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Purpose Retinal microvascular endothelial dysfunction is thought to be of importance in the development of ocular vascular diseases. Obstructive sleep apnoea (OSA) causes macrovascular endothelial dysfunction, but the effect of OSA on retinal microvascular endothelial function is not known. We aimed to determine the effect of OSA on retinal microvascular function. Methods We conducted a multi-centre, double-blind, randomised, parallel, controlled trial in patients with known moderate-to-severe OSA, established on continuous positive airway pressure (CPAP). Participants were randomised to 14 nights of either continued CPAP or sham CPAP to generate a return of OSA. Retinal vascular responses to flickering light were measured using dynamic vessel analysis both at baseline and after 14 nights of intervention. The primary outcome was the change from baseline to follow-up in the area under the curve of the arteriolar response to flickering light, sham CPAP versus continued CPAP. Results Nineteen patients were randomised to sham CPAP, and 18 patients were randomised to continued CPAP. There was no significant effect of CPAP withdrawal and return of OSA on retinal responses, with a change in the area under the curve of the arteriole response to flickering light of + 3.8 arbitrary units (95% CI − 10.6 to + 18.2, p = 0.59), sham CPAP versus continued CPAP. Conclusions CPAP withdrawal and a return of OSA had no significant effect on retinal microvascular responses. This contrasts with the effect of CPAP withdrawal on macrovascular endothelial function and suggests that OSA has different effects on macrovascular and microvascular endothelial function. ISRCTN 78082983, 23/10/2014, Prospectively registered.

Obstructive sleep apnoea (OSA) was traditionally thought to be mainly caused by obesity and upper airway crowding, and hence OSA management was not personalised according to particular characteristics, with most symptomatic patients receiving continuous positive airway pressure therapy. Recent advances in our understanding have identified additional potential and distinct causes of OSA (endotypes), and subgroups of patients (phenotypes) with increased risk of cardiovascular complications. In this review, we discuss the evidence to date as to whether there are distinct clinically useful endotypes and phenotypes of OSA, and the challenges to the field in moving towards delivering personalised therapy in OSA.

Introduction The severity of obstructive sleep apnoea (OSA) is highly variable on a night-to-night basis. Patients are commonly categorised based on the severity of their OSA, and this is then used to influence management and reimbursement, including continuous positive airway pressure (CPAP). We aimed to establish to what extent the OSA severity category changes during two periods of OSA, based on mean and maximum oxygen desaturation index (ODI). Methods Patients with a diagnosis of moderate to severe OSA who had been on CPAP for greater than 1 year were included in this study. Subjects underwent two periods of CPAP withdrawal for four nights each. Results Twenty-five patients completed the study. Based on the mean ODI of the four nights, 14 (56%) patients changed OSA severity categorisation, with three (12%) changing category to mild. Based on the maximum ODI of the four nights, nine (36%) patients changed OSA severity categorisation, with one (4%) changing category to mild. One third to a half of patients’ OSA severity category changed between the two periods of four night’s CPAP withdrawal. Conclusions OSA is highly variable on a period-to-period basis as well as on a night-to-night basis. We believe the concept of patients having a definable and ‘real’ level of OSA severity is therefore flawed. OSA severity should be based mainly on symptoms, as these are the dominant reasons for treatment, and the sleep study should be used qualitatively to ascertain whether respiratory events are the likely cause of the symptoms. Trial Registration ISRCTN17987510.

We describe a 40-year-old female who presented with progressive breathlessness and hypercapnic respiratory failure during pregnancy secondary to undiagnosed muscle-specific kinase myasthenia gravis. Her presentation was progressive and protracted, having over five contacts with healthcare professionals over nine months, many of these predating her pregnancy. Her atypical presentation for myasthenia with minimal limb weakness led to consideration of other causes of hypercapnic respiratory failure. Once diagnosed, she was treated with intravenous immunoglobulin and non-invasive ventilation. She gave birth to a pre-term infant by planned caesarean section. Her insidious presentation and the progressive nature of her breathlessness were unusual and our report highlights the predominant involvement of respiratory muscles in muscle-specific kinase myasthenia. Her pregnancy may have further delayed her diagnosis due the attribution of some symptoms to normal pregnancy. Early recognition and treatment of myasthenia gravis are important to prevent life-threatening complications.

