Opioid - signs of use
IV - needletracks, infection, endocarditis
intoxication, OD , pinpoint pupils
rule out Wernickes, Korsakoff psychosis
Assessment of patient seeking benzodiazepines
- Risk
-intoxicated?
-signs of overdose - pinpoint pupils, slurred speech, ataxia (BZDs)
-suicide attempts, self harm, aggression, forensic, current hx - Substance use
-sx leading to prescription of BZD, diagnoses
-when first prescribed, by who, history over time of dose, escalation
-dependence, craving, withdrawal, tolerance, salience - substance use seeking behaviour overtakes other domains
-other substance use - Mental illness
-anxiety disorders, depression
-for anxiety or short term
-symptoms of MI that need additional tx and f/u - Psychosocial (4)
-employment
-supports
-relationship
-finances - Collateral & safescript
-from GP, D&A services, private psychiatrist, family members
-dr shopping line
Stages of change and author
Prochaska
- Pre-contemplation: continuous use with no interest in quitting in past 6 months
- Contemplation: continuous use with ambivalent interest in quitting
- Preparation: continuous use with interest in quitting in the next 30 days
- Action: active attempt to quit
- Maintenance: abstinent for more than 3 months but less than 5 years
Opioid use in pregnancy - effects
-Reduction of foetal growth -> resulting in LBW, prematurity and foetal and noenatal death
-Clinical signs of opioid neonatal abstinence syndrome occur in 48–94% of infants exposed to opioids in utero: GI disturbances, irritability, hyperactivity, feeding and sleeping disturbances (child may need to be monitored for 3 days after delivery)
-Transmitted HIV, hep B, hep C
BZD use in pregnancy - effects
High dosage use - cleft lip, cleft palate, ‘floppy baby syndrome’
Ix of Pt who drinks (RANZCP)
Markers of heavy drinking. Consider: GGT; MCV (high); uric acid; AST/ALT ratio>2
Evidence of pancreatitis.
Macrocytosis
DDx of pt drinking with double gaze (RANZCP)
Wernicke’s encephalopathy (AKA Wernicke fluent encephalopathy) characterised by acute confusion, ataxia and ocular motility disturbance (eye signs such as diplopia and nystagmus on lateral gaze).
Alcohol withdrawal (mild or moderate)
Consider: recency of alcohol cessation; withdrawal may include hallucinations/visual disturbance, agitation and physical signs.
Alcohol withdrawal (severe)
Consider: extreme autonomic dysfunction, agitation, confusion; alcohol withdrawal delirium indicating greater severity (includes criteria for delirium as well as withdrawal); includes delirium tremens (extreme autonomic hyperactivity, tremulousness,
hallucinations/illusions/delusions, associated with heavy drinking).
Acute or chronic head injury (extradural, subdural) as falls are common in those with alcoholism.
Delirium associated with other causes: acute pancreatitis, postictal or hepatic encephalopathy as she is confused, seizures are common in alcohol dependence as is liver disease.
Other disorders:
Consider: other disorders that may be associated with alcohol use (e.g. anxiety disorders, mood disorders, trauma-related syndromes); other disorders that may explain symptoms (e.g. primary psychotic disorder, intellectual disability).
Mx of Wernickes (RANZCP)
Context of request:
Identifies and addresses the consultation question of the treating general medical team
Decision to admit:
Admission justified – e.g. diplopia (possible Wernicke’s) and perceptual symptoms (possible delirium) suggest possible severe withdrawal.
Care approach on unit:
* Environment. Safe, calm environment supports recovery from delirium. Consider: avoid stimulus overload and stimulus deprivation; single room, close observations; daytime/night-time cues assist sleep wake cycle, clock/calendar/date visible.
* Staffing. Optimise staff continuity (medical, nursing) so patient is familiar with staff; calm supportive stance; avoid non-related conversations in earshot.
* Family and trusted others. Presence of family members experienced as safe may assist in supporting the person (minimising escalations) and in orientation. Opportunity to support key family/social network members.
* Communication and physical wellbeing. Consider: need for glasses/hearing aids; pen/paper as alternative to verbal communication; where possible encourage physical activity to avoid pressure sores, assist with orientation; ensure adequate rest.
* Monitoring and observations. Alcohol withdrawal scale or equivalent; observations.
