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Abstract
A woman in her mid-70s presented with worsening dyspnoea, cough and fatigue initially treated for pneumonia. Despite antibiotics, her condition deteriorated, prompting further investigation. Medical history included previous breast implants, the latter of which had ruptured years earlier and was subsequently removed prior to the current presentation. Imaging revealed bilateral lung consolidations and lymphadenopathy. Bronchoalveolar lavage indicated macrophagic alveolitis, while biopsies showed chronic inflammation and the presence of silicone. Diagnosis of chronic pulmonary silicone embolism was made, a rare condition linked to the migration of silicone particles into the lungs, causing inflammation. Treatment involved corticosteroids, leading to symptom resolution. This case highlights the diagnostic challenges of silicone pneumonitis, which can manifest years after implant rupture and removal. Clinicians should be aware of this condition to avoid misdiagnosis and delayed treatment, as symptoms may persist even after implant removal due to irreversible lung fibrosis.
- Interstitial lung disease
- Global Health
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Background
Silicone breast implants are widely used for both cosmetic enhancement and reconstructive surgery, with millions of procedures performed globally each year. Despite their popularity, concerns regarding the long-term safety of silicone implants have emerged, including complications such as chronic pulmonary silicone embolism (CPSE). This condition, while rare, can develop years after implant rupture and removal, leading to significant respiratory issues that are often misdiagnosed.
CPSE presents a unique challenge for physicians, as its symptoms—including dyspnoea, cough and fever—are non-specific and may mimic other pulmonary diseases. The diagnosis is complicated further by the delayed onset of symptoms, often occurring years after the initial surgical procedure. This case underscores the importance of recognising the potential for silicone-related lung complications in patients with a history of breast implants, especially when conventional treatments fail.
The key message of this manuscript is the need for heightened awareness among clinicians regarding CPSE as a potential cause of respiratory disease in patients with a history of breast implants. Early consideration of this diagnosis may facilitate timely management and improve patient outcomes.
Case presentation
A woman in her mid-70s was referred to the emergency department with worsening dyspnoea, persistent dry cough and asthenia. Her general practitioner suspected pneumonia and started antibiotic therapy with co-amoxicillin 1 g three times a day for a total of 7 days, which ended 4 days before admission. Medical history was relevant for ischaemic heart disease with two coronary stents, atrial fibrillation anticoagulated with rivaroxaban and bilateral breast implants inserted 50 years ago. The last prosthetic replacement was 20 years ago, and both breast implants have definitively been removed 1 year ago following invasive carcinoma of the right breast, now considered to be in remission. She also has Poland syndrome, a rare congenital malformation consisting of partial or complete agenesis of the pectoralis major muscle and of the breast resulting in pectus excavatum for which she had undergone multiple interventions and reconstruction with a silicone implant 50 years ago (figures 1 and 2).
Patient’s first CT showing multiple bilateral peripheral condensations.
Patient’s second CT, 7 days later, showing an increase in the extent of bilateral peripheral pulmonary condensations, with the appearance of adjacent ground-glass areas.
On evaluation, the patient was irregularly tachycardic at 102 beats per minute with normal blood pressure and afebrile. The respiratory rate was 16 breaths per minute with a peripheral oxygen saturation of 92% on room air. Pulmonary auscultation revealed coarse rales up to the right mid-pulmonary fold. Blood tests showed elevated C-reactive protein (108 mg/L), normal white cell count and negative procalcitonin (0.06 ug/L). A chest CT scan (figure 1) showed multiple bilateral peripheral condensations, predominantly on the right, suggestive of pneumonia and a pre-sternal silicone implant. Ceftriaxone 2 g once daily and clarithromycin 500 mg twice daily were started, and the patient was admitted to the internal medicine ward.
The clinical course was unfavourable with the development of hypoxemia requiring supplemental oxygen (2 L/min) and fever, as well as the persistence of the inflammatory syndrome. Antibiotic therapy was switched to piperacillin-tazobactam 4.5 g three times a day.
