⌚ Fat Embolism Syndrome Case Studies

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Fat Embolism Syndrome Case Studies



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The importance of recognizing fat embolism syndrome in patients with hemoglobinopathy

Fat embolism is the presence of fat particles within the microcirculation, while FES is the systemic manifestation of fat emboli within the microcirculation. Common systemic manifestations include respiratory distress, altered mental status, and a rash. FES is most often associated with orthopedic trauma. Rare cases of FES have been reported to occur following bone marrow transplantation, osteomyelitis, pancreatitis, alcoholic fatty liver, and even liposuction.

Fat embolization occurs frequently following orthopedic trauma. Hypoxemia may suggest fat embolization causing subclinical FES. Almost all patients monitored with continuous pulse oximetry following a long-bone fracture will have episodes of hypoxemia. Further embolization may occur during operative fixation. While almost all patients will have fat globules detected in the blood or develop transient hypoxia, the incidence of FES is much lower.

Fat particles enter the circulation and cause damage to capillary beds. While the pulmonary system is most frequently affected, fat embolism can occur in the microcirculation of the brain, skin, eyes, and heart can be involved. The two leading theories for the formation of fat embolism are the mechanical theory and biochemical theory. The mechanical theory proposes that obstruction of the systemic vasculature by fat embolism occurs from the direct release of bone marrow into the venous system following trauma. An elevated intramedullary pressure following trauma leads to the release of fat through open venous sinusoids.

The embolized fat obstructs capillary beds. While this accounts for embolisms within the pulmonary capillaries, the theory does not explain embolisms within the systemic capillaries beds. Patients have been shown to have systemic fat embolization without a patent foramen ovale. The biochemical theory provides an alternate explanation for fat embolization. This theory proposes that the inflammatory response to trauma causes the release of free fatty acids from the bone marrow into the venous system. The elevated free fatty acids as well as the inflammatory mediators cause damage to capillary beds.

Elevated free fatty acid levels have been associated with hypoxemia. Regardless of the mechanism initiating fat embolism, the end result is an intense inflammatory response. Capillary beds develop increased permeability and inflammatory mediators damage surrounding tissues. In the lungs, this induces lung injury that is indistinguishable from ARDS. Embolized fat droplets can travel to microvasculature throughout the body.

FES is, therefore, a multiorgan disease and can damage any microcirculatory system within the body. Fat has been reported to embolize to the lungs, brain, skin, retina, kidneys, liver, and even the heart. Presenting signs are nonspecific and include tachypnea, tachycardia, and fever. Patient may have a petechial rash. Specific symptoms are dependent on the organ systems involved. Patients may decompensate rapidly to respiratory failure, especially during manipulation of fractures whilemoving the patient or setting the fracture in the operating room. This must especially be taken into consideration while in the operating room; an anesthetized patient may develop acute hypoxia secondary to FES.

FES can cause nonspecific neurological symptoms. Symptoms are believed to arise from cerebral edema rather than ischemia, so symptoms are nonlateralizing. In the setting of severe cerebral edema the patient may become unresponsive. While the torso is most commonly affected, the entire dermis and even mucosal membranes can be involved. Patients may also develop thrombocytopenia or a decrease in hemoglobin in FES. Since FES is a heterogeneous disease with no pathognomonic features, its diagnosis can be challenging. Gurd proposed a of clinical criteria for diagnosing FES in that he later modified with Wilson[ 4 , 5 ] [ Table 1 ].

Schonfeld has suggested a scoring system to helpin diagnosis[ 24 ] [ Table 2 ], while Lindeque proposed that FES can be diagnosed based on respiratory changes alone[ 25 ] [ Table 3 ]. None of these criteria have been validated or have been universally accepted. In the acute setting respiratory distress is the most clinically significant feature of FES. Laboratory and imaging tests can helpin the diagnosis, but are nonspecific. Patients will demonstrate hypoxemia while on room air on arterial blood gas. Chest x-ray will often show diffuse interstitial infiltrates while chest CT scan will show diffuse areas of vascular congestion and pulmonary edema.

Attempts at developing specific test for FES have been disappointing. Biologic markers such as lipase, free fatty acids, and phospholipase A2 have all been shown to be elevated in patients with FES; however, this elevation is nonspecific in patients with lung injury. Microscopic examination of blood, urine, or sputum may show fat globules, but again this finding is nonspecific. BAL though is invasive and time intensive. It has not become widely used in diagnosing FES. With the absence of specific tests or criteria the diagnosis of FES is dependent on the clinical acumen of the treating physician. It should be clinically suspected in patients with respiratory distress or a petechial rash and are at high risk for developing FES.

Therapeutic treatments developed specifically for FES have been largely unsuccessful. Early experiments attempted to use dextrose to decrease free fatty acid mobilization or ethanol to decrease lipolysis; however, neither have shown clinical benefits. Corticosteroidtherapy has been proposed as a potential therapy for FES by limiting free fatty acid levels, stabilizing membranes, and inhibiting complement mediated leukocyte aggregation.

