A Hussain. A Fatal Fat Embolism. The Internet Journal of Anesthesiology. 2003 Volume 8 Number 2.
Fat Embolism and the associated Fat Embolic Syndrome is a serious and potentially life threatening condition. It tends to occur most frequently after fractures or intramedullary instrumentation of long bones particularly the femur and tibia. Some other non-traumatic conditions such as Diabetes Mellitus sever Burns, SLE and Pancreatitis etc. can also result in Fat Embolic Syndrome. Young adults irrespective of sex are commonly affected. Its classical presentation consists of an asymptomatic interval followed by pulmonary and neurological manifestations combined with petechail haemorrhages. The diagnosis largerly depends on high index of suspicions and exclusion of other conditions. Treatment of this condition remains supportive. Mortality associated with this condition is significant, ranging from 10-20 %.
Here is a description of such a fatal case.
This 21 year old, male Yemeni, weighing 89.0 kg was brought to the Accident and Emergency Department by RED CRESCENT after sustaining multiple injuries in a road traffic accident between two cars coming at high speed in opposite directions. The primary injuries were
Superficial laceration on forehead 3x4 cm.
Two longitudinal parallel burses on right 5th and 6th ribs anteriorly each measuring 2x4 cm .
Swelling of left mid thigh.
Open wound measuring 5x5cm on right lower leg with exposed tibia and fibula.
The patient was thoroughly evaluated by Surgical Trauma Team and management started accordingly.
On arrival, the patient was fully awake and well oriented in time, space and person. There was no sign of airway obstruction. He had history of momentary loss of consciousness for 5 minutes at the scene. He had no history of vomiting, convulsions or bleeding from ear, nose and throat. Higher mental functions, all cranial nerves, as well as motor and sensory systems were intact. The neck area was non-tender.
The patient was breathing spontaneously at the rate of 22 breaths per minutes. Oxygen Saturation was 95% on room air. The trachea was central and apex beat at its normal position. On auscultation of the chest, breathing was vesicular, equal in intensity with normal vocal resonance on both sides of chest. Pulse was 88/minutes, regular and moderate in volume. All the peripheral pulses were palpable. Blood Pressure was 99/60 mmHg. Temperature was 37.1 ° C. The abdomen was soft. Tenderness and guarding were absent.
Blood was sent to the laboratory and the results are shown in the tables. CT Scan brain, X-rays cervical spine, chest and both lower limbs were done and these are shown in figures. Ultrasonography of abdomen revealed normal architecture of liver, spleen and kidneys. There was no evidence of free fluid in peritoneal or pelvic cavity.
Management In The Accident And Emergency Unit
O2 inhalation 4/Lwith simple facemask
Lactated Ringer's Solution 2000 ml I/V fast
Then 100 ml/hour
Blood two units of Packed Red Blood Cells
Injection Morphine 5 mg IV prn
Injection Metoclopramide 10 mg I/V slow stat
Injection Pethidine 75 mg I/M stat
Injection Ceforoxime 1.5 I/V stat then
750 mg I/V 8 hourly
Injection Metronadazole 500 mg I/V 8 hourly
Prophylaxis against Tetanus:
Injection Tetanus Toxoid 0.5 ml I/M stat
Dressing of the wounds
Back slab made of Plaster of Paris was applied on the whole right Lower limb
Splinting (immobilization) with metallic frame on left lower limb
The patient was kept under keen observations. He could not be transferred to the surgical floor due to unavailability of beds. He was quite stable for about 12 hours. Around 14:00, his heart and respiratory rates then increased gradually and oxygen saturation decreased. However, he was maintaining blood pressure and conscious level. At this point, oxygen therapy was changed to a non-rebreathing face mask. At 17:50 he became drowsy and lost his conscious level completely at 18:00. Heart rate was 140/minute, respiratory rate >35/minute, SpO2 78% on FiO2 0.8 and BP 110/55 mmHg. He was intubated with pre-oxygenation, Inj. Fentanyl 100µg I/V, Inj. Midazolam 5.0 mg I/V and Inj. Rocurinum 50 mg I/V. Cricoid pressure was maintained with modified Sellick's maneuver. An endotracheal tube sized 8.5 mm ID was passed and fixed at the 20 cm mark at an angle of the mouth after confirmation with an EtCO2 detector device. Mechanical ventilation was started with a tidal volume of 600 ml and a rate of 12/minute. I: E ratio was kept at 1:2.
