Objective: Cerebral edema is common in severe hepatic encephalopathy and may be life threatening. Bolus 23.4% hypertonic saline improves surveillance neuromonitoring scores, although its mechanism of action is not clearly established. We investigated the hypothesis that bolus hypertonic saline decreases cerebral edema in severe hepatic encephalopathy utilizing a quantitative technique to measure brain and cerebrospinal fluid volume changes. Design: Retrospective analysis of serial CT scans, and clinical data for a case-control series were performed. Setting: ICUs of a tertiary care hospital. Patients: Patients with severe hepatic encephalopathy treated with 23.4% hypertonic saline and control patients who did not receive 23.4% hypertonic saline. Interventions: 23.4% hypertonic saline bolus administration. Measurements and Main Results: We used clinically obtained CT scans to measure volumes of the ventricles, intracranial cerebrospinal fluid, and brain using a previously validated semiautomated technique (Analyze Direct, Overland Park, KS). Volumes before and after 23.4% hypertonic saline were compared with Wilcoxon signed rank test. Associations among total cerebrospinal fluid volume, ventricular volume, serum sodium, and Glasgow Coma Scale scores were assessed using Spearman rank correlation test. Eleven patients with 18 administrations of 23.4% hypertonic saline met inclusion criteria. Total cerebrospinal fluid (median, 47.6?mL [35.1–69.4 mL] to 61.9?mL [47.7–87.0 mL]; p < 0.001) and ventricular volumes (median, 8.0?mL [6.9–9.5 mL] to 9.2?mL [7.8–11.9 mL]; p = 0.002) increased and Glasgow Coma Scale scores improved (median, 4 [3–6] to 7 [6–9]; p = 0.008) after 23.4% hypertonic saline. In contrast, total cerebrospinal fluid and ventricular volumes decreased in untreated control patients. Serum sodium increase was associated with increase in total cerebrospinal fluid volume (r = 0.83, p < 0.001), and change in total cerebrospinal fluid volume was associated with ventricular volume change (r = 0.86; p < 0.001). Conclusions: Total cerebrospinal fluid and ventricular volumes increased after 23.4% hypertonic saline, consistent with a reduction in brain tissue volume. Total cerebrospinal fluid and ventricular volume change may be useful quantitative measures to assess cerebral edema in severe hepatic encephalopathy.

Objective: To determine the relation between high arterial oxygen tension levels (PaO2) and long-term mortality in patients with spontaneous intracerebral hemorrhage treated in the ICU. Design: National observational multicenter cohort study. Setting: Twenty-one ICUs in Finland. Patients: A total of 3,033 adult patients. Interventions: None. Measurements and Main Results: Patients were divided into high (> 150?mm Hg), intermediate (97.5–150?mm Hg), and low (< 97.5?mm Hg) PaO2 groups based on the lowest measured PaO2/FIO2 ratio during the first 24 hours after ICU admission: 63% (n = 1,923) were in the low group, 29% (n = 892) were in the intermediate group, and 7% (n = 218) were in the high group; 80% were mechanically ventilated. The primary outcome was 6-month mortality, which occurred in 49% of patients and was significantly more frequent in the high PaO2 group than in the intermediate and low PaO2 groups (61% vs 52% and 46%, respectively, p < 0.001). In univariate analysis, patients in the high PaO2 group had a significantly increased risk of 6-month mortality compared with the low PaO2 group (odds ratio, 1.82; 95% CIs, 1.36–2.42; p < 0.001), but this statistically significant relation was lost after adjusting for markers of severity of illness in a logistic mixed-effects regression model (odds ratio, 1.10; 95% CI, 0.76–1.60; p = 0.598). Conclusions: No significant relation between PaO2 levels and long-term mortality was found. The clinical role of hyperoxemia in patients with intracerebral hemorrhage treated in the ICU remains controversial and warrants further studies.

Objectives: Shared decision making is endorsed by critical care organizations; however, there remains confusion about what shared decision making is, when it should be used, and approaches to promote partnerships in treatment decisions. The purpose of this statement is to define shared decision making, recommend when shared decision making should be used, identify the range of ethically acceptable decision-making models, and present important communication skills. Design: The American College of Critical Care Medicine and American Thoracic Society Ethics Committees reviewed empirical research and normative analyses published in peer-reviewed journals to generate recommendations. Recommendations approved by consensus of the full Ethics Committees of American College of Critical Care Medicine and American Thoracic Society were included in the statement. Main Results: Six recommendations were endorsed: 1) Definition: Shared decision making is a collaborative process that allows patients, or their surrogates, and clinicians to make healthcare decisions together, taking into account the best scientific evidence available, as well as the patient’s values, goals, and preferences. 2) Clinicians should engage in a shared decision making process to define overall goals of care (including decisions regarding limiting or withdrawing life-prolonging interventions) and when making major treatment decisions that may be affected by personal values, goals, and preferences. 3) Clinicians should use as their “default” approach a shared decision making process that includes three main elements: information exchange, deliberation, and making a treatment decision. 4) A wide range of decision-making approaches are ethically supportable, including patient- or surrogate-directed and clinician-directed models. Clinicians should tailor the decision-making process based on the preferences of the patient or surrogate. 5) Clinicians should be trained in communication skills. 6) Research is needed to evaluate decision-making strategies. Conclusions: Patient and surrogate preferences for decision-making roles regarding value-laden choices range from preferring to exercise significant authority to ceding such authority to providers. Clinicians should adapt the decision-making model to the needs and preferences of the patient or surrogate.

