ANATOMY

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.

FIGURE 15-2 Forearm compartments: transverse sections through the left forearm at various levels.

(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.

ETIOLOGY: NERVE INJURY

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

CLINICAL DIAGNOSIS

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.

TREATMENT

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.

ETIOLOGY: ISCHEMIA

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.

FIGURE 15-6 A 3-year-old boy who sustained a supracondylar fracture. At the time of cast removal, his forearm had poor sensation and was contracted in the pronated and flexed position.

(From Mubarak, S. J., and Hargens, A. R.: Compartment Syndromes and Volkmann’s Contracture. Philadelphia, W. B. Saunders, 1981, p. 88.)

FIGURE 15-7 Causes of Volkmann’s contracture in 58 limbs (55 children). In this study, the supracondylar fractures accounted for half of these complications in the upper extremity.

(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.

FIGURE 15-8 Pathogenesis of postischemia-initiated compartment syndrome.

(From Mubarak, S. J., and Hargens, A. R.: Compartment Syndromes and Volkmann’s Contracture. Philadelphia, W. B. Saunders, 1981.)

CLINICAL DIAGNOSIS

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.

Symptoms and Signs of Arterial Injury

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.

Symptoms of Compartment Syndrome

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.

Signs of Compartment Syndrome

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.)

DIFFERENTIAL DIAGNOSIS

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.

TABLE 15-1 Typical Clinical Findings of Compartment Syndrome, Arterial Occlusion, and Neurapraxia

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.

TREATMENT

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.

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.

FIGURE 15-10 A and B, Simple realignment of an ischemic limb may reduce the tension on the brachial artery and restore the distal circulation.

(From Herring, J. A.: Tachdjian’s Pediatric Orthopedics, 3rd ed., 2002, p. 2148.)

FIGURE 15-11 Scheme for management of supracondylar fractures associated with upper extremity ischemia.

(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 explored five brachial arteries and found a similar ratio of luminal damage, laceration, and entrapment of the arteries. One patient was treated with ligation, and had long-term claudication symptoms. Eight of 11 patients who initially had an absent radial pulse demonstrated a return of the pulse after the closed reduction. In three children, the radial pulse did not return, but no further treatment was required because the forearm and hand remained pink without any further neurologic deficits. This is known in the orthopedic literature as the “pulseless pink hand.”

The Vancouver study group reviewed the pulseless pink hand in 13 patients following closed reduction and percutaneous pinning of the supracondylar fracture.⁶⁵ They recommended color flow duplex scanning and MRA as a noninvasive safe technique for evaluating brachial artery patency and collateral circulation around the elbow. The vascular injuries in the 13 patients were studied; four had a thrombus or intimal tear. These patients underwent vein patch graft angioplasty. Urokinase infusion was used intra-arterially in four patients, and open thrombectomy was used in one. At follow-up, MRA studies of these patients showed a high rate of asymptomatic reocclusion and residual stenosis of the brachial artery. Thus, the investigators called into question the need for vascular reconstruction of intimal tears when the patient has a pink, well-perfused hand and MRA or other noninvasive studies that demonstrate adequate collateral circulation. They strongly recommended observation as the mainstay of treatment for these patients.

In a recent survey of pediatric orthopedic surgeons, 60.5% of responding surgeons would monitor a pulseless pink hand for at least 24 hours following reduction and pinning. If the hand remained pulseless after 24 hours, the majority of respondents (61.2%) would continue to observe the extremity and monitor for adequate collateral circulation.⁴⁹

Compartment Syndrome

When the patient is cooperative, most compartment syndromes can be diagnosed clinically, and intracompartmental pressure measurement is only confirmatory. There are three groups of patients in whom difficulties in eliciting or interpreting the physical findings make measurement of intracompartmental pressure particularly valuable as a criterion for decompression:

1. Uncooperative or unreliable patients. A child with a supracondylar fracture will often be so frightened that careful motor and sensory evaluation is not possible.

2. Unresponsive patients. A patient with a head injury or one who is sedated and on a respirator with a swollen limb needs pressure measurement.

