Clinical Focus

  • Pediatric Critical Care Medicine

Boards, Advisory Committees, Professional Organizations

  • Member, Maternal and Child Health Research Institute (MCHRI) (2018 - Present)
  • Member, American Academy of Pediatrics (2010 - Present)
  • Member, Society of Critical Care Medicine (2013 - Present)
  • Faculty, SCCM Critical Care Ultrasound (2014 - Present)

Professional Education

  • Residency:University of Washington Pediatric Residency (2013) WA
  • Medical Education:University of Missouri Kansas City School of Medicine Registrar (2010) MO
  • Board Certification: Pediatric Critical Care Medicine, American Board of Pediatrics (2016)
  • Fellowship:Johns Hopkins University Pediatric Critical Care Fellowship (2016) MD
  • Board Certification: Pediatrics, American Board of Pediatrics (2013)

Research & Scholarship

Current Research and Scholarly Interests

Our current research is focused on evaluation of cardiac bioenergetics and cardiac mechanics in pediatric sepsis. In particular, we have focused our efforts on the identification of developmental variability in cardiac bioenergetic reserve and mitochondrial oxidative stress in the setting of sepsis. Additionally we explore the role of mitochondrial dynamics in critical illness.


All Publications

  • Western diet regulates immune status and the response to LPS-driven sepsis independent of diet-associated microbiome. Proceedings of the National Academy of Sciences of the United States of America Napier, B. A., Andres-Terre, M., Massis, L. M., Hryckowian, A. J., Higginbottom, S. K., Cumnock, K., Casey, K. M., Haileselassie, B., Lugo, K. A., Schneider, D. S., Sonnenburg, J. L., Monack, D. M. 2019; 116 (9): 3688–94


    Sepsis is a deleterious immune response to infection that leads to organ failure and is the 11th most common cause of death worldwide. Despite plaguing humanity for thousands of years, the host factors that regulate this immunological response and subsequent sepsis severity and outcome are not fully understood. Here we describe how the Western diet (WD), a diet high in fat and sucrose and low in fiber, found rampant in industrialized countries, leads to worse disease and poorer outcomes in an LPS-driven sepsis model in WD-fed mice compared with mice fed standard fiber-rich chow (SC). We find that WD-fed mice have higher baseline inflammation (metaflammation) and signs of sepsis-associated immunoparalysis compared with SC-fed mice. WD mice also have an increased frequency of neutrophils, some with an "aged" phenotype, in the blood during sepsis compared with SC mice. Importantly, we found that the WD-dependent increase in sepsis severity and higher mortality is independent of the microbiome, suggesting that the diet may be directly regulating the innate immune system through an unknown mechanism. Strikingly, we could predict LPS-driven sepsis outcome by tracking specific WD-dependent disease factors (e.g., hypothermia and frequency of neutrophils in the blood) during disease progression and recovery. We conclude that the WD is reprogramming the basal immune status and acute response to LPS-driven sepsis and that this correlates with alternative disease paths that lead to more severe disease and poorer outcomes.

    View details for PubMedID 30808756

  • Deciphering the Effects of Performing Ultrasound on Critically Ill Emergency Department Patients Critical Care Explorations Bhargava, V., Haileselassie, B., Su, E. 2019
  • Fragmented mitochondria released from microglia trigger A1 astrocytic response and propagate inflammatory neurodegeneration. Nature neuroscience Joshi, A. U., Minhas, P. S., Liddelow, S. A., Haileselassie, B., Andreasson, K. I., Dorn, G. W., Mochly-Rosen, D. 2019; 22 (10): 1635–48


    In neurodegenerative diseases, debris of dead neurons are thought to trigger glia-mediated neuroinflammation, thus increasing neuronal death. Here we show that the expression of neurotoxic proteins associated with these diseases in microglia alone is sufficient to directly trigger death of naive neurons and to propagate neuronal death through activation of naive astrocytes to the A1 state. Injury propagation is mediated, in great part, by the release of fragmented and dysfunctional microglial mitochondria into the neuronal milieu. The amount of damaged mitochondria released from microglia relative to functional mitochondria and the consequent neuronal injury are determined by Fis1-mediated mitochondrial fragmentation within the glial cells. The propagation of the inflammatory response and neuronal cell death by extracellular dysfunctional mitochondria suggests a potential new intervention for neurodegeneration-one that inhibits mitochondrial fragmentation in microglia, thus inhibiting the release of dysfunctional mitochondria into the extracellular milieu of the brain, without affecting the release of healthy neuroprotective mitochondria.

