Anesthetic Considerations for Patients with Hereditary Neuropathy with Liability to Pressure Palsies: A Narrative Review.

Hereditary neuropathy with liability to pressure palsies (HNPP) is an autosomal dominant demyelinating neuropathy characterized by an increased susceptibility to peripheral nerve injury from trauma, compression, or shear forces. Patients with this condition are unique, necessitating distinct considerations for anesthesia and surgical teams. This review describes the etiology, prevalence, clinical presentation, and management of HNPP and presents contemporary evidence and recommendations for optimal care for HNPP patients in the perioperative period. While the incidence of HNPP is reported at 7-16:100,000, this figure may be an underestimation due to underdiagnosis, further complicating medicolegal issues. With the subtle nature of symptoms associated with HNPP, patients with this condition may remain unrecognized during the perioperative period, posing significant risks. Several aspects of caring for this population, including anesthetic choices, intraoperative positioning, and monitoring strategy, may deviate from standard practices. As such, a tailored approach to caring for this unique population, coupled with meticulous preoperative planning, is crucial and requires a multidisciplinary approach.

Hospital discharge hemoglobin values and posthospitalization clinical outcomes in transfused patients undergoing noncardiac surgery.

BACKGROUND: Red blood cell (RBC) transfusion is common in surgical patients, yet optimal transfusion targets are incompletely defined in the perioperative period. Hemoglobin levels at the time of hospital discharge may provide insight into transfusion practices, anemia management, and patient outcomes. STUDY DESIGN AND METHODS: This is an observational cohort study of adults receiving RBC transfusion during noncardiac surgery from 2010 to 2014. Multivariable regression was used to assess the relationships between hospital discharge hemoglobin concentrations, anemia severity (severe: <8 g/dL; moderate: 8-10 g/dL; mild/none: ≥10 g/dL), and clinical outcomes, including a primary outcome of 30-day hospital readmission and secondary outcomes of posthospitalization RBC transfusion, composite stroke or myocardial infarction, and mortality. RESULTS: A total of 3129 patients were included: 165 (5%) with severe discharge anemia, 1962 (63%) moderate, and 1002 (32%) with mild/none. Five hundred ninety-two (19%) were readmitted, with the highest rates observed with severe anemia (26% vs 19% for mild/none). Readmissions were not significantly different after multivariable adjustment (overall P = .216); however, in those receiving postoperative intensive care, severe anemia was associated with increased readmission rates (hazard ratio [HR], 1.72; 95% confidence interval [CI], 1.09-2.71; reference mild/none]. Posthospitalization RBC transfusion rates were highest with severe anemia (25% vs 10% for mild/none; adjusted HR, 2.2; 95% CI, 1.5-3.3; P < .001). There were no significant differences in composite stroke/myocardial infarction, or mortality. RBC transfusion volumes did not modify anemia-outcome relationships. CONCLUSION: Hospital discharge hemoglobin values for transfused surgical patients were not associated with hospital readmission rates except for those receiving postoperative intensive care. Further evaluation is warranted to understand downstream consequences of postsurgical anemia.

Transmission pathways and mediators as the basis for clinical pharmacology of pain.

INTRODUCTION: Mediators in pain transmission are the targets of a multitude of different analgesic pharmaceuticals. This review explores the most significant mediators of pain transmission as well as the pharmaceuticals that act on them. Areas covered: The review explores many of the key mediators of pain transmission. In doing so, this review uncovers important areas for further research. It also highlights agents with potential for producing novel analgesics, probes important interactions between pain transmission pathways that could contribute to synergistic analgesia, and emphasizes transmission factors that participate in transforming acute injury into chronic pain. Expert commentary: This review examines current pain research, particularly in the context of identifying novel analgesics, highlighting interactions between analgesic transmission pathways, and discussing factors that may contribute to the development of chronic pain after an acute injury.

Pain transduction: a pharmacologic perspective.