Investigations
PCR testing on nasopharyngeal swabs for Chlamydia pneumoniae, Mycoplasma pneumoniae, influenza A and B, respiratory syncytial virus, SARS-CoV-2 and a complete respiratory panel (adenovirus, bocavirus, coronavirus 229E, HKU1, NL63, OC43, human metapneumovirus, parainfluenza 1–4, rhinovirus, Bordetella pertussis) were negative. HIV screening test was negative. Laboratory tests for anti-neutrophilic cytoplasm antibody, anti-nuclear factor, rheumatoid factor and anti-ribonucleoprotein antibodies were negative.
A chest CT scan at day 7 (figure 2) showed a worsening of bilateral peripheral pulmonary condensations with the appearance of adjacent ground-glass areas. There were also multiple axillary lymph nodes and bilateral internal mammary chains with a reactive appearance.
Cryptogenic organising pneumonia was suspected and indicated bronchoalveolar lavage (BAL) and transbronchial biopsies (TBBs). BAL fluid was dominated by macrophages (92%) without significant alteration of cell distribution. Bacteriological, fungal, mycobacterial and legionella species cultures were negative.
Histo-pathological analysis of the TBBs showed a foreign body type gigantocellular reaction on the material of exogenous, globular, transparent appearance suggesting silicone (figure 3a). Focally in the surrounding area, intraluminal fibrin balls associated with fibromyxoid plugs and chronic pneumonitis were noted, suggesting acute fibrinous and organising pneumonia (figure 3b).
Histo-pathological analysis of the transbronchial biopsies showing a foreign body type gigantocellular reaction, partly on material of exogenous appearance suggesting silicone (arrow, 3a). Intraluminal fibrinous plugs with chronic pneumonitis suggesting acute fibrinous and organising pneumonia (circle, 3b) in close association with giant cell containing exogenous material suggesting silicone (arrow). HE, 20x
Treatment, outcome and follow-up
The catamnesis revealed that the left breast implant, which had been replaced 20 years ago, ruptured during a cardiac massage because of acute myocardial infarction 10 years before removal. Two breast MRI studies that had been performed before removal revealed an intracapsular rupture of the left retro-pectoral breast prosthesis associated with axillary and intramammary adenopathy. A breast MRI carried out just before removal had shown multiple left axillary lymph node silicomas associated with the previous rupture. Thus, the patient had been wearing the ruptured left breast implant for 5 years before it was replaced and finally removed 1 year before actual presentation. The pre-sternal implant shows no signs of rupture. She had no history of silicone injections and no other significant past exposure.
The patient was started on prednisone (1 mg/kg). The oxygen was rapidly weaned off, the fever resolved, the inflammatory syndrome regressed and the patient was discharged 3 weeks after admission in good general condition.
During follow-up, the patient describes a clear improvement in her general condition and dyspnoea, which unfortunately persists on exertion and remains disabling. A follow-up chest CT (figure 4) performed 4 months after hospitalisation showed complete disappearance of pulmonary condensations and ground glass opacities.
Patients’s follow-up CT, taken 4 months after the introduction of corticosteroid therapy, showing resolution of bilateral peripheral pulmonary condensations and adjacent ground-glass areas.
