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[Rupture of the diaphragm in closed traumas: apropos of 28 cases].

Twenty-eight cases of ruptured diaphragm due to blunt trauma are reported, including three with rupture on the right. Most of the patients were young men and rupture was an isolated lesion in only 6 patients, all others having multiple trauma. One patient died during surgery (3.6%) and complications, mostly respiratory, occurred in 17 patients (60.7%). Mid-term functional digestive and respiratory sequellae were evaluated. The gravity of ruptured diaphragm is basically related to the severity of the trauma and associated lesions. The diagnosis remains unrecognized in an important number of cases emphasizing the importance of repeated chest X-rays.

Abdominal Injuries↗

Changes in blood and bronchoalveolar lavage fluid components in calves with experimentally induced pneumonic pasteurellosis.

Pneumonic pasteurellosis was experimentally induced in calves by inoculation of 5 x 10(8) Pasteurella haemolytica organisms into the right diaphragmatic lung lobe. Blood and bronchoalveolar lavage fluid samples were obtained prior to inoculation and at postinoculation hour (PIH) 2, 4, and 6. Calves developed acute lung injury, characteristic of pneumonic pasteurellosis. Lesions were found only in the right diaphragmatic lobe. By PIH 4, significant (P less than 0.01) increases were detected in lavage fluid total cell count, neutrophil count, total protein and albumin concentrations, and alkaline phosphatase (ALP) and lactic dehydrogenase (LD) activities. Myeloperoxidase and elastase activities did not increase. Neutrophil depletion ameliorated the lung lesions and prevented the increase in lavage fluid cell count, total protein, and albumin concentrations and ALP and LD activities. Treatment with the iron chelator, deferoxamine mesylatehydroxyethyl starch, attenuated the increase in total protein and albumin concentrations and ALP and LD activities at PID 4, but not PIH 6. Treatment with a neutrophil function inhibitor, pentoxifylline, prevented the increase in lavage fluid neutrophil numbers, but accentuated the increase in total protein and albumin concentrations, and ALP, LD, myeloperoxidase, and elastase activities.

Animals↗

Respiratory muscle activity in the assessment of bronchial responsiveness in asthmatic children.

We investigated whether an increase in transcutaneous electromyographic (EMG) activity of the diaphragm and intercostal muscles corresponds with the concentration of histamine that induces a 20% fall in the forced expiratory volume in one second (FEV1; PC20). Eleven asthmatic children (mean age 11.9 yr) were studied after they were given histamine challenge. EMG activity at PC20 or at the highest histamine concentration was compared with activity at baseline by calculating the ratio of the mean peak-to-peak excursion at the highest histamine dose to that at baseline [EMG activity ratio (EMGAR)]. In all children reaching PC20, an increase in diaphragmatic and intercostal EMGAR was observed. No increase was found at the dose step before PC20 was reached. In six challenges, no fall in FEV1 was induced, and no increase in EMGAR was seen. In two challenges, no fall in FEV1 was induced, but increase in diaphragmatic or intercostal EMGAR was observed. Increase in the electrical activity of the diaphragm and intercostal muscles in asthmatic children corresponds closely to a 20% fall in FEV1 induced by histamine challenge.

Administration, Inhalation↗

[Epicardial fatty tissue of the right ventricle--morphology, morphometry and functional significance].

