BRACHIAL PLEXUS INJURY AND COSTOCLAVICULAR SYNDROMEDR BHAVIN MANDOWARA

ANATOMY OF BRACHIAL PLEXUS

ANATOMY AND PATHOLOGIC BASIS The plexus can be divided into regions that include (from

proximal to distal) trunks, divisions, cords, branches, and nerves. Trunks and divisions are further subdivided with a nomenclature based on overall relationships with other upper extremity anatomic structures and include upper, lower, and middle trunks, and posterior and anterior cords.

 The pathologic basis and histologic changes seen with brachial plexus lesions vary with the underlying cause, which include compression, transection, ischemia, inflammation, metabolic abnormalities, neoplasia, and radiation therapy.

SYMPTOMS AND SIGNS The onset of symptoms from brachial plexopathies may vary from

acute to insidious. Acute onset is usually characterized by pain in the shoulder or upper arm, while insidious onset can manifest as progressive pain, evolving numbness, weakness of selected muscles, or any combination. Acute onset, in the absence of trauma, favors a metabolic or inflammatory process

Chronic progression of symptoms in patients with a history of cancer and radiation treatment suggests either as a cause. Clinical signs include muscle weakness, atrophy, and sensory loss

The primary pathologic lesion in most plexopathies is axonal loss, with demyelination and conduction block as secondary processes

ETIOLOGY Traumatic injuries are the most common cause of brachial

plexus lesions in children and adults. Motor vehicle accidents, industrial accidents, falls, objects falling on a shoulder, and sports injuries are among the many causes of closed brachial plexus trauma

Open traumatic brachial plexus injuries result from gunshot wounds, lacerations, and animal bites. Open injuries are frequently associated with secondary injury from expanding hematomas, pseudoaneurysms, and arteriovenous fistulas

Nontraumatic brachial plexopathies include neuralgic amyotrophy, hereditary brachial plexopathy, neoplastic and radiation induced plexopathy, thoracic outlet syndrome, and brachial plexopathy related to diabetes

NEURALGIC AMYOTROPHYNeuralgic amyotrophy is characterized clinically by the onset of severe pain followed by patchy weakness in the distribution of the upper and/or middle brachial plexus, usually involving winging of the scapula. The time to onset of weakness is highly variable. Sensory symptoms occur in a majority of patients, most commonly manifesting as hypesthesia and/or paresthesia, and usually involving the lateral shoulder and arm and/or the hand

Hereditary brachial plexopathy

Hereditary brachial plexopathy is a rare autosomal dominant disorder characterized by recurrent, painful brachial plexopathies. In some families the cause has been identified as mutations in the SEPT9 gene

NEOPLASM AND RADIOTHERAPY Breast and lung cancers are the most frequent

neoplasms leading to brachial plexopathy. Pain in the shoulder and axilla is the most common presenting symptom of neoplastic brachial plexopathy. Invasion of the lower plexus (inferior trunk and medial cord) occurs more frequently than invasion of the upper trunk

Radiation-induced brachial plexopathy is a consideration in patients with cancer who develop plexopathy after radiation therapy in the vicinity of the brachial plexus. Either cancer recurrence or radiation therapy can cause a brachial plexopathy in this setting.

THORACIC OUTLET SYNDROMES Thoracic outlet syndrome (TOS) is a term used to

denote a variety of upper extremity syndromes, with only a small number having a neurologic basis. TOS is generally divided into true neurogenic TOS, vascular TOS (with arterial vascular and venous vascular subtypes), and disputed (nonspecific) TOS

DIABETIC PLEXOPATHY

Plexopathies related to diabetes mellitus usually involve the lumbosacral plexus, but upper extremity involvement has also been observed as part of the syndrome. In contemporary series, upper extremity involvement occurs in up to one-third of patients and may be in the form of mononeuropathies of the ulnar and median nerves, or at more proximal sites in the brachial plexus

IATROGENIC BRACHIAL PLEXOPATHIES

Iatrogenic brachial plexopathies related to surgery and other medical procedures account for approximately 7 to 10 percent of all brachial plexopathies. Examples include classic postoperative paralysis, postmedian sternotomy plexopathy, and medial fascial compartment syndrome

