fat embolism Syndrome

Fat Chuk blood clot syndrome (Fat embolism syndrome)

2010-07-07T09:21:00.000-07:00

Fat Chuk blood clot syndrome (Fat embolism syndrome) is a syndrome. Caused by changes that occur after Homeostasis fracture After surgery, the orthophosphate Ping disc or conditions other than problems orthophosphate Ping disc. I happen to like Severe infection blunt injury, blood tranfusion as a condition caused a drop of fat, small blood and obstruction of blood vessels of organs important, such as lung brain heart kidney as tissue, organs ischemia. to culture. The work of organs that fail the group appeared out clinical symptoms are many Depending on the fat emboli to go to what obstructive incidence fat embolism.

In patients with limb bones were broken percent from 0.5 to 2.2 and in the case of multiple fracture the culture together with a pelvic fracture is found percentage 50-10%.

Fat embolism syndrome is a condition of critical illness in the growth and mortality rates as high as 5000 per year and the show symptoms at birth are different. Occur within 12 hours about 25 percent during the 36 hours, 75 percent and the 85 per cent within 48 hours causes the occurrence of fat embolism.

Causes are unknown. But the theory that most people believe is a bone marrow emboli that is when the tear of blood vessels in the bone marrow and fat tissue in the bone marrow into the blood drop. Fat droplets that come off (fat globules) combines with platlets, fibrin or red cell in blood vessels causing obstruction of blood vessels. Vascular wall cells and secrete substances destroyed. Thromboplastin, fatty acid and adenosine diphosphate which these materials will accelerate the coagulation of blood. Typically, the coagulation of blood could be the breakdown of the work of the fibrinolysis system, but in patients with depressed level of fat embolism substance that helps the body process of fibrinolysis is less blood clot break down.

Coagulation of the blood increased. The ability to break down blood clot. The patients had low hemoglobin and the erythrocyte sedimentation rate. thrombocytopenia. Detected the bleeding or blood spots under eyes and body lining signs and symptoms.

Signs and symptoms will be much less depending on the emboli to plug in various positions with much. Very little if any symptoms will disappear by themselves. For patients with severe changes of the system are different symptoms and signs that appear in various systems follows.

1. The obstructive respiratory system of capillary gas exchange will be reduced. The condition of low blood oxygen (Hypoxia), which is to stimulate the respiratory control center. Giving patients breathe faster, breathing hard and pant I may have a blood (blood sputum) gas pressure in the artery is reduced PO2 and PCO2 increased.

2. Cardiovascular system. Of the obstructive coronary artery. The pulmonary circulation changes. The increase in pulmonary vascular resistance. So it works right ventricles increased strength to resist. And the pressure increased. Pressure of the right ventricles increased. The right auricle to the squeezing force. Hypoxia and physical condition when trying to adapt. By increasing the amount of blood from the heart The heart is squeezing more. Cause symptoms fast pulse (tachycardia) may have some chest pain from symptoms of myocardial ischemia if blood pressure is very low and right ventricles fail

3. The nervous system caused by cerebral fat emboli not allow enough blood to the brain. Patients with symptoms restless confusion and absorption into insensibility. May have symptoms of muscle contraction spasms or part of a serious nature decerebrate rigidity may be destroyed only the brain tissue. Disability until the later treatment, such as urine does not hold one. Or Alzheimer's disease

4. Skin symptoms may not change And are often found in recently, if patients have severe symptoms. Patients may die before Symptoms include the skin. Of the blood spots (petichiae) found that the neck. Followed by chest shoulder arms lining eye (conjunctiva) of the lower eyelid.

5. Kidneys were not changed often. Conditions often associated with shock. There is little urine (oliguria) until it no urine (anuria) diagnosis Fat embolism syndrome.

1. The history and symptoms of the patient. Often in younger patients. Injured several of the fast breathing, fever, fast pulse restless confusion.

2. The laboratory to determine Aterial blood gas because state hypoxia is measure the most important condition fat embolism was the PO2 below 60 mmHg for P CO2 less than 55 mmHg or pH less than 7.3 ESR higher found. Hemoglobin decreased 3-5 gm% Platelet count lower than 150,000 / mm3 Hematocrit values lower than normal prothrombin time value is lower than normal blood was free fatty acid, chloesterol, triglyceride and fat found in urine, sputum

3. Radiography of the lung will find a ceiling look like white snow (snow storm) and From the electrocardiogram (EKG) was invert T wave and depressd ST segment due to Rt.Bundle branch block guidelines for treatment.

No drugs. Syndrome is directly However, treatment to relieve symptoms. The following treatment.

1. Of the oxygen. When was the first state Hypoxia and respiratory care. The adequacy of the blood. To adjust pH and electrolyte balance in the body. The nutrient that has enough power.

2. Chest physical therapy. To prevent infection, pneumonia lung deflation airbags.

3. To eliminate movement and mend the broken, especially in patients with multiple fracture in Finland. Surgical Steel was put firmly bone fixation (rigid internal fixation) to form long bones (long bone) in patients with multiple injury can reduce the incidence of fat embolism syndrome from 22% down to 4.5%.

