Barrier Enclosure during Endotracheal Intubation Canelli, Robert; Connor, Christopher W; Gonzalez, Mauricio ...
The New England journal of medicine,
05/2020, Volume:
382, Issue:
20
Journal Article
Peer reviewed
Open access
A four-sided plexiglass box with access holes for an operator was used to provide additional protection for an operator performing intubation. The box reduced the amount of material expelled from a ...simulated patient cough that ended up on the operator. This letter is accompanied by a video showing the simulation.
Barrier Enclosure during Endotracheal Intubation Canelli, Robert; Connor, Christopher W; Gonzalez, Mauricio ...
New England journal of medicine/The New England journal of medicine,
05/2020, Volume:
382, Issue:
20
Journal Article
Intranasal Naloxone Administration Ortega, Rafael; Nozari, Ala; Baker, William ...
The New England journal of medicine,
03/2021, Volume:
384, Issue:
12
Journal Article
Peer reviewed
Intranasal naloxone is used to treat patients with respiratory and central nervous system depression that is known or suspected to be caused by an opioid overdose. This video demonstrates the ...administration of intranasal naloxone.
Summary Migraine attacks with auras are sometimes associated with underlying hereditary or acquired cerebrovascular disorders. A unifying pathophysiological explanation linking migraine to these ...conditions has been difficult to identify. On the basis of genetic and epidemiological evidence, we suggest that changes in blood vessels, hypoperfusion disorders, and microembolisation can cause neurovascular dysfunction and evoke cortical spreading depression, an event that is widely thought to underlie aura symptoms. In fact, recent experimental data have indicated that focal, mild, and transient ischaemia can trigger cortical spreading depression without an enduring tissue signature. Although migraine with aura has many causes (eg, neuronal network excitability), it seems that migraine and stroke might both be triggered by hypoperfusion and could therefore exist on a continuum of vascular complications in a subset of patients who have these hereditary or acquired comorbid vascular conditions.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
Renal protection is a critical concept for anesthesiologists, nephrologists, and urologists, since anesthesia and renal function are highly interconnected and can potentially interfere with one ...another. Therefore, a comprehensive understanding of anesthetic drugs and their effects on renal function remains fundamental to the success of renal surgeries, especially transplant procedures. Some experimental studies have shown that some anesthetics provide protection against renal ischemia/reperfusion (IR) injury, but there is limited clinical evidence.
The effects of anesthetic drugs on renal failure are particularly important in the context of kidney transplantation, since the conditions of preservation following removal profoundly influence the recovery of organ function. Currently, preservation procedures are typically based on the usage of a cold-storage solution. Some anesthetic drugs induce anti-inflammatory, anti-necrotic, and anti-apoptotic effects. A more thorough understanding of anesthetic effects on renal function can present a novel approach for developing organ-protective strategies. The aim of this review is to discuss the effects of different anesthetic drugs on renal function, with particular focus on IR injury. Many studies have demonstrated the organ-protective effects of some anesthetic drugs, specifically propofol, which indicate the potential of some anesthetics to introduce novel organ protective targets. This is not surprising, since lipid emulsions are major components of propofol, which accumulating data show provide organ protective effects against IR injury. Key Messages: Thorough understanding of the interaction between anesthetic drugs and renal function remains fundamental to the delivery of safe perioperative care and to optimizing outcomes after renal surgeries, particularly transplant procedures. Anesthetics can be repurposed for organ protection with more information about their effects, especially during transplant procedures. Here, we review the effects of different anesthetic drugs - specifically those that contain lipids in their structure, with special reference to IR injury.
Objective
Patent foramen ovale and pulmonary arteriovenous shunts are associated with serious complications such as cerebral emboli, stroke, and migraine with aura. The pathophysiological mechanisms ...that link these conditions are unknown. We aimed to establish a mechanism linking microembolization to migraine aura in an experimental animal model.
Methods
We introduced particulate or air microemboli into the carotid circulation in mice to determine whether transient microvascular occlusion, insufficient to cause infarcts, triggered cortical spreading depression (CSD), a propagating slow depolarization that underlies migraine aura.
Results
Air microemboli reliably triggered CSD without causing infarction. Polystyrene microspheres (10μm) or cholesterol crystals (<70μm) triggered CSD in 16 of 28 mice, with 60% of the mice (40% of those with CSD) showing no infarcts or inflammation on detailed histological analysis of serial brain sections. No evidence of injury was detected on magnetic resonance imaging examination (9.4T; T2 weighted) in 14 of 15 selected animals. The occurrence of CSD appeared to be related to the magnitude and duration of flow reduction, with a triggering mechanism that depended on decreased brain perfusion but not sustained tissue damage.
