Delirium

Nurse pages med student: ..Mr. Smith pulled out his NG tube and cant seem to sit still. Last night after his surgery he was fine, reading the paper and talking to his familytoday I dont even think he knows where he is can you come see him? Med student says: sounds like DELIRIUM- good thing you calledIll be right there.

Case Study
Mrs. M. is a 70 year old woman with a history of thalamic CVA, bipolar illness, chronic pain, and osteoarthritis. She takes Tylenol with codeine, valproate, lithium, conjugated estrogens with progesterone, and aspirin. Two months ago, her daughter died unexpectedly, and she has been more depressed. One week ago, she became agitated and uncooperative. She was seen in the ER, where labs and CXR were normal. A consulting psychiatrist recommended Clonazepam.

Case Study
Despite the clonazepam, she worsened, and became uncontrollable at home. She went back to the ER, where she had a fluctuating level of consciousness. CBC, renal panel, and CXR were normal. An EKG showed a LBBB (old) with slight ST changes from last EKG. Troponin level was 2.9. On further questioning, the patient admitted that she has some shortness of breath 5 days prior. The admitting team concluded that her delirium was due to ischemia/infarction. She was treated with aspirin and beta blockers and did well.

Learning Objectives
Recognize that delirium is a common presentation of disease in the elderly Recognize that delirium is associated with adverse outcomes Know how to distinguish between delirium and other diagnoses (dementia, depression) Identify risk factors for delirium and strategies for risk reduction Discuss management strategies, recognizing the limitations of current data

Delirium
A sudden and significant decline in mental functioning not better accounted for by a pre existing or evolving dementia. Disturbance of consciousness with reduced ability to focus, sustain, and shift attention.

Definition
an acute disorder of attention and cognition (de lira off the path) Standard definition not use until 1980 with publication of DSM III Other terms used include organic brain syndrome, metabolic encephelopathy, toxic psychosis, acute mental status change, exogenous psychosis, sundowning

History
Written descriptions of patients who would meet the current definitions of delirium date back at least 2,500 years.
In the Books of Epidemics, circa 400 BC, Hippocrates, Paul of Aegina, circa the seventh century AD, Almost 300 years ago, delirium was described by Richard Morton, circa the 18th century AD described persons having delirium.

History
Almost 50 years ago, George L. Engel and John Romano postulated that delirium was a reversible cerebral insufficiency due to decreased brain metabolic activity, based on electroencephalogram (EEG) slowing in patients with delirium. In 1980, the third edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III) was the first attempt to standardize delirium nomenclature.

Introduction
A significant public health problem that forebodes poor outcome, delirium is associated with cognitive and functional decline, complicates medical course, and increases resource use and mortality risk. Unfortunately, delirium is under recognized by health care workers.

Delirium is present in 1 percent of adults in the community, in at least 10 percent of emergency department patients, in 40 percent of terminally ill patients, and in as much as one-half of hospitalized patients.

Introduction
Prevalence increases with patient age, complexity of medical comorbidities, and the number and frequency of medications prescribed. Delirium is most often caused by multiple etiologies, such as infection, metabolic abnormalities, endocrinopathies, substance intoxication, and withdrawal. There are several theories proposed to explain its Pathophysiology. These include Neurochemical abnormalities, inflammatory changes, oxidative stress, bloodbrain barrier dysfunction, and interactions between these factors.

Definition
Delirium is defined by the acute onset of fluctuating cognitive impairment and a disturbance of consciousness with reduced ability to attend.
There are frequent associated perceptual abnormalities, sleepwake cycle disturbances, disorganized thought process, and abnormal psychomotor activity.

ICD-10 CLASSIFICATION
F00-F09 Organic, including symptomatic, mental disorders

F00 : Dementia in Alzheimer's disease

F00.0 Dementia in Alzheimer's disease with early onset F00.1 Dementia in Alzheimer's disease with late onset F00.2 Dementia in Alzheimer's disease, atypical or mixed type F00.8 Dementia in Alzheimer's disease, unspecified

F01 : Vascular dementia

F01.0 Vascular dementia of acute onset F01.1 Multi-infarct dementia F01.2 Sub cortical vascular dementia F01.3 Mixed cortical and sub cortical vascular dementia F01.8 Other vascular dementia F01.9 Vascular dementia, unspecified

