Search

Purpose In acute respiratory distress syndrome (ARDS), dead space fraction has been independently associated with mortality. We hypothesized that early measurement of the difference between arterial and end-tidal CO2 (arterial-ET difference), a surrogate for dead space fraction, would predict mortality in mechanically ventilated patients with ARDS. Methods We performed two separate exploratory analyses. We first used publicly available databases from the ALTA, EDEN, and OMEGA ARDS Network trials (N = 124) as a derivation cohort to test our hypothesis. We then performed a separate retrospective analysis of patients with ARDS using University of Chicago patients (N = 302) as a validation cohort. Results The ARDS Network derivation cohort demonstrated arterial-ET difference, vasopressor requirement, age, and APACHE III to be associated with mortality by univariable analysis. By multivariable analysis, only the arterial-ET difference remained significant (P = 0.047). In a separate analysis, the modified Enghoff equation ((PaCO2–PETCO2)/PaCO2) was used in place of the arterial-ET difference and did not alter the results. The University of Chicago cohort found arterial-ET difference, age, ventilator mode, vasopressor requirement, and APACHE II to be associated with mortality in a univariate analysis. By multivariable analysis, the arterial-ET difference continued to be predictive of mortality (P = 0.031). In the validation cohort, substitution of the arterial-ET difference for the modified Enghoff equation showed similar results. Conclusion Arterial to end-tidal CO2 (ETCO2) difference is an independent predictor of mortality in patients with ARDS.

Rationale:Early mobilization and physical rehabilitation improve functional outcomes and are essential to high quality critical care. Despite its importance, it is common for rehabilitation to be deferred in the critically ill due to a variety of barriers, including infection with SARS-CoV-2. We present a single academic center's experience providing physical and occupational therapy to critically ill patients infected with SARS-CoV-2. Methods:All patients with Coronavirus Disease 2019 (COVID-19) associated illness admitted to the intensive care unit (ICU) from March 1st to July 31st, 2020 were identified in this retrospective chart review. Patients who received at least one therapy treatment session were included in the study. Results:Three-hundred and seventy-nine physical and occupational therapy sessions were conducted with 116 patients. The majority (85%) of patients were admitted to the ICU for hypoxemic respiratory failure. The median number of treatment sessions during ICU admission per patient was 2, (IQR: 1-4). The median time from ICU admission to first PT session was 4 days (IQR, 3-5). The median percentage of ICU days with physical and occupational therapy treatment was 33% (IQR, 21-50). The median session length was 25 minutes (IQR, 25-30min). Sitting was achieved in 353 sessions, (93%) standing was achieved in 261 sessions (69%), walking was achieved in 185 sessions (48%), and sitting in the bedside chair 118 times (31%).Patients with respiratory failure completed therapy sessions while receiving mechanical ventilation (21% of sessions), high flow nasal cannula (45% of sessions), non-invasive positive pressure ventilation by helmet and facemask (7% of sessions), and ECMO (12% of sessions). Patients requiring vasoactive medications (4%) and continuous renal replacement therapy (6%) were also treated by physical and occupational therapy. Delirium, determined by confusion assessment method (CAM-ICU), was frequently encountered by the physical and occupational therapy teams and was not an absolute barrier (32%) (Table 1). Discharge destinations included: home (n=57, 61%), acute rehabilitation units (n=16, 17%), long term acute care hospitals (n=9, 10%), sub-acute care centers (n=8, 8%), and skilled nursing facilities (n=4, 4%). No members of the therapy team were diagnosed with SARS-CoV-2 during the study period. Conclusions:This report demonstrates the feasibility of conducting physical and occupational therapy in COVID-19 specific ICUs. Providing therapy services appeared to be safe for patients and members of the therapy team, as adverse events were rare and no therapist was diagnosed with COVID-19.