For patients at risk of severe fat embolism to assess every patient on admission. Keeping track changes to various symptoms, including temperature, pulse rate, respiratory rate and blood pressure level of consciousness. Changes in neurological symptoms. Blood spots out of the body. If you see something wrong. The medical report and mend the broken. To the bone is still broken. To reduce the movement of the bone This is important to prevent fat embolism, or when the condition is then they will not cause more severe symptoms Principles of Nursing.

When severe fat embolism in the hospital, then follows.

1. Recorded vital signs every 15 minutes, and assessed symptoms. Symptoms of various systems.

2. Respiratory care to open The patient received oxygen treatment plan. The patient may receive O2 mask or respirator. The need to take care of the machine working efficiently.
3. View the follow-up blood gas PO2 and PCO2 and pH values to determine if the abnormal condition Hypoxia doctors to report immediately. To help And trace the other laboratories, such as CBC, electrolyte, Hematocrit, Hemoglobin.

4. Care to receive blood or fluid of the medical treatment plan. To prevent and correct conditions ¾ channel and blood Edit shock conditions adjust the pH balance in the body. In order to drain fat from the body. Prevent renal failure. And care to get enough nutrients. As well as drugs. Plan of medical treatment.

5. Rub the body to reduce fever.

6. Record amount of fluid the body has. Body fluid volume and drive out.

7. The patient has symptoms of restless confusion careful absorption into the accident. Must maintain close

8. Trace Others, such as chest X-ray, EKG.

9. To psychological care.

10. To prevent pressure ulcers and complications of pulmonary fat embolism syndrome, when conditions have been treated to provide relief. The patient has recovered. Perceived better Breathing itself is usually normal pulse of blood gas and chest X-ray and EKG is normal for doctors consider surgery to fixing broken bones.