Efforts were made to transfer the patient to the Surgical Intensive Care Unit. At 22:00 one bed in the SICU was arranged for this patient. On the way from the Accident and Emergency Department to the SICU another CT Scan of the brain (plain) was done which is shown in figures below.
Management In The Surgical Intensive Care Unit
At 23:00, the patient was admitted in the SICU sedated, intubated and ventilated. On arrival in the SICU his heart rate was 145/minute, SpO2 91% on FiO2 1.0, blood pressure 95/60 mmHg. The chest was full of crackles. Ventilation continued with the same ventilatory parameters. Injections of Fentanyl 100µg, Midazolam 2mg and Rocurium 50 mg I/V were given. Sedation and analgesia was started with Propofol 2mg/kg/hour and Fentanyl 50µg/hour infusions respectively. Blood was sent to the laboratory. The results are shown in the tables below.
Different levels of PEEP (0-15cm of water) were also tried. A dobutamine infusion 0-20 mg/kg/minute was started. Senior help was called. Furosemide 100mg and Morphine 20 mg I/V were given. Four units of Red Blood Cells and 500 ml of 5% Albumin were transfused. The central venous line was changed to a pulmonary artery catheter. X-rays of the chest done in the SICU are shown in the following figures.
The cardiac out put was 8.1 L/minute, cardiac index 3.86 L/minute/m2, system vascular resistance 483 dynes.s.cm-5, pulmonary artery pressure 68/53 mmHg, central venous pressure +7 mmHg, temperature 38.3 °C and pulmonary capillary wedge pressure 13 mm Hg reflecting early sepsis as well. At this point a Nor-adrenaline infusion with 0-20µg/minute was started. The blood pressure dropped to 80/45 mmHg at 01:00 hours. An adrenaline infusion of 0-20µg/minute was also started. He also received some boluses of Metaraminol 0.5-1.0 mg I/V prn. Serial arterial blood gases (ABGs) were done showing progressive acidosis, hypercapnia and severe hypoxemia. Sodium Bicarbonate 8.4% 50 ml was also given. The results of the ABGs are shown in the table below.
At 03:25 hours, the patient developed bradycardia and hypotension. Five minutes later, cardiac arrest occurred. Code Blue was initiated and full cardiopulmonary resuscitation performed for 30 minutes. He was declared dead at 04:00 hours.
In 1861, Zenker1 described the presence of fat droplets in the lungs of a railway worker who had suffered a severe thoraco-abdominal crush injury at autopsy and later in 1873, Bergmann2 clinically diagnosed Fat Embolic Syndrome in a patient with fracture of the femur. The work continued on understanding the pathophysiology and pathogenesis of fat embolism throughout the early 20th century and in 1969, Peltier3 published his work on the pulmonary consequences of fat rmbolism and its treatment. Gurd4 in 1970 put together the various clinical manifestations, which he later called the Fat Embolic Syndrome.
The risk of Fat Embolic Syndrome is the greatest in the multiply injured patient, especially those with femoral fractures accompanied by other long bone fractures. Magerl et al5 in 1966 studied 4,197 fractures and found the incidence of Fat Embolism Syndrome to be 0.9%, where as in a similar study by Peltier et al 6 in 1974 an incidence of 1-2.2% for tibia and femur fractures was described. Ganong7 in 1993 found much higher rates of fat embolism. The overall incidence rate of fat embolism was found to be 23% (19 % in tibia versus 75% in femur bone fractures). Collins et al8 reported that closed fractures had a higher incidence of Fat Embolic Syndrome compared to open fractures. This was thought to be because the intramedullary bone pressure is lower in case of open fractures, which reduces the bulk of fat emboli propelled into the blood stream.
Two events promote entrance of marrow contents into the circulation following a fracture: movement of unstable bone fragments and reaming of the medullary cavity for the placement of an internal fixation device. Fat Embolic Syndrome is also reported after non-traumatic lesions such as DM, severe burns, pancreatitis etc. Age seems to be a factor in the development of Fat Embolic Syndrome; young men with fractures are at increased risk.