F02 : Dementia in other diseases classified elsewhere

F02.0 Dementia in Pick's disease F02.1 Dementia in Creutzfeldt-Jakob disease F02.2 Dementia in Huntington's disease F02.3 Dementia in Parkinson's disease F02.4 Dementia in human immunodeficiency virus [HIV] disease F02.8 Dementia in other specified diseases classified elsewhere

F03 : Unspecified dementia

A fifth character may be used to specify dementia in F00-F03, as follows: .x0 Without additional symptoms .x1 With other symptoms, predominantly delusional .x2 With other symptoms, predominantly hallucinatory .x3 With other symptoms, predominantly depressive .x4 With other mixed symptoms A sixth character may be used to indicate the severity of the dementia: .xx0 Mild .xx1 Moderate .xx2 Severe

F04 Organic amnesic syndrome, not induced by alcohol and other psychoactive substances

F05 Delirium, not induced by alcohol and other psychoactive substances F05.0 Delirium, not superimposed on dementia, so described F05.1 Delirium, superimposed on dementia F05.8 Other delirium F05.9 Delirium, unspecified

F06 Other mental disorders due to brain damage and dysfunction and to physical disease F06.0 Organic hallucinosis F06.1 Organic catatonic disorder F06.2 Organic delusional [schizophrenia-like] disorder F06.3 Organic mood [affective] disorder .30 Organic manic disorder .31 Organic bipolar disorder .32 Organic depressive disorder .33 Organic mixed affective disorder

 F06.4 Organic anxiety disorder F06.5 Organic dissociative disorder F06.6 Organic emotionally labile [asthenic] disorder F06.7 Mild cognitive disorder .70 Not associated with a physical disorder .71 Associated with a physical disorder F06.8 Other specified mental disorders due to brain damage and dysfunction and to physical disease F06.9 Unspecified mental disorder due to brain damage and dysfunction and to physical disease

F07 Personality and behavioural disorders due to brain disease, damage and dysfunction F07.0 Organic personality disorder F07.1 Postencephalitic syndrome F07.2 Postconcussional syndrome F07.8 Other organic personality and behavioural disorders due to brain disease, damage and dysfunction F07.9 Unspecified mental disorder due to brain disease, damage and dysfunction
F09 Unspecified organic or symptomatic mental disorder

ICD-10 CRITERIA FOR DELIRIUM

FO5: DELIRIUM, NOT INDUCED BY ALCOHOL AND OTHER PSYCHOACTIVE SUBSTANCES

A. Clouding of consciousness, i.e. reduced clarity of awareness of the environment, with reduced ability to focus, sustain, or shift attention. B. Disturbance of cognition, manifest by both: (1) impairment of immediate recall and recent memory, with relatively intact remote memory; (2) disorientation in time, place or person.

ICD-10 CRITERIA
C. At least one of the following psychomotor disturbances: (1) rapid, unpredictable shifts from hypo-activity to hyper-activity; (2) increased reaction time; (3) increased or decreased flow of speech; (4) enhanced startle reaction.

ICD-10 CRITERIA
D. Disturbance of sleep or the sleep-wake cycle, manifest by at least one of the following: (1) insomnia, which in severe cases may involve total sleep loss, with or without daytime drowsiness, or reversal of the sleep-wake cycle; (2) nocturnal worsening of symptoms; (3) disturbing dreams and nightmares which may continue as hallucinations or illusions after awakening.

ICD-10 CRITERIA
E. Rapid onset and fluctuations of the symptoms over the course of the day. F. Objective evidence from history, physical and neurological examination or laboratory tests of an underlying cerebral or systemic disease (other than psychoactive substance-related) that can be presumed to be responsible for the clinical manifestations in A-D.

Comments
Emotional disturbances such as depression, anxiety or fear, irritability, euphoria, apathy or wondering, perplexity, disturbances of perception (illusions or hallucinations, often visual) and transient delusions are typical but are not specific indications for the diagnosis. Use the fourth character to indicate whether the delirium is superimposed on dementia or not: F05.0 Delirium, not superimposed on dementia F05.1 Delirium, superimposed on dementia F05.8 Other delirium F05.9 Delirium, unspecified

COMPARATIVE NOSOLOGY
Delirium by Other Names: Intensive care unit psychosis Acute confusional state Acute brain failure Encephalitis Encephalopathy Toxic metabolic state Central nervous system toxicity Cinchonism Paraneoplastic limbic encephalitis Sundowning Cerebral insufficiency Organic brain syndrome