This meta-analysis, though, included only one recent trial. A randomized trial found no difference in incidence of FES between patients treated with methylprednisolone. Placement of inferior venal cava filters has been advocated as a method to reduce showering of emboli to the pulmonary vasculature. Once a patient develops FES the only proven treatment is supportive care of the involved organ systems. Supplemental oxygen may be required to improve oxygenation. If ARDS develops the patient may require mechanical ventilation while recovering from lung injury. Patients may require intravenous fluid for resuscitation to avoid developing shock. In severe cases, in which a fat pulmonary embolism causes, right ventricular failure ionotropic support with dobutamine may be necessary.

Patients with neurological manifestations require frequent neurological examinations and documentation of Glascow Coma Scale to assess for neurologic deterioration. Rapid deterioration may develop from increased cerebral edema. Early operative fixation of long-bone fractures is advocated to reduce the incidence of FES. The use of internal fixation devices for treatment of long bone fractures was accompanied by a reduction in the incidence of FES. Increased intramedullary pressure during fixation increases the amount of fat emboli entering the circulation.

While reaming may increase intramedullary pressure, reaming has not been shown to increase the incidence of FES. A randomized trial comparing pulmonary complications in patients undergoing fixation with reamed nailing and unreamed nailing found no difference between the two groups. Surgical techniques to reduce embolization including drilling holes in the cortex to reduce intramedullary pressure, lavaging bone marrow prior to fixation to reduce marrow for embolization, venting of the femur, use of a bone-vacuum, and use of tourniquets to prevent embolization have been attempted.

None of these have clearly been shown to reduce FES. With supportive care and early fixation FES has a favorable outcome. The most significant morbidity is associated with the development of ARDS. However, most patients can expect a complete recovery of pulmonary, neurologic, and retinal abnormalities. FES most commonly presents with respiratory distress in orthopedic trauma patients.

No specific diagnostic tests or criteria exist, so the syndrome is most often a diagnosis of exclusion. Therapy is most often directed at treatment of ARDS and support of other organ systems affected by fat embolization. Early operative fixation long-bone fractures have reduced the incidence of FES. Source of Support: Nil. Conflict of Interest: None declared. National Center for Biotechnology Information , U.

Michael E. Kwiatt and Mark J. Mark J. Author information Copyright and License information Disclaimer. Address for correspondence: Dr. E-mail: ude. This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3. This article has been cited by other articles in PMC. Abstract Fat embolism syndrome FES is an ill-defined clinical entity that arises from the systemic manifestations of fat emboli within the microcirculation.

Keywords: Fat embolism, fat embolism syndrome, trauma. Open in a separate window. Table 2 Schonfeld's scoring system for FES. Table 3 Lindeque's criteria for FES. Supportive treatment Once a patient develops FES the only proven treatment is supportive care of the involved organ systems. Operative fixation Early operative fixation of long-bone fractures is advocated to reduce the incidence of FES. Morbidity and mortality With supportive care and early fixation FES has a favorable outcome. Scuderi CS. Naturally, these antibodies attack foreign invaders, but when these begin to harm the phospholipid-binding proteins, the blood coagulates unusually.

The syndrome is considered primary when this happens in the nonexistence of other associated disease. More commonly, the disease is secondary as it occurs in conjunction with an autoimmune disorder, systemic lupus erythematosus for instance. In very uncommon circumstances, lupus anticoagulant syndrome causes a person to develop rapid organ failure as a result of generalized thrombosis. This stage of condition is referred as catastrophic antiphospholipid syndrome. Phospholipids are fat molecules that contain phosphorus which are typically found all over the body, specifically in living cells and cell membranes. Once a patient develops the disease, the immune system releases antibodies against phospholipids. Normally, clotting is a basic body process. It assists in closing up minute cuts on the walls of the blood vessels, avoiding too much blood loss.

In lupus anticoagulant syndrome, on the other hand, there are unnecessary thrombi forming in the arteries and veins, blocking the circulation of blood, oxygen and nutrients to the organs and tissues. While the disease was first documented to be present in individuals with systemic lupus erythematosus, at this time, it is understood that majority of these patients do not have the latter. The main etiology is not wholly determined. Yet, it is known to reduce the concentration of annexin V, a protein attaching to phospholipids which also has a strong anticoagulant activity.

Its decline is assumed to be the potential factor which enhances the predisposition of blood to thicken. Anticardiolipin in addition is related to a drop of prostacyclin concentration, which is essential in inhibiting the clumping together of platelets. Treatment is directed at stopping clot and thrombus formation. The condition is regularly treated by administering a combination of blood thinning drugs. Classically, the patient receives a shot of heparin combined with Coumadin.

Warfarin is used to inhibit clotting factor synthesis. After a few days of receiving combined drugs, the patient will only receive warfarin as heparin is discontinued. In some instances, aspirin is added to the treatment regimen in order to inhibit platelet activation thus preventing intra-vessel clotting. Treatment involves daily administration of low dose of aspirin 75 mg. Treatment for pregnant mothers is predominantly complicated as this is costly, involves repeated injections and incorporates a number of adverse reactions. For pregnant women, the pharmacologic treatment comprises of low molecular weight heparin and aspirin in low dose as a replacement for warfarin as this drug tends to be teratogenic as it can cross the placenta.

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