3. Patients with nerve deficits. When there is an associated nerve injury or arterial injury at the elbow, intracompartmental pressure measurement frequently is required to differentiate these problems from a compartment syndrome.

Mubarak and colleagues recommend that any intracompartmental pressure greater than 30 to 35 mm Hg be considered for fasciotomy if it is combined with the clinical findings of a compartment syndrome. However, one must remember that any threshold pressure is a relative indication for decompression that should be tempered by the patient’s overall condition, blood pressure, and peripheral perfusion; the trend of the symptoms and signs; the trend of the intracompartmental pressures; and the cooperation and reliability of the patient.⁵⁷

Bardenheuer² was the first to report on fasciotomy in the forearm. Eichler and Lipscomb¹³ described an approach to a patient with a forearm compartment syndrome that included a division of forearm skin, subcutaneous tissue, and fascia. In 1972, Eaton and Green¹¹ described a specific operative technique in which the skin incision began distal to the elbow flexion crease and medial to the bicipital tendon, extending distally in the longitudinal axis of the midforearm to the transverse flexion crease at the wrist. The forearm fascia was incised longitudinally along its full length. The epimysium of all poorly vascularized muscles was sectioned. The fascia was left open, and delayed closure with split-thickness skin grafts and relaxing incisions was performed 48 to 72 hours later.

Neumeyer and Kilgore’s incision began adjacent to the medial epicondyle, extended obliquely across the antecubital fossa over the volar mobile wad, and returned to the midline in the distal forearm.⁵⁹ It continued in a curvilinear fashion across the carpal canal to the midpalm. This report recommended wide exposure of all three possible areas of involvement: the volar and dorsal compartments of the forearm and the intrinsic compartments of the hand. Closure was accomplished by split-thickness skin grafts after several days.

Whitesides and associates⁷⁷ described another operative approach in which the incision began above the elbow laterally and was carried transversely across the an-tecubital fossa to the proximal-medial forearm. The incision was continued distally along the ulnar border of the forearm to the wrist, where it curved laterally in the flexor crease of the wrist and extended into the palm in the thenar crease. The fascia was opened from above the elbow to the midpalm. The carpal tunnel and all neurovascular and muscular envelopes were opened fully. They noted that subcutaneous fasciotomy should never be performed in the forearm. The fascia was left open and was closed by split-thickness skin grafts 48 to 72 hours later. Similarly, Matsen and associates used the volar-ulnar approach. They frequently performed carpal tunnel release and epimysiotomy, as recommended by Eaton and Green.¹¹ The advantage of this volar-ulnar approach is that the flexor tendons and median nerve are not left exposed in the distal forearm.

The effectiveness of the volar forearm fasciotomy was evaluated initially in a series of cadaver experiments.²¹ The incisions used were the volar-ulnar incision described by Whitesides and associates⁷⁷ and the curvilinear midline volar incision. Both incisions were effective in lowering pressures in the volar forearm, and both also lowered pressure within the mobile wad and dorsal regions in approximately half of the limbs. However, the curvilinear incision allowed easier exposure of the arteries and nerves of the forearm and the mobile wad. The volar forearm pressure generally fell to normal values when the antebrachial fascia had been divided from the lacertus fibrosus to the junction of the middle and distal thirds of the forearm. When the dorsal pressures remained elevated following volar fasciotomy, a dorsal fasciotomy was performed.

A Volkmann contracture is the major complication of a compartment syndrome. Fortunately, the incidence of that complication following supracondylar fractures, as previously noted, has declined significantly in the past 40 years. With proper treatment of the elbow injury and early recognition and treatment of ischemia, Volkmann’s contracture is a rarely seen sequela of a supracondylar fracture. Many large series on the treatment of supracondylar fractures report no cases of Volkmann’s contracture when treated by Dunlap’s traction,¹⁰ overhead pin traction,⁶ or percutaneous pinning.^14,43,69,70

Gelberman and colleagues²⁰ reported no cases of Volkmann’s contracture in a study of supracondylar fractures. However, they noted that crush injuries or severe open injuries, when associated with compartment syndromes, resulted in considerable disability with decreased strength and limitation of forearm and hand motion. In these cases, much of the functional loss can be attributed to the crush injury alone; the compartment syndrome is an additional insult.²⁰

A complete discussion of the treatment of an established contracture is covered by Gelberman^20,21 and others,⁵⁷ and is beyond the scope of this discussion.

