Biomedical subjects
Publications and source records attributed to T K Lim.
We describe two patients with group A beta hemolytic streptococcal septicemia from minor foci in the skin. They developed extreme toxemia, mental obtundation and multi-system organ failure associated with diffuse erythema. They both survived after appropriate antibiotic and intense supportive therapy. These are examples of the "toxic strept syndrome" which is similar to staphylococcal toxic shock.
The extent of air-space destruction caused by emphysema is very variable in severe chronic obstructive pulmonary disease (COPD), constituting one of the most obvious differences between COPD and asthma. Differences in the static deflation pressure-volume curve between COPD and asthma can easily be shown, but it has been surprisingly difficult to find distinctive mechanical features of impaired airway function caused by air-space destruction. This may be because in mild airway obstruction related to smoking--particularly in younger subjects--emphysema may be absent, and the predominant site of airway narrowing in the smallest bronchi and respiratory bronchioles may be the same as that found in asthma in remission. In more severe obstruction caused by COPD there is almost always very severe intrinsic disease of the airways and this may so dominate the functional abnormality that it is difficult to detect any additional change because of airspace destruction. Overall, few studies have set out to detect specific effects of parenchymal destruction on airway function.
A 23 year old man with glottic dysfunction presented as recurrent bronchial asthma. His symptoms were aggravated by application of a noseclip and associated with asynchronous thoraco-abdominal wall motion. The glottic dysfunction was corrected by sedation but not continuous positive airway pressure. This is the first report of vocal cord dysfunction triggered by application of a noseclip and associated with asynchronous thoraco-abdominal wall motion.
Real time X-ray diffraction was used to examine the gel bilayer to disordered bilayer phase transition in fully hydrated dipalmitoyltrehalose. The L beta to L alpha phase transition was shown to proceed via a second-order thermodynamic process involving incommensurate mesophase bilayer repeat structures and the formation of an intermediate rectangular acyl chain packing subcell. This phenomenon has only been previously shown to occur for dihexadecylphosphatidylcholine (DHPC) and dipalmitoylphosphatidylcholine (DPPC) dihydrates undergoing stepwise (i.e., noncontinuous) temperature changes. It can thus be inferred that the presence of trehalose-trehalose intra-bilayer interactions is a sufficient condition to modify the acyl chain structural rearrangements within the bilayer as a function of temperature.
Ventilatory function and airway reactivity of 20 firefighters were studied one hour before and one hour after exposure in a smoke chamber. None showed an increase in airway reactivity to inhaled histamine before exposure. Eight (80%) of the regular firefighters, however, had an increase in airway reactivity after exposure in the smoke chamber. After six hours, three of the firefighters still had increased airway reactivity. All were non-reactive after 24 hours but the ventilatory function of the three firefighters who were reactive after six hours did not return to baseline values. The duration of service as a firefighter is the major contributing factor to the change in airway reactivity. This increase in airway responsiveness among regular firefighters suggests that some form of chronic epithelial injury is needed before an increase in airway responsiveness is seen.
Patients with chronic obstructive pulmonary disease [COPD] breath at large lung volumes because of dynamic hyperinflation. Their end-tidal lung volumes will then be much above the equilibrium position of the respiratory system and the elastic recoil pressure would be above zero at end-tidal exhalation. This auto or intrinsic positive end-expiratory pressure [auto-PEEP] contributes to the elastic work of inspiration and the sensation of dyspnoea. The purpose of this study was to offset the auto-PEEP in patients with exacerbated chronic airflow obstruction by applying continuous positive airway pressure via the nose [nasal-CPAP]. Nine out of 14 patients experienced alleviation of dyspnoea while on nasal-CPAP [4 to 8 cmH2O]. These 9 patients had significantly more severe hyperinflation than the 5 patients who did not respond positively to nasal-CPAP. While there is a complex relationship between intrinsic and extrinsically applied PEEP in patients with COPD, the result of this study is consistent with the notion that CPAP may alleviate dyspnoea by reducing auto-PEEP, improving lung mechanics and unloading the inspiratory muscles. Nasal-CPAP may have a potential therapeutic role in exacerbations of COPD.
All the information regarding the forced expiratory manoeuvre are contained in the simple volume-time spirogram. Flow-volume and time-domain indices could be derived by digitising the volume-time spirogram. This paper describes an electronic means of digitising the spirogram and demonstrates its capability in deriving flow-volume and time-domain spirometric indices. The spirograms of 118 granite quarry workers were digitised using an electronic digitising pen. The volume and time data are stored in a micro-computer and a programme written in dBASEIII Plus is used to smoothen and derive the standard volume-time, flow-volume and time domain indices. There was good agreement between digitised and hand-read values (intraclass correlation coefficients, rI, greater than 0.9) for the forced expiratory flow in one second (FEV1) and forced vital capacity (FVC) irrespective of the pulmonary status. There was a small but statistically significant difference between digitised and hand-read FEV1 for those with normal and restrictive pulmonary function groups (-115 ml/sec and 19 ml/sec respectively). There was however, no evidence of systematic bias between the two methods. The technique described herein provides a rapid and accurate means for deriving flow-volume and time domain indices from a volume-time spirogram. It also provides the opportunity to reanalyse previously collected volume-time spirograms and allow for the assessment of small airways function of these subjects using newer flow-volume and time domain indices.