Rationale:Patients with COVID-19 frequently develop severe respiratory disease and may require invasive mechanical ventilation. A study of primarily white patients intubated for COVID-19 associated respiratory failure found predictors of 28-day mortality to be respiratory system compliance, age, tidal volume, arterial pH and heart rate. Little is known about the outcomes of minority populations with severe COVID-19 pneumonia. Therefore, we present an analysis of the predictors of mortality in a group of primarily African American patients with COVID-19 associated respiratory failure. Methods:All adult patients admitted to the University of Chicago COVID-19 intensive care unit receiving invasive mechanical ventilation between March 1st and June 31st, 2020 were identified. Patients were included in the study if they had at least one recorded measure of plateau airway pressure while receiving volume-controlled ventilation allowing determination of driving pressure and lung compliance. Univariable analysis was conducted comparing survivors with those who died in-hospital followed by construction of a multivariable logistic regression model predicting in-hospital mortality based on significant factors from univariable analysis, excluding colinear variables. Results:Eighty-five patients were included in this retrospective study. Patients were primarily African American (n=73, 86%). Among all study patients, median tidal volume was 6.0 cc/kg ideal body weight (IQR 5.8-6.2), PEEP was 8 cm H2O (IQR 5.0-10), and driving pressure was 14 cm H2O (IQR 11-16). Median respiratory system compliance was 27 ml/cm H2O (IQR 21-34). Salvage therapies for refractory hypoxemia in the cohort included prone positioning (27%), paralysis (27%), inhaled pulmonary vasodilators (19%), and extracorporeal membrane oxygenation (1%). In the multivariable logistic regression model, age (OR 1.077, 95% CI 1.031 to 1.125, p=0.001) and driving pressure (OR 1.174, 95% CI 1.009 to 1.366, p=0.038) were found to be independent predictors of mortality. Conclusions:In a predominantly African American patient population with COVID-19 pneumonia requiring invasive mechanical ventilation, higher driving pressure was predictive of overall mortality. These finding are consistent with the work of Botta et al (2020), who demonstrated reduced lung compliance was predictive of mortality among a largely white group of patients with severe COVID-19 pneumonia. While minority populations infected with COVID-19 have been found worse outcomes, early lung mechanics appear to be comparable to white patients. These findings support that higher driving pressures and low lung compliance are indicative of serious lung injury which may lead to death.

Background Reduced body weight at the time of intensive care unit (ICU) admission is associated with worse survival, and a paradoxical benefit of obesity has been suggested in critical illness. However, no research has addressed the survival effects of disaggregated body constituents of dry weight such as skeletal muscle, fat, and bone density. Methods Single-center, prospective observational cohort study of medical ICU (MICU) patients from an academic institution in the USA. Five hundred and seven patients requiring CT scanning of chest or abdomen within the first 24 h of ICU admission were evaluated with erector spinae muscle (ESM) and subcutaneous adipose tissue (SAT) areas and with bone density determinations at the time of ICU admission, which were correlated with clinical outcomes accounting for potential confounders. Results Larger admission ESM area was associated with decreased odds of 6-month mortality (OR per cm2, 0.96; 95% CI, 0.94–0.97; p 2, 0.98; 95% CI, 0.96–0.99; p = 0.012). Higher bone density was similarly associated with lower odds of mortality (OR per 100 HU, 0.69; 95% CI, 0.49–0.96; p = 0.027) and disability at discharge (OR per 100 HU, 0.52; 95% CI, 0.37–0.74; p Conclusion In our cohort, ICU admission skeletal muscle mass measured with ESM area and bone density were associated with survival and disability at discharge, although muscle area was the only component that remained significantly associated with survival after multivariable adjustments. SAT had no association with the analyzed outcome measures.

Background Lidocaine is used to alleviate procedural pain but paradoxically increases pain during injection. Pain perception can be modulated by non-noxious stimuli such as temperature or touch according to the gate control theory of pain. We postulated that lidocaine dripped onto the skin prior to injection would cool or add the sensation of touch at the skin surface to reduce pain perception from the procedure. Methods A randomized clinical trial of patients referred to the procedure service from February 2011 through March 2015 was conducted. All patients received 1% subcutaneous lidocaine injection. Patients randomized to the intervention group had approximately 1 to 2 ml of lidocaine squirted onto the skin surface prior to subcutaneous lidocaine injection. Patients were blinded to the details of the intervention and were surveyed by a blinded investigator to document the primary outcome (severity of pain from the procedure) using a visual analog scale. Results A total of 481 patients provided consent and were randomized to treatment. There was a significant improvement in the primary outcome of procedural pain (control, 16.6 ± 24.8 mm vs 12.2 ± 19.4 mm; P = .03) with the intervention group as assessed by using the visual analog scale score. Pain scores were primarily improved for peripherally inserted central catheters (control, 18.8 ± 25.6 mm vs 12.2 ± 18.2 mm; P = .02) upon subgroup analysis. Conclusions Bedside procedures are exceedingly common. Data regarding the severity of procedural pain and strategies to mitigate it are important for the informed consent process and patient satisfaction. Overall, pain reported from common bedside procedures is low, but pain can be further reduced with the addition of lidocaine onto the skin surface to modulate pain perception. Trial Registry ClinicalTrials.gov; No.: NCT01330134; URL: www.clinicaltrials.gov.

