Selasa, 2008 Juni 24

DELIRIUM

Delirium

A. Pendahuluan
Delirium sering terjadi, kadang-kadang tidak dikenali, suatu sindrom pada 30% pasien yang
dirawat rumah sakit, dengan risiko besar pada usia tua. Delirium mungkin bisa sebagai diagnosis
atau komplikasi perawatan di rumah sakit untuk berbagai kondisi. Dalam DSM-IV terdapat daftar
kriteria untuk diagnosis delirium (Acute confusional state). Hal ini penting untuk mengenali dan
merawat pasien secara tepat, karena para pasien yang dirawat di rumah sakit mempunyai resiko
untuk terjadi komplikasi, seperti dehidrasi, malnutrisi, aspirasi, ulkus, jatuh, dan perawatan di
rumah sakit yang lebih lama. Tingkat mortalitas jugs tinggi (kira-kira 8%), yang berhubungan
dengan kondisi medis yang mendaasarinya.

B. Sub tipe Klinis

Delirium dapat dibagi menjadi sub tipe hiperaktif dan hipoaktif, tergantung dari aktivitas
psikomotornya. Keduanya dapat terjadi bersamaan pada satu individu.
a. Delirium hiperaktif
Delirium hiperaktif merupakan delirium yang paling sering terjadi. Pada pasien terjadi agitasi,
psikosis, labilitas mood, penolakan untuk terapi medis, dan tindakan dispruptif lainnya. Kadang
diperlukan pengawas karena pasien mungkin mencabut selang infus atau kathether, atau mencoba
pergi dari tempat tidur. Pasien delirium karena intoksikasi, obat antikolinergik, dan alkohol
withdrawal biasanya menunjukkan perilaku tersebut.
b. Delirium hipoaktif
Adalah bentuk delirium yang paling sering, tapi sedikit dikenali oleh para klinisi. Pasien tampak
bingung, lethargia, dan malas. Hal itu mungkin sulit dibedakan dengan keadaan fatigue dan
somnolen, bedanya pasien akan dengan mudah dibangunkan dan dalam berada dalam tingkat
kesadaran yang normal. Rangsang yang kuat diperlukan untuk membangunkan , biasanya bangun
tidak komplet dan transient. Penyakit yang mendasari adalah metabolit dan enchepalopati.

C. Patofisiologi
Patofisiologi dari delirium belum bisa diterangkan secara jelas. Delirium dianggap sebagai
kelainaan umum otak, yaitu metabolism dan neurotransmitter (disfungsi bihemisferik). Beberapa
jalur spesifik neural juga dianggap sebagai penyebab delirium, hal ini diketahui dengan adanya
beberapa obat yang yang bekerja pada jalur spesifik neural (misalnya antikolinergik) dapat memicu
terjadinya delirium.

D. Diagnosis banding
Delirium harus dibedakan dengan kelainan kognitif global.
Tabel 1. Kriteria DSM-IV untuk delirium
Gangguan kesadaran
Penurunan derajat kewaspadaan
Tidak bisa memusatkan perhatian
Tidak bisa menggeser perhatian
Gangguan kognitif
Defisit memori
Disorientasi
Gangguan bahasa
Berkembang dalam waktu pendek
Jam dan hari
Fluktuatif, sundowning
Hal-hal tersebut di atas berubah berdasar kondisi medik, intoksikasi, dan atau pengobatan
a. Demensia
Demensia berbeda karena onsetnya adalah gradual (biasanya tahun), dan persisten. Demensia
tidak menyebabkan penurunan kewaspadaan sampai late stages (dapat diketahui dari anamnesa).
Pasien dengan dengan demensia mudah menjadi delirium, walaupun demikian, kondisi akut pada
pasien demensia bisa delirium atau kondisi akut lainnya. Demensia lewy bodies bisa disertai
dengan halusinasi dan psikosis.
b. Depresi
Depresi bisa terjadi mimic hypoactive deliriumdengan penolakan yang jelas, retardasi psikomotor,
melambatnya pembicaraan, apatis, dan pseudodemensia. Depresi tidak mempengaruhi derajat
kesadaran.
c. Psikosis
Psikosis bisa terjadi mimic hyperactive delirium. Psikosis fungsoinal berbeda karena halusinasi
suara. Lebih banyak khayalan, dan lebih sedikit fluktuatif.
d. CVA
CVA jarang disertai dengan delitium, atau salah dianggap sebagai delirium. Contohnya, aphasia
mungkin salah dianggap sebagai kebingungan. Juga kelainan difus pada atensi karena stroke
pada daerah temporooccipital, parietal, prefrontal, atau region sub kortikal pada hemisfer kanan.
Keadaan akut mungkin memperburuk tanda neurologis fokal karena CVA lama.

