Michael Birch
Royal Victoria Infirmary
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Featured researches published by Michael Birch.
Journal of Glaucoma | 2005
Sukhpal S. Sandhu; Sandip Chattopadhyay; Michael Birch; Neeta Ray-Chaudhuri
Purpose:To investigate how quickly Goldmann applanation tonometers used in clinical practice develop calibration errors, and to determine the frequency of checks required to detect these errors. Materials and Methods:Prospective check of the calibration error of all Haag-Streit Goldmann applanation tonometers in the department at month zero, month one, and month four. The tonometers were checked according to the Haag-Streit method using a standard calibration check weight bar by two independent observers. Calibration errors were classed as ±0.5 to 2.5 mm Hg, ±3 to 4 mm Hg, or >±4 mm Hg. Tonometers with a calibration error greater than ±2.5 mm Hg were returned to the manufacturer for re-calibration. Results:At month zero 2 of 34 (5.9%), at month one 3 of 29 (10.3%), and at month four 0 of 33 (0.0%) tonometers fell within the manufacturers recommended calibration range of ±0.5 mm Hg. A total of 14 of 34 (41.2%) tonometers at month zero, 10 of 29 (34.5%) tonometers at month one, and 17 of 33 (51.5%) tonometers at month four were identified to have calibration errors greater than ±2.5 mm Hg. Conclusions:Goldmann applanation tonometers are not as accurate as the manufacturers recommended calibration error tolerance of ±0.5 mm Hg would suggest. Calibration error of less than ±2.5 mm Hg is clinically acceptable. Calibration error checks should be carried out once monthly and tonometers with calibration error greater than ±2.5 mm Hg returned to the manufacturer for re-calibration. Additional checks should be made if tonometers suffer specific damage. Ideally individual ophthalmologists should check calibration before each session.
Journal of Medical Genetics | 2004
Thomas Ressiniotis; Philip G. Griffiths; Michael Birch; Sharon Keers; Patrick F. Chinnery
Primary open angle glaucoma (POAG) is the second commonest cause of blind registration in the United Kingdom and affects approximately 70 million people worldwide.1,2 The major risk factors are intraocular pressure, ethnicity, refractive errors, and vascular function. There is also clear evidence from population, case control, and twin studies of a heritable element to POAG.3,4 The genes encoding myocilin and optineurin have been be linked to POAG in large families with autosomal dominant inheritance, and a number of chromosomal loci are being studied for a possible genetic association with glaucoma.5–10 It appears that POAG is a complex trait and multiple genes contribute to the phenotype and increase individuals’ susceptibility to glaucomatous optic neuropathy. Quite independently, a number of recent studies suggest that apoptosis of the retinal ganglion cells is an important mechanism behind glaucoma.11,12 Apoptosis is a form of genetically controlled, programmed cell death, which is under extensive research, especially in cancer,13–15 neuronal injury,16 and neurodegenerative disorders.17,18 During the primary regulatory steps of apoptosis, a signal of cellular distress activates the tumour suppressor protein p53. This protein acts like a “guardian of the genome”, regulating subsequent apoptotic events through several oncogenes, principally bax and bcl-2 .13 Further apoptotic events include changes in mitochondria with cytochrome c release and activation of cystein proteases (caspases), which digest the dying cell from within.19 It is therefore of great interest that one study showed an association between genetic polymorphic variants of the p53 gene and POAG. In a Chinese study, a cytosine (C) residue at codon 72 of the p53 gene was significantly more common in POAG patients than control subjects.20 In another study carried out on an Indian cohort, a second polymorphism (a 16 bp duplication in …
BMC Ophthalmology | 2005
Thomas Ressiniotis; Philip G. Griffiths; Sharon Keers; Patrick F. Chinnery; Michael Birch
BackgroundPrimary open angle glaucoma (POAG) is considered to be a neurodegenerative optic neuropathy, in which cell death occurs by apoptosis. p21, is an important protective component of the apoptotic pathway, regulating cellular arrest in the presence of DNA damage. An unstable or altered p21 protein could modify the cellular response to genomic injury and abolish the effect of p21. A previous study on a Chinese cohort suggested that the p21 codon 31 polymorphism may alter the state of apoptosis in glaucomatous optic neuropathy, failing to protect the ganglion cells. The aim of this study was to test the hypothesis that a p21 codon 31 polymorphism is associated with POAG on a Caucasian cohort.Methods140 POAG patients and a control group of 73 healthy individuals were included in the study. All the subjects were of Caucasian origin. Genomic DNA was amplified by polymerase chain reaction, followed by enzymatic restriction fragment length polymorphism technique (PCR-RFLP). Patients and controls were genotyped for a single nucleotide polymorphism (C/A transversion) in the third base of codon 31 of p21, which leads to a serine (Ser)/arginine (Arg) substitution.ResultsThe distribution of the genotypes in the POAG patients showed 128 (91.4%) Ser homozygotes, 10 (7.1%) Ser/Arg heterozygotes and 2 (1.5%) Arg homozygotes. In the control cohort, there were 61 (83.6%) Ser homozygotes and 12 (16.4%) Ser/Arg heterozygotes. No Arg homozygotes were present amongst the control group. Both the allelic and genotypic frequencies of the Ser or Arg residues at codon 31 were not significantly different between POAG patients and controls (Fishers exact test, P = 0.20 for alleles and P = 0.0561 for genotypes).ConclusionThis study suggests that the p21 codon 31 polymorphism does not contribute to the risk of POAG in the Caucasian population.