    View details for DOI 10.1038/s41593-019-0486-0

    View details for PubMedID 31551592

  • Drp1/Fis1 interaction mediates mitochondrial dysfunction in septic cardiomyopathy. Journal of molecular and cellular cardiology Haileselassie, B., Mukherjee, R., Joshi, A. U., Napier, B. A., Massis, L. M., Ostberg, N. P., Queliconi, B. B., Monack, D., Bernstein, D., Mochly-Rosen, D. 2019


    Mitochondrial dysfunction is a key contributor to septic cardiomyopathy. Although recent literature implicates dynamin related protein 1 (Drp1) and its mitochondrial adaptor fission 1 (Fis1) in the development of pathologic fission and mitochondrial failure in neurodegenerative disease, little is known about the role of Drp1/Fis1 interaction in the context of sepsis-induced cardiomyopathy. Our study tests the hypothesis that Drp1/Fis1 interaction is a major driver of sepsis-mediated pathologic fission, leading to mitochondrial dysfunction in the heart.H9C2 cardiomyocytes were treated with lipopolysaccharide (LPS) to evaluate changes in mitochondrial membrane potential, oxidative stress, cellular respiration, and mitochondrial morphology. Balb/c mice were treated with LPS, cardiac function was measured by echocardiogaphy, and mitochondrial morphology determined by electron microscopy (EM). Drp1/Fis1 interaction was inhibited by P110 to determine whether limiting mitochondrial fission can reduce LPS-induced oxidative stress and cardiac dysfunction.LPS-treated H9C2 cardiomyocytes demonstrated a decrease in mitochondrial respiration followed by an increase in mitochondrial oxidative stress and a reduction in membrane potential. Inhibition of Drp1/Fis1 interaction with P110 attenuated LPS-mediated cellular oxidative stress and preserved membrane potential. In vivo, cardiac dysfunction in LPS-treated mice was associated with increased mitochondrial fragmentation. Treatment with P110 reduced cardiac mitochondrial fragmentation, prevented decline in cardiac function, and reduced mortality.Sepsis decreases cardiac mitochondrial respiration and membrane potential while increasing oxidative stress and inducing pathologic fission. Treatment with P110 was protective in both in vitro and in vivo models of septic cardiomyopathy, suggesting a key role of Drp1/Fis1 interaction, and a potential target to reduce its morbidity and mortality.

    View details for PubMedID 30981733

  • ROLE OF DRP1/FIS1-MEDIATED MITOCHONDRIAL FRAGMENTATION IN SEPSIS-INDUCED MYOCARDIAL DYSFUNCTION Society of Critical Care Medicine Congress Haileselassie, B., Joshi, A., Mukherjee, R., Napier, B., Massis, L., Ostberg, N., Monack, D., Bernstein, D., Mochly-Rosen, D. 2019: 21
  • Low Left Atrial Strain Is Associated With Adverse Outcomes in Hypertrophic Cardiomyopathy Patients. Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography Vasquez, N., Ostrander, B. T., Lu, D. Y., Ventoulis, I., Haileselassie, B., Goyal, S., Greenland, G. V., Vakrou, S., Olgin, J. E., Abraham, T. P., Abraham, M. R. 2019


