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Congenital stenosis of individual pulmonary veins is uncommon. Of the 49 cases reported, four were seen at the IWK Hospital for Children and are reported here. Plain radiographs show a shift of the heart toward the side of major involvement, Kerley B lines, fluid in the fissures, and interstitial edema of the affected lobes. These findings, while subtle, should nevertheless suggest stenosis. Technetium-99m macro-aggregate lung perfusion scans show absence of or diminished perfusion of the affected lobes. The diagnosis can usually be confirmed with angiography. Congenital stenosis of individual pulmonary veins should be considered in children with repeated pulmonary infections, dyspnea, failure to thrive, hemoptysis, or unexplained pulmonary hypertension.

Kidney transplant biopsies in the diagnosis and management of acute rejection reactions. In 68 consecutive renal transplant biopsies, histopathologic changes and clinical status of the graft recipient, both at the time of biopsy as well as one month later, were evaluated by independent observers. Nine histologic features were graded semiquantitatively (scale, 0 to 4): glomerular endothelial swelling, proliferation, exudation and necrosis; interstitial edema and infiltrate; vascular endothelial edema, infiltration and necrosis. The total score for each biopsy was termed the acute rejection index (ARI). The validity of the ARI as a means of evaluating rejection reactions was established by correlating the ARI with a second, overall histopathologic categorization. Clinical status at the time of biopsy was classified by retrospective analysis of all clinical data except the biopsy. The mean ARI of patients with an acute clinical rejection was significantly higher than those of patients with just a chronic clinical rejection or no clinical rejection. The utility of the biopsy in predicting the response of the graft recipient to therapy was evaluated in those 46 patients in whom an acute rejection was diagnosed clinically and in whom a full and complete course of therapy for the acute clinical rejection was given. Of the 28 patients whom the pathologist predicted would respond to therapy, 27 did show substantial improvement of their renal function up to one month following institution of treatment. Of the 18 patients whom the pathologist predicted would not respond to therapy, 15 had no clinical response. The data suggest that the transplant biopsy is helpful in 1) establishing the diagnosis of an acute rejection and 2) indicating whether or not the graft recipient will respond to standard immunosuppressive treatment for an acute rejection. Biopsies de reins transplantes dans le diagnostic et le traitement de reactions de rejet aigu. Dans 68 transplantations renales consecutives les modifications histologiques du transplant et l'etat clinique du receveur ont ete evalues par des observateurs independants a la fois au moment de la biopsie puis un mois plus tard. Neuf aspects histologiques ont ete apprecies de maniere semiquantitative (echelle de 0 a 4): le gonflement de l'endothelium glomerulaire, la proliferation, l'exsudation et la necrose; l'oedeme interstitiel et l'infiltration; l'oedeme endothelial, l'infiltration et la necrose des vaisseaux. Le total dans chaque biopsie a ete appele index de rejet aigu (ARI). La validite de ARI dans l'evaluation des reactions de rejet a ete etablie en correlant ARI avec une deuxieme classification histologique globale. L'etat clinique au moment de la biopsie a ete classe par l'analyse retrospective de tous les documents cliniques a l'exception de la biopsie. Le ARI moyen des malades atteints de rejet aigu est significativement superieur a celui des malades atteints seulement de rejet clinique chronique ou indemnes de rejet clinique. L'utilite de la biopsie dans le pronostic de la reponse du receveur au traitement a ete evaluee pour les 46 malades chez lesquels un traitement de rejet aigu a ete pleinement realise en doses et en duree. Parmi les 28 malades pour lesquels l'anatomo-pathologiste avait prevu qu'ils repondraient au traitement 27 ont eu une amelioration substantielle de la fonction renale dans le mois qui a suivi l'institution du traitement. Parmi les 18 malades pour lesquels l'anatomo-pathologiste avait prevu qu'ils ne repondraient pas au traitement 15 n'ont eu aucun effet clinique. Les observations suggerent que la biopsie du transplant est utile pour 1) etablir le diagnostic de rejet aigu et 2) indiquer si le receveur repondra au traitement immunosuppresseur habituel du rejet aigu.

Groups of 6 cats were curarized and maintained under assisted ventilation with either air or a 35% oxygen mixture. Lungs were then fixed and divided in small pieces, some of which were chosen at random for histological studies. Pulmonary lesions after assisted ventilation with air were rather discrete, even after 72 h. On the contrary, after the same period of ventilation with 35% O2, all cats showed capillary dilatation, interstitial edema and intra-alveolar hemorrhagic exsudate.

To determine whether interstitial pulmonary edema occurs or not in experimental cirrhotic rats, male Sprague-Dawley rats were given carbon tetrachloride subcutaneously in order to induce liver cirrhosis. The percent lung water content of the cirrhotic rats increased to 79.1 +/- 0.7% compared to 77.4 +/- 0.9% in control rats (p less than 0.001). Microscopically, 8 of 10 cirrhotic rats show the pulmonary interstitial thickening with lymphocytic infiltration. Moreover, perivascular edema with dilatation of lymphatics was frequently recognized. This suggested that fluid retention of pulmonary interstitial tissue would occur in the cirrhotic rats, and then perivascular edema would compress the small airways of the lung in cirrhotic rats.

