Delirium in ICU

Critical Care Asia

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A Publication of Critical Care Education Foundation

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April-Sept, 2003 Volume 1 Issue 2


. . . The First “Claris International


Critical Care



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Oration was delivered by Dr. Jamshed ; Sunavala. The Plaque and cash award of Rs. 50,000 was presented to Dr Sunavala by Mr. Sushil Honda, Chairman, Claris Lifesciences Ltd. . ..


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Critical Care Asia

2Delerium in ICU :An overview

Dr. Ashutosh B. Shah,

D.N.B. (PSY.), D.P.M (MUMBAI), M.B.B.S. (MUMBAI), PGDMLS Consultant Psychiatrist, Mumbai.


threatening situation. Delirium is often unrecognized and frequently goes untreated. This substantially increases morbidity and mortality2·’ . Advanced technology in the ICU at times appears to take priority over the functional health of the brain and the emotional trauma

• • 6,7 experiencing.


Delirium is a syndrome that has

multiple causes. Little has been achieved

to prevent it. It frequently occurs in

patients with life threatening medical /

surgical illnesses. Delirium in this

population is often unrecognized and

frequently goes untreated despite the

fact that it is a medical emergency. The

estimated prevalence of delirium in the

ICU is 15% to 40% and is increasing with

an increase in the number of elderly and

more severely ill patients being admitted

to the ICU. In this setting, delirium impaired consciousness, disordered

contributes to an increased morbidity. It is associated with a poor prognosis and the mortality rate varies between 10% to 30%. Medical management of delirium consists of diagnosing the syndrome, removing the underlying cause(s), and symptomatic/ supportive treatment.


attention and cognitive function and abnormalities of perception and affect. There may be increased or decreased psychomotor activity, and a disordered sleep-wake cycle.

Delirium has two variants: hyperactive and hypoactive. Patients with hyperactive delirium have restlessness and agitation whereas patients with the

Acute confusional slate, metabolic

encephalopathy, organic brain hypoactive variant have decreases in syndrome, ICU psychosis, consultation consciousness and psychomotor liaison psychiatry, behavioral

disturbance in ICU.


The word delirium is derived from the Latin delirare: “lo act crazy,” or “off the track”. Hippocrates, around 500 BC, first described the manifestations of delirium. Celsus probably introduced the term into the medical literature in the first century AD.’ Delirium represents a medical emergency.

Illnesses requiring admission to an ICU can be stressful enough to endanger patients’ physiological and psychological health and stability. Consequently, delirium in the ICU may incorrectly be perceived by doctors as a “normal” reaction by patients to a potentially life-

activity”. Some patients experience a mixture of hyperactive and hypgactive delirium and their emotional state may fluctuate widely in an irregular and unpredictable manner during the course of a single day.’


Delirium has been called “every man’s psychosis” to emphasize that everyone is potentially susceptible.8 The elderly and men have an increased risk of delirium, particularly after cardiac surgery.’· ‘0 The estimated prevalence of deliriumintheICUis15%to40%’·11• In this setting, delirium contributes to an increased morbidity. It is associated with a poor prognosis, and carries a mortality rate of 10%to 30%. 12• ‘ 3

critically ill patients may be

Delirium is defined as an acute, reversible syndrome manifesting with

t IaUS;

Risk Fadors General fadors

1. Dehydration

2. Advanced age

3. Chronic alcohol use

4. Liver disease

5. Fractures of major joints 6. Preoperative electrolyte


Postoperative fadors

1. Low cardiac output 2. Perioperative

hypotension 3. Postoperative



No difference between general vs. epidural

vs. spinal.