Authors’ Prefered Fasciotomy Technique

We prefer a single longitudinal curvilinear incision for decompression of the volar forearm (Fig. 15-12). This incision allows an easy approach to the antebrachial fascia and the transverse carpal ligament, as well as to the neurovascular structures of the forearm and the mobile wad. The incision is nearly identical to McConnell’s combined exposure of the median and ulnar neurovascular bundles, as described by Henry.³¹ A straight longitudinal incision is used for the dorsal compartment of the forearm (see Figs. 15-2 and 15-13). Technique and postoperative care are described in detail elsewhere.^20,21,57

FIGURE 15-12 Dorsal and volar forearm incisions.

(From Gelberman, R. H., Garfin, S. R., Hergenroeder, P. T., Mubarak, S. J., and Menon, J.: Compartment syndromes of the forearm: diagnosis and treatment. Clin. Orthop. 161:252, 1981.)

FIGURE 15-13 Cross-section of left forearm with wick catheter illustrating its position and fasciotomy incision. W, Wick catheter; 1, ulnar nerve; 2, ulna; 3, radius; 4, median nerve; 5, radial artery; 6, forearm fascia.

(From Gelberman, R. H., Garfin, S. R., Hergenroeder, P. T., Mubarak, S. J., and Menon, J.: Compartment syndromes of the forearm: Diagnosis and treatment. Clin. Orthop. 161:252, 1981.)

It is clear that many factors influence the result of a supracondylar fracture associated with ischemia. However, the treating orthopedic surgeon must carefully assess the clinical findings and document them in the medical records. When appropriate, laboratory instruments such as Doppler blood flow studies, MRA (for a possible arterial injury), and intracompartmental pressure measurements (for possible compartment syndrome) should be performed to clarify the diagnosis. Treating these causes for forearm and hand ischemia promptly will result in the best results.

SURGICAL TIMING AND NEUROVASCULAR COMPLICATIONS

A number of recent studies have investigated the association between surgical timing and perioperative complications in the treatment of closed, well-perfused, displaced supracondylar humerus fractures in children.^28,51,75 The groups from Cincinnati and Los Angeles were unable to identify any significant differences in the need for open reduction (2% to 13%), or the rates of pin tract infection (1% to 4%), iatrogenic nerve injury (2% to 4%), vascular injury recognized after surgery (2%), and compartment syndrome leading to Volkmann’s ischemic contracture (0%) when comparing patients with closed, well-perfused, displaced supracondylar humerus fractures treated 8 to 12 hours following the initial injury with those treated more than 8 to 12 hours after injury.^28,51

More recently, a group from Edinburgh, Scotland, did demonstrate an increased need to perform an open reduction in patients with closed, well-perfused, Gartland type III supracondylar humerus fractures when surgery was delayed more than 8 hours following injury (33%) compared with those treated in less than 8 hours from the time of injury (11.5%), P = 0.05.⁷⁵

All of these studies specifically excluded two of the most common indications that prompt the emergent treatment of supracondylar humerus fractures: open fracture and extremity ischemia. We do not recommend delayed treatment in those situations. At present, we will allow an 8- to 12-hour delay in the treatment of displaced supracondylar humerus fractures provided that the skin is intact and the neurovascular examination is normal. These patients are splinted in a position of comfort and are admitted for elevation/observation until definitive surgical treatment. Some fractures with marked displacement can be provisionally reduced in the emergency room to improve patient comfort and fracture position before splinting. Patients in whom the skin is compromised, the swelling is severe, or the neurovascular examination is abnormal are treated with closed reduction and pinning emergently.

