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Wk 19 – Drug Overdose MECHANISMS OF UNCONSCIOUSNESS 1. List the most common causes of unconsciousness. For each, outline the mechanism by which unconsciousness is precipitated Our state of arousal is influenced by the central ascending reticular formation, which extends from the lower brainstem to the thalamus. Our conscious state is a product of complex interactions between the RAS, cortex, brainstem and the sensory stimuli reaching them. Some terms Consciousness means a state of wakefulness with awareness of self and surroundings. Clouding of consciousness means reduced wakefulness and/or self-awareness, sometimes with confusion; the term is used more in psychiatry than clinical neurology. Confusion is the state of altered consciousness in which the subject is bewildered and misinterprets his or her surroundings. Stupor is an abnormal, sleepy state from which the subject can be aroused by stimuli, applied vigorously or repeatedly. The term is also used to describe various psychiatric states, e.g. catatonic and depressive stupor. Delirium is a state of high arousal (seen typically in delirium tremens) in which there is confusion and often visual hallucination. States of unresponsiveness Coma: Global event or specific interruption to the midbrain (RAS) and GCS <9. It is a state of unarousable unresponsiveness Persistent vegetative state (PVS): Loss of sentinent behaviour – patient perceives little or nothing yet lies apparently awake, breathing spontaneously. The brainstem is normal “Locked in” syndrome: State of unresponsiveness due to massive rd brainstem damage below the 3 nerve nuclei. Patient has a functioning cortex and unlike a PVS patient, is fully aware, but can‘t move or communicate except by vertical eye movement Brainstem death: Irreversible loss of the capacity for consciousness with the irreversible loss of the capacity to breathe. Mechanisms of Coma/unconsciousness Altered consciousness is produced by 3 mechanisms affecting the brainstem, Reticular formation and cerebral cortex: 1. Diffuse brain dysfunction – generalised severe metabolic or toxic disorders which depress/inhibit overall brain function, or cause inadequate substrate delivery to brain (blood, O 2, glucose) a. Drug OD, alcohol abuse, CO poisoning, hypo/hyper-glycaemia, hypoxic/ischaemic brain injury, severe uremia, hepatocellular failure, respiratory failure with CO 2 retention, hyper/hypo-calcaemia, hypo/hyper- natremia, hypo-adrenalism, pituitarism, thyroidism, metabolic acidosis, hypothermia, hyperpyrexia, Trauma (following closed head injury), encephalitis, epilepsy, septicaemia, subarachnoid haemorrhage, cerebral oedema from chronic hypoxia 2. Direct effect within the brainstem – a lesion within the brainstem itself which damages/inhibits the RAS a. Brainstem haemorrhage/infarction, neoplasm, brainstem demyelination, Wernicke-Korsakoff syndrome, trauma 3. Pressure effect on the brainstem – A mass lesion within the cerebral hemisphere or cerebellum compresses the brainstem, inhibiting the RAS a. Hemisphere tumour, infarction, abscess, haematoma, encephalitis, trauma, cerebellar mass lesions CAUSES A Alcohol & Drugs Depression of the CNS (GABA relationship???) Worse when combined with drugs due to respiratory depression E Endocrine/exocrine, electrolytes Hypoadrenalism – (Addison’s crisis or cessation of steroid treatment) – results in severe hypotension and dehydration Hypopituitarism/hypothyroidism – rare Hyponatremia – due to salt loss, dilution (H2O), or endocrine problems – causes an influx of water into brain cells (Hyper- natremia is less of a problem) Hypokalaemia – due to diuretic effect, increases frequency of cardiac ectopic beats Hyperkalaemia – can cause a metabolic acidosis I Insulin Hypoglycaemia - glucose for brain cellular function (and ketone can cause acidosis) Hyperglycaemia (when >35) causes dehydration & coma O Oxygen & opiates Oxygen – hypoxia so neurons die Opiates – depress CNS function U Uraemia, renal & hypertension Uraemia – inhibits cerebral function due to cytotoxicity, cell swelling and depletion of glutamate (from chronic renal failure – pyelonephritis, diabetes, hypertension etc) T Trauma (e.g. closed head injury, penetrating Direct pressure on RAS or blood supply head injury, hypoxia/hypovolemia) I Infection (neuro/systemic) Neurological infection (meningitis/encephalitis) – swelling and intracranial pressure Systemic – may be due to dehydration? P Psychological, poisons, porphyria Anxiety related??? S Space occupying lesion, stroke, Space occupying lesions (tumour) – pressure effect on RAS subarachnoid haemorrhage, shock, Stroke - blood supply seizure SAH – inflammation and pressure effect Shock - blood supply Seizure – following Grand Mal seizures – probably due to depletion of glutamate and other NTs More detailed mechanisms Coma due to cerebral mass lesions and herniations Compression of blood vessels ischemia neuronal cell death/dysfunction inability of RAS coma Metabolic disorders Interrupting the delivery of energy substrates inability of reticular activating system coma o E.g. hypoxia, ischemia, hypoglycaemia, hyperosmolarity, hypercapnia, hypercalcemia o Cerebral neurons rely on a blood supply of oxygen and glucose (remember they only metabolise glucose and not fatty acids or protein). o Brain stores of glucose provide energy for approximately 2 minutes after blood flow is interrupted and oxygen stores last 8-10 seconds Interrupted removal of wastes inability of reticular activating system coma o E.g. the high brain [ammonia] of hepatic coma interferes with cerebral energy metabolism and the Na, K- ATPase pump, increase the number and size of astrocytes, alters nerve cell function and causes increased concentrations of potentially toxic products of ammonia metabolism By altering neuronal excitability (drug and alcohol intoxication, anaesthesia and epilepsy). Hepatic encephalopathy Results from the inability to adequately detoxify metabolites of protein metabolism → ↑ [NH4] → affects CNS by: o Interferes with neuronal metabolism and Na/K/ATP-ase pump o ↑ number and size of astrocytes o ↑ [toxic products of NH4] → abnormalities of neurotransmitters o NH4 and other metabolites can bind to GABA receptors → ↑ neuronal inhibition by endogenous mechanisms Renal Failure Results in the inability of the kidneys to excrete waste products (e.g. urea) results in ↑ permeability of the BBB → brain exposure to organic acids and ↑ brain Ca and ↑ CSF PO4 2+ - Abnormalities of Osmolarity Seizures and coma as a result of DKA, and non-ketotic hyperosmolar states, and hyponatraemia Hypercapnia Results in a ↓ LOC proportional to ↑ CO2 Due to CO2 + H2O → diffuse across the BBB → H2CO3 → H and HCO3 → leads to an ↑ [H ] → changes in the + - + normal functions of cellular proteins (eg ion pumps) Drug induced- CNS depressants, anesthetics, → suppression of the RAS and the cerebral cortex Epilepsy: 1 disturbance of electrical activity of the brain, with continuous discharges of the cortex → coma even in the o absence of convulsions PHARMACOLOGY 1. Describe the mechanisms of action and clinical effects of the commonly used mood altering illicit drugs General groupings: CNS depressants – alcohol, benzodiazapines CNS psychostimulants – amphetamine, cocaine, prescription stimulants Opiates/Opiods – heroin, morphine, methadone, pethidine Cannabis – marijuana, hashish Hallucinogens – LSD, Ecstasy Inhalants – aerosol sprays, glues, paint Other – OTC (e.g. anti-histamines), phencyclidine (PCP) Problems with different drugs: Drug class Toxicity/OD W/d Delirium Psychosis Flashbacks Dep/Anxiety Depressants ++ ++ ++ + - ++ Stimulants ++ + - ++ - ++ Opiates ++ ++ - - - + Cannabis - - - ++ + + Hallucinogens + - - - ++ + Inhalants ++ - ++ - - - PCP + - ++ - - - OTC + - + - - + ++ - Likely and dramatic syndrome + -Problems might occur but