Ophthalmology | 2009
Sukhpal S. Sandhu; Sandip Chattopadhyay; George Amariotakis; Fillipos Skarmoutsos; Michael Birch; Neeta Ray-Chaudhuri
OBJECTIVES With normal clinical use, Goldmann applanation tonometers frequently develop calibration errors. Only the manufacturer can perform recalibration. This study aimed to assess whether intraocular pressure (IOP) measured by Goldmann applanation tonometers with known small calibration errors could be adjusted to reflect true IOP to allow continued clinical use. DESIGN Evaluation of diagnostic test. PARTICIPANTS Patients under regular review who had undergone previous applanation tonometry. METHODS Patients with a range of IOPs underwent IOP measurement using a gold standard 0-error tonometer and tonometers with known calibration errors in a randomized blind fashion. The calibration errors of the tonometers ranged 0 to +5 mmHg. MAIN OUTCOME MEASURES Intraocular pressure. RESULTS For the first part of the study, 125 eyes of 125 patients with a mean IOP of 18.5 mmHg (range, 8-43 mmHg) were tested. Mean IOP measured by the tonometer with an error of +1 mmHg was +1.0 (95% confidence interval [CI], 0.3-1.7 mmHg; P = 0.0076, compared with gold standard 0-error), with the +2 mmHg error was +1.2 (95% CI, 0.8-1.7 mmHg; P<0.0001), with the +3 mmHg error was +1.6 (95% CI, 1.2-1.9 mmHg; P<0.0001), with the +4 mmHg error was +3.6 (95% CI, 2.9-4.2 mmHg; P<0.0001), and with the +5 mmHg error was +3.3 (95% CI, 2.9-3.8 mmHg; P<0.0001). In the second part of the study, IOP measured by each of the tonometers with +2 mmHg error was +0.6 mmHg (95% CI, 0.1-1.1 mmHg; P = 0.0241), +1.5 mmHg (95% CI, 1.0-2.0 mmHg; P<0.0001), and +1.5 mmHg (95% CI, 1.9-2.1 mmHg; P<0.0001). CONCLUSIONS There is a relationship between calibration error and clinical error in IOP measured, but it is not a one-to-one relationship. The error overestimates IOP and is consistent over a clinical range of IOPs. In certain circumstances where resources are limited, it may be clinically acceptable to use tonometers with calibration errors of less than +3 mmHg, because they do not overestimate IOP by more than 2 mmHg. FINANCIAL DISCLOSURE(S) The author(s) have no proprietary or commercial interest in any materials discussed in this article.
British Journal of Ophthalmology | 2006
Richard M. Andrews; Thomas Ressiniotis; Douglass M. Turnbull; Michael Birch; Sharon Keers; Patrick F. Chinnery; Philip G. Griffiths
Aim: To investigate a possible association between mitochondrial haplogroups and primary open angle glaucoma (POAG). Methods: Genomic DNA was extracted from 140 POAG patients and 75 healthy individuals. Restriction enzyme digest analysis of polymerase chain reaction (PCR) amplified fragments was used to determine the mitochondrial haplogroup of each patient and control. Results: The median age was 73 years for the POAG patients (range 51–87, SD 8.01) and 78 years for the controls (range 68–90, SD 4.4). Mean IOP was 20.8 mm Hg for the patients (SD 2.6) and 16.2 mm Hg for the controls (SD 3.4). Median cup/disc ratio was 0.8 and 0.3 for patients and controls respectively. No statistically significant difference was found in the haplogroup distribution between the POAG patients and the healthy individuals (Fisher’s exact test). Conclusion: In this cohort, mitochondrial haplogroups do not appear to contribute to the pathogenesis of POAG.