The COVID-19 pandemic changed continuous positive airway pressure (CPAP) setup pathways. We evaluated patients commenced on CPAP in 2019 (prepandemic) and 2020 (post-first UK wave). Face-to-face (F2F) setup numbers, with CPAP turned on, decreased from 613 patients (98.9%) in 2019, to 6 (1.1%) in 2020. In 2020, setups were F2F without CPAP turned on (403 (71.1%)), or remote (158 (27.9%)). Prepandemic median CPAP usage at first follow-up was 5.4 (2.7–6.9) hours/night and fell by 0.9 hours/night (95% CI 0.5 to 1.2, p

P217 Table 1A comparison of first and second wave characteristics, treatment and outcome data First wave Second wave Mean difference (95%CI) X2 (df) P value Age (years) 69.0 (52.0, 80.0) 62.0 (52.0, 71.0) -3.4 (-7.8 to +1.1) - 0.14 Sex: - Male - Female 49 (69.0%) 22 (31.0%) 180 (65.0%) 97 (35.0%) - 0.4 (1) 0.52 BMI (kg/m2) 28.5 (24.9, 33.6) 29.6 (24.8, 34.9) +0.6 (-1.7 to +2.9) - 0.63 Clinical Frailty Score: - 1 to 2 (fit) 18 (25.4%) 132 (47.7%) - 15.6 (5) 0.008 CT severity score - Moderate/severe - Severe 11 (29.7%) 23 (62.2%) 131 (52.2%) 113 (45.0%) - 16.0 (3) 0.0012 CRP prior to rHDU admission (mg/L) 180.6 (118.0, 210.0) 124.1 (78.1, 175.6) -44.1 (-66.9 to -21.3) - 0.0002 Spike gene testing - VOC B.1.1.7 variant - Wild-type - Ambiguous - - - 143 (67.1%) 57 (26.8%) 13 (6.1%) - - - Dexamethasone 3 (4.2%) 266 (96.0%) - 271.4 (1)

For obstructive sleep apnoea (OSA), few mechanical treatment options are available and no pharmacotherapy is approved [1–3]. However, safe and efficacious pharmacotherapy would have substantial appeal for many people with OSA., BAY 2253651 is a nasally applied genioglossus muscle activator via pharyngeal mucosal receptor stimulation (potassium channel blocker) aimed to treat obstructive sleep apnoea. Although well-tolerated and safe, there was no significant therapeutic effect. https://bit.ly/3zDbyia

Retinal microvascular endothelial dysfunction is thought to be of importance in the development of ocular vascular diseases. Obstructive sleep apnoea (OSA) causes macrovascular endothelial dysfunction, but the effect of OSA on retinal microvascular endothelial function is not known. We aimed to determine the effect of OSA on retinal microvascular function.We conducted a multi-centre, double-blind, randomised, parallel, controlled trial in patients with known moderate-to-severe OSA, established on continuous positive airway pressure (CPAP). Participants were randomised to 14 nights of either continued CPAP or sham CPAP to generate a return of OSA. Retinal vascular responses to flickering light were measured using dynamic vessel analysis both at baseline and after 14 nights of intervention. The primary outcome was the change from baseline to follow-up in the area under the curve of the arteriolar response to flickering light, sham CPAP versus continued CPAP.Nineteen patients were randomised to sham CPAP, and 18 patients were randomised to continued CPAP. There was no significant effect of CPAP withdrawal and return of OSA on retinal responses, with a change in the area under the curve of the arteriole response to flickering light of + 3.8 arbitrary units (95% CI - 10.6 to + 18.2, p = 0.59), sham CPAP versus continued CPAP.CPAP withdrawal and a return of OSA had no significant effect on retinal microvascular responses. This contrasts with the effect of CPAP withdrawal on macrovascular endothelial function and suggests that OSA has different effects on macrovascular and microvascular endothelial function. ISRCTN 78082983, 23/10/2014, Prospectively registered.

Damage to the blood vessels supplying the lung accompanies several systemic disorders, and their classification can be confusing. This chapter clearly explains the different presentations, the different blood tests available, and the pathology (mainly based on size of vessel involved) associated with diseases such as granulomatosis with polyangiitis (Wegener’s), microscopic polyangiitis, Goodpasture’s disease, Churg-Strauss syndrome (eosinophilic granulomatosis with polyangiitis), and the rarer arteritides such as Takayasu’s.

Ideally, communicate with ICU early, as it is much better that they know about a potentially sick patient who may need ICU input than to find your patient (and you!) in difficulty later on, with no ICU bed. Previously, multiple different scoring systems for the early recognition of sick patients were in use in hospitals, enabling doctors and nursing staff to readily identify and assess a deteriorating patient, including response to treatment.