are unlikely to be dramatic - Lack of substantial evidence (doesn‘t mean these won‘t occur) Public perception – the “Drug problem” Heroin, marijuana, alcohol, amphetamines, tobacco, cocaine, ecstasy, LSD Deaths from drug abuse 1/5 of deaths in Australia have a drug-related cause (mostly tobacco, then alcohol, then ilicits) 10% total burden of disease is attributed to tobacco smoking Influences influencing mortality Impact on the community depends on the percentage using and quantity of use Other factors – drug effect, drug purity, context of use DSM-IV: INTOXICATION Reversible substance specific syndrome due to recent ingestion (or exposure) to a substance Clinically relevant behavioural or psychological changes that are due to the effect of the substance on the CNS DSM-IV: SUBSTANCE ABUSE (Over 1 of the following in the last 12m) Recurrent use and failure to fulfil obligations Recurrent use when physically hazardous Recurrent substance-related legal problems Continued use despite persistent/recurrent social or interpersonal problems DSM-IV: SUBSTANCE DEPENDENCE (3 or more of the following in the last 12m) Increased tolerance Repeated withdrawal symptoms Taken in larger amounts over longer period than initially intended Persistent desire to cut down/unsuccessful attempts Great deal of time getting, using or recovering Important activities given up or reduced Continued use despite physical or psychological problems Summary: TOXIDROMES Stimulants Sedative/hypnotic Opiates Anticholinergics Cholingerics (amphetamines) Restlessness Sedation Pinpoint pupils Blurred vision Salivation Excessive Confusion Unresponsive Mydriasis Lacrimation speech/motor Paraesthesia Slow and shallow Dry skin Urination Tremor Diplopia RR Urinary retention Defecation Insomnia Blurred vision Bradycardia Flushing Diarrhoea Tachycardia Slurred speech Bowel sounds Fever Vomiting Hallucinations Ataxia Hypothermia Tachycardia Bradycardia Nystamgus Hallucinations Hallucinations Psychosis Coma 1. Describe the mechanisms of action and clinical effects of the commonly used mood altering illicit drugs CNS Depressants (Alcohol, barbiturates, BDZ, opiates) General OD presentation for all depressants: Sluggishness, incoordination, difficulty thinking, slow speech, faulty judgment, drowsiness, ataxia, hypothermia and in severe cases – respiratory & CNS depression (coma) Drug Pharmacological mechanism Effects Tolerance Dependence Withdrawal Presentation of Management of OD OD Alcohol Not fully understood, activity of Slurred speech, Acute occurs w/in 1 Moderate Phase 1 (8-24h): Hypoglycaemia, ABC etc Ca channels? staggering gait, drinking session. likelihood of Nervous, metabolic acidosis, - Glucagon or IV intellectual + motor Cellular tolerance to the Physical & apprehensive, blood osmolality, glucose for impairment, mood in membrane lipid Psychological tremor, nausea acute renal failure hypoglycemia changes, sedation, fluidity in amount of Phase 2 (2-4d): - Haemodialysis in euphoria EtOH required to Agitated, muscle severe cases esp. become intoxicated cramps, N/V, with severe Pharmacokinetic HTN, tachycardia, metabolic acidosis changes in severe insomnia alcoholics Phase 3 (2-4+ d): confusion, disorientation, DTs, convulsions (can be fatal) BDZ (Vals, Potentiate action of GABA (-) at Anxiolytic, sedative, Limited cellular tolerance Moderate Anxiety, insomnia, Rarely cause severe Flumazanil if severe xanies, GABAA receptors in the raphe hypnotic, as an anti-convulsant likelihood of convulsions, panic poisoning except in respiratory Roofies, nuclei ( 5HT firing) and RF anticonvulsant, physical & attacks elderly/chronic depression BUT this rophy, rope, (sedation) euphoria if IV psychological respiratory disease may provoke downers) Watch for respiratory epileptic fits depression Barbiturates Potentiate GABA at GABAA Euphoria, anxiolytic, Rapid – both cellular and Strong Anxiety, insomnia, CVS depression (Barbs, receptors (different site & less sedation, hypnotic, pharmacokinetic likelihood of sweating, DTs, Christmas specific than BDZ) – same areas anticonvulsant, GA, physical & confusion, tree, pinks, as for BDZ CVS, respiratory Less tolerance to psychological convulsions sleepers, depression respiratory depression tootsies) (BAD) Opiates Ventral tegmental area ( opioid Analgesia, euphoria Cellular tolerance to N/V, Physical and Physical w/d Constricted pupils, Naloxone IV (repeat (smack, receptors – cause firing of DA (VTA/NA effects), euphoria, analgesia & psychological symptoms: hypoglycaemia, every 2min until horse, junk, neurons release of DA in respiratory respiratory depression Diarrhoea, N/V, convulsions in breathing is H, Mexican nucleus acumbens – receptors depression, constrict abdo cramps, conjunction with adequate) -This brown, china here too) – euphoria/ pupils, constipation, No tolerance to sweating, HTN, track marks reverses respiratory white, dope, Periaqueductal grey area N/V constipation & pupil convulsions, depression & coma downtown, (analgesia) constriction goose-bumps (last Rarely, non- dollies, miss Area postrema (inc. chemo-R about 14d) cardiogenic An infusion may be Emma, trigger zones) pulmonary oedema required as the t1/2 Morpho, Big RF (sedation, resp. depression) Anxiety, agitation, of naloxone is less H, brown apprehension, than that of the sugar, white craving (lasts m- opiate lady) yrs) Psychomotor Stimulants (Amphetamines, cocaine, nicotine, caffeine) Drug Pharmacological Effects Tolerance Dependence Withdrawal Presentation of Management of OD mechanism OD Amphetamines Stimulate nucleus Euphoria, alternis, dry Cellular Powerful psychological Craving, anxiety, Convulsions Reassure and rehydration (Uppers, A, acumbens mouth, anorexia, dilated tolerance to dependence depression, sleep Hyper or hypo- Diazepam/Chlorpromazine speed, crank, (euphoria/depend), pupils, tachycardia, HTN, some effects disturbance, tension for severe whiz, sulph, HTH (appetite, T), RF tremor, agitation, (e.g. effect on irritability, suicidal Hyperthermia agitation/convulsions hearts, dexies, (alertness) sweating, appetite BP over time) ideation, self- Cardiac Dantrolene for crystal, ice, harm arrhythmias hypothermia glass, meth) Causes release of Worse – hyperthermia, DIC B-blockers? and DA, NA, 5-HT in arrhythmias, Rhabdomyolysis these areas and convulsions, (so measure CK Some deaths have been Ecstasy related to CEREBRAL causes inhibition of hyponatremia, DIC, levels) (―E‖, pills, doves, OEDEMA secondary to DA transporter and cerebral haemorrhage Renal failure fantasy, adam) excess water ingestion (the inhibits MOA at high Deaths (even from doses just ONE tablet). drug also has an anti- diuretic effect on the kidney). Effects may be exacerbated or precipitated by associated physical activity & sweating/ thirst. Cocaine Stimulates Nucleus Euphoria, altertness, dry To some, but Very high likelihood for Depression, Reassurance (Coke, ―C‖, acumbens, HTH, RF mouth, dilated pupils, not all effects psychological anxiety, irritability, Diazepam for severe crack, rock, Inhibition of tachycardia, (tolerance to (esp. IV or smoked as insomnia, self- agitation/convulsions nose-candy) transporters (DAT, hypertension, tremor, euphoria etc. ―Crack‖) harm Active external cooling for NET, SERT) – agitation, sweating, but not to CVS hyperthermia potentiates central hallucinations depression) - Intense sx on w/d No physical w/d effects of then craving & anxiety syndrome catecholamines & 5ht Severe – arrhythmias, (no physical w/d) hyperthermia, convulsions, AMI, cerebral haem. Nicotine Stimulates nicotinic Mild psychostimulant - Acute tolerance Very high likelihood of Cravings, receptors (reward alertness, performance – no evidence developing irritability, effect) – nucleus and stress for required dependence (craving performance & acumbens, ventral doses lasts many months- concentration tegmental areas, yrs) hippocampus, RF Some