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Transcript
Emergency Psychiatry
(The Acutely Disturbed Patient)
A/Professor David Ash
Senior Visiting Consultant
Intensive Care Unit
Glenside Hospital
Introduction
1. A/Professor David Ash
• Overview
• Setting
• Cedars Psychiatric Intensive Care Unit
• Violence and aggression
• Pharmacotherapy
–
–
–
–
–
Agitated, psychotic patient
Mania, schizomania
Bipolar depression, schizodepression
Unipolar depression
Patient perspective
• ECT
• Substance abuse
A/Professor David Ash
2
Overview
• Emergency psychiatry is a subspecialty of
psychiatry that has evolved over the last 30
years.
• Reduction in inpatient beds has resulted in
the growth of psychiatric emergency services
and an increase in the numbers of people
seen in the community.
• Principles of crisis intervention.
A/Professor David Ash
3
Psychiatric Emergencies
• No single condition or illness
• Any situation requiring immediate assessment
and rapid intervention
• Involve behavioural disturbance, threat of
behavioural disturbance, physiological
disturbance, high risk assessment
A/Professor David Ash
4
Psychiatric Emergencies
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Suicidal Presentations
Aggression and Violence
Acute psychosis
Mood disorders – mania and depression
Personality disorders in crisis
Major disasters
A/Professor David Ash
5
Psychiatric Emergencies
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Alcohol / substance abuse or intoxication
Medical conditions
Delirium
Neuroleptic Malignant Syndrome
Serotonin syndrome
Lithium toxicity
A/Professor David Ash
6
Psychiatric Emergencies
•
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Alcohol / substance abuse or intoxication
Medical conditions
Delirium
Neuroleptic Malignant Syndrome
Serotonin syndrome
Lithium toxicity
A/Professor David Ash
7
Risk Assessment
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Self harm
Self neglect
Victim of aggression, violence
Suicide
Disinhibition
Impulsivity
Restlessness, agitation
Harassment, verbal aggression
Threatened / actual aggression, violence
Absconding risk
Available support
Insight
Ability to work with treating clinicians
Availability of suitable accommodation
Substance use
Alcohol
A/Professor David Ash
8
The Setting
•
•
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Community
Crisis units / short stay units/ crisis beds
Emergency department
Inpatient unit
High dependency unit (HDU) / Intensive care
unit (ICU)
A/Professor David Ash
9
The Community
• Location – community clinic, patient’s home
• Preferred by patients
• Able to assess person’s capacity to cope in familiar
home environment
• Presence of family, neighbours, friends
• Safety issues
– Work in pairs
– Risk assessment prior to visit, if necessary police
in attendance
– Weapons
– Ensure front door not deadlocked
– Decision to detain – end interview – ensure that
ambulance, police in attendance
A/Professor David Ash
10
I didn’t knowA/Professor
they made
house calls
David Ash
11
Emergency Department
• Triage
• Safe environment for emergency evaluation
– Weapon screening
– Rooms in which the examiner cannot be easily
trapped
– Open vs enclosed interview area
– Method to call for help
– Adequate personnel to respond if help is needed
including trained security personnel
A/Professor David Ash
12
Crisis Units / Short Stay Units/
Crisis Beds, PECCU
• Location – community, mental health
centres, psychiatric hospitals (Ash,
Galletly), general hospitals (Frank et al)
• Short term crisis admission, triage,
transfer
• Early discharge, community treatment
A/Professor David Ash
13
Inpatient Units
•
•
•
•
•
Higher acuity
Aggression and violence
Substance abuse
Forensic issues
Homelessness (Ash, Galletly et al)
A/Professor David Ash
14
Inpatient Units
•
•
•
•
•
•
Safe environment for patients / staff
Time out, restraint, seclusion
Guidelines for risk management
Staff training / staff morale
Leadership / support
Linkage and communication with community
resources
A/Professor David Ash
15
Not much of a psychiatric unit, though, is it?
