Conference Lectures

           Dr. Gurumoorthi P
FAT EMBOLISM SYNDROME(FES)-AN UPDATE
Fat embolism refers to the presence of fat droplets within the peripheral and lung microcirculation with or without clinical sequelae. However, not all fat emboli progress to FES.The clinical signs and symptoms of FES are nonspecific. Bergman's Triad: dyspnea,neurologic impairment,petechial rash.The differential diagnosis for each of these signs can be broad, and typically the diagnosis of FES is a diagnosis of exclusion.
Three criteria used to define fat embolism syndrome
1.Gurd and Wilson (FES = 1 major + 4minor + fat microglobulinemia)
Major criteria
Respiratory insufficiency,Cerebral involvement, Petechial rash
Minor criteria
Pyrexia,Tachycardia,Retinal changes,Jaundice,Renal changes(anuria or  liguria) Thrombocytopenia (a drop of>50% of the admission thrombocyte value)High erythrocyte sedimentation rate, Fat macroglobulinemia
2.Schonfeld’s criteria (FES = 5 or more points)
Diffuse petechiae (5 points)Alveolar infiltrates (4 points)
Hypoxemia (<70 mm Hg) (3 points)Confusion (1 point)
Fever 38 ⁰C
Heart rate >120/min
Respiratory rate >30/min
3.Lindeque criteria ( FES= femur fracture+or - tibia fracture +1 feature)
A sustained PaO2 <60 mm Hg
A sustained PaCO2 >55mmHg) or pH <7.3
A sustained respiratory rate >35/min even after adequate sedation
Increased work of breathing judged  by dyspnea, use of accessory muscles,tachycardia and anxiety.

Risk factors for fat embolism syndrome
General factors
Males,Age 10–39 yrs,Posttraumatic hypovolumic state,Reduced cardiopulmonary reserve
Injury-related factors
Multiple fractures,Bilateral femur fractures,Femur shaft fractures,Lower extremity fractures,Traumatic fractures,Concomitant pulmonary injury
Surgery-related factors
Intramedullary reamed and unreamed nailing after femoral fracture, Joint replacement after femoral fracture, Bilateral procedures, Joint replacement with high-volume prosthesis
CLINICAL PRESENTATION
FES usually manifests as a multisystem disorder. A latent period of 12 to 48 hours may precede any clinical manifestations.
Respiratory
Up to 75% of patients presenting with FES have some degree of respiratory dysfunction,ranging from tachypnea and mild hypoxemia to respiratory failure requiring ventilator support.
Central Nervous System
Perioperative central nervous system dysfunction is yet another nonspecific sign of FES. In an awake patient, cerebral signs are usually nonspecific,nonlateralizing and mimic diffuse encephalopathy.Fortunately these neurologic changes are usually reversible.
Cardiovascular
Cardiovascular changes after pulmonary fat embolization are characterized by an increase in pulmonary artery pressure, systemic arterial hypotension, a decrease in cardiac output, and arrhythmias
Skin
Petechial rash is also associated with FES in 25% to 95% of cases. However, the rash is typically located on the upper anterior torso, and is also evident on oral mucous membranes, conjunctiva, skin folds of the neck, and axillae. The rash tends to be transient and disappears within 24 hours. This condition is due to engorgement of dermal vessels and increased endothelial fragility, as well as platelet damage resulting from FFAs.
Eyes
Retinopathy has been reported in 50% of patients with FES and in 4% of patients with long bone fractures presenting with a subclinical syndrome.Typical lesions consist of cotton-wool spots and flamelike hemorrhages, and are attributed to microvascular injury and microinfarction of the retina. Retinal lesions disappear after a few weeks, although scotomas may persist.
Platelets
Thrombocytopenia (platelet count <150,000/ml) and unexplained anemia are not uncommon. A correlation has been demonstrated between increases in A-a gradient and thrombocytopenia, even in asymptomatic fracture patients the diagnosis of FES is based on a constellation of clinical and laboratory findings, and exclusion of other potential diagnoses.
Laboratory Tests
Blood gas analysis
Arterial Blood gas analysis initially reveals hypoxia with hypocarbia and respiratory alkalosis. Later on, as respiratory muscle fatigue develops, there may be carbon dioxide retention and respiratory acidosis. An increased alveolar- arterial shunt fraction, in the absence of ARDS, within 24-48 h of a potentially causative event is strongly suggestive of FES.
Imaging studies
Chest XRay-Diffuse, evenly distributed interstitial and alveolar densities are typical findings. Patchy infiltrates in the perihilar and basilar areas resemble pulmonary edema, without vascular congestion and cardiomegaly.
Comparable changes on the computed tomography (CT) scan can also be seen with multiple mottled perfusion defects. Ventilation-perfusion scans also demonstrate subsegmental perfusion defects, and are highly suggestive of clinical note.
