Conservative surgical management of a large eyelid tumour.
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Biomedical subjects
Publications and source records attributed to R F Taylor.
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BACKGROUND: Significant morbidity and mortality result from the ineffective evacuation of empyema. Failure of conventional first line treatment with closed intercostal tube drainage and antibiotic therapy may result in fibrin deposition and loculated empyema. Enzymatic debridement using intrapleural instillation of streptokinase is a non-invasive therapeutic option which may obviate the need for surgical intervention. METHODS: Eleven adults with multiloculated post-pneumonic empyemas who had failed to respond satisfactorily to intercostal tube drainage and antibiotic therapy were treated with intrapleural streptokinase between November 1992 and January 1994. A small catheter was inserted under ultrasound guidance into a loculation within the pleural space. Aliquots of 250,000 units of streptokinase in 100 ml normal saline were instilled into the pleural cavity and the tube clamped for four hours. Response was assessed by clinical outcome, measurement of drain output after unclamping, and subsequent pleural ultrasound, chest radiography, or both. RESULTS: Streptokinase enhanced drainage in all patients. Complete resolution of the empyema with re-expansion of the underlying lung was effected in eight patients, all of whom remain well. Further resolution of minimal pleural thickening was shown on subsequent chest radiographs. Two patients with considerably thickened visceral pleura following empyema drainage underwent successful decortication. The other, with myocarditis and a pyopneumothorax, underwent surgery for non-resolution of the pneumothorax but died perioperatively from cardiac failure. The number of streptokinase instillations per patient ranged from two to six (median three), and the volume of empyema fluid drained per patient ranged from 100 ml to 4870 ml (median 900 ml). Streptokinase was well tolerated in all patients. CONCLUSIONS: Intrapleural streptokinase is an effective adjunct in the management of complicated empyema and may reduce the need for surgery.
The antimicrobial prescribing practices of 26 physicians from the U.K. and Eire who care for patients with cystic fibrosis (CF) were assessed by postal questionnaire. Our main aim was to delineate divergent practices which may reveal a need for controlled prospective studies. For first-line intravenous (i.v.) therapy of acute exacerbations associated with Pseudomonas aeruginosa, 20 physicians (76.9%) combine a penicillin derivative with an aminoglycoside, in contrast to five (19.2%) who regularly use i.v. monotherapy with ceftazidime and one who combines i.v. ceftazidime with an aminoglycoside. When i.v. therapy is considered inappropriate, oral ciprofloxacin is sometimes used by all clinicians and oral broad spectrum agents are used in addition by 13, chloramphenicol being prescribed most often. Excluding allergy, the most important factor influencing choice of agents by 19 (73.1%) physicians is the most recent sputum susceptibility results. For maintenance therapy, 21 prescribe oral anti-staphylococcal agents if Staphylococcus aureus is isolated; of these, eight do so only if lung function deteriorates, nine after repeated isolation and four after first isolation of S. aureus. The remaining five physicians give anti-staphylococcal drugs to all patients once the diagnosis of CF is made. For maintenance of lung function in patients with persistent P. aeruginosa, all physicians used nebulized antibiotics, the indications for which vary between units. There was general concordance in the therapy of exacerbations associated with P. aeruginosa, whereas the use of agents to maintain lung function is more varied. We suggest that prospective studies address practices which vary greatly, such as the route, the duration and the timing of initiating antibiotic therapy given to maintain lung function.
