Chapter 4: Complications

Nearly 200,000 people are affected with a compartment syndrome each year in the United States.¹ Although there are many causes, the clinical pathway in the development of this syndrome is the same.

Muscle groups in the body are surrounded by fascial sheaths that enclose the muscles within a defined space or compartment. When an injury occurs to the muscles within a compartment, swelling ensues. Because the tight fascial sheaths allow little room for expansion, the pressure within the compartment begins to increase. Eventually, blood flow is compromised and irreversible muscle injury follows. One must suspect a compartment syndrome early to prevent contracture deformities (i.e., Volkmann’s ischemic contractures) that result from ensuing muscle and nerve necrosis.

The most common locations for compartment syndrome are the forearm and leg.¹ Other sites that have been implicated include the hand, shoulder, back, buttocks, thigh, abdomen, and foot. A discussion specific to each of these muscle compartments is included elsewhere in the text.

In approximately 70% of cases, compartment syndrome develops after a fracture and half of those are caused by tibia fractures.² Other commonly associated fractures include the tibia, humeral shaft, forearm bones, and supracondylar fractures in children.^3,4 Other causes of acute compartment syndrome include crush injury, constrictive dressings/casts, seizures, intravenous infiltration, snakebites, infection, prolonged immobilization, burns, acute arterial occlusion or injury, and exertion.^2,5 A venous tourniquet can produce compartment syndrome in as little as 90 minutes if it is accidentally left in place.⁶ Patients with a coagulopathy (i.e., Coumadin, hemophilia) are at increased risk and may develop compartment syndrome after minimal trauma.

Clinical Features

The diagnosis of compartment syndrome is primarily a clinical one. Patients will exhibit pain out of proportion to the underlying injury, sensory symptoms, and muscle weakness. Pain is the earliest and most consistent sign. It is usually persistent and not relieved by immobilization. It is critical that the emergency physician recognizes this condition by its early features, and before other signs and symptoms develop, to prevent permanent injury.

Pain that is aggravated by passive stretching is the most reliable sign of compartment syndrome.² Diminished sensation is the second most sensitive examination finding for compartment syndrome. Sensory examination of the nerves coursing through the affected compartments will reveal diminished two-point discrimination or light touch. Both of these tests are more sensitive than pinprick. Palpation of the compartment will disclose tenderness and “tenseness” over the ischemic segments. The distal pulses and capillary filling may be entirely normal in a patient with significant muscle ischemia and, therefore, these findings should not be used to rule out the existence of a compartment syndrome.

To summarize, disproportionate pain is the earliest symptom, whereas pain with passive stretching of the involved muscles is the most sensitive sign of compartment syndrome. Paresthesias or hypesthesias in nerves traversing the compartment are also important signs of a developing compartment syndrome. Orthopedic consultation should be obtained as soon as compartment syndrome is a consideration.

Compartment Pressure Measurement

The decision to perform a fasciotomy is based on a combination of clinical findings, as previously outlined, and measurement of elevated compartment pressures. If one suspects a compartment syndrome, frequent reexamination in the hospital and measurement of compartment pressures must be carried out. Compartment pressures are most commonly performed using the commercially developed Stryker STIC device (Fig. 4–1 and Videos 4–1 and 4–2).^2,7,8

If this device is unavailable, a backup technique, such as the infusion technique, can be performed with materials readily found in most emergency departments.⁸ The necessary equipment include (1) a blood pressure manometer, (2) 20-mL syringe, (3) three-way stopcock, (4) 18-gauge needle, (5) normal saline, and (6) two intravenous extension tubes.

