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Fat embolism Syndrome
- 1. FAT EMBOLISM SYNDROME DR. PRAMESH PRASAD SHRESTHA FCPS RESIDENT DEPARTMENTOF ORTHOPEDICS
- 2. HISTORY 1861The condition was first diagnosed by Zenker. 1865,Wagner described the correlation of fat embolism with fractures, and attributed the origin of fat in the lungs to the bone marrow 1873,Von Bergmann is considered the first individual to clinically diagnose fat embolism Friedrich Albert von Zenker 13 March 1825 - 13 June 1898 Zenker FA. Beitrage zur anatomie und physiologie der lunge. J Braunsdorf 1861.
- 3. DEFINITION Fat embolism refers to the presence of fat droplets within the microcirculation with or without clinical sequelae Fat Embolism Syndrome (FES) is a clinically relevant syndrome that occurs in the presence of intravasation of fat in the pulmonary tree, and is characterized by clear signs and symptoms. NOT ALL PATIENTS WITH FAT EMBOLISM DEVELOP FES Only 3 – 5 % of all patients with long bone fractures develop FES.
- 4. FAT EMBOLISM SYNDROME Clinical diagnosis Mostly associated with long bone and pelvic fractures More in closed fractures than open fractures Chances increases with number of fractures Onset 12-72 hours on initial trauma Presence of 20-50ml of fat globules is required in the blood stream Mortality: 5-15%
- 5. ETIOLOGY Trauma (95%) Fractures Orthopedic procedures Soft tissue injuries Burns Liposuctions Bone marrow harvesting and transplant Extracorporeal Membrane Oxygenation
- 6. ETIOLOGY NonTrauma (5%) • Pancreatitis • Diabetes Mellitus • Osteomyelitis • Panniculitis • Bone tumor lysis • Sickle cell hemoglobinopathies • Alcoholic Fatty liver disease • Lipid Infusion • Intraosseous infusion • Steroid therapy
- 7. RISK FACTORS General Factors • Males • Age 10-39Y • Post traumatic hypovolemic state • Reduced cardiopulmonary reserve • Preexisting vascular condition Injury related Factors • Multiple Fractures • Low Extremity Fractures • Femur Shaft Fractures • Concomitant Pulmonary Injury Surgery Related Factors • Intramedullary Nails • Joint Replacement surgeries • Bilateral Procedures • HighVolume Prosthesis Stein PD, et al. Fat embolism syndrome. Am J Med Sci 2008;336(6):472–7.
- 8. PATHOPHYSIOLOGY UNKNOWN 3 theories are proposed MechanicalTheory (Gauss’Theory) BiochemicalTheory (Lehmann and Moore’sTheory) CoagulationTheory
- 9. PATHOPHYSIOLOGY Mechanical Theory (Gauss’Theory) Fat from marrow directly passes into the blood stream Increase in intramedullary pressure forces marrow particles, fat, or bone fragments into the circulation Normal Intramedullary pressure : 65 mmHg Gauss H.The pathology of fat embolism. Arch Surg. 1924;9:592–605
- 13. PATHOPHYSIOLOGY Biochemical Theory (Lehmann and Moore’sTheory) Fat embolus is broken down by Lipoprotein Lipase in the blood and form FFA FFA is directly damages the pneumocytes and lung endothelial cells, increasing lung permeability Results inARDS and pulmonary edema Lehman, E.P. and Moore, R.M. (1927) Fat embolism including experimental production without trauma. Arch. Surg., 14: 621
- 14. PATHOPHYSIOLOGY Coagulation theory Tissue thromboplastin is released with marrow elements following long bone fractures. Activates intravascular coagulation Fibrin and fibrin degradation products, leukocytes, platelets and fat globules combine to increase pulmonary vascular permeability Results inARDS Soloway HB, Robinson EF. The coagulation mechanism in experimental pulmonary fat embolism. J Trauma 1972; 12:630-31
- 16. CLINICAL FEATURES DIAGNOSIS IS ALWAYS CLINICAL AND NOT CHEMICAL Typically manifests 12-72 hours after trauma Extremely heterogeneous pattern of presentation, therefore, the precise diagnosis continues to be elusive
- 17. SYMPTOMS Rapid breathing Shortness of breath Mental Confusion Lethargy Decreased consciousness Skin rashes Fever
- 18. PULMONARY SIGNS 75% of patients with FES Tachypnea Hypoxia, Rales, Pleural friction rub Auscultation: Loud harsh breath sounds with crepitus and wheeze 50% of patients who develop FES may requires Mechanical ventilation Bulger,Archives of Surgery 1997; 132: 435-9
- 19. CHEST RADIOLOGY Normal in most cases Chest X-ray: “Snow Storm Appearance” HRCT of Chest: Ground Glass Opacities
- 20. CHEST RADIOLOGY Normal in most cases Chest X-ray: “Snow Storm Appearance” HRCT of Chest: Ground Glass Opacities
- 21. NEUROLOGY SIGNS Usually occur after pulmonary signs Occurs in 80% of patients with FES Usually minor symptoms are present: Drowsiness, anxiety, restlessness and rigidity But may progress: Seizures, Stupor, Confusion and coma. Neurological signs are attributed to cerebral edema secondary to hypoxia, or ischemia due to fat embolism or due to damage of cerebral vessels by FFAs and other inflammatory molecules Butteriss DJ, et al. Reversible cytotoxic cerebral edema in cerebral fat embolism. AJNR Am J Neuroradiol 2006;27(3):620–3.
