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Management of compartmental syndrome
Management of Compartmental Syndrome Diagnostic and Surgical Considerations
Bok Y. Lee, MD, FACS, Castle Point, New York Richard F. Brancato, BA, Castle Point, New York In H. Park, MD, FACS, Castle Point, New York William W. Shaw, MD, FACS, Valhalla, New York
Compartmental syndrome is a frequent cause of functional impairment after trauma to the legs. In this condition, posttraumatic swelling within a closed anatomic space increases intracompartmental pressure, leading to a compromise of circulation and tissue function within that space. The development of this syndrome has frequently been associated with such diverse conditions as arterial and venous injuries, fractures, massive soft tissue trauma, phlegmasia cerulea dolens, arterial embolization, and arterial reconstructive procedures. Unless this syndrome is recognized promptly and treated by surgical decompression, permanent neuromuscular deficits may result. In some instances, the diagnosis of compartmental syndrome may be made from clinical signs and symptoms alone. Frequently, however, early clinical evidence of this syndrome is difficult to assess, and at the onset of obvious neuromuscular deficits or the obliteration of palpable pulses, ischemia is frequently established and irreversible tissue damage has already occurred. In these instances, monitoring of intramuscular pressures may be a valuable tool in the early diagnosis and clinical evaluation of patients at risk for this syndrome. For the prevention of irreversible muscle and nerve damage that can result from compartmental syndrome, it is imperative that the diagnosis be made early and that circulation to the ischemic muscle be reestablished as soon as possible. We present herein our experience with the diagnosis and successful management of compartmental syndrome and a review of the literature deFrom the Departments of Swgmy. Veterans Administration Medical Center. Castle Point, New York, and New York Medical college. Valhalla, New Yak. Fieqw&forreprlntsshouldbeadrfessedtoBokY.Lee,~,~ of Swgwy, Veterans Administrationhtedlc.alCenter. Castle Point. New York 12511.
vohms
MB, B8gtembu 1984
scribing the clinical characteristics, surgical management, and etiologic factors contributing to this syndrome. Clinical Characteristics The clinical diagnosis of compartmental syndrome is often difficult because of (1) its frequent association with conditions that produce pain, (2) the difficulty in quantitating the degree of swelling that, like pain, would be expected to be present in any traumatized leg, (3) the relatively late onset of hypoesthesia that can develop at different rates, (4) a difficult differential diagnosis, including cellulitis, thrombophlebitis, tibia1 stress fractures, osteomyelitis, tenosynovitis, and an ill-defined condition frequently referred to as shin splints, and (5) the loss of palpable pulses which may occur late or sometimes not at all in the course of this syndrome. Specifically, however, any of the aforementioned symptoms may be absent. One factor that is present in all cases of compartmental syndrome is an increase in tissue pressure. Thus, an objective measurement of intracompartmental pressure may indicate the onset of the syndrome before it becomes manifest clinically. Normal tissue pressures are reported to be approximately 0 mm Hg [I]. Experimental studies conducted by Jennings [2] using tissue compression as an indirect measure of tissue pressure showed that tissue perfusion decreases progressively as tissue compression increases. Although there is some debate concerning the exact level that tissue pressures must reach before tissue perfusion ceases, most investigators agree that blood flow ceases in the microcirculation when tissue pressure within a closed compartment increases to levels equal to the diastolic blood pressure. In the normotensive patient, it is apparent that tissue
383
Lee et al
Ftgure 1. Basic apparatus ussd for intramuscularpressure measurements.
