Acute compartment syndrome following a minor athletic injury

Acute compartment syndrome following a minor athletic injury

TheJournal of Emergency Medicine, Vol. 7, pp. 353-357,1989 ACUTE COMPARTMENT Printed in the USA ??Copyright 0 1989 Maxwell Pergamon Macmillan plc S...

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TheJournal of Emergency Medicine, Vol. 7, pp. 353-357,1989

ACUTE COMPARTMENT

Printed in the USA ??Copyright 0 1989 Maxwell Pergamon Macmillan plc

SYNDROME

Talmage D. Egan,

MD,*

FOLLOWING

A MINOR ATHLETIC

and Steven M. Joyce,

INJURY

MD, FACEPt

*Department of Anesthesiology, and tAssociate Professor of Medicine (Clinical), Division of Emergency Medicine, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, Utah Reprint address: Steven M. Joyce, MD, Emergency Department, University of Utah Hospital, 50 North Medical Drive, Salt Lake City, UT 84132

0 Abstract-An athletic young male presented with right calf pain following a twisting injury during a soccer game. Other than apparently severe calf pain, no symptoms or signs of compartment syndrome were noted. The patient later returned with lateral and anterior compartment syndrome, and suffered partial loss of peroneal nerve and muscle function despite fasciotomy. Although rare, acute compartment syndrome resulting from seemingly minor injury or exertion has been reported. Pain out of proportion to the apparent injury and a history of chronic leg pain with exertion may be helpful in identifying these patients prior to development of more obvious signs and symptoms. The diagnosis of acute compartment syndrome may be confirmed by compartmental pressure measurement. Prompt intervention is indicated once the diagnosis is established. 0 Keywords-acute injury

injury that illustrates the importance of physician awareness in early diagnosis and treatment. CASE REPORT

A 23-year-old white male presented to the emergency department complaining of severe right leg pain following a soccer game. The patient was an avid amateur athlete who was in good physical condition and played soccer frequently. He noted a sudden sharp pain in his lateral right calf near the knee when he twisted the leg. He denied direct trauma. A tearing sensation in the upper lateral calf worsened over the following several hours. Examination showed a male in moderate pain unable to ambulate. Palpation of the calf elicited marked tenderness along the length of the fibula where a slight proximal swelling was noted. There was no other swelling, and the anterior and lateral muscle groups were supple. There was no pain with passive movement of the ankle, and distal neurovascular function was intact, including sensation. Radiographs of the tibia and fibula were normal. Because of the mechanism of injury and paucity of physical findings, a diagnosis of stress fracture of the fibula versus leg strain was made, and the patient was discharged in a posterior splint with codeine analgesics and instructions to elevate and apply ice to the leg. Because of steadily increasing pain unresponsive to the above measures, the patient returned for re-examination in two days. At that time the patient had swelling and tenderness of the lateral and anterior calf, with loss of ankle eversion and toe extension and loss of sensation on the dorsomedial foot. Pressures were measured in the lateral and anterior compart-

compartment syndrome; athletic

INTRODUCTION

Acute compartment syndrome is a well-described entity and is most commonly associated with fractures in the leg (1). Exercise and athletic trauma, while perhaps less commonly known, are also recognized as potential causes of acute compartment syndrome. Most cases of exercise-induced compartment syndrome have been reported in association with dramatic and prolonged increases in exertion in unconditioned individuals such as military recruits (“march gangrene”) (2,3). However, physicians must also be aware of the rare occurrence of acute compartment syndrome following moderate exercise or minor athletic trauma (4). We report a case of acute compartment syndrome (ACS) resulting from a minor athletic

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Talmage D. Egan and Steven M. Joyce

354

ments and were found to be 105 and 63 mmHg, respectively. Normal pressure would be expected to be less than 30 mmHg (usually 10 to 20 mmHg) in a recumbent, normotensive adult, in any compartment. A diagnosis of acute compartment syndrome was made, and the patient was immediately taken to the operating room where a four-compartment fasciotomy was performed. The lateral compartment was noted to be ecchymotic, and delayed debridement of 60% of the peroneal muscles was necessary. The anterior and posterior compartments were not affected. Follow-up at eight months showed numbness of the dorsum of the foot and marked weakness of the peroneal muscles, severely limiting the patient’s athletic activities. With physical therapy the patient is expected to make slow improvement, although full leg function may never be regained.

