Transcript Emergency Room Psychiatry

Emergency Room Psychiatry
Professor Moruf Adelekan
Consultant Psychiatrist
Royal Blackburn Hospital
Blackburn
United Kingdom
The interview: Some possible constraints
– Time limitation
– Sense of urgency to assess the risk
– Lack of collateral information
– Patient’s distress
– Patient’s long and rambling accounts of their
problems
– Pressure from carers
– A&E or ward targets/limitations
The interview
 Psychiatrist’s relationship with the patient influences the
interview.
 Back to basics:
 Techniques of questioning
 Observation
 Interpretation
 Being straight forward, honest, calm and non-threatening
helps.
 Ability to convey to the patient that you are in control and will
act indecisively to protect them and others.
 Communicate clearly your impression and management plan.
The setting
• Safety: Be very conscious of your safety and that of other
staff (How?)
• Sitting arrangement: how far from patient, at what level
and angle?
• The room: door, alarm system
• Interview style and approach:
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calm manner
quiet voice
avoid eye contact, if this will aggravate patient
sit rather than stand
• Avoid the attitudes and behaviours that increase patient
anxiety and frustration
General Strategy
• Self protection
– Know as much as possible about patient.
– Be alert for aggression.
– Attend to safety of physical surroundings.
– Have others present during the interview if
needed.
– Have others in vicinity.
– Attend to developing alliance with the patient.( do
not threaten or confront patients with paranoia)
General Strategy (contd.)
 Prevent harm
 Prevent self harm or suicide. Use whatever safe
methods to prevent them from harming themselves.
 Prevent violence towards others. Consider the
following:
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Inform patient that violence is not acceptable.
Approach patient in nonthreatening manner.
Reassure.
Offer medication.
Inform patient that restraint is used if necessary.
When patients are restrained observe their vitals closely.
Administer immediate treatment for agitation
History, MSE, PE and Investigations
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What are the key areas to check in the history?
What about MSE?
General PE
PE where cerebral pathology is suspected
– Level of consciousness: from fully awake, to
drowsiness, stupor, semi-comatose, deep coma
– Clouding of consciousness, delirium and fugue
– Language ability etc.
• Investigations: Bloods; Illicit drug screen, ECG,
Brain scan
The pitfalls
 The physical health problems
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Head trauma
Seizures
Metabolic abnormalities
Infections etc.
 Substance use/misuse disorders
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Acute intoxication
Withdrawals
Delirium
Wernicke’s encephalopathy etc.
 Medication related
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Intoxication
Withdrawals
Allergic reactions
Overdoses etc.
DELIBERATE SELF HARM: EPIDEMIOLOGY
• 1% of patients who deliberately self-harm commit suicide in
the first year.
• Of DSH patients, 10% ultimately commit suicide
• 50% of completed suicides have a history of DSH
DSH: ASSESSMENT
• Interview informants, family and friends
• The following point to intention:
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Planned
Precautions taken to being found
Was help sought
Had the patient considered that he or she had taken sufficient to kill
self or be dangerous
– Suicide note
– Active hostility aimed at another
• Present intention:
– Still present?
– Precipitant to DSH
Factors that increase risk
• History of harm (to self/others)
• Pre-existing vulnerabilities: Male, Young, Disrupted or Abusive Childhood,
Antisocial, Suspicious, Impulsive, Irritable
• Social and Interpersonal factors: Poor social network, Lack of education,
Lack of work skills, Rootless, Poverty, Homelessness
• Mental disorders (mania, schizophrenia, depression, psychopathic
disorders etc) particularly characterised by:
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active symptoms
poor compliance
poor engagement with services
treatment resistance
lack of insight
• Substance Misuse (past but more importantly current)
Factors that increase risk (contd.)
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Mental state
– thoughts of self harm or violence
– paranoid thoughts
– command hallucinations
– mood disturbance
– delusions evoking fear, provoking indignation, provoking jealousy, involving injury/threat
from close relative or companion
– ideas of influence
– clouding consciousness and confusion
Situational triggers
– Availability of weapons
– Loss
– Demands and expectations
– Confrontation
– Change
– Physical illness
– Other provocation
Specific poisoning
• Check what to do with the following:
– Benzodiazepine
– Carbon Monoxide
– Cyanide
– Opiates
– Paracetamol
– SSRIs
– Lithium
Violence and assaultative behaviour
 Ascertain cause.
