2. PLAN OF PRESENTATION
• DEFINITION
• HISTORY
• COMPARATIVE NOSOLOGY
• EPIDEMIOLOGY
• PREDISPOSING FACTORS
• ETIOLOGY
• PATHOPHYSIOLOGY
• TYPES OF DELIRIUM
• INVESTIGATIONS
• PHARMACOLOGICAL MANAGEMENT
• MANAGEMENT IN SOME SPECIAL CASES
• CONCLUSION
• BIBLIOGRAPHY
Dr.Subrata Naska
3. WHAT IS DELIRIUM ?
• DELIRIUM IS CHARACTERIZED BY AN ACUTE DECLINE IN BOTH THE LEVEL
OF CONSCIOUSNESS AND COGNITION WITH PARTICULAR IMPAIRMENT
IN ATTENTION.
• A LIFE THREATENING, YET POTENTIALLY REVERSIBLE DISORDER OF THE
CENTRAL NERVOUS SYSTEM (CNS), DELIRIUM OFTEN INVOLVES
PERCEPTUAL DISTURBANCES, ABNORMAL PSYCHOMOTOR ACTIVITY,
AND SLEEP CYCLE IMPAIRMENT.
4. ACCORDING TO DSM IV-TR
• FOREMOST A DISTURBANCE OF CONSCIOUSNESS, ATTENTION, COGNITION, AND PERCEPTION.
• IT IS A COMMON PSYCHIATRIC SYNDROME WHICH COMMONLY HERALDS AN INCREASE IN MORBIDITY
AND MORTALITY. PATIENTS WITH DELIRIUM REMAIN IN THE HOSPITAL LONGER AND ARE MORE
COMMONLY DISCHARGED TO LONG-TERM CARE FACILITIES.
• BEHAVIORAL MANIFESTATIONS OF DELIRIUM MAY INTERFERE WITH TREATMENT COMPLIANCE AND ARE
OFTEN PRECIPITANTS FOR PSYCHIATRIC CONSULTATION.
• A PSYCHIATRIST SHOULD PROVIDE AND/OR ADVOCATE FOR THE APPROPRIATE TREATMENT BEYOND
SIMPLE MEDICAL EXPEDIENCE.
Dr.Subrata Naska
5. HISTORY
• THE EARLIEST KNOWN REFERENCES TO DELIRIUM IN MEDICAL LITERATURE
ARE FOUND IN THE WRITINGS OF HIPPOCRATES. SOME 2,400 YEARS AGO,
IN HIS BOOK OF EPIDEMICS, HIPPOCRATES DESCRIBED IT FIRST.
• TRADITION HOLDS THAT THE WORD DELIRIUM WAS FIRST USED IN THE
FORMAL MEDICAL CONTEXT BY CELSUS IN THE FIRST CENTURY AD.
• HOWEVER, CELSUS USED THE TERM DELIRIUM TO DESCRIBE A SPECTRUM OF MENTAL
DISORDERS RANGING FROM GENERAL INSANITY TO ACUTE TRANSIENT STATES OF MENTAL
DISTURBANCE, INCLUDING PHRENITIS, LETHARGUS, HYSTERIA, MELANCHOLIA, AND
MANIA.
Dr.Subrata Naska
6. HISTORY
• THE ANCIENT GREEK TERMS phrenitis AND lethargus HAVE
GIVEN RISE TO THE MODERN ENGLISH WORDS FRENZY AND
LETHARGY, RESPECTIVELY.
• THIS DISTINCTION FIRST MADE BY ARETAEUS MAY REPRESENT
THE FIRST RECORDED DESCRIPTION OF BOTH THE
HYPERACTIVE AND HYPOACTIVE MOTOR ELEMENTS OF
DELIRIUM.
Dr.Subrata Naska
7. HISTORY
• CENTURIES LATER IN 1583 PHILIPS BARROUGH IN HIS
TEXTBOOK “ THE METHOD OF PHYSICK” CLARIFIED THE
CONCEPT OF DELIRIUM.
• BARROUGH PROPOSED THAT DELIRIUM CONSTITUTED A
DERANGEMENT OF SOME COMBINATION OF THREE MAIN
INTERNAL SENSES, INCLUDING IMAGINATION, COGNITION,
AND MEMORY.
Dr.Subrata Naska
8.
9. HISTORY
• THE CONCEPT OF DERANGED SENSES WAS ELABORATED BY
THOMAS WILLIS IN HIS 1672 “treatise de anima brutorum”.
WILLIS ESTABLISHED THAT DELIRIUM WAS IN FACT A SPECIFIC
SET OF SYMPTOMS AND NOT A DISEASE.
• IN THE 18TH CENTURY, ERASMUS DARWIN AND JOHN HUNTER
MADE SIGNIFICANT CONTRIBUTIONS TO THE THEORY OF
DELIRIUM.
• DARWIN WAS THE FIRST TO COMPARE THE DELIRIUM WITH THE
DREAM STATE, NOTING THAT BOTH STATES CONSTITUTED AN
INTERRUPTION OF “VOLUNTARY POWER” AND A SUSPENSION
OF THE ABILITY TO ATTEND TO ONE'S EXTERNAL ENVIRONMENT.
Dr.Subrata Naska
10. HISTORY
• JAMES SIMS FURTHER DISTINGUISHED TWO SPECIES OF DELIRIUM, WHICH HE REFERRED TO AS LOW OR RAVING, WHICH CORRESPOND ALMOST
PERFECTLY WITH THE MODERN CONCEPT OF HYPOACTIVE AND HYPERACTIVE MOTOR SUBTYPES OF DELIRIUM.
• ARGUABLY THE MOST IMPORTANT CONTRIBUTION IN DEVELOPMENT OF THE CONCEPT OF DELIRIUM TOOK PLACE IN THE 20TH CENTURY IN LIGHT OF
THE WORK OF GEORGE ENGEL AND JOHN ROMANO.
• THEY WERE ABLE TO DEMONSTRATE THAT DELIRIUM IS DUE TO A REDUCTION IN THE METABOLIC ACTIVITY OF THE BRAIN.
• ENGEL AND ROMANO ILLUSTRATED THIS POINT THROUGH THE USE OF ELECTROENCEPHALOGRAMS (EEGS), AS BACKGROUND ACTIVITY WAS
OBSERVED TO SLOW IN CONJUNCTION WITH METABOLIC RATE.
• THIS DECREASE WAS OBSERVED TO CORRESPOND PROPORTIONATELY WITH DECREASES IN COGNITION, MEMORY, AND ATTENTION.
• INTERESTINGLY, THESE FINDINGS OF REDUCED ACTIVITY WERE CONSISTENT IN ALL SUBTYPES OF DELIRIUM, REGARDLESS OF THE LEVEL OF
PSYCHOMOTOR ACTIVITY.
