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Diagnosis and Treatment of Delirium in 2006

Diagnosis and Treatment of Delirium in 2006

The preceding decade yielded a
worldwide surge in studies of
delirium with improving methodology.
This progress was possible
because of the robust foundation
prepared by investigators such as Engel,
Lipowski, Trzepacz, and Inouye. The
next 10 years are primed to deliver a
striking evolution in the care of patients
with delirium.

The current DSM-IV-TR model
portrays delirium as an acute, reversible
neuropsychiatric syndrome caused by
medical illness and/or drug-related
activity.1 A recent survey confirmed
that many clinicians believe delirium
to be transient and lacking in long-term
consequences for the brain.2 This belief,
however, is in conflict with emerging
evidence on several fronts. For one, delirium
has been shown to markedly and
independently affect patient outcomes
such as length of stay and loss of independent
living, among others.3-8 Equally
striking are studies suggesting new and
persistent cognitive deficits,4,9-14 which
may be linked to known15,16 and hypothesized17-
21
pathologic processes occurring
within the delirious brain.

Delirium is epidemic among hospitalized
patients, especially in the elderly
and chronically ill, with rates reported
between 12% and 80% depending on
the subpopulation. Because of its pervasiveness
and its associated risks for
morbidity and mortality, it is imperative
that delirium is diagnosed accurately,
prevented, and treated.22-24

DIAGNOSIS

Clinical diagnosis remains the mainstay
in practice. A DSM-IV-TR diagnosis
requires an acute disturbance in
consciousness, new cognitive dysfunction
or perceptual anomalies, and a
tendency to fluctuate. Subspecifiers are:

  • Delirium caused by a general medical
    condition.
  • Substance intoxication or withdrawal
    delirium.
  • Delirium resulting from multiple
    causes.1

While the DSM-IV-TR approach to
delirium is a clear upgrade from the
DSM-3R, I would argue that it is still
slightly delira, or off-track.

Inconsistency abounds in the published
and clinical language as to what
distinguishes a cause from a risk factor
for delirium. This arbitrariness is
reflected in the current DSM and in the
1999 American Psychiatric Association
treatment guidelines.25 The phrases "cause," "risk factor," "associated conditions,"
and "underlying etiology" have
been and often still are used interchangeably
and without scientific precision.
The cerebral etiopathology of
delirium has yet to be sufficiently elucidated,
and thus we cannot identify a
cause. The term "precipitant," however,
can justifiably be used to subsume risk factors that are generally transient or
acute (eg, a urinary tract infection).
Similarly, "baseline vulnerability" is a
term coined by Inouye26 to describe the
risk factors that are, by definition,
chronic and innate to the patient (eg,
dementia). Thus, it is proposed that there
are numerous and widely varying
precipitants that can activate delirium
(or acute brain failure according to
Lipowski) in susceptible patients (those
with high baseline vulnerability).

Inouye and Charpentier26 eloquently
supported this concept in their landmark
1996 study. They separated out baseline
risks present at admission (eg,
previous cognitive impairment) from
precipitants affecting the patient after
admission (eg, new-onset respiratory
insufficiency). Robust patients with less
baseline vulnerability ("more cerebral
reserve") were more resilient in the face
of new precipitants after admission.
The reverse was true as well. The more
baseline vulnerability a patient had, the
higher the likelihood of delirium developing
if his or her frail homeostasis
("less cerebral reserve") was stressed
with additional precipitants. Hence, the
brain-delirium relationship was demonstrated
to behave much like other mechanisms
of organ failure.

This would suggest that comorbid
disease states and even medications
may precipitate, but do not necessarily
cause, delirium in vulnerable patients.
The vast number and disparate nature
of the identified precipitants innately
argue against their having direct causal
links to delirium. Exceptions may exist,
of course, in which select precipitants
have direct causative links, such as
medications with hefty anticholinergic
or pro-dopaminergic activity. The question remains how and where to fit delirium
tremens and sedative withdrawal
states into the larger delirium paradigm.
Behavioral similarities are manifested
between these clinical states and
"regular" delirium, yet neurochemistry,
electroencephalographic (EEG) patterns,
and treatments are seemingly
disparate.

Electroencephalography

The EEG is useful in the uncommon
situation in which one is trying to distinguish
delirium from other psychiatric
states, such as catatonia, conversion
disorder, or malingering. EEG findings
in delirium (not delirium tremens or
benzodiazepine withdrawal) consistently
show diffuse disorganization and
flattening, followed by reorganization
at frequencies slower than normal for
that person.27,28

Diagnostic scales and tools

The reader is referred to the excellent
review by Smith and colleagues29 for
more details on the numerous instruments
that have been developed
to diagnose delirium objectively in
research and clinical settings. The
most robust of these instruments are
described below.