AVASCULAR NECROSIS

Despite the rich vascular supply, AVN has been reported in the distal fragment following a supracondylar humerus fracture.⁵⁵ AVN of the capitellum as well as the trochlea has been reported, although both are extremely rare. The occurrence of AVN is much more likely to be associated with a condylar fracture, medial or lateral, than with a supracondylar humerus fracture. Condylar fractures require early and accurate diagnosis as well as prompt management to maximize successful osseous healing and minimize the development of future deformity. Even in widely displaced type III supracondylar fractures, Morrissy and Wilkins⁵⁵ did not find a correlation between severity of the fracture and the extent of avascular changes, which are very rare. Because the capitellar blood supply enters the distal humerus laterally and distally, a fracture that exits the lateral column very distally may lead to avascular changes in this region. Similarly, low fractures exiting medially may be at increased risk for avascularity associated with the trochlea.

Distal humeral AVN and the fishtail deformity may be associated with decreased range of motion, the development of a cubitus valgus deformity, and, occasionally, a subsequent tardy ulnar nerve palsy. Depending on which of the two vascular supplies to the growth centers is compromised, different deformities may develop. With elimination of the more lateral trochlear blood supply, such as may occur with a supracondylar humerus fracture with T intercondylar extension, a classic fishtail deformity of the distal humerus may occur (Fig. 15-14). The fishtail deformity is more frequently associated with an inadequately treated lateral condyle fracture. The deformity includes the loss of the normal crista dividing the capitellum from the trochlear groove and central involution of the distal articular surface. The central involution allows the proximal ulna to “settle” into the distal humerus. Clinically, the prominence of the olecranon normally seen during maximal flexion of the elbow is absent (Fig. 15-15).

FIGURE 15-14 Trochlear blood supply. Medial and lateral vessels feed the trochlea; the severity of avascular changes as well as the type of resulting deformity is dependent on which vessel is injured. In this illustration, a central deficiency and fishtail deformity of the distal humerus would be expected to develop.

(From Rockwood, C. A., Wilkins, K. E., and Beaty, J. H.: Fractures in Children, 4th ed., Vol. 3. Philadelphia, Lippincott-Raven, 1996.)

FIGURE 15-15 Fishtail deformity—loss of the olecranon prominence. Clinical findings of avascular necrosis (AVN) of the distal humerus can include depression of the prominence of the olecranon secondary to a central deficiency as demonstrated in this silhouette of flexed elbows as viewed from the patient’s head. Also cubitus varus or less likely valgus and diminished range of motion may be seen with AVN of the distal humerus.

If both vessels feeding the distal humeral fragment have been compromised, complete aplasia of the trochlea may result. This condition will most likely lead to a progressive cubitus varus deformity and potential posterolateral rotatory instability of the ulnohumeral articulation. A tardy ulnar nerve palsy may also develop. Causative factors include instability of the ulnar nerve over a hypoplastic medial condylar region and scarring or tethering as the nerve enters the flexor carpi ulnaris.¹⁶ In time, this leads to abnormal traction, stretching, and friction of the ulnar nerve as it moves over the medial epicondyle, producing a gradual progressive ulnar neuropathy.³⁴

Management of the sequelae of distal humeral AVN is rarely satisfying. Surgical intervention for improvement of motion may be indicated in specific cases, if a vigorous physical program is unsuccessful. Cases of tardy ulnar nerve palsy are managed with anterior transposition of the ulnar nerve. Progressive angular deformity of the distal humerus may be attributable to either AVN or physeal injury. Physeal arrest, sporadically reported in conjunction with even mild supracondylar humerus fractures, appears similar to a nonunion but is rare.^37,60 If it is detected early and the degree of physeal involvement is limited, physeal bar resection, although technically demanding, may be considered. Although the fishtail deformity itself is not amenable to surgical correction, cubitus varus or valgus, which may occur in conjunction with either physeal arrest or AVN, can be corrected with a supracondylar osteotomy. Because the restoration of growth potential may not be possible in cases of AVN, as in some cases of physeal arrest, recurrent angular deformity may occur, depending on the age of the child, requiring multiple osteotomies over time.