Objectives Many survivors of acute respiratory distress syndrome have poor long-term outcomes possibly due to supportive care practices during "invasive" mechanical ventilation. Helmet noninvasive ventilation in acute respiratory distress syndrome may reduce intubation rates; however, it is unknown if avoiding intubation with helmet noninvasive ventilation alters the consequences of surviving acute respiratory distress syndrome. Design Long-term follow-up data from a previously published randomized controlled trial. Patients Adults patients with acute respiratory distress syndrome enrolled in a previously published clinical trial. Setting Adult ICU. Intervention None. Measurements and main results The primary outcome was functional independence at 1 year after hospital discharge defined as independence in activities of daily living and ambulation. At 1 year, patients were surveyed to assess for functional independence, survival, and number of institution-free days, defined as days alive spent living at home. The presence of ICU-acquired weakness and functional independence was also assessed by a blinded therapist on hospital discharge. On hospital discharge, there was a greater prevalence of ICU-acquired weakness (79.5% vs 38.6%; p = 0.0002) and less functional independence (15.4% vs 50%; p = 0.001) in the facemask group. One-year follow-up data were collected for 81 of 83 patients (97.6%). One-year mortality was higher in the facemask group (69.2% vs 43.2%; p = 0.017). At 1 year, patients in the helmet group were more likely to be functionally independent (40.9% vs 15.4%; p = 0.015) and had more institution-free days (median, 268.5 [0-354] vs 0 [0-323]; p = 0.017). Conclusions Poor functional recovery after invasive mechanical ventilation for acute respiratory distress syndrome is common. Helmet noninvasive ventilation may be the first intervention that mitigates the long-term complications that plague survivors of acute respiratory distress syndrome managed with noninvasive ventilation.

We present areas of uncertainty concerning intensive care unit-acquired weakness (ICUAW) and identify areas for future research. Age, pre-ICU functional and cognitive state, concurrent illness, frailty, and health trajectories impact outcomes and should be assessed to stratify patients. In the ICU, early assessment of limb and diaphragm muscle strength and function using nonvolitional tests may be useful, but comparison with established methods of global and specific muscle strength and physical function and determination of their reliability and normal values would be important to advance these techniques. Serial measurements of limb and respiratory muscle strength, and systematic screening for dysphagia, would be helpful to clarify if and how weakness of these muscle groups is independently associated with outcome. ICUAW, delirium, and sedatives and analgesics may interact with each other, amplifying the effects of each individual factor. Reduced mobility in patients with hypoactive delirium needs investigations into dysfunction of central and peripheral nervous system motor pathways. Interventional nutritional studies should include muscle mass, strength, and physical function as outcomes, and prioritize elucidation of mechanisms. At follow-up, ICU survivors may suffer from prolonged muscle weakness and wasting and other physical impairments, as well as fatigue without demonstrable weakness on examination. Further studies should evaluate the prevalence and severity of fatigue in ICU survivors and define its association with psychiatric disorders, pain, cognitive impairment, and axonal loss. Finally, methodological issues, including accounting for baseline status, handling of missing data, and inclusion of patient-centered outcome measures should be addressed in future studies.

The international pandemic of coronavirus disease 2019 (Covid-19) has caused unprecedented strain on healthcare systems worldwide and threatens to deplete the available supply of mechanical ventilators. In addition to ventilator allocation protocols, a potential way of addressing this problem is ventilator sharing, also termed split- or co-ventilation, a concept that has gained recent attention in anticipation of dire equipment shortages. Co-ventilation was initially proposed by Neyman and Irvin in 2006 as a method of increasing surge capacity needs during disasters resulting in mass casualty respiratory failure. They demonstrated the technical feasibility of using one ventilator on four mechanical lungs, and proposed use as a last resort only after depletion of ventilators and staff available for manual ventilation to temporarily bridge to the arrival of disaster relief.1 Similar circuits have since been used in both sheep models and more sophisticated mechanical lung models.2 3 Tonetti and colleagues describe a simple circuit which can be used to ventilate two patients with one ventilator and report on its use in mechanical lung models of differing compliance and resistance.4 While this report again demonstrates the technical feasibility of ventilating multiple patients with a single ventilator, there are many areas of caution to consider before widespread implementation of this technique in the current pandemic. Tonetti and colleagues, as well as the protocol recently published by New York Presbyterian Hospital, have attempted to address many of the technical challenges of co-ventilation, although many still remain.4 5 Front and centre among these problems is the inability to titrate mechanical ventilation to the individual patient physiology. Close matching of ventilatory settings—such as minute ventilation, positive end-expiratory pressure and fraction of inspired oxygen—to patient characteristics such as pulmonary mechanics (static compliance, resistance); oxygen consumption and carbon dioxide production; acid-base balance; and haemodynamics—is necessary to optimise …