pressures in the 40 to 60 mm Hg range are capable of producing decreased or totally absent blood flow in the microcirculation. Using compartmental pressures as a criterion, Whitesides et al [3] have recommended surgical decompression when compartmental pressure is within 30 mm Hg of the diastolic pressure. When compartmental pressure is equal to the diastolic pressure, surgical decompression is mandatory. Intramuscular Pressure Monitoring The apparatus used for monitoring intramuscular pressure is shown in Figure 1. A standard pressure transducer is connected to a stripchart recorder and is calibrated before each procedure. A 24 gauge needle is attached to the distal end of a length of rigid plastic tubing that is proximally fastened to the dome of the transducer. A syringe filled with sterile physiologic saline solution is connected through a stopcock to the other dome outlet. The system is flushed to remove any air bubbles. At the time the needle is inserted into the muscular compartment, a slow, steady manual infusion of approximately 0.1 ml fluid is passed through the needle to prevent tissue fluid entry and to maintain patency. The pressure monitored by the transducer is then observed until equilibrium is attained and documented by the stripchart recorder. The pressure measurements may be repeated as often as needed, with flushing of the system before each measurement. Treatment If the patient demonstrates clinical evidence of compartmental syndrome, all circumferential dressings should be removed immediately and the affected leg raised to heart level to assure maximum local arterial pressure without compromising venous drainage. If prompt resolution of the signs of ischemia does not occur and tissue pressure remains ele-
304
vated, immediate surgical decompression is indicated. In this procedure, all potentially limiting envelopes (for example, fascia and skin) should be surgically opened to allow tissue perfusion and the return of venous pressure to within normal limits. When fasciotomy is performed for an acute compartmental syndrome, the procedure should be carried out without a tourniquet to avoid prolonging the period of ischemia, while allowing the surgeon to judge the response of the compressed muscle to deGood surgical exposure facilitates compression. evaluation of the condition of the muscle, permits early excision of necrotic areas, and allows adequate hemostasis. Fasciotomy is most effective if it is performed early in the course of the syndrome. In a retrospective study by Sheridan and Masten [4], 46 legs with acute compartmental syndrome treated by fasciotomy were reviewed. In those legs decompressed within 12 hours of appearance of the syndrome, 31 percent showed residual functional deficits at follow-up. In contrast, in those legs having late decompression, 91 percent showed residual functional losses, 54 percent developed complications, and 20 percent required amputation. The time from diagnosis of compartmental syndrome to fasciotomy was determined from the time the earliest evidence of the syndrome appeared. If surgical intervention is performed early in the course of the syndrome, the compromised circulation of the leg can be restored and symptoms will disappear shortly after operation. A reduction in pain should occur within several hours, and the restoration of mobility and sensibility in the course of 2 weeks. Clinical Material The diagnosis of a compartmental syndrome may be so apparent that tissue pressure measurementa are not necessary to confirm the need for fasciotomy. However, there are some patients in whom the use of tissue pressure measurements has been extremely helpful. The following case reports have been selected to illustrate a variety of clinical conditions associated with compartmental syndrome and surgical treatment for delayed decompression and healing.
Illustrative Case Reports Case 1. In April 1979, a 68 year old diabetic white man with a history of bilateral femoropopliteal bypass and below-knee amputation of the left leg secondary to peripheral vascular disease was admitted to the Veterans Administration Medical Center, Castle Point, New York. Physical examination at the time of admission revealed ulceration of the left below-knee stump with severe ischemia of the right lower leg. Noninvasive external magnetic flowmetry measurements at the right thigh and calf showed a reduced peak pulsatile flow rate of 126 ml/ min and 35 ml/min, respectively. Segmental Doppler examination showed complete absence of distal pressures, which indicated occlusion of the right femoropopliteal bypass. Arteriography demonstrated arteriosclerotic changes in the abdominal,aorta, with complete occlusion
The American Journal ol Surgery
Compartmental
of the left common iliac and superficial femoral arteries, and arteriosclerotic changes of the right common iliac artery. Embolectomy of the right femoropopliteal bypass was carried out with restoration of normal blood flow. Twenty-six hours postoperatively, signs of acute right anterior tibial compartment syndrome developed. The clinical presentation included pain and swelling localized to the right anterior tibial compartment with erythematous discoloration. Doppler systolic pressures of the posterior tibial and dorsahi pedis arteries were 54 mm Hg and 46 mm Hg, respectively. Intramuscular pressure measurement of the anterior tibial compartment was 38 mm Hg and of the thigh compartment 0 mm Hg. The positive tissue pressure generated in the anterior tibial compartment was apparently sufficient to compromise blood flow to the distal thiid of the right leg. An emergency fasciotomy was performed with two longitudinal incisions approximately 1.5 inches in length at the upper third and lower third lateral aspect of the leg. The fascia was opened from the knee to the ankle. The muscles of the anterior tibial compartment appeared slightly cyanotic. Postoperatively, segmental Doppler systolic pressures showed