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Lactate dehydrogenase and creatine kinase activities in isolated edema fluid and peripheral blood in cold-induced brain edema.

A study of the alterations in lactate dehydrogenase and creatine kinase isoenzyme patterns in isolated grey and white matter edema fluid and in peripheral blood is described with a view to possible clinical use in severe brain-injury. The breakdown of the blood-brain barrier, caused by the infliction of a cold injury to the cerebral cortex of cats, resulted in a shift in the LD isoenzyme distribution in favour of the faster moving fractions and the appearance of brain-type CK in the peripheral blood. Total lactate dehydrogenase activity demonstrated no statistical significant changes during the experiment and total creatine kinase showed only slight increased values in the samples collected simultaneously with the infliction of a cold lesion. This strongly suggests that measurements of these parameters in peripheral blood are of little value as indicators of brain damage. Alterations in isoenzyme patterns observed in edema fluids are reflected in peripheral blood. The presence, therefore, of brain-type creatine kinase accompanied by a relative high amount of lactate dehydrogenase H-sub unit in peripheral blood, can be considered as adequate indices of severe brain damage.

Animals↗

Omega-oxidized leukotriene B4 detected in the broncho-alveolar lavage fluid of patients with non-cardiogenic pulmonary edema, but not in those with cardiogenic edema.

Leukotriene (LT) generation has been implicated in the pathogenesis of the acute respiratory distress syndrome, ARDS. In the present study, we analysed broncho-alveolar lavage fluids of patients on mechanical ventilation because of ARDS (17 samples taken from 9 patients) or because of cardiogenic edema (8 samples taken from 6 patients) and of healthy volunteers (10 samples from different donors). LTs were separated as methylated and non-methylated compounds using different HPLC procedures, and were identified by chromatographic mobility, on-line UV-spectrum analysis and post HPLC immunoreactivity. In the lavage samples of the healthy volunteers and the patients with cardiogenic edema, no LTs were detected by these techniques (detection limit congruent to 0.1-0.2 ng/ml lavage fluid). By contrast, in 15 out of 17 samples from patients with ARDS LTB4 or its metabolites 20-OH-LTB4 and 20-COOH-LTB4 were detected. The endproduct of omega-oxidation, 20-COOH-LTB4, represented the quantitatively predominant compound, detected in the range of 0.3-2.6 ng/ml perfusate. We conclude that the chemotactic agent LTB4 may be involved in the amplification of inflammatory events encountered in ARDS, and that the oxidized metabolites of LTB4 are particularly suitable for monitoring lung leukotriene generation under conditions of neutrophil efflux and oxidative stress.

Adult↗

[Severe necrotic and haemorrhagic edema of the upper limbs revealing remitting seronegative symmetrical synovitis with pitting edema].

BACKGROUND: RS3PE (Remitting Seronegative Symmetrical Synovitis with Pitting Edema) syndrome is characterized by bilateral and symmetrical tenosynovitis of the distal extremities. It occurs with acute onset in older patients aged over 50 years. This heterogeneous entity can be isolated or can reveal various rheumatic diseases and neoplastic conditions. We report a case of RS3PE syndrome associated with unusually severe cutaneous necrotic and haemorrhagic lesions, and revealing malignant monoclonal IgM proliferation. CASE REPORT: A 62-year-old man was admitted for acute and symmetrical synovitis of both hands and forearms associated with fever and increased acute phase reactants. Severe necrotic and haemorrhagic edema developed simultaneously. Laboratory tests ruled out infectious disease and collagen vascular disorder. Clinical symptoms responded promptly to corticosteroids to reveal severe erosive arthropathy of both wrists. The monoclonal IgM proliferation discovered during the acute phase evolved into a malignant medullary plasmocytosis. After adequate treatment of this proliferation, no haematological, cutaneous or articular relapse occurred during the two-year follow-up period. DISCUSSION: This type of cutaneous symptoms has never been reported during the course of RS3PE syndrome. It may be supposed that the severity of the initial clinical picture was linked in this patient to the paraneoplastic nature of this.

Arm↗

Experimental brain tumors and edema in rats. III. Peritumorous edema.

In rats experimental brain tumors were produced by intracerebral implantation of a glioma cell clone. Peritumorous edema was investigated by light and electron microscopy, using exogenous tracers [human serum albumin (HSA), horseradish peroxidase] and immuno-histochemical methods for localization of endogenous serum proteins. An infiltration by serum proteins was observed in peritumoral grey and white matter. Peroxidase was found in pinocytotic vesicles of vascular endothelial cells, in pericytes and diffusely in the extracellular space. High concentrations of endogenous rat serum proteins and exogenous human serum albumin were also found in neurons of the grey matter and in oligodendrocytes of the white matter. A cellular uptake of extravasated proteins, therefore, may contribute to edema resolution.