physical dependence (leads to w/d syndrome that lasts 2-3 weeks) Psychotomimetics (Hallucinogens) – Cannabis, LSD, phencyclidine, mescaline - Cause alterations in perception/thought/mood (most don‘t consistently produce hallucinations) Drug Pharmacological Effects Tolerance Dependence Withdrawal Presentation of Management of OD mechanism OD Atropine, Competitive ―Red as beet, dry as bone, blind as a bat, Primarily supportive – Scopolamine (Anti- antagonists to ACh mad as a hatter & hot as a hare‖ – for the calm reassurance and cholinergics) – Angel’s at peripheral & anti-cholinergic toxidrome non-threatening trumpet, deadly central Muscarinic environment with nightshade receptors at a Onset 30-60m after ingestion and may minimal stimuli common binding site continue for 24-48hr because of delayed gastric emptying & absorption Reassure that anxiety LSD (also mescaline, Acts on 5HT and DA Onset of effects w/in 30-60 mins (lasts 12- Only short No No Hyperthermia, is due to the drug and psilocybin) receptors 24h) term dependence/a withdrawal HTN, coma, effect will wear off Hallucinogenic tolerance ddiction, respiratory (Taken: Orally activity thought to be ―Trip‖ – changes in mood/perception. aversive arrest, bleeding Physical/chemical (tasteless, colourless mediated by effect rather than reported, cardiac restraint if danger to liquid) – often liquid on serotonin 2 Boundaries b/w user & environment reinforcing arrest, self/others (But note impregnated blotter receptors. blurred, time distortion, objects flow or properties polyneuropathy that prolonged restrain paper, gelatine pulsatile, heightened colour perception, can contribute to squares or tiny tablets Acts post- threatening/stress environment may Greatest risk = hyperthermia, rhabdo, Also –intranasal, synaptically to inhibit provoke feelings of severe anxiety/paranoia behaviour related acidosis, exacerbate parenteral, sublingual, 5HT release and = ―bad trip‖ (often reason medical attn trauma rather paranoia) inhalation, retention of 5HT at sought). than toxicity conjunctival routes 5HT2R (net effect = If severe – 5HT agonist) paralysation and Psilocybin, psilocin Similar structure to Altered perception (w/in 30m and) Frequent Present with fear, endotracheal – magic mushrooms, LSD (structural use may agitation, intubation shrooms, caps, silly analogues of 5HT) Varying CNS effects – euphoria, visual cause confusion & fun guys, cubies hallucinations (including perceived motion elevations delerium, Rhabdo – fluid of stationary surfaces/objects). of hepatic psychosis and repletion and urinary enzymes schizophrenia alkalinisation Nausea and sympathomimetic activity (e.g. like syndromes tachycardia, mydriasis) BDZ if Nausea & anxious/agitated sympathomimetic Supportive activity (mydriasis, tachycardia) Agitation can fever Cannabinoids Psychomimetic and Central: Relaxation, sensory awareness, Mild w/d (Tetrahydrocannabinol depressant effects ST memory, confidence but not syndrome (THC) – Marijuana performance, motor coordination, due to some (leaves) or hashish Stimulate catalepsy, analgesia, anti-emetic & physical (extracted resin) cannabinoid (CB1) appetite dependence receptors in - Nausea, hippocampus, Peripheral: tachycardia, vasodilation, agitation, cerebellum, sub bronchodilation irritability, nigra, mesolimbic sweating, region, cortex confusion, CB2 – peripheral tachycardia (lymphoid tissue - immune response?) Ketamine (Special K, Dissociative Believe they are outside body and Tremendous ―K‖, Kit-Kat, Cat anaesthetic – blocks anasthetic properties prevent normal injuries without valium, ―Jet‖) NMDA receptor feedback that would limit physical activity perceived pain channel or And PCP (Angel dust) frequency of channel Fluctuate b/w combative/anxious and opening by binding sedated/somnolent to outside of receptor Mixed nystagmus (horizontal, vertical, rotary), mild-mod HTN, tachycardia, confusion, altered perceptions, visual hallucinations MANAGEMENT 1. Describe the principles of the major treatment options for substance abuse Treatment options include: Abstinence vs. Harm Minimisation (e.g. methadone, needle exchange etc) Individual vs. self-help groups Detoxification – medical vs. non-medical Therapeutic communities Voluntary (free will) vs. in-voluntary Diversion programs Drugs of dependence records Oral vs. implants (e.g. opiates) New – drug ―vaccinations‖ (e.g. cocaine) Drug Psychological interventions Pharmacological interventions Alcohol CBT Acamprosate & Naltrexone Motivational enhancement therapy Antabuse (Disulfiram) Brief (psyc) interventions 12-step programs Therapeutic communities Nicotine CBT Nicotine replacement therapies MET Zyban (Bupropion) Smoking cessation programs/workshops SSRIs Hypnosis Complementary medicines Quitline Acupuncture Massage Cannabis CBT Currently none MET Counselling for co-morbid conditions (e.g. depression & anxiety) – often the most important problems with these drugs Heroin/Opiates CBT (? Evidence) Methadone maintenance MET (?) Naltrexone (oral, depot/injection, implant) Long term in-patient treatment Buprenorphine Cocaine (limited CBT Currently none use in Australia) MET Experimental research into a cocaine vaccine – Counselling for co-morbid conditions (depression, blockade of cocaine effects peripherally anxiety) – big problems with these drugs Amphetamines CBT Currently none MET Pharmacological treatment of co-morbid Counselling for co-morbid conditions psychological conditions (e.g. SSRIs) Psychological Therapy CBT Employs active and directive techniques such as teaching, suggestion, persuasion & homework assignments – they challenge clients to substitute a rational belief system for an irrational one Cognitive – involves attempts to restructure thinking. It makes the patient aware of their attributional style (negative, self defeating attitudes) and gets them to make a conscious effort to change it with positive self talk. It also involves assertiveness training Challenges false beliefs re. Misinterpretation of somatic symptoms Behavioural – attempts to change consequences of actions by removing reinforces for the problem behaviour and adding new reinforcers for more adaptive behaviour The ABC paradigm: o A = event exposed to o B = thoughts, beliefs or self-verbalisations person engages in response to A o C = emotional & behavioural responses to B Motivational Enhancement Therapy/Motivational Interviewing MET is a systematic intervention approach for evoking change. It is based on principles of motivational psychology and is designed to produce rapid, internally-motivated change It employs motivational strategies to mobilise the client‘s own change resources. It may be delivered as an intervention in itself, or may be used as a prelude to further treatment Stages of Behavioural Change 1. Precontemplation – individuals who are not considering change in their problem behaviour 2. Contemplation – entails the person‘s beginning to consider both the existence of a problem & the feasibility & costs of changing the problem behaviour 3. Determination – where the decision is made to take action and change 4. Action – the individual begins to modify the problem behaviour (normally continues for 3-6m) 5. Maintenance or sustained change 6. Relapse – if these efforts fail, the individual begins another cycle The MET approach begins with the assumption that the responsibility and capability for change lies within the client. MET seeks to support intrinsic motivation for change, which will lead the client to initiate, persist in and comply with behaviour change efforts. Five basic motivational principles underlie such an approach: 1. Express empathy – therapist‘s role is a blend of supportive companion & knowledgeable consultant 2. Develop discrepancy – where the patient is now, compared to where they want to be 3. Avoid argumentation – the client, not the therapist, should voice the arguments