Association Between Survival and Time of Day for Rapid Response Team Calls in a National Registry. (Patel)

Churpek MM, et al. Association Between Survival and Time of Day for Rapid Response Team Calls in a National Registry. Crit Care Med. 2017 Oct;45(10):1677-1682.

OBJECTIVES: Decreased staffing at nighttime is associated with worse outcomes in hospitalized patients. Rapid response teams were developed to decrease preventable harm by providing additional critical care resources to patients with clinical deterioration. We sought to determine whether rapid response team call frequency suffers from decreased utilization at night and how this is associated with patient outcomes.

DESIGN: Retrospective analysis of a prospectively collected registry database.

SETTING: National registry database of inpatient rapid response team calls.

PATIENTS: Index rapid response team calls occurring on the general wards in the American Heart Association Get With The Guidelines-Medical Emergency Team database between 2005 and 2015 were analyzed.

INTERVENTIONS: None.

MEASUREMENTS AND MAIN RESULTS: The primary outcome was inhospital mortality. Patient and event characteristics between the hours with the highest and lowest mortality were compared, and multivariable models adjusting for patient characteristics were fit. A total of 282,710 rapid response team calls from 274 hospitals were included. The lowest frequency of calls occurred in the consecutive 1 AM to 6:59 AM period, with 266 of 274 (97%) hospitals having lower than expected call volumes during those hours. Mortality was highest during the 7 AM hour and lowest during the noon hour (18.8% vs 13.8%; adjusted odds ratio, 1.41 [1.31-1.52]; p < 0.001). Compared with calls at the noon hour, those during the 7 AM hour had more deranged vital signs, were more likely to have a respiratory trigger, and were more likely to have greater than two simultaneous triggers.

CONCLUSIONS: Rapid response team activation is less frequent during the early morning and is followed by a spike in mortality in the 7 AM hour. These findings suggest that failure to rescue deteriorating patients is more common overnight. Strategies aimed at improving rapid response team utilization during these vulnerable hours may improve patient outcomes.

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Individualizing Thresholds of Cerebral Perfusion Pressure Using Estimated Limits of Autoregulation. (Patel)

Donnelly J, et al. Individualizing Thresholds of Cerebral Perfusion Pressure Using Estimated Limits of Autoregulation. Crit Care Med. 2017 Sep;45(9):1464-1471.

OBJECTIVES: In severe traumatic brain injury, cerebral perfusion pressure management based on cerebrovascular pressure reactivity index has the potential to provide a personalized treatment target to improve patient outcomes. So far, the methods have focused on identifying “one” autoregulation-guided cerebral perfusion pressure target-called “cerebral perfusion pressure optimal”. We investigated whether a cerebral perfusion pressure autoregulation range-which uses a continuous estimation of the “lower” and “upper” cerebral perfusion pressure limits of cerebrovascular pressure autoregulation (assessed with pressure reactivity index)-has prognostic value.

DESIGN: Single-center retrospective analysis of prospectively collected data.

SETTING: The neurocritical care unit at a tertiary academic medical center.

PATIENTS: Data from 729 severe traumatic brain injury patients admitted between 1996 and 2016 were used. Treatment was guided by controlling intracranial pressure and cerebral perfusion pressure according to a local protocol.

INTERVENTIONS: None.

METHODS AND MAIN RESULTS: Cerebral perfusion pressure-pressure reactivity index curves were fitted automatically using a previously published curve-fitting heuristic from the relationship between pressure reactivity index and cerebral perfusion pressure. The cerebral perfusion pressure values at which this “U-shaped curve” crossed the fixed threshold from intact to impaired pressure reactivity (pressure reactivity index = 0.3) were denoted automatically the “lower” and “upper” cerebral perfusion pressure limits of reactivity, respectively. The percentage of time with cerebral perfusion pressure below (%cerebral perfusion pressure < lower limit of reactivity), above (%cerebral perfusion pressure > upper limit of reactivity), or within these reactivity limits (%cerebral perfusion pressure within limits of reactivity) was calculated for each patient and compared across dichotomized Glasgow Outcome Scores. After adjusting for age, initial Glasgow Coma Scale, and mean intracranial pressure, percentage of time with cerebral perfusion pressure less than lower limit of reactivity was associated with unfavorable outcome (odds ratio %cerebral perfusion pressure < lower limit of reactivity, 1.04; 95% CI, 1.02-1.06; p < 0.001) and mortality (odds ratio, 1.06; 95% CI, 1.04-1.08; p < 0.001).

CONCLUSIONS: Individualized autoregulation-guided cerebral perfusion pressure management may be a plausible alternative to fixed cerebral perfusion pressure threshold management in severe traumatic brain injury patients. Prospective randomized research will help define which autoregulation-guided method is beneficial, safe, and most practical.