A/Professor David Ash
16
ICU / HDU
Admission to the ICU / HDU is indicated for:
Dangerous, aggressive self harming behavior, not able to be
contained in a less restrictive environment
Aim for brief admission with:
• Intensive treatment
• High nurse / patient ratios
• Calming environment
• Recovery based services
Potential disadvantages of ICU / HDU:
• Risk of assault
• Overmedication
• Overstimulation
• Worsening of symptoms
A/Professor David Ash
• PTSD
17
Options
1. Central, stand alone ICUs
2. Smaller HDU / ICUs in inpatient units
Flexibility, closed / open options
3. Intensive nursing 1:1 in open ward
Associated Issues
•
•
consumer involvement
how to reduce trauma associated with inpatient care in the
HDU / ICU
• safety care plans
• sensory modulation
• debriefing, counselling following seclusion and restraint
A/Professor David Ash
18
Cedars PICU - Adelaide
• Intake from: CNAHS (North, East), overflow from West
Rural and Remote (on Glenside Campus) + all indigenous
people
• 10 beds
Cedars PICU:
Psychiatrist 1.1 FTE
Psychiatric Registrars 1 – 2 FTE
CSC 1 FTE
CN 1 FTE
Primary Nurses 4
Social Worker 1 FTE
Drug and Alcohol Clinician 0.2 FTE
Carer Support Worked 0.5 FTE
•
•
•
Daily handover meetings and clinical review
Experienced nursing staff
Non-pharmacological interventions include:
•
•
One to one counselling and support
Recovery-focussed care
Early intervention/de-escalation techniques
Psycho-education
Drug and alcohol counselling
Judicious use of medication, restraint, seclusion
Communication with patients, family,
support networks,
A/Professor
David Ash treating teams (clinicians)
19
Cedars PICU - Adelaide
Routine monitoring of electrolytes, renal
function, liver function, glucose,
cholesterol, lipid profile, ECG, BMI
A/Professor David Ash
20
Treatment of Behavioural Emergencies –
summary of expert consensus guidelines
Preferred initial interventions for an imminently
violent patient:
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•
•
•
•
Verbal intervention
Voluntary medication
Show of force
Emergency medication
Offer food, beverage, other assistance
Alternate Interventions:
• Physical restraint
• Locked or unlocked quiet room, seclusion
A/Professor David Ash
21
-
Treatment of Behavioural Emergencies summary of
expert consensus guidelines
When to use physical restraint:
Extremely or usually appropriate:
• Acute danger to other patients, bystanders, staff or self
Sometimes appropriate:
• To prevent an involuntary patients from leaving prior to
assessment or transfer to a locked facility
Rarely or never appropriate:
•
•
•
•
Lack of resources to supervise patient adequately
To prevent a voluntary patient from leaving prior to assessment
To maintain an orderly treatment environment
History of previous self-injury or aggression
A/Professor David Ash
22
A/Professor David Ash
23
Illusion - self deception
in regard to the memory
of a past experience
A/Professor David Ash
24
Violence and Aggression
Aggression: Hostile or destructive behaviour or actions
Violence: Physical force exerted for the purpose of
violating, damaging, or abusing
Contemporary concerns
•
•
•
Unprovoked, haphazard violence
Violence by people suffering from mental illness
Terrorism
A/Professor David Ash
25
Models of Aggression
• Don Grant
dehumanization
acceptance of violence
rage and its control
• Learning Theory
Bandura - imitation and modeling of aggression
• Megargee
over vs under controlled personality
• Group dynamics
primitive, murderous rage
A/Professor David Ash
26
Psychodynamic Concepts of
Aggression
•
•
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•
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aggression as an innate drive
ambivalence of primary love object
deficits in superego development
defence against feelings of inferiority or impotence
splitting
displacement
projection
projective identification
A/Professor David Ash
27
Social and Cultural Aspects
• Young men in low socioeconomic groups have an
increased risk of violence and of being a victim of violence
• USA – nonwhites are more likely to be offenders and
victims of violence
• There are differences between countries (e.g. Europe
compared to USA)
• Culture:
• Subcultures of violence
• Regional cultures of violence
• Societal values and violence
• Economic inequality and criminal violence
• Inequality of opportunity and criminal violence
A/Professor David Ash
28
Biological
• Lorenz – aggression is an inherent tension-producing
drive
• Amygdala, hypothalamus, prefrontal cortex, limbic
system
• Cortical dysfunction e.g. abnormal EEG in antisocial
personality disorder
• Genetic e.g. sex chromosome abnormalities
• Hormonal
• Neurotransmitters
 GABA,  serotonin,  noradrenalin and 
dopamine are associated with increased aggression
• Alcohol, substance abuse
A/Professor David Ash
29
Developmental Factors
Associated with Adult Violence
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Abuse by parents
Truancy, school failure, lower IQ
Delinquency as an adolescent
Arrest for prior assaults
Childhood hyperactivity
First psychiatric hospitalization by age 18 years
Fire setting and animal cruelty
History of being a childhood bully
A/Professor David Ash
30
Risk Factors for Aggression or
Violence
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•
•
•
•
young, male
developmental factors
less education
lack of sustained employment
lower socioeconomic status
history of substance abuse
acute intoxication with alcohol and / or psychoactive
substances
past history of violence, aggression
violent fantasies
forensic history
A/Professor David Ash
31
Risk Factors for Aggression and
Violence (continued)
• chronic anger towards others
• recent sense of being unfairly treated.
