CHAPTER 15 Complications of Supracondylar Fractures of the Elbow
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 (acute), or in the osseous structures, such as malalignment (chronic). In this chapter, we first discuss the anatomy of this area, then neurovascular problems, and finally bony complications of supracondylar humerus fractures in children.
Anterior to the supracondylar area of the distal humerus is the median nerve (Fig. 15-1). In the proximal forearm, the anterior interosseous branch separates to innervate the flexor 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.
FIGURE 15-1 Major neurovascular structures of the elbow.
(From Mubarak, S. J., and Hargens, A. R.: Compartment Syndromes and Volkmann’s Contracture. Philadelphia, W. B. Saunders, 1981, p. 24.)
The radial nerve lies posterolateral to the usual location of supracondylar fractures and, thus, is less commonly involved (see Fig. 15-1). The ulnar nerve with its posterior location is uncommonly involved with a typical extension-type supracondylar fracture.
The forearm consists of two basic compartments: volar and dorsal (Fig. 15-2). 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.
(From Mubarak, S. J., and Hargens, A. R.: Compartment Syndromes and Volkmann’s Contracture. Philadelphia, W. B. Saunders, 1981, p. 28.)
The median and ulnar nerves traverse the forearm between the superficial and deep flexor groups. The major arteries about the elbow include the brachial artery, which bifurcates 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 the brevis muscles. This group of muscles is physically and functionally distinct; it lies between the dorsal and volar forearm compartments and probably 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 recent study by Louahem et al,46 the most commonly injured nerve was the anterior interosseous branch of the median nerve. This is likely due to its anatomic arrangement of the exclusively motor posterior fascicles which are exposed to the zone of injury, and its tight tethering to the proximal forearm musculature. The second-most commonly involved nerve was the ulnar, followed by the radial nerve. Ulnar nerve injury was most commonly associated with posterolateral fracture patterns due to direct contusion and stretching 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 stretching from the laterally displaced proximal humeral fragment.
Ulnar nerve injury also occurred iatrogenically in 5% of patients during medial percutaneous pin placement in a recent large series.69 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.63 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.69 A displaced supracondylar fracture presenting with an absent radial pulse has a 50% to 60% incidence of associated nerve injury at fracture presentation.19
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 autonomous zones of the median, ulnar, and radial nerve.
After reduction of the fracture and stabilization with percutaneous pinning, re-evaluation of the neurovascular examination is mandatory. On rare occasions, the compromised nerve may recover before the patient’s discharge, but in most incidents, 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 to evaluate the status of recovery 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.19
Advances in surgical techniques with lateral pin entry fixation have demonstrated significant decreases in iatrogenic ulnar nerve injury and satisfactory mechanical stability in Gartland type II, III and IV fractures.43,69,70 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 result from supracondylar fractures or other injuries to the elbow region that can lead to forearm ischemia: (1) arterial injury and (2) compartment syndrome from hemorrhage or postischemic swelling (Fig. 15-3). An arterial injury may result from laceration, thrombus, embolus, intimal tear, or pseudoaneurysm (Fig. 15-4). Such an injury may cause nerve and muscle ischemia directly or may result in postischemic swelling or hemorrhage, thereby causing a compartment syndrome.
(From Mubarak, S. J., and Hargens, A. R.: Compartment Syndromes and Volkmann’s Contracture. Philadelphia, W. B. Saunders Co., 1981, p. 22.)
The muscles of the extremities are grouped into compartments that are enclosed by a relatively noncom-pliant osteofascial envelope. Muscle swelling causes increased pressure within the compartment that is not easily dissipated owing 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 the 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’s contracture is the popular term that refers to the end stage of an ischemic injury to the muscles and nerves of the limb (Fig. 15-5). Untreated compartment syndromes and arterial injuries are the primary causes of Volkmann’s contracture. The term Volkmann’s ischemia is nonspecific and should not be used.
In general, the most common traumatic event that produces a compartment syndrome or an arterial injury about the elbow is the supracondylar fracture of the distal humerus (Fig. 15-6). In 1956, Lipscomb noted that supracondylar fractures were the cause of 48% of Volkmann’s contractures in 92 cases from the Mayo Clinic.45 In 1967, Ehrlich and Lipscomb, in a review of 32 more cases of Volkmann’s contracture, reported that 34% were due to supracondylar fractures and 22% were due to forearm fractures.13 In 1979, Mubarak and Carroll, reporting on 58 Volkmann’s contractures in children (Fig. 15-7), found that supracondylar fractures had caused only 16% of these contractures.56 In most recent studies, compartment syndromes are extremely unusual because of the advent of early closed reduction and percutaneous pinning.
(From Mubarak, S. J., and Hargens, A. R.: Compartment Syndromes and Volkmann’s Contracture. Philadelphia, W. B. Saunders, 1981, p. 88.)
