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Pectus excavatum: Etiology and evaluation

Pectus excavatum: Etiology and evaluation
Author:
Oscar H Mayer, MD
Section Editor:
Gregory Redding, MD
Deputy Editor:
Alison G Hoppin, MD
Literature review current through: Jan 2024.
This topic last updated: Oct 09, 2023.

INTRODUCTION — Pectus excavatum (PE), or "funnel chest," is a deformity of the chest wall characterized by a sternal depression (picture 1). The clinical significance of PE depends on three issues:

Severity of the chest wall defect

Cardiopulmonary morbidity

Psychosocial impact, because the defect alters the patient's appearance

Despite decades of experience with surgical and nonsurgical treatment and efforts to quantify outcomes in each of these areas, the decision of when and how to treat PE remains controversial. These issues are discussed in a separate topic review. (See "Pectus excavatum: Treatment".)

This topic review will discuss the epidemiology, clinical features, and evaluation of PE.

The diagnosis and treatment of pectus carinatum (in which the sternum protrudes above the chest) and other chest wall deformities are reviewed separately. (See "Pectus carinatum and arcuatum" and "Chest wall diseases and restrictive physiology".)

DEFINITION — Pectus excavatum (PE), or "funnel chest," is a deformity of the chest wall characterized by a sternal depression typically beginning over the midportion of the manubrium and progressing inward through the xiphoid process (picture 1). The deformity may be symmetric or asymmetric.

EPIDEMIOLOGY — PE accounts for 90 percent of anterior chest wall disorders [1]. The incidence of PE is 1 in every 400 to 1000 live births [1,2]. It is three to five times more prevalent in males than females. It is usually sporadic but may be associated with connective tissue disorders, neuromuscular disease, and some genetic conditions. (See 'Etiology' below.)

ETIOLOGY — While there is no consensus for what causes PE, there have been a number of hypotheses, ranging from disproportionate muscular force putting abnormal stress and strain on the sternum and costal cartilages, to defective cartilage structure and growth, abnormal rib growth, or combinations thereof [3].

An early theory that PE is caused by abnormal diaphragmatic connections was discarded because surgical interventions to release the central tendon and substernal ligament in early childhood were not effective [4]. (See "Pectus excavatum: Treatment", section on 'Historical approaches'.)

PE is usually sporadic [1], but it has been associated with connective tissue disorders (particularly Marfan syndrome, Ehlers-Danlos syndrome, and osteogenesis imperfecta) [5,6] and neuromuscular disease (eg, spinal muscular atrophy). It also can be seen in a variety of other genetic conditions, including Noonan syndrome, Turner syndrome, neurofibromatosis type 1 and multiple endocrine neoplasia type 2b [7,8]. (See "Genetics, clinical features, and diagnosis of Marfan syndrome and related disorders".)

The increased prevalence of PE in connective tissue disorders suggests the possibility that it is caused by abnormal cartilage development [9]. In particular, some authors have hypothesized that the deformity is caused by abnormalities of cartilage remodeling due to an imbalance between cartilage growth-promoting and growth-inhibiting genes [1]. Genetic contributors to PE seem likely, and familial patterns of inheritance have occasionally been reported [10,11]. Several different genes affecting cartilage growth are associated with syndromic causes of PE (eg, fibrillin1 gene in Marfan syndrome and genes in the RasMAPK pathway in Noonan syndrome). However, no specific genetic triggers for abnormal cartilage growth in nonsyndromic (isolated) PE have been identified [12]. Cartilage samples from patients with PE have normal histology [9].

PE may also occur in response to underlying pulmonary conditions. Patients with a repaired congenital diaphragmatic hernia are prone to PE, presumably because the axis of contraction of the diaphragm is more horizontal than vertical, so that the diaphragm pulls the lower edge of the sternum inward [9]. Patients with spinal muscular atrophy type 1 are also prone to developing PE, presumably because the chest wall is highly compliant and unable to resist intrapleural pressure variation during respiration; these forces gradually deform the sternum over time. PE also can occur in children with subglottic stenosis and bronchopulmonary dysplasia [13]. The proposed mechanism is that the chronic abnormal negative intrathoracic pressures in these conditions contribute to the development of PE in infants, whose chests walls are compliant. It is possible that this mechanism also applies to young children with obstructive sleep apnea, based on limited evidence [14]. (See "Congenital diaphragmatic hernia in the neonate" and "Spinal muscular atrophy".)