improvement in the ischemic index on the right side, and tissue pressure measurement of the anterior tibia1 compartment was 6 mm Hg. Comment: The development of severe compartmental syndrome after reconstructive vascular surgery is relatively rare but should not be overlooked when certain circumstances prevail. In our experience, emergency fasciotomy is indicated if swelling is progressive for several hours after reconstructive vascular surgery and if it is associated with elevated compartment pressures above 35 mni Hg, continued paralysis and anesthesia of the leg, and observation of peripheral pulses on Doppler examination. If peripheral pulses subsequently disappear, reembolization or thrombosis can be ruled out by arteriography, reexploration, or both. Case 2. In December 1930, a 60 year old diabetic man was admitted with chief complaints of swelling, erythema, and mild pain of the left ankle after having fallen on ice
Vo*nw 148. Sapi-
1984
Syndrome
approximately 24 hours before admission. Physical examination revealed massive swelling, cellulitis, and color changes, with blister formation over the entire lower left leg (Figure 2). Palpable pulses and sensation below the left ankle were absent. Segmental Doppler pressures and digital pbotoplethysmography showed severe reduction of the left posterior tibia1 and dorsalis pedis arterial systolic pressures. Digital thermistor thermometry showed the left toes to be approximately 4OC cooler than the right toes. Radiographic examination of the left leg showed a trimalleolar fracture of the ankle with anterior displacement of the tibia and fibula. An emergency fasciotomy was performed for limb salvage, followed by concomitant closed reduction of the dislocated left ankle. Medial and lateral incisions were made through the subcutaneous tissue and fascia from the ankle to the knee (Figure 3). After opening the fascia, there was immediate protrusion and separation of the ischemic muscles of the anterior compartment. The dislocated ankle joint was reduced and maintained with a Steimann’s pin through the calcaneus to the ankle joint and into the distal half of the tibia. Postreduction radiographic examination of the left ankle showed restoration of anatomic alignment of the bony fragments. Postoperatively, the color of the leg improved and sensation with active movement of the toes returned. Digital thermistor thermometry and photoplethysmography demonstrated excellent improvement in skin temperatures and tissue perfusion at the toes. Subsequent secondary closure of the wounds of the left leg and application of a split-thickness skin graft were carried out, with excellent healing (Figure 4). Comment: The development of signs and symptoms of an acute anterior tibial compartmental syndrome after fracture of the tibia, fibula, or ankle is not an uncommon occurrence. Clinicahy, the classic complex of pain, swelling, and tenderness over the anterior tibia1 compartment in addition to weakness or paralysis of the compartment musculature are invariably present. Pallor and loss of pulses, however, may not prove useful in the early diagnosis of the compartment syndrome. In the presence of diminished photoplethysmographic waveforms and Doppler
385
Ftgure 3. Surgtcal decompresskm resuffed In immediate pfvtfusfon and separatkm of the b&em/c nnSc~oftheante&f V, wldhexceffent improvement In skin temperatureand tissue pertuston.
systolic pressures, arterial occlusion may be difficult to differentiate from compartment syndrome. However, in the presence of a tight compartmental envelope, we recommend emergency surgical decompression first. If an arterial lesion is still suspected, an arteriogram may then be obtained. Case 3. In February 1979, a 36 year old white man with an 8 year history of anterior tibial compartment syndrome was referred to our hospital. The patient had previously
undergone recurrent operations of the right anterior tibia with numerous unsuccessful skin grafts. Physical examination at the time of admission showed the anterior aspect of the right lower legs to be severely ulcerated and sunken, with dense scar tissue at the site of previous surgery (Figure 5). To correct the defect, wide excision of the dense scar tissue and coverage with a healthier skin flap were indicated. Photoplethysmographic study of the right lower leg demonstrated the presence of good pulsatile waveforms superior, inferior, medial, and lateral to the site of ulceration, indicating good healing potential. A tensor fascia lata myocutaneous microvascular free flap with anastomosis of the lateral circumflex femoral artery and vein to the peroneal artery and vein was carried out. Preoperative photoplethysmographic waveforms obtained at the donor site demonstrated good pulsatile flow, and preoperative arteriography demonstrated an acceptable lateral femoral circumflex artery. Intraoperatively, blood flow at the lateral circumflex femoral artery was measured using standard electromagnetic flowmetry. Blood flow measured before tensor fascia lata myocutaneous free flap transfer was 19 ml/min. After anastomosis of the lateral circumflex femoral artery to the peroneal artery, blood flow was 37 ml/min. Postoperatively, the myocutaneous flap was warm and photoplethysmography demonstrated excellent pulsatile waveforms over the lateral circumflex artery (Figure 6). At last follow-up two years postoperatively, viability of the myocutanous flap was excellent. Comment: On rare occasions, patients with a history of compartmental syndrome have had necrosis of the skin overlying the compartment. In such instances, the necrotic tissue may become infected and the entire limb may be threatened. When local blood supply is inadequate, skin grafts often prove to be inadequate. Under these circumstances, a myocutaneous free flap provides a well-vascularized living tissue that seals off the wound, prevents further infection, and brings a rich blood supply to an area of ischemic necrosis.
