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BTS Clinical Statement on Pulmonary Arteriovenous Malformations

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BTS Clinical Statement on Pulmonary Arteriovenous Malformations Downloaded from http://thorax.bmj.com/ on November 15, 2017 - Published by group.bmj.com BTS Clinical Statement British Thoracic Society Clinical Statement on Pulmonary Arteriovenous Malformations Claire L Shovlin,1,2 Robin Condliffe,3 James W Donaldson,4 David G Kiely,3,5 Stephen J Wort,6,7 on behalf of the British Thoracic Society 1NHLI Vascular Science, Imperial EXECUTIVE SUMMARY high cardiac output.16 PAVMs of any size allow College London, London, UK Pulmonary arteriovenous malformations (PAVMs) are paradoxical emboli that may cause ischaemic 2Respiratory Medicine, and structurally abnormal vascular communications that strokes,17 18 myocardial infarction,18–20 cerebral VASCERN HHT European 17 21–23 Reference Centre, Hammersmith provide a continuous right-to-left shunt between (brain) and peripheral abscesses, discitis and Hospital, Imperial College pulmonary arteries and veins. Their importance stems migraines.24–26 Less frequently, PAVMs may cause Healthcare NHS Trust, London, from the risks they pose (>1 in 4 patients will have haemoptysis, haemothorax27–29 and/or maternal UK 29 3 a paradoxical embolic stroke, abscess or myocardial death in pregnancy. Due to compensatory adap- Pulmonary Vascular Disease Unit, Royal Hallamshire Hospital, infarction while life-threatening haemorrhage affects tations, respiratory symptoms are frequently absent Sheffield, UK 1 in 100 women in pregnancy), opportunities for risk or not recognised until PAVM treatment has led 4 Dept of Respiratory Medicine, prevention, surprisingly high prevalence and under- to improvement or resolution.1 13–16 26 However, Derby Teaching Hospitals NHS appreciation, thus representing a challenging condition at least one in three patients with PAVMs will Foundation Trust, Derby, UK 5Department of Infection, for practising healthcare professionals. The driver for the have more severe migraines, nosebleeds, respira- Immunity and Cardiovascular current Clinical Statement was the plethora of new data tory, cardiac or other symptoms than they would Disease, University of Sheffield, since previous hereditary haemorrhagic telangiectasia if PAVMs were treated. Risk–benefit analyses are Sheffield, UK 30–32 6 (HHT) guidelines generated in 2006 and a systematic almost always in favour of treatment. There Pulmonary Hypertension Cochrane Review for PAVM embolisation in 2011. The Department, Royal Brompton is evidence for risk reduction for many PAVM 13–17 24 26 29 Hospital, London, UK British Thoracic Society (BTS) identified key areas in which complications, although contraindica- 7NHLI Vascular Science, Imperial there is now evidence to drive a change in practice. tions should be considered. Additionally, recent College London, London, UK Due to the paucity of data in children, this Statement evidence reminds of the potential levels33 and focused on adults over 16 years. The Statement spans consequences1 34 of iatrogenic radiation exposure Correspondence to the management of PAVMs already known to be present incurred in delivery of these health benefits. Professor Claire L Shovlin, (interventional and medical), screening and diagnosis (for Professor of Practice (Clinical HHT, the most common cause of PAVMs, is a and Molecular Medicine), NHLI PAVMs and HHT) and follow-up of patients following a multisystemic vascular disorder.6–9 HHT is inher- Vascular Science, Imperial first diagnosis, intervention or negative screen for PAVMs. ited as an autosomal dominant trait and most College London, Imperial The Good Practice Points (in bold) were generated commonly results from a pathogenic sequence Centre for Translational for a target audience of general respiratory, medical and Experimental Medicine, variant in ENG encoding endoglin (HHT type 1/ Hammersmith Campus, Du Cane and specialist clinicians and were approved by the HHT1), ACVRL1 encoding ALK-1 (HHT type 2/ Rd, London W12 0NN, UK; c. BTS Standards of Care Committee, before formal peer HHT2) or SMAD4.35–37 Frequent nosebleeds are the shovlin@ imperial. ac. uk review and public consultation. The Statement spans hallmark of HHT. Approximately 50% of patients embolisation treatment, accessory medical management with HHT have CT-detectable PAVMs38 and most Received 14 July 2017 and issues related to the likelihood of underlying HHT. Revised 1 September 2017 have systemic arteriovenous malformations (AVMs) Accepted 4 September 2017 in sites such as the liver, gastrointestinal tract or brain.6–9 35 37–39 All HHT genotypes predispose to INTRODUCTION AVMs, bleeding from mucocutaneous and gastroin- testinal telangiectasia, and iron deficiency anaemia Pulmonary arteriovenous malformations (PAVMs) 40 are structurally abnormal