 Look for predictors:
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Recent acts
Verbal/physical threats
Carrying weapons/objects
Progressive agitation
Catatonic excitation
Substance intoxication
Impulse dyscontrol etc.
 Assess the risk for violence
 Consider past history
 Overt stressors
 Consider intention, wish, availability of means etc..
General principles of management of violence
• Ensure sufficient staff are present. Request support from security
personnel, if indicated. Disarm weapons
• Verbal talk-down, e.g. for half an hour – may not work if psychotic or
organic
• Physical restraint/seclusion, e.g. for drug free evaluation
• Treat psychiatric illnesses appropriately
• Medication as emergency:
– Neuroleptic antipsychotics in sedative doses
• Choice depends on the protocol used in treatment unit
• Caution: possible brain damage as increased side effect; akathisia which may be misdiagnosed
as agitation
– Benzodiazepines
• Can be combined with neuroleptics e.g. lorazepam/clonazepam + haloperidol
• Risk of confusion and disinhibition of violence, especially at high doses and in brain damage
• Staff debriefing following serious untoward incident
Rapid tranquilization (RT)
• The use of psychotropic medication to control agitated,
threatening or destructive psychotic behaviour.
• This procedure can be used in the Emergency Unit as well as
Inpatient Unit.
• However, staff have to be adequately trained and the
procedures should be meticulously implemented to ensure
good results and safety of everyone (the patient, staff and
other patients)
• An example of the Policy Guide from Lancashire care NHS
Trust is available for a full study of what the RT entails
ACUTE PSYCHOSIS
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Severe mental illness
Disorder of thinking and perception
Loss of contact with reality
Lack of insight
Patient usually frightened of his or her
experiences, thus limiting engagement with
mental health professionals
ACUTE PSYCHOSIS: SIGNS AND SYMPTOMS
• POSITIVE SYMPTOMS: delusions, hallucinations, formal
thought disorder
• NEGATIVE SYMPTOMS: flat affect, poverty of thought, lack of
motivation, social withdrawal
• COGNITIVE SYMPTOMS: distractability, impaired working
memory, impaired executive function
• MOOD SYMPTOMS: depression, elevation
• ANXIETY/PANIC/PERPLEXITY
• AGGRESSION/HOSTILITY/SUICIDAL BEHAVIOUR
ACUTE PSYCHOSIS:AETIOLOGY
• PRIMARY FUNCTIONAL PSYCHOTIC DISORDERS
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SCHIZOPHRENIA
BIPOLAR DISORDER
DEPRESSION
SCHIZOPHRENIFORM DISORDER
SCHIZOAFFECTIVE DISORDER
DELUSIONAL DISORDER
ACUTE AND TRANSIENT PSYCHOTIC DISORDERS
• SECONDARY (ORGANIC) PSYCHOTIC DISORDERS
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DEMENTIA
ACUTE CONFUSIONAL STATE
PSYCHOSIS RESULTING FROM AN ORGNIC (PHYSICAL) DISORDER
ALCOHOL-INDUCED
DRUG INDUCED
ACUTE PSYCHOSIS:INVESTIGATIONS
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Detailed History and MSE
Blood tests and full blood count
Urea and Electrolytes
Random blood sugar
Liver, kidney and thyroid function tests
Urine drug screen
Pregnancy test
ECG
EEG
Brain imaging (CT or where available MRI scan)
ACUTE PSYCHOSIS:MANAGEMENT
• Assess danger for self and others
• Consider disposal options (admission, immediate treatment
followed by community follow-up etc.
• Antipsychotic medication (several options): note principles of
usage
• Treat anxiety, agitation and insomnia with short-term
diazepam. CPZ and Quetiapine can also be used
• For mania, prescribe a mood stabiliser
• If depressed, consider use of adjunctive antidepressant
• Consider long-acting depots where compliance or poor
response from oral meds is an issue
• Psychological intervention, social intervention, rehabilitation
etc.
