Capsular Contracture Management

Capsular contracture (CC) remains a leading cause for reoperation after breast reconstruction. The cause of CC is likely multifactorial, and there are many working theories in the current peer-reviewed literature related to causes. There are several modifiable risk factors for CC as well. Techniques such as capsulotomy and capsulectomy are employed, with capsulotomy often preferred for its shorter duration and quicker recovery, especially in cases with thinner capsules. Although capsulectomy is the gold standard, it poses greater risks. Despite potential improvements in esthetics and quality of life, reoperations carry risks of complications, including bleeding and further distortion of breast architecture.

Key points

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Capsular contracture is a common complication following implant-based breast reconstruction and augmentation.
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The genesis of capsular contracture is secondary to an inflammatory response to the implantation of a foreign body with the natural breast anatomy.
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Pharmacologic interventions (antimicrobials and leukotriene antagonists) and superior surgical technique may be used to attempt to prevent the formation of capsular contracture perioperatively.
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Prior capsular contracture increases the patient’s risk of having subsequent capsular contracture after surgical correction of the initial contracture event.
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Many novel technological and surgical advancements using implantable scaffolding show promise in the prevention and treatment of capsular contracture.

Abbreviations

ADMs	Acellular Dermal Matrices
BII	Breast Implant Illness
CC	Capsular Contracture
HOCl	Hypochlorous Acid
TAS	Triple Antibiotic Solution
TLRs	Toll-Like Receptors

Introduction

Capsular contracture (CC) is a common complication following implant-based breast augmentation. Soft, thin capsule formation around the implant is expected due to the immune system reacting to foreign body placement. CC occurs when this response is exaggerated, causing increased thickening and fibrosis of the capsule that may lead to hardening, breast shape distortion, and pain. ^,^, The mechanism of contracture is not well-understood, although over the last 50 years both etiology and epidemiology have been studied extensively with likely several overlapping causes identified, such as immunobiological, patient-specific, and implant-related risk factors. ^, Implant material and texture, as well as location of access incision, have been shown to be associated with rate of CC. ^, CC severity is evaluated through the widely accepted Baker Scale, with criteria evaluating pain, appearance, and breast firmness. ^,

Etiology

Although the etiology is likely multifactorial, the cornerstone of CC genesis is thought to be chronic inflammatory reaction. The first and most commonly accepted reason for CC is the immune response to the implant as a foreign body. From a pathophysiological perspective, the innate immune system is thought to elicit CC formation, with macrophages secreting interleukin-8 and tumor necrosis factor-α, which have been associated with more severe Baker grade contractures. Additionally, transforming growth factor (TGF)-beta release from mast cells has been studied as the instigator of phosphorylation cascades that lead to CC. Mast cells may also play a role in activating fibroblasts to secrete collagen via paracrine signaling. Fibroblasts are numerous within the capsule, and it has been found that as CC worsens, the collagen fibers increase in diameter and orient themselves into a helical orientation that thickens the capsule. Although not well understood, Toll-like receptors (TLRs), which are activated by recognizing invading pathogens or endogenous signals, have been reported to be present in all grades of Baker contracture. It is unclear whether bacteria (pathogen-associated molecular patterns [PAMPs]), damage-associated molecular patterns (DAMPs), or genetics are the main triggers for TLR activation. Moreover, there are several other intracellular pathways that drive specific immune responses and would need to be investigated to pinpoint the exact pathway that drives CC formation. ^,

Another studied theory of CC development is subclinical bacterial infection of the surgical site that leads to biofilm formation on the implant. Propionibacterium acnes , Escherichia coli , Staphylococcus aureus , and Staphylococcus epidermidis (most common) are some of the species of bacteria that have been cultured from patients undergoing revision breast surgery after CC. These bacteria may enter the breast pocket via implant insertion by the surgeon or from the skin surface or breast gland tissue. The implant itself has a large, hydrophilic surface that allows biofilms to form. Biofilms are defined as bacteria that adhere to a prosthetic surface and each other via an extracellular matrix. Although bacteria like E coli and S epidermidis may be susceptible to antibiotics, biofilms are known to persist despite antibiotic treatment and elicit an immune response. This response is similar to the one discussed earlier; with the difference being that the fighting off of the infection causes the secretion of inflammatory signals leading to an excessive fibrotic reaction and capsule formation. ^, Notably, there are arguments against this proposed etiology of CC given that bacteria has been found on implants that have not been complicated by contracture, suggesting that there is some mechanism that converts this benign bacteria presence to a pathologic one. However, pathogenesis could simply be due to increased bacterial load. Histologically, studies show that CC has maximum collagen density at 5 years postsurgery, which may also contradict that infection has to be present as the timeline is too long, unless it is a chronic infection. ^, Moreover, a 2013 cohort study showed that the rates of CC in patients treated with triple antibiotic irrigation therapy versus those who were not, did not have statistically different rates of CC. There is the suggestion that biofilm formation may increase the rate of CC but is not the main cause, as a fibrotic response will happen with or without infection present. ^,