DISCUSSION Acute exercise-induced compartment syndrome was first described by Vogt in 1943 (5), and has been known by a variety of terms including march gangrene (3), exercise-induced compartment syndrome (6), and exertional compartment syndrome (7). As mentioned, most causes are associated with dramatic increases in exertion in unconditioned individuals. We were able to find fewer than 20 cases of ACS associated with minor exertion or common athletic injuries in the English literature (3,4,11,12,15-17). Over half of these cases resulted from injuries sustained in amateur rugby games (3). Increased pressure within the compartment is thought to be the central pathogenic factor in all types of compartment syndromes (8). High compartment pressure impairs tissue perfusion, which initially causes pain, swelling, numbness, and weakness, and may eventually culminate in tissue necrosis. Fortunately, the reversible changes induced by increased compartmental pressures precede the nerve and muscle nercrosis by a matter of hours and thus make intervention possible if the diagnosis is made early (9). Left untreated, the prolonged ischemia of acute compartment syndrome can result in Volkmann’s contracture, neural deficit, and gangrene. There is evidence that increased pressure can result from a muscle tear with subsequent intracompartmental bleeding (10,ll). We believe a muscle tear was probably the cause of our patient’s increased compartmental pressure, though the amount of necrosis found at operation made anatomical confirmation impossible.

Many different muscle compartments can be involved in exertional ACS (Table 1). ACS secondary to moderate exertion has been reported in the hand (12) and forearm (6). Exertional ACS in the leg, which comprises the majority of reported cases, is most common in the anterior compartment (2), whereas isolated lateral or posterior syndromes are unusual (11,lS). In our patient, swelling and increased compartmental pressure were noted in both the lateral and anterior compartments. Only the lateral compartment sustained necrosis. The diagnosis of acute compartment syndrome of any etiology can usually be made on clinical grounds. There are a number of symptoms and signs that have proved useful in making the diagnosis. Pain out of proportion to that normally anticipated for a given clinical situation is perhaps the cardinal symptom (9). Other complaints might include weakness of the muscles and numbness in the distribution of nerves that pass through the involved compartment (1). Additional historical factors can be of value in suggesting the diagnosis of exertional ACS. The syndrome is more likely to occur in patients unaccustomed to vigorous exercise or at the start of a sport season when patients are relatively out of condition (2). The acute syndrome is also thought to develop more commonly in patients who suffer from chronic exercise-induced compartment syndrome. This chronic syndrome is characterized by recurrent, exertional compartment pain that resolves with rest. This disorder is thought to be due to relative ischemia of the affected compartment due to increased oxygen demand during exercise, which may in turn be secondary to deficient vascular autoregulation of unknown etiology (15). In one study, as many as 8 of 52 patients who developed exertional ACS had a history of episodic pain in the leg when exercising (2). However, our patient was a conditioned athlete who denied any history of leg pain with exercise. It is important to recall that a wide variety of sporting, recreational, and exercise activities can lead to exertional ACS. Cases have been reported in patients relating no apparent injury or relatively minor athletic trauma while participating in tennis (4), basketball (15), football, (1 l), dancing (16), and hiking (3). A case has even been reported in a debilitated elderly woman undergoing physical therapy (17). The case described in this report involved an apparently minor soccer injury. On physical examination, palpable tenseness and tenderness of the muscle compartment and pain on passive stretch of the involved muscles may be demonstrated (14). In addition, paralysis of the muscle group and hypoesthesia in the distribution of sensory

Exertional ACS

355

Table 1. Compartmental syndromes and assoclated physical signs’

