Study objective We sought to determine, using video review, the frequencies of first attempt success and adverse effects during rapid sequence intubation (RSI) in a large, tertiary care pediatric emergency department (ED). Methods We conducted a retrospective study of children undergoing RSI in the ED of a pediatric institution. Data were collected from pre-existing video and written records of care provided. The primary outcome was successful intubation on the first attempt at laryngoscopy. The secondary outcome was the occurrence of any adverse effect during RSI, including episodes of physiologic deterioration. We collected time data from the RSI process using video review. We explored the association between physician type and first attempt success. Results We obtained complete records for 114 of 123 (93%) children who underwent RSI in the ED over 12 months. Median age was 2.4 years and 89 (78%) were medical resuscitations. Of the 114 subjects, 59 (52%) were successfully intubated on the first attempt. Seventy subjects (61%) had one or more adverse effects during RSI; 38 (33%) suffered oxyhemoglobin desaturation and two required cardiopulmonary resuscitation after physiologic deterioration. Fewer adverse effects were documented in the written records than were noted on video review. The median time from induction through final endotracheal tube placement was 3 minutes. After adjusting for patient characteristics and illness severity, attending level providers were 10 times more likely to be successful on the first attempt than all trainees combined. Conclusions Video review of RSI revealed that first attempt failure and adverse effects were much more common than previously reported for children in an ED.

There is substantial evidence that Kaposi sarcoma-associated herpesvirus (KSHV) plays an important role in the pathogenesis of all forms of Kaposi sarcoma (KS). It has been noted that KS commonly occurs in locations, such as the feet, where tissue may be poorly oxygenated. On the basis of this observation, the potential role of hypoxia in the reactivation of KSHV replication was explored by studying 2 KSHV-infected primary effusion lymphoma B-cell lines (BC-3 and BCBL-1) latently infected with KSHV. Acute and chronic exposure of these cells to hypoxia (1% O 2 ) induced KSHV lytic replication, as indicated by an increase in intracellular lytic protein expression and detection of virus in cell supernatants by Western immunoblotting. In addition, hypoxia increased the levels of secreted viral interleukin-6. Moreover, hypoxia enhanced the lytic replication initiated by the viral inducer 12-O-tetradecanoylphorbol-13-acetate. Desferoxamine and cobalt chloride, 2 compounds that increase the intracellular levels of hypoxia-inducible factor 1, were also able to induce KSHV lytic replication. These studies suggest that hypoxia is an inducer of KSHV replication. This process may play an important role in the pathogenesis of KS. ( IntroductionKaposi sarcoma (KS) is a multifocal proliferative disease of vascular origin. KS lesions are characterized by proliferation and growth of spindle-shaped neoplastic cells that appear to be of lymphatic endothelial cell origin. [1][2][3] KS is the most common neoplasm in human immunodeficiency virus type 1-infected individuals. 1 Even before the advent of acquired immunodeficiency syndrome (AIDS), KS was known to be more prevalent in certain geographic areas and groups of patients (classic and endemic KS). A classic form of KS is described as occurring in elderly men in southern Italy and other Mediterranean countries, 4 and an endemic form of KS has been observed to occur in sub-Saharan Africa. 5,6 In addition, transplant recipients and other immunosuppressed patients are at risk for developing KS. 4 Since the discovery of Kaposi sarcoma-associated herpesvirus (KSHV), also called human herpesvirus-8 (HHV-8), in 1994, 7 substantial evidence has been accumulated that implicates it as an essential factor in the pathogenesis of all forms of KS. 8,9 It is also involved in the pathogenesis of primary effusion lymphoma (PEL) and certain cases of multicentric Castleman disease. 10 KSHV DNA is detected in nearly all KS lesions. 7,11,12 As with other human herpesviruses, infection with KSHV can be latent or lytic. Activation of viral replication in latently infected B cells, endothelial cells, or other target cells may be responsible for viral spread and contribute to the development of KS. 4 KSHV encodes for several cellular gene mimics that are produced during lytic replication and that have proangiogenic activity. [13][14][15][16] The virus also encodes several cellular protein mimics with oncogenic potential, such as v-cyc, a D-type cyclin, and a member of the interferon regulatory factor ...

Following the simultaneous introduction of four interventions in a paediatric ED, RSI was performed more reliably, successfully and safely.