Emergency Room Psychiatry

Professor Moruf AdelekanConsultant Psychiatrist

Royal Blackburn HospitalBlackburn

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 questioningObservationInterpretation

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:

– 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:

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

• 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 problemsHead traumaSeizuresMetabolic abnormalitiesInfections etc.

Substance use/misuse disordersAcute intoxicationWithdrawalsDeliriumWernicke’s encephalopathy etc.

Medication relatedIntoxicationWithdrawalsAllergic reactionsOverdoses 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:

– 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:– 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.)• 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:

Recent actsVerbal/physical threatsCarrying weapons/objectsProgressive agitationCatatonic excitationSubstance intoxicationImpulse dyscontrol etc.

Assess the risk for violenceConsider past historyOvert stressorsConsider 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

• 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– SCHIZOPHRENIA– BIPOLAR DISORDER – DEPRESSION– SCHIZOPHRENIFORM DISORDER– SCHIZOAFFECTIVE DISORDER– DELUSIONAL DISORDER– ACUTE AND TRANSIENT PSYCHOTIC DISORDERS

• SECONDARY (ORGANIC) PSYCHOTIC DISORDERS– DEMENTIA– ACUTE CONFUSIONAL STATE– PSYCHOSIS RESULTING FROM AN ORGNIC (PHYSICAL) DISORDER– ALCOHOL-INDUCED– DRUG INDUCED

ACUTE PSYCHOSIS:INVESTIGATIONS

• 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?

• 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

• Up to 1 in 10 admissions to general medical wards, and up to one-third in those over 65

• 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

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 reactionsTorticollis, 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.

AkathisiaUnpleasant 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 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 Autonomic dysfunction (hyperthermia, labile BP, pallor, sweating, tachycardia) Fluctuating level of consciousness (stupor) Muscular rigidity Urinary incontinence

Investigations: Blood tests may show raised serum creatine kinase, leucocytosis Management

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.