Emergency Situations 2 Its 0800 and the outpatient clinic where you work as RN has just opened.

RW, a 40 y/o man hops into the clinic c/o severe pain and swelling in his right lower leg. He tells you he was walking between two cars the night before, when one of the cars was backed up, catching his lower leg between the bumpers. He states he didnt think it was hurt that bad and went home to wash the abrasions. He woke up at approx 0400, and states, my leg was killing me. Symbol, terms, abbreviation Diagnoses/medical conditions Lower leg fractures Meaning/ definition Description/meaning of the diagnosis or medical problem

Lower leg fractures include fractures of the tibia and fibula. Of these two bones, the tibia is the only weightbearing bone. Fractures of the tibia generally are associated with fibula fracture, because the force is transmitted along the interosseous membrane to the fibula. The skin and subcutaneous tissue are very thin over the anterior and medial tibia and as a result of this, a significant number of fractures to the lower leg are open. Even in closed fractures, the thin, soft tissue can become compromised. In contrast, the fibula is well covered by soft tissue over most of its course with the exception of the lateral malleolus. The tibia and fibula articulate at the proximal tibia-fibular syndesmosis. Fractures of the tibia can involve the tibial plateau, tibial tubercle, tibial eminence, proximal tibia, tibial shaft, and tibial plafond.

Acute compartment syndrome

Acute compartment syndrome occurs when the tissue pressure within a closed muscle compartment exceeds the perfusion pressure and results in muscle and nerve ischemia. It typically occurs subsequent to a traumatic event, most commonly a fracture. The cycle of events leading to acute compartment syndrome begins when the tissue pressure exceeds the venous pressure and impairs blood outflow. Lack of oxygenated blood and accumulation of waste products

result in pain and decreased peripheral sensation secondary to nerve irritation. Late manifestations of compartment syndrome include the absence of a distal pulse, hypoesthesia, and extremity paresis, because the cycle of elevating tissue pressure eventually compromises arterial blood flow. If left untreated or if inadequately treated, the muscles and nerve within the compartment undergo ischemic necrosis, and a limb contracture, called a Volkmann contracture, results. Severe cases may lead to renal failure and death. The literature is somewhat confusing because of the interchangeable use of the terms acute, subacute, chronic, and recurrent compartment syndrome; crush syndrome; and Volkmann ischemic contracture. Crush syndrome is distinct from compartment syndrome; it is defined as a severe systemic manifestation (eg, rhabdomyolysis) of trauma and ischemia involving soft tissues, principally skeletal muscle, as a result of prolonged severe crushing. Crush syndrome trauma or rhabdomyolysis may also lead to an acute compartment syndrome.

Pathophysiology of leg fractures

History Mechanisms of injury for tibia-fibula fractures can be divided into 2 categories:

Low-energy injuries such as ground levels falls and athletic injuries High-energy injuries such as motor vehicle injuries, pedestrians struck by motor vehicles, and gunshot wounds

Patient may report a history of direct (motor vehicle crash or axial loading) or indirect (twisting) trauma. Patient may complain of pain, swelling, and inability to ambulate with tibia fracture. Ambulation is possible with isolated fibula fracture.

Tibial plateau fractures occur from axial loading with valgus or varus forces, such as in a fall from a height or collision with the bumper of a car. The lateral tibial plateau is fractured more frequently than the medial plateau. Tibial tubercle fractures usually occur during jumping activities such as basketball, diving, football, and gymnastics. This type of fracture is more common in adolescents than in adults. Tibial eminence fractures occur with trauma to the distal femur while the knee is flexed such as falling off of a bicycle. Another mechanism for this fracture is hyperextension. Tibial eminence avulsion fractures occur most often in children aged 8-14 years but can occur in a skeletally mature patient. Tibial shaft fractures usually present with a history of major trauma. An exception to this is a toddler's fracture, which is a spiral fracture that occurs with minor trauma in children who are learning to walk. Tibial plafond fractures refer to fractures involving the weightbearing surface of the distal tibia. This type of injury usually results from high-energy axial loading but may result from lowerenergy rotation forces. Maisonneuve fractures are rare and considered unstable ankle injuries. This type of injury usually involves a pronation-external rotation force. Stress fractures of the tibia and fibula may occur as a result of repetitive submaximal stresses that may occur while participating in athletics. The history may reveal some change in training routine. Patients with osteoporosis may have a seemingly innocent mechanism of injury and still sustain fracture.[3] Physical When examining a patient for a lower leg fracture one should first examine the patient for edema, ecchymosis, and point tenderness. Gross deformities should be noted and splinted. A careful neurovascular assessment should be performed, and an emergent fracture reduction should be performed if neurovascular deficits are present. A careful examination should be performed for open wounds. Open fractures require antibiotics and an emergent orthopedic consultation. Tibial plateau fractures often present with a knee effusion. Tenderness will be present along the medial or lateral tibial plateau. Approximately 20% of tibial plateau fractures are associated with ligamentous injuries.