Includes: Administration of sedation, drugs used for sedation, sedation in specific circumstances.

These common infections are typically self-limiting and managed in the community but, in the immunocompromised, can be devastating (especially with suppressed T-cell function such as following organ transplant). Viral pathogens discussed include influenza, cytomegalovirus (CMV), adenovirus, measles, human metapneumovirus, parainfluenza, respiratory syncitial virus (RSV), varicella pneumonia, hantavirus. Severe acute respiratory syndrome (SARS), and Middle East respiratory syndrome (MERS) are covered and reflect recent developments. The circumstances surrounding these infections and appropriate laboratory tests are discussed in detail, as imaging of the lung is rarely diagnostic.

This chapter covers all aspects of the diagnosis and management of community and hospital acquired pneumonia. Community-acquired pneumonia represents the commonest infectious cause of death in the UK and USA. Up to 10% require ITU admission where mortality remains at 50%. The predisposing conditions are discussed. This chapter includes guidance on community-acquired pneumonia severity scores and antibiotic choice, based on the recent British Thoracic Society guidelines. Strategies for patients who may need ITU care, who fail to respond to initial antibiotics, and who need follow-up after pneumonia are discussed. Other forms of respiratory infection are covered, including their aetiology and their management. These include ventilator-acquired pneumonia (VAP), aspiration pneumonia, lung abscess (including Lemierre’s syndrome), nocardiosis, actinomycosis, anthrax, tularaemia, melioidosis, and leptospirosis. The differential diagnosis of fever and CXR infiltrates in a patient on ITU is highlighted.

This is usually performed as an adjunct to assisted ventilation. Such patients are now often returned to respiratory wards for ‘decannulation’ with the potential for complications to occur there.

Pulmonary rehabilitation (PR) is a well-established evidence-based multidisciplinary programme of care for patients with symptomatic chronic respiratory impairment, targeting the extrapulmonary manifestations of the disease. The programme is individually tailored and should contain high-intensity progressive aerobic training, strength training, and self-management education. PR is probably the most cost-effective intervention for COPD. It interrupts the vicious cycle of dyspnoea leading to inactivity, subsequent deconditioning, and further worsening dyspnoea on more minimal exertion.

Difficulty in intubating patients often arises unexpectedly, even in those predicted to be low risk. The Difficult Airway Society have produced guidelines to help planning for difficulty and to produce a standardized approach. Cricothyroidotomy or ‘emergency front of neck access’ is the Plan D on these guidelines. It should be performed in after plans A–C have failed, a situation termed ‘can’t intubate can’t oxygenate’ (CICO). Cricothyroidotomy should only be performed by those with appropriate skills and training. The descriptions in this chapter are included to describe the technique and to outline the equipment required.

Includes: Emergency oxygen therapy, home oxygen therapy, practical issues with home oxygen, long-term oxygen therapy (LTOT), ambulatory oxygen therapy (AOT), short burst oxygen therapy (SBOT)

This chapter covers three diagnostic tests in common use that are not described elsewhere in this Handbook. Skin prick tests are still used, although some units have replaced them with the more expensive RAST tests for specific IgE. A full description of how to do and read them is included. The simple technique of induced sputum for TB and PCP is less frequently used although likely to increase in use as specific new biomarkers of disease are identified in sputum. Bronchoprovocation testing to measure bronchial reactivity is also done by many units to help in the diagnosis of asthma, and a full description of the various techniques is included in this chapter.

The aim of pleurodesis is to seal visceral to parietal pleura with adhesions to prevent pleural fluid or air accumulating. Pleurodesis is dependent upon lung re-expansion following removal of pleural fluid or air, which allows the apposition of visceral and parietal pleura. This may be encouraged by applying suction to an intercostal drain. Inflammation of the pleural surfaces and local activation of coagulation, required to produce pleural fibrosis and adhesions. May be induced by chemical sclerosing agent or by mechanical pleural abrasion at VATS.

This chapter considers pneumothorax aspiration. 1° pneumothorax: Consider aspiration if patient breathless, hypoxic, and pneumothorax large. 2° pneumothorax: Consider aspiration if evidence of underlying lung disease (or patient with significant smoking history, aged >50 years), with small pneumothorax and breathlessness.

