A Quality Improvement Initiative to Increase Confirmation of Prehospital Endotracheal Tube Placement at Emergency Department Transfer of Care.

OBJECTIVES: Rates of prehospital unplanned extubation (UE) range from 0 to 25% and are the result of many factors, including patient movement. Transfer of care of intubated patients to the emergency department (ED) involves significant patient movement and represents a high-risk event for UE. Frequent confirmation of endotracheal tube (ETT) placement is imperative for early recognition of UE and to minimize patient harm. METHODS: Local Practice-Our baseline rate of verbal ETT position confirmation with a member of the ED team during ED transfer of care was 74%. Our goal was to increase this practice to >90% in six months. This project was completed in partnership with Toronto Paramedic Services. Prehospital electronic patient care records (ePCRs) were reviewed weekly to determine the proportion of intubated patients who had ETT placement confirmed in the ED at transfer of care. Interventions-Pre- and post-project paramedic focus groups were conducted to identify potential drivers, change ideas, and project feedback. Three staggered interventions were introduced over five months: (1) memorandums to paramedics, ED chiefs and respiratory therapy leads, (2) individualized paramedic feedback e-mails, and (3) ePCR changes and closing rules. RESULTS: The pre-project focus group identified several potential drivers, such as physical barriers, interprofessional relationships, and communication. ETT confirmation remained ≥90% for the last eight weeks and interventions resulted in special cause variation. Median cases without verbal confirmation between paramedics and ED staff reduced from 5/week (IQR 2.5, 6.5) to 1/week (IQR 0, 2). UE was identified in 0.6% (2/340) of patients with ETT confirmation. The post-project focus group noted improvements in perceived accountability, interprofessional relationships, and satisfaction with interventions. CONCLUSION: Through a series of interventions, we improved the rate of ETT confirmation during ED transfer of care. Although rates of UE were low, improvement in ETT confirmation may lead to faster recognition of UE when it does occur thereby mitigating complications. The observed improvement was sustained after interventions ended.

Intrasac pressure waveforms after endovascular aneurysm repair (EVAR) are a reliable marker of type I endoleaks, but not type II or combined types: an experimental study.

PURPOSE: To ascertain the nature of the pressure wave transmitted through aneurysm thrombus and the changes produced after endovascular repair and the development of type I and II endoleaks. METHODS: A 25 mm Talent endovascular graft was deployed in a latex model of an abdominal aortic aneurysm, which was incorporated in a pulsatile flow unit. The graft was surrounded by thrombus analogue to simulate conditions in vivo. Pressure waveforms in the sac were captured over 5s at 1000 Hz in these settings: (i) no endoleaks (baseline), after introduction of (ii) type I (iii) type II and (iv) combined type I and II endoleaks. The arterial blood pressure settings used were 140/100 and 130/90 mmHg, denoted the high and low settings, respectively. ANOVA in Minitab 13 was applied for statistical analysis. RESULTS: Pulsatile waveforms were transmitted through the thrombus. Intrasac pressure after stent-grafting reduced to 110/107, 99/96 mmHg (p<0.001) (high, low settings, respectively). Introduction of a type I endoleak caused this to rise to 120/112, 115/107 mmHg (p<0.001, vs. baseline); after producing a type II endoleak these were 101/98, 91/88 mmHg (p<0.001, vs. baseline). A combined type I and II endoleak produced intrasac pressures identical to that of a type I endoleak. CONCLUSIONS: Intrasac pressure waveforms following EVAR are easily defined following a type I endoleak. Waveforms obtained following type II endoleak simulation resemble the baseline waveform in an attenuated form. Intrasac pressures are, therefore, a reliable marker for type I, but not a type II endoleak. In the case of a combined endoleak, the type I endoleak waveform effectively masks that of the type II. Intrasac thrombus faithfully transmits intrasac pressures.

Aneurysmal hypertension and its relationship to sac thrombus: a semi-qualitative analysis by experimental fluid mechanics.

OBJECTIVES: To ascertain the effect of aneurysm thrombus and luminal diameter on arterial blood pressure within the abdominal aortic aneurysm lumen and at the sac wall. METHODS: A life-like abdominal aortic aneurysm was incorporated in a pulsatile flow unit, using systemic blood pressure settings of 140/100 mmHg and 130/90 mmHg (denoted the high and low settings, respectively). Aneurysm sac pressure was measured in the absence of thrombus within the sac. This was repeated after a thrombus analogue (gelatine) was introduced into the aneurysm model in an asymmetric fashion. Luminal and sac wall pressures were compared to the systemic pressure, and to each other, in both blood pressure settings. Statistical analysis was performed using ANOVA in Minitab 13. RESULTS: In the empty sac, the luminal and sac wall pressures were identical to the systemic pressures at the high and low settings. After introduction of thrombus, pressure was transmitted in a monophasic pulsatile fashion, measuring 166/142/151 mmHg (SP/DP/MP) at the sac wall, while the corresponding intraluminal pressure was 164/136/145 mmHg (p<0.001, high setting). By contrast, in the low setting, these readings were 157/133/141 (sac wall) and 160/128/138 mmHg (lumen; p<0.001). The sac wall pressures were significantly higher than the luminal pressures for both high and low settings (p<0.001). CONCLUSIONS: Thrombus has a significant effect on the intraaneurysmal lumen itself and causes localised hypertension with high intraluminal pressures. The differences between the sac wall/luminal pressures may affect regional aneurysm wall biomechanics, but needs further study.