Pediatric Postoperative Pulse Oximetry Monitoring During Transport to the Postanesthesia Care Unit Reduces Frequency of Hypoxemia.

BACKGROUND: The standard use of pulse oximetry during the transport of postoperative patients from the operating room (OR) to the postanesthesia care unit (PACU) is not routinely practiced. A study was conducted to determine if the frequency of hypoxemia on admission to the PACU decreased after implementation of routine use of transport pulse oximeters for postoperative patients being transferred to the PACU. METHODS: In this prospective cohort study, which was conducted at an academic pediatric hospital, the primary outcome measure was the frequency of hypoxemic events on arrival to the PACU. RESULTS: A total of 506 patients in the preintervention phase and 597 in the postintervention phase met the inclusion criteria. Six hypoxemic events on arrival to the PACU were identified in preintervention phase versus zero in the postintervention period, p = 0.009. Use of oxygen monitors during transport from the OR to the PACU increased from 0% to 100%, p < 0.0001, in the postintervention phase. The median duration of unmonitored time during transport decreased from 272 seconds to 13 seconds, p < 0.0001. Of the 605 patients who met the inclusion criteria for sustainment audits-conducted 18 months after the postimplementation evaluation-99.8% were transported to the PACU with a pulse oximeter, and there were zero reported hypoxemic patients on PACU admission. CONCLUSION: The routine use of portable oxygen monitoring when transferring patients from the OR to the PACU is a low-cost, noninvasive safety measure that should be considered at any institution performing pediatric general anesthesia.

Dexmedetomidine for sedation in the parturient with respiratory failure requiring noninvasive ventilation.

Dexmedetomidine is a selective alpha-2 receptor agonist that possesses both sedative and analgesic properties, with minimal respiratory depression. We report the successful administration of dexmedetomidine on a 16-year-old primigravida woman that allowed the patient to tolerate application of bi-level positive airway pressure ventilation in treatment of acute hypoxemic respiratory failure.

Use of hypothermia to allow low-tidal-volume ventilation in a patient with ARDS.

Low-tidal-volume ventilation reduces mortality in patients with ARDS, but there are often challenges in implementing lung-protective ventilation, such as acidosis from hypercapnia. In a patient with severe ARDS we achieved adequate ventilation with a very low tidal volume (4 mL/kg ideal body weight) by inducing mild hypothermia (body temperature 35-36°C).

Overexpression of mitochondrial Hsp70/Hsp75 protects astrocytes against ischemic injury in vitro.

Mitochondrial heat shock protein 70 (mtHsp70/Hsp75/Grp75/mortalin/TRAP-1/PBP74) is an essential mitochondrial chaperone and a member of the heat shock protein 70 (HSP70) family. Although many studies have shown the protective properties of overexpression of the cytosolic inducible member of the HSP70 family, Hsp72, few studies have investigated the protective potential of Hsp75 against ischemic injury. Mitochondria are one of the primary targets of ischemic injury in astrocytes. In this study, we analyzed the effects of Hsp75 overexpression on cellular levels of reactive oxygen species (ROS), mitochondrial membrane potential, ATP levels, and viability during the ischemia-like conditions of oxygen-glucose deprivation (OGD) or glucose deprivation (GD) in primary astrocytic cultures. We show that Hsp75 overexpression decreases ROS production and preserves mitochondrial membrane potential during GD, and preserves ATP levels and cell viability during OGD. These findings indicate that Hsp75 can provide protection against ischemia-like in vitro injury and suggest that it should be further studied as a potential candidate for protection against ischemic injury.

Regulation of apoptotic and inflammatory cell signaling in cerebral ischemia: the complex roles of heat shock protein 70.

Although heat shock proteins have been studied for decades, new intracellular and extracellular functions in a variety of diseases continue to be discovered. Heat shock proteins function within networks of interacting proteins; they can alter cellular physiology rapidly in response to stress without requiring new protein synthesis. This review focuses on the heat shock protein 70 family and considers especially the functions of the inducible member, heat shock protein 72, in the setting of cerebral ischemia. In general, inhibiting apoptotic signaling at multiple points and up-regulating survival signaling, heat shock protein 70 has a net prosurvival effect. Heat shock protein 70 has both antiinflammatory and proinflammatory effects depending on the cell type, context, and intracellular or extracellular location. Intracellular effects are often antiinflammatory with inhibition of nuclear factor-kappaB signaling. Extracellular effects can lead to inflammatory cytokine production or induction of regulatory immune cells and reduced inflammation.