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1.
Spine Deform ; 12(3): 739-746, 2024 May.
Article in English | MEDLINE | ID: mdl-38413472

ABSTRACT

INTRODUCTION: Pedicle screws are the primary method of vertebral fixation in scoliosis surgery, but there are lingering concerns over potential malposition. The rates of pedicle screw malposition in pediatric spine surgery vary from 10% to 21%. Malpositioned screws can lead to potentially catastrophic neurological, vascular, and visceral complications. Pedicle screw positioning in patients with neuromuscular scoliosis is challenging due to a combination of large curves, complex pelvic anatomy, and osteopenia. This study aimed to determine the rate of pedicle screw malposition, associated complications, and subsequent revision from screws placed with the assistance of machine vision navigation technology in patients with neuromuscular scoliosis undergoing posterior instrumentation and fusion. METHOD: A retrospective analysis of the records of patients with neuromuscular scoliosis who underwent thoracolumbar pedicle screw insertion with the assistance of machine-vision image guidance navigation was performed. Screws were inserted by either a staff surgeon, orthopaedic fellow, or orthopaedic resident. Post-operative ultra-low dose CT scans were used to assess pedicle screw accuracy. The Gertzbein classification was used to grade any pedicle breaches (grade 0, no breach; grade 1, <2 mm; grade 2, 2-4 mm; grade 3, >4 mm). A screw was deemed accurate if no breach was identified (grade 0). RESULTS: 25 patients were included in the analysis, with a mean age of 13.6 years (range 11 to 18 years; 13/25 (52.0%) were female. The average pre-operative supine Cobb angle was 90.0 degrees (48-120 degrees). A total of 687 screws from 25 patients were analyzed (402 thoracic, 241 lumbosacral, 44 S2 alar-iliac (S2AI) screws). Surgical trainees (fellows and orthopaedic residents) inserted 46.6% (320/687) of screws with 98.8% (4/320) accuracy. The overall accuracy of pedicle screw insertion was 98.0% (Grade 0, no breach). All 13 breaches that occurred in the thoracic and lumbar screws were Grade 1. Of the 44 S2AI screws placed, one screw had a Grade 3 breach (2.3%) noted on intra-operative radiographs following rod placement and correction. This screw was subsequently revised. None of the breaches resulted in neuromonitoring changes, vessel, or visceral injuries. CONCLUSION: Machine vision navigation technology combined with careful free-hand pedicle screw insertion techniques demonstrated high levels of pedicle screw insertion accuracy, even in patients with challenging anatomy.


Subject(s)
Pedicle Screws , Scoliosis , Spinal Fusion , Humans , Scoliosis/surgery , Scoliosis/diagnostic imaging , Retrospective Studies , Adolescent , Female , Spinal Fusion/instrumentation , Spinal Fusion/methods , Spinal Fusion/adverse effects , Male , Child , Lumbar Vertebrae/surgery , Lumbar Vertebrae/diagnostic imaging , Thoracic Vertebrae/surgery , Thoracic Vertebrae/diagnostic imaging , Surgery, Computer-Assisted/methods , Tomography, X-Ray Computed
3.
Spine Deform ; 11(6): 1539-1542, 2023 Nov.
Article in English | MEDLINE | ID: mdl-37306937

ABSTRACT

It is a historic and common practice while performing spine surgery on patients with a VNS has been to have the patient's neurologist turn off the VNS generator in the pre-operative anesthetic care unit and to use bipolar rather than monopolar electrocautery. Here we report a case of a 16-year-old male patient with cerebral palsy and refractory epilepsy managed with an implanted VNS who had scoliosis surgery (and subsequent hip surgery) conducted with the use of monopolar cautery. Although VNS manufacturer guidelines suggest that monopolar cautery should be avoided, perioperative care providers should consider its selective use in high-risk instances (with greater risks of morbidity and mortality due to blood loss which outweigh the risk of surgical re-insertion of a VNS) such as cardiac or major orthopedic surgery. Considering the number of patients with VNS devices presenting for major orthopedic surgery is increasing, it is important to have an approach and strategy for perioperative management of VNS devices.