E. Gejala klinis
a. Gangguan tingkat kesadaran
Adalah diagnostik karakteristik dari delirium. Pasien mungkin terjadi penurunan kewaspadaan dan
kesukaran untuk berkonsentrasi. Kemampuan untuk menjaga dan memusatkan perhatian secara
tepat dipengaruhi juga, sehingga pasien menjadi mudah dikacaukan dan tidak bisa mengindahkan
rangsang.
b. Gangguan kognitif
Manifestasi dengan gangguan memori (bermasalah pada register dan proses dari informasi) dan
gangguan fungsi eksekutif. Pasien mempunyai kesulitan dalam merencanakan tugas dan
mengatasi masalah.
c. Gangguan persepsi dan sensori
Sering terjadi pada pasien muda. Bisa terjadi pada bentuk hiperaktif dan hipoaktif. Halusinasi yang
terjadi biasan ya visual ( berbeda dengan halusinasi suara byang sering terjadi pada skizofrenia.
Paranoid dan khayalan penyiksaan mungkin terjadi.

d. Gejala somatik
Predominan pada pasien tua. Termasuk inkontinensia urin, gangguan gait, tremor, gangguan
bahasa, (reseptif atau ekspresif aphasia), dan gangguan tidur (pembalikan pola tidur, tidur ringkas,
dan terpotong-potong)
e. Tanda neurologis fokal
Mungkin muncul, tapi dengan gangguan CNS. Tanda fokal diasosiasikan dengan CVA lama atau
kondisi akut
f. Gangguan emosi
Mungkin terjadi labilitas mood dan depresi

F. Faktor resiko
Faktor resiko pada perkembangan demensia termasuk ketuaan dan demensia. Etiologi (Tabel 2)
juga bisa disebut faktor resiko
Tabel 2. Etiologi Delirium
Infeksi : UTI, pneumonia
Obat : antikolinergik (antihistamin, klonidin, antidepressant trisiklik), narkotika (meperidin),
benzodiazepine, H2 Bloker, steroid, teofilin, digoksin, ati parkinson, sindrom neuroleptik maligna
Withdrawal : etanol, narkotika, benzodiazepine
Abnormalitas elektrolit : terutama hiper dan hiponatremia serta hiperkalsemia, tapi bisa juga pada
koreksi berlebihan dan cepat pada hiper dan hipotonus yang menghasilkan edma serebri dan
myelonisis pontin
Post operasi : analgesi, hipotensi, anesthesia, gangguan cairan dan elektrolit
Gangguan metabolit : uremia, ensefalopati portosistemik, defisiensi vitamin B12, sindrom
Wernicke-Korsakoff, hiper atau hipoglikemia, hiper atau hipotiroid, hipoksia, hiperkapnea
CNS : CVA, vaskulitis, hematoma suddural, neoplasma (primer atau metastase), meningitis,
ensefalitis, neurosifilis, hipotensi relative
Lingkungan : hipertermia, hipotermia, trauma, luka bakar, fraktur

G. Diagnosis
a. Anamnesa
Anamnesis menjadi sulit pada pasien delirium. Pasien biasanya bingung dan tidak bisa bercerita,
mereka sepertinya tidak mengenali masalah yang terjadi. Bisa dilakukann allow anamnesis pada
keluarga dan teman dekat dan anamnesis harus focus pada poin-poin tertentu (Tabel 3)
b. Pemeriksaan fisik
Berguna untuk mengetahui adanya penyebab atau adanya tanda neurologis fokal. Confussion
Association Method (CAM)menyediakan alat untuk menilai pasien delirium.
c. Riwayat penyakit dahulu
Status mental dasar ( adakah penurunan kognisi progresif seperti demensia?)
Riwayat delirium
Riwayat cedera kepala atau terjatuh
Obat – obatan
Alkolhol
Tanda vital mungkin mendasari masalah. Pada pemeriksaan fisik cari tanda – tanda infeksi,
dehidrasi dan cedera kepala. Nilai adakah retensi urin atau feses.
Short blessed test digunakan untuk mengetahui disfungsi kognisi dimana score lebih dari 8
abnormal.
Pemeriksaan passif pada perilaku pasien yang penting ditanyakan :
Aktivitas motorik : adakah aktivitas yang berlebihan misalnya mengamuk atau adakah aktivitas
yang menurun ( retardasi psikomotorik? ).
Kesadaran : apakah pasien letargi, sejauh mana rangsangan yang dibutuhkan untuk
menyadarkan pasien, berapa lama ?
 Perhatian : dapatkah pasien mengalihkan perhatiannya ke rangsangan yang baru?
Kemampuan berbicara : apakah pasien merasa curiga atau delusi?
d. Etiologi
Penyebab utama dari delirium diantaranya infeksi saluran
kemih,pneumonia,obstipasi,hipoksia,hiptensi relatif, obat-obatan khususnya antikolinergik tapi
meskipun demikian terdapat multifaktor yang mendasari etiloginya.
e. Pemeriksaan laboratorium
Termasuk didalamnya pemeriksan elektrolit ( Ca dan BUN/Cr ), LFT dan CBC.rontgent torax untuk
menyingkirkan pneumonia bila perlu. AGD,EKG,kadar alkohol dan screening toksikologi.
f. Pemeriksaan neuroimaging
CT kepala non kontras harus dilakukan bila terdapat defisit neurologi fokal atau bila ada riwayat
trauma untuk menyingkirkan SAH. MRI diindikasikan untuk mengevaluasi stroke akut.
g. Lumbal punctie
Lumbal punctie untuk menyingkirkan meningoencephalitis diindikasikan untuk pasien dengan
perubahan status mental yang tidak dapat dijelaskan. Misalnya,bila ditemukan demam,leukositosis
atau tanda – tanda sepsis lainnya tapi belum ditemukan sumber infeksi.
h. EEG
Tidak dilakukan secara rutin. Yang ditemukan dari derilium biasanya tidak spesifik, aktivitas
gelombang yang lambat dan difus.