Epidemiology
Population Prevalence Range (%) Incidence Range (%)

General medical inpatients

Medical and surgical inpatients General surgical inpatients

1030
515 N/A

316
1055 915 postoperatively

Critical care unit patients

Cardiac surgery inpatients Orthopedic surgery patients

16
1634 33

1683
734 1850

Emergency department
Terminally ill cancer patients Institutionalized elderly

710
2328 44

N/A
83 33

Prevalence
Hospitalized medically ill Hospitalized elderly Postoperative patients Near-death terminal patients 10-30% 10-40% up to 50% up to 80%

4 major causes
Underlying medical condition Substance intoxication Substance withdrawal Combination of any or all of these

Delirium Risk Factors

Age Cognitive impairment 25% delirious are demented 40% demented in hospital delirious Male gender Severe illness Hip fracture Fever or hypothermia Hypotension Malnutrition Alcoholism High number of meds Sensory impairment Psychoactive medications Use of lines and restraints Metabolic disorders: Azotemia Hypo- or hyperglycemia Hypo- or hypernatrmiea Depression Pain

Delirium Risk Model

Patient Factors + Extrinsic Factors
Incidence of delirium per day

Baseline Risk Group

12 10 8 6 4 2 0 High Low

High Low

Low Intermediate High

Precipitating Factor Group

Inouye JAMA 1996

Pathophysiology
Nonspecific manifestation of a widespread reduction in cerebral metabolism & derangement of neurotransmission due to: Cholinergic deficiency GABA Dopamine NE Specific receptors ( e.g., steroid) Alteration of blood flow, inflammation

Hypotheses about Delirium Pathophysiology

Decreased oxidative metabolism :- Abnormal second messenger that uses neurotransmitter as first messenger Reduced cholinergic function:- Change in bloodbrain barrier permeability Dopamine excess Nor epinephrine or Glutamate excess and Serotonin imbalance:- Endocrine abnormality (e.g., hypothalamic-pituitaryadrenal axis and thyroid hormone) - Amino butyric acid imbalance :- Decreased somatostatin like reactivity. Inflammatory hypothesis with cytokine increase Decreased beta endorphin Abnormal signal transduction

Etiology
Although there has been research looking for 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.

To date, the proposed theories for delirium pathophysiology involve neurochemical abnormalities, alterations in metabolism, involvement of cytokines and acute phase reactants, and changes in the permeability of the bloodbrain barrier.
Interestingly, these systems are not mutually exclusive and may have considerable interactions.

Neurochemical Theories
Neurochemical changes in acetylcholine, dopamine, glutamate, - aminobutyric acid (GABA), and serotonin are found in patients with delirium. ACETYLCHOLINE The cholinergic system has been extensively studied in delirium, as it is involved with rapid eye movement (REM) sleep, attention, arousal, and memory. Anticholinergic agents have been found to cause delirium in humans and behavioral and EEG changes in animals.

Dopamine
Dopamine is involved in maintaining and shifting attention via modulation of the frontal cortex. Antipsychotic agents that block dopamine receptors provide symptomatic relief for delirious patients and may result in a relative decrease in dopamine levels. Substances that increase dopamine, such as psychostimulants, carbidopa and levodopa (Sinemet), bupropion (Wellbutrin), or amantadine (Symmetrel), may cause delirium. As dopamine levels increase, cholinergic levels decline, possibly contributing to delirium through the interaction of the two neurotransmitter systems. Additionally, reduction in dopaminergic function is associated with alterations in oxidative metabolism.

Glutamate
Glutamate abnormalities are inferred in the pathophysiology of delirium. Glutamate excitatory neurotoxicity via the N-methyl-D-aspartate (NMDA) receptor may cause apoptosis and neuronal death and has been associated with alcohol intoxication and withdrawal, conditions that are associated with delirium. Wernicke's encephalopathy is example of a delirium that may involve glutamate abnormalities. Wernicke's encephalopathy is due to thiamine deficiency. Thiamine is a cofactor of several enzymes. Evidence suggests that such enzyme deficits result in focal lactic acidosis, cerebral energy impairment, and depolarization of neurons resulting from glutamate excitotoxicity.

GABA
Alterations in GABA activity have been associated with delirium.

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.