Immunocompromised patients are at high risk for developing severe sepsis. Currently, there are no validated strategies for identifying this group of patients in large administrative databases.We set out to define and validate a method that could be used to identify immunocompromised patients with severe sepsis in administrative databases.Patients were categorized as immunocompromised based on the presence of International Classification of Diseases, 9th revision discharge diagnosis codes and medication data. We validated this strategy by comparing the discriminatory ability of the search algorithm to that of manual chart review.We identified 4,438 patients at a single academic center with severe sepsis using a definition applied to administrative data described by Angus and colleagues. There were 1,185 (26.7%) who were categorized as immunocompromised based on our novel administrative data search strategy. Compared with identification by medical record review, the new administrative data search strategy had positive and negative predictive values of 94.4% (95% confidence interval [CI], 88.8-97.7%) and 94.3% (95% CI, 91.0-96.6%). The sensitivity and specificity were 87.4% (95% CI, 80.6-92.5%) and 97.6% (95% CI, 95.0-99.9%).Patients who are immunosuppressed are a large subgroup of those with severe sepsis. Following its validation as a search strategy using other large databases, and its adaptation for International Classification of Diseases, 10th revision, this novel method may allow researchers to account for a patient's immune state when examining outcomes.

Immunosuppressive medical conditions are risk factors for mortality from severe infections. It is unknown whether hospital characteristics affect this risk.To determine whether the odds of death for an immunosuppressed patient with sepsis relative to a nonimmunosuppressed patient with sepsis varies according to the hospital's yearly case volume of immunosuppressed patients with sepsis.Patients with sepsis at hospitals in the Vizient database were characterized as immunosuppressed or not immunosuppressed on the basis of diagnosis codes and medication use. Hospitals were grouped into quartiles based on their average volumes of immunosuppressed patients with sepsis per year. Multilevel logistic regression with clustering of patients by hospital was used to determine whether the odds of in-hospital death from sepsis owing to a suppressed immune state varied by hospital quartile.There were 350,183 patients with sepsis at 60 hospitals in the Vizient database from 2010 to 2012. Immunosuppressed patients with sepsis at the 15 hospitals in the lowest quartile (64 to 224 immunosuppressed patients with sepsis per year) had an increased odds of in-hospital death relative to nonimmunosuppressed patients with sepsis at these hospitals (adjusted odds ratio, 1.38; 95% confidence interval, 1.27-1.50; P 0.001). The odds of in-hospital death for immunosuppressed patients with sepsis relative to nonimmunosuppressed patients with sepsis was similar for patients at hospitals in the second, third, and fourth quartiles (225 to 1,056 immunosuppressed patients with sepsis per year). The adjusted odds of death from sepsis owing to a suppressed immune state of 1.21 (95% confidence interval, 1.18-1.25; P 0.001) for patients at these 45 hospitals was significantly less than for patients at the 15 hospitals in the lowest quartile (P = 0.004 for difference).The risk of death from sepsis owing to a suppressed immune state was greatest at hospitals with the lowest volume of immunosuppressed patients with sepsis. Further study is needed to determine whether this finding is related to differences in patient characteristics or in care delivery at hospitals with different amounts of exposure to immunosuppressed patients.

Background The dysregulated host immune response that defines sepsis varies as a function of both the immune status of the host and the distinct nature of the pathogen. The degree to which immunocompromising comorbidities or immunosuppressive medications affect the immune response to infection is poorly understood because these patients are often excluded from studies about septic immunity. The objectives of this study were to determine the immune response to a single pathogen (Staphylococcus aureus) among a diverse case mix of patients and to determine whether comorbidities affect immune and clinical outcomes. Methods Blood samples were drawn from 95 adult inpatients at multiple time points after the first positive S. aureus blood culture. Cox proportional hazards modeling was used to determine the associations between admission neutrophil counts, admission lymphocyte counts, cytokine levels, and 90-day mortality. A nested case-control flow cytometric analysis was conducted to determine T-helper type 1 (Th1), Th2, Th17, and regulatory T-cell (Treg) subsets among a subgroup of 28 patients. In a secondary analysis, we categorized patients as either having immunocompromising disorders (human immunodeficiency virus and hematologic malignancies), receiving immunosuppressive medications, or being not immunocompromised. Results Higher neutrophil-to-lymphocyte count ratios and higher Th17 cytokine responses relative to Th1 cytokine responses early after infection were independently associated with mortality and did not depend on the immune state of the patient (HR 1.93, 95% CI 1.17–3.17, p = 0.01; and HR 1.13, 95% CI 1.01–1.27, p = 0.03, respectively). On the basis of flow cytometric analysis of CD4 T-helper subsets, an increasing Th17/Treg response over the course of the infection was most strongly associated with increased mortality (HR 4.41, 95% CI 1.69–11.5, p