The Epidemiology of Hospital Death Following Pediatric Severe Sepsis: When, Why, and How Children With Sepsis Die. (Dodd)

Weiss SL, et al. The Epidemiology of Hospital Death Following Pediatric Severe Sepsis: When, Why, and How Children With Sepsis Die. Pediatr Crit Care Med. 2017 Sep;18(9):823-830.

OBJECTIVE: The epidemiology of in-hospital death after pediatric sepsis has not been well characterized. We investigated the timing, cause, mode, and attribution of death in children with severe sepsis, hypothesizing that refractory shock leading to early death is rare in the current era.

DESIGN: Retrospective observational study.

SETTING: Emergency departments and ICUs at two academic children’s hospitals.

PATIENTS: Seventy-nine patients less than 18 years old treated for severe sepsis/septic shock in 2012-2013 who died prior to hospital discharge.

INTERVENTIONS: None.

MEASUREMENTS AND MAIN RESULTS: Time to death from sepsis recognition, cause and mode of death, and attribution of death to sepsis were determined from medical records. Organ dysfunction was assessed via daily Pediatric Logistic Organ Dysfunction-2 scores for 7 days preceding death with an increase greater than or equal to 5 defined as worsening organ dysfunction. The median time to death was 8 days (interquartile range, 1-12 d) with 25%, 35%, and 49% of cumulative deaths within 1, 3, and 7 days of sepsis recognition, respectively. The most common cause of death was refractory shock (34%), then multiple organ dysfunction syndrome after shock recovery (27%), neurologic injury (19%), single-organ respiratory failure (9%), and nonseptic comorbidity (6%). Early deaths (≤ 3 d) were mostly due to refractory shock in young, previously healthy patients while multiple organ dysfunction syndrome predominated after 3 days. Mode of death was withdrawal in 72%, unsuccessful cardiopulmonary resuscitation in 22%, and irreversible loss of neurologic function in 6%. Ninety percent of deaths were attributable to acute or chronic manifestations of sepsis. Only 23% had a rise in Pediatric Logistic Organ Dysfunction-2 that indicated worsening organ dysfunction.

CONCLUSIONS: Refractory shock remains a common cause of death in pediatric sepsis, especially for early deaths. Later deaths were mostly attributable to multiple organ dysfunction syndrome, neurologic, and respiratory failure after life-sustaining therapies were limited. A pattern of persistent, rather than worsening, organ dysfunction preceded most deaths.

Dexmedetomidine for Sedation During Noninvasive Ventilation in Pediatric Patients. (Dodd)

Venkatraman R, et al. Dexmedetomidine for Sedation During Noninvasive Ventilation in Pediatric Patients. Pediatr Crit Care Med. 2017 Sep;18(9):831-837.

OBJECTIVES: To describe the use of dexmedetomidine for sedation in a large cohort of nonintubated children with acute respiratory insufficiency receiving noninvasive ventilatory support.

DESIGN: Single-center, retrospective, observational cohort study.

SETTING: A large quaternary-care PICU.

PATIENTS: The study cohort included 202 children receiving noninvasive ventilatory and a dexmedetomidine infusion within 48 hours of PICU admission over a 6-month period.

INTERVENTIONS: None.

MEASUREMENTS AND MAIN RESULTS: The primary respiratory diagnoses in the cohort (median age, 2 yr) included status asthmaticus (60%) and bronchiolitis (29%). Dexmedetomidine was infused for a median of 35 hours with a median hourly dose across the patient cohort of 0.61 μg/kg/hr (range, 0.4-0.8 μg/kg/hr). The target sedation level was achieved in 168 patients (83%) in the cohort for greater than or equal to 80% of the recorded values over the entire noninvasive ventilatory course, with dexmedetomidine as the only continuously administered sedative agent. While vital signs were frequently abnormal relative to age-based norms, clinical interventions were needed rarely to treat bradycardia (13%), hypotension (20%), and hypopnea (5%). The most frequently used of these interventions was a dexmedetomidine dose reduction, fluid bolus, and titration of noninvasive ventilatory support. Five patients (2.5%) required endotracheal intubation: three due to progression of their respiratory illness, one with septic shock, and one with apnea requiring resuscitation. In 194 of 202 patients (96%), the outcome of the noninvasive ventilatory course was successful with the patient being weaned from noninvasive respiratory support to nasal cannula or room air.

CONCLUSIONS: Dexmedetomidine was often effective as a single continuous sedative infusion during pediatric noninvasive ventilatory. Cardiorespiratory events associated with its use were typically mild and/or reversible with dose reduction, fluid administration, and/or noninvasive ventilatory titration. Prospective studies comparing dexmedetomidine with other agents in this setting are warranted.