11. COMPARATIVE NOSOLOGY
DUE TO THE VARIETY OF ETIOLOGIES
THAT MAY LEAD TO THE DEVELOPMENT
OF DELIRIUM, THERE ARE MANY
SYNONYMS FOR DELIRIUM THAT HAVE
BEEN INTRODUCED AND ADOPTED BY
MEDICAL PRACTITIONERS.
ACUTE CONFUSIONAL STATE
ACUTE BRAIN FAILURE
ENCEPHALITIS
ENCEPHALOPATHY
INTENSIVE CARE UNIT PSYCHOSIS
TOXIC METABOLIC STATE
CENTRAL NERVOUS SYSTEM TOXICITY
PARANEOPLASTIC LIMBIC ENCEPHALITIS
SUNDOWNING
CEREBRAL INSUFFICIENCY
ORGANIC BRAIN SYNDROME
Dr.Subrata Naska
12. EPIDEMIOLOGY
• DELIRIUM IS A COMMON DISORDER IN ELDERLY PATIENTS, WITH MOST
INCIDENCE AND PREVALENCE RATES REPORTED IN THE ELDERLY.
AGE PREVALENCE
55 YEARS AND MORE 1%
85 YEARS AND MORE 13%
ELDERLY EMERGENCY ROOM SUBJECTS 5-10 %
Dr.Subrata Naska
13. EPIDEMIOLOGY
TYPE PREVALENCE
GENERAL SURGICAL PATIENTS 10-15%
HIP FRACTURES 50%
INTENSIVE CARE UNITS 70-87%
END OF LIFE CARE 83%
PATIENTS IN NURSING HOMES OR
POSTACUTE CARE SETTINGS
60%
• Yale- New Haven study (Inouye S. Ann Intern Med 1993: 119-474)
• 65% unrecognized by Physicians
• 43% unrecognized by Nurses
Dr.Subrata Naska
14. • DEMOGRAPHIC
CHARACTERISTICS
• AGE 65 AND OLDER
• MALE SEX
• COGNITIVE STATUS
• DEMENTIA
• COGNITIVE IMPAIRMENT
• HISTORY OF DELIRIUM
• DEPRESSION
• FUNCTIONAL STATUS
• FUNCTIONAL DEPENDENCE
• IMMOBILITY
• HISTORY OF FALLS
• LOW LEVEL OF ACTIVITY
• SENSORY IMPAIRMENT
• HEARING
• VISUAL
• DECREASED ORAL INTAKE
• DEHYDRATION
• MALNUTRITION
• DRUGS
• TREATMENT WITH PSYCHOACTIVE DRUGS
• TREATMENT WITH DRUGS WITH ANTICHOLINERGIC PROPERTIES
• ALCOHOL ABUSE
• COEXISTING MEDICAL CONDITIONS
• SEVERE MEDICAL DISEASES
• CHRONIC RENAL OR HEPATIC DISEASE
• STROKE
• NEUROLOGICAL DISEASE
• METABOLIC DERANGEMENTS
• INFECTION WITH HUMAN IMMUNODEFICIENCY VIRUS
• FRACTURES OR TRAUMA
• TERMINAL DISEASES
PREDISPOSING FACTORS FOR DELIRIUM
Dr.Subrata Naska
15. COMMON ETIOLOGIES OF DELIRIUM
• CENTRAL NERVOUS SYSTEM DISORDER
• SEIZURE (POSTICTAL, NONCONVULSIVE STATUS, STATUS)
• MIGRAINE
• HEAD TRAUMA
• BRAIN TUMOR
• SUBARACHNOID HEMORRHAGE
• SUBDURAL, EPIDURAL HEMATOMA
• ABSCESS
• INTRACEREBRAL HEMORRHAGE
• CEREBELLAR HEMORRHAGE
• NONHEMORRHAGIC STROKE
• TRANSIENT ISCHEMIA
Dr.Subrata Naska
20. ETIOLOGY
• RENAL
• RENAL FAILURE, UREMIA, SIADH
• HEPATIC
• HEPATITIS, CIRRHOSIS, HEPATIC FAILURE
• NEOPLASM
• NEOPLASM (PRIMARY BRAIN, METASTASES, PARANEOPLASTIC SYNDROME)
• DRUGS OF ABUSE
• INTOXICATION AND WITHDRAWAL
• TOXINS
• INTOXICATION AND WITHDRAWAL
• HEAVY METALS AND ALUMINUM
21. PATHOPHYSIOLOGY
• THE PATHOPHYSIOLOGY OF DELIRIUM REMAINS POORLY UNDERSTOOD.
• ALTHOUGH THERE HAS BEEN RESEARCH TO FIND A FINAL COMMON
PATHWAY THAT EXPLAINS ALL DELIRIUM, GIVEN THE HETEROGENEITY OF THE
ETIOLOGIES AND THE PRESENTATIONS OF DELIRIUM, THERE MAY NOT BE ONE
MECHANISM THAT ENCOMPASSES THE ENTIRE SYNDROME.
• EEG STUDIES HAVE DEMONSTRATED DIFFUSE SLOWING OF CORTICAL
BACKGROUND ACTIVITY, WHICH DOES NOT CORRELATE WITH UNDERLYING
CAUSES.
Dr.Subrata Naska
22. NEUROCHEMICAL
• PATIENTS WITH DELIRIUM HAVE SHOWN EVIDENCE OF NEUROCHEMICAL
CHANGES IN
• ACETYLCHOLINE
• DOPAMINE
• GLUTAMATE
• γ-AMINOBUTYRIC ACID (GABA)
• SEROTONIN SYSTEMS.
Dr.Subrata Naska
23. ACETYLCHOLINE
• EXTENSIVE EVIDENCE SUPPORTS THE ROLE OF CHOLINERGIC DEFICIENCY IN DELIRIUM AS IT IS
INVOLVED IN RAPID EYE MOVEMENT (REM) SLEEP, ATTENTION, AROUSAL, AND MEMORY.
• ADMINISTRATION OF ANTICHOLINERGIC DRUGS CAN INDUCE DELIRIUM IN HUMANS AND
ANIMALS, AND SERUM ANTICHOLINERGIC ACTIVITY IS INCREASED IN PATIENTS WITH DELIRIUM.
• PHYSOSTIGMINE (ANTILIRIUM), A CHOLINERGIC AGENT, REVERSES DELIRIUM ASSOCIATED WITH
ANTICHOLINERGIC DRUGS.
• THIS SUGGESTS THE POSSIBILITY OF INTERACTIONS BETWEEN OTHER SYSTEMS AND THE
CHOLINERGIC SYSTEM IN THE PATHOPHYSIOLOGY OF DELIRIUM.
