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The diaphragm is the main breathing muscle. If the nerve supplying it is damaged, that side stops working and the floppy muscle gets sucked upwards each time you breathe in, squashing the lung above it. Plication stitches the slack diaphragm flat and tight so it stops moving the wrong way. It does not make the muscle work again, but it usually improves breathlessness — especially lying down.
The problem being fixed
The diaphragm generates the majority of tidal volume in quiet breathing. When its motor supply fails, the muscle becomes flaccid and, instead of descending on inspiration, is drawn upward by the negative intrathoracic pressure the other muscles create. This paradoxical motion both fails to contribute volume and actively steals it, compressing the ipsilateral lower lobe and displacing the mediastinum.
Common causes include phrenic nerve injury after cardiac surgery (typically from cold cardioplegia or traction), neuralgic amyotrophy, cervical spine or brachial plexus pathology, malignant infiltration, birth trauma in children, and congenital eventration, in which the diaphragm is thin and elevated without true denervation. A substantial minority are idiopathic.
The clinical picture differs sharply by laterality, and this determines urgency:
| Unilateral paralysis | Bilateral paralysis | |
|---|---|---|
| Typical symptoms | Exertional breathlessness; often minimal at rest. Many are asymptomatic and found incidentally on chest radiograph | Marked orthopnoea, breathlessness at rest, disturbed sleep, morning headache |
| Fall in forced vital capacity, upright to supine | Around 15–25% | Frequently over 30–50% |
| Ventilatory failure | Uncommon in isolation | Common, particularly during sleep |
| First-line management | Observation; many recover over 12–24 months | Non-invasive ventilation, not surgery first |
Making the diagnosis properly
An elevated hemidiaphragm on a chest radiograph is a finding, not a diagnosis — lobar collapse, subpulmonic effusion and eventration all mimic it. The confirmatory assessments a physiotherapist should expect to see, and can help interpret, are:
- Spirometry sitting and supine. A fall in forced vital capacity (FVC) greater than 20% on lying flat indicates significant diaphragmatic weakness, and is the single most useful bedside test.1 It is frequently omitted.
- Maximal inspiratory pressure and sniff nasal inspiratory pressure. Non-invasive global inspiratory muscle measures, interpreted together because each has failure modes.1
- Diaphragm ultrasound — thickening fraction and excursion, increasingly the investigation of choice, being bedside, radiation-free and repeatable.2
- Fluoroscopic sniff test for paradoxical motion, and phrenic nerve conduction studies where the site of the lesion is in question.
Distinguishing recoverable neuropraxia from permanent injury matters, because plication is largely irreversible and spontaneous recovery over one to two years is common after cardiac surgery and neuralgic amyotrophy. Most units therefore wait, unless symptoms are severe or the cause is known to be permanent.
What the operation involves
The redundant diaphragm is folded and sutured under tension — usually thoracoscopically, sometimes open or laparoscopically — to flatten it, lower its resting position and abolish paradoxical movement. Nothing is reinnervated. The lung above it re-expands into the recovered volume, and the chest wall no longer has to work against an upward-moving floor.
In selected patients with bilateral paralysis, diaphragm pacing is an alternative where the phrenic nerve and muscle remain viable, but non-invasive ventilation remains the mainstay.
What plication achieves
Observational series consistently report improvement rather than normalisation. Long-term follow-up in adults with unilateral paralysis showed sustained gains in FVC and FEV1 of roughly 10–20% of predicted, improved dyspnoea scores and durable benefit at five years.3 Systematic review confirms the direction and magnitude across series while noting the absence of randomised comparison.4
Expectation-setting is part of the treatment. The realistic outcome is less breathlessness on exertion and lying flat, not a normal diaphragm or a normal spirogram.
Physiotherapy before and after plication
Before
- Establish the baseline that matters. Upright and supine FVC, inspiratory pressures, exercise capacity and a symptom measure. Repeat over months if surgery is being deferred for possible recovery — the trend is the decision-making information.
- Position for symptom relief. Sleeping more upright, and side-lying on the affected side, often reduce orthopnoea meaningfully.
- Screen for sleep-disordered breathing, particularly with bilateral involvement or a large supine fall — see Non-Invasive Ventilation.