    Paroxysmal atrial fibrillation (PAF) and left atrial (LA) structural remodeling are common in hypertrophic cardiomyopathy (HCM) patients, who are also at risk for adverse cardiovascular outcomes.We assessed whether PAF and/or LA remodeling was associated with adverse outcomes in HCM.We retrospectively studied 45 HCM patients with PAF (PAF group) and 59 HCM patients without atrial fibrillation (AF; no-AF group). LA/left ventricular (LV) function and mechanics were assessed by echocardiography. Patients were followed for development of the composite endpoint comprising heart failure, stroke, and death.Clinical/demographic characteristics, degree of LV hypertrophy, and E/e' were similar in the two groups The PAF group had significantly higher LA volume, but lower LA ejection fraction (LAEF), LA contractile, and reservoir strain/strain rate than the no-AF group. During follow-up, 27 patients developed the composite endpoint. Incidence of the composite endpoint was similar in the two groups. Absolute values of 23.8% for reservoir strain and 10.2% for conduit strain were the best cutoffs for the composite endpoint, using receiver operating characteristic analysis. Kaplan-Meier survival analysis showed lower event-free survival in patients with reservoir strain ≤23.8% or conduit strain ≤10.2%. Univariate Cox analysis revealed an association between female sex, LAEF, LA reservoir/conduit strain, and LV global longitudinal strain with the composite endpoint. The association between LA reservoir/conduit strain and the composite endpoint persisted after controlling for age, sex, LAEF, and LV global longitudinal strain.In this pilot HCM patient study, PAF was associated with a greater degree of LA myopathy, and low LA reservoir and conduit strain were associated with higher risk for adverse cardiovascular outcomes.

    View details for PubMedID 30904367

  • Interaction of mitochondrial fission factor with dynamin related protein 1 governs physiological mitochondrial function in vivo. Scientific reports Kornfeld, O. S., Qvit, N., Haileselassie, B., Shamloo, M., Bernardi, P., Mochly-Rosen, D. 2018; 8 (1): 14034


    Mitochondria form a dynamic network governed by a balance between opposing fission and fusion processes. Because excessive mitochondrial fission correlates with numerous pathologies, including neurodegeneration, the mechanism governing fission has become an attractive therapeutic strategy. However, targeting fission is a double-edged sword as physiological fission is necessary for mitochondrial function. Fission is trigged by Drp1 anchoring to adaptors tethered to the outer mitochondrial membrane. We designed peptide P259 that distinguishes physiological from pathological fission by specifically inhibiting Drp1's interaction with the Mff adaptor. Treatment of cells with P259 elongated mitochondria and disrupted mitochondrial function and motility. Sustained in vivo treatment caused a decline in ATP levels and altered mitochondrial structure in the brain, resulting in behavioral deficits in wild-type mice and a shorter lifespan in a mouse model of Huntington's disease. Therefore, the Mff-Drp1 interaction is critical for physiological mitochondrial fission, motility, and function in vitro and in vivo. Tools, such as P259, that differentiate physiological from pathological fission will enable the examination of context-dependent roles of Drp1 and the suitability of mitochondrial fission as a target for drug development.

    View details for PubMedID 30232469

  • Clinical Outcomes in Patients With Nonobstructive, Labile, and Obstructive Hypertrophic Cardiomyopathy. Journal of the American Heart Association Lu, D., Pozios, I., Haileselassie, ., Ventoulis, I., Liu, H., Sorensen, L., Canepa, M., Phillip, S., Abraham, R. M., Abraham, T. P. 2018: e006657.

    View details for DOI 10.1161/JAHA.117.006657.

  • Drp1/Fis1-mediated mitochondrial fragmentation leads to lysosomal dysfunction in cardiac models of Huntington's disease. Journal of molecular and cellular cardiology Joshi, A. U., Ebert, A. E., Haileselassie, B., Mochly-Rosen, D. 2018; 127: 125–33


    Huntington's disease (HD) is a fatal hereditary neurodegenerative disorder, best known for its clinical triad of progressive motor impairment, cognitive deficits and psychiatric disturbances, is caused by CAG-repeat expansion in exon 1 of Huntingtin (HTT). However, in addition to the neurological disease, mutant HTT (mHTT), which is ubiquitously expressed in all tissues, impairs other organ systems. Not surprisingly, cardiovascular dysautonomia as well as the deterioration of circadian rhythms are among the earliest detectable pathophysiological changes in individuals with HD. Mitochondrial dysfunction in the brain and skeletal muscle in HD has been well documented, as the disease progresses. However, not much is known about mitochondrial abnormalities in the heart. In this study, we describe a role for Drp1/Fis1-mediated excessive mitochondrial fission and dysfunction, associated with lysosomal dysfunction in H9C2 expressing long polyglutamine repeat (Q73) and in human iPSC-derived cardiomyocytes transfected with Q77. Expression of long polyglutamine repeat led to reduced ATP production and mitochondrial fragmentation. We observed an increased accumulation of damaged mitochondria in the lysosome that was coupled with lysosomal dysfunction. Importantly, reducing Drp1/Fis1-mediated mitochondrial damage significantly improved mitochondrial function and cell survival. Finally, reducing Fis1-mediated Drp1 recruitment to the mitochondria, using the selective inhibitor of this interaction, P110, improved mitochondrial structure in the cardiac tissue of R6/2 mice. We suggest that drugs focusing on the central nervous system will not address mitochondrial function across all organs, and therefore will not be a sufficient strategy to treat or slow down HD disease progression.