Discussion
We present the case of a patient with subacute, worsening dyspnoea, inflammatory syndrome associated with radiologically progressive multifocal pneumonitis leading to respiratory failure, several years after a documented rupture of a breast prosthesis and its removal before the onset of symptoms. To our knowledge, only seven cases of pathologically confirmed pneumonitis due to CPSE have been reported.1–6
In USA, it is estimated that 1% of women have breast implants, which represents 3.5 million people.7 It is the second most frequently performed plastic and reconstructive surgery procedure, and it is estimated that 2.2 million breast augmentations were performed worldwide in 2023.7 Silicone implants are widely used for cosmetic and reconstructive purposes because of the presumed benign nature of the substance and its lack of immunogenicity.2 Safety of silicone implants became a concern after the first case of silicone pneumonitis reported in 1976.2 8 Concerns about their safety are rising as the prevalence of all-type complications (auto-immune diseases, hypersensitivity reactions, granulomas, lymphadenopathy) is approximately 20%, according to the Food and Drug Administration (FDA).9 10 The actual incidence of pulmonary silicone pneumonitis is unknown.9 The main pulmonary vascular complication is acute or chronic pulmonary silicone particles embolization.9
The majority of pulmonary complications associated with silicone injection are due to acute pulmonary silicone embolism. This rare but well-known entity occurs within 72 hours of the injection of subcutaneous liquid silicone, which is currently prohibited by the FDA.1 6 8 9 11–13
CPSE is even rarer and occurs years after implants’ insertion, most often in patients with a history of prosthetic rupture, as in our patient’s case.3 4 9 The prevalence of CPSE in women with breast augmentation is unknown.1 These pulmonary complications are a real diagnostic challenge since the clinical and radiological manifestations occur years after initial implantation and diagnosis is often delayed.10 The clinical presentation (dyspnoea, cough and possibly fever) is not specific. In most cases, infectious pneumonia is first suspected, and silicone pneumonitis is later considered after several courses of antibiotics and multiple investigations.9 Imaging often reveals diffuse ground-glass opacities with condensations, also opening the way to a broad differential diagnosis, including infections and organising pneumonia.1 2 9 Diagnosis is confirmed by the presence of silicone surrounded by inflammation on lung biopsy.1 2 9
The pathophysiological hypothesis of silicone pneumonitis is the migration of microdroplets through the blood and lymphatic circulation to the lungs, creating inflammation around foreign bodies, mimicking interstitial lung disease.1 4 6 9 The histo-pathological features are clear, non-birefringent globules characteristic of silicone emboli, silicone plaques or translucent vacuolated globular deposits of silicone.1–3 5 6 8 In our case, histo-pathological examination showed a foreign body type gigantocellular reaction, partly on the material of exogenous, globular, transparent appearance suggesting silicone, consistent with findings in the literature (figure 3).
The diagnosis of silicone pneumonitis can easily be missed. The distribution of silicone in the lung is probably not homogeneous, and biopsy may reveal only an aspecific inflammatory reaction, which would be classified as idiopathic fibrosis. We believe that this diagnosis should be considered in patients with a history of prosthesis presenting with unclear pulmonary disease.
Treatment is based on corticosteroid therapy and ventilatory support with oxygen therapy when necessary. In most cases described in the literature, the silicone implants have been removed, with no improvement in symptoms due to the irreversible fibrotic process that had set in.3 4 8
Patient’s perspective
So first I had breast cancer, which left me devastated and tired, and for which I had a long course of treatment and surgery. Then I was hospitalised for pneumonia.
I couldn’t eat, I was breathless without getting out of bed and I couldn’t make any effort, I even needed oxygen to breathe. First, I had antibiotics, which had no effect on the illness.
I didn’t know that the silicone in my implants could be the cause of my symptoms and my illness. I would have liked to have been warned of this risk when the prostheses were implanted. Nobody told me.
Since I’ve been taking the cortisone, I feel much better. It’s like night and day. Now I can walk and build up my leg muscles again, I’ve been able to eat again and I’ve been able to sleep.
As soon as I walk for more than 10 min, I have to stop because I’m out of breath and I have a cough with persistent sputum.
The cortisone is being gradually and very slowly reduced and I’m coping well with it.
I’d like to be able to do without cortisone in the long term, but I don’t know if that will be possible.
I’ve also had side-effects from cortisone: oral candidiasis and shingles, so I’d prefer to be able to stop this treatment 1 day.
I’m glad that my case can help other doctors to help patients who have the same thing as me.
Learning points
Diagnosis of silicone pneumonitis years after a documented breast rupture remains a challenge due to the lack of specificity of the clinical-radiological presentation and is easy to miss.
Chronic pulmonary silicone embolization after breast implant rupture is a rare and probably underdiagnosed cause of acute fibrinous organising pneumonia.
This is essential that clinicians and pathologists are familiar with this pathology to avoid delayed or missed diagnoses.
In most of the cases described, the symptoms improved with corticosteroid therapy, but the fibrosing sequelae are irreversible even after the removal of the causative agent (implant).
Ethics statements
Patient consent for publication
Footnotes
Contributors CVG wrote the first version of the manuscript. SY provided the histopathological images and their interpretation. All authors read and approved the final version of the manuscript. POB supervised the writing of the manuscript and is its guarantor.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.