NATURAL HISTORY — Information on the evolution of untreated PE is based upon limited retrospective data and reports of clinical impressions [15-17]. The following observations are generally accepted:

Approximately one-third of cases of PE present in infancy [9].

Spontaneous regression of PE in infancy has been reported but is rare [2]. The frequency of spontaneous improvement decreases even further after one year of age, and no spontaneous improvement can be expected after six years of age.

After 12 years of age, the PE deformity worsens in one-third of patients during the adolescent growth spurt and remains the same in two-thirds [15,18]. There are no reliable markers to predict progression.

As PE worsens, simple symmetrical lesions may progress to more complex asymmetric deformities [18-21].

No debilitating physiologic disabilities or deaths have been attributed to PE in children or young adults [15]. In adults, complaints of exercise intolerance are common; no deaths have been attributed to the isolated deformity.

CLINICAL FEATURES

Cosmetic concerns — Concerns about physical appearance are common among patients with PE who seek medical attention [1,2]. Female patients are more likely to express concern over their appearance than male patients (68 versus 40 percent) [22]. However, there is poor correlation between the severity of PE and concern about appearance [22]. One longitudinal study suggests that cosmetic concerns subside over time: Among patients with mild PE who did not undergo surgery, the concern about appearance usually subsided by 18 to 20 years of age [23].

Symptoms — Among a large group of patients evaluated for severe PE, most of whom were in the pediatric age range, the following symptoms were reported [24]:

Exercise intolerance – 82 percent

Chest pain – 68 percent

Poor endurance – 67 percent

Shortness of breath – 42 percent

In a separate study, similar frequencies of these problems were reported in a group of 50 adults with PE [23]. While young children are less likely to display these symptoms, they may develop during adolescence, sometimes in as little as six months [24].

INDICATIONS FOR SPECIALTY CONSULTATION — The clinical significance of a patient's PE depends upon the severity of the chest wall defect, cardiopulmonary morbidity, and its psychosocial impact (patient's concern about his or her appearance).

In patients with mild PE (see 'Physical examination' below), cardiopulmonary function is almost always normal and the presence or absence of cosmetic concerns is the primary indication for consultation for possible surgical correction.

Patients with moderate or severe PE and/or with complaints suggesting cardiorespiratory compromise should be evaluated by computed tomography (CT) to quantify the severity of PE. They should also undergo pulmonary function testing to assess for restrictive respiratory disease, and selected patients should be referred for exercise testing and a cardiac evaluation. (See 'Evaluation' below.)

The timing for referral also depends on the patients age. PE rarely improves after six years of age, and one-third of cases progress during the adolescent growth spurt (see 'Natural History' above). If surgery is performed to correct the defect, the optimal timing is late childhood or early adolescence. (See "Pectus excavatum: Treatment", section on 'Timing'.)

EVALUATION — Patients with PE should be evaluated to estimate the severity of the deformity and whether there are associated anomalies.

Patients with moderate or severe PE and/or with complaints suggesting cardiorespiratory compromise should be evaluated by CT to quantify the severity of PE. A low threshold for evaluation is appropriate; one retrospective study demonstrated that the level of physical symptoms correlated poorly with severity of deformity on chest CT imaging [25]. Patients with any respiratory complaints or who are surgical candidates should also undergo pulmonary function testing to assess for restrictive respiratory disease. Selected patients should have exercise testing to assess for cardiopulmonary limitation. Patients with significant displacement of the heart or cardiopulmonary limitation should be evaluated with echocardiography and electrocardiography.

For patients not deemed to be candidates for surgical correction after the initial evaluation, it is important to repeat the focused physical examination and imaging periodically. This is especially important during periods of rapid growth, such as adolescence, because the deformity and associated symptoms may increase markedly [26]. (See 'Natural History' above.)