In contrast, decreases in CNS GABA levels are observed in patients with delirium resulting from benzodiazepine and alcohol withdrawal.

Serotonin
Excess and attenuated serotonin has been implicated in delirium.

Support for this hypothesis comes from the classic serotonin syndrome, which is a delirium with tachycardia, tremor, diaphoresis, shivering, diarrhea, hyper reflexia, fever, ataxia, and myoclonus.
Additionally, patients with hepatic pathology and delirium have elevations in serotonin. Patients who are withdrawing from serotoninergic agents may also present with delirium, suggesting that the absolute levels of a single neurotransmitter may not explain delirium.

Oxidative Metabolism
Alterations in oxidative metabolism may result in delirium via a number of proposed mechanisms: Neuronal injury Reduced dopaminergic function Reduction of the synthesis and release of acetylcholine Reduced glucose utilization.

The abnormalities in oxidative metabolism may be a final common pathway for the neurotransmitter abnormalities in delirium.

BloodBrain Barrier Alterations

Delirium may be related to capillary endothelial changes that result in the disruption of the bloodbrain barrier. These alterations in permeability may contribute to the pathophysiology of delirium. Cortical biopsies in patients with traumatically induced delirium from epidural and subdural hematomas demonstrate bloodbrain barrier dysfunction. Other studies have proposed bloodbrain barrier dysfunction in delirium tremens and primary hyperparathyroidism, a condition with many neuropsychiatric manifestations, including delirium.

Causes: I WATCH DEATH

I nfections W ithdrawal A cute metabolic T rauma C NS pathology H ypoxia D eficiencies E ndocrinopathies A cute vascular T oxins or drugs H eavy metals

I WATCH DEATH
Infections: encephalitis, meningitis, sepsis Withdrawal: ETOH, sedative-hypnotics, barbiturates Acute metabolic: acid-base, electrolytes, liver or renal failure Trauma: brain injury, burns

I WATCH DEATH
CNS pathology: hemorrhage, seizures, stroke, tumor (dont forget metastases) Hypoxia: CO poisoning, hypoxia, pulmonary or cardiac failure, anemia Deficiencies: thiamine, niacin, B12 Endocrinopathies: hyper- or hypoadrenocortisolism, hyper- or hypoglycemia

I WATCH DEATH

Acute vascular: hypertensive encephalopthy and shock Toxins or drugs: pesticides, solvents, medications, (many!) drugs of abuse
anticholinergics, narcotic analgesics, sedatives

Heavy metals: lead, manganese, mercury

Drugs of abuse
Alcohol Amphetamines Cannabis Cocaine Hallucinogens Inhalants Opiates Phencyclidine (PCP) Sedatives Hypnotics

Clinical features
Prodrome Fluctuating course Attention deficits Arousal /psychomotor disturbance Impaired cognition Sleep-wake disturbance Altered perceptions Affective disturbances

Prodrome
Restlessness Anxiety Sleep disturbance

Fluctuating course
Develops over a short period (hours to days) Symptoms fluctuate during the course of the day (SYMPTOMS WAX AND WANE)
Levels of consciousness Orientation Agitation Short-term memory Hallucinations

Attentional deficits
Easily distracted by the environment
May be able to focus initially, but will not be able to sustain or shift attention

Arousal/psychomotor disturbance
Hyperactive (agitated, hyperalert) Hypoactive (lethargic, hypoalert) Mixed

Impaired cognition
Memory Deficits Language Disturbance Disorganized thinking Disorientation
Time of day, date, place, situation, others, self

Sleep-wake disturbance
Fragmented throughout 24-hour period Reversal of normal cycle

Altered perceptions
Illusions Hallucinations - Visual (most common) - Auditory - Tactile, Gustatory, Olfactory Delusions

Affective disturbance
Anxiety / fear Depression Irritability Apathy Euphoria Lability

Duration
Typically, symptoms resolve in 10-12 days or may last up to 2 months Dependent on underlying problem and management

Determining the Causes of Delirium

Gather history from patient, health care providers, friends, and family Establish extent and acuity of the medical co-morbidities with labs and diagnostic studies as appropriate. Review the medication list. Consider the medications that were recently stopped, as withdrawal may be a factor. Review for substances of abuse and dependence. Urine or serum toxicology.