Lung weight, extravascular water content, hemoglobin content as an index of blood congestion, and DNA content as an index of cellular content, were determined for 57 patients dying from multiple, extrathoracic trauma. This report, which confirms previous publications, concerns itself in particular with the problems of determination of the "normal" lung weight. Studies of the influence of survival time on the lung showed that lung weight may significantly increase to twice its value after very short times up to one hour after trauma as a result of blood congestion, and following longer survival may be elevated several times as a result of developing interstitial edema. Early appearing interstitial edema is morphometrically detectable already 10 minutes after the beginning of shock. Normal weights were obtained from 10 cases after immediate death following severe cranial trauma or decapitation by being run over. Our results show that normal lungs have an average weight of 234 g (s +/- 39). Literature values for "normal" lung weight are approximately twice as high.

To evaluate the potential risk of pulmonary damage due to aerial spraying of the insecticide fenitrothion, rat lungs were examined under light and electron microscopy at 3, 7, 21, and 60 days after exposure. Rats were exposed by a “nose-only” apparatus for 1 hr to 2 or 500 mg/m 3 of aerosolized fenitrothion (15%) mixed with solvent Cyclosol 63 (35%) and diluent oil 585 (50%). Aerosol size particles were monitored by a light scattering apparatus. Only minor modifications of lung alveolar tissues were observed after exposure to the high concentration. At 3 days, discrete foci of mild inflammation were detected, including interstitial edema, cellular infiltration, and increased number of alveolar macrophages. At 7 days, signs of irritation were diminished while at 21 and 60 days alveolar tissues were essentially normal. Exposure to lower concentration induced more limited changes at 3 days; no modifications were seen at later periods. It is concluded that a single exposure to this fenitrothion mixture at 500 mg/m 3 presents no serious hazard of pulmonary toxicity.

It has been shown that simultaneous administration of norepinephrine (10mug/kg/min) and drotaverine (200 mug/kg/min) does induce interstitial myocardial edema which tends to increase left ventricular diastolic stiffness. These results suggest that in myocardial ischaemia temporary increase of left ventricular diastolic stiffness may be caused by interstitial edema.

Adult respiratory distress syndrome (ARDS) from overdose of tricyclic antidepressants (TCA) has been reported but is not well known. During a 1-year period, 81 patients with serious overdose from tranquilizers and other psychotropic drugs were examined. TCA alone induced overdose in 30 patients or were combined with other drugs in 26 patients. Twenty-five (31%) patients had overdose from drugs other than TCA. Chest radiography revealed that 30 (54%) patients with TCA overdose and six (24%) patients with non-TCA overdose had abnormalities. Clinical and radiographic findings consistent with ARDS were noted in five (9%) patients with TCA overdose and none of the patients with non-TCA overdose. Five patients with TCA overdose and one (4%) patient with non-TCA overdose had interstitial edema that never progressed to ARDS. TCA should be added to the list of drugs associated with the development of ARDS.

We have investigated the relative effects of lung edema and of increases in pulmonary blood volume (PBV) on lung compliance (CL), and also the effects of selective elevations of pulmonary arterial (Ppa) and left atrial (Pla) pressures on PBV and on CL, using an isolated, perfused, and ventilated rabbit lung preparation. Lung weight was continuously recorded. A step rise in Pla at constant flow caused a rapid rise in PBV accompanied by an immediate fall in CL. With maintained high vascular pressures interstitial edema accumulated with no further fall in CL. Not until 3 times the normal amount of extra-vascular fluid had accumulated did a further, secondary reduction in CL occur. When Ppa was elevated to the same level by 1) a rise in flow and 2) a rise in Pla, the latter type of experiment gave 3–5 times larger increases in PBV. Pla elevations with or without rise in Ppa (flow adjusted) gave almost the same rises in PBV. The fall in CL was related to rises in PBV regardless of how such rises were obtained. Our conclusion is that increases in PBV, but not accumulation of interstitial edema, reduced CL in this preparation.

In ovalbumin-sensitized, mepyramine-treated guinea pigs protracted anaphylactic shock was elicited by i.v. injection of antigen. Diffuse or focal necrosis of myocardial cells was found in animals which died in protracted shock, as well as perivascular and interstitial edema. The antigen effects could be partially imitated by i.v. infusion of high amounts of adrenaline into nonsensitized guinea pigs. When adrenaline was infused during protracted anaphylactic shock, the catecholamine effects did not add to the histological effects of the antigen. Rather, the morphological alterations in the hearts were reduced, whereas the survival times were not increased, but decreased. - The findings are discussed in view of the nature of protracted anaphylactic shock.

Pulmonary lymphatics in a group of SIDS cases were compared with a control group of a similar age distribution. The causes of death in the controls were known to be associated with varying degrees of pulmonary edema. The surface areas of pleural, interstitial, peribronchial, periarterial and perivenous lymphatics were planimetrically measured. The data were statistically tested. The tests showed that the pulmonary lymphatics of the SIDS group were significantly more distended than those of the control group as expressed by highly significant differences in their surface areas. On the whole 2142 lymphatics were measured; 1255 in the SIDS group, which consisted of slides from 10 cases and 887 in the control group which consisted of slides from 11 controls. Although the sample size imposes a limit on the general applicability of the results, the clear distinction between the two groups as shown by the tests do indicate a possible feature of SIDS--lymphatic stasis--which might be secondary to some impairment of lymphatic drainage. This in turn could induce subtle fibrotic changes in the connective tissue framework of these lungs. The results are presented in the light of the forensic significance of the signs of asphyxia frequently found in SIDS and the diagnostic difficulties encountered in differentiating between SIDS and mechanical asphyxia e.g. due to smothering.

