Volkmann Contracture 

In 1881, Richard von Volkmann published an article in which he attempted to ascribe irreversible contractures of the flexor muscles of the hand to ischemic processes in the forearm. He believed that the problem was caused by massive venous stasis and simultaneous arterial insufficiency secondary to overly tight bandages. In 1906, Hildebrand first used the term "Volkmann ischemic contracture" to describe the final result of any untreated compartment syndrome, and he was the first to suggest that elevated tissue pressure may be causally related to ischemic contracture.

In 1909, Thomas reviewed the 112 published cases of Volkmann ischemic contracture and found fractures to be the predominant cause. However, he also noted that tight bandages, an arterial embolus, or arterial insufficiency could also lead to the problem. Since then, much has been learned about the etiologies of Volkmann contracture, and more important, much has been learned about its preventive therapies.

In 1914, Murphy was the first to suggest that fasciotomy might prevent Volkmann contracture. He also suggested that tissue pressure and fasciotomy were related to the development of contracture. During World War II and subsequent years, many cases of Volkmann contracture occurred as a result of high-velocity gunshot wounds that caused fractures. Unfortunately, the arterial spasm accompanying the fracture was seen as the cause; therefore, more attention was directed to treating arterial spasm than to the need for fasciotomy.

Surgical exploration of the artery often led to reversal of an acute impending compartment syndrome. It is now thought that this outcome occurred because vascular surgeons were actually performing limited fasciotomies during exposure of the vasculature. Appreciation of the importance of fasciotomy grew during the Vietnam War, and, in 1967, Chandler and Knapp suggested that long-term results might have improved if the surgeons had included routine fasciotomy with arterial repairs.

Originally, most studies of ischemic contractures were focused on those of the upper extremity. In 1958, Ellis reported a 2% incidence of compartment syndrome with tibia fractures, and increased attention was paid to contractures involving the lower extremities. Initially, the focus was on the anterior compartment of the leg, but the work of Seddon, Kelly, and Whitesides in the mid-1960s demonstrated the existence of 4 compartments in the leg and the need to decompress more than just the anterior compartment.^{[1, 2]} Since then, compartment syndrome has been shown to affect many areas of the body, including the hand, foot, thigh, and buttocks.

Frequency

Overall, Volkmann contractures are rare, with an incidence of about 0.5%. Blakemore et al reviewed 978 consecutive upper-extremity long-bone fractures in children admitted to the hospital over a 13-year period.^[3] Thirty-three were noted to have a supracondylar fracture. Three (7%) developed a compartment syndrome requiring fasciotomies. In a subgroup analysis, 9 children had ipsilateral displaced, extension, supracondylar humerus fractures or displaced forearm fractures. In this subgroup, the prevalence of Volkmann contracture was 33%.

Any process that leads to increased compartmental pressure can lead to a compartment syndrome.^[4] For example, decreased compartment size with no change in volume results in increased pressure. This change can be secondary to closure of fascial defects, localized external pressure, or overly tight dressings. Many processes lead to increased compartment content without a corresponding increase in compartment volume, thereby increasing pressure. Bleeding into a closed compartment can be due to a major vascular injury or a bleeding disorder, congenital or acquired.^[5]

Increased capillary permeability can be due to exercise, burns, hypoalbuminemia, intra-arterial drugs, surgery, seizures and eclampsia, exercise, and trauma (without major vascular injury). Exercise, venous obstruction, and use of a long-leg brace can lead to increased capillary pressure. Muscle hypertrophy or neoplastic processes can increase the volume and, therefore, the pressure within a compartment. Finally, infiltrated infusions are an unfortunate iatrogenic cause.

Volkmann ischemic contracture is usually seen in children with displaced supracondylar fractures of the humerus or forearm fractures.^{[6, 7, 8, 9]} It results from severe injury to the deep tissues and muscles of the volar compartment secondary to increased compartmental pressures.^{[10, 11]}

Three types of Volkmann contracture have been described: mild, moderate, and severe. The mild type involves wrist flexors. The moderate type involves injury to the flexor digitorum profundus, flexor digitorum superficialis, flexor pollicis longus, flexor carpi radialis, and flexor carpi ulnaris. The severe type involves both the flexors and the extensors.

A variant of Volkmann ischemic contracture known as pseudo-Volkmann contracture has also been described in the literature. This is due to tethering of the flexor digitorum profundus secondary to fractures of the ulna. It has been described to occur 2 days to 16 years after the closed reduction of fractures of the shafts of the radius and ulna. None of the patients had nerve palsies or undue pain after reduction of the fractures.^[12]

A routine check of the passive range of motion of all fingers immediately after closed reductions of fractures of the radius and ulna is recommended. If muscle tethering is detected, repeat manipulation of the fracture is required to release the muscle. If unsuccessful, surgical release through a small incision should be attempted to normalize the length, excursion, and function of the flexor digitorum profundus. Function can be restored by untethering the muscle and its tendons from the ulnar fracture by means of early manipulation or late localized myotenolysis.

The clinical presentation of Volkmann contracture includes what is commonly referred to as the 5 P s. These are pain, pallor, pulselessness, paresthesias, and paralysis. Pain is the earliest sign.^[13]

On physical examination, pain accentuated by passive stretching seems to be the most reliable finding. Firmness of the tissues often is noted on palpation. Pulselessness and paralysis are late findings. Induration of the forearm is another useful diagnostic finding.

Some argue about which compartment pressure readings are indications for fasciotomy. However, most agree that patients with compartment pressures exceeding 30 mm Hg should be taken to the operating room for emergency fasciotomy.^[14]

The relevant anatomy of Volkmann contracture includes the superficial and deep flexor muscles.

Superficial flexor muscles

• Pronator teres - Median innervation
• Flexor carpi radialis - Median innervation
• Flexor carpi ulnaris - Ulnar innervation
• Flexor digitorum superficialis - Median innervation
• Palmaris longus - Median innervation

Deep flexor muscles

• Flexor pollicis longus - Median (anterior interosseous) innervation
• Pronator quadratus - Median (anterior interosseous) innervation
• Flexor digitorum profundus - Median (anterior interosseous) and ulnar innervation

There are no absolute contraindications to immediate decompression for Volkmann contracture in the acute setting.