Determining the Causes of Delirium

Consider the substances that were recently stopped, as withdrawal may be a factor (e.g., alcohol, benzodiazepines, and opiates). Consider over-the-counter medications, herbal preparations, and teas. Establish whether there was recent exposure to anesthesia or surgery. Evaluate vital signs for autonomic changes. Check all indwelling catheters for signs of infection. Check skin for evidence of breakdown or infection.

Determining the Causes of Delirium

Evaluate for pain severity, duration, and intensity. Evaluate for constipation or diarrhea. Evaluate for urinary tract infection. Evaluate for acidbase disturbance. Consider deep venous thrombosis or pulmonary embolus. Consider seizure or postictal state; consider electroencephalogram. Review laboratory studies for evidence of renal, cardiac, hepatic, pulmonary, or hematological dysfunction.

Determining the Causes of Delirium

Check nutritional status. Consider whether there is sensory overload or deprivation (e.g., too close to the nursing station or agitated roommate vs. glasses or hearing aide misplaced or absent). Consider structural neuroimaging. Consider cerebrospinal evaluation. Consider additional body fluid analyses . Consider medicationmedication interactions. Consider medicationover-the-counter medication interactions.

Differential Diagnosis
CNS pathology Dementia, particularly frontal lobe Other Psychiatric disorders Psychosis Depression: 41% misdiagnosed as depression
Farrell Arch Intern Med 1995

Bipolar disorder Aconvulsive status epilepticus Akathisia Overall, 32-67% missed or misdiagnosed

Workup
History Interview- also with family, if available Physical, cognitive, and neurological exam Vital signs, fluid status Review of medical record
Anesthesia and medication record review temporal correlation?

Mini-mental state examination

Tests orientation, short-term memory, attention, concentration, constructional ability 30 points is perfect score
< 20 points suggestive of problem Not helpful without knowing baseline

Workup
Electrolytes CBC EKG CXR EEG- not usually necessary Arterial blood gas or Oxygen saturation Urinalysis +/- Culture and sensitivity Urine drug screen Blood alcohol Serum drug levels (digoxin, theophylline, phenobarbital, cyclosporin, lithium, etc)

CAM
(Confusion Assessment Method)
1. Acute change & fluctuation in mental status and behavior AND 2. Inattention AND EITHER 3. Disorganized thinking OR 4. Altered consciousness (not alert) (Inouye SK et al. Ann Intern Med 1990;113:941-948.)

Diagnostic Tools
Sensitivity Specificity

CAM* Delirium Rating Scale* Clock draw

.46-.92 .82-.94 .87

.90.92 .82-.94 .93

MMSE (23/24 cutoff) Digit span test

.52-87 .34

.76-.82 .90

*validated for delirium & capable of distinguishing delirium from dementia

Diagnosis
MMSE & Clock draw
-Not designed for delirium -Useful at separating normal from abnormal -Not specific for distinguishing delirium from dementia -May be useful as change from baseline

Delirium versus Dementia

Delirium
Rapid onset Primary defect in attention Fluctuates during the course of a day Visual hallucinations common Often cannot attend to MMSE or clock draw

Dementia
Insidious onset Primary defect in short term memory Attention often normal Does not fluctuate during day Visual hallucinations less common Can attend to MMSE or clock draw, but cannot perform well

Medications and Delirium

Sedative-hypnotics, especially benzos Narcotics, especially meperidine Anticholinergic Miscellaneous
Lidocaine Amiodorone H2 Blockers Steroids NSAIAs -Propranolol -Digoxin -Lithium -Metoclopromide -Levodopa

Consider any drug a possible cause

Can Interventions Prevent Delirium?

Risk factor reduction strategy targeting: cognitive impairment sleep deprivation immobility visual impairment dehydration

Intervention Protocol
Cognition Sleep Immobility Vision Hearing Dehydration ::Orientation, activities Bedtime drink, massage, music, noise reduction Ambulation, exercises Visual aids and adaptive equipment Portable amplifiers, cerumen disimpaction BUN, volume repletion

::::-

Outcome
May progress to stupor, coma, seizures or death, particularly if untreated Increased risk for postoperative complications, longer postoperative recuperation, longer hospital stays, long-term disability Elderly patients 22-76% chance of dying during that hospitalization Several studies suggest that up to 25% of all patients with delirium die within 6 months.