Assessment of extravascular lung water (EVLW) is imprecise in vivo, yet of both clinical and investigative relevance in patients with cardiac disease. Recently, a double-indicator method using thermal-green dye has been proposed as a nondestructive technique for in vivo quantification of EVLW. In our 5-yr study, indocyanine green dye was used as the intravascular indicator and heat as the diffusible indicator in 44 control dogs, 74 dogs administered intravenous oleic acid, 63 dogs in whom left atrial pressure was altered with a left atrial balloon, and 31 dogs with low-output cardiac failure (electrical shock and complete heart block). In these animals, in vivo measures of EVLW correlated closely with standard gravimetric techniques (r = 0.87, p less than .001), although the indicator dilution technique tended to underestimate actual lung water at higher volumes. In an additional 26 dogs, fluid (lactated Ringer's solution) was administered directly into a distal pulmonary airway, producing alveolar rather than interstitial edema. In these animals, as the infused volume was increased, the thermal technique underestimated consistently the actual amount of infused fluid. Nonetheless, we conclude that in most clinical and experimental situations where moderate changes in lung water are anticipated, this technique can provide reasonable estimates of extravascular fluid accumulation.

The morphological changes in the adrenal cortex and renal juxtaglomerular apparatus have been examined in pregnant sheep subjected to sodium depletion or loading. These changes were similar to those found in non-pregnant sheep in response to sodium depletion or loading, with the additional finding of interstitial edema in the zona glomerulosa of sheep with twin fetuses. As in non-pregnant sheep, sodium depletion resulted in evidence of juxtaglomerular peripolar cell granule release. The major finding was that sodium depletion in sheep with twin fetuses triggered the onset of ovine toxemia or "twin lamb disease".

In our study of 14 patients with adult respiratory distress syndrome (ARDS), we measured A-aDO 2 , Vd/Vt, arterial-to-end tidal Pco 2 difference (a-etPco 2 ), effective dynamic compliance, and pulmonary vascular resistance on a daily basis. At the onset of ARDS, all patients showed bilateral interstitial edema on the chest x-ray films, P(A-a)O 2 of more than 500 mm Hg, marked decrease in effective dynamic compliance, a moderate increase in Vd/Vt, and a normal value of a-etPco 2 . Pulmonary vascular resistance was low. After seven days, all of those who subsequently died had developed persistent elevation of P(A-a)O 2 , significant increase in Vd/Vt, a-etPco 2 and pulmonary vascular resistance, and significant decrease in effective dynamic compliance compared to the values at the onset of ARDS. Those abnormalities diverged significantly from the findings in those who survived. By evaluating sequential changes of those parameters, we might be able to predict an accurate prognosis of ARDS.

Changes in the morphology of myocardial cells during reperfusion after long cardiac ischemia were studied as a sensitive indicator of myocardial damage. Observations were made by light and electron microscopy on specimens of atrial myocardium from 20 patients undergoing uneventful coronary bypass surgery with global hypothermic (less than 18 degrees C) cardioplegic protection. The findings in biopsy specimens taken before and immediately after cardiac arrest and following 20 and 60 min of reperfusion were arbitrarily graded in a semiquantitative scoring system. More than 60 min of cold cardioplegic arrest resulted in foci of altered myocardial structure, as seen in biopsies prior to reperfusion. After 20 min of reflow, intracellular and interstitial edema was found and no regression of the subcellular changes had taken place. (Worsening was observed in 7 cases.) After 60 min of reperfusion the myocardial ultrastructure had normalized in all the patients who had had ischemic cardiac arrest for less than two hours. In two hearts with longer ischemia (120 and 140 min), scattered areas of myocytes undergoing progressive changes were seen, although the postoperative myocardial performance was normal. Provided that the observed atrial changes were representative of left and right ventricle, the study indicates that reperfusion per se may enhance edema and cellular derangement, and that reperfusion for more than 20 min is usually necessary for normalization of the myocardium after more than one hour of ischemia.

By means of magnetic resonance imaging (MRI), the proton spin-lattice relaxation times (T1 values) of the skeletal muscles were measured in Duchenne muscular dystrophy (DMD) carriers and normal controls. The bound water fraction (BWF) was calculated form the T1 values obtained, according to the fast proton diffusion model. In the DMD carriers, T1 values of the gluteus maximus and quadriceps femoris muscles were significantly higher, and BWFs of these muscles were significantly lower, than in normal control. Degenerative muscular changes accompanied by interstitial edema were presumed responsible for this abnormality. No correlation was observed between the muscle T1 and serum creatine kinase values. The present study showed that MRI could be a useful method for studying the dynamic state of water in both normal and pathological skeletal muscles. Its possible utility for DMD carrier detection was discussed briefly.

T MERE IS no doubt that roentgen examination is by far the most valuable single method for diagnosis of diseases of the pleura, but it also has very sharp limitations. Changes in the pleura may indicate abnormalities in other structures, particularly the lungs, mediastinum, heart, and certain subdiaphragmatic organs. Because early abnormal changes in the pleura may be well exhibited roentgenographically before other specific signs are evident, the method is excellent for detection of those conditions that manifest themselves by pleural reaction. A striking example is our ability to find pleural edema or a minimal amount of pleural effusion as one of the earliest signs of left heart failure, often before there is obvious evidence of interstitial edema or even before clear-cut symptoms appear. On the other hand, determination of the nature of the process that is affecting the pleura may be far more difficult. This is especially true in determining the etiology or background of a pleural effusion, the most common abnormality of the pleura. The pleura is also affected by primary diseases, i.e., those that arise in the membrane itself. These, too, can be detected at an early stage by roentgen examination, but again the problem of etiology arises, and it may be extraordinarily difficult to determine their exact nature.