There are two theories about the pathogenesis of Fat Embolism, which are widely accepted among the physicians.
The mechanical theory states that Fat Embolic Syndrome results from physical obstruction of the pulmonary and systemic vasculature with embolized fat. In the pulmonary vasculature, they cause ventilation / perfusion mismatch leading to shunting effect.
The biochemical theory states that circulating free fatty acids derived from fat droplets are directly toxic to pneumocytes and capillary endothelium in the lungs, causing interstitial hemorrhage, edema and chemical pneumonitis.
The possibility of co-existing Shock, Hypovolemia and Sepsis, all of which reduce liver flow, facilitate the pathogenesis of Fat Embolic Syndrome by exacerbating the toxic effects of free fatty acids cannot be ignored.
A thorough knowledge of the signs and symptoms of the syndrome and a high index of suspicion are needed to make the diagnosis.
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 with in few hours of injury.
The respiratory findings range from nearly asymptomatic hypoxemia to ARDS requiring Ventilatory support. Fat droplets are entrapped in the pulmonary capillary beds causing shunting effect (right to left intrapulmonary shunting of deoxygenated blood). These shunts can be obtained by the use of shunt equation
Q·s/Q·t = CćO2 –CaO2 / CćO2 - C v--O2
CćO2 =Oxygen content of ideal pulmonary-end capillaries. (Derived from Alveolar Gas Equation.
CaO2 = Arterial O2 content (obtained from Arterial Blood Gases)
C v--O2 =mixed venous content of O2 (obtained from Pulmonary Artery Catheter)
Shunt lines as shown in figure 9. Note that there is little benefit in increasing FiO2 in patients with very large shunts. Oxygen therapy do not play any role if the shunt is >30%.
Moreover, these substances produce local ischemia and inflammation with concomitant release of inflammatory mediators, platelet aggregation, and vasoactive amines.
A whole series of central nervous system disturbance can occur from Cerebral Fat Embolism. The fat droplets that travel through arteriovenous shunts to the brain produce local ischemia and inflammation. Central nervous system dysfunction initially manifest as agitated delirium but may progress to stupor, seizures, or coma and is usually unresponsive to correction of hypoxia. Retinal hemorrhages with intra–arterial fat globules are visible upon fundoscopic examination. Adams9 described that these changes can occur within the first 24 hours and consists of “cotton wool” exudates and small streaky hemorrhages along the retinal vessels and in the macula region. Also, diffuse edema and pallor also occur in the macula zone.
Tachycardia is one sign that is invariably present in all patients with Fat Embolic Syndrome. This is due to right ventricular strain and is often resistant to therapy. Rarely, systemic fat emboli can affect the heart leading to mottled myocardial necrosis. This can be detected by some non-specific ECG changes such as ST depression, T wave flattening, Av block and bundle–branch patterns.
A petechial rash that appears on the upper anterior portion of the body including chest, neck, upper arm, axillae, shoulders, oral mucous membrane and conjunctivae is considered to be a pathognomic sign of Fat Embolic Syndrome. Gossling et al10 suggested that they occur in 50-60% of patients. Kaplan ET al11 found that they appear on the second or third day after injury and are secondary symptoms. They results from occlusion of dermal capillaries by fat and increased capillary fragility.
Systemic fever is a common early sign of Fat Embolic Syndrome. It is often mild but may reach up to 39.0 °C. Later the onset of pulmonary infection may lead to an additional temperature increase.
There is no pathognomic test during the course of a Fat Embolic Syndrome, but a high index of suspicion is helpful in diagnosis. Close observations should be kept for the clinical signs and symptoms of Fat Embolic Syndrome on any patient at risk. However, some investigations can be helpful in conjunction with the clinical features.
ABGs may show a low PaO2 and PaCO2 with a respiratory alkalosis in the early stages but in later stages hypoxemia and hypercapnia with respiratory acidosis may be prominent feature due to diffusion defects.
2. Urine and sputum examination.
Samples may contain aft globules but these tests are non-specific.
3. Haemotological Tests.
During the acute phase of Fat Embolic Syndrome, there may be increase in FDPs, positive D-Dimer test, thrombocytopenia and other coagulation abnormalities. Patients often have a mild anemia.
4. Biochemical tests
Liver and renal function tests should performed. Serum electrolytes are mandatory. Hypocalcemia may be present due to saponification of the circulating unbound free fatty acids.
