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between services. Excessive hyperventilation can easily
worsen cerebral ischemia or contribute to tearing of
bridging veins after evacuation of an intracranial hematoma. Review of the neurological exam and any imaging
of an acute intracranial process should be performed so
that the anesthesiologist can assess the degree of injury,
midline shift, hematoma size, location of the injury, and
potential for associated cervical spine injuries in the case
of trauma. Quick and efficient collection of this information and any pertinent past medical history, medications,
vital signs, and laboratory values is crucial to successful
treatment. These details will help the anesthesiologist
determine the need for a general anesthetic versus monitored anesthesia care, the need for cervical spine precautions during intubation and positioning, the likelihood
of intraoperative hemodynamic problems, selection of
appropriate vasoactive medications and the need for
direct arterial blood pressure monitoring, and the likelihood of large fluid shifts, coagulopathy, and need for
transfusion, which will guide selection of appropriate
intravenous access. Unless adequate peripheral venous
access is impossible to obtain, central venous catheters
are not typically used for these cases, as the additional
delay can contribute to significantly poorer neurologic
outcomes.
Diagnosis of an acute intracranial event is particularly
challenging to the anesthesia team intraoperatively and
postoperatively because of the many anesthesia medications that can aect the mental status and cardiovascular
and respiratory systems. In addition, acute illnesses such as
sepsis or liver failure can alter the mental status. Knowledge
of the baseline mental status and motor exam coupled with
the ability to perform a quick gross neurological exam
with pupillary light reexes and a Glasgow Coma Scale
assessment for speech, motor, and orientation will guide
the primary workup. Prior medical history is also critical information to know, as patients who have recovered
strength aer a stroke may exhibit transient weakness of the
same limb(s) in the immediate postoperative period aer a
general anesthetic. New focal decits such as a facial droop,
unilateral weakness, or expressive aphasia, particularly aer
nonneurosurgical procedures, are especially concerning for
an acute stroke.
is section discusses some of the more common or
more critical acute neurologic events that an anesthesiologist may encounter throughout the hospital and that
should be part of the dierential diagnosis for acute neurologic changes. Each chapter presents a specic diagnosis,
its pathophysiology, and the appropriate approach to treatment of that disorder.
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SECTIONA
CEREBRALORIGIN
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62.
DELIRIUM
Bret D. Alvis and Christopher G.Hughes
CLINICALCASE
specically in surgical patients focusing on delirium in
the rst few postoperative days have found similar results,
A 77- year- old male with a history of hypertension and
dementia presents for emergent repair of his unstable pelvic
fracture. He has a past surgical history of coronary artery
including associations with increased length of stay, higher
cost of care, prolonged cognitive impairment, and increased
mortality.
5,12,13
bypass graing (CABG) 10years prior without anesthetic
complications. Initial plan is to perform a rapid sequence
intubation and general endotracheal tube anesthetic.
BACKGROUND
DEFINITION
e clinical syndrome of delirium consists of inattention,
disorganized thinking, disorientation, and/ or altered lev-
els of consciousness.14 While no consensus denitions
Delirium occurs when a patient experiences uctuations
in mental status caused by acute cerebral dysfunction. All
hospitalized patients are at risk for the development of
delirium, with a reported incidence of 11%– 25% in elderly
patients and as high as 80% in the critically ill.
1,2
Patients
in the perioperative setting are no exception, and the risk
of developing postoperative delirium appears dependent
on age, preexisting comorbid conditions, severity of concurrent illness, and the severity of the surgical process.
Because of a lack of clearly dened distinction between
emergence and postoperative delirium, however, there is a
wide discrepancy in the literature regarding the actual rates
of delirium aer surgery.3 Up to 45% of patients will experience delirium symptoms in the postanesthesia care unit
(PACU) aer surgery, many of whose symptoms persist at
PACU discharge, which predicts further brain dysfunction
during the hospitalization.
4– 6
Postoperative delirium in the
ward or intensive care unit (ICU) has been reported to
occur in up to 50% of patients aer both cardiac and noncardiac surgery, and it typically develops within the rst to
second day of admission.
7
Delirium in the hospital is independently associated
with signicant morbidity and mortality, such that as the
duration of delirium increases, a patient is at higher risk for
cognitive and executive dysfunction at 3 and 12 months
and for decreased short- and long- term survival.