Plane choice in alloplastic breast augmentation may also increase the risk of CC. It was found that the rate of CC was 3 times higher with more severe correlating Baker grade in subpectoral implant patients compared to those who received prepectoral placement. This is thought to result from the disruption and increased scarring of the pectoral muscles in the subpectoral position. ^, The longer the implant has been in place correlates to an increased risk of CC. ^,^, Subglandular placement is correlated with increased capsular formation and contracture compared to the subpectoral placement in breast augmentation patients; however, there has been no demonstrated increase in risk with subfascial placement. ^,^, A large systematic review and meta-analysis of subfascial implant placement demonstrated that subfascial augmentation offers the advantage of lower CC rates, while also preventing the discomfort and potential animation deformity associated with subpectoral augmentation. Histologically, collagen content does not differ greatly from patients who did not have radiation, although there was an observed increased quantity of elastin and cellular infiltrates. ^,

Hematoma formation and different types of implant shell surfaces have also been studied as potential instigators of CC development. ^,^, There have been several studies on the rate of CC in patients who receive smooth versus textured implants. Smooth implants have thinner capsules and easily change position in the breast. Textured implants have a thicker capsule and rougher surface that keep them stationary within the breast pocket. The surface also integrates with the natural breast tissue. A 1993 study found a statistically significant decrease in CC favoring textured silicone implants (21% for smooth vs 4% rate of CC in textured). However, various following studies report different results. For example, a 1997 study suggested that there was no difference in incidence of CC between smooth and textured saline implants. Recently, a 2022 article looking at 506 implants reported that there was no difference in CC rate with smooth versus textured implants, but the subfascial plane patients had a statistically significantly greater rate of contracture with smooth implants. Lastly, TLR-4 and CD90 expression and previous episodes of fibrosis are risk factors for CC. There are also modifiable risk factors that increase the incidence of CC, including smoking in both the preoperative and postoperative period, as well as incision choice by the surgeon, with inframammary fold incision posing the lowest risk of developing CC in the breast. ^,^,

Clinical presentation

Since 1978, the main grading criteria for evaluating CC has been a subjective system called the Baker Scale. The originally invented scale with grades I through IV is most widely used to evaluate CC associated with breast augmentation ( Table 1 ). Grade I contracture is asymptomatic with the breast maintaining its natural texture and soft feel. Grade II exhibits breasts that are increasingly firm; however, the patient does not have pain. In grade III, there is minimal discomfort, but the patient can feel the capsule. At this point, the breast may look harder and rounder, and the nipple contour may change. Severe contracture is categorized by grade IV, which causes the breast to be tender and painful. The contracture is visible from the outside, and the breast is hard and tense to the touch. There are some limitations when extrapolating use of this scale when assessing patients who have undergone breast augmentation. For example, there is some degree of firmness that is associated with the implant itself, which may lead the original criteria to misclassify certain breasts as having contracture.

Table 1

Baker scale for capsular contracture after breast augmentation

Class	Baker Scale Physical Findings	Patient Symptoms	Reoperation
I	Completely natural appearing breast	None	Not indicated
II	Minimal contracture present, patient does not feel	None	Not indicated
III	Moderate contracture, patient can feel	Symptomatic	May be indicated
IV	Severe contracture obvious, patient can feel painfully	Symptomatic	Required

Management

Perioperative Interventions

Over the years, several studies have investigated pharmacologic and nonpharmacologic measures at all stages of operation to prevent CC. Antimicrobial agents have been evaluated extensively, as one of the main theories of the basis of CC is bacterial biofilm formation and surgical site infection due to S aureus or even methicillin-resistant S aureus . Topical antiseptics applied preoperatively have been shown to decrease the rate of CC, with chlorhexidine gluconate proving more effective than povidone-iodine. Perioperatively, a triple antibiotic solution (TAS), which consists of bacitracin, Ancef, and gentamicin irrigated into the breast pocket for 5 minutes, was associated with lower rate of contracture. Betadine, which had the warning removed by the Food and Drug Administration in 2017 regarding its risk with implants, is also considered to be antimicrobial and can be used interchangeably or simultaneously with TAS. Similarly, leukotriene antagonists (eg, montelukast and zafirlukast) have been used to reduce CC rates. Glucocorticoids, antifibrotic drugs, and nonsteroidal anti-inflammatory drugs have also been shown to decrease inflammatory and foreign body response to implant placement. While preoperative 1 time doses of cefazolin is common practice, postoperative administration, implant-grafted drug substances within the shell or the filler, and irrigation of the implant prior to placement are other antibiotic administration methods being evaluated. ^, Pocket irrigation with hypochlorous acid (HOCl) has also been proposed by some, with one study demonstrating a significant decrease in the incidence of CC after 1 year. Similar to other irrigants, HOCl kills pathogens via oxidative damage and inhibition of cell growth locally.