Two groups of 10 patients with systemic arterial hypertension were studied by respiratory function tests before and after acute administration of diazoxide or furosemide. Small airways obstruction was present in a high percentage of patients and was partially reversed after the acute administration either of diazoxide or of furosemide. Systemic arterial hypertension seems to influence small airways caliber, through pulmonary vascular distension and/or pulmonary interstitial edema

Summary Suspensions of Salmonella typhimurium, Shigella dysenteriae and Botulinum-A-toxin or saline for controls resp. have been injected to 132 male Wistar rats. The basal function of the adrenal was altered by 2 I. U./100 g ACTH and 5 × 0,02 mg/100 g/die dexamethason resp. in 32 animals each. The animals are sacrificed after 2, 6, 10 and 14 hours after injection. Glutaraldehyde-OsC4-fixation of the adrenals by immersion. Araldite embedding. Zeiss EM 9 S 2. Both endotoxins rapidly cause aggregation of thrombocytes and formation of fibrin, release of monocytes into the circulation, disturbance of permeability of the capillary wall with interstitial edema and interstitial fibrin deposits. Lesions of cortical cells and endothelial cells are not visible. Intracortical hemorrhage 14 hours after injection of toxins is regarded as the result of consumption-coagulopathia. The functional state of the cortical cells has no influence on the hemorrhage. But hemorrhage can be forced by isolated dexamethason depending blockade of the RHS of the adrenal as a special case of generalized Sanarelli-Shwartzman reaction. Botulinum-A-toxin does not lead to early alteration of thrombocytes. Platelet aggregation appears first after 14 hours. With Botulinum-A-toxin hemorrhage in the adrenal can be produced only, if at the same time the RHS is blocked. In our study this was done by dexamethason induced regressive transformation of the adrenal cortex.

The chest radiograms and the arterial $${\text{P}}_{{\text{O}}_{\text{2}} }$$ values were studied in 61 patients suffering from severe acute CO poisoning. 22 patients (36.1%) showed abnormalities on chest film taken at the time of admission. The radiologic pulmonary abnormalities were classified into three patterns: 1. ground glass density, 2. interstitial edema, and 3. intraalveolar edema. Particular emphasis was placed on the diffuse, homogenous and hazy density like ground glass on chest films, as the patients who presented “ground glass density” showed marked hypoxemia at the time of admission. Clinical symptoms of pulmonary edema were manifested in 4 eases (6.6%) in this series of patients. Pulmonary edema in acute CO poisoning is far commonner than previously considered, and possible mechanism to develop it was discussed.

Chest films, right sided heart catheterization, and measurement of the regional lung perfusion, using 133Xe, were carried out 31 times on patients with mitral valve disease. A relationship was found between the radiologic evaluation in 3 grades, and the values of pulmonary wedge pressure and the apical and basal perfusion. Changes in flow distribution as reflected in altered appearance of the vessels and the presence of interstitial edema were found to be the most sensitive factors in the evaluation of pulmonary wedge pressure. Chest radiography was thus found suitable for the evaluation of pulmonary wedge pressure in mitral valve disease.

A case is presented of total anomalous pulmonary venous connection below the diaphragm, with roentgenographic evidence of pulmonary edema, interstitial edema and a normal cardiac silhouette. These findings led to a diagnosis of pulmonary venous obstruction proximal to the mitral valve. Our findings confirm that the morphologic substratum of Kerley B lines is predominantly edema of the interlobular septum.

In an effort to determine whether the lung has any role in the catabolism of gastrin, the synthetic heptadecapeptide was infused into a series of isolated perfused canine lungs. The results indicate that the normal lung does not catabolize gastrin. When interstitial edema supervenes, loss of gastrin from the perfusion mixture occurs which appears to be reversible. Under these circumstances, transudation but not catabolism appears to be occurring.

In this paper there are described the histopathological features of lesions induced in rabbit testes by single standard cryoinjuries inflicted between a few minutes and 4 days earlier. The most important events determined by the thermal insult consist of a sudden coagulation necrosis of the directly affected parenchyma, and an acute, unspecific inflammatory reaction in the rest of the gonad, characterized by interstitial edema and histiocytic-polynuclear infiltration. As reported in an earlier publication, this inflammatory-reparative process ends in about 1 month after the cryoinjury, with fibrous replacement of the necrotic tissue and reestablishment of the normal morphological and functional conditions in the rest of the gonad.

Summary The clinical and pathologic findings in early myositis ossificans progressiva occurring in homozygotic twins are presented. This is the second reported instance of this disease in identical twins. The early lesions consist of marked interstitial edema and connective tissue proliferation in the involved mesodermal structures. Degenerative changes in the skeletal muscle fibers are probably secondary to the surrounding connective tissue reaction. The progress of the disease appears to be unaffected by steroid therapy, even when instituted early, except for a transient response during the more acute phases.

