AJTCCM VOL. 29 NO. 4 2023 147
EDITORIAL
Extracorporeal membrane oxygenation (ECMO) is a specialised life
support technology that utilises an external membrane oxygenator
and centrifugal pump to maintain oxygenation (venovenous,
VV‑ECMO) and haemodynamics and oxygenation (venoarterial,
VA‑ECMO) in patients with severe respiratory or cardiac failure,
respectively.[1,2] Owing to its inherent complexity and the intensive
personnel and resources it requires, ECMO is typically used as a last
resort when other treatments have failed, and should be oered in
specialised referral centres with the necessary expertise. Access to
ECMO, particularly in the private sector, is expanding, and while the
true number of ECMO‑capable hospitals in South Africa (SA) is not
known, only 5 centres (1 public and 4 private) in Cape Town, Durban,
Johannesburg and Pretoria are registered with the international
Extracorporeal Life Support Organization (ELSO).[3]
e indications for VV‑ECMO encompass most causes of acute
respiratory failure and include, but are not limited to, any cause of
acute respiratory distress syndrome (ARDS), severe pneumonia,
aspiration, reperfusion injury aer pulmonary endarterectomy for
chronic thromboembolic pulmonary hypertension, and primary
gra dysfunction following lung transplantation.[4,5] ECMO as a
modality for respiratory support rst gained traction during the
H1N1 inuenza pandemic in 2009 and was also widely employed
during the COVID‑19 pandemic, with in‑hospital mortality of
~40%.[6‑8] Incontrast, VA‑ECMO can provide temporary support in
patients with cardiogenic shock, myocarditis, massive pulmonary
embolism, failure to wean from cardiopulmonary bypass, or severe
heart failure as a bridge to heart transplantation or implantation of
a ventricular assist device.[9,10] VA‑ECMO generally carries a higher
risk of complications due to arterial cannulation and the strict
requirement for therapeutic anticoagulation, and may have a lower
survival rate because of the additive organ failures (respiratory and
cardiac) of the conditions it supports.[11,12]
In this issue of AJTCCM, Van Zijl et al.[13] retrospectively report
the outcomes of all patients supported with VV‑ and VA‑ECMO at
Netcare Milpark Hospital, a high‑volume centre (dened as >20cases
per year[14]) in Johannesburg, SA, that treated 107 patients over
>2years during a period predating the COVID pandemic. Most
patients (73%) had respiratory failure as their indication for ECMO,
with 54% of the cohort receiving VV‑ECMO. Overall, survival to
hospital discharge in the cohort was 44%. As Milpark Hospital is also
a centre for thoracic transplantation, 29% of the patients in this study
were being supported for primary gra dysfunction aer either heart
or lung transplantation; when these were excluded, outcomes between
patients treated for respiratory and cardiac failure were broadly similar
(42% v. 35%, respectively).
While the relatively small sample size and the heterogeneous mix of
indications for both modalities make interrogation of the risk factors
associated with poor outcome and comparisons of mortality with
international studies challenging, the authors are nevertheless to be
commended on publishing the rst report of ECMO outcomes in the
SA context. ere is a pressing need for more comprehensive local data
on this treatment modality from both the private and public sectors,
as outcomes can vary greatly depending on patient selection, timing
of ECMO initiation, institutional protocols and access to critical care
infrastructure. In addition, further reports on the outcomes of ECMO
for severe COVID‑associated ARDS from the SA setting are eagerly
awaited. e ECMO and broader critical care community need these
data to guide eorts to align practices with international best practices,
potentially improving outcomes.
e scarcity of data on ECMO outcomes in SA underscores the
importance of contribution to international registries (such as the
ESLO registry) to better understand ECMO ecacy, challenges and
potential usefulness. Such eorts are essential for rening clinical
practices, optimising patient selection, and enhancing the overall
quality of care. Contributing to registries also allows SA to add to
global research eorts and collaborate with experts worldwide. is
rst report acts as a catalyst, drawing attention to the urgency of
the further research and data gathering that is needed to ultimately
contribute to better patient outcomes and more informed decision‑
making among healthcare providers using ECMO in SA.
