fat embolism


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fat embolism

a respiratory distress syndrome that can occur during long bone fractures that result from the release of bone marrow elements into the circulatory system that accumulate in the lungs to affect gas exchange adversely. See: bone marrow embolism.
Synonym(s): oil embolism

fat embolism

a circulatory condition characterized by the blocking of an artery by a plug of fat. The plug enters the circulatory system after the fracture of a long bone or, less commonly, after traumatic injury to adipose tissue or to a fatty liver. Fat embolism usually occurs suddenly 12 to 36 hours after an injury and is characterized by symptoms related to the site occluded, such as severe chest pain, pallor, dyspnea, tachycardia, delirium, prostration, and in some cases coma. Anemia and thrombocytopenia are common. Systemic fat embolism may occur after extensive trauma, since lipid metabolism is altered by the injury and free fatty acids are released, resulting in vasculitis with obstruction of many small pulmonary and cerebral arteries. Classic signs of systemic fat embolism are petechial hemorrhages on the neck, shoulders, axillae, and conjunctivae that appear 2 or 3 days after the injury. Radiographic findings include patchy diffuse opacities throughout the lungs. There is no specific therapy for systemic fat embolism. The patient is placed in a high Fowler's position and given oxygen, corticosteroids, blood transfusion, respiratory assistance, or other supportive care as needed. Compare air embolism, gas embolism.

fat embolism

An embolus containing fat, an event that follows long bone fractures, and less commonly, hepatic trauma; embolic fat 'metastasizes' to the lungs, causing dyspnea, shock, to the brain causing coma, to the kidneys causing lipiduria. See Embolism.

fat em·bo·lism

(fat em'bŏ-lizm)
The occurrence of fat globules in the circulation following fractures of a long bone, in burns, in parturition, and in association with fatty degeneration of the liver; the emboli most commonly block pulmonary or cerebral vessels when symptoms referable to either or both of these regions appear.

fat embolism

The release of fat into the blood and its movement with the circulation to a point where blockage of small arteries occurs. Fat embolism usually follows fractures of long bones. Obstruction of vital arteries such as those in the brain, the lungs or in the coronary arteries of the heart is a serious complication. The acidic products of fat breakdown can also cause permanent damage to the linings of the arteries.

Fat Embolism

DRG Category:175
Mean LOS:6.6 days
Description:MEDICAL: Pulmonary Embolism With Major CC

An embolism is any undissolved mass that travels in the circulation and occludes a blood vessel. A fat embolism, which is an unusual complication from a traumatic injury, occurs when fat droplets enter the circulation and lodge in small vessels and capillaries, particularly in the lung and brain. Two theories exist that explain the pathophysiology of fat emboli: the mechanical theory and the biochemical theory. The mechanical theory states that trauma disrupts fat cells and tears veins in the bone marrow at the site of a fracture. Fat droplets enter the circulation because of increased pressure of the interstitium at the area of injury. The biochemical theory states that a stress-related release of catecholamines after trauma mobilizes fat molecules from a tissue. These molecules group into fat droplets and eventually obstruct the circulation. In addition, free fatty acids destroy pulmonary endothelium, increase capillary permeability in the lungs, and lead to pulmonary edema.

The result of either theory is the accumulation of fat droplets that are too large to pass easily through small capillaries, where they lodge and break apart into fatty acids, which are toxic to lung tissues, the capillary endothelium, and surfactant. Pulmonary hypertension, alveolar collapse, and even noncardiac pulmonary edema follow. Mortality rates are approximately 10% to 20%. Patients with increased age, underlying medical conditions, and poor physiological reserves have poorer health outcomes than other patients.

Causes

Fat embolism is associated with severe traumatic injury with accompanying long-bone (tibial or femoral) or pelvic fractures and generally occurs within 3 days of the fracture. It has also been reported in patients with severe burns, head injury, or severely compromised circulation. Nontraumatic disease states that have occasionally been associated with fat embolism include acute pancreatitis, alcoholism, diabetes mellitus, and osteomyelitis. Procedures such as liposuction, orthopedic surgery, joint replacement, abdominal surgery, and cardiac massage (closed chest) are also associated with fat embolism. It is also associated with parenteral lipid infusion and corticoid administration. Fat embolisms are the most common nonthrombotic cause of pulmonary emboli.

Genetic considerations

No clear genetic contributions to susceptibility have been defined.

Gender, ethnic/racial, and life span considerations

Many patients who develop the disorder are under age 30 and have severe associated traumatic injuries. Males are more likely than females to have a significant traumatic injury. Older adults have a poorer outcome than their younger counterparts. No racial or ethnic considerations are known to be associated with fat embolism.

