Research Publications Spotlight

Keenan JE, Benrashid E, Kale E, Nicoara A, Husain AM, Hughes GC. Neurophysiological Intraoperative Monitoring During Aortic Arch Surgery. Semin Cardiothorac Vasc Anesth. 2016 Oct 4. pii: 1089253216672441. [Epub ahead of print]

Abstract

Circulatory management during replacement of the aortic arch is complex and involves a period of circulatory arrest to provide a bloodless field during arch vessel anastomosis. To guard against ischemic brain injury, tissue metabolic demand is reduced by systemically cooling the patient prior to circulatory arrest. Neurophysiological intraoperative monitoring (NIOM) is often used during the course of these procedures to provide contemporaneous assessment of brain status to help direct circulatory management decisions and detect brain ischemia. In this review, we discuss the characteristics of electrocerebral activity through the process of cooling, circulatory arrest, and rewarming as depicted through commonly used NIOM modalities, including electroencephalography and peripheral nerve somatosensory-evoked potentials. Attention is directed toward the role NIOM has traditionally played during deep hypothermic circulatory arrest, where it is used to define the point of electrocerebral inactivity or maximal cerebral metabolic suppression prior to initiating circulatory arrest while also discussing the evolving utility of NIOM when systemic circulatory arrest is initiated at more moderate degrees of hypothermia in conjunction with regional brain perfusion. The use of cerebral tissue oximetry by near-infrared spectroscopy as an alternative NIOM modality during surgery of the aortic arch is addressed as well. Finally, special considerations for NIOM and the detection of spinal cord ischemia during hybrid aortic arch repair and emerging operative techniques are also discussed.


Gamble JF, Kurian DJ, Udani AG, Greene NH. Airway Management in a Patient with Wolf-Hirschhorn Syndrome. Case Rep Pediatr. 2016;2016:7070125. Epub 2016 Sep 26.

Abstract

We present a case of a 3-month-old female with Wolf-Hirschhorn syndrome (WHS) undergoing general anesthesia for laparoscopic gastrostomy tube placement with a focus on airway management. WHS is a rare 4p microdeletion syndrome resulting in multiple congenital abnormalities, including craniofacial deformities. Microcephaly, micrognathia, and glossoptosis are common features in WHS patients and risk factors for a pediatric airway that is potentially difficult to intubate. We discuss anesthesia strategies for airway preparation and management in a WHS patient requiring general anesthesia with endotracheal intubation.


Li Y, Pan K, Chen L, Ning JL, Li X, Yang T, Terrando N, Gu J, Tao G. Deferoxamine Regulates Neuroinflammation and Iron Homeostasis in a Mouse Model of Postoperative Cognitive Dysfunction. J Neuroinflammation. 2016 Oct 12;13(1):268.

Abstract

BACKGROUND: Postoperative cognitive dysfunction (POCD) is a common complication after surgery, especially amongst elderly patients. Neuroinflammation and iron homeostasis are key hallmarks of several neurological disorders. In this study, we investigated the role of deferoxamine (DFO), a clinically used iron chelator, in a mouse model of surgery-induced cognitive dysfunction and assessed its neuroprotective effects on neuroinflammation, oxidative stress, and memory function.

METHODS: A model of laparotomy under general anesthesia and analgesia was used to study POCD. Twelve to 14 months C57BL/6J male mice were treated with DFO, and changes in iron signaling, microglia activity, oxidative stress, inflammatory cytokines, and neurotrophic factors were assessed in the hippocampus on postoperative days 3, 7, and 14. Memory function was evaluated using fear conditioning and Morris water maze tests. BV2 microglia cells were used to test the anti-inflammatory and neuroprotective effects of DFO.

RESULTS: Peripheral surgical trauma triggered changes in hippocampal iron homeostasis including ferric iron deposition, increase in hepcidin and divalent metal transporter-1, reduction in ferroportin and ferritin, and oxidative stress. Microglia activation, inflammatory cytokines, brain-derived neurotropic factor impairments, and cognitive dysfunction were found up to day 14 after surgery. Treatment with DFO significantly reduced neuroinflammation and improved cognitive decline by modulating p38 MAPK signaling, reactive oxygen species, and pro-inflammatory cytokines release.

CONCLUSIONS: Iron imbalance represents a novel mechanism underlying surgery-induced neuroinflammation and cognitive decline. DFO treatment regulates neuroinflammation and microglia activity after surgery.