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Fat Embolism Syndrome in a Patient Who Underwent Unilateral Total Knee Replacement Vaishali S Kulkarni

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Fat Embolism Syndrome in a Patient Who Underwent Unilateral Total Knee Replacement Vaishali S Kulkarni RIA Vaishali S Kulkarni 10.5005/jp-journals-10049-0051 CASE REPORT Fat Embolism Syndrome in a Patient who Underwent Unilateral Total Knee Replacement Vaishali S Kulkarni ABSTRACT surgery.3 So, we present an interesting case of FES of Fat embolism syndrome (FES) is known to be relatively common a patient who developed sudden dyspnea and disori- in cases of multiple traumatic fractures; it is rare in cases of total entation after total knee replacement. knee arthroplasty. We describe a case of a 61-year-old female who underwent unilateral total knee arthroplasty, 5 hours later CASE REPORT she developed slurring of speech, disorientation subsequently desaturated, requiring intubation. The clinical diagnosis of A 61-year-old female patient weighing 80 kilograms was fat embolism syndrome was made by criteria of exclusion. diagnosed with osteoarthritis of both knees and admitted Fat embolism syndrome can occur unexpectedly in elective for left total knee replacement. She had type 2 diabetes reconstructive orthopedic procedures. One should have a high degree of clinical suspicion of fat embolism syndrome when a mellitus, hypertension, and hypothyroidism for 3 years. patient deteriorates perioperatively. The treatment is primarily She had an episode of acute angina 1 year earlier for supportive. which angioplasty was done, and three coronary stents Keywords: Fat embolism syndrome, Local anesthetics, Total were placed. The patient was on thyroxine, antihyper- knee replacement, Pulmonary embolism. tensives, oral hypoglycemic agents, tablet clopidogrel and aspirin daily. Tablet clopidogrel was stopped five How to cite this article: Kulkarni VS. Fat Embolism Syndrome in a Patient who Underwent Unilateral Total Knee Replacement. days before surgery. Preoperative blood and biochemis- Res Inno in Anesth 2018;3(2):56-59. try tests performed before surgery were within normal ranges. Similarly, no special findings were observed on Source of support: Nil X-ray chest and electrocardiogram. The preoperative Conflict of interest: None echocardiogram showed good left ventricular function with a left ventricular ejection fraction (LEVF)–50% and INTRODUCTION grade 1 diastolic dysfunction. Fat embolism is caused by the release of fat globules The patient received tablets thyroxine 50 mg, amlodi- into the systemic circulation and is a known complica- pine 5 mg, nicorandil 10 mg 2 hours before surgery. tion after pelvic and long bone fractures; however, it With standard monitoring in the operation theatre and can also present within the setting of elective ortho- a baseline BP of 160/80 mm Hg, PR of 80/min and a pedic surgery, severe burns, liver injury, closed-chest room air saturation of 99%, she was made to sit, and the cardiac massage, and liposuction.1 Fat embolism may subarachnoid block was given under aseptic precautions be asymptomatic but in 1–5%, it results in fat embo- at the L3 L 4 interspace using a 25 G Quincke’s needle. lism syndrome which ranges from mild respiratory Cerebrospinal fluid (CSF) was clear, and 3.4 mL of 0.5% distress to multiorgan dysfunction involving the lung, of heavy bupivacaine was given. The intravenous fluid brain, and skin with a triad of symptoms that include used was Plasma-Lyte and preoperatively iv cefuroxime dyspnea, petechial hemorrhages, and neurological 1.5 gm, iv gentamycin 80 mg and iv tranexamic acid abnormality.2 Although fat embolism is common fol- 1.5 gm was given. During surgery, 4L/min oxygen was lowing long bone fractures and orthopedic surgery, FES administered via Hudson faces mask. Vital signs of the with serious clinical manifestations known to occur patient were stable throughout the entire surgery. Pulse in only 0.1% of patients undergoing joint replacement oxygen saturation was maintained at 100. Left side knee replacement was done without using a tourniquet. Operation time was 2 hours and 45 minutes. At the end Consultant of surgery, an adductor canal block was given under Department of Anesthesia, Global Hospital, Mumbai, Mumbai, ultrasound guidance, and aseptic precautions with 20 mL Maharashtra, India of 0.125% bupivacaine and 1% lignocaine and a catheter Corresponding Author: Vaishali S Kulkarni, Consultant, were secured in the canal. Postoperatively patient was Department of Anesthesia, Global Hospital, Mumbai, Mumbai, conscious, oriented, comfortable and moving both lower Maharashtra, India, email: [email protected] limbs. 