• residential instability – homeless mentally ill more
likely to offend
• antisocial / borderline personality disorder
• mania
• acute psychosis – delusional beliefs involving
particular individuals
• command hallucinations
• delirium
• dementia
A/Professor David Ash
32
A/Professor David Ash
Paranoia – delusions of persecution
33
Assessing the Aggressive,
Violent Patient
Aims:
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•
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To ensure your own safety
To ensure the safety of staff and other patients
To keep the patient safe
To detect the presence of acute medical problems
To detect the presence of psychiatric illness
To achieve rapid stabilization and disposition of the
patient
A/Professor David Ash
34
Clinical Evaluation
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Remain at a safe distance
Privacy but not isolation
Offer food, drink, universal language of hospitality
Look and listen, be respectful
Talk with an even, concerned tone of voice
Consider the timing of questions and directions
Ask simple questions
Avoid being provocative
Agree to disagree
Maintain observational awareness – warning signs
Obtain collateral history
A/Professor David Ash
35
Clinical Evaluation
• The environment should not be fragile
• Know where the alarms are located and how to
activate them
• Ensure availability, presence of adequately trained
staff and security personnel
• Ensure a means of escape
A/Professor David Ash
36
Predictors of Impending Violence
Include:
•
•
•
•
•
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Refusal to cooperate
Intense staring
Motor restlessness
Purposeless movements
Labile affect
Loud speech
Irritability
Intimidating behavior
Damage to property
Demeaning or hostile verbal behavior
Direct threat of assault
A/Professor David Ash
37
Hillard and Zatek
Management
• Establish differential diagnosis
• Attempt where possible to initiate treatment with
medication to treat underlying illness.
• Assess risk to others (specific threats) – duty to warn
• Weapons – firearms notification
• Where to treat?
• Voluntary or detained?
• Use verbal strategies initially; if necessary use
restraint, emergency medication, seclusion
• Liaise with treating team/clinicians (if any)
• If no evidence of psychiatric or medical illness –
consider involving the police.
A/Professor David Ash
38
Pharmacotherapy – General Principles
Choice of medication is based on:
•
•
•
•
diagnostic assessment,
past history,
medical comorbidities,
substance abuse and intoxication
A/Professor David Ash
39
Choice of Medication
Consider:
• speed of onset
• oral vs IM
• duration of action
• side effects
• past response
• patient preference
A/Professor David Ash
40
Consumer Perspective
• Consumers stress the importance of staff treating them with respect,
communicating, listening, involving them in treatment decisions (Allen)
• Expert Consensus Guidelines (Behavioral Emergencies), (Allen):
- Verbal interaction
- Collaborative approach
- Oral medication if possible – guided by consumer’s problems, medication
experiences and preferences
• IM medication – can be a symbolic assault involving
– Physical trauma
– emotional trauma
– Risk of side effects
Compromises the clinician – patient relationship
May reduce future medication adherence
A/Professor David Ash
41
Consumer Perspective
• 1/5 of a consumer panel attributed their
emergency contact to lack of access to more
routine mental health care
• almost 50% of consumers said they wanted
medication and benefited from medication
• Many complained about forced administration
and unwanted side effects
A/Professor David Ash
42
Consumer Panel Stressed the Importance
of:
•
•
•
•
Alternatives to traditional emergency room services
Increased use of advance directives
More comfortable physical environments
Improved training of emergency unit staff to foster a
humane, person-centres approach
• Collaboration between practitioners and consumers
• Improved discharge planning and reliable , consistent
aftercare
A/Professor David Ash
43
Benzodiazepines
Exercise caution in the use of benzodiazepines:
•
•
•
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•
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elderly
patients with respiratory disease
acute intoxication with alcohol
severe impairment of hepatic or renal function
depressed level of consciousness,
