NOVEMBER 1992, VOL 56, NO 5
AORN JOI!RNAL
Compartment Syndrome A CLOSER LOOKAT ETIOLOGY, TREATMENT Lorena Perry Good, RN
C
ompartment syndrome is a condition in which neuromuscular deficits develop after an injury or surgery to an extremity. It occurs when there is increased pressure within a limited anatomic space. which leads to compromised circulation and function of the tissues within that space. To develop compartment syndrome, there must be a limiting sleeve surrounding the neuromuscular tissue and a cause for the increased pressure in the space.' The extremities are susceptible to compartment syndrome because muscles, nerves, blood vessels, and bone are surrounded and protected by fascia (ie. tough. inelastic, fibrous tissue).
The fascia creates a closed space or compartment. The fascia cannot expand; therefore, any condition that increases the contents of the compartment or decreases the size of the compartment puts the patient at risk for developing compartment syndrome. Human anatomy makes the extremities vulnerable to compartment syndrome. The most common sites for compartment syndrome are the deep volar compartments of the forearm (Fig I ) , the interosseous compartments of the hand (Fig 2), and the four compartments of the lower leg (Fig 3). In the leg, the anterior compartment is the most common site.
Etiology
C Lorena Perry Good, R N . is u ci-iricul cure instr.r~torut Luncuster- ( P u ) General Hospital. S / r c mi-tied /lei. t i i r t - s i n g diplomu at Lnrikeriuir Hospitul .%hool of'Nirrsirig, Philadelphin. The c r i d i o r thutrks Sirsuri Fiiclis for the illirstrations uriti Pun? Wile! f o r her help in preparing this niutiiisrript.
ompartment syndrome can develop for a variety of reasons. Most often it is the result of some type of trauma to the extremity (eg, bums, fractures, crush injuries). Traumatic injuries increase intracompartmental c o n t e n t s a s a r e s u l t of the i n f l a m m a t o r y response. Thermal injuries increase compartment contents because plasma colloids and proteins leak into the interstitial space. Nephrotic syndrome, with its concomittant loss of proteins, decreases oncotic pressure and also can cause compartment syndrome. The body senses decreased oncotic pressure as a loss of intravascular volume and activates the renin-angiotension-aldosteronesystem to cons e r v e s o d i u m a n d w a t e r . T h i s r e s u l t s in increased hydrostatic pressure, which results in edema.' Other causes of compartment syn-
drome include surgical closure of muscle fascia, vascular injury, excess traction, animal or human bites, external pressure, and postischemic swelling (Table 1). Compartment syndrome also can develop from localized external pressure caused by mast trousers, air splints, or positioning (eg, an unconscious patient lying on an extremity, a patient in the lithotomy position during long surgical procedures). Flexing of the knees and hips during surgery restricts arterial and venous flow; when the position is released, the postischemic swelling can lead to compartment ~yndrome.~
Pathophysiology
A
fter an injury, fluid accumulates in the muscle compartment. The inelastic fas.cia cannot expand to accommodate the increased volume, and pressure within the compartment rises. As tissue pressure increases in the closed space, the venous pressure also rises. This results in a decreased arteriovenous (A-V) gradient, which decreases local blood supply and results in tissue hypoxia. The body responds to tissue hypoxia by releasing histamine in an attempt to dilate capillaries and increase blood flow to the affected area. Histamine, in addition to vasodilatation, also increases capillary membrane permeabiliFig 1.The deep volar compartment of the forety. This allows fluids (ie, plasma colloids, proarm is a common site for compartment sydrome. teins) to leak out of the blood vessels and into (Adaptedfrom RN 52 (February 19891,R surrounding tissues, further increasing compartLavin, with permissionfrom M Reingold} mental pressure. As tissue pressure within the /-) compartment continues to rise and exceeds the capillary perfusion pressure, venous blood flow is impaired. If pressure continues to rise, arterial capillary blood flow will fall to a point where it no longer can meet the basic metabolic needs of the tissue. This condition leads to ischemia Fig 2. The interosseous compartments of the hand are susceptiand necrosis of muscles, nerves, ble to compartment syndrome. (Adaptedfrom Journal of Emergency Nursing 14 (SeptemberlOctober I988),J Proehl, and other tissues. Normal compartmental pres- with permission from Mosby-Year Book, Inc) 905
