[Diagnosis of acute pulmonary embolism. Recommendations of the German Society of Pneumology].
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Publications and source records attributed to P Dorow.
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STUDY OBJECTIVE: To explore the role of MRI in the differential diagnosis of pleural disease. PATIENTS: Forty-two patients with pleural disease were included. METHOD: Retrospective study. All patients were examined with both CT and MRI. The morphologic features of pleural lesions and magnetic resonance signal intensity on T1-weighted, T2-weighted, and contrast-enhanced T1-weighted images were evaluated. RESULTS: Mediastinal pleural involvement, circumferential pleural thickening, nodularity, irregularity of pleural contour, and infiltration of the chest wall and/or diaphragm were most suggestive of a malignant cause both on CT and MRI. Pleural calcification on CT was suggestive of a benign cause. Contrary to what has been previously reported in the literature, neither on CT nor on MRI, pleural thickness >1 cm revealed significant difference between malignant and benign pleural disease (p>0.05, chi(2) test). High signal intensity in relation to intercostal muscles on T2-weighted and/or contrast-enhanced T1-weighted images was significantly suggestive for a malignant disease. Using morphologic features in combination with the signal intensity features, MRI had a sensitivity of 100% and a specificity of 93% in the detection of pleural malignancy. CONCLUSION: When signal intensity and morphologic features are assessed, MRI is more useful and therefore superior to CT in differentiation of malignant from benign pleural disease.
This randomized, double-blind, parallel-group study compared the efficacy and tolerability of as-required salbutamol 100 microg administered from either a chlorofluorocarbon (CFC) pressurized metered dose inhaler (pMDI; Ventolin) or from a non-CFC hydrofluoroalkane (HFA) 134a pMDI (Ventolin CFC-free) in patients with mild to moderate asthma. All patients (n = 423) continued with their standard asthma therapy, and recorded their daily use of study medication, morning and evening peak expiratory flow (PEF) and symptom scores, throughout the 4-week treatment period. Clinic lung function was measured at 2-week intervals. The median daily use of inhaled study medication remained constant at four actuations per day throughout the study in both treatment groups and statistical analysis indicated that the two formulations were equivalent. Small improvements in both treatment groups were reported in mean morning and evening PEF, clinic forced expiratory volume in 1 sec and clinic PEF and there were no significant differences between the two groups. Both formulations were well tolerated. This study indicates that as-required salbutamol 100 microg administered via a HFA 134a pMDI is as effective and safe as the currently available CFC-propelled formulation.
A central apnea is a disorder characterized by apneic events during sleep with no associated ventilatory effort. Central sleep apnea syndrome is characterized by repeated apneas during sleep resulting from loss of respiratory effort. Although the etiology of central apnea remains obscure in most cases, current investigations into breathing control system during sleep and association with certain diseases have pointed out possible mechanisms. Ventilation during sleep is highly dependent on the nonbehavioral control system. As a result, any diseases affecting this control system could influence the breathing patterns while the patient is asleep. As our results show, most patients with central sleep apnea and without congestive heart failure had quantifiable abnormalities like diminished carbon dioxide response curves. Neurological diseases affecting the brainstem are able to produce breathing pattern disorders in sleep. Well-known neurological diseases such as arteriosclerosis in the elderly, infarctions, tumors, hemorrhage, accidents with damage of this region, encephalitis, poliomyelitis or other infectious diseases may cause central apnea during sleep, even if in wakefulness no abnormalities of breathing patterns are present. Apneas cause hypoxemia, hypercapnia and increased sympathicotonia. This may result in development of pulmonary artery hypertension or systemic hypertension. Published results demonstrate that medical treatment is ineffective in these patients. Implantation of a diaphragm pacing device is an invasive measure, the efficacy of the diaphragm pacing has not been proven by long-term trials, however. Mechanical ventilation was shown to be the most efficient treatment. A therapeutic procedure using a timed n-BiPAP device is able to normalize blood gases during sleep. The n-BiPAP prevented the development of severe pulmonary artery hypertension during sleep.
Kinins are potent inflammatory mediators, liberated from kininogens by different kininogenases. The aim of this study was to investigate the kinin generation pathways in acute and chronic inflammation of the lower airways. We studied bronchoalveolar lavage fluid (BALF) of patients with acute pneumonia, patients with chronic bronchitis and healthy controls. Kinins were determined by radioimmunoassay (RIA). Plasma kallikrein (pl-Kal), alpha2-macroglobulin (alpha2-M) and toluenesulphonylarginine methyl ester (TAME) esterase activity (TAME-ea) were studied in BALF before and after gel filtration chromatography. Plasma kallikrein and alpha2-M were measured using two newly developed sandwich enzyme-linked immunosorbent assays (ELISAs). TAME-ea was measured by a radiochemical assay. After gel filtration, inhibition of TAME-ea with benzamidine, soy-bean-trypsin inhibitor (SBTI) and aprotinin was performed. Kinins and TAME-ea did not differ significantly between acute pneumonia and chronic bronchitis, whereas pl-Kal and alpha2-M values were significantly higher in acute pneumonia. Gel filtration revealed the highest TAME-ea peak in acute pneumonia corresponding with the first alpha2-M peak at approximately 800 kDa, whereas in chronic bronchitis the highest peak was found at approximately 40 kDa. The inhibition test showed that the TAME-ea peak at approximately 800 kDa was due to pl-Kal and the TAME-ea peak at approximately 40 kDa was mainly due to tissue kallikrein. High peaks of alpha2-M and pl-Kal were found in pneumonia and only small peaks were seen in chronic bronchitis. We conclude that in acute airway inflammation kinins seem to be mainly generated by plasma kallikrein whereas in chronic inflammation, kininogenases other than plasma kallikrein, such as tissue kallikrein, seem to be more important.