Global health considerations

No data are available.

Assessment

History

Elicit a history of recent traumatic injury. In most patients, the injury is obvious because of the presence of casts or traction. Some patients exhibit changes in mental status such as restlessness, delirium, or drowsiness progressing to coma and even seizures. Others complain of fever, anxiety, unexplained discomfort, or respiratory distress (shortness of breath, cough).

Fat embolization may be classified into three distinct forms based on the patient’s progression of symptoms: subclinical, classic, and fulminant. Approximately half of patients with uncomplicated fractures have subclinical fat emboli, which resolve spontaneously within a few days. Patients with the classic form generally have a latent period of 1 to 2 days, followed by the development of symptoms that include mental status changes, shortness of breath, fever, tachycardia, and petechiae. The fulminant form is characterized by an early onset of neurological and respiratory deterioration as well as the onset of signs of right ventricular failure (distended neck veins, liver congestion, peripheral edema). A rapid onset of neurological deterioration in patients who sustained severe injuries and multiple fractures but who were initially conscious suggests a fat embolism.

Physical examination

The most common symptoms are related to cardiopulmonary function and include tachycardia, dyspnea, fever, and signs of hypoxemia, including restlessness, agitation, confusion, or even stupor. Some patients may have a seizure. Note that neurological changes usually occur 6 to 12 hours before respiratory system changes and rarely without impending respiratory involvement.

Inspect the patient’s skin for petechiae, a classic sign that appears 1 to 2 days after injury in more than half of patients with fat embolism. Petechiae are of short duration, last only 4 to 6 hours, and appear most commonly on the neck, upper trunk, conjunctivae, or retina. An ophthalmic examination may reveal fat globules in the retinal vessels. Approximately half of the patients who display neurological symptoms also develop micro-infarcts of the retina. When auscultating the patient’s heart and lungs, a rapid heart rate and respiratory rate with rales, rhonchi, and possibly a pleural friction rub are usually heard.

Psychosocial

Because fat embolism is a complication of other disease processes or traumatic injuries, the addition of another life-threatening complication could be the final breaking point for the family or significant others involved. Evaluate the patient’s social network to determine what support is available during the acute illness.

Diagnostic highlights

TestNormal ResultAbnormality With ConditionExplanation
Platelet count150,000–400,000 mm3Decreased < 15,000 mm3Platelets are used up in the clotting process
Pao280–100 mm Hg< 60 mm HgHypoxemia occurs because of problems with ventilation and perfusion due to obstruction of pulmonary circulation
ElectrocardiogramNormal rate; rhythm; and P, Q, R, S, and T wavesTachycardia, right bundle branch block, depressed ST segmentsObstruction of the pulmonary circulation leads to right heart strain

Other Tests: Increased serum lipase, fat in the urine, fibrinogen, complete blood count, patchy infiltrates on chest x-ray, ventilation perfusion scans, computed tomography and magnetic resonance imaging, pulse oximetry to detect arterial oxygen saturation, calcium levels, arterial blood gas analysis

Primary nursing diagnosis

Diagnosis

Impaired gas exchange related to pulmonary capillary inflammation and arteriovenous shunting

Outcomes

Respiratory status: Gas exchange; Respiratory status: Ventilation; Symptom control behavior; Treatment behavior: Illness or injury; Comfort level

Interventions

Airway management; Anxiety reduction; Oxygen therapy; Airway suctioning; Airway insertion and stabilization; Cough enhancement; Mechanical ventilation; Positioning; Respiratory monitoring

Planning and implementation

Collaborative

support for airway and breathing.
Management of the patient almost always requires support of the patient’s airway and breathing with supplemental oxygen and possibly endotracheal intubation and mechanical ventilation. Patients who do not exhibit changes in mental status or pulmonary edema may benefit from supplemental oxygen by nasal cannula or face mask. Patients with a deteriorating mental status, dropping arterial oxygen saturations, and decreasing levels of Pao2 (less than 50 mm Hg) usually need positive pressure ventilation with positive end-expiratory pressure and possibly pressure control ventilation.

