Adult Chest Surgery

Chapter 118. Overview 

This section on chest wall disorders encompasses benign disorders of the skeletal and muscular chest wall, including congenital deformities of the chest wall, a group of compressive disorders known collectively as thoracic outlet syndrome, and management of chest wall infections (Fig. 118-1).

Figure 118-1.


Muscular (A) and skeletal (B) anatomy of the chest, anterior view.


Congenital chest wall deformities may be categorized as (1) pectus excavatum, (2) pectus carinatum, (3) Poland's syndrome, (4) sternal defects, and (5) miscellaneous anterior chest wall defects. While most patients present during childhood, some may present in early adulthood as well.


Pectus excavatum, or "funnel chest," is a congenital deformity characterized by posterior depression of the middle to inferior portion of the sternum and posterior curvature of the associated costal cartilages. Generally, the manubrium and first and second ribs are normal. The severity of the depression varies and is usually asymmetric with a deviation to the right side. Shamberger and colleagues reported that most cases (86%) are diagnosed at or within a few weeks of birth.Although it was once commonly believed that children would "grow out of" this deformity, the severity of the sternal depression may increase as the child grows.

Pectus excavatum is the most common congenital chest wall deformity in children. The incidence generally is reported to range from 1 in 300 or 400 to 1 in 1000 live births. In addition, boys are reported to be affected three times as often as girls.The etiology of this deformity is unknown. Theories include intrauterine pressure, rickets, and abnormalities of the diaphragm.Shamberger and colleagues note that 35% of patients report a positive family history for chest wall deformities.1

Pectus excavatum may be accompanied by other abnormalities. In a study of 704 children with pectus excavatum, 18% had other musculoskeletal abnormalities, such as scoliosis or kyphosis. Pectus excavatum also has been associated with Marfan's syndrome and congenital heart defects (1.5%).Patients may be asymptomatic or may complain of dyspnea on exertion or chest pain. Although asymptomatic, children may experience psychological distress as a consequence of their cosmetic appearance. In a recent multicenter prospective trial, shortness of breath on exertion was reported by 66% of patients. Limited exercise tolerance (64.5%), shortness of breath at rest (62.1%), chest pain on exertion (51.1%), chest pain unrelated to exertion (32%), and palpitations (11%) also were reported. Pain on exertion and at rest was presumably musculoskeletal in origin.3

Physical examination reveals a middle to inferior sternal depression of varying severity. Usually the depression is asymmetric, with deviation to the right side being most common. The heart is often rotated more to the left because of the depression. Many studies have investigated the altered cardiac function by means of electrocardiogram (ECG), echocardiogram, nuclear medicine test, and angiogram. Most of these studies have shown decreased exercise tolerance consequent to decreased stroke volume. At rest, the cardiac index is normal, but the response to moderate exertion is below predicted values.

Given the common subjective complaints of shortness of breath, pulmonary function testing has been used in numerous studies to quantify any abnormality.4–6 In most patients, a mild to moderate (10–15%) reduction in forced expiratory volume in 1 second and vital capacity is identified.The severity of symptoms does not often correlate well with objective findings in pulmonary and cardiac function.

Several methods of "grading" the severity of sternal depression by radiographic investigations have been described. The pectus (or Hallerindex is a ratio between the transverse chest diameter at its widest point and the distance from the posterior aspect of the sternum and the anterior spine at its closest point.Another method compares the distance from the point closest to the posterior sternum to the anterior spine and the distance between the spine and sternum at the angle of Louis.Unfortunately, neither method consistently correlates the severity of symptoms to an objective index.

Surgery has been the primary form of therapy for these patients. While the cosmetic benefit cannot be debated, the effect on pulmonary and cardiac function is less clear. A recent meta-analysis of the effect of surgery on pulmonary function suggests that it may improve in the short term, but most patients experience a decrease in pulmonary function on long-term follow-up.Presumably, this is related to loss of chest wall compliance. The effect of surgery on cardiac function is less clear, with conflicting data.8,9 The surgical treatment of pectus excavatum is detailed in Chapters 119 and 120.


