, with bilateral dilated and fixed pupils and flaccid paralysis of the limbs. There was no retinal bleeding. He showed ataxic respiration with severe stridor and massive discharge of foamy fluid pinkish in colour from the trachea characteristic in pulmonary edema was significant. Chest x-ray film demonstrated perihilar densities suggesting pulmonary edema. CT scan showed extremely small ventricle on both sides without manifestations of intracranial hematomas or cerebral contusion. With an intensive medical treatments including corticosteroids, alkalizing agents and alpha-blocker were administered under controlled respiration, the discharge of edema fluid was gradually decreased and the findings on blood gases were also improved. However neurological signs were aggravated and he died 8 hours after the injury. Central venous pressure was maintained at the level between 8 to 10 cm. From these clinical findings the pulmonary edema was concluded as neurogenic. Direct or indirect injury to the hypothalamic efferent pathway at the level of lower brain stem seemed to be important as the cause of neurogenic pulmonary edema in this case. The possible pathophysiology of neurogenic pulmonary edema associated with brain stem injury and intracranial hypertension was discussed with other related literature.

Brain Concussion↗
PubMed1980

[Focal edema of the intima as a preatherosclerotic arterial lesion].

A number of histological, histochemical and immunomorphological methods were used to study focal edema of the aortal intima in children and young subjects and its association with the development of atherosclerotic alterations. The main manifestations of the focal edema of the intima include focal accumulation of insudate consisting of serous or serous-fibrinous liquid, accumulation of metachromatic substances, damage of collagen and elastic fibers, proliferation of smooth muscle cells and their fatty metamorphosis. Later, signs of organization and sclerosis of the edematous zone develop. The following stages of the development of focal intimal edema may be distinguished: simple or serous edema; serous-fibrinous edema; proliferation of smooth muscle cells followed by their fatty degeneration and extracellular release of lipids; organization or sclerosis of the edema focus. It is assumed that late stages of the development of focal edema of the intima are associated with fibrous and fibrous-lipid atherosclerotic plaques.

Adolescent↗
PubMed1980

[Effect of various kinds of glucocorticoids on experimental brain edema (author's transl)].

Although the effectiveness of glucocorticoids for the treatment of cerebral edema has been widely accepted in neurosurgical practice, but its mechanism is still obscure. Also the dose equivalent of various kinds of glucocorticoid preparation is still uncertain. Only the dose equivalent determined by the test examining an antiinflammatory effect on a growth of glanulation, has been applied for the treatment of brain edema. The authors attempted to establish the dose equivalent of each kinds of glucocorticoid for the treatment of cerebral edema. Cold induced cerebral edema was produced by touching a metal probe at the temperature of -90 degrees C for 3 minutes on the right parietal cortex of rat brain. Hydrocortisone (16 mg/kg), prednisolone (3.2 mg/kg), methylprednisolone (3.2 mg/kg), dexamethasone (0.8 mg/kg) and betamethasone (0.8 mg/kg) were administered at the time of 3 hours prior or after the cold injury. The animals were sacrificed 24 hours after injury and the grade of brain edema was determined by the changes of water content in the brain tissue. For this purpose, the authors developed a new method of measuring water content in the brain tissue using tritiated water and a liquid scintillation counter. In the group of animals which were treated with prednisolone, dexamethasone or betamethasone, the water content was significantly decreased compared to the value of non-treated animals. But in the animals treated with hydrocortisone or methylprednisolone, no significant changes of the water content was observed. But in the animals treated with double doses of hydrocortisone (32 mg/kg) or methylprednisolone (6.4 mg/kg), cerebral edema was improved significantly. From these results the authors concluded that the dose equivalent of each kinds of glucocorticoid for the treatment of the brain edema was as follows: hydrocortisone: prednisolone: methylprednisolone: dexamethasone: betamethasone = 40 : 4 : 8 : 1 : 1.

Animals↗
PubMedDate not supplied

The genesis of peritumoral vasogenic brain edema and tumor cysts: a hypothetical role for tumor-derived vascular permeability factor.