The nurse and trauma surgeon or orthopedist work together to prevent fat emboli whenever possible by encouraging adequate gas exchange; this entails clearing secretions and promoting good ventilation. Discuss the patient’s activity restrictions with the physician. To limit the effects of immobilization, turn the patient frequently and, when he or she is ready, get the patient out of bed. If the injuries allow, encourage dangling or ambulation. Maintain the patient’s hydration by intravenous or enteral fluids, as prescribed, and provide prophylaxis for deep venous thrombosis and stress-related gastrointestinal bleeding.

pharmacologic.
Diuretics may be needed if pulmonary edema develops. Many experts recommend prophylactic use of corticosteroids for patients at high risk for fat emboli, but they seem less effective after fat emboli develop. Some experts suggest that the introduction of steroids may help treat pulmonary manifestations by decreasing the inflammatory response of the pulmonary capillaries as well as by stabilizing lysosomal and capillary membranes. Analgesics are also necessary to manage the pain of the traumatic injury.

The best treatment of fat emboli is preventing their occurrence. Surgical stabilization of extremity fractures to reduce bone movement probably minimizes the release of fatty products from the bone marrow. The location of the fracture determines whether the surgeon uses internal or external fixation techniques.

Pharmacologic highlights

General Comments: Medications provide supportive management rather than curative measures.

Medication or Drug ClassDosageDescriptionRationale
Corticosteroids, often methylprednisoloneVaries with drugAnti-inflammatoriesDecrease inflammatory response of pulmonary capillaries; stabilize lysosomal and capillary membranes

Other Drugs: Analgesics are also necessary to manage the pain of the traumatic injury.

Independent

The highest priority is maintaining the airway, breathing, and circulation. Ongoing monitoring of the cardiopulmonary system is essential, coupled with interventions such as suctioning, placement of an oral airway if appropriate, and immediate notification of the trauma service if the airway, breathing, or circulation becomes impaired.

The patient needs to be an active participant in her or his care. Before she or he undergoes activity or coughing and deep-breathing exercises, make sure that the patient’s pain is controlled. In addition to administering prescribed medications, explore nonpharmacologic alternatives to pain management, such as diversionary activities and guided imagery.

The patient’s and family’s level of anxiety is apt to be exacerbated by the critical care environment. Explain all the equipment and answer questions honestly and thoroughly. If the patient has to undergo endotracheal intubation, provide a method for communication, such as a magic slate or point board. Work with the family to allow as much visitation as the patient’s condition allows. Remember that although young people in their late teens often appear to be adults, they often regress during a serious illness and need a great deal of support from their parents and significant others.

Evidence-Based Practice and Health Policy

Bederman, S.S., Bhandari, M., McKee, M.D., & Schemitsch, E.H. (2009). Do corticosteroids reduce the risk of fat embolism syndrome in patients with long-bone fractures? A meta-analysis. Canadian Journal of Surgery, 52(5), 386–393.

  • A meta-analysis of seven quasi-randomized controlled trials including 389 patients provides evidence that a corticoidsteroid regimen following a long-bone fracture reduces the risk of developing fat embolisms.
  • The relative risk of developing fat embolism syndrome (FES) decreased by 58% to 89% among patients receiving corticosteroids when compared to patients who did not. The pooled relative risk reduction across all the studies was 78% (95% CI, 43% to 92%).
  • Corticosteroid dosing regimens in the studies ranged from 6 to 90 mg/kg. A sensitivity analysis revealed that lower doses of corticosteroids (6 to 9 mg/kg) demonstrated improved results over higher doses (> 30 mg/kg).

Documentation guidelines

  • Physical responses: Vital signs, cardiopulmonary assessment, neurological assessment, mental status, presence or absence of petechiae
  • Emotional response: Coping strategies, mood, affect, flexibility, cooperation
  • Presence of complications: Fever, infection, skin breakdown, loss of consciousness
  • Ongoing monitoring: Pulse oximetry or arterial blood gases results that are abnormal, abnormal laboratory findings
  • Response to treatment: Mechanical ventilation, response to fluid replacement and medications, response to supplemental oxygen

Discharge and home healthcare guidelines

A patient who has recovered from the underlying disease process or injury is no longer at risk for developing fat embolism and can be discharged. Teach the patient about any medications and treatments needed before he or she leaves the hospital. Explain the disease process and how it occurred and note that recurrence is doubtful unless the patient experiences another traumatic injury. Arrange for any follow-up care with the primary healthcare provider.

fat em·bo·lism

(fat em'bŏ-lizm)
The occurrence of fat globules in the circulation following fractures of a long bone, in burns, in parturition, and in association with fatty degeneration of the liver.