G Calligaro, BSc Hons, MB BCh, FCP (SA), MMed (Med), Cert
Pulm (SA)
Division of Pulmonology, Department of Medicine, Groote Schuur
Hospital and Faculty of Health Sciences, University of Cape Town,
South Africa
greg.calligar[email protected]
D omson, MB ChB, FCS (SA), MMed (Surg), Cert Critical Care (SA)
Division of Critical Care, Department of Anaesthesia and Periopera-
tive Medicine, Groote Schuur Hospital and Faculty of Health Sciences,
University of Cape Town, South Africa
1. White A, Fan E. What is ECMO? Am J Respir Crit Care Med 2016;193(6):9‑10. https://
doi.org/10.1164/rccm.1936P9
2. Wrisinger WC, ompson SL. Basics of extracorporeal membrane oxygenation. Surg
Clin North Am 2022;102(1):23‑35. https://doi.org/10.1016/j.suc.2021.09.001
3. Extracorporeal Life Support Organization. Map of ELSO centres with ECMO
availability. 2023. https://www.elso.org/membership/ecmoavailabilitymap.aspx
(accessed 15 September 2023).
4. Faccioli E, Terzi S, Pangoni A, et al. Extracorporeal membrane oxygenation in
lung transplantation: Indications, techniques and results. World J Transplant
2021;11(7):290‑302. https://doi.org/10.5500/wjt.v11.i7.290
5. Ndubisi N, van Berkel V. Veno‑venous extracorporeal membrane oxygenation for the
treatment of respiratory compromise. Indian J orac Cardiovasc Surg 2023;39(Suppl
1):1‑7. https://doi.org/10.1007/s12055‑022‑01467‑3
6. Bertini P, Guarracino F, Falcone M, et al. ECMO in COVID‑19 patients: A systematic
review and meta‑analysis. J Cardiothorac Vasc Anesth 2022;36(8 Pt A):2700‑2706.
https://doi.org/10.1053/j.jvca.2021.11.006
7. Chong WH, Saha BK, Medarov BI. A systematic review and meta‑analysis
comparing the clinical characteristics and outcomes of COVID‑19 and inuenza
patients on ECMO. Respir Investig 2021;59(6):748‑756. https://doi.org/10.1016/j.
resinv.2021.07.006
8. Ramanathan K, Shekar K, Ling RR, et al. Extracorporeal membrane oxygenation for
COVID‑19: A systematic review and meta‑analysis. Crit Care 2021;25:211. https://doi.
org/10.1186/s13054‑021‑03634‑1
9. Rivers J, Pilcher D, Kim J, Bartos JA, Burrell A. Extracorporeal membrane oxygenation
for the treatment of massive pulmonary embolism: An analysis of the ELSO database.
Resuscitation 2023;191:109940. https://doi.org/10.1016/j.resuscitation.2023.109940
10. Saxena A, Curran J, Ahmad D, et al. Utilisation and outcomes of V‑AV ECMO: A
systematic review and meta‑analysis. Artif Organs 2023;47(10):1559‑1566. https://
doi.org/10.1111/aor.14610
Bridging hope: South Africas ECMO reporting journey begins
148 AJTCCM VOL. 29 NO. 4 2023
EDITORIAL
11. Alba AC, Foroutan F, Buchan TA, et al. Mortality in patients with cardiogenic shock
supported with VA ECMO: A systematic review and meta‑analysis evaluating the impact
of etiology on 29,289 patients. J Heart Lung Transplant 2021;40(4):260‑258. https://doi.