8– 11
Studies
exist, emergence delirium typically refers to agitation aer
discontinuation of an inhaled anesthetic, PACU delirium refers to delirium occurring aer emergence but during the initial recovery phase, and postoperative delirium
refers to delirium that occurs aer the patient meets PACU
discharge criteria or has been discharged from the PACU.
Manifestations of delirium always include uctuations
in mental status and can present with a wide spectrum of
1,3
symptoms that can include, but are not limited to, sleep
disturbances, abnormal psychomotor activity, acute psychosis, decreased psychomotor activity, hallucinations, and
emotional disturbances such as fear, depression, and/ or
anxiety.
14,15
is syndrome of brain dysfunction can be categorized
into three motoric subtypes: hyperactive, hypoactive, or
mixed. Hyperactive delirium is least common; however, it is
the most common perception of delirium to clinicians.
Patients with hyperactive delirium display prominent agitated motor behaviors that can be witnessed easily. e most
common form is hypoactive delirium, and it is the most difcult to diagnose, typically requiring validated deliriumassessment tools to diagnose.15 Hypoactive delirium is
characterized by slow patient movements, decreased speed
of cognition, and decreased alertness, and this motor subtype may be associated with worse outcomes.18 Patients are
oen overlooked, however, because they are not displaying
16,17
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the disruptive behaviors that frequently trigger delirium in
the dierential diagnosis.
DIAGNOSIS
18
ere are validated instruments that allow clinicians to assess
a patient’s level of arousal and content of consciousness even
when a patient is mechanically ventilated. e Richmond
Agitation Sedation Scale (RASS) (Table 62.1) and the Riker
Sedation Agitation Scale (SAS) are commonly used tools
that can be used to assess level of arousal.
19,20
Importantly,
assessment for delirium cannot occur if the patient is deemed
unresponsive by the sedation scales (RASS - 4 or - 5 or SAS
of 1 to 2). Once a patient can respond to verbal stimuli, they
TABLE62.2 CONFUSION ASSESSMENT METHOD(CAM)
Diagnosis— requires BOTH A& B along with EITHER feature C
or D
(A) Acute onset or
Fluctuating course
(B) Inattention * Does the patient:
(C) Disorganized
thinking
* Acute change in mental status from
baseline?
* Does this abnormal behavior:
1. Fluctuate overtime?
2. Come andgo?
3. Increase/ decrease in severity?
1. Have difculty focusing?
2. Become easily distracted?
3. Having difculty keeping track of what
is said?
* Patient’s thinking:
1. Disorganized
2. Incoherent
can be assessed using tools such as the Confusion Assessment
Method (CAM),21 the 4AT,22 the Confusion Assessment
Method for Intensive Care Unit (CAM- ICU),23 or the
Intensive Care Delirium Screening Checklist (ICDSC).24
e CAM assessment includes an evaluation of the patient
for the key features of delirium such as an acute onset, uctuating course, and inattention (Table 62.2).21 e 4AT is a brief
(D) Altered level of
consciousness
SOURCE:Adapted from Inouye etal.
* Is the patient:
1. Alert
2. Vigilant
3. Lethargic
4. Stuporous
5. Comatose
21
TABLE62.1 RICHMOND AGITATION SEDATION
SCALE(RASS)
Score
+4 Combative Combative, violent, immediate danger
+3 Very Agitated Pulls or removes tube(s) or
+2 Agitated Frequent or nonpurposeful movements,
+1 Restless Anxious but movements not
0 Alert and Calm
- 1 Drowsy Not fully aler t, but has sustained
- 2 Light Sedation Briey awakens with eye contact to
- 3 Moderate
- 4 Deep Sedation No response to voice, but movement
- 5 Unarousable No response to voice or physical
SOURCE:Adapted from Sessler etal.
Terminology
Sedation
Clinical Description
to staff
catheters(s)— aggressive
ghts ventilator
aggressive/ vigorous
awakening (eye opening/ contact) to
voice (>10 seconds)
voice (<10 seconds)
Movement or eye opening to voice (but
no eye contact)
or eye opening to physical stimulation
stimulation
19
tool that assesses alertness, orientation, attention, and change
in mental status.22 If the patient is critically ill or mechanically ventilated, the CAM- ICU and ICDSC scales are the
most validated. e CAM- ICU assess the same four features
as the CAM examination in a more abbreviated manner to
t the needs of ICU patients— acute changes/ uctuations
in mental status, inattention, disorganized thinking, and an
altered level of consciousness.23 e ICDSC uses eight diagnostic features to make the diagnosis of delirium, for which
the patient needs only four of those features.
