|
Project Title:
Mechanical Ventilation and Delirium
Funding Agency:
NIH
Total Project Period:
Jul 1, 2005 - Jun 30, 2006
Principal Investigator:
Eric Milbrandt, MD;
Mentor/Collaborators:
Derek C Angus, MD; Fernando Boada, MD; Patrick Kochanek, MD; Bruce Pollock, MD; Lisa Weissfeld, PhD.
Project Summary:
Two major developments frequently linked during many patients’ ICU course are the need for mechanical ventilation and the development of delirium. Also known as acute encephalopathy,15 delirium occurs in as many as 80% of mechanically ventilated medical ICU patients.2-5,16 Most clinicians consider ICU delirium to be expected, iatrogenic, and without consequence.17 Recent data, however, associate delirium with increased duration of mechanical ventilation and ICU stay, increased medical complications, such as ventilator-associated pneumonia, and worse patient outcomes, such as increased 6-month mortality.2-5,18 After addressing any underlying causes, the correct treatment for delirium is an antipsychotic, such as intravenous haloperidol.19 However, current practice is characterized by infrequent use of antipsychotics and prolific use of sedatives, such as benzodiazepines or opiates.17 The current belief regarding why delirium is associated with unwanted complications is that untreated delirium and the associated excessive sedation impair the patient’s ability to wean from the ventilator, increasing exposure to the complications of prolonged mechanical ventilation.16,18 Consequently, recent national guidelines recommend “routine assessment for the presence of delirium” in all mechanically ventilated ICU patients and treatment with haloperidol.19 This approach is based on expert opinion and some limited case series but has never been prospectively evaluated in a randomized controlled trial.19,20 In observational preliminary work, I have shown a 15.3% absolute reduction in 28-day mortality for mechanically ventilated patients who received their first dose of haloperidol within the first 2 days of mechanical ventilation as compared to those who never received haloperidol despite similar baseline severity of illness and comorbidity. It is possible that unmeasured differences between groups, including indication bias, could account for this association. Nevertheless, these results are quite provocative; requiring confirmation in a prospective randomized controlled trial.
|
|