vascular communications due to chronic blood loss. Visceral AVMs are between pulmonary arteries and veins that range usually silent but have the potential for site-specific in size and complexity and provide an anatomic complications. By reducing systemic vascular resis- right-to-left shunt.1–4 PAVMs allow a proportion tance, visceral AVMs require supranormal cardiac of the right ventricular stroke volume to bypass outputs to maintain arterial blood pressure, with gas exchange, filtration and other functions of the cardiac demands increased further by coexisting pulmonary capillary bed. Limited prevalence data iron deficiency, anaemia, hypoxaemia, exercise, 41–46 suggest that PAVMs may affect many as 1 in 2600 pregnancy and sepsis. Despite their haemor- individuals (95% CIs 1 in 1315 to 1 in 5555).5 rhagic phenotype, patients with HHT are at risk of ► http:// dx. doi. org/ 10. 1136/ The majority of PAVMs are due to hereditary venous thromboemboli (VTE), particularly if serum thoraxjnl- 2017- 211072 47 47 48 haemorrhagic telangiectasia (HHT),6–9 but there is iron is low and/or factor VIII high. Patients 10 evidence for underappreciation of both PAVMs with HHT often tolerate anticoagulation or anti- 49 and HHT.11 PAVMs may be present from birth platelet therapy well. Recently described reduced and have usually completed major development rates of specific cancers,34 50 51 better survival by adult life, although they can enlarge later in outcomes for cancer patients who have HHT52 and 20 T Shovlin CL,o cite: life, for example, during pregnancy or other alter- low myocardial infarction rates await explanation. 12 Condliffe R, Donaldson JW, ations in pulmonary haemodynamics. The size The HHT phenotype is subtly different between et al. Thorax of the right-to-left shunt determines the degree HHT genotypes, for instance patients with HHT2 2017;72:1154–1163. of hypoxaemia,13 14 exuberant ventilation15 and are less likely to have PAVMs and more likely to 1154 Shovlin CL, et al. Thorax 2017;72:1154–1163. doi:10.1136/thoraxjnl-2017-210764 Downloaded from http://thorax.bmj.com/ on November 15, 2017 - Published by group.bmj.com BTS Clinical Statement have hepatic AVMs than patients with HHT1 or SMAD4-related the revised document was reapproved by the BTS Standards of HHT.37 39 In addition, many rarer HHT complications appear to Care Committee in June 2017 before final Thorax review and be relatively genotype specific, for example, pulmonary arterial publication. hypertension (ACVRL153–55), juvenile polyposis (SMAD437 56) and aortopathy (SMAD437 57). Non-HHT patients can develop sporadic PAVMs, when they SECTION 1: INTERVENTIONS are generally solitary. Single and multiple PAVMs commonly 1A: Management overview occur following surgical treatment of complex cyanotic congen- All patients with radiographically-visible PAVMs should be ital heart disease if a lung receives no or minimal hepatic considered for referral to interventional colleagues experienced venous return58–60 and more rarely as part of other inherited in PAVM embolisation. Due to the small diameter of many vasculopathies. Radiological differential diagnoses of a PAVM PAVM feeding arteries and the possibility of reperfusion or reca- include a bronchocoele, bronchopulmonary sequestration, nalisation, medical management and follow-up is also required pulmonary varix, pulmonary arterial aneurysm and aberrant (see Sections 2 and 4). systemic to pulmonary communications.2 Other causes of right- Embolisation treatment is recommended even for asymp- to-left shunts detectable by contrast echocardiography include tomatic patients.31 PAVM treatment reduces risks from para- intermittent shunting through intracardiac defects (when right- doxical emboli and improves oxygenation, other physiological side pressures exceed left, most commonly after a Valsalva parameters, symptoms exacerbated by right-to-left shunting manoeuvre61), the hepatopulmonary syndrome62 and functional and haemorrhage.13–17 24 26 Patients should not undergo embo- shunting (present in ~10% of the general population at rest, lisation expecting improved exercise tolerance, although this rising on exercise,63 after adrenergic stimuli64 and in response may be observed. Patients with concurrent chronic obstructive 65 to low PaO2 ). pulmonary disease, asthma or cardiovascular disease, or patients pursuing activities when exuberant ventilation is required CLINICAL STATEMENT METHODOLOGY to clear carbon dioxide, are more likely to note symptomatic 13 66 The Clinical Statement Group (CSG) was chaired by Professor benefit from embolisation. Claire Shovlin (CLS) and comprised the three most recent Right-to-left shunts detectable only by contrast echocar- 67 chairs of the British Thoracic Society (BTS) Pulmonary Vascular diography carry lower risks, but for radiologically-visible Specialist Advisory Group and an
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