David Luyt
Leicester Royal Infirmary
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Featured researches published by David Luyt.
Pediatric Allergy and Immunology | 2011
Heidi Ball; David Luyt; Kristian Bravin; Kerrie Kirk
To cite this article: Ball H, Luyt D, Bravin K, Kirk K. Single nut or total nut avoidance in nut allergic children: outcome of nut challenges to guide exclusion diets. Pediatr Allergy Immunol 2011: 22: 808–812.
Chronic Illness | 2011
Emma Pitchforth; Simon Weaver; Janet Willars; Emilia Wawrzkowicz; David Luyt; Mary Dixon-Woods
Objectives: The aim of this study was to explore, using qualitative methods, the experiences of children and their parents living with nut allergy. Methods: Children with a confirmed diagnosis of peanut allergy were identified from a database of patients maintained at an allergy clinic at a large teaching hospital. Interviews with 26 families were conducted involving 11 children, 25 mothers and 12 fathers. Results: The diagnosis of nut allergy signalled a critical transition—or biographical disruption—in the life of the family. Parents took on the role of ‘alert assistant’ and sought to create ‘safe places’ where nuts were not permitted, but often struggled when outside the home environment. The option of ‘passing as normal’, often used by people with a chronic illness to avoid stigma, was not available to them. Consequently, parents often reported being treated as faddy, demanding, and neurotic, and children suffered from teasing and exclusion. The social consequences of nut allergy were worsened by poor labelling and control of foods and products containing nuts. Discussion: In many ways, nut allergy may be considered a form of disability, because it imposes social barriers on participating fully in society.
Journal of Paediatrics and Child Health | 2006
Arani V Sridhar; Sanjiv Nichani; David Luyt; Shawqui Nour
Abstract: Candida peritonitis is a rare but potentially fatal complication of early dislodgement of percutaneous endoscopic gastrostomy (PEG) feeding tube. We report the case of 12‐year‐old boy who developed Candida peritonitis subsequent to early dislodgement of PEG tube. PEG tubes may be prone to accidental dislodgement or removal by patients or carers. This complication has to be recognized early in order to avoid the risk of peritonitis. In our case the patient initially developed coliform peritonitis followed by peritoneal and systemic candidiasis. The patient needed ventilatory support, inotropic support, broad‐spectrum antibiotics, total parenteral nutrition and antifungal agents liposomal amphotericin and flucytosine.
IEEE Journal of Biomedical and Health Informatics | 2017
Luis Hernandez-Munoz; Sandra I. Woolley; David Luyt; Gary Stiefel; Kerrie Kirk; Nick Makwana; Cathryn Melchior; Tom C. Dawson; Gabriel Wong; Tim Collins; Lavanya Diwakar
Anaphylaxis is an increasingly prevalent life-threatening allergic condition that requires people with anaphylaxis and their caregivers to be trained in the avoidance of allergen triggers and in the administration of adrenaline autoinjectors. The prompt and correct administration of autoinjectors in the event of an anaphylactic reaction is a significant challenge in the management of anaphylaxis. Unfortunately, many people do not know how to use autoinjectors and either fail to use them or fail to use them correctly. This is due in part to deficiencies in training and also to the lack of a system encouraging continuous practice with feedback. Assistive smartphone healthcare technologies have demonstrated potential to support the management of chronic conditions such as diabetes and cardiovascular disease, but there have been deficiencies in their evaluation and there has been a lack of application to anaphylaxis. This paper describes AllergiSense, a smartphone app and sensing system for anaphylaxis management, and presents the results of a randomized, controlled, prepost evaluation of AllergiSense injection training and feedback tools with healthy participants. Participants whose training was supplemented with AllergiSense injection feedback achieved significantly better practiced injections with 90.5% performing correct injections compared to only 28.6% in the paper-only control group. In addition, the results provide insights into possible self-efficacy failings in traditional training and the benefits of embedding self-efficacy theory into the technology design process.
Scopus | 2004
David Luyt; J Pridgeon; Justin Brown; Giles J. Peek; Richard K. Firmin; Hitesh Pandya
OBJECTIVE To describe the short-term outcome of children with meningococcal sepsis treated with extracorporeal membrane oxygenation (ECMO) in a single centre. DESIGN Retrospective analysis of case notes. SETTING The Heartlink ECMO Centre, Glenfield Hospital, Leicester. PATIENTS Eleven children (8 boys) out of a total caseload of 800 patients were treated for meningococcal sepsis with ECMO. INTERVENTIONS Extracorporeal membrane oxygenation. RESULTS All children with meningococcal sepsis treated with ECMO had a Glasgow Meningococcal Septicaemia Prognostic Score (GMSPS) > or = 12 (positive predictive risk of death of approximately 90%). Five children had adult respiratory distress syndrome (ARDS) and six had refractory shock with multi-organ dysfunction syndrome (MODS) at presentation for ECMO. All five children in the ARDS group survived, four of five receiving veno-venous (VV-) ECMO therapy. In contrast, only one of six children with refractory shock with MODS survived, all of whom required veno-arterial (VA-) ECMO therapy. CONCLUSIONS Most children with meningococcal sepsis and severe ARDS can be successfully treated with VV-ECMO. In contrast, children with refractory shock and MODS die despite treatment with VA-ECMO. This report does not resolve whether ECMO therapy offers any advantage over conventional therapy in treating severe meningococcal sepsis.