Tibial tubercle fracture will have tenderness over the anterior tibia approximately 3 cm distal to the articular surface. In more severe tibial tubercle fractures, full extension of the knee is not possible. The patella may be high riding.

Tibial eminence fracture may present with a knee effusion and pain and may represent an avulsion of the tibial attachment of the anterior cruciate ligament. Tibial shaft fractures are the most common long bone fracture and usually involve the fibula as well. Tibial fractures present with localized pain, swelling, and deformity. Maisonneuve fractures involve a fracture of the proximal fibula in association with a fractured medial malleolus (or injured deltoid ligament) and diastasis of the distal tibiofibular syndesmosis. Patients present with proximal fibular pain in addition to medial ankle pain. This is an unstable ankle injury. Tibial plafond fractures will have tenderness along the distal tibial and may have severely decreased range of motion in the ankle. Causes Causes include the following:

Direct forces such as those caused by falls and MVCs Indirect or rotational forces

Differential Diagnoses

Ankle Injury, Soft Tissue Compartment Syndrome, Extremity Fractures, Ankle Fractures, Knee Knee Injury, Soft Tissue Pediatrics, Child Abuse Pediatrics, Limp Peripheral Vascular Injuries Trauma, Peripheral Vascular Injuries

Workup Imaging studies

Radiography
Perform radiographs of the knee, tibia/fibula, and ankle as indicated

Computed tomography
Computed tomography is indicated for severely injured patients if unable to get diagnostically sufficient radiographs of the knee. In patients with tibial plateau fractures and tibial plafond fractures, computed tomography can help further evaluate the extent of the fracture.

In tibial plateau fractures, radiographs may underestimate the degree of articular depression when compared with computed tomography. This is important because articular depression of greater than 3 mm may be considered for surgery.

For stress fractures

Radiographic findings are usually seen after 2-8 weeks of symptoms, and radiographs may not be very sensitive during the early stages of symptoms. Radionucleotide scanning and MRI are more sensitive in diagnosing stress fractures and stress injuries than radiographs.

Other Tests
Pedestrians struck by motor vehicles with lower extremity fractures have a high incidence of concomitant spine, chest, or intra-abdominal injuries.[4] These patients may need additional radiographic tests to rule out these injuries when clinically indicated.

Prehospital Care
Address airway, breathing, and circulation. Check and document neurovascular status. Apply sterile dressing to open wounds. Apply gentle traction to reduce gross deformities; splint the extremity. Administer parenteral analgesics for an isolated extremity injury in a hemodynamically stable patient.

Emergency Department Care

Parenteral analgesia should be administered when appropriate. Although management of pain has improved, pain due to long bone fractures is notably undertreated in the emergency department.[3] Open fractures must be diagnosed and treated appropriately (also see Tibia Fractures, Open). Tetanus vaccination should be updated, and appropriate antibiotics should be given in a timely manner. Some recommend antibiotics within 3 hours of the accident.[5] This should involve antistaphylococcal coverage and consideration of an aminoglycoside for more severe wounds. Orthopedics should be consulted for emergent debridement and wound care. Fractures with tissue at risk for opening should be protected to prevent further morbidity.

Compartment syndrome
Compartment syndrome can develop in fractures of the lower leg.

Signs of compartment syndrome include crescendo symptoms, pain with passive movement of involved muscles, paresthesias, and pallor, and a very late finding is pulselessness. Increased compartment pressure is present during compartment syndrome; therefore, external palpation frequently aids in the diagnosis. However, a soft extremity on palpation does not rule out compartment syndrome. Serial examinations should be performed on patients with high-risk injuries or patients with equivocal symptoms. If compartment syndrome is suspected, obtain an emergent orthopedic consult and measure compartment pressures. Compartment syndrome must be treated promptly with an emergency surgical fasciotomy. If untreated, the increased compartment pressures can cause ischemia and necrosis of the structures within that facial compartment and permanent disability. Risk factors for compartment syndrome of the lower leg include tibial diaphysis fracture, softtissue injury, and crush injury.[6] Open fractures in pediatric patients have a significantly increased risk of developing compartment syndrome.[6]

Tibial plateau fracture

Immobilize nondisplaced fractures and have the patient remain nonweightbearing. Obtain an orthopedic consultation for displaced (depressed) fractures, which require open reduction and internal fixation. Articular depression of greater than 3 mm may be considered for surgery.

