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Management of violent patient in emergency
- 1. MANAGEMENT OF VIOLENT PATIENT IN EMERGENCY DEPARTMENT SUDARSHAN PANDEY INTERN, MBBS KUSMS
- 2. Violence and Aggression • Violence and aggression refer to a range of behaviours or actions that can result in harm, hurt or injury to another person, regardless of whether the violence or aggression is physically or verbally expressed, physical harm is sustained or the intention is clear
- 3. Causes Organic Diseases Drugs Psychiatric Hypoxia CNS infection Seizure CVA Trauma Neoplasm Electrolyte abnormality Delirium Dementia Hypo/hyperthermia Endocrine disorder •Alcohol (intoxication and withdrawal) •Sedative-hypnotics (intoxication or withdrawal) •Amphetamine/Cocaine •LSD •Anticholinergics •Aromatic hydrocarbons (e.g., glue, paint, •Steroids •Schizophrenia •Paranoid ideation •Catatonic excitement •Mania •Personality disorders(Borderline/ Antisocial) •Delusional Depression •PTSD •Decompensating OCD •Homosexual panic
- 4. OTHER FACTORS Social factors: • history of violence • Little impulse control • low self-esteem • frustration • delays in treatment • in police custody/gang affiliation • victim of crime
- 6. PRODROME OF VIOLANCE Phase 1: Anxiety Phase 2: Defensive behavior Phase 3: Physical aggression
- 7. ANXIOUS BEHAVIOUR • Pacing /hand-wringing • body tensing, • Facial tension, • fidgety behavior, • Asking repetitive questions • speaking in a loud voice • exhibiting pressured speech
- 8. DEFENSIVE BEHAVIOR • Verbal abuse, • profanity, • Power struggle • chanting, staring /darting eyes, mumbling, flushed face, clenching hands, • repeated approach to staffs
- 9. PHYSICAL AGGRESSION • completely lost control over emotions and behaviors • Physically violent acts : a danger to property, staff, other patients, visitors, and themselves
- 10. MANAGEMENT OF VIOLENT PATIENT • CONTAINMENT & SAFETY • ASSESSMENT • NON VIOLENT DE- ESCALATION • INTERVENTION • TAKE DOWN AND RESTRAINT
- 12. • The American Psychiatric Association recommends that the presence of any one of the following in a violent patient should prompt a search for an organic etiology: 1. a patient >40 years of age with no previous psychiatric history; 2. disorientation, lethargy, or stupor; 3. abnormal vital signs; 4. visual hallucinations.
- 13. INVESTIGATION • Pulse oxymetry • Blood glucose • ECGs • Chest Xray • blood Biochemistries, • toxicology screening, • CT head scans • lumbar puncture
- 14. DE-ESCALATION DE-ESCALATION The use of techniques (including verbal and non verbal communication skills) aimed at defusing anger and averting aggression DE-ESCALATORY SKILLS • Explain intentions to patients and others; • Try to appear calm and self- controlled; • Ensure own non-verbal communication is non-threatening; • Engage in conversation, acknowledge concerns and feelings; • Ask open-ended questions; • Ask for any weapons to be put down (not handed over)’ and • Know how to call for help in an emergency.
- 15. PHYSICAL RESTRAIN MANUAL STRAIN • team approach to manual restraint • When using manual restraint, avoid taking the subject to the floor, but ‘if this becomes necessary’, use the supine (face up) position if possible, and if face down position does have to be used, use it for as short a time as possible MECHANICAL STRAIN • managing extreme violence directed at other people or • limiting self-injurious behaviour of extremely high frequency or intensity. • Using Handcuffs , Restraining belts
- 19. MEDICATION/CHEMICAL RESTRAINT Chemical restraint refers to the administration of a medication that is used to control behavior or freedom of movement but that is not a part of a patient’s daily medication regimen Rapid tranquilization refers to giving medication every half hour to every hour to target symptoms of agitation,hostility, and motor excitement
- 20. Drugs Adult Dosage Route Adverse Effects Benzodiazepines Lorazepam 2–4 mg IV, IM, PO C/I in alcohol intoxication, respiratory and neurologic depression, coma Midazolam 0.01–0.07 mg/kg IV, IM Respiratory and neurologic depression, amnesia, hypotension Typical antipsychotics Haloperidol 2–5 mg IV, IM EPS, QT-interval prolongation, NMS, tardive dyskinesia with long-term use Atypical antipsychotics Olanzapine 5–10 mg IM, PO Drowsiness, agitation, dizziness, akathisia Risperidone 2-8 mg PO Anaphylactoid reactions,hypotension, NMS
- 22. Dangers of Emergency sedation 1. Sedative drugs may mask important signs of underlying illness, eg an intracranial haematoma requiring urgent treatment. 2. The normal protective reflexes (including airway refl exes, such as gag and cough response) will be suppressed. 3. Respiratory depression and the need for tracheal intubation and IPPV may develop. 4. Adverse cardiovascular events (eg hypotension and arrhythmias) may be provoked, particularly in a struggling, hypoxic individual. 5. Individual side effects of the drugs
- 23. SECLUSION • The supervised confinement of a patient in a room, which may be locked. • Its sole aim is to contain severely disturbed behaviour that is likely to cause harm to others
- 24. Algorithm for decision making regarding use of seclusion and restraint.
- 26. Phineas Gage
- 27. REFERENCE • Violence and aggression: NICE guideline Draft for consultation, November 2014 • Tintinalli's Emergency Medicine 7th edition • Management of the Acutely Violent Patient, Jorge R. Petit, MD
Editor's Notes
- Sanfilippo syndrome, or mucopolysaccharidosis III (MPS-III) is a rare autosomal recessive lysosomal storage disease. It is caused by a deficiency in one of the enzymes needed to break down the glycosaminoglycan heparan sulfate (which is found in the extra-cellular matrix and on cell surface glycoproteins). The disease manifests in young children. Affected infants are apparently normal, although some mild facial dysmorphism may be noticeable. The stiff joints, hirsuteness and coarse hair typical of other mucopolysaccharidoses are usually not present until late in the disease. After an initial symptom-free interval, patients usually present with a slowing of development and/or behavioral problems, followed by progressive intellectual decline resulting in severe dementia and progressive motor disease.[6] Acquisition of speech is often slow and incomplete. The disease progresses to increasing behavioural disturbance including temper tantrums, hyperactivity, destructiveness, aggressive behaviour, pica and sleep disturbance. As affected children have normal muscle strength and mobility, the behavioural disturbances are very difficult to manage. The disordered sleep in particular presents a significant problem to care providers. In the final phase of the illness, children become increasingly immobile and unresponsive, often require wheelchairs, and develop swallowing difficulties and seizures. The life-span of an affected child does not usually extend beyond late teens to early twenties. Although the clinical features of the disease are mainly neurological, patients may also develop diarrhea, carious teeth, and an enlarged liver and spleen. There is a broad range of clinical severity. The disease may very rarely present later in life as a psychotic episode Vogt–Koyanagi–Harada disease (VKH), also known as Vogt–Koyanagi–Harada syndrome and uveomeningitis syndrome,[1] is a multisystem disease of presumed autoimmune cause, that affects pigmented tissues, which have melanin. The most significant manifestation is bilateral, diffuse uveitis, which affects the eye.[2][3] VKH may variably also involve the inner ear with effects on hearing, the skin, and the meninges of the central nervous system