PubMed | 2006
K Khambekar; Sanjiv Nichani; David Luyt; Giles J. Peek; Richard K. Firmin; David Field; Hitesh Pandya
Objective: To describe the later health status of newborn infants who received extracorporeal membrane oxygenation (ECMO) for acute respiratory failure in the era after the UK ECMO trial. Design: Prospective follow up study of newborn infants who received ECMO at a single centre between January 1997 and January 2001. Setting: Departments of ECMO and Paediatric Intensive Care, University Hospitals of Leicester. Patients: All babies who received ECMO within 14 days of birth. Interventions: Neurodevelopment screening using the schedule for growing skills-II (SGS-II) assessment tool. Main outcome measures: Survival at 12 months of age by disease and functional development at follow up. Results: A total of 145 neonates received ECMO for treatment of respiratory failure. Of these, 108 (75%) were alive at 1 year of age. There were no deaths in children treated for respiratory failure secondary to meconium aspiration syndrome (73/145). Ninety three (86% of survivors) infants attended a follow up visit at 11–19 months postnatal age. Eighty two were classed as normal, seven as having “impairment”, and four as having “severe disability”. Conclusions: Most newborn infants with acute respiratory failure treated with ECMO will have a normal neurodevelopment screening assessment at 11–19 months of postnatal age. There is no evidence to suggest that changes in neonatal practice since the UK ECMO trial have led to changes in outcome of infants undergoing ECMO therapy.
Archives of Disease in Childhood-fetal and Neonatal Edition | 2005
Kiran Khambekar; Sanjiv Nichani; David Luyt; Giles J. Peek; Richard K. Firmin; David Field; Hitesh Pandya
Objective: To describe the later health status of newborn infants who received extracorporeal membrane oxygenation (ECMO) for acute respiratory failure in the era after the UK ECMO trial. Design: Prospective follow up study of newborn infants who received ECMO at a single centre between January 1997 and January 2001. Setting: Departments of ECMO and Paediatric Intensive Care, University Hospitals of Leicester. Patients: All babies who received ECMO within 14 days of birth. Interventions: Neurodevelopment screening using the schedule for growing skills-II (SGS-II) assessment tool. Main outcome measures: Survival at 12 months of age by disease and functional development at follow up. Results: A total of 145 neonates received ECMO for treatment of respiratory failure. Of these, 108 (75%) were alive at 1 year of age. There were no deaths in children treated for respiratory failure secondary to meconium aspiration syndrome (73/145). Ninety three (86% of survivors) infants attended a follow up visit at 11–19 months postnatal age. Eighty two were classed as normal, seven as having “impairment”, and four as having “severe disability”. Conclusions: Most newborn infants with acute respiratory failure treated with ECMO will have a normal neurodevelopment screening assessment at 11–19 months of postnatal age. There is no evidence to suggest that changes in neonatal practice since the UK ECMO trial have led to changes in outcome of infants undergoing ECMO therapy.
Journal of the Royal Society of Medicine | 2003
David Luyt
Whenever the possibility of an inherited metabolic disease is broached on the ward round, I shudder. These children are usually very sick and young, offering few diagnostic clues. My first instinct is to seek advice from my esteemed colleagues in the biochemistry laboratory, hoping that annual leave or travel to a congress will not rob me of salvation from this source. But Dr Clarkes concise yet inclusive book has made me feel less dependent on such help. The number of disorders that have been attributed to inherited point defects in metabolism now exceeds 500. These are individually rare but collectively account for a substantial proportion of illness, especially in children. I had often asked myself how the non-expert clinician could ever get a grip on this complex topic. ‘Had’ because Clarke offers a problem-oriented approach that includes the investigations required and exhaustive tabulation of differential diagnoses. After an introductory chapter on disease mechanisms he groups the syndromes by clinical presentation—neurological (chronic and acute encephalopathy, stroke, movement disorder, myopathy and psychiatric); metabolic acidosis; hepatic (jaundice, hepatomegaly, hypoglycaemia, hepatocellular dysfunction); cardiac (cardiomyopathy, arrhythmias, coronary artery disease); storage syndromes; and dysmorphism. Then follow chapters on acute metabolic illness in the newborn, newborn screening, laboratory investigations and treatment. So that is the scope, but what about the content. Does the text lead the perplexed clinician towards the right conclusion? Take metabolic acidosis—a common presentation that has the ability to mystify and deceive when it may be no more than severe shock with poor perfusion and lactic acidosis. It is also a common presenting or coincident feature of many inherited metabolic diseases. Clarke elegantly guides the reader towards timely diagnostic decisions. Some of his clinical ‘pearls’ are: that metabolic acidosis may be ‘so mild that the generally recognized clinical signs, such as tachypnea, are absent or so subtle that they are missed’; that ‘In other cases, the patient presents with an episode of acute, severe, even life-threatening, acidosis, and the underlying persistence of the condition is only recognised after resolution of the acute episode’; and that ‘the most frustrating presentation is infrequent bouts of recurrent, acute acidosis separated by long intervals of apparent good health during which diagnostic tests show no significant abnormality’. In his approach to metabolic acidosis, Clarke first asks whether it is a result of abnormal losses of bicarbonate or accumulation of acid; in other words, is the anion gap normal or expanded? This division is crucial as it is the latter in which inherited metabolic diseases reside, so the reader learns at an early stage the direction of the investigation. Accumulated acids are lactic acids, ketoacids or organic acids. The differential diagnosis and description of these is exhaustive; a three-page table of the organic acidurias is just one example. There is not space here to offer accounts of the other chapters, all of which are just as impressive. If your clinical work brings you into contact with patients who may be hiding an inherited metabolic disease, Clarkes Guide is for you. Clearly it will be of greatest help to paediatricians. My friends in the biochemistry laboratory will be allowed to borrow my copy, on the understanding that I get it back before they go away.
Journal of the Royal Society of Medicine | 2000
David Luyt; Helena Dunbar; Heidi Baker
Paediatrics and Child Health | 2016
David Luyt; Heidi Ball; Kerrie Kirk; Gary Stiefel