Comments
F&e 4. Wfth subsequenlsecondarycksun,ofthemwrndsofths fefl leg and applfcatfon of a splft-thickness graft, healing was excellant.
386
As a result of the clinical observation that marked bulging of the underlying muscle occurs after fasciotomy, many investigators have suggested that increased pressure within the compartment resulting from any case may initiate the syndrome. The increase in tissue pressure may be caused either by a decrease in size of the compartment or by an increase in the volume of its contents. The fascia of the legs
The American
Journal of Surpy
Compartmental
has been most commonly implicated as the envelope of limited compliance in compartmental syndrome, although associations with tight external dressings, skin, and epimysium have been reported [5-S]. This syndrome has been caused by postischemic swelling after arterial occlusion or prolonged aortofemoral bypass, fracture, soft tissue trauma, excessive muscular work, and closure of fascial defects. Clinical evidence and experimental evidence re-
F@m8.~,attertenswfsebr,latamyocut~ fen#oral artery and wfn to the pamneal attery and
vohmw
140, %ep4w
1904
Syndrome
ported by Benjamin [5] and Eaton and Green [6] have demonstrated that elevated intracompartmental pressures compromise local circulation by producing arterial spasm. Burton [I] has reported the existence of an arteriolar critical closing pressure as the determinant in circulatory compromise. Masten and Krugmire [9] have reported that both of these mechanisms are dependent on sustained active contraction of vascular segments in the presence of
anaMmo&
ftWVV8SUd8f~~~wllh
vein, excellent
pftot@etftysmograpf#k
pulsatffe
waveforms
of tfm lateral chcumffex were obtained.
387
Lee et al
ischemia, which is usually a potent stimulus for vasodilation. These investigators have also provided the following mechanism as an explanation for the compromise of tissue blood flow that results from increased tissue pressure: Veins are collapsible tubes, thus, the pressure in patent veins cannot be less than that in tissue. As long as perfusion persists, increased tissue pressure leads to increased venous pressure. Local tissue perfusion is primarily dependent on the local arteriovenous gradient and local vascular resistance. An increase in venous pressure associated with increased tissue pressure diminishes the arteriovenous gradient. When changes in local vascular resistance can no longer compensate for a decrease in the arteriovenous gradient, local tissue perfusion decreases. When local tissue perfusion is reduced to a point at which the metabolic demands of the tissue can no longer be maintained, diminished tissue function and viability become evident. Summary Compartmental syndrome is a condition in which swelling within a closed anatomic space increases the intracompartmental pressure to compromise the circulation and function of tissue within that space. Unless this condition is recognized early and treated by prompt surgical decompression, permanent neuromuscular deficits may result. In those instances in which early clinical evidence of this syndrome is difficult to assess, monitoring of intramuscular
388
pressures may be a valuable adjunct in the clinical evaluation of patients at risk for this syndrome. The association of compartmental syndrome with a wide variety of circumstances and the importance of an early diagnosis make it essential that all physicians be familiar with this condition. As physician awareness and recognition of this condition increase, the complications associated with it can be greatly reduced. References 1. Burton AC. On the physical equilibrium of small blood vessels. Am J Physiol 1951;164:319-29. 2. Jennings Ah%. Some observations on critical closing pressures in the peripheral circulation of anesthetized patients. Br J Anaesth 1964;36:683-93. 3. Whitesides TE, Haney TC, Morimoto K. Tissue pressure measurements as a determinant for the need of fasciotomy. Clin Orthop 1975;113:42-51. 4. Sheridan GW, Masten FA. Fasciotomy in the treatment of the acute compartment syndrome. J Bone Joint Surg [Am] 1976;58:112-5. 5. Benjamin A. The relief of traumatic arterial spasm in threatened Volkmann’s ischemic contracture. J Bone Joint Surg [Br] 1957;39:71 l-3. 6. Eaton RG, Green WT. Epimysiotomy and fasciotomy in the treatment of Volkmann’s ischemic contracture. Orthrop Clin North Am 1972;3:175-86. 7. Bowden RM, Gutman E. Fate of voluntary muscle after vascular injury in man. J Bone Joint Surg [Br] 1949;31:356-68. 8. Patman RD, Thompson JE. Fasciotomy in peripheral vascular surgery. Arch Surg 1970;101:663-72. 9. Masten FA, Krugmire RB. Compartmental syndrome. Surg Gynecol Obstet 1978;147:943-8.
