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Biomedical subjects

H Hay

Publications and source records attributed to H Hay.

8 recordsLinked to original sources
PubMed2000

Rapidly developing airway obstruction resulting from achalasia of the oesophagus.

Megaoesophagus resulting from achalasia is a rare but serious cause of airway obstruction. The exact aetiology remains unclear. Although 29 cases have previously been reported, the potential need for urgent treatment has not been sufficiently emphasized. Some forms of treatment with drugs or decompression with a fine tube have been advocated but emergency tracheal intubation may become necessary. A 90-year-old lady had a bolus of food lodged in her oesophagus but with no respiratory symptoms. The bolus was removed under anaesthesia. Six weeks later she suffered similar symptoms after eating but developed severe airway obstruction over 10 min. Emergency intubation of the trachea was necessary before removing the food bolus under general anaesthesia. This case demonstrates the urgency with which these patients may need to be treated. The condition can rapidly worsen due to swallowing of air and saliva.

Aged↗
PubMed2000

Contamination of piped medical gas supply with water.

The failure of anaesthetic equipment as a result of maintenance is extremely rare. The ingress of water into the flowmeters of an anaesthetic machine from the piped medical air supply is reported and is possibly unique. The piped medical air supply was open to the atmosphere during maintenance. Water condensed in the gas pipeline and this was not noticed during subsequent testing. Water was seen leaking from the orthopaedic air tools used for surgery but was assumed to be from the autoclaving process. Later the same day, when medical air from the piped source was used as part of the gas mixture for a general anaesthetic, water was seen filling the barrel of the flowmeter air control valve. This could have had far-reaching and dangerous consequences for the patient, which were fortunately averted.

Air↗
PubMed2000

Delivery of an hypoxic gas mixture due to a defective rubber seal of a flowmeter control tube.

The delivery of an hypoxic gas mixture to a patient during general anaesthesia is a rare event due to contemporary standards of monitoring, equipment design and alarm features. An incident is described where a split occurred in a rubber seal round the top of a flowmeter control tube. This resulted in a downstream oxygen leak and the delivery of an hypoxic gas mixture to the patient. The bobbin on the oxygen flowmeter did not accurately reflect the amount of oxygen being delivered. A paramagnetic oxygen analyser and a fuel cell oxygen electrode indicated that the inspired oxygen concentration was lower than intended. The anaesthetic machine was exchanged, and the operation continued uneventfully. The faulty anaesthetic machine subsequently passed a formal pressure test by the hospital engineers and also close examination of the flowmeter control valves. The importance of monitoring equipment and the interpretation of the information that they provide is emphasized.

Adult↗
PubMed2000

Oxygen delivery failure resulting from interference with a Bain breathing system.

A critical incident is described where the expiratory (scavenging) port of an obsolete version of a Bain-type breathing system valve assembly was inadvertently connected to the common gas outlet of an anaesthetic machine. This resulted in the patient being deprived of a supply of fresh gas. This misconnection was made possible by adding a plastic connector to the valve scavenging port and subsequent wrongful misconnection. The patient fortunately suffered no harm. The case highlights the danger of equipment that has been subjected to unauthorized interference.

Adult↗
PubMed1989

Modulation of antibody-mediated glomerular injury in vivo by bacterial lipopolysaccharide, tumor necrosis factor, and IL-1.

