Impact of ASA score misclassification on NSQIP predicted mortality: a retrospective analysis.

BACKGROUND: The ASA physical classification score has a major impact on the observed/expected (O/E) mortality ratio in the NSQIP General Vascular Mortality Model. The difference in predicted mortality is greatest between ASAs 3 and 4. We hypothesized under-classified ASA scores significantly affect the O/E mortality. METHODS: We conducted a retrospective review of NSQIP essential surgery cases from January 2014 to December 2014 (n = 1264) with mortality sub-analysis (n = 33) at our institution. We recorded transfer and emergency status and independently calculated the ASA score for mortalities using published definitions. A random sample of 50 survivors and 10 emergency survivors were reviewed and ASA recalculated. We performed statistical modeling to simulate the effects of ASA misclassifications. Statistical analysis was performed using JMP 10 and SAS 9.4. RESULTS: ASA was under-classified in 18.2% of mortalities, most commonly ASAs 3 and 4. Sixteen percent of ASA 3 survivors were misclassified, including 60% in the emergency subgroup (p < 0.05 vs. elective cases). Patients transferred from other institutions were more likely to be emergency cases than non-transferred patients (43.5 vs. 7.84%, p < 0.05). Transferred patients had a higher proportion of ASAs 3-5 vs. ASAs 1-2 compared with non-transfers (84.38 vs. 49.76%, p < 0.05) Simulation data showed ASA misclassification underestimated predicted mortality by 2.5 deaths on average. CONCLUSION: ASA misclassification significantly impacts O/E mortality. With accurate ASA classification, observed mortality would not have exceeded expected mortality in our institution. Education regarding the impact of ASA scoring is critical to ensure accurate O/E mortality data at hospitals using NSQIP to assess surgical quality.

The role of high airway pressure and dynamic strain on ventilator-induced lung injury in a heterogeneous acute lung injury model.

BACKGROUND: Acute respiratory distress syndrome causes a heterogeneous lung injury with normal and acutely injured lung tissue in the same lung. Improperly adjusted mechanical ventilation can exacerbate ARDS causing a secondary ventilator-induced lung injury (VILI). We hypothesized that a peak airway pressure of 40 cmH2O (static strain) alone would not cause additional injury in either the normal or acutely injured lung tissue unless combined with high tidal volume (dynamic strain). METHODS: Pigs were anesthetized, and heterogeneous acute lung injury (ALI) was created by Tween instillation via a bronchoscope to both diaphragmatic lung lobes. Tissue in all other lobes was normal. Airway pressure release ventilation was used to precisely regulate time and pressure at both inspiration and expiration. Animals were separated into two groups: (1) over-distension + high dynamic strain (OD + HDS, n = 6) and (2) over-distension + low dynamic strain (OD + LDS, n = 6). OD was caused by setting the inspiratory pressure at 40 cmH2O and dynamic strain was modified by changing the expiratory duration, which varied the tidal volume. Animals were ventilated for 6 h recording hemodynamics, lung function, and inflammatory mediators followed by an extensive necropsy. RESULTS: In normal tissue (NT), OD + LDS caused minimal histologic damage and a significant reduction in BALF total protein (p < 0.05) and MMP-9 activity (p < 0.05), as compared with OD + HDS. In acutely injured tissue (ALIT), OD + LDS resulted in reduced histologic injury and pulmonary edema (p < 0.05), as compared with OD + HDS. CONCLUSIONS: Both NT and ALIT are resistant to VILI caused by OD alone, but when combined with a HDS, significant tissue injury develops.

Limiting ventilator-associated lung injury in a preterm porcine neonatal model.

PURPOSE: Preterm infants are prone to respiratory distress syndrome (RDS), with severe cases requiring mechanical ventilation for support. However, there are no clear guidelines regarding the optimal ventilation strategy. We hypothesized that airway pressure release ventilation (APRV) would mitigate lung injury in a preterm porcine neonatal model. METHODS: Preterm piglets were delivered on gestational day 98 (85% of 115day term), instrumented, and randomized to volume guarantee (VG; n=10) with low tidal volumes (5.5cm3kg-1) and PEEP 4cmH2O or APRV (n=10) with initial ventilator settings: PHigh 18cmH2O, PLow 0cmH2O, THigh 1.30s, TLow 0.15s. Ventilator setting changes were made in response to clinical parameters in both groups. Animals were monitored continuously for 24hours. RESULTS: The mortality rates between the two groups were not significantly different (p>0.05). The VG group had relatively increased oxygen requirements (FiO2 50%±9%) compared with the APRV group (FiO2 28%±5%; p>0.05) and a decrease in PaO2/FiO2 ratio (VG 162±33mmHg; APRV 251±45mmHg; p<0.05). The compliance of the VG group (0.51±0.07L·cmH2O-1) was significantly less than the APRV group (0.90±0.06L·cmH2O-1; p<0.05). CONCLUSION: This study demonstrates that APRV improves oxygenation and compliance as compared with VG. This preliminary work suggests further study into the clinical uses of APRV in the neonate is warranted. LEVEL OF EVIDENCE: Not Applicable (Basic Science Animal Study).

The 30-year evolution of airway pressure release ventilation (APRV).