Restless-legs syndrome and periodic movements during sleep are associated with sleep apnoea syndrome. Similar to sleep apnoea syndrome, restless-legs syndrome and periodic movements during sleep may cause severe hyposomnia and hypersomnia. Exact diagnosis may partly fail in severe obstructive sleep apnoea syndrome if only cardiorespiratory polygraphy is performed. Simultaneous videorecordings and EMG of mm. tibialis ant. ensure diagnosis. Therapeutic regime may be difficult due to failure or side effects, however. We report on our experience in an one-year follow-up of 12 patients with sleep apnoea syndrome and restless-legs syndrome and/or periodic movements during sleep. Despite adequate interdisciplinary initiation of therapy and monitoring, these patients are often subject to therapy changes, failures or side effects. There was no correlation between jerks and the complaints of the patients.
Patients suffering from severe heart failure may develop breathing disorders during sleep. Results may be heavy disturbances in sleep architecture, worsening of haemodynamics and of the prognosis of these patients. Causes of breathing disorders are probably instability of breathing regulation caused by hypoxaemia, hypocapnia, and prolonged blood circulation time. This study examined the influence exercised by different concentrations of continuously applied oxygen during night time on breathing disorders, oxygen saturation and sleep architecture in patients with severe heart failure (NYHA III-IV). All patients showed an improvement in sleep architecture. Total sleeping time increased significantly. Fragmentations of sleep by arousal reactions decreased, time of REM-sleep and non-REM-sleep III and IV increased significantly.
Own results of 23,174 patients suffering from sleep apnoea syndrome showed that about 4 per cent of these patients have an increase of bronchial reactivity. In 60 patients with assured bronchial hyperreactivity we performed an inhalative bronchial provocation test using carbachol. Tests were performed before and after two days of treatment with nCPAP in the early morning. 23 of our 60 patients showed a decrease of PD20 FEV1 after nCPAP. The other patients did not show any significant differences. Our results demonstrate that in patients with increased bronchial reactivity, nCPAP therapy may aggravate bronchial hyperreactivity.
Our own investigations comprising 23,174 patients suffering from sleep apnoea showed that about 4 per cent of these patients suffer from a hyperreactive bronchial system. In some of these patients treatment with nCPAP causes coughing or mild dyspnoea even after having been previously asymptomatic. Loss of water and heat on the surface of bronchial mucosa may induce reversible bronchoconstriction. We examined in 60 patients suffering from obstructive sleep apnoea whether mechanical treatment with nCPAP would cause a change in bronchial reactivity. Cold air hyperventilation was used in provocation testing. Provocation tests were performed before and after a 3-day treatment with nCPAP in the early morning. In some patients with previously positive reaction, application of nCPAP alone decreased the lung function. Cold air hyperventilation challenge may be helpful to detect possible risks in patients using nCPAP, and to minimise such risks.
7 patients aged 30-56 years with the perception of subjective increased fitness 4-22 months after single lung transplantation were tested for the objective benefit. Using a standardized ergometric test protocol cardiopulmonary parameters (ventilation, blood gases, gas exchange, blood pressure, ECG) were measured 5 males and 2 females. After transplantation in all patients the objective fitness was increased by 30-60 watts and the blood gases were markedly improved. The physical fitness of the subjects under study was probably limited by the reduced lung function of the native lung, the reduced mobility of the diaphragm in elderly patients and the impaired muscular strength and endurance.
Of the 8,973 patients with sleep related breathing disorders examined in our department, about 4% were found to have a hyperreagible bronchial system. Provocation tests were performed before and after a 3-day CPAP therapy in 8 male patients with confirmed bronchial hyperreagibility. Two of these 8 patients revealed a marked increase of the respiratory path resistance and a decrease in FEV1.0 of 30% in the provocation test after 3 days. This did not occur with the other patients. From these findings, it is concluded that CPAP therapy can lead to an increase in the hyperreagibility in some patients with hyperreagible bronchial systems. However, further investigations are needed to identify the underlying causal relationships.