Includes: Indications and risks, bleeding and bronchoscopy, patient preparation, bronchial washings, bronchial brushings, bronchial biopsies, bronchoalveolar lavage (BAL), transbronchial lung biopsy (TBB), central airway obstruction, diagnostic procedures, TBNA, EBUS, Radial EBUS, autofluorescence bronchoscopy, rigid bronchoscopy, navigation bronchoscopy, therapeutic procedures, bronchial laser resection, electrocautery, argon–plasma coagulation (APC), and cryotherapy/cryoextraction, photodynamic therapy (PDT), tracheobronchial stent insertion, and rachytherapy.

Includes: Aims of smoking cessation interventions, NRT, non-nicotine replacement therapy, drugs, hypnosis, acupuncture/acupressure, electronic cigarettes

Respiratory physicians are often involved in making difficult decisions about the appropriateness of treatment and the prolongation of life in patients with chronic underlying lung disease. Sometimes, artificial ventilation may prolong the dying process; life has a natural end, and the potential to prolong life in the ICU can cause dilemmas. In other cases, these interventions are valuable at prolonging life with a reversible complication.

Thoracic ultrasound (TUS) is increasingly used for bedside evaluation of the pleural space and thorax. Given improved safety, NPSA and BTS guidance ‘strongly recommend’ TUS for pleural fluid procedure site selection. TUS also gives useful diagnostic information that may alter management (e.g. a patient with a transudative effusion who has pleural nodularity, suggestive of malignancy).

Includes: Positive pressure ventilators, CPAP, high-flow nasal oxygen (HFNO), indications, acute exacerbation of COPD, acute cardiogenic pulmonary oedema, decompensated OSA and obesity hypoventilation, respiratory failure from neuromuscular weakness, Immunocompromised patients, CAP, contraindications, chest wall deformity and neuromuscular weakness, sleep apnoea, cystic fibrosis, COPD, NIV end-of-life weaning

Sickle cell disease is an autosomal recessive condition resulting in a substitution of a valine for glycine in the β‎-globin subunit of Hb, forming HbS. HbS is less soluble under reduced O2 tensions and leads to deformation of red blood cells (sickling) when deoxygenated (e.g. in atelectatic lung), resulting in chronic haemolysis and vascular occlusion with tissue infarction in individuals homozygous for the β‎-globin gene mutation (sickle cell anaemia/disease).

Revised and updated for its third edition, the Oxford Handbook of Respiratory Medicine is concise, practical, and designed for rapid access to essential information. It covers the latest clinical guidelines and developments in the field and features unique sections on practical procedures, as well as a symptoms section to aid in differential diagnosis and clinical management. Practical advice on management is integrated throughout and a dedicated section on respiratory emergencies ensures the ability to cope with any eventuality. New sections include thoracic ultrasound, indwelling pleural catheters, safe sedation, and cardiopulmonary exercise testing, and this new edition covers all major respiratory diseases and symptoms.

The multiplicity of inhaler devices on the market is often bewildering, as companies vie to increase their market share. The different devices have a role for those unable to use conventional inhalers. This chapter details the different devices, both their advantages and disadvantages. It is nearly impossible to remember the specific usage instructions for each type of inhaler, and this chapter contains a useful table for quick reference when helping patients to use their particular device. The place of nebulizers is also discussed.

Includes: Acute upper airway obstruction, anaphylaxis, upper respiratory tract infections, laryngeal and tracheal disorders

Includes: Simple airway adjuncts, oropharyngeal airway (Guedel), nasopharyngeal airway, supra-glottic airway devices (SGAD), intubation, endotracheal tube

Chest drain insertion is associated with significant morbidity and mortality, and careful consideration should be given to the precise indication for drainage. Out-of-hours drain insertion should be avoided, unless an emergency. Ultrasound guidance should be used for all drains inserted for fluid, but is not required for pneumothorax.

Many fungi can affect the lung through direct invasion or immunological mechanisms. This chapter covers the range of fungi and the mechanisms by which they can cause damage, as well as the factors provoking invasion, such as immunosuppression, HIV, infection, bone marrow suppression, and use of biological therapies like infliximab. Aspergillus is the most common and covered in detail, including simple allergic asthma, allergic bronchopulmonary aspergillosis, invasive Aspergillus disease, aspergilloma, and hypersensitivity pneumonitis due to Aspergillus. The role of steroids and antifungal agents is explored. Pneumocystis pneumonia (PCP) is also covered in detail, particularly its treatment in different settings. The endemic mycoses (histoplasmosis, blastomycosis, coccidioidomycosis and paracoccidioidomycosis), cryptococcosis, and candidal pneumonia are all discussed, with sections on their presentation, diagnosis, and treatment.