- 22. BRAIN RADIOLOGY NCCT head: Normal in most cases MRI Brain: DWI: early (most common at 1-4 days): scattered punctate foci of cytotoxic edema (starfield pattern) Later (most common at 5-14 days): confluent areas of cytotoxic edema in the white matter SWI Wallnut KernelAppearance
- 23. BRAIN RADIOLOGY NCCT head: Normal in most cases MRI Brain: DWI: early (most common at 1-4 days): scattered punctate foci of cytotoxic edema (starfield pattern) Later (most common at 5-14 days): confluent areas of cytotoxic edema in the white matter SWI Wallnut KernelAppearance
- 24. OTHER SIGNS Skin: Petechial Rashes Pathognomic, along with respiratory and neurological symptoms Occurs in 20-50% of patients with FES Can occur anywhere in the body, main in the eyes, axilla and neck Cardiovascular Right heart failure, usually secondary to pulmonary hypertension Eyes: Retinopathy (50%) Cotton wool lesions, flame like hemorrhages
- 25. TRIAD OF FAT EMBOLISM SYNDROME Fat Embolism Syndrome Hypoxia Neurological Abnormalities Petechial Rashes
- 26. DIAGNOSIS Based on a constellation of clinical signs, laboratory findings and exclusion of other diseases Lab tests Arterial blood gas analysis PaO2 <60mmHg Thrombocytopenia UnexplainedAnemia Urine Cytology: Fat globules Peripheral blood smear: Fat Globules Sputum: Fat Globules Signify fat embolus, but does not indicate Fat Embolism Syndrome
- 27. DIAGNOSIS Bronchoalveolar Lavage Quantification of cells containing fat droplets in bronchial alveolar lavage (BAL) fluid within the first 24 hours after trauma have also been shown to correlate with clinical fat embolism in some studies. >30% of macrophages laden with fat globules in BAL fluid is highly suggestive of FES • Mimoz O, Edouard A, Beydon L, et al. Contribution of bronchoalveolar lavage to the diagnosis of posttraumatic pulmonary fat embolism. Intensive Care Med 1995;21(12):973–80. • Chastre J, Fagon JY, Soler P, et al. Bronchoalveolar lavage for rapid diagnosis of the fat embolism syndrome in trauma patients.Ann Intern Med 1990;113(8): 583–8.