Airway pressure release ventilation (APRV) was first described in 1987 and defined as continuous positive airway pressure (CPAP) with a brief release while allowing the patient to spontaneously breathe throughout the respiratory cycle. The current understanding of the optimal strategy to minimize ventilator-induced lung injury is to "open the lung and keep it open". APRV should be ideal for this strategy with the prolonged CPAP duration recruiting the lung and the minimal release duration preventing lung collapse. However, APRV is inconsistently defined with significant variation in the settings used in experimental studies and in clinical practice. The goal of this review was to analyze the published literature and determine APRV efficacy as a lung-protective strategy. We reviewed all original articles in which the authors stated that APRV was used. The primary analysis was to correlate APRV settings with physiologic and clinical outcomes. Results showed that there was tremendous variation in settings that were all defined as APRV, particularly CPAP and release phase duration and the parameters used to guide these settings. Thus, it was impossible to assess efficacy of a single strategy since almost none of the APRV settings were identical. Therefore, we divided all APRV studies divided into two basic categories: (1) fixed-setting APRV (F-APRV) in which the release phase is set and left constant; and (2) personalized-APRV (P-APRV) in which the release phase is set based on changes in lung mechanics using the slope of the expiratory flow curve. Results showed that in no study was there a statistically significant worse outcome with APRV, regardless of the settings (F-ARPV or P-APRV). Multiple studies demonstrated that P-APRV stabilizes alveoli and reduces the incidence of acute respiratory distress syndrome (ARDS) in clinically relevant animal models and in trauma patients. In conclusion, over the 30 years since the mode's inception there have been no strict criteria in defining a mechanical breath as being APRV. P-APRV has shown great promise as a highly lung-protective ventilation strategy.

Trauma transfers to a rural level 1 center: a retrospective cohort study.

BACKGROUND: The regionalization of trauma care, the Emergency Medical Treatment and Active Labor Act of 1986, the advent of Accountable Care Organizations and bundled payments have brought Level 1 trauma centers (TC) to a new crossroads. By protocol, injured patients are preferentially transferred to designated TCs when a higher level of care is indicated. Trauma transfers frequently come during off hours and may not always appear to be related to injury severity. Based on this observation, we hypothesized patients transferred from regional hospitals to Level 1 TCs would have lower injury severity scores (ISS) and unfavorable payor status. METHODS: We queried our TC registry to identify trauma transfers (TTP) and primary trauma patients (PTP) treated at our level 1 TC between 2004 and 2012. Demographics, payor status, length of stay (LOS), injury severity score (ISS), and discharging service were compared. RESULTS: 5699 TTP and 11147 PTP were identified. Uninsured patients comprised 11 % (n = 602) of TTP compared with 15 % (n = 1,721) of PTP (P < 0.0001). Surprisingly 52 % of TTP were Medicare or HMO (n = 3008) beneficiaries, versus 42 % of PTP being Medicare or HMO (n = 4614) recipients (P < 0.0001). Patients were discharged predominantly by neurosurgery and orthopedic surgery (i.e.: General Adult and General Pediatric comprised <50 % of discharges) for all trauma admissions. Adult and Pediatric Trauma services accounted for 29 % (n = 1674) of TTP versus 45 % of PTP (n = 5045) discharges (P < 0.0001). Mean Injury Severity Score of TTP was found to be 11.5 ± 0.11, in comparison to 11.6 ± 0.11 in PTP (P = 0.42), while mean LOS was 5.6 ± 0.1 days for TTP and 5.9 ± 0.1 days for PTP (P = 0.06). CONCLUSIONS: These data suggest designated trauma centers should continue to encourage and accept appropriate transfer of trauma patients for surgical subspecialty care. The perception trauma transfers increase institutional fiscal burden is unsubstantiated.

The effects of airway pressure release ventilation on respiratory mechanics in extrapulmonary lung injury.

BACKGROUND: Lung injury is often studied without consideration for pathologic changes in the chest wall. In order to reduce the incidence of lung injury using preemptive mechanical ventilation, it is important to recognize the influence of altered chest wall mechanics on disease pathogenesis. In this study, we hypothesize that airway pressure release ventilation (APRV) may be able to reduce the chest wall elastance associated with an extrapulmonary lung injury model as compared with low tidal volume (LVt) ventilation. METHODS: Female Yorkshire pigs were anesthetized and instrumented. Fecal peritonitis was established, and the superior mesenteric artery was clamped for 30 min to induce an ischemia/reperfusion injury. Immediately following injury, pigs were randomized into (1) LVt (n = 3), positive end-expiratory pressure (PEEP) 5 cmH2O, V t 6 cc kg(-1), FiO2 21 %, and guided by the ARDSnet protocol or (2) APRV (n = 3), P High 16-22 cmH2O, P Low 0 cmH2O, T High 4.5 s, T Low set to terminate the peak expiratory flow at 75 %, and FiO2 21 %. Pigs were monitored continuously for 48 h. Lung samples and bronchoalveolar lavage fluid were collected at necropsy. RESULTS: LVt resulted in mild acute respiratory distress syndrome (ARDS) (PaO2/FiO2 = 226.2 ± 17.1 mmHg) whereas APRV prevented ARDS (PaO2/FiO2 = 465.7 ± 66.5 mmHg; p < 0.05). LVt had a reduced surfactant protein A concentration and increased histologic injury as compared with APRV. The plateau pressure in APRV (34.3 ± 0.9 cmH2O) was significantly greater than LVt (22.2 ± 2.0 cmH2O; p < 0.05) yet transpulmonary pressure between groups was similar (p > 0.05). This was because the pleural pressure was significantly lower in LVt (7.6 ± 0.5 cmH2O) as compared with APRV (17.4 ± 3.5 cmH2O; p < 0.05). Finally, the elastance of the lung, chest wall, and respiratory system were all significantly greater in LVt as compared with APRV (all p < 0.05). CONCLUSIONS: APRV preserved surfactant and lung architecture and maintenance of oxygenation. Despite the greater plateau pressure and tidal volumes in the APRV group, the transpulmonary pressure was similar to that of LVt. Thus, the majority of the plateau pressure in the APRV group was distributed as pleural pressure in this extrapulmonary lung injury model. APRV maintained a normal lung elastance and an open, homogeneously ventilated lung without increasing lung stress.