Cerebral edema and fluid-filled cysts are common accompaniments of brain tumors. They contribute to the mass effect imposed by the primary tumor and are often responsible for a patient's signs and symptoms. Cerebral edema significantly increases the morbidity associated with tumor biopsy, excision, radiation therapy, and chemotherapy. Both edema and cyst formation are thought to result from a deficiency in the blood-brain barrier, with consequent extravasation of water, electrolytes, and plasma proteins from altered tumor microvessels. The resultant expansion of the cerebral interstitial space contributes to the elevated intracranial pressure observed with brain tumors. Departure from the typical blood-brain barrier microvascular architecture may only partially explain the occurrence of edema and tumor cyst formation. Biochemical mediators have also been implicated in vascular extravasation. Vascular permeability factor or vascular endothelial growth factor (VPF/VEGF) is a protein that has recently been isolated from a variety of tumors including human brain tumors. VPFb is an extraordinarily potent inducer of both microvascular extravasation (edemagenesis) and the formation of new blood vessels (angiogenesis). Its role in tumor growth and progression would therefore appear pivotal. Herein, the author presents an updated account of the investigation of VPF. Historical and clinical perspectives of the study and treatment of tumor associated edema are provided. The efficacy of high-dose dexamethasone in the treatment of neoplastic brain edema is discussed. A hypothetical role for VPF in edemagenesis is presented and discussed. It is hoped that an expanded understanding of the mechanisms responsible for the genesis of edema will ultimately facilitate therapeutic intervention.

Blood-Brain Barrier↗
PubMed1995

Myocardial edema and compromised left ventricular function attributable to dirofilariasis and cardiopulmonary bypass in dogs.

We investigated the relation between left ventricular dysfunction and myocardial edema in dogs with heartworm (Dirofilaria immitis) infection that were undergoing cardiopulmonary bypass. Dogs with and without D immitis were anesthetized by continuous thiopental infusion and were mechanically ventilated. Sonomicrometry crystals were placed on the long and short axes of the left ventricle, and a Millar pressure transducer was placed in the left ventricular chamber. Pressure-volume loops were digitized and continuously recorded. Dogs with and without D immitis were placed on standard hypothermic cardiopulmonary bypass, with 1 hour of aortic cross-clamp. Wet-to-dry weight ratio corrected for residual blood volume was used to quantitate the volume of myocardial edema. Preload recruitable stroke work was used as a preload-independent index of systolic function. Tau, the isovolumic relaxation time constant, was determined to assess diastolic relaxation. Dogs with D immitis had increased baseline myocardial wet-to-dry weight ratio. After cardiopulmonary bypass, myocardial edema increased in all dogs. Acute edema attributable to cardiopulmonary bypass decreased preload recruitable stroke work in all dogs of both groups, and dogs with D immitis could not be weaned from cardiopulmonary bypass. Myocardial edema increased diastolic relaxation times (tau) in dogs with and without D immitis. We conclude that cardiopulmonary bypass and heartworm infection induce myocardial edema. This edema compromises left ventricular systolic and diastolic function making D immitis an important confounding factor in weaning dogs from cardiopulmonary bypass.

Analysis of Variance↗
PubMed1994

Correlation between sex hormone receptors and peritumoral edema in intracranial meningiomas.

Fifty patients with intracranial meningiomas, verified histologically, are retrospectively analyzed to correlate the peritumoral brain edema with the positivity of estrogen receptors and progesterone receptors. The extent of edema was quantified on CT scan and/or MR. Monoclonal antibodies were used to test the estrogen receptors and the dextran-coated charcoal method was used to test the progesterone receptors. Significant levels of both receptors were found in 41 (82%) specimens. 80% of the cases with positive receptors had brain edema, in contrast to only 2 among 9 cases with negative receptors. Thus, the presence of brain edema has resulted to be correlated to the positivity of sex hormone receptors, although we did not find significant correlation between the amount of receptors and the amount of edema. The suggested mechanisms responsible for the brain edema surrounding intracranial meningiomas are discussed. We can suggest that progesterone may induce the secretion of some substances from meningioma cells, such as prostaglandins and biogenic amines, which may result in vagogenic edema.

Adult↗
PubMed1994

Corneal edema recovery dynamics in diabetes: is the alloxan induced diabetic rabbit a useful model?

