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Reducing Surgery for Pediatric Posttonsillectomy Hemorrhage Using Tranexamic Acid: A Quality Improvement Initiative
Get PDFObjective: Evaluate the use of tranexamic acid (TXA) and observation as a management option for pediatric patients presenting with posttonsillectomy hemorrhage (PTH). Study Design: Retrospective analysis of a prospectively implemented quality improvement initiative with a historical control comparison group. Setting: Tertiary children\u27s hospital. Methods: Patients \u3c 18 years of age who underwent adenotonsillectomy (AT) and returned to the Emergency Department for PTH were included. Patients who were stable without large volume or active bleeding were given intravenous TXA and admitted for overnight observation. Data were compared in a before-and-after analysis: preprotocol (April 2022 to March 2023) versus postprotocol (April 2023 to March 2024). For cost-effectiveness analysis, we analyzed aggregated claims data from a commercial claims database. Results: Preprotocol 1800 adenotonsillectomies were performed, and 40 procedures were performed for control of hemorrhage (2.2 per 100 AT). Postprotocol 2356 adenotonsillectomies were performed, and 30 procedures were performed to control hemorrhage (1.3 per 100 AT) showing a significant reduction in return to the operating room (relative risk [RR] = 0.59, 95% confidence interval [CI] [0.358, 0.916], P-value.020). There were no reported adverse events attributable to TXA. An estimated 21 surgeries were avoided, and 26 additional patients were observed in the hospital during the postprotocol period, for an estimated net cost savings of $174,970. Conclusion: The implementation of a standardized TXA protocol significantly reduced the need for return to the operating room for PTH in pediatric patients, without complications and with net cost savings to the health care system
History of psychedelic drug science and molecular pharmacology
No full textClassic psychedelics have been used by various cultures for millennia for healing and religious purposes. The modern era of psychedelic science began with the first empirical experiments by Dr. Arthur Heffter in 1898 to determine just what they are when he discovered the active alkaloid in the peyote cactus responsible for its intoxicating effects and named it mescaline. As with many aspects of society there has been a dramatic and often contentious relationship between ‘western’ society and psychedelics. In the early to mid-20th century, they were seen as valuable medicines with great potential for healing, and as scientific tools for understanding in the nascent field of neuroscience. As the counterculture of the 1960s embraced psychedelics as elements of youthful protest, governments around the world labeled them as dangerous, with no medical value. That ultimately led to severe legal penalties for their possession and essentially halted any significant scientific advances. No clinical studies were carried out for nearly 20 years, with very few preclinical studies performed by only a handful of researchers. As the political climate changed, clinical trials were once again allowed, culminating in several high profile published studies on the efficacy of psychedelics to treat psychiatric disorders. Around that time a paradigm shift in the acceptance of psychedelics as medicines to benefit society began to occur, spurring the rapid growth of the ecosystem surrounding psychedelics research. This review presents an overview of the last 125 years of psychedelic science, with key events and findings along the way highlighted leading to a greater understanding of their pharmacology, chemistry, and therapeutic potential
Direct Naloxone Distribution in the Emergency Department Increases Naloxone Access for Patients Following Accidental Overdose
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Role of Perinasal Musculature in Ipsilateral Nasal Obstruction During Synkinesis Progression
No full textBackground: Facial synkinesis can lead to unintended activation of perinasal muscles, contributing to dynamic nasal obstruction. Objective: To determine whether targeted botulinum toxin injections, compared to no treatment, reduce new ipsilateral nasal obstruction symptoms in patients with facial synkinesis, as measured by patient-reported outcomes and the Nasal Obstruction Symptom Evaluation (NOSE) scale. Methods: A retrospective review was conducted of patients presenting with ipsilateral nasal obstruction and synkinesis at a multidisciplinary facial nerve clinic. Botulinum toxin (2-2.5 units) was injected into the supra-alar nasalis and depressor septi muscles. Symptom improvement was assessed at 4 weeks using patient-reported outcomes and the NOSE scale. Results: Of 99 treated synkinetic patients, 23 (23.5%) reported new-onset nasal obstruction. Following chemodenervation, 74% experienced symptom relief, 4% had no improvement, and 22% were indeterminate. NOSE scores significantly improved from a mean of 44.86 to 28.93, with a mean difference of 15.93 (95% confidence interval: 2.86-29.00). Conclusion: Botulinum toxin injections targeting the perinasal musculature significantly improved nasal obstruction symptoms in patients with facial synkinesis
Meconium Periorchitis and Pathological Associations With Testicular and Scrotal Development: Three Case Reports and Review
No full textMeconium periorchitis, while often benign, has been associated with testicular abnormalities and scrotal defects. We present three cases exhibiting these associations. Case one presented with a right neonatal torsion. Exploration demonstrated a necrotic right testicle with an obliterated cord and a meconium-stained left testicle without torsion that later atrophied. Cases 2 and 3 both presented at birth with bilateral scrotoschisis, transverse ectopia, and meconium staining. Meconium periorchitis may have a role in testicular loss and scrotal defects. The resulting defects may lead to transverse testicular ectopia and scrotoschisis. If discovered in utero, a prompt testicular exam may be warranted after birth