INTRODUCTION: Pain represents a necessary physiological function yet remains a significant pathological process in humans across the world. The transduction of a nociceptive stimulus refers to the processes that turn a noxious stimulus into a transmissible neurological signal. This involves a number of ion channels that facilitate the conversion of nociceptive stimulus into and electrical signal. AREAS COVERED: An understanding of nociceptive physiology complements a discussion of analgesic pharmacology. Therefore, the two are presented together. In this review article, a critical evaluation is provided on research findings relating to both the physiology and pharmacology of relevant acid-sensing ion channels (ASICs), transient receptor potential (TRP) cation channels, and voltage-gated sodium (Nav) channels. Expert commentary: Despite significant steps toward identifying new and more effective modalities to treat pain, there remain many avenues of inquiry related to pain transduction. The activity of ASICs in nociception has been demonstrated but the physiology is not fully understood. A number of medications appear to interact with ASICs but no research has demonstrated pain-relieving clinical utility. Direct antagonism of TRPV1 channels is not in practice due to concerning side effects. However, work in this area is ongoing. Additional research in the of TRPA1, TRPV3, and TRPM8 may yield useful results. Local anesthetics are widely used. However, the risk for systemic effects limits the maximal safe dosage. Selective Nav antagonists have been identified that lack systemic effects.

Arterial Catheterization and Infection: Toll-like Receptors in Defense against Microorganisms and Therapeutic Implications.

Radial artery catheterization has become a preferred route over femoral artery catheterization, in order to monitor the blood pressure of hemodynamically unstable patients or for repeated sampling of arterial blood gases. While the incidence of catheter-related infection is lower in the radial artery than the femoral artery, infection remains a major issue that requires attention. In this review of the literature, we discuss infectious complications of radial artery catheterization, with a focus on various risk factors and establishing the most common causative agents. We also critically review the role of the innate immune system involving Toll-like receptors (TLRs) in host-defense, with the goal of establishing a common pathway used by the innate immune system via TLRs to combat the pathogens that most commonly cause infection in radial artery catheterization. If this pathway can be therapeutically manipulated to preemptively attack pathogenic agents, immunomodulation may be an option in reducing the incidence of infection in this procedure.

Therapeutic Basis of Clinical Pain Modulation.

Pain is a hallmark of almost all bodily ailments and can be modulated by agents, including analgesics and anesthetics that suppress pain signals in the central nervous system. Defects in the modulatory systems, including the endogenous pain-inhibitory pathways, are a major factor in the initiation and chronicity of pain. Thus, pain modulation is particularly applicable to the practice of medicine. This review summarizes the existing literature on pain modulation. Here, we critically reviewed the literature from PubMed on pain modulation published primarily within the past 5 years in high impact journals. Specifically, we have discussed important anatomical landmarks of pain modulation and outlined the endogenous networks and underlying mechanisms of clinically relevant pain modulatory methods. The Gate Control Theory is briefly presented with discussion on the capacity of pain modulation to cause both hyper- and hypoalgesia. An emphasis has been given to highlight key areas in pain research that, because of unanswered questions or therapeutic potential, merit additional scientific scrutiny. The information presented in this paper would be helpful in developing novel therapies, metrics, and interventions for improved patient management.

Effect of sedative-hypnotics, anesthetics and analgesics on sleep architecture in obstructive sleep apnea.

The perioperative care of obstructive sleep apnea (OSA) patients is currently receiving much attention due to an increased risk for complications. It is established that postoperative changes in sleep architecture occur and this may have pathophysiological implications for OSA patients. Upper airway muscle activity decreases during rapid eye movement sleep (REMS). Severe OSA patients exhibit exaggerated chemoreceptor-driven ventilation during non-rapid eye movement sleep (NREMS), which leads to central and obstructive apnea. This article critically reviewed the literature relevant to preoperative screening for OSA, prevalence of OSA in surgical populations and changes in postoperative sleep architecture relevant to OSA patients. In particular, we addressed three questions in regard to the effects of sedative-hypnotics, anesthetics and analgesics on sleep architecture, the underlying mechanisms and the relevance to OSA. Indeed, these classes of drugs alter sleep architecture, which likely significantly contributes to abnormal postoperative sleep architecture, exacerbation of OSA and postoperative complications.