Animals↗

Comparison of measured and calculated colloid osmotic pressure of serum and pulmonary edema fluid in patients with pulmonary edema.

Serum and pulmonary edema fluid samples of 26 patients with pulmonary edema were examined. The correlation coefficient comparing measured colloid osmotic pressure (COPm) to calculated colloid osmotic pressure (COPc) (Landis and Pappenheimer equation) was 0.84. Significant differences between COPm and COPc were noted when total protein (TP) concentrations were less than or greater than 5 g/dl (p < 0.001 and p < 0.01, respectively). Twenty-one of 69 samples (30%) had a greater than 4 mm Hg difference between measured and calculated values. COP should be measured rather than calculated for accurate determinations.

Adult↗

Edema development and recovery in neurogenic pulmonary edema.

We determined the time course of changes in extravascular lung water (EVLW) that occur after massive sympathetic activation produced by intracisternal veratrine administration in chloralose-anesthetized dogs. Three groups of dogs were studied. In the first group (n = 9), acute increases in EVLW (occurring within minutes) were determined both by measuring extravascular thermal volume and by gravimetric analysis. In the second (n = 6) and third (n = 7) groups, changes in EVLW were followed for 2-3 h after veratrine administration. Extravascular thermal volume was measured in the second group. In the third group, right atrial injections of a vascular indicator (125I-labeled serum albumin) and an extravascular indicator (3HOH) were made while blood was sampled from the pulmonary artery (PA) and left atrium, and EVLW was determined by deconvolution of the left atrial and PA concentration-time curves. Indicator-dilution and gravimetric EVLW increased acutely only in dogs in which PA pressure exceeded 60 Torr, with two- to four-fold increases in EVLW being observed in dogs that developed the highest PA pressures (maximum 94 Torr). Thus, severe edema can develop rapidly after massive sympathetic nervous system activation but requires extreme degrees of pulmonary hypertension. In several dogs after the acute increase in EVLW associated with the pulmonary hypertension, the indicator-dilution EVLW decreased with time. These decreases appear to effect clearance of edema fluid rather than alterations in perfusion.

Animals↗

Elevated levels of interleukin-8 and leukotriene B4 in pulmonary edema fluid of a patient with reexpansion pulmonary edema.

We experienced a case of reexpansion pulmonary edema (RPE) after surgical treatment of pneumothorax. In this case, protein leakage and polymorphonuclear leukocyte (PMN) accumulation were observed in the reexpanded lung. Interleukin-8 and leukotriene B4 in edema fluid were increased at the onset of RPE. PMN elastase was also increased, though its peak was delayed. The plasma level of P-selectin, which mediates adhesion between PMN and endothelium, was elevated. We speculate that some of these fluid mediators may play important roles in chemotaxis and activation of PMN in the development of RPE.

Adult↗

[Reimplantation edema in the transplanted lung. Reperfusion-ischemia or hydrostatic edema?].

The development of non cardiogenic pulmonary edema or pulmonary reimplantation response after lung transplantation has been well described. The cause is ischemic vascular injury of the allograft, results in increased permeability of the lung after reperfusion, in turn leading to interstitial and alveolar edema. We report two cases of pulmonary reimplantation response after bilateral sequential lung transplantation. Massive pink frothy fluid was noted in the orifice of the double-lumen endobronchial tube. Blood and endobronchial fluid samples were collected for protein electrophoresis. We conclude that, in spite of the severity of reimplantation response, this complication can be resolved early when the cause is mainly hydrostatic.

Blood Proteins↗

[Distribution and constitutional changes of edema fluid in cytotoxic brain edema analyzed by electron microscopy and differential scanning calorimetry].

To understand the pathogenesis of brain edema, we studied distribution and constitutional changes of brain-tissue water by morphological and thermoanalytical methods in cytotoxic brain edema induced by 6-aminonicotinamide (6-ANA). Ninety-two Wistar rats were divided into three groups; Group I rats receiving physiological salt solution intraperitoneally served as controls. Group II and III animals were intraperitoneally given 120 mg/kg and 36 mg/kg of 6-ANA respectively. All animals were starved after injection of drugs to exclude differences in water intake. Then they were decapitated at 3, 6, 12, 24, 36 or 48 hours to measure specific gravity (SG) of large brain tissue (1.1-1.5 g), and to evaluate water content (WC) and free water ratio (FWR) of small brain-tissue samples (15-35 mg) taken from the frontal cortex; WC was measured by a drying-weighing method, and FWR was analyzed with a differential scanning calorimeter. Moreover morphological changes of the frontal cortex of the brain were studied in Group II (n = 12) at 3, 6, 12, 24 and 48 hours with an electron microscope. Neurological status of animals administered 6-ANA (Group II and III) deteriorated with time. Morphological studies showed that perivascular astrocytes and astrocytic processes in the cerebral cortex were swollen most remarkably at 48 hours. However neuronal and endothelial cells were almost intact. The FWR of Group I decreased significantly about four per cent (p less than 0.001) after being starved for 48 hours. But the SG and WC of the group showed little change.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Aminonicotinamide↗