Immunosuppressive drugs are used mainly in the management of pulmonary vasculitis, but also in asthma, sarcoidosis, and ILD. The chapter also covers corticosteroids, azathioprine, methotrexate, cyclophosphamide, rituximab

A multi-system disorder of unknown cause, likely resulting from the interplay of environmental and genetic factors, characterized by non-caseating granulomata and CD4+ Th1-biased T cell response in affected organs. Commonly involves the respiratory system but can affect nearly all organs. Fifty to sixty per cent of people have spontaneous remissions; others may develop chronic, and sometimes progressive, disease.

Using image guidance (either CT or US), a cutting needle takes several 1–2 cm cores along the long axis of any parietal pleural pathology. PET/CT may have a role guiding pleural biopsy in patients with diffuse pleural abnormality to increase sensitivity. US-guided pleural biopsies increase microbiological diagnosis in pleural infection but this is not routine practice. Using thoracoscopic biopsy (medical thoracoscopy/VATS), multiple biopsies are taken of visually abnormal parietal pleura. Using a pleural biopsy needle in a ‘blind’ percutaneous fashion to take multiple biopsies. Not advocated for diagnosing malignancy. May have utility in resource-limited settings for diffuse pleural diseases, but thoracoscopy still preferred.

Palliative care is defined by the World Health Organization (WHO) as an approach that improves the QoL of patients and their families facing the problems associated with life-threatening illness, through the prevention and relief of suffering by means of early identification, impeccable assessment, and treatment of pain and other problems, including physical, psychosocial, and spiritual.

Includes: Statutory sick pay (SSP), employment and support allowance (ESA), personal independence payment (PIP), direct payments, carer’s allowance, NHS continuing healthcare, income support ± disability premiums, working tax credit (with extra credit for disability), disabled students’ allowance (DSA), access to work grant, disabled facilities grant, other transport assistance, industrial injuries disablement benefit, reduced earning allowance.

Introduction In patients treated with non-invasive ventilation (NIV) for exacerbations of COPD (ECOPD), late failure, defined as recurrent respiratory acidaemia during NIV but after 24 hours following normalisation of pH, or relapse, defined as recurrence of respiratory acidaemia during admission but after 24 hours following cessation of NIV, are associated with poor survival and frailty.1 However, the UK prevalence and outcome of late failure and relapse is unknown. Methods Unique, consecutive patients who had spirometry confirmed ECOPD requiring NIV for respiratory acidaemia were prospectively recruited to the NIV Outcomes study (ISRCTN22921168) in 10 NHS trusts. The prevalence and outcomes of patients with late failure and/or relapse was investigated. Results Of the 733 patients recruited, 41(5.6%) developed late failure alone, 48(6.5%) experienced relapse alone and 4 (0.5%) developed both. The time to late failure was 2.8(1.8–5.8) days from NIV starting and 2.3(1.5–3.6) days from initial pH correction. Population descriptors are shown in the table 1. Following late failure, NIV was continued in 95.6% of patients, with 60% having changes to ventilatory settings and 31.1% having changes to improve patient-ventilator synchrony. Only 2.2% were invasively ventilated following late failure. Overall hospital mortality was 31.7% in late failure patients, 37.5% in patients who relapsed and 75% if both occurred. This compares with 17.7% mortality in patients without late failure or relapse. Discussion Late failure and/or relapse is relatively common, occurring in around 10% of NIV patients and is associated with worse hospital mortality. Both the prevalence of late failure, and inpatient mortality are lower here than described in a previous single centre study.2Patients with late failure/relapse tend towards worse lung function, lower BMI, more LTOT and left ventricular systolic dysfunction. The majority continued on NIV following optimisation of ventilatory settings, and 60–70% survived to discharge. It may be that in patients who have optimised NIV (ventilator settings or synchrony) failure to improve is not due to failure of the ventilatory interface (NIV rather than invasive ventilation), but rather failure of the lungs due to the severity of the underlying disease and acute insult. References Lancet Respir Med 2018;6:935–47 Thorax 2000;55(10):819–25