Medication options:
* Thiamine. For example, 500mg intravenous bd/tds for 3-5 days to avoid Wernicke-Korsakoff syndrome. The immediate management is intravenous thiamine. Thiamine is useful in preventing Wernicke encephalopathy and Korsakoff Syndrome.
W.E is an acute disorder due to thiamine deficiency manifested by confusion, ataxia, and ophthalmoplegia. K.S. is manifested by memory impairment and amnesia. Thiamine has no effect on the symptoms or signs of alcohol withdrawal or on the incidence of
seizures or DTs. Oral Thiamine is poorly absorbed enterally in those with alcohol abuse histories.
* Benzodiazepines. For example, diazepam, lorazepam. Preventative for delirium tremens. Preventative for withdrawal-induced seizure risk (peaks on day 2 in mild withdrawal, or days later in severe withdrawal). Consider intravenous loading dose and as per protocol.
* Multivitamin/folate. Where concerned about diet. Folate deficiency may lead to peripheral neuropathy; B group vitamins and minerals (e.g. Mg) may affect lipid and glucose metabolism.
* Symptomatic treatments. Fluids/electrolytes if dehydrated; antiemetics for nausea/vomiting; paracetamol, NSAIDs for aches/pains; night sedation; acute sedation options e.g. benzodiazepines, haloperidol; sleep e.g. temazepam.
* Medication precautions. (If raised, may contribute to this section.) For example propranolol, clonidine may mask features of withdrawal.
CLINICAL FEATURES OF WERNICKE’S ENCEPHALOPATHY
- Ataxia
- Confusion
- Ophthalmoplegia / nystagmus (abducens or sixth nerve palsy)
- Hypothermia or hypotension
- Memory disturbance
- Coma/Unconsciousness
FEATURES OF KORSAKOFF SYNDROME
- Severe retrograde and anterograde amnesia particularly anterograde
- Telescoping of events
- Confabulation
- Polyneuropathy
- Lack of insight
- Apathy
- Deficiency of thiamine
- Necrosis and haemorrhage in the mamillary bodies
CLINICAL FEATURES OF DELIRIUM TREMENS
- Medical emergency
- Usually occurs in 48–72 hrs after abstinence from alcohol but may occur up to seven
days later - Exaggerated features of simple withdrawal in 75% of cases, i.e., anxiety, dehydration,
sweating, tachycardia, headaches, insomnia and tremor. - Autonomic instability
- Hyperthermia
- Seizures
- Coarse tremor
- Disorientation and confusion
- Hallucinations- Lilliputian type (EMQ)
- Paranoid delusions
- Complications; arrythmias, HT, pneumonia, renal failure
PSYCHOLOGICAL AND SOCIAL TREATMENTS FOR ALCOHOL DEPENDENCE
- Alcoholics Anonymous
- Motivational enhancement therapy
- CBT
- Social skills training; larger repertoire of coping skills will reduce the stress of highrisk
situations and provide alternatives to alcohol use. Techniques involve
assertiveness training, modelling, and role playing of skills such as refusal of alcohol
and dealing with interpersonal problems. - Social behaviour and network therapy (UKATT study); Combination of cognitive
behavioural approach and community reinforcement approach, behavioural marital
and family therapy. - Contingency management:
Clinician arranges the environment such that alcohol use is readily detectable
Reinforcers are arranged to reward abstinence
Incentives are withheld following alcohol use
Reinforcement from alternative sources (employment, family or social) is increased to
compete with that from alcohol - Cue exposure – repeated exposure to stimuli to extinguish cravings
- Therapeutic communities and residential rehabilitation
BIOLOGICAL TREATMENTS FOR ALCOHOL DEPENDENCE
- Disulfiram
a. Prevents breakdown of alcohol by aldehyde dehydrogenase
b. Can cause liver dysfunction and thyroid dysfunction
c. Principle of negative reinforcement - Naltrexone - Opiate receptor antagonist that reduces the pleasurable effects of
drinking - Acamprosate - GABA analogue
Opioid dependence meds
- Methadone maintenance. Opioid agonist, 20–100 mg oral
- Buprenorphine- Partial Agonist – 8–24 mg sublingually
- Naltrexone- Opioid antagonist
- Clonidine and Lofexidine. Alpha-2 adrenergic agonist
- LAAM- Longer acting opioid agonist than methadone
- Recently, Buprenorphine-naloxone combination (Suboxone) as a long acting tablet.