AORN JOCRNAL
sures range from 0 to 20 mm HE. When tissue pressures reach 30 mm Hg or more, blood flow to the microcirculation is impaired. Irreversible damage to nerves and muscles may occur within four to 12 hours after the onset of impaired perfusion. If left untreated, compartment syndrome may result in irreversible damage..' The ischemia produced by hypoperfusion is influenced by many factors, including the metabolic rate of the tissues, vascular tone, duration of elevated pressure, and local arterial blood pressure.5 Compartment syndrome may
Fig 3 Compartment syndrome may occur in any of the four compartments of the lower leg. The anterior compartment is the most common 5ite. (Aduptedfionr R N 52 (February 1989). R L c i i ~ t iM. rth pelmission from M Reingold) 906
NOVEMBER 1992, VOL 56. NO 5
be aggravated by local arterial blood pressure that may be already reduced by peripheral vascular disease, hypotension and shock, hemorrhage, arterial occlusion, or elevation of the extremity above the level of the h e a t 6
Signs, Symptoms
E
arly diagnosis of compartment syndrome is important, because prompt treatment can preserve the function and viability of the nerves and tissues in the affected compartment. Clinical assessments are helpful but may not reflect changes until permanent damage has occurred. Assessment can be very difficult in an unconscious or an uncooperative patient. Pain is the most common and most important presenting symptom in the conscious patient. The pain that results from compartment syndrome is out of proportion to the magnitude of the injury and is caused by muscle ischemia and necrosis. Patients often describe the pain as deep, burning, and unrelenting. The pain is progressive and poorly localized, a n d it may require increasing amounts of analgesics until neither narcotics nor positioning of the extremity provide relief. Absence of pain, however, does not rule out compartment syndrome. Patients with compartment syndrome may experience pain with passive movement, such as stretching or extending their fingers or toes. This stretch pain often is referred pain related to the affected compartment and also is caused by muscle ischemia. Patients may experience muscle weakness with compartment syndrome. An ischemic muscle weakens rapidly, and eventually movement becomes impossible. The ability to move fingers and toes, however, does not always indicate normal muscle function. While assessing a patient, it is important to palpate and compare both limbs. As compartment pressures rise, muscles will feel full and tense. The patient may complain of tightness, pressure, or tenderness in the affected extremity. This may or may not be accompanied by redness or warmth. Other indicators include
NOVEMBER 1992, VOL 56, NO 5
AORN JOURNAL
I Table 1
Etiologies of Compartment Syndrome
I
Increased compartment content Bleeding Major vascular injury Coagulation defect Bleeding disorder Anticoagulant therapy Increased capillary filtration Reperfusion after ischemia Arterial bypass grafting Embolectom y Ergotamine ingestion Cardiac catheterization Lying on limb Trauma Fracture Convulsion Intensive use of muscles Exercise Seizures Eclampsia Tetany Bums Thermal Electrical Intra-arterial drug injection Orthopedic surgery Tibia1 osteotomy Hauser procedure
Reduction and internal fixation of fractures Snakebite
Increased capillary pressure Intensive use of muscles Venous obstruction Phlegmasia cerulea dolens (ie, acute inflammation and edema of the legs) 111-fitting leg brace Venous ligation Diminished serum osmolarity (ie, nephrotic syndrome)
Decreased compartment volume Closure of fascia1 defects Excessive traction on fractured limbs Miscellaneous Infiltrated infusion Pressure transfusion Leaky dialysis cannula Muscle hypertrophy Popliteal cyst External pressure Tight casts, dressings, or air splints Lying on limb
(Adapted “ith permission of F A Matsen, Compartmental Syndromes (1980) Grune and Stratton, Inc, Neu! Yo14City) I
numbness, loss of sharp/dull discrimination, and diminished two-point discrimination of the affected area. Nerve conduction is affected rapidly by ischemia. When pressure develops, muscles and nerves begin to deteriorate within several hours.’ Skin color, temperature, and capillary refill time are unreliable indicators. The patient’s larger arteries remain patent until compartment pressure is very high; therefore, pulses may be
palpable on physical examination. Pallor and loss of pulses are late and ominous signs.