Anxiety
• Anxiety could be a manifestation of most major psychiatric conditions
• Other causes include:
– Substance misuse disorders – alcohol and drug withdrawal
– Intoxication: Drugs (e.g. penicillin); Caffeine; Poisons (e.g. Arsenic, Hg)
– Intracranial: Brain tumours, Head injury, CVD, Subarachnoid haemorrhage,
Encephalitis
– Endocrine: Pituitary, Thyroid, Parathyroid, Adrenal Dysfunctions;
Phaeochromocytoma, Hypoglycaemia
– Hyperventilation: hyperpnoea or tachypnoea with palpitations, dizziness, tinnitus, chest
pain, paraesthesia
– Impending myocardial infarction
– Hypoglycaemia
– Cardiac arrhythmias
– Pulmonary embolism
– Post ictal etc.
Management of acute anxiety
• Aim at treating the underlying cause
• Explain the nature of the symptoms to the patient, e.g. palpitations and
chest pain because of fear of heart attack
• Reassure the patient
• Breathing exercises can be given: make use of of a paper bag into which
the patient can rebreathe to help reduce the resp. alkalosis that worsen
the condition
• Relaxation techniques – these may involve progressive muscular relaxation
• Patient should be encouraged to keep a diary of daily activities and
progress made. Longer term psychological treatment
• Benzodiazepines: rapid anxiolytic effect; start low dose; avoid long-term
use and dependency; rebound withdrawal symptoms
Suspecting medical cause for any presentation?
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Acute onset
First episode
Geriatric age
Current medical illnesses/injury
Substance misuse, Overdoses
Non auditory disturbances of perception
Neurological signs:
– Loss of consciousness seizures, change in pattern of headache, head
injury etc.
• Mental status signs:
– Diminished alertness, disorientation, impaired attention etc.
Acute organic brain syndrome/Ac. Confusional states/delirium
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Up to 1 in 10 admissions to general medical wards, and up to one-third in those
over 65
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Associated with increased morbidity and mortality rates, and increased length of stay in
hospital
Clinical presentation
– An acute onset
– A fluctuating course
– Inattention
– Wandering thoughts
– A fluctuating level of consciousness
– Hallucinations, particularly visual, illusions and nightmares
– Drowsy or agitated or restless
– Clinical picture usually worse at night
– Short-term memory impairment
– Lability of mood
– Fear and apprehension
– Disturbed or apparently “strange” behaviour
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Acute OBS: Aetiology
• Causes are organic and theoretically reversible, although could be
superimposed on chronic organic mental disorders
• Common causes:
– Infection: Cerebral malaria, UTI, HIV
– Metabolic disturbance: causes include hypoxia, electrolyte imbalance, and
respiratory, cardiac and renal failure
– Endocrine disorders: diabetes mellitus, including insulin-induced
hypoglycaemia; Cushing’s syndrome
– Vitamin deficiencies: Thiamine in alcoholics and vit B12 in pernicious anaemia
– Neurological: head injury, ictal or post-ictal states in epilepsy, space occupying
lesions, raised intracranial pressure, cerebrovascular disease
– Drugs: Psychotropics (may be used to treat AOBS but may exacerbate them);
Benzodiazepines (intoxication or withdrawal); antipsychotic medication;
antidepressants; Cardiac meds such as digoxin or diuretics; Antiparkinsonian
drugs such as L-dopa; Corticosteroids; Opiates for analgesia
– Alcohol withdrawal: delirium tremens
– Postoperative: including from the effects of general anaesthesia
Acute OBS: Principles of Management
• Identification and treatment of underlying cause
• Attention to nursing and environment: Keep surroundings well lit
and continuously orientating the patient to time and place; introduce new
staff; give explanations and reassurance about procedures
• Drug treatment:
– Sedative medication can clearly aggravate an ACS and may exacerbate
underlying medical conditions such as hypoxia through sedation
– However, haloperidol, when judiciously used, can control an otherwise
unmanageable or aggressive behaviour
• Be aware of drug interactions: for example prescribed psychotropic
drugs and drugs prescribed for underlying medical and surgical conditions;
and the effects of liver disease on drug metabolism
Immediate medical treatment
 Common global neurological disorders:
 Wernicke’s encephalopathy – confusion, ataxia and opthalmoplegia
- Thiamine 100 mg i.v immediately
• Opioid intoxication – pin point pupils not responding
• naloxone 4 mg i.v
• Hypoglycemia – i.v Dextrose or Glucagon
• Delirium Tremens (Latin for shaking frenzy)
• Develop 2-3 days after cessation of heavy drinking. Life threatening.
