When does fat embolism occur after fracture?

Fat Embolism

Another reasonably frequent and dramatic form of nonthrombotic embolism is fat embolism. A rather characteristic syndrome follows entry of neutral fat into the vascular system creating mechanical emboli and focal ischemia, resulting in a triad of symptoms consisting of respiratory distress, petechiae, and altered mental status. There is a variable lag time of 12 to 72 hours in the onset of the syndrome after the inciting event.420

By far the most common inciting event is traumatic fracture of marrow-containing long bones; the incidence of fat embolism rises with the number of fractures. However, orthopedic procedures and trauma to other fat-laden tissues (e.g., fatty liver) occasionally are followed by the same syndrome.

The reasons for the variability in incidence of the syndrome after apparently comparable injuries are not clear. Perhaps variations in incidence and severity relate to the amount of fat released. The pathophysiologic consequences appear to derive from two events: (1) actual vascular obstruction by neutral particles of fat and (2) the injurious effects of free fatty acids released by the action of lipases on the neutral fat.421 The latter effect is probably the more important, causing a diffuse vasculitis with leakage from cerebral, pulmonary, and other vascular beds.422

The diagnosis of fat embolism syndrome is a clinical one suggested by the onset of dyspnea, neurologic abnormalities, petechiae, and fever in the proper clinical context (seeFig. 127.2 andeFig. 127.2). Petechiae, typically distributed over the head, neck, anterior chest, and axillae, are present in only 20–50% of cases.423 Therefore, their absence should not preclude consideration of the disease. No laboratory test is diagnostic of the syndrome.

Although a variety of treatments have been suggested (e.g., IV ethanol, albumin, dextran, heparin), none has proved effective. There is some evidence to suggest that corticosteroid therapy might prevent the onset of fat embolism syndrome after an inciting event, but controlled studies are sparse, and the topic remains controversial.424 Supportive treatment, including mechanical ventilatory support, when necessary, is the primary approach and, with meticulous supportive care, survival among most cases of fat embolism is common.425 However, severe fat embolism syndrome, manifested by widespread opacities on chest CT and acute respiratory distress syndrome, is often life-threatening.426

Risk

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Long bone fractures, pelvic fractures

80–100% fat embolism

0.2–19% fat embolism syndrome (FES)

Male > female

Adult >> pediatric

Multiple fractures > single fractures

Pathologic fractures > traumatic fractures

Total hip, total knee replacement, intramedullary nailing:

27–100% fat embolism

Unknown incidence FES

Unusual causes: Liposuction, fat injection, bone marrow harvest and/or transplantation, vertebroplasty, cardiopulmonary bypass, CPR, burns, pancreatitis, sickle cell disease, osteomyelitis, fatty liver, soft tissue injury

Perioperative Risks

•

FES: 7–20% mortality

Pre-existing FES: Respiratory failure/ARDS, RV dysfunction, shock, coagulopathy, neurologic dysfunction

Intraop fat embolism: Shock, hypoxemia

Worry About

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Pre-existing FES: Hypoxemia, reduced pulm compliance, hypotension, cardiac arrest, Pulm Htn, RV failure, abnormal CNS response to anesthetic, coagulopathy

Intraop embolism: Hypotension, right ventricular failure, hypoxemia, paradoxical embolization, neurologic dysfunction

Overview

•

Fat particles (globules of marrow fat) traveling into blood and lung

Must distinguish fat embolism, which is common, from FES, a much less common consequence of fat embolism

FES can produce mild pulm dysfunction to severe ARDS.

Pulm Htn and acute right ventricular failure may occur in severe cases of FES.

Typically, the onset of signs and symptoms of FES is delayed up to 72 hr following injury.

Fat embolism occurs commonly during femoral reaming and cementing in hip arthroplasty.

FES is confounded with cement reaction during arthroplasty.

ICD9-CM: 673.8 (Other pulmonary embolism)

Etiology

•

Most frequently follows orthopedic trauma with release of marrow fat into venous circulation

Pathology produced by mechanical obstruction by intravascular fat passing into the pulm and systemic arterial circulation and by production of endogenous inflammatory mediators

Usual Treatment

•

Early fracture fixation to decrease embolization

Use of noncemented prosthesis or venting of femoral shaft may reduce embolization during hip arthroplasty

Unreamed nailing for fracture fixation to reduce embolization

O2 therapy to maintain SaO2 >90%

Low tidal volume ventilation strategy with PEEP for ARDS

Aggressive hemodynamic support with fluid and/or inotropes for shock and/or RV failure

