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OBJECTIVE: To revise the "Clinical Practice Guidelines for the Sustained Use of Sedatives and Analgesics in the Critically Ill Adult" published in Critical Care Medicine in 2002. METHODS: The American College of Critical Care Medicine assembled a 20-person, multidisciplinary, multi-institutional task force with expertise in guideline development, pain, agitation and sedation, delirium management, and associated outcomes in adult critically ill patients. The task force, divided into four subcommittees, collaborated over 6 yr in person, via teleconferences, and via electronic communication. Subcommittees were responsible for developing relevant clinical questions, using the Grading of Recommendations Assessment, Development and Evaluation method (http://www.gradeworkinggroup.org) to review, evaluate, and summarize the literature, and to develop clinical statements (descriptive) and recommendations (actionable). With the help of a professional librarian and Refworks database software, they developed a Web-based electronic database of over 19,000 references extracted from eight clinical search engines, related to pain and analgesia, agitation and sedation, delirium, and related clinical outcomes in adult ICU patients. The group also used psychometric analyses to evaluate and compare pain, agitation/sedation, and delirium assessment tools. All task force members were allowed to review the literature supporting each statement and recommendation and provided feedback to the subcommittees. Group consensus was achieved for all statements and recommendations using the nominal group technique and the modified Delphi method, with anonymous voting by all task force members using E-Survey (http://www.esurvey.com). All voting was completed in December 2010. Relevant studies published after this date and prior to publication of these guidelines were referenced in the text. The quality of evidence for each statement and recommendation was ranked as high (A), moderate (B), or low/very low (C). The strength of recommendations was ranked as strong (1) or weak (2), and either in favor of (+) or against (-) an intervention. A strong recommendation (either for or against) indicated that the intervention's desirable effects either clearly outweighed its undesirable effects (risks, burdens, and costs) or it did not. For all strong recommendations, the phrase "We recommend …" is used throughout. A weak recommendation, either for or against an intervention, indicated that the trade-off between desirable and undesirable effects was less clear. For all weak recommendations, the phrase "We suggest …" is used throughout. In the absence of sufficient evidence, or when group consensus could not be achieved, no recommendation (0) was made. Consensus based on expert opinion was not used as a substitute for a lack of evidence. A consistent method for addressing potential conflict of interest was followed if task force members were coauthors of related research. The development of this guideline was independent of any industry funding. CONCLUSION: These guidelines provide a roadmap for developing integrated, evidence-based, and patient-centered protocols for preventing and treating pain, agitation, and delirium in critically ill patients.

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BACKGROUND: Delirium (acute brain dysfunction) is a potentially life threatening disturbance in brain function that frequently occurs in critically ill patients. While this area of brain dysfunction in critical care is rapidly advancing, striking limitations in use of terminology related to delirium internationally are hindering cross-talk and collaborative research. In the English literature, synonyms of delirium such as the Intensive Care Unit syndrome, acute brain dysfunction, acute brain failure, psychosis, confusion, and encephalopathy are widely used. This often leads to scientific "confusion" regarding published data and methodology within studies, which is further exacerbated by organizational, cultural and language barriers. OBJECTIVE: We undertook this multinational effort to identify conflicts in terminology and phenomenology of delirium to facilitate communication across medical disciplines and languages. METHODS: The evaluation of the terminology used for acute brain dysfunction was determined conducting communications with 24 authors from academic communities throughout countries/regions that speak the 13 variants of the Romanic languages included into this manuscript. RESULTS: In the 13 languages utilizing Romanic characters, included in this report, we identified the following terms used to define major types of acute brain dysfunction: coma, delirium, delirio, delirium tremens, délire, confusion mentale, delir, delier, Durchgangs-Syndrom, acute verwardheid, intensiv-psykose, IVA-psykos, IVA-syndrom, akutt konfusion/forvirring. Interestingly two terms are very consistent: 100 % of the selected languages use the term coma or koma to describe patients unresponsive to verbal and/or physical stimuli, and 100% use delirium tremens to define delirium due to alcohol withdrawal. Conversely, only 54% use the term delirium to indicate the disorder as defined by the DSM-IV as an acute change in mental status, inattention, disorganized thinking and altered level of consciousness. CONCLUSIONS: Attempts towards standardization in terminology, or at least awareness of differences across languages and specialties, will help cross-talk among clinicians and researchers.