56 RIA Fat Embolism Syndrome in a Patient who Underwent Unilateral Total Knee Replacement Five hours later, the patient developed slurring of DISCUSSION speech, became drowsy and disoriented and had two The pathophysiology of fat embolism syndrome is episodes of vomiting, and the saturation was at 87% unclear, but two mechanisms have been suggested. One on room air and oxygen by Hudson mask 4 liters was mechanism suggests that physical obstruction of the started after which the saturation of 100% was attained. systemic vasculature is caused by fat globules released The patient was then advised to get a computed tomog- from the bone marrow of long bones due to increased raphy (CT) brain and then shifted to intensive care unit intramedullary pressure after trauma or orthopedic (ICU) for further management. During the transfer, surgery such as placement of intramedullary rods.4 The the patient developed two episodes of GTCS which other is a biochemical mechanism that suggests that was treated with IV midazolam and IV levetiracetam. hydrolyzation of the fat, over a few hours, in plasma to In the ICU the patient then became restless dyspneic, free fatty acids can cause a local inflammatory response developed bilateral wheeze. Due to deteriorating GCS and direct toxicity to the lung or capillary endothelium.5 and respiratory distress, the patient was intubated and Last, the coagulation theory proposed that the release mechanically ventilated. A chest X-ray showed right- of tissue thromboplastin, following traumatic long bone sided patch and the arterial blood gas showed a pH injury, result in activation of the complement system and of 7.28, pO2-71, pCO2-32, HCO3-17 and lactate of 5.8. extrinsic coagulation pathways and factor VII activation Electrocardiogram and a fresh echocardiogram showed that leads to intravascular coagulation and subsequently no abnormality. CT brain showed some evidence of lead to an increase in pulmonary permeability of the fat pituitary hemorrhage for which the neurologist was globules.6 consulted and a magnetic resonance imaging (MRI) The initial trigger for FES in TKR surgery was pro- brain was done which showed no abnormality. She was posed to be due to cementing techniques and increased started on fentanyl and midazolam infusions and insulin systemic monomer. On the contrary, the development of infusion as per her blood sugar level and Nitroglycerin FES was described to be due to release of the bone marrow infusion in view of elevated blood pressure. She was fat globules into circulation before cement application started on low molecular weight heparin, IV leveti- after placement of the intramedullary femoral align- racetam after consulting the neurologist. ment guide during TKA. The modification of surgical Computed tomography (CT) chest showed large techniques to cementless TKR, and staging (unilateral vs. patchy collapse consolidation of both lower lobes and bilateral) TKR procedures or the use of computer-assisted mild bilateral pleural effusion and pulmonary angiogram navigation has not been associated with a lower incidence and D-dimer was done which were both normal. There of FES.3 The time onset of the clinical development of was difficulty to wean the patient off the ventilator due FES following knee arthroplasty was variable from an to increased irritability on stopping the sedation and a intraoperative cardiorespiratory collapse, before or after persistent V/Q mismatch, and her respiratory condition deflating the tourniquet, to the development of respira- further deteriorated on the 3rd postoperative day. She was tory, cardiovascular and cerebral dysfunction minutes to treated as ARDS with aspiration pneumonitis with N ace- hours in the postoperative period. tylcysteine and regular nebulization, chest physiotherapy The presentation of the FES can be subclinical, clinical and antibiotics. Urine analysis and fundoscopy was done or fulminating. There is no specific sign, symptom nor and showed no fat globules. On the 5th postoperative test, which is pathognomonic to the FES. The diagnosis day, the patient developed a petechial rash over the trunk. of fat embolism is usually a clinical diagnosis of exclusion The patient developed consumption coagulopathy, the and requires a vigilant high index of suspicion. Christie hemoglobin dropped from 10 mg/dL postoperative to et al. documented embolic evidence of fat on echocar- 6.7 mg/dL and she was transfused two unit of packed red diography in 97 out of 110 patients having reaming of a blood cells. Due to patient persistent respiratory distress fractured femur or tibia.7 Despite the regular occurrence she was sedated and ventilated for two more days. On of microscopic fat embolization, FES with multiorgan the 7th postoperative day she was gradually weaned off involvement is rare. The basic triad of FES includes res- the ventilator, and after confirmation of good neurologi- piratory distress, neurological abnormality, and petechial cal status, the patient was extubated. The postextubation rash, and other associated features include thrombocyto- patient was started on incentive spirometry
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