Evidence of cardiac damage was found in 17 out of 26 Bantu goldminers with heatstroke. Myocardial injury was diagnosed on the basis of serum lactic dehydrogenase (LDH) isoenzyme patterns and electrocardiographically. A significant increase in the percentage of LDH-1 was present in 69 per cent of the patients. Electrocardiographic tracings were abnormal in 58 per cent of the cases. The changes consisted mainly of sinus tachycardia and nonspecific S-T segment and T-wave abnormalities, which were reversible in those patients who were followed up. A good correlation (75 per cent) was found between the isoenzyme and the electrocardiographic evidence of cardiac damage. Pathological examination of the heart in the 2 patients who died in the acute stage showed interstitial edema and degeneration of the muscle fibers. Although myocardial damage occurred in the majority of the cases, in none was it severe enough to cause overt cardiac failure.

Lungs of patients in cases of mitral insufficiency were studied to observe the influences of cardiopulmonary bypass. In addition to preoperative pathological conditions of lungs, more marked changes were noted in the type II alveolar epithelial cells and the interstitium postoperatively.Dilatation of capillaries and interstitial edema became evident. Concomitantly, a decreased number of granules containing lamellar structures, enlargement and fusion of these granules, and invasions of swollen and coarse lamellar structures to a granule forming a bulky conglomeration were notable. Other changes demonstrated in the cytoplasmic matrix were an increase of electron density and a dilatations of granular endoplasmic reticulum. No definite conclusion was drawn from the present investigations alone, however, structural alterations described in the paper are suggestive of resulting changes of lung surfactant, which will be a cause of pulmonary syndrome because of poor ability to keep the alveoli open.

Objective The aim of work is to evaluate the role of magnetic resonance imaging in the assessment of different entities of inflammatory breast disorders. Materials and methods Eighty-one non-lactating patients with mastitis had been evaluated by post contrast MR imaging; their ages ranged from 22 to 70 years (Average age: 41.6 years). MRI data analysis was performed regarding qualitative criteria and parametric color maps for image post processing. Diagnosis was made up regarding resolution in follow up sessions for simple mastitis and biopsy were done for cases with suspicious imaging findings. Results Mammary interstitial edema with no masses or abnormal enhancement was elicited in 28.4% ( n = 23/81). T2-weighed and post contrast series were the sequences of choice to rely upon in evaluation. T2 had demonstrated lesions in 64.2% ( n = 52/81) and contrast uptake was detected in 68% ( n = 55/81). Quantitative analysis was overlapping. MR imaging had displayed sensitivity, specificity and accuracy of 87.5%, 72.3%, and 75.4% respectively in differentiating benign forms of mastitis from malignant ones. Conclusion In inflammatory breast disorders, MR imaging can precisely delineate disease extent and monitor response to therapy. Immediate distinction between infectious/non-infectious and malignant mastitis is difficult to be obtained.