The American Journal of Surgery
Bok Y. Lee, MD, FACS, Castle Point, New York Richard F. Brancato, BA, Castle Point, New York In H. Park, MD, FACS, Castle Point, New York William W. Shaw, MD, FACS, Valhalla, New York
Compartmental syndrome is a frequent cause of functional impairment after trauma to the legs. In this condition, posttraumatic swelling within a closed anatomic space increases intracompartmental pressure, leading to a compromise of circulation and tissue function within that space. The development of this syndrome has frequently been associated with such diverse conditions as arterial and venous injuries, fractures, massive soft tissue trauma, phlegmasia cerulea dolens, arterial embolization, and arterial reconstructive procedures. Unless this syndrome is recognized promptly and treated by surgical decompression, permanent neuromuscular deficits may result. In some instances, the diagnosis of compartmental syndrome may be made from clinical signs and symptoms alone. Frequently, however, early clinical evidence of this syndrome is difficult to assess, and at the onset of obvious neuromuscular deficits or the obliteration of palpable pulses, ischemia is frequently established and irreversible tissue damage has already occurred. In these instances, monitoring of intramuscular pressures may be a valuable tool in the early diagnosis and clinical evaluation of patients at risk for this syndrome. For the prevention of irreversible muscle and nerve damage that can result from compartmental syndrome, it is imperative that the diagnosis be made early and that circulation to the ischemic muscle be reestablished as soon as possible. We present herein our experience with the diagnosis and successful management of compartmental syndrome and a review of the literature deFrom the Departments of Swgmy. Veterans Administration Medical Center. Castle Point, New York, and New York Medical college. Valhalla, New Yak. Fieqw&forreprlntsshouldbeadrfessedtoBokY.Lee,~,~ of Swgwy, Veterans Administrationhtedlc.alCenter. Castle Point. New York 12511.
vohms
MB, B8gtembu 1984
scribing the clinical characteristics, surgical management, and etiologic factors contributing to this syndrome. Clinical Characteristics The clinical diagnosis of compartmental syndrome is often difficult because of (1) its frequent association with conditions that produce pain, (2) the difficulty in quantitating the degree of swelling that, like pain, would be expected to be present in any traumatized leg, (3) the relatively late onset of hypoesthesia that can develop at different rates, (4) a difficult differential diagnosis, including cellulitis, thrombophlebitis, tibia1 stress fractures, osteomyelitis, tenosynovitis, and an ill-defined condition frequently referred to as shin splints, and (5) the loss of palpable pulses which may occur late or sometimes not at all in the course of this syndrome. Specifically, however, any of the aforementioned symptoms may be absent. One factor that is present in all cases of compartmental syndrome is an increase in tissue pressure. Thus, an objective measurement of intracompartmental pressure may indicate the onset of the syndrome before it becomes manifest clinically. Normal tissue pressures are reported to be approximately 0 mm Hg [I]. Experimental studies conducted by Jennings [2] using tissue compression as an indirect measure of tissue pressure showed that tissue perfusion decreases progressively as tissue compression increases. Although there is some debate concerning the exact level that tissue pressures must reach before tissue perfusion ceases, most investigators agree that blood flow ceases in the microcirculation when tissue pressure within a closed compartment increases to levels equal to the diastolic blood pressure. In the normotensive patient, it is apparent that tissue
383
Lee et al
Ftgure 1. Basic apparatus ussd for intramuscularpressure measurements.