The height (thickness) of epicardial fat has been measured in histological slides at 10 standard "measuring points" in 200 human hearts. The 172 male and 28 female hearts were obtained from unselected autopsy material of the Institut of Pathology of the hospital groups "Bergmannsheil" in Bochum. The thickness of the epicardial fat on the surface of the right ventricle varies in histological paraffin slides between 0 and 13.6 mm. The mean of all 2,000 measurements is 2.19 mm, the median 1.7 mm. The mean values of the measurements at each of the standard points ranges between 0.851 mm at point No. 6 (dorso-caudal at the middle of the septum) and 4.12 mm at point No. 2 (sharp heart edge close to the bases). The lowest mean figure of the fat layer thickness is found in the dorso-caudal (diaphragmatic) region of the ventricular wall alongside the septum. At this point 0 thickness (fat-free area) is observed most frequently. The highest mean value and also the highest absolute measurement of fat layer thickness are found along the sharp heart edge - the ventro-lateral edge of the right ventricle - decrease from the heart bases to the apex. The average values of the standard "measuring points" along the ventral surface of the ventricular wall which decrease gradually from the heart bases to the apex, lie somewhere between the average values of the test points of the ventricle edge and the dorso-caudal surface close to the septum. In women, the epicardial fat layer on the right ventricle is, on average, thicker than that in men - ratio 1.65:1. A correlation can be seen between the thickness of the subcutaneous and epicardial fatty tissue layers. The weight of the ventricle wall can be increased in the case of marked fat development, and in exceptional cases the whole heart weight may be positively affected. Between age of 40 and death the thickness of the epicardial fat generally undergoes no statistical change. There is no statistical influence of the thickness of epicardial fat on the age at death, no is there any correlation between cause of death and thickness of the epicardial fat, and the epicardial fat is not diminished in deceased cancer patients. In the case of hypertrophy of the right ventricle there are no differences in the thickness of the fat layer as compared with the non-hypertrophic left ventricle. Chronic decompensated insufficiency of the right ventricle is associated with thinning of the fatty layer. No relationship is found between epicardial fat layer thickness and pathological silicosis in ex-miners.

Adipose Tissue↗

Feline hepatic disease.

Species differences in anatomy, physiology, and biochemistry lead to many dissimilarities between the canine and feline liver. Major differences exist in the interpretation of liver function tests, the significance of biochemical jaundice, the consequences of anorexia, and the efficiency of hepatic metabolic systems. Biochemical alterations in total bilirubin, ALT, and SAP may indicate the presence of disease in the feline liver. It is, however, impossible to make accurate diagnoses without liver biopsy. A liver biopsy can provide a diagnosis and prognosis and can guide the therapeutic plan. The feline hepatic diseases most frequently seen in our hospital are hepatic lipidosis, cholangiohepatitis complex, toxic hepatopathy, and hepatic neoplasia. Less common diseases of the feline liver include extrahepatic biliary obstruction, portacaval vascular anomalies, hepatic parasites, hepatic cysts, and diaphragmatic hernia. Systemic diseases that can effect the liver of cats are feline infectious peritonitis, multicentric lymphosarcoma, myeloproliferative diseases, hemolytic anemia, infectious panleukopenia, and systemic fungal infections.

Animals↗

Diaphragm sarcolemmal injury is induced by sepsis and alleviated by nitric oxide synthase inhibition.

Endotoxemia is associated with impaired diaphragm contractility, and increased nitric oxide (NO) production has recently been implicated in this phenomenon. However, the precise nature of sepsis-related alterations in diaphragm myofiber function remains unclear. We tested the hypothesis that enhanced NO synthesis during sepsis produces diaphragm sarcolemmal injury with attendant abnormalities of myofiber membrane electrophysiology. Two different rat sepsis models were employed: acute (4 h) intraarterial endotoxin (LPS; 20 mg/kg) and subacute (24 h) peritonitis induced by cecal ligation and perforation (CLP). Diaphragm damage occurred after both LPS and CLP, as indicated by hyperpermeability of myofibers to a low molecular weight tracer dye, which is normally unable to penetrate the sarcolemma. Sarcolemmal injury was significantly correlated with reductions in the resting membrane potential (Em) of single diaphragm myofibers. Western analysis revealed increased diaphragmatic expression of the inducible isoform of NO synthase (iNOS) after LPS and CLP. An inhibitor of NOS activity, LNMMA, significantly decreased morphologic as well as electrophysiologic signs of myofiber membrane injury and dysfunction. Therefore, we conclude that both acute endotoxemia and subacute peritonitis models of sepsis lead to significant sarcolemmal damage and altered Em in diaphragm myofibers. These changes appear to be mediated, at least in part, through the pathway of increased nitric oxide production.

Animals↗

Central respiratory carbon dioxide chemosensitivity does not decrease during sleep.