patients using other sedating medications
A/Professor David Ash
44
Midazolam
• Midazolam 2 – 10 mg (IM/IV) is often used in the
emergency department for agitated, aggressive
patients
• Midazolam IM is also used in ICU – Brentwood
• Risk of respiratory depression – requires close
monitoring and ideally pulse oximetry
• Onset of action 1 – 15 minutes (depending on route
of administration)
• Half life 1 – 2.8 hours
A/Professor David Ash
45
Clonazepam
• Clonazepam (0.5 – 2 mg) is a longer acting IM
alternative to midazolam – but risks associated with
excessive sedation, ataxia
• Onset of action 5 – 15 minutes
• Peak plasma levels in less than 4 hours
• Half life 20 – 40 hours
A/Professor David Ash
46
Lorazepam
• Lorazepam (0.5 – 2.5 mg) is often favoured over
diazepam because of the shorter half life
• Onset of action 5 – 15 minutes
• Peak plasma levels in 2 hours (oral and IM have a
similar absorption profile)
• Half life 10 – 20 hours
• Less respiratory depression than Diazepam and
Midazolam
A/Professor David Ash
47
Diazepam
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•
•
•
Diazepam (2.5 – 10 mg) is well absorbed orally
IM absorption is erratic
Onset of action (oral) up to 30 minutes
Half life 14 - 60 hours (has multiple active
metabolites)
A/Professor David Ash
48
Antipsychotic Medication
First Generation Antipsychotics –
Low Potency
 sedation
postural hypotension
 EPS
Chlorpromazine (oral)
•
•
•
Onset of action up to 20 minutes with oral medication
Peak plasma levels -2-4 hours
Half life 24 hours (range 8-35 hours)
Intermediate Potency
e.g. perphenazine
A/Professor David Ash
49
First Generation Antipsychotics – High Potency
tranquilization
 EPS
Haloperidol (oral / IM)
• Time of Onset of action depends on route of
administration
– IV – immediate
– Oral - up to 60 minutes
• Half life 24 hours
A/Professor David Ash
50
Zuclopenthixol
• Zuclopenthixol HCl (Clopixol) 10, 25mg tablets
• Onset of action 10-30 minutes
• Peak plasma levels in less than 4 hours
• Half life 24 hours
A/Professor David Ash
51
Droperidol
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•
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•
•
Droperidol is a high potency Butyrophenone
Parenteral preparation
Maximum dose 30 mg over 24 hours
Onset action (IM) 1 – 20 minutes
Duration of action 2 – 4 hours
Half life 2.2 hours
Prolongation QT interval
A/Professor David Ash
52
Acuphase (Zuclopenthixol
acetate)
• Acuphase (Zuclopenthixol acetate) – short acting
depot used when IM medication is required, with
tranquilization lasting 24 to 72 hours
• Onset of action 4 to 6 hours
• Monitor for EPS
• Exercise caution in treatment naive patients
A/Professor David Ash
53
Second Generation
Antipsychotics (SGAs)
• Risperidone (tablets, quicklets, depot)
• Paliperidone (tablets, depot)
• Olanzapine (tablets, wafers, short-acting IM,
depot)
• Amisulpride (tablets, syrup)
• Aripiprazole (tablets, short-acting IM)
• Quetiapine IR, XR (tablets)
• Ziprasidone (tablets, short-acting IM)
• Clozapine (tablets, syrup)
A/Professor David Ash
54
Second Generation
Antipsychotics
• Until recently research suggested SGAs have
superior efficacy for negative symptoms, cognition
and mood in schizophrenia.
• First episode psychosis (low dose)
• SGAs are also used
–
–
–
–
For tranquilization and to reduce hostility in agitated patients
In mania and depression
As mood stabilizers
In anxiety disorders including GAD and social anxiety
disorder
– As augmentation treatments in OCD and treatment-resistant
depression
– As monotherapy / augmentation in PTSD and borderline
personality disorder
– Behavioral disturbance
in dementia
A/Professor
David Ash and brain injury
55
Second Generation Antipsychotics
• Less likely to cause EPS, although can occur with 2nd
generation antipsychotics esp. Risperidone, Amisulpride
in higher doses (Aripiprazole – restlessness)
• EPS less likely with Quetiapine and Clozapine
• Metabolic syndrome (predominantly Clozapine,
Olanzapine)
• Cardiovascular / cerebrovascular events in the elderly
?class effect
• Postural hypotension (Risperidone, Quetiapine)
• Hyperprolactinemia (Risperidone, Amisulpride)
• QTc prolongation (e.g. Ziprasidone, Amisulpride,
Quetiapine)
A/Professor David Ash
56
Second Generation Antipsychotics –
Controversies, Unresolved Issues
• Drug development studies have focused on
reduction in symptoms severity with restrictive
inclusion / exclusion criteria.