H. PENATALAKSANAAN
a. Perawatan
Perawatan supportif sampai penyebab utamanya diketahui.
Pengobatan sebelumnya : menghentikan pengobatan yang mungkin memperburuk delirium.
Rawat bersama bagian geriatri.
Tingkatkan keamanan sekitar dari jatuh.
Kurangi aktivitas fisik berlebihan.
Hindari tidur yang tidak nyenyak.
Sediakan keluarga untuk merawat pasien.
Nilai sensoriknya :
1. Hindari rangsangan ekstrim.
2. Hindari dua pasien delirium pada ruang yang sama.
3. sediakan alat bantu pendengaran dan penglihatan.
4. Gunakan jendela untuk orientasi pasien siang atau malam.
5. Apakah pasien kesakitan?
b. Terapi medikamentosa
Tidak semua delirium membutuhkan terapi medicamentosa yang spesifik.pengobatan hanya
diindikasikan untuk gangguan perilaku yang membahayakan.
Neuroleptic agent, berguna bagi pasien hiperaktif yang membahayakan dirinya atau paramedis.
Obat ini mempunyai efek minimal pada tekanan darah dan pernapasan jangan diberikan pada
pasien parkinsonisme. Memungkinkan adanya reaksi berkebalikan termasuk
distonia,akatisia,katatonia,diskinesiatardife dan sindrom neurolleptic malignant.
Haloperidol, adalah drug of choice dari derilium hiperaktif dimana dosis permulaannya harus
rendah (0.5-1mg) diberikan secara parenteral. Dimana dapat dinaikkan dosisnya dua kali sampai
deriliumnya terkontrol. Sesuai dengan keadaan pasien dapat diberikan dolsis ulangan 4-8 jam.
Untuk konversi beri 50-100% dari dosis parenteral yang dibutuhkan dalam 24 jam terbagi.
Benzodiazepine kerja menengah, sebagai pengganti antipsikotik agent diindikasikan untuk agitasi
yang berat,insomnia dan withdrawl sindrom. Kerja benzodiazepine onsetnya bisa lebih cepat
dibanding antipsikotik bila diberikan secara parenteral tapi mengakibatkan sedasi dan depresi
nafas. Beberapa pasien dengan delirium dapat mengalami peningkatan paradoksal agitasi ketika
diberikan golongan benzodiazepin. Agen dengan intermediet acting lebih dipilih, misalnya
lorazepam (activan), karena short-acting agent beresiko terjadinya agitasi paradoksal setelah obat
dihentikan. Inisial dosis untuk pasien geriatri adalah 0.5-2 mg lorazepam per oral. Efek samping
obat berupa depresi, hipotensi, dam delirium.
Kontrol nyeri pada pasien delirium merupakan persoalan suatu managemen yang sulit. Walaupun
nyeri bisa merupakan salah satu penyebab delirium, sedangkan analgesik opioid sebagai obat
yang sering digunakan, justru dapat menyebabkan perburukan keadaan. Terapi yang paling sesuai
adalah menggunakan agen non narkotik sebagai terapi inisial; apabila terapi tersebut tidak
berhasil, maka hendaknya dicoba agen short-acting misalnya fentanyl dan pantau keadaan pasien
dengan ketat.

I. Perjalanan klinis dan pemantauan pasien

Perjalanan klinis delirium sangat bervariasi dan bergantung kepada etiologi yang mendasarinya.
Perjalanan klinis cenderung untuk fluktuatif dalam jam dan hari; derajat keparahan dan menifestasi
klinisnya mempunyai banyak perbedaan pada waktu yang berbeda. Walaupun gejala dan
tanda`klinis yang ada harus diterapi bersamaan dengan sebab yang mendasari, namun gejala dan
tanda bisa menetap untuk beberapa minggu dan bahkan beberapa bulan setelah kejadian. Pasien
harus dimonitor sampai 3 – 6 bulan pasca kejadian delirium untuk memastikan keadaan perbaikan.
J. Kesimpulan
- Delirium adalah kondisi yang banyak ditemukan dan serius pada pasien geriatri dengan angka
mortalitas yang tinggi.
- Delirium didefinisikan sebagai gangguan kognisi dan kesadaran, fluktuatif, dan mempunyai satu
atau lebih presipitan.
- Delirium dapat hiperaktif atau hipoaktif. Hipoaktif delirium lebih sulit untuk dikenali.
- Pengobatan primer untuk delirium adalah terapi suportif ketika underlying disease telah diketahui
dan teratasi.
- Harus dilakukan review medikasi pasien untuk mengetahui hal-hal yang mempengaruhi delirium;
dan harus berhati-hati ketika dilakukan perubahan medikasi.
- Pemeriksaan fisik yang berlebihan dan sering, dapat berakibat cedera iatrogenik dan harus
dihindari.
- Intrvensi farmakologi dengan neuroleptik atau benzodiazepin harus diresepkan untuk
penggunaan jangka pendek, hal tersebut dilakukan untuk menghindari spesifik disruptif atau
kebiasaan yang berbahaya.

Background

Delirium or acute confusional state is a transient global disorder of cognition. The condition is a
medical emergency associated with increased morbidity and mortality rates. Early diagnosis and
resolution of symptoms are correlated with the most favorable outcomes. Therefore, it must be
treated as a medical emergency.

Delirium is not a disease but a syndrome with multiple causes that result in a similar constellation
of symptoms. Delirium is defined as a transient, usually reversible, cause of cerebral dysfunction
and manifests clinically with a wide range of neuropsychiatric abnormalities. The clinical hallmarks
are decreased attention span and a waxing and waning type of confusion.

Delirium often is unrecognized or misdiagnosed and commonly is mistaken for dementia,

depression, mania, an acute schizophrenic reaction, or part of old age (patients who are elderly are
expected to become confused in the hospital).