Background Vasoactive medications are commonly used in the treatment of critically ill patients, but their impact on the development of ICU-acquired weakness is not well described. The objective of this study is to evaluate the relationship between vasoactive medication use and the outcome of ICU-acquired weakness. Methods This is a secondary analysis of mechanically ventilated patients (N = 172) enrolled in a randomized clinical trial of early occupational and physical therapy vs conventional therapy, which evaluated the end point of ICU-acquired weakness on hospital discharge. Patients underwent bedside muscle strength testing by a therapist blinded to study allocation to evaluate for ICU-acquired weakness. The effects of vasoactive medication use on the incidence of ICU-acquired weakness in this population were assessed. Results On logistic regression analysis, the use of vasoactive medications increased the odds of developing ICU-acquired weakness (odds ratio [OR], 3.2; P = .01) independent of all other established risk factors for weakness. Duration of vasoactive medication use (in days) (OR, 1.35; P = .004) and cumulative norepinephrine dose (μg/kg/d) (OR, 1.01; P = .02) (but not vasopressin or phenylephrine) were also independently associated with the outcome of ICU-acquired weakness. Conclusions In mechanically ventilated patients enrolled in a randomized clinical trial of early mobilization, the use of vasoactive medications was independently associated with the development of ICU-acquired weakness. Prospective trials to further evaluate this relationship are merited. Trial Registry ClinicalTrials.gov; No.: NCT01777035; URL: www.clinicaltrials.gov

Vital signs and composite scores, such as the Modified Early Warning Score, are used to identify high-risk ward patients and trigger rapid response teams. Although age-related vital sign changes are known to occur, little is known about the differences in vital signs between elderly and nonelderly patients prior to ward cardiac arrest. We aimed to compare the accuracy of vital signs for detecting cardiac arrest between elderly and nonelderly patients.Observational cohort study.Five hospitals in the United States.A total of 269,956 patient admissions to the wards with documented age, including 422 index ward cardiac arrests.None.Patient characteristics and vital signs prior to cardiac arrest were compared between elderly (age, 65 yr or older) and nonelderly (age,65 yr) patients. The area under the receiver operating characteristic curve for vital signs and the Modified Early Warning Score were also compared. Elderly patients had a higher cardiac arrest rate (2.2 vs 1.0 per 1,000 ward admissions; p0.001) and in-hospital mortality (2.9% vs 0.7%; p0.001) than nonelderly patients. Within 4 hours of cardiac arrest, elderly patients had significantly lower mean heart rate (88 vs 99 beats/min; p0.001), diastolic blood pressure (60 vs 66 mm Hg; p=0.007), shock index (0.82 vs 0.93; p0.001), and Modified Early Warning Score (2.6 vs 3.3; p0.001) and higher pulse pressure index (0.45 vs 0.41; p0.001) and temperature (36.4°C vs 36.3°C; p=0.047). The area under the receiver operating characteristic curves for all vital signs and the Modified Early Warning Score were higher for nonelderly patients than elderly patients (Modified Early Warning Score area under the receiver operating characteristic curve 0.85 [95% CI, 0.82-0.88] vs 0.71 [95% CI, 0.68-0.75]; p0.001).Vital signs more accurately detect cardiac arrest in nonelderly patients compared with elderly patients, which has important implications for how they are used for identifying critically ill patients. More accurate methods for risk stratification of elderly patients are necessary to decrease the occurrence of this devastating event.

In this review, we seek to highlight how critical illness and critical care affect longer-term outcomes, to underline the contribution of ICU delirium to cognitive dysfunction several months after ICU discharge, to give new insights into ICU acquired weakness, to emphasize the importance of value-based healthcare, and to delineate the elements of family-centered care. This consensus of 29 also provides a perspective and a research agenda about post-ICU recovery., SCOPUS: re.j, info:eu-repo/semantics/published

We tested the power of clinicians' predictions that a medical ICU patient would "die before hospital discharge" for both survival to discharge and for outcomes at 6 months.We restricted our analyses to patients who had been in the medical ICU at least 72 hours and for whom we had follow-up at 6 months after medical ICU admission. For 350 medical ICU patients, on each medical ICU day, we asked their attending physician, fellow, resident, and primary nurse one question-"do you think this patient will die in hospital or survive to be discharged"? We correlated these responses with 6-month outcomes (death and/or Barthel score for survivors).We obtained over 6,000 predictions on 2,271 medical ICU patient-days. Of 350 medical ICU patients who stayed more than 72 hours, 143 patients (41%) had discordant predictions-that is, on the same medical ICU day, at least one provider predicted survival, whereas another predicted death before discharge. As we have shown previously, predictions of "death before discharge" were imperfect-only 104 of 187 of patients with a prediction of death (56%) actually died in hospital. However, this is the central finding of our study, and predictions of death before discharge were much more accurate for 6-month outcomes. Of 120 patients with a corroborated prediction of death before discharge (93%), 112 patients had died within 6 months of medical ICU discharge, and only 4% were functioning with a Barthel score more than 70. In contrast, 67 of 163 patients who did not have any prediction of death before discharge (41%) were alive with Barthel score more than 70 at 6 months.Fewer than 4% of medical ICU patients who required 72 hours of medical ICU care and had a corroborated prediction of death before discharge were alive at 6 months and functioning with a Barthel score more than 70.