After
- Standard thoracotomy or thoracoscopy care applies — analgesia adequate for deep breathing, early mobilisation, shoulder girdle range of movement on the operated side.
- Expect basal atelectasis above the plication and treat it with volume rather than force: sustained maximal inspiration, positioning and walking.
- Recheck supine spirometry before discharge and at follow-up. It is the objective evidence that the operation did what it was intended to do.
- Inspiratory muscle training has no established role here. The diaphragm is denervated, so loading it cannot strengthen it; any benefit would come from accessory and intercostal muscles, and that has not been tested after plication. If trialled, be explicit that it is empirical.
Role of the physiotherapist
Push for supine spirometry — it is cheap, decisive and frequently missed, and a physiotherapist is often the person who thinks of it. Track the trend across months so that the choice between waiting for recovery and operating is made on data. Afterwards, treat the predictable basal atelectasis, restore shoulder movement, and re-measure supine vital capacity to confirm the mechanical problem has actually been corrected. Be clear with the patient that the aim was to stop the diaphragm being pulled the wrong way, not to make it work again.
Evidence summary
Framing. Plication is a mechanical remedy for a neuromuscular lesion: it abolishes paradoxical motion and lowers diaphragm resting position without restoring contractile function. Evidence is observational and consistent, and the principal clinical decisions — whom to operate on and when — turn on distinguishing recoverable from permanent denervation.3,4
Evidence — assessmentThe European Respiratory Society statement on respiratory muscle testing supports supine–upright spirometry, maximal inspiratory pressure and sniff nasal inspiratory pressure as complementary non-invasive measures, with a supine FVC fall above 20% indicating significant diaphragmatic weakness.1 Diaphragm ultrasound (thickening fraction, excursion) has become the preferred bedside imaging modality and correlates with functional measures.2
Evidence — plicationLong-term adult follow-up after plication for unilateral paralysis reported sustained improvement in FVC, FEV1 and dyspnoea to five years.3 Systematic review across series found consistent physiological and symptomatic gains with acceptable morbidity, but no randomised comparison against conservative management, and heterogeneous selection.4 In bilateral disease, non-invasive ventilation remains first-line and plication is adjunctive.5
Physiotherapy implicationsPerform and advocate supine spirometry; it is the most informative and most neglected measure in this population. Serial measurement over 12–24 months informs the wait-versus-operate decision after cardiac surgery or neuralgic amyotrophy. Post-operatively, anticipate basal atelectasis and treat with volume-based techniques and mobilisation. Do not present inspiratory muscle training as evidence-based after plication — the target muscle is denervated and no post-surgical data exist.
Evidence gapsNo randomised trial compares plication with conservative management, and selection criteria vary widely between series. Optimal timing after phrenic injury is undefined. No study has examined physiotherapy content or dose after plication, and the role of inspiratory muscle training in diaphragmatic paralysis, with or without surgery, is unresolved.
References & evidence base
- Laveneziana P, Albuquerque A, Aliverti A, et al. ERS statement on respiratory muscle testing at rest and during exercise. Eur Respir J 2019;53(6):1801214.
- Boussuges A, Rives S, Finance J, Brégeon F. Assessment of diaphragmatic function by ultrasonography: current approach and perspectives. World J Clin Cases 2020;8(12):2408–2424.
- Freeman RK, Van Woerkom J, Vyverberg A, Ascioti AJ. Long-term follow-up of the functional and physiologic results of diaphragm plication in adults with unilateral diaphragm paralysis. Ann Thorac Surg 2009;88(4):1112–1117.
- Kokatnur L, Rudrappa M. Diaphragmatic palsy. Diseases 2018;6(1):16.
- Ricoy J, Rodríguez-Núñez N, Álvarez-Dobaño JM, Toubes ME, Riveiro V, Valdés L. Diaphragmatic dysfunction. Pulmonology 2019;25(4):223–235.
References are numbered in citation order (Vancouver/BMJ style) and were current at the time of writing. Guidelines are living documents — verify against the latest version before clinical use.
Physiotherapy around major chest, cardiac and upper abdominal procedures — from open surgery to bronchoscopic, catheter-based and bedside treatments — aims to reduce chest complications and shorten the return to normal function.
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