    View details for DOI 10.1016/j.yjmcc.2018.12.004

    View details for PubMedID 30550751

  • Left Atrial Strain Predicts Adverse Outcomes in Hypertrophic Cardiomyopathy Circulation, American Heart Association's 2018 Scientific Sessions Vasquez, ., Ostrander, B., Lu, D., Ventoulis, I., Haileselassie, B., Goyal, S., Vakrou, S., Abraham, T. P., Abraham, R. M. 2018: A17186
  • Diagnostic Bedside Ultrasound Program Development in Pediatric Critical Care Medicine: Results of a National Survey. Pediatric critical care medicine : a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies Conlon, T. W., Kantor, D. B., Su, E. R., Basu, S., Boyer, D. L., Haileselassie, B., Petersen, T. L., Su, F., Nishisaki, A. 2018


    To assess current diagnostic bedside ultrasound program core element (training, credentialing, image storage, documentation, and quality assurance) implementation across pediatric critical care medicine divisions in the United States.Cross-sectional questionnaire-based needs assessment survey.Pediatric critical care medicine divisions with an Accreditation Council of Graduate Medical Education-accredited fellowship.Divisional leaders in education and/or bedside ultrasound training.None.Fifty-five of 67 pediatric critical care medicine divisions (82%) with an Accreditation Council of Graduate Medical Education-accredited fellowship provided responses. Overall, 63% of responding divisions (34/54) were clinically performing diagnostic bedside ultrasound studies with no difference between divisions with large versus small units. Diagnostic bedside ultrasound training is available for pediatric critical care medicine fellows within 67% of divisions (35/52) with no difference in availability between divisions with large versus small units. Other core elements were present in less than 25% of all divisions performing clinical studies, with a statistically significant increase in credentialing and documentation among divisions with large units (p = 0.048 and 0.01, respectively). All core elements were perceived to have not only high impact in program development but also high effort in implementation. Assuming that all structural elements could be effectively implemented within their division, 83% of respondents (43/52) agreed that diagnostic bedside ultrasound should be a core curricular component of fellowship education.Diagnostic bedside ultrasound is increasingly prevalent in training and clinical use across the pediatric critical care medicine landscape despite frequently absent core programmatic infrastructural elements. These core elements are perceived as important to program development, regardless of division unit size. Shared standardized resources may assist in reducing the effort in core element implementation and allow us to measure important educational and clinical outcomes.

    View details for PubMedID 30113518

  • Certification in Critical Care Echocardiography: The Evolution of an Emerging PICU Practice PEDIATRIC CRITICAL CARE MEDICINE Su, E., Haileselassie, B., Hernandez, A., Diaz-Gomez, J. L. 2018; 19 (1): 88

    View details for PubMedID 29303901

  • E/e' ratio and outcome prediction in hypertrophic cardiomyopathy: the influence of outflow tract obstruction. European heart journal cardiovascular Imaging Lu, D. Y., Haileselassie, B., Ventoulis, I., Liu, H. Y., Liang, H. Y., Pozios, I., Canepa, M., Phillip, S., Abraham, M. R., Abraham, T. 2018; 19 (1): 101–7