• RECENT REPORTS INDICATE THAT CHOLINESTERASE INHIBITORS APPEAR TO HAVE SOME BENEFIT
EVEN IN CASES OF DELIRIUM THAT ARE NOT INDUCED BY DRUGS. Dr.Subrata Naska
24. DOPAMINE
• DOPAMINERGIC EXCESS ALSO APPEARS TO CONTRIBUTE TO DELIRIUM,
POSSIBLY OWING TO ITS REGULATORY INFLUENCE ON THE RELEASE OF
ACETYLCHOLINE.
• ONE SUGGESTED MECHANISM IS THE INVOLVEMENT OF DOPAMINE IN
MAINTAINING AND SHIFTING ATTENTION.
• DOPAMINERGIC DRUGS (E.G., LEVODOPA AND BUPROPION ARE
RECOGNIZED PRECIPITANTS OF DELIRIUM, AND DOPAMINE ANTAGONISTS
(E.G., ANTIPSYCHOTIC AGENTS) EFFECTIVELY TREAT DELIRIUM SYMPTOMS.
Dr.Subrata Naska
25. GLUTAMATE
• GLUTAMATE, THROUGH ITS EXCITATORY NEUROTOXICITY EFFECTS (MEDIATED
VIA THE N-METHYL-D-ASPARTATE [NMDA] RECEPTOR), MAY CAUSE
NEURONAL DEATH AND CAN BE ASSOCIATED WITH DELIRIUM.
• DRUGS THAT ARE NMDA ANTAGONISTS, SUCH AS KETAMINE AND
PHENCYCLIDINE (PCP) ARE ASSOCIATED WITH DELIRIUM.
• ONE PROPOSED MECHANISM OF WERNICKE'S ENCEPHALOPATHY IS
THROUGH GLUTAMATE ABNORMALITIES.
Dr.Subrata Naska
26. GABA
• GABA, AN INHIBITOR OF BRAIN ACTIVITY, HAS BEEN IMPLICATED IN
CONTRIBUTING TO DELIRIUM SECONDARY TO BENZODIAZEPINE AND
ALCOHOL WITHDRAWAL.
• HEPATIC ENCEPHALOPATHY HAS BEEN ASSOCIATED WITH INCREASED
SERUM AMMONIA AND GABA LEVELS.
Dr.Subrata Naska
27. OTHER NEUROTRANSMITTERS
• PERTURBATIONS OF OTHER NEUROTRANSMITTERS, SUCH AS NOREPINEPHRINE,
SEROTONIN, GABA, GLUTAMATE, AND MELATONIN, MAY ALSO HAVE A ROLE IN THE
PATHOPHYSIOLOGY OF DELIRIUM, BUT THE EVIDENCE IS LESS WELL DEVELOPED. THESE
NEUROTRANSMITTERS MAY EXERT THEIR INFLUENCE THROUGH INTERACTIONS WITH THE
CHOLINERGIC AND DOPAMINERGIC PATHWAYS.
• OXIDATIVE METABOLISM
DISTURBANCE IN BRAIN OXYGEN SUPPLY VERSUS DEMAND HAS BEEN ONE OF THE
THEORIES PROPOSED FOR DELIRIUM. IMPAIRED OXIDATIVE METABOLISM APPEARS TO BE
A PREDISPOSING FACTOR FOR LATER DEVELOPMENT OF DELIRIUM.
Dr.Subrata Naska
28. BLOOD–BRAIN BARRIER ALTERATIONS
• ONE HYPOTHESIS OF DELIRIUM IS THAT IT IS A CNS RESPONSE TO SYSTEMIC
INFLAMMATION DURING A STATE OF BLOOD–BRAIN BARRIER
COMPROMISE.
• IN POSTCARDIAC SURGERY PATIENTS, CHEMOKINES, WHICH IS AN
INFLAMMATORY MARKER, HAVE BEEN ASSOCIATED WITH DELIRIUM BY
DISRUPTING THE BLOOD–BRAIN BARRIER.
• SIMILAR ALTERATIONS HAVE BEEN FOUND IN PATIENTS DEVELOPING
DELIRIUM AFTER TRAUMA, PRIMARY HYPERPARATHYROIDISM AND
DELIRIUM TREMENS.
Dr.Subrata Naska
30. AMMONIA
• HEPATIC ENCEPHALOPATHY IS CAUSED BY MANY FACTORS.
• ONE FACTOR IDENTIFIED IN THE PATHOGENESIS OF THIS SYNDROME HAS BEEN AMMONIA.
• AMMONIA AND SEVERAL OTHER FACTORS ARE KNOWN TO INDUCE AND AGGRAVATE
ASTROCYTE SWELLING, WHICH INITIATE A CASCADE OF EVENTS LEADING TO DELIRIUM.
• ONE OTHER MECHANISM COULD BE THAT ELEVATED AMMONIA LEVELS CAN CONTRIBUTE
TO INCREASED GLUTAMATE AND GLUTAMINE LEVELS, WHICH ARE PRECURSORS TO GABA.
• CYTOKINES, INCLUDING INTERLEUKIN-1, INTERLEUKIN-2, INTERLEUKIN-6, TUMOR NECROSIS
FACTOR-Α (TNF-Α), AND INTERFERON, MAY CONTRIBUTE TO DELIRIUM BY INCREASING THE
PERMEABILITY OF THE BLOOD–BRAIN BARRIER AND ALTERING NEUROTRANSMISSION.
Dr.Subrata Naska
31. • FINALLY, CHRONIC STRESS BROUGHT ON BY ILLNESS OR TRAUMA
ACTIVATES THE SYMPATHETIC NERVOUS SYSTEM AND HYPOTHALAMIC–
PITUITARY–ADRENOCORTICAL AXIS, RESULTING IN INCREASED CYTOKINE
LEVELS AND CHRONIC HYPERCORTISOLISM.
• CHRONIC HYPERCORTISOLISM HAS DELETERIOUS EFFECTS ON
HIPPOCAMPAL SEROTONIN (5-HYDROXYTRYPTAMINE) 5-HT1A
RECEPTORS, WHICH MAY CONTRIBUTE TO DELIRIUM.