• Down regulation of GABA and up regulation of excitatory neuro transmitters
like noradrenaline, dopamine etc..
• Adrenergic storm-hypertension, tachycardia, hyperreflexia, diaphoresis,
hyperthermia, anxiety, paranoia and panic attacks and neurotoxicity.
• Primarily visual hallucinations but could be tactile – Formication.
• Associated with metabolic disturbances and seizures.
• Symptomatic Rx and Benzo regimen e.g. Valium/Librium.
• Treat Seizures symptomatically.
• Never volunteer to treat on Psychiatric ward.
Extra pyramidal side effects
 Acute dystonic reactions
 Torticollis, oculogyric crisis, spasms of back, tongue or jaw.
 Painful and frightening.
 More common in young males, neuroleptic naïve and high potent first
generation antipsychotics.
 Occurs within hours of taking oral and minutes of i.m.
 Anticholinergics (Procyclidine), antiparkisonian drugs (Trihexyphenidyl) or
muscle relaxants (diazepam)
 i.m or oral depends on severity of symptoms.
 Remember patient might not be able to swallow.
 Akathisia
 Unpleasant sensations of "inner" restlessness that manifests itself with an
inability to sit still or remain motionless.
 Foot stamping when seated, constant crossing/uncrossing legs, rocking and
constantly pacing up and down.
 Anticholinergics (Procyclidine) and Propranolol.
Extra pyramidal side effects
 Parkinsonian SEs
 Muscular lead-pipe rigidity, bradykinesia/akinesia, resting tremor, bradyphrenia, salivation and
postural instability.
 Occur days to weeks after antipsychotic drug Rx
 Consider other neurological conditions.
 Anticholinergics might play a role in relief of symptoms.
 Tardive dyskinesia
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Long-term extrapyramidal SEs of antipsychotic use
Prevalence of 15-25%, and starts months or years after commencing antipsychotic use
Non-drug related cases in the elderly reported
Risk factors: female sex, affective disorder, organic brain disease, parkinsonian side effects during
acute treatment, alcohol abuse, negative symptoms of schizophrenia and increasing age
Symptoms: Lip smacking or chewing, tongue protrusion, choreifrom hand movements(pill rolling) or
pelvic thrusting. Severe orofacial movements-difficulty speaking, eating or breathing.
Management: Difficult. Dose reduction; Benzodiazepines (e.g. Clonazepam)and muscle relaxants,
tetrabenazine (a dopamine-depleting agent), vitamin E (a free radical scavenger) and lithium. Weak
evidence base for all the strategies.
In severe cases, switch to clozapine.
Use minimum effective dose of drugs, preferably where possible, oral form.
Neuroleptic malignant syndrome
 Medical emergency, life-threatening and requires immediate treatment
 Occurs most often with drugs which act directly on central dopaminergic systems
(haloperidol, CPZ) but has also been reported with other drugs such as antidepressants
(e.g. Dothiepin)
 Likely an idiosyncratic reaction; some patients have been cautiously re-challenged on
same drug without recurrence
 Marked and sudden reduction in dopamine activity:
 Withdrawal of dopaminergic agents
 Blocking dopamine receptors
 05-1% of patients on neuroleptics will develop NMS, with most developing it shortly
after initial exposure (90% within 2 weeks)
 Clinical features
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Autonomic dysfunction (hyperthermia, labile BP, pallor, sweating, tachycardia)
Fluctuating level of consciousness (stupor)
Muscular rigidity
Urinary incontinence
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Clinical emergency
Stop offending antipsychotic drug immediately
Admit patient to a medical ward where maximal supportive care is available
Sometimes, Dantrolene or Bromocryptine (a dopamine agonist Haloperidol and Chlorpromazine are
greatest risk.
 Investigations: Blood tests may show raised serum creatine kinase, leucocytosis
 Management