Diagnosis
T
o confirm a diagnosis of compartment syndrome, tissue pressure should be directly measured and monitored, in addition to the clinical assessment of signs and symptoms. Monitoring tissue pressure is espe-
NOVEMBER 1992. VOL 56, NO 5
AORN JOURNAL
nique is a quick, easy way to measure one-time pressure or intermittent pressures, but it cannot be used for continuous monitoring. Other systems use continuous infusion via needles or wickes and transducer monitoring systems. An intracompartmental pressure monitor can be used for either one-time or continuous pressure monitoring (Fig 5). Each setup is different and may not be familiar to all institutions.
mercury manometer
4 - 2 0 mL syringe
Treatment Fig 4 . The Whitesides technique is a quick, easy way to measure one-time or intermittent tissue pressure. (Adapredfiom Clinical Orthopedics and Related Research 43 (Januaiy 1985),T Whitesides et al. with permission from J B Lippincott Co, Phildelphia)
I
ntracompartmental pressures of more than 30 mm Hg with the presence of clinical findings indicate the need for intervention. Surgical decompression via a fasciotomy of the affected compartment is the treatment of choice. In a fasciotomy, the fascia is slit the entire length of the compartment, allowing the
cially important in an unconscious or uncooperative patient who cannot verify pain or changes in movement ability or sensation. When a diagnosis cannot be verified based on clinical signs, increased intracompartmental pressures help differentiate compartment syndrome from other conditions that may mimic its clinical signs and symptoms (eg, arterial occlusion, phlebitis, nerve damage from trauma or surgery). Several techniques are used to measure intracompartmental pressures. The Whitesides technique was developed by Thomas Whitesides, Jr, MD, in the 1970s. It uses a mercury manometer, IV tubing, a three-way stopcock, and a Fig 5. An intracompartmental pressure monitor can be used for either syringe filled with normal one-time or continuous pressure monitoring. (Photograph courtesy of saline (Fig 4). This tech- Str-yker Instruments, Kalaniazoo, Mich) 910
NOVEMBER 1992, VOL 56, NO 5
swollen muscle to bulge out through the incision. This decompresses the compartment and allows restoration of normal perfusion. The contents of the compartment usually will be soft to palpation when decompression is adequate. One or all of the compartments of the affected extremity are opened while the patient is anesthetized to prevent increased pressure from developing in another compartment. After surgical decompression, the wound is covered with sterile dressings, splinted in a functional position, and elevated. The wound is monitored and debrided as necessary for several days postoperatively to determine if delayed primary closure or skin grafting will be necessary. Free radical scavengers also have been used to limit tissue injury after ischemia. Oxygenderived free radicals have been implicated as a cause of tissue injury after ischemia. As oxygen is supplied to an extremity during reperfusion, reactive compounds are generated and attack cell membranes. This leads to increased capillary membrane permeability, edema, and tissue necrosis. Free radical scavengers reduce free radicals to less toxic products and thereby limit tissue injury. Two free radical scavengers that have been shown to reduce muscle necrosis in skeletal muscle are mannitol (ie, a dydroxyl radical scavenger) and superoxide dismutase (ie, an oxygen radical scavenger).8
Complications
T
he most common complication of compartment syndrome treatment is infection. This may be caused if diagnosis is delayed or if skin closure is attempted over devitalized tissue. Renal failure may occur because excessive amounts of myoglobin are released from necrotic muscle and accumulate in the renal tubules. The patient’s urine turns a dark reddish brown until the myoglobin is cleared from the body. Hyperkalemia can occur as potassium is released from the cells of the damaged muscle. If the patient experiences renal failure, potassium retention may compound the problem. This may lead to high
AORN JOURNAL
serum potassium and potentially life-threatening cardiac rhythm disturbances. Necrotic muscle tissue also releases lactic acid, which can lead to metabolic acidosis and other acid/base disturbances. Compartment syndrome patients also may experience muscle weakness, paralysis, nerve damage, contractures, and gangrene (which ultimately could result in amputation).