This retrospective study reviews the patterns of P. cepacia pulmonary infection in 75 of a total of 872 mainly adults with cystic fibrosis, registered here during the 4 years 1987-1990; 35 (47%) were female. During this period, 55 patients acquired P. cepacia and the annual incidence and prevalence rates have remained between 1.6 and 3.1%, and 4.1 and 5.9%, respectively. The mean age at the time of the first isolation of P. cepacia was 23 years, ranging 11-45 years. Sixty-eight percent of the initial isolates were multi-resistant (sensitive to fewer than three of 15 anti-pseudomonal agents). Prior to acquisition of P. cepacia, 28 (50.9%) patients already had severe lung disease and only three had normal lung function. Infection was transient in 39.1% of patients. Initial multi-resistance of P. cepacia to anti-pseudomonal agents was significantly associated with persistent infection. Clinical outcome was unaffected by age, sex and early intravenous antibiotic therapy but was significantly adversely affected by increasing severity of lung disease at the onset of P. cepacia infection and by initial multi-resistance, and persistence of the organism. Thus, all patients with normal or mild lung disease at the outset of infection have remained clinically stable, whereas, only six of 28 patients with severe disease remained stable, three of whom were transiently infected with P. cepacia. The prevalence of P. cepacia at the time of death fluctuated between 12.5% and 26.9% during the study period.
BACKGROUND: Pseudomonas aeruginosa has been located in the endobronchiolar spaces of patients with cystic fibrosis where nutrients may be limited. In these sites it is thought that adaptation of the pathogen might occur and growth factors, present in relative excess, may thus promote survival of the organism. Auxotrophy of pulmonary isolates of P aeruginosa has previously been shown to be a feature of cystic fibrosis and chronic lung sepsis; auxotrophic isolates have additional nutritional requirements to the prototrophic "wild types" of the species. A study was therefore carried out to determine whether the proportion of auxotrophs differs between stable and acutely ill patients, or correlates with the extent of underlying disease. METHODS: Sputum samples were cultured for P aeruginosa and tested for auxotrophy by spreading serial dilutions of homogenised sputum on to a minimal medium which supports only prototrophs, and a complete medium which supports both nutritional types. The proportion of auxotrophs to prototrophs was determined and growth factors of confirmed auxotrophs were identified. RESULTS: Thirty two (86%) of 37 adults with cystic fibrosis infected with P aeruginosa harboured auxotrophs; methionine dependent mutants were isolated from seven of 16 patients tested (44%). More than 50% of the total number of colonies were auxotrophic in 19 of 26 samples (73%) from patients with acute exacerbations and in only six of 15 samples (40%) from clinically stable patients. In four patients from whom samples in both the acute and stable states were available, the proportion of auxotrophs fell in the sample taken when stable. Auxotrophs predominated in all samples from 11 of those patients with very severe underlying lung disease, in contrast to 13 of 30 samples from patients with less severe disease. There was no association between the percentage of auxotrophs and the presence of other respiratory pathogens. CONCLUSIONS: The majority of adults with cystic fibrosis infected with P aeruginosa harbour auxotrophs in the sputum. A significant proportion of acutely ill patients and those with severe underlying disease have a preponderance of auxotrophs in the sputum compared with stable patients and those with less severe disease.
This study examines the extent to which the cerebrum and other suprapontine structures modulate the respiratory response to added mechanical resistive loads to breathing. Nine adult cats were anesthetized with thiopental sodium, tracheotomized, and instrumented with diaphragm electromyographic (EMGdi) recording electrodes. Two levels of resistive loads and tracheal occlusion were applied at the onset of inspiration in random order before and after decerebration. The integrated signal of the EMGdi (integral of EMGdi) was used to detect changes in respiratory timing and as an index of respiratory motor drive. The results showed that, compared with intact cats, decerebration did not significantly change baseline values for peak integral of EMGdi, respiratory timing, systemic blood pressure, or arterial blood gases. Although the percent changes in the peak integral of EMGdi elicited by the added loads were still significantly greater than those elicited by unloaded control breaths after decerebration, the magnitude of the responses was significantly attenuated at all load levels compared with the intact preparation. It is concluded that the cerebrum and/or other suprapontine structures provide information that is facilitatory to the respiratory pattern generator with little effect on timing.
