Forearm Compartment Syndrome

Article Author:
Andreea Jimenez
Article Editor:
Raghavendra Marappa-Ganeshan
Updated:
4/1/2020 2:59:06 AM
PubMed Link:
Forearm Compartment Syndrome

Introduction

Compartment syndrome is a condition in which increased tissue pressure within a limited space compromises the circulation and function of the contents of that space. This happens when pressure is elevated over a certain level for some time sufficient to reduce capillary perfusion. The inadequate tissue perfusion then leads to inadequate tissue oxygenation to the nerves as well as muscles within the affected compartment.[1]

Compartment syndrome was first described in 1881 by Richard von Volkmann, a German surgeon, who first described the Volkmann contracture in a publication called 'Non-infective ischaemic conditions of various fascial compartments in the extremities.' He believed at the time that the contracture was not due to nerve damage but rather to ischemia.

The anatomy of the forearm is very complex. The ulna and the radius represent the bony structure. There are 3 compartments of muscles.[2]

The three compartments are:

1. The anterior compartment contains the hand and wrist flexors which are divided into a superficial group (flexor carpi radialis FCR, palmaris longus PL, flexor carpi ulnaris FCU, pronator teres PT, flexor digitorum superficialis FDS) and a deep group (flexor digitorum profundus FDP, flexor policis longus FPL, pronator quadratus PQ). The muscles are largely involved with flexion of the wrist and fingers and pronation. The superficial muscles have their origin on the common flexor tendon on the medial epicondyle of the humerus. The ulnar nerve and artery are also contained within this compartment. The flexor digitorum superficialis lies in between the other four muscles of the superficial group and the three muscles of the deep group. This is why, in some literature, it is classified as the intermediate group.

2. The posterior compartment contains 9 muscles which are responsible for extension of the wrist and digits, and supination of the forearm. It is separated from the anterior compartment by the interosseous membrane between the radius and ulna. It is divided into 3 groups: superficial group (extensor carpi ulnaris ECU, anconeus), intermediate group (extensor digitorum, extensor digiti minimi), and deep group (abductor policis longus APL, extensor policis longus EPL, extensor policis brevis EPB, extensor indicis, supinator). Extensor tendons pass through the extensor retinaculum at the wrist joint in 6 compartments. The supinator and the anconeus are the two muscles in the posterior compartment of the forearm that does not pass through the wrist extensor compartments.

3. The lateral compartment contains the mobile wad of Henry, which is represented by the brachioradialis, extensor carpi radialis longus ECRL, and extensor carpi radialis brevis ECRB. 

The nerves that supply the forearm are the radial nerve, the median nerve, and the ulnar nerve with their sensory and motor branches.

The vascular supply is provided by the radial artery and the ulnar artery and their anastomotic vessels.[1][3]

Etiology

The most common causes include:

1. Trauma is, by far, the most common cause. Within the trauma spectrum, fractures of the midshaft radius and/or ulna, distal radius fractures, or supracondylar humerus fractures are the most common causes in children. Other types of trauma include crush injuries, contusions, or gunshot wounds to the forearm.

2. Tight casts, dressings, or external wrappings

3. Extravasation of intravenous fluids/infusions[4][5]

4. Burns

5. Bleeding disorders

6. Post-ischemic swelling

7. Arterial injuries[6]

8. Intensive use of muscles during exercise, seizures, eclampsia, tetany

9. Intravenous drug administration

10. Anticoagulation therapy increases the risk of compartment syndrome in patients who sustain an injury to their forearm.[7]

11. Rare causes such as snake bites or carbon monoxide intoxication[8]

Epidemiology

Compartment syndrome in the forearm is most commonly seen after trauma associated with fractures, crush injuries, head injuries, and burns.[9] The National Trauma Data Bank (U.S.A.) reveals 1.22% of forearm fractures, and 3.79% of tibial fracture patients underwent fasciotomy for compartment syndrome.[7] Young patients with a mean age of 32 years in males and a mean of 44 years in females are likely to be affected, while the overall incidence of acute compartment syndromes is 3.1 per 100000 population per year in the western world.[10] Incidence is increased in men compared to women with a ratio of 10 to 1.

Pathophysiology

There is more than one theory to describe the pathophysiology of compartment syndrome.[11] Amongst them, the common factor tends to be anoxia at the cellular level following a cascade of events.[12] The increased pressure within the osseofascial compartment affects the venous return system, which results in decreased arterial pressure and an increase in venous pressure. This leads to a shift in the interstitial and cellular osmolality, creating a vicious cycle of cellular anoxia, leading to chemical mediators further increasing capillary permeability.

