Docstoc

Wk 19 – Drug Overdose

Document Sample
Wk 19 – Drug Overdose Powered By Docstoc
					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) hyperventilationsustained 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 signsComa 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.
 ToneUnilateral 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.

				
DOCUMENT INFO
Shared By:
Categories:
Tags:
Stats:
views:23
posted:10/30/2011
language:English
pages:21