JUSTIFICATIVA E OBJETIVOS: Disfunção respiratória é frequente em crianças com cardiopatias congênitas acianóticas com hiperfluxo pulmonar (CCAHP), porém pouco é conhecido sobre a estrutura pulmonar destes pacientes. O objetivo deste estudo foi quantificar os volumes de gás e tecido e a distribuição da aeração pulmonar nesta população. MÉTODOS: Após aprovação do Comitê de Ética institucional e obtenção do consentimento escrito pós-informado, foram obtidas tomografias computadorizadas torácicas em sete crianças com CCAHF. As imagens pulmonares direita e esquerda foram contornadas em todas as imagens e os volumes e pesos pulmonares foram computados a partir dos dados volumétricos. As comparações entre esquerda e direita foram analisadas usando teste t de Student pareado e as correlações através de regressão exponencial. RESULTADOS: A idade mediana foi 20 meses e o peso foi de 9,9 kg. Volume pulmonar total (VPT) foi de 66,7 ± 23,1 mL.kg-1, o de tecido 33,5 ± 15,7 mL.kg-1 e o de gás 33,1 ± 8,3 mL.kg-1. O pulmão direito representou 57,9% e o pulmão esquerdo 42,1% do VPT (p < 0,001). O volume pulmonar de gás à direita foi 60,5% do volume de gás total (p< 0,001) e a quantidade de parênquima pulmonar normalmente aerado foi significativamente menor à esquerda (27,6 ± 6,8 vs . 18,1 ± 8% p < 0,001). CONCLUSÕES: As crianças portadoras de CCAHP apresentaram aumento no volume de tecido pulmonar maior que o esperado, possivelmente por edema intersticial. A aeração pulmonar está reduzida no pulmão esquerdo pela compressão imposta pelo coração ao pulmão subjacente. BACKGROUND AND OBJECTIVES: Respiratory dysfunction is common in children with acyanotic congenital heart defects (ACHD) with pulmonary hyperflow; however, little is known about the pulmonary structure of those patients. The objective of this study was to quantify the volumes of air and tissue, as well as the distribution of pulmonary aeration in this population. METHODS: After approval by the Ethics Committee of the institution and signing of an informed consent, seven children with ACHD with pulmonary hyperflow underwent computed tomographies of the chest. All images included the left and right pulmonary contour, and pulmonary volumes and weight were calculated using volumetric data. Paired Student t test was used to compare left and right, and exponential regression was used for correlations. RESULTS: Patients had a mean age of 20 months and weight of 9.9 kg. Total pulmonary volume (TPV) was 66.7 ± 23.1 mL.kg-1, tissue volume of 33.5 ± 15.7 mL.kg-1, and air volume of 33.1 ± 8.3 mL.kg-1. The right lung represented 57.9% of TPV and the left, 42.1% (p < 0.001). The pulmonary volume of air on the right was 60.5% of the total air volume (p < 0.001), and the volume of pulmonary parenchyma normally aerated was significantly lower on the left (27.6 ± 6.8 vs . 18.1 ± 8%, p < 0.001). CONCLUSIONS: The volume of lung tissue was greater than expected in children with ACHD with pulmonary hyperflow, possibly due to interstitial edema. Pulmonary aeration is reduced in the left lung due to the compression of the lung by the heart. JUSTIFICATIVA Y OBJETIVOS: La disfunción respiratoria es frecuente en niños con cardiopatías congénitas acianóticas con hiperflujo pulmonar (CCAHP), sin embargo, se conoce muy poco sobre la estructura pulmonar de esos pacientes. El objetivo de este estudio, fue cuantificar los volúmenes de gas y tejido y la distribución de la aeración pulmonar en esa población. MÉTODOS: Después de la aprobación por parte del Comité de Ética Institucional y de la obtención del consentimiento escrito informado, se obtuvieron tomografías computadorizadas torácicas en siete niños con CCAHF. Las imágenes pulmonares derecha e izquierda fueron perfiladas en todas las imágenes, y los volúmenes y los pesos pulmonares fueron computados a partir de los datos volumétricos. Las comparaciones entre izquierda y derecha fueron analizadas usando el test t de Student pareado y las correlaciones a través de regresión exponencial. RESULTADOS: La edad mediana fue de 20 meses y el peso fue de 9,9 kg. El volumen pulmonar total (VPT) 66,7 ± 23,1 mL.kg-1, y del tejido 33,5 ± 15,7 mL.kg-1 y el del gas 33,1 ± 8,3 mL.kg-1. El pulmón derecho representó un 57,9% y el pulmón izquierdo 42,1% del VPT (p < 0,001). El volumen pulmonar de gas a la derecha fue de un 60,5% del volumen de gas total (p < 0,001) y la cantidad de parénquima pulmonar normalmente aerado fue significativamente menor a la izquierda (27,6 ± 6,8 vs . 18,1 ± 8%, p < 0,001). CONCLUSIONES: Los niños portadores de CCAHP presentaron un aumento en el volumen de tejido pulmonar mayor que lo esperado, posiblemente por edema intersticial. La aeración pulmonar está reducida en el pulmón izquierdo por la compresión impuesta por el corazón al pulmón subyacente.

To the Editor.— Smith and Cho (233:861, 1975) reported cytomegalovirus interstitial pneumonitis in a case of sudden infant death syndrome (SIDS) and referred to two other cases from the literature. I can add two more cases (unpublished) from Wayne County, Michigan. Cytomegalovirus is known to cause respiratory tract infections in the first year of life (Proc Soc Exp Biol Med132:957, 1969). I agree with the authors that some may be missed in SIDS. Virus isolations from postmortem material in SIDS have been unrewarding and inconclusive. During the same period and time when SIDS incidence is at a peak, however, infants hospitalized for respiratory tract infections have yielded a high rate of respiratory pathogens.1Double virus infections are not uncommon. In infants less than 1 year of age, the respiratory syncytial virus was more frequently isolated, and with lesser frequency, rhinovirus, adenovirus, parainfluenza, enterovirus, and influenza virus.Mycoplasma pneumoniae

É relatada a observação de uma paciente de 44 anos de idade com quadro clínico de edema de pulmão secundário a meningioma situado na fossa posterior. São feitos comentários sobre a importância da gasometria arterial realizada no período pré e pós-operatório e especialmente sobre o gradiente alvéolo-arterial de oxigênio que serve de guia na avaliação clínica do paciente neurocirúrgico, particularmente nos casos de edema pulmonar não cardiogênico. A case of a 44-year-old woman presenting pulmonary edema secondary to posterior fossa meningioma is reported. The authors have tried to demonstrate the relationship between a lesion occupying space in the posterior fossa and important pulmonary abnormality such as interstitial edema based on increasing A-aD02 (oxygen alveolar arterial gradient) in this peculiar case. A-aD02 is easily measured and represents a good guide for evaluating the efficiency of medical and neurosurgical management when it is done in the serial way, particularly in those cases of non cardiogenic pulmonary edema.

The mildest form of acute pancreatitis is characterized by interstitial edema associated with a mild inflammatory exudate composed of either polymorphonuclear leukocytes or lymphocytes. Acinar tissue and ductular structures remain intact. There may be slight interstitial fibrosis. Occasionally there is a slight degree of fat necrosis. It is possible for this type of inflammatory process to recur on several occasions and resolve each time without residual histologic abnormality. This sequence is termed “relapsing acute pancreatitis” and is typical of the majority of instances of pancreatitis associated with biliary tract disease.

Experimental cardiac transplantation using various animals preceded the first human-to-human cardiac transplant in 1967. Such experimental work provided a sound basis for our understanding of the clinical and pathological features of cardiac rejection and their modification by immunosuppressive agents. Pioneering experimental work in animals was performed by Carrel and Guthrie1, Mann et al. 2, Downie3, Lower et al.4,and Blumenstock et al.5. Cooper6 has reviewed the many stages of the experimental development of cardiac transplantation which span this century, and Uys and Rose7 list key references to the cardiac pathology of experimental cardiac transplantation in dogs, rats, rabbits and baboons. Thomson8, in 1968, was the first to describe the pathology of a transplanted human heart, and this was followed shortly thereafter by the report of Lower et al.9.