The apparatus is set up such that the syringe and two extension tubes are attached to the ports of the three-way stopcock (Fig. 4–2). The plunger of the syringe is opened to the 15-mL mark. One extension tube is connected to the blood pressure device, whereas the other is connected to the 18-gauge needle. Saline is drawn up through the needle to fill one-half of the tubing and the stopcock is closed off so the saline will not be lost. The needle is then sterilely inserted into the muscle of the compartment to be measured. At this time, the stopcock is turned such that the syringe is opened to both extension tubes. As the syringe plunger is slowly depressed, the manometer reading will begin to rise. When the meniscus of the saline within the extension tubing is first noted to move, the pressure read from the manometer is the compartment pressure.⁸

Erroneous pressure readings can result in several situations. For this device to read accurately, the top of the column of saline must be placed at the same level as the tip of the needle. If the pressure is read while saline is being injected into the muscle, a falsely elevated reading will be obtained.⁸

Normal compartment pressures are below 10 mm Hg. At pressures >20 mm Hg, capillary blood flow within the compartment may be compromised. Traditional teaching had been to perform fasciotomy at pressures >30 mm Hg. However, in experimental studies, it has been shown that patients with higher diastolic blood pressures have a reduced likelihood of ischemic necrosis because of higher perfusion pressures. For this reason, many authors now recommend fasciotomy when the compartment pressure reaches a point that is 20 mm Hg below the mean arterial pressure or 30 mm Hg below the diastolic pressure.^2,5

Measurements should be made in all of the compartments of the extremity in question. Multiple measurements within a single compartment may be necessary as evidence suggests that pressures at different locations within the same compartment are not uniform. Distances as short as 5 cm result in significantly different pressure readings that will alter clinical decision making. The highest pressure recorded should be used.^2,8,9 Also given that the highest compartment pressures are often found after 12 to 36 hours, multiple measurements over time may be necessary.⁵

Several noninvasive methods of measuring compartment pressures are under investigation. Promising technology includes ultrasound with a pulsed phase-locked loop, laser Doppler flowmetry, and near-infrared spectroscopy.^2,10,11

To summarize, compartment syndrome is a challenging diagnosis to make. Compartment pressure measurement is an adjunct to clinical examination. Controversy exists over cutoffs of compartment pressure that require immediate fasciotomy. The patient with an equivocal examination and indeterminate compartment measurements requires at a minimum prompt orthopedic consultation and clinical observation with serial examinations.

Treatment

The treatment of compartment syndrome requires immediate fasciotomy. Delays may result in irreversible damage to muscles and nerves. In general, nerves and muscles can tolerate up to 4 hours of total ischemia. After 8 hours, damage is irreversible.⁸ However, there is evidence that pediatric patients may still have reasonably good outcomes despite delayed presentations.¹²

In addition to arranging for fasciotomy, the emergency physician must remove all circular constrictive dressings and splints and relieve flexion if the elbow and forearm are involved. The affected limb should be placed at the level of the heart to avoid reduction in arterial flow and increase in compartment pressure due to dependent edema. Hypotension must be avoided and treated aggressively.^2,5 In partially reduced supracondylar fractures, skeletal traction is recommended. If relief is not obtained within 30 minutes, then surgery is indicated. One must not “watch and wait,” as the goal is to restore circulation before irreparable damage ensues. Rhabdomyolysis may complicate compartment syndrome, and adequate hydration to maintain urinary output is essential. See Chapter 1 for further discussion of rhabdomyolysis.

Osteomyelitis is a suppurative process in bone caused by pyogenic organisms.^13–19 It is most common in patients younger than 20 years or older than 50 years. Bone infection occurs secondary to bacteria that are spread (1) hematogenously, (2) from a contiguous focus, or (3) secondary to vascular insufficiency. Osteomyelitis is accompanied by bone destruction that may be limited to a single portion of bone or may involve several regions, including the marrow, cortex, periosteum, and surrounding soft tissues.

Hematogenous osteomyelitis occurs most commonly in children. The infection is acute in nature and is localized to the bony metaphysis and then spreads into the subperiosteal space. The most frequently affected bones are the proximal tibia and distal femur.¹⁸ In adult patients, the vertebrae are the most common sites of hematogenous spread of infection. The reader is referred to Chapter 6 for further details about this condition.