Management
Identify and treat the underlying etiology. Increase observation and monitoring vital signs, fluid intake and output, oxygenation, safety. Discontinue or minimize dosing of nonessential medications. Coordinate with other physicians and providers. Monitor and assure safety of patient and staff - suicidality and violence potential - fall & wandering risk - need for a sitter - remove potentially dangerous items from the environment - restrain when other means not effective

Management
Assess individual characteristics and family psychosocial

Establish and maintain an alliance with the family and other clinicians Educate the family temporary and part of a medical condition not crazy Provide post-delirium education and processing for patient

Management
Environmental interventions - Timelessness - Sensory impairment (vision, hearing) - Orientation cues - Family members - Frequent reorientation - Nightlights

Management
Pharmacologic management of agitation - Low doses of high potency Neuroleptic (i.e. haloperidol) p/o, IM or IV - Atypical antipsychotics (Risperidone) - Inapsine (more sedating with more rapid onset than haloperidol IM or IV only monitor for hypotension) Haloperidol and inapsine have been associated with sudden death by lengthening the QT interval; avoid or monitor by telemetry if corrected QT interval is greater than 450 m sec or greater than 25% from a previous EKG.

Neuroleptics
Considered agents of choice for most cases of delirium RCTs in agitation and dementia suggest benefit (NNT = 5) Side effects can include extra pyramidal SEs, hypotension, sedation, Akathisia Sedation effect before antipsychotic effect Haloperidol, droperidol Atypical: Risperidone, Olanzapine

Use of Haloperidol
Lowest possible dose, e.g., .5-1.0 BID tapering down as delirium clears 0.5mg, repeat every 30 minutes until agitation is controlled Some advocate doubling of dose every 30 minutes until agitation is controlled (probably not wise in elderly!) Droperidol can be used IV - more rapid onset Caution: sedation, hypotension, less anti-psychotic than haloperidol

Atypical Neuroleptics
Risperidone: for those with side effects from haloperidol or contraindications Starting dose: 0.5mg HS or BID
Olanzapine: agent of choice for patients with PD with hallucinations/delirium Starting dose 2.5mg PO HS or BID

Benzodiazepines
Should usually be avoided. Agents of choice for ETOH, benzodiazepines withdrawal More rapid onset than Neuroleptics. Peak effects brief, sedation more common, can prolong delirium May be useful in terminal delirium associated with high dose narcotics and myoclonus Lorazepam 0.5-1 mg IV or PO (t1/2 15-20 hours)

Other agents
? Trazadone 25-100mg Physostigmine (dont try this) reverses delirium due to Anticholinergic activity SEs: bradycardia, asystole, bronchospasm, seizures ? Donepezil ? Mood stabilizers Narcotics and pain medications (empiric use in patients with dementia often helpful)

Delirium in the ICU

Unlikely to be entirely preventable due to burden of illness, interventions, and environment
Restraints less humane than sedation (my opinion) Depth of sedation? Sedative of choice?

Prevention is the Best Medicine

All evidence suggests that it is easier to PREVENT delirium than to TREAT delirium Prevention of delirium is least likely to be possible in the intensive care unit Treatment of delirium in the intensive care unit is particularly challenging and most likely to require medications or physical restraints

Management
Benzodiazepines Treatment of choice for delirium due to benzodiazepine or alcohol withdrawal. May worsen confusion in delirium Contraindicated in delirium due to hepatic encephalopathy

Nursing Interventions
Eliminate extra medicines, reverse metabolic abnormalities, hydration, nutrition Geriatric consultation? Education of patients and family Re-orientation by staff, family, sitters, clocks, calendars Remove nonessential lines and tubes Quiet, non interrupted sleep at night Stimulation (but not too much) during day Discharge home?

What we seecommon cases

Homeless male, hx. ETOH abuse, 2 days post-op 82 year-old women with UTI Burn victim after multiple med changes Mildly demented 71 year-old after hip replacement

Summary
Delirium is common and is often a harbinger of death- especially in vulnerable populations. It is a sudden change in mental status, with a fluctuating course, marked by decreased attention. It is caused by underlying medical problems, drug intoxication/withdrawal, or a combination. Recognizing delirium and searching for the cause can save the patients life.

Summary
Delirium is common in older inpatients, associated with poor outcomes, and commonly missed or misdiagnosed Prevention is the best approach Management involves treating underlying causes, minimizing medications, supportive care, and avoidance of restraints when possible ICU delirium poses particular challenges Further research and RCTs are needed