pressures in the 40 to 60 mm Hg range are capable of producing decreased or totally absent blood flow in the microcirculation. Using compartmental pressures as a criterion, Whitesides et al [3] have recommended surgical decompression when compartmental pressure is within 30 mm Hg of the diastolic pressure. When compartmental pressure is equal to the diastolic pressure, surgical decompression is mandatory. Intramuscular Pressure Monitoring The apparatus used for monitoring intramuscular pressure is shown in Figure 1. A standard pressure transducer is connected to a stripchart recorder and is calibrated before each procedure. A 24 gauge needle is attached to the distal end of a length of rigid plastic tubing that is proximally fastened to the dome of the transducer. A syringe filled with sterile physiologic saline solution is connected through a stopcock to the other dome outlet. The system is flushed to remove any air bubbles. At the time the needle is inserted into the muscular compartment, a slow, steady manual infusion of approximately 0.1 ml fluid is passed through the needle to prevent tissue fluid entry and to maintain patency. The pressure monitored by the transducer is then observed until equilibrium is attained and documented by the stripchart recorder. The pressure measurements may be repeated as often as needed, with flushing of the system before each measurement. Treatment If the patient demonstrates clinical evidence of compartmental syndrome, all circumferential dressings should be removed immediately and the affected leg raised to heart level to assure maximum local arterial pressure without compromising venous drainage. If prompt resolution of the signs of ischemia does not occur and tissue pressure remains ele-
304
vated, immediate surgical decompression is indicated. In this procedure, all potentially limiting envelopes (for example, fascia and skin) should be surgically opened to allow tissue perfusion and the return of venous pressure to within normal limits. When fasciotomy is performed for an acute compartmental syndrome, the procedure should be carried out without a tourniquet to avoid prolonging the period of ischemia, while allowing the surgeon to judge the response of the compressed muscle to deGood surgical exposure facilitates compression. evaluation of the condition of the muscle, permits early excision of necrotic areas, and allows adequate hemostasis. Fasciotomy is most effective if it is performed early in the course of the syndrome. In a retrospective study by Sheridan and Masten [4], 46 legs with acute compartmental syndrome treated by fasciotomy were reviewed. In those legs decompressed within 12 hours of appearance of the syndrome, 31 percent showed residual functional deficits at follow-up. In contrast, in those legs having late decompression, 91 percent showed residual functional losses, 54 percent developed complications, and 20 percent required amputation. The time from diagnosis of compartmental syndrome to fasciotomy was determined from the time the earliest evidence of the syndrome appeared. If surgical intervention is performed early in the course of the syndrome, the compromised circulation of the leg can be restored and symptoms will disappear shortly after operation. A reduction in pain should occur within several hours, and the restoration of mobility and sensibility in the course of 2 weeks. Clinical Material The diagnosis of a compartmental syndrome may be so apparent that tissue pressure measurementa are not necessary to confirm the need for fasciotomy. However, there are some patients in whom the use of tissue pressure measurements has been extremely helpful. The following case reports have been selected to illustrate a variety of clinical conditions associated with compartmental syndrome and surgical treatment for delayed decompression and healing.
Illustrative Case Reports Case 1. In April 1979, a 68 year old diabetic white man with a history of bilateral femoropopliteal bypass and below-knee amputation of the left leg secondary to peripheral vascular disease was admitted to the Veterans Administration Medical Center, Castle Point, New York. Physical examination at the time of admission revealed ulceration of the left below-knee stump with severe ischemia of the right lower leg. Noninvasive external magnetic flowmetry measurements at the right thigh and calf showed a reduced peak pulsatile flow rate of 126 ml/ min and 35 ml/min, respectively. Segmental Doppler examination showed complete absence of distal pressures, which indicated occlusion of the right femoropopliteal bypass. Arteriography demonstrated arteriosclerotic changes in the abdominal,aorta, with complete occlusion
The American Journal ol Surgery
Compartmental
of the left common iliac and superficial femoral arteries, and arteriosclerotic changes of the right common iliac artery. Embolectomy of the right femoropopliteal bypass was carried out with restoration of normal blood flow. Twenty-six hours postoperatively, signs of acute right anterior tibial compartment syndrome developed. The clinical presentation included pain and swelling localized to the right anterior tibial compartment with erythematous discoloration. Doppler systolic pressures of the posterior tibial and dorsahi pedis arteries were 54 mm Hg and 46 mm Hg, respectively. Intramuscular pressure measurement of the anterior tibial compartment was 38 mm Hg and of the thigh compartment 0 mm Hg. The positive tissue pressure generated in the anterior tibial compartment was apparently sufficient to compromise blood flow to the distal thiid of the right leg. An emergency fasciotomy was performed with two longitudinal incisions approximately 1.5 inches in length at the upper third and lower third lateral aspect of the leg. The fascia was opened from the knee to the ankle. The muscles of the anterior tibial compartment appeared slightly cyanotic. Postoperatively, segmental Doppler systolic pressures showed