(From Mubarak, S. J., and Carroll, N. C.: Volkmann’s contracture in children: aetiology and prevention. J. Bone Joint Surg. 61B:285, 1979.)
An arterial injury can produce nerve and muscle ischemia directly or the additional problem of a compartment syndrome by one of two mechanisms (see Fig. 15-3).57 First, if the major vessel is lacerated, hemorrhage into the compartment may produce the syndrome. Second, a compartment syndrome may result from postischemic swelling if there is inadequate collateral circulation or if the vessel is only partially occluded, for example, from an arterial spasm or an intimal tear. In this situation, the decreased perfusion and ischemia of both capillaries and muscles will cause an increase in the permeability of the capillary walls. The resulting edema will then cause more ischemia, and a vicious circle may ensue. When there is complete arterial occlusion, a compartment syndrome may develop from postischemic swelling or reperfusion injury after the circulation is restored (Fig. 15-8). When complete arterial occlusion is secondary to massive emboli or prolonged use of a tourniquet in which the circulation is not restored, gangrene rather than compartment syndrome will likely result.
There is an association between supracondylar fractures, an absent radial pulse, and Volkmann’s contracture. When the concepts of compartment syndrome as a cause for Volkmann’s contracture became popular, forearm fasciotomies became the accepted treatment method to prevent this devastating complication. An absent radial pulse, which is most commonly associated with arterial injury, began to merge with the notion of compartment syndrome. This misconception has no doubt caused many physicians to delay treatment for a compartment syndrome while waiting for the radial pulse to disappear. Owing to these misconceptions, the signs and symptoms of arterial injury compared with those of compartment syndrome will be discussed in detail.
As with a compartment syndrome, pain out of proportion to that expected for the injury is the earliest symptom of arterial ischemia. The earliest clinical sign for an arterial injury is pain with passive stretch of the involved muscles. This usually will be associated with absent or decreased pulses, poor skin color, and decreased skin temperature. Other early findings are weakness and hypesthesia in a glove-like distribution.
The early diagnosis of a compartment syndrome depends on recognition of the signs and symptoms of increased intracompartmental pressure. The first and most important symptom of an impending compartment syndrome is pain that is greater than that expected from the primary problem (e.g., the fracture or contusion). The pain is usually described as a feeling of increased pressure and is localized to the affected compartment. It is not relieved by immobilization. Pain may be lacking if a central or peripheral sensory nerve deficit is superimposed. Other early symptoms include swelling, numbness, and weakness.
The earliest and most objective finding is a tense compartment that is a direct manifestation of the increased intracompartmental pressure. The tenseness should be evident throughout the involved compartments. To evaluate this, all dressings must be removed. Although it is not possible, even with experience, to estimate consistently by palpation the degree to which intracompartmental pressures are elevated, the presence of significant tenseness throughout the compartment boundaries suggests a compartment syndrome. Conversely, if the compartment is palpably soft, the examiner may be reassured that, for the moment, compartment pressures are not elevated.
Pain with passive stretch of the muscles in the involved compartment is a common finding that is usually associated with muscle ischemia. However, direct muscle injury or contusion may elicit this clinical finding.
The volar compartment of the forearm is traversed by nerves (radial, ulnar, and median) that have a distal sensory distribution in the hand. The first sign of nerve ischemia is alteration of sensation, which is manifest early by subjective paresthesia in the distribution of the involved nerve, followed by hypesthesia and, later, anesthesia. Unless there is a superimposed sensory or peripheral nerve deficit, decreased sensation to light touch or pinprick in the distal sensory distribution is a very reliable sign of ischemia. The dorsal compartment of the forearm is not associated with a specific sensory nerve.
Paresis secondary to nerve or neuromuscular junction ischemia and elevated intracompartmental pressure is a common finding. The paresis may be confusing, however, because it may be secondary to proximal nerve injury or guarding secondary to pain rather than to intracompartmental ischemia.
Except in the presence of major arterial injury or disease, peripheral pulses and capillary filling are routinely intact in compartment syndrome patients. Although intracompartmental pressures may become high enough to cause ischemia of the muscle and nerve by occluding the microcirculation within the compartment, the pressures are rarely high enough to occlude the major arteries (Fig. 15-9). In our experience, the intracompartmental pressures usually do not exceed 80 mm Hg and are more commonly between 40 and 60 mm Hg. It has been suggested that absent pulses may result from vascular spasm secondary to elevated intracompartmental pressures.12 Mubarak and colleagues have demonstrated that pressurization to as high as 80 mm Hg of the entire anterolateral compartment in a number of dogs produced only occasional transient spasm of the midsize vessels on angiography.
FIGURE 15-9 Schematic view of forearm compartment syndrome. Intracompartmental pressures are rarely high enough to occlude the major arteries of the compartment. However, the pressure is sufficient to cause ischemia of muscle and nerve by occluding the microcirculation within the compartment.