Compartment Forearm Dorsal Volar Hand lnterosseus

Leg Anterior Lateral

Sensory Loss Ulnar/median nerves

Deep peroneal nerve

Superficial posterior

Superficial and deep peroneal nerves -

Deep posterior

Posterior tibia1 nerve

Gluteal

Muscles Weakened

(Rarely sciatic)

*This table has been adapted from table 75-2 in reference

Painful Passive Motion

Tenseness Location

Digital extensors Digital flexors

Digital flexion Digital extension

Dorsal forearm Volar forearm

lnterosseus

Abductladduct (metacarpophalangeal joints)

Dorsum hand between metacarpals

Toe extensors Tibialis anterior Peroneal muscles

Toe flexion

Anterior aspect leg

Foot inversion

Soleus and gastrocnemius Toe flexors Tibialis posterior

Foot dorsiflexion

Lateral aspect leg over fibula Calf

Gluteals, piriformis, or tensor fascia lata

Toe extension

Hip flexion

Distal medial leg between Achilles tendon and tibia Buttock

19.

nerves passing through the compartment may be noted (Table 1). Interestingly, capillary refill and peripheral pulses are frequently normal in acute compartment syndrome (8). It has been suggested that an objective sensory deficit is perhaps the most reliable physical sign of acute compartment syndrome, while a palpably tense compartment is the earliest finding (1). It should be emphasized that not all of these symptoms and signs are present in each patient with acute compartment syndrome (9). Extreme pain in the setting of a seemingly minor injury was the most prominent aspect of the case described in this report. The diagnosis, though initially based on clinical findings, can be confirmed by compartment pressure measuring techniques (13,14). These objective techniques are especially valuable with uncooperative or unreliable patients, or with patients in whom the physical findings are equivocal or confusing (13). Several methods of measuring compartment pressures are available (19). Perhaps the most practical for diagnostic use in the emergency department is the needle method described by Whitesides and coauthors in 1975 (Figure 1). A mercury manometer, 2Occ syringe, and intravenous extension tubing partially filled with saline are connected via an open three-way stopcock. An 18-gauge needle, attached to the intravenous tubing and flushed with saline, is inserted perpendicularly into the compartment. Pressure is slowly applied to the system using the syringe. When the system pressure equals the compartment pressure, the air-saline meniscus in the intravenous tubing is observed to move. The manometer reading at this point

represents the compartment pressure. Readings may be repeated at the same or different sites within the compartment; checks for tissue plugs or clots may be carried out between readings. Minimal volume of injection will prevent further increase in tissue pressure. This method is reportedly accurate to within *3 mmHg of actual compartment pressure. Other more accurate measures of tissue pressure measurement utilize the wick or split catheters and provide for continuous tissue pressure monitoring via a low-pressure transducer. These latter methods are accurate to within * 1 mmHg of actual pressure, but due to their complexity and expense are perhaps best suited for continuous in-patient tissue pressure monitoring. Fasciotomy should be considered when sustained compartment pressures of greater than 30 to 40 mmHg are noted (14). Pressures at which the syndrome develops may be lower in hypotensive and higher in hypertensive patients, so that correlation with clinical signs and symptoms is always important. The diagnosis of ACS in the patient reported herein was confirmed by compartment pressure measurement. It is unknown whether compartment pressures would have been elevated at the time of his initial presentation, given the absence of swelling or tenderness. However, whenever the diagnosis is suspected, compartment pressures should be measured.

SUMMARY

A delay in the diagnosis of acute compartment syndrome of any etiology can be catastrophic in terms of

Talmage

356

D. Egan and Steven

M. Joyce

2Occ syringe i

.sterile

air

‘-plastic

saline

IV extension

(a)

3 way stop cock open to syringe and both extension tubes

Figure 1. Needle technique for measurement of compartmental pressures. (a) Aspiration of saline column into intravenous tubing. (b) With needle tip positioned in compartment muscle, syringe plunger Is depressed and pressure read immediately as saline meniscus begins to move. (Redrawn from reference 20. Used by permission.)

