Fat embolism syndrome : A diagnostic dilemma

Abstract

Fat embolism syndrome (FES) is a constellation of clinical manifestations following fracture of long bones. In retrospective review, incidence of FES was less than 1% [1]. Fat embolism syndrome is a clinical diagnosis. This condition is often misdiagnosed and fatal if the treatment is delayed. We present two cases of fat embolism syndrome to highlight problems of missed diagnosis. Case 1 A 19 year old male sustained bilateral closed tibial and fibular fracture. Plaster of Paris (POP) slab was applied over both lower limbs and surgery planned. While awaiting fixation of fractures patient developed high grade fever from second day. Surgery was deferred to investigate fever. No specific cause for fever could be found and empirical treatment for malaria administered. Four days after the injury, patient suddenly developed tachypnea (breath rate 55/minute), tachycardia (pulse 145/minute), and altered sensorium. Oxygen saturation on pulse oximetry (SpO2) was 60% with high flow oxygen by facemask. He was intubated and mechanically ventilated with 100 % oxygen using anaesthesia circuit and later placed on ventilator in control mode with positive end expiratory pressure (PEEP). As oxygen saturation did not improve, PEEP was gradually increased to 20 cm of H2O. The high level PEEP resulted in pneumothorax for which an intercostal chest drain was inserted and patient was shifted to a tertiary care hospital. On arrival to the intensive care unit quick clinical evaluation revealed marked pallor, pulse 140/minute, blood pressure of 130/70 mm Hg, SpO2 90%, breath rate and neurological status could not be ascertained as patient was under effect of muscle relaxants. Patient was placed on Seimens Servo i ventilator in synchronized intermittent mandatory ventilation (SIMV) mode with PEEP. Initial ventilator settings were tidal volume 350 ml, mandatory breath rate 16/minute, fraction of inspired oxygen (FiO2) 0.7 and PEEP 10 cm H2O. With these settings peak inspiratory pressure of 23 cm H2O, plateau pressure of 20 cm H2O, mean airway pressure of 12 cm H2O and dynamic compliance of 30 ml/cm H2O was recorded. There were no petechial or subconjuctival haemorrhages. Chest auscultation revealed bilateral extensive crepitations and bronchial breath sounds. Fundoscopy revealed multiple haemorrhages along the vessel in entire field of both eyes. Doppler study of lower limb showed no evidence of venous thrombosis. Investigations revealed haemoglobin (Hb) 6.8 gm %, chest radiograph showed bilateral non homogenous opacities with predominant basal distribution (Fig. 1). Arterial blood gas (ABG) showed pH of 7.25, partial pressure of oxygen in arterial blood (PaO2) 55 mm Hg, partial pressure of carbon dioxide in arterial blood (PaCO2) 35 mmHg, bicarbonate (HCO3) 18 mmol/L and PaO2/FiO2 ratio of 78. Other investigations were within normal limits. Right internal jugular vein was cannulated and central venous pressure (CVP) of 12 cm of saline was recorded. Frank blood was noted on endotracheal suction. Fig. 1 Chest radiograph (antero-posterior view) shows bilateral non homogenous opacities in a predominantly basal distribution On the basis of clinical background, chest radiograph and arterial blood gas analysis report, the case was diagnosed as fat embolism syndrome with acute respiratory distress syndrome (ARDS). Patient was kept sedated, muscle relaxants discontinued and mechanical ventilation continued. Tachycardia and tachypnea settled down after eight hours of ventilation and patient started responding to simple verbal commands. The case was discussed with orthopaedic surgeon for fixation of fractures on fifth day. A consensus decision was taken to wait for some time. Next day while on ventilator, patient suddenly desaturated (SpO2 70%), became restless and developed tachypnea (breath rate 60/minute) and tachycardia (heart rate 150/minute). There were no specific changes on electrocardiogram and transthoracic echocardiography did not show any evidence of right ventricular strain. Patient improved within one hour with readjustment of ventilator settings. This episode was thought to be fresh episode of fat embolism. In view of recurring fat embolism, it was decided to fix fractures early. On sixth day bilateral open reduction and dynamic compression plating of both fractures was done under general anesthesia. Intraoperative course was uneventful. Postoperatively, ventilation, adequate analgesia, and antibiotics were continued. On seventh day patient improved and he was placed on oxygen mask. After eight hours of extubation patient again developed tachycardia, tachypnea, diaphoresis, and mild desaturation (SpO2 90%). This time noninvasive ventilation was used to tide over the crisis. After six hours of mask ventilation SpO2 improved to 97%. Thereafter he made an uneventful recovery.