Laryngoscopy should be performed in unresponsive patients if non-invasive airway clearance techniques are unsuccessful. Laryngoscopy involves placing a device in the mouth to visualize the back of the airway. If the foreign body can be seen, it can be removed with forceps. An endotracheal tube should then be placed in order to prevent airway compromise from resulting inflammation after the procedure. If the foreign body cannot be visualized, intubation, tracheotomy, or needle cricothyrotomy can be done to restore an airway for patients who have become unresponsive due to airway compromise.If non-invasive measures do not dislodge the foreign body, and the patient can maintain adequate ventilation, rigid bronchoscopy under general anesthesia should be performed. Supplemental oxygen, cardiac monitoring, and a pulse oximeter should be applied to the patient. Efforts should be made to keep the patient calm and avoid agitating the patient to prevent further airway compromise. Flexible rather than rigid bronchoscopy might be used when the diagnosis or object location are unclear. When flexible bronchoscope is used, rigid bronchoscope is typically on standby and readily available as this is the preferred approach for removal. Rigid bronchoscopy allows good airway control, ready bleeding management, better visualization, and ability to manipulate the aspirated object with a variety of forceps. Flexible bronchoscopy may be used for extraction when distal access is needed and the operator is experienced in this technique.
This report further expands the phenotypic spectrum to include the possibility of normal intelligence as corroborated by formal, longitudinal psycho-educational testing.The presence of two homologous low copy repeats either side of the deletion break-point suggests that non-allelic homologous recombination is the likely mechanism underlying this syndrome. Genetics
The microdeletion, around 1.6 million base pairs, in length and encompasses 5 known genes and 17 uncharacterised transcripts. These include transferrin receptor, choline-phosphate cytidylyltransferase A, RNF168, serine/threonine-protein kinase, nuclear cap-binding protein complex, melanotransferrin, DLG1 and D-beta-hydroxybutyrate dehydrogenase

Research
Research on the risk for developing schizophrenia in Ashkenazi Jews and other populations showed that 3q29 microdeletion syndrome leads to a significant higher rate of schizophrenia. In addition, a deletion at 3q29 was found to confer an increase to the odds of developing schizophrenia in a study of copy number variants and their effect on that disorder. References
External links

DECIPHER database entry for 3q29 microdeletion syndrome