Pectus carinatum is a congenital deformity characterized by sternal protrusion with anterior displacement of the middle and lower sternum and associated costal cartilages. Pectus carinatum may be classified as chondrogladiolar (symmetric or asymmetric), mixed pectus carinatum and excavatum, and chondromanubrial. The chondrogladiolar type is described as an anterior protrusion of the body of the sternum with protrusion of the lower costal cartilages. As reported by Shamberger and colleagues, the symmetric type is more common.The mixed type is often composed of both elements of carinatum and excavatum. The chondromanubrial type, also referred to as "pouter pigeon," involves an anterior protrusion of the manubrium along with the second and third costal cartilages.

In contrast to pectus excavatum, pectus carinatum is not usually recognized until adolescence. It is seven times less common than pectus excavatum,10 with a reported incidence of 0.6 to 0.97 cases per 1000. Like pectus excavatum, it, too, is much more common in males than in females (4:1). A family history again is present in approximately 30% of patients. Scoliosis is the most commonly associated musculoskeletal deformity, whereas fewer than 5% of patients with pectus carinatum also have congenital heart disease. Symptoms are uncommon in childhood but may progress into adolescence. Shortness of breath, it has been suggested, may be related to decreased chest wall compliance with increased chest diameter. In pectus carinatum, there is increased residual volume and reduced vital capacity, which may account for symptoms.

Again, surgical repair by osteotomy is the main form of therapy. Surgical therapy provides excellent results in as many as 97% of patients with low morbidity.11 The surgical treatment of pectus carinatum is discussed in Chapter 119.


Poland's syndrome is the congenital absence of the pectoralis major and minor muscles associated with syndactyly (fused fingers). It is also associated with abnormalities of the ribs, chest wall depressions, and abnormalities of the breasts. Abnormalities may range from hypoplasia to complete absence. Poland's syndrome occurs in 1 in 30,000–32,000 live births and is not often familial.12 The etiology is not well understood.


Sternal defects may be classified as cleft sternum or ectopic cordis. A cleft sternum results from nonfusion of the sternal plates. The remainder of the sternum is normal, as is the diaphragm, pericardium, and location of the heart. It usually involves the superior portion of the sternum. In ectopic cordis, the sternal cleft involves the inferior portion of the sternum and is associated with abnormal diaphragm, pericardium, and location of the heart. In thoracic ectopic cordis, the heart is exterior to the chest and without its pericardial coverage. Thoracoabdominal ectopic cordis is associated with an inferior sternal cleft, anterior diaphragmatic defect, absence of pericardium at the diaphragmatic defect, an omphalocele, and intrinsic cardiac abnormalities.13 The surgical management of sternal defects is discussed in Chapter 119.


Thoracic sympathectomy has been described for disorders such as hyperhidrosis, reflex sympathetic dystrophy, upper extremity ischemia, Raynaud disease, and splanchnicectomy for pancreatic pain. Hyperhidrosis is a disorder of excessive sweat production. The disorder most commonly affects the axillae, hands, feet, and face. The prevalence of palmar and plantar hyperhidrosis is estimated as 0.6–1%, with axillary hyperhidrosis affecting 1.4%. Although diagnostic tests do exist, history provides the diagnosis in most cases. The typical patient is a young adult who is able to give a typical history of consistent excessive sweating causing social embarrassment and interference with normal day-to-day activities. A family history may be present in as many as 65%.22

The pathophysiology of hyperhidrosis is not well understood. Eccrine glands are distributed around the body, with high concentrations in areas such as the palms, soles, and forehead. These glands are innervated by the cholinergic fibers of the sympathetic nervous system. Patients with hyperhidrosis do not demonstrate any histopathologic changes in the sweat glands or changes in their numbers. Up to two-thirds of patients report a positive family history. Hyperhidrosis must be differentiated from secondary effects from neurologic, endocrinologic, metabolic, and other such disorders, as well as febrile illness, malignancy, and drugs.

A wide array of modalities is available to treat hyperhidrosis. These include nonsurgical (i.e., topical or systemic) and surgical treatments. Patients with hyperhidrosis generally are offered topical agents that contain aluminum chloride, which may help in mild cases. Occasionally, a trial of iontophoresis is appropriate if the patient can tolerate the side effects of tingling and electric shocks. Medications may have some benefit in selected patients in certain situations. Beta blockers and cholinergics may provide some relief of symptoms; however, the duration of these effects may be short. Propranolol (10 mg, two to four times daily) can be quite helpful. Alternatively, glycopyrrolate (0.5–1 mg) may help patients who can tolerate dry mouth, the most frequent side effect. Botox injections may be useful in palmar and axillary hyperhidrosis.