Physical examination

Sternal depression – The sternal depression can be qualitatively assessed on visual examination (picture 1). Some clinicians also measure the chest quantitatively using calipers to measure the distance between point of maximal sternal depression and the spine, and the transverse thoracic diameter (figure 1). However, there are no standards for defining PE severity based on these measurements, so the primary use is to document the deformity including chest asymmetry and monitor changes over time [27]. Caliper measurements cannot be used as a substitute for CT-based measurements of PE severity.

Proposed, but not established, uses for caliper measurements include:

Ratio of transverse thoracic diameter to diameter at maximal sternal depression – This has been called the chest severity index (CSI) [28], which is analogous to the CT-based pectus severity index (PSI) (see 'Imaging' below). Although CSI is correlated with PSI, it cannot be used as a substitute, and there are no standards correlating CSI with indications for surgical correction.

Depth of the sternal depression – This is the difference between caliper measurements at the point of maximal sternal depression and a measurement laterally in each midclavicular line [29]. One author suggested that a depth of >2.5 cm constitutes a moderate to severe defect [29].

Thoracic abnormalities – In addition to the sternal depression, patients with PE often have a narrowed chest wall diameter in the sagittal (anteroposterior) plane and a flat, broad, and often kyphotic chest [30]. Between 10 and 39 percent of patients with PE also have associated scoliosis, which may be severe [2,9,24,31,32]. Scoliosis may present early or late in the course of PE, and it is unclear whether chest wall repair affects the onset or progression of scoliosis.

Respiratory symptoms – Resting tachypnea has been reported by up to 98 percent of patients and can be more prominent in adolescence [2]. Patients with more severe forms of PE are much more likely to have reduced aerobic capacity. Upper or lower respiratory abnormalities are uncommon findings on physical examinations. However, an association between laryngomalacia and PE has been reported, especially in infants [5]. In a retrospective study of children presenting with laryngomalacia, 6.6 percent were found to have PE [33]. This suggests that the pectus deformity may develop in response to prolonged increased inspiratory work and is not always a primary deformity. (See 'Etiology' above and 'Pulmonary function' below.)

Cardiac examination – Abnormalities of the cardiac examination are unusual in patients with isolated PE. Cardiovascular anomalies are more likely in patients with PE and associated syndromes (eg, Noonan or Marfan) [6]. (See "Genetics, clinical features, and diagnosis of Marfan syndrome and related disorders" and "Causes of short stature", section on 'Noonan syndrome'.)

Patients with severe PE can have tachycardia due to a reduced stroke volume, depending on the distortion and displacement of the heart [27]. Functional systolic murmurs are heard in approximately 18 percent of patients, probably due to compression of the left ventricular outflow tract [2]. Mitral valve prolapse has been reported in 7 to 20 percent of patients with PE [2,5].

Imaging — Plain radiographs in the anteroposterior and lateral planes have limited value in assessing the pectus defect, but they can be useful in evaluating for coincident kyphoscoliosis or lung disease.

Computed tomography scan — CT is typically reserved for patients with moderate to severe deformity or cardiorespiratory compromise, in whom they help to accurately determine the severity of the pectus defect and its impact on the lungs, heart, and large vessels [9]. Three-dimensional reconstructions can be performed to assess the defect from a variety of different thoracic measurements [34]. Magnetic resonance imaging (MRI) also has been successfully used for this purpose and has the advantage of avoiding radiation exposure [35]. Conventional radiographs are used to measure PSI in some health care systems but are less well standardized than CT and may be less accurate for measurements of asymmetric chests [36,37].

Pectus severity index (PSI) – The PSI, also known as the Haller index, describes the depth of the pectus defect by comparing the ratio of the lateral diameter of the chest to the sternum-to-spine distance, at the point of maximal depression (figure 2 and image 1) [38]. The chest CT scan should be performed at full inspiration to maximize the intrathoracic dimensions and to provide standardization to permit comparison with subsequent scans. A normal chest has a PSI of ≤2.5 [39]. Among patients referred for surgery based on clinical criteria (ie, without consideration of CT scan results), all patients had a PSI of ≥3.25, whereas patients with PE who were not referred for surgery had PSI <3.25 [38].