PURPOSE: To compare the contact lens-induced corneal edema recovery dynamics of human subjects with type 1 diabetes with those of age- and sex-matched normal human subjects; to compare the human data with previously reported data from alloxan-induced diabetic rabbit. METHODS: Corneal edema was induced by 2 hours of closed eye wear with a thick, soft contact lens. After removal of the contact lens, central corneal thickness measurements were made at 30-minute intervals for 3 hours using optical pachometry. RESULTS: Human subjects with type 1 diabetes demonstrated a significantly slower rate of corneal edema recovery than age- and sex-matched human controls. The rate of corneal edema recovery found in this study for human subjects with type 1 diabetes is similar to that previously reported for alloxan-induced diabetic rabbits. CONCLUSIONS: The decreased corneal edema recovery ability of the patient with type 1 diabetes suggests that care should be taken when prescribing contact lens use in these people. The similarity between corneal edema recovery rates in the human subject with type 1 diabetes and the alloxan-induced diabetic rabbit supports the use of the alloxan-induced diabetic rabbit as an animal model for studies of corneal edema recovery dynamics in diabetes.

Adolescent↗
PubMed1996

Reexpansion pulmonary edema.

Reexpansion pulmonary edema is a rare complication attending the rapid reexpansion of a chronically collapsed lung, such as occurs after evacuation of a large amount of air or fluid from the pleural space. The condition usually appears unexpectedly and dramatically-immediately or within 1 h in 64% of patients and within 24 h in the remainder. The clinical manifestations are varied; they range from roentgenographic findings alone in asymptomatic patients to severe cardiorespiratory insufficiency. The radiographic evidence of reexpansion pulmonary edema is a unilateral alveolar filling pattern, seen within a few hours of reexpansion of the lung. The edema may progress for 24-48 h and persist for 4-5 days. Human data on the pathophysiology of reexpansion pulmonary edema derive from small series of patients, case reports, and reviews of the literature. On the other hand, a larger body of data exists on experimental reexpansion pulmonary edema in cats, monkeys, rabbits, sheep, and goats. This review examines the clinical and experimental evidence for reexpansion pulmonary edema. In addition, we detail the historical background, clinical setting, treatment, and outcome of reexpansion pulmonary edema.

Animals↗
PubMed1996

Effect of macular edema on surgical visual outcome in eyes with idiopathic epiretinal membrane.

OBJECTIVE: To determine whether macular edema affects the surgical outcome in eyes with idiopathic epiretinal membrane. DESIGN: Case series. SETTING: University-based referral practice in Vancouver. PATIENTS: Sixty-one patients (63 eyes) (37 women and 24 men ranging in age from 47 to 96 [mean 70] years) who underwent pars plana vitrectomy with membrane peeling for idiopathic epiretinal membrane. OUTCOME MEASURES: Degree of macular edema on preoperative fluorescein angiograms (none, mild or severe), as rated independently by two masked observers, and preoperative and postoperative Snellen visual acuity. RESULTS: Of the 63 eyes 32 had no macular edema, 21 had mild edema, and 10 had severe edema. Fifty-two eyes (83%) had an improvement in visual acuity. The mean number of lines of improvement in visual acuity for the three groups was 2.2, 3.7 and 2.6 respectively. Multiple regression analysis showed that the factor with the greatest adverse effect on visual outcome was intraoperative macular hole formation. The presence of macular edema preoperatively did not significantly affect visual outcome. CONCLUSIONS: Our results suggest that even eyes with significant macular edema secondary to idiopathic epiretinal membranes may benefit from vitrectomy with membrane peeling.

Aged↗
PubMed1998

Analysis of lymphatic drainage in various forms of leg edema using two compartment lymphoscintigraphy.

