The safety and efficacy of sugammadex for reversing neuromuscular blockade in younger children and infants.

INTRODUCTION: Sugammadex, a novel selective antagonist of non-depolarizing neuromuscular blocking agents, has been shown to rapidly and effectively reverse moderate and deep paralysis in adults and pediatric patients over age 2, improving patient recovery and reducing the risk of postoperative complications. AREAS COVERED: Since the use of sugammadex in patients under age 2 is not widely studied, we aim to provide an overview on the drug's application and potential use in infants and neonates. There is a limited but growing body of evidence for the safe, efficacious use of sugammadex in children under age 2. Relevant studies were identified from the most updated data including case reports, clinical trials, systematic reviews, and meta analyses. EXPERT OPINION: The results suggest that at a dose of 2 to 4 mg/kg of sugammadex can be safely used to rapidly and effectively reverse neuromuscular blockade in neonates and infants; it is non-inferior based on incidence of adverse events compared to neostigmine. Additionally, sugammadex doses between 8 and 16 mg/kg may be used as a rescue agent for infants during 'can't intubate, can't ventilate' crisis. Overall, sugammadex offers new value in the perioperative care of patients under age 2, with further studies warranted to better understand its application and full effect in the pediatric population.

Traumatic carotid artery injury caused by a metal sipping straw in a pediatric patient: Anesthetic management and considerations.

CNS injury following a traumatic intraoral injury is a rare but potentially catastrophic occurrence in pediatrics. For example, intraoral trauma resulting in acute ischemic stroke (AIS) secondary to carotid artery dissection has only been described by a limited number of case reports [1]. We report the case of a 4-year-old boy who suffered a penetrating right internal carotid injury after a fall resulting in a metal straw perforating the neck and oropharynx. The patient presented in hemorrhagic shock with altered consciousness. CT Angiography revealed a right internal carotid traumatic rupture with flow occlusion and right cerebral hemispheric hypoperfusion. The patient underwent emergent neuroradiologic intervention under general anesthesia with successful reconstruction of the right carotid artery through the use of five flow diverting pipeline stents. The patient was extubated one week later with the only neurologic sequala being slight left upper extremity weakness. Anesthetic management played a vital part in this outstanding outcome. Thoughtful management is required to ensure both survival and the best possible neurologic recovery. Despite the rarity of these events, there is sufficient evidence from similar interventions and neurophysiology to guide sound management. This case report highlights these principles and areas for further investigation. Our experience may be instructive in the support of safe care under similarly rare but challenging circumstances.

Anesthesia, the developing brain, and dexmedetomidine for neuroprotection.

Anesthesia-induced neurotoxicity is a set of unfavorable adverse effects on central or peripheral nervous systems associated with administration of anesthesia. Several animal model studies from the early 2000's, from rodents to non-human primates, have shown that general anesthetics cause neuroapoptosis and impairment in neurodevelopment. It has been difficult to translate this evidence to clinical practice. However, some studies suggest lasting behavioral effects in humans due to early anesthesia exposure. Dexmedetomidine is a sedative and analgesic with agonist activities on the alpha-2 (ɑ2) adrenoceptors as well as imidazoline type 2 (I2) receptors, allowing it to affect intracellular signaling and modulate cellular processes. In addition to being easily delivered, distributed, and eliminated from the body, dexmedetomidine stands out for its ability to offer neuroprotection against apoptosis, ischemia, and inflammation while preserving neuroplasticity, as demonstrated through many animal studies. This property puts dexmedetomidine in the unique position as an anesthetic that may circumvent the neurotoxicity potentially associated with anesthesia.

Paradoxical reduction of plasma lipids and atherosclerosis in mice with adenine-induced chronic kidney disease and hypercholesterolemia.

Background: Atherosclerotic cardiovascular disease is prevalent among patients with chronic kidney disease (CKD). In this study, we initially aimed to test whether vascular calcification associated with CKD can worsen atherosclerosis. However, a paradoxical finding emerged from attempting to test this hypothesis in a mouse model of adenine-induced CKD. Methods: We combined adenine-induced CKD and diet-induced atherosclerosis in mice with a mutation in the low-density lipoprotein receptor gene. In the first study, mice were co-treated with 0.2% adenine in a western diet for 8 weeks to induce CKD and atherosclerosis simultaneously. In the second study, mice were pre-treated with adenine in a regular diet for 8 weeks, followed by a western diet for another 8 weeks. Results: Co-treatment with adenine and a western diet resulted in a reduction of plasma triglycerides and cholesterol, liver lipid contents, and atherosclerosis in co-treated mice when compared with the western-only group, despite a fully penetrant CKD phenotype developed in response to adenine. In the two-step model, renal tubulointerstitial damage and polyuria persisted after the discontinuation of adenine in the adenine-pre-treated mice. The mice, however, had similar plasma triglycerides, cholesterol, liver lipid contents, and aortic root atherosclerosis after being fed a western diet, irrespective of adenine pre-treatment. Unexpectedly, adenine pre-treated mice consumed twice the calories from the diet as those not pre-treated without showing an increase in body weight. Conclusion: The adenine-induced CKD model does not recapitulate accelerated atherosclerosis, limiting its use in pre-clinical studies. The results indicate that excessive adenine intake impacts lipid metabolism.