org/10.1016/j.healun.2021.01.009
12. Ostadal P, Rokyta R, Karasek J, et al. Extracorporeal membrane oxygenation in the therapy
of cardiogenic shock: Results of the ECMO‑CS randomised clinical trial. Circulation
2023;147(6):454‑464. https://doi.org/10.1161/CIRCULATIONAHA.122.062949
13. Van Zijl NLJ, Janson JT, Sussman M, Geldenhuys A. Extracorporeal membrane oxygenation
in South Africa: Experience from a single centre in the private sector. Afr J orac Crit Care
Med 2023;29(4):e211. https://doi.org/10.7196/AJTCCM.2023.v29i4.211
14. Ng PY, Ip A, Fang S, et al. Eect of hospital case volume on clinical outcomes of patients
requiring extracorporeal membrane oxygenation: A territory‑wide longitudinal observational
study. J orac Dis 2022;14(6):1802‑1814. https://doi.org/10.21037/jtd‑21‑1512
Afr J Thoracic Crit Care Med 2023;29(4):e1727. https://doi.
org/10.7196/AJTCCM.2023.v29i4.1727
Ventilator-associated pneumonia is ubiquitous and troublesome
Hospital‑acquired infections are a source of increased morbidity and
mortality in patients admitted for all severities of disease.[1] Patients
requiring intensive care are at signicantly increased risk owing to
the nature of their illness and the need for invasive procedures that
include mechanical ventilation, vascular access, and drainage tubes
of all kinds. Ventilator‑associated pneumonia (VAP) is one of the
most common manifestations of hospital‑acquired infection and is
associated with increased intensive care and hospital stay, as well as
increased mortality.[2]
Mazwi etal.[3] have added a useful description of VAP from an
intensive care unit (ICU) in the developing world. ey demonstrated
a moderate rate of VAP, in line with gures from other parts of the
world (16.4 per 1 000 ventilator days), with global gures ranging
between 9.0 and 18.0 per 1 000 ventilator days.[2] Later‑onset VAP
was associated with the isolation of multidrug‑resistant organisms
and significantly increased mortality. This study was conducted
between March 2013 and December 2015, aer the time when global
awareness of VAP increased and various care bundles were introduced
that have been associated with a decreased prevalence of VAP.[4] is
was also shortly before the current problems of increasingly drug‑
resistant organisms with carbapenem‑resistant Enterobacteriaceae
and Acinetobacter species.
VAP remains a difficult problem for intensivists. A number of
ICU‑related events can mimic pneumonia, and colonisation of
patients with organisms is extremely common. ese make diagnosis
dicult, with no universally accepted denition for VAP. One of
the most widely used clinical approaches uses clinical suspicion of
pneumonia with an inltrate on the chest radiograph plus any one of
leucocytosis, fever >38.3°C, or purulent tracheobronchial secretions.[5]
is method lacks precision, with an autopsy study showing that it had
sensitivity of 69% and specicity of 75%.[6] e Clinical Pulmonary
Infection Score[7] was similarly imprecise, with sensitivity of 77% and
specicity of 42%. Adding detection of organisms may increase the
diagnostic precision, but this oen requires invasive investigation with
lavage and quantitative culture.[8] Although more rapid detection and
determination of resistance patterns of signicant organisms by novel
technologies that include polymerase chain reaction multiplex panels
are potentially useful, studies to date have not demonstrated major
improvements in outcome compared with conventional techniques.[9]
e lack of specicity for the diagnosis of VAP has been of concern
over the years, partly because of the lack of an appropriate gold
standard other than histopathology. e Centers for Disease Control
attempted to formalise a surveillance denition of VAP in 2012.[10]
Acknowledging the wide dierential diagnosis of pulmonary‑based
complications in ventilated patients, a ventilator‑associated event
(VAE) surveillance definition was formulated. The first level was
ventilator‑associated condition (VAC), marked by a deterioration in