for change 4. Roll with resistance – don‘t meet resistance head-on, client should suggest solutions, not the therapist 5. Support self-efficacy – client‘s specific belief that he/she can change Pharmacological therapy Methadone Can be used short-term to blunt opiate w/d or as long term substitution for opiate addiction Pharmacologically similar to morphine, but longer half life (>24h) Less sedative action Physical w/d is less acute than with morphine or other short acting drugs, though physical dependence is no less pronounced In the presence of methadone, an injection of morphine don‘t cause normal euphoria and lack of physical abstinence syndrome makes it possible to wean addicts off morphine Buprenorphine (partial -receptor agonist) Liable to cause respiratory depression Long duration of action, produces minimal w/d symptoms, has a low potential for OD and the ability to block heroin effects Naloxone (opioid antagonist) Affinity for all 3 opioid receptors, it blocks the actions of endogenous opioids as well as those of morphine-like drugs Produces very little effect in normal subjects, but produces rapid reversal of the effects of morphine & other opioids Can cause hyperalgesia under conditions of stress or inflammation due to blockage of endogenous opioids Used to treat respiratory depression caused by opioid OD Precipitates w/d symptoms in addicts Effects last only 2-4 hours so may need to be given repeatedly Naltrexone (similar to naloxone, but longer duration of action). May be of use in addicts who have detoxified as it nullifies the effects of a further dose of opiate Disulfiram Inhibits aldehyde dehydrogenase so makes alcohol consumption unpleasant Produces no marked affect when given alone Ethanol consumption in the presence of disulfiram is followed by a severe reaction involving flushing, tachycardia, hyperventilation and considerable panic and distress – due to accumulation of acetaldehyde in the bloodstream Although the reaction is extremely unpleasant, it is not harmful and so can be used as an aversion therapy in alcoholics BDZ Used to alleviate acute abstinence syndrome of alcohol (sedative effect reduces symptoms of w/d) BUT are addictive Acamprosate Used to reduce cravings for alcohol Weak antagonist at NDMA receptors – exact MOA not known, but it decreases glutamatergic transmission & modulates neuronal hyper-excitability during w/d from alcohol May work by interfering in some way with synaptic plasticity Pitfalls & problems in history ASSESSMENT OF DELIBERATE DRUG OD taking Be aware of: Patient won‘t talk to you a) the importance of the history and mental status examination of the patient who (DOCUMENT) has taken a deliberate drug overdose; Patient can‘t talk (sedation, delirium, intoxication) (b) how suicide risk can be assessed; Homicidally Duty of care vs. civil liberty OD and substance abuse in general Containing affect Documentation Advice and referral Be aware that the patient may not easily or invariability give an reliable report – continued use of the substance becomes important to the patient even at the expense of health, safety and social functioning – patient will protect their ability to continue use by minimising, denying or even lying about the extent of their use and the problems resulting from it. Doctor needs to be alert to characteristic defences and take note of what the patient is trying to hid Should directly address the patient‘s concerns re. Disclosure of info to family, employers, legal authorities etc Avoid questions that are likely to make the patient defensive First review patient‘s life history, including successes and problems experienced at work, school, family, friendships etc WITHOUT linking these problems to use of substance Then a parallel chronology of the patient‘s use of alcohol/other substances specific questions have to be asked about each category of psychoactive drugs and with prescribed drugs (determine if they were taken only for prescribed reason) Then specifically look at the relationship b/w drug use and the patient‘s problems – may reveal a correlation the patient has not previously seen Attention to any medical, social, emotional or psychological complications of use history of treatment for substance abuse, family history of substance abuse/psychiatric disorders Mental State Exam – assessment of: Item What is assessed, described or observed General Description Appearance Including clothing, body build, posture, grooming, hygiene, tattoos and facial expression. Behaviour Appropriateness, abnormal motor behaviour (tics, mannerisms), restlessness, agitation, retardation. Attitude towards examiner Response, cooperation, disclosure, hostility, seductiveness, inappropriateness. Mood and Affect Mood Describe depth, intensity, duration and fluctuations of mood. May be neutral, euphoric, depressed, anxious, irritable etc. Affect The way a patient conveys their emotional state. May be full, blunted, restricted or inappropriate. Appropriateness Are the pt‘s responses appropriate to the matter being discussed? Speech Tempo, modulation and quality, dysphasia or dysarthria Perceptual disturbances Hallucinations (auditory, visual, gustatory, tactile) Thought Thought form Quantity of ideas and the way in which they are produced. Logical and relevant or fragmented and irrelevant Thought content Preoccupation, obsessions, delusions – suicidal, homicidal, paranoid, hypochondriacal, omnipotence Sensorium and Cognition Alertness and level of consciousness Clouding or fluctuating Orientation Time, place and person – ask day, date, month and year, Ask where pt is and if pt knows who they are. Short-term memory Ask pt to recall list of 3 objects after 3-5mins Long-term memory Ask pt to recall events of previous few days and 1 year ago Concentration Subtract 7 from 100 and keep going or spell ‗world‘ backwards General knowledge and intelligence Simple arithmetic, assess literacy Judgement and Insight Judgement Describe hypothetical situation and ask how pt would behave (eg. What would you do if you smelt smoke in a cinema?) Insight Determine whether pt is aware that he/she has a problem and their level of understanding of this. Deliberate OD/Suicide Attempt – Format Demographics HPC Systems review Past psych history o Past attempts (details), admissions, Dx, Tx, psych systems review, substance abuse, FHx (suicide & psych Hx) Past medical history Substance abuse Personal developmental, social, occupation MSE Summary and Dx Plan for the future Suicide Assessment 1. Details of attempt How serious was this attempt? How, why and what were the expectations? What did they take, how did they take it, where did they take it, how many attempts, planned vs. impulsive, intoxicated, telling someone prior, note, what did they do after? WHY?? Stressors, emotions (hopeless, desperate, in pain, angry), illness? POSSIBLE MOTIVES INCLUDE: 2. What about now? Intent to die (preparation, chance What‘s the ongoing risk? Ideation, current intent, disappointed they failed, of discovery, lethality of method, planning, why did it fail, aftermath) availability of means, what‘s changed, safety network who‘s at home, follow- up arranged Relief from a stressful situation 3. Mental illness Seeking care Screen by asking about recent mood, anxiety problems, substance use Coercive/angry problems Testing fate 4. Mental state Indifferent/ambivalent 5. Collateral BUT may not be able to 6. Psych opinion explain why!! FACTOR POINTS ASSIGNED Sex (male) 1 Age (<19 or >45) 1 Depression or hopelessness 2 Previous attempts or psychiatric care 1 Excessive alcohol or drug use 1 Rational thinking loss 2 Separated, divorced, or widowed 1 Organized or serious attempt 2 No social supports 1 Stated future intent 2 Five points or less: questionable outpatient treatment; six or more points: emergency psychiatric treatment/evaluation; more than nine points: psychiatric hospitalisation. SUICIDE ASSESSMENT Before doing this, build rapport: PEARLS P = partnership E=empathy A=apology R=respect L=legitimisation/listen S=support Ask about MOOD (and take not of affect) If adolescent – ―how are things at school?