Conclusion
C
ompartment syndrome is not a common condition encountered by perioperative nurses. Early recognition of high-risk situations and clinical findings, however, can lead to prompt diagnosis and early intervention, which can preserve function and viability of a patient’s limb. 0 Notes 1. F A Matsen, “Compartmental syndromes,” Hospital Practice 15 (February 1980) 113-117. 2. M Larson, J Leigh, L Wilson, “Detecting compartmental syndrome using continuous pressure monitoring,” Focus on Critical Care 13 (October 1986) 51-56. 3. R Lavin, “The high pressure demands of compartment syndrome,” RN 52 (February 1989) 22-25. 4. J Proehl, “Compartment syndrome,” Journal of Emergency Nursing 14 (September/October 1988) 283-292. 5. Larson, Leigh, Wilson, “Detecting compartmental syndrome using continuous pressure monitoring,” 51-56. 6. Proehl, “Compartment syndrome,” 283-292. 7. M A Ricci et al, “Are free radical scavengers beneficial in the treatment of compartment syndrome after acute arterial ischemia?” Journal of Vascular Surgery 9 (February 1989) 244-249. 8. Ibid.
911
AORN JOI!RNAL
Compartment Syndrome A CLOSER LOOKAT ETIOLOGY, TREATMENT Lorena Perry Good, RN
C
ompartment syndrome is a condition in which neuromuscular deficits develop after an injury or surgery to an extremity. It occurs when there is increased pressure within a limited anatomic space. which leads to compromised circulation and function of the tissues within that space. To develop compartment syndrome, there must be a limiting sleeve surrounding the neuromuscular tissue and a cause for the increased pressure in the space.' The extremities are susceptible to compartment syndrome because muscles, nerves, blood vessels, and bone are surrounded and protected by fascia (ie. tough. inelastic, fibrous tissue).
The fascia creates a closed space or compartment. The fascia cannot expand; therefore, any condition that increases the contents of the compartment or decreases the size of the compartment puts the patient at risk for developing compartment syndrome. Human anatomy makes the extremities vulnerable to compartment syndrome. The most common sites for compartment syndrome are the deep volar compartments of the forearm (Fig I ) , the interosseous compartments of the hand (Fig 2), and the four compartments of the lower leg (Fig 3). In the leg, the anterior compartment is the most common site.
Etiology
C Lorena Perry Good, R N . is u ci-iricul cure instr.r~torut Luncuster- ( P u ) General Hospital. S / r c mi-tied /lei. t i i r t - s i n g diplomu at Lnrikeriuir Hospitul .%hool of'Nirrsirig, Philadelphin. The c r i d i o r thutrks Sirsuri Fiiclis for the illirstrations uriti Pun? Wile! f o r her help in preparing this niutiiisrript.