The anatomical and functional status of the epifascial and subfascial lymphatic compartments was analyzed using two compartment lymphoscintigraphy in five groups of patients (total 55) with various forms of edema of the lower extremities. Digital whole body scintigraphy enabled semiquantitative estimation of radiotracer transport with comparison of lymphatic drainage between those individuals without (normal) and those with leg edema by calculating the uptake of the radiopharmaceutical transported to regional lymph nodes. A visual assessment of the lymphatic drainage pathways of the legs was also performed. In patients with cyclic idiopathic edema, an accelerated rate of lymphatic transport was detected (high lymph volume overload or dynamic insufficiency). In those with venous (phlebo) edemas, high volume lymphatic overload (dynamic insufficiency) of the epifascial compartment was scintigraphically detected by increased tracer uptake in regional nodes. In patients with deep femoral venous occlusion (post-thrombotic syndrome). subfascial lymphatic transport was uniformly markedly reduced (safety valve lymphatic insufficiency). On the other hand, in the epifascial compartment, lymph transport was accelerated. In those patients with recurrent or extensive skin ulceration, lymph transport was reduced. Patients with lipedema (obesity) scintigraphically showed no alteration in lymphatic transport. This study demonstrates that lymphatic drainage is notably affected (except in obesity termed lipedema) in various edemas of the leg. Lymphatic drainage varied depending on the specific compartment and the pathophysiologic mechanism accounting for the edema. Two compartment lymphoscintigraphy is a valuable diagnostic tool for accurate assessment of leg edema of known and unknown origin.

Adult↗
PubMed1998

[Orbital edema induced by psychotropic drugs?].

INTRODUCTION: Drugs known to be responsible for orbital edema are calcium channel blockers, rifampicin, atracurarium, methylprednisolone and mannitol. We describe three patients with orbital edema induced by psychotropic drugs administrated for a long period of time. OBSERVATIONS: These patients were aged 51 to 73 years, and had orbital edema predominant in the morning, but persisting during the day. All the other causes of orbital edema--including steatoblepharon--were ruled out by medical history and investigations. In one case the edema decreased after the interruption of nearly all psychotropic drugs. DISCUSSION: The exclusive orbital localization of the edema suggests a local or regional mechanism that could be an exacerbation of the physiological morning orbital edema induced by decreased lymphatic flow. This flow is usually enhanced by gravity and automatic palpebral blinking.

Aged↗
PubMed1975

[Nonhemodynamic pulmonary edema due to toxins].

Lesional pulmonary edema caused by substances which are directly caustic for the gastrointestinal pathways (strong acids and bases, inhaled vomit) are opposed by their immediate and long-term gravity with those due to cardiotropic medicamentatous toxins or volemic overloading which lead to curable pulmonary edema. Material and human factors, in favour of accidental intoxication are compensated for by the fact that many toxins produce vapours which are strongly irritant for the upper respiratory pathways: this prevents prolonged exposure and therefore wards off edema. Drug intoxication by ingestion can lead to pulmonary edema by relative or absolute volemic overload, by allergic accidents or by immaturity of the enzyme degradation systems. It seems to us that the notions of "neurological" and "metabolic" toxic edema should be abandoned. In lesional edema the treatment is that of the acute respiratory failure. The combination of pethidine, promethazine, and chlorpromazine gives good immediate results. Owing to careful follow-up, hemodynamic pulmonary edema should most frequently be avoided.

Acute Kidney Injury↗
PubMed1981

Acute mountain sickness and the edemas of high altitude: a common pathogenesis?

Within days of ascent to high altitude when symptoms of acute mountain sickness (AMS) are common, pulmonary and cerebral edema may also develop. Although peripheral edema of the hands, face or feet may also appear, its association with AMS is unclear. In addition, persons with high altitude pulmonary edema often report an antidiuresis. Hence, altitude sickness appears to result from abnormalities in the handling of body water. To test this hypothesis, we studied 102 men and women who were trekking in the Mount Everest region of Nepal. Most were seen both at low (1377 m) and at high (4243 m) altitude. Severity of AMS was measured by an established Symptom Score derived from a questionnaire and physical examination. Change in body water was inferred from change in body weight in less than 10 days. Peripheral edema was assessed separately by physical examination. AMS Symptom Score correlated directly with weight change; those who remained well lost weight, whereas increasing signs and symptoms of AMS occurred in those with increasing weight gain. The symptomatic subjects also developed peripheral edema and reported decreased urinary output. These findings support the hypothesis that with rapid ascent to high altitude, abnormalities in the handling of body water, with antidiuresis, result in fluid retention (weight gain) manifest as peripheral, pulmonary, and/or cerebral edema.

Adolescent↗
PubMed1991

Attenuation of IL-2-induced multisystem organ edema by phalloidin and antamanide.