Other potential etiologies for loss of range of motion include myositis ossificans, soft tissue contracture or scar formation, osseous deformity producing a bone block to motion, and angulation at the fracture site.

In cases in which the fracture has healed but flexion or extension is believed to be limited structurally by a bony block, excision of the tip of the olecranon with enlargement of the olecranon fossa may occasionally prove beneficial (Fig. 15-16). Osseous impingement is an uncommon cause of motion loss. The technique has been well described for the management of the more common impingement from degenerative changes of the elbow by Morrey.⁵⁴

FIGURE 15-16 A, Teenage patient with open reduction and internal fixation of left supracondylar humerus fracture with markedly limited motion postoperatively secondary to arthrofibrosis as well as impingement of both the coronoid and olecranon fossae due to healing with collapse of the medial and lateral columns of the distal humerus. B, Three-dimensional computed tomography scan of elbow showing impingement of the olecranon fossa. C, Distal humeral osteoplasty was performed with removal of the tip of the olecranon, foraminotomy of the distal humerus, and débridement of impinging distal humerus proximal to the capitellum. The arc of motion of the elbow increased by 50 degrees postoperatively.

MYOSITIS OSSIFICANS

Myositis ossificans is a potential complication of supracondylar humerus fractures, which if extensive, results in poor elbow motion. The phenomenon is not common and may even be self-limiting, with resolution over a 1- to 2-year course (Fig. 15-17). Siris⁷¹ found a 2% incidence in a 1939 review of 330 supracondylar humerus fractures, whereas more recent studies have reported an incidence of less than 1% and 0% by most authors. The occurrence and severity would intuitively be expected to be increased in cases treated with open reduction, particularly if the surgery is delayed from the time of the injury. In supracondylar humerus fractures treated with open reduction acutely, only one report identifies myositis as a postoperative complication.²² Even with delayed open management, Lal and Bhan⁴² found no cases of myositis ossificans in their report of 20 fractures treated with open reduction 11 to 17 days after injury. Surgical excision of the affected tissue should be performed only if the ectopic bone is clearly demonstrated to be causative of motion loss, conservative attempts to regain motion have failed, and adequate time from that of the injury has transpired such that the lesion is quiescent. Bone scan has been recommended in assessing the metabolic activity level of the lesion, but the editor favors the plain radiographic features of clear marginal delineation and trabecularization. Attempts to prevent heterotopic bone formation with low-dose external beam irradiation, and administration of oral nonsteroidal anti-inflammatory agents or oral disphosphonates are not warranted due to the rarity and self-limiting nature of this complication.³⁰

FIGURE 15-17 Myositis ossificans. A, Supracondylar fracture with myositis ossificans and a rigid elbow. B, Spontaneous resorption and remodeling with restoration of motion, lacking 20 degrees of flexion 7 months after injury.

ANGULAR DEFORMITY

Angular deformity of the elbow is the most common significant adverse sequela of a supracondylar humerus fracture. This condition may arise from growth disturbances such as a physeal injury or AVN, as outlined previously, or from the position in which the fracture healed. Malunion may result in either a flexion or extension deformity in the sagittal plane; a varus or valgus deformity in the coronal plane; and rotational deformity in the horizontal plane. Deformity may occur in any single plane or in a combination of planes. Although some remodeling of sagittal plane deformity can be expected, no significant improvement in coronal and horizontal deformity should be anticipated.^4,15,40,52

Although cubitus valgus has been reported in association with supracondylar fractures of the humerus,⁸ cubitus varus is far more commonly reported as a complication of the management of these fractures.

Cubitus varus has been termed a cosmetic sequela by numerous authors. This characterization may limit indications for corrective surgery, particularly in the modern medical environment. Tardy ulnar nerve palsy has been described in association with cubitus varus, although it is more commonly found secondary to cubitus valgus.¹⁷ Functional deficits and a potential increased risk of new injury as well as limitations of motion and discomfort have been well described in patients with cubitus varus. A correlation between re-sidual cubitus varus following supracondylar humerus fractures and subsequent lateral condyle fractures has been noted.⁷ Thus, although the indications for surgical correction of cubitus varus do include poor cosmesis of an unsightly deformity, one must also consider future function of the extremity and the risk for new injuries due to altered biomechanics of the elbow in varus.