oxygenation (need for an increase in the fraction of inspired oxygen
or positive end‑expiratory pressure 48 hours aer stability has been
achieved). However, VAC can include many ICU‑related events, but
the suspicion of infection (new fever or leucocytosis) coupled with
starting a new antimicrobial agent elevated the grading to infection‑
related VAC, which could then be classied as possible or probable
VAP depending on the ndings on microbiological investigation.[10]
Despite the logical nature of this surveillance denition, a number
of studies have shown that it too has problems, and a recent meta‑
analysis suggested that the VAE approach missed up to 50% of cases
of VAP with overall sensitivity <50%, although specicity reached
80%.[11] e lack of precision of the VAE surveillance approach for the
diagnosis may have implications for epidemiology and intervention
studies, and the discordance between VAE and VAP at the clinical
level needs to be recognised.[12] Consensus diagnostic criteria are still
lacking, which makes comparison of VAP incidence rates between
institutions and nations dicult.[2]
e increasing burden of multidrug‑resistant organisms and the
mortality and morbidity associated with VAP make prevention
paramount. e many processes involved in management of critically
ill patients make VAP likely, and considerable attention has been paid
to various interventions and bundles of care to prevent VAP. ere
has been considerable success with these approaches, with a marked
decline in VAP rates, although zero VAP may not be achievable.[13]
Mazwi etal.[3] discuss prevention of VAP as an essential component
of management. A number of interventions have been suggested as
part of prevention strategies and bundles, some of which, such as
venous thromboembolism prophylaxis, may reduce VAC but not
VAP. A particular area of concern related to VAP prevention in less
well‑resourced countries is ICU stang levels, with an increased
sta‑to‑patient ratio associated with an increased incidence of VAP,
particularly late‑onset VAP.[14] Eective VAP prevention approaches
to date have included non‑pharmacological measures related to
endotracheal tube management and patient positioning. Shortening
the duration of intubation using sedation and weaning policies[15]
and avoiding intubation by the use of non‑invasive ventilation or
high‑ow nasal cannula oxygen administration are eective, as are
semi‑recumbent positioning and subglottic secretion drainage.[16,17]
Pharmacological measures, including selective oral or digestive tract
AJTCCM VOL. 29 NO. 4 2023 149
EDITORIAL
decontamination, have been eective in some areas, but are oen
dicult to implement and are costly.[18] e most important and cost‑
eective recommendation for prevention of all hospital‑acquired
infections remains hand hygiene.[19]
Richard I Raine, MB ChB, MMed (Med), FCP (SA)
Department of Pulmonology, Division of Medicine, Groote Schuur Hospital and
University of Cape Town, South Africa
1. Rosenthal VD, Yin R, Lu Y, etal. e impact of healthcare‑associated infections on mortality
in ICU: A prospective study in Asia, Africa, Eastern Europe, Latin America, and the Middle
East. Am J Infect Control 2023;51(6):675‑682. https://doi.org/10.1016/j.ajic.2022.08.024
2. Papazian L, Klompas M, Luyt CE. Ventilator‑associated pneumonia in adults: Anarrative
review. Intensive Care Med 2020;46(5):888‑906. https://doi.org/10.1007/s00134‑020‑05980‑0
3. 3Mazwi S, van Blydenstein SA, Mukansi M. Ventilator‑associated pneumonia in an
academic imtensive care unit in Johannesburg, South Africa. Afr J orac Crit Care Med
2023;29(4):e154. https://doi.org/10.7196/AJTCCM.2023.v29i4.154
4. Martinez‑Reviejo R, Tejada S, Jansson M, etal. Prevention of ventilator‑associated
pneumonia through care bundles: A systematic review and meta‑analysis. J Intensive Med
2023;3(4):352‑364. https://doi.org/10.1016/j.jointm.2023.04.004
5. Johanson WG Jr, Pierce AK, Sanford JP, omas GD. Nosocomial respiratory infections