Tibial eminence fracture

For nondisplaced fractures (and stable knee joint), immobilize the knee. Obtain an orthopedic consultation for an unstable knee, or displaced fracture for possible surgical fixation.

Tibial tubercle fracture

For nondisplaced fractures, immobilize the knee. Obtain an orthopedic consultation for a displaced fracture to consider open reduction and internal fixation.

Proximal tibia fractures

Intra-articular fractures require reduction and internal fixation. Other methods to surgically repair proximal tibia fractures include external fixation, plating, and intramedullary nailing.

Closed treatment involves reduction and the placement of a long leg cast. Intact extensor mechanisms can make it difficult to maintain good fracture alignment. Tibial shaft fractures that are closed may be treated with cast immobilization if alignment is good or with intramedullary nailing.

Isolated midshaft or proximal fibula fracture

Immobilization in a long leg cast generally is not required. Recommend a few days without weightbearing activity until swelling resolves, followed by weightbearing activity as tolerated. Short leg walking cast usually is not required; however, some orthopedists may prefer a short leg walking cast or cam walker with weight bearing.

Tibia and fibula stress fractures

The keystone of treating stress fractures is the temporary cessation of the offending activity. Crutches may be used initially to allow the patient to be nonweight-bearing.

Consultations
Obtain emergent orthopedic consultation for open fractures. Consultation is also generally indicated for closed fractures. Emergent consultation is needed in suspected compartment syndrome. Advise patient to obtain orthopedic follow-up care of isolated fibula fractures

Medication Summary
Drugs used to treat fractures include nonsteroidal anti-inflammatory agents and analgesics. In addition, administer proper antibiotics and tetanus prophylaxis for open fractures. www.emedicine.com/emerg/topic207.htm

Acute compartment syndrome

Anatomy

Compartment syndrome may develop wherever a compartment is present. Possible sites include the lower leg, forearm, wrist, and hand.

Lower leg

The lower leg is divided into 4 compartments. A fifth compartment has been documented, but the clinical significance of this compartment has yet to be established. The 5 compartments are as follows:

Anterior Lateral Superficial posterior Deep posterior Tibialis posterior

Anterior compartment Muscles in the anterior compartment are as follows:

Tibialis anterior Extensor digitorum longus Extensor hallucis longus Peroneus tertius

The borders of the anterior compartment are as follows:

Tibia Fibula Interosseous membrane Anterior intermuscular septum

Lateral compartment The lateral compartment includes the peroneus longus and brevis. Within the compartment lie the common peroneal nerve and its superficial and deep branches. The borders of this compartment are as follows:

Anterior intermuscular septum Fibula Posterior intermuscular septum Deep fascia

Superficial posterior compartment The superficial posterior compartment contains the gastrocnemius, soleus, and plantaris. It is surrounded by the deep fascia of the leg. Deep posterior compartment The muscles within the deep posterior compartment are as follows:

Flexor digitorum longus Flexor hallucis longus

Popliteus Tibialis posterior

Also within this compartment lie the posterior tibial artery and vein and the tibial nerve. The borders of the deep posterior compartment are as follows:

Tibia Fibula Deep transverse fascia Interosseous membrane

Tibialis posteriorcompartment The tibialis posterior compartment is a more recently described subdivision of the deep posterior compartment. It consists of the tibialis posterior, which has been shown to have its own fascial layer.

Forearm
Four interconnected compartments of the forearm are recognized, as follows:

Superficial volar (flexor) Deep volar Dorsal (extensor) compartment Compartment containing the mobile wad of Henry

The deep volar compartment contains the flexor digitorum profundus, flexor pollicis longus, and pronator quadratus muscles and tendons. The mobile wad of Henry comprises the brachioradialis, extensor carpi radialis brevis (ECRB), and extensor carpi radialis longus muscles and tendons. Elevated pressures most commonly affect the volar compartments, but the dorsal and mobile wad compartments may also be involved, alone or in addition to the volar compartments. It is usually difficult to clinically differentiate isolated or combined involvement of the deep and superficial volar compartments.

