Acute Delirium

FIGURE 17.1 Assessment of level of sedation and delirium in the ICU. RASS, Richmond Agitation Sedation Scale (see Table 17.3); CAM-ICU, Confusion Assessment Method for the ICU: delirium is diagnosed by the presence of 3 of the 4 diagnostic features.

TABLE 17.1 The Richmond Agitation Sedation Scale for the Assessment of Depth of Sedation

+4	Very combative, violent, dangerous to staff
+3	Pulling catheters and tubes, aggressive
+2	Frequent nonpurposeful movements, fights ventilator
+1	Anxious but movements not aggressive or vigorous
0	Alert and calm
–1	Awakes (eye contact) for > 10 seconds in response to voice
–2	Awakes (eye contact) for < 10 seconds in response to voice
–3	Eye opening or movement to voice without eye contact
–4	No response to voice, but eye opening or movement to physical stimulation
–5	No response to voice or physical stimulation

Sedation holidays (stopping all sedatives at regular intervals) have been shown to decrease the duration of mechanical ventilation and the length of ICU stay. They also decrease the incidence of delirium. Still, the need for sedation holidays is not sufficiently appreciated. In fact, it has been our experience that precisely the sickest patient is the one at highest risk for delirium and in whom sedation holidays are less frequently used.

We still know little about the causes and mechanisms of delirium in critically ill patients, but there is emerging research. Studies have definitively demonstrated that prolonged exposure to psychoactive drugs in general and sedative drugs in particular increase the risk and severity of delirium. Benzodiazepines are particularly prone to exacerbate delirium and they are only indicated for the treatment of delirium related to alcohol withdrawal. Dexmedetomidine may be a safer option. Antidopaminergic agents are the best medications for agitation; the relative value of haloperidol versus atypical antipsychotics (such quetiapine or olanzepine) is not well studied in the ICU population. The risk of delirium with opiates has been less studied, but we often find them to be a major contributing factor. The general principle is that we should be using all sedatives very judiciously, prescribing the lowest possible doses and stopping them as soon as they are no longer truly necessary. In fact, a good first step would be to ensure that we avoid sedating critically ill patients who are already drowsy (when not stuporous or comatose), an everyday error in many ICUs today.

As neurologists we are often consulted to evaluate these patients in the medical or the surgical ICU and we can be very useful. Table 17.2 lists some of the diagnoses to consider when evaluating “encephalopathic” patients in general ICUs. The experienced clinician will look for brainstem or lateralizing signs, subtle manifestations of seizures, and features of major toxidromes (see chapter 14). Adventitious movements such as multifocal myoclonus (more common with uremia) and asterixis (more common with liver failure) are good markers of a metabolic derangement, albeit nonspecific. Severe muscle rigidity with clonus should raise suspicion for serotonin syndrome, neuroleptic malignant syndrome, and when accompanied by high fever, malignant hyperthermia.

Our approach to the evaluation of patients with ICU delirium is summarized in Table 17.3. In essence, after reviewing the history and examining the patient, we try to answer the following questions:

Do I have a diagnosis?
Should the patient have more blood tests?
Should the patient have brain imaging? If so, which one?
Should the patient have a lumbar puncture?
Should the patient have an electroencephalogram? If so, is there a need for continuous monitoring?
Are there any medications in the regimen that should be reduced or stopped?
Do I need to recommend specific treatment for agitation?

In the case presented, we found that the patient had mixed delirium with multifocal myoclonus, but normal brainstem reflexes and no lateralizing signs on examination. Muscle tone was normal. Deep tendon reflexes were decreased in the legs, consistent with his long history of diabetes. He had no meningeal signs or clinical manifestations of seizures. We requested a serum ammonia level, which was normal, and decided to follow his clinical evolution without recommending further testing. We did ask the primary team to stop the infusion of midazolam and to use intravenous haloperidol (2–5 mg every 4 hours) for the patient’s episodic agitation. We also strongly advised to stop the infusion of fentanyl that the patient had been receiving since surgery. With these simple changes, the patient began to improve despite further increase in his BUN for two more days (to reach a peak of 58 mg/dL) before it started to decline. Once off sedatives, he was extubated without complications. Upon discharge 2 weeks later, his intellectual function was nearly normal.

TABLE 17.2 Differential Diagnoses in ICU Patients with Encephalopathy