Fat Embolism Syndrome in a Surgical Patient

2010-06-24T09:58:00.000-07:00

James L. Glazer, MD, and Daniel K. Onion, MD, MPH
Fat embolism syndrome, a condition characterizedby hypoxia, bilateral pulmonary infiltrates, andmental status change, is commonly thought of inassociation with long-bone trauma. Fat embolizationcan frequently take place, however, within thesetting of elective and semiacute orthopedic procedures.1 In particular, there is a high incidence of fatembolization during placement of hip prostheses.Although studies suggest that embolization eventsinfrequently result in a clinically apparent fat embolismsyndrome,1,2 clinicians should be vigilant inconsidering fat embolism syndrome as a causativeagent of postoperative respiratory distress.Case ReportAn 80-year-old woman with a history of hip fractureand prosthesis placement of the left hip cameto the emergency department after a fall. A displacedfemoral neck fracture of the right hip wasdiagnosed based on clinical examination and radiologicfindings. The patient was admitted to thehospital by the orthopedics service.The patient was scheduled for operative placementof a bipolar prosthesis of her right hip on theday following admission. Her preoperative coursewas uneventful. An electrocardiogram (ECG)showed Q waves in leads III, aVF, and V3, whichwere interpreted as an old inferior infarction. Shewas afebrile, her blood pressure was 160/82 mmHg, and her oxygen saturations were 93% on roomair. In the operating room, she was sedated withmidazolam and fentanyl and received spinal anesthesia.Placement of a cemented hip stem (Johnson &Johnson Ultima) and femoral head component(Johnson & Johnson), bipolar shell, and bipolarliner was uneventful. The procedure lasted 96 minutes,during which the patient maintained oxygensaturations of 98% to 100% on 10 L of oxygen.Her blood pressure ranged between 90 and 135mm Hg systolic, and her pulse was less than 100beats per minute. Approximately 10 minutes postoperatively,the patient abruptly developed a sinustachycardia with a pulse of 135 beats per minute.Her blood pressure was 122/88 mm Hg and heroxygen saturations were 85% to 86% on room airat a respiratory rate of 36/min. At this point, consultationby the family practice service was requestedby the orthopedic surgeon.An ECG, complete blood count, and cardiacprofile were all obtained. The ECG showed sinustachycardia without acute ST or T wave changes.Her hematocrit was stable, cardiac enzyme levelswere negative, and a thyroid-stimulating hormonelevel was within normal limits. The patient’s tachycardiaand tachypnea continued, with her pulseranging from 135 to 140 beats per minute andrespirations between 24 and 36/min. Two hourspostoperatively, she developed a fever of 101.7° Fand systolic hypertension of 165 mm Hg.A diagnosis of pulmonary embolus was considered,and arterial blood gas readings and a chestradiograph were obtained. Arterial blood gas on 4L of inspired oxygen showed a pH of 7.41, carbondioxide 36 mm Hg, and oxygen 81 mm Hg, with97% saturation calculated. A chest radiographshowed bilateral perihilar fullness but a lack ofinfiltrate. Based on the patient’s persistent oxygenrequirement and her continued tachycardia andtachypnea, a d-dimer assay and ventilation-perfusionscan were obtained. Four hours postoperativelythe patient had oxygen saturations of 78% onroom air and 91% on 4 L of inspired oxygen.The d-dimer assay results were between 1,500and 2,000 mg/L, a positive result. The ventilationperfusionscan was read as intermediate probabilitywith matched segmental and subsegmental defectsbilaterally, predominately at the lung bases andworse on the left. The patient was given heparin.Approximately 1 hour before her initial bolus of saturations suddenly began to improve, from 89%to 95% on 4 L of oxygen. Her pulse returned to100 beats per minute, and her systolic blood pressurestabilized in the range of 125 to 135 mm Hg.During the next 24 hours, she was weaned fromoxygen, her low-grade temperature resolved, andher blood pressure remained stable. Several newpetechiae were noted on the patient’s anterior chestwall. A skin biopsy of the petechial lesions revealedintravascular fat, and a diagnosis of fat embolismsyndrome was made. A review of her symptomsfrom the previous night indicated the patient metfive of Gurd and Wilson’s criteria for fat embolismsyndrome, including petechiae, hypoxemia, pyrexia,tachycardia, and relative thrombocytopenia.3The heparin was discontinued.The patient did suffer some bleeding from herwound site and required a transfusion of 2 U ofpacked red blood cells. She had no hematoma andbegan to make excellent progress with physicaltherapy. She was released from the hospital 8 dayspostoperatively.At her 6-month follow-up, the patient was doingwell. She had suffered no complications of theprosthesis itself and was progressing well in physicaltherapy, with good return of function to heraffected hip. She had no long-term sequelae of herembolization event.DiscussionThe workup of a patient with acute onset of shortnessof breath after an orthopedic operative procedureshould include consideration of pulmonarythromboembolism and fat embolism as possiblecauses. Fat embolus is a common occurrence inmany orthopedic procedures. Although it has beendescribed extensively in the setting of long-bonefractures and multiple trauma, fat embolism syndromehas not been widely reported as a complicationof total hip arthroplasty.1,3–5In the patient described above, the diagnosis offat embolism syndrome was entertained after thepossibility of pulmonary thromboembolism wasruled out. The fat embolism syndrome was firstdescribed clinically by Von Bergmann,6 who caredfor a man with a broken femur and symptoms of thesyndrome in 1873. The prevalence of fat embolismsyndrome among all fracture patients is reported tobe between 0.25% and 1.25%.7 Among patientswith multiple bone fractures, the prevalence canreach 5% to 10%.8,9The pathophysiology of fat embolism syndromehas not yet been definitively characterized. A mechanicaltheory holds that the embolization eventresults from a transient rise in pressure in a fatcontainingcavity in association with torn bloodvessels, allowing escape of marrow or adipose fatcells into the circulation.10 Two alternative biochemicaltheories posit explanations for fat embolismsyndrome, both of which could account for theobservation of the syndrome in nontraumatic settings.In one, fat droplets already in the circulationare broken down at distal sites to free fatty acids,which then exert a local toxic effect on the tissues.This theory explains the appearance of petechiaeand the histologic changes in pneumocytes in associationwith fat-embolism–induced acute respiratorydistress syndrome (ARDS).11 The obstructiveexplanation for fat embolism syndrome proposesthat free fatty acids are mobilized by circulatingcatecholamines. Fat droplets in the circulationeventually coalesce and embolize, causing destructiveeffects.12Fat embolism syndrome can occur in immediateconjunction with a precipitating factor or it can bedelayed for up to 3 days, although 85% of cases areapparent within 48 hours.13 The diagnostic workupof a patient suspected of having fat embolism syndromeshould include serial arterial blood gas measurements,as hypoxemia is one of the cardinalfeatures. Serial chest radiographs can be used toobserve the progression of ARDS infiltrates in thelungs, although it should be noted that chest radiographicchanges are often not apparent in the initialstages of the syndrome. An ECG might show a newright bundle-branch block or nonspecific T-wavechanges. A late laboratory marker of fat embolismsyndrome is serum lipase, which becomes elevated3 to 5 days after embolization and peaks at 5 to 8days.Gurd and Wilson3 proposed the most widelyaccepted guidelines for the diagnosis of fat embolismsyndrome, which require at least one sign fromthe major and at least four signs from the minorcriteria (Table 1). An alternative set of standardswas later proposed by Lindeque et al,14 who believedthat the criteria of Gurd and Wilson weretoo restrictive. The criteria of Lindeque et al areseldom used among clinicians, in part because of
they are unable to distinguish fat embolism syndrome
from other causes of respiratory distress.15
The histologic diagnosis of fat embolism syndrome
relies on observing fat globules in vascular
spaces. This finding is most reliably obtained by a
biopsy of superficial cutaneous petechial lesions.
Fat globules can also be found in sputum and urine,
although this evidence is made more elusive by the
fact that fat must be actively circulating at the time
the sample is collected.
The treatment of fat embolism syndrome is primarily
supportive. As with other causes of ARDS,
maintaining adequate tissue oxygenation and an
arterial oxygen saturation of more than 90% should
be the clinician’s goal. The patient’s lung disease
might necessitate the use of positive airway pressure
or even mechanical ventilation. Because many
patients suffer fat embolism syndrome in conjunction
with multiple trauma, general supportive measures,
including hemodynamic stabilization, maintenance
of normal electrolyte values, and prompt
attention to orthopedic and soft-tissue injury
should be maintained.
The effects of steroids on patients with fat embolism
syndrome have long been debated in the
literature. The theoretical basis for using corticosteroids
is sound; they are thought to stabilize granulocyte
membranes, reduce catecholamine levels,
retard platelet aggregation, inhibit the activation of
complement system, and protect the capillary endothelium.
Corticosteroids have been shown to reduce
the incidence of fat embolism syndrome when
given prophylactically in the emergency department,
16 although data showing a therapeutic role
for them once clinically apparent fat embolism syndrome
has developed have remained elusive.
Orthopedic surgeons might be able to reduce
their patients’ risk of fat embolism syndrome. Early
fracture fixation has decreased the incidence of pulmonary
complications17 and fat embolism syndrome18
related to long-bone trauma. Using a distal
drain hole or a proximal and distal vacuum
during the cementing stage of total hip arthroplasty
has been associated with markedly reduced embolization.
Recent studies using ultrasound have detected
embolic events in routine total hip replacement
operations in 94% and 100% of patients
studied.1,19 No patients in either group, however,
showed clinically observable symptoms, underscoring
the complexity of the factors that contribute to
the genesis of the fat embolism syndrome.
It is thought that the technique used to cement
the intramedullary component of the prosthesis
causes embolic events during total hip arthroplasty.
5,20,21 In the traditional method, the femoral
canal is first reamed out. Next, glue is inserted into
the intramedullary canal, then the stem of the prosthesis.
This technique generates tremendous pressures
in the canal, which might cause the extravasation
of marrow or cement into the vasculature.
Use of a distal drain hole or vacuum greatly reduces
the intermedullary pressures during total hip arthroplasty.
Although such new approaches seem to
reduce a patient’s risk of fat embolism syndrome,
surgeons caution that operative techniques which
use a distal port might be associated with increased
incidence of cement failure and femoral shaft fracture.
Conclusion
Long thought to be a problem unique to trauma
patients, the fat embolism syndrome is common in
other settings as well (Table 2). In particular, it
should be considered in the differential diagnosis of
shortness of breath that occurs after any orthopedic
surgical procedure. It can be encountered in old
patients as well as young, and by family physicians
as well as surgeons and intensivists.