Exertional ACS

357

disability and deformity. Although most commonly associated with fractures and other severe injuries, the condition has been caused occasionally by strenuous exercise, usually in unconditioned individuals. Only rarely has acute compartment syndrome (ACS) been described in persons sustaining minor injuries or following moderate exertion. The emergency physician must be alert to the possibility of ACS arising

under these conditions. A history of previous exertional muscle pain and the finding of pain out of proportion to the apparent injury may be helpful in these cases. The diagnosis is usually made by history and physical exam, and can be confirmed by compartment pressure measurement. Once the diagnosis is reached, decompressive fasciotomy should be performed as quickly as possible.

REFERENCES 1. Mubarak SJ, Hargens AR. Acute compartment syndromes. Surg Clin of North Am. 1983;63:539-65. 2. Reneman RS. The anterior and the lateral compartmental syndrome of the leg due to intensive use of muscles. Clin Orthop. 1975;113:69-80. 3. Blandy JP, Fuller R. March gangrene: ischaemic myositis of the leg muscles from exercise. J Bone Joint Surg. 1957;39B: 679-92. 4. Kennedy JC, Roth JH. Major tibia1 compartment syndromes following minor athletic trauma. Am J Sports Med. 1979;7: 201-3. 5. Horn CE. Acute ischaemia of the anterior tibia1 muscle and the long extensor muscles of the toes. J Bone Joint Surg. 1945;27: 615-22. 6. lmbriglia JE, Boland DM. An exercise induced compartment syndrome of the dorsal forearm-a case report. J Hand Surg. 1984;9A:142-3. I. Garfin S, Mubarak SJ, Owen CA. Exertional anterolateral compartment syndrome. J Bone Joint Surg. 1977;59A(3):4045. 8. Matsen FA III. Compartmental syndrome: a unified concept. Clin Orthop. 1975;113:8-14. 9. Matsen FA III, Krugmire RB Jr. Compartmental syndromes. Surg Gynecol Obstet. 1978;147:943-9. 10. Straehley D, Jones WW. Acute compartment syndrome (anterior, lateral, and superficial posterior) following tear of the medial head of the gastrocnemius muscle: a case report. Am J Sports Med. 1986;14:96-9. 11. Arciero RA, Shishido NS, Parr TJ. Acute anterolateral com-

partment syndrome secondary to rupture of the peroneus longus muscle. Am J Sports Med. 1984;12:366-7. 12. Reid RL, Travis RT. Acute necrosis of the second interosseous compartment of the hand. J Bone Joint Surg. 1973;55A:10957. 13. Mubarak SJ, Owen CA, Hargens AR, Garetto LP, Akeson WH. Acute compartment syndromes: Diagnosis and treatment with the aid of the wick catheter. J Bone Joint Surg. 1978;60A: 1091-5. 14. Matsen FA III, Winquist RA, Krugmire RB Jr. Diagnosis and management of compartmental syndromes. J Bone Joint Surg. 1980:62A:286-91. 15. Leach RE, Hammond G, Stryker WS. Anterior tibia1 compartment syndrome. J Bone Joint Surg. 1967;49A:451-61. 16. Lunceford EM Jr. The peroneal compartment syndrome. South Med J. 1965;58:621-3. 17. Sweeney RC, Chadwick CJ, Bagnall WE. Exercise induced anterior tibia1 compartment compression syndrome in the elderly. Postgrad Med J. 1981;57:537-8. 18. Mubarak SJ, Owen CA, Garfin S, Hargens AR. Acute exertional superficial posterior compartment syndrome. Am J Sports Med. 1978;6:287-90. 19. Van Ryn DE: Compartmental syndrome. In: Roberts JR, Hedges JR, eds. Clinical procedures in emergency medicine. Philadelphia: WB Saunders; 1085. 20. Whitesides TE, Haney TC, Morimoto K, et al. Tissue pressure measurements as a determinant for the need for fasciotomy. Clin Orthop. 1975;113:43.