For patients undergoing thoracoscopic sympathectomy, the place where the chain is divided also can depend on the primary symptom and underlying disease (see Chap. 121). Patients with facial sweating or blushing generally require division of the chain high over the T2 rib, whereas patients undergoing operation for thoracic outlet syndrome/reflex sympathetic dystrophy generally undergo sympathectomy at T2 to T3. Patients referred for splanchnicectomy for chronic pancreatic pain will need division of the T4 to T10 levels. Indications for sympathectomy other than hyperhidrosis are not as common. Thoracoscopic sympathectomy from the T2 to T4 levels was performed in 25 patients with severe Raynaud disease. The basal capillary flow and maximal refilling time were measured and compared with the same measurements obtained in a group of 50 healthy individuals. The basal capillary flow and maximal refilling time improved after the sympathectomy to levels similar to those in the control group. Furthermore, the effect was maintained during the 5-year follow-up period. The patients' symptom severity scores diminished to zero in the early postoperative period and increased to 28% of their initial value 5 years after the operation.23


Thoracic outlet syndrome is a constellation of symptoms that result from compression of elements of the neurovascular bundle as they pass through the thoracic outlet.


The thoracic outlet has three potential spaces for neurovascular compression. These include the interscalene triangle, the costoclavicular space, and the retropectoralis minor space. The interscalene triangle is bounded anteriorly by the anterior scalene muscle, posteriorly by the middle and posterior scalene muscles, and inferiorly by the first rib. The subclavian artery and the three trunks of the brachial plexus traverse the triangle. The subclavian vein runs beneath the anterior scalene muscle. The costoclavicular space is bounded superiorly by the clavicle, anteriorly by the subclavius muscle, and posteriorly by the first rib and middle scalene muscle. The retropectoralis minor space is bounded anteriorly by the pectoralis minor muscle and posteriorly and superiorly by the subscapularis muscle, and posteriorly and inferiorly by the anterior chest wall.

Radiographic imaging has shown that in normal subjects, upper extremity elevation does not produce a change in the interscalene triangle but does narrow the costoclavicular and retropectoralis minor spaces.14 Arterial compression occurs most frequently in the costoclavicular space, followed by the interscalene triangle, whereas neurologic compression occurs equally in the two.14

Clinical Presentation

Thoracic outlet syndrome typically occurs in patients between 20 and 40 years of age. Females are affected four times more often than males.15 Three syndromes may be encountered depending on which element(s) of the neurovascular bundle are being compressed: the neurologic, arterial, and venous thoracic outlet syndrome. Signs and symptoms may include pain, numbness, tingling, and weakness. Neurogenic thoracic outlet syndrome occurs in roughly 90% of patients, with arterial and venous thoracic outlet syndrome accounting for the remaining 5–10%.16

There are four basic maneuvers that may be performed to elicit signs or symptoms of thoracic outlet syndrome. These include the Adson test, the costoclavicular test, the Roos test, and the Wright test. The Adson (or scalene) test contracts the anterior and middle scalene muscles, resulting in a decrease in the interscalene triangle. To perform the maneuver, the patient is asked to take and hold a deep breath while extending the neck fully and turning the head toward the side. The costoclavicular test narrows the costoclavicular space by narrowing the area between the clavicle and first rib. The maneuver is performed by having the patient hold the shoulders down and backward. The Roos test is performed by holding both arms at 90 degrees of abduction and external rotation with the shoulders drawn back. The patient is instructed to open and close the hands slowly for 3 minutes. The hyperabduction, or Wright, test is performed with the shoulders hyperabducted and externally rotated. As with most clinical tests, these maneuvers are not specific for thoracic outlet syndrome, and 56% of normal patients may have at least one positive test.17

In neurogenic thoracic outlet syndrome, symptoms may include pain, paraesthesia, or even weakness. Generally these symptoms follow an ulnar nerve pattern. In arterial thoracic outlet syndrome, symptoms may include cold, weakness, and pain. Venous thoracic outlet syndrome may present as edema, cyanosis, or venous distention. Often the symptoms overlap, blurring the distinction between neurologic and vascular thoracic outlet syndrome.