The word delirium is derived from the Latin term meaning "off the track." This syndrome was
reported during Hippocrates' time, and, in 1813, Sutton described delirium tremens. Later,
Wernicke described the encephalopathy that bears his name.

Pathophysiology

Based on the state of arousal, 3 types of delirium are described. Hyperactive delirium is observed
in patients in a state of alcohol withdrawal or intoxication with to phencyclidine (PCP),
amphetamine, and lysergic acid diethylamide (LSD). Hypoactive delirium is observed in patients in
states of hepatic encephalopathy and hypercapnia. In mixed delirium, individuals display daytime
sedation with nocturnal agitation and behavioral problems.

The mechanism of delirium still is not fully understood. Delirium results from a wide variety of
structural or physiological insults. The neuropathogenesis of delirium has been studied in patients
with hepatic encephalopathy and alcohol withdrawal. Research in these areas still is limited. The
main hypothesis is reversible impairment of cerebral oxidative metabolism and multiple
neurotransmitter abnormalities. The following observations support the hypothesis of multiple
neurotransmitter abnormalities.

Acetylcholine

Data from animal and clinical studies support the hypothesis that acetylcholine is one of the critical
neurotransmitters in the pathogenesis of delirium. 1 Clinically, good reasons support this hypothesis.
Anticholinergic medications are a well-known cause of acute confusional states, and patients with
impaired cholinergic transmission, such those with Alzheimer disease, are particularly susceptible.
In patients with postoperative delirium, serum anticholinergic activity is increased.

Dopamine

In the brain, a reciprocal relationship exists between cholinergic and dopaminergic activities. In
delirium, an excess of dopaminergic activity occurs. Symptomatic relief occurs with antipsychotic
medications such as haloperidol and other neuroleptic dopamine blockers.

Other neurotransmitters
Serotonin: Human and animal studies have found that serotonin is increased in patients with
hepatic encephalopathy and septic delirium. Hallucinogens such as LSD act as agonists at the site
of serotonin receptors. Serotoninergic agents also can cause delirium.

Gamma-aminobutyric acid (GABA): In patients with hepatic encephalopathy, increased inhibitory

GABA levels also are observed. An increase in ammonia levels occurs in patients with hepatic
encephalopathy, which causes an increase in the amino acids glutamate and glutamine, which are
precursors to GABA. Decreases in CNS GABA levels are observed in patients with delirium
resulting from benzodiazepine and alcohol withdrawal.

Cortisol and beta-endorphins: Delirium has been associated with the disruption of cortisol and
beta-endorphin circadian rhythms. This mechanism has been suggested as a possible explanation
for delirium caused by exogenous glucocorticoids.

Inflammatory mechanism

Recent studies have suggested a role for cytokines, such as interleukin-1 and interleukin-6, in the
pathogenesis of delirium. Following a wide range of infectious, inflammatory, and toxic insults,
endogenous pyrogen, such as interleukin-1, is released from the cells. Head trauma and ischemia,
which frequently are associated with delirium, are characterized by brain responses that are
mediated by interleukin-1 and interleukin-6.

Stress reaction mechanism

Studies indicate psychosocial stress and sleep deprivation facilitate the onset of delirium.

Structural mechanism

The specific neuronal pathways that cause delirium are unknown. Imaging studies of metabolic
(eg, hepatic encephalopathy) and structural (eg, traumatic brain injury, stroke) factors support the
hypothesis that certain anatomical pathways may play a more important role than others. The
reticular formation and its connections are the main sites of arousal and attention. The dorsal
tegmental pathway projecting from the mesencephalic reticular formation to the tectum and the
thalamus is involved in delirium.

Disrupted blood-brain barrier can allow neurotoxic agents and inflammatory cytokines to enter the
brain and may cause delirium. Contrast-enhanced MRI can be used to assess the blood-brain
barrier.2, 3

History

The diagnosis of delirium is clinical. No single test is successful. Obtaining a thorough history is
essential.
 Because delirious patients often are confused and unable to provide accurate information,
getting a detailed history from family, caregivers, and nursing staff is particularly important.
Nursing notes can be very helpful for documentation of episodes of disorientation,
abnormal behavior, and hallucinations. Learning to record accurate and specific findings in
mental status as well as the particular time the finding was observed is imperative for the
staff. Staff should not just report "he was confused."
 Delirium always should be suspected when an acute or subacute deterioration in behavior,
cognition, or function occurs, especially in patients who are elderly, demented, or
depressed.
 Patients may have visual hallucinations or persecutory delusions as well as grandiose
delusions.
 Some patients with delirium also may become suicidal or homicidal. Therefore, they should
not be left unattended or alone.
 Delirium is mistaken for dementia or depression, especially when patients are quiet or
withdrawn. However, by Diagnostic and Statistical Manual of Mental Disorders, Fourth
Edition, Text Revision (DSM-IV-TR) criteria, dementia cannot be diagnosed with certainty
when delirium is present. Health professionals can do Mini-Mental Status Exam (MMSE)7,
depression assessment screening using DSM-IV-TR criteria8, or the Geriatric Depression
Scale (GDS)9. They can also assess for suicidal and homicidal risk if necessary. Health
professionals can directly ask patients about suicidal or homicidal ideation (thoughts),
intent, and plan.
 Depression symptoms are commonly seen with delirium. In a recent study, patients having
symptoms of dysphoric mood and hopelessness are at risk for incident delirium while in
the hospital.10 On the other hand, hypoactive delirium may be mistaken for depression. Up
to 42% of patients referred to psychiatry services for suspected depressive illness in the
hospital may have delirium.11 Screening for depression in the presence of delirium is quite
challenging.
 Delirium is a common cause for psychotic symptoms, bizarre delusions, abnormal
behavior, and thought disorders. Agitated patients are at risk for violent and abnormal
behavior and in rare circumstances, agitation can lead to attempts of homicide.
 The mental status is a bedside or interview assessment that dramatically fluctuates.
It includes the patient's appearance, affect (mood), thoughts (especially the presence of
hallucinations and delusions), inquiry into self-destructive behavior, homicidal behavior,
judgment and, in this diagnosis, orientation, immediate, recent, and long-term memory.
 Main symptoms