Wrist
In the wrist, most of the soft tissues are bound within rigid compartments. The volar wrist tendons, for the most part, are tightly constrained within the carpal tunnel (thumb and finger long flexor tendons), except for the flexor carpi radialis, flexor carpi ulnaris, and palmaris longus tendons, which are in separate compartments. The dorsal compartments are primarily channels for tendons and are rarely afflicted by compartment syndrome. The dorsal extensor tendons pass under an extensor retinaculum and are divided into 6 compartments, as follows:

Radial wrist abductor (abductor pollicis longus tendon) and thumb extensor (extensor pollicis brevis tendon) dorsal to the trapezium bone Radial wrist extensors (extensor carpi radialis longus and ECRB tendons) dorsal and radial to the trapezoid bone Extensor pollicis longus tendon Common finger extensors (extensor digitorum communis [EDC] tendon) dorsal to the capitotrapezoid articulation Extensor digiti minimi tendon to the fifth digit Ulnar wrist extensor (extensor carpi ulnaris tendon) in a groove adjacent to the ulnar styloid

Hand
The hand has 10 compartments, as follows:

Dorsal interossei (4 compartments) Palmar interossei (3 compartments) Adductor pollicis compartment Thenar compartment Hypothenar compartment

Pathophysiology
Compartment syndrome results primarily from increased intracompartmental pressure. The mechanism involved in the development of increased pressure depends on the precipitating event. Two distinct types of compartment syndrome have been recognized. The first type is associated with trauma to the affected compartment, as seen in fractures or muscle injuries. The second form, called exertional compartment syndrome, is associated with repetitive loading or microtrauma related to physical activity.[11, 12, 13, 14, 15, 16, 17, 18] Thus, compartment syndrome may be acute or chronic in nature. Tissue perfusion is proportional to the difference between the capillary perfusion pressure (CPP) and the interstitial fluid pressure, which is stated by the following formula: LBF = (PA - PV)/R In the formula above, LBF is local blood flow, PA is local arterial pressure, PV is venous pressure, and R is local vascular resistance. Normal myocyte metabolism requires a 5-7 mm Hg oxygen tension, which can readily be obtained with a CPP of 25 mm Hg and an interstitial tissue pressure of 4-6 mm Hg.[19] When fluid is introduced into a fixed-volume compartment, tissue pressure increases and venous pressure rises. When the interstitial pressure exceeds the CPP (a narrowed arteriovenous [AV] perfusion gradient), capillary collapse and muscle and tissue ischemia occur.

Skeletal muscle responds to ischemia by releasing histaminelike substances that increase vascular permeability. Plasma leaks out of the capillaries, and relative blood sludging in the small capillaries occurs, worsening the ischemia. The myocytes begin to lyse, and the myofibrillar proteins decompose into osmotically active particles that attract water from arterial blood. One milliosmole (mOsm) is estimated to exert a pressure of 19.5 mm Hg; therefore, a relatively small increase in osmotically active particles in a closed compartment attracts sufficient fluid to cause a further rise in intramuscular pressure. When tissue blood flow is diminished further, muscle ischemia and subsequent cell edema worsen. This vicious cycle of worsening tissue perfusion continues to propagate. Some reduction in the local AV gradient can be compensated for by changes in local vascular resistance (autoregulation). However, compartment tamponade occurs as arterial blood flow is occluded. Shrier and Magder questioned this traditional hypothesis for the pathophysiology of compartment syndrome and postulated that within muscle compartments, a critical closing pressure exists (similar to West zone II in lung physiology).[20] These authors showed that the increase in this critical closing pressure, which they called Pcrit, rather than an increase in arterial resistance, results in decreased blood flow. The transmural pressure at which blood flow ceases depends on adrenergic tone as well as the interstitial pressure; the pressure at which this occurs is still under debate. However, in general, compartmental pressures higher than 30 mm Hg require surgical intervention. If such high compartmental pressures are left untreated, within 6-10 hours, muscle infarction, tissue necrosis, and nerve injury occur. For unclear reasons, compartment syndrome that is associated with surgical positioning may manifest later, with a mean time to presentation of 15-24 hours or longer postoperatively.[21] Pressure-induced functional deficits are likely caused by decreased tissue perfusion rather than a direct mechanical effect. Therefore, the amount of pressure a limb can tolerate depends on limb elevation, blood pressure, hemorrhage, and arterial occlusion. In addition to local morbidity caused by muscle necrosis and tissue ischemia, cellular destruction and alterations in muscle cell membranes lead to the release of myoglobin into the circulation. This circulating myoglobin results in renal injury. Advanced compartment syndrome may result in rhabdomyolysis, and conversely, rhabdomyolysis may result in compartment syndrome.[22] Mortality is usually due to renal failure or sepsis from difficult wound management. The mechanism of compartment syndrome following vascular trauma may differ slightly from the above scenario because most cases occur with reperfusion. This reperfusion syndrome is likely related to the ischemic depletion of high-energy phosphate forms and ischemic muscle injury. Muscle has considerable ability to regenerate by forming new muscle cells. Therefore, it is extremely important to decompress ischemic muscle as early as possible. Compartment pressures return to normal after a fasciotomy.[23]