Factor replacement for coagulopathy with bleeding

Corticosteroids, heparin, ethanol, dextran, aspirin, prophylactic vena caval filter: Unproven benefit

Fat embolism

Fat embolism is a rare entity, but occurs most commonly as a result of long bone fractures and polytrauma. It may be related to excessive pseudomotion of unstable fracture or internal fixation with IM nail. It is most common in young males aged 10–40 years and is rare in children and the elderly. This may be related to the low fat content of bone marrow in children and the minimal trauma fractures that tend to occur in the elderly.66

Two theories regarding the pathophysiologic mechanism of fat embolism syndrome (FES) exist – the mechanical hypothesis and the biochemical hypothesis. The mechanical hypothesis postulates that an increase in IM pressure forces marrow particles, fat, or bone fragments into the circulation via the open venous sinusoids. This leads to obstruction of peripheral and lung microcirculation. This results in ventilation–perfusion mismatch, low partial pressure of oxygen, and low oxygen saturation. Cerebral and renal embolization may contribute to the symptoms. The biochemical hypothesis postulates that physiochemical alteration occurs when fat globules are acted upon by lipoprotein lipase, resulting in the release of free fatty acids. This results in the release of toxic intermediates that can cause direct injury to pneumocytes and lung endothelial cells.67

FES is characterized by progressive respiratory insufficiency, deteriorating mental status, and petechial rash (major diagnostic criteria). Minor diagnostic criteria include pyrexia, tachycardia, retinal changes, jaundice, oliguria/anuria, thrombocytopenia, high erythrocyte sedimentation rate, and fat macroglobulinemia. According to Gurd and Wilson, the diagnosis of FES involves two major criteria, or one major plus four minor criteria plus fat microglobulinemia.68 Typically, FES occurs within 24–72 h after injury and is largely a clinical diagnosis. Laboratory investigations may include an arterial blood gas to diagnose hypoxemia and cytologic examination of urine, blood, or sputum looking for fat globules. Chest radiography may be normal in these patients, prompting investigation with chest CT or bronchoalveolar lavage looking for fat-laden macrophages.69 Because of the lack of specific diagnostic criteria or investigations, the incidence of FES is likely to be underestimated.

Once FES is suspected, the management is largely supportive and usually involves management of the hypoxemia. Prophylactic measures in those considered at risk for FES are most important. These include early stabilization of long bone/pelvic fractures, minimizing IM pressures during reaming, and irrigation of marrow prior to insertion of prostheses. Pharmacologic therapies have been disappointing and, despite initial interest in using steroids, there have not been any level 1 studies supporting their use.

Laboratory Studies:

Arterial blood gas demonstrates an alveolar-to-arterial oxygen tension difference, which, when drawn within 24 to 48 hours of a sentinel event, can be suggestive of fat embolism. Thrombocytopenia, anemia, and hypofibrinogenemia are nonspecific findings. Urinary fat stains are not thought to be sensitive or specific.

Fat Embolism

Fat embolism is another potential complication of IO insertion.3,72 However, this condition is rare and has been reported only in adult patients.65 Animal studies have found no changes in blood gases during IO infusion and limited evidence of fat globule collections in the lungs.69,70 In a swine cardiac arrest model, there was no difference in the risk for fat emboli in pigs that had an IO line inserted versus those receiving IV medications.131,132 Because the marrow in infants and children is primarily hematopoietic, this potential complication is unlikely to occur in this population.

Epidemiology

Fat embolism occurs in nearly all patients with bone fractures and during many orthopedic procedures.4,5 However, most patients with fat emboli are asymptomatic, and less than 20 percent develop overt fat embolism syndrome.5 The true incidence of fat embolism syndrome remains unknown, because many mild cases go unrecognized.

Fat embolism syndrome is most likely to occur after severe trauma. Multiple skeletal fractures increase the risk of fat embolism syndrome, because a larger amount of fat is released into the marrow vessels.5 In individuals with significant trauma, the incidence of fat embolism syndrome is estimated at 20 percent when multiple fractures are present, and 0.5 to 20 percent with a single fracture.5,6 Fat embolism syndrome is more likely to occur after closed, rather than open, fractures and in patients with fractures involving the middle and proximal parts of the femoral shaft. However, fat embolism syndrome can occur following minor injury, particularly in patients with underlying pulmonary vascular disease.

In addition to trauma, fat embolism can occur following liposuction or in patients with pancreatitis, fatty liver, or osteomyelitis.1–3 Furthermore, fat emboli may be a cause of acute chest syndrome associated with sickle cell disease7 (see Chapter 12).