    Diastolic dysfunction is thought to be an important pathophysiologic component of hypertrophic cardiomyopathy (HCM). However, there are conflicting data on the potential value of the mitral E/e' ratio. We examined whether left ventricular outflow tract (LVOT) obstruction influences the value of E/e' in predicting outcomes in HCM.Patients who met diagnostic criteria for HCM were enrolled. Diastolic function was assessed with complete two-dimensional and Doppler echocardiography. A composite clinical outcome including new onset atrial fibrillation, sustained ventricular tachycardia/fibrillation, heart failure, transplantation, and death was examined over a mean follow-up period of 4.2 years. Among 604 patients, 206 patients had an E/e' level ≥20. Patients with higher septal E/e' level were older, with more severe NYHA class, and more severe LVOT obstruction. Higher E/e' was associated with worse event-free survival in non-obstructive group and total HCM cohort. In addition, E/e' and LVOT pressure gradient were highly correlated in non-obstructive and total HCM, but not in labile or obstructive group. During follow-up period, 95 patients underwent myectomy. Post-op E/e' correlated significantly with LVOT pressure gradient (R = 0.306, P = 0.004). In these patients, post-op E/e' was associated with worse event-free survival (log-rank P = 0.030).Assessment of E/e' is useful for risk stratification in HCM patients. Nevertheless, the predictive power is confounded by dynamic LVOT obstruction. Higher E/e' predicts worse clinical outcomes in non-obstructive HCM and in labile/obstructive after myectomy.

    View details for DOI 10.1093/ehjci/jex134

    View details for PubMedID 28977350

  • Certification in Critical Care Echocardiography: The Evolution of an Emerging PICU Practice. Pediatr Crit Care Med. Su, E., Haileselassie, B., Hernandez, A., Díaz-Gómez, J. L. 2018 ; 19 ((1))
  • Myocardial oxidative stress correlates with left ventricular dysfunction on strain echocardiography in a rodent model of sepsis. Intensive care medicine experimental Haileselassie, B., Su, E., Pozios, I., Niño, D. F., Liu, H., Lu, D., Ventoulis, I., Fulton, W. B., Sodhi, C. P., Hackam, D., O'Rourke, B., Abraham, T. 2017; 5 (1): 21-?


    Recognition of cardiomyopathy in sepsis can be challenging due to the limitations of conventional measures such as ejection fraction (EF) and fractional shortening (FS) in the context of variable preload and afterload conditions. This study correlates myocardial function using strain echocardiography (SE) with cardiomyocyte oxidative stress in a murine model of sepsis.C57BL/6J mice were randomized into control (n = 10), sham (n = 25), and a cecal ligation and puncture (CLP) (n = 33) model of sepsis. Echocardiography was performed pre-, 12, 24, and 48 h post-injury. Cardiac pro-inflammatory cytokines and mitochondrial redox scavenger expression were evaluated in a subset of each arm. To evaluate the influence of redox scavenger upregulation on oxidative injury and cardiac function, CLP was performed on mitochondrial catalase-upregulated C57BL/6J MCAT(+/+) mice (n = 12) and wild-type (WT) animals for comparison.Septic C57BL/6J mice exhibited depressed longitudinal strain (LS) when compared to sham and control at 24 h (p < 0.01) and 48 h (p = 0.04) post-CLP despite having a preserved EF. Furthermore, there was a significant association between increased odds of mortality and depressed LS (OR = 1.23, p = 0.04). Septic C57BL/6J mice concomitantly demonstrated increased expression of cardiomyocyte pro-inflammatory cytokines and decreased expression of redox scavengers at 24 and 48 h. When comparing C57Bl/6 MCAT (+/+) mice and C57BL/6J WT mice, a significant decrease in LS was identified in the WT mice at 24 h (MCAT = -23 ± 5% vs. WT = -15 ± 4% p < 0.01) and 48 h (MCAT = -23 ± 7% vs. WT = -15 ± 4.3% p = 0.04) post-CLP which correlated with significant increase in the level of cardiac oxidative stress following CLP.In this sepsis model, SE identified cardiomyopathy despite normal EF. SE depression temporally coincides with upregulation of inflammatory cytokines and decreases expression of key mitochondrial ROS scavengers. Upregulation of redox scavenger (CAT) abrogates oxidative stress and cardiac dysfunction in this sepsis model.