improvement in the ischemic index on the right side, and tissue pressure measurement of the anterior tibia1 compartment was 6 mm Hg. Comment: The development of severe compartmental syndrome after reconstructive vascular surgery is relatively rare but should not be overlooked when certain circumstances prevail. In our experience, emergency fasciotomy is indicated if swelling is progressive for several hours after reconstructive vascular surgery and if it is associated with elevated compartment pressures above 35 mni Hg, continued paralysis and anesthesia of the leg, and observation of peripheral pulses on Doppler examination. If peripheral pulses subsequently disappear, reembolization or thrombosis can be ruled out by arteriography, reexploration, or both. Case 2. In December 1930, a 60 year old diabetic man was admitted with chief complaints of swelling, erythema, and mild pain of the left ankle after having fallen on ice
Vo*nw 148. Sapi-
1984
Syndrome
approximately 24 hours before admission. Physical examination revealed massive swelling, cellulitis, and color changes, with blister formation over the entire lower left leg (Figure 2). Palpable pulses and sensation below the left ankle were absent. Segmental Doppler pressures and digital pbotoplethysmography showed severe reduction of the left posterior tibia1 and dorsalis pedis arterial systolic pressures. Digital thermistor thermometry showed the left toes to be approximately 4OC cooler than the right toes. Radiographic examination of the left leg showed a trimalleolar fracture of the ankle with anterior displacement of the tibia and fibula. An emergency fasciotomy was performed for limb salvage, followed by concomitant closed reduction of the dislocated left ankle. Medial and lateral incisions were made through the subcutaneous tissue and fascia from the ankle to the knee (Figure 3). After opening the fascia, there was immediate protrusion and separation of the ischemic muscles of the anterior compartment. The dislocated ankle joint was reduced and maintained with a Steimann’s pin through the calcaneus to the ankle joint and into the distal half of the tibia. Postreduction radiographic examination of the left ankle showed restoration of anatomic alignment of the bony fragments. Postoperatively, the color of the leg improved and sensation with active movement of the toes returned. Digital thermistor thermometry and photoplethysmography demonstrated excellent improvement in skin temperatures and tissue perfusion at the toes. Subsequent secondary closure of the wounds of the left leg and application of a split-thickness skin graft were carried out, with excellent healing (Figure 4). Comment: The development of signs and symptoms of an acute anterior tibial compartmental syndrome after fracture of the tibia, fibula, or ankle is not an uncommon occurrence. Clinicahy, the classic complex of pain, swelling, and tenderness over the anterior tibia1 compartment in addition to weakness or paralysis of the compartment musculature are invariably present. Pallor and loss of pulses, however, may not prove useful in the early diagnosis of the compartment syndrome. In the presence of diminished photoplethysmographic waveforms and Doppler
385
Ftgure 3. Surgtcal decompresskm resuffed In immediate pfvtfusfon and separatkm of the b&em/c nnSc~oftheante&f V, wldhexceffent improvement In skin temperatureand tissue pertuston.
systolic pressures, arterial occlusion may be difficult to differentiate from compartment syndrome. However, in the presence of a tight compartmental envelope, we recommend emergency surgical decompression first. If an arterial lesion is still suspected, an arteriogram may then be obtained. Case 3. In February 1979, a 36 year old white man with an 8 year history of anterior tibial compartment syndrome was referred to our hospital. The patient had previously
undergone recurrent operations of the right anterior tibia with numerous unsuccessful skin grafts. Physical examination at the time of admission showed the anterior aspect of the right lower legs to be severely ulcerated and sunken, with dense scar tissue at the site of previous surgery (Figure 5). To correct the defect, wide excision of the dense scar tissue and coverage with a healthier skin flap were indicated. Photoplethysmographic study of the right lower leg demonstrated the presence of good pulsatile waveforms superior, inferior, medial, and lateral to the site of ulceration, indicating good healing potential. A tensor fascia lata myocutaneous microvascular free flap with anastomosis of the lateral circumflex femoral artery and vein to the peroneal artery and vein was carried out. Preoperative photoplethysmographic waveforms obtained at the donor site demonstrated good pulsatile flow, and preoperative arteriography demonstrated an acceptable lateral femoral circumflex artery. Intraoperatively, blood flow at the lateral circumflex femoral artery was measured using standard electromagnetic flowmetry. Blood flow measured before tensor fascia lata myocutaneous free flap transfer was 19 ml/min. After anastomosis of the lateral circumflex femoral artery to the peroneal artery, blood flow was 37 ml/min. Postoperatively, the myocutaneous flap was warm and photoplethysmography demonstrated excellent pulsatile waveforms over the lateral circumflex artery (Figure 6). At last follow-up two years postoperatively, viability of the myocutanous flap was excellent. Comment: On rare occasions, patients with a history of compartmental syndrome have had necrosis of the skin overlying the compartment. In such instances, the necrotic tissue may become infected and the entire limb may be threatened. When local blood supply is inadequate, skin grafts often prove to be inadequate. Under these circumstances, a myocutaneous free flap provides a well-vascularized living tissue that seals off the wound, prevents further infection, and brings a rich blood supply to an area of ischemic necrosis.