Material modifications to the breast implant itself have also been reported to prevent CC. Biological matrices (eg, acellular dermal matrices [ADMs] and polymeric meshes) and synthetic meshes (eg, vicryl and TIGR matrix) placed around the implant are routinely used to decrease incidence of CC. Zwitterionic polymers are another type of biomaterial being studied for this purpose as well. With respect to surgical techniques, the “no touch” method using an insertion funnel limits bacterial growth and contact once the surgeon removes the implant from its packaging. In the actual surgery itself, the periareolar approach versus inframammary approach for implant placement is associated with a higher incidence of grade III and IV CC.

The use of nipple shields has also been advocated in breast surgery since the late twentieth century, although no concrete evidence to date demonstrates a decrease in infection risk. The most common technique remains covering the nipples with a clear occlusive dressing, with this dressing demonstrating positive bacterial contamination in several studies when cultures were taken of the dressing after removal. ^,^, Similar to the concern for seeding the breast pocket with skin flora, the no-touch technique has been developed to minimize this risk. ^, Innovations such as the breast-implant funnel have been popularized in the last decade in order for the surgeon, and patients skin, to avoid ever touching the implant.

Although commonly used in practice, the use of postoperative drains has also demonstrated significant increase in the risk of postoperative infection and contamination of the breast pocket in several studies. This may be a source of seeding for the development of CC, and some surgeons have begun to advocate for a drainless technique. Should a seroma develop, these can be serially aspirated with the aid of ultrasound.

Operative Intervention

Since CC has been one of the leading causes for reoperation after breast implant placement for decades, the focus on reoperative success is rightfully emphasized. With hopes of effectively addressing the breast (or breasts) affected by CC, initial surgical intervention includes techniques like capsulotomy, open partial capsulectomy and total capsulectomy as potentially effective means of addressing the affected capsule. Capsulectomy takes more time due to length of dissection (often an additional hour compared to unilateral capsulotomy). Removal of excess tissue can be difficult and also cause complications due to resulting lack of tissue cover for the implant and risk of pneumothorax in the case of implants in the subpectoral plane.

Capsulotomy is another option for treatment of CC and is technically less challenging to perform than capsulectomy. While older articles, such as Young and colleagues in 1998, report higher rates of CC recurrence with open capsulotomy, Swanson and colleagues in a retrospective study from 1996 to 2016 of open capsulotomies reported recurrence rates after capsulotomy of 22.7% and 25% to 53.4% for capsulectomy. As such, for patients who have thin capsules from saline implants, especially in the submuscular plane, capsulotomy is often suggested because the capsule can be resorbed naturally with low associated seroma rate. Capsulectomy can be used for thicker capsules that exhibit visible calcification. In addition to thin capsules, other relative contraindications to total capsulectomy include thin mastectomy flap (risk of mastectomy flap compromise) and cases when a capsular flap is needed to improve implant malpositioning or esthetic outcome, such as correcting the inframammary crease. ^,

Occasionally, the senior author may initially attempt capsulotomy without removing the implant. Fat grafting with capsulotomy has been shown as an effective means of addressing the contracted capsule without having to remove or replace the implant. This technique involves addressing the patient’s pain level while simultaneously working to correct the cosmetic alterations imposed by CC. Lipofilling in and around the contracted capsule has been shown to aid in relieving the pain caused by CC as well as addressing some of the misshapen architecture that is present in the breast tissue. This technique has been demonstrated to allow patients to achieve pain relief as well as moving their breasts toward a less severe Baker classification of capsular contraction. Therefore, the cosmetic and quality of life improvements that result from this approach significantly decrease the need for the replacement of an alloplastic prosthesis.