- 28. GURD ANDWILSON’S CRITERIA Gurd AR. Fat embolism:An aid to diagnosis. J Bone Joint Surg Br. 1970; 52:732–7 Gurd AR,Wilson RI.The fat embolism syndrome. J Bone Joint Surg Br. 1974; 56B:408–16 Major Criteria Respiratory Insufficiency Cerebral involvement Petechial rash Minor Criteria Pyrexia Tachycardia Retinal Changes Jaundice Renal Changes (Anuria/Oliguria) Thrombocytopenia (A drop of >50% of admission thrombocytes) High ESR Fat macroglobulinemia
- 29. SCHONFELD’S SCORING SYSTEM Also known as Fat Embolism Index Schonfeld’s Scoring System (Fat Embolism Index) Diffuse Petechiae 5 points Alveolar infiltrates 4 points Hypoxemia (<70mmHg PaO2) 3 points Confusion 1 point Fever >38°C 1 point Heart Rate >120/min 1 point Respiratory Rate >30/min 1 point Schonfeld SA, PloysongsangY, DiLisio R, Crissman JD, Miller E, Hammerschmidt DE, et al. Fat embolism prophylaxis with corticosteroid:A prospective study in high-risk patients. Ann Intern Med. 1983;99:438–43
- 30. LINDEQUE’S CRITERIA Femur Fracture ±Tibia Fracture + 1 feature A Sustained PaO2 <60mmHg 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 Lindeque BG, Schoeman HS, Dommissen GF, Boeyens MC,Vlok AL. Fat embolism syndrome: A double blind therapeutic study. J Bone Joint Surg Br. 1987;69:128–31.
- 31. SEVITT’S CLASSIFICATION 1. Subclinical FES (Incomplete and Partial Syndrome) 2. Non Fulminant FES (the Classical Syndrome) 3. Fulminant FES (Fulminating Cases) Sevitt S.The significance and classification of fat-embolism. The Lancet. 1960 Oct 15;276(7155):825-8. • 3 Days after trauma • Probably occurs in almost all long bone fractures of Lower extremity • Decrease in PaO2, Platelet counts and Hemoglobin • No clinical signs or symptoms 1. Subclinical FES (Incomplete and Partial Syndrome) 2. Non Fulminant FES (the Classical Syndrome) 3. Fulminant FES (Fulminating Cases)
- 32. SEVITT’S CLASSIFICATION 1. Subclinical FES (Incomplete and Partial Syndrome) 2. Non Fulminant FES (the Classical Syndrome) 3. Fulminant FES (Fulminating Cases) Sevitt S.The significance and classification of fat-embolism. The Lancet. 1960 Oct 15;276(7155):825-8. • Any time up to 6 days after trauma • Clinical signs and symptoms are clearly evident 1. Subclinical FES (Incomplete and Partial Syndrome) 2. Non Fulminant FES (the Classical Syndrome) 3. Fulminant FES (Fulminating Cases)
- 33. SEVITT’S CLASSIFICATION 1. Subclinical FES (Incomplete and Partial Syndrome) 2. Non Fulminant FES (the Classical Syndrome) 3. Fulminant FES (Fulminating Cases) Sevitt S.The significance and classification of fat-embolism. The Lancet. 1960 Oct 15;276(7155):825-8. • Occurs suddenly and progresses rapidly, often resulting in death, within few hours of initial trauma • Clinical Features of ARDS, Cor pulmonale and neurological changes present • Rapidly progresses and death is usually inevitable 1. Subclinical FES (Incomplete and Partial Syndrome) 2. Non Fulminant FES (the Classical Syndrome) 3. Fulminant FES (Fulminating Cases)
- 34. MANAGEMENT No Definitive therapy Treatment is largely supportive Prevention is better than Cure
- 35. PREVENTIVE MEASURES AVOIDTRAUMA Early stabilization of the fracture Preventative pharmacologic therapies has limited role Preventive measures in Surgery: Cementless prostheses, Bone vacuum cementing techniques, less reaming Venting/ drilling the cortex to prevent high intramedullary pressure Marrow Lavage Svenningsen S, et al. Prevention of fat embolism syndrome in patients with femoral fractures— immediate or delayed operative fixation? Ann Chir Gynaecol 1987;76(3):163–6.
- 36. PREVENTIVE MEASURES Albumin: Albumin has been recommended for volume resuscitation Restores blood volume Binds fatty acids and may decrease the extent of lung injury. MG Abbott. Fat embolism syndrome : An in-depth review. Asian Journal of Critical Care 2005;1:19-24.
