Michael Badellino

Lehigh Valley Health Network, Allentown, Pennsylvania, United States

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Publications (8)31.99 Total impact

  • Margaret M Moore · Michael D Pasquale · Michael Badellino ·
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    ABSTRACT: Of the 500,000 brain injuries in the United States annually, 80% are considered mild (mild traumatic brain injury). Unfortunately, 2% to 3% of them will subsequently deteriorate and result in severe neurologic dysfunction. Intracerebral changes in the elderly, chronic oral anticoagulation, and platelet inhibition may contribute to the development of intracranial bleeding after minor head injury. We sought to investigate the association of age and the use of anticoagulation and antiplatelet therapy with neurologic deterioration and the need for neurosurgical intervention in patients presenting with mild traumatic brain injury. A retrospective review of all adult (>14 years) patients admitted to our Level I trauma service with a Glasgow Coma Scale (GCS) score of 14 to 15 who underwent neurosurgical intervention during their hospital stay was performed. Patients were stratified into two groups, age <65 years and age ≥ 65 years. Each group was then further stratified by the use of anticoagulants: warfarin, aspirin, clopidogrel, or a combination. Mechanism of injury, prehospital complaints, admission GCS, type of neurosurgical intervention, intensive care unit length of stay, hospital length of stay, and discharge disposition were evaluated. Z test and logistic regression were used to compare proportions or percentages from different groups. Of the 7,678 patients evaluated during the study period, 101 (1.3%) required neurosurgical intervention. The ≥ 65 years population underwent significantly more interventions as did those patients on anticoagulants. All patients aged 65 years or older who present with a GCS score of >13 after head trauma should undergo a screening computed tomography of the head regardless of prehospital use of anticoagulation. Patients younger than 65 years can be selectively screened based on presenting complaints and mechanism of injury provided they are not on anticoagulation.
    05/2012; 73(1):126-30. DOI:10.1097/TA.0b013e31824b01af
  • Erik J Teicher · Rovinder S Sandhu · Dale A Dangleben · Michael M Badellino ·

    The American surgeon 07/2010; 76(7):780-2. · 0.82 Impact Factor
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    ABSTRACT: A monoacetyldiglyceride (MADG) markedly improves survival in a murine model of abdominal sepsis. MADGs have been shown to stimulate hematopoiesis in vitro. We examined effects of MADG administration in setting of cecal ligation and puncture (CLP) and hypothesized that oral (p.o.) administration of MADG would result in alterations of cytokine and chemokine expression after CLP. Four groups of 20 mice: sham group underwent celiotomy but not CLP; control group underwent CLP and administration of phosphate buffer solution; simultaneous treatment group had administration of 50 mg/kg MADG p.o. Immediately, before CLP and at 24, 48, and 72-hour post-CLP, posttreatment group had initial administration of MADG at 1-hour post-CLP, and at 24, 48, and 72-hour postoperative. We followed survival to 10-day postoperative. Serum and tissue levels of pro- and anti-inflammatory cytokines were measured. Serum levels of chemokines stromal cell-derived factor (SDF-1) and stem cell factor (SCF) were measured to ascertain if effects of MADG involve stimulation of bone marrow stromal and stem cells. Polymerase chain reaction was used to measure SDF and SCF mRNA expression in liver and lung. Administration of MADG (p.o.) significantly improved survival in mice after CLP with associated systemic alterations of a variety of cytokines. Increased levels of mRNA coding for SCF and SDF in lung and liver were found after CLP. Administration of MADG (p.o.) after CLP results in marked improvement in survival. Cytokine level changes demonstrate associated immunomodulatory effects. These effects may be mediated by bone marrow stromal and stem cell activation, evidenced by increases in SDF and SCF. Further study of behavior of bone marrow-derived stem cells in setting of sepsis is warranted. MADG may hold promise for use in treatment of sepsis.
    The Journal of trauma 01/2010; 68(1):62-8. DOI:10.1097/TA.0b013e3181c3fede · 2.96 Impact Factor
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    ABSTRACT: Hepatic angiography (HA) and hepatic angioembolization (HAE) are increasingly used to diagnose and treat intrahepatic arterial injuries. This study was performed to review indications, outcomes, and complications of HA/HAE in blunt trauma patients who underwent HAE as adjunct management of hepatic injury. A retrospective review of consecutive cases of HA/HAE at a Level I trauma center during an 8-year period. Data include demographics, physiologic condition, liver injury grade, HA/HAE indications, outcomes, morbidity, and mortality. Seventy-nine patients underwent diagnostic HA; 31 (39%) had subsequent HAE. Fifty-eight hemodynamically stable patients had computerized axial tomographic (CT) scan followed by HA. HA was performed for contrast blush on CT in 30 (52%) of 58 patients, high-grade liver injury in 4 (7%), subsequent hemodynamic instability in 15 (27%), and angiography planned for other purpose in 9 (17%). HA confirmed arterial injury and led to HAE in 50% of patients with contrast blush on CT or high-grade liver injury. HA was negative when performed for hemodynamic instability or for other primary purposes. Twenty-one hemodynamically unstable patients underwent emergent laparotomy followed by postoperative HA with 11 (50%) requiring HAE. Overall mortality in HAE group was 16%, and liver-related morbidity was 29% usually presenting as gallbladder or liver necrosis. HA/HAE should be used when CT scan suggests associated intrahepatic arterial or high-grade injury in the management of hepatic injuries and should also be considered after laparotomy and perihepatic packing to control inaccessible intrahepatic hemorrhage. Mortality related to HAE is uncommon, but morbidity occurs frequently.
    The Journal of trauma 10/2009; 67(4):769-73. DOI:10.1097/TA.0b013e3181b5ce7f · 2.96 Impact Factor

  • Critical Care Medicine 12/2005; 33(Supplement). DOI:10.1097/00003246-200512002-00145 · 6.31 Impact Factor

  • Critical Care Medicine 12/2005; 33(Supplement). DOI:10.1097/00003246-200512002-00167 · 6.31 Impact Factor

  • Critical Care Medicine 12/2005; 33(Supplement). DOI:10.1097/00003246-200512002-00011 · 6.31 Impact Factor

  • Critical Care Medicine 12/2005; 33(Supplement). DOI:10.1097/00003246-200512002-00144 · 6.31 Impact Factor