THORACIC OUTLET SYNDROMES Thoracic outlet syndrome (TOS) refers to a constellation of signs

and symptoms that arise from compression of the neurovascular bundle by various structures in the area just above the first rib and behind the clavicle, within the confined space of the thoracic outlet

several names have been coined to describe pathology involving the thoracic outlet which are

• cervical rib syndrome • scalene anticus syndrome • costoclavicular syndrome • hyperabduction syndrome

The term “thoracic outlet syndrome” was coined to collectively encompass the spectrum of syndromes related to the general region of the thoracic outlet

TERMINOLOGY OF TOS Neurogenic (nTOS) from brachial plexus compression(95%) Venous (vTOS) from subclavian vein compression (3%) Arterial (aTOS) from subclavian artery compression(1%)

Compression of the brachial plexus leads to upper extremity numbness, dysesthesia and weaknessVenous compression may cause deep vein thrombosis and extremity swellingArterial compression can lead to distal thromboembolism, arm pain with exertion (‘claudication’) or acute arterial thrombosis

ETIOPATHOGENESIS Thoracic outlet syndromes are due to rib anomalies,

muscular anomalies, or a result of injury. Cervical ribs predispose the patient to TOS after hyperextension-flexion (whiplash) injury. The absence of a rib anomaly makes the diagnosis of arterial thoracic outlet syndrome less likely. Many patients with nTOS have a prior history of neck trauma or repetitive occupational physical stress. Similarly, vTOS is highly associated with repetitive movements, particularly with repetitive overhead upper extremity movements

CLINICAL EXAMINATION Symptoms of neurogenic TOS include upper extremity pain,

dysesthesia, weakness, and numbness in the hand, arm, or shoulder. Progressive unilateral atrophic weakness of the hypothenar hand muscles and numbness in the distribution of the ulnar nerve and medial antebrachial cutaneous nerves can occur, but very rarely. Tenderness over the scalene muscles is often present

Arterial TOS typically presents as thromboembolism to the hand or arm. Features of arm/hand ischemia include pain, paresthesia, pallor, and coolness

Venous TOS is easily differentiated from the other forms of TOS because venous compression may lead to upper extremity venous thrombosis, swelling, and cyanosis even in the absence of thrombosis. Due to swelling, some patients may complain of hand paresthesias

DIAGNOSIS

Diagnosis of nTOS is often clinical, but electrodiagnostic and imaging can exclude other diagnosis

Arterial or venous duplex ultrasounds are the initial diagnostic tests for aTOS or vTOS, respectively

The role for computed tomographic or magnetic resonance imaging is evolving and provides important diagnostic information especially when ultrasound results are equivocal

Conventional arteriography (aTOS) and venography (vTOS) remain useful diagnostic modalities especially when initiation of thrombolysis is considered

MANAGEMENT Patients with nTOS should be managed conservatively with

physical therapy and weight loss supplemented by medical therapy unless they have progressive neurologic weakness or disabling pain and paresthesia. Patients who have not responded to conservative treatment may become candidates for thoracic outlet decompression; however, the patient needs to understand that the long-term success rates for thoracic outlet decompression for nTOS diminish over time.

For patients with deep vein thrombosis due to vTOS, thrombolysis and early thoracic outlet decompression are performed to relieve extrinsic vein compression. In properly selected patients, long-term outcomes are excellent following thrombolysis and thoracic outlet decompression

MANAGEMENT (contd…)

Patients with aTOS are treated according to the nature of their symptoms and initial presentation. Patients with signs and symptoms of upper extremity thromboembolism undergo thoracic outlet decompression in conjunction with embolectomy, thrombolytic therapy, or anticoagulation. Arterial TOS is nearly always associated with a correctable anatomic bony abnormality, and, without decompression, the rate of recurrent thromboembolism is high. The supraclavicular approach offers direct access to the subclavian artery. Occasionally, arterial reconstruction (ie, surgical bypass) may be needed.

THANK YOU