‖ ―How are things at home?‖ THEN IF SAD/DEPRESSED, PROCEED TO: 1. INTENT Have you ever thought about hurting yourself/ ending your life? (suicidal ideation) Frequency of these thoughts 2. PLAN How well thought out and specific is the plan Place, time, others present/absent 3. MEANS To carry out plan e.g. rope, tablets 4. PREVIOUS ATTEMPTS Failed previous attempts make an individual more likely to try a second time 5. CO-EXISTING PSYCHIATRIC CONDITIONS 6. HISTORY OF ABUSE 7. CONTRIBUTING FACTORS Personal loss – especially suicide of relative/friend Family conflict Problems with peers – rejection/humiliation Loss of job Reasons or motive→ Revenge (―They‘ll be sorry when I‘ve gone.‖) → Reunion (―I‘ll join my mother in heaven.‖) → Rebirth (―After I die, I can start again.‖) → Atonement (―I will punish myself for what I have done.‖) → Escape (―I want to be free of my body and my life.‖) → Altruistic (―My death will bring them together.‖) → Control (―I am unafraid of death.‖) 8. ASSESS PROTECTIVE FACTORS Extent of social support –friends/family Whether friends/family are aware of the ideation, and its seriousness Whether the adolescent has strong religious adherence Whether they will enter a contract agreement not to commit suicide Whether they have any insight into their ideation and its causation FINALLY, Categorise plans/attempts according to: Lethality – e.g. Gun worse than OD Intention – did they really want to kill themselves or did they want to hurt someone else to get attention It usually goes: Thoughts plans attempts (Mood disorders, depressed people etc.) OR Threats self-harm attempts (Angry people like personality disorders, people who want to “get back” at the world) An example: BE SENSITIVE BUT DIRECT! Ok Sarah you seem a bit down… Have you ever thought that life was not worth living? Or Have you ever felt so bad that you have considered ending it all? If yes … Have you thought about killing yourself? Have you thought how you might do this? Have you made any plans for doing this? Have you ever tried to hurt yourself before? c) The potential sequelae of overdose with commonly prescribed medications Paracetamol Single doses >150 mg/kg may result in severe liver damage (may be fatal), hypoglycaemia and acute renal tubular necrosis Benzodiazepines causes prolonged sleep without serious respiratory or CNS depression BUT in the presence of other CNS depressants eg alcohol can cause severe respiratory depression Opioids acute overdose produces coma and respiratory depression with characteristic constricted pupils. Naloxone for morphine OD, Barbiturates non-selective CNS depressants producing sedation and reduction of anxiety in therapeutic doses and unconsciousness and death from respiratory and cardiovascular failure in OD Tricyclics blocks the uptake of amines by nerve terminals by binding to the site of the carrier protein. Initial effect of OD is excitement, delirium and possibly convulsions. This is followed by coma and respiratory depression lasting for some days before recovery. Cardiac dysrhythmias are common and sudden death may result from ventricular fibrillation. Not commonly used due to dire effects in OD…. and you don’t want to be giving depressed possibly suicidal Pts something that would be great to OD on… HISTORY TAKING 1. Demonstrate the ability to take a comprehensive history of prescribed and non-prescribed substance abuse Doctors encounter patients with substance use disorders in all clinical settings. It can either be intoxication, abuse or dependence. Despite the prevalence, these disorders are often undetected & undiagnosed . Thus a thorough & accurate substance use history should be a part of ANY medical or psychiatric interview. There are a number of factors which influence the accurate identification, assessment & diagnosis of substance use disorders. These include: The clinical setting o Ensure privacy & reassure patient on confidentiality The style of interviewing o Vital to build rapport & communicate well, reflect emotion, etc o Start off with less threatening issues before going onto more sensitive areas (ask about prescription medications, non-prescription or over-the-counter, herbal/ natural/ complementary then finally ask about ‗social‘ or ‗recreational‘ drugs. The attitude of the doctor o Non-confrontational & non-judgemental words/tones o Avoid calling it ‗illicit‘ drugs – will either not understand you or it will put fear into them – risk them not admitting to it o Avoid ‗labelling‘ people (eg ‗drug user‘ or ‗alcoholic‘) o Ask, ―how has cocaine caused you problems?‖ rather than, ―how has your use of cocaine been a problem?‖ o Instead of ―why do you drink alcohol then?‖ ask, ―how were you feeling before you drank?‖ ―do you think there were any specific circumstances or triggers to drinking at the time?‖ Patient characteristics o Age, gender, partner or marital status, legal & employment status & ethnicity o Degree of insight into & explanation for the nature of their problem o Medical or psychiatric co morbidity o Stage of use/abuse of the substance (eg current intoxication, early withdrawal, early abstinence, sustained abstinence or recent relapse) o Stage of readiness for change & motivation rd The psychiatric history & mental state examination are combined with history from 3 parties & physical examination to help shape the differential Dx, investigations & management plan. Also try to “normalise” your questions, this also gives warning about the forthcoming question. eg “now with these next few questions, I ask them of ALL my patients to make sure I get a complete history. They may not necessarily apply to you OK? Have you ever used any social or recreational drugs?” Important Information to obtain on substance abuse includes: Types of drugs used May need to jot down common names & research later Many drug users take a variety of drugs May have one preferred but supplement with others depending on availability Major categories are: Depressants (alcohol, barbiturates, benzodiazepines) Stimulants (amphetamines, cocaine, phencyclidine) Opioids/opiates (heroin/diamorphine, morphine, codeine, oxycodone, methadone) Cannabis (marijuana & hashish) Hallucinogens (LSD, mescaline, mushrooms) Nicotine (cigarettes, chewing tobacco/dips & snuff) Inhalants (paint thinners, gasoline, glue & cleaning fluids) Designer drugs (MDMA or Ecstasy, ketamine & γ-hydroxybutyrate or GHB) Age when first started using substances Gives you an idea about their history & also has diagnostic & prognostic implications Early onset (<15yo) is associated with subsequent ‗abuse‘ & ‗dependence‘ Also hints at childhood psychopathology (such as abuse which may have triggered event) Age at first use of nicotine – nicotine often precedes experimentation with illicit drugs & is more prevalent in individuals with other substance abuse disorders Establish PATTERN of use (frequency, amount, route) “it would be helpful for me to understand the pattern of your alcohol/ cocaine/ marijuana/ etc use. As you know, people’s use of alcohol/ cocaine/ marijuana/ etc varies greatly & it would help me to understand the usual pattern for you” Frequency of use Constant Situational – eg only used when at Rave party or at friends‘ houses, etc. Amount being used at start & now (tolerance occurs for most substances) Gives you an idea of the patient‘s ‗progression‘ (eg from sniffing 1 bag of heroin per week to injecting 2 bags per week) If unsure, might be helpful to ask about how much they would spend each day/week Route of administration Oral, sublingual, snort/sniff, IV (& which veins they use) Important to check because specific routes associated with certain medical