24
e immediate postoperative setting, especially the
PACU, requires additional attention, because the diagnosis
of delirium can be very challenging, as emergence from general anesthesia oen presents with signs similar to delirium.
A recent study found that signs of delirium were highest
upon arrival to the PACU (>30%) and decreased over time;
however, 4% of patients still had persistent signs of delirium
at time of PACU discharge despite meeting discharge criteria.2 Another study of high- risk elderly patients found
PACU delirium rates of 45% even aer patients met PACU
discharge criteria.4 Unfortunately, no specic delirium
assessment tool has been validated in the PACU. Neither the
CAM- ICU nor the Nursing Delirium Symptom Checklist
(NuDESC) was very sensitive in the PACU in one study,
but specicity was >90%;4 thus, patients testing positive
with these assessment tools are highly likely to have delirium,
but a few patients may be missed. When one considers that
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451
over 230million surgical cases occur per year worldwide, it
is easy to conclude that there are likely a substantial number
of patients who leave the PACU with altered brain function
and are at risk for persistent delirium.
ETIOLOGY
2
ere are many proposed mechanisms for the development
TABLE62.4 PERIOPERATIVE RISK FACTORS FORDELIRIUM
Surgery Anesthesia
Major abdominal ASA >3 Classication
Cardiac Benzodiazepine premedication
Emergency vs. elective General anesthesia?
Open vs. endovascular Deeper sedation?
Increased duration Opioid administration?
of delirium. Systemic and central nervous system inammation, cholinergic deciency, and disturbances in neurotransmitters such as serotonin and norepinephrine are a
few of the proposed mechanisms.25 Studies have shown that
there are neuroanatomical changes, including brain atrophy
and white matter changes, in patients with delirium.
26,27
e
white matter changes persist even aer hospital discharge
and may be the cause of long- term cognitive impairment in
these patients.
25
It is important for clinicians to understand the risk
factors and precipitants for delirium in order to prevent
it from occurring. e most common medical conditions
that precipitate delirium in hospitalized patients are infections of the urinary tract and the lungs.3 ese two etiologies alone may be present in 34%– 64% of the hospitalized
patients with delirium.3 Other etiologies include dehydration, electrolyte abnormalities, acute kidney injury or liver
failure, ethanol or benzodiazepine withdrawal, central nervous system insults, and seizures (Table 62.3). Congestive
heart failure and acute myocardial infarction have also been
implicated as delirium precipitants.3 A recent systematic
review of risk factors identied age, dementia, hypertension, coma, delirium on the previous day, emergency surgery, mechanical ventilations, polytrauma, and metabolic
acidosis as having the strongest evidence as delirium risk
factors.28 Along with risk factors, precipitants of delirium
include physical restraints, bladder catheters, polypharmacy, sleep disturbances, and medications with anticholinergic properties. Despite this list of common etiologies,
there are plenty of patients who develop delirium in the
hospital where no obvious etiological agents can befound.
e incidence and risk factors of postoperative delirium
reported in the literature appear to be strongly inuenced by
the severity of the surgical insult, comorbidities, and sedative
and/ or analgesic drug exposure (Table 62.4).3 e risk correlates with the type of operation:otolaryngological (12%),
general surgery (13%), aortic (29%), major abdominal (50%),
and cardiac (up to 51%).3 Furthermore, increased surgical
duration, emergency surgery, and open (versus endovascular)
surgery also appear to increase risk.3 Along with the type of
surgery, other reported risk factors for postoperative delirium
include increasing age, preexisting cognitive impairment,
increased cardiovascular comorbidities (including diabetes),
and severity of illness (American Society of Anesthesiologists
classications >3).3 Benzodiazepine administration in the
perioperative setting has been strongly associated with
emergence and postoperative delirium, similar to studies of
29– 34
Opioid adminis-
TABLE62.3 DELIRIUM RISK FACTORS AND PRECIPITANTS
Risk Factors Precipitants
mechanically ventilated ICU patients.
tration has been associated with delirium in the postoperative and ICU settings;
2,35,36
however, data on this association
is inconsistent, as others have shown opioids to be protective,
Increasing age Infection
Preexisting cognitive impairment Dehydration
when used to appropriately control pain, or to have no association with delirium.
