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Introduction: Little is known about the incidence and etiology of fat embolism in pediatric patients. We sought to determine the incidence, time course, and associated factors of pulmonary fat embolism (PFE), cerebral fat embolism (CFE), and kidney fat embolism (KFE) in trauma and nontrauma pediatric patients at the time of autopsy., Methods: Retrospectively, a convenience sample of consecutive pediatric patients (age, ≤10 years) who had undergone autopsy between 2008 and 2012 were evaluated for fat embolism. Patients who had no documented cause of death or who were hospital births and died during the same hospitalization were excluded. Formalin-fixed paraffin sections were reviewed by a forensic pathologist for evidence of fat embolism and nuclear elements. Autopsy reports were used to determine cause of death, injuries, resuscitative efforts taken, sex, height, weight, and age., Results: Sixty-seven decedents were evaluated. The median age was 2.0 years (interquartile range, 0.75-4), median body mass index (BMI) was 18.0 kg/m(2) (interquartile range, 15.7-19.0 kg/m(2)), and 55% of the patients were male. Pulmonary fat embolism, CFE, and KFE were present in 30%, 15%, and 3% of all patients, respectively. The incidence of PFE was not significantly different by cause of death (trauma 33%, drowning 36%, burn 14%, medical 28%). Patients with PFE but not CFE had significantly higher age, height, weight, and BMI. Half of the PFE and 57% of the CFE occurred in patients who lived less than 1 hour after beginning of resuscitation. Seventy-one percent of patients with CFE did not have a patent foramen ovale. Multivariate regression revealed an increased odds ratio of PFE based on BMI (1.244 [95% confidence interval, 1.043-1.484], P = .015). None of the samples evaluated demonstrated nuclear elements., Conclusions: Pulmonary fat embolism, CFE, and KFE are common in pediatric trauma and medical deaths. Body mass index is independently associated with the development of PFE. Absence of nuclear elements suggests that fat embolism did not originate from intramedullary fat., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Background: Traumatically injured patients have multiple causes for acute respiratory decompensation. We reviewed the use of computed tomography pulmonary angiography (CTPA) in critically injured patients to evaluate the results and impact on patient care., Methods: The charts of trauma patients (age >16 years) admitted to our intensive care unit for greater than 48 hours, who underwent CTPA for acute respiratory decompensation, were reviewed to determine the results of these studies and the effect on patient care., Results: We identified 188 patients who underwent CTPA for acute physiologic changes. Pertinent clinical finding were identified in 95% of studies and included atelectasis/collapse (56%), pleural effusion (18%), pneumonia (15%), and pulmonary embolus (18%). These results prompted interventions designed to improve patient outcome. The most frequent interventions were modifications of ventilator therapy (52%), antibiotic therapy (28%), mini-bronchoalveolar lavage (15%), or bronchoscopy (15%). Diagnostic agreement between chest x-ray and CTPA was poor to moderate (κ = 0.013-0.512)., Conclusions: Computed tomography pulmonary angiography is valuable in the evaluation of cardiopulmonary deterioration in critically ill traumatically injured patients. Computed tomography pulmonary angiography offers the ability to identify causes of acute physiologic changes not detected using standard chest x-ray. The results of these studies provide insight into the underlying pathophysiology and offer an opportunity to direct subsequent patient care., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Background: To determine the incidence, time course, and severity of pulmonary fat embolism (PFE) and cerebral fat embolism (CFE) in trauma and nontrauma patients at the time of autopsy., Methods: Prospectively, consecutive patients presenting for autopsy were evaluated for evidence pulmonary and brain fat embolism. The lung sections were obtained from the upper and lower lobe of the patients' lungs on the right and left and brain tissue. This tissue was prepared with osmium tetroxide for histologic evaluation. The number of fat droplets per high power field was counted for all sections. The autopsy reports and medical records were used to determine cause of death, time to death, injuries, if cardiopulmonary resuscitation (CPR) was attempted, sex, height, weight, and age., Results: Fifty decedents were evaluated for PFE and CFE. The average age was 45.8 years ± 17.4 years, average body mass index was 30.1 kg/cm² ± 7.0 kg/cm², and 68% of the patients were men. The cause of death was determined to be trauma in 68% (34/50) of decedents, with 88% (30/34) blunt and 12% (4/34) penetrating. CPR was performed on 30% (15/50), and PFE was present in 76% (38/50) of all patients. Subjects with PFE had no difference with respect to sex, trauma, mechanism of injury, CPR, external contusions, fractures, head, spine, chest, abdominal, pelvic, and extremity injuries. However, subjects without PFE had significantly increased weight (109 ± 29 kg vs. 86 ± 18 kg; p = 0.023) but no difference in height or body mass index. PFE was present in 82% (28/34) of trauma patents and 63% (10/16) nontrauma patients. Eighty-eight percent of nontrauma patients and 86% of trauma patients who received CPR had PFE. Trauma patients with PFE showed no significant difference in any group. Eighty-eight percent of trauma patients died within 1 hour of injury, and 80% (24/30) of them had PFE at the time of autopsy. CFE was present only in one patient with a severe head and cervical spine injury., Conclusion: PFE is common in trauma patients. CPR is associated with a high incidence of PFE regardless of cause of death. PFE occurs acutely within the "golden hour" and should be considered in traumatically injured patients. Further studies are needed to evaluate the pathogenesis of PFE.

Background: Timing and type of chemoprophylaxis (CP) that should be used in patients with traumatic brain injury (TBI) remains unclear. We reviewed our institutions experience with low-molecular-weight heparin (LMWH) and unfractionated heparin (UFH) in TBI., Methods: The charts of all TBI patients with a head abbreviated injury severity score >2 (HAIS) and an intensive care unit length of stay >48 hours admitted during a 42-month period between 2006 and 2009 were reviewed. CP was initiated after intracranial hemorrhage was considered stable. We reviewed all operative notes and radiologic reports in these patients to analyze the rate of significant intracranial hemorrhagic complications, deep venous thrombosis, or pulmonary embolus., Results: A total of 386 patients with TBI were identified; 158 were treated with LMWH and 171 were treated with UFH. HAIS was significantly different between the LMWH (3.8 ± 0.7) and UFH (4.1 ± 0.7) groups; the time to initiation of CP was not. The UFH group had a significantly higher rate of deep venous thrombosis and pulmonary embolus. Progression of ICH that occurred after the initiation of CP was significantly higher in the UFH-treated patients (59%) when compared with those treated with LMWH (40%). Two patients in the UFH group required craniotomy after the initiation of CP., Conclusion: LMWH is an effective method of CP in patients with TBI, providing a lower rate of venous thromboembolic and hemorrhagic complications when compared with UFH. A large, prospective, randomized study would better evaluate the safety and efficacy of LMWH in patients suffering blunt traumatic brain injury.