problems o Intravenous - Hep B&C, thrombophlebitis, infective endocarditis, etc. o Snorting - nasal septum necrosis, epistaxis, etc. What they think the substance(s) does for them Reason for taking it could be peer pressure, numbing depressed feelings, etc Consequences associated with substance use Changes in academic performance Occupational functioning Interpersonal relationships (impact on family & friends) Medical problems Legal problems – how do they get their substances? How do they get the $$$? Previous attempt(s) at quitting Treatment history Past hospital admissions for detoxification, admission to ‗therapeutic communities‘ Participation in various treatment or support programs Outpatient programs run by hospitals Group or individual psychotherapy (CBT, MET – motivational enhancement therapy) Pharmacological therapies (eg oral naltrexone, methadone program, acamprosate, etc) History of withdrawal symptoms Periods of abstinence Relapse(s) & the circumstances/ triggers for it Information about abstinence & relapse indicates the patient‘s ‗progression‘ or ‗regression‘ with respect to substance use It also identifies the severity of the disorder & external factors such as relationship difficulties, psychiatric symptoms, legal or medical problems & reasons for treatment failure that may have influenced the return to substance use Assess the patient’s level of motivation for change precontemplation, contemplation, preparation, action & maintenance Summarise your understanding at the end & ask patient if they have anything to add or clarify Ask if they have any concerns or questions for you Finally thank them for their participation CLINICAL REASONING/PRACTICE 1. Describe the clinical approach to assessment of the unconscious patient including the use of Guedel airway PRIMARY SURVEY A. Airway and CX spine immobilisation o Clear/maintain airway if necessary use Guedel airway o Intubation via RSI Cricoid cartilage is pushed backwards to block oesophagus. Drugs given to induce unconsciousness while holding oesophagus closed Endotracheal tube inserted and ring inflated to protect from aspiration and keep in place Release of cricoid cartilage o Put collar on to protect C spine B. Breathing & ventilation o Respiratory rate and pattern and chest wall movement C. Circulation & haemorrhage control o PR and BP CPR if absent D. Disability neuro assessment E. Exposure, environment and events o Important to take temperature and log roll pt F. Family and Friends While performing survey it is important try and obtain more information on time course & a quick medical Hx from friends/families witnesses and ambos. Time course Quick History When last seen and with whom A - allergies Any witnessed trauma or seizure M - medications Any EtOH - quantity & type P - past medical history What drugs - when, how much? L - last ate E – environment/events what’s actually happened SECONDARY SURVEY- FURTHER EXAMINATION Depth of coma assessed and recorded via Glasgow coma scale (GCS) Full general and neurological examination should be carried out Clues to cause of coma can be gleamed from examination Temperature Raised in infection and hyperpyrexia and subnormal in hypothermia Skin Look for cyanosis, jaundice, purpura, rashes, pigmentation, injection marks and trauma and Skin texture which can be coarse and dry in hypothyroidism Breath Sniff breath for ketones, alcohol, hepatic and uraemic fetor Respiration Some respiratory patterns are of diagnostic importance… Cheyne-Stokes alternating hyperpnoea & apnoea. o In primary neuro disease it suggests bilateral cerebral dysfunction, usually deep in hemispheres or upper brainstem, sign of incipient coning. o Also occurs in metabolic comas, if there‘s CO2 retention from pulmonary disease, with chronic hypoxia at high altitudes (>3500m) and in normal people during sleep. Kussmaul (acidotic) Respiration sighing hyperventilation seen in diabetic ketoacidosis and uraemia Central neurogenic (pontine) hyperventilationsustained rapid deep breathing seen with pontine lesions, may be episodic (switches abruptly on and off) Ataxic respiration Shallow halting irregular respiration that occurs when the medullary respiratory centre is damaged…it frequently proceeds death. Vomiting, hiccup and excessive yawning often indicates lower brainstem lesion in a stuporose pt. NEURO EXAM IN COMA Head, Neck and Spine Look for trauma, skull burr-holes, cranial bruits, neck stiffness Pupils Record size and reaction to light and look for patterns Dilatation of one pupil, which becomes fixed to light, indicates herniation of the uncus of the temporal lobe (coning) rd which compresses the 3 nerve NEUROSURGICAL EMERGENCY (possible subdural or extradural haematoma) Horner’s Syndrome (ipsilateral pupillary constriction an ptosis) occurs with lesions of the hypothalamus and also rarely in coning. Bilateral and midpoint reactive pupils (NORMAL) metabolic comas and following most CNS depressant drugs (except opiates) Bilateral light fixed dilated pupils Cardinal sign of brain stem death, also occur in deep coma of any cause but particularly in response to barbiturate intoxication or hypothermia Bilateral pinpoint light fixed pupils Opiate drugs and pontine lesions (eg pontine haemorrhage) that interrupt sympathetic pathways Bilateral mid-position light fixed or slightly dilated light fixed pupils sometimes irregular are seen when brainstem damage interrupts the light reflex Fundi Look for papilloedema and retinal haemorrhage Ocular Movements Ocular axes usually slightly divergent, slow, roving, side to side eye movements are seen in light coma Vestibulo-ocular reflexes Passive head turning produces conjugate ocular deviation away from direction of induced head rotation (dolls head reflex), this is lost in deep coma and is absent in brainstem lesions and thus brainstem death (practical value in coma is limited) Calorics Slow tonic ocular deviation towards ice cold water irrigated ear indicates intact brainstem (used to test for brainstem death) Abnormalities of conjugate gaze o Sustained conjugate lateral deviation occurs towards the side of a destructive frontal lesion (eyes look towards normal limbs). Rarely and irritative lesion in one frontal region (eg epileptic focus from a glioma) drives the eyes away from the side of the lesion Sustained lateral deviation away lesion can occur with pontine brainstem lesions, when one paramedian pontine reticular formulation (PPRF) is damaged & the opposite is active. o Skew deviation One eye up one down indicates brainstem or cerebellar lesion o Ocular blobbing sudden, brisk, downward diving eye movements seen in pontine or cerebellar haemorrhage. Other spontaneous eye movements (other than roving eye movements) are distinctly unusual in coma of any cause Lateralizing signsComa makes it difficult to recognize focal neurological signs but there are some signs that can be helpful in indicating the side of a lesion: Response to visual threat in a stuporose patient Asymmetry suggests hemianopia. Facial appearance Drooping of one side, unilateral dribbling, or blowing in and out of the paralysed cheek. ToneUnilateral flaccidity or spasticity may be the only sign of hemiparesis. Asymmetrical response to painful stimuli Asymmetry of plantar responses. Both are often extensor in deep coma of any cause. Asymmetry of tendon reflexes Asymmetry of decerebrate and decorticate posturing INVESTIGATIONS If after Hx and examination the cause remains unclear, further investigations are needed. Blood and urine Drugs screen (e.g. salicylates, diazepam, narcotics, amfetamines) Routine biochemistry (urea, electrolytes, glucose, calcium, liver biochemistry) Metabolic and endocrine studies (TSH, serum cortisol) Blood cultures Rarities, such as cerebral malaria (thick blood film) or porphyria, are often forgotten. Imaging CT or MR brain imaging may indicate an otherwise