Guest Foreword
Hypoactive Delirium Is More Appropriately Named
as “Acute Apathy Syndrome”
Jan N. M. Schieveld, MD, PhD
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Department of Psychiatry and Psychology
Division of Child and Adolescent Psychiatry and Psychology
Maastricht University Medical Center;
Maastricht University
School for Mental Health & Neuroscience (MHeNS),
Division 2;
Department of Psychiatry & Neuropsychology
South Limburg Mental Health Research & Teaching Network;
Maastricht, The Netherlands; and
Mutsaersstichting
Institution for Child & Youth Mental Health Care
Venlo, The Netherlands
Jacqueline J. M. H. Strik, MD, PhD
Department of Psychiatry and Psychology
Division of Child and Adolescent Psychiatry and Psychology
Maastricht University Medical Center;
School for Mental Health & Neuroscience (MHeNS),
Division 2; and
Maastricht, The Netherlands
W
hen two patients who share a surname appear in an
ICU, critical care professionals make extra efforts
to avoid name confusion. Paradoxically, those same
professionals frequently confuse two neuropsychiatric states
solely because they share the same surname: hyperactive delir-
ium and hypoactive delirium.
Both forms of delirium are neurocognitive disorders attrib-
utable to some combination of 1) the underlying critical illness,
2) the “sickness behavior” (adaptive responses to the illness), and
3) the polypharmacy (including opiates and benzodiazepines)
that is common in the ICU. Both forms of delirium are char-
acterized by a fluctuating clinical course with clarity alternating
with periods of hyperactivity or of hypoactivity. Occasionally,
patients will present with both abnormal activity patterns.
Hyperactive delirium tends to command immediate atten-
tion because that disorder threatens the safety of the patient
(self-injury and unplanned removal of support devices) and
of providers. Although the patient is brought under control,
Key Words: apathy; critical illness; delirium; hypoactive
The authors have disclosed that they do not have any potential conflicts
of interest.
Copyright © 2018 by the Society of Critical Care Medicine and Wolters
Kluwer Health, Inc. All Rights Reserved.
DOI: 10.1097/CCM.0000000000003334
Critical Care Medicine www.ccmjournal.org 1561
Copyright © 2018 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.
providers often use the familiar “I WATCH DEATH” mne-
monic to identify, exclude, and treat the underlying causes
(1). We will not discuss hyperactive delirium further, except
to observe that the name is a reasonable label for the behavior
that accompanies that neurocognitive disorder.
Hypoactive delirium, which is much more prevalent, is less
familiar and more forbidding. Many intensivists recall their
initial encounter with delirium terminale, the apathy that
many patients exhibit in the hours and days prior to death from
advanced cancer, and which can be accompanied by intermit-
tent psychotic episodes "(psychosis of the dying)". The empty
gaze, reduced responsiveness, and lessened motor activity are
troubling to family and staff. Yet, such apathy does not always
herald death, even in the ICU. Neuropsychiatrists recognize at
least seven causes for acute apathy, including:
1) apathy syndrome,
2) catatonic inhibition,
3) major depressive disorder,
4) negative symptom complex of e.g., nontraumatic brain
injury and/or schizophrenia,
5) nonconvulsive status epilepticus,
6) excessive sedation due to antipsychotic medications and/or
opioids, and
7) neuroleptic-induced deficit syndrome (2).
Even in pure psychiatric cases where the patient is somatically
“well,” several of these disorders overlap in presentation, in their
response to elicitation of signs, and in the specific diagnostic cri-
teria. Critical illness, the adaptive “sickness behavior,” and inter-
current medications further confound assessment and diagnosis.
The common elements—diminished will, diminished action,
diminished communication—have resulted in a convenient, but
unfortunately misguiding, label: “hypoactive delirium” (3).
The common elements should properly be labeled “acute
apathy syndrome in critical illness.” Once properly labeled, we
can suggest several steps and observations.
1) There should be prompt attention to ruling out immediately
reversible causes of acute apathy such as subclinical status
epilepticus and adverse effects of current medications.
2) There should be an explicit evaluation: is the patient suffering
owing to the apathetic state? Apathy, in and of itself, may not
cause suffering. Further, apathy itself cannot be treated, only
an underlying cause can be treated. However, well-inten-
tioned, nonspecific treatments have potential for harm.
3) If the cause of the apathy is major depression, are conventional
antidepressive medications—which often require weeks to be
Guest Foreword

Figure 1. The neuropsychiatry of critical illness: the algorithm of brain reactions.

effective—ever indicated in the setting of critical illness? Alter-
natively, is there a role for a trial of ketamine infusion?
4) If the patient has severe depression and even catatonia, might
the patient respond to electroconvulsive therapy? Does the
potential benefit outweigh the risk in critically ill patients?
5) The negative symptoms of schizophrenia can respond well
to clozapine provided the diagnosis is accurate, but again
response takes time and the medication carries additional
risk of side effects and interactions.
Such questions and observations illustrate the need for a
more pragmatic classification of brain reactions to critical ill-
ness, including agitation and inhibition syndromes.
Figure 1 represents one way of classifying these reactions by
type and progressive severity. In their most severe forms, either
can lead to coma and even death.
We reiterate that neurocognitive problems in the ICU are
important but difficult to diagnose and more difficult to treat.
Nevertheless, lumping them under the common surname
“delirium” obscures fundamental differences in cause and in
appropriate treatment. By labeling acute apathy for what it is,
we intend to shift the naming and thinking paradigm around
faulty neurocognition in the ICU toward a more disciplined
approach to recognition, classification, and intervention.
ACKNOWLEDGEMENT
We acknowledge the support of Jolien Nivelle, medical secre-
tary, for her help with Figure 1.
REFERENCES
1. Wise MG: Delirium. Textbook of Neuropsychiatry. Hales RE, Yudofsky
SC (Eds). Washington, DC, The American Psychiatry Press, 1987, pp
89–106
2. Stahl S: Psychopharmacology of Antipsychotics. Stahl S (Ed). London,
UK, Dunitz M Ltd, 2001, pp 41
3. Hermus IP, Willems SJ, Bogman AC, et al: “Delirium” is no delirium: On
type specifying and drug response. Crit Care Med 2015; 43:e589

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