fat

1. the adipose or fatty tissue of the body.
2. neutral fat; a triglyceride (or triacylglycerol), which is an ester of fatty acids and glycerol (a trihydric alcohol). Each fat molecule contains one glycerol residue connected by ester linkages to three fatty acid residues, which may be the same or different. The fatty acids may have no double bonds in the carbon chain (saturated fatty acids), one double bond (monounsaturated), or two or more double bonds (polyunsaturated).

fat absorption test
assesses the absorptive capacity of the small intestine, quantitatively by measuring serum lipid levels or qualitatively by plasma turbidity, at timed intervals after the oral administration of fats.
animal fat
a most important abattoir by-product providing edible fat for the human food chain. Products include oleo oil and oleo stearin used in margarine manufacture and dripping for commercial baking. Nonedible fats go to leather dressings, glycerol manufacture and lubricants. Beef and pork fat are the valuable ones, mutton fat having too strong a flavor for edible fat.
boiling (burning) fat
see acrolein poisoning.
fat cattle
a class of beef cattle of any age but usually greater than one year, well-covered and judged ready for slaughter to provide prime cuts of beef.
fat cow syndrome
a syndrome of anorexia and ketonuria that occurs in overfat cows at calving. Precipitated by events that interfere with the cow's feed intake for even short periods. A poor response to treatment and many cows die.
Enlarge picture
Fatty liver in fat cow syndrome. By permission from Blowey RW, Weaver AD, Diseases and Disorders of Cattle, Mosby, 1997
crude fat
that part of a feed that is extractable by ether. Includes fat, oil, wax, resin and some pigments.
dietary fat
a rich source of energy for carnivores and omnivores and to a limited extent ruminants. Are usually too expensive for widespread use other than as excipients. They aid in the formation of pellets and in reducing dustiness. Their problem is a tendency to rancidification unless an antioxidant is added.
fat embolism
lesion created by a fat embolus.
fat embolus
globules of fat, sufficient to act as emboli occur usually after trauma or surgery, but can also occur in hyperlipemia, myositis and atherosclerosis.
fat ewe pregnancy toxemia
occurs when there is a voluntary restriction of food intake in late pregnancy associated with lack of ruminal expansion potential caused by excess abdominal fat and multiple fetuses. It is common in hobby sheep farms where it is thought that ewes should lamb with body condition scores greater than 4 rather than less than 3.5.
leaf fat
the best edible fat from a pig carcass, from under the peritoneum.
fat marbling
deposition of fat between muscle fibers. A highly desirable characteristic in beef. Is a guarantee of a carcass from a young animal.
fat necrosis
necrosis in which fat is broken down into fatty acids and glycerol, usually occurring in subcutaneous tissue as a result of trauma. See also lipomatosis.
orbital fat
fat located deep to the eyeball; substantial amounts provide good shock-absorbent surroundings.
perivaginal fat prolapse
during a difficult parturition in a fat cow or heifer perivaginal fat is pushed caudally and bursts through the vaginal wall into the vagina.
fat phanaerosis
conversion in the tissues of invisible fatty substances into fat which can be stained and thus become visible.
fat prolapse
see perivaginal fat prolapse (above).
fat sheep
a class of meat sheep of any age but usually greater than one year, well-covered and judged ready for slaughter to provide prime cuts of mutton.
References in periodicals archive ?
Free fatty acids, cathecolamines, and arterial hypoxia in patients with fat embolism.
Fat embolism syndrome: prospective evaluation in 92 fracture patients.
Unfortunately, as the echocardiographic appearance of fat, thrombi and tumour are similar, it is not possible to reliably diagnose fat embolism intraoperatively.
The clinical diagnosis of intraoperative fat embolism would be supported by the subsequent development of fat embolism syndrome, however this did not occur in our patient.
The detection of fat embolism by transoesophageal echocardiography during reamed intramedullary nailing.
Peter R, Schopfer A, Le Coultre B, Hoffmeyer P Fat embolism and death during prophylactic osteosynthesis of a metastatic femur using an unreamed femoral nail.
Fatal pulmonary fat embolism in the early postoperative period.
Key Words: pulmonary embolism, hypoxia, trauma, respiratory system, fat embolism
Fat embolism syndrome is a rare, poorly understood but serious complication which occurs after the direct entry of fat globules into the systemic circulation.
As opposed to computed tomography (CT) findings in other forms of ARDS, radiological features have only been described occasionally in severe fat embolism syndrome.
In this report, we present a case of severe fat embolism syndrome with unique CT findings including subpleural and centrilobular nodules.
MRI of the brain showed no focal lesions but diffuse atrophy suggestive of severe preceding hypoxaemia, probably caused by cerebral fat embolism.