o Clouding of consciousness
o Difficulty maintaining or shifting attention
o Disorientation
o Illusions
o Hallucinations
o Fluctuating levels of consciousness
 Symptoms tend to fluctuate over the course of the day, with some improvement in the
daytime and maximum disturbance at night. Reversal of the sleep-wake cycle is common.
 Neurological symptoms

 o Dysphasia
o Dysarthria
o Tremor
o Asterixis in hepatic encephalopathy and uremia
o Motor abnormalities
 Patients with delirium who are hyperactive have an increased state of arousal,
psychomotor abnormalities, and hypervigilance. In contrast, patients with delirium who are
hypoactive are withdrawn, less active, and sleepy.
 Hypoactive delirium sometimes is misdiagnosed as dementia or depression. Mixed states
also occur.
 In patients who are elderly, delirium often is the presenting symptom of an underlying
illness.

Physical

 A careful and complete physical examination including a mental status examination is

necessary. Testing vital signs such as temperature, pulse, blood pressure, and respiration
is mandatory.
o Patients have difficulty sustaining attention, problems in orientation and short-term
memory, poor insight, and impaired judgment. Key elements here are fluctuating
levels of consciousness.
o Impaired attention can be assessed with bedside tests that require sustained
attention to a task that has not been memorized, such as reciting the days of the
week or months of the year backwards, counting backwards from 20, or doing
serial subtraction.
 DSM-IV-TR8 diagnostic criteria for delirium
o Disturbance of consciousness (ie, reduced clarity of awareness of the
environment) occurs, with reduced ability to focus, sustain, or shift attention.
o Change in cognition (eg, memory deficit, disorientation, language disturbance,
perceptual disturbance) occurs that is not better accounted for by a preexisting,
established, or evolving dementia.
o The disturbance develops over a short period (usually hours to days) and tends to
fluctuate during the course of the day.
o Evidence from the history, physical examination, or laboratory findings is present
that indicates the disturbance is caused by a direct physiologic consequence of a
general medical condition, an intoxicating substance, medication use, or more
than one cause.
 Other diagnostic instruments are the Delirium Symptom Interview (DSI) and the Confusion
Assessment Method (CAM).12
 Delirium symptom severity can be assessed by the Delirium Rating Scale (DRS) and the
Memorial Delirium Assessment Scale (MDAS).
 Table 1. Differentiating Features of Delirium and Dementia
Features Delirium Dementia

Onset Acute Insidious

 Course Fluctuating Progressive

Duration Days to weeks Months to years

Consciousness Altered Clear

Attention Impaired Normal, except for severe dementia

Psychomotor changes Increased or decreased Often normal

Reversibility Usually Rarely

 To make an accurate diagnosis, periodic application of diagnostic criteria such as CAM or
DSM-IV criteria and knowledge of the patient's baseline mental status is imperative.
 A simple cognitive test like the Mini-Cog can be a predictor of inhospital delirium. At the
time of admission to the hospital, if the elderly patient does not have a history of dementia
or cognitive impairment, the Mini-Cog can be used to identify patients at high risk for
inhospital delirium.
 The Confusion Assessment Method for the Intensive Care Unit (CAM-ICU) offers the
clinician the opportunity to identify delirium in critical care patients, especially patients on
mechanical ventilation. The CAM-ICU makes use of nonverbal assessments to evaluate
the important features of delirium.
 Another instrument that can be used in ICU settings is the Intensive Care Delirium
Screening Checklist (ICDSC). The severity of delirium in the ICU can be estimated by
the Delirium Detection Scale (DDS).

Causes

Almost any medical illness, intoxication, or medication can cause delirium. Often, delirium is
multifactorial in etiology, and the physician treating the delirium should investigate each cause
contributing to it. Medications are the most common reversible cause of delirium.