Dr.Subrata Naska
32. THEORIES FOR POST OP DELIRIUM
• ACETYLCHOLINE INTERACTION WITH MEDICATIONS USED DURING SURGERY
• INCREASE OF NEUROTRANSMITTERS, SEROTONIN AND DOPAMINE DURING
SURGERY
• PREVIOUS ABNORMALITY LEVELS OF MELATONIN
• DAMAGE TO NEURONS BY OXIDATIVE STRESS OR INFLAMMATION CAUSED BY
A SURGICAL PROCEDURE
• POST OP ABNORMAL BRAIN WAVES Dr.Subrata Naska
34. TYPES
• DSM IV-TR CLASSIFIES DELIRIUM INTO 5 SUBTYPES DEPENDING
ON THE ETIOLOGY:
I. DELIRIUM DUE TO A GENERAL MEDICAL CONDITION.
II. DELIRIUM DUE TO SUBSTANCE INTOXICATION
III. DELIRIUM DUE TO SUBSTANCE WITHDRAWAL
IV. DELIRIUM DUE TO MULTIPLE ETIOLOGIES
V. DELIRIUM NOT OTHERWISE SPECIFIED
Dr.Subrata Naska
35. DIAGNOSTIC CRITERIA OF THOSE SUBTYPES
WHATEVER THE TYPE IS 3 CRITERIAS HAS TO BE REMEMBERED
THESE 3 CRITERIAS WILL BE THE SAME IN ALL 5 VARIETIES
2. A CHANGE IN COGNITION (SUCH AS MEMORY DEFICIT, DISORIENTATION, LANGUAGE
DISTURBANCE) OR THE DEVELOPMENT OF A PERCEPTUAL DISTURBANCE THAT IS NOT BETTER
ACCOUNTED FOR BY A PREEXISTING, ESTABLISHED, OR EVOLVING DEMENTIA.
1. DISTURBANCE OF CONSCIOUSNESS (I.E., REDUCED CLARITY OF AWARENESS OF THE
ENVIRONMENT) WITH REDUCED ABILITY TO FOCUS, SUSTAIN, OR SHIFT ATTENTION.
3. THE DISTURBANCE DEVELOPS OVER A SHORT PERIOD OF TIME (USUALLY HOURS TO
DAYS) AND TENDS TO FLUCTUATE DURING THE COURSE OF THE DAY. Dr.Subrata Naska
36. ADDITIONAL CRITERIAS FOR INDIVIDUAL
CATEGORIES
DELIRIUM DUE TO GENERAL MEDICAL CONDITION
• THERE IS EVIDENCE FROM THE HISTORY, PHYSICAL EXAMINATION, OR
LABORATORY FINDINGS THAT THE DISTURBANCE IS CAUSED BY THE DIRECT
PHYSIOLOGICAL CONSEQUENCES OF A GENERAL MEDICAL CONDITION.
SUBSTANCE INTOXICATION DELIRIUM
• THERE IS EVIDENCE FROM THE HISTORY, PHYSICAL EXAMINATION, OR
LABORATORY FINDINGS OF EITHER (1) OR (2):
• THE SYMPTOMS IN CRITERIA A AND B DEVELOPED DURING SUBSTANCE INTOXICATION
• MEDICATION USE IS ETIOLOGICALLY RELATED TO THE DISTURBANCE*
*CRITERIA A - DISTURBANCE OF CONSCIOUSNESS (I.E., REDUCED CLARITY OF AWARENESS OF THE ENVIRONMENT) WITH REDUCED ABILITY
TO FOCUS, SUSTAIN, OR SHIFT ATTENTION.
CRITERIA B - A CHANGE IN COGNITION (SUCH AS MEMORY DEFICIT, DISORIENTATION, LANGUAGE DISTURBANCE) OR THE DEVELOPMENT
OF A PERCEPTUAL DISTURBANCE THAT IS NOT BETTER ACCOUNTED FOR BY A PREEXISTING, ESTABLISHED, OR EVOLVING DEMENTIA.
Dr.Subrata Naska
37. ADDITIONAL CRITERIAS FOR INDIVIDUAL
CATEGORIES
SUBSTANCE WITHDRAWAL DELIRIUM
• THERE IS EVIDENCE FROM THE HISTORY, PHYSICAL EXAMINATION, OR
LABORATORY FINDINGS THAT THE SYMPTOMS IN CRITERIA A AND B
DEVELOPED DURING, OR SHORTLY AFTER, A WITHDRAWAL SYNDROME.
DELIRIUM DUE TO MULTIPLE ETIOLOGIES
• THERE IS EVIDENCE FROM THE HISTORY, PHYSICAL EXAMINATION, OR
LABORATORY FINDINGS THAT THE DELIRIUM HAS MORE THAN ONE
ETIOLOGY (E.G., MORE THAN ONE ETIOLOGICAL GENERAL MEDICAL
CONDITION, A GENERAL MEDICAL CONDITION PLUS SUBSTANCE
INTOXICATION OR MEDICATION SIDE EFFECT). Dr.Subrata Naska
38. ADDITIONAL CRITERIAS FOR INDIVIDUAL
CATEGORIES
DELIRIUM NOT OTHERWISE SPECIFIED
• THIS CATEGORY SHOULD BE USED TO DIAGNOSE A DELIRIUM THAT DOES NOT MEET
CRITERIA FOR ANY OF THE SPECIFIC TYPES OF DELIRIUM DESCRIBED IN THIS SECTION.
•
EXAMPLES INCLUDE A CLINICAL PRESENTATION OF DELIRIUM THAT IS SUSPECTED TO
BE DUE TO A GENERAL MEDICAL CONDITION OR SUBSTANCE USE BUT FOR WHICH
THERE IS INSUFFICIENT EVIDENCE TO ESTABLISH A SPECIFIC ETIOLOGY
• DELIRIUM DUE TO CAUSES NOT LISTED IN SECTION DESCRIBED PREVIOUSLY (E.G.,
SENSORY DEPRIVATION)
Dr.Subrata Naska
39. DELIRIUM DUE TO SUBSTANCE INTOXICATION.
DRUGS OF ABUSE
• INTOXICATION WITH A VARIETY OF DRUGS OF ABUSE IS
KNOWN TO CAUSE DELIRIUM.
• COCAINE
• PCP
• HEROIN
• ALCOHOL
• NITROUS OXIDE
• AMPHETAMINE AND ITS DERIVATIVES (E.G., SPEED AND ECSTASY)
• MARIJUANA.
Dr.Subrata Naska
40. • EXPERIMENTATION WITH DRUGS OF ABUSE EXTENDS TO SYNTHETIC COMPOUNDS KNOWN AS
RAVES, WHICH ARE OFTEN USED IN DANCE CLUBS
• 3,4-METHYLENE-DIOXYMETHAMPHETAMINE (MDMA), ALSO KNOWN AS ECSTASY, A
METHAMPHETAMINE ANALOG, HAVE BEEN ASSOCIATED WITH DELIRIUM AND FATALITIES.