1 Ph . actori I


1. Sedatives

2. Anticholinergics 3. Corticosteroids 4. Cardiac


5. Narcotic analgesics


Hospitalization f

Delirium has a multi-factorial etiology. It is due to· the brain’s nonspecific reaction to disruption of the internal environment necessary for normal function. ‘

Environmental factors in the ICU that may induce or add to the cerebral dysfunction include sleep deprivation, sensory overload, lack of meaningful verbal or cognitive stimulation, and immobilization. ” ·” ·”

The various factors can be categorized in lo:

1. Infectious – Encephalitis, meningitis,

and syphilis

2. Withdrawal of alcohol, barbiturates,


3. Acute metabolic -Acidosis, alkalosis,

electrolyte disturbance, hepatic

failure, and renal failure

4. Trauma – Heat stroke, postoperative,

and severe burns

5. CNS pathology – Abscesses

hemorrhage, normal pressur~ hydrocephalus, seizures, stroke, tumors, vasculitis

6. Hypoxia – Anemia, carbon monoxide poisoning, hypotension, and pulmonary or cardiac failure

7. Deficiencies – Vitamin Bl 2, niacin, and thiamine

8. Endocrinopathies . Hyper- or

hypoadrenocorticism and hyper. or


9. Acute vascular – Hypertensive

encephalopathy, shock

10.Toxins or drugs – Medications,

pesticides, and solvents

11.Heavy metals – Lead, manganese,

and mercury


Optimal brain function requires

normal anatomic structures, on intact

and integrated neural pathway,

transmission of electrical impulses, and

a stable biochemical environment.

Cerebral oxidative metabolism requires

sufficient supplies of oxygen and

glucose. Neurohumoral function, which

includes circulating cortisol, growth

hormone, and dopamine and central

noradrenergic activity, must olso be ‘”

balance. Adequate cerebral blood flow . I h bainwith

~ icalcCore A_. i “SIQ

· ys1cal restraints 2. Malnutrition

3. More than three medications

4. Bladder catheter

5. Iatrogenic events


1snecessarytosuppyIe r these hormones and nutrients.”·”


. 1 cturallY

produced in the cere ra e .. d 11 Thecogn,t,ve the pons, and the me u a. nd

process takes pIace in

e c ‘d the

. d h I

the brain stem an t a amu

activating mechanism. .

sprov, e


depends on continuous .

interoc tho! prov,

between the mechanisms arousal and awarene modulated by input from the brain

l!Effllb1udlil !ID •

1s s ru

b I h mispheres,

. th erebrum, a

C0 nsciousne tion

ss on

·de d is . stef11

MW¥ &r



Critical Care Asia

ascending reticular activating system (ARAS), which has a broad connection to the cerebral hemispheres. Neurotransmitters link the brain with perception of external events and regulate higher integroted intellectual responses.1•11·20 The exact mechanism by which delirium emerges is still unclear. Some of the main pathophysiological features associated with development of cognitive dysfunction are summarized:

Known associated features

1. Widespread reduction of cerebrol oxidative mechanism

2. Neurohumoral imbolonce

3. Disruption in synaptic lronsmission

4. Damage to cell membranes

5. Reduction in CSF levels of


Possible associated features

1. Increase in circulating concentrations of cortisol, growth hormone, dopamine

2. Hyperfunction of beta-endorphins

3. Modulation of norodrenergic, dopaminergic, serotonergic



Delirium is a clinical diagnosis based primarily on the patient’s behavior. Evidence of cognitive and attentional deficits is elicited and observed at the bedside. Various mental assessment tools may assist in diagnosing delirium. These are:

1. Mini Mental Stole Examination (MMSE)

9. Reaction confusionol scale

l O. Nursing delirium roting scale 11 . Saskatoon delirium checklist 12. Confusion assessment method

Fluctuating levels of consciousness mean that individual tests provide only a reflection of the patient’s condition at any particular time. Patients may appear lucid at the time of testing, and this situation may delay the diagnosis of delirium.’.,·’ A detailed history of a patient’s pre-morbid mental state is needed in order to elucidate any new changes in the patient’s mental condition.•·• Information about the patient’s prescription and over the counter (OTC) medications is essential. 15

The best study for diagnosis of delirium is electroencephalography (EEG). EEGs of patients in delirium show diffuse slowing of background activity, indicating cerebral insufficiency. Although these changes ore not specific to delirium, they ore in general on early indicator of encephalopathy in patients with any form of cerebral metabolic change. Serial EEGs ore recommended to determine the level of change from the pre-morbid EEG. Continuous computer- processed EEG monitoring of cerebral function provides a means of assessment even in patients who ore sedated and may be useful in diagnosing delirium.” ·” Computed tomography and magnetic resonance imaging of the brain may be used to exclude cerebral pathologic changes.’