The formation of interstitial edema is a complex phenomenon that involves not only increased capillary filtration into the tissues, but also the changes that can occur in the tissue’s ability to hold water coupled to the lymphatic drainage characteristics of the particular organ. Fifty years ago, Landis (1934) developed the concept that capillary pressure, usually controlled experimentally by altered venous pressure, must be elevated to some critical level before observable interstitial edema develops. He postulated that tissues react to increased capillary filtration by raising their tissue pressure, lowering their tissue colloid osmotic pressure (Starling, 1896) and increasing their lymphatic draining to provide the organ with a “margin of safety” in which observable edema is avoided even when capillary pressure increases by 15 to 20 mm Hg.

Permanent renal damage following extracorporeal shock wave lithotripsy (ESWL†) of renal calculi has not been reported. However, several studies have shown that temporary acute functional and morphologic changes can be noted immediately after ESWL treatment. Shock wave therapy has been directly associated with the development of intrarenal hematomas, interstitial edema, and temporary tubular dysfunction. The occurrence of reversible acute tubular necrosis following bilateral, simultaneous ESWL therapy in a nonobstructive system is herein reported.

Eighteen of 62 patients with acute carbon monoxide poisoning showed abnormal chest roentgenograms.The ground-glass appearance was the most common finding, representing the initial manifestation.Perihilar haze and peribronchial and perivascular cuffing were the second most frequent pulmonary changes.Intra-alveolar edema was the third manifestation.Cardiac enlargement and elevation of the night hemidiaphragm were also noted.The ground-glass appearance in acute carbon monoxide poisoning might be considered as parenchymal interstitial edema caused by tissue hypoxia and/or the toxic effect of carbon monoxide on alveolar membranes. Perihilar haze was often accompanied by cardiac enlargement and seemed to be of cardiac origin. Elevation of the right hemidiaphragm indicated enlargement of the liver.The outcome following hyperbaric oxygen therapy was favorable in cases with normal chest findings or the ground-glass appearance. Perihilar haze or intra-alveolar edema signified a poor prognosis. When abnormal chest r...

Anatomically two types of acute inflammation of the pancreas can be distinguished; the mild form is characterized by interstitial edema and peripancreatic fat necrosis. The severe type shows extensive peripancreatic fat necrosis and pancreatic parenchymal necrosis, local or diffuse. This necrotizing type develops in 8%– 15% of patients with acute pancreatitis.

Morphometric data from stable (nonedematous) isolated dog lungs, perfused with nearly cell-free perfusates, were compared to similar stereological evaluations of isolated dog lungs after induction of severe acute hydrostatic edema. In the edematous lungs, capillary surface and volume densities were substantially increased. Alveolar surface density was also increased. Thicknesses of the endothelial and type I epithelial cellular compartments of the air-blood barrier were unchanged. Thickness of the interstitial compartmemt of the air-blood barrier was substantially increased and this, in turn, caused an overall increase in mean thickness of the barrier. Volume densities of the nonparenchymal connective tissue spaces surrounding the extra-alveolar vessels and airways were also increased. In both the endothelial and type I epithelial cells cytoplasmic volume densities of pinocytotic vesicles were increased. In addition, the number of vesicles opening onto the luminal and albuminal cellular surfaces increased signficantly. Transendothelial vesicular passage may contribute to interstitial edema formation, and transepithelial vesicular transport may contribute to alveolar flooding in isolated perfused dog lungs.

Three atypical cases of pulmonary malaria are presented and discussed. Radiologically, they were manifested by very subtle thickening of interlobular septae or by more overt interstitial edema and pleural effusion. They were all relatively mild and cleared completely on antimalarial drugs. This is in contrast to most reported cases which were severe and fatal. This resultant widening of the clinical and radiologic spectrum of pulmonary malaria leads to the conclusion that such a complication is likely more common than previously recognized. The radiologist can suggest the correct diagnosis by being aware of its many manifestations and by having a high index of suspicion.

The major mechanisms of tumor invasion in vivo are discussed in the present review. A special emphasis is placed on tumor dedifferentiation which has proved to be of paramount importance for the invasion process. Based on in vivo observations obtained from various human and animal tumors a concept for the mechanism of tumor invasion is proposed which mainly comprises the following basic events: the first and essential step in tumor invasion is the tumor dedifferentiation and dissociation at the invasion front. This apparently temporary and reversible process mobilizes the tumor cells out of the main tumor bulk and enables them to invade the host tissue by active locomotion. This mechanism is essentially supported by an interstitial edema in the host tissue adjacent to the tumor periphery, which causes an 'opening and widening' of the host intercellular spaces. Enzymatic changes in the micromilieu of the extracellular matrix may contribute to this process. The tumor cell proliferation completes the invasion process in so far, as the invading tumor cells are still able to proliferate, leading this way to expanding tumor cell nests in the host tissue which have the potency to redifferentiate. The expansive growth of these tumor cell nests results in a progressive atrophy of the host tissue, mainly caused by an increasing compression and a competitive withdrawal of oxygen and other nutrients by the tumor cells. The overall picture of tumor invasion can therefore be considered as a repetitive cycle of active tumor cell locomotion followed by focal tumor cell proliferation in the host tissue.

