Recurrent pleural effusions occurring in association with immunoglobulin light chain amyloidosis and not associated with amyloid cardiomyopathy are rare. These portend an overall poor prognosis with mean survival time of approximately 1.8 months. We hereby report a case of a 59-year-old Caucasian female with recurrent pleural effusions and an ultimate diagnosis of pulmonary amyloidosis in association with plasma cell myeloma. The optimal treatment for recurrent pleural effusions in amyloidosis has not been determined; however, our patient responded to therapy with Cyclophosphamide-Bortezomib- (Velcade-) Dexamethasone (CyBorD) and had no repeat hospitalizations or recurrence of pleural effusion at four-month follow-up after initiation of therapy.

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Fat embolism syndrome (FES) is a known complication of long bone fractures especially femur fractures. The incidence is about 3-4%. Herein, we report a case of a young male who suffered FES and the resultant cerebral fat embolism.CASE PRESENTATION: Twenty-year-old male presented with a left thigh deformity after a bike accident. He was found to have femoral and tibial fractures which required surgery. On admission, CT head was normal. In the post-op period, he began seizing so he remained intubated for airway protection and moved to the ICU for further care. Repeat CT head was still normal. Patient underwent usual ICU care but when sedation was turned off, the patient continued to have posturing movements and poor response to stimuli. While awaiting MRI brain, his lab work began showing several derangements including a precipitous drop in hemoglobin, without any obvious source of bleeding, and platelets. CT abdomen, pelvis, and lower extremity showed no retroperitoneal bleed or hematoma. Chest X-ray was normal. MRI brain showed small foci of diffusion restriction in both cerebral hemispheres, midbrain, and cerebellum. Given the clinical picture, this was most consistent with FES. Transesophageal Echo (TEE) was performed to assess for PFO or shunts and none were noted. It was assumed that the patient had fat emboli to the brain through pulmonary vasculature translocation. Patient was able to be extubated and transferred to the floor where he continued to work with physical therapy. He was discharged to an acute rehabilitation facility.DISCUSSION: Fat embolism syndrome requires a high clinical suspicion. There is no agreed upon diagnostic criteria, but many clinicians use Gurd and Wilson's criteria. Diagnosis is suggested when there are 2 major criteria or 1 major and 4 minor criteria. Our patient had cerebral involvement, sudden drop in hemoglobin and platelets, and tachycardia. The neurologic complications can be devastating. They usually begin as agitation but can progress to seizures and coma as they did in our patient. Fat droplets of small diameters can pass through the pulmonary capillaries to reach the cerebral circulation. We feel this was the mechanism of cerebral fat embolism in our patient. CONCLUSIONS:The clinician must be vigilant when assessing a patient with long bone fracture. Agitation or altered mentation can be a manifestation of cerebral fat embolism.

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