Page 20 - Delaware Medical Journal - May 2017
P. 20
Fat Emboli Syndrome
Isha Misra MD, Justin Glasgow MD, and Farid Moosavy MD
CASE PRESENTATION
A 33-year-old male with a reported history of sickle cell trait who had not seen a doctor in some time presented to the hospital
with the acute onset of low back pain. He reported a history of heavy lifting at work but no recent trauma. Two evenings prior
to presentation, he had noted a “twinge” in his low back while leaving work, but did not have any concerns about the pain. However, he did awake later that evening in the middle of the night with severe pain in the center of back with radiation to both sides. He did not have any radiation of the pain into his legs, any lower extremity weakness, equina syndrome. When pain persisted for over 24 hours and he was unable to eat, presented to the emergency department
for evaluation.
In addition to the above HPI, his review
of symptoms did reveal recent upper respiratory infection symptoms with some associated pleuritic chest pain that was treated with an antibiotic by an urgent care center. Vitals were notable for a low grade fever, sinus tachycardia with a heart rate of 103, and episodic desaturation on 2L NC to an oxygen saturation of 80%. On physical exam, he was uncomfortable but not in any acute distress, lungs were clear and he had spinous process and paraspinal tenderness to palpation in
the lumbar spine with no strength or
Initial ED work-up was remarkable for a leukocytosis with 2% bands, a microcytic anemia with a hemoglobin of 8.8, a basic metabolic panel within normal limits,
a CTA of chest negative for pulmonary embolism with an incidental 3mm right upper lobe lung nodule, and a CT abdomen and pelvis demonstrating enlarged lymph nodes adjacent to the splenic hilum felt
to be likely reactive in nature. Given the lack of localizing symptoms or diagnosis, medicine was asked to evaluate the patient after drawing blood cultures and ordering additional MRI imaging of lumbar spine to evaluate for an abscess.
were marked by rapid worsening of his oxygenation status leading to pulmonary consultation and initiation of broad the hospital, a rapid response was called for respiratory distress. That evaluation included a chest x-ray showing pulmonary edema for which he was given a dose
of IV furosemide, placed on BIPAP
and transferred to a higher level of care
for closer monitoring of his respiratory status. He did not adequately respond to treatment, and a few hours later a second rapid response was called for altered mental status. At this time he was minimally arousable to sternal rub. He was not hypoglycemic, did not respond to a reversal dose of Narcan and had an STAT CT of
his head with no acute abnormalities. He did have a respiratory acidosis on ABG
and given the progressive decline in
mental status and respiratory status he was transferred to a medical intensive care unit where he was intubated.
The patient was noted to have several lab abnormalities at this point, including worsening liver function tests, LDH, and
thrombocytopenia. Infectious Diseases was consulted for persistent fevers with unknown source. Hematology was consulted for worsening pancytopenia, elevated LDH and ferritin, and nucleated red blood cells on peripheral smear. Fat Emboli Syndrome was suspected, however the patient only had a reported history of sickle cell trait as opposed to HgbSS or
SC disease. As such, a hemoglobin electrophoresis was performed, and SC disease. Given strong suspicion for Fat Emboli Syndrome at this point, a dialysis catheter was placed and red cell exchange was urgently performed.
His hospital course was further complicated by worsening AKI and ventilator dyssynchrony. The next
day, lumbar puncture was done due to persistent fevers and encephalopathy. EEG was also completed. MRI obtained but unfortunately only a limited view was able to be obtained due to technical issues with the MRI scanner.
The next morning, the patient was noted to
pupils. Stroke alert was called and a stat noncontrast CT head was performed.
This showed diffuse cerebral edema and hypodensities in the bilateral temporal lobes. There was obliteration of the cisterns and compression of the 4th ventricle. Hypertonic saline was initiated. Neurology evaluated the patient and noted their exam to be consistent with brain death. Apnea diagnosis of brain death due to patient was conducted by nuclear medicine. The
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Del Med J | May 2017 | Vol. 89 | No. 5