Fat Embolism: Diagnosis and Treatment

2010-06-16T09:55:00.001-07:00

Introduction
Fat embolism syndrome follows long bone fractures. Its classic presentation consists of an asymptomatic interval followed by pulmonary and neurologic manifestations combined with petechial hemorrhages. The syndrome follows a biphasic clinical course. The initial symptoms are probably caused by mechanical occlusion of multiple blood vessels with fat globules that are too large to pass through the capillaries. Unlike other embolic events, the vascular occlusion in fat embolism is often temporary or incomplete since fat globules do not completely obstruct capillary blood flow because of their fluidity and deformability. The late presentation is thought to be a result of hydrolysis of the fat to more irritating free fatty acids which then migrate to other organs via the systemic circulation.
Etiology
Many aspects of the fat embolism syndrome remain poorly understood, and disagreement about its etiology, pathophysiology, diagnosis and treatment persists. It is therefore difficult to determine the incidence of this complication. It ranges from less than 2% to 22% in different studies. Fat embolism has been associated with many nontraumatic disorders. It is most common after skeletal injury, and is most likely to occur in patients with multiple long bone and pelvic fractures. Patients with fractures involving the middle and proximal parts of the femoral shaft are more likely to experience fat embolism. Age also seems to be a factor in the development of FES: young men with fractures are at increased risk.
Fat embolism and FES are also more likely to occur after closed, rather than open, fractures. Two events promote entrance of marrow contents into the circulation following a fracture: movement of unstable bone fragments and reaming of the medullary cavity during placement of an internal fixation device. Both of these cause distortion of and increased pressure within the medullary cavity, permitting entry of marrow fat into torn venous channels that remain open even in shock because they are attached to the surrounding bone.
Multiple fractures release a greater amount of fat into the marrow vessels than do single fractures, increasing the liklihood of FES.
Pathophysiology
There are two theories which have gained acceptance:
1 The mechanical theory: FES results from physical obstruction of the pulmonary and systemic vasculature with embolized fat. Increased intramedullary pressure after injury forces marrow into injured venous sinusoids, from which the fat travels to the lung and occludes pulmonary capillaries. Fat emboli can cause cor pulmonale if adequate compensatory pulmonary vasodilation does not occur.
1 The biochemical theory: Circulating free fatty acids are directly toxic to pneumocytes and capillary endothelium in the lung, causing interstitial hemorrhage, edema and chemical pneumonitis.
It is also possible that coexisting shock, hypovolemia and sepsis, all of which reduce liver flow, facilitate the development of FES by exacerbating the toxic effects of free fatty acids.
Clinical Presentation
A thorough knowledge of the signs and symptoms of the syndrome and a high index of suspicion are needed if the diagnosis is to be made.
An asymptomatic latent period of about 12-48 hours precedes the clinical manifestations. The fulminant form presents as acute cor pulmonale, respiratory failure, and/or embolic phenomena leading to death within a few hours of injury.
Clinical fat embolism syndrome presents with tachycardia, tachypnea, elevated temperature, hypoxemia, hypocapnia, thrombocytopenia, and occasionally mild neurological symptoms.
A petechial rash that appears on the upper anterior portion of the body, including the chest, neck, upper arm, axilla, shoulder, oral mucous membranes and conjunctivae is considered to be a pathognomonic sign of FES, however, it appears late and often disappears within hours. It results from occlusion of dermal capillaries by fat, and increased capillary fragility.
CNS signs, including a change in level of consciousness, are not uncommon. They are usually nonspecific and have the features of diffuse encephalopathy: acute confusion, stupor, coma, rigidity, or convulsions. Cerebral edema contributes to the neurologic deterioration. Hypoxemia is present in nearly all patients with FES, often to a Pa02 of well below 60 mmHg. Arterial hypoxemia in these patients has been attributed to ventilation-perfusion inequality and intrapulmonary shunting. Acute cor pulmonale is manifested by respiratory distress, hypoxemia, hypotension and elevated central venous pressure.
The chest X-ray may show evenly distributed, fleck-like pulmonary shadows (Snow Storm appearance), increased pulmonary markings and dilatation of the right side of the heart.
Laboratory Tests
Laboratory tests are mostly nonspecific:

2010-06-13T11:18:00.001-07:00

Fat Embolism Syndrome

2010-06-13T10:53:00.000-07:00

Fat Embolism Syndrome
Description
Fat embolism syndrome (FES) occurs when embolic fat macroglobules pass into the small vessels of the lung and other sites, producing endothelial damage and resulting respiratory failure (ARDS-like picture), cerebral dysfunction and a petechial rash. It can be difficult to diagnose.The initial symptoms are probably caused by mechanical occlusion of multiple blood vessels with fat globules that are too large to pass through the capillaries. The vascular occlusion in fat embolism is often temporary or incomplete, as fat globules do not obstruct capillary blood flow completely because of their fluidity and deformability. The late presentation is thought to be a result of hydrolysis of the fat to more irritating free fatty acids which then migrate to other organs via the systemic circulation. It has also been suggested that paradoxical embolism occurs from shunting.
Aetiology
Fat embolism syndrome (FES) most often follows a closed fracture of a long bone but there are many other causes:
Fractures - closed fractures produce more emboli than open fractures. Long bones, pelvis and ribs cause more emboli. Sternum and clavicle furnish less. Multiple fractures produce more emboli
Orthopaedic procedures - most commonly intramedullary nailing of the long bones, hip or knee replacements
Massive soft tissue injury
Severe burns
Bone marrow biopsy
Nontraumatic settings occasionally lead to fat embolism. These include conditions associated with:
Liposuction
Fatty liver
Prolonged corticosteroid therapy
Acute pancreatitis
Osteomyelitis
Conditions causing bone infarcts, especially sickle cell disease
Epidemiology
The given incidence of this complication ranges from less than 2% to 22% in different studies. It varies considerably according to the cause. One large study found that patients with multiple fractures of the femur (excluding neck) were more likely to have fat embolism syndrome (FES) than those with isolated fractures (1.29% versus 0.54%). Patients with isolated fractures of the tibia and fibula had a lower incidence (0.30%) and patients with isolated fractures of the neck of the femur were even lower (0.06%). Minimal incidence was seen in isolated fractures of the pelvis, ribs, humerus, radius and ulna. Nonorthopaedic conditions rarely, if ever, were accompanied by FES.Men were more likely to develop the condition than women and it was rare in children aged 0 to 9 years. The age range most commonly affected was 10 to 39 years.
Presentation
There is usually a latent period of 24 to 72 hours between injury and onset. The onset is then sudden, with:
Breathlessness ± vague pains in the chest. Depending on severity this can progress to respiratory failure with tachypnoea, increasing breathlessness and hypoxia.
Fever - often in excess of 38.3°C with a disproportionately high pulse rate.
Petechial rash -commonly over the upper anterior part of the trunk, arm and neck, buccal mucosa and conjunctivae. The rash may be transient, disappearing after 24 hours.
Central nervous system symptoms, varying from a mild headache to significant cerebral dysfunction (restlessness, disorientation, confusion, seizures, stupor or coma).
Renal - oliguria, haematuria, anuria.
Drowsiness with oliguria is almost pathognomonic.
There is a fulminant form which presents as acute cor pulmonale, respiratory failure and/or embolic phenomena leading to death within a few hours of injury.4
Diagnostic criteria (combined from various sources)
Diagnostic criteria were first devised by Gurd and have been modified several times since. Major criteria
Respiratory insufficiency
Cerebral involvement
Petechial rash
Minor criteria
Tachycardia
Pyrexia (usually >39°C)
Confusion
Sustained pO2 <8 kPa
Sustained respiratory rate >35/minute, in spite of sedation
Retinal changes - cotton wool exudates and small haemorrhages, occasionally fat globules seen in retinal vessels
Jaundice
Renal signs
Thrombocytopenia
Anaemia
High ESR
Fat macroglobulinemia
Diffuse alveolar infiltrates 'snow storm appearance' on chest X-ray
Differential diagnosis
Dyspnoea, hypoxia and abnormal chest X-ray can occur with thromboembolism and pneumonia.
Investigations
Cytological examination of urine, blood and sputum may detect fat globules that are either free or in macrophages. This test has low sensitivity and a negative result does not exclude fat embolism.
The chest X-ray may show evenly distributed, fleck-like pulmonary shadows (snow storm appearance), increased pulmonary markings and dilatation of the right side of the heart.
Blood gases will show hypoxia, pO2 usually less than 8 kPa (60 mmHg) and hypocapnia. Continuous pulse oximeter monitoring may enable hypoxia from fat embolism to be detected in at-risk patients before it is clinically apparent (suggested by recurrent desaturations below 90%).
Platelets are reduced. Decreased haematocrit occurs within 24 to 48 hours and is attributed to intra-alveolar haemorrhage. Lipase is elevated but this is not pathognomonic, as it occurs in any bone trauma. Calcium is reduced.
Brain MRI scan may help in the diagnosis of cerebral fat embolism.
Transoesophageal echocardiograph (TEE) may be of value in detecting intraoperative release of marrow contents into the bloodstream during intramedullary reaming and nailing.
Management
Management of fat embolism syndrome (FES) is supportive and consists primarily of ensuring good arterial oxygenation. High flow rate of oxygen is given to maintain the arterial oxygen tension in the normal range. Restriction of fluid intake and the use of diuretics can minimise fluid accumulation in the lungs so long as circulation is maintained.On the other hand, maintenance of intravascular volume is important because shock can exacerbate the lung injury caused by FES. Albumin has been recommended for volume resuscitation in addition to balanced electrolyte solution, because it not only restores blood volume but also binds fatty acids and may decrease the extent of lung injury.Mechanical ventilation and positive end-expiratory pressure (PEEP) may be required to maintain arterial oxygenation.
Drugs
High-dose corticosteroids have been effective in preventing development of FES in several trials but controversy on this issue still persists. Lower doses may also be effective There is also dispute as to whether steroids are effective at all.
Surgical
Prompt surgical stabilisation of long bone fractures reduces the risk of the syndrome.
Prognosis
The mortality rate from fat embolism syndrome (FES) is 5 to 15%. Even severe respiratory failure associated with fat embolism seldom leads to death.
Neurological deficit and coma may last for days or weeks. Residual deficits may include personality changes, memory loss and cognitive dysfunction.
Pulmonary sequelae usually resolve completely within a year, although residual diffusion capacity deficits may exist.
Prevention
Early immobilisation of fractures seems to be the most effective way of reducing the incidence of this condition.
Historical
Fat embolism was first described as an autopsy finding by Zenker in 1862. In 1873 von Bergmann described it as a clinical syndrome for the first time.