So-called "peribronchial cuffing" in acute pulmonary edema appears to be caused by edema involving the bronchila wall as well as the peribronchial interstitial space, and this was confirmed at autopsy in a patient with acute left heart failure. Edema of the bronchial wall indicates transdation from capillaries derived from the bronchial rather than the pulmonary atery, which may well explain all of the radiological manifestations of acute interstitial edema. The possible role of this circulation in the production of acute alveolar edema is also discussed. The significance of the bronchial artery circulation in the production of acute pulmonary edema warrants reevaluation.

Magnetic resonance imaging (MRI) of kidneys was performed prior to extracorporeal shock wave lithotripsy (ESWLT), within 48 hours of treatment (immediate), and three months post-ESWL (intermediate) in 14 patients. Five patients underwent bilateral treatments for a total of 19 treated kidneys. With the pre-ESWL study serving as a control, immediate and intermediate examinations were evaluated for changes in renal volume, development of abnormalities in the corticomedullary junction (CMJ), development of intrarenal, subcapsular, or perinephric fluid, and alterations in the perinephric tissue and renal fascia. A statistically significant increase in renal volume occurred in the immediate post-ESWL period. This increase may have been secondary to parenchymal interstitial edema which resolved within three months. Thirty-two percent developed subcapsular bleeding and fascial and perinephric tissue prominence. All abnormalities identified on the immediate studies attributable to the ESWL treatment had resolved by the three-month study. No new cases of hypertension had developed within a three-month follow-up period.

The admission to anaesthesiological intensive care units is most often required by respiratory difficulties and pulmonary malfunctions. Even today one of the main causes of death among these patients remains the intractable respiratory insufficiency. Undoubtedly — shock be it a septic or hypovolemic traumatic shock -is one of the major factors in the development and perpetuation of pulmonary complications. Nowhere in the body the manifestations of shock can so easily be observed as in the lungs, where clinical findings, x-ray visualization and physiological measurements allow the concomitant interpretation of functional and morphological data. Independent of the basic illness a uniform clinical, pathophysiological and morphological pattern can be seen in the course of shock complicated by the insufficiency of pulmonary gas exchange. Depending on the course of the illness several well defined phases can be identified and are easily mistaken for distinct pathological entities. Despite the great number of terms used for shock induced respiratory malfunction I would like to emphasize the uniformity of this clinico-pathological process. Moreover this lack of a common name for a common problem reflects our lack of understanding of the underlying etiologic and pathogenetic process.

A validated computer simulation of pulmonary microvascular exchange (J.L. Bert and K.L. Pinder, Microvasc. Res., 27 (1984) 51-70) has been extended to include exchange with the air space (alveoli). Equations which hypothetically describe characteristics associated with this additional compartment and the exchange of both fluid and plasma proteins between the lung tissue and the alveolar space are presented. These are incorporated into the simulation which has been used to predict the behavior of the pulmonary microvascular exchange system including alveolar flooding. The predicted trends associated with alveolar flooding are reasonable. However, due to the lack of specific experimental or clinical findings, the simulation remains essentially unvalidated. The effect on alveolar flooding and interstitial edema of the parameters associated with the additional relationships is presented and discussed. Primarily, results for perturbations in circulatory pressure are presented. Additionally, changes in permeability characteristics are shown and discussed.

CARDIOVASCULAR disturbances in poliomyelitis were first described in 1910 by Robertson and Chesley,1 who commented on the presence of interstitial edema and swelling of the fibers in the myocardium of patients dying of the infection. The earliest clinical report of heart involvement was published in 1912 by Hertz, Johnson and Depree2; they observed a patient who recovered from an attack of infantile paralysis in which myocarditis was present. Although the presence of cyanosis, rapid pulse, and cardiac arrhythmias in severe cases had been noted in passing by many students of this disease, it remained for Saphir and Wile3 in . . .

In terms of patient survival, the immediate period of “shock,” or low perfusion, from whatever cause, is not our real problem. We get patients through this phase quite well, although undoubtedly the stage is set for the progressive, multisystem organ dysfunction which becomes our therapeutic challenge. Survival is determined by the severity of vital organ damage during and immediately after the shock episode. This is true for the respiratory system as for the other vital organ systems. Such damage can obviously be ameliorated or worsened by therapeutic interventions.

Histological and ultrastructural studies were made on 17 excised canine hearts after 0 (control), 3, 14, 18, and 24 hours of preservation by perfusion with cold filtered plasma. These were correlated with function as measured by an isovolumetric balloon technique. Variations in structure and function were observed within each group of preserved hearts, but function and structure correlated well in individual hearts: when function was excellent, structure was excellent; when function was poor, changes in the sarcoplasmic reticulum and mitochondria were prominent. The presence of marked angulations in the mitochondrial cristae correlated with high dp/dt values. Interstitial edema was present in all preserved hearts. The three control hearts, one 3-hour heart, and two 14-hour hearts showed excellent morphology and function. Of the five 18-hour hearts, function and morphology were excellent in three and barely adequate in one; a severely damaged heart could not be defibrillated. Of the six 24-hour hearts, morphology and function were excellent in three and poor in two; one heart with diffuse mitochondrial damage could not be defibrillated. These studies demonstrate good morphological preservation of canine hearts for 24 hours.