The Delirium Rating Scale-Revised
(DRS-R-98) is a 16-item, 46-point clinician-
rated scale.30 It can serve to diagnose,
rate the severity of, and track
delirium changes over time. The best
cutoff score is 15 for the severity subscale
and 18 for the total score (sensitivity
and specificity in the mid-90
percentiles). It has excellent internal
validity and the capacity to discriminate
delirium from dementia. This scale
is an upgraded version of the original
DRS,31 which lacked expanded functionality
for repeated measurements or
for discriminating motoric subtypes
(hypoactive or hyperactive).

The Confusion Assessment Method
(CAM) is designed for detection of delirium
by nonpsychiatrists.32 It is an algorithm-
based tool that operationalized
DSMdiagnostic criteria. Sensitivity and specificity are both above 90%, and
interrater reliability between trained lay
interviewers and experts is high.33 The
5-minute CAM-ICU34 can be used for
ventilated patients, and had a sensitivity
of 73% and a specificity of 100%
in one validation study.35

The Memorial Delirium Assessment
Scale
(MDAS) of Breitbart and associates36
is a 10-item, 30-point clinician
scale that is best suited for rating severity.
A cutoff score of 13 gives a sensitivity
of 71% and a specificity of 94%
for delirium. The MDAS correlates very
well with the DRS and clinician's severity
ratings, and the scale is well suited
for serial administration. It is often used
as a severity scale, with the CAM or
the DRS serving to objectify the delirium
diagnosis.

The Nursing Delirium Screening
Scale
is an intriguing instrument still
in development.37 This 1-minute, 5-
item, 10-point nurse-scored instrument
has shown a sensitivity and specificity
of 86% at a 2-point cutoff, and has excellent
potential for repeated or "continuous"
measurement. The results of this
test also correlate well with those of the
MDAS and DSM-IV. This scale still
needs further evaluation in older patients
and for its ability to differentiate delirium
from dementia.

With regard to the Mini-Mental State
Examination (MMSE),38 Ross and
colleagues39 reported the mean MMSE
score to be 14.3 for delirious patients
versus 29.6 for controls. The first elements
of the MMSE in their relatively
young cohort to show deficits were the
reverse calculation, orientation, and
recall items. A single MMSE is not
sensitive (33%) for identifying delirium40
and is incapable of discriminating
delirium from dementia. Serial
MMSEs, on the other hand, can help
identify improvement or worsening of
delirium, as demonstrated in a 2005
study by O'Keefe and coworkers,41 and
assist in delirium screening when baseline
MMSE scores are known.42

TREATMENT

A useful construct to guide delirium
management in 2006 is the precipitantvulnerability-
brain failure model presented
earlier. After the diagnosis is
made, the first task of the psychiatrist
is to avoid recommending that the
primary team "search for an underlying
cause of delirium" and to avoid
automatically recommending antipsychotics
if the patient is agitated. Our
first duty is to be a diligent observer
and to appreciate where the patient is
at clinically.

Once we are better aware of our
patient's situation, we can more selectively selectively
seek to address modifiable precipitants,
and to decide whether and which
pharmacologic agents would best serve
the patient. Modifiable precipitants
may, for example, be an undetected
urinary tract infection, pneumonia,
organ failure, sepsis, or a host of medications.
Anticholinergics, benzodiazepines, corticosteroids, powerful
dopamine agonists, and certain opioids
are best limited when feasible,43,44
although some uncertainty remains in
this arena.45Tact and diplomacy are critical
skills for the psychiatrist to exercise
when addressing these precipitants
with the patient's primary care physician.
In the end, the goal of treating
delirium is not to control agitation or
hallucinations alone, but to reverse the
delirium and thus mitigate associated
morbidity and mortality risks.

Intervention programs

Several comprehensive, primarily nonpharmacologic
intervention protocols
have been published. Regrettably, only
a few of these reports are methodologically
sound. The largest and bestdesigned
is the Elder Life Program of
Inouye and associates.46 In this prevention
program, they selected 426
nondelirious patients at risk for delirium
and sought to address baseline
cognitive impairment, sleep, mobility,
vision, hearing, and dehydration. They
reported a 5% decrease in delirium incidence
compared with a usual-care
control group. One year after discharge,
the intervention group also demonstrated
a 15% reduction in costs and
length of stay at nursing homes compared
with the controls.47

Naughton and colleagues48 reported
reducing delirium incidence from 41%
to 19%, and reducing length of stay for
delirious patients in a specialty geriatrics
unit by means of their intervention
program. This program sought to
maximize provider coordination,
knowledge, and awareness, and used
both medication-based and non-
medication-based interventions. The raters in this study were not blind to
the treatment group.

Using the less specific Organic Brain
Syndrome Scale, an early prevention
study described a reduction in delirium
incidence, duration, severity, and hospital
length of stay for postoperative
patients.49 This protocol consisted chiefly of oxygen therapy and prevention
of perioperative hypotension. On
the other hand, one group found their
comprehensive nonpharmacologic intervention
program to be ineffective in
reducing delirium incidence.50

Overall, environmental and nursing
measures have been suggested to have
an important role in delirium management,
particularly if smartly targeted at
modifiable precipitants; these measures
are inclusive of delirium recognition and
education-promoting components.

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