Jeff Garrett
Jeff has been a practising Respiratory Physician since 1987. He has been in private practice since 1988 and held appointments at both Green Lane Hospital and Middlemore Hospital as a Respiratory Physician. He was Clinical Director of Respiratory Services at Green Lane Hospital between 1992 and 1999 and has been Clinical Director of Medicine at Middlemore Hospital since 2002. Jeff was President of the New Zealand Branch of the Thoracic Society of Australia and New Zealand for 5 years from 2002. He has chaired or been a member of a number of national respiratory committees including the National Respiratory Standards Committee, National COPD, Lung Cancer and Oxygen Service Committees and National Asthma Standards Committee. He sat on the European Respiratory Society Committee as an overseas delegate for 5 years, the Asian Pacific Asthma Advisory Committee, the International Advisory Committee on inhaler therapy and the Australian Lung cancer Guidelines committee. He has published 70 papers in peer reviewed journals and written 5 book chapters.
Better Outcomes for Lung Cancer in Family Practice Main Session  Friday, 13 June 2014 Start 9:10am Duration: 25mins Baytrust Lung cancer remains the leading cause of cancer death in New Zealand causing 19% of all cancer deaths (1500 annually). Maori have especially poor outcomes. Relative to other cancers, lung cancer has poor survival outcomes and New Zealand’s 5 year survival rates are only 10.2% and 3-6% behind other developed countries. Differences in survival outcomes between countries are considered mainly due to differences in delays of diagnosis. Improvements in outcome across developed countries have been mainly attributed to better co-ordinated care. Audits undertaken in the Northern region in 2000, 2004 and 2008 have been informative and have contributed to the development of national standards of care with the following aims: 1. To achieve lung cancer outcomes comparable with other countries 2. To diagnose and treat cancer at an earlier stage 3. To improve treatment rates. A variety of processes are required to achieve this and include: 1. Improve GP and public’s awareness of lung cancer symptoms and outcomes (if diagnosed early) 2. Identification of patients at high risk of lung cancer (COPD, FH/PH cancer, >15 pack year history, >45 years), CT scan screening is under review. 3. Clinical Pathways (Integrated) and which are auditable 4. Improved communication (e-referrals, GP access to hospital records) 5. Improved coordination of care 6. Prompt assessment and work-up by respiratory team with multidisciplinary discussion 7. Accurate and timely selection of patients for potentially curative treatment 8. Improved information and support for patients Since the implementation of the Standards in the Northern region important changes have occurred. With the introduction of e-referrals has come improved timeliness of referral to OP clinics and GP access to CT scanning with more rapid diagnosis, staging and management of patients. The MDT meetings are electronic, imbedded in the hospital record, auditable and sent to patient’s GPs. In 2013 the Australian wiki based Lung cancer Guidelines were published (http://wiki.cancer.org.au/australia/Guidelines:Lung) and follow a question and answer format for each tumour type (Non Small Cell/Small Cell), stage (TNM), and treatment (surgery, radiation therapy, chemotherapy). They are very informative and are regularly updated. Currently the Northern region is developing a static integrated (between primary and secondary care) clinical pathway which will eventually evolve into a dynamic pathway and be imbedded in the GPs electronic health record. The presentation will concentrate on the standards and processes identified above rather than on new treatment modalities (stereotactic radiation therapy, microwave ablation, new chemotherapy agents), or investigational aids (CT/PET, EndoBronchial Endoscopic Ultrasound,testing for EGFR mutations) or even the need for Advance Care Plans but which is available through the Australian Lung Cancer Guideline above. Targeting Small Airways - New Paradigms of Treatment Concurrent Workshop Repeated Friday, 13 June 2014 Start 2:00pm Duration: 55mins Room 1 Start 3:05pm Duration: 55mins Room 1 The small airways (<2mm in size) are important components of all inflammatory airways disorders (COPD, asthma, bronchiectasis) yet have captured little attention over the years. Less than 20 publications were generated in the 1990s but since 2010 there have