Pectus correction index (PCI) – The correction index is the percentage of the chest depth represented by the pectus deformity (figure 2). PCI may be superior to PSI as a measure of pectus deformity in individuals with nonstandard chests, ie, unusually broad or narrow chests [40]. A PCI of ≥28 percent is correlated with PSI of ≥3.25 and has been used as a threshold for surgical correction.

Other measures – Other CT protocols have been developed to assess the pectus defect at different levels through the thorax, evaluating asymmetry by comparing the anteroposterior diameter at each midaxillary line to the lateral diameter [41]. One report demonstrated that the sensitivity and specificity were maximal with a combination of PSI measured at the sternal-xiphoid junction and the right-to-left asymmetry measured at the sternomanubrial junction [42].

Other indices have been proposed to measure thoracic and cardiac distortion in an effort to quantify the severity of PE and define thresholds for surgical intervention [43-45]. As an example, the pectus gracilis index (PGI) is the ratio of the lateral diameter of the chest to the sternum-to-spine distance at the gladiolus-manubrial junction (ie, at a point above the maximal sternal depression) [43]. The PGI correlates with PSI in patients with PE and is also independently correlated with forced vital capacity (FVC), reflecting narrowing of the upper thorax.

Photographic imaging — Developing data describe a nonradiographic approach to assess the severity of PE based on external three-dimensional photographic reconstruction of the thorax, in which the "external" PSI (external Haller index) was defined as the widest external thoracic transverse diameter divided by the sagittal distance between the external point of maximum depression and back surface [46]. In a study of 92 patients, external PSI of ≥1.83 was closely correlated with a radiographic PSI of ≥3.25. Similarly, external PCI of ≥15.2 percent correlated with radiographic PCI of ≥28 percent. While there is promise in this technique, the equipment is not widely available and represents a potential direction for evaluation in the future.

Pulmonary function — Pulmonary function testing is indicated for patients with moderate to severe PE or for those with respiratory symptoms.

Although a majority of patients with PE have some sort of subjective respiratory complaint (shortness of breath, chest pain, or exercise intolerance), pulmonary function abnormalities are found in less than one-third of patients with PE, and the correlation between the two is weak [23,43]. In patients with moderate or severe PE, the mean FVC is usually within the normal range, although the mean is somewhat lower than in patients without PE [9,39,47]. As an example, in one case series, mean FVC, forced expiratory volume in one second (FEV1), and mean ventilatory volume (MVV) were normal at 86, 87, and 82 percent predicted, respectively [39] (see "Overview of pulmonary function testing in children", section on 'Restrictive disease'). However, it is important to remember that normal results of pulmonary function testing does not exclude the possibility of cardiopulmonary limitation during exercise.

Further evaluation for selected patients

Exercise testing — Exercise testing is indicated for patients with moderate to severe PE or for those with significant respiratory symptoms. For detecting cardiopulmonary abnormalities, exercise testing is more sensitive than spirometry or thoracic gas volume measurements performed at rest [1,48]. This may be because exercise testing evaluates the interplay between the cardiac and pulmonary systems.

Exercise testing demonstrates mild impairment in some patients with severe PE, and the degree of impairment correlates with the severity of the defect. In patients with PE, small case series have shown reduced maximal exercise capacity (as measured by maximal oxygen uptake [VO2max]) due to low stroke volume [49] and reduced VO2max and threshold for lactate accumulation [39]. In another study, the tidal volume/FVC was lower and the respiratory rate higher during exercise testing in patients with PE as compared with normal controls, perhaps indicating a higher metabolic cost of breathing in a mechanically inefficient system [50].

Cardiac function — Patients with significant displacement of the heart on imaging or cardiopulmonary limitation, should have a cardiology evaluation with echocardiography and electrocardiography. A cardiac evaluation is also appropriate for patients with syndromes associated with cardiac malformations, such as Turner or Noonan syndrome. Patients with PE commonly have cardiac displacement to the left. In one large series of female patients, 68 percent had electrocardiographic evidence of right ventricular strain [51]. Electrocardiographic evidence of right axis deviation and ST segment depression in patients with severe PE usually reflects rotation and compression of the heart rather than an intrinsic myocardial abnormality [2].