History
Patients with compartment syndrome typically present with pain whose severity appears out of proportion to the injury. The pain is often described as burning. The pain is also deep and aching in nature and is worsened by passive stretching of the involved muscles. The patient may describe a tense feeling in the extremity. Pain, however, should not be a sine qua non of the diagnosis. In severe trauma, such as an open fracture, it is difficult to differentiate between pain from the fracture and pain resulting from increased compartment pressure. Paresthesia or numbness is an unreliable early complaint[10] ; however, decreased 2-point discrimination is a more reliable early test and can be helpful to make the diagnosis. Botte and Gelberman reported that 4 of 9 awake patients with compartment pressures higher than 30 mm Hg had median nerve 2-point discrimination of more than 1 cm.[15] Correlation has also been reported between diminished vibration sense (256 cycles/s) and increasing compartment pressure. Importantly, note that these symptoms assume a conscious patient who did not suffer any additional injury that hinders sensory input (eg, spinal cord injury). In young children, the ability to gather a history of complaints is limited. Determine the mechanism of injury. High-velocity injuries are particularly worrisome, as are long-bone fractures and crush injuries. Penetrating injuries (eg, gunshot wounds, stabbings) can cause arterial injury, which can quickly lead to compartment syndrome. Venous injury may also cause compartment syndrome, however, so the clinician should not be misled by the presence of palpable pulses. Anticoagulation therapy and bleeding disorders (eg, hemophilia) significantly increase the likelihood of compartment syndrome. Remember to ask if patients are anticoagulated for any reason. Compartment syndrome requiring fasciotomy has been observed after simple venipuncture in an anticoagulated patient. Vigorous exertion may lead to compartment syndrome. Compartment syndrome has been found in soldiers and athletes without any trauma. This can be acute or chronic, with acute compartment pressures as high as those found in severe trauma. If compartment syndrome is suspected, check intracompartmental pressure, even in the absence of any trauma

Physical Examination
On physical examination, evidence of trauma and gross deformity should alert the physician to the possibility of a developing compartment syndrome. Comparison of the affected limb to the unaffected limb is useful. Excessively vigorous examination of a tibial fracture should be avoided because this may exacerbate irritation of the deep posterior compartment. Common symptoms observed in compartment syndrome include a feeling of tightness and swelling. Pain with certain movements, particularly passive stretching of the muscles, is the earliest clinical indicator of compartment syndrome. A patient may report pain with active flexion. The traditional 5 P's of acute ischemia in a limb (ie, pain, paresthesia, pallor, pulselessness, poikilothermia) are not clinically reliable; they may manifest only in the late stages of

compartment syndrome, by which time extensive and irreversible soft tissue damage may have taken place. Peripheral pulses and capillary refill remain normal in most cases of upper extremity acute compartment syndrome. The most important diagnostic physical finding is a firm, wooden feeling on deep palpation. Bullae may also be seen; however, so-called fracture blisters are common in the absence of compartment syndrome. In cases involving the leg, a soft tissue mass may be noticed as a result of herniation of fat and/or muscle tissue from the fascial defect that is often found in the lower third of the leg. In cases of trauma and gross deformity, a claw-toe deformity might occur; therefore, the patient should be evaluated for such a condition. If a patient complains of pain, determine whether any neural compromise is present. Sensory nerves tend to be affected before the motor nerves, and selected nerves may be more susceptible than others in the same compartment. For example, in acute anterior lower leg compartment syndrome, the first sign to develop may be numbness between the first 2 toes (superficial peroneal nerve). Decreased 2-point discrimination is the most consistent early finding, and correlation has also been reported between diminished vibration sense (as measured with a 256 cycle per second tuning fork). If objective evidence of a major sensory deficit, a motor deficit, or loss of peripheral pulse is found, the syndrome is far advanced.