• Short term, narrowly focused trials provide
limited information about the effectiveness of
drugs in clinical practice.
• Recent studies have raised questions about
the advantages of SGAs in schizophrenia:
(CATIE, CAFÉ, CUtLASS 1, EUFEST,
Goldberg et al)
A/Professor David Ash
57
Risperidone
•
•
•
•
•
•
•
Oral, quicklets
0.5 – 2 mg stat dose
Onset action 10 - 30 minutes
Peak plasma levels 1-2 hours
Duration of action 6 - 10 hours
Half life 19 hours
Postural hypotension, EPS (high
dose), hyperprolactinemia
A/Professor David Ash
58
Paliperidone
• Active metabolite of risperidone
• Prolonged release tablet
• Peak plasma concentrations about 24 hours after oral
dosing
• Elimination half-life of about 23 hours
• Similar side effects to risperidone
A/Professor David Ash
59
Olanzapine
•
•
•
•
Oral, wafers, IM
2.5 – 10 mg stat dose
Onset of action 15 - 60 minutes
Peak plasma levels 15 minutes -8 hours (depending
on route of administration)
• Half life 27 hours
• Metabolic syndrome, sedation
A/Professor David Ash
60
Amisulpride
•
•
•
•
Oral – tablets, syrup
Peak plasma level 1 – 4 hours
Half life 12 hours
EPS, hyperprolactinemia and QTc prologation at
high dose
Aripiprazole
•
•
•
•
•
Oral – tablets
Onset action 1 – 3 hours
Peak plasma level 3-5 hours
Half life 75 hours
Restlessness
A/Professor David Ash
61
Quetiapine IR
•
•
•
•
•
•
•
•
Oral - tablets
50-150mg stat dose
Onset of action 10 - 30 minutes
Peak plasma level 1-5 hours
Duration of Action 4 - 12 hours
Half life 6-7 hours
Postural hypotnesion,sedation
? QTc prologation at high dose
XR form now available, longer half life.
A/Professor David Ash
62
Ziprasidone
•
•
•
•
•
80 – 160 mg / day
Must be taken with food
Low incidence weight gain
Akathisia
QTc prologation
A/Professor David Ash
63
Clozapine
•
•
•
•
Oral - tablets
Peak plasma levels 2-5 hours
Half life 12 hours
Agranulocytosis, myocarditis,
cardiomyopathy, metabolic syndrome,
lower seizure threshold – balance
benefit against risk.
A/Professor David Ash
64
Antipsychotics and Risk of Sudden Death
Straus et al. 2004
Precise mechanism uncertain, suggestions include:
•
•
•
•
•
Peripheral vasodilatation and cardiovascular collapse
Oral laryngeal / pharyngeal dystonia
Acute myocarditis
Cardiomyopathy
QTc prolongation
A/Professor David Ash
65
Antipsychotics and Risk of Sudden
Death
Straus et al. 2004
• Integrated Primary Care Information Project
• 554 cases of sudden cardiac death
• Current use of antipsychotics was associated
with a 3 fold increase in the risk of sudden
cardiac death
• Risk highest with butyrophenone antipsychotics
(e.g. haloperidol / droperidol) and short term
use
A/Professor David Ash
66
QTc Interval
• Dose dependant prolongation of QTc interval may
potentiate risk of serious ventricular arrhythmias such as
Torsade de Pointes (rare occurrence < 0.01%)
• Risk enhanced by existence of
– bradycardia (< 55)
– hypokalaemia
– congenital prolongation of QTc interval
– treatment with medications that produce pronounced
bradycardia, slowing of intracardiac conduction or
prolongation of QTc interval
– should not be given with drugs that induce arrythmias
such as amiodorone, quinidine, sotolol, cisapride,
thioridazine and erythromycin
A/Professor David Ash
67
Medication for agitated, psychotic
patients
Generally involves a combination of:
• Oral atypical antipsychotic
• Oral benzodiazepine in the first instance
If compliance is an issue:
• Olanzapine / risperidone dissolvable wafers or
• Risperidone / amisulpride syrup
A/Professor David Ash
68
Parenteral Medication
If patient more agitated or unwilling to accept oral medication:
• IM olanzapine or IM haloperidol plus
• IM lorazepam / clonazepam /midazolam
If patient extremely agitated and presents an ongoing threat
to self or others or has not responded to IM olanzapine / IM
haloperidol consider use of:
• zuclopenthixol acetate plus
• IM lorazepam / clonazepam / midazolam
Monitor level of sedation, respiration. Ideally pulse oximetry if
using midazolam.