MRI of the brain seems to be more sensitive in detecting abnormalities in patients with FES.MRI brain T 2 weighted images show areas of high intensity early in the course of FES.  Many FES cases with normal brain CT have been found to have small cerebral infarctions on MRI. Fat embolism syndrome lesions are characteristically located deep in the white matter, brain stem and cerebellum ganglia. In cases where MRI of brain is totally normal, a diagnosis of brain FES can be safely excluded.  MRI Brain can also be used in follow up of patients as an improvement in images is always associated to a clinical improvement.
Fat globules in BAL(broncho alveolar lavage) may signify circulating fat globules of fat embolism and need not point on to FES. The absence of fat globules in BAL macrophages has a high negative predictive value and may help in ruling out fat embolism. Fat droplets in BAL have also been reported in patients with sepsis, hyperlipidemia, and patients on lipid infusions
MANAGEMENT
There is no definitive therapy for FES.
Before any clinical syndrome develops, it is possible to initiate certain measures that may prevent or decrease the severity of FES. Early stabilization of the fracture involving the pelvis or long bones is probably the single most important prophylactic measure that has been shown to result in a decrease in the incidence of FES.
The use of preventative pharmacologic therapies has been disappointing.It has been shown that in those patients who are likely to develop FES preoperatively,are also likely to experience exacerbations intraoperatively. Some institutions delay any definitive operative fixation until clinical improvement has been observed.One alternative is to stabilize fractures by external fixation (if possible) initially and then perform the definitive fixation once the clinical situation allows.Although early stabilization of fractures is the preferred option in uncomplicated cases, it is unclear whether this is an optimal option in patients who are already showing signs of FES or have sustained significant trauma and lung contusion.
Although the signs of intraoperative FES can be nonspecific, sudden development of cardiopulmonary instability, pulmonary edema that is temporarily related to fracture manipulation, and intramedullary nailing of long bone fractures should alert the clinician to the possibility of FES.Careful surgical technique that focuses on limiting the medullary canal pressurization associated with reaming is helpful.Lavaging the marrow before inserting the prosthesis similarly may decrease the amount of marrow available for embolization.Venting before the insertion of prosthesis has also been suggested as one strategy to decrease intramedullary pressure and the incidence of FES.
Albumin for volume resuscitation is recommended because it helps in restoring euvolumia and also binds to free fatty acids and reduces further injury of lungs.Although various agents (aspirin, hypertonic saline, low molecular weight dextran,and steroids) have all been suggested, none have been definitively proven to help.Though the role of steroids is controversial,during early stage of FES, low dose methyl prednisolone (6mg/kg/day for 3 days)has role in preventing the hypoxia.Once the syndrome develops, the clinical dysfunction is treated symptomatically. Initial respiratory dysfunction is managed using supplemental oxygen to prevent hypoxemia. Respiratory failure (ARDS/ALI) is managed by ventilator support modes.
 1. Spontaneous ventilation
The initial management of hypoxia associated with pulmonary fat embolism should be spontaneous ventilation. Oxygen inhalation using facemask and highflow gas delivery system can be used to deliver FIO2 of 50 – 80%.
2. CPAP and noninvasive ventilation
CPAP may be added to improve PaO2 without increasing FIO2.Mechanical ventilation may also be applied via CPAP mask and has been used successfully in patients.
3. Mechanical ventilation and PEEP
If a FIO2 of >60% and CPAP of > 10 cm are required to achieve a PaO2 > 60mm Hg, then endotracheal intubation, mechanical ventilation with PEEP should be considered.The use of steroids in the treatment of FES is controversial and is not supported by large, randomized control trials. Inotropes (epinephrine, norepinephrine,vasopressin, phenylephrine) and fluids are typically used to manageintraoperative hypotension and cardiovascular collapse. Management of right heart failure secondary to increased pulmonary hypertension is challenging. In addition to inotropic support, it may require specific pulmonary vasodilators. There are reports showed that patients with fulminant FES with cardiovascular collapse successfully resuscitated by using PCPS(percutaneous pulmonary support) and administration of PGE1.
ANAESTHETIC CONSIDERATIONS
No significant differences have been noted in FES outcomes in patients receiving general or regional anesthesia. Although the incidence of deep vein thrombosis is decreased with regional anesthesia, the choice of anesthetic should be decided by the clinical condition of the patient.
Anesthesiologists occasionally may encounter mental status changes, significant emergence delirium, irritability, and confused state in the postoperative care unit or postoperatively. In the appropriate clinical setting,the diagnosis FES must be entertained, and patients should be evaluated with an MRI scan to rule out FES. Management of cerebral dysfunction is primarily supportive, with the aim of optimizing the intracranial pressure, cerebral perfusion pressure and oxygen delivery.