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PURPOSE: To describe a minimally invasive alternative to conventional mechanical ventilation, using a small size uncuffed nasotracheal tube (translaryngeal open ventilation) paired with pressure control ventilation, in acute respiratory failure complicating chronic obstructive pulmonary disease (COPD). CLINICAL FEATURES: Two cooperative COPD patients, who failed noninvasive mechanical ventilation, were intubated nasotracheally. Mechanical ventilation was initiated in pressure control mode via an uncuffed 6 mm tube. RESULTS: Respiratory rate improved after 1 hour (from 44 to 28 breaths*min(-1) in case 1 and from 32 to 25 breaths*min(-1) in case 2); PaC0(2) decreased (from 120 to 62 mmHg in case 1 and from 69 to 51 mmHg in case 2); with pressure control mode levels of 45 cm H(2)O and 55 cm H(2)O respectively. PaO(2) increased from 40 mmHg (with FIO(2) 0.3) to 55 mmHg (with FIO(2) 0.3) in the first patient and from 55 mmHg (with FIO(2) 0.4) to 60 mmHg (with FIO(2) 0.4 ) in the second patient; pH improved from 7.18 to 7.31 in case 1 and from 7.22 to 7.39 in case 2. Patients were able to trigger the ventilator, speak, swallow and to clear secretions spontaneously. Both patients were ventilated for three days in this manner without any adverse effects. Both survived and were discharged home after 20 and 18 days in hospital respectively. CONCLUSION: This very preliminary report suggests that, in carefully selected patients who fail mask ventilation, mechanical support with translaryngeal open ventilation can improve gas exchange, breathing pattern and tachypnea, without hindering glottic function.

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We compared crural diaphragm electrical activity (EAdi) with transdiaphragmatic pressure (Pdi) during varying levels of pressure support ventilation (PS) in 13 intubated patients. With changing PS, we found no evidence for changes in neuromechanical coupling of the diaphragm. From lowest to highest PS (2 cm H(2)O +/- 4 to 20 cm H(2)O +/- 7), tidal volume increased from 430 ml +/- 180 to 527 ml +/- 180 (p < 0.001). The inspiratory volume calculated during the period when EAdi increased to its peak did not change from 276 +/- 147 to 277 +/- 162 ml, p = 0.976. Respiratory rate decreased from 23.9 (+/- 7) to 21.3 (+/- 7) breaths/min (p = 0.015). EAdi and Pdi decreased proportionally by adding PS (r = 0.84 and r = 0.90, for mean and peak values, respectively). Mean and peak EAdi decreased (p < 0.001) by 33 +/- 21% (mean +/- SD) and 37 +/- 23% with the addition of 10 cm H(2)O of PS, similar to the decrease in the mean and peak Pdi (p < 0.001) observed (34 +/- 36 and 35 +/- 23%). We also found that ventilator assist continued during the diaphragm deactivation period, a phenomenon that was further exaggerated at higher PS levels. We conclude that EAdi is a valid measurement of neural drive to the diaphragm in acute respiratory failure.

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OBJECTIVES: (1) To establish risk factors for the development of delirium in an intensive care unit (ICU) and (2) to determine the effect of delirium on morbidity, mortality and length of stay. DESIGN: Prospective study. SETTING: Sixteen-bed medical/surgical ICU in a university hospital. PATIENTS: Two hundred and sixteen consecutive patients admitted to the ICU for more than 24 h during 5 months were included in the study. INTERVENTIONS: Medical history, selected laboratory values, drugs received and factors that may influence patient psychological and emotional well-being were noted. All patients were screened with a delirium scale. A psychiatrist confirmed the diagnosis of delirium. Major complications such as self-extubation and removal of catheters, as well as mortality and length of stay were recorded. RESULTS: Forty patients (19%) developed delirium; of these, one-third were not agitated. In the multivariate analysis hypertension, smoking history, abnormal bilirubin level, epidural use and morphine were statistically significantly associated with delirium. Traditional factors associated with the development of delirium on general ward patients were not significant in our study. Morbidity (self-extubation and removal of catheters), but not mortality, was clearly increased. CONCLUSION: Predictive risk factors for the development of delirium in studies outside the ICU may not be applicable to critically ill patients. Delirium is associated with increased morbidity. Awareness of patients at risk may lead to better recognition and earlier intervention.

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OBJECTIVE: Delirium in the intensive care unit is poorly defined. Clinical evaluation is difficult in the setting of unstable, often intubated patients. A screening tool may improve the detection of delirium. METHOD: We created a screening checklist of eight items based on DSM criteria and features of delirium: altered level of consciousness, inattention, disorientation, hallucination or delusion, psychomotor agitation or retardation, inappropriate mood or speech, sleep/wake cycle disturbance, and symptom fluctuation. During 3 months, all patients admitted to a busy medical/surgical intensive care unit were evaluated, and the scale score was compared to a psychiatric evaluation. RESULTS: In 93 patients studied, 15 developed delirium. Fourteen (93%) of them had a score of 4 points or more. This score was also present in 15 (19%) of patients without delirium, 14 of whom had a known psychiatric illness, dementia, a structural neurological abnormality or encephalopathy. A ROC analysis was used to determine the sensitivity and specificity of the screening tool. The area under the ROC curve is 0.9017. Predicted sensitivity is 99% and specificity is 64%. CONCLUSION: This study suggests that the Intensive Care Delirium Screening Checklist can easily be applied by a clinician or a nurse in a busy critical care setting to screen all patients even when communication is compromised. The tool can be utilized quickly and helps to identify delirious patients. Earlier diagnosis may lead to earlier intervention and better patient care.