Osteomyelitis that develops from a contiguous source of infection most commonly follows trauma (open fracture or puncture wound) or surgery (joint replacement or fracture fixation). The hand and the foot are the most common sites for this type of osteomyelitis. Vascular insufficiency, as a cause of osteomyelitis, is most often due to diabetes. In this scenario, a soft-tissue infection of the foot is the nidus for the spread of infection to the bone. In adults with contiguous osteomyelitis or osteomyelitis in the presence of vascular insufficiency, the process is usually subacute or chronic in nature.

Bacteriology

The bacterium most often isolated in cases of osteomyelitis is Staphylococcus aureus (S. aureus). Infecting organisms differ according to the age of the patient.¹⁸ S. aureus and streptococci are common causes in neonates. Haemophilus influenzae and Escherichia coli also occur in neonatal osteomyelitis. Gram-negative rods are seen in elderly patients, whereas fungal osteomyelitis is a complication of immunocompromised patients. Patients with sickle cell disease frequently have infection due to S. aureus or Salmonella species.¹⁸ A mixed flora (S. aureus, streptococci, and anaerobic bacteria) may be noted when osteomyelitis is secondary to spread directly from an adjacent wound, as in the diabetic patient with a foot ulcer.

Clinical Presentation

The typical clinical features in all forms of osteomyelitis are chills, fever, malaise, local pain, and swelling. Constitutional symptoms are more common in children than in adults or patients with chronic osteomyelitis. In the contiguous form, pain and edema as well as erythema are noted around the wound and drainage occurs in most cases. As the process progresses, the involved extremity is held in slight flexion and passive movement is resisted secondary to pain. Initially, there is no swelling; however, the soft tissues later become edematous as a subperiosteal abscess develops. Eventually, as chronic osteomyelitis develops, a sinus tract breaks through the skin and drains infectious material.

In diabetic patients with an infected foot ulcer, osteomyelitis can be assumed to be present whenever bone is exposed in the ulcer bed or gentle advancement of a sterile probe contacts bone.^19,20 Exposed bone or probe-to-bone has a sensitivity of 60% and a specificity of 91% in diabetic patients with foot ulcers.²¹

Diagnosis

Isolating causative organisms is the most important step in diagnosis and treatment; however, this information is rarely available to the emergency physician. Blood cultures should be obtained and are positive in 50% of cases of hematogenous osteomyelitis.¹⁷ Cultures of material from the wound or sinus tract can be performed, but may be misleading as many of the cultured microorganisms will represent colonizing bacteria.¹⁹ Surface swab cultures of infected diabetic feet have no diagnostic utility.²⁰

Laboratory tests are usually not very helpful. The leukocyte count is not a sensitive marker for osteomyelitis. The erythrocyte sedimentation rate (ESR) is elevated in 90% of patients with osteomyelitis, but this test lacks specificity.¹⁷ A normal ESR in a patient with a low clinical suspicion may help the clinician rule out the diagnosis. The C-reactive protein is another nonspecific inflammatory marker that has the advantage that it will increase within the first 24 hours of the disease course and return to normal levels within 1 week of effective treatment. Ultimately, a needle aspiration of the bone is required to reveal the infecting organism in almost 90% of cases.²⁰ An open biopsy may be required to obtain sufficient material.

Plain radiographs are the initial study of choice in patients with osteomyelitis, although they are of little value early in the disease process. A negative radiograph, therefore, does not rule out osteomyelitis. Less than one-third of patients with symptomatic osteomyelitis for 7 to 10 days will have radiographic findings. Rarefaction, indicating diffuse demineralization, requires 30% to 50% of the bone mineral to be lost before it is seen on a radiograph. Demineralization and periosteal elevation followed by sclerosis is rare until after 10 to 21 days of infection, but by 28 days, 90% of patients will demonstrate plain-film abnormalities (Fig. 4–3). The most common finding in early infection is soft-tissue swelling, followed by periosteal elevation. Periosteal elevation is less commonly seen in adults due to a more fibrous and adherent periosteum. Late findings of osteomyelitis on plain films are lytic areas surrounded by sclerotic bone.^18,20