The ventilatory response to CO2 decreases during slow-wave sleep (SWS) and rapid-eye-movement (REM) sleep compared with awake levels. However, it is not known to what extent this can be attributed to decreased sensitivity of the CO2 chemoreflex. Mechanical factors during sleep may decrease ventilatory output, or PCO2 at the central chemoreceptor may not increase to the same degree as PaCO2, particularly during REM sleep when brain blood flow (BBF) is increased. In 10 goats, we measured the ventilatory (VI), diaphragmatic electromyogram (EMGdI), and BBF responses to CO2 rebreathing during each sleep-wake state. delta VI/delta PaCO2 decreased from wakefulness to SWS (p less than 0.05) and REM sleep (p less than 0.05). In contrast, delta EMGdI/delta PaCO2 was decreased only during REM sleep (p less than 0.05). Concurrently, delta BBF/delta PaCO2 increased during REM sleep (p less than 0.05) compared with the awake state or SWS. A significant reciprocal correlation existed between delta EMGdI/delta PaCO2 and delta BBF/delta PaCO2 across sleep states (r = -0.786). When EMGdI was related to directly measured cerebral venous PCO2 (n = 4), a single linear function (r = 0.894) was found, independent of sleep-wake state. Similar results were obtained during quasi-steady-state hypercapnia. We conclude that central CO2 chemosensitivity is intact during sleep.

Animals↗

Developmental toxicity of clarified slurry oil, syntower bottoms, and distillate aromatic extract administered as a single oral dose to pregnant rats.

Clarified slurry oil (CSO), syntower bottoms (STB), and distillate aromatic extract (DAE) are refinery streams produced by processing crude oil. Each of these refinery streams is rich in both hydrocarbons having carbon numbers of C20 or greater and polycyclic aromatic compounds. Available data indicate that some refinery streams are developmentally toxic (manifested primarily as increased embryolethality and growth retardation) by the dermal route of exposure. However, there is no conclusive evidence for their being teratogenic. The present studies were designed to further explore the suspected teratogenic potency of refinery streams while at the same time limiting embryolethality. To profile teratogenic effects as a function of gestation day, pregnant rats received a single oral dose (2000 mg/kg) of CSO, STB, or DAE on one of gestation days (GD) 11-14; DAE and STB were also administered on GD 15. To profile effects as a dose response function, rats received a single oral dose of CSO, DAE, or STB on GD 12 at 125, 500, and 2000 mg/kg. Control animals were similarly treated but were administered tap water. On GD 20, dams were necropsied and the fetuses evaluated for normal development. In general, evidence of maternal toxicity (i.e., decreased body weight gain, decreased thymus weight) was observed at doses greater than or equal to 500 mg/kg. For each refinery stream tested, the incidence of resorption was greatest on GD 11. A common pattern of fetal malformations was observed for all of the refinery streams tested and included cleft palate, diaphragmatic hernia, and paw and tail defects. The incidence and type of malformation observed were influenced by the gestation day of exposure. The incidences of external and skeletal malformations were greatest on GD 11 and 12 for fetuses exposed to CSO; on GD 13 and 14, the incidence of malformation was comparable for CSO- and STB-exposed fetuses. The incidence of visceral anomalies was greatest on GD 11-13 for fetuses exposed to CSO and STB; on Gestation D 14, the incidence was comparable for each of the refinery streams tested. In general, the ability to produce adverse effects on development was greatest for CSO and least for DAE. Effects produced by STB were comparable to or less severe than those observed for CSO.

Abnormalities, Drug-Induced↗

The pathophysiology of gastro-oesophageal reflux disease: an overview.

