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I have a few questions about the patient example. On day 2, the patient was found to be positive for hyperactive delirium and was given lorazepam. What is the reasoning for using lorazepam if it could have caused or could potentiate the delirium? Also, didn’t they succeed only in sedating him? I understand that it is probably more beneficial to the patient to have hypoactive rather than hyperactive delirium but are we actually treating the delirium by sedating him? Many of the patients in the ICU suffer with sleep deprivation and can behave similarly to those your article defined as having delirium. Are these conditions in fact the same thing or does sleep deprivation only contribute to the delirium?
Working in the ICU, it is often difficult to assess patients secondary to intubation and mechanical ventilation. The CAM-ICU tool does offer an alternative assessment option that may be appropriate for some patients in the ICU. Patients with anxiety or delirium still need our assistance in the recovery process.
We would like to thank this reader for her insightful questions and comments. The case example included in our article, Monitoring Delirium in Critically Ill Patients, was intended as an example of how to use the CAM-ICU to monitor for delirium in patients receiving mechanical ventilation, rather than a model of how to treat delirium. The example was chosen to represent a typical ICU patient’s course, which often includes heavy use of benzodiazepines to suppress any hyperactivity. We agree with the reader that administering lorazepam to sedate a hyperactive patient may only succeed in producing a hypoactive form of delirium. Hypoactive delirium may not be an improvement; data from the non-ICU population indicate that patients with hypoactive delirium may have a worse prognosis than those with hyperactive delirium.1 These hypoactive patients may experience increased time on the ventilator as well as prolonged length of stay in the ICU and the hospital.2 In addition, these patients may experience long-term neuropsychological impairment,3 yet the exact relationship between delirium and long-term neuropsychological impairment is not known. Although some authors still recommended benzodiazepines as the treatment of choice for delirium,4 others have commented that these agents are known to precipitate delirium and should be avoided.5,6 Both Society of Critical Care Medicine (SCCM) and American Psychiatric Association clinical practice guidelines recommend haloperidol, a typical antipsychotic agent, with a grade C recommendation based on case series and expert opinion for the treatment of delirium.5,6 However, we find that benzodiazepines continue to be used, perhaps because haloperidol is not sedating enough to protect against self-extubation or disruption of invasive devices. Concern over the adverse effects of haloperidol (ie, QT prolongation, arrhythmias, and extrapyramidal effects) may also limit its use. We hope that the implementation of standardized sedation/analgesic protocols that include targeted delivery and daily awakening trials along with new tools for the treatment of delirium, particularly the atypical antipsychotics, will prove to be effective in minimizing and perhaps even preventing delirium.
It is important to emphasize that the first step to treat delirium is the removal of deliriogenic medications and correction of any known risk factors for delirium such as hypox-emia, anemia, electrolyte abnormalities, or sleep deprivation (as pointed out by the reader). It should be noted that investigations of sleep architecture in the ICU are in their infancy,7 which limits our ability to comment further on this seemingly very important aspect of delirium risk.
On a final note, we share the reader’s belief that the CAM-ICU is complementary to the traditional neurological examination. In our ICUs, we now monitor patients routinely for pain, anxiety, and delirium. Since the publication of the SCCM guidelines, the CAM-ICU is being incorporated by many other ICUs around the world.
References
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