A/Professor David Ash
69
Mania / Schizoaffective Disorder with
Mania
Medications which have efficacy include:
•
•
•
•
•
Lithium Carbonate
Sodium Valproate
Carbamazepine
Olanzapine
ziprasidone
•
•
•
•
Quetiapine
Risperidone
Aripiprazole
Clozapine
In practise second generation antipsychotics are often used in
combination with anticonvulsants / lithium carbonate.
Concurrent use of oral / parenteral benzodiazepines to sedate
and reduce arousal.
A/Professor David Ash
70
Sodium Valproate:
• loading dose 20-30 mg/kg.
• If no response after 7 - 10 days consider alternative
mood stabilizer
• more efficacious in patients with:
mixed affective states
rapid cycling
comorbid substance abuse
A/Professor David Ash
71
Bipolar Depression /
Schizoaffective Disorder with Depression
• Optimize mood stabilizer
• Antidepressant medication – ? Efficacy in BP
depression
• Benzodiazepines to reduce arousal / agitation
• SGA to reduce arousal / agitation and/or psychotic
symptoms, augment treatment of depression
• If compliance has not been an issue consider an
alternative mood stabilizer
• Lamotrigine has efficacy in prophylaxis of bipolar
depression – however has limited value in the acute
setting
• Monitor mood / suicidal ideation – provision of
treatment in safe environment
A/Professor David Ash
• SGA monotherapy in bipolar depression
72
Unipolar Depression
• Antidepressant medication
• Second generation antipsychotic monotherapy
(quetiapine)
• Second generation antipsychotic to reduce
arousal / agitation and / or psychotic symptoms
• Benzodiazepines to reduce arousal / agitation
• Monitor mood / suicidal ideation – provision of
treatment in safe environment
• Consider augmentation strategies e.g. lithium,
thyroxine, secondA/Professor
generation
antipsychotic etc.
David Ash
73
Schizophrenia
RANZCP Clinical Practice Guidelines, McGorry et al 2005
• SGA – treatment of first choice
• Conventional antipsychotic in low dosage where there is
remission, good tolerability, or depot medication unavoidable
• Consider clozapine if there is incomplete remission with at least
2 other antipsychotic agents
• Psychosocial interventions – assertive community treatment,
medication adherence therapy, (cognitive remediation therapy)
• Consumer involvement
• Physical health – prevention and early treatment of medical
illness
• Shared care with GP.
A/Professor David Ash
74
Treatment Resistant
Schizophrenia
Also:
• Clozapine / amisulpride combination
• Clozapine / aripiprazole combination
• Clozapine / ECT
A/Professor David Ash
75
ECT - Indications
Depression
Bipolar depression
Unipolar depression
Psychotic features
Lack of response to pharmacotherapy
Severe illness with significant risk to self through
suicide or self neglect
Mania
Severe mania unresponsive to pharmacotherapy
A/Professor David Ash
76
ECT - Indications
Schizophrenia
Catatonia
Associated depression
Inadequate response to pharmacotherapy
Severe illness, risk to self, others
Evidence for combined clozapine and ECT in
treatment refractory schizophrenia
A/Professor David Ash
77
Shock treatment – therapy used to alter favorably the course
A/Professor David Ash
78
of a mental illness
Substance Abuse
• Two to three times more common among
those with psychiatric illness than in general
population.
• Negative attitudes towards this subset of the
population hinders the provision of effective
care.
• Urine drug screening helpful
A/Professor David Ash
79
Common Substances of Abuse
•
•
•
•
•
•
•
•
Alcohol
Cocaine
Amphetamine
Methamphetamine
MDMA (3,4 methylene dioxymethamphetamine), (ecstasy)
Ketamine
Cannabis
Opiates
A/Professor David Ash
80
The Drug Abusing Patient
• Patient may present with intoxication or withdrawal
symptom.
• Stimulant intoxication may induce paranoid
symptoms, delirium.