• SPECIAL K, OR KETAMINE, AN ANESTHETIC AGENT OFTEN USED BY VETERINARIANS
• PCP (ALSO KNOWN AS ANGEL DUST) ARE NMDA RECEPTOR ANTAGONISTS AND ARE OTHER
EXAMPLES OF STREET DRUGS ASSOCIATED WITH DELIRIUM.
• FLUNITRAZEPAM (ROHYPNOL) AND γ-HYDROXYBUTYRATE (GHB) ARE OTHER COMMON
CHOICES OF RECREATIONAL DRUG USERS WITH THE POTENTIAL FOR DELIRIUM
Dr.Subrata Naska
41. DELIRIUM DUE TO SUBSTANCE WITHDRAWAL
ALCOHOL WITHDRAWAL
• THE CLASSIC AGITATED WITHDRAWAL DELIRIUM IS DELIRIUM TREMENS.
• THIS SYNDROME, SYNONYMOUS WITH SEVERE ALCOHOL WITHDRAWAL, PRESENTS
WITH
• DELIRIUM
• AUTONOMIC HYPERACTIVITY
• FREQUENT VISUAL AND TACTILE HALLUCINATIONS
• CARRIES A SIGNIFICANT RISK OF SEIZURES AND DEATH IF UNTREATED.
• PATIENTS ADMITTED TO THE HOSPITAL MAY PRESENT SEVERAL DAYS INTO
ADMISSION WITH ALCOHOL WITHDRAWAL AND MAY BE AT RISK FOR
DELIRIUM TREMENS.
Dr.Subrata Naska
42. BENZODIAZEPINE WITHDRAWAL
• BENZODIAZEPINE WITHDRAWAL MAY APPEAR SIMILAR TO ALCOHOL
WITHDRAWAL AND MAY ALSO BE ACCOMPANIED BY SEIZURES.
• THE ONSET OF SYMPTOMS IS DEPENDENT ON THE HALF-LIFE OF THE
PARTICULAR BENZODIAZEPINE.
• EXAMPLE: ALPRAZOLAM WITHDRAWAL (SHORT HALF-LIFE) MAY PRESENT IN
1 TO 2 DAYS
• DIAZEPAM (VALIUM) WITHDRAWAL (LONG HALF-LIFE) MAY PRESENT 5 TO 7
DAYS AFTER THE LAST DOSE.
Dr.Subrata Naska
43. OPIATE WITHDRAWAL
• OPIATE WITHDRAWAL PRESENTS WITH
• SEVERE FLU-LIKE SYNDROMES
• GASTROINTESTINAL (GI) CRAMPING
• DIARRHEA
• DIAPHORESIS
• AUTONOMIC HYPERACTIVITY
• CRAVING.
• DELIRIUM MAY ALSO OCCUR WITH OPIOID WITHDRAWAL AND HAS BEEN
REPORTED WITH SWITCHING OF OPIATES EG: FROM TRANSDERMAL
FENTANYL TO MORPHINE.
• THE PRESENTATION MAY OCCUR BECAUSE OF UNKNOWN PRIOR USE OF
OPIATES IN THE CONTEXT OF ABUSE. Dr.Subrata Naska
44. DELIRIUM IN POST-OP PATIENTS
DELIRIUM FOLLOWING CORONARY ARTERY BYPASS GRAFT
• THE INCIDENCE OF DELIRIUM AFTER CORONARY ARTERY BYPASS (CABG)
PROCEDURE HAS RANGED FROM 3 TO 35 PERCENT.
• SEVERAL FACTORS PLAY A ROLE IN THE DEVELOPMENT OF DELIRIUM IN POST
CABG PATIENTS.
• IN ONE STUDY DELIRIUM WAS DETECTED IN 74 OF 220 (33.6 PERCENT) PATIENTS
UNDERGOING CABG PROCEDURE.
Dr.Subrata Naska
45. • MULTIPLE RISK FACTORS WERE IDENTIFIED FOR DELIRIUM IN THIS STUDY.
• INCREASING AGE
• BLOOD UREA LEVEL
• CARDIO-THORACIC INDEX
• HYPERTENSION
• SMOKING HABITS
• BLOOD REPLACEMENT DURING BYPASS
• ATRIAL FIBRILLATION (AF)
• PNEUMONIA
• BLOOD BALANCE IN THE POSTOPERATIVE PERIOD WERE ALL
ASSOCIATED WITH DELIRIUM.
• INTERESTINGLY, NO SPECIFIC FACTOR ASSOCIATED WITH THE CABG
PROCEDURE ITSELF (PERFUSION PRESSURE, NUMBER OF GRAFTS) WAS
CORRELATED WITH AN INCREASED RISK FOR DELIRIUM POSTOPERATIVELY.
• THE LENGTH OF STAY WAS TWICE AS LONG IN THE DELIRIOUS GROUP.
Dr.Subrata Naska
46. DELIRIUM FOLLOWING HIP/JOINT REPLACEMENT
• DELIRIUM IS A COMMON ADVERSE EVENT IN PATIENTS UNDERGOING HIP
REPLACEMENT, WITH ESTIMATES IN THE RANGE OF 15 TO 60 PERCENT.
• SEVERAL STUDIES HAVE INDICATED THAT POST–HIP REPLACEMENT DELIRIUM
HAS BEEN ASSOCIATED WITH INCREASED MORBIDITY AND MORTALITY.
• STUDIES SHOW THAT COGNITIVE IMPAIRMENT AT ADMISSION HAD THE
HIGHEST PREDICTIVE VALUE FOR POSTOPERATIVE DELIRIUM, AND CONTRARY
TO PREVIOUS FINDINGS, AGE WAS AN INDEPENDENT PREDICTIVE FACTOR
FOR DELIRIUM.
• POSTOPERATIVE DELIRIUM WAS FOUR TIMES AS FREQUENT IN ACUTE PATIENTS
AS IN ELECTIVE HIP REPLACEMENT PATIENTS. Dr.Subrata Naska
47. CARDINAL CLINICAL FEATURES
• ALTERED CONSCIOUSNESS
• ALTERED ATTENTION
• DISORIENTATION (ESPECIALLY TO TIME AND SPACE)
• MEMORY IMPAIRMENT
• PERCEPTUAL DISTURBANCES SUCH AS ILLUSIONS AND HALLUCINATIONS
• CAN ACCOMPANY BOTH HYPOACTIVE AND HYPERACTIVE SUBTYPES
• HALLUCINATIONS ARE USUALLY VISUAL
• DELUSIONS IF PRESENT ARE OFTEN PARANOID OR PERSECUTIONAL
• PSYCHOMOTOR HYPERACTIVITY AND HYPOACTIVITY
• THE HYPOACTIVE (DECREASED PSYCHOMOTOR ACTIVITY) VARIANT OF DELIRIUM IS MORE COMMON
THAN HYPERACTIVE DELIRIUM IN ELDERLY PATIENTS
• DISRUPTION OF THE SLEEP WAKE CYCLE
• MOOD ALTERATIONS (FROM SUBTLE IRRITABILITY TO OBVIOUS DYSPHORIA,
ANXIETY, OR EVEN EUPHORIA) Dr.Subrata Naska
48. CLINICAL FEATURES
• ALTERED NEUROLOGICAL FUNCTION (E.G., AUTONOMIC HYPERACTIVITY OR
INSTABILITY, MYOCLONIC JERKING, AND DYSARTHRIA).