 DSM-IV-TR classification of delirium

o Delirium due to general medical condition
o Substance intoxication delirium
o Substance withdrawal delirium
o Delirium due to multiple etiologies
o Delirium not otherwise specified
 Some of the other common reversible causes include the following:
o Hypoxia
o Hypoglycemia
o Hyperthermia
o Anticholinergic delirium
o Alcohol or sedative withdrawal
 Other causes of delirium include the following:
o Infections
 o Metabolic abnormalities
o Structural lesions of the brain
o Postoperative states
o Miscellaneous causes, such as sensory deprivation, sleep deprivation, fecal
impaction, urinary retention, and change of environment
 In persons who are elderly, medications at therapeutic doses and levels can cause
delirium.
 Although numerous risk factors have been described, a recent study identified 5 important
independent risk factors.
o Use of physical restraints
o Malnutrition
o Use of a bladder catheter
o Any iatrogenic event
o Use of 3 or more medications
 Dementia is one of the strongest most consistent risk factors. Underlying dementia is
observed in 25-50% of patients. The presence of dementia increases the risk of delirium 2-
3 times. Low educational level, which may be an indicator of low cognitive reserve, is
associated with increased vulnerability to delirium.
 Dysphoric mood and hopelessness are also risk factors for incident delirium.
 Structural changes
o Closed head injury or cerebral hemorrhage
o Cerebrovascular accidents, such as cerebral infarction, subarachnoid
hemorrhage, and hypertensive encephalopathy
o Primary or metastatic brain tumors
o Brain abscess
 Metabolic causes
o Fluid and electrolyte abnormalities, acid-base disturbances, and hypoxia
o Hypoglycemia
o Hepatic or renal failure
o Vitamin deficiency states (especially thiamine and cyanocobalamin)
o Endocrinopathies associated with the thyroid and parathyroid
 Hypoperfusion states
o Shock
o Congestive heart failure
o Cardiac arrhythmias
o Anemias
 Infectious causes
o CNS infections such as meningitis
o Encephalitis
o HIV-related brain infections
o Septicemia
o Pneumonia
o Urinary tract infections
 Toxic causes
o Substance intoxication - Alcohol, heroin, cannabis, PCP, and LSD
o Medication-induced delirium
  Anticholinergics (Benadryl, tricyclic antidepressants)
 Narcotics (meperidine)
 Sedative hypnotics (benzodiazepines)
 Histamine-2 (H2) blockers (cimetidine)
 Corticosteroids
 Centrally acting antihypertensives (methyldopa, reserpine)
 Anti-Parkinson drugs (levodopa)
o Substance withdrawal from alcohol, opioids, and benzodiazepines
 Other causes
o Postictal state
o Unfamiliar environment
 Operation-related delirium
o Preoperative (dementia, polypharmacy, drug withdrawal, fluid and electrolyte
imbalance)
o Intraoperative (meperidine, long-acting benzodiazepines, anticholinergics such as
atropine; however, medications such as glycopyrrolate can be used because, in
contrast to atropine, they do not cross the blood brain barrier)
o Postoperative (hypoxia, hypotension)
o Drugs are a common risk factor for delirium, and drug-induced delirium is
commonly seen in medical practice, especially in hospital settings. The risk of
anticholinergic toxicity is greater in elderly persons, and the risk of inducing
delirium by medications is high in frail, elderly persons and in those with dementia.

Other Problems to be Considered

Dementia
AIDS-related complex
Psychosis

Dementia is one of the most important risk factors for delirium. It often coexists in patients who are
hospitalized. Delirium may be a risk factor or marker for the development of dementia. The safest
rule is to consider delirium when recent changes in an elderly patient's level of consciousness and
cognition have occurred in an acute setting.

Patients with hypoactive withdrawn delirium may be misdiagnosed as depressed. Depressed

patients also may have cognitive symptoms, but the patient's level of consciousness is normal.

Delirium may have to be differentiated from psychosis because both have psychotic features. In
delirium, the patient usually does not have a previous history of serious psychiatric illness. The
onset of symptoms of delirium is acute or subacute, the hallucinations predominantly are visual and
fluctuate, and the patient has impaired memory and orientation and clouding of consciousness

Lab Studies
  Complete blood cell count with differential - Helpful to diagnose infection and anemia
 Electrolytes - To diagnose low or high levels
 Glucose - To diagnose hypoglycemia, diabetic ketoacidosis, and hyperosmolar nonketotic
states
 Renal and liver function tests - To diagnose liver and renal failure
 Thyroid function studies - To diagnose hypothyroidism
 Urine analysis - Used to diagnose urinary tract infection
 Urine and blood drug screen - Used to diagnose toxicological causes
 Thiamine and vitamin B-12 levels - Used to detect deficiency states of these vitamins
 Tests for bacteriological and viral etiologies - To diagnose infection
 Sedimentation rate
 Drug screen including alcohol level
 HIV tests
 Tests for other infectious causes if necessary or clinically indicated (These tests are not
performed routinely, even though 30-40% of hospitalized patients with HIV infection
develop delirium during hospitalization. 13)

Imaging Studies

 Neuroimaging
o Perform CT scan of the head.
o Magnetic resonance imaging (MRI) of the head may be helpful in the diagnosis of
stroke, hemorrhage, and structural lesions.
 Electroencephalogram
o In delirium, generally, slowing of the posterior dominant rhythm and increased
generalized slow-wave activity are observed on electroencephalogram (EEG)
recordings.
o In delirium resulting from alcohol/sedative withdrawal, increased EEG fast-wave
activity occurs.
o In patients with hepatic encephalopathy, diffuse EEG slowing occurs.
o The type of patterns observed includes triphasic waves in toxicity or metabolic
derangement, continuous discharges in nonconvulsive status epilepticus, and
localized delta activity in focal lesions.
 Chest x-ray is used to diagnose pneumonia or congestive heart failure.

Other Tests

 Lumbar puncture is indicated when CNS infection is suspected as a cause of delirium or

when the source for the systemic infection cannot be determined.
 Pulse oximetry is used to diagnose hypoxia as a cause of delirium.
 Electrocardiogram is used to diagnose ischemic and arrhythmic causes.

Medical Care
When delirium is diagnosed or suspected, the underlying causes should be sought. Despite every
effort, no cause for delirium can be found in approximately 16% of patients. Components of
delirium management include supportive therapy and pharmacological management.