Effects of inspiratory tracheal occlusion (TO) on respiratory duration (inspiratory and expiratory duration), ventilation, and the peak integrated diaphragm electromyographic (integral of EMGdi) response were tested in 16 anesthetized cats before and after decerebellation with and without vagal input. The same protocols were repeated in the decerebrate preparation. Decerebellation did not significantly affect the baseline or the loaded values [tracheal occlusion (TO)] for respiratory duration, tidal volume, or magnitude of the integral of EMGdi response. Vagal blockade eliminated the load-compensating responses in the intact and the decerebrate preparation. However, vagal blockade in concert with decerebellation resulted in a significant (P < 0.05) reversible inhibition of the peak integral of EMGdi response during inspiratory TO. This suggests that removal of vagal and cerebellar influences during loaded breathing unmasked inhibitory inputs to the respiratory pattern generator. With vagus intact, decerebellation before or after decerebration abolished the attenuation of the peak integral of EMGdi response to TO observed with decerebration alone. We conclude that the cerebellum does play a role in determining the pattern of the respiratory response to TO. This influence may be direct and/or indirect via interaction with information emanating from suprapontine, vagal, and nonvagal sources.
In a previous study, we reported that inspiratory tracheal occlusion (TO) significantly inhibited the motor drive to the diaphragm in a decerebellated bilaterally vagotomized preparation (J. Appl. Physiol. 75:675-681, 1993). The hypothesis to be tested in the present study was that respiratory muscle afferents activated by inspiratory TO provided the inputs responsible for the observed inhibition. Adult cats were anesthetized, tracheotomized, and instrumented with diaphragm electromyographic (EMGdi) recording electrodes. The cerebellum, vagi, and dorsal spinal cord (C2-T2) were surgically exposed. Inspiratory TO was applied before and after cold blockade of the dorsal cord (C6) or dorsal root (C3-6) transection in the intact and decerebellated vagotomized cat. Respiratory timing (inspiratory and expiratory duration) was determined from the EMGdi record, and the peak integrated EMGdi (integral of EMGdi) response was used as an index of respiratory motor drive. Our results showed that 1) cold blockade at the dorsal C6 level in an intact preparation significantly increased the peak of the integral of EMGdi response to TO and was reversible upon rewarming; 2) as previously reported, decerebellation coupled with bilateral vagotomy significantly decreased the peak integral of EMGdi response to TO with no effect on timing; 3) cold blockade (-1 degree C) of the dorsal cord at C6 significantly attenuated this inhibition, and subsequent dorsal rhizotomy at C3-6 completely abolished this inhibition; and 4) decerebellation, cold blockade of the dorsal cord (C6), and dorsal rhizotomy (C3-6) did not significantly affect baseline values in bilaterally vagotomized cats.(ABSTRACT TRUNCATED AT 250 WORDS)
Two Asian patients admitted to hospital with acute severe asthma had been chewing betel nut immediately before the attacks. Arecoline, a cholinergic alkaloid, is a major constituent of Areca catechu (betel) nut and causes the euphoric effects. We sought an association between betel-nut chewing and bronchoconstriction in asthmatic patients. In vitro, arecoline caused dose-related contraction of human bronchial smooth-muscle strips, with one-tenth the potency of methacholine. In a double-blind challenge study, inhalation of arecoline caused bronchoconstriction in six of seven asthmatic patients and one of six healthy subjects; methacholine caused bronchoconstriction in all the asthmatic patients and in five controls. The geometric mean concentrations of arecoline and methacholine that caused 20% falls in the forced expiratory volume in 1 s (PC20 FEV1) in the asthmatic subjects were 5.2 mg/ml and 1.6 mg/ml, respectively. We then studied four Bengali asthmatic patients, regular users of betel nut, during a betel-nut challenge. Three showed no adverse effects, but one showed a 30% fall in FEV1 by 150 min after chewing; the effect was reproducible. In the UK, the rate of hospital admission for acute asthma is higher among Asians than among other groups in the population; betel-nut chewing may be one of several factors that affect asthma control and severity of attacks.