• FOCAL NEUROLOGIC SIGNS CAN ALSO OCCUR BUT USUALLY SUGGEST AN
UNDERLYING CEREBROVASCULAR EVENT.
• INCOHERENT SPEECH AND A DIMINISHED ABILITY TO SEQUENCE ACTIONS
PROPERLY
Dr.Subrata Naska
57. NERVOUS SYSTEM
REFLEXES ASYMMETRY WITH BABINSKI'S SIGNS
MASS LESION
CEREBROVASCULAR
DISEASE
PREEXISTING DEMENTIA
ABDUCENT NERVE
(SIXTH CRANIAL NERVE) WEAKNESS IN LATERAL GAZE INCREASED INTRACRANIAL
PRESSURE
LIMB STRENGTH ASYMMETRICAL
MASS LESION
CEREBROVASCULAR
DISEASE
AUTONOMIC NERVOUS SYSTEM HYPERACTIVITY Dr.Subrata Naska
58. LABORATORY WORKUP
STANDARD STUDIES
• BLOOD CHEMISTRIES (INCLUDING
ELECTROLYTES, RENAL AND HEPATIC INDEXES,
AND GLUCOSE)
• COMPLETE BLOOD COUNT WITH WHITE CELL
DIFFERENTIAL
• THYROID FUNCTION TESTS
• SEROLOGIC TESTS FOR SYPHILIS
• HUMAN IMMUNODEFICIENCY VIRUS (HIV)
ANTIBODY TEST
• URINALYSIS
• ELECTROCARDIOGRAM
• ELECTROENCEPHALOGRAM
• CHEST X-RAY
• BLOOD AND URINE DRUG SCREENS
• ADDITIONAL TESTS WHEN INDICATED
• BLOOD, URINE, AND CEREBROSPINAL FLUID
(CSF) CULTURES
• B12, FOLIC ACID CONCENTRATIONS
• COMPUTED TOMOGRAPHY OR MAGNETIC
RESONANCE IMAGING BRAIN SCAN
• LUMBAR PUNCTURE AND CSF EXAMINATION
Dr.Subrata Naska
59. RATING SCALES IN DELIRIUM
CONFUSION ASSESSMENT METHOD
• CONFUSION ASSESSMENT METHOD (CAM) HAS BEEN VALIDATED IN A NUMBER OF
SETTINGS, INCLUDING THE INTENSIVE CARE UNIT IN ELDERLY
• 95 PERCENT SENSITIVITY AND 88 PERCENT SPECIFICITY.
• THE ADMINISTRATION TIME IS APPROXIMATELY 2 MINUTES.
• THE INSTRUMENT DETECTED DELIRIUM IN 83.3 PERCENT OF PATIENTS IN THE INTENSIVE
CARE UNIT, THE HIGHEST PUBLISHED RATE IN THE INTENSIVE CARE UNIT SETTING.
Dr.Subrata Naska
60. DELIRIUM RATING SCALE (DRS)
3 ITEMS IN SCALE
• ITEM 1: TEMPORAL ONSET OF SYMPTOMS
• ITEM 2: PERCEPTUAL DISTURBANCES
• ITEM 3: THE PRESENCE OF ANY TYPE OF HALLUCINATION IS RATED.
Dr.Subrata Naska
62. DIFFERENTIAL DIAGNOSIS
DELIRIUM SHOULD BE DIFFERENTIATED FROM
• DEMENTIA
• DEPRESSION
• PSYCHOTIC DISORDER
• SCHIZOPHRENIFORM DISORDER
ALL OF THEM CAUSE GLOBAL COGNITIVE DEFICIT.
• DISSOCIATIVE DISORDERS Dr.Subrata Naska
63. FEATURE DEMENTIA DELIRIUM
ONSET SLOW RAPID
DURATION MONTHS TO YEARS HOURS TO WEEKS
ATTENTION PRESERVED FLUCTUATES
MEMORY IMPAIRED REMOTE MEMORY IMPAIRED RECENT AND
IMMEDIATE MEMORY
SPEECH WORD-FINDING DIFFICULTY INCOHERENT (SLOW OR
RAPID)
SLEEP WAKE CYCLE FRAGMENTED SLEEP FREQUENT DISRUPTION (E.G.
DAY NIGHT REVERSAL)
THOUGHTS IMPOVERISHED DISORGANIZED
AWARENESS UNCHANGED REDUCED
ALERTNESS USUALLY NORMAL HYPERVIGILANT OR
REDUCED VIGILANCE
OCCASIONALLY, DELIRIUM OCCURS IN A PATIENT WITH DEMENTIA, A CONDITION KNOWN AS
BECLOUDED DEMENTIA.
Dr.Subrata Nask
64. • HYPOACTIVE DELIRIUM CAN RESEMBLE DEPRESSION. HOWEVER CLOUDING
OF CONSCIOUSNESS IS ABSENT IN DEPRESSION
• HYPERACTIVE DELIRIUM CAN MIMIC ACUTE PSYCHOSIS. HOWEVER IN
DELIRIUM HALLUCINATIONS ARE PREDOMINANTLY VISUAL AND DELUSION ARE
NOT WELL SYSTEMATIZED.
• AN EEG CAN DIFFERENTIATE IT FROM BOTH DEPRESSION & PSYCHOSIS
Dr.Subrata Nask
66. • IN TREATING DELIRIUM, THE PRIMARY GOAL IS TO TREAT THE UNDERLYING
CAUSE.
• THE OTHER IMPORTANT GOAL OF TREATMENT IS TO PROVIDE PHYSICAL,
SENSORY, AND ENVIRONMENTAL SUPPORT.
• PHYSICAL SUPPORT IS NECESSARY SO THAT DELIRIOUS PATIENTS DO NOT GET INTO
SITUATIONS IN WHICH THEY MAY HAVE ACCIDENTS.
• PATIENTS WITH DELIRIUM SHOULD BE NEITHER SENSORY DEPRIVED NOR OVERLY
STIMULATED BY THE ENVIRONMENT.