Differential Diagnosis

The differential diagnosis of delirium includes dementia, depression, and schizophrenia . Whereas dementia develops slowly and is permanent, delirium has on acute onset, and patients usually recover completely. The

2. 3. 4. 5. 6. 7. 8 .

Glasgow Coma Scale (GCS) Clinical assessment of confusion Confusion roting scale

Delirium symptom checklist Delirium roting scale

Delirium assessment scale Organic brain syndrome scale

.~llillriJJ 7P


hypoactive form of delirium may be mistaken for depression, but delirious patients have indications of disorientation not seen in depression. Acutely schizophrenic patients may appear to be confused, but on examination, they do not have cognitive deficits and most likely have auditory ratherthanvisualhallucinations.”

Clinical Manifestations

Delirium is a frightening experience, both for patients and patients’ relatives. However, because of the impairment of short-term memory in delirium, patients may have no recollection of a delirious episode once the episode has subsided .”· ” · 26 Infrequently, patients are aware that something is wrong and are afraid of “going crazy.• Patients may try to hide the change in their mental state from themselves and from others by confabulation and denial.”

The symptoms range from confusion, sleep disturbance, disorientation to time, place, person and occasionally self, memory impairment, mood and perceptual changes including fragmentary delusions and fleeting visual, auditory hallucinations.

Because of cognitive dysfunction, delirious patients may misperceive the environment as hostile or threatening. Increased psychomotor activity in hyperactive delirious patients may bring about attempts at escape that require physical or chemical restraint. Patients have an increased risk of unintentional self-harm because they may dislodge critical life-support and monitoring equipment.”·” Such unintentional self- harm may prolong the length of an ICU stay and necessitate further invasive treatment, thus adding to the list of potential complicaiions. 13 Delirious

patients may also try to assault visitors.”

Slaff and

Hypoactive delirious patient

. s usuall

are quiet, sleepy and slow in res d’ Y

h . Pan 1ng ese patients may experience .. · hII . . .h v,v,d


.d’. h Ord

a ucmat1ons wit out any autw

in 1cat1on as to t e seriousness of h condition.12 t e

Physiological arousal accompanyin delirium may include tachycard’ 9

, 10, hypertension, tachypnea, and increased

oxygen consumption. This arousal con accelerate hemodynamic and respiratory deterioration .” Agitation leading to hypermetabolism ot the muscular level contributes to metabolic acidosis, which may result in worsening organ dysfunction. Physiological arousal can then be sufficient to push an already critically ill patient “over the brink’ and result in a fatal outcome.22· ” · 2•

Medical Management

Medical management of delirium consists of diagnosing the syndrome, removing the underlying causes, and treating the signs and symptoms. Investigations include complete blood count, Serum electrolytes, random blood sugar, liver and renal functions tests, EEG, arterial blood gas analysis, urine examination. Further tests may be done as clinically indicated e.g. thyroid assay, brain imaging etc.

Doses of medications used to treat a patient’s primary condition that may be

. · hould be contributing to the deI,rium s .

Of drug15 reduced if possible. If use a d

· ilar ru9 unavoidable, a change to a s,m aY

with less risk of delirious side effects nn

be advisable. . and Adequate relief from pau,_ the anxiety must also be included ,n d

t ess an treatment. Pain causes s r


Critical Care Asia

The nursing instrudions are summarized:


Sleep Disruption Noise



Support Systems


Nursing Implication

Dimming of lights at night.

decreases total sleep time and quality

0.25 mg /day given orally which can be stepped up if required. A watch is kept for extra-pyramidal symptoms, which usually happen once a dose of 3 mg I

and therefore enhances the risk delirium.”


Medical treatment of delirium day is exceeded. Benzodiazepines requires use of pharmacological particularly lorazepam is given in

agents.’· ” · 15 Neuroleptic drugs such as haloperidol is the medication of choice. A patient’s possible co-morbid conditions must be considered when selecting medication.’0·” · ” Haloperidol is thought to have diffuse suppressive effects on spontaneous musculoskeletal hyperactivity and behavior. It also acts as a dopamine antagonist, without pronounced sedative or hypotensive effects.”·”·” ·’• The dose of haloperidol used is kept low, starting with

combination with haloperidol. This practice allows use of smaller and safer dosages of either of the two (neuroleptic agents and benzodiazepines) with greater effectiveness and fewer side effects.’· ” ·”

Delirious patients may also have co- morbid psychiatric conditions such as dementia, psychosis, and depression, wh ich should not be overlooked. Referral to a psychiatrist for further assessment and treatment may be appropriate.

