Obstructive sleep apnoea in adultsBMJ 2009; 338 doi: https://doi.org/10.1136/bmj.b1165 (Published 07 April 2009) Cite this as: BMJ 2009;338:b1165
All rapid responses
Obstructive sleep apnoea (OSA) in adults is quite a common problem, and by far its management is still short of the expectations in this modern era. We would like to extend our sincere thanks to Dr. Sophie D West, Dr. Helen A McBeath, and Prof John R Stradling, for a thorough and unparalleled practice lesson .
May we be given an opportunity to present our views and a new and simple technique for managing OSA. Possibly we are overlooking the way some extra and excess weight overlying the throat in affected individuals, which comes down bearing over the hyoid bone during sleep, when the throat muscles relax. Besides, any obstruction in the nasopharynx, oropharynx, hypopharynx, and larynx, it could also possibly lead to obstructive sleep apnoea.
Management of this common problem is not satisfactory as yet. Collar size has to be watched, and overweight and obese persons will benefit by reducing their weight. Available text is replete with the risk factors, and likewise we also have various ways of management. Lifestyle changes like losing weight, exercising regularly, avoidance of smoking and alcohol, etc, may help to an extent. For those who continue to have problems due to OSA, other modalities have been in use, ranging from surgery which involves with removal of tissue, termed uvulopalatopharyngoplasty (UPPP), jaw repositioning, plastic implants in the soft palate, tracheostomy, removal of tonsils, adenoids, correction of deviated nasal septum or nasal polypectomy, etc. Supplemental oxygen, CPAP (continuous positive airway pressure), bilevel positive airway pressure (BPAP), adaptive servo-ventilation (ASV), expiratory positive airway pressure (EPAP), oral appliances to keep throat open, adjustable airway pressure devices, etc.
As is almost usual with us, this technique was used for the first time in our first author’s case [Figure 1]. The primary author used to snore heavily during his sleep, and was waking up abruptly during his sleep due to suffocation. He had noticed that his shirts were no more fitting him, as his neck circumference had increased considerably. Plus he had also developed a double chin. He stopped smoking, and tried reducing his weight and did go back to regular exercises, but it did not help. Then he tried removing the double chin and extra flab over his neck, by the non-invasive and painless technique that we have developed for removal of excess flab that was published in your rapid response, the “Dr S. Arulrhaj’s technique” . The results were remarkable after two sittings that in ten days, and required just about 10 minutes in each sitting [Figure 1]. The results were equally remarkable on some other patients who were harried by snoring and apnoeic spells during sleep, who now have markedly reduced spells of waking up abruptly during sleep, and snoring has reduced. We have been calling this absolutely new technique, being showcased to the world for the first time, as the “Mainpuri Technique”. Mainpuri is a remote and neglected district in Uttar Pradesh, India, where the first authors originates.
We know that this technique is a novel concept, that can take care of most patients who suffer from snoring and sleep apnoea, and we would like to place this technique to the world through you, BMJ. Lot more research needs to be done to make this technique perfect, precise, absolutely free from any complications, and more acceptable as a simple, absolutely painless technique that does not require anaesthesia or sharps, needles, etc. There is no need of hospitalization. By bringing this technique on to your platform BMJ, we would like research groups and research and teaching hospitals to take on from here, as we don’t have any resources whatsoever. We could do this out of our own initiative, own accord, own resources, and with no help from any other source, private, governmental, or international. We are positive that this “MAINPURI TECHNIQUE for OSA” is going to help out most of the patients who are suffering from OSA.
Dr (Lt Col) Rajesh Chauhan
Hon’ National Professor IMA CGP, India.
Dr. Ajay Kumar Singh Parihar
Dr. Shruti Chauhan
Email : firstname.lastname@example.org
1. West SD, McBeath HA, Stradling JR. Obstructive sleep apnoea in adults. BMJ 2009;338:b1165
2. Chauhan R, Parihar AKS, Chauhan S. Obesity revisited : Dr. S. Arulrhaj’s non-invasive, quick and painless technique for flab and cellulite removal. BMJ 9 May 2013. http://www.bmj.com/content/346/bmj.f1050/rr/644779 (Accessed on 20 May 2013)
Competing interests: No competing interests
We congratulate the authors for their article on the ‘easily missed’
condition of obstructive sleep apnoea hypopnoea syndrome (OSAHS). (1) They
present a summary of the disease manifestations, assessment and treatment.
However, we would like to suggest that the consequences of OSAHS are not
just limited to driving and cardiovascular risk. It is recognized that the
pathophysiological consequences of OSAHS are diverse, affecting almost
every organ of the body. (2) We summarise below the ophthalmic
manifestations which can be significant and indeed can be the initial
presentation of the disease.