ompartment syndrome can develop for a variety of reasons. Most often it is the result of some type of trauma to the extremity (eg, bums, fractures, crush injuries). Traumatic injuries increase intracompartmental c o n t e n t s a s a r e s u l t of the i n f l a m m a t o r y response. Thermal injuries increase compartment contents because plasma colloids and proteins leak into the interstitial space. Nephrotic syndrome, with its concomittant loss of proteins, decreases oncotic pressure and also can cause compartment syndrome. The body senses decreased oncotic pressure as a loss of intravascular volume and activates the renin-angiotension-aldosteronesystem to cons e r v e s o d i u m a n d w a t e r . T h i s r e s u l t s in increased hydrostatic pressure, which results in edema.' Other causes of compartment syn-
drome include surgical closure of muscle fascia, vascular injury, excess traction, animal or human bites, external pressure, and postischemic swelling (Table 1). Compartment syndrome also can develop from localized external pressure caused by mast trousers, air splints, or positioning (eg, an unconscious patient lying on an extremity, a patient in the lithotomy position during long surgical procedures). Flexing of the knees and hips during surgery restricts arterial and venous flow; when the position is released, the postischemic swelling can lead to compartment ~yndrome.~
Pathophysiology
A
fter an injury, fluid accumulates in the muscle compartment. The inelastic fas.cia cannot expand to accommodate the increased volume, and pressure within the compartment rises. As tissue pressure increases in the closed space, the venous pressure also rises. This results in a decreased arteriovenous (A-V) gradient, which decreases local blood supply and results in tissue hypoxia. The body responds to tissue hypoxia by releasing histamine in an attempt to dilate capillaries and increase blood flow to the affected area. Histamine, in addition to vasodilatation, also increases capillary membrane permeabiliFig 1.The deep volar compartment of the forety. This allows fluids (ie, plasma colloids, proarm is a common site for compartment sydrome. teins) to leak out of the blood vessels and into (Adaptedfrom RN 52 (February 19891,R surrounding tissues, further increasing compartLavin, with permissionfrom M Reingold} mental pressure. As tissue pressure within the /-) compartment continues to rise and exceeds the capillary perfusion pressure, venous blood flow is impaired. If pressure continues to rise, arterial capillary blood flow will fall to a point where it no longer can meet the basic metabolic needs of the tissue. This condition leads to ischemia Fig 2. The interosseous compartments of the hand are susceptiand necrosis of muscles, nerves, ble to compartment syndrome. (Adaptedfrom Journal of Emergency Nursing 14 (SeptemberlOctober I988),J Proehl, and other tissues. Normal compartmental pres- with permission from Mosby-Year Book, Inc) 905
AORN JOCRNAL
sures range from 0 to 20 mm HE. When tissue pressures reach 30 mm Hg or more, blood flow to the microcirculation is impaired. Irreversible damage to nerves and muscles may occur within four to 12 hours after the onset of impaired perfusion. If left untreated, compartment syndrome may result in irreversible damage..' The ischemia produced by hypoperfusion is influenced by many factors, including the metabolic rate of the tissues, vascular tone, duration of elevated pressure, and local arterial blood pressure.5 Compartment syndrome may
Fig 3 Compartment syndrome may occur in any of the four compartments of the lower leg. The anterior compartment is the most common 5ite. (Aduptedfionr R N 52 (February 1989). R L c i i ~ t iM. rth pelmission from M Reingold) 906
NOVEMBER 1992, VOL 56. NO 5
be aggravated by local arterial blood pressure that may be already reduced by peripheral vascular disease, hypotension and shock, hemorrhage, arterial occlusion, or elevation of the extremity above the level of the h e a t 6
Signs, Symptoms
E