 Fluid and nutrition

o These should be given carefully because the patient may be unwilling or physically
unable to maintain a balanced intake.
o For the patient suspected of having alcohol toxicity or alcohol withdrawal, therapy
should include multivitamins, especially thiamine.
 Environmental modifications
o Reorientation techniques or memory cues such as a calendar, clocks, and family
photos may be helpful.
o The environment should be stable, quiet, and well-lighted. Support from a familiar
nurse and family should be encouraged.
o Family members and staff should explain proceedings at every opportunity,
reinforce orientation, and reassure the patient.
o Sensory deficits should be corrected, if necessary, with eyeglasses and hearing
aids.
o Physical restraints should be avoided. Delirious patients may pull out intravenous
lines, climb out of bed, and may not be compliant. Perceptual problems lead to
agitation, fear, combative behavior, and wandering. Severely delirious patients
benefit from constant observation (sitters), which may be cost effective for these
patients and help avoid the use of physical restraints.
o These patients should never be left alone or unattended.

Consultations

Psychiatric consultation may be indicated for management of behavioral problems such as

agitation or aggressive behavior.

Delirium that causes injury to the patient or others should be treated with medications. The most
common medications used are neuroleptics. Benzodiazepines often are used for withdrawal states.

Drug Category: Neuroleptics

The medication of choice in the treatment of psychotic symptoms. Older neuroleptics

such as haloperidol, a high-potency antipsychotic, are useful but have many adverse
neurological effects. Newer neuroleptics such as risperidone, olanzapine, and quetiapine
relieve symptoms while minimizing adverse effects. Initial doses may need to be higher
than maintenance doses. Use lower doses in patients who are elderly. Discontinue these
medications as soon as possible. Attempt a trial of tapering the medication once
symptoms are in control. Neuroleptics can be associated with adverse neurological effects
such as extrapyramidal symptoms, neuroleptic malignant syndrome, and tardive
dyskinesia. Doses should be kept as low as possible to minimize adverse effects.
Paradoxical and hypersensitivity reactions may occur.
 Drug Name Haloperidol (Haldol)
A butyrophenone high-potency antipsychotic. One of
most effective antipsychotics for delirium. High-
Description potency antipsychotic medications also cause less
sedation than phenothiazines and reduce risks of
exacerbating delirium.
Moderate symptomatology: 0.5-2 mg PO bid/tid
Severe symptomatology: 3-5 mg PO bid/tid
Adult Dose
Geriatric and debilitated: 0.5-2 mg PO bid/tid; 2-5
mg IM q4-8h
3-12 years: 0.05 mg/kg/d or 0.25-0.5 mg/d PO
bid/tid initially and increase by 0.25-0.5 mg q5-7d
Maintenance dose: 0.05-0.15 mg/kg/d PO in 2-3
divided doses; not to exceed 0.15 mg/kg/d
Pediatric Dose
6-12 years: 1-3 mg/dose IM q4-8h, not to exceed
0.15 mg/kg/d; change to PO therapy as soon as
possible
>12 years: Administer as in adults
Documented hypersensitivity, Parkinson disease,
Contraindications
severe depression, comatose states
May increase tricyclic antidepressant serum
concentrations and hypotensive action of
antihypertensive agents; rifampin, phenobarbital,
and carbamazepine may decrease effects;
Interactions coadministration with anticholinergics may increase
intraocular pressure; encephalopathiclike syndrome
is associated with concurrent administration with
lithium; Haldol can potentiate CNS depressant
effects of alcohol, opiates, and anesthetics
C - Fetal risk revealed in studies in animals but not
Pregnancy established or not studied in humans; may use if
benefits outweigh risk to fetus
Monitor for extrapyramidal symptoms (reduce dose
if these occur); avoid anticholinergics; severe
neurotoxicity manifesting as rigidity or inability to
walk or talk may occur in patients with thyrotoxicosis
also receiving antipsychotics; if IV/IM, watch for
Precautions
hypotension; caution in diagnosed CNS depression
or cardiac disease; if history of seizures, benefits
must outweigh risks; significant increase in body
temperature may indicate intolerance to
antipsychotics (discontinue if it occurs)
Drug Name Risperidone (Risperdal)
 A newer antipsychotic with fewer extrapyramidal
adverse effects than Haldol. Binds to dopamine D2-
receptor with 20 times lower affinity than for 5-HT2-
Description
receptor. Improves negative symptoms of
psychoses and reduces incidence of adverse
extrapyramidal effects.
0.5-2 mg PO qd or bid
0.5 mg PO bid for elderly debilitated patients with
Adult Dose
severe renal or hepatic failure or predisposed to
hypotension
Pediatric Dose Not established
Contraindications Documented hypersensitivity
Coadministration with carbamazepine may
Interactions decrease effects; may inhibit effects of levodopa;
SSRIs and clozapine may increase levels
C - Fetal risk revealed in studies in animals but not
Pregnancy established or not studied in humans; may use if
benefits outweigh risk to fetus
Can cause orthostatic hypotension, seizures,
hyperprolactinemia, and body temperature
regulation abnormalities; has potential for
Precautions
proarrhythmic effects by prolonging QT interval; > 2
mg/d may increase adverse extrapyramidal effects
in elderly patients

Drug Category: Short-acting sedatives

Reserved for delirium resulting from seizures or withdrawal from alcohol or sedative
hypnotics. Coadministration with neuroleptics is considered only in patients who tolerate
lower doses of either medication or have prominent anxiety or agitation. Benzodiazepines
are preferred over neuroleptics for treatment of delirium resulting from alcohol or
sedative hypnotic withdrawal. They also may be used when unknown substances may
have been ingested and may be helpful in delirium from hallucinogen, cocaine, stimulant,
or PCP toxicity. Use special precaution when using benzodiazepines because they may
cause respiratory depression, especially in patients who are elderly, those with pulmonary
problems, or debilitated patients.