Bedside equipment (e.g., ventilators and monitors) should be moved away from the patient whenever possible and alarms are turned down.

The noise from telephones, doors, and movement of equipment should be reduced, especially at night, to optimize undisturbed sleep.

Conversation among staff members should be kept to a minimum at nighttime.

Use of simple sentences and a calm voice. The person talking should face the patient. Use of medical terminology that the patient does not understand should be avoided. Procedures should be explained in clear, simple terms beforehand.

Placing a clock and a calendar within a patient’s field of vision. Ensuring that patients are provided with glosses and/or hearing aids as required.

Radios and televisions can help alleviate sensory deprivation and orient patients to reality, but the programs chosen should be appropriate lo and favored by the patient. Minimizing the number of visitors to a patient

Appropriate family members may reassure a patient by both communication and tactile stimulation. The family requires an understanding of the inappropriate, bizarre, and offensive behavior of the patient. The family should be reassured that the syndrome is transient and usually without permanent psychiatric sequel.

Relieve pain adequately. Procedures, especially endotracheal suctioning, may be associated with discomfort or pain, particularly for postoperative patients.

~!ml[@]~•. .

Most treatment of

t2> J


emp1nca Y ·

. rtant preventive and curative are 1mpo



Delirium remains a persistent problem in all ICUs. Many underlying conditions cannot be altered in the ICU, and much of the clinical management of delirious patients is directed toward life- saving procedures.

Educating ICU staff about the early

recognition and treatment of delirium is

2 essential to good management. ·• Such

an educational program should be given prominence in orientation curricula for n e w s t a f f m e m b e r s a n d i n I C U c o u r s e s , in conjunction with the technical aspects of the ICU environment.1•

Consideration should be given to the structural design of any new ICU or to refurbishing existing ICUs. Features to be considered include windows, o p t i ~ a l acoustics, single rooms, and noise- diminishing measures such as cho .

lreatment of anxiety in the ICU patio t I nrtion a'<I Irwin RS, Fink MP, Cerra FB Eds n j t”‘ RipPe JI,\ Medicine. 3rded.Boston,Mass’. littl~Bn•nsive eo,; 1996:2497-2506. r – &Co1,..

lO. Jacobson S, Schreibman B. Behavi ‘ pharmacologic treatment of deliriu oral and Physician. 1997; 56:2005-2012. m. Am Fa~

11 . Crippen OW. Pharmacologic treatmenl of br . . and delirium. Crit Care Clin. 1994; l0:73J.7~; 1011’-‘e

12 Cnppen OW. Neuralog1c monitoring in the •· . careunit. NewHoriz. 1994; 2:107-120. inten,;.,,

f f i c i e n t

t o

a v e r t




are not Su

development of delirium, but all of th~m

. · osing noise-reduced equipment with safe

indelirium.Acta PsychiatrScand. 1994;89:329-334. 20 Bird TD. Memory loss and dementia. In: Fauci lo, Braunwald E, lsselbocher KJ, et al, Eds. Harrison’s P r i n c i p l e s o f I n t e r n a l M e d i c i n e . 1 4 t h e d . N e w Y o r k , N Y:

McGraw-Hill; 1998: 142-150.

21 Power BM, Forbes AM, van Heerden PY, llett Kf.

Pharmacokinetics of drugs used in critically ill odults.

Clin Pharmacokinet. 1998; 34:25-56.

22 Blacher RS. The psychological and psychiatric consequences of the ICU stay. Eur J Anaesthesiol Supp.

1997; 15:45-47.

23 McCartney JR, Boland RJ. Anxiety and delirium inlhe

intensive care unit. Crit Care Clin. 199-4; l 0:673-680. 24 Tesar GE, Stern TA. Diognosisondtreatmentafogitation and delirium in the ICU patient. In: Rippe JM, Irwin RS, Fink MP, Cerra F8, Eds. Intensive Care Medicine. 3rd ed.