unsuspected mass lesion or intracranial haemorrhage. CSF examination Lumbar puncture performed in coma only after risk assessment to check for contraindications, CT done to rule out intracranial mass lesion. CSF examination is likely to alter therapy only if undiagnosed meningoencephalitis or other identifiable infection is present. Electrophysiological tests EEG is of some value in the diagnosis of metabolic coma, and encephalitis. M ANAGEMENT Comatose or stuporose pts need immediate care before full diagnosis can be made, careful nursing, meticulous attention to the airway, & frequent monitoring of vital functions are mandatory. Longer-term requirements are: skin care - turning, removal of jewellery, avoidance of pressure sores and pressure palsies oral hygiene - mouth washes, suction eye care - taping of lids, prevention of corneal damage, irrigation fluids - intragastric or i.v. fluids calories - liquid diet through a fine intragastric tube, 1255 kJ (3000 kcal) daily sphincters - catheterization only when essential (Paul's tubing if possible); avoid constipation (evacuate rectum). GUEDEL AIRWAY Sits in the oropharynx & maintains the airway by holding the tongue & soft tissues forward (stops tongue swallowing). Comes in different sizes – measure from tragus of ear to corner of their mouth Does NOT protect against aspiration Airway is inserted upside down then rotated into position Pt must be unconscious otherwise will not tolerate & will vomit/retch 1. Eyes Open Spontaneously 4 To loud verbal command 3 To pain 2 No response 1 2. Best motor response To verbal command Obeys 6 To painful stimuli Localises pain 5 Flexion – withdrawal 4 Abnormal flexion posturing 3 Extension posturing 2 No response 1 3. Best verbal response Oriented 5 Confused, disoriented 4 Inappropriate words 3 Incomprehensible sounds 2 None 1 COMMUNICATION SKILLS 1. Demonstrate the ability to communicate with families of seriously ill patients 1. Identify the problem and factors contributing to the responses to illness such as: The patient may feel overwhelmed if they are suddenly thrust into a crisis, are in pain, there is a threat to their life etc. There may be an element of guilt (e.g. for not watching their daughter carefully enough) Ignorance/lack of information may contribute and helping them understand what is happening may enable them to deal with the situation Stigma/apprehension about the illness/diagnosis and what it means (e.g. ―our daughter is a drug addict‖ + all the stereotypes etc. that go with that) Personality style – whether they like to be in control, blame others etc. Past experiences of loss – can make them more sensitive/worried Past history or psychiatric problems/substance abuse etc Social context – supports/employment/finances etc – many ―minor‖ problems can combine and influence how the patient copes. One more issue to deal with amongst background stressors may just be the final straw 2. Consider staff contribution and responses. Education & Training (COMMUNICATION SKILLS) – poor communication with patients and their families/avoidance of them may make existing problems worse Membership of a multidisciplinary team – if hard cases can be discussed and solutions developed by a wide range of people, the individuals involved are less likely to dump distress/frustration/concerns onto patients Motivation to work in the area and expectations of professional performance – unrealistic expectations = disappointments in our performance Administrative and other responsibilities Emotional morbidity – e.g. depression (if we are depressed, everything is too much effort) 3. Recognise the powerlessness of patients & families in the medical setting and look at means by which their sense of control can be improved, for example: Provide appropriate information Encourage them to ask questions Acknowledge the burden of grief Explain why tests/investigations/treatments are necessary 4. Attention to practical issues Difficult, angry patients often have severe pain or delirium which needs to be investigated and/or treated Remember – OFTEN FEAR PRESENTS AS ANGER 5. Recognise the origins of difficult behaviours – this may reduce the sense of being personally attacked 6. Need for self-reflection – is this really a problem, or is it just my perception? 7. In responding to patients/family who are angry etc. it is important to: Introduce yourself Speak calmly and clearly Explain your role Listen to the person/family Clarify the cause of the difficulty and the precise nature of their concerns Acknowledge the distress they are experiencing Good communication skills are essential and often just allowing the person to talk (without criticising or judging them) allows them to regain control and behave more appropriately Never place yourself/other staff members at risk 2. Discuss reasons why patients or families may demonstrate aggressive or disruptive behaviour in medical settings Patients When faced with complex problems, pain etc it is common to regress i.e. behave in a less mature manner eg become more demanding, childlike etc. If staff fail to understand this they may not offer appropriate support Most people avoid talking about emotionally difficult issues – presumably a patient is frightened, but may be pressured by parents, friends to be brave, and her anxiety may be manifest as rude or demanding behaviour Not everyone who is sick was well-adjusted before his or her diagnosis! People may become disinhibited when intoxicated, or angry and abusive. This may also apply when withdrawing from substances. Parents Parents may feel overwhelmed/guilty that they hadn‘t acted sooner (and as parents they are ―expected‖ to help her, even though she is an adult), and instead dump their anger onto staff. Parents may not know the full history and may blame staff for the patient‘s situation. They may have had other adverse experiences in the health care setting, or have experienced other losses, and are very sensitive and fearful. STAFF ISSUES IN ICU 1. Describe the psychological, emotional, and ethical issues which affect staff working in environments such as ICU ICU -Patients in intensive care units are critically ill. ICU is a high stress, heavy workload environment where life and death hang in the balance and emotions run high. ETHICAL ISSUES Consent Patients in ICU are often too ill to consent to procedures themselves (intubated, LOC /mental state level lowered). Reliance is on family members/next of kin to make decisions. This is stressful for these people and can lead to emotion charged conversations and situations. In the absence of a next of kin this decision may need to be made by the medical staff in charge at the time. This can be very stressful, always remember that there are ethics committees in large hospitals (where most ICU are located) and part of their job is to resolve issues related to ethical situations ie whether or not to turn off a ventilator, insert a feeding tube, give TPN, etc Euthanasia What are the boundaries of euthanasia and allowing a patient to comfortably slip away? Who is capable of making the decision on behalf of the patient? Who knows the patient best? What is our ethical and moral duty to the patient? Should we make a decision in this regard? If you are not comfortable, don‘t do it, refer to someone else (consultant, ethics team) Availability of the service Who has a right to a bed in ICU? Who determines who is sick enough to have the bed? ICU is a limited resource? Where are patients to go when they are discharged from ICU – HDU, general ward, morgue? Cost benefit analysis? How much is too much? Who makes that decision? What is futility? Boundary issues Working in close contact with family members who may see you as the patients only means of survival. Lots of stress experienced, may be overwhelming degrees of gratitude from family members that needs to be dealt with when the member