Differentials

Cellulitis Cnidaria Envenomation Deep Venous Thrombosis Emergent Management of Necrotizing Fasciitis Gas Gangrene in Emergency Medicine Peripheral Vascular Injuries Physical Medicine and Rehabilitation for Stress Fractures Rhabdomyolysis in Emergency Medicine

Approach Considerations
In a patient with the classic compartment syndrome presentation and physical examination findings, no further diagnostic workup is needed. Laboratory results are often normal, are not necessary to diagnose compartment syndrome, and are not helpful to rule out compartment syndrome. However, in acute compartment syndrome, especially with trauma, consider performing a workup for rhabdomyolysis, with measurement of the following:

Creatine phosphokinase (CPK) Renal function studies Urinalysis Urine myoglobin

A CPK concentration of 1000-5000 U/mL or greater or the presence of myoglobinuria can suggest compartment syndrome. Serial CPK measurements may show rising levels indicative of a developing compartment syndrome. Urinalysis may be used to help identify causes of acute renal failure. Patients with rhabdomyolysis should have serum chemistry studies done. Complete blood cell count and coagulation studies should be part of the preoperative workup. Anemia worsens tissue oxygenation. Disseminated intravascular coagulation is a rare but possible complication. Measurement of intracompartmental pressures remains the standard for diagnosis of compartment syndrome. Perform this procedure as soon as the diagnosis of compartment syndrome is considered. Imaging studies are usually not helpful in making the diagnosis of compartment syndrome. However, such studies are used in part to eliminate disorders in the differential diagnosis. Standard radiographs are obtained to determine the occurrence and nature of fractures. Stress fractures and periostitis can be diagnosed with plain radiographs, bone scans, computed tomography (CT) scans, or magnetic resonance imaging (MRI) scans.[47] CT scanning may be useful if pelvic or thigh compartment syndrome is part of the differential diagnosis. Muscle tears can be observed using MRI or ultrasonography.[48] MRI may show increased signal intensity in an entire compartment on T2-weighted, spin-echo sequences. Doppler ultrasound may be used to evaluate arterial flow and to rule out deep venous thrombosis, particularly in the lower extremities. In addition, the loss of normal phasic patterns of tibial venous blood flow has been shown to accurately predict the need for surgical fasciotomy.[49] Ultrasonography alone is not useful in diagnosing compartment syndrome, but it aids in the exclusion of other disorders. In the lower leg, partial vascular occlusion may cause a pseudocompartment syndrome. Angiography may be needed to exclude adductor canal compression syndrome and popliteal artery entrapment. Pulse oximetry is helpful in identifying limb hypoperfusion. However, it is not sensitive enough to exclude compartment syndrome. In unusual cases, muscle biopsies may be necessary in primary muscle disorders. Histology is usually not helpful, but if necrotizing fasciitis is in the differential diagnosis, intraoperative cultures and a Gram stain may be of benefit.

Renal Function and Serum Chemistry Studies

Blood urea nitrogen (BUN) and creatinine levels are used to assess the patient's hydration status in cases of rhabdomyolysis. Measurement of the potassium level is needed in cases of rhabdomyolysis, as severe hyperkalemia may result in a wide-complex, possibly fatal arrhythmia. Purines released from cell nuclei result in hyperuricemia and nephrotoxicity. Coexisting oliguria, aciduria, and uricosuria worsen nephrotoxicity. An anion gap may indicate other underlying etiologies (eg, drug overdose) for the compartment syndrome. Sodium, potassium, bicarbonate, and phosphate levels are used to assess lactic acidosis and other metabolic acids. In addition, hyperphosphatemia aggravates hypocalcemia. Metastatic calcification is possible.

Approach Considerations
The treatment of choice for acute compartment syndrome is early decompression. If the tissue pressure remains elevated in a patient with any other signs or symptoms of a compartment syndrome, adequate decompressive fasciotomy must be performed as an emergency procedure. Following fasciotomy, fracture reduction or stabilization and vascular repair can be performed, if needed. If a developing compartment syndrome is suspected, place the affected limb or limbs at the level of the heart. Elevation is contraindicated because it decreases arterial flow and narrows the arterial-venous pressure gradient.[51, 52] In patients with tibial fracture and suspected compartment syndrome, immobilize the lower leg with the ankle in slight plantar flexion, which decreases the deep posterior compartment pressure and does not increase the anterior compartment pressure. (Postoperatively, the ankle is held at 90 to prevent equinus deformity.) All bandages and casts must be removed. Releasing 1 side of a plaster cast can reduce compartment pressure by 30%, bivalving can produce an additional 35% reduction,[44] and complete removal of the cast reduces the pressure by another 15%, for a total decrease of 85% from baseline.[53] Cutting undercast padding (Webril, Kendall Healthcare Products Co) may decrease compartmental pressure by 10-30%.[54, 44, 9] Administer antivenin in cases of snake envenomation; this may reverse a developing compartment syndrome. Correct hypoperfusion with crystalloid solution and blood products. Relative hypertension and correction of acute anemia may help prevent the development of an impending acute compartment syndrome. Ongoing research continues to examine the role of nitric oxide. In the setting of an acute compartment syndrome, capillary permeability is altered after 3 hours, resulting in postischemia tissue swelling of 30-60%. The role of mannitol in decreasing tissue edema is still under investigation; it may reduce compartment pressures and lessen reperfusion injury.[55, 56, 57] Vasodilator drugs or sympathetic blocking drugs appear to be ineffective, probably because maximal local vasodilatation is already present in this condition.