Background ICU-acquired weakness (ICU-AW) has immediate and long-term consequences for critically ill patients. Strategies for the prevention of weakness include modification of known risk factors, such as hyperglycemia and immobility. Intensive insulin therapy (IIT) has been proposed to prevent critical illness polyneuropathy. However, the effect of insulin and early mobilization on clinically apparent weakness is not well known. Methods This is a secondary analysis of all patients with mechanical ventilation (N = 104) previously enrolled in a randomized controlled trial of early occupational and physical therapy vs conventional therapy, which evaluated the end point of functional independence. Every patient had IIT and blinded muscle strength testing on hospital discharge to determine the incidence of clinically apparent weakness. The effects of insulin dose and early mobilization on the incidence of ICU-AW were assessed. Results On logistic regression analyses, early mobilization and increasing insulin dose prevented the incidence of ICU-AW (OR, 0.18, P = .001; OR, 0.001, P = .011; respectively) independent of known risk factors for weakness. Early mobilization also significantly reduced insulin requirements to achieve similar glycemic goals as compared with control patients (0.07 units/kg/d vs 0.2 units/kg/d, P Conclusions The duel effect of early mobilization in reducing clinically relevant ICU-AW and promoting euglycemia suggests its potential usefulness as an alternative to IIT.

Many patients who are evaluated and treated for sepsis have histories of recent infections. The prognostic implications of surviving an infectious process are not well understood. We undertook this study to determine the clinical impact of prior infections among patients with hematological malignancies, a population at high risk for developing and dying from sepsis. The medical records of 203 patients with hematological malignancies and blood-stream infections admitted over a 3-year period to an urban teaching hospital were retrospectively reviewed. The 30-day mortality after blood-stream infection in these high-risk patients was 24 %. There were 46 patients (23 %) who had inpatient infections in the 90 days prior to the index blood-stream infection. History of recent infection portended worse prognosis from blood-stream infection under multivariable analysis [odds ratio (OR) 2.60, p = 0.04, 95 % confidence interval (CI) 1.04-6.47]. There were 86 patients (42 %) who had subsequent infections in the first 90 days after the index blood-stream infection. Patients with subsequent infections had greater mortality during days 91-365 than patients without subsequent infections [hazard ratio (HR) 1.97, p = 0.02, 95 % CI 1.13-3.44]. Recent infections prognosticate worse outcomes from subsequent blood-stream infections for this high-risk population. Further research into the clinical and biochemical reasons for this observation may lead to targets for intervention, and, ultimately, improvements in long-term mortality from sepsis.

Stays in intensive care units are commonly accompanied by muscle weakness. This article reviews the basis for these changes and provides guidance on how to prevent, diagnose, and treat this condition.

Rationale: Intensive care unit (ICU) delirium is associated with ventilator, ICU, and hospital days; discharge functional status; and mortality. Whether rapidly reversible, sedation-related delirium (delirium that abates shortly after sedative interruption) occurs with the same frequency and portends the same prognosis as persistent delirium (delirium that persists despite a short period of sedative interruption) is unknown.Objectives: To compare rapidly reversible, sedation-related delirium and persistent delirium.Methods: This was a prospective cohort study of 102 adult, intubated medical ICU subjects in a tertiary care teaching hospital. Confusion Assessment Method for the ICU evaluation was performed before and after daily interruption of continuous sedation (DIS). Investigators were blinded to each other’s assessments and as to whether evaluations were before or after DIS. The primary outcome was proportion of days with no delirium versus rapidly reversible, sedation-related delirium versus persisten...

