Background and Aims Obesity‐induced pathogenesis of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) is associated with increased de novo lipogenesis (DNL) and hepatic glucose production (HGP) that is due to excess fatty acids. Acyl‐coenzyme A (CoA) thioesterase (Acot) family members control the cellular utilization of fatty acids by hydrolyzing (deactivating) acyl‐CoA into nonesterified fatty acids and CoASH. Approach and Results Using Caenorhabditis elegans, we identified Acot9 as the strongest regulator of lipid accumulation within the Acot family. Indicative of a maladaptive function, hepatic Acot9 expression was higher in patients with obesity who had NAFLD and NASH compared with healthy controls with obesity. In the setting of excessive nutrition, global ablation of Acot9 protected mice against increases in weight gain, HGP, steatosis, and steatohepatitis. Supportive of a hepatic function, the liver‐specific deletion of Acot9 inhibited HGP and steatosis in mice without affecting diet‐induced weight gain. By contrast, the rescue of Acot9 expression only in the livers of Acot9 knockout mice was sufficient to promote HGP and steatosis. Mechanistically, hepatic Acot9 localized to the inner mitochondrial membrane, where it deactivated short‐chain but not long‐chain fatty acyl‐CoA. This unique localization and activity of Acot9 directed acetyl‐CoA away from protein lysine acetylation and toward the citric acid (TCA) cycle. Acot9‐mediated exacerbation of triglyceride and glucose biosynthesis was attributable at least in part to increased TCA cycle activity, which provided substrates for HGP and DNL. β‐oxidation and ketone body production, which depend on long‐chain fatty acyl‐CoA, were not regulated by Acot9. Conclusions Taken together, our findings indicate that Acot9 channels hepatic acyl‐CoAs toward increased HGP and DNL under the pathophysiology of obesity. Therefore, Acot9 represents a target for the management of NAFLD.

INTRODUCTION:Over the past decade the use of e-cigarettes has risen dramatically, particularly among teenagers. They have been proven to cause lung injury and hypoxic respiratory failure. A less commonly studied pulmonary effect of vaping is significant bullous disease with the potential to cause a spontaneous pneumothorax.CASE PRESENTATION: This is a 22 year-old male with no significant medical history presented due to sudden onset left-sided pleuritic chest pain that was unprovoked and associated with dyspnea. He smokes 1 joule every 4 days and has been smoking for 4 years. On arrival, he was found to be tachycardic and appeared uncomfortable. Electrocardiogram showed normal sinus rhythm. Computed tomography was done and revealed a large left sided pneumothorax and left lung collapse. He had a chest tube placed to suction with improvement in his symptoms. Repeat chest radiography showed significant improvement in the pneumothorax with a small apical left sided pneumothorax.The chest tube remained to suction with a continuous leak observed without resolution of the apical pneumothorax that remained stable in size. On day 8 of hospitalization, he underwent a video-assisted thoracoscopic surgery (VATS) with left upper lobe wedge resection and talc pleurodesis. A new chest tube was placed intra operatively and repeat chest radiography showed resolution of the pneumothorax with no air leak observed. Intra operative findings were suggestive of significant bullous lung disease with blebs. On day 11, the chest tube was removed successfully without recurrence of pneumothorax. He was discharged home breathing comfortably on room air.DISCUSSION: E-cigarettes contain propylene glycol and vegetable glycerin, which decompose when exposed to high temperatures generating harmful carbonyl compounds. These compounds have been shown to cause oxidative stress and release of inflammatory markers causing airway epithelial injury and impaired gas exchange. The addition of flavoring agents further causes epithelial injury and reduction in ciliary beat frequency leading to decreased mucociliary clearance and increased colonization. The indications for VATS include recurrent pneumothoraces, large bullae, incomplete expansion of the lung, and bilateral involvement. VATS has been associated with decreased hospital length of stay and rehabilitation time.CONCLUSIONS: This case highlights the need for thorough exposure history in patients with an unclear etiology for respiratory symptoms, particularly among young adults. Early recognition of candidates for VATS also leads to improved outcomes. Vaping has been associated with bullous disease, although there have not been many cases of rapidly progressing bullous disease causing pneumothorax.

A 24-year-old woman, G5P4, presented for a routine checkup at 28 weeks gestation. Ultrasound of the fetus showed a neck mass with no other anomalies and no polyhydramnios. Magnetic resonance imaging (MRI) of the fetus showed a cystic mass suggestive of a neck teratoma. She was continued with her pregnancy as planned and was scheduled for a cesarean section at 37 weeks gestation. Ex utero intrapartum treatment (EXIT) procedure was performed. There were no intraoperative or postoperative complications. How to cite this article Al-Baghdadi R, Kika N, Ahmed B, Porovic S. Ex utero Intrapartum Treatment Procedure for Fetal Neck Teratoma. Donald School J Ultrasound Obstet Gynecol 2017;11(3):227-229.