• Opiate withdrawal marked by pupillary dilatation,
lacrimation, diarrhoea, cramping
• Patient may present with physical symptoms and
demand opiates for pain relief
A/Professor David Ash
81
Amphetamine –
Methamphetamine Abuse
• Clinical Presentation:
–
–
–
–
–
–
–
–
–
Acute anxiety
Paranoid ideation
Loud, demanding behaviour
Motor agitation, aggression
Stereotypic behaviours –sniffing, teeth clenching,
purposeless searching, picking of skin
May be evidence of needle marks
Pulse, BP, respiration rate, increased and dilated pupils
Exacerbation, precipitation of mania/psychosis
Persisting delusional state
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Treatment
•
•
•
•
Support, verbal de-escalation
Safety first – potential for aggression
Benzodiazepines – to reduce arousal
Second generation antipsychotics
• i.e. Olanzapine - Quetiapine
•
•
•
•
Monitor for orthostatic hypertension with SGAs
ECG – QTc
General medical including hydration, malnutrition
Routine screens including Biochemistry, CBP, Hep
screens, HIV
• Assess need for inpatient treatment
• Referral to specialist drug, alcohol service where
appropriate
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Case Presentation
Mrs B. 52 year old married woman, lives in a country town
200km from Adelaide. 2 sons aged 28, 33 years.
1995: sexual assault by chiropractor, later developed severe
illness with mood disturbance, auditory and ?olfactory
hallucinations, passivity experiences, religious
delusions, delusions of reference.
Past History: postpartum depression; social anxiety disorder
No family history of psychiatric illness
Emotional deprivation, physical aggression and neglect by
parents esp. father.
History of sexual assaults in childhood, adolescence and
adult life
Husband emotionally abusive, controlling, similarities to
father
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Case Presentation cont.
Employed as registered nurse, managed several
successful businesses prior to illness onset.
Self esteem linked to work, parenting, physical
appearance.
Since 1995: chronic, fluctuating psychotic symptoms with
episodic mood disturbance. Ongoing social anxiety and
posttraumatic symptoms.
Underlying Axis 2 issues although functioned well prior to
illness onset.
Organic screens including EEG, CT head, MRI head,
ECG, echocardiogram NAD.
A/Professor David Ash
85
Case Presentation cont.
Intensive outpatient treatment including:
Supportive psychotherapy
Psychoeducation
Marital counselling
Theological input
CBT
Cautious exploration of past traumas and underlying dynamic
issues
Pharmacotherapy
Second and third opinions
Inpatient treatment:
numerous admissions including ICU due to psychotic symptoms
and risk of self harm
Traumatic experience in hospital
A/Professor David Ash
86
Case Presentation cont.
Pharmacotherapy
•
•
•
•
FGAs – oral / depot
SGAs – including clozapine
Mood stabilisers
Antidepressants
Current medication
•
•
•
•
•
Amisulpride 1,000 mg daily
Seroquel 300 mg bd
Benztropine 2-3 mg daily
Lorazepam 1.5 mg daily
Temapzepam 10 mg prn nocte
Psychotic symptoms have settled, mood stable for
last 6 months.
Still has moderately severe social anxiety.
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88
References
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Crisis Beds: The Interface Between the Hospital and the Community. Ash et al.
International Journal of Social Psychiatry 43: 193 -198, 1997
Development of Australia’s first psychiatric emergency centre. Frank et al
Australasian Psychiatry, 13: 266 - 272, 2005
A survey of violence, self harm, victimisation and homelessness in patients
admitted to an acute regional inpatient unit in South Australia. Ash et al.
International Journal of Social Psychiatry 49 112-118, 2003
Self reported forensic histories amongst patients admitted to an acute psychiatric
unit. Ash et al. Psychiatry, Psychology and the Law 6:197-202, 1999
Emergency Psychiatry ed Hillard and Zitek; McGraw and Hill
Psychotropic Drug Directory ed Basire 2003/2004
Acute Inpatient Psychiatric Care A Source Book –Treatment Protocol Project
WHO – Andrews
Safety and Tolerability of Oral Loading Divalproex Sodium in Acutely Manic
Bipolar Patients Hirschfeld et al, J Clin Psychiatry 1999; 60, 815-818
Managing the Agitated Psychotic Patient – an Update. Forster, Emergency
Psychiatry 8; 2, 2002
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•
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Efficacy of Atypical Antipsychotics in Bipolar Disorder Berk and Dodd
Drugs 2005 65 (2); 257-269
Review and Update of the American Psychiatric Association Practice
Guidelines for Bipolar Disorder James C-Y. Chou, Primary Psychiatry Sept.