Seventy-four of 403 (18.4%) sputum isolates of Pseudomonas aeruginosa from 49 of 136 (36.0%) adults with cystic fibrosis (CF) were auxotrophic mutants. Two of 11 (18.2%) isolates of P. aeruginosa taken from patients with non-CF bronchiectasis were also auxotrophic. All 99 strains taken from non-bronchiectatic sources were prototrophic. Forty-six of 55 (83.6%) CF auxotrophs required one or more of 36 growth factors tested; the requirements for the remaining 9 isolates were not identified. Methionine was the sole factor required by 17 of 22 (77.3%) isolated which depended on a single factor. We conclude that auxotrophy is a feature of P. aeruginosa infection in cystic fibrosis.
Ribotyping of 25 isolates of Pseudomonas cepacia taken from the sputum of 21 adults with cystic fibrosis (CF) who were registered at the Royal Brompton Hospital between 1987 and 1991, revealed that seven patients (33.3%) shared strains of a similar ribotype pattern with others, while 14 patients (63.7%) harboured strains unique to each individual. Constancy of sputum strain carriage was seen in two of three patients sampled twice over a 3-month period. Although no evidence for patient-to-patient transmission of P. cepacia within this group of patients was found, the fact that one third of CF patients shared strains of the same ribotype with others, suggests that nosocomial acquisition of this organism may have occurred.
Twelve courses of intravenous temocillin were given in combination with an intravenous aminoglycoside to five patients with cystic fibrosis (CF) for pulmonary exacerbations associated with Pseudomonas cepacia. All patients were infected concurrently with Pseudomonas aeruginosa in addition to P. cepacia. Improvement occurred after six of seven courses given to three patients in which temocillin was used as first-line therapy and following three of five courses given to two patients after failure of other antipseudomonal agents. All ten pre-treatment isolates of P. cepacia were resistant to aminoglycosides and eight were sensitive to temocillin. Clinical improvement was seen on both occasions in which the pre-treatment isolates were resistant to temocillin.
BACKGROUND: Pseudomonas aeruginosa infection is seldom eradicated in patients with cystic fibrosis despite intensive antipseudomonal treatment. Upper airway sites of infection may contribute to perpetuation of lower airways infection. This study was designed to find out which extrapulmonary sites are infected and whether the strains at these sites are identical to those in the lungs. METHODS: Sputum and upper airway samples from 42 patients were cultured for P aeruginosa and stool samples from 20 patients were also tested. Nineteen isolates from sputum and extrapulmonary sites from four patients were genotyped with the pCM tox probe. RESULTS: P aeruginosa was isolated from the sputum of 36 patients, 34 of whom had infection in the upper airways. Six of the 20 patients tested were positive for P aeruginosa in the stool. The nasopharynx was colonised in 30 patients, the oropharynx in 29, the middle meatus in 13, the external nares in six, and the inferior turbinate in four. Three of four patients tested had the same strain of P aeruginosa (a different one in each individual) in the sputum and the upper airways, and in two of the three the stool isolate was a different strain. CONCLUSION: Most adults with cystic fibrosis and P aeruginosa pulmonary infection have upper airway reservoirs of the organism and strains from these sites are identical to those in the lungs.
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Measurement of the potential difference (PD) across the airways provides an indication of the viability and integrity of the lining epithelium. PD was recorded from the lower airways in "diseased controls" and in patients following heart-lung transplantation. Diseased controls showed a high PD centrally which fell (became less negative) peripherally (trachea -15.8 mV (SEM 1.0), lobar bronchi -12.6 mV (1.2), segmental bronchi -9.8 mV (1.2]. Following heart-lung transplantation (HLT) the profile of PD with airway size was altered in comparison to non-transplanted patients with reduced values in the large airways. Host tracheal values above the anastomosis were similarly reduced. Two episodes of rejection were associated with a lower mean airway PD; no significant changes were found with infection. In patients with cystic fibrosis (CF), values in the donor lung did not differ from those in non-CF transplanted patients up to one year following transplantation, although nasal PD in the host remained elevated. HLT selectively alters the PD profile only of larger airways, which may relate to the interruption of the bronchial arterial supply to these sites.