37– 39
Hypertension Electrolyte abnormalities
Congestive heart failure Acute kidney failure
Acute myocardial infarction Acute liver failure
Mechanical ventilation Ethanol/ drug withdrawal
Polytrauma Fragmented sleep
Metabolic acidosis Central ner vous system insults
Existing coma/ delirium Benzodiazepines
DELIRIUM 451
EVALUATION
Once a patient is suspected of suering from delirium, they
should be evaluated with a thorough history and physical examination. e history can help a clinician identify
possible targets for intervention such as drug ingestions,
alcohol/ drug withdrawal, and metabolic derangements.
Importantly, it may help dierentiate between dementia
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or baseline cognitive impairment and new- onset delirium.
e examination should evaluate possible sources of infection and volume status.
Potentially indicated testing includes electrolyte panel,
complete blood count, liver function tests, thyroid function tests, electrocardiogram, infection work- up including
chest radiograph, urinalysis, and culture data. Hypoxemia
and hypercarbia should also be excluded, especially in the
PACU and postoperative setting.
patient’s environment.44 Sleep hygiene and patient reorientation should be performed for all patients to prevent
delirium.44 Other environmental factors include removal
of catheters/ restraints, nonpharmacologic sleep protocols,
early mobilization, providing regular stimulating activities,
and attention to hydration.44 Always ensure patient safety
while removing any unnecessary medical devices and pharmacologic therapies.
Specic pharmacological agents are not supported by
denitive guidelines or evidence to support their use as
TREATMENT
therapies for delirium.7 Popular pharmacologic treatments
used by clinicians include dexmedetomidine and/ or an
antipsychotic medication such as haloperidol, olanzapine,
e Benjamin Franklin adage “An ounce of prevention is
worth a pound of cure” is apropos with regard to delirium,
as no denitive therapy has been proven. e rst thing a
clinician should attempt to do is modify the several risk
factors for delirium by improving sleep hygiene, providing appropriate pain control, executing appropriate sedative regimens, and avoiding medications that might trigger
delirium (Table 62.5).40 ese medications include benzodiazepines, anticholinergics, and sedating agents. Aer the
history and examination, a clinician should promptly treat
any causes identied— metabolic derangements, infections,
hypoxemia, hypercarbia, and soforth.
Symptom management is important but can prove
challenging.41 e critical care literature supports a systematic approach to pain, agitation, and delirium management in their recent guidelines.1 is includes focusing
on the ABCDEs:(A) assess, prevent, and manage pain;
(B) both spontaneous awakening trials and spontaneous breathing trials; (C)choice of sedation; (D)delirium
monitoring and management; and (E) early mobility
and exercise.15 Sedation protocols and early physical and
occupational therapy have been shown to reduce delir-
42,43
ium.
Another treatment category is optimization of the
or quetiapine (Table 62.5).41 e Maximizing Ecacy of
Targeted Sedation and Reducing Neurological Dysfunction
(MENDS) trial compared lorazepam and dexmedetomidine for sedation in critically ill patients, and patients who
received dexmedetomidine for sedation had more days free
of delirium.33 e Safety and Ecacy of Dexmedetomidine
Compared with Midazolam (SEDCOM) trial showed that
dexmedetomidine patients experienced fewer episodes of
delirium.
