Week 11 Flashcards
what are the steps in the risk assessment-based aproach to poisoning?
- resuscitation
- risk assessment
- supportive care and monitoring
- Investigations
- Decontamination
- Enhanced elimination
- Antidotes
- Disposition
what is involved in RESUSCITATION in the risk assessment-based aproach to poisoning?
Airway Breathing Circulation Control seizures Correct hypoglycaemia Correct hyperthermia Consider resuscitation antidotes
what is involved in RISK ASSESSMENT in the risk assessment-based aproach to poisoning?
Agent Dose Time since ingestion Clinical features Progress of the symptoms Patient factors
What are the S&S of ANTIcholinergic toxicity?
Red as a beet
- flushed
Dry as a bone
- Anhydrosis
Hot as a hare
- Anhydrotic hyperthermia
Mad as a hatter
- Delerium/hallucinations
Full as a flask
- urinary retention
Tachycardia
Decreased/no bowel sounds
What are the S&S of CHOlinergic toxicity?
SLUDGE BBB
Salivation Lacrimation Urination Defecation Gastric Emesis Bronchoraehea Bronchospasm Bradycardia
What causes cholinergic toxicity?
insecticides containing organophosphates
what are the keys to overdose resus?
Resuscitation should continue until expert advice can be obtained on the
poison – can be prolonged.
Transport early if in cardiac arrest and continue CPR to hospital
Attempts at decontamination does NOT take priority over CPR
What should be noted about seizures in an overdose?
– if present, usually generalised. If partial seizures, this indicates a focal neurological
problem that requires further investigation.
– Common causes – Venlafaxine, bupropion, tramadol, amphetamines
– We treat with Midazolam.
What should be noted in ABC’s of overdose resus
– Patients can deteriorate quickly so monitor closely and be prepared for change in vitals, including cardiac arrest
– Attention to airway, breathing and circulation is paramount
– There is an increased risk of aspiration in these patients (been noted at GCS of 12).
what supportive care and monitoring is required ofr overdose?
Drugs normally affect the respiratory system, cardiovascular system, the central nervous system.
Respiratory system
– Full RSA needed.
– Intubation may be required if there is a lowered LOC.
– Secure the airway while you wait for MICA.
– Monitor ventilations regularly. Have bag mask at the ready.
Cardiovascular system: – 12 lead ECG essential – rate, rhythm, PRI, QRS width, ST, – Some drugs will cause arrhythmias – Fluids – Monitor closely
GCS – closely monitor. If changes start your ABCs again
Whata re the types of CNS depressants?
Opiates – morphine, heroin, codeine, tramadol, methadone
Sedative-hypnotic drugs - benzodiazepines & barbiturates
GHB - Gamma Hydroxybutyrate
Alcohol
What is the clinical presentation of an Opioid OD?
LIKELY:
Lowered level of consciousness (drowsy)
Respiratory depression leading to failure & death
Pinpoint pupils
POTENTIALLY:
Could be hypotensive
May have vomited or be vomiting
Check setting and history!
Tramadol OD on the increase
– Doses > 500 mg may cause seizures in adults.
– Deaths have occurred following ingestion of