Targeting Kinin B1R Attenuates Hypertension Through AT1R-Dependent Mechanisms
No full textBACKGROUND: Neurogenic hypertension is chronically high blood pressure that is initiated and maintained through excessive sympathetic nervous system activity and has been associated with increased B1R (kinin B1 receptor) activation. We previously reported a central role for B1R in mediating inflammatory pathways in the development of deoxycorticosterone acetate salt hypertension. Additionally, we identified a causal relationship between B1R expression after Ang II (angiotensin II) stimulation, and that B1R can mediate the bidirectional interaction between neuroinflammation and oxidative stress. However, whether there are any interactions between AT1R (Ang II-type I receptor) and B1R, and if B1R can mediate the effects of Ang II-induced hypertension, has not yet been investigated. METHODS: We used a well-established mouse model of Ang II-induced hypertension to test the hypothesis that B1R activation contributes to increased sympathoexcitation, autonomic dysfunction, oxidative stress, and inflammation, potentially through interactions with AT1R. Wild-type and BIR knockout mice were infused with Ang II or saline via osmotic minipump for 28 days, then functional and molecular changes in response to Ang II were assessed. RESULTS: Ang II in wild-type mice led to significant increases in B1R expression associated with sympathoexcitation, autonomic dysfunction, impaired baroreflex sensitivity, and enhanced blood pressure, whereas these changes were attenuated in B1R gene-deficient mice. B1R was shown to directly interact with AT1R, and activation of B1R was involved with microglial activation and subsequent neuroinflammation, increased neuronal firing, and altered synaptic density. We further used pharmacological blockade of B1R to dismiss potential developmental alterations in gene-deficient mice. Specific B1R antagonist attenuated Ang II-induced increases in blood pressure, supporting the role of B1R in blood pressure regulation. CONCLUSIONS: Our data provide the first evidence of the role of B1R in Ang II-induced hypertension and its interactions with AT1R, highlighting B1R as a potential therapeutic target for hypertension
Should we subtype gastric intestinal metaplasia in gastric biopsies, a single institution\u27s experience
No full textGastric intestinal metaplasia (GIM) is considered a risk factor for gastric dysplasia and adenocarcinoma. While surveillance endoscopies are often performed, particularly for incomplete GIM, the clinical value of histologic subtyping (complete, incomplete, or mixed) remains unclear. This study evaluated the progression risk of different GIM subtypes diagnosed through random gastric biopsies and their association with various clinical factors. Archived pathology data from 206 gastric biopsy cases were analyzed, including 52 negative controls, 56 complete GIM, 54 incomplete GIM, and 44 mixed GIM. Histologic slides were reviewed for subtype confirmation and other pathological changes; clinical data were extracted from medical records. Multiple linear regression was conducted for correlation analysis, and Analysis of Variance was used to compare group means. GIM was predominantly located in the antrum. Over a mean follow-up period of 52.2 months, none of the patients, including 12 under mapping surveillance, developed gastric neoplasia. Significant associations were found between Helicobacter pylori (H. pylori) and all types of GIM. H. pylori infection was also significantly associated with the extent of the GIM. Hypertension showed a trend toward significance in correlation with GIM, but no other associations were identified between GIM and demographic or clinical factors such as gender, age, smoking, diabetes mellitus, or hyperlipidemia. Our findings suggest that the routine subtyping GIM in pathology reports may not be necessary, given the lack of progression to any type of neoplasia within the follow-up period. However, the redemonstrated association between H. pylori and GIM emphasizes the importance of eradication therapy
The Interplay of Oxidative Stress, Mitochondrial Dysfunction, and Neuroinflammation in Autism Spectrum Disorder: Behavioral Implications and Therapeutic Strategies
No full textAutism spectrum disorder (ASD) deals with several symptoms, including language and speech impairment and developmental delays. The main brain regions affected could be the prefrontal cortex (PFC) or the temporal lobe. The detrimental features could include oxidative stress, mitochondrial dysfunction, and neuroinflammation. Most often, these phenomena are interrelated and can lead to one another, creating a vicious cycle. They also influence the regulation of certain genes involved in the pathogenesis of ASD or related behavior. In the brain regions prone to these detrimental features, a cascade of free radicals, inflammatory cytokines, and mitochondrial energy disruptions is initiated. These actions during the prenatal or developmental stage of the child potentially lead to ASD symptomatic features, such as social isolation, communication difficulty, speech and language impairment, cognitive dysfunction, and intellectual disability. The more recent theories, including genetics, epigenetics, and the gut-brain axis, have been demonstrated to play a greater role in ASD pathology, often being associated with the more common ones as mentioned above. We also introduced some of the neurological disorders possessing shared genetic and behavioral traits with ASD. Many genes playing a role in ASD-like features and their potential targeted drugs were explained briefly. However, there are limited therapeutic options, and molecular pathways related to this disorder are less explored. Currently, researchers and therapists are racing to uncover a concrete remedy. This review also provides a brief outline of potential antioxidant, mitochondrial, and anti-inflammatory therapies. We finally included some novel strategies to diagnose and manage autistic pathology and symptoms