Intraoperative surfactant administration during neonatal sacrococcygeal teratoma resection.

A very preterm infant with a prenatally diagnosed sacrococcygeal teratoma presented for urgent resection. Intraoperatively, he required massive transfusion due to hemorrhage with progressive decline in lung compliance and hypoxia. Rescue surfactant was given with immediate improvement in ventilation and oxygenation. Surgery was successfully completed without complications.

Resection of a Posterior Mediastinal Mass in a 4-Year-Old Child Complicated by Difficult Airway Management and Emergent Use of Extracorporeal Membrane Oxygenation.

Literature on posterior mediastinal masses is limited. Furthermore, they have traditionally been described to pose lower cardiopulmonary risks compared with anterior mediastinal masses. Studies on posterior mediastinal masses are even more limited in the pediatric population. We present a case of a large posterior mediastinal mass in a 4-year-old child who presented with extremely difficult airway management during endobronchial intubation due to severe external compression that led to use of an adapted airway management technique with a rigid airway exchanger for lung isolation. Due to the pathology of the mass, a tracheal tear was encountered during surgical dissection and the patient required emergent venovenous extracorporeal membrane oxygenation to allow for successful airway repair and complete resection of the mass.

Urinary neutrophil gelatinase-associated lipocalin (NGAL) distinguishes sustained from transient acute kidney injury after general surgery.

BACKGROUND: This prospective study tests the hypothesis that after general surgery urinary NGAL can distinguish between sustained acute kidney injury (AKI), typical of nephron damage, from transient AKI, commonly seen with hemodynamic variation and prerenal azotemia. METHODS: Urine was collected in 510 patients within 2-3 hr after general surgery and urinary NGAL was determined using ELISA. Patients who met AKIN Stage 1 criteria of AKI were sub-classified into those with sustained AKI (serum creatinine elevation for more than 3 days), and those with transient AKI (serum creatinine elevation for less 3 days). RESULTS: Seventeen of 510 patients (3.3%) met the Stage 1 AKIN criteria within 48 hrs of surgery. Elevations in serum creatinine were sustained in 9 and transient in 8 patients. Urinary NGAL was significantly elevated only in patients with sustained AKI (204.8+/-411.9 ng/dL); patients with transient AKI had urinary NGAL that was indistinguishable from patients who did not meet AKIN criteria at all (30.8 ±36.5 ng/dL vs. 31.9 ±113 ng/dL). The area under the curve (AUC) of the receiver operating characteristic (ROC) curve of urinary NGAL to predict sustained AKI was 0.85 [CI (95%): 0.773 to 0.929, p<0.001]. CONCLUSIONS: Urinary NGAL levels measured 2-3 hr after surgery were able to distinguish the kinetics of creatinine (sustained AKI vs transient AKI) over the subsequent week. Transient AKI is an easily reversible state that is likely not associated with substantial tubular injury and therefore NGAL release. Using AKIN criteria, both transient and sustained AKI are classified as AKI even though our data demonstrates that they are possibly different entities.

Activation of the AXL kinase causes resistance to EGFR-targeted therapy in lung cancer.

Human non-small cell lung cancers (NSCLCs) with activating mutations in EGFR frequently respond to treatment with EGFR-targeted tyrosine kinase inhibitors (TKIs), such as erlotinib, but responses are not durable, as tumors acquire resistance. Secondary mutations in EGFR (such as T790M) or upregulation of the MET kinase are found in over 50% of resistant tumors. Here, we report increased activation of AXL and evidence for epithelial-to-mesenchymal transition (EMT) in multiple in vitro and in vivo EGFR-mutant lung cancer models with acquired resistance to erlotinib in the absence of the EGFR p.Thr790Met alteration or MET activation. Genetic or pharmacological inhibition of AXL restored sensitivity to erlotinib in these tumor models. Increased expression of AXL and, in some cases, of its ligand GAS6 was found in EGFR-mutant lung cancers obtained from individuals with acquired resistance to TKIs. These data identify AXL as a promising therapeutic target whose inhibition could prevent or overcome acquired resistance to EGFR TKIs in individuals with EGFR-mutant lung cancer.