Renal Protection
Ischemia that lasts 4 hours leads to significant myoglobinuria, which reaches a maximum about 3 hours after the circulation is restored but persists for as long as 12 hours. In the face of rhabdomyolysis, IV fluid administration and, potentially, bicarbonate may be used to keep urine output at 1-2 mL/kg/hr. The combination of hypovolemia, acidemia, and myoglobinemia may cause acute renal failure. Alkalization of the urine and diuresis appear to be renal-protective, presumably because hemoglobin and myoglobin are more soluble in an alkaline solution. Patients who survive almost always recover renal function, even those patients who require prolonged hemodialysis. Current recommendations are as follows:

Correct hypovolemia with crystalloid solution Infuse 500 mL/hr of crystalloid solution and 22.4 mEq bicarbonate (12 L/day, forcing diuresis of approximately 8 L/day) If diuresis is less than 300 mL/hr, administer mannitol dose of 1 g/kg If blood pH is greater than 7.45, administer 250 mg acetazolamide Monitor vital signs and urine pH level and volume hourly Assess osmolarity and electrolytes and arterial blood gas every 6 hours

Indications for Fasciotomy

The definitive surgical therapy for compartment syndrome is emergent fasciotomy to release the involved compartment, with subsequent fracture reduction or stabilization and vascular repair, if needed. When compartment pressures are elevated, especially in acute settings, prompt surgical evaluation should be performed, since elevated pressures can, over a prolonged period, cause irreversible damage.[58, 59] However, no consensus exists regarding the exact pressure at which fasciotomy should be performed.[13, 15, 17, 18, 60] Whitesides et al advised that fasciotomy should be performed when the compartment pressure rises to within 10-30 mm Hg of the patient's diastolic blood pressure (the so-called delta-P).[61, 62] McQueen and Court-Brown, studying compartment syndrome in dogs, affirmed the difference of 30 mm Hg between the compartment pressure and the diastolic blood pressure as a more reliable measure than absolute pressure measurements.[38] Currently, many surgeons use a measured compartment pressure of 30 mm Hg as a cutoff for fasciotomy. Multiple pressure readings are often obtained, and the clinician must decide how to incorporate these readings with the clinical picture in the decision-making process. Mubarak and Hargens recommended that fasciotomy be performed for the following patients[24] :

Those who are normotensive with positive clinical findings, who have compartment pressures of greater than 30 mm Hg, and whose duration of increased pressure is unknown or thought to be longer than 8 hours Those who are uncooperative or unconscious, with a compartment pressure of greater than 30 mm Hg Those with low blood pressure and a compartment pressure of greater than 20 mm Hg

The tolerance of tissue to prolonged ischemia varies depending on the type of tissue that is involved. Matsen showed that muscles have functional impairment after 2-4 hours of ischemia and irreversible functional loss after 4-12 hours.[10] Nerve tissue shows abnormal function after 30 minutes of ischemia, with irreversible functional loss after 12-24 hours. Additional experimental data, however, have shown significant changes in somatosensory potentials as early as 45 minutes after compartment pressure increases up to 30 mm Hg. If the compartment pressure is greater than 40 mm Hg, a fasciotomy is usually performed emergently, and fasciotomy is indicated if the pressure remains 30-40 mm Hg for longer than 4 hours. As a rule, when in doubt, the compartment should be released.

