In 1881, Volkmann described a condition involving muscle ischemia and necrosis that subsequently led to fibrosis and contracture of the forearm ^[1]. In 1909, Thomas ^[2] collected 107 cases that had been reported in the literature and among these were cases in which no splint or bandage had been applied. Brooks ^[3] described a similar condition and believed that venous obstruction was the main factor involved in contracture formation. It is now well recognized that ischemic contractures can develop from many different injuries, as long as the injuries cause swelling of the soft tissues that are contained in relatively non-distensible Osseo-fascial compartments ^[4]. As a result of this swelling, intramuscular pressure is elevated to a magnitude sufficient to occlude capillary perfusion. The compartments with the least ability to expand are most severely affected by this ischemic insult. Because the deep flexor compartment of the forearm lies next to the bone, it is the first and most severely affected variable levels of necrosis and fibrosis, though to a lesser degree, may also be evident in the flexor digitorum superficialis and the superficially located muscles, such as the wrist flexors. The muscle degeneration which follows is most marked in the middle and its extent decreases peripherally, so that a so-called ellipsoid-shaped infarct as described by Seddon may be the end result. Nerve trunks running in the ischemic zone also suffer damage; this is initially caused by ischemia but is later aggravated by the subsequent muscle fibrosis. The incidence of Volkmann’s contracture is low and it is considered as a rare condition with an incidence of 0.5%. The treatment of an established contracture is complicated and depends on the severity of the infarct and the affected muscle and nerve tissue ^[5]. It includes physiotherapy, splinting, muscle sliding, tendon transfer, neurolysis, fibrotic tissue excision, muscle grafting and osteotomy ^[6]. In our case report the Volkmann ischemic contracture (VIC) was caused by excessively tight splint wrapped around the forearm fracture applied by a traditional bonesetter treated successfully with Max page muscle sliding operation.

Here is a 14-year-old boy came to orthopedic department at BGS Global Institute of Medical Sciences hospital (GIMS) with complaints of pain in the left forearm and inability to move left forearm for 6 months. Patient gives history of fall from bicycle after which patient sustained injuries to left elbow for which he took osteopath treatment for 1 week where herbs and cardboard was used. Following which patient developed soakage of wound dressing then took him to other private hospital where X-ray was done, wound was managed and advised for follow-up after 6 months for deformity correction. Later patient came to BGS GIMS for further management. On examination, wasting of the thenar and hypothenar eminence noted, a hypopigmented scar of about 7 × 5 cm present over volar aspect of proximal forearm, hypoesthesia noted over palmar aspect of hand. Movements at elbow both supination and pronation were reduced. There was a flexion deformity at left elbow and wrist joint, hyperextension at the metacarpophalangeal joint, flexion at the proximal interphalangeal, and distal interphalangeal joints. (Fig. 1,2)

Later X-ray was done which showed 6-month-old supracondylar fracture (Figure 1) and diagnosed VIC of the left upper limb, moderate degree based on Tsuge classification (Table 1). Patient was treated with analgesics, antibiotics and other supportive measures. Later under general anesthesia Max Page release surgery was done (Fig. 3). Post-operatively antibiotics, analgesics were continued and good correction was seen at 6months follow up (Fig. 4). A splint was applied to maintain correction (Fig. 5).

VIC is a permanent flexion deformity caused by ischemia that results in a claw-like presentation of the hand. The key precipitating event was acute compartment syndrome, which may occur due to decrease in compartment size or an increase in the volume of the compartment, which can lead to a decrease in blood flow to the muscles and nerves within that compartment. Any cause of compartment syndrome may result in VIC. Intercompartmental pressures of >30 mmHg significantly impair the arterial circulation and are indicative of compartment syndrome ^[7]. VIC is late sequelae of compartment syndrome that occurs when there is sustained ischemic damage to the muscles ^[8]. Acute compartment syndrome is predominantly caused by acute fracture trauma, but it may also result from soft tissue crush injuries or vascular complications [9-11]. The etiology of traumatic hand compartment syndrome into three groups: Soft tissue injury-related, fracture-related, and vascular injury-related causes. The most common etiology of hand compartment was related to soft tissue injuries, which constituted 86.8 % of all etiologies ^[12]. Supracondylar humerus fracture and forearm fracture were the most associated fractures with the development of compartment syndrome and VIC afterward ^[13]. Other rare causes mentioned in the literature [14-16] include intoxication, infusion of hypertonic dextrose extra venously, chemotherapy perfusion for therapy of malignant cancers, and following excision of congenital radioulnar synostosis. VIC has a wide clinical spectrum based on the degree of the nerve injury and the level of muscle necrosis. The signs and symptoms of compartment syndrome include the following: Pain (out of proportion to what one would expect, especially with passive stretch of the muscles). This is the most common complaint. Paresthesia, paralysis, pallor (pale color), poikilothermia (cold distal extremity compared to the contralateral side) and pulselessness. Patients with an ischemic contracture, in contrast to those with acute compartment syndrome, do not experience pain; instead, they have deformity of the wrist, hand, and fingers that causes the hand to have a claw-like appearance, decreased sensation, paleness of the skin, muscle weakness and loss (atrophy) and dysfunction brought on by the ischemia episode and the ensuing muscle scarring and fibrosis. The treatment of ischemic contracture depends on the severity of the condition and the underlying cause ^[17,18]. Mild ischemic contracture can be treated with splinting and hand therapy, while moderate ischemic contracture can be treated with surgical techniques, such as flexor tendons lengthening or tendons transfer. Severe ischemic contracture requires surgery, which can be graded according to the severity of the deformity. Max Page in 1923 stated that if the muscle bellies are spared, one can perform the release of muscle insertions, achieving excellent results ^[19]. This technique was later popularized by Scaglietti ^[20] and Gosset ^[21]. Since then, this technique has produced remarkable results as compared to infarcted muscle excision and muscle lengthening ^[22,23].Post-intervention care may include splinting and rehabilitation to optimize outcomes. Splints are used in rehabilitation to help maintain finger and wrist position and prevent further contracture. (Fig. 5).

Immediate identification of the compartment syndrome and its early treatment is mandatory to avoid its devastating consequences, such as VIC. Once the contracture sets in, the prognosis is always guarded, even after long and intensive physiotherapy and various restorative surgical techniques. Good functional outcomes were achieved in majority of moderate VIC’s operated with Max Page muscle sliding operation.  We therefore recommend Max Page muscle sliding operation as the operation of first choice to treat moderate VIC of the forearm.

Proper assessment and surgical release of Volkmann’s Ischemic Contracture gives good functional outcome of hand