We have investigated the effects of LPS, human rTNF (hrTNF) and human rIL-1 beta (hrIL-1 beta) pretreatment on the intensity of antibody-mediated injury in vivo by using a passive model of anti-glomerular basement membrane (GBM) antibody-mediated nephritis in rats. The experiments show that all three pretreatments exacerbate injury in this model whether judged by albuminuria or the prevalence of glomerular capillary thrombi. The effect on albuminuria was dose dependent with all three treatments. The lowest effective dose of LPS was 0.025 microgram while those for hrTNF and hrIL-1 beta were 0.4 microgram and 0.5 microgram, respectively. All three pretreatments also increased the prevalence of glomerular capillary thrombi which were rare in rats injected with anti-GBM antibodies without pretreatment. LPS pretreatment appeared to be more effective in causing glomerular capillary thrombi than hrTNF or hrIL-1 beta and this was reflected in the correlations between albuminuria and the proportion of glomeruli with capillary thrombi. This relation was linear for all three pretreatments but the slope was appreciably greater for rats pretreated with LPS (0.37) when compared with results from rats given either hrTNF (0.22) or hrIL-1 beta (0.29). Pretreatment of nephritic rats with both cytokines increased the slope to 0.42 demonstrating a synergistic effect. The synergism of hrTNF with hrIL-1 beta was also demonstrated by the effective doses needed to induce albuminuria which was evident in rats treated with 0.05 microgram of IL-1 beta and 0.4 microgram of TNF. Neither the cytokines nor LPS caused clinical, morphologic, or biochemical evidence of renal toxicity when given alone in the dose used here but they did cause a transient increase in the number of neutrophils marginated in glomerular capillaries. Pretreatment of rats with LPS or cytokines increased the glomerular neutrophil influx after anti-GBM antibodies by roughly sixfold. Our experiments show that TNF and IL-1 can increase the severity of glomerular injury in nephritis; they may be important in modulating glomerular injury clinically.

Albuminuria↗
PubMed1989

Leukotrienes, LTC4 and LTB4, in bronchoalveolar lavage in bronchial asthma and other respiratory diseases.

Leukotrienes (LTs) C4 and B4 are potent proinflammatory mediators with a wide variety of biologic activities, including smooth muscle contraction, mucus hypersecretion, and leukocyte activation, which may be of particular relevance to the pathology of asthma and other respiratory diseases. We measured the concentrations of LTC4 and LTB4 in bronchoalveolar lavage fluid from 16 atopic subjects with asthma (eight symptomatic and eight asymptomatic) and from 14 control subjects without asthma (six with hay fever and eight nonatopic). The amounts detected in symptomatic subjects with asthma were significantly higher than in control subjects (LTB4, 0.58 +/- 0.06 versus 0.36 +/- 0.05 pmol/ml, p less than 0.05; LTC4, 0.36 +/- 0.1 versus 0.12 +/- 0.02 pmol/ml, p less than 0.01). LTC4 and LTB4 were also measured in 17 patients: nine with interstitial lung disease of varying etiology (cryptogenic fibrosing alveolitis [CFA] or idiopathic pulmonary fibrosis), three with sarcoidosis, one with extrinsic allergic alveolitis, one with sulphonamide-induced pneumonia, and one patient with eosinophilic granuloma. The concentrations of LTB4 (but not LTC4) were significantly greater in patients with CFA compared with normal control subjects (0.69 +/- 0.3 versus 0.36 +/- 0.05 pmol/ml, p less than 0.01). There was a significant correlation (p less than 0.05) between the percentage of neutrophils and the concentration of LTB4 in the bronchoalveolar lavage fluid) of the group with interstitial lung disease as a whole. This study provides evidence for a role for LTs in the airways of subjects with day-to-day asthma and suggests that LTB4 may also be involved in the recruitment of granulocytes into the lung in patients with CFA.

Adult↗
PubMed1989

Studies on the specificity of the L929 cell bioassay for the measurement of tumour necrosis factor.

We report a study of the specificity of the L929 cell cytotoxicity assay for tumour necrosis factor (TNF) in clinical samples. Normal human serum caused marked killing and detachment of L929 cells. Despite heating at 56 degrees C for 30 min, followed by dilution, normal human serum still retained significant activity that could not be neutralized by a monoclonal antibody to TNF. In part this latter cytotoxicity was spurious, and related to detachment and clumping of viable cells. Recombinant human interleukin 1-beta (rhIL1-beta) and interferon-gamma (rhIFN-gamma) were not cytocidal, and did not synergize with recombinant human TNF (rhTNF) in the L929 cell bioassay. Although an antibody to TNF may be used to confirm specific activity, it is important to be aware of the limitations imposed by non-specific activity in serum and of the potential for synergy between TNF and other cytokines.

Animals↗