been upwards of 200 publications on small airways. The earliest evidence of damage in a number of conditions (eg smoking related COPD, whooping cough, LAM, chronic rejection post lung transplant) is often centred in the small airways and the earliest evidence of remodelling in chronic asthma occurs in the small airways. A degree of dogma and bias has long been held by both researchers and doctors with a number of false assumptions: eg the large airways formulate the largest part of airways resistance so small airways unimportant, asthma is a smooth muscle disorder and there is no smooth muscle around the small airways, there is no inflammation in the small airways in asthma….. Small airways disease can contribute to greater severity of symptoms in asthma and is associated with more exacerbations. Small airways damage can occur in isolation particularly in childhood when the airways are more prone to damage and possibly as a result of infections (whooping cough, adenovirus, >?influenza virus, chicken pox,?bronchiolitis) and possibly as a result of a genetic predisposition or passive smoking. Such children may go on to suffer winter bronchitis often labelled as episodic asthma and often lose their tendency during adolescence. However, they often relapse later in life with recurring episodes of bronchitis or unexplained breathlessness (due to dynamic hyperexpansion). Invariably they have well preserved lung function but evidence of small airways damage as identified by a reduced FEF 25-75 on spirometry or an increase in Residual Volume or reduced FVC/SVC on detailed lung volume testing. They can also be shown to have a heterogeneous pattern of gas trapping on an expiratory HRCT scan of the chest. Such patients most usually exhibit neutrophilic inflammation on testing and whilst pathogenic bacteria are only cultured in 20% of instances are usually found to be colonised with pathogenic bacteria on mRNA testing. They remain a poorly studied group of patients and although macrolide antibiotics remain the best theoretical treatment we must also be guarded about their overuse. In asthma (eosinophilic inflammation) the small airways should also be considered for targeted therapy and there is emerging evidence of increased efficacy with use of ultrafine MDIs which deposit 60% of their dose within the airways and to all airways compared with standard MDIs/powdered devices which deposit only 20% into the airways and to the first 5 generations. Are the Concepts of Asthma and COPD Outmoded? Nurses Programme  Saturday, 14 June 2014 Start 11:00am Duration: 30mins Sportsdrome Whilst there are benefits in defining COPD and asthma as distinct clinical entities there are considerable overlaps. Patients with asthma invariably develop an element of re-modelling and in time fixed airways obstruction. A proportion of people with smoking related airways disease have a moderate degree of reversibility and will behave somewhat like patients with longstanding asthma. Patients with functional small airways damage (often occurring in childhood or as an initial consequence of smoking) and bronchiectasis are often mislabelled as having asthma or COPD and subsequently placed on ineffective medication. Conversely a proportion of patients with smoking related COPD and asthma develop bronchiectasis. It is therefore more important to consider the inflammatory cell present. This is best assessed by way of induced sputum testing using hypertonic saline or spontaneous sputum sampling which is not feely available outside of research laboratories or NZRSI in Auckland. This allows an assessment of whether there are inflammatory cells present ie eosinophils or neutrophils. Whist we await the development of a point of care test, the best surrogate remains a straightforward Full Blood Count and which is superior to FeNO (unless patient steroid naïve). An eosinophil count of >0.35 is associated with an 80% likelihood that eosinophils are present whereas an eosinophil count of <0.2 is associated with a 76% likelihood that neutrophils are present. Two forms of treatment are available: bronchodilators and anti-inflammatory agents. If eosinophils are present then the most effective form of therapy is inhaled steroid therapy. If patients do not achieve adequate control of inflammation with 1000ug BDP equivalent a day then in 25% it is because of poor inhaler technique and in 50%, poor adherence. Use of the smartinhaler (WiFi based) is one way of assessing adherence, another is through evaluation of dispensing information (>8 ICS inhalers/year using testsafe data). If eosinophilic inflammation is present and patients are fully compliant with 1000µg BDP equivalent per day then the dose needs to be doubled. Further benefit might be derived from “ultrafine” inhalers (eg QVAR MDI) which are not yet freely available in New Zealand but which were registered here in the 1990’s. Conversely if neutrophilic inflammation is present it is as a consequence of either an irritation or bacterial infection. Although bacteria are only cultured in 10-20% of cases (predominantly due to low counts), pathogenic bacteria are invariably present using mRNA technology. In this setting inhaled or oral steroids will exert no benefit and a prolonged course of a macrolide antibiotic is usually required. In the New Zealand context we are overprescribing inhaled steroids in COPD (>60%) vs 15-20% who would benefit yet not maximising in patients with moderate to severe asthma. Further, higher dose inhaled steroids in COPD have been shown to increase the risk of pneumonia. Although we need to remain respectful of the potential for antibiotic resistance targeted use of longer courses of macrolide antibiotics is reasonable. This presentation will reinforce the need for spirometry in primary care, will identify the potential benefits of validated questionnaires (eg CCQ and ACT) and will introduce the audience to a dynamic clinical pathway for COPD under development/assessment. Inflammatory Airway Disorders- How Can We Direct Therapy Better? Concurrent Workshop Repeated Saturday, 14 June 2014 Start 2:00pm Duration: 55mins Room 9 Start 3:05pm Duration: 55mins Room 9 Whether treating asthma, COPD, or chronic cough it is important to consider the inflammatory cell present. This is best assessed by way of induced sputum (using nebulised hypertonic saline) or spontaneous sputum sampling and which has not evolved further than research laboratories worldwide but which has limited availability through Middlemore Hospital and NZRSI (funded by Southern Cross) in Auckland. This allows an accurate assessment of whether there are inflammatory cells present and if so what type ( eosinophils or neutrophils or a combination). Whist we await the development of a point of care test, the best surrogate remains a straightforward Full Blood Count and which is superior to FeNO (unless patient inhaled steroid naïve). An eosinophil count of >0.35 is associated with an 80% likelihood that eosinophils are present whereas an eosinophil count of <0.2 is associated with a 76% likelihood that neutrophils are present. If eosinophils are present then the most effective form of therapy is inhaled steroid therapy. If patients do not achieve adequate control of inflammation with 1000ug BDP equivalent a day then in 25% it is because of poor inhaler technique and in 50%, poor adherence. Use of the smartinhaler (WiFi based) is one way of assessing adherence, another is through evaluation of dispensing information (>8 ICS inhalers/year using testsafe data). If eosinophilic inflammation is present and patients are fully compliant with 1000µg BDP equivalent per day then the dose needs to be doubled. Despite this requirement, current NZ asthma guidelines are ambiguous and, possibly as a consequence of combination therapy (LABA/ICS) available, 50% of patients with severe asthma attending the Middlemore Outpatient clinic were not on maximal therapy. Further benefit might be derived from “ultrafine” inhalers (eg QVAR MDI) which are not yet freely available in New Zealand but which were registered here in the 1990’s. Conversely if neutrophilic inflammation is present it is as a consequence of either an irritation or bacterial infection. Although bacteria are only cultured in 10-20% of cases (predominantly due to low counts), pathogenic bacteria are invariably present using mRNA technology. In this setting inhaled or oral steroids exert no benefit and a prolonged course of a macrolide antibiotic is preferred. In the New Zealand context we are overprescribing inhaled steroids in COPD patients (>60%) yet clinical studies indicate that obvious benefit is only accrued in the 15-20% who have eosinophilic inflammation present. In fact high dose inhaled steroids in non eosinophilic COPD may actually increase the risk of pneumonia. Further, higher dose inhaled steroids in COPD have been shown to increase the risk of pneumonia. Although we need to remain respectful of the potential for antibiotic resistance targeted use of longer courses of macrolide antibiotics is reasonable.