Gastro-oesophageal reflux disease (GORD) is a multifactorial disease. Although it is primarily a motility disorder, several other disturbances can interfere and contribute to determine the severity of symptoms and the degree of lesions. In normal subjects, as in patients with pathological reflux, nearly all the episodes of reflux obey one of the following three mechanisms: (a) a transient complete relaxation of the lower oesophageal sphincter (TLOSR), (b) a transient increase in intra-abdominal pressure which overcomes the resistance of the antireflux barrier ('stress reflux') and, (c) a spontaneous reflux through a permanently hypotonic sphincter. Gastric distension is the major factor that can induce TLOSRs. Whereas, at rest, the diaphragm probably plays little role in cardial competence, diaphragmatic contraction may help prevent reflux in conditions resulting in increased abdominal pressure such as during physical activity and abdominal staining. The presence of a hiatal hernia increases susceptibility to reflux. A delayed gastric emptying may also facilitate reflux and represents a factor of resistance to antireflux therapy. Most studies in humans have shown that motor abnormalities remain unchanged after healing of oesophagitis. Acid and pepsin are the most noxious agents of the upper gastrointestinal secretions that can participate in the pathogenesis of oesophagitis. However, there is no evidence that patients with reflux have greater acid secretion than subjects without reflux. The clearance function is a two-stage phenomenon requiring first a reduction in volume by peristalsis and then chemical neutralization by saliva. Primary peristalsis is mainly responsible for the clearance of acid in both the upright and the supine positions. It takes longer to clear acid in patients with non-reducing hiatal hernia. The layer of mucus which carpets the mucosa comes from the saliva and also from the submucosal glands of the oesophagus. The paracellular pathway is the major route by which mucosal HCl enters and then damages the oesophageal epithelium. Only a minority of acid reflux episodes are accompanied by symptoms. The acid exposure during the time period that precedes a reflux episode (i.e. the acid burden) is a key factor determining whether that reflux episode will be symptomatic or asymptomatic.

Animals↗

Pleural effusions and diseases of the pleura.

There are four factors that govern fluid movement to or from the pleural space: hydrostatic pressure, colloid osmotic pressure, filtration coefficient, and lymphatic function. When any of these factors are altered, fluid accumulates within the pleural space. Congestive heart failure, pancreatitis, neoplasia, hypoalbuminemia, and pulmonary thromboembolism can evoke pleural effusions by altering normal fluid transport mechanisms. This approach to pleural effusion helps to explain fluid accumulation. Chylothorax, hemothorax, and empyema are also covered in the article.

Animals↗

Measurement of ventilation and respiratory mechanics during continuous positive airway pressure (CPAP) treatment in infants.

A new method has been evaluated for measuring ventilation and lung mechanics in spontaneously breathing infants by means of a face chamber. Airway flow is measured with a pneumotachograph inserted between the face chamber and a stable pressure source. Oesophageal pressure is measured via a water-filled oesophageal catheter. The method is suitable for use in conjunction with continuous positive airway pressure (CPAP) treatment in neonatal intensive care. A flat frequency response curve up to 15 Hz for the two measuring systems (i.e., airway flow and oesophageal pressure), and a time shift between the two respective signals of less than 2 msec are prerequisites for correct evaluation of respiratory mechanics. In preterm infants with chest distortion, the inhomogeneity of pleural pressure affects the significance of resistance and compliance values, as calculated from oesophageal pressure. Supra-diaphragmatic pressure variations reflect the resistive and elastic load on the diaphragm exerted by the lungs and thorax. Thus, oesophageal pressure is still useful in studies of respiratory mechanics in preterm infants.

Apnea↗

Hypercapnic coma due to diaphragmatic involvement in a patient with dermatomyositis.

We report an acute respiratory distress by diaphragmatic involvement due to dermatomyositis. A fifty year-old patient with typical dermatomyositis presented an acute respiratory insufficiency with hypercapnic coma due to diaphragmatic muscle involvement. Respiratory state required mechanical ventilation initially and improved secondarily gradually upon corticosteroids and intravenous immunoglobulins. Only few cases of acute respiratory distress in dermatomyositis due to respiratory muscle involvement are reported in literature.

Coma↗

[The clinical and pathophysiological characteristics of the combined use of diaphragmatic electrostimulation and ultrasonic inhalation in patients with obstructive bronchitis].