Fat Embolism

2010-05-22T21:35:00.000-07:00

The quantity was referred to in the last program of the common ABC telly broadcast "House" and since then people somebody been really eager to cognise writer nigh the term. Considering the fact that friendly networking place Chirrup has transmute the most touristed modality of connexion, group are also tweeting on the subject.Thanks to the video periodical, fill are now conversation of modification caused by an nausea that was supposedly not regularize heard of before. According to examination history, fat embolism was rank perceived in the twelvemonth 1873. Doctors explained that the syndrome was the ending of an accruement of fat instruction globules in the rare tracts of the lungs which leads to breathing problems as the fat in the lungs coil the respiratory piece.Fat embolism according to doctors is a really extraordinary disease and is also real catchy to notice in a organism. Though the venture for the employment of such a disease may be a limited breakage, a paper unhealthiness, vaudevillian on the cutis or any respiratory disarray, more of us are quite unacquainted with the quantity. After the recent cite of fat interval by one of the characters in "House", the communal man seems to mortal turn addicted to the point and is on the track for sources which may helpfulness them to get a gambler statement of the medical statement, an statement that was not provided in the broadcast.In the closing programme of "House", the role of Hannah dies of fat embolism, which is caused by an amputation activity. Since then grouping hit been on the watch for an statement to fat interval.