    View details for DOI 10.1186/s40635-017-0134-5

    View details for PubMedID 28405943

  • Role of Global Longitudinal Strain in Predicting Outcomes in Hypertrophic Cardiomyopathy. The American journal of cardiology Liu, H., Pozios, I., Haileselassie, B., Nowbar, A., Sorensen, L. L., Phillip, S., Lu, D. Y., Ventoulis, I., Luo, H., Abraham, M. R., Abraham, T. P. 2017; 120 (4): 670–75


    Global longitudinal strain (GLS) is a sensitive indicator of global left ventricular function particularly in those with normal ejection fraction. We examined the potential value of GLS in predicting outcomes in hypertrophic cardiomyopathy (HC). Conventional and strain echocardiography was performed in 400 patients with HC followed for a median 3.1 years (interquartile range 1.2 to 5.6). Peak systolic strain from 3 apical views was averaged to calculate GLS. Patients were divided based on a previously published cutoff value of -16%. Additionally, we identified 4 HC subgroups based on GLS: GLS ≤ -20%, -20% < GLS ≤ -16%, -16% < GLS ≤ -10%, and GLS > -10%. The primary end point was a composite of new-onset sustained ventricular tachycardia/fibrillation, heart failure, cardiac transplantation, and all-cause death. Patients with GLS > -16% had significantly more events (17% vs 7%, p = 0.002). In the 4-group analysis, event rates increased with worsening GLS (5%, 7%, 14%, and 33%, respectively, p = 0.001). Event-free survival was significantly superior in those with GLS ≤ -16% versus GLS > -16% (p = 0.004); similarly, GLS > -10% portended a significantly worse event-free survival compared with each of the other 3 groups (p <0.01 for all pairwise comparisons). By univariate and multivariate Cox regression analysis, GLS remained significantly associated with the composite end point. GLS > -10% had 4 times the risk of events compared with GLS ≤ -16% (p = 0.006). In conclusion, echo-based GLS is independently associated with outcomes in HC. Patients with GLS > -10% have significantly higher event rates.

    View details for DOI 10.1016/j.amjcard.2017.05.039

    View details for PubMedID 28687124

  • Impact of peak provoked left ventricular outflow tract gradients on clinical outcomes in hypertrophic cardiomyopathy. International journal of cardiology Lu, D. Y., Hailesealassie, B., Ventoulis, I., Liu, H., Liang, H. Y., Nowbar, A., Pozios, I., Canepa, M., Cresswell, K., Luo, H. C., Abraham, M. R., Abraham, T. P. 2017; 243: 290–95


    Hypertrophic cardiomyopathy (HCM) is traditionally classified based on a left ventricular outflow tract (LVOT) pressure gradient of 30mmHg at rest or with provocation. There are no data on whether 30mmHg is the most informative cut-off value and whether provoked gradients offer any information regarding outcomes.Resting and provoked peak LVOT pressure gradients were measured by Doppler echocardiography in patients fulfilling guidelines criteria for HCM. A composite clinical outcome including new onset atrial fibrillation, ventricular tachycardia/fibrillation, heart failure, transplantation, and death was examined over a median follow-up period of 2.1years.Among 536 patients, 131 patients had resting LVOT gradients greater than 30mmHg. Subjects with higher resting gradients were older with more cardiovascular events. For provoked gradients, a bi-modal risk distribution was found. Patients with provoked gradients >90mmHg (HR 3.92, 95% CI 1.97-7.79) or <30mmHg (HR 2.15, 95% CI 1.08-4.29) have more events compared to those with gradients between 30 and 89mmHg in multivariable analysis. The introduction of two cut-off points for provoked gradients allowed HCM to be reclassified into four groups: patients with "benign" latent HCM (provoked gradient 30-89mmHg) had the best prognosis, whereas those with persistent obstructive HCM had the worst outcome.Provoked LVOT pressure gradients offer additional information regarding clinical outcomes in HCM. Applying cut-off points at 30 and 90mmHg to provoked LVOT pressure gradients further classifies HCM patients into low-, intermediate- and high-risk groups.

    View details for DOI 10.1016/j.ijcard.2017.04.039

    View details for PubMedID 28747034

  • Strain Echocardiography Parameters Correlate With Disease Severity in Children and Infants With Sepsis PEDIATRIC CRITICAL CARE MEDICINE Haileselassie, B., Su, E., Pozios, I., Fiskum, T., Thompson, R., Abraham, T. 2016; 17 (5): 383-390