recovers enough to move from ICU. PSYCHOLOGICAL AND EMOTIONAL ISSUES Dealing with death Due to the severity of illness faced by patients in ICU, many die. Due to the intimate nature of ICU (one on one nursing in many centres, high doctor patient ratios, and large amounts of contact with family) staff are faced with more boundary issues and staff need to establish coping mechanisms for this. Many hospitals have debriefing sessions for staff to help them deal with issues relating to death of patients and risks they may be putting their families at. (Has been seen especially in times of disaster eg Bali bombing and SARS outbreak) Work hours Hours are often long to maintain continuity of care (25 hour shifts to allow for an hour overlap for doctors). Means long time away from home, family and friends. Can lead to working tired and sleep deprived when extremely busy. Dealing with Families and the unknown Different people cope with grief, stressful situations differently. Anger is often a representation of this grief/worry. ICU staff need to recognise this and not take outbursts as personal although they may seem so. Good communication skills are a must. Knowledge ICU is an area of frequently evolving protocols, information and knowledge. Staying abreast of this can add to the stresses of staff in these environments. Staffing issues The complexities of the cases in ICU are bound to result in disagreements of patient care. Always ensure discussions are held away from patients and family if heated with a mediator if possible. (YES they can be that heated) Always remember that everyone has the patients best interests at heart. High staff turnover in these areas due to burnout is common. This can add to the stress of the working environment due to the need to establish new working relationships and friendships frequently. SUBSTANCE ABUSE (PPH) 1. What are the commonly used illicit substances in Australia? 1. Marijuana 2. Amphetamines 3. Ecstasy 4. Cocaine 5. Heroin 2. Describe the prevalence of illicit substance abuse in Australian teenagers Marijuana/cannabis was used at least once by 28% of persons aged 14–17 years. Around 5% of 14–17-year-olds had used amphetamines and 4% had used ecstasy/designer drugs at least once in their lifetime. At each age, marijuana/cannabis was the most prevalent illicit drug, used at least once by 12% of 14-year-olds, ranging up to 39% of 17-year-olds. Illicit drug use in the last 12 months by young people aged 14–17 years also increased with age. Overall, 21% of persons aged 14–17 years had used marijuana/cannabis in the last 12 months, 4% had used amphetamines and 3% had used ecstasy/designer drugs. Marijuana/cannabis was used at least once in the last 12 months by 10% of 14-year-olds, ranging up to 29% of 17- year-olds. WHY USE DRUGS? Pleasurable, positive effects Modelling use by others Culturally consistent Perceived social benefits Experimentation and curiosity 3. Outline the risk factors which predispose to substance abuse in young people From Lecture: Individual Risk of Abuse/Dependence Genetics Physiological Vulnerability Psychological Factors Personality Factors Social and Psychosocial Factors From RACGP: - Factors for substance ABUSE Most adolescents use drugs for the same reasons as anybody else — to experience the positive effects of the drug. Early experimenting behaviour with drugs is often related to curiosity, typical adolescent risk taking and to peer influences. Individual (inherent & external) factors Adolescence Genetic vulnerability Anti-social behaviour Knowledge Being male Lack of social bonding Childhood physical and sexual assault Poor school performance Early age of first use Familial Poor quality family relationships & parental skills Socio-demographic Associating with substance abusing peers Being labelled as a substance abuser High stress and lack of coping/support mechanisms Low socio-economic status 4. Discuss the consequences (physical, psychological and social) of substance abuse for (a) the individual, (b) his/her family, and (c) the community Individual Mortality and morbidity are associated with the direct effects of the drug, the mode of administration or from environmental factors associated with drug use such as crime, violence and poor standards of living. The consequences of illicit drug use include physical health outcomes such as kidney, liver and heart damage, loss of memory or concentration, depression, the transmission of viruses through sharing needles, as well as psychological and physical addiction. Some illicit drugs can lead to increased aggression or hostility. Domestic - loss of friends, deterioration of marriage/relationships, psychological impact on spouse (eg. anxiety, stress), arguments, domestic violence, neglect of children, divorce. Occupational – absenteeism, poor performance, unexplained absences during day, failure to be promoted, demotion, dismissal, unemployment. Financial – loss of regular income, hardship from money spent on alcohol, gambling debts, victim of fraud. Legal – Drink-driving, drunk and disorderly, loss of licence, assault, homicide Family Family effects include family breakdown or division, financial problems/ruin, stress on family members. Feelings of inadequacy for parents – ―I should have known‖ or ―what did I do to make him/her like this‖. Other siblings may be forced to take on parental responsibilities, which may occur prematurely. Other siblings can be pressured into experimenting and then develop similar problems. Family may be shunned or embarrassed socially. Community Community problems include crime and danger involved with addictions, including needle stick injuries Increased health costs for hospitalisations and rehabilitation. Decreased productivity from the individual. Public health impact The economic cost of drug use in 1998-99 was $34.4B. (42% alcohol, 47% tobacco and 11% illicit drugs) Health care services Loss of production Welfare costs Road accidents Law enforcement Loss of life 5. What community resources are available to assist individuals with substance abuse, and their families/carers? Support groups (e.g. AA) Detoxification – detox centres, in/out-patient programs/clinics in public and private hospitals Self-help Controlled use programs Pharmacotherapy (e.g. naltrexone and methadone) Drug and alcohol specific services General mental health services Family counselling and support services Child and adolescent services School guidance counsellors 6. What are the notification obligations for a medical practitioner in relation to patients with known/suspected prescription drug dependency? In Queensland, there is no obligation to report a person with a drug dependency (prescription or otherwise) to the police. However, a doctor must notify the Chief Executive of Queensland Health of any patient who is being or will be treated with a controlled drug for longer than two months. The doctor also must notify the Chief Executive if he/she reasonably suspects that the patient has been treated with a controlled drug for more than two months by another doctor(s), and wishes to continue the treatment of the patient with a controlled drug. A doctor must not prescribe, administer etc. a controlled drug or restricted drug of dependency to or for a person the doctor reasonably believes to be drug dependent without the written approval of the Chief Executive. A doctor wishing to treat a drug dependent person must report the circumstances of the case to the Chief Executive. If approval is granted, the doctor must not administer, prescribe etc. a controlled drug or a restricted drug of dependency in excess of the quantity approved by the Chief Executive. Importantly, doctors themselves have a high rate of self-medication with strong opioids, and some practitioners do become dependent. This can lead to a finding of impairment by a medical board.
"Wk 19 – Drug Overdose"