About us Editorial board Search Ahead of print Current issue Archives Submit article Instructions Subscribe Contacts Login 
Home Print this page Email this page Users Online: 1420

 Table of Contents  
Year : 2015  |  Volume : 15  |  Issue : 3  |  Page : 281-284

Multiorgan dysfunction due to traumatic fat embolism syndrome: Critical care and perioperative issues

1 Department of Anaesthesiology and Chief of Critical Care Medicine Division, R G Kar Medical College, Kolkata, West Bengal, India
2 Department of Anaesthesiology and Critical Care, R G Kar Medical College, Kolkata, West Bengal, India
3 Department of Physiology, Burdwan Medical College, Burdwan, West Bengal, India

Date of Web Publication2-Sep-2015

Correspondence Address:
Arunima Chaudhuri
Department of Physiology, Burdwan Medical College, Burdwan - 713 102, West Bengal
Login to access the Email id

DOI: 10.4103/1319-6308.164316

Rights and Permissions

Fat embolism is the presence of fat droplets within the circulation following trauma with or without clinical sequel. Fat embolism syndrome (FES) is a rare, but serious sequel of fat embolism usually occurring within 24 h of trauma and mostly causing petechial rashes, respiratory insufficiency, and central nervous system dysfunction. We report a young male who developed clinical FES while awaiting surgery for definitive fixation of bilateral closed tibial fracture following initial stabilization with long leg slab, was treated in the intensive care unit and underwent internal fixation under epidural anesthesia after clinical improvement. FES is a multisystem disorder with variable clinical presentation. Timely organ support improves prognosis. Epidural anesthesia can be a safe option for definitive fixation of lower limb fractures after improvement of organ dysfunctions.

  Abstract in Arabic 

عطب أعضاء متعددة نتيجة للانسداد الدهني بعد الإصابة
يعرّف الانسداد الدهني بوجود قطرات من الدهن بالدورة الدموية بعد التعرّض للإصابة مع عدم وجود عواقب طبية . متلازمة الانسداد الدهني نادرة و لكن عواقبها تظهر خلال 24 ساعة من الإصابة و تسبب طفحا بثوريا و ضيقا في التنفس و اختلالا في الحهاز العصبي المركزي.
تقرير الحالة. سجلت حالة متلازمة الانسداد الدهني عند شاب أثناء انتظاره لإجراء عملية جراجية دقيقة لتثبيت كسر مغلق ثنائي الجانب لعظم الساق الأعظم بعد تثبيت ابتدائي بجبيرة طويلة للساق و قد عولج بوحدة العناية المكثفة مع إجراء العملية تحت التخدير النصفي يعد تحسن حالته الصحية. الخلاصة: تتسبب متلازمة الانسداد الدهني في اعتلال العديد من الأجهزة و تظهر بأعراض سريرية مختلفة. دعم الأعضاء وقتيا يحسن من فرص النجاة وكذلك التخدير النصفي قد يكون الخيار الأسلم لعمليات التثبيت الدقيقة لكسور الأطراف السفلية بعد تحسن عطب العضو

Keywords: Fat embolism syndrome, multiorgan dysfunction, perioperative management

How to cite this article:
Dasgupta S, Das S, Chaudhuri A. Multiorgan dysfunction due to traumatic fat embolism syndrome: Critical care and perioperative issues. Saudi J Sports Med 2015;15:281-4

How to cite this URL:
Dasgupta S, Das S, Chaudhuri A. Multiorgan dysfunction due to traumatic fat embolism syndrome: Critical care and perioperative issues. Saudi J Sports Med [serial online] 2015 [cited 2020 Jul 8];15:281-4. Available from: http://www.sjosm.org/text.asp?2015/15/3/281/164316

  Introduction Top

Fat embolism syndrome (FES) is a rare but catastrophic complication of trauma or surgery involving long bones and pelvis. Fat embolism is the presence of fat droplets within the circulation following trauma with or without clinical sequelae. FES is a rare but serious complications of fat embolism usually occurring within 24 h of trauma and mostly causing petechial rashes, respiratory insufficiency, and central nervous system dysfunction. [1],[2],[3] However, clinical features are highly variable, most diagnostic tests are nonspecific and hence FES is largely a diagnosis of exclusion. Treatment is supportive. With early fixation of fractures and timely organ support, the mortality from FES is below 10%. [1],[2],[3],[4]