European Journal of Ophthalmology | 2014
Saurabh Ghosh; Sridhar Manvikar; Neeta Ray-Chaudhuri; Michael Birch
Purpose To study the effect on central vision of transscleral diode laser cyclophotocoagulation (TSDLC) for the reduction of intraocular pressure (IOP) in patients with visual acuity (VA) better than 6/18. Methods Retrospective chart review was conducted of patients undergoing cyclophotocoagulation between 2000 and 2008. Patients who underwent TSDLC with VA of 6/18 or better and at least 24 months follow-up were included. Primary outcome was decrease of 2 or more lines at 24 months. Secondary outcome was IOP control with or without treatment. Results A total of 46 eyes of 44 patients were included with VA ranging from 6/18 to 6/5 (median VA 6/12). Mean IOP was 24 mm Hg (range 12-35). A mean of 1.3 treatments were given per eye, with 12 eyes (26%) requiring retreatment. At 24 months, the median VA was 6/18 (range light perception—6/5). Eighteen eyes (39.1%) retained the same VA, 35 eyes (76.1%) retained VA of 6/18 or better, in 7 eyes (19.4%) VA was <6/60. Loss of ≥2 lines was recorded in 11 eyes (23.9%), and loss of 1 line in 13 eyes (28.3%). Mean IOP at 24 months was 17.2 mm Hg (range 12-28). Thirty-nine (84.8%) patients had IOP ≤21 mm Hg. Conclusions This study suggests a role of TSDLC as an effective, safe, and rapid method of treatment in patients with good vision over a 24-month period. The loss of VA in some patients is similar to previously reported studies in patients having cyclodiode, trabeculectomy, or tube surgery.
Retina-the Journal of Retinal and Vitreous Diseases | 2007
Sukhpal S. Sandhu; Michael Birch; Philip G. Griffiths; S.J. Talks
Purpose: To assess the short-term effects of argon laser on retinal thickening as demonstrated by optical coherence tomography (OCT). Methods: A prospectively collected consecutive series of patients undergoing routine focal argon laser treatment for sight-threatening diabetic maculopathy had bilateral OCT performed before laser treatment and 1 hour, 24 hours, and 2 weeks after treatment. The main outcome measure was change in retinal thickness in the region of laser treatment. Results: Forty-six eyes were analyzed. There was a small increase in retinal thickness in the treated area 1 hour after laser treatment, with a mean change from before laser treatment of +2.6 &mgr;m (95% confidence interval [CI], +0.2 to + 5.0). However, there was a larger change 24 hours after treatment of +39.0 &mgr;m (95% CI, +31.6 to + 46.4) and a significant decrease 2 weeks after treatment of −14.6 &mgr;m (95% CI, −21.6 to −7.7) from before laser treatment values. Conclusion: Focal argon laser treatment remains the first-line treatment for sight-threatening diabetic maculopathy. This study shows that in the short-term, areas of retinal thickening worsen before settling in response to argon laser treatment as demonstrated by OCT.
Eye | 2003
Zoe Johnson; Philip G. Griffiths; Michael Birch
AbstractAims/purpose To investigate a nurse-led assessment clinic of new referrals of possible glaucoma. To determine the potential for nurse prescribing. To review the background literature about nurse prescribing.Methods Audit of the outcomes of patients attending the nurse-led glaucoma assessment clinic during two defined periods (169 patients). An audit of all patients started on timolol or latanoprost treatment by a nurse following a protocol.Results A total of 46 patients were commenced on treatment at the clinic, 31 on timolol, 14 on latanoprost, and one on brimonidine. Four of these had the treatment stopped at the review clinic in order to reassess the diagnosis. Four patients in the timolol group developed side effects requiring a change in medication, but these could not have been predicted from their past medical history. Nine patients had treatment changed or added to because the intraocular pressure was felt to be inadequately controlled. During the two 3-month audits, a further 11 patients were commenced on treatment for glaucoma at the review clinic.Conclusions Initial data from this clinic suggest that nurses possess the diagnostic skills necessary to prescribe for new glaucoma patients. The legal and administrative frame works are developing for more nurses to be able to prescribe. With the newer prostaglandin treatments for glaucoma being available, nurses may usefully and safely be able to prescribe first-line treatments for glaucoma.
British Journal of Ophthalmology | 2011
Jaswant Sandhu; Sreekumari Pushpoth; Michael Birch; Neeta Ray-Chaudhuri
In April 2009, the National Institute of Clinical Excellence (NICE) issued guidelines on the diagnosis, monitoring and treatment of glaucoma and ocular hypertension (OHT).1 The publication of these guidelines has resulted in a large national increase of referrals with OHT or suspect chronic open angle glaucoma (COAG) beyond the 28% predicted by NICE.2 Our own referrals have increased by 91.2%. Optometrists complying with legal advice are recommended …
Clinical and Experimental Ophthalmology | 2007
George Amariotakis; Thomas Ressiniotis; Gerasimos M. Voros; Michael Birch
Herein a case is reported of a full‐thickness scleral burn in the left eye of a 61‐year‐old man, following contact trans‐scleral cyclodiode laser treatment for traumatic aphakic glaucoma, unresponsive to maximal medical treatment. The defect was successfully repaired by scleral suturing under local anaesthetic.