4.
Transfus Apher Sci ; 59(5): 102851, 2020 Oct.
Article in English | MEDLINE | ID: mdl-32571640

ABSTRACT

Throughout storage, red blood cells (RBCs) undergo detrimental changes in viability and their ability to effectively transport oxygen. RBC storage lesions are mediated, in part, by a progressive loss of cell deformability, and associated with the release of extracellular vesicles (EVs). Accumulation of EVs during the storage of RBCs correlates with a decrease in RBC surface area to volume ratio. Similarly, the loss of RBC-deformability is associated with loss of RBC surface area to volume ratio. In this study we thus tested whether loss of RBC-deformability is associated with increased RBC-EV production during blood storage. EVs obtained by differential centrifugation of stored RBCs (non-leukoreduced non-irradiated or leukoreduced γ-irradiated RBCs stored 35 or 28 days respectively) were enumerated by high-sensitivity flow cytometry. RBC deformability was quantified, using a cell-flow-properties-analyzer, by measuring the median cell elongation ratio (MER) and percentage of low and high deformable cells in the population (%, LDFC, and HDFC, respectively). The number of EVs was inversely correlated with the MER and positively correlated with the %LDFC with both measures showing highly significant logarithmic dependence with EV levels in stored RBCs. Considering how highly deformable cells did not correlate with EV formation as compared with low deformable RBCs we propose that the formation of EVs is a key factor leading to increased RBC-rigidity.


Subject(s)
Blood Preservation/methods , Erythrocytes/metabolism , Extracellular Vesicles/metabolism , Humans
6.
Anaesthesia ; 74(9): 1130-1137, 2019 09.
Article in English | MEDLINE | ID: mdl-30932171

ABSTRACT

Haemostatic activation during cardiopulmonary bypass is associated with prothrombotic complications. Although it is not possible to detect and quantify haemostatic activation directly, platelet dysfunction, as measured with point-of-care-assays, may be a useful surrogate. In this study, we assessed the association between cardiopulmonary bypass-associated platelet dysfunction and adverse outcomes in 3010 cardiac surgical patients. Platelet dysfunction, as measured near the end of the rewarming phase of cardiopulmonary bypass, was calculated as the proportion of non-functional platelets after activation with collagen. Logistic regression and multivariable analyses were applied to assess the relationship between platelet dysfunction and a composite of in-hospital death; myocardial infarction; stroke; deep vein thrombosis or pulmonary embolism; and acute kidney injury (greater than a two-fold increase in creatinine). The outcome occurred in 251 (8%) of 3010 patients. The median (IQR [range]) percentage platelet dysfunction was less for those without the outcome as compared with those with the outcome; 14% (8-28% [1-99%]) vs. 19% (11-45% [2-98%]), p < 0.001. After risk adjustment, platelet dysfunction was independently associated with the composite outcome (p < 0.001), such that for each 1% increase in platelet dysfunction there was an approximately 1% increase in the composite outcome (OR 1.012; 95%CI 1.006-1.018). This exploratory study suggests that cardiopulmonary bypass-associated platelet dysfunction has prognostic value and may be a useful clinical measure of haemostatic activation in cardiac surgery.


Subject(s)
Blood Platelet Disorders/epidemiology , Cardiac Surgical Procedures , Postoperative Complications/epidemiology , Adolescent , Adult , Aged , Aged, 80 and over , Canada/epidemiology , Cluster Analysis , Comorbidity , Female , Humans , Male , Middle Aged , Retrospective Studies , Risk Factors , Treatment Outcome , Young Adult
7.
J Pharmacol Exp Ther ; 296(2): 312-21, 2001 Feb.
Article in English | MEDLINE | ID: mdl-11160612

ABSTRACT

The stress-activated mitogen-activated protein kinase (MAPK) p38 has been linked to the production of inflammatory cytokines/mediators/inflammation and death/apoptosis following cell stress. In these studies, a second-generation p38 MAPK inhibitor, SB 239063 (IC(50) = 44 nM), was found to exhibit improved kinase selectivity and increased cellular (3-fold) and in vivo (3- to 10-fold) activity over first-generation inhibitors. Oral SB 239063 inhibited lipopolysaccharide-induced plasma tumor necrosis factor production (IC(50) = 2.6 mg/kg) and reduced adjuvant-induced arthritis (51% at 10 mg/kg) in rats. SB 239063 reduced infarct volume (48%) and neurological deficits (42%) when administered orally (15 mg/kg, b.i.d.) before moderate stroke. Intravenous SB 239063 exhibited a clearance of 34 ml/min/kg, a volume of distribution of 3 l/kg, and a plasma half-life of 75 min. An i.v. dosing regimen that provided effective plasma concentrations of 0.38, 0.75, or 1.5 microg/ml (i.e., begun 15 min poststroke and continuing over the initial 6-h p38 activation period) was used. Significant and dose-proportional brain penetration of SB 239063 was demonstrated during these infusion periods. In both moderate and severe stroke, intravenous SB 239063 produced a maximum reduction of infarct size by 41 and 27% and neurological deficits by 35 and 33%, respectively. No effects of the drug were observed on cerebral perfusion, hemodynamics, or body temperature. Direct neuroprotective effects from oxygen and glucose deprivation were also demonstrated in organotypic cultures of rat brain tissue. This robust in vitro and in vivo SB 239063-induced neuroprotection emphasizes the potential role of MAPK pathways in ischemic stroke and also suggests that p38 inhibition warrants further study, including protection in other models of nervous system injury and neurodegeneration.


