Histopathologic features of fat embolism in fulminant fat embolism syndrome.

A 76-yr-old-man with a right femoral neck fracture was scheduled to undergo bipolar hip arthroplasty during general anesthesia. The patient has been under appropriate medication for hepatitis C, hypertension, and diabetes mellitus. We prepared the patient for general anesthesia with minimum monitoring devices for noninvasive blood pressure, blood oxygen saturation, end-tidal carbon dioxide, electrocardiogram, and body temperature. The patient went through induction with 200 mg thiopental, 0.1 mg fentanyl, 6 mg vecuronium, and 5% sevoflurane uneventfully. After induction, we changed the patient to the right-side-up position and added a sacral block (20 mg lidocaine [1%] and 3 mg morphine) for the postoperative pain. The operation started with this position, and anesthesia was maintained with sevoflurane. Soon after compressive insertion of a metal stem device with bone cement into the femoral bone canal, the end-tidal carbon dioxide decreased suddenly from 35 mmHg to 15 mmHg, and a shock state followed. The surgery was stopped, and we quickly returned the patient to the supine position. While central venous blood access was being placed, the patient’s heart rate decreased to less than 40 beats/min. His blood pressure decreased unmeasurably lower; a state of pulseless electrical activity followed. Cardiopulmonary resuscitation in conformity with Advanced Cardiac Life Support 2005 was started. Five minutes after the initial pulseless state, blood pressure was 70/30 mmHg, and heart rate increased to 120 beats/min. An arterial catheter was placed at this point to the brachial artery for arterial blood pressure monitoring. We executed transesophageal echocardiography. A huge thrombus in the right atrium and massive dilation of the right atrium and ventricle were revealed. Despite an almost maximal dose of pharmacologic support (0.5 g kg 1 min 1 epinephrine and 10 g kg 1 min 1 dobutamine), the cardiopulmonary condition remained unstable, and the blood pressure continued to decrease. We decided to place a portable PCPS (Capiox EBS; Terumo, Tokyo, Japan) with an 18-French drainage cannula into the femoral vein and a 16-French infusion cannula into the femoral artery. The PCPS started with the initial rotation rate at 1,500 rpm, but we could not achieve sufficient blood flow output for poor venous drainage. After increasing the rotation rate to 3,000 rpm, the blood drainage improved to obtain enough blood flow (3.5 l/min). We observed compact clusters trapped in the artificial lung of the PCPS device (fig. 1). Approximately 10 min after PCPS was started, the vital signs became stable. We tried a second observation of the heart with transesophageal echocardiography and found normalization of the right chambers. Approximately 1 h after PCPS was started, we began decreasing PCPS blood flow gradually to 0.5 l/min. The cardiopulmonary condition remained stable. So we decided to remove the PCPS from the patient. Even after the removal of the PCPS, the patient’s hemodynamic condition remained unchanged long enough; the patient was transferred from the operating room to the intensive care unit. He was discharged from the hospital 2 months after the surgery. The compact clusters in the artificial lung were analyzed histopathologically in the following procedure: (1) Make a hole in the artificial lung and remove the compact clusters as specimens. (2) Fix them with 10% formalin. (3) Make some of them into paraffin sections and stain the sections with hematoxylin and eosin. (4) Make some of them into frozen sections and stain the sections with oil red O. (5) Examine the stained sections under the light microscope. Figures 2–4 show that the compact clusters in the artificial lung were mixed thrombus with large quantities of lipid granules.