OBJECTIVES Sleep is regulated by circadian and homeostatic processes and is highly organized temporally. Our study was designed to determine whether this organization is preserved in patients receiving mechanical ventilation (MV) and intravenous sedation. DESIGN Observational study. SETTING Academic medical intensive care unit. PATIENTS Critically ill patients receiving MV and intravenous sedation. METHODS Continuous polysomnography (PSG) was initiated an average of 2.0 (1.0, 3.0) days after ICU admission and continued ≥ 36 h or until the patient was extubated. Sleep staging and power spectral analysis were performed using standard approaches. We also calculated the electroencephalography spectral edge frequency 95% SEF₉₅, a parameter that is normally higher during wakefulness than during sleep. Circadian rhythmicity was assessed in 16 subjects through the measurement of aMT6s in urine samples collected hourly for 24-48 hours. Light intensity at the head of the bed was measured continuously. MEASUREMENTS AND RESULTS We analyzed 819.7 h of PSG recordings from 21 subjects. REM sleep was identified in only 2/21 subjects. Slow wave activity lacked the normal diurnal and ultradian periodicity and homeostatic decline found in healthy adults. In nearly all patients, SEF₉₅ was consistently low without evidence of diurnal rhythmicity (median 6.3 [5.3, 7.8] Hz, n = 18). A circadian rhythm of aMT6s excretion was present in most (13/16, 81.3%) patients, but only 4 subjects had normal timing. Comparison of the SEF₉₅ during the melatonin-based biological night and day revealed no difference between the 2 periods (P = 0.64). CONCLUSIONS The circadian rhythms and PSG of patients receiving mechanical ventilation and intravenous sedation exhibit pronounced temporal disorganization. The finding that most subjects exhibited preserved, but phase delayed, excretion of aMT6s suggests that the circadian pacemaker of such patients may be free-running.

Background Pneumonia is the leading infectious cause of death. Early deterioration and death commonly result from progressive sepsis, shock, respiratory failure, and cardiac complications. Recent data suggest that cardiac arrest may also be common, yet few previous studies have addressed this. Accordingly, we sought to characterize early cardiac arrest in patients who are hospitalized with coexisting pneumonia. Methods We performed a retrospective analysis of a multicenter cardiac arrest database, with data from > 500 North American hospitals. We included in-hospital cardiac arrest events that occurred in community-dwelling adults with pneumonia within the first 72 h after hospital admission. We compared patient and event characteristics for patients with and without pneumonia. For patients with pneumonia, we also compared events according to event location. Results We identified 4,453 episodes of early cardiac arrest in patients who were hospitalized with pneumonia. Among patients with preexisting pneumonia, only 36.5% were receiving mechanical ventilation and only 33.3% were receiving infusions of vasoactive drugs prior to cardiac arrest. Only 52.3% of patients on the ward were receiving ECG monitoring prior to cardiac arrest. Shockable rhythms were uncommon in all patients with pneumonia (ventricular tachycardia or fibrillation, 14.8%). Patients on the ward were significantly older than patients in the ICU. Conclusions In patients with preexisting pneumonia, cardiac arrest may occur in the absence of preceding shock or respiratory failure. Physicians should be alert to the possibility of abrupt cardiopulmonary collapse, and future studies should address this possibility. The mechanism may involve myocardial ischemia, a maladaptive response to hypoxia, sepsis-related cardiomyopathy, or other phenomena.

Background Current rapid response team activation criteria were not statistically derived using ward vital signs, and the best vital sign predictors of cardiac arrest (CA) have not been determined. In addition, it is unknown when vital signs begin to accurately detect this event prior to CA. Methods We conducted a nested case-control study of 88 patients experiencing CA on the wards of a university hospital between November 2008 and January 2011, matched 1:4 to 352 control subjects residing on the same ward at the same time as the case CA. Vital signs and Modified Early Warning Scores (MEWS) were compared on admission and during the 48 h preceding CA. Results Case patients were older (64 ± 16 years vs 58 ± 18 years; P = .002) and more likely to have had a prior ICU admission than control subjects (41% vs 24%; P = .001), but had similar admission MEWS (2.2 ± 1.3 vs 2.0 ± 1.3; P = .28). In the 48 h preceding CA, maximum MEWS was the best predictor (area under the receiver operating characteristic curve [AUC] 0.77; 95% CI, 0.71-0.82), followed by maximum respiratory rate (AUC 0.72; 95% CI, 0.65-0.78), maximum heart rate (AUC 0.68; 95% CI, 0.61-0.74), maximum pulse pressure index (AUC 0.61; 95% CI, 0.54-0.68), and minimum diastolic BP (AUC 0.60; 95% CI, 0.53-0.67). By 48 h prior to CA, the MEWS was higher in cases (P = .005), with increasing disparity leading up to the event. Conclusions The MEWS was significantly different between patients experiencing CA and control patients by 48 h prior to the event, but includes poor predictors of CA such as temperature and omits significant predictors such as diastolic BP and pulse pressure index.