Alternate methods for diagnosing osteomyelitis include radionuclide bone scanning, computed tomography (CT), and magnetic resonance imaging (MRI). Bone scan typically turns positive within 24 to 48 hours after onset of symptoms.^18,19 A normal bone scan makes the diagnosis very unlikely. CT is more sensitive than plain radiography. It is helpful in detecting necrotic bone (sequestra) in patients with chronic osteomyelitis and this may help the orthopedic surgeon plan treatment. Of all imaging studies, MRI is the best test for diagnosing osteomyelitis.²² MRI is also favored for any patient suspected of having vertebral involvement.^18–24

Treatment

Antibiotics, used alone, have the potential to be curative only in patients with hematogenous osteomyelitis. Empiric intravenous antibiotics should be administered by the emergency physician in patients with (1) hematogenous osteomyelitis, (2) a toxic appearance, (3) suspicion of vertebral osteomyelitis, or (4) partially treated or recurrent disease at the request of a consulting orthopedist. Antibiotic regimens should be tailored to culture and sensitivity findings. Methicillin-susceptible S. aureus may be treated with penicillinase-resistant penicillin, such as Nafcillin. Methicillin-resistant S. aureus and coagulase-negative staphylococcus are treated with vancomycin. Gram-negative organisms, including Pseudomonas, may be treated with a fluoroquinolone or a third-generation cephalosporin. Patients with sickle cell disease and osteomyelitis should receive a fluoroquinolone or a third-generation cephalosporin to cover Salmonella. Typical empiric coverage includes vancomycin plus coverage for gram-negative organism.¹⁹

In adults with contiguous spread or vascular insufficiency (i.e., diabetic foot), cure cannot be achieved without debridement of infected bone. In the case of a patient with prosthesis or other foreign material, removal is generally required. Patients are treated with antibiotic therapy for a total of 4 to 6 weeks following the last debridement surgery.¹⁹

Prevention

The prevention of possible future complications, such as osteomyelitis, in patients presenting with trauma is a vital task of the emergency physician. Open fractures require thorough irrigation and debridement, commonly in the operating room. Prophylactic antibiotics and tetanus immunization should be administered promptly. Antibiotic therapy directed against gram-positive and gram-negative organisms should be administered within 6 hours after open trauma to reduce the risk of osteomyelitis.²⁵

Cellulitis

This infection affects the skin and subcutaneous tissues and is most often caused by S. aureus and beta-hemolytic streptococci.^26,27 Other organisms may be present and polymicrobial infection is especially common in diabetic patients. Pseudomonas should be suspected after puncture wounds to the foot.

Clinical features are consistent and include pain, tenderness, warmth, induration, and erythema (Fig. 4–4). Lymphangitis and lymphadenopathy are often associated (Fig. 4–5). The clinician should consider the possibility of an abscess cavity and palpate for the presence of a fluctuant area. Ultrasound or needle aspiration may be necessary if an abscess is suspected (Fig. 4–6).²⁸

Treatment with an oral antibiotic to cover methicillin-resistant S. aureus and beta-hemolytic streptococci for 7 to 10 days is appropriate in nonimmunocompromised, nontoxic patients with mild infection. For animal or human bites, amoxicillin clavulanate (Augmentin) is the agent of choice for outpatient treatment. Cellulitis originating from a puncture wound to the foot is treated with ciprofloxacin or ceftazidime.

Necrotizing Infections

Patients with necrotizing soft-tissue infections typically present with a short clinical course that rapidly deteriorates to septic shock and death if not treated promptly. The initial management of all necrotizing soft-tissue infections is the same. Important treatment principles include high clinical suspicion, early surgical debridement, and broad-spectrum antibiotics.²⁹ Plain radiography may reveal the presence of gas (Fig. 4–7). CT will better delineate the extent of the infection, but should not delay treatment (Fig. 4–8).