arly diagnosis of compartment syndrome is important, because prompt treatment can preserve the function and viability of the nerves and tissues in the affected compartment. Clinical assessments are helpful but may not reflect changes until permanent damage has occurred. Assessment can be very difficult in an unconscious or an uncooperative patient. Pain is the most common and most important presenting symptom in the conscious patient. The pain that results from compartment syndrome is out of proportion to the magnitude of the injury and is caused by muscle ischemia and necrosis. Patients often describe the pain as deep, burning, and unrelenting. The pain is progressive and poorly localized, a n d it may require increasing amounts of analgesics until neither narcotics nor positioning of the extremity provide relief. Absence of pain, however, does not rule out compartment syndrome. Patients with compartment syndrome may experience pain with passive movement, such as stretching or extending their fingers or toes. This stretch pain often is referred pain related to the affected compartment and also is caused by muscle ischemia. Patients may experience muscle weakness with compartment syndrome. An ischemic muscle weakens rapidly, and eventually movement becomes impossible. The ability to move fingers and toes, however, does not always indicate normal muscle function. While assessing a patient, it is important to palpate and compare both limbs. As compartment pressures rise, muscles will feel full and tense. The patient may complain of tightness, pressure, or tenderness in the affected extremity. This may or may not be accompanied by redness or warmth. Other indicators include
NOVEMBER 1992, VOL 56, NO 5
AORN JOURNAL
I Table 1
Etiologies of Compartment Syndrome
I
Increased compartment content Bleeding Major vascular injury Coagulation defect Bleeding disorder Anticoagulant therapy Increased capillary filtration Reperfusion after ischemia Arterial bypass grafting Embolectom y Ergotamine ingestion Cardiac catheterization Lying on limb Trauma Fracture Convulsion Intensive use of muscles Exercise Seizures Eclampsia Tetany Bums Thermal Electrical Intra-arterial drug injection Orthopedic surgery Tibia1 osteotomy Hauser procedure
Reduction and internal fixation of fractures Snakebite
Increased capillary pressure Intensive use of muscles Venous obstruction Phlegmasia cerulea dolens (ie, acute inflammation and edema of the legs) 111-fitting leg brace Venous ligation Diminished serum osmolarity (ie, nephrotic syndrome)
Decreased compartment volume Closure of fascia1 defects Excessive traction on fractured limbs Miscellaneous Infiltrated infusion Pressure transfusion Leaky dialysis cannula Muscle hypertrophy Popliteal cyst External pressure Tight casts, dressings, or air splints Lying on limb
(Adapted “ith permission of F A Matsen, Compartmental Syndromes (1980) Grune and Stratton, Inc, Neu! Yo14City) I
numbness, loss of sharp/dull discrimination, and diminished two-point discrimination of the affected area. Nerve conduction is affected rapidly by ischemia. When pressure develops, muscles and nerves begin to deteriorate within several hours.’ Skin color, temperature, and capillary refill time are unreliable indicators. The patient’s larger arteries remain patent until compartment pressure is very high; therefore, pulses may be
palpable on physical examination. Pallor and loss of pulses are late and ominous signs.
Diagnosis
T
o confirm a diagnosis of compartment syndrome, tissue pressure should be directly measured and monitored, in addition to the clinical assessment of signs and symptoms. Monitoring tissue pressure is espe-
NOVEMBER 1992. VOL 56, NO 5
AORN JOURNAL
nique is a quick, easy way to measure one-time pressure or intermittent pressures, but it cannot be used for continuous monitoring. Other systems use continuous infusion via needles or wickes and transducer monitoring systems. An intracompartmental pressure monitor can be used for either one-time or continuous pressure monitoring (Fig 5). Each setup is different and may not be familiar to all institutions.