- 37. MEDICAL MANAGEMENT Corticosteroids: Anti-Inflammatory: reduces peri-vascular hemorrhage and edema Mainly as a prophylactic measure Initiation after development of FES unclear High-dose Methylprednisone (90 mg/kg over 4 days) or a lower dose prophylactically (6 mg/kg over 2 days) has shown some clinical efficacy in improving outcomes Amandeep Gupta, Charles S. Reilly. Fat Embolism. Cont Edu Anaesth Crit Care & Pain 2007;7:148-51 Babalis GA, et al. Prevention of posttraumatic hypoxaemia in isolated lower limb long bone fractures with a minimal prophylactic dose of corticosteroids. Injury 2004;35(3):309–17
- 38. TREATMENT SUPPORTIVE: ABC Adequate Oxygenation IV Access, peripheral or central (Correct fluid deficit) Consider NG intubation to aspirate gastric content to prevent aspiration and causing ARDS. Monitor: Vitals Strict: I/O chart: maintain output 50-100 ml/hr. CVP monitoring to avoid fluid overload ABG monitoring
- 39. MEDICAL MANAGEMENT Many drugs have been tried, with limited to no demonstrable benefits Aspirin Has been shown to normalize blood gas, coagulation proteins, and platelet count Amandeep Gupta, Charles S. Reilly. Fat Embolism. Cont Edu Anaesth Crit Care & Pain 2007;7:148-51
- 40. MEDICAL MANAGEMENT Heparin Imitates lipase activity, that may destroy fat globules, (solves Mechanical theory) Use is controversial, as the destroyed fat globules may give rise to FFA and cause more harm (may cause Biochemical theory) Possibility of increased risk of bleeding Amandeep Gupta, Charles S. Reilly. Fat Embolism. Cont Edu Anaesth Crit Care & Pain 2007;7:148-51
- 41. MEDICAL MANAGEMENT N-acetylcysteine: In animal study, N-acetylcysteine reduced the severity of Acute Lung Injury caused by Fat embolism Ethanol: Lipase inhibitor, prevents formation of FFA Liu DD, Kao SJ, Chen HI. N-Acetylcysteine attenuates acute lung injury induced by fat embolism. Crit Care Med 2008;36(2):565–71.
- 42. MEDICAL MANAGEMENT Hypertonic Glucose: Blocks mobilization of FFA Sildenafil: has been shown to prevent an increase in pulmonary pressures after bone marrow embolization in one experimental model Krebs J, et al. Sildenafil prevents cardiovascular changes after bone marrow fat embolization in sheep. Anesthesiology 2007;107(1):75–81.
- 43. VENTILATION SpontaneousVentilation: Initially with face masks, high flow masks Target FiO2: 50 – 80%
- 44. VENTILATION CPAP and Non invasiveVentilation Increases PaO2 without increasing FiO2 Mechanical Ventilation 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
- 45. PROGNOSIS The duration of FES is difficult to predict. Prognosis is good except in fulminant cases. Most morbidity is associated with Pulmonary dysfunction Residual neurologic deficits and residual diffusion capacity deficits may persist. Mortality is estimated to be 5-15% overall, but most patients will recover fully.
- 46. TAKE HOME MESSAGE FAT EMBOLISM SYNDROME is a poorly understood disease However, its consequences are well recognized Mainly associated with long bone fractures, therefore is mostly encountered by Orthopedic surgeons. Prevention is the best way to deal with FES Treatment is mainly supportive
Hinweis der Redaktion
- Starting from the beginning, Fat embolism was first diagnosed by a german pathologist Friedrich Albert von Zenker, during an autopsy in 1861 A few years later, in 1865 Wagner described the correlation of fat embolism with fractures, and attributed the origin of fat in the lungs to bone marrow Then again in 1873, Von Bergmann was able to diagnose Fat embolism clinically.
- Fat embolism refers to the presence of fat droplets within the microcirculation with or without clinical sequelae And can be seen in up to 90% of all long bone fractures Fat Embolism Syndrome (FES) is a clinically relevant syndrome that occurs in the presence of intravasation of fat in the pulmonary tree, and is characterized by clear signs and symptoms.
