Background and Purpose-The optimal hemoglobin (Hgb) target after aneurysmal subarachnoid hemorrhage is not precisely known. We sought to examine the threshold of Hgb concentration associated with an increased risk of cerebral metabolic dysfunction in patients with poor-grade subarachnoid hemorrhage. Methods-Twenty consecutive patients with poor-grade subarachnoid hemorrhage who underwent multimodality neuromonitoring (intracranial pressure, brain tissue oxygen tension, cerebral microdialysis) were studied prospectively. Brain tissue oxygen tension and extracellular lactate/pyruvate ratio were used as markers of cerebral metabolic dysfunction and the relationship between Hgb concentrations and the incidence of brain hypoxia (defined by a brain tissue oxygen tension Ͻ20 mm Hg) and cell energy dysfunction (defined by a lactate/pyruvate ratio Ͼ40) was analyzed.

Background and Purpose-The purpose of this study was to analyze whether fever control attenuates cerebral metabolic distress after aneurysmal subarachnoid hemorrhage (SAH). Methods-Eighteen SAH patients, who underwent intracranial pressure (ICP) and cerebral microdialysis monitoring and were treated with induced normothermia for refractory fever (body temperature Ն38.3°C, despite antipyretics), were studied. Levels of microdialysate lactate/pyruvate ratio (LPR) and episodes of cerebral metabolic crisis (LPR Ͼ40) were analyzed during fever and induced normothermia, at normal and high ICP (Ͼ20 mm Hg). Results-Compared to fever, induced normothermia resulted in lower LPR (40Ϯ24 versus 32Ϯ9, PϽ0.01) and a reduced incidence of cerebral metabolic crisis (13% versus 5%, PϽ0.05) at normal ICP. During episodes of high ICP, induced normothermia was associated with a similar reduction of LPR, fewer episodes of cerebral metabolic crisis (37% versus 8%, PϽ0.01), and lower ICP (32Ϯ11 versus 28Ϯ12 mm Hg, PϽ0.05). Conclusions-Fever control is associated with reduced cerebral metabolic distress in patients with SAH, irrespective of ICP.

After severe TBI, PbtO2 correlates with PF ratio. Acute lung injury is associated with an increased risk of compromised PbtO2, independent from intracerebral and systemic injuries. Our findings support the use of lung-protective strategies to prevent brain hypoxia in TBI patients.

Background: Full-fixed appliance orthodontic treatment (commonly called braces) increases plaque accumulation and the risk of gingivitis and periodontitis. However, little consensus exists on changes to subgingival microbiota and specific periodontopathogens during treatment with braces. Prior studies have been hampered by selection biases due to dependence on culture conditions, candidate-based PCR and shallow sequencing methods. Objective:The objective was to provide the first longitudinal, culture-free and deepsequence profiling of subgingival bacteria in subjects during early stages of full-fixed orthodontic treatment. Methods:We performed 16S rRNA next-generation sequencing (NGS) on 168 subgingival samples collected at 4 distinct mandibular tooth sites per subject before (0 weeks) and during (6 and 12 weeks) orthodontic intervention in 9 experimental and 5 control subjects not undergoing treatment.Results: Overall, we noted that orthodontic intervention led to increased microbial richness, accompanied by an increased incidence of localized gingivitis/mild periodontitis in subjects requiring orthodontic treatment compared to controls, as well as significant baseline variations in subgingival microbiomes in all subjects. Moreover, we confirmed individual-and site-dependent microbiome variability (in particular, the lingual site harboured higher microbiome diversity than buccal sites) that orthodontic bands may lead to more prolonged shifts in microbial changes compared to brackets, and evidence of adaptive enrichment of consensus bacteria with orthodontic intervention (12 novel, consensus bacterial species were identified). Conclusion:Our study, along with evolving global profiling methods and data analyses, builds a strong foundation for further analyses of subgingival microbiomes during full-fixed orthodontic treatment.

Hecht Syndrome is an autosomal dominant distal arthrogryposis caused by mutation in the MYH8 locus characterized by trismus and pseudocamptodactyly. Hecht-associated trismus is thought to result from bilateral hyperplasia of the mandibular coronoid processes. Although several interventions to address trismus have been pursued, no consensus exists regarding optimal management. In this report, the authors present a 7-month-old male with Hecht Syndrome referred for management of trismus. By age 2, interincisal opening had progressively decreased from 12 to 5 mm despite physical therapy. Nutrition was limited to liquids, oral hygiene was compromised, and aspiration risk was present. Computed tomography examination revealed enlarged coronoid processes extending medially and superiorly to the zygomatic arches. To release bony impaction of the coronoid processes against the zygoma and to prevent reossification of the temporalis tendon insertion, resection of the enlarged coronoids and distal temporalis muscles as well as placement of Alloderm spacers were performed via an open craniofacial transzygomatic approach. Jaw motion rehabilitation was used following surgery. Two years postoperatively, the patient had no signs of recurrence and good functional stability of jaw excursion. He was able to chew and swallow solid foods, protrude his tongue, use utensils, and perform regular oral hygiene, none of which were possible before surgery. This case demonstrates that open bilateral coronoidectomy can be a successful and durable management option for trismus in patients with Hecht Syndrome. The open transzygomatic approach is safe, has low morbidity, and provides direct access and adequate exposure for coronoid resection, spacer placement, and prevention of temporalis reinsertion.