mercury manometer
4 - 2 0 mL syringe
Treatment Fig 4 . The Whitesides technique is a quick, easy way to measure one-time or intermittent tissue pressure. (Adapredfiom Clinical Orthopedics and Related Research 43 (Januaiy 1985),T Whitesides et al. with permission from J B Lippincott Co, Phildelphia)
I
ntracompartmental pressures of more than 30 mm Hg with the presence of clinical findings indicate the need for intervention. Surgical decompression via a fasciotomy of the affected compartment is the treatment of choice. In a fasciotomy, the fascia is slit the entire length of the compartment, allowing the
cially important in an unconscious or uncooperative patient who cannot verify pain or changes in movement ability or sensation. When a diagnosis cannot be verified based on clinical signs, increased intracompartmental pressures help differentiate compartment syndrome from other conditions that may mimic its clinical signs and symptoms (eg, arterial occlusion, phlebitis, nerve damage from trauma or surgery). Several techniques are used to measure intracompartmental pressures. The Whitesides technique was developed by Thomas Whitesides, Jr, MD, in the 1970s. It uses a mercury manometer, IV tubing, a three-way stopcock, and a Fig 5. An intracompartmental pressure monitor can be used for either syringe filled with normal one-time or continuous pressure monitoring. (Photograph courtesy of saline (Fig 4). This tech- Str-yker Instruments, Kalaniazoo, Mich) 910
NOVEMBER 1992, VOL 56, NO 5
swollen muscle to bulge out through the incision. This decompresses the compartment and allows restoration of normal perfusion. The contents of the compartment usually will be soft to palpation when decompression is adequate. One or all of the compartments of the affected extremity are opened while the patient is anesthetized to prevent increased pressure from developing in another compartment. After surgical decompression, the wound is covered with sterile dressings, splinted in a functional position, and elevated. The wound is monitored and debrided as necessary for several days postoperatively to determine if delayed primary closure or skin grafting will be necessary. Free radical scavengers also have been used to limit tissue injury after ischemia. Oxygenderived free radicals have been implicated as a cause of tissue injury after ischemia. As oxygen is supplied to an extremity during reperfusion, reactive compounds are generated and attack cell membranes. This leads to increased capillary membrane permeability, edema, and tissue necrosis. Free radical scavengers reduce free radicals to less toxic products and thereby limit tissue injury. Two free radical scavengers that have been shown to reduce muscle necrosis in skeletal muscle are mannitol (ie, a dydroxyl radical scavenger) and superoxide dismutase (ie, an oxygen radical scavenger).8
Complications
T
he most common complication of compartment syndrome treatment is infection. This may be caused if diagnosis is delayed or if skin closure is attempted over devitalized tissue. Renal failure may occur because excessive amounts of myoglobin are released from necrotic muscle and accumulate in the renal tubules. The patient’s urine turns a dark reddish brown until the myoglobin is cleared from the body. Hyperkalemia can occur as potassium is released from the cells of the damaged muscle. If the patient experiences renal failure, potassium retention may compound the problem. This may lead to high
AORN JOURNAL
serum potassium and potentially life-threatening cardiac rhythm disturbances. Necrotic muscle tissue also releases lactic acid, which can lead to metabolic acidosis and other acid/base disturbances. Compartment syndrome patients also may experience muscle weakness, paralysis, nerve damage, contractures, and gangrene (which ultimately could result in amputation).
Conclusion
C
ompartment syndrome is not a common condition encountered by perioperative nurses. Early recognition of high-risk situations and clinical findings, however, can lead to prompt diagnosis and early intervention, which can preserve function and viability of a patient’s limb. 0 Notes 1. F A Matsen, “Compartmental syndromes,” Hospital Practice 15 (February 1980) 113-117. 2. M Larson, J Leigh, L Wilson, “Detecting compartmental syndrome using continuous pressure monitoring,” Focus on Critical Care 13 (October 1986) 51-56. 3. R Lavin, “The high pressure demands of compartment syndrome,” RN 52 (February 1989) 22-25. 4. J Proehl, “Compartment syndrome,” Journal of Emergency Nursing 14 (September/October 1988) 283-292. 5. Larson, Leigh, Wilson, “Detecting compartmental syndrome using continuous pressure monitoring,” 51-56. 6. Proehl, “Compartment syndrome,” 283-292. 7. M A Ricci et al, “Are free radical scavengers beneficial in the treatment of compartment syndrome after acute arterial ischemia?” Journal of Vascular Surgery 9 (February 1989) 244-249. 8. Ibid.
911