with Gram‑negative bacilli: e signicance of colonization of the respiratory tract. Ann
Intern Med 1972;77(5):701‑706. https://doi.org/10.7326/0003‑4819‑77‑5‑701
6. Fabregas N, Ewig S, Torres A, etal. Clinical diagnosis of ventilator associated pneumonia
revisited: Comparative validation using immediate post‑mortem lung biopsies. orax
1999;54(10):867‑873. https://doi.org/10.1136/thx.54.10.867
7. Pugin J, Auckenthaler R, Mili N, Janssens JP, Lew PD, Suter PM. Diagnosis of ventilator
associated pneumonia by bacteriologic analysis of bronchoscopic and nonbronchoscopic
‘blind’ bronchoalveolar lavage uid. Am Rev Respir Dis 1991;143(5Pt 1):1121‑1129. https://
doi.org/10.1164/ajrccm/143.5_Pt_1.1121
8. Torres A, Niederman MS, Chastre J, etal. International ERS/ESICM/ESCMID/ALAT
guidelines for the management of hospital‑acquired pneumonia and ventilator‑associated
pneumonia: Guidelines for the management of hospital‑acquired pneumonia (HAP)/
ventilator‑associated pneumonia (VAP) of the European Respiratory Society (ERS),
European Society of Intensive Care Medicine (ESICM), European Society of Clinical
Microbiology and Infectious Diseases (ESCMID) and Asociación Latinoamericana del Tórax
(ALAT). Eur Respir J 2017;50(3):1700582. https://doi.org/10.1183/13993003.00582‑2017
9. Luyt C‑E, Hékimian G, Bonnet I, etal. Usefulness of point‑of‑care multiplex PCR to rapidly
identify pathogens responsible for ventilator‑associated pneumonia and their resistance to
antibiotics: An observational study. Crit Care 2020;24:378. https://doi.org/10.1186/s13054‑
020‑03102‑2
10. Magill SS, Klompas M, Balk R, etal. Developing a new, national approach to surveillance for
ventilator‑associated events. Crit Care Med 2013;41(11):2467‑2475. https://doi.org/10.1097/
CCM.0b013e3182a262db
11. Fan Y, Fang G, Wu Y, Zhang J, Zhu M, Xiong L. Does ventilator‑associated event surveillance
detect ventilator‑associated pneumonia in intensive care units? A systematic review and
meta‑analysis. Crit Care 2016;20(1):338. https://doi.org/10.1186/s13054‑016‑1506‑z
12. Klompas, M. Ventilator‑associated events: What they are and what they are not. Respir Care
2019;64(8):953‑961. https://doi.org/10.4187/respcare.07059
13. Colombo SM, Palomeque AC, Li Bassi G. e zero‑VAP sophistry and controversies
surrounding prevention of ventilator‑associated pneumonia. Intensive Care Med
2020;46(2):368‑371. https://doi.org/10.1007/s00134‑019‑05882‑w
14. Cimiotti JP. Stang level: A determinant of late‑onset ventilator‑associated pneumonia. Crit
Care 2007;11(4):154. https://doi.org/10.1186/cc6085
15. Girard TD, Kress JP, Fuchs BD, etal. Ecacy and safety of a paired sedation and ventilator
weaning protocol for mechanically ventilated patients in intensive care (Awakening and
Breathing Controlled trial): A randomised controlled trial. Lancet 2008;371(9607):126‑134.
https://doi.org/10.1016/S0140‑6736(08)60105‑1
16. Drakulovic MB, Torres A, Bauer TT, Nicolas JM, Nogue S, Ferrer M. Supine body position as
a risk factor for nosocomial pneumonia in mechanically ventilated patients: A randomised
trial. Lancet 1999;354(9193):1851‑1858. https://doi.org/10.1016/S0140‑6736(98)12251‑1
17. Maertens B, Lin F, Chen Y, Rello J, Lathyris D, Blot S. Eectiveness of continuous cu
pressure control in preventing ventilator‑associated pneumonia: A systematic review and
meta‑analysis of randomized controlled trials. Crit Care Med 2022;50(10):1430‑1439.
https://doi.org/10.1097/CCM.0000000000005630
18. Minozzi S, Pieri S, Brazzi L, Pecoraro V, Montrucchio G, D’Amico R. Topical antibiotic
prophylaxis to reduce respiratory tract infections and mortality in adults receiving
mechanical ventilation. Cochrane Database Syst Rev 2021, Issue 1. Art. No.: CD000022.
https://doi.org/10.1002/14651858.CD000022.pub4
19. World Health Organization. WHO guidelines on hand hygiene in health care. 15January
2009. https://www.who.int/publications/i/item/9789241597906 (accessed 8 November
2023).