Boston, Mass: little Brown & Co Inc; l 996:2487-2496. 25 Slaby AE, Erle SR. Dementia and delirium. Inc Stoudemire A, Fogel BS, eds. Psychiatric Care ol lhe Medical Patient. New York, NY: Oxford Un~ersity Press;

1993 :431-444.

26 Root JD, Plum F. Evaluation of the comatose patient. In:

Ayres SM, Grenvik A Holbrook PR, Shoemaker WC, Eds. Textbook of Critic~I Care. 3rd ed. Philodelp/,io, Po, WBSaundersCo; 1995:1562-1571 . .

27 Keep P, James J, Inman M. Windows in the intens,.<e therapyunit.Anaesthesia. 1980;35:257-262. ed

28 Kimball CP. Intensive care units. In: Cheren S,and

Psychosomatic Medicine : Practice. Madison, Conn : Press Inc, 1989:786-792.

alarm systems that do not disturb th sleep of patients.”

References :

1. LipowskiZJ.Delirium·anor a .


Delirium: :4,cute Co~fusion~I ~~a;:ntol syndrome. In:

Oxford University Press; 1990:3-228 . New York, NY: 2, Eden BM, Foreman MO. Problem. . ‘

underrecognition of delirium i .~ associated with

study.Heart lung. l996·25·388n cnt1cal core: o case 3. Inouye SK, van Dyck CH . . -400.

Horwitz RI. Clarifyin , Alessi CA, Balkin S, Siegal AP. assessment method Ang Icon us1an: the confusio~

Theo,y, Physiol~, .tieS International UnrvefSI


4. A~m~trang SC,

18: 113-129. . ,edonOll and . n ntern Mod. 1990; 113:941 – 30 Berger I, Waldhorn RE. Analgesia, Ph icion-

m1~1agnosis of

Coua KL


‘p Watanabe KS. The

poralysis in the intensive core unit. Arn Forn ys 1995; 51 :166-1 72.


5. Haskell RM, Frankel HL

6. flin Issues. 1997; 8: 335-~o~~ndo MF. Agitation. AACN

aston C, MacKenzi F. 0 I’ . .

198B;17:229.237 °·

7. ~ngel GL, Roma . . . eart ung.

insufficJe no J.. Delirium, a s d


sychosomatics. 1997 . •

e irium in the ICU. H L

B. Rop~r AHncy. JMChmn1c Dis. 1959 . f.26r0om2e of cerebral • ort1n JB Ac ‘ · – 77.

coma. In: Fauci AS B . ute confusional st t

, rounwald E I Iba a es and , sse cher KJ, et al,

deliriu~ is

Eds. Harrison’s Principles of Internal Med· .

NewYork, NY:McGraw-Hill; 1998:125./~~ne.14tt,ed. . . II based Nursing interventions 9. Pollack MH, labbate LA, Stern TA. Recog ..

13 14

15 16


18 19

Inaba-Roland _KE, Maricle RA. Assessing delirium i acute care setting. Heart lung. 1992; 21:48-55 nth, Kis~i.Y, l”.”” Y, Takez””.’a K, Kurosawa H,·Endo Delmum in cnhcal care unit patients admitted 1hr

on emergency room. Gen Hosp

patient with •intensive core unit psychosis! Hear1

1984; 13:59-65. ng. Cardy J, Matta 8. Brain failure. Curr Opin CrnCore. 1997;3:273-278.

Bowden P. Psychiatric aspects of intensive care. In: Tinker J, Rapin M. Care of the Critically Ill Patient New yo,1 NY: Springer-Verlag; 1983:787-797. ‘ lipowski ZJ. Delirium (acufe conlusional states).JNM. 1987; 258:1789-1792.

Koponen HJ, Leinonen E, lepola U, Reikkinen PJ.Alo,g-

term follow-up study of cerebrospinal fluid somatostotin

C.. I

nt1ca CareAs· IQ

1995;17:371 -379.

Hansell HN. The behavioral effects of noise on ma ·the

· :: co~siderations in the management of og,to 1998;

29 Hassan E, Fontaine DK, Neorman “HS. TI,ero delirious critically ill patients. Pharmocotheropy.

Psy h.°”9 C IOI~.


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