Vascularisation in the middle of muscle belly is more affected, and that is when muscle degeneration occurs. Muscles centered around the anterior interosseous artery are the most commonly affected, particularly FPL and FDP. In the acute stage, nerves are involved because of ischemia, and in later stages, damage occurs due to entrapment of nerves in the fibrous tissue. Muscles can retain the electrical response for up to 3 hours. They can tolerate ischemia for up to 4 hours, and irreversible damage occurs at 8 hours. Nerves can conduct impulses for up to 1 hour. They can survive up to 4 hours (neuropraxia), and at 8 hours, irreversible damage occurs.[7]

When sustained vascular compromise occurs, the muscle undergoes necrosis, fibrosis, and contracture. Associated nerve damage causes further muscle dysfunction, sensory deficits, and may result in chronic pain. The result is a dysfunctional muscle compartment with local and distant manifestations that depend on the compartment involved and the degree of muscle contracture as well as nerve damage.[1]

History and Physical

Compartment syndrome of the forearm is primarily a clinical diagnosis. Most often, patients present within a few hours of the inciting event, sometimes even within 48 hours. They present with a swollen, tense, tender forearm with overlying skin that is often pink. Pain that is out of proportion to the injury is the pathognomonic sign, especially on passive stretching of the fingers. Pain is usually not relieved by rest, analgesia, or anti-inflammatory medication. Pain can, however, disappear in late stages or presentations or chronic compartment syndrome. A few patients who present a few hours after the onset of compartment syndrome present with hemorrhagic blisters in addition to the above mentioned.

Sensory deficits or paresthesias are usually a sign of nerve ischemia in the affected compartment and can be present. Paralysis is often a late sign.

Radial and ulnar pulses are usually intact, given the systolic arterial pressure (around 120 mmHg) usually exceeds the pressure within the involved compartment. The absence of pulses is usually a late finding, and amputations are considered when there is a significant amount of ischaemic tissue death.

In children, anxiety associated with increasing analgesic requirements is a reliable indicator of compartment syndrome.[13]

Be aware pain can sometimes be difficult to asses or be absent if there is nerve damage, in polytrauma patients, a patient who is unconscious or sedated and in children or in patients who have had some form of regional nerve blocks for pain relief.[1][14]

Evaluation

Using a combination of clinical diagnosis and intracompartmental pressure measurements increases both the sensitivity and specificity of diagnosing the forearm compartment syndrome.[15]

Measurements of the affected compartment can be done using a transducer connected to a catheter, which is inserted 5 cm into the affected area of the forearm. Normal intracompartmental pressures vary between 0 to 8 mmHg, and critical pressure is considered anything above 30 mmHg.

A pressure higher than 30 mmHg of the diastolic blood pressure (delta p) of the patient is associated with compartment syndrome, and fasciotomy is indicated in that case. The delta p (delta pressure) is the difference between the diastolic blood pressure of the patient and the compartment pressure. A delta p of less than 30 mmHg strongly suggests acute compartment syndrome.

Compartment pressure measurements are indicated in polytrauma patients, patients not alert or unreliable, or if there are inconclusive physical examination findings. Positive clinical findings should prompt urgent surgical intervention without the need for compartment measurements.[1]

Other investigations to aid diagnosis include forearm radiographs or MRI scans of the forearm (mainly in chronic compartment syndrome rather than acute settings).

Treatment / Management

Patients with suspected acute compartment syndrome of the forearm should be assessed following the advanced trauma life support principles and managed in a multidisciplinary approach. A senior review must be done as soon as possible after the patient has arrived in the emergency department. First steps can be taken on initial assessment such as oxygen administration, elevating the arm in a sling, splitting or removing a tight cast or dressing, ensuring the patient is normotensive as hypotension reduces perfusion pressure and causes further tissue injury. The definitive treatment of acute compartment syndrome is a surgical intervention in the form of urgent forearm compartment fasciotomies.[1][16]