[Hereditary angioneurotic edema (Quincke's edema). Report of a case and literature review].

Familiar angioneurotic edema or Quincke's edema is an uncommon variant of urticaria, associated or not, that involves the subcutanean cell tissue and mucous of the face and upper airdigestive tract. It can produce an acute dyspnea and risk of suffocation with intubation or tracheostomy up to a 20% of the cases. The disease is a result of deficit in C esterasa inhibitor which autosomal dominant inheritance. We are reporting one clinical case confirmed as such corresponding to a 81 years-old male whom was operated by tracheotomy after sending from UCI with an emergency coniotomy and failure for orotracheal intubation.

Aged↗

Tracheal mucosal edema in hydrostatic pulmonary edema.

Airway edema has been described in heart failure, and, in animal experiments, airway narrowing was observed with elevated left atrial pressure (Pla). On the basis of double-indicator-dilution principles using helium and dimethylether, we were able to measure a water compartment of the tracheal mucosa (VH2O) in dogs. Hypervolemia with an attendant increase in Pla caused by infusion of 2 liters of dextran increased VH2O from 368 +/- 71 (SE) to 794 +/- 177 microliters (P < 0.01). Pulmonary arterial wedge and central venous pressures (Pcv) rose concomitantly. Increases in pulmonary arterial wedge and Pcv by a left atrial balloon catheter produced similar increases in VH2O, whereas increases in Pcv alone by a right atrial balloon did not increase VH2O. Increasing VH2O by dextran infusion was associated with an increase in pulmonary resistance from 1.16 +/- 0.19 to 2.15 +/- 0.24 cmH2O.l-1.s (P < 0.01). These observations show that fluid accumulation in the lung during pulmonary congestion also involves extraparenchymal airways and is related to Pla rather than right atrial pressure. This indicates that sufficient collateral drainage exists during right-sided but not left-sided pressure elevations.

Anesthesia↗

Measurement of edema in the nervous system. Use of Percoll density gradients for determination of specific gravity in cerebral cortex and white matter under normal conditions and in experimental cytotoxic brain edema.

A method is presented by which density measurements can be performed on samples from cerebral cortex and white matter of normal and intoxicated animals using nontoxic ingredients as an alternative to the bromobenzene-kerosene technique described by Nelson et al. (1971). A continuous density gradient is prepared in a calibrated glass cylinder by using a new product, Percoll, which consists of colloidal silica particles coated with polyvinyl pyrrolidone. The gradient is stable and the same column can be used for repeated experiments over a long period of time. Interactions between the gradient media and the samples are evaluated and various methodological aspects concerning removal and handling of the tissue samples are presented. Experiments with acute triethyltin (TET) intoxication in the mouse and the hamster show that the Percoll technique can be used as an alternative to the bromobenzene-kerosene method in quantitative studies on cytotoxic brain edema.

Animals↗

[Negative pressure pulmonary edema. Post-obstructive lung edema after use of a laryngeal mask].

A 31-year-old male patient was scheduled for surgical treatment of a distal radius fracture under general anaesthesia using a laryngeal mask airway and spontaneous ventilation. The intraoperative course was uneventful. During recovery, the patient strongly bit the laryngeal mask, producing a complete obstruction of the artificial airway in combination with very forceful inspiratory efforts until the mask was removed. In the recovery room the patient developed dyspnea and desaturation. A portable chest radiograph demonstrated bilateral alveolar infiltration suggesting pulmonary edema. The patient was transferred to the intensive care unit where drug therapy (furosemide and hydrocortisone) and treatment with the continuous flow continuous positive airway pressure (CF-CPAP) system led to complete recovery within 24 h.

Adult↗

Focal reexpansion pulmonary edema after drainage of large pleural effusions: clinical evidence suggesting hypoxic injury to the lung as the cause of edema.