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Bronchial hyperresponsiveness (BHR) in smokers is believed to be a consequence of airway wall inflammation. We have examined the effects of treatment with nonsteroidal anti-inflammatory drugs (NSAID) on BHR to inhaled histamine, measured as the provocative concentration reducing forced expiratory volume in one second (FEV1) by 20% (PC20), in middle-aged male cigarette smokers in two separate double-blind, placebo-controlled, cross-over trials. Baseline FEV1 in these smokers ranged from 41-117% predicted values. In the first study 15 men (mean age 58 yrs, FEV1 2.20 l) were examined before and one hour after a single dose of 1.2 g aspirin. There was no significant change in PC20 (geometric mean 1.88 mg.ml-1 pre-aspirin, 1.89 mg.ml-1 post-aspirin) or baseline FEV1 and we observed no tachyphylaxis to the effects of inhaled histamine at one hour after placebo. In the second study 10 men (mean age 60 yrs, FEV1 2.53 l) were examined before and after three days' treatment with the NSAID flurbiprofen 50 mg t.d.s. Baseline PC20 was higher in this group than in the first study. There was no relationship between the excretion of urinary thromboxane metabolites and the intensity of BHR under baseline conditions; flurbiprofen greatly reduced the urinary excretion of thromboxane metabolites, but baseline FEV1 was not altered. Analysis of change in PC20 was complicated by a difference in baseline PC20 before the two treatments, but treatment with flurbiprofen did not significantly attenuate BHR. The results suggest that thromboxane or other cyclo-oxygenase products of arachidonic acid metabolism do not play an important role in the short-term maintenance of BHR to histamine in middle-aged male cigarette smokers.
We studied 22 Asian patients with steroid dependent asthma. Using a clinical approach to the addition of high dose inhaled budesonide and tapering of systematic steroid, we were able to substitute 5 to 20 mg prednisolone with 800 micrograms per day of inhaled budesonide in all patients. There was also a greater reduction in nocturnal symptoms and awakenings and a smaller overnight fall in PEFR during treatment with budesonide than with prednisolone. Inhaled budesonide was an effective long term substitute for prednisolone in chronic asthma.
Asthmatic patients who came to hospital for treatment of severe attacks were assessed for level of obstruction and the effects of a deep inhalation (DI) on degree of obstruction at various stages of their treatment and after recovery over several days. The more severe the obstruction, the greater was the constrictor effect of a DI; as lung function improved with intensive treatment, including corticosteroids, the constrictor effect diminished. Thus, we believe the constrictor effects of a DI relate to the degree of inflammation in the obstructive process. These longitudinal data relating severity to the effects of a DI were nearly identical to previously published cross-sectional data in a group of patients with spontaneous asthma with widely different levels of lung function. It is possible that the response to a DI in a given asthmatic subject serves as a functional marker for the predominant mechanism for obstruction.
We describe the course of illness in two middle-aged diabetic men who died suddenly from primary lung abscesses. They were in apparent good health and presented with fever, cough and small lung abscess [less than 5 cm] on chest radiographs. While receiving standard antimicrobial therapy in hospital, they experienced sudden respiratory arrest from aspiration of purulent material presumably following the drainage of lung abscess contents. This is a very unusual complication and the similar clinical features between these two cases prompted this report.
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This paper describes 19 consecutive episodes (18 patients) of status asthmaticus managed in a medical intensive care. Eleven patients required mechanical ventilatory support [MV] and 2 (11%) died. Most patients had acute respiratory acidosis although arterial blood gases alone could not predict the need for MV. The peak inspiratory airway pressure measured during MV was a useful index of the severity of underlying lung disease. The most serious complication of MV was barotrauma. On follow up studies, two distinctive patterns of chronic asthma could be identified. One group of patients had highly labile pulmonary function with unpredictable and wide changes in peak flow rates while another group had poorly reversible obstruction.
Bronchial hyperresponsiveness to inhaled histamine in smokers is associated with an accelerated annual decline in FEV1 and low baseline FEV1 values. The evolution of bronchial hyperresponsiveness and whether it precedes or follows the accelerated decline in FEV1 and reduction in FEV1 is unknown. Measurements of the provocative concentration of inhaled histamine required to reduce FEV1 by 20% (PC20) were repeated after a four year interval in 27 male smokers (mean age 59 years, smoking on average 27 cigarettes a day in 1986) and 16 men who were ex-smokers in 1982 and who remained non-smokers until 1986 (mean age 53 years in 1986). These men were originally recruited to a prospective study in 1974 and had their first PC20 measurement in 1982. PC20 was positively related to baseline FEV1 in both smokers and ex-smokers in both 1982 and 1986 (r ranging from 0.56 to 0.76, p less than 0.01). In smokers mean FEV1 fell from 83% to 77% predicted (p less than 0.001) and geometric mean PC20 from 7.11 to 3.27 mg/ml (p less than 0.001) between 1982 and 1986. The change in PC20 in individual smokers over the four years was related to change in FEV1 (p = 0.012). In ex-smokers mean FEV1 was 93% predicted both in 1982 and in 1986 and there was no significant difference in geometric mean PC20 between 1982 (6.68 mg/ml) and 1986 (5.98 mg/ml). Thus in smokers there was an accelerated annual decline in FEV1 and an increase in bronchial hyperresponsiveness as FEV1 fell. The ex-smokers had comparable levels of bronchial hyperresponsiveness in 1982. Mean PC20 values were unchanged in 1986 in these men, who showed a normal age related decline in FEV1. These longitudinal results emphasise the importance of baseline airway geometry in influencing bronchial hyperresponsiveness to histamine in middle aged smokers and ex-smokers.
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In a double-blind double-placebo study 10 asthmatics exercised on a treadmill after treatment for 1 week with placebo, or ketotifen 1 mg twice daily, or SCG 10 mg four times daily. The post-exercise percentage fall in FEV1 after SCG but not after ketotifen was significantly smaller than after placebo. A 1-week treatment with SCG but not ketotifen protected against EIA.