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1.
Global Spine J ; 13(6): 1658-1670, 2023 Jul.
Article in English | MEDLINE | ID: mdl-36562179

ABSTRACT

STUDY DESIGN: Systematic Review and Meta-analysis. OBJECTIVE: Postoperative urinary retention (POUR) is a common complication following lumbar spine surgery (LSS) and timely recognition is imperative to avoid long-term consequences. The aim of the current meta-analysis was to systematically review the literature in order to identify risk factors associated with POUR after LSS. METHODS: In accordance with PRISMA guidelines, a systematic review of the literature was performed using Pubmed, EMBASE, and MEDLINE database for articles on POUR following LSS. A meta-analysis was performed comparing patients with and without POUR; and the factors associated with this adverse event were analyzed. The pooled data were reported as mean differences with 95% confidence intervals (CI; P < .05). Heterogeneity among the studies was evaluated using the I2 statistic. RESULTS: The meta-analysis included 10 studies compromised of 30,300 patients. Based on our analysis, patients who were male, were older in age, underwent instrumented fusion, had diabetes mellitus, coronary artery disease, or benign prostatic hypertrophy had significantly higher risk of developing POUR. Additionally, patients in who developed POUR had significantly longer surgical times and higher volumes of intra-operative fluid administration, as compared with non-POUR patients. The POUR patients also had a significantly higher association with urinary tract infection. Prior surgery, BMI, length of stay, and smoking status did not reveal any statistical association with POUR. CONCLUSIONS: Risk factors associated with POUR following LSS include male gender, older age, longer surgical times, fusion procedures, larger volumes of intraoperative infusions, and associated comorbidities like DM, CAD, and BPH.

2.
Am J Case Rep ; 22: e932048, 2021 Jul 08.
Article in English | MEDLINE | ID: mdl-34234096

ABSTRACT

BACKGROUND Brugada syndrome is a rare ion channelopathy that can lead to sudden cardiac death and lethal arrhythmias in patients without a structural cardiac defect, the most common of which being the gain-of-function mutation of the SCN5a sodium ion channel involving phase 0 of the cardiac action potential. In 2012, BrS electrocardiogram findings were redefined and classified as either congenital Brugada syndrome (BrS) or Brugada phenocopies (BrP). Several etiologies of BrP have been reported, such as metabolic derangements, electrolyte abnormalities, cardiovascular diseases, and pulmonary embolism. CASE REPORT A 28-year-old man presented to the Emergency Department unresponsive. An initial ECG taken by Emergency Medical Services (EMS) was interpreted as a STEMI. An initial ECG in the ED showed a Brugada type I ECG pattern in leads V1-V2 and hyperacute T wave abnormalities, among other findings. Additionally, the patient had a serum potassium level of 9 mmol/L, glucose level of 1375 mmol/L, and peak cardiac troponin-I of 20.452 µg/L. All underlying medical conditions were stabilized, electrolyte and metabolic abnormalities were corrected, and subsequent normalization of electrocardiographic findings was achieved. CONCLUSIONS Distinguishing congenital Brugada syndrome from Brugada phenocopies can be difficult, especially when patients present to the ED with severe underlying conditions. Several factors can be used to direct clinical suspicion towards one or the other; however, confirmation may require EP studies and further tests. In this case, the following findings were suggestive of BrP: presence of an identifiable underlying abnormality, correction of the underlying condition resolves the ECG pattern, and the absence of family history of sudden cardiac death.


Subject(s)
Alcoholic Intoxication , Brugada Syndrome , Diabetic Ketoacidosis , Hyperkalemia , Adult , Brugada Syndrome/diagnosis , Diabetic Ketoacidosis/complications , Diabetic Ketoacidosis/diagnosis , Electrocardiography , Humans , Hyperkalemia/diagnosis , Hyperkalemia/etiology , Male
3.
Mol Pain ; 14: 1744806918796763, 2018.
Article in English | MEDLINE | ID: mdl-30178698

ABSTRACT

Chronic orofacial pain is a significant health problem requiring identification of regulating processes. Involvement of epigenetic modifications that is reported for hindlimb neuropathic pain experimental models, however, is less well studied in cranial nerve pain models. Three independent observations reported here are the (1) epigenetic profile in mouse trigeminal ganglia (TG) after trigeminal inflammatory compression (TIC) nerve injury mouse model determined by gene expression microarray, (2) H3K9 acetylation pattern in TG by immunohistochemistry, and (3) efficacy of histone deacetylase (HDAC) inhibitors to attenuate development of hypersensitivity. After TIC injury, ipsilateral whisker pad mechanical sensitization develops by day 3 and persists well beyond day 21 in contrast to sham surgery. Global acetylation of H3K9 decreases at day 21 in ipsilateral TG . Thirty-four genes are significantly ( p < 0.05) overexpressed in the ipsilateral TG by at least two-fold at either 3 or 21 days post-trigeminal inflammatory compression injury. The three genes most overexpressed three days post-trigeminal inflammatory compression nerve injury are nerve regeneration-associated gene ATF3, up 6.8-fold, and two of its regeneration-associated gene effector genes, Sprr1a and Gal, up 174- and 25-fold, respectively. Although transcription levels of 25 of 32 genes significantly overexpressed three days post-trigeminal inflammatory compression return to constitutive levels by day 21, these three regeneration-associated genes remain significantly overexpressed at the later time point. On day 21, when tissues are healed, other differentially expressed genes include 39 of the top 50 upregulated and downregulated genes. Remarkably, preemptive manipulation of gene expression with two HDAC inhibitors (HDACi's), suberanilohydroxamic acid (SAHA) and MS-275, reduces the magnitude and duration of whisker pad mechanical hypersensitivity and prevents the development of a persistent pain state. These findings suggest that trigeminal nerve injury leads to epigenetic modifications favoring overexpression of genes involved in nerve regeneration and that maintaining transcriptional homeostasis with epigenetic modifying drugs could help prevent the development of persistent pain.


Subject(s)
Facial Pain/complications , Gene Expression Regulation/physiology , Histone Deacetylase Inhibitors/therapeutic use , Hyperalgesia/etiology , Hyperalgesia/prevention & control , Activating Transcription Factor 3/genetics , Activating Transcription Factor 3/metabolism , Animals , Benzamides/therapeutic use , Cornified Envelope Proline-Rich Proteins/genetics , Cornified Envelope Proline-Rich Proteins/metabolism , Disease Models, Animal , Facial Pain/etiology , Facial Pain/pathology , Functional Laterality , Ganglia, Spinal/pathology , Gene Expression Regulation/drug effects , Histone Deacetylases/metabolism , Male , Mice , Mice, Inbred BALB C , Nerve Tissue Proteins/genetics , Nerve Tissue Proteins/metabolism , Nylons , Pain Threshold/drug effects , Physical Stimulation/adverse effects , Pyridines/therapeutic use , Pyrroles/therapeutic use , Trigeminal Nerve Injuries/complications , Vibrissae/innervation
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