  Case Report Top

A 35-year-old male, injured by road traffic accident at midnight was admitted 10 h later with bilateral closed tibial fracture. He was immediately stabilized by long leg slab, and urgent definitive fixation was planned. With no history of head injury, he had a Glasgow Coma Scale (GCS) of 15/15. Respiratory and hemodynamic parameters were normal. While awaiting surgery, at around 2 h after admission, he suddenly developed drowsiness, respiratory distress, and hypotension. On evaluation, the patient was found to have tachycardia (120/min), tachypnea (40/min), hypotension (90/60 mmHg), and SpO 2 of 76% on room air. There was no fever or pallor. Scattered crepitations and loud heart sound with a II/VI midsystolic murmur were found. GCS was 8/15 (E2V2M4) by then, with nonreactive plantars, diminished jerks, and no lateralizing signs. Pupils and fundus were normal. No petechiae were found. ABG on oxygen (6l/min) through face mask showed the hypoxemia (pH 7.46, PCO 2 27 mmHg, PaO 2 51 mmHg, SaO 2 85%, HCO 3 20 mmol/L, BE − 3.2). Computed tomography (CT) scan of the head was normal [Figure 1]. With the GCS fast declining to 6/15 (E1V1M4), the patient was shifted to Intensive Care Unit, intubated and ventilated. The only abnormality detected in primary blood investigations was a thrombocytopenia (110,000/cumm). Electrocardiogram showed sinus tachycardia. Chest X-ray revealed bilateral diffuse infiltrates [Figure 2]. We performed an early magnetic resonance imaging (MRI) brain to exclude cerebral fat embolism (CFE). T2 fluid-attenuated inversion recovery (FLAIR) and diffusion-weighted images (DWI) showed bilaterally scattered nodular hyperintensities mainly in white matter, suggestive of microinfarcts due to CFE Takahashi et al. Grade-2 [1] [Figure 3] and [Table 1]. Bronchoalveolar lavage (BAL) revealed fat droplets in more than 30% macrophages. No fat globules were detected in blood or urine. Echocardiography showed mild right ventricular dilatation, tricuspid regurgitation, pulmonary artery systolic pressure of 54 mmHg, left ventricular ejection fraction of 64% and ruled out any shunts or patent foramen ovale. Considering Gurd's criteria, [2],[3] [Table 2] diagnosis of FES with CFE and acute respiratory distress syndrome (ARDS) was made. The patient was treated supportively. Hemodynamic instability was managed with cautious fluids and titrated infusions of noradrenaline and dobutamine. Ventilation was managed following ARDSNet. [4] Steroids were not administered. The patient was extubated on day 10 after significant clinical improvement and was shifted to high dependency unit (HDU) on day 12 without any residual neurodeficit. Bilateral closed reduction and internal fixation with tibial interlocking nail were done 3 days later under epidural anesthesia. An 18G epidural catheter was introduced through a 16G Tuohy needle inserted at L3-L4 interspace and following drugs were administered: Lignocaine 2% with adrenaline (1:200,000) 10 ml, bupivacaine 0.5% 6 ml and fentanyl 50 μg to achieve a sensory block up to T 10 and Bromage score of 4. Standard monitors were used along with invasive arterial pressure (IAP) and central venous pressure (CVP) monitoring. No sedation was given. After an uneventful surgery, he was shifted to HDU again, where postoperative analgesia was maintained with titrated epidural infusion of bupivacaine 0.0625% and fentanyl. The epidural catheter was removed after 72 h, and the patient was shifted to ward on day 20 on oral paracetamol. He was discharged home after 3 days.
Figure 1: Normal plain computed tomography scan head

Click here to view
Figure 2: Bilateral diffuse infiltrates on chest X-ray

Click here to view
Figure 3: "Star field/Starry sky" pattern of scattered bright spots on a darker background on diffusion-weighted magnetic resonance imaging

Click here to view
Table 1: Takahashi grading according to size and distribution of T2 MRI lesions: Correlates with GCS at onset and degree of clinical neurological improvement

Click here to view
Table 2: Diagnosis of Fat embolism syndrome according to major and minor Gurd's criteria for diagnosis of FES

