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Complications associated with supracondylar humerus fractures can be divided into broad categories. The etiology of a complication may be due to the injury itself or the management of the injury. The complication may be associated with the soft tissues, such as a neurovascular problem, or in the osseous structures, such as malalignment. In this chapter, we first discuss the anatomy of this area, then neurovascular problems, and finally bony complications of supracondylar humerus fractures in children. In 2014, the American Academy of Orthopaedic Surgeons (AAOS) adopted appropriate use criteria (AUC) for the management of pediatric supracondylar humerus fractures, and in 2015 adopted the AUC for pediatric supracondylar humerus fractures with vascular injury. These AAOS references should be reviewed prior to engaging in the treatment of a pediatric supracondylar humerus fracture.
Anterior to the supracondylar area of the distal humerus is the median nerve ( Fig. 28.1 ). In the proximal forearm, the anterior interosseous branch separates to innervate the flexor digitorum profundus to the index finger and the flexor pollicis longus and then terminates with the innervation of the pronator quadratus. There is no sensory branch for this nerve. The remainder of the median nerve traverses the forearm and supplies the sensation to the palmar aspect of the thumb, the index finger, the long finger, and the radial aspect of the ring finger.
The radial nerve is posterolateral to the usual location of supracondylar fractures and thus is less commonly involved (see Fig. 28.1 ). The ulnar nerve with its posterior location is uncommonly involved with the typical extension-type supracondylar fracture.
The forearm consists of two basic compartments: volar and dorsal ( Fig. 28.2 ). The volar compartment includes the flexors and pronators of the forearm and wrist, which may be further divided into superficial and deep muscle groups. The superficial muscles include the flexor carpi ulnaris, the palmaris longus, the flexor carpi radialis, and the pronator teres. The deeper group of muscles consists of the flexor digitorum superficialis and profundus, the flexor pollicis longus, and the pronator quadratus.
The median and ulnar nerves traverse the forearm between the superficial and deep flexor groups. The major arteries of the elbow consist of the brachial artery, bifurcating in the region of the radial head to form the radial and ulnar arteries.
The dorsal compartment consists mainly of the wrist and finger extensors. The mobile wad of Henry includes the brachioradialis and the extensor carpi radialis longus and brevis muscles. This group of muscles is physically and functionally distinct; it lies between the dorsal and volar forearm compartments and should be considered a separate compartment. The major nerve of the dorsal compartment is the posterior interosseous nerve, a continuation of the radial nerve. The major artery of the dorsal compartment is the posterior interosseous artery.
Most nerve injuries are associated with type III displaced supracondylar fractures. In a 2010 study by Babal et al., the most commonly injured nerve was the anterior interosseous branch of the median nerve. This is likely due to the anatomic arrangement of the exclusively motor posterior fascicles, which are exposed to the zone of injury, as well as to its tight tether to the proximal forearm musculature. The second most commonly involved nerve was the ulnar nerve, followed by the radial nerve. Ulnar nerve injury was most commonly associated with posterolateral fracture patterns due to direct contusion and stretch of the nerve from the medially displaced proximal humeral fragment or edema within the cubital tunnel. Radial nerve injury was consistently associated with posteromedial fractures, due to contusion and stretch from the laterally displaced proximal humeral fragment.
Ulnar nerve injury also occurred iatrogenically in 4% of patients during medial percutaneous pin placement in a recent large metaanalysis. The causes of iatrogenic ulnar nerve injury include (1) direct penetration of the nerve or its sheath by the medial pin, (2) constriction of the cubital tunnel by the pin while the elbow is in flexion, (3) medial pin injury to an unstable ulnar nerve, which subluxates or dislocates anteriorly when the elbow is in flexion, and (4) nerve contusion and edema. In 2001, Skaggs et al. reported on 345 extension-type supracondylar humerus fractures in children treated with closed reduction and percutaneous pin fixation. The use of a medial pin was associated with an iatrogenic ulnar nerve injury in 15% of patients in which the pin was placed with the elbow positioned in hyperflexion. Only 4% of patients sustained nerve injury when the medial pin was placed without hyperflexion, and no iatrogenic injuries occurred in patients treated with all lateral entry pin fixation. A displaced supracondylar fracture presenting with an absent radial pulse has a 50% to 60% incidence of associated nerve injury at fracture presentation.
The diagnosis of anterior interosseous nerve injury is easily missed. The inability to flex the distal segment of the thumb and the index fingers is an indication of this nerve being damaged. With a pure anterior interosseous nerve injury, there is no sensory deficit. Sensory examination by light touch and two-point discrimination is recommended for children, especially in the median, ulnar, and radial nerve distributions.
After reduction of the fracture and stabilization with percutaneous pinning, reevaluation of the neurovascular examination is mandatory. On rare occasions, the compromised nerve may recover before the patient's discharge, but in most cases, the neurapraxia requires observation and will gradually return over the ensuing months. If after 4 to 6 months no return of function is noted, electromyelographic and nerve conduction studies are recommended. Only rarely have cases been reported of permanent nerve deficits requiring later neurolysis, grafting, or tendon transfer. Nearly all nerves will return to normal function within the first 6 months following the injury.
Advances in surgical techniques with lateral pin entry fixation have significantly decreased rates of iatrogenic ulnar nerve injury with satisfactory mechanical stability in Gartland type II, III, and IV fractures. Authors recommend two-pin lateral-entry fixation as the primary mode of percutaneous fixation in all unstable supracondylar humerus fractures, with the addition of a third lateral-entry pin or medial pin as needed to achieve fracture stability.
Two basic pathologic processes may lead to forearm ischemia in the setting of supracondylar fractures or other injuries to the elbow region: (1) arterial injury and (2) compartment syndrome from hemorrhage or swelling ( Fig. 28.3 ). An arterial injury may result from laceration, thrombus, embolus, intimal tear, vasospasm, or extrinsic compression/kinking from injured adjacent soft tissues ( Fig. 28.4 ). Such an injury may cause nerve and muscle ischemia directly or may result in postischemic swelling or hemorrhage, thereby causing a compartment syndrome.
The muscles of the extremities are grouped into compartments that are enclosed by a relatively noncompliant osteofascial envelope. Muscle swelling causes increased pressure within the compartment that is not easily dissipated due to the relatively inelastic nature of the surrounding fascia. If the pressure remains sufficiently high for several hours, loss of function of intracompartmental nerves and muscles due to ischemia may result. A compartment syndrome is a condition in which the high pressure within the compartment compromises the circulation to the nerves and muscles within the involved compartment. In either event, nerve and muscle ischemia may result, possibly leading to a forearm contracture.
To prevent permanent loss of nerve and muscle function, this condition must be diagnosed promptly and treated correctly. Volkmann contracture is the popular term that refers to the end stage of an ischemic injury to the muscles and nerves of the limb ( Fig. 28.5 ). Untreated compartment syndromes and arterial injuries are the primary causes of Volkmann contracture. The term Volkmann ischemia is nonspecific and should not be used.
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