NON PHARMACOLOGICAL
Dr.Subrata Nask
67. TREATMENT
• FAMILIAR PICTURES AND DECORATIONS, THE PRESENCE OF A CLOCK OR A CALENDAR, AND
REGULAR ORIENTATIONS TO PERSON, PLACE, AND TIME HELP MAKE PATIENTS WITH DELIRIUM
COMFORTABLE.
• CONTINUITY IN BOTH NURSING AND MEDICAL STAFF CAN HELP DECREASE PATIENT FEARS AND
PARANOIA BECAUSE OF UNFAMILIAR FACES.
• DELIRIUM CAN SOMETIMES OCCUR IN OLDER PATIENTS WEARING EYE PATCHES AFTER
CATARACT SURGERY, SUCH PATIENTS CAN BE HELPED BY PLACING PINHOLES IN THE PATCHES
TO LET IN SOME STIMULI OR BY OCCASIONALLY REMOVING ONE PATCH AT A TIME DURING
RECOVERY.
• INTERRUPTIONS OF SLEEP SHOULD BE MINIMIZED WHEN POSSIBLE.
• ADEQUATE NUTRITION IS IMPORTANT FOR RECOVERY FROM THE DELIRIUM AND THE
UNDERLYING ILLNESS, AS WELL AS FOR PROVIDING USEFUL ORIENTATION.
Dr.Subrata Nask
68. TREATMENT
• PSYCHOSOCIAL SUPPORT CAN BE PROVIDED BY BOTH STAFF AND FAMILY OR
FRIENDS.
• PHYSICAL RESTRAINS SHOULD BE AVOIDED WHENEVER POSSIBLE
• FAMILY MEMBERS MAY BE AVAILABLE TO PROVIDE CONSTANT OBSERVATION,
WHICH CAN MINIMIZE THE NEED FOR PHYSICAL RESTRAINTS.
Dr.Subrata Nask
69. • PSYCHOACTIVE MEDICATIONS ARE INDICATED FOR DELIRIUM ASSOCIATED
WITH DRUG WITHDRAWAL OR FOR BEHAVIORS THAT POSE A SAFETY RISK
FOR THE PATIENT AND OTHERS.
• TWO GENERAL CLASSES OF AGENTS—THE ANTIPSYCHOTICS AND THE
BENZODIAZEPINES—ARE MOST FREQUENTLY USED.
• ANTIPSYCHOTICS ARE BENEFICIAL IN PATIENTS HAVING
• PERCEPTUAL DISTURBANCES ASSOCIATED WITH
• SLEEP–WAKE CYCLE ABNORMALITIES
• BEHAVIORAL DYSCONTROL
PHARMACOLOGICAL
Dr.Subrata Nask
70. • HALOPERIDOL IS THE MOST PREFERRED DRUG AMONGST THE ANTIPSYCHOTICS
• REASON:
• HIGHLY POTENT
• FEWER ANTICHOLINERGIC FEWER INCIDENT OF HYPOTENSION
• DISADVANTAGE:
• FREQUENCY OF EXTRAPYRAMIDAL SIDE EFFECTS IS HIGHER
• CANT BE USED IN PATIENTS LIKE DELIRIUM WITH PARKINSONISM
Dr.Subrata Nask
71. FACTS ABOUT HALOPERIDOL DOSAGE
• THE INITIAL DOSE 2 TO 6 MG INTRAMUSCULAR INJECTION.
• REPEATED IN AN HOUR IF THE PATIENT REMAINS AGITATED.
• ORAL MEDICATION IN LIQUID CONCENTRATE OR TABLET FORM SHOULD BEGIN AS SOON AS
POSSIBLE
• TWO DAILY ORAL DOSES SHOULD SUFFICE, WITH TWO THIRDS OF THE DOSE BEING GIVEN AT
BEDTIME.
• TO ACHIEVE THE SAME THERAPEUTIC EFFECT, THE ORAL DOSE SHOULD BE APPROXIMATELY 1.5
TIMES THE PARENTERAL DOSE.
• THE EFFECTIVE TOTAL DAILY DOSE OF HALOPERIDOL MAY RANGE FROM 5 TO 40 MG FOR MOST
PATIENTS WITH DELIRIUM.
Dr.Subrata Nask
72. • OTHER ANTIPSYCHOTIC DRUGS FOUND EQUALLY EFFECTIVE AS
HALOPERIDOL
• THIORIDAZINE
• DROPERIDOL
• CHLORPROMAZINE
• HOWEVER, ANTICHOLINERGIC SIDE EFFECTS ARE MORE PROMINENT WITH
THEIR USAGE.
Dr.Subrata Nask
73. ATYPICAL ANTIPSYCHOTICS
• ATYPICAL ANTIPSYCHOTICS HAVE SHOWN SOME PROMISE IN BEING
EFFECTIVE IN MANAGING DELIRIUM
• DRUGS COMMONLY USED
• RISPERIDONE
• OLANZAPINE
• QUETIAPINE
• ALL IN LOW DOSE HAS BEEN FOUND TO BE EFFECTIVE IN MANAGING
AGGRESSION IN DELIRIUM
Dr.Subrata Nask
74. ATYPICAL ANTIPSYCHOTICS
ALL CAN PROLONG QTC DURATION
0.5–1 MG A DAY
RISPERIDONE EPS CONCERNS LIMITED DATA IN DELIRIUM
OLANZAPINE 5–10 MG A DAY HIGHER MORTALITY IN DEMENTIA
QUETIAPINE 25–150 MG A DAY
PATIENTS WITH PARKINSON'S DISEASE AND DELIRIUM WHO REQUIRE ANTIPSYCHOTIC MEDICATIONS, CLOZAPINE OR
QUETIAPINE HAVE SOME SUPPORT IN THE LITERATURE AND ARE LESS LIKELY TO EXACERBATE PARKINSONIAN SYMPTOMS
Dr.Subrata Nask
75. BENZODIAZEPINES
• BENZODIAZEPINES ARE USED IN THE MANAGEMENT OF DELIRIUM TO SEDATE
THE AGITATED PATIENT.
• WHEN THE AGITATION IS ASSOCIATED WITH SEDATIVE-HYPNOTIC WITHDRAWAL
(SUCH AS ALCOHOL, BENZODIAZEPINES, BARBITURATES), BENZODIAZEPINES
ARE THE TREATMENT OF CHOICE.
• INSOMNIA IS BEST TREATED WITH BENZODIAZEPINES WITH SHORT OR
INTERMEDIATE HALF-LIVES (E.G., LORAZEPAM 1 TO 2 MG AT BEDTIME).