Echocardiography has demonstrated subtle right ventricular outflow obstruction and reduced right ventricular systolic function in patients with severe PE [52,53], and these measures improve after surgical treatment [54,55]. Accordingly, a study using intraoperative transesophageal echocardiography demonstrated relief of right heart chamber compression and improved cardiac output immediately after surgical repair [56] (see "Pectus excavatum: Treatment", section on 'Outcomes'). The cardiac distortion may be associated with conduction abnormalities, such as bundle branch block, which were present in 16 percent of patients in one series [9].

In a case series of patients with severe PE (PSI 5.2±1.3), cardiac MRI testing showed cardiac strain in the mid- and apical ventricles and smaller ventricular volumes compared with unaffected controls [57].

Dynamic imaging — Dynamic resonance imaging technology is an emerging technique that can assess the movement of the chest during breathing. This technology is not widely available, and data are limited on its clinical utility in patients with PE. One case series showed that quiet expiration is the best phase for determining thoracic indices in static measurements (ie, CT-based PSI) [58]. Other potential uses of dynamic imaging are to assess the motion of the chest wall relative to the pectus deformity, which might inform surgical decisions.

SUMMARY AND RECOMMENDATIONS

Definition – Pectus excavatum (PE) is a deformity of the chest wall characterized by a sternal depression beginning over the midportion of the manubrium and progressing inward toward the xiphoid process (picture 1). The deformity may be symmetric or asymmetric. (See 'Definition' above.)

Etiology – PE is usually sporadic, but it has been associated with connective tissue disorders (such as Marfan syndrome and Ehlers-Danlos syndrome), neuromuscular disease, and a variety of other genetic conditions, including Noonan syndrome and Turner syndrome. The pathogenesis of PE and reasons for these associations are not well established. (See 'Etiology' above.)

Natural history – PE can be present at birth and, in some cases, may resolve. However, it tends to worsen during the rapid growth of adolescence. (See 'Natural History' above.)

Clinical presentation – Patients with PE typically present with cosmetic concerns, but some patients also report exercise intolerance and shortness of breath. (See 'Clinical features' above.)

Initial evaluation – Evaluation of a patient with moderate or severe PE includes quantification of the sternal depression using measurements from a chest CT scan, particularly the pectus severity index (PSI) and pectus correction index (PCI) (figure 2 and image 1). A typical candidate for surgery usually has a PSI of ≥3.25 or PCI ≥28 percent. (See 'Imaging' above.)

Further evaluation – Further testing depends on the severity of PE and other symptoms (see 'Evaluation' above):

Pulmonary function tests – Patients with moderate to severe PE are candidates for possible surgical intervention and should undergo pulmonary function testing. On pulmonary function testing, lung volumes such as forced vital capacity (FVC) are often normal. (See 'Pulmonary function' above.)

Exercise testing – Exercise testing is indicated for patients with moderate to severe PE or for those with significant respiratory symptoms. For these patients, exercise testing often demonstrates mild impairment. The impairment correlates with the severity of the defect and is consistent with cardiovascular dysfunction rather than ventilatory limitation or physical deconditioning. (See 'Exercise testing' above.)

Cardiac evaluation – Patients with significant displacement of the heart on imaging or cardiopulmonary limitation should have a cardiology evaluation with echocardiography and electrocardiography. Electrocardiography may demonstrate right axis deviation and ST segment depression, which reflects rotation and compression of the heart. Some patients have conduction abnormalities, such as bundle branch block. Echocardiography may demonstrate subtle right ventricular outflow obstruction and reduced right ventricular systolic function in patients with severe PE. (See 'Cardiac function' above.)

Referral for surgery – The decision of whether and when to refer a patient for specialty consultation depends on the severity of the defect and the patient's age and cardiopulmonary symptoms (see 'Indications for specialty consultation' above). Surgery is typically performed during late childhood or early adolescence. Indications for surgery are discussed separately. (See "Pectus excavatum: Treatment", section on 'Indications'.)

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Topic 6361 Version 22.0

References

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