Comments
F&e 4. Wfth subsequenlsecondarycksun,ofthemwrndsofths fefl leg and applfcatfon of a splft-thickness graft, healing was excellant.
386
As a result of the clinical observation that marked bulging of the underlying muscle occurs after fasciotomy, many investigators have suggested that increased pressure within the compartment resulting from any case may initiate the syndrome. The increase in tissue pressure may be caused either by a decrease in size of the compartment or by an increase in the volume of its contents. The fascia of the legs
The American
Journal of Surpy
Compartmental
has been most commonly implicated as the envelope of limited compliance in compartmental syndrome, although associations with tight external dressings, skin, and epimysium have been reported [5-S]. This syndrome has been caused by postischemic swelling after arterial occlusion or prolonged aortofemoral bypass, fracture, soft tissue trauma, excessive muscular work, and closure of fascial defects. Clinical evidence and experimental evidence re-
F@m8.~,attertenswfsebr,latamyocut~ fen#oral artery and wfn to the pamneal attery and
vohmw
140, %ep4w
1904
Syndrome
ported by Benjamin [5] and Eaton and Green [6] have demonstrated that elevated intracompartmental pressures compromise local circulation by producing arterial spasm. Burton [I] has reported the existence of an arteriolar critical closing pressure as the determinant in circulatory compromise. Masten and Krugmire [9] have reported that both of these mechanisms are dependent on sustained active contraction of vascular segments in the presence of
anaMmo&
ftWVV8SUd8f~~~wllh
vein, excellent
pftot@etftysmograpf#k
pulsatffe
waveforms
of tfm lateral chcumffex were obtained.
387
Lee et al
ischemia, which is usually a potent stimulus for vasodilation. These investigators have also provided the following mechanism as an explanation for the compromise of tissue blood flow that results from increased tissue pressure: Veins are collapsible tubes, thus, the pressure in patent veins cannot be less than that in tissue. As long as perfusion persists, increased tissue pressure leads to increased venous pressure. Local tissue perfusion is primarily dependent on the local arteriovenous gradient and local vascular resistance. An increase in venous pressure associated with increased tissue pressure diminishes the arteriovenous gradient. When changes in local vascular resistance can no longer compensate for a decrease in the arteriovenous gradient, local tissue perfusion decreases. When local tissue perfusion is reduced to a point at which the metabolic demands of the tissue can no longer be maintained, diminished tissue function and viability become evident. Summary Compartmental syndrome is a condition in which swelling within a closed anatomic space increases the intracompartmental pressure to compromise the circulation and function of tissue within that space. Unless this condition is recognized early and treated by prompt surgical decompression, permanent neuromuscular deficits may result. In those instances in which early clinical evidence of this syndrome is difficult to assess, monitoring of intramuscular
388
pressures may be a valuable adjunct in the clinical evaluation of patients at risk for this syndrome. The association of compartmental syndrome with a wide variety of circumstances and the importance of an early diagnosis make it essential that all physicians be familiar with this condition. As physician awareness and recognition of this condition increase, the complications associated with it can be greatly reduced. References 1. Burton AC. On the physical equilibrium of small blood vessels. Am J Physiol 1951;164:319-29. 2. Jennings Ah%. Some observations on critical closing pressures in the peripheral circulation of anesthetized patients. Br J Anaesth 1964;36:683-93. 3. Whitesides TE, Haney TC, Morimoto K. Tissue pressure measurements as a determinant for the need of fasciotomy. Clin Orthop 1975;113:42-51. 4. Sheridan GW, Masten FA. Fasciotomy in the treatment of the acute compartment syndrome. J Bone Joint Surg [Am] 1976;58:112-5. 5. Benjamin A. The relief of traumatic arterial spasm in threatened Volkmann’s ischemic contracture. J Bone Joint Surg [Br] 1957;39:71 l-3. 6. Eaton RG, Green WT. Epimysiotomy and fasciotomy in the treatment of Volkmann’s ischemic contracture. Orthrop Clin North Am 1972;3:175-86. 7. Bowden RM, Gutman E. Fate of voluntary muscle after vascular injury in man. J Bone Joint Surg [Br] 1949;31:356-68. 8. Patman RD, Thompson JE. Fasciotomy in peripheral vascular surgery. Arch Surg 1970;101:663-72. 9. Masten FA, Krugmire RB. Compartmental syndrome. Surg Gynecol Obstet 1978;147:943-8.
The American Journal of Surgery