Thoracic outlet syndrome may be caused by congenital or acquired anatomic abnormalities. Congenital anatomic abnormalities include cervical rib, elongated C7 transverse process, exostosis of the first rib, fibrous band, and supranumerary muscles. A cervical rib is an extra rib originating from the seventh cervical vertebra. In the general population, a cervical rib is present in fewer than 1% and in only 5–9% of patients with thoracic outlet syndrome.18 Fibrous bands arising from the first or cervical rib also may contribute to neurovascular compression. Acquired anatomic abnormalities include traumatic injuries, postoperative scarring, and tumors.


Apart from a history and physical examination, assessment of a patient with symptoms consistent with thoracic outlet syndrome should include x-rays of the cervical spine and chest to identify a cervical rib, CT scan with intravenous contrast material or MRI to define the anatomy of the thoracic outlet, and nerve conduction testing. Rarely, angiography is required.

CT or MRI examination is performed in the neutral position as well as with the arms extended above the head to attempt to reproduce symptoms. This permits better detection of thoracic outlet syndrome.19,20

Nerve conduction velocity testing measures the motor conduction of the ulnar, median, and radial nerves. On average, the ulnar nerve conduction velocity is 85 m/s, whereas patients with thoracic outlet syndrome average 53 m/s.21


Generally, patients diagnosed with thoracic outlet syndrome are advised to undertake physiotherapy, including heat massages, active neck massages, scalene anticus muscle stretching, strengthening of the upper trapezius and shoulder girdle, and proper posture instruction. As a rule, patients with an ulnar nerve conduction velocity of greater than 60 m/s do very well with conservative measures, whereas patients with an ulnar nerve conduction velocity of less than 60 m/s do less well and often require surgical intervention. Surgery for thoracic outlet syndrome is discussed in Chapters 122, 123, and 124.


An aspect of thoracic outlet syndrome that deserves special attention is Paget-Schroetter syndrome, also known as effort thrombosis of the axillary-subclavian vein. This condition is said to occur following excessive or unusual use of the extremities in the presence of one or more compressive elements. Initially, management consisted of exercise and anticoagulation, but morbidity was high. The current suggested management includes the use of thrombolytic agents, such as heparin, followed by early surgical decompression. Results with surgical management have been very good, and there is less morbidity than with nonoperative management. The surgical treatment of Paget-Schroetter syndrome is described in Chapter 125.


Infections of the chest wall may be classified as soft tissue infections, infections invading the chest wall, or infections of the cartilage or bony structures.

Soft Tissue Infections

Chest wall soft tissue infections may originate from direct inoculation or hematogenous spread. These infections may be classified as bacterial or nonbacterial or necrotizing or nonnecrotizing. The clinical presentation varies from only a mildly symptomatic patient to a frankly septic patient. The clinical presentation, as well as treatment, often is dictated by the offending organism. Chapter 126 discusses this topic in greater detail.

Empyema Necessitas

Chest wall infections also may originate in the lung parenchyma or pleural space and "invade" the chest wall. This entity was much more common in the days before antimicrobial therapy. Therapy relies on treatment of the underlying infection and usually requires surgical debridement.

Cartilage or Bony Infections


Primary sternal osteomyelitis is a rare condition. Most of the recent cases have been reported in IV drug abusers. The diagnosis should be suspected in a young patient presenting with acute inflammatory swelling over the sternum. It is further supported by leukocytosis and positive Gram's stain. Empirical antibiotic coverage for Staphylococcus aureus should be initiated prior to culture and sensitivity reports. Secondary sternal osteomyelitis such as postoperative deep sternal infection occurs in 1–3%. Risk factors such as diabetes, bilateral internal mammary artery grafts, and renal failure have been identified. Treatment relies on IV antibiotics to cover methicillin-resistant S. aureus and debridement. Deep sternal infections may require greater debridement and may benefit from soft tissue transposition to aid healing.