Fat Embolism Syndrome in a Surgical Patient: Discussion

2010-05-21T06:20:00.000-07:00

The workup of a patient with acute onset of shortness of breath after an orthopedic operative procedure should include consideration of pulmonary thromboembolism and fat embolism as possible causes. Fat embolus is a common occurrence in many orthopedic procedures. Although it has been described extensively in the setting of long-bone fractures and multiple trauma, fat embolism syndrome has not been widely reported as a complication of total hip arthroplasty.
In the patient described above, the diagnosis of fat embolism syndrome was entertained after the possibility of pulmonary thromboembolism was ruled out. The fat embolism syndrome was first described clinically by Von Bergmann,who cared for a man with a broken femur and symptoms of the syndrome in 1873. The prevalence of fat embolism syndrome among all fracture patients is reported to be between 0.25% and 1.25%. Among patients with multiple bone fractures, the prevalence can reach 5% to 10%.
The pathophysiology of fat embolism syndrome has not yet been definitively characterized. A mechanical theory holds that the embolization event results from a transient rise in pressure in a fat-containing cavity in association with torn blood vessels, allowing escape of marrow or adipose fat cells into the circulation.Two alternative biochemical theories posit explanations for fat embolism syndrome, both of which could account for the observation of the syndrome in nontraumatic settings. In one, fat droplets already in the circulation are broken down at distal sites to free fatty acids, which then exert a local toxic effect on the tissues. This theory explains the appearance of petechiae and the histologic changes in pneumocytes in association with fat-embolism-induced acute respiratory distress syndrome (ARDS).The obstructive explanation for fat embolism syndrome proposes that free fatty acids are mobilized by circulating catecholamines. Fat droplets in the circulation eventually coalesce and embolize, causing destructive effects.
Fat embolism syndrome can occur in immediate conjunction with a precipitating factor or it can be delayed for up to 3 days, although 85% of cases are apparent within 48 hours. The diagnostic workup of a patient suspected of having fat embolism syndrome should include serial arterial blood gas measurements, as hypoxemia is one of the cardinal features. Serial chest radiographs can be used to observe the progression of ARDS infiltrates in the lungs, although it should be noted that chest radiographic changes are often not apparent in the initial stages of the syndrome. An ECG might show a new right bundle-branch block or nonspecific T-wave changes. A late laboratory marker of fat embolism syndrome is serum lipase, which becomes elevated 3 to 5 days after embolization and peaks at 5 to 8 days.
Gurd and Wilson proposed the most widely accepted guidelines for the diagnosis of fat embolism syndrome, which require at least one sign from the major and at least four signs from the minor criteria ( Table 1). An alternative set of standards was later proposed by Lindeque et al, who believed that the criteria of Gurd and Wilson were too restrictive. The criteria of Lindeque et al are seldom used among clinicians, in part because of they are unable to distinguish fat embolism syndrome from other causes of respiratory distress.
The histologic diagnosis of fat embolism syndrome relies on observing fat globules in vascular spaces. This finding is most reliably obtained by a biopsy of superficial cutaneous petechial lesions. Fat globules can also be found in sputum and urine, although this evidence is made more elusive by the fact that fat must be actively circulating at the time the sample is collected.
The treatment of fat embolism syndrome is primarily supportive. As with other causes of ARDS, maintaining adequate tissue oxygenation and an arterial oxygen saturation of more than 90% should be the clinician's goal. The patient's lung disease might necessitate the use of positive airway pressure or even mechanical ventilation. Because many patients suffer fat embolism syndrome in conjunction with multiple trauma, general supportive measures, including hemodynamic stabilization, maintenance of normal electrolyte values, and prompt attention to orthopedic and soft-tissue injury should be maintained.
The effects of steroids on patients with fat embolism syndrome have long been debated in the literature. The theoretical basis for using corticosteroids is sound; they are thought to stabilize granulocyte membranes, reduce catecholamine levels, retard platelet aggregation, inhibit the activation of complement system, and protect the capillary endothelium. Corticosteroids have been shown to reduce the incidence of fat embolism syndrome when given prophylactically in the emergency department, although data showing a therapeutic role for them once clinically apparent fat embolism syndrome has developed have remained elusive.
Orthopedic surgeons might be able to reduce their patients' risk of fat embolism syndrome. Early fracture fixation has decreased the incidence of pulmonary complications and fat embolism syndrome related to long-bone trauma. Using a distal drain hole or a proximal and distal vacuum during the cementing stage of total hip arthroplasty has been associated with markedly reduced embolization. Recent studies using ultrasound have detected embolic events in routine total hip replacement operations in 94% and 100% of patients studied. No patients in either group, however, showed clinically observable symptoms, underscoring the complexity of the factors that contribute to the genesis of the fat embolism syndrome.
It is thought that the technique used to cement the intramedullary component of the prosthesis causes embolic events during total hip arthroplasty. In the traditional method, the femoral canal is first reamed out. Next, glue is inserted into the intramedullary canal, then the stem of the prosthesis. This technique generates tremendous pressures in the canal, which might cause the extravasation of marrow or cement into the vasculature. Use of a distal drain hole or vacuum greatly reduces the intermedullary pressures during total hip arthroplasty. Although such new approaches seem to reduce a patient's risk of fat embolism syndrome, surgeons caution that operative techniques which use a distal port might be associated with increased incidence of cement failure and femoral shaft fracture.