• BENZODIAZEPINES WITH LONG HALF-LIVES AND BARBITURATES SHOULD BE
AVOIDED UNLESS THEY ARE BEING USED AS PART OF THE TREATMENT FOR THE
UNDERLYING DISORDER (E.G., ALCOHOL WITHDRAWAL).
0.5–3 MG/DAY AND AS NEEDED EVERY 4 HR
LORAZEPAM
BEST USE IN DELIRIUM SECONDARY TO
ALCOHOL/BENZODIAZEPINE WITHDRAWAL
CAN WORSEN DELIRIUM
Dr.Subrata Nask
76. • PATIENTS EXPERIENCING ALCOHOL WITHDRAWAL SHOULD BE GIVEN THIAMINE
INTRAMUSCULARLY OR INTRAVENOUSLY TO PREVENT KORSAKOFF'S SYNDROME
• PATIENTS WITH BENZODIAZEPINE INTOXICATION CAN BE GIVEN INJ.FLUMAZENIL
• DOSE:
• 0.2MG IV OVER 15-30 SEC.
• IF AFTER 30 SEC NO RESPONSE ADMINISTER 0.3MG OVER 30 SEC 1 MINUTE LATER
• IF NO RESPONSE THEN 0.5MG OVER 30 SEC AT 1 MINS INTERVAL.
• MAX DOSAGE 3 MG.
Dr.Subrata Nask
77. • USE OF CHOLINESTERASE INHIBITORS, SUCH AS PHYSOSTIGMINE, HAS BEEN
SHOWN TO REDUCE THE SEVERITY OF THE DELIRIUM, PARTICULARLY IN
PATIENTS WITH ANTICHOLINERGIC POISONING
• CURRENTLY TRIALS ARE ONGOING TO COMPARE IF DEXMEDETOMIDINE IS A
MORE EFFECTIVE MEDICATION THAN HALOPERIDOL IN THE TREATMENT OF
AGITATION AND DELIRIUM IN PATIENTS RECEIVING MECHANICAL VENTILATION
IN AN INTENSIVE CARE UNIT
Dr.Subrata Nask
78. ELECTROCONVULSIVE THERAPY (ECT)
• ECT IS ALSO A TREATMENT FOR DELIRIUM WHEN OTHER APPROACHES HAVE
FAILED. .
• IT HAS BEEN USED AS A LAST RESORT FOR DELIRIOUS PATIENTS WITH SEVERE
AGITATION WHO ARE NOT RESPONSIVE TO PHARMACOTHERAPY, SUCH AS
HIGH DOSES OF IV HALOPERIDOL.
SLEEP–WAKE CYCLE
• ATTEMPTS TO RESTORE SLEEP INTEGRITY
• MOVING THE SCHEDULE OF EXISTING SEDATING MEDICATIONS TO THE HOUR OF SLEEP
• REDUCING OR MOVING ACTIVATING MEDICATIONS AND STIMULANTS SUCH AS CAFFEINE
TO THE MORNING.
• BRIEF, JUDICIOUS USE OF SEDATING AGENTS, SUCH AS ZOLPIDEM OR TRAZODONE, TO RESET
THE SLEEP–WAKE CYCLE MAY BE APPROPRIATE.
Dr.Subrata Nask
79. TREATMENT IN SPECIAL POPULATIONS
PARKINSON'S DISEASE
• THE ANTIPARKINSONIAN AGENTS ARE FREQUENTLY IMPLICATED IN CAUSING DELIRIUM
• DECREASING THE DOSAGE OF THE ANTIPARKINSONIAN AGENT HAS TO BE WEIGHED AGAINST
A WORSENING OF MOTOR SYMPTOMS
• IF THE DELIRIUM PERSISTS AFTER ATTENUATION OF THE ANTIPARKINSONIAN AGENTS,
CLOZAPINE IS RECOMMENDED
• IF A PATIENT IS NOT ABLE TO TOLERATE CLOZAPINE, ALTERNATIVE ANTIPSYCHOTIC AGENTS
SHOULD BE CONSIDERED.
Dr.Subrata Nask
80. TERMINALLY ILL PATIENTS
THE FOCUS INITIALLY SHOULD BE AGGRESSIVE SEARCH FOR THE ETIOLOGY
PALLIATION
COMFORT
ASSISTANCE WITH DYING
Dr.Subrata Nask
81. RECENT STUDIES
• RECENT STUDIES SHOW THAT DELIRIUM STRONGLY PREDICTS FUTURE NEW-
ONSET DEMENTIA, AS WELL AS ACCELERATING EXISTING DEMENTIA.
• NEWER STUDIES ON ACH ENHANCERS
• STUDIES DONE ON RIVASTIGMINE SHOW PROMISING RESULTS, BUT SHOULD BE
COMMENCED BEFORE ONSET IF POSSIBLE
• SOME EVIDENCE FOR DONEPEZIL
• 5HT ANTAGONIST - ODANSETRON (8MG/DAY) HAS BEEN FOUND EFFECTIVE
ESPECIALLY IN HYPOACTIVE TYPE, BUT EFFICACY IS FOUND IN BOTH TYPES.
• STIMULANTS ARE NOW FOUND TO BE EFFECTIVE IN HYPOACTIVE TYPE -
MODAFINIL, METHYLPHENIDATE, DEXAMPHETAMINE
Dr.Subrata Nask
82. RECENT STUDIES
• DRUG MODIFYING NE TRANSMISSION
• ALPHA 2 AGONISTS - CLONIDINE, DEXMEDETOMIDINE
• NE RELEASED ESPECIALLY IN WITHDRAWAL STATES AND HYPOXIC
DAMAGE IS SEVERELY NEUROTOXIC
• NEW STUDIES ON DEXMEDETOMIDINE PRE OP AND POSTOP SHOWS IT
REDUCES TRANSITION TO DELIRIUM FROM 40% TO 3-4% AND REDUCED
NEED FOR OPIATE ANALGESICS POST OP
(MALDONADO ET AL, PSYCHOSOMATICS 2009)
Dr.Subrata Nask
83. SUMMARY
• DELIRIUM IS A STATE CHARACTERIZED BY AN ACUTE DECLINE IN BOTH THE
LEVEL OF CONSCIOUSNESS AND COGNITION WITH PARTICULAR
IMPAIRMENT IN ATTENTION.
• THERE ARE MULTIPLE ETIOGIES OF DELIRIUM
• 65% UNRECOGNIZED BY PHYSICIANS
• EARLY DIAGNOSIS AND EVALUATION OF CAUSE IS ESSENTIAL
• TREATMENT INCLUDE PHARMACOLOGICAL AND NON
PHARMACOLOGICAL ASPECT
• NON PHARMACOLOGICAL APPROACH IS MORE ESSENTIAL IN TREATMENT
Dr.Subrata Nask