Ocular associations reported with OSAHS include floppy eyelid
syndrome, blepharoptosis, lower lid ectropion, blepharochalasis, eyelash
ptosis, lacrimal gland prolapse, papillary conjunctivitis, filamentary or
infectious keratitis, recurrent corneal erosion, keratoconus, optic
neuropathy, papilloedema and glaucoma. (3-5) In addition, leaking masks
used for continuous positive airway pressure (CPAP) treatment can cause
ocular irritation and even induce conjunctivitis. (6-7)
The effect of OSAHS treatment on the ocular manifestations is less
well documented and needs further studies. But isolated case reports have
suggested reversal of symptoms of FES accompanied with significant weight
loss (8) and initiation of CPAP. (9) And more recently effects of CPAP on
intraocular pressure and performance in visual field testing have been
reported. (10, 11) We would therefore recommend that as part of their
treatment, patients with OSAHS should also be advised to see their
optometrist to screen for potentially blinding manifestations of their
Conversely, studies using polysomnography, screening tools (Berlins
or Sleep Disorders Questionnaire (SA-SDQ) questionnaire) or even a simple
sleep history have shown a high prevalence of sleep disorders in patients
with ocular disorders including non- arteritic anterior ischaemic optic
neuropathy (NAION), primary open angle glaucoma (POAG), normal tension
glaucoma (NTG), floppy eye lid syndrome (FES) and more recently central
serous chorio-retinopathy (CSCR).(12) However a lack of training and
awareness is responsible for a sleep history rarely being considered in
the Ophthalmic clinics.
To conclude, clinical presentation in OSAHS may often be to non-sleep
specialists with symptoms that are not immediately attributable to sleep
apnoea (2) and this is probably the underlying cause for a large number of
undiagnosed OSAHS patients. We stress the importance of a simple sleep
history (± scoring system) becoming part of the normal systems review and
not just for use in the most obvious case scenario of an obese middle-aged
1)West SD, McBeath HA, Stradling JR. Obstructive sleep apnoea in
adults. BMJ 2009; 338: 946-8.
2)Schlosshan D, Elliott MW. Sleep.2: Clinical presentation and diagnosis
of the obstructive sleep apnoea hypopnoea syndrome. Thorax 2004; 59: 347-
3)McNab AA. The eye and sleep. Clin Experimental Ophthalmol 2005; 33: 117-
4)Mojon DS, Goldblum D, Fleischhauer J, Chiou AGY, Freuh BE, Hess CW et
al. Eyelid, conjunctival and corneal findings in sleep apnoea syndrome.
Ophthalmology. 1999, 106: 1182-1185.
5)Mojon DS, Hess CW, Goldblum D, et al. High prevalence of glaucoma in
patients with sleep apnoea syndrome. Ophthalmology 1999; 106: 1009-12.
6)Stauffer JL, Fayter NA, MacLurg BJ. Conjunctivitis from nasal CPAP
apparatus (letter). Chest 1984; 86: 802.
7)Fayers T, Simcock DE, Wilkins MR. Reactivation of recurrent corneal
erosion syndrome by continuous positive pressure ventilation. Cornea 2007;
8)Parunovic A. Floppy eyelid syndrome. Br J Ophthalmol 1983; 67: 264-266.
9)McNab AA. Reversal of floppy lid syndrome with treatment of obstructive
sleep apnoea. Clin Experiment Ophthalmol 2000; 28(2): 125-6.
10)Sebastian RT, Johns S, Gibson RA. Treating obstructive sleep apnoea
syndrome: does it improve visual field changes? Eye 2006; 20: 118-120.
11)Kiekens S, De Groot V, Coeckelbergh T, Tassignon MJ, van de Heyning P,
De Backer W, Verbraecken J. Continuous positive airway pressure therapy is
associated with an increase in intraocular pressure in obstructive sleep
apnoea. Invest Ophthal Vis Sc 2008; 49: 934-40.
12)Kadyan A, Sandramouli S. Sleep apnoea in the eye clinic. Br J
Ophthalmol 2009; 93: 132-3.
Competing Interest: None declared.
Competing interests: No competing interests
We are the father and uncle of Toby Tweddell, who was killed on the
M62 motorway on the edge of Liverpool on 8 August 2006, his car crushed
from behind by a Large Goods Vehicle (LGV); the driver had fallen asleep
at the wheel, and was subsequently found to be suffering from sleep
We are glad that the paper by West, McBeath and Stradling “Easily
missed? Obstructive sleep apnoea in adults” was printed in the 18/4/2009
issue of the BMJ.
In the four months from October 2007, at least four cases came before
the UK courts of LGV drivers accused of causing death by dangerous driving
(nine people in total killed); all four LGV drivers were suffering from
sleep apnoea which was only diagnosed after their accidents.
Sleep apnoea is therefore an important cause of fatal road accidents,
which GPs need fully to understand, since they play such a pivotal role in
declaring vocational drivers fit to drive.
The inquest into Toby’s death took place on 25 July 2008. Coroner
Sumner’s 5 August 2008 verdict reported that the driver of the LGV that
killed Toby had visited his GP during April 2006 complaining of tiredness.
“Blood and urine samples were taken to ascertain if he was a diabetic”,
reported the Coroner. When these were returned indicating that the patient
did not suffer from diabetes, “his G.P. advised him that he was most
probably suffering from stress.” “Critically, no diagnosis of sleep apnoea
was made”, said the Coroner. Nor was the driver referred to a consultant
in sleep medicine.