FAT EMBOLISM SYNDROME

Fat embolism is a frequent occurrence following hip and knee replacement, but the clinical syndrome of fat emboli is rare [48]. The majority occur following the use of long-stemmed implants or intramedullary instrumentation for limb alignment [49]. Fat embolism syndrome has been seen more commonly in rheumatoid arthritis [50].

Mortality is high following fat embolism syndrome and thus measures must be taken to prevent its occurrence. When using intramedullary instrumentation, it is recommended that gentle insertion, overdrilling of the canal, and slotted alignment stems should be used to reduce intramedullary pressures that may lead to fat emboli. During preparation for cemented stem insertion, canal plugging and removal of loose intramedullary debris may help minimize fat emboli [48].

Fat embolism syndrome often presents as confusion secondary to hypoxemia during the first few days following surgery. Other causes of confusion must be ruled out [51]. The classic axillary and subconjunctival petechiae are often not present on physical examination. Several authors have tried to establish criteria to make the diagnosis of fat embolism syndrome [52,53]. Once established, fat embolism syndrome is treated with hemodynamic and respiratory support. Corticosteroids have been used in some cases.

Fat embolism syndrome

Fat embolism syndrome (FES) was first described in 1861 as a spectrum of clinical findings in certain patients suffering from fractures of medullated bones.135 This syndrome is clinically recognized in approximately 50% of patients with long-bone fractures; it affects multiple organ systems and may be fatal in 20% of severe cases.136 Systemic involvement includes a petechial rash, respiratory insufficiency, radiographic changes, and central nervous system involvement. Purtscher's retinopathy manifests retinal lesions similar to FES, and fat embolism has been suggested as a pathogenic mechanism.

An estimated 50% of patients with overt FES have retinal abnormalities, which include cottonwool spots and retinal hemorrhages. In a prospective study, Chuang and associates136 examined 100 consecutive patients with long-bone fractures but with no clinical or laboratory evidence of FES. They noted retinal findings in four patients and suggested that ophthalmoscopy may identify subclinical FES in patients at risk. Although the visual prognosis for patients with fundus lesions in FES is generally good, permanent visual scotomata have been reported.136

Fat embolism syndrome

Fat embolism syndrome (FES) was first described in 1861 by Zeuker.81 FES can be a complication of fractures of long bones, such as the femur, and is associated with various neurologic signs including paralysis, tremor, delirium, stupor, and coma. FES has been diagnosed in 5% of all patients with fractures. Clinical features usually commence between 24 and 48 hours after the injury, and the mortality rate has been reported to be as high as 30%.82 It was suggested that FES is caused by the delayed release of fat droplets from pulmonary fat emboli, by repeated influx of emboli from an inadequately fixed fracture, or by fatty acid hydrolyzed from neutral fat. The pathologic changes in FES are produced by combined mechanical damage induced by fat droplets and biochemical damage induced by fatty acids.82

Retinopathy has been reported in 50% of patients with FES and in 4% of patients with long-bone fractures presenting with a subclinical syndrome. Typical lesions consist of cotton-wool spots and flame-like hemorrhages, and are attributed to microvascular injury and microinfarction of the retina. Retinal lesions disappear after a few weeks, although scotomas may persist.83

Pulmonary and Systemic Fat Embolism

Fat embolism may be an important sequel to soft tissue or bony trauma. Whereas in the past fat globules were believed to be extruded from the edges of bony fractures into the systemic circulation, it is now believed that fat embolism may reflect the instability of lipoproteins in the plasma with coalescence into macroglobules of lipid. Fat globules are not uncommonly seen in lung tissue following fatal trauma or in deaths following orthopedic procedures which are not directly related to the surgery. Pulmonary fat embolism detected microscopically is usually not associated with respiratory failure and the degree of fat embolism must be interpreted in the context of other factors such as the presence of other injuries and underlying natural disease processes.

Globules of fat within the pulmonary circulation may result in vascular obstruction, local vasoconstriction and pulmonary edema. To establish fat embolism as a significant contributing factor to the cause of death one must identify systemic embolism.

It was previously universally accepted that systemic fat embolism occurs when the pulmonary capillaries and veins become ‘saturated’ with fat globules and thus allow fat to appear within the arterial system. Another possible route for systemic fat embolism is a patent foramen ovale. More recently the suggestion has been made that fat embolism may also relate to an alteration in the activity of lipase or phospholipase which is caused by the embolic fat. This alteration then leads to the precipitation of serum fat in the vessels of the different organs.

Systemic fat embolism results in vascular obstruction and inflammation with petechiae seen within the brain and skin and demonstrable fat on microscopic examination of the brain and kidney using special stains and processing techniques.