fat embolism(redirected from oil embolism)
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fat embolismAn 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)
fat embolismThe 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.
|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.
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.
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.
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.
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.
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.
|Test||Normal Result||Abnormality With Condition||Explanation|
|Platelet count||150,000–400,000 mm3||Decreased < 15,000 mm3||Platelets are used up in the clotting process|
|Pao2||80–100 mm Hg||< 60 mm Hg||Hypoxemia occurs because of problems with ventilation and perfusion due to obstruction of pulmonary circulation|
|Electrocardiogram||Normal rate; rhythm; and P, Q, R, S, and T waves||Tachycardia, right bundle branch block, depressed ST segments||Obstruction 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
DiagnosisImpaired gas exchange related to pulmonary capillary inflammation and arteriovenous shunting
OutcomesRespiratory status: Gas exchange; Respiratory status: Ventilation; Symptom control behavior; Treatment behavior: Illness or injury; Comfort level
InterventionsAirway management; Anxiety reduction; Oxygen therapy; Airway suctioning; Airway insertion and stabilization; Cough enhancement; Mechanical ventilation; Positioning; Respiratory monitoring
Planning and implementation
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.
General Comments: Medications provide supportive management rather than curative measures.
|Medication or Drug Class||Dosage||Description||Rationale|
|Corticosteroids, often methylprednisolone||Varies with drug||Anti-inflammatories||Decrease inflammatory response of pulmonary capillaries; stabilize lysosomal and capillary membranes|
Other Drugs: Analgesics are also necessary to manage the pain of the traumatic injury.
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).
- 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.