This may show evidence of right hear strain or ischemic patters if the myocardial muscle is involved.
6. Bronchoalveolar lavage (BAL)
Bronchopulmonary lavage with staining of alveolar macrophages fat to aid in the diagnosis or to predict like hood of fat embolic syndrome is controversial.
1. X-ray chest
The classical chest x-ray of fat embolism syndrome shows multiple flocculent shadows (snow storm appearance). However, the spectrum includes a diffuse, ground glass appearance or military dissemination of very fine shadows. Later, the picture may be complicated by infection or pulmonary edema.
Transesophageal echocardiography has been used to detect fat embolism in patients who are undergoing invasive intramedullary procedures.
3. CT Scan Brain.
CT Scan brain (plain) may be normal or may reveal diffuse white-matter petechial haemorrhages consistent with microvasvular injury.
4. Spiral CT Scan chest.
Helical CT Scan chest may be normal as the fat droplets are lodged in capillary beds. Parenchymal changes consistent with lung contusion. Acute lung injury, or ARDS may be evident.
Scant data exist regarding MRI findings in patients with fat embolic syndrome.
The differential diagnosis includes pulmonary embolism, cardiac or pulmonary contusion, septic shock, hypervolemia, intracranial injury, aspiration pneumonitis, ARDS and transfusion reactions.
On the basis of clinical and laboratory signs, Gurd 4 has classified major and minor criteria for the diagnosis of Fat Embolic Syndrome.
Hypoxemia (PaO2 <60 mmHg; FiO2 <0.4)
Central Nervous System depression (disproportionate to hypoxia)
Retinal fat emboli
Urinary fat globules
Decreased platelet count/haematocrit (unexplained)
Fat globules in sputum
Criteria for diagnosis of fat embolic syndrome require at least one sign
From major criteria and four sigh from minor criteria categories.
Fat Embolic Syndrome is a self-limiting disease and the treatment is supportive in nature.
Mechanical Ventilatory Support
This is indicated for those patients who cannot maintain PaO2 above 60 mmHg or there is evidence of respiratory distress, hypercapnia and exhaustion. PEEP therapy may be helpful.
Adequate circulatory volume with the judicious use of colloids, crystalloids. Diuretics are necessary. Volume depletion may precipitate shock and organ dysfunction, but volume overload may worsen hypoxia. Albumin has been recommended for volume resuscitation because it not only restore blood volume but also binds free fatty acids, and may decrease the extent of lung injury.
Prophylaxis of deep vein thrombosis.
Prevention of stress related gastrointestinal bleeding.
High dose corticosteroids have been effective in preventing development of Fat Embolic Syndrome in several trials, but controversy on this issue still persists. Preliminary studies support a possible role of corticosteroids, methylprednisolone 30mg/kg I/V twice on the day of admission, which have been shown to improve oxygenation by blocking the adverse effects of vasoactive substances. This may relieve pulmonary vascular spasm and reduce interstitial edema
Dexran, Aspirin and Heparin.
These agents may exacerbate bleeding. No clinical benefit has been conclusively demonstrated with any of these agents
Prophylaxis Of Fat Embolic Syndrome
Riska et al 15 has provided convincing evidence that the incidence of fat embolic syndrome can be reduced by
Adequate immobilization of the fracture prior to transport and early operative fixation of long bone fractures.
Use of oxygen
Our patient was 21 years old with history of long bone fractures closed as well as open fractures obtained in a road traffic accident. Other conditions such as brain and lung pathologies were excluded. When we look at the Gurd ‘s criteria three out of four signs namely hypoxemia, CNS depression and pulmonary edema from major criteria and three out of seven, tachycardia, hyperthermia, fall in haematocrit/platelet count from minor criteria were present. Someone said
“ Diseases do not read the text books” but in our case it seems to be they seem to have done it.
Dr. ALTAF HUSSAIN MBBS; DA; MCPS; FCPS. Department of Anaesthesiology (41) King Khalid University Hospital Post Box No. 7805 Al-Riyadh 11472 Saudi Arabia E-mail: email@example.com
Many thanks to Mr. Sagheer Ahmad secretary Surgical ICU for providing clinical data and radiological images regarding this case.