Afr J Thoracic Crit Care Med 2023;29(4):e1611. https://doi.
org/10.7196/AJTCCM.2023.v29i4.1611
e hidden epidemic of post-tuberculosis bronchiectasis
In this issue of AJTCCM, Titus etal.[1] report on a retrospective
cohort of adult patients with non‑cystic fibrosis bronchiectasis
in the pulmonology unit at Charlotte Maxeke Johannesburg
Academic Hospital, South Africa (SA). In doing so, they respond
to the paucity of epidemiological data on the disease, particularly
in high tuberculosis (TB)/HIV burden settings such as SA. Given
the intensity of respiratory insults across the life stages of people in
these settings, it is unsurprising that most epidemiological estimates
suggest that the true burden of post‑infectious bronchiectasis
is largely unrecognised. During the two centuries that followed
René Laënnec’s rst reports of the disease in 1819, relatively little
attention has been given to bronchiectasis, which has been rising in
incidence and prevalence globally and is associated with substantial
socioeconomic costs.[2] e increasing prevalence of bronchiectasis
may partly be due to improved imaging technologies, including
computed tomography, but is undoubtedly also driven by the
increasing cumulative prevalence of its underlying causes.
e noteworthy ndings of the report by Titus etal. were: (i)the
median (interquartile range) age of the cohort was 49 (38 ‑ 60)
years; (ii) there was a slight male predominance (51.2%); (iii) chest
radiography was used to support the diagnosis of bronchiectasis in
44.6% of the patients; (iv) TB was the most common attributable
cause (77.0%); (v) the majority of the patients experienced at least
one exacerbation (62.9%); (vi) over half the cohort received inhaled
corticosteroids; and (vii) immunomodulatory macrolide therapy was
used in only 10.6% of the patients.
The precise prevalence of bronchiectasis in SA is not known –
there have been no large population‑based prevalence studies, and
there is no national registry for the disease. Globally, the prevalence
of the disease varies across geographical regions, reecting regional
dierences in socioeconomic factors, the epidemiology of contributory
or underlying conditions (particularly the relative prevalence of
infectious v. non‑infectious lung disease), and the demographic prole
of the populations. e prevalence of bronchiectasis in the USA, based
150 AJTCCM VOL. 29 NO. 4 2023
EDITORIAL
on historical medical records and claims data, has been estimated to
be between 139 and 213 cases per 100000 persons, and the prevalence
in the UK, estimated from a population‑based cohort, to be 566 cases
per 100000 women and 485 per 100000 men.[3,4] e prevalence of
bronchiectasis in these settings is increased in older persons and in
women, patterns that are also consistent with data from Germany, Spain
and Singapore.[5‑7] e highest prevalence estimates of bronchiectasis are
reported in China, where there are 1 200 cases per 100000 population
>40 years of age.[8] In India, as in other parts of the world where post‑
infectious bronchiectasis predominates, patients with bronchiectasis
were signicantly younger and more likely to be male compared with
their counterparts in the US and UK, even aer accounting for the
generally older general population demographics of the latter.[9,10] e
methods used to establish these prevalence gures vary considerably,
and population‑based studies from Africa are conspicuously lacking.
The finding that post‑TB lung disease is a leading cause of
bronchiectasis in this Johannesburg cohort is consistent with the
conclusion made by a recent systematic review, which identied post‑
infectious bronchiectasis as the most common identiable cause of non‑
cystic bronchiectasis in adults.[9] In Asia, for example, more than two‑
thirds of adult bronchiectasis was attributable to prior TB, consistent
with the ndings of Titus etal. It is now widely accepted that post‑TB
lung disease is underestimated, underdiagnosed and under‑reported.