Interpretation
In a mouse model, microemboli triggered CSD, often without causing microinfarction. Paradoxical embolization then may link cardiac and extracardiac right‐to‐left shunts to migraine aura. If translatable to humans, a subset of migraine auras may belong to a spectrum of hypoperfusion disorders along with transient ischemic attacks and silent infarcts. ANN NEUROL 2010;67:221–229
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
Background Over 1.4 million US adults identify as transgender when gender identity differs from the sex assigned at birth 1. Although transgender patients face adverse health outcomes, they remain an ...understudied population 2. A 2017 study surveyed 411 practicing clinicians and found that 80% had been involved in treating a transgender patient, but 80.6% had never received training on transgender care 3. The purpose of this report is to describe prolonged desaturation in one case of a transgender patient who wore a chest binder intraoperatively owing to a lack of preoperative recognition. Case presentation A 19-year-old transgender male of African-American descent with anxiety and class 3 obesity presented for an esophagogastroduodenoscopy to evaluate a 2-year history of upper abdominal pain unresponsive to proton pump inhibitor therapy, with a plan for monitored anesthesia care. His medications included sertraline, pantoprazole, zolpidem, ergocalciferol, leuprolide, and testosterone cypionate. Preoperatively, the patient was instructed to remove all clothing and to don a patient gown while in the bathroom. The attending anesthesiologist then conducted the interview and examination in the preoperative holding area. The patient was induced with 250 mg of propofol, and reassuring respirations were noted by capnography. Respirations and oxygen saturation remained stable upon insertion of the endoscope. Four minutes later, the patient's oxygen saturation rapidly decreased to 50% and end-tidal capnography was lost. The endoscope was removed, and the patient was given 200 mg of propofol and 20 mg succinylcholine. His oxygen saturation recovered to 80% and 100% after 2 and 5 minutes, respectively, of ventilation with 100% inspired oxygen. No further oxygen desaturation was noted throughout the procedure, and the patient was closely monitored for signs of respiratory difficulty during an uneventful postoperative course. After full emergence, it was revealed that the patient had been wearing a chest binder throughout the operative procedure. The patient was counseled on the necessity to communicate the presence of this accessory prior to all future procedures. Conclusion In the clinical narrative, a healthy patient was observed to have prolonged oxygen desaturation after induction of anesthesia. Laryngospasm was suspected clinically owing to the sudden absence of end-tidal carbon dioxide. Prolonged oxygen desaturation despite appropriate interventions suggests the contribution of additional factors. We speculate that the presence of a chest binder intraoperatively predisposed the patient to more rapid oxygen desaturation less responsive to typical therapy. A chest binder would introduce mechanical restriction to the patient's breathing owing to its inherent design to compress. Although the patient was asked to remove all clothing, specific instructions were not provided regarding the removal of a chest binder. The presence of chest binding was also absent in the electronic health record, despite the documented presence of the patient's preferred gender, hormonal therapy regimen, and medical history. Ultimately, this case reflects the gap between practitioner knowledge and hospital guidelines and the practices of transgender patients. In reviewing existing literature and the potential for atelectasis with external compression, we would consider that patients refrain from chest binding for 12-24 hours before surgical procedures, resume no sooner than 24 hours after ambulation, and participate in diagnostic incentive spirometry pre- and postoperatively. Keywords: Ambulatory surgery, Chest binder, Endoscopy, Perioperative guidelines, Transgender medicine
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
Efforts to develop a treatment for bupivacaine cardiotoxicity led to the discovery that Intralipid, a popular brand of intravenous lipid emulsion, could be used not only as an effective treatment for ...anesthetic-induced cardiac arrest, but also as a means of reversing many other toxicities. Contradictory data exist regarding the mechanism of action of lipid emulsion, a combination of fatty acids traditionally used in parenteral nutrition. Some researchers attribute the effects to lipophilicity and the individual characteristics of the lipids, while other data demonstrate a direct empowering mechanism through cellular upstream and downstream pathways. Understanding the underlying mechanism of action of this safe source of calories may assist in the development of novel organ protective agents. In this review, some of the direct cardiac effects of lipid emulsion are briefly discussed. This article is open to POST-PUBLICATION REVIEW. Registered readers (see "For Readers") may comment by clicking on ABSTRACT on the issue's contents page.
Spontaneous spreading depolarizations are frequent after various forms of human brain injury such as ischemic or hemorrhagic stroke and trauma, and worsen the outcome. We have recently shown that ...supply-demand mismatch transients trigger spreading depolarizations in ischemic stroke. Here, we examined the mechanisms triggering recurrent spreading depolarization events for many days after subarachnoid hemorrhage. Despite large volumes of subarachnoid hemorrhage induced by cisternal injection of fresh arterial blood in rodents, electrophysiological recordings did not detect a single spreading depolarization for up to 72 h after subarachnoid hemorrhage. Cortical susceptibility to spreading depolarization, measured by direct electrical stimulation or topical KCl application, was suppressed after subarachnoid hemorrhage. Focal cerebral ischemia experimentally induced after subarachnoid hemorrhage revealed a biphasic change in the propensity to develop peri-infarct spreading depolarizations. Frequency of peri-infarct spreading depolarizations decreased at 12 h, increased at 72 h and normalized at 7 days after subarachnoid hemorrhage compared with sham controls. However, ischemic tissue and neurological outcomes were significantly worse after subarachnoid hemorrhage even when peri-infarct spreading depolarization frequency was reduced. Laser speckle flowmetry implicated cerebrovascular hemodynamic mechanisms worsening the outcome. Altogether, our data suggest that cerebral ischemia is required for spreading depolarizations to be triggered after subarachnoid hemorrhage, which then creates a vicious cycle leading to the delayed cerebral ischemia syndrome.
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NUK, OILJ, SAZU, UKNU, UL, UM, UPUK
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