Aim is to prevent diversion and facilitate unsupervised dosing programmes
Opioid dependence psychological tx
- Psychoeducation – Identify harmful behaviours
§ Needle sharing
§ Where do they buy heroin from?
§ Variation in purity
§ Injection sites - Education about risks of overdose, risk of transmission of illness, managing overdose,
medical illness and contraception - Counselling about less risky practices and needle exchange services
- Screening for HIV, Hepatitis B and C
- Encourage vaccination for all patients
- CBT
- Contingency management
- Psychodynamic and Interpersonal therapies- Psychodynamically oriented group
therapy, modified for substance-dependent patients, appears to be effective in promoting abstinence when combined with behavioural monitoring and individual
supportive psychotherapy. - Family therapy – enhance treatment adherence and facilitate implementation and
monitoring of contingency contracts with opioid-dependent patients - Twelve-step programmes
FEATURES OF OPIOID WITHDRAWAL
- Lacrimation (tear secretion)
- Rhinorrhoea
- Agitation
- Perspiration
- Piloerection (goose flesh)
- Tachycardia
- Vomiting
- Shivering
- Yawning /10 min
- Dilated pupils (cf. pinpoint pupils in overdose)
- Clinical institute Narcotic assessment (Withdrawal scale)
MANAGEMENT OF OPIOID WITHDRAWAL
- Methadone substitution, with gradual methadone tapering
- Abrupt discontinuation of opioids, with use of clonidine to suppress withdrawal symptoms
- Clonidine-naltrexone detoxification, where withdrawal symptoms are precipitated by naltrexone and then suppressed by clonidine
- Buprenorphine substitution (12-18 hours after short acting agonists such as heroin or endone to avoid precipitated withdrawal)
- Use of other medications to treat the symptoms of opioid withdrawal.
-loperamide for diarrhea
-promethazine for N+V
-nurofen for myalgia
PRINCIPLES IN METHADONE TREATMENT
- Confirm dependence and opioid use; history, physical examination, urine tests and
corroborative sources - Obtain informed consent from patient prior to commencement
- Nature of treatment
- Purpose of treatment
- Side effects
- Risks associated with administration
- Benefits
- Risks associated with not having
- Can withdraw consent at any time
- Programme policies and expectations
- Leaflets and drug and alcohol team involvement
- If patient already on methadone following conditions to be met before administration
of dose:
I. Confirm dose with prescriber
II. Last consumption confirmed and supervised
III. Prescriptions not being issued elsewhere
IV. Patient comfortable on dose
V. No other CI present - LFTs and ECG- risk of hepatic or renal dysfunction can affect excretion and
methadone can prolong QT interval - Start low, 5–10 mg for moderate withdrawal. Remember that doses > 30 mg have a
high potential for overdose and death if opioid naive - Further incremental doses can be given in 5–10 mg increments according to
withdrawal scale - Always prescribe under supervision
- Stabilisation usually achieved within 6 weeks. And between 60–120 mg/day
- Overdose- naloxone IV- 0.4–2 mg. Effect can reverse in 20 min to 1 hr. so monitor
and repeat administration.
Ax of gambling
o History
Initiation of the gambling
Progression
Frequency
Severity
Types of games
Maintaining factors
Dependence factors
o Features
‘Chasing ones losses’
Preoccupied with gambling
Lies to conceal extent of involvement with gambling
Relies on others to provide money to relieve desperate financial situations caused by gambling
Restless or irritable when attempting to cut down or stop gambling
Has made repeated unsuccessful efforts to control or cut back or stop gambling
o Consequences of gambling – financial, interpersonal, vocational, social, legal, etc.
o Assessment suicide/risk
o Motivation to change
o Questionnaires – SOGS – south oaks gambling screen
Mx of gambling
o Pharmacological
SSRIS – all SSRI’s have been sown to be better than placebo
Naltrexone
* U receptor antagonist – effective to help impulsive behaviours and disorders such as kleptomania , reducing high urge and craving states in people with alcohol or heroin – modulates the mesolimbic dopamine pathway involved in reward and reinforcement
Mood stabilisers – lithium
o Psychological
CBT
* Training in assertiveness
* Problem solving
* Social skills
* Relapse prevention
* Relaxation
Gamblers anonymous
Behavioural therapy
* Aversion therapy
* Imaginal desensitisation
* Imaginal relaxation
* Behavioural monitoring
* Covert sensitisation
* Spousal contingency contracting