If more conservative measures like these fail, patients can agree to subsequently undergo capsulectomy that includes removing a portion or the entirety of the offending capsule. Once the contracted capsule has been addressed, surgeons, as is deemed technically relevant, can choose to exchange implants, alter implant size, revise with mastopexy, apply internal structural support with sutures, or even graft autologous tissue as a means to pursue ideal surgical outcomes. Revisional mastopexy is a viable alternative to the reintroduction of implants. ^,^,^,^,

Kühn and colleagues demonstrated that CC is strongly correlated with a desire for implant replacement and implant removal. Notably, this study found that patients with more severe contracture (ie, Baker III and IV) desired implant replacement more often when compared with patients with lesser degrees of contracture that desired permanent implant removal. Nonetheless, this study demonstrated a significantly larger portion (77.5%) of revisional procedures addressing CC involved implant replacement.

CC is also thought to exacerbate instances of breast implant illness (BII), leaving many patients to favor explanation and concomitant capsulectomy. BII refers to a constellation of systemic symptoms reported by some individuals with breast implants including fatigue, arthralgias, myalgias, cognitive difficulties, psychiatric disturbances, and various other widespread complaints. The underlying mechanisms of BII remain unclear, though it is believed to involve immune system reactions, potentially linked to biofilm formation on implants and subsequent immune activation. A review of 31 studies involving 39,505 breast implant patients demonstrated 72.4% of patients elected to have their implants removed, and 83.5% of those who underwent explantation reported improvement in symptomatology. Of note, 53% of patients who had their implants removed also elected to receive a total capsulectomy. Recent data even demonstrate a lack of significant difference in systemic symptom improvement for patients that undergo explantation with or without capsulectomy (partial and total), further highlighting the nuance that goes into surgical management of CC. ^,^,^,

Postoperative

To reduce the risk of CC both after the index operation and corrective surgery, patients may employ several interventions to prevent or reduce risk of recurrence. First and foremost, smoking cessation is of utmost importance, as this has been demonstrated as having positive correlation to the development of CC, with many arguing for at least 4 weeks preop, and 4 weeks of postoperatively smoking and nicotine cessation. Patients may also need to be counseled that common over-the-counter vape products also contain nicotine and can be harmful to the breast capsule. ^, Massage techniques such as gentling massaging the implant in the pocket for 5 minutes, 2 to 3 times per day, starting as early as 2 weeks postoperatively. Several studies have investigated earlier massage, as early as 2 days postop; however, there are no significant data to demonstrate any difference in the development of CC in these patients. In fact, to date, there has been no study that has demonstrated a meaningful reduction in CC when comparing patients that undergo implant massage to those that do not. Massage technique remains controversial for this reason but proves no additional risk and has the added benefit of patient comfort in actively participating in their care.

Postoperative pharmacologic prophylaxis has gained additional headway. Many surgeons have begun prescribing Montelukast or Zafirlukast in the postoperative period to prevent capsular inflammation and long-term contracture. Several series have been published demonstrating that 20 mg Zafirlukast or 10 mg Montelukast twice a day for 3 months has been beneficial in producing a soft capsule. In addition to the use of antimicrobial irrigants intraoperatively, some surgeons have been anecdotally treating patients with up to 3 months of oral doxycycline, supplemented by vitamin E to bolster immune response and protect the breast capsule from bacterial growth. ^,

Challenges

While the aforementioned approaches do have potential to correct contracture, they are not without complication. For any reoperation of the breast and surrounding tissue, there are always risks of complications and no guarantee that the next outcome will be more favorable than the last. The primary operation has likely distorted some breast architecture, affected skin integrity and created scar tissue burden that will certainly be encountered in a reoperation to address CC. Notably in patients that have had implants for a longer duration, anatomic changes and skin distortion contribute to possible capsular formation over time. As has been shown, the risk of developing CC is most likely during the first year, but the overall occurrence of this complication increases over time. This likely has implications for surgical success when addressing CC. Let it also not be lost that the secondary or tertiary operations done to address the contracted capsule are many times not done by the same surgeon who performed the initial operation. This poses another unique challenge especially if the original techniques performed are not known.

Similarly to the initial surgical intervention, these corrective methods can still lead to bleeding, further distortion of breast architecture, rupture of implant, infection, patient dissatisfaction, and recurrence of CC. Recurrence of CC after one of the aforementioned interventions has been demonstrated to be as high as 30%, as patients with previous CC are at an increased risk to develop the condition again. ^,

For particularly difficult or more affected capsules, there are special risks to consider. Patients that experience contracture after a submuscular implantation may have a capsule that is firmly attached to the chest wall. Dissection of this capsule requires careful and precise surgical intervention, posing a risk of damaging axillary structures or intercostal musculature, causing a pneumothorax, or even inciting major bleeding. These adverse effects can ironically increase the risk of future contraction of the breast capsule.

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