Surgical intervention is performed under general anesthetic. The fasciotomy approaches are volar and dorsal. The volar incision starts just radial to FCU at the wrist and extends proximally to the medial epicondyle. The fascia over the deep muscle compartment needs to be dissected. This approach decompresses the anterior compartment and the posterior compartment as well. The incision can extend distally also to release the carpal tunnel. The dorsal incision starts 2 cm distal to the lateral epicondyle toward the midline of the wrist. It decompresses the mobile wad of Henry and the posterior compartment. Usually, the wounds are left open and covered in sterile dressings, and the patient will require a second look intervention at 48 to 72 hours. During the second look procedure, the dead muscle tissue needs to be debrided, and delayed primary closure of the wounds can be attempted. If the operating team is unable to close the wounds, a negative pressure dressing should be considered followed at a later stage by split-thickness skin grafting.[17][13]

Differential Diagnosis

Patients with spreading cellulitis can present with pain, swelling, and redness over the forearm. In such scenarios, the cellulitis might be spreading from hand (distal to proximal) or the arm or olecranon. There might be a history of trauma/penetrating injury/insect bites that precipitated the cellulitis. The forearm compartments remain soft and passive stretch of muscles dodo not tend to cause excruciating pain as it does in compartment syndrome with a firm to palpate compartments.

Prognosis

The most important prognostic value in patients with acute compartment syndrome of the forearm is the time to diagnosis and fasciotomy. Reports suggest a rate of fasciotomy between 2% to 24% in acute compartment syndrome patients. This is mainly due to uncertainties in diagnosing this condition. The timing of the diagnosis and immediate surgical intervention is critical and limb saving. Delayed diagnosis can have devastating consequences on the patient. Prognosis varies from full recovery to amputation depending on the time of presentation, symptoms at presentation (absent pulses, as well as paralysis of the affected limb, are signs associated with late presentations), time to diagnosis, and surgical intervention.[1]

Complications

Failure to relieve the pressure in time can lead to tissue death in the affected compartment.

The most common complication is Volkmann ischemic contracture, which is an irreversible muscle contracture in the forearm, wrist, and hand that results from muscle damage and necrosis. Patients usually present with particular clinical features, which include elbow flexion, forearm pronation, wrist flexion, thumb adduction, metacarpophalangeal joints extension, and interphalangeal joints flexion. Volkmann contracture can be classified using the Tsuge classification into mild (when only finger flexor muscles are affected), moderate (when wrist and finger flexors are affected), and severe (when wrist, finger flexors, and extensors are all affected). Treatment options for this condition range from dynamic splinting to excision of necrotic tissue and tendon transfers.[17]

Other complications include nerve damage, gangrene, chronic regional pain syndrome, and rhabdomyolysis, which in turn can then lead to kidney failure. Rhabdomyolysis has been reported in up to 23% of cases diagnosed with acute compartment syndrome in general. Rhabdomyolysis presents clinically as a triad of symptoms, which include muscle stiffness, muscle pain (particularly back pain), and poor urine output or dark-colored urine.[14][18]

Deterrence and Patient Education

Compartment syndrome of the forearm is a surgical emergency that can be clinically challenging to diagnose. Patients who present with signs and symptoms of compartment syndrome have to be informed of the complications associated with this condition. Where clinical signs and symptoms are not conclusive, compartment measurements should be taken early on to diagnose the condition. In patients who do not have the capacity, are sedated or unconscious, the best interest decision should be made involving their families where possible (and if time allows). 

Enhancing Healthcare Team Outcomes

Diagnosing forearm compartment syndrome as well as treating the condition, can be difficult for any clinician. Early diagnosis is fundamental, and patients can present with an array of signs and symptoms, which can be challenging. Early measures can be taken from the moment they come into the emergency department by the emergency care team. They involve administration of analgesia, removal of any splints or dressings, and elevation of the arm. Patients should be reviewed early in their presentation by a senior clinician. Where clinical suspicions are significant, the surgical team should be informed straight away. The theatre team, as well as the anesthetic team, should be involved early on as well in the management of these patients as often surgical intervention, is required urgently. Where clinical findings indicate a pulseless limb, the vascular surgical team should be involved and ideally present during surgical intervention. Where time allows early radiographs of the affected limb can be taken to aid diagnosis, and this should be liaised with the radiology team. Following surgical intervention, it is essential patients have adequate pain relief, and close monitoring on the ward and pharmacy advice should be sought where necessary. The nursing team looking after the patient should be given a clear management plan following surgical intervention as their input is essential in the recovery of the patient. In certain cases where secondary wound closures are difficult, the involvement of the plastic surgery team is advisable to help with further management and wound healing.


References

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