Subject(s)
Brain/pathology , Enzyme Inhibitors/therapeutic use , Imidazoles/therapeutic use , Ischemic Attack, Transient/drug therapy , Ischemic Attack, Transient/pathology , Mitogen-Activated Protein Kinases/antagonists & inhibitors , Neuroprotective Agents/therapeutic use , Pyrimidines/therapeutic use , Animals , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Body Temperature/drug effects , Cerebrovascular Circulation/drug effects , Hemodynamics/drug effects , Hippocampus/pathology , Inflammation/pathology , Inflammation/prevention & control , Organ Culture Techniques , Pyridines/therapeutic use , Rats , Rats, Inbred Lew , Rats, Inbred SHR , p38 Mitogen-Activated Protein Kinases
8.
J Cardiovasc Pharmacol ; 33(5): 703-10, 1999 May.
Article in English | MEDLINE | ID: mdl-10226856

ABSTRACT

The hemodynamic and cardioprotective properties of the novel adenosine A1/A2 receptor agonist AMP 579 (IS-[1a,2b,3b,4a(S*)]-4-[7-[[1-[(3-chloro-2-thienyl)methyl]propylamino]- 3H-imidazo[4,5-b]pyridin-3-yl]-N-ethyl-2,3-dihydroxy cyclopentanecarboxamide) were studied in two canine models designed to simulate (a) mild single-vessel coronary artery disease, and (b) myocardial ischemia/reperfusion injury. In the first model, a moderate stenosis was placed on the left circumflex coronary artery (LCCA), and the effects of AMP 579 on regional myocardial blood flow were assessed. AMP 579, 10 micrograms/kg/min, i.v., for 10 min, induced coronary dilation without causing endocardial steal. In the model of ischemia/reperfusion injury (60 min LCCA occlusion/5 h reperfusion), AMP 579, 10 micrograms/kg/min, i.v., administered for 15 min before ischemia significantly decreased myocardial infarct size. Control infarct size to area at risk (IS/AAR) equaled 34 +/- 3% (n = 9); IS/AAR for AMP 579-treated dogs equaled 16 +/- 4% (n = 9). Preconditioning (5 min LCCA occlusion + 10 min reperfusion) immediately before the 60-min LCCA occlusion also resulted in a marked decrease in IS/AAR: 9 +/- 3% (n = 6). The selective A1 agonist CPA reduced infarct size when administered at 3 micrograms/kg/min, i.v., for 15 min before LCCA occlusion: IS/AAR = 11 +/- 3% (n = 5). Pretreatment of animals with the adenosine-receptor antagonist 8-SPT, 10 mg/kg, i.v., attenuated the myocardial protective effects associated with preconditioning, CPA, and AMP 579, resulting in IS/AAR values of 28 +/- 7% (n = 7), 28 +/- 4% (n = 8), and 26 +/- 3% (n = 8), respectively. The ability of 8-SPT to block the cardioprotective effects suggests that these effects were mediated through an interaction with adenosine receptors. These experimental results indicate that AMP 579 is an effective coronary vasodilator, which also can protect the heart from ischemic injury. Thus AMP 579 has the potential to be useful in cardiovascular therapeutics.