- Now coming to the overview of Fat embolism syndrome, It a clinical diagnosis, mostly associated with long bone fracture of the lower limb and pelvic fractures. Seen more in closed fractures than open fracture, Usually seen 12-72 hours after trauma, rare beyond this range, however, if present before 12 hours, it is usually fulminant type. One Femur of adult contains 70-100ml of fat, and presence of only 20-50 ml of fat in the circulation is sufficient to cause Fat embolism syndrome Mortality rate is around 5-15%
- Cause of Fat embolism syndrome can be divided into Traumatic and Non traumatic. Traumatic causes contributes to 95% of total cases. And these can be because of…
- Non traumatic causes contributes to 5% of total cases,
- Male are 4 times more likely to develop FES than females Rare in <10 years and >40 years. Low fat content in bones of young children, Hypovolemic state results in higher concentration of fat in the blood stream. Pre existing vascular conditions such as atherosclerosis and reduced cardiopulmonary reserve tends to increase the chances of development of FES Multiple fractures, mainly of the long bones of lower extremities, and even among them, Femur fractures are known for their tendency in development of FES. Concommitant pulmonary injury along with these facture, leads to even higher chances of development of FES. Following the fractures, there is a high chance of development of FES after orthopedic surgery such as Intramedullary nails, Joint replacement, procedures in bilateral limbs and high volume prosthesis.
- The exact mechanism of the disease process is unknown, however 3 theories has been proposed and I will be going through them individually
- The Mechanical theory was proposed by Gauss in 1924 According to this theory, Fat from the marrow directly passes into the blood stream after fractures. Also increase in Intramedullary pressure, forces marrow particles, fat or bone fragments into the circulation during orthopedics procedures. The normal intramedullary pressure is 65mmHG and it can increase up to 500 mmHg during intramedullary nailing and up to 1400 mmHg during Hip Arthroplasty.
- IN pre operative state: long bone contains yellow bone marrow, filled with adipose tissue containing fat Following trauma when there is a fracture, the fat in the marrow sips into the circulation forming a fat embolus which can be 10 – 40 um in diameter The embolus reaches the heart and the lungs (most commonly) where there are small capillaries measuring <20um. In vessels with pre existing atherosclerosis or because of narrow lumen, the fat embolus gets impacted, obstructing the vessel and giving rise to symptoms
- IN pre operative state: long bone contains yellow bone marrow, filled with adipose tissue containing fat Following trauma when there is a fracture, the fat in the marrow sips into the circulation forming a fat embolus which can be 10 – 40 um in diameter The embolus reaches the heart and the lungs (most commonly) where there are small capillaries measuring <20um. In vessels with pre existing atherosclerosis or because of narrow lumen, the fat embolus gets impacted, obstructing the vessel and giving rise to symptoms
- IN pre operative state: long bone contains yellow bone marrow, filled with adipose tissue containing fat Following trauma when there is a fracture, the fat in the marrow sips into the circulation forming a fat embolus which can be 10 – 40 um in diameter The embolus reaches the heart and the lungs (most commonly) where there are small capillaries measuring <20um. In vessels with pre existing atherosclerosis or because of narrow lumen, the fat embolus gets impacted, obstructing the vessel and giving rise to symptoms
- In 1927, Lehmann and Moore proposed the biochemical theory. According to this theory, the fat globules that passes in to the circulation is acted upon by lipoprotein lipase which is released during inflammatory process, which then form FFA…
- Then in 1972, Soloway and Robinson proposed the Coagulation theory, and according to this theory, Tissue thromboplastin is released along with marrow elements following bone fractures and activates intravascular coagulation cascade, leading to production of Fibrin, fibrin degradation products, leukocytes, platelets and fat globules which combine to increase the pulmonary vascular permeability, resulting in pulmonary edema, and ARDS
- In all proposed theory, the primary organ to be involved in the lungs, however, Fat embolism syndrome can affect other organ systems as well. In the lungs, it causes V/Q mismatch leading to decrease in PaO2, ARDS causing respiratory failure and Acute Pulmonary hypertension causeing right heart failure From the lungs, the fat emboli may pass into the systemic circulation. however The exact pathway of transfer of embolusfrom pulmonary to systemic circulation is unknown. it is thought to be from bronchopulmonary shunt, patent foramen ovale or by direct flow from pulmonary capillaries. Once in the systemic circulation, It may affect the brain causing neurological dysfunction, kidneys causing Oliguria/anuria, Heart, causing MI, Eyes causing retinal/conjunctival hemorrhage or skin causing petechial rashes
- Pulmonary signs are Present in 75% of patients who develop Fat embolism syndrome and it is the first clinical signs to appear.. Patients usually has tachypnea, hypoxia with oxygen saturation below 90%, rales and pleural friction rubs may be audible On auscultation, loud harsh breath with crepitus and wheeze may be heard. 50% of all patient who develop FES may require Mechanical ventilation.
