Faculty Bibliography

BACKGROUND: The aim of this study was to determine the incidence, outcomes, and risk factors for synechia formation after endoscopic sinus surgery (ESS) and middle turbinate medialization with and without FloSeal. METHODS: A retrospective review was performed of patients who underwent primary ESS with middle turbinate medialization, with or without the placement of FloSeal. Medialization was performed with the placement of an absorbable conchopexy suture and silastic splint. Operative variables and outcomes were analyzed to identify risk factors for synechia formation. RESULTS: One hundred thirty-five patients underwent medialization alone and 37 patients underwent medialization with placement of FloSeal. Overall, synechia formation was noted in 16 patients (9.3%). A statistically significant higher incidence of synechia formation was noted in patients who underwent middle turbinate medialization with the placement of FloSeal versus medialization alone (18.9% versus 6.7%). The incidences of intraoperative complications (6.2% versus 4.7%) and postoperative complications (6.2% versus 7%) were similar between patients with and without synechia, respectively. Patients experiencing synechia, however, underwent a statistically significant higher rate of revision procedures (25% versus 5.1%). CONCLUSION: Despite adequate prevention with middle turbinate medialization, synechia formation after ESS may result in higher rates of revision procedures. The placement of FloSeal in conjunction with middle turbinate medialization may result in a higher incidence of synechia formation

In vivo reconstitution of the dTDP-D-desosamine pathway of the megalomicin gene cluster from Micromonospora megalomicea was achieved by expression of the genes in Escherichia coli. LC/MS/MS analysis of the dTDP-sugar intermediates produced by operons containing different sets of genes showed that production of dTDP-D-desosamine from dtdp-4-keto-6-deoxy-D-glucose requires only four biosynthetic steps, catalysed by MegCIV, MegCV, MegDII and MegDIII, and that MegCII is not involved. Instead, bioconversion studies demonstrated that MegCII is needed together with MegCIII to catalyse transfer of D-desosamine to 3-alpha-mycarosylerythronolide B.

OBJECTIVES/OBJECTIVE:Congenital anterior skull base defects with meningoencephaloceles causing nasal obstruction are rare clinical entities. Nasal obstruction in children may also be a symptom of multiple benign nasal and allergic disorders, making the initial diagnosis of meningoencephalocele difficult. Traditionally, skull base defects have been repaired via a bifrontal craniotomy approach. With the advent of pediatric endoscopic instrumentation, more of these lesions are accessible via an intranasal endoscopic approach, even in the infant population. However, owing to the rarity of these lesions, there is a paucity of data demonstrating successful adaptation of endoscopic skull base techniques to the pediatric population. METHODS:Retrospective review of two cases of endoscopic repair of anterior skull base defects with meningoencephaloceles at a tertiary care medical center. RESULTS:Two children, ages 15 months and 6 years, underwent successful endoscopic closure of their anterior skull base defects and resection of their intranasal meningoencephalocele with resolution of their nasal obstruction and cerebrospinal fluid rhinorrhea. CONCLUSIONS:Pediatric nasal meningoencephaloceles with anterior skull base defects can be successfully repaired via a transnasal endoscopic technique, thus minimizing the complications associated with craniotomy and frontal lobe retraction. Triplanar computed tomographic and magnetic resonance imaging is paramount to evaluate the caliber of the skull base defect, consistency of the herniated intracranial contents, as well as the presence of cerebral vasculature.

Nerve injury elicits both universal and limited responses. Among the former is regenerative growth, which occurs in most peripheral neurons, and among the latter is the long-term hyperexcitability that appears selectively in nociceptive sensory neurons. Since positive injury signals communicate information from the site of an injury to the cell body, we hypothesize that a nerve injury activates both universal and limited positive injury signals. Studies in Aplysia indicate that protein kinase G is a limited signal that is responsible for the induction of long-term hyperexcitability. Given that long-term hyperexcitability contributes to chronic pain after axotomy in rodent neuropathic pain models, we investigated its underlying basis in the rat peripheral nervous system. Using biochemical assays, Western blots, and immunocytochemistry we found that the Type 1alpha protein kinase G is the predominant isoform in the rat periphery. It is present primarily in axons and cell bodies of nociceptive neurons, including populations that are isolectin B4-positive, isolectin B4-negative, and those that express transient receptor potential vanilloid receptor-1. Surprisingly, protein kinase G is not present in the facial nerve, which overwhelmingly contains axons of motor neurons. Crushing the sciatic nerve or a cutaneous sensory nerve activates protein kinase G in axons and results in its retrograde transport to the neuronal somata in the DRG. Preventing the activation of protein kinase G by injecting Rp-8-pCPT-cGMPS into the crush site abolished the transport. The protein kinase A inhibitor Rp-8-pCPT-cAMPS had no effect. Extracellular signal-related kinases 42/44 are also activated and transported after nerve crush, but in both motor and sensory axons. Chronic pain has been linked to long-term hyperexcitability following a nerve inflammation in several rodent models. We therefore injected complete Freund's adjuvant into the hindpaw to induce an inflammation and found that protein kinase G was activated in the sural nerve and transported to the DRG. In contrast, the extracellular signal-related kinases in the sensory axons were not activated by the complete Freund's adjuvant. These studies support the idea that the extracellular signal-related kinases are universal positive axonal signals and that protein kinase G is a limited positive axonal signal. They also establish the association between protein kinase G, the induction of long-term hyperexcitability, and chronic pain in rodents.

We present a case of successful separation of craniopagus conjoined twins. The procedure was staged to permit each child to develop adequate independent cerebral venous drainage and to prevent deleterious, perioperative cerebral edema. Surgical hemorrhage, blood product delivery, and hemodilution were minimized.