INTRODUCTION:Tracheoesophageal fistula (TEF) is a known but serious complication of prolonged intubation. There are various clinical consequences associated with TEF and achieving successful repair can be difficult.CASE PRESENTATION: This is a 61 year-old female with a history of multiple medical problems who presented initially after being found down outside. She was hypothermic on admission and required active rewarming. She was intubated for hypoxic and hypercapnic respiratory failure. Her hospital course was complicated by septic shock due to Klebsiella and Pseudomonas pneumonia, which required prolonged intubation. Tracheostomy was attempted on day 20 of intubation however a 1cm TEF was seen in the subglottic region and the procedure was aborted. She had a repeat bronchoscopy as she developed a constant leak with volume loss on the ventilator along with increased gastric secretions via endotracheal tube. This showed that the fistula had increased in size and therefore a tracheostomy tube was surgically placed with the cuff beyond the level of the TEF. Her course was soon complicated by episodes of severe respiratory distress due to dislodged tracheostomy into the esophagus due to further increasing size of the fistula, now extending from just below the vocal cords to slightly beyond the mid-trachea. Endoscopic repair with gastrointestinal over-the-scope-clipping (OTSC) was attempted but failed. She eventually underwent TEF repair with a left sternocleidomastoid flap to repair the posterior membrane of the trachea and primary repair of the esophagus. She was subsequently placed on veno-venous Extracorporeal membrane oxygenation (V-V ECMO) during the procedure. Her course was then complicated by hemoptysis and bleeding around the TEF surgical repair site causing obstruction by blood clots in the distal tracheostomy tube. She was given tranexamic acid nebulizers and an endotracheal tube was left with the distal tip beyond the distal end of the tracheostomy tube about 1 cm above the carina. She is currently still in the intensive care unit, off of ECMO, recovering.DISCUSSION: Management of benign TEFs includes surgical flap with either muscle flaps or full thickness skin grafts. Surgical complications include wound dehiscence, recurrent fistulas, and tracheal stenosis with an 11% mortality rate. Patients requiring surgical intervention may benefit from V-V ECMO preoperatively to allow for ultra protective ventilation with low airway pressure to allow healing. Those who are not a candidate for surgery can receive tracheal or esophageal stenting. A newer intervention is OTSC with promising results, that our patient unfortunately failed.CONCLUSIONS: TEFs are an uncommon but severe complication of prolonged intubation. In the era of COVID-19 there has been a rise in reported cases of such complications due to prolonged intubation. This case demonstrates the severity of such complications.

Bronchiectasis is a chronic condition with pathogenic airway dilation and bronchial wall thickening that has been associated with many different causes. One of the less studied causes is silicone exposure.CASE PRESENTATION: This is a 33 year-old female with a history of supraventricular tachycardia, chronic respiratory failure due to bronchiectasis, and pulmonary hypertension group 3 presented with increased work of breathing and lethargy. She appeared uncomfortable with tachypnea and hypoxia requiring an increase of her baseline home oxygen. ABG was consistent with acute hypercapnic respiratory failure and thus she was placed on Bi-level with improvement in hermental status. Chest radiograph showed hyperinflated lungs and diffuse bronchiectasis bilaterally. Computed tomography showed extensive severe bilateral cystic bronchiectasis. She had multiple recurrent admissions for hypercapnic respiratory failure due to progression of her bronchiectasis with superimposed bacterial pneumonia and colonization. She had an extensive work up to assess for an underlying etiology for her bronchiectasis which began at age 18 with mild disease. Full rheumatologic evaluation was unrevealing. Her pulmonary function tests revealed a severe mixed defect with an FEV1/FVC of 58, FEV1 0.57 (22%), and FVC 0.98 (33%), TLC 4L. However, her respiratory status declined rapidly after she had a silicone gluteal augmentation surgery in 2015 which was "botched." She was treated with steroids and intravenous antibiotics and was discharged home on home oxygen. DISCUSSION: In recent years there has been a rise in cases of silicosis due to modern industries; however, a less studied phenomenon is that of lung disease as a complication of silicone breast and gluteal implants. The pathogenesis of silicosis is due to sIlica particles deposited in the distal airways, engulfed by alveolar macrophages leading to an upregulation of pro inflammatory and pro fibrotic pathways. Further silica ingestion by the macrophages leads to autophagy and release of intracellular silica thus attracting more macrophages with the release of cytotoxic antioxidants, proteases, and inflammatory cytokines. This leads to fibrosis and alveolitis. Bronchiectasis results from the destruction of connective tissue due to proteases with chronic inflammation leading to a host susceptible to recurrent infections, leading to further inflammation and progression of bronchiectasis.CONCLUSIONS: This case highlights the need for physicians to be aware of the potential adverse pulmonary effects, although rare, of silicone implants. This particular patient most likely suffered progression of bronchiectasis with both a restrictive and obstructive disease due to silicosis from the gluteal implants.