Two examples of necrotizing soft-tissue infections, necrotizing fasciitis and clostridial myonecrosis, are considered subsequently. These entities differ in the depth of the infectious process and the pathogens that cause disease.

Necrotizing Fasciitis

This condition is a rare—but often fatal—soft-tissue infection that involves the superficial fascial layers of the extremities, abdomen, or perineum.^30,31 Risk factors include the immunocompromised host (e.g., diabetes), peripheral vascular disease, intravenous drug use, older age, and recent trauma or surgery. Two types are considered, depending on the infectious agents involved.

Type I necrotizing fasciitis accounts for the majority of cases of necrotizing fasciitis. The causative agents are polymicrobial. Gram-positive, gram-negative, and anaerobic bacteria act synergistically to produce extensive tissue destruction. In the early stages, it may be mistaken for a simple cellulitis or abscess. The appearance of the skin may range from mild erythema early on to red-purple blebs with foul-smelling watery discharge. Pain is almost universally present and is often out of proportion and beyond the visible signs of skin infection.^30,31 Gas may or may not be present in the subcutaneous tissues. One commonly recognized form of this entity occurs in the perineum, and is termed Fournier gangrene (Fig. 4–9).

Type II necrotizing fasciitis is caused by beta-hemolytic streptococci, commonly group A. This infection represents 25% to 45% of cases of necrotizing fasciitis. Particularly virulent subtypes have given this pathogen the distinction of the title “flesh-eating bacteria” by the lay press. Type II necrotizing fasciitis is more likely to occur in younger, healthier patients without predisposing illnesses. In over a third of patients, no portal of entry is identified.^30,31 Characteristic findings of this infection include a rapidly progressive necrosis, the rare presence of gas, and a high incidence of streptococcal toxic shock syndrome.

Necrotizing fasciitis is a clinical diagnosis. A high index of suspicion must be maintained to avoid a delay due to nonspecific findings. Adjunctive tests are available to support clinical suspicion; however, currently the only way to completely confirm or rule out the diagnosis is surgical exploration. CT may identify signs of necrotizing fasciitis, such as deep fascial thickening, enhancement, fluid and gas in the soft-tissue planes in and around the superficial fascia.³² Though much better than plain radiography, the sensitivity may be as low at 80%,³⁰ whereas more recent data suggests the sensitivity of the newer generation scanners is much better.³³ MRI sensitivity is believed to be quite high, but its usefulness is limited due to test availability, time required to obtain the study, and controversy regarding its low specificity.³² Investigation of the utility of ultrasound is ongoing. A scoring system (laboratory risk indicator for necrotizing fasciitis [LRINEC]) was developed to place patients in low-, intermediate-, and high-risk categories for necrotizing fasciitis.³⁴ The calculation is based on C-reactive protein, WBC, hemoglobin, Na⁺, serum creatinine, and serum glucose levels. Initial findings appeared promising. However, subsequent analyses failed to confirm the study results.^29,35 Further investigation is required prior to the routine application of the LRINEC score.

Treatment of necrotizing fasciitis consists of early debridement of necrotic tissue and antibiotic therapy. Antibiotic agents of choice include carbapenem or beta-lactam/beta-lactamase inhibitor and clindamycin in combination with coverage against methicillin-resistant S. aureus until culture results are available.²⁹

Clostridial Myonecrosis (Gas Gangrene)

This is a distinct necrotizing infection of muscle caused by Clostridium perfringens or septicum. The most common predisposing factors include trauma and surgery. As the name implies, gas formation and crepitus are prominent features. This condition can present in a similar manner to other forms of necrotizing soft-tissue infections, but distinctive features include a bronze-brown skin discoloration, bullae formation, and copious foul-smelling drainage. The course of clostridial myonecrosis is rapid, with an incubation period of less than 24 hours.^29,34

The treatment is prompt surgical decompression and debridement. The antibiotic agents of choice are penicillin and clindamycin.²⁹ Hyperbaric oxygen is thought to be of greater benefit in clostridial infections than other forms of necrotizing soft-tissue infections, though randomized controlled trials are lacking.