In a study of patients with clinical signs of compartment syndrome after revascularization surgery for lower limb ischemia, Arato et al reported that measurement of intracompartmental pressure and tissue oxygenation (measured with near-infrared spectroscopy) could be used to determine whether fasciotomy was needed.[63] Patients with pressure below 40 mm Hg and normal tissue oxygen saturation were treated conservatively. With compartment syndrome in the hand, surgeons should have a lower threshold for decompression; a compartmental pressure of greater than 15-20 mm Hg is a relative indication for release. If compartment syndrome is diagnosed late, fasciotomy is of no benefit. In fact, fasciotomy probably is contraindicated after the third or fourth day following the onset of compartment syndrome. When fasciotomy is performed late, severe infection usually develops in the necrotic muscle. However, if the necrotic muscle is left alone and the compartment is not open, it can heal with scar tissue. This may result in a more functional extremity with fewer complications. However, if the duration of compartment syndrome is unclear, the surgeon should elect to decompress the indicated compartments. In the setting of a vascular injury, a fasciotomy should be performed on high-risk patients before arterial exploration. High-risk patients include those with prolonged ischemia time, significant preoperative hypotension, associated crush injury, combined arterial and venous injury, or the need for a major venous ligation in the popliteal or femoral area.

Complications
With late diagnosis, irreversible tissue ischemia can develop in the acute setting. Thus, permanent muscle and nerve damage, along with chronic pain, may occur. Peroneal nerve palsy, in particular, may develop. With muscle damage, muscle contractures may be observed. For more information on management of contractures, see the Medscape Reference article Volkmann Contracture. Hypesthesia and painful dysesthesia can also result from compartment syndrome. These may resolve slowly with time. Phenytoin (Dilantin), gabapentin (Neurontin), or carbamazepine (Tegretol) may be of some value in making the patient more comfortable.

Medication Summary
Opioids, nonopioids, and nonsteroidal anti-inflammatory drugs (NSAIDs) can be used for pain management in compartment syndrome.[70] Side effects and patient profiles should be considered when choosing medications. Acetaminophen can result in liver damage. Narcotics can produce gastrointestinal distress, constipation, and sedation, and they have addictive potential. NSAIDs can result in gastrointestinal upset, gastrointestinal bleeding, renal damage, and impaired coagulation.

1. How would you transport RW to the examining room? Transport RW by stretcher. Dont make him walk or sit by wheelchair RW is placed in the examining room and asked to remove his trousers and put on a gown. RW is unable to lay his leg on the exam table room without pain. You observe that his right lower leg is grossly edematous and pale 2. What should your next priority be? Note and splint gross deformities. Obtain neuro assessment. There are no pulses in the distant extremity, sensation is diminished, the extremity is cold to touch, and any movement is extremely painful 3. What should your next action be? notify physician for any neuro deficit observed. The physician is with another patient, and asks you to wait a minute. 4. How should you respond? The patient has no pulses in the distant extremity, sensation is diminished, the extremity is cold to touch, and any movement is extremely painful. It seems it really needs urgent attention on this. After assessing the patient the physician determines that RW should be transported to the nearest ED. The clinic physician notifies the ED physician the RW is coming in by ambulance with possible compartment syndrome of the right lower leg. 5. Explain the pathophysiology of compartment syndrome and clarify its significance Compartment syndrome results primarily from increased intracompartmental pressure.

When fluid is introduced into a fixed-volume compartment, tissue pressure increases and venous pressure rises. When the interstitial pressure exceeds the CPP (a narrowed arteriovenous [AV] perfusion gradient), capillary collapse and muscle and tissue ischemia occur. Skeletal muscle responds to ischemia by releasing histaminelike substances that increase vascular permeability. Plasma leaks out of the capillaries, and relative blood sludging in the small capillaries occurs, worsening the ischemia. The myocytes begin to lyse, and the myofibrillar proteins decompose into osmotically active particles that attract water from arterial blood.
6. How is compartment syndrome be treated?

The treatment of choice for acute compartment syndrome is early decompression. If the tissue pressure remains elevated in a patient with any other signs or symptoms of a compartment syndrome, adequate decompressive fasciotomy must be performed as an emergency procedure. Following fasciotomy, fracture reduction or stabilization and vascular repair can be performed, if needed.

7. How will you manage fasciotomy once it has been performed? Prevent possible infection from open wound. Meticulous dressing Manage pain Monitor nutritional status to promote wound healing Recognize emotional aspects that an open wound may have on the patient and the family

Critical care nursing: synergy for optimal outcomes

By Roberta Kaplow,Sonya R. Hardin Given that this is a crush injury, the physician orders a urine for myoglobin on RW 8. What is the rationale behind this order Urinalysis for myoglobin may be used to help identify causes of acute renal failure 9. How is rhabdomyolysis treated? . fluid resuscitation and prevention of end-organ complications http://emedicine.medscape.com/article/827738-treatment#a1126