    In the progression of severe sepsis, sepsis-induced myocardial dysfunction contributes to severity of illness and ultimate mortality. Identification of sepsis-induced myocardial dysfunction causing depressed cardiac function during critical illness has implications for ongoing patient management. However, assessing pediatric cardiac function traditionally relies on echocardiographic qualitative assessment and measurement of left ventricular ejection fraction or fractional shortening. These metrics are often insensitive for detecting early or regional myocardial dysfunction. Strain echocardiography is a contemporary echocardiographic modality that may be more sensitive to perturbations in cardiac function. This investigation hypothesizes that strain echocardiography metrics correlate with severity of illness in pediatric sepsis despite normal fractional shortening.Single-center retrospective observational study.Tertiary 36-bed medical/surgical PICU.Pediatric patients admitted with sepsis.None.Twenty-three children with sepsis received an echocardiogram in the study period. Patients with sepsis demonstrated abnormal peak systolic longitudinal strain for age (mean = -0.13 ± 0.07; p < 0.01) and low normal peak systolic circumferential strain (mean = -0.17 ± 0.14; p = 0.02) compared with internal controls as well as previously published normal values. Depressed strain was demonstrated in the septic patients despite having normal fractional shortening (mean = 0.41; 95% CI, 0.38-0.43). On initial echocardiographic imaging, worsening peak systolic longitudinal strain was associated with increasing lactate (p = 0.04).Pediatric patients with sepsis demonstrate evidence of depressed strain echocardiography parameters not shown by fractional shortening that correlate with clinical indices of sepsis severity. Whether strain echocardiography could eventually assist in grading pediatric sepsis severity and affect management is an area for potential future investigation.

    View details for DOI 10.1097/PCC.0000000000000683

    View details for Web of Science ID 000379595900008

    View details for PubMedID 26963758

    View details for PubMedCentralID PMC4856561

  • Oropharyngeal dermoid cyst in an infant with intermittent airway obstruction. A case report. The neuroradiology journal Wagner, M. W., Haileselassie, B., Kannan, S., Chen, C., Poretti, A., Tunkel, D. E., Huisman, T. A. 2014; 27 (5): 627-631


    Dermoid cysts are benign epithelial inclusions and cystic lesions that may occur in several locations including the oropharynx. We describe the case of a two-month-old baby girl who presented with progressive respiratory distress, hypoxemia, and feeding difficulties because of an oropharyngeal dermoid cyst. The child had an airway work-up that included laryngoscopy. However, the mass remained undetected. This is most likely explained by the mobile nature of the lesion, prolapsing into the high nasopharynx in supine position. In our patient, magnetic resonance imaging (MRI), initially performed to rule out brainstem pathology, revealed an oropharyngeal dermoid cyst. This case shows the potential role of neuroimaging in the diagnostic work-up of a young child presenting with respiratory distress by excluding a central nervous system lesion and diagnosing an "unexpected" nasopharyngeal mass lesion. In addition, MRI allowed exclusion of skull base lesions of neural origin such as an anterior meningoencephalocele or heterotopic neuroglial tissue which would be managed differently from pharyngeal masses.

    View details for DOI 10.15274/NRJ-2014-10085

    View details for PubMedID 25260210

    View details for PubMedCentralID PMC4237111

  • Fat Embolism: Evolution of Histopathological Changes in the Rat Lung JOURNAL OF ORTHOPAEDIC RESEARCH McIff, T. E., Poisner, A. M., Herndon, B., Lankachandra, K., Schutt, S., HaileSelassie, B., Patel, S., Quinn, T., Adler, F., Molteni, A. 2010; 28 (2): 191-197


    The pathophysiology of Fat Embolism Syndrome (FES) is poorly understood and subject to some controversy. Evaluation of the evolution of histological changes in the lungs of patients with FES is impractical. The current theories of FES were established through acute clinical observations and acute animal experiments, but sequential changes in the histology of lungs over a prolonged period have not been made. The progressive effects of fat embolization of the lungs were examined in a rat model over a period of 11 days. Triolein, a major bone marrow fat, was administered to conscious Sprague-Dawley rats via the caudal vein. Rats were euthanized at 24, 48, 96 h, and 11 days, but some died within a few hours. Histomorphometric evaluations of lung tissue were made, including stains for fat, collagen, and smooth muscle actin. Arterial and arteriolar patency decreased progressively up to 96 h, but returned toward normal after 11 days. A striking finding was the very early presence of inflammation and fibrosis after only several hours, persisting up to 11 days. The results of this study provide evidence of both very early and prolonged changes due to fat embolization.

    View details for DOI 10.1002/jor.20963

    View details for Web of Science ID 000273675700008

    View details for PubMedID 19688870