Most recently known as reflex sympathetic dystrophy, the term complex regional pain syndrome (CRPS) was created to better describe this condition. Earlier names include algodystrophy, algoneurodystrophy, Sudeck atrophy, and causalgia.^36,37

CRPS is a painful condition of an extremity that follows trauma, infection, or surgery. The peak incidence is in people aged 55 to 75 years and occurs in women more frequently than in men by a ratio of 3.5:1. The syndrome is more common in the upper extremity, but the lower extremity also may be affected.³⁸ In some cases, the traumatic event is minimal in severity, such as following venipuncture or an intramuscular injection. A precipitating event is not identified in 10% of cases.³⁸

The pathophysiology of CRPS is not fully understood. Three major pathophysiological pathways have been identified: aberrant inflammatory mechanisms, vasomotor dysfunction, and neuroplastic changes within the CNS.³⁸ A detailed description of the pathways is outside the scope of this text.

The diagnosis of CRPS is based primarily on history and physical examination. A history of recent or remote trauma followed by the characteristic triad of symptoms is suggestive of CRPS. The triad includes autonomic, sensory, and motor disturbances.³⁹ In the acute phase, the injured limb is usually painful, commonly described as “burning” or “tearing.” The limb is also red, warm (though occasionally it may be cool), and swollen. Allodynia and hyperalgesia; changes in sweating; changes in skin, hair, and nail growth; and muscle weakness may also be present. Over time, if the disorder persists, symptoms change. Pain continues and may spread. However, patients may also experience numbness. Voluntary motor control may be reduced. The warm limb often becomes cold. Dystonia, tremor, and myoclonus might develop. The Budapest criteria are used to score the signs and symptoms to determine a diagnosis of CRPS.³⁸ Radiographs commonly show demineralization of the bone.³⁶

Approximately 80% of those with CRPS who begin treatment within 1 year of injury have considerable improvement in their symptoms, but only approximately 50% of those treated after 1 year improve substantially.³⁶ Early treatment is paramount to allow for improved prognosis.

Multiple modalities are used in the treatment of CRPS. Physical therapy is considered a first-line treatment and may be more important than drug therapy. Medications that are commonly used to treat CRPS include nonsteroidal anti-inflammatory drugs, anticonvulsants (gabapentin, pregabalin), bisphosphonates/calcitonin, oral glucocorticoids, tricyclic antidepressants (amitriptyline, nortriptyline), alpha adrenergic blocking agents, and calcium channel blockers. Of note, opioids have minimal effect on pain. Patients who do not respond to initial therapy may require more invasive treatment, such as intrathecal injections, sympathectomy, and spinal cord stimulation.³⁹ Cognitive behavior techniques are also employed.³⁶ No emergency treatment is required. However, it is incumbent on the emergency physician to recognize this condition and refer the patient appropriately in order that the patient receives early treatment.

Emergency physicians are in a unique position to aid in the prevention of CRPS. Studies suggest that, when appropriate, early immobilization reduces the risk of CRPS. Also, Vitamin C in higher doses (500 mg/d) has been shown to decrease the risk of CRPS in patients after a distal radius fracture.⁴⁰

Fat embolism occurs in almost all patients who sustain a pelvic or long bone fracture. However, clinical signs and symptoms of fat embolism syndrome (FES) occur in only 0.5% to 10% of patients.⁴¹ Mortality rates of FES are currently thought to be about 10%.⁴² FES is characterized by a classic triad of respiratory insufficiency, cerebral involvement, and a petechial rash that typically develops within 72 hours of injury. The incidence increases in young adults with multiple injuries and rarely occurs in children or patients with upper-extremity fractures.⁴³ Open fractures are less likely to develop FES compared with closed fractures, as higher pressures are more likely to develop in the latter.⁴²