Successful TB treatment is narrowly dened as the achievement of
bacteriological cure or the completion of treatment, irrespective of
permanent and/or progressive functional decits resulting from an
episode of TB. The large number of people who have survived an
episode of TB represent a population vulnerable and susceptible to
chronic respiratory disease, and their numbers will continue to increase
until TB is eradicated. e current paradigm of perceiving an episode of
TB as a discrete life event is challenged by estimates suggesting that an
average of 3.6 potential years of life are lost aer a fully treated episode
of tuberculosis, and that TB survivors bear an excess mortality burden
compared with risk‑matched controls who have never had TB.[11‑13]
e incidence of bronchiectasis following an episode of TB has been
found to range from 16% to 65%, and superimposition by other bacterial
infections is a potential risk factor for the development of bronchiectasis.
[14] In a well‑characterised cohort from Malawi, bronchiectasis developed
in 44% of people who completed TB treatment.[15] Given that 54 million
people have been treated for TB since the year 2000 globally, and that
there are an estimated 300000 new cases of TB in SA each year,[16] the
implications for bronchiectasis are staggering.
e aetiological spectrum of bronchiectasis in SA and other low‑ and
middle‑income settings is to be contrasted with that in Europe, North
America and Australia, where idiopathic bronchiectasis predominates
and post‑TB bronchiectasis is exceedingly rare. ese dierences present
major limitations to generalising research ndings, care strategies and
clinical guidelines across settings, and emphasise the importance of
generating local data. Few, if any, of the recommendations in the timely
South African oracic Society position statement on the management
of non‑cystic brosis bronchiectasis were based on high‑quality local
or regional evidence.[17]
The roles of inhaled corticosteroids, bronchodilators,
immunomodulators, mucoactive agents, targeted eradication therapy,
suppression of
colonising pathogens, and airway clearance techniques
are particularly dicult to evaluate in post‑TB bronchiectasis owing
to the pathological heterogeneity of the disease. TB bronchitis,
bronchial obstruction by regional lymphadenopathy, and traction
bronchiectasis from neighbouring parenchymal brosis all contribute
to the total burden of post‑TB bronchiectasis, but are unlikely to
respond uniformly to therapeutic interventions. In contrast to the
common use of inhaled corticosteroids in the cohort reported by Titus
etal., most guidelines recommend against the use of inhaled steroids
for bronchiectasis unless there is coexisting asthma, owing to their
association with increased exacerbation frequency, mycobacterial
infection and mortality.[18‑20]
The work by Titus et al. reminds us that without local
epidemiological data, it is difficult to advocate for the resources
needed to develop context‑specic preventive, diagnostic, therapeutic
and care strategies for patients with the disease. In particular,we
need a greater focus on primary and adjunctive treatment options
(including host‑directed therapies) for tuberculosis aimed at limiting
the development of post‑TB lung disease in the rst instance. For
those now living with post‑TB bronchiectasis and other forms of post‑
infectious bronchiectasis, we need therapeutic trials or high‑quality
cohort data to establish the usefulness of bronchodilators, inhaled
corticosteroids, and macrolide therapy. Even the well‑intentioned
universal application of airway clearance techniques with nebulised
saline brings substantial direct and indirect costs to patients and
health services, and we should interrogate whether those costs are
outweighed by the assumed benets in our patients, especially those
with dry bronchiectasis.In pursuing this work, the authors have issued
a call for greater commitment to advancing locally relevant science
aimed at informing the care of patients with neglected respiratory
diseases in our setting.
Rubeshan Perumal, MB ChB, MMed (Int Med), MPhil, MPH, PhD,
FCP (SA), Cert Pulmonology (SA)
Department of Pulmonology and Critical Care, Division of Internal Medicine,
School of Clinical Medicine, College of Health Sciences, University of KwaZulu-
Natal, Durban, South Africa; Centre for the AIDS Programme of Research in
South Africa, Durban, South Africa
1. Titus G, Hassanali S, Feldman C. Non‑cystic brosis bronchiectasis: A single‑centre
retrospective study in Johannesburg, South Africa. Afr J orac Crit Care Med
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