BACKGROUND: The purposes of this study were to review possible causes of reexpansion pulmonary edema (RPE) and to attempt to explain atypical distributions of RPE after drainage of large pleural effusions. METHODS: Five patients had focal RPE after routine drainage of large pleural effusions. In these cases, pleural effusion did not completely fill the hemithorax, and part or all of the ipsilateral upper lobe remained aerated. Reexpansion was accomplished by chest tube drainage with -20 cm H2O suction in four cases and by percutaneous needle aspiration without application of negative intrapleural suction in one. RESULTS: In all five cases, RPE developed in the portion of the lung that had been collapsed but did not develop in the portion of the lung that remained aerated. CONCLUSIONS: This suggests that hypoxic injury to the atelectatic lung, rather than mechanical stress, is the most plausible explanation for RPE.

Aged↗

MR imaging of bone marrow edema pattern: transient osteoporosis, transient bone marrow edema syndrome, or osteonecrosis.

The bone marrow edema (BME) pattern of signal intensity changes on magnetic resonance (MR) images (decreased on T1-weighted and increased on T2-weighted) is a nonspecific finding encountered with several entities, including transient osteoporosis of the hip, transient BME syndrome, osteonecrosis, trauma, infection, and infiltrative neoplasm. Transient osteoporosis, an unusual but distinct syndrome characterized by self-limited pain and radiographically evident osteopenia, can be distinguished from other causes of the BME pattern, particularly osteonecrosis, on the basis of clinical findings and the development of radiographically evident focal osteopenia within 8 weeks after the onset of pain. This is an important distinction, since all patients with transient osteoporosis recover completely, without intervention. The term transient BME syndrome can be used to describe any patient in whom a reversible BME pattern is seen on MR images. Although the transient BME syndrome is also self-limited and quite likely related to transient osteoporosis, the authors believe that to avoid confusion, this nonspecific term should be reserved only for patients who do not develop radiographically evident osteopenia.

Adult↗

Capillary permeability factor secreted by malignant brain tumor. Role in peritumoral brain edema and possible mechanism for anti-edema effect of glucocorticoids.

Conditioned media from two human malignant gliomas, C6 rat glioma, Walker 256 carcinosarcoma, and normal human glia were concentrated 50-fold to create a culture supernatant (SUP-C). The effect of SUP-C on rat brain capillary permeability was investigated by measuring the entry of 14C-aminoisobutyric acid (14C-AIB) by means of quantitative autoradiography. The SUP-C contained proteins with a molecular weight of 10 kD or greater. The SUP-C from all tumor cells markedly increased brain capillary permeability, indicating the presence of a permeability factor, whereas that from normal glial cells did not. Glioma cells produced more factor after incubation for 20 hours than 4 hours. The activity of capillary permeability factor in the SUP-C was inhibited by pretreatment of animals with BW755C (lipoxygenase inhibitor), but not with indomethacin (cyclo-oxygenase inhibitor). Pretreatment of animals with dexamethasone prior to intracerebral infusion of tumor SUP-C significantly reduced the factor-induced increase in capillary permeability. On the other hand, coincubating glioma cells with dexamethasone produced SUP-C with a permeability activity that was about one and a half times greater than that without dexamethasone. These results indicate that glucocorticoids produce their anti-edema effects by directly acting on capillary endothelial cells, possibly through the inhibition of phospholipase A2 activity, resulting in a decrease of lipoxygenase rather than cyclo-oxygenase products. The production of capillary permeability factor by tumor cells was not inhibited, but rather enhanced, by administration of glucocorticoids.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗

Radiographical investigations of organic lesions of the hypothalamus in patients suffering from neurogenic pulmonary edema due to serious intracranial diseases: relationship between radiographical findings and outcome of patients suffering from neurogenic pulmonary edema.

Radiographical investigations of the hypothalamus by computerized tomography (CT) have rarely been performed despite the fact that the damage to the hypothalamus owing to serious intracranial organic diseases may cause neurogenic pulmonary edema (NPE). We presented 22 consecutive cases of patients suffering from NPE caused by serious intracranial organic diseases and investigated the relationship between NPE and abnormal radiographical findings of the hypothalamus. In 11 cases, organic lesions were noted in the hypothalami and 10 of these patients died of NPE (91.0%). In contrast, of the remaining 11 cases without significant radiographical findings of organic lesions in the hypothalami, only 2 patients were lost (18.2%). In general, various factors including systemic ones are considered to contribute to the prognosis of the patients suffering NPEs caused by serious intracranial diseases. It was concluded that hypothalamic damage was not always found by radiograph in patients with NPE due to critical intracranial diseases, but once abnormal findings in their hypothalamus of these patients were noted, their prognosis would become significantly poor (p < 0.05).

Adult↗