- Chest Xrays are usually normal, however, in some cases, Snow storm appearance of the bilateral lung field may be seen, by micronodular opacities High resolution CT scan of the chest shows ground glass opacities with geographical distribution and in present context, the findings can be very similar to chest findings of COVID-19
- Chest Xrays are usually normal, however, in some cases, Snow storm appearance of the bilateral lung field may be seen, by micronodular opacities High resolution CT scan of the chest shows ground glass opacities with geographical distribution and in present context, the findings can be very similar to chest findings of COVID-19
- Neurological signs are usually seen after the onset of pulmonary signs. It is present in ~80% of patients who develop FES And are usually limited to minor symptoms like drowsiness, anxiety, restlessness and muscle rigidity. These symptoms usually recover fully. However it may progress to seizures, stupor, confusion and coma which may lead to patients having a persistent neurological deficit even after recover from fat embolism.
- NCCT of head is normal in most cases However, there may be specific findings in MRI In early Diffuse weighted image, done within 1-4 days, there may be scattered punctate foci of cytotoxic edema known as starfield pattern Later, in 5-14 confluent areas of cytotoxic edema in the white matter can be seen In Susceptibility weighted image, Wallnut kernel appearance can be seen, which are small focal hypointensities spread throughout the cerebral cortex.
- NCCT of head is normal in most cases However, there may be specific findings in MRI In early Diffuse weighted image, done within 1-4 days, there may be scattered punctate foci of cytotoxic edema known as starfield pattern Later, in 5-14 confluent areas of cytotoxic edema in the white matter can be seen In Susceptibility weighted image, Wallnut kernel appearance can be seen, which are small focal hypointensities spread throughout the cerebral cortex.
- Other signs include Petechial rashes in the skin which, can occur anywhere in the body but mainly in the conjunctiva, axilla and the neck. It Occurs due to obstruction of the microvasculatures and resultant capillary hemorrhages. Capillary hemorrhages occurs even in internal organs. This is a pathognomic sign of FES, however, it appears late after 4-5 days and last until day 7, and is present only in 20-50% of patients Right heart failure may be present with changes in the ECG such as ST segment depression and features of RBBB…
- With all these myriad of symptoms that can occur, Hypoxia, neurological abnormalities and Petechial rashes has been described as the Triad of Fat embolism syndrome
- Diagnosis is based on a constellation of clinical signs, laboratory findings and exclusion of other diseases. Lab tests… Thrombocytopenia : that is more than 50% decrease in platelet count as compared to admission Fat globules are seen in Urine Cytology, Peripheral blood smear and Sputum. However, these tests signify the presence of fat embolus which can be seen in 90% of patient after long bone fracture and not necessarily indicate fat embolism syndrome.
- Since the diagnosis of FES is very elusive, multiple criteria for diagnosis is used, the first and the most commonly used is the Gurd and Wilson’s criteria. This criteria was first developed by GURD in 1970, and later modified by gurd himself with Wilson in 1974 The Major Criteria includes… IN gurd and Wilson’s criteria, Presence of 1 major and 4 minor criteria including Fat Macroglobinemia, is diagnostic of FES
- Score of 5 or more is diagnosed as FES
- In MOST Cases, Fat embolism syndrome is classified as Pulmonary or Cerebral, however, this does not give any information regarding severity and prognosis of the disease. Therefore, Sevitt developed the classification based on severity of FES in 1960
- In MOST Cases, Fat embolism syndrome is classified as Pulmonary or Cerebral, however, this does not give any information regarding severity and prognosis of the disease. Therefore, Sevitt developed the classification based on severity of FES in 1960
- In MOST Cases, Fat embolism syndrome is classified as Pulmonary or Cerebral, however, this does not give any information regarding severity and prognosis of the disease. Therefore, Sevitt developed the classification based on severity of FES in 1960
- The only way to absolutely prevent FES is to avoid traumatic incidents altogether. However, that is not always possible. Therefore, following trauma, 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
- IN a study mentioned in the article, out of 58 patient, use of aspirin resulted in early normalization of blood gas, coagulation proteins and platelet counts as compared to controls
- However, most of these drugs have been found to be of only theoretical use and of no practical benefits.
- Reservoir masks can deliver between FiO2 of 60 – 80%