Very good clinicians often use a form of self-doubt to avoid the dangers of overconfidence in the diagnosis and management of disease. Asking the questions ‘‘What does not fit with this patient’s clinical course?’’ and ‘‘What am I missing?’’—especially when things seem obvious or fully explained—is a useful tool for a physician. Perhaps even more important is to ask ‘‘What did I do wrong and how can I make sure it won’t happen again?’’ The benefits of doing so are many: it helps dispel the myth of infallibility; it is a useful teaching tool; and it helps the past inform the future, hopefully to the benefit of our patients. In this commentary, we attempt to address the question ‘‘What ten big mistakes have we made in the field of intensive care medicine?’’ There is no question that our choices are subjective, and therefore somewhat arbitrary. To address this shortcoming, we encourage readers to extend our list.

Speaking for the remarkable number of mentees of Lawrence D. H. Wood, MD, PhD, who are productive and creative contributors to the fi eld of critical care medicine, of which Dr Wood is a primary founder, I feel both delighted and humbled to off er some thoughts about this extraordinary man. Many others could and should add their own refl ections on knowledge and inspiration received from him, and I acknowledge this as but a single step in that process. I believe that all of us regard Dr Wood as a leader in applying rigorous science to test hypotheses or answer questions arising at the bedside of critically ill patients.

Critical care medicine has matured greatly as a field in the past decade. Much has been learned concerning the institution of life support therapies to sustain patients with diverse and multiple organ failures, thus providing patients with a window of opportunity to recover from potentially life-ending insults. The management of critically ill patients has increasingly involved creation of a highly controlled environment by care providers, with patients immobilized, tethered to devices, and receiving multiple drugs to facilitate the entire process. Although it has been assumed that such control of the patient has been necessary to implement essential therapies and to tailor life support systems such as mechanical ventilation, this assumption may be unfounded or at least overplayed, as knowledge of the adverse effects of this approach have been identified and quantified. Extant information, based on observational studies and a few interventional trials, would suggest a radically different approach to care is warranted, even given the difficulties in reversing the current culture of critical care management. Specifically, methods to avoid entirely, or minimize, neuromuscular blockade and sedation are supported by recent literature. These methods include the use of noninvasive ventilation in appropriately selected patients, the development of mechanical ventilators more synchronous with patient efforts and needs, and the use of sedation strategies to avoid drug accumulations with protracted effects. These methods, in turn, afford opportunities to avoid extreme immobilization and institute physiotherapy earlier than previously had been thought possible. In addition to the neuropsychiatric and neuromuscular benefits that could derive from minimizing opiate administration in critically ill patients, gut hypomotility could be avoided. This, in turn, could facilitate earlier and more complete enteral nutrition. Even when opioids have to be administered in generous amounts for control of pain that may accompany critical illness, it is now possible to block the peripheral actions of these medications with the μ-receptor antagonist methylnaltrexone. Other new drugs being introduced into the critical care unit such as dexmedetomidine may also provide a greater ability to achieve analgesia and anxiolysis without some of the adverse concomitant effects seen with more traditional drug regimens. The ultimate goal of this multipronged program to facilitate the maintenance of patients who are more interactive with their care providers, and the life support provided in the intensive care unit would be to speed the pace of recovery and to diminish the need for the protracted rehabilitation that often follows survival from critical illness.

Severe weakness is being recognized as a complication that impacts significantly on the pace and degree of recovery and return to former functional status of patients who survive the organ failures that mandate life-support therapies such as mechanical ventilation. Despite the apparent importance of this problem, much remains to be understood about its incidence, causes, prevention, and treatment.Review from literature and an expert round-table.The Brussels Round Table Conference in 2009 convened more than 20 experts in the fields of intensive care, neurology, and muscle physiology to review current understandings of intensive care unit-acquired weakness and to improve clinical outcome.Formal electrophysiological evaluation of patients with intensive care unit-acquired weakness can identify peripheral neuropathies, myopathies, and combinations of these disorders, although the correlation of these findings to weakness measurable at the bedside is not always precise. For routine clinical purposes, bedside assessment of neuromuscular function can be performed but is often confounded by complicating factors such as sedative and analgesic administration. Risk factors for development of intensive care unit-acquired weakness include bed rest itself, sepsis, and corticosteroid exposure. A strong association exists between weakness and long-term ventilator dependence; weakness is a major determinant of patient outcomes after surviving acute respiratory failure and may be present for months, or indefinitely, in the convalescence phase of critical illness.Although much has been learned about the physiology and cell and molecular biology of skeletal and diaphragm dysfunction under conditions of aging, exercise, disuse, and sepsis, the application of these understandings to the bedside requires more study in both bench models and patients. Although a trend toward greater immobilization and sedation of patients has characterized the past several decades of intensive care unit care, recent studies have demonstrated that early physical and occupational therapy, including during the period of intubation and ventilator support, can be safely performed and will likely improve patient outcomes with regard to functional status.

Regulatory agencies evaluate hospitals' care of patients with sepsis according to their completion of the SEP-1 performance measure. Pepper and colleagues found that evidence is lacking to support ...