Interleukin 2 (IL-2) is a potent cytokine with diverse effects, including the ability to stimulate lymphocyte differentiation into cells capable of lysing tumor. Its therapeutic efficacy is limited because of side effects such as breakdown of the microvascular barrier and edema. Control of the microvascular barrier is in part regulated by endothelial cell cytoskeletal contractile proteins. This study tests whether the cyclopeptides that maintain actin filament organization and distribution and reduce macromolecular flux across the endothelial cell junction in vitro would similarly maintain barrier tightness and prevent early edema produced by IL-2 in vivo. Anesthetized rats were treated at 30-min periods with intravenous saline (0.5 ml, n = 41), phalloidin (20 micrograms in 0.5 ml, n = 21), or antamanide, (20 micrograms in 0.5 ml, n = 21), starting 30 min before the 1-h infusion of 10(6) U of recombinant human IL-2 or saline. Six hours after the start of IL-2, there was edema in the saline/IL-2 group, as measured by increased wet-to-dry ratios (W/D) in the lungs, heart, and kidney. With saline/IL-2, bronchoalveolar lavage (BAL) fluid contained an elevated protein concentration and higher plasma thromboxane levels compared with controls. The number of neutrophils sequestered in the lungs was more than twice that of saline controls. Phalloidin significantly attenuated edema in lung and reduced BAL protein leak. Antamanide treatment was as effective in limiting lung and heart edema, but, in contrast to phalloidin, antamanide prevented kidney edema and did not lead to an alteration in the liver W/D. Antamanide also prevented BAL fluid protein leak.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1999

Airway obstruction due to late-onset angioneurotic edema from angiotensin-converting enzyme inhibition.

PURPOSE: Angioneurotic edema is a well-documented complication of angiotensin-converting enzyme inhibitors (ACEI). We report a case of acute airway obstruction from a late-onset, probable ACEI-related angioneurotic edema and its subsequent management. CLINICAL FEATURES: A 48-yr-old obese man presented for transurethral resection of a bladder tumour (TURBT). His past medical history included hypertension controlled with hydrochlorothiazide and quinapril which had been started 13 mo earlier. Previous surgery was uncomplicated. Midazolam was used for premedication and for intraoperative sedation together with fentanyl and propofol. After uneventful spinal anesthesia with bupivacaine, operation and recovery, he was transferred to the floor. Five hours later he developed severe edema of his face, tongue and neck, with drooling, that progressed into airway obstruction and respiratory arrest. Ventilation was restored via immediate cricothyroidotomy, and a subsequent tracheotomy was completed uneventfully in the operating room. His serum C1 esterase inhibitor levels at 1, 5 and 23 days later were normal. The angioneurotic edema was attributed to the ACEI treatment. The edema resolved after 48 hr, and further follow-up was unremarkable. CONCLUSION: This observation is consistent with other reports that angioneurotic edema from ACEI can occur many months after the initiation of treatment. This can involve the airway and may produce life-threatening respiratory compromise. Physicians should be aware of this association and the possible need for immediate surgical intervention for the establishment of an airway in case of worsening edema or respiratory arrest.

Airway Obstruction↗
PubMedDate not supplied

Bilateral disc edema and unilateral macular hole in a patient with retinitis pigmentosa.

PURPOSE: A unique case of retinitis pigmentosa (RP) associated with bilateral disc edema and unilateral macular hole is presented. METHODS: A 49-year-old woman, a known RP patient, was found to have bilateral disc edema and a macular hole in the left eye during routine clinical examination. Fluorescein angiography revealed hyperfluorescent leakage of the optic nerve head significantly OD and minimally OS. There was staining in the macular regions which was consistent with retinal pigment epithelium atrophy OD and cystoid macular edema (CME) OS. Cerebrospinal fluid pressure and examination by lumbar puncture was normal. Disc edema spontaneously decreased bilaterally during follow-up. DISCUSSION: Bilateral disc edema was thought to be secondary to inflammation caused by rapid degeneration of photoreceptors and retinal pigment epithelium and macular hole was secondary to CME. CONCLUSIONS: Inflammatory response in the course of retinitis pigmentosa may result in disc edema and cystoid macular edema, which may further progresses to macular hole.

Female↗