34
Antipsychotics have also been looked at for the treatment and/ or prevention of delirium. e Modifying the
Incidence of Delirium (MIND) study compared ziprasidone with haloperidol and placebo and found no difference in delirium outcomes.45 uetiapine has been
compared to placebo in a small trial of critically ill patients
with delirium, with both patient groups receiving haloperidol as a rescue medication.46 e quetiapine arm did show
a decrease in number of hours to resolution of the delirium symptoms and a reduction in the amount of rescue
medications required.46 When comparing dexmedetomidine to haloperidol in hyperactive delirium, mechanically
ventilated patients showed earlier time to extubation and
shorter ICU length of stay in the dexmedetomidine arm.47
Haloperidol for delirium prophylaxis in the ICU has not
been shown to be eective in reducing delirium incidence
TABLE62.5 DELIRIUM PREVENTION AND TREATMENT
OPTIONS
Pharmacological Environment Optimization
Dexmedetomidine Sleep hygiene
Haloperidol? Patient reorientation
Quetiapine? Remove catheters/ restraints
Olanzapine? Early mobilization
Risperidone? Appropriate hydration
Statins? Sedation protocol
and may lead to more oversedation.48 Risperidone has
been evaluated in one randomized controlled trial, where
a single dose given sublingually aer cardiac surgery was
more eective than placebo in prevention of delirium.41
Statin therapy has shown some promise in delirium secondary to pleiotropic anti- inammatory properties, targeting a diminished neuroinammation.49 ere is also
evidence that statin use can reduce the risk of delirium in
the ICU
27,48
and that withdrawal of statin therapy in prior
users greatly increases the risk of delirium.27 Prior evidence has shown that high levels of anticholinergic activity and decits in cholinergic function are associated with
452 SECTION A. CEREBRAL ORIGIN
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453
delirium, but prophylactic rivastigmine (a cholinesterase
inhibitor) has been shown to be ineective in reducing
delirium aer cardiac surgery and in the ICU and may have
increased mortality in the ICU.
50– 53
reduce delirium, however, is less compelling than the evidence that adequate pain control reduces delirium.61 Astudy
of femoral nerve blockade in addition to patient- controlled
analgesia demonstrated a lower incidence of postoperative
delirium aer total knee replacement.65 Asmall randomized
ANESTHETIC CONSIDERATIONS
controlled trial in patients having spine surgery compared
prophylactic gabapentin to placebo and found that gaba-
pentin reduced delirium.66 A fast- track surgery model for
With regard to anesthetic management and risk of delirium,
studies have demonstrated that benzodiazepine administration is associated with emergence and postoperative delir-
54– 57
ium.
In the postoperative cardiac surgery patient, there
has been promising research showing a decrease in delirium
rates when patients are sedated with dexmedetomidine
knee and hip arthroplasty found minimal delirium when
the nonopioid medications gabapentin, acetaminophen,
and celecoxib were primarily used for pain management.67
Finally, a recently published study found that only approximately 3% of patients developed delirium aer an enhanced
recovery fast- track model for colonic surgery.
68
versus propofol or midazolam58 and decreased delirium
duration with dexmedetomidine sedation versus morphinebased sedation.59 Existing data is not clear regarding the
CASE- BASED LEARNING DISCUSSION
association between analgesics and postoperative delirium
despite studies examining variable opioid types, routes, and
patient populations.
3
e evidence is inconclusive regarding the eects of
anesthesia type or depth of anesthesia on the development
of postoperative delirium. When a total intravenous propofol general anesthetic was performed and compared to desurane, there was no dierence in postoperative delirium
rates.60 ere have been two low- quality randomized clinical trials with high risk of bias that found a lower incidence
of delirium in patients who received regional anesthesia
for lower- extremity surgeries,61 and a Cochrane review did
suggest that regional anesthesia may decrease postoperative confusion in hip surgery patients.62 Alarge prospective
study of elderly hip surgery patients, however, did not nd
an increased risk of postoperative delirium with general
anesthesia versus regional anesthesia, and a neither did a
more recent meta- analysis.63 Spinal anesthesia with lighter
sedation versus deeper sedation for hip surgery has been
studied in elderly patients and did show a decrease in the
incidence of postoperative delirium in patients receiving
lighter sedation.
64
1. Is the anesthetic plan acceptable? Would you change to
a spinal anesthetic technique with low- dose sedation?
What is your analgesic plan if using general anesthesia?
What is your analgesic plan if using spinal anesthesia?
2. e case goes without any complications under general
anesthesia with an endotracheal tube. What are the
patient’s risk factors for postoperative delirium? What
would you be looking for in the PACU to make the
diagnosis? Is there anything you would do to try and
prevent postoperative delirium?
3. e patient wakes up and is unable to follow commands
to verbal stimuli. What validated tools can you use to
help you make a delirium diagnosis? ese tools are
used, and it is deemed that this patient is experiencing
postoperative delirium. What can you do to treat this
diagnosis?
4. e patient starts to pick at his IV and is tachypneic
and tachycardic. Can this be secondary to his delirium?
What would be your treatment plan? Should you
inform the surgeons of this diagnosis and his condition?
Despite these limitations, the clinical guidelines for
postoperative delirium prevention in the elderly state that
regional anesthesia can improve pain control and help pre-
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nonopioid alternatives to manage postoperative pain to
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