Objective: Excellence is an important goal for all physicians. Unfortunately, it is hard to define, evaluate, and achieve. To provide a concise interpretive review of excellence in intensive care medicine, with a focus on those key characteristics that excellent physicians possess but are seldom discussed. Data Sources: Electronic search of the PubMed database using the search terms “excellence,” “role models,” “compassion,” “commitment,” “dedication,” and “passion.” Study Selection: Publications or studies of excellence, role models, compassion, commitment, dedication, and passion. Two reviewers evaluated each term. Data Extraction: Publications or studies were abstracted independently and in duplicate. Data Synthesis: Excellence in critical care can be achieved through deliberate practice, feedback, and effective evaluation. Excellence embodies numerous characteristics, which include compassion, commitment, and passion. Conclusions: Awareness of the fundamental characteristics of excellence can help young students and doctors determine what they should strive for to become excellent physicians as well as encourage experienced doctors to rekindle the spark that initially motivated them to become physicians.

Objectives: Circadian rhythms are severely disrupted among the critically ill. These circadian arrhythmias impair mentation, immunity, autonomic function, endocrine activity, hormonal signaling, and ultimately healing. In this review, we present a modern model of circadian disruption among the critically ill, discuss causes of these circadian arrhythmias, review observational and intervention studies of the effects of circadian-rhythm–restoring factors on medical outcomes, and identify needed key trials of circadian interventions in the critically ill. Data Sources: MEDLINE, EMBASE, PsychINFO, Google Scholar through December 2014. Study Selection: Articles relevant to circadian rhythms, melatonin, and light in the critically ill were selected. Data Extraction and Data Synthesis: Articles were synthesized for this review of circadian arrhythmia and the use of circadian-rhythm–restoring interventions among the critically ill. Conclusions: Circadian disruption often demonstrates serial degradation: initially, the amplitude attenuates along with delayed circadian phase. With increasing acuity of illness, circadian rhythmicity may be lost entirely. Causes of chronodisruption may be environmental or internal to the patient. In particular, inadequate daytime illumination and nocturnal light pollution disrupt healthy circadian periodicity. Internal causes of circadian arrhythmia include critical illness itself and subjective experience of distress and pain. Observational studies of windowed rooms and real-time ambient lighting have found that physiologic light-dark patterns may support recovery from critical illness. Studies of early morning bright light or evening melatonin agonists have found improved rates of delirium, enhanced sleep, and lower arrhythmia prevalence. The current evidence base emphasizes that lighting and melatoninergic interventions deserve to be tested in full-scale trials.

Objective: Alterations in neutrophil morphology (size, shape, and composition), mechanics (deformability), and motility (chemotaxis and migration) have been observed during sepsis. We combine summarizing features of neutrophil morphology, mechanics, and motility that change during sepsis with an investigation into their clinical utility as markers for sepsis through measurement with novel technologies. Data Sources: We performed an initial literature search in MEDLINE using search terms “neutrophil,” “morphology,” “mechanics,” “dynamics,” “motility,” “mobility,” “spreading,” “polarization,” “migration,” and “chemotaxis.” We then combined the results with “sepsis” and “septic shock.” We scanned bibliographies of included articles to identify additional articles. Study Selection and Data Extraction: Final selection was done after the authors reviewed recovered articles. We included articles based on their relevance for our review topic. Data Synthesis: When compared with resting conditions, sepsis causes an increase in circulating numbers of larger, more rigid neutrophils that show diminished granularity, migration, and chemotaxis. Combined measurement of these variables could provide a more complete view on neutrophil phenotype manifestation. For that purpose, sophisticated automated hematology analyzers, microscopy, and bedside microfluidic devices provide clinically feasible, high-throughput, and cost-limiting means. Conclusions: We propose that integration of features of neutrophil morphology, mechanics, and motility with these new analytical methods can be useful as markers for diagnosis, prognosis, and monitoring of sepsis and may even contribute to basic understanding of its pathophysiology.

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Objectives: Virulent and multidrug-resistant Pseudomonas aeruginosa causes a lethal pneumonia, especially in patients who are artificially ventilated. It has been reported that the virulence mechanism used by P. aeruginosa, which is linked to acute lung injury, is strongly associated with the type III secretion system, and specific antibodies targeting this system have shown a protective effect in both experimental and clinical settings. We investigated the effect of administering IV immunoglobulins on P. aeruginosa pneumonia, including its associated bacteremia and mortality, although focusing especially on type III secretion system–associated P. aeruginosa virulence. Design: Prospective randomized and controlled animal study. Setting: University laboratory. Subjects: Male ICR mice. Interventions: Mice were infected intratracheally with a lethal dose of the virulent P. aeruginosa PA103 strain. IV immunoglobulin administration was examined in three different settings: 1) premixed; 2) pre-IV, prophylactic administration before bacterial infection; and 3) post-IV, therapeutic administration after bacterial infection. The effect of specific antigen titer depletion of IV immunoglobulins was also examined. Measurements and Main Results: Survival and body temperature were monitored for 24 hours. Bacteremia, cytokine concentration, myeloperoxidase activity, WBC counts in the blood, and lung bacterial load were evaluated. Survival improved significantly in mice that received IV immunoglobulins (p < 0.05). Lung edema, lung bacteriologic load, and bacteremia decreased significantly in the IV immunoglobulin–treated mice (p < 0.05). The mechanism of protection was associated with the presence of antibodies against both PcrV and some bacterial surface antigens in the IV immunoglobulins. Conclusions: IV immunoglobulin administration had a significantly protective effect against lethal infection from virulent P. aeruginosa. Prophylactic IV immunoglobulin administration at the highest dose was comparable with that achieved by administrating a specific anti-PcrV polyclonal IgG into the mice. The mechanism of protection is likely to involve the synergic action of anti-PcrV titers and antibodies against some surface antigen(s) that block the type III secretion system–associated virulence of P. aeruginosa.