One-hundred and six cases of rib osteomyelitis were reported by Bishara and colleagues.24 Most cases occurred in children and young adults. Common clinical signs were fever (73%), soft tissue mass (64%), and chest pain (60%). The routes of infection were contiguous spread in 68% and hematogenous spread in 38%. Mycobacterial and bacterial infections accounted for the majority of cases. Therapy entails antimicrobial therapy with or without debridement and resection.


The sternoclavicular joint is an unusual site of septic arthritis in healthy persons but is commonly involved in septic arthritis in IV drug users. Sternoclavicular osteomyelitis usually presents with a slow, progressive onset of chest pain that is localized to the sternoclavicular joint or pain referred to the shoulder or neck. The area is tender to palpation. Fever and leukocytosis are not always present.

In a review of 180 cases of sternoclavicular septic arthritis, the most common risk factor was IV drug use (21%), followed by infection at a distant site (15%), diabetes mellitus (13%), trauma (12%), and infected central venous access (9%). No underlying medical condition was found in 23% of patients.25 S. aureus was the offending organism in 49% of patients, whereas Pseudomonas aeruginosa was found in 10%.

A CT scan or MRI should be obtained routinely in all cases of sternoclavicular joint arthritis. If there is extensive bony destruction with chest wall phlegmon or abscess, retrosternal abscess, mediastinitis, or pleural extension, joint resection is indicated. Medical management, such as IV antibiotics, is seldom effective. Incision and debridement, if not en bloc resection of the joint, are often required. A hockey-stick incision is made from the medial third of the clavicle down the midline of the manubrium, and en bloc resection of the joint is performed, with debridement of bone and soft tissues until they appear healthy. The subclavian vein may be densely adherent to the posterior aspect of the joint capsule. Small wounds can be permitted to heal by secondary intention. Larger wounds may require a soft tissue or muscle flap for coverage. The flap improves wound vascularity and healing, and it protects the great vessels from trauma.

Specific antibiotic therapy should be based on culture data and continued for 4 weeks in uncomplicated sternoclavicular septic arthritis and for 6 weeks in cases complicated by osteomyelitis or mediastinitis. Functional outcomes generally are excellent, even after sternoclavicular joint resection.26


Benign tumors of the chest wall comprise roughly half the primary chest wall tumors. They may be classified by soft tissue origin or bone and cartilage origin. Benign chest wall tumors typically manifest as slow-growing, palpable masses in asymptomatic patients. The slow growth rate that typifies most benign chest wall tumors is evidenced on radiologic images by well-defined tissue planes and sometimes by pressure erosions on adjacent bone.27

Benign Soft Tissue Tumors

These lesions are not uncommon and are comprised of lipomas, fibromas, neurofibromas, lymphangiomas, and hemangiomas. Often these lesions are asymptomatic. Surgical excision is indicated for enlarging masses and for definitive diagnosis.

Benign Bone and Cartilage Tumors

Osteochondroma, chondroma, and fibrous dysplasia are the most common forms of benign bone and cartilage tumors of the chest wall. Others include eosinophilic granuloma, giant cell tumor, chondroblastoma, and osteoblastoma.

Osteochondromas are the most common benign rib tumors, comprising roughly 50%. They occur commonly in the metaphyseal region of the rib in the bony cortex at the costochondral junction. The tumors are characteristically pedunculated, with osseous protuberances arising from the surface of the parent bone. Radiographs may show a cap composed of hyaline cartilage, which may be calcified. Surgical resection is indicated for definitive diagnosis.

Chondromas account for approximately 15% of benign rib lesions. Clinically and radiographically, they cannot be distinguished from chondrosarcomas and thus should be resected for definitive diagnosis and treatment.

Fibrous dysplasia is a skeletal developmental anomaly in which mesenchymal osteoblasts fail to undergo normal morphologic differentiation and maturation. The ribs are commonly affected, and the clavicle is involved occasionally. Radiographs characteristically show unilateral fusiform enlargement and deformity with cortical thickening and increased trabeculation of one or more ribs with amorphous or irregular calcification.27 Readers are referred to Part 15 (Chaps. 114, 115, 116, and 117) for surgical techniques used to resect and reconstruct chest wall tumors.


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