Table 1. Criteria for Fat Embolism Syndrome by Gurd and Wilson
Major Criteria Minor Criteria
Petechiae in a vest distribution Tachycardia (heart rate > 110 beats per minute)
Hypoxemia with PaO2 <> 38.5°C)
FI02 < /= 0.4
Central nervous system depression Emboli visible in retina
disproportionate to hypoxemia
Pulmonary edema Fat in urine
Fat in sputum
Unexplained drop in hematocrit or platelet count
Increasing erythrocyte sedimentation rate
PaO
2
- arterial oxygen pressure, FIO
2
- forced inspiratory oxygen.

fat embolism syndrome

2010-05-19T05:35:00.000-07:00

Emboli composed of fat are common, relatively innocuous and may occur in alcoholism, BM biopsy, cardiopulmonary bypass, compression injury, DM, lymphangiography, pancreatitis, sickle cell anemia, corticosteroid therapy; contrarily, the FES is neither common nor trivial; clinically significant FE may be endogenous or exogenous in origin; most are due to major fractures, especially of long bones, and trauma to parenchymal organs–eg, the liver–most deaths in the immediate post-trauma period have significant fat embolism, burns, blast injury, severe infections, especially α-toxin-producing Clostridium spp Clinical Hypoxia–50% of femoral shaft fractures have ↓ arterial PO2 within the first few days, acute onset of dyspnea, tachypnea, cyanosis, tachycardia with sudden onset of right-sided cardiac failure, showers of petechiae, thrombocytopenia, cerebral embolism–with changes in personality, confusion, drowsiness, weakness, agitation, spasticity, defects of the visual field, and rarely, extreme pyrexia Diagnosis It had been reported that fat droplets in a BAL was indicative of fat embolism, a finding which in one small–34 group of Pts proved to have a low specificity of 26.5%; > 3% oil red O positive macrophages in the BAL are often found in trauma Pts, and may indicate FES or silent FE Treatment No therapy is effective.

fat embolism

2010-05-18T05:51:00.000-07:00

embolism /em·bo·lism/ (em´bŏ-lizm) the sudden blocking of an artery by a clot or foreign material which has been brought to its site of lodgment by the blood current.

air embolism that due to air bubbles entering the veins from trauma, surgical procedures, or severe decompression sickness.
cerebral embolism embolism of a cerebral artery.
coronary embolism embolism of a coronary artery.
fat embolism obstruction by a fat embolus, occurring especially after fractures of large bones.
miliary embolism embolism affecting many small blood vessels.
paradoxical embolism blockage of a systemic artery by a thrombus originating in a systemic vein that has passed through a defect in the interatrial or interventricular septum.
pulmonary embolism obstruction of the pulmonary artery or one of its branches by an embolus.
fat embolism n.
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.

X-ray Image of Fat Embolism

2010-05-18T05:46:00.000-07:00

Fat embolism in a 58-year-old woman who presented with sudden dyspnea. The patient had undergone intramuscular injection of some fatty materials into the buttock several days earlier. (a) Radiograph shows bilateral ground-glass areas of increased opacity. (b) Thin-section (1-mm collimation) CT scan obtained at the level of the aortic arch shows widespread patchy ground-glass attenuation and consolidation. A follow-up radiograph obtained 10 days later (not shown) revealed complete resolution of the ground-glass patterns.
But what is Fat Embolism?
Fat Embolism is an infrequent complication of long bone fracture, occurring in 1%–3% of patients with simple tibial or femoral fractures but in up to 20% of individuals with more severe trauma. Less common causes include hemoglobinopathy, major burns, pancreatitis, overwhelming infection, tumors, blood transfusion, and liposuction. The mechanisms are not completely understood but presumably are twofold. The first mechanism is the production of free fatty acids, which initiates a toxic reaction in the endothelium. The process is further complicated by the accumulation of neutrophils and other inflammatory cells, which causes damage to the vasculature. The second mechanism is the mechanical obstruction of the pulmonary vasculature by fat globules and aggregates of red blood cells and platelets.

Fat Embolism: The News

2010-05-18T05:43:00.000-07:00

Fat obstruction: mean? - Many people now look for the word "fat clogged" after seeing last season House '. After searching it seems that obstruction in the lipid environment into the circulatory system of physical injury or surgery. One of the most common examples of fats clog occurs when the fracture Fat obstruction that occurs when the body fat in the blood flow and cause difficulties. Symptoms fatty obstruction of medical education, including lung, skin and nervous system, hematology I think this is one of the consequences is fat We will take care of their health, especially broken bones or injuries, or our Below is a picture of fatty blockages. You can see clearly the accumulation of fat in the blood drops causing serious disease.

Fat Embolism: Things to Know About Fat Embolism

2010-05-18T01:50:00.000-07:00

Fat Embolism: What Does It Mean? – A lot of people are now looking for the phrase “Fat Embolism” after watching House’ season finale.

After researching for it, it turns out that Fat Embolism is a condition where in fats enter the circulatory system because of a physical trauma or a surgery. One of the most common examples of a fat embolism happens when a bone was fractured. The Fat Embolism here happens when fatty bone marrow enters the blood stream and causes blockage to the continuous blood flow.

Symptoms of Fat Embolism according to medical studies include pulmonary, neurological, dermatological, and haematological conditions. I guess this is one of the consequences of being fat. Therefore, we should then take good care of our health most especially our bones not to have fractures or trauma.

Below is an picture of a Fat Embolism. You can clearly see the accumulation of fat globules in the blood stream which can cause severe health conditions.