Drug Name Lorazepam (Ativan)

Description Preferable because it is short acting and has no
active metabolites. In addition, can be used in both
IM and IV forms. When patient needs to be sedated
for longer than 24 h, this medication is excellent.
Commonly used prophylactically to prevent delirium
 tremens.
0.5-2 mg PO/IV/IM; frequent repeat dosing (q2-4h)
Adult Dose
may be needed in cases of delirium tremens
Pediatric Dose Not established
Documented hypersensitivity; preexisting CNS
depression; hypotension; narrow-angle glaucoma;
Contraindications
sleep apnea syndrome; severe respiratory
insufficiency
Toxicity of benzodiazepines in CNS increases when
Interactions used concurrently with alcohol, phenothiazines,
barbiturates, and MAOIs
D - Fetal risk shown in humans; use only if benefits
Pregnancy
outweigh risk to fetus
Caution in limited pulmonary reserve, patients who
are elderly, and very ill patients; can cause hypoxic
Precautions cardiac arrest; caution also needed in patients with
myasthenia gravis, organic brain syndrome, or
Parkinson disease

Drug Category: Vitamins

Patients with alcoholism and patients with malnutrition are prone to thiamine and vitamin
B-12 deficiency, which can cause delirium.

Drug Name Thiamine hydrochloride (Thiamilate)

For alcohol withdrawal and in cases of Wernicke
Description
encephalopathy.
Adult Dose 100 mg IV initially, followed by 50-100 mg/d IV/IM
Pediatric Dose 50 mg IV initially, followed by 10-25 mg/d IV/IM
Contraindications Documented hypersensitivity
Interactions None reported
A - Fetal risk not revealed in controlled studies in
Pregnancy
humans
Sensitivity reactions can occur (intradermal test-
dose recommended in suspected sensitivity);
deaths have resulted from IV use; sudden onset or
worsening of Wernicke encephalopathy may occur
Precautions
following glucose administration in patients who are
thiamine-deficient; administer before or together
with dextrose-containing fluids in suspected
thiamine deficiency
 Drug Name Cyanocobalamin (Crystamine, Cyomin, Nascobal)
Vitamin B-12 deficiency can cause confusion or
delirium in patients who are elderly.
Deoxyadenosylcobalamin and hydroxocobalamin
are active forms of vitamin B-12 in humans.
Description Vitamin B-12 is synthesized by microbes but not
by humans or plants. Vitamin B-12 deficiency may
result from intrinsic factor deficiency (pernicious
anemia), partial or total gastrectomy, or diseases
of the distal ileum.
Maintenance dose: 1000 mcg IM monthly or 500
mcg/wk intranasally or 100 mcg/d PO
Adult Dose
Load initially if deficient (100 mcg IM injections for
1 wk, then every wk for 6 mo)
10-50 mcg/d IM for 5-10 d, followed by 100-250
Pediatric Dose
mcg/dose IM q2-4wk
Documented hypersensitivity; hereditary optic
Contraindications
nerve atrophy
Interactions None reported
C - Fetal risk revealed in studies in animals but not
Pregnancy established or not studied in humans; may use if
benefits outweigh risk to fetus
Intradermal test dose recommended before
parenteral administration (anaphylactic shock and
death reported with parenteral administration);
hypokalemia and thrombocytosis can occur upon
Precautions conversion from severe megaloblastic anemia to
normal erythropoiesis after cyanocobalamin
therapy; monitor serum potassium levels and
platelet count; vitamin B-12 therapy can unmask
polycythemia vera

Further Inpatient Care

 Carefully assess patients to determine their level of care needs. Assessment should
include behavior (24 h), daily mental status, potential for injury, and underlying medical and
metabolic status.

Further Outpatient Care

 Following recovery, patient's memories of events of the delirium are variable.

 Educate the patient, family, and primary caregivers about future risk factors.
 It is not unusual for patients who are elderly to require 6-8 weeks or longer for full recovery.
Deterrence/Prevention

 Prevention should be the goal because delirium is associated with adverse outcomes and
high health care costs.
 A multicomponent intervention study that targeted cognitive impairment, sleep deprivation,
immobility, visual impairment, hearing impairment, and dehydration showed significant
reduction in the number and duration of episodes of delirium in older patients who were
hospitalized.
 Patients who are at high risk for delirium should be monitored closely as outpatients,
during hospitalization, and throughout surgical procedures.
 Physicians should become familiar with prescribing practices for patients who are elderly,
keeping dosages low and avoiding medications that cause delirium.
 Monitoring the patient's mental status as a vital sign helps diagnose delirium early.

Complications

 Malnutrition, fluid and electrolyte abnormalities

 Aspiration pneumonia
 Pressure ulcers
 Weakness, decreased mobility, and decreased function
 Falls and combative behavior leading to injuries and fractures
 Wandering and getting lost

Prognosis

 Resolution of symptoms may take longer in patients with poor premorbid cognitive
function, incorrect or incomplete diagnosis of contributing factors, and structural brain
diseases treated with large doses of psychoactive medications prior to the onset of acute
medical illness.
 For some patients, the cognitive effects of delirium may resolve slowly or not at all