Click here to view

  Discussion Top

Fat embolism syndrome is a multisystem disorder mainly involving the lungs, brain and skin. The organ dysfunction in FES results from the entry of fat globules into the circulation due to high intramedullary pressures and direct injury to capillary endothelium by free fatty acids liberated by lipolysis. FES can occur in the absence of right to left shunts or patent foramen ovale as in our patient, where tiny fat droplets reach left heart traversing the pulmonary circulation or via pulmonary - bronchial shunts. [3] Clinical features are highly variable. Pulmonary features include ventilation perfusion mismatch, shunts, and ARDS. Central nervous system features are nonspecific including confusion, convulsions, drowsiness and even coma. Transient petechiae, typically on the upper torso and mucous membranes, found in 25-95% cases are pathognomonic. [5] Hemodynamic derangements are mainly due to acute cor pulmonale. Gurd's diagnostic criteria are widely accepted, and our patient was accordingly diagnosed despite lacking petechiae. Most diagnostic tests are nonspecific and nonreliable. The BAL finding in our patient, although very suggestive, was also nonspecific. [6] For CFE, MRI brain with DWI and T2 FLAIR is more sensitive than CT, which is usually normal. [7] The "starfield" pattern of bright spots on a dark background in DWI depicting cytotoxic edema and pathognomonic of cerebral microinfarcts appears earlier than T2 hyperintensities suggestive of vasogenic edema. [7] The efficacy of methylprednisolone in routine prophylaxis or treatment is unproved. [3] Management of CFE is aimed toward optimization of intracranial and cerebral perfusion pressure. Early stabilization of the fracture is the most important measure to prevent FES. [8] However, internal fixation may worsen established FES, and it may be delayed in such cases till clinical improvement occurs, as we did. [8] However, the appropriate timing of fixation remains uncertain. [8] The prophylactic surgical measures to control high intramedullary pressures include venting, drilling cortical holes or marrow lavaging, the latter two being followed in our case. [3] Epidural anesthesia without sedation was preferred over general anesthesia because of decreased incidence of deep vein thrombosis, improved postoperative analgesia, better pulmonary toilet, and for continuous monitoring of sensorium in view of risks of repeat CFE episodes. [9] However, no significant outcome difference has been demonstrated between these anesthetic modes, and clinical condition of the patient should guide anesthetic choice. [3] We used intraoperative IAP and CVP monitoring in view of recent cardiopulmonary issues. Although intraoperative transesophageal echocardiography is sensitive for detecting subclinical FES by demonstrating embolic particles in the right heart coupled with any drop in SpO 2 , [3] we avoided it in the awake patient. The mortality from FES is <10%. [10] Most of the organ dysfunctions are reversible except few cases of severe CFE, who are left with residual neurodeficits.

  Conclusion Top

Possibility of FES should be considered in all cases of cardiorespiratory and neurologic deterioration during and following trauma or orthopedic surgery. Early MRI is the key to diagnose CFE. Timely organ support improves prognosis. Epidural anesthesia can be a safe option for definitive fixation of lower limb fractures after improvement of organ dysfunctions in established FES.

  References Top

Takahashi M, Suzuki R, Osakabe Y, Asai JI, Miyo T, Nagashima G, et al. Magnetic resonance imaging findings in cerebral fat embolism: Correlation with clinical manifestations. J Trauma 1999;46:324-7.  Back to cited text no. 1
Gurd AR, Wilson RI. The fat embolism syndrome. J Bone Joint Surg Br 1974;56B: 408-16.  Back to cited text no. 2
Akhtar S. Fat embolism. Anesthesiol Clin North Am 2009;27:533-50.  Back to cited text no. 3
Brower RG, Matthay MA, Morris A, Schoenfeld D, Thompson T, Wheeler A. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000;342:1301-8.  Back to cited text no. 4
Capan LM, Miller SM, Patel KP. Fat embolism. Anesthesiol Clin North Am 1993;11:25-54.  Back to cited text no. 5
Mimoz O, Edouard A, Beydon L, Quillard J, Verra F, Fleury J, et al. Contribution of bronchoalveolar lavage to the diagnosis of posttraumatic pulmonary fat embolism. Intensive Care Med 1995;21:973-80.  Back to cited text no. 6
Stoeger A, Daniaux M, Felber S, Stockhammer G, Aichner F, zur Nedden D. MRI findings in cerebral fat embolism. Eur Radiol 1998;8:1590-3.  Back to cited text no. 7
Pape HC, Regel G, Dwerger A, Sturm JA, Tscherne H. Influence of thoracic trauma and primary femoral intramedullary nailing on the incidence of ARDS in multiple trauma patients. Injury 1993;24:S82-103.  Back to cited text no. 8
Dutton RP, McCunn M, Grissom TE. Anesthesia for trauma. In: Miller RD, Eriksson LI, Fleisher LA, Wiener-Kronish JP, Young WL, editor. Miller's Anesthesia. 7 th ed. Philadelphia: Churchill Livingstone; 2010. p. 2277-311.  Back to cited text no. 9
Taviloglu K, Yanar H. Fat embolism syndrome. Surg Today 2007;37:5-8.  Back to cited text no. 10


  [Figure 1], [Figure 2], [Figure 3]

  [Table 1], [Table 2]


Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

  In this article
Case Report
Article Figures
Article Tables

 Article Access Statistics
    PDF Downloaded94    
    Comments [Add]    

Recommend this journal