2004; 11 (9), 73-84
Treatment options for Bipolar Mania Kasper and Attarbaschi, Clinical
Approaches in Bipolar Disorders 2004; 3. 24-32
RANZCP Clinical Practice Guidelines – Summary of guidelines for the
treatment of bipolar disorder P Mitchell et al, Australasian Psychiatry, Vol
11, No.1, March 2003
A Meta-analysis of the Efficacy of Second Generation Antipsychotics John
Davis, Nancy Chen, Ina Glick. Arch. Gen. Psychiatry Vol 60; June 2003,
553-564
RANZCP Clinical Practice Guidelines Summary of Guidelines for the
treatment of Schizophrenia McGorry et al; Australasian Psychiatry; Vol 11
No 2, June 2003, 135-150
What Do Consumers Say They Want and Need During a Psychiatric
Emergency Allen et al, J Psychiatr Pract. 2003 9 (1), 39-58
Treatment of Behavioural Emergencies: a summary of the expert consensus
guidelines Allen et al , J Psychiatr Pract. 2003 9 (1), 16-38
Goldberg et al Cognitive improvement after treatment with secondgeneration antipsychotic medications in first-episode schizophrenia: is it a
practice effect? Arch Gen Psychiatry 2007 64 1115-22
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Atypical antipsychotics in the treatment of schizophrenia – systematic
overview and metaregression analysis Geddes et al 2000, BMJ 321, 13711376
The European First Episode Schizophrenia Trial (EUFEST) Rationale and
design of the trial. Fleischhacker et al 2005 Schizophrenia Research 78,
147-156
Antipsychotics and the Risk of Sudden Cardiac Death. Straus et al, Arch Int
Med 2004 164: 1293-1297.
The Usefulness and Use of Second Generation Antipsychotic Medication
Sartorius et al 2002 Current Opinion in Psychiatry 15, S1-S51
The Usefulness and Use of Second Generation Antipsychotic Medication
Sartorius et al 2003 Current Opinion in Psychiatry 16, S44
Guidance on New (Atypical) Antipsychotic Drugs for the Treatment of
Schizophrenia – National Institute of Clinical Excellence (NICE) Barnett
2002
Effectiveness of Antipsychotic Drugs in Patients With Chronic
Schizophrenia Lieberman et al New England Journal of Medicine 2005 353
12; 1209-1223
Clinical Trials for Antipsychotic Drugs; design conventions, dilemmas and
innovations. Stroup et al, Nature Reviews Drug Discovery 2006 5, 133-146
Randomised Controlled Trial of the Effect on Quality of Life of Second –vs
First-Generation Antipsychotic Drugs in Schizophrenia, CUtLASS 1, Arch
Gen Psychiatry, Vol 63, Oct 2006.
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Treatment of a first episode of psychotic illness with quetiapine. An
analysis of 2 year outcomes. Kopola et al. Schizophrenia Research 81
(2006) 29-39.
Higher than Physician’s Desk Reference (US) doses on atypical
antipsychotics, Goodnick, Expert Opinion Drug Saf. (2005) 44): 653-668
Clinical experience with atypical antipsychotics in an acute inpatient unit.
Focus on quetiapine. Keks et al., International Journal of Psychiatry in
Clinical Practice, 2006; 10(2): 0-00.
RANZCP Clinical Practice Guidelines – Summary of guidelines for the
treatment of bipolar disorder Mitchell et al, Australasian Psychiatry, Vol 11,
No.1, March 2003
Amisulpride augmentation of Clozapine – an open non-randomized study in
patients with schizophrenia partially responsive to Clozapine Munro et al,
Acta Psychiatrica Scand. 2004; 110, 292-298
Co-administration of Clozapine and Amisulpride in patients with
Schizophrenia. Ziegenbein et al; 58th Annual Convention Biol. Psychiatry;
May 2003
Combination of Clozapine and Amisulpride in Treatment Resistant
Schizophrenia –case reports and review of the literature Zink et al,
Pharmacopsychiatry 2004; 27, 20-31
Differential effects of high-dose amisulpride versus flupenthixol on latent
dimensions of depressive and negative symptomatology in acute
schizophrenia: an evaluation using confirmatory factor analysis Muller et
al., Int. Clin. Psychopharmacol 2002 Sep, 17 (5) 249-61
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