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BACKGROUND: The risk for venous thromboembolism (VTE) and the risk for bleeding among critically ill surgical patients are both important in the early postoperative period. MATERIALS AND METHODS: To record VTE prophylaxis prescribed for surgical patients in the intensive care unit (ICU) within the first postoperative week. We conducted a prospective observational cross-sectional study of Canadian university affiliated ICUs. RESULTS: Of 29 ICU Directors approached, 28 (96.6%) participated, representing 34 ICUs and 589 ICU beds across Canada. Among 89 patients, surgical procedures were 32 abdominal (36.0%), 19 vascular (21.3%), 10 orthopedic (11.2%), 9 trauma (10.1%), 8 neurologic (9.0%), 5 thoracic (5.6%), 5 gynecologic (5.6%), and 1 for necrotizing fasciitis (1.1%). VTE prophylaxis with unfractionated heparin, low molecular weight heparin, and intermittent pneumatic compression was used in 35 of 89 (39.3%), 8 of 89 (9.0%), and 9 of 89 (10.1%) patients, respectively, whereas 8 of 89 (9.0%) patients were receiving therapeutic anticoagulation. Two methods of VTE prophylaxis were prescribed for 20 of 89 (22.5%) patients. Prophylaxis with unfractionated or low molecular weight heparin was significantly less likely to be prescribed for postoperative ICU patients requiring mechanical ventilation compared with those weaned from mechanical ventilation (odds ratio [OR] 0.36, P =.03). The use of intermittent pneumatic compression devices was significantly associated with current hemorrhage (OR 13.5, P =.02), and risk for future hemorrhage (OR 19.3, P =.001). CONCLUSIONS: VTE prevention for surgical ICU patients within the first postoperative week appear to be individualized, and influenced by current and future risks of thrombosis and bleeding.

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1. The effects of the calcium channel blockers, verapamil and nifedipine on myocardial ischaemia and oedema evoked by endothelin-1 (ET-1) or IRL 1620, an ETB receptor-selective agonist were studied in anaesthetized and conscious rats. 2. Bolus injection of ET-1 (1 nmol kg-1, i.v.) or IRL 1620 (1 nmol kg-1, i.v.) to conscious chronically catheterized rats evoked a transient depressor response followed by a prolonged pressor effect. Corresponding to changes in blood pressure, a transient tachycardia and a sustained bradycardia were observed. Pretreatment of the animals with verapamil (1 mg kg-1, i.v.) or nifedipine (200 micrograms kg-1, i.v.) produced on average 5 mmHg decrease in mean arterial blood pressure. Both verapamil and nifedipine inhibited by 63 and 44% the pressor actions of ET-1 or IRL 1620 (1 nmol kg-1), respectively, and the accompanying bradycardia. Both verapamil and nifedipine potentiated the magnitude of the depressor action of ET-1 and IRL 1620 without affecting the accompanying tachycardia. Decreasing mean arterial blood pressure with hydralazine (0.2 - 0.3 micromol kg-1, i.v.) to levels comparable to those observed after verapamil or nifedipine had no significant effects on the haemodynamic responses to ET-1 or IRL-1620. 3. Intravenous bolus injection of ET-1 or IRL 1620 (0.1-2 nmol kg-1) into anaesthetized rats produced dose-dependent ST segment elevation of the electrocardiogram without causing arrhythmias. ST segment elevation developed within 30-50s and persisted for at least 10-20 min following injection of the peptides. 4. Pretreatment of the animals with verapamil (1 mg kg-1, i.v.) or nifedipine (200 micrograms kg-1, i.v.) inhibited on average by 79 and 76% the ST segment elevation elicited by ET-1 (1 nmol kg-1), respectively. Verapamil and nifedipine also attenuated IRL 1620 (1 nmol kg-1)-induced ST segment elevation on average by 71 and 74%, respectively. In contrast, no significant inhibition was observed with hydralazine (0.2-0.3 mumol kg-1). 5. Both ET-1 and, to a lesser extent, IRL 1620 (0.1-2 nmol kg-1) evoked albumin accumulation in cardiac tissues in a dose-dependent fashion as measured by the local extravascular accumulation of Evans blue dye in conscious rats. ET-1 and IRL 1620 (1 nmol kg-1) enhanced albumin extravasation by 109 and 82%, and 34 and 44% in the left ventricle and right atrium, respectively. ET-1 or IRL 1620-induced albumin extravasation was completely prevented by verapamil (1 mg kg-1) or nifedipine (200 micrograms kg-1) in these vascular beds. In contrast, hydralazine (0.2-0.3 mumol kg-1) failed to modify the effects of ET-1 or IRL 1620 on albumin extravasation. 6. These results show that verapamil and nifedipine are highly effective in protecting the myocardium against the pro-ischaemic and microvascular permeability enhancing effects of ET-1 and suggest that ETA and constrictor ETB (tentatively termed ETB2) receptors mediating these actions of ET-1 are coupled to calcium influx through dihydropyridine-sensitive calcium channels.