Introduction Non-invasive ventilation (NIV) is life-saving in exacerbations of COPD complicated by acute hypercapnic respiratory failure (AHRF). These episodes indicate advanced disease and patients who survive the acute episode show significant morbidity and high one-year mortality.1 In this group, clinicians can be prognostically pessimistic about outcome and quality of life (QoL); understanding predictors of poor outcome six months following an episode of AHRF treated with NIV could help clinical decision making. Methods Unique, consecutive patients were prospectively recruited to the NIV Outcomes study (ISRCTN22921168) in 10 NHS trusts. Consenting patients surviving to discharge were followed up monthly with QoL assessed using validated QoL questionnaires including the COPD Assessment Test (CAT). Poor outcome was defined as a pre-discharge CAT score in the worst 50% of responses (CAT=24–40) with subsequent clinically significant decline (≥2 points), or death, within six months. Multivariate logistic regression identified independent predictors. Continuous variables were subsequently dichotomised, and regression rerun. Results 553 patients survived to discharge; 253 consented and 239 provided >1 QoL assessment. Median(IQR) follow up time was 359(171–367) days, with 8(3–11) months of questionnaires completed, and NIVO score of 3(1–3.75). Mean(SD) age 68.9(9.1) years and FEV136.8(14.7)% predicted. 34.2% had previously received NIV, 24.6% were prescribed LTOT, and 47.1% were unable to leave the house unassisted. 56.6% had persistent hypercapnia post-ventilation. 67/239 suffered poor outcome. Independent predictors of poor outcome were LTOT, Left Ventricular Systolic Dysfunction, Diaphragm height ≤2.3 cm, confusion pre-ventilation, admission haemoglobin ≤14 g/dL, Pre-discharge HADS-depression Score ≥8, Pre-discharge Nottingham Extended Activities of Daily Living score ≤30 (Table 1). A simple tool (1 point assigned to each variable) demonstrated an area under the receiver operating characteristic curve of 0.809 (95% CI’s: 0.747–0.871). Discussion These routinely available clinical indices, which include a measure of hyperinflation, and two simple patient completed questionnaires demonstrate independent prediction of poor outcome in this population. A clinical tool from these indices shows promise but would require external validation before clinical use. If this occurred, it may help challenge prognostic pessimism and with predicting patients who require specialist palliative input. Reference BTS/ICS AHRF Guideline. Thorax(2016);71:ii1–ii35.

The SARS-CoV-2 can lead to severe illness with COVID-19. Outcomes of patients requiring mechanical ventilation are poor. Awake proning in COVID-19 improves oxygenation, but on data clinical outcomes is limited. This single-centre retrospective study aimed to assess whether successful awake proning of patients with COVID-19, requiring respiratory support (continuous positive airways pressure (CPAP) or high-flow nasal oxygen (HFNO)) on a respiratory high-dependency unit (HDU), is associated with improved outcomes. HDU care included awake proning by respiratory physiotherapists. Of 565 patients admitted with COVID-19, 71 (12.6%) were managed on the respiratory HDU, with 48 of these (67.6%) requiring respiratory support. Patients managed with CPAP alone 22/48 (45.8%) were significantly less likely to die than patients who required transfer onto HFNO 26/48 (54.2%): CPAP mortality 36.4%; HFNO mortality 69.2%, (p=0.023); however, multivariate analysis demonstrated that increasing age and the inability to awake prone were the only independent predictors of COVID-19 mortality. The mortality of patients with COVID-19 requiring respiratory support is considerable. Data from our cohort managed on HDU show that CPAP and awake proning are possible in a selected population of COVID-19, and may be useful. Further prospective studies are required.

Background: The efficacy of CPAP at the mildest end of the OSA spectrum is unclear. The MERGE trial investigated the effect of CPAP on quality of life in patients with mild OSA (Wimms et al. 2019). This subset analysis aimed to determine the effectiveness of CPAP in a subset of patients with ‘very9 mild OSA, defined as having mild OSA according to the sensitive AASM 2012 criteria, but no OSA using the earlier AASM 2007 criteria (i.e. AHI >5 to Methods: The MERGE trial randomised patients with mild OSA (AHI >5 to ≤15 events/hr, AASM 2007 or 2012) in parallel to receive either CPAP plus Standard Care or Standard Care alone for 3 months. A subset of 95 of 301 patients were identified as having ‘very9 mild OSA. Results: The subset of 95 ‘very9 mild OSA patients had a median (IQR) AHI 6.80(5.7, 8.8) events/hr, and were symptomatic (Vitality 41.9(10.9); ESS 10.3(4.7)). 50 of 95 were allocated to CPAP, and 45 to Standard Care. ‘Very9 mild OSA patients had significantly improved Vitality after 3 months of CPAP, compared to Standard Care (+9.2 points, 95% CI +5.6 to +12.7; p Conclusions: This subset analysis has shown the clinical effectiveness of CPAP treatment in patients at the mildest end of the disease spectrum, with 9very9 mild but symptomatic OSA. The results were similar to those observed in the primary analysis of the MERGE trial.