Subject(s)
Coronary Circulation/drug effects , Heart/drug effects , Imidazoles/pharmacology , Purinergic P1 Receptor Agonists , Pyridines/pharmacology , Animals , Coronary Disease/physiopathology , Dogs , Heart/physiopathology , Ischemic Preconditioning, Myocardial , Myocardial Infarction/pathology , Myocardial Infarction/physiopathology , Myocardial Ischemia/pathology , Myocardial Ischemia/physiopathology , Myocardial Reperfusion Injury/pathology , Myocardial Reperfusion Injury/physiopathology , Regional Blood Flow/drug effects
9.
Thromb Haemost ; 78(4): 1278-85, 1997 Oct.
Article in English | MEDLINE | ID: mdl-9364998

ABSTRACT

A canine model of electrolytic injury-induced coronary artery thrombosis and rtPA-induced thrombolysis was used to evaluate the relative antithrombotic efficacy of enoxaparin (a low molecular weight heparin), conventional therapy (heparin or heparin plus aspirin), and hirulog (a direct thrombin inhibitor), when used as adjunctive therapy during thrombolysis. After 60 min of clot aging, adjunctive therapy was begun at doses which elevated APTT approximately 2-fold over baseline. Fifteen minutes after the start of adjunctive therapy, recombinant tissue plasminogen activator (rtPA) was administered (100 microg/kg i.v. bolus + 20 microg/kg/min for 60 min). Adjunctive therapy continued for 1 h after termination of rtPA and blood flow was monitored for two additional hours. Enoxaparin (1 mg/kg i.v. bolus + 30 microg/kg/min, n = 10 for each treatment group) was the only adjunctive treatment that significantly increased the total minutes of flow (143 +/- 25 min out of a possible 240 min, vs 54 +/- 25 min for vehicle, p <0.05) and decreased thrombus mass (6.0 +/- 1.3 mg vs 11.8 +/- 3.2 mg for vehicle). Although hirulog (2 mg/kg i.v. bolus + 40 microg/kg/min) did not significantly increase the minutes of flow (120 +/- 27 min, p <0.06) or decrease thrombus mass (8.7 +/- 1.7 mg) compared to vehicle, these values were not significantly different than those measured in the enoxaparin group. However, the results with hirulog were achieved at the expense of a significantly greater increase in template bleeding time than that measured during enoxaparin treatment. Minutes of flow for heparin (50 U/kg i.v. bolus + 0.6 U/kg/min) and heparin plus aspirin (5 mg/kg i.v. bolus) were 69 +/- 20 and 60 +/- 23 min, respectively; thrombus masses were 8.2 +/- 1.3 and 7.3 +/- 1.0 mg, respectively. In summary, enoxaparin was more effective than conventional therapy in this model in terms of vessel patency and thrombus mass, and was as effective as hirulog, at least at a dose of hirulog that only modestly impaired hemostasis. Therefore, enoxaparin may prove to be a safe and effective alternative agent for adjunctive therapy during thrombolysis with rtPA.


Subject(s)
Coronary Thrombosis/drug therapy , Enoxaparin/therapeutic use , Fibrinolytic Agents/therapeutic use , Heparin/therapeutic use , Hirudins/analogs & derivatives , Peptide Fragments/therapeutic use , Platelet Aggregation Inhibitors/therapeutic use , Thrombolytic Therapy , Tissue Plasminogen Activator/therapeutic use , Adenosine Diphosphate/pharmacology , Animals , Aspirin/administration & dosage , Aspirin/pharmacology , Aspirin/therapeutic use , Aspirin/toxicity , Bleeding Time , Collagen/pharmacology , Dogs , Drug Evaluation, Preclinical , Drug Synergism , Drug Therapy, Combination , Enoxaparin/administration & dosage , Enoxaparin/pharmacology , Enoxaparin/toxicity , Factor Xa Inhibitors , Female , Fibrinolytic Agents/administration & dosage , Fibrinolytic Agents/pharmacology , Fibrinolytic Agents/toxicity , Hemorrhage/chemically induced , Hemostasis/drug effects , Heparin/administration & dosage , Heparin/pharmacology , Heparin/toxicity , Hirudin Therapy , Hirudins/administration & dosage , Hirudins/pharmacology , Hirudins/toxicity , Male , Partial Thromboplastin Time , Peptide Fragments/administration & dosage , Peptide Fragments/pharmacology , Peptide Fragments/toxicity , Platelet Aggregation/drug effects , Platelet Aggregation Inhibitors/administration & dosage , Platelet Count/drug effects , Prothrombin/antagonists & inhibitors , Prothrombin Time , Recombinant Proteins/administration & dosage , Recombinant Proteins/pharmacology , Recombinant Proteins/therapeutic use , Recombinant Proteins/toxicity , Recurrence , Safety , Thrombin/pharmacology , Tissue Plasminogen Activator/administration & dosage , Tissue Plasminogen Activator/pharmacology , Tissue Plasminogen Activator/toxicity
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