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Hypertension is common following coronary artery bypass surgery. The safety of labetalol, a recently released combined alpha-1 and beta-adrenergic blocking agent for treatment of hypertension in this clinical situation is controversial. The authors compared the hemodynamic effects of labetalol with those of sodium nitroprusside (SNP) in 91 patients with good left ventricular function and equally severe coronary artery disease and in whom coronary artery bypass surgery had been just completed. They were anesthetized using fentanyl, diazepam, and enflurane. If hypertension developed postoperatively, patients were randomized to receive labetalol, 2 mg/min to a maximum of 300 mg (20 patients) or sodium nitroprusside in 0.5 micrograms.kg-1.min-1 increments by infusion (20 patients) to return blood pressure to normal. Compared with control values, labetalol brought about significant (P less than 0.05) reductions in heart rate, and cardiac index. No change was noted in stroke volume or systemic vascular resistance, but slight increases were found in central venous pressure and pulmonary capillary wedge pressure. Sodium nitroprusside treatment caused significant increases in heart rate and cardiac index while reducing diastolic blood pressure, central venous pressure, and pulmonary capillary wedge pressure. Stroke volume remained unchanged. Following the study period, blood pressure was controlled in all patients with SNP. Total doses of SNP in the 16 h following the study period were significantly less in the labetalol group (46.6 +/- 11.7 mg) versus (116.1 +/- 10.3 mg) in the SNP group (P less than 0.05). In this clinical circumstance, labetalol can be safe and effective for controlling hypertension, but its mechanism of achieving this effect varies from that for sodium nitroprusside.(ABSTRACT TRUNCATED AT 250 WORDS)

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Surgical ventriculomyectomy and ventriculomyotomy by the aortic approach are safe and effective methods of relieving symptoms and obstruction to left ventricular outflow in patients with hypertrophic obstructive cardiomyopathy. With the addition of Doppler ultrasound to the routine follow-up assessment of these patients an unexpectedly high occurrence of aortic regurgitation was found in the postoperative patients. Because aortic regurgitation has been reported to rarely accompany this condition, 67 patients with hypertrophic obstructive cardiomyopathy were studied clinically and with Doppler echocardiography for the presence and severity of aortic regurgitation. Severity of the regurgitation was quantitated by pulsed or color Doppler echocardiography according to the length and width of the regurgitant jet in at least two views. In 37 patients with hypertrophic obstructive cardiomyopathy who did not undergo surgery, aortic regurgitation was detected in only 1 (3%) by Doppler ultrasound and in none clinically. In 52 patients who did undergo surgery and were studied a mean of 7.8 years postoperatively, aortic regurgitation of trivial to moderate degree was common, being detected in 28 (54%) by Doppler ultrasound and in 6 (12%) clinically. In a subgroup of 22 patients who were studied preoperatively and again early postoperatively (mean 6 weeks), new aortic regurgitation was found in 8 (36%) and was graded as trivial in all. Aortic regurgitation is a common complication related to ventriculomyectomy and ventriculomyotomy in patients with hypertrophic obstructive cardiomyopathy. Although initially trivial, the regurgitation may progress in severity over time. The regurgitation has been well tolerated in all patients studied to date.

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Data from previous experiments in rats indicate that release of serotonin in the central nervous system increases renin and corticosterone secretion. To determine which serotonergic neurons are involved, lesions of the dorsal or median raphe nuclei were produced by local injections of 5,7-dihydroxytryptamine (5,7-DHT) in rats, and 2 weeks later, the renin responses to parachloroamphetamine (PCA) were determined. Plasma corticosterone was also measured. PCA produced significant increases in plasma renin activity and plasma corticosterone in sham-lesioned animals and animals with median raphe lesions. The plasma corticosterone response to PCA was also normal in rats with dorsal raphe lesions but the renin response was significantly reduced. The data support the hypothesis that serotonergic neurons in the dorsal raphe nucleus are part of a neural pathway mediating increased renin secretion, and that the stimulatory effect of serotonin on corticosterone secretion is mediated by a different pathway.

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