So yes, OSA is easily missed by GPs, with dreadful consequences.
The situation is exacerbated by inaction by the Department for
Transport and the Driver Vehicle Licensing Agency (DVLA). LGV drivers have
a higher than average incidence of obesity, with which OSA is positively
correlated. Yet in the “information and useful notes”
(http://www.dvla.gov.uk/media/pdf/leaflets/inf4d.pdf - last accessed 4 May
2009) that DVLA publishes for use with the Medical Examination Report D4
form which GPs complete with applicants for vocational driving licences,
there is no mention of obesity as being positively correlated with the
incidence of OSA; and DVLA states, bizarrely, that “at least three in
every thousand men have OSA” (amongst applicants for and renewers of
vocational licenses the incidence of OSA is probably nearer to one in
Following Toby’s inquest, Coroner Sumner took the unusual step of
issuing a Rule 43 Report to the Lord Chancellor’s Department. This called
for a toughening of the licensing regime for commercial drivers, as it
relates to OSA. Coroner Sumner stated that OSA is no respecter of age, and
criticised the absence of any provision “for a lorry driver to have to
undergo any form of routine medical examination from the time of their
qualification to drive until their 45th birthday”, noting that “lorry
driving involves little physical effort and there is evidence of obesity
within the industry”, and that “apart from other medical complications
arising from obesity, there is evidence to suggest that overweight people
are more likely to suffer from sleep apnoea”.
As yet the Department for Transport and DVLA continue to resist
pressure to change the licensing regime for vocational drivers to focus
more sharply on identifying sufferers from sleep apnoea, and getting them
treated before they cause an accident.
What is needed is a coherent and evidence-based (rather than evidence
-ignoring!) framework that:
i) makes clear the connection between obesity and the incidence of
ii) accurately indicates the likely prevalence of OSA, taking account
of the prevalence of obesity amongst vocational drivers;
iii) encourages GPs (as your article does) to spot potential cases of
sleep apnoea and to ensure that any such potential cases are properly
investigated, thereby increasing the proportion of sufferers who are
successfully diagnosed and treated;
iv) requires vocational drivers to be regularly screened, rather than
for this to happen only once they reach age 45.
Irrespective of whether such changes are made to the framework, GPs
with greater awareness of OSA have a crucial role to play in identifying
vocational drivers who may be suffering from OSA, and in ensuring that
their condition is investigated and suitably treated.
Nic Tweddell and Seb Schmoller
Competing interests: No competing interests
Obstructive sleep apnoea may be even more likely, and even less
detectable, among schizophrenics (such as myself). We are notorious for
being difficult patients who do not always conform to medical advice. We
are not readily treated and healed.
The fatal nexus between obstructive sleep apnoea and anti- psychotic
drugs is- the metabolic syndrome (1). The tragic terms reeled off in the
article by West, McBeath and Stradling are unhappily connected to the side
effects of the atypical anti- psychotics in particular: 'obesity ...
hypertension, hyperlipidaemia, insulin resistance, type 2 diabetes, and
the metabolic syndrome, and therefore cardiovascular disease.' (2)
References to obstructive sleep apnoea are not generally found in the
psychiatric literature, with the exception of the radical and sceptical
book by David Healey, 'Psychiatric Drugs Explained' (3).
I would very tentatively suggest this ailment as a possible elephant
in the room. Like a torpedo, it is under the surface, and, like a torpedo,
it can kill. It has not been promptly spotted even though it may be a
cause of the sudden death syndrome among schizophrenics that has been
attributed mostly to cardiovascular disease (4).
Undiagnosed obstructive sleep apnoea could be a potential deadly
bridge between anti- psychotic drugs, cardiovascular disease, and the
unexplained sudden deaths that haunt psychiatric units.
One might consider a case study on a single patient. Alternatively,
there would be a retrospective case- control survey of the incidence of
obstructive sleep apnoea on schizophrenics under psychiatric medication,
perhaps compared to neuroleptic naive patients just diagnosed. Maybe a
grim 'a priori' correlation exists between schizophrenia itself and sleep
apnoea. Any case control analysis is painfully difficult to adequately
Success will not happen without creative linkages across many fields
of medicine. The narrow window of the mere specialist is extremely
inferior to the general perspective(though the latter is far from easy to
(1) The metabolic syndrome and schizophrenia. J.M.Meyer, S.M.Stahl.
Acta Psychiatr Scand 2009: 119: 4-14.
(2)Easily Missed? Obstructive sleep apnoea in adults. Sophie D West,
Helen A McBeath, John R Stradling. BMJ 2009;338:b1165.
(3)Psychiatric Drugs Explained. David Healey. Elsevier. Fifth
Edition. 2009. Chapter 13. Sleep disorders and insomnia. Pg. 173.
(4)Sudden death in psychiatric patients. D. Ruschena et al. BJPsych
(1998), 172, 331-336
Competing interests: No competing interests