There are two main theories concerning the etiology of FES.⁴⁴ Following a fracture, intramedullary fat is released into the venous circulation. These fat globules subsequently embolize to end organs such as the lungs, brain, and skin. Mechanical obstruction of the end-organ capillary beds has been proposed as a potential source of injury in FES. However, the 24- to 72-hour delay between injury and the emergence of symptoms cannot be explained by mechanical obstruction alone. This fact has given rise to a second theory that fat emboli cause an inflammatory cascade that damages end-organ tissues. In this theory, fat emboli are metabolized to free fatty acids that, when present in high concentrations, induce an inflammatory reaction that damages end organs. It is still unclear why this syndrome develops in some patients and not in others, although the likelihood does seem to increase in patients with more significant fractures.

Clinical Manifestations

All cases have a latent period that ranges from 12 to 48 hours after the injury.⁴⁴ Pulmonary involvement is the earliest feature and is present in 75% of patients.⁴⁵ It manifests as tachypnea and dyspnea that may be confused with pulmonary embolism. Hypoxia is present and the PO₂ is often <60 mm Hg.⁴² Moist rales may be noted over the lung fields on examination. The chest radiograph is normal in mild-to-moderate cases, but after an initial delay, bilateral diffuse pulmonary edema develops in severe cases.⁴⁵ The findings of high-resolution CT in mild cases of FES demonstrate ground-glass opacities.⁴⁶ Mechanical ventilation will be necessary in 10% of patients.⁴⁵ Pulmonary function recovers completely within 1 week.

Neurologic symptoms range from restlessness to confusion or convulsions. Prolonged coma due to cerebral fat embolism has been reported, but in the majority of cases, symptoms resolve spontaneously⁴² Recovery of higher cortical functions may be delayed. CT scan of the brain may reveal cerebral edema or be entirely normal, but MRI may help in diagnosing cerebral fat embolism by revealing high-intensity signal abnormalities in watershed areas.

Petechiae are observed in 20% to 50% of patients with FES.⁴⁵ The low specific gravity of fat globules is thought to pre-dispose to embolization in nondependent areas of the skin. Therefore, petechiae are initially observed over the anterior axillary folds and the anterior surface of the neck and chest. They are also found in the buccal mucosa and conjunctiva. The distribution and intensity of the rash varies and resolution is usually noted within 1 week.

FES is a clinical diagnosis. The diagnostic criteria developed by Gurd and Wilson⁴⁷ can aid in making the diagnosis and are the most widely used. The clinical features of the disorder are divided into major and minor categories (Table 4–1). The major features include respiratory insufficiency, cerebral involvement, and petechial rash. Minor features include pyrexia, tachycardia, retinal changes, jaundice, and renal insufficiency. At least two of the major features or one major plus four minor features must be present to make the diagnosis of FES.^42,47 Other laboratory features include anemia, thrombocytopenia, or a high ESR.

Treatment

The cornerstone of treatment is prevention and early detection. Early resuscitation, stabilization, and operative treatment are thought to have decreased the incidence of FES in recent years. Immobilization with no excessive motion permitted has been shown to decrease the incidence of FES. In addition, open reduction with internal fixation within 24 to 48 hours of injury will decrease fat embolism.⁴² Of patients who do develop FES, one-third of cases are mild and require only supportive treatment. The management of respiratory failure secondary to fat embolism is similar to the management of the adult respiratory distress syndrome. Respiratory support with oxygen is employed to keep the PaO₂ above 70 mm Hg. There is insufficient controlled data to confirm the value of parenteral steroids in the treatment of this inflammatory condition, although some authors recommend intravenous methylprednisolone. The mainstay of treatment, however, is respiratory support, which must be started early.