In 30 patients with suspected or, respectively 27 patients with confirmed, sleep apnea syndrome, 24-h esophagus pH metering was carried out. The patients were divided into two groups (number of apnea per 6 h > or < 100). A pH value of < 4 was defined as a pathological reflux when it occurred in total in at least 4% of the measuring period. Pathological reflux was encountered in 76% of the light SAS group and in 68% of the patients with severe SAS. Positional variations through upright and supine positions were apparent but not significant. Further investigations are therefore necessary to evaluate the relationships between degree of severity, position, and accompanying diseases.
We report of five patients, suffering from central sleep-apnea. All patients had a global respiratory failure during day-time and developed severe pulmonary artery hypertension during sleep. Therapy with n-BiPAP leeds to an improvement of blood gases and a decrease of pulmonary artery hypertension during sleep.
We examined circadian blood pressure rhythm before and two days after onset of n-CPAP therapy in 50 patients, suffering from polysomnograhpically ensured severe obstructive sleep-apnea-syndrome. Measurements were performed using a non-invasive blood pressure registration. Patients with normal circadian blood pressure conditions and those with disturbed circadian rhythm could be differentiated. N-CPAP therapy may normalize circadian blood pressure conditions in some patients.
Uvulo-palato-pharyngo-plastic is one possibility for treatment of obstructive sleep-apnea. We examined in a prospective study design 36 patients, suffering from polysomnographically ensured obstructive sleep-apnea-syndrome, who were undergone uvulo-palato-pharyngo-plastic. We analysed pre- und postoperative polysomnographic data. Most of patients demonstrated a decrease of amount of apneas, duration of apneas and an increase of minimal oxygen-desaturation. Patients who had high amounts of apneas (AI > 40/h) or who had a Broca-index > 140 p.c. gained not as much from surgical treatment as other patients did.
In 1,150 patients with sleep apnea syndrome, the apnea number, the morning theophyllin level, the symptom of morning exhaustion were recorded for the first night of theophyllin therapy and in the follow-up period of up to 5 years; in addition, side effects were noted at the end of the observation period. Prior to start of the therapy, the average apnea number was 97 per night; this decreased to 25 per night in the initial therapy. In the observation period of between 3 and 28 months, the number of apnea phases increased slightly on average. The symptoms of morning exhaustion initially decreased to 60% but increased again by about 20% over the next five years. In responders, theophyllin reduces the number of apnea in the long term course; however, frequent therapy controls are needed to determine the optimal dosage. Longitudinally, patients with an apnea index < 20/profited most from this drug therapy.
UNLABELLED: Gastroesophageal reflux (GER) may be associated with pulmonary diseases. The aim of this study was to investigate the role of GER in patients with sleep apnea syndrome (SAS). We evaluated, therefore, in patients with SAS the occurrence of GER during simultaneous apnea monitoring, and whether GER is related to the severity of SAS. METHODS: 17 consecutive patients with proven SAS were divided into two groups according to the severity of SAS: (A) apnea index > or = 5 and < 15, n = 8; (B) apnea index > or = 15, n = 9. All patients underwent 24 hours pH-metry in the proximal and distal esophagus and simultaneous apnea monitoring during the night. RESULTS: There was a high occurrence of GER in patients with SAS, but no significant difference was found between the two groups with respect to reflux times at the distal or at the proximal esophageal site. Reflux episodes and apnea periods were not timely correlated. Most of the patients of both groups were obese. CONCLUSIONS: Patients with SAS often have GER. However, there is neither a relation of GER with the severity of SAS nor a timely association between GER- and SAS-episodes. Thus, it is unlikely that there is a direct link between GER and SAS. However, there may be factors predisposing for both diseases.
The long-term efficacy and tolerability of azelastine (CAS 58581-89-8) nasal spray (0.14 mg/nostril b.i.d.) was investigated in patients suffering from perennial allergic rhinitis. 185 patients entered an initial 6 months' study; 35 of them continued in a follow-up for a further 30 to 60 weeks' treatment. Azelastine both attenuated the severity and reduced the incidence of rhinitis symptoms, with the highest rate of improvement during the first month with some additional improvement during the following months. The most marked effects were on those symptoms which were initially most severe: nasal obstruction, mucosal swelling, rhinorrhoea, sneezing and nasal itching. Signs of rhinitis identified by rhinoscopic examination improved in parallel to symptoms. 84.1% of patients reported 'good' or 'very good' efficacy as did 94.3% during the follow-up. Approximately 96% of patients rated the tolerability of treatment as 'very good' or 'good'. The incidence of adverse events of possibly causal relationship to azelastine treatment was low during the first 6 months. The most frequent events were the experience of application site reactions (e.g. burning) and bitter or unpleasant taste, specific to azelastine. No unwanted effects were reported by patients continuing treatment. In addition, results of nasal biopsies indicate that with the dose used azelastine nasal spray is a safe drug for long-term treatment of perennial allergic rhinitis.