(From Rang, M.: Children’s Fractures. Philadelphia, J. B. Lippincott Co., 1974.)
Many traumatic events that precipitate a compartment syndrome or arterial injury can also produce a painful, swollen extremity. The diagnosis of the underlying problem (e.g., fracture or contusion) is obvious; the diagnosis of a superimposed ischemia is more difficult. Pain out of proportion to that expected for the injury and any sensory deficit must be explained. A compartment syndrome or an arterial injury also must be differentiated from a nerve injury, which is usually a neurapraxia when it is associated with a closed elbow fracture or dislocation. The clinical findings of these three entities overlap, frequently making the diagnosis difficult, if not impossible, by clinical means. All of these problems may be associated with motor or sensory deficits and pain. Careful clinical evaluation is necessary to differentiate these entities (Table 15-1). As noted earlier, an arterial injury usually results in absent pulses, poor skin color, and decreased skin temperature. In contrast, a compartment syndrome routinely presents with intact peripheral circulation unless the underlying etiology is an arterial injury. A diagnosis of nerve injury is usually made by exclusion of the other two entities. Doppler blood flow studies, arteriography, and pressure measurements are frequently required to aid in the differential diagnosis of these three entities, especially if these problems are present in combination.
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From Mubarak, S. J., and Carroll, N. C.: Volkmann’s contracture in children: aetiology and prevention. J. Bone Surg. 61B:290, 1979.
Differentiation of these entities is important because therapy for each is radically different. The neurapraxia accompanying a closed fracture is usually best treated by observation. Arterial injuries warrant immediate operative repair of the vessel, and a compartment syndrome necessitates immediate decompressive fasciotomy.
When evaluating a patient with a traumatized limb and a neurocirculatory deficit, the physician should document carefully the time of injury and examination. A thorough examination should include motor, sensory, and circulatory evaluation. In the case of a young child, in which patient cooperation is not possible, observations of finger movement should be documented while the circulation is objectively assessed by palpation of the pulses and by Doppler examination. When a neurologic deficit is observed in a painful, traumatized, and swollen limb, the physician must evaluate and treat the patient promptly. At this stage, one must differentiate the troublesome problems of compartment syndrome, neurapraxia, and arterial injury.
When an arterial injury associated with a supracondylar fracture is suspected, a Doppler examination should be performed. The velocity Doppler is an integral instrument in assessing the presence of peripheral pulses and is very useful for noninvasive documentation of pulses in the presence of a markedly swollen extremity. A quantitative Doppler technique has been described by Schoenecker and colleagues66 to detect significant asymmetry between the injured and an uninjured extremity in children with type III supracondylar humerus fractures. Arteriography is not recommended in an acute situation.67 Shaw and associates noted the risk of arteriography to be the following: (1) prolongation of ischemic time between fracture and reduction; (2) arterial damage at the catheter insertion site; and (3) allergy to contrast material.67
After confirmation of distal forearm ischemia, an attempt to better align the fracture fragments should be made immediately in the emergency room. In extension-type fractures, this is accomplished by extending the elbow, correcting any coronal plane deformity, and reducing the fracture by bringing the proximal fragment posteriorly and the distal fragment anteriorly (Fig. 15-10). Often, this simple maneuver will immediately restore distal circulation.33 If the distal circulation is not restored, a vascular surgeon should be notified, and the patient should be taken immediately to the operating room. All authors agree that the fracture should be reduced and stabilized by percutaneous pinning or, if necessary, open reduction and fixation. If the radial pulse does not return within 30 minutes, and signs of forearm and hand ischemia continue to be evident, then exploration of the brachial artery at the fracture site is recommended. In these circumstances, prophylactic fasciotomy of the forearm should be considered after brachial artery repair if the period of ischemia is more than 4 hours. An algorithm for the treatment of supracondylar humerus fractures associated with forearm and hand ischemia is represented in Figure 15-11.
(From Herring, J. A.: Tachdjian’s Pediatric Orthopedics, 3rd ed., 2002, p. 2148.)
(From Mubarak, S. J., and Hargens, A. R.: Compartment Syndromes and Volkmann’s Contracture. Philadelphia, W. B. Saunders, 1981, p. 144.)
Shaw and colleagues67 explored three cases and documented intimal tears with thrombus obstructing the brachial artery lumen. In two patients, the injured segment was excised and replaced by a saphenous vein graft; and prophylactic fasciotomy was also performed. One patient was noted to have brachial artery entrapment at the fracture site that was appropriately released.
Schoenecker and associates66 recommend brachial artery exploration if Doppler-detectable pulses did not return within 30 minutes after fracture reduction. A vascular surgeon assisted with the exploration. Three of seven patients demonstrated interluminal damage or transsection, requiring saphenous vein graft. Four others demonstrated kinking or entrapment of the artery at the fracture site, with re-establishment of the pulses after mobilization. Garbuz and coworkers19