Efficiency of diaphragm electrostimulation (DES) in combination with ultrasound inhalations (USI) was tried in 172 patients with chronic obstructive bronchitis (COB) in the exacerbation phase. They were divided into 3 groups by the degree of respiratory distress (RD) and circulatory insufficiency (CI). Group 1 consisted of 61 patients with RD of the first degree, group 2--of 57 patients with RD of the second degree and CI stage I, group 3--of 54 patients with RD of the second degree and CI stage IIA. Each group was subdivided into 3 subgroups exposed to DES + USI, USI, DES (subgroups 1, 2 and 3, respectively). Before and after the treatment, the patients underwent spirography, ECG, stimulation electromyography of the diaphragm, x-ray of the chest. Positive effects of DES + USI were reported on respiration mechanics, diaphragm contractility, pulmonary ventilation, function of the bronchopulmonary system and diaphragm. This combination promoted also deeper inhalation of the aerosol, faster relief of clinical symptoms. DES in COB patients is contraindicated unless bronchospasm is properly reduced.

Administration, Inhalation↗

Pulmonary function and electromyographic study of respiratory muscles in myotonic dystrophy.

Ten adult myotonic dystrophy patients underwent measurements of lung function, maximal dynamic and static ventilatory efforts, and respiratory muscle electromyography (EMG). EMG studies were performed during spontaneous breathing or when subjects breathed through high inspiratory or expiratory resistive loads. Present results show that (1) a moderate restriction of lung volumes with hypoxemia plus normocapnia is often observed; (2) patients sustain dynamic ventilatory efforts more easily than static work; and (3) abnormalities in respiratory muscle EMG exist with spontaneous expiratory and inspiratory intercostal activities during quiet breathing and changes in muscular response to resistive loads. Inspiratory loading evokes contraction of expiratory muscles, with a marked decrease in inspiratory activities. Expiratory resistive loads prolong the diaphragmatic contraction throughout the expiratory time, and in some patients, relaxation of the diaphragm does not occur during the loaded run. These EMG data suggest that the reciprocal inhibition among respiratory neurons is enhanced in myotonic dystrophy and that myotonia also occurs in the diaphragm when loads oppose its relaxation.

Adult↗

Architecture and function of the gastroesophageal barrier in the piglet.

We describe the anatomy and function of the gastroesophageal barrier in the piglet. Male piglets underwent dissection (N = 6) and gastroesophageal muscle layer histometry (N = 6). Sedated, nonintubated animals (N = 13) underwent four-probe perfusion esophageal manometry and the pressure profiles were related to the muscular thickness in the four quadrants. Hiatal and gastroesophageal anatomy are similar to our own. The muscle is thicker at the point where the clasp (on the right side) and sling fibers (on the left) concentrate. The pressure profiles were axially and radially asymmetric in coincidence with the thickness variations of the corresponding muscle layers. Sphincteric pressure was recorded as a plateau, whereas diaphragmatic crural pressure appeared as phasic oscillations in synchrony with respiration. The sphincter relaxed upon deglutition. In conclusion, the gastroesophageal structure and physiology are so similar in men and piglets that piglets are excellent models for research in this area.

Animals↗

Successful diaphragmatic pacing for idiopathic alveolar hypoventilation.

We describe the case of a 17-year-old woman noted to have idiopathic alveolar hypoventilation, with multiple Intensive Care Unit (ICU) admissions because of acute respiratory failure (ARF) due to respiratory infections. After two years of diaphragmatic pacing arterial blood gases have substantially improved, without obstructive apnoea. Signs of right ventricular enlargement and pulmonary hypertension have decreased. Morning headache and diurnal somnolence have disappeared, and she is also able to perform more physical and mental activity, allowing her to enjoy a better quality of life.

Adolescent↗

Atrioventricular septal defect: quantitative anatomy of the left ventricle.

A morphometric study was performed in 18 human hearts with atrioventricular septal defect not associated with other anomalies; 16 hearts had common atrioventricular orifices, and 2 presented separate right and left atrioventricular orifices. A total of eight parameters were analyzed, characterizing ventricular wall thickness, length and circumference of the inflow and outflow tracts, and circumference of the left orifice and aortic orifice. The data were compared with previously published patterns of normality. In addition, the volume of the aortic outflow tract was calculated. The inflow tract was shorter than the outflow tract, and the length of the diaphragmatic wall was equal to the sum of the lengths of the inflow tract and ventricular wall thickness at the level of the apex.

Cadaver↗