SURGICAL APPROACH

In considering surgical correction of a distal humeral deformity, one of the first steps is deciding on the surgical approach. A medial approach, which allows visualization and protection of the neurovascular bundles, has been advocated by some authors.³⁹ One potential detraction from this approach is that manipulation of the neurovascular structures is necessary to gain access to the distal humerus. Also, particularly for cubitus varus, an osteotomy with lateral closing is difficult from the medial approach.

The posterior approach has been advocated by several authors. This can be accomplished through a triceps-splitting, triceps-tendon transecting,^27,61 or triceps-sparing technique.^27,61 Avascularity of the distal fragment has been reported to be associated with this tendon transection.²⁷ The posterior approach, particularly the first two techniques, affords excellent visualization of the distal humerus, being used with some frequency in displaced intercondylar distal humeral fractures. A long incision is necessary, as well as significant dissection, which risks postoperative adhesion formation. In one study of supracondylar humeral fractures, stiffness was noted in 21% of those managed with closed techniques but in 50% of those treated with open reduction through a posterior approach.⁶¹ In addition, intraoperative assessment of the magnitude of correction of the carrying angle can be difficult in the prone or lateral position.

The lateral approach is the most frequently used and advocated approach to the distal humerus for the correction of cubitus varus.^* The dissection is brought to the shaft of the humerus, distal to the area in which the radial nerve exits laterally from around the shaft. A subperiosteal plane is used to expose the humerus, as well as avoid injury to the medial neurovascular structures (Fig. 15-18).

FIGURE 15-18 Lateral approach to the distal humerus. The lateral approach is used to expose the distal humerus. The triceps is taken posteriorly; the brachioradialis and extensor carpi radialis longus are mobilized anteriorly from lateral supracondylar ridge; and the brachialis is dissected off the anterior distal humerus. The radial nerve passes laterally around the humeral shaft just proximal to this dissection, passing between the brachialis and brachioradialis before entering the supinator to become the posterior interosseous nerve.

(Modified from Hoppenfeld, S.: Surgical Exposures in Orthopedic Surgery: The Anatomic Approach, 2nd ed. Philadelphia, J. B. Lippincott, 1984.)

OSTEOTOMY TECHNIQUES

The next step in planning the correction of a distal humeral deformity is the nature of the osteotomy. As already outlined, there are various techniques to consider. The lateral closing wedge osteotomy is the most widely used and recommended technique. With a lateral closing wedge osteotomy, correction of the three aspects of distal humeral deformity following supracondylar fracture malunion are possible: cubitus varus, hyperextension, and rotation (Fig. 15-19). Some authors advocate a simple laterally based closing wedge, leaving the medial cortex intact as a hinge.^{3,23,39,50,62} Although this approach may have value in certain cases with limited deformity, flexion and extension are not well addressed, nor is rotational deformity. Wong and Balasubramaniam⁸⁰ argue that correction of the rotational component is unnecessary. Also, as the size of the wedge required to achieve appropriate valgus alignment increases, so does the prominence of the distal fragment laterally.⁷⁸ Owing to these constraints, a corrective closing wedge osteotomy that is laterally and anteriorly based with medial translation of the distal fragment is preferred to obtain optimal results (Fig. 15-20).^* If desired for greater osseous contact, a spike can be left laterally on the distal fragment to interlock with the proximal shaft, similar to a Wiltse distal tibial varus osteotomy.⁷⁹

FIGURE 15-19 Osteotomy templating. Distal humeral closing wedge osteotomy planned to remove more bone anteriorly to correct any extension deformity, as well as more laterally to correct cubitus varus. The magnitude of anterior closing wedge equals the difference in maximal elbow flexion comparing the injured elbow with contralateral. The magnitude of lateral wedge resection needed equals the degrees of ulnohumeral varus plus degrees of carrying angle of the contralateral elbow.

(Modified from Hollinshead, W. J.: Anatomy for Surgeons, Vol. 3: The Back and Limbs, 3rd ed. Philadelphia, Harper & Row, 1982.)

FIGURE 15-20 Fragment reduction and fixation. In correction of the deformity, the distal fragment is flexed to eliminate hyperextension, rotated to correct varus and provide the planned degree of valgus, and medialized to minimize lateral prominence of the capitellum. Fixation is provided with two to three threaded Steinmann pins, either solely from the lateral aspect of the humerus, or two from the lateral and one from medial, spaced as widely as possible at the osteotomy site for maximal rotational control.

(Modified from Hollinshead, W. J.: Anatomy for Surgeons, Vol. 3: The Back and Limbs, 3rd ed. Philadelphia, Harper & Row, 1982.)

Uchida and associates⁷² described a three-dimensional osteotomy for the correction of cubitus varus. A posterolateral approach is used, and a complex biplane, tridirectional step cut osteotomy is performed, with fixation provided by screws. Although elegant in design and execution, this technically demanding osteotomy differs from a lateral closing wedge flexion osteotomy only in the extent and angle of bone surface contact. If poor postosteotomy healing is a concern, this technique offers extensive surface contact for osseous bridging.

A dome osteotomy has been described that involves a posterior approach, marking the planned dome from a reference Kirschner wire, and uses K-wire fixation.³⁸ This technique allows correction of malrotation and avoids a potentially prominent lateral epicondylar re-gion, but it does not address flexion/extension of the distal fragment. Also, this procedure is more technically demanding than that using the laterally based closing wedge osteotomy. In their report of 11 patients, Kanaujia and associates found that the outcome for all was satisfactory.

FIXATION TECHNIQUES

The final consideration in surgical correction of the distal humerus malunion is fixation options for the osteotomy fragments. These include smooth Kirschner wires,^62,71 threaded Steinmann pins, screws,⁷² screws with a wire tension band,^3,16,45,50 plates and screws,^9,32 and external fixation.⁴² The smooth Kirschner wire fixation has proven to be less than reliable, with a greater incidence of loss of correction compared with threaded fixation (Fig. 15-21). Adequate fixation and maintenance of alignment is reliably obtained and the buried pins can be retrieved in the future, particularly if the physis was crossed for optimal fixation. In the older, larger child, crossed screws may be used, although great care must be exercised to avoid unplanned translation of the fragments. The technique of screws paralleling the osteotomy, connected with a tension band wire, can be used only if good medial cortical integrity remains following the closing wedge osteotomy. Neither medial translation nor derotation is possible if this fixation is chosen. In the older adolescent, one-third tubular or 3.5-mm pelvic reconstruction plates with screws may be necessary to gain adequate fixation, particularly if early range of motion is planned postoperatively. External fixation is another option, although the size of the distal fragment is such that at most two pins could be used. Also, the inherent difficulties with pin tract care exist, which limits the attractiveness of this option.

FIGURE 15-21 A, A 6-year-old boy with cubitus varus of the right elbow following supracondylar fracture. B, Anteroposterior (AP) view of his right distal humerus. C, AP view of the patient’s normal left distal humerus. D, AP view following closing wedge valgus and flexion osteotomy to correct cubitus varus. E, Lateral view 4 weeks postoperatively demonstrating restoration of sagittal alignment, distal humerus.

In summary, distal humeral malunion is not an uncommon complication of supracondylar humerus fractures. The most common deformity is cubitus varus, with varying components of extension and rotation of the distal fragment. The deformity is not purely cosmetic, because it alters the biomechanics of the elbow and may increase the risk to the patient of a future lateral condyle fracture. Corrective osteotomy with attention to detail is reliable and safe. An anterolaterally based closing wedge osteotomy with medial translation of the distal fragment is the treatment of choice. Subdermal threaded Steinmann pin fixation has proved adequate for the vast majority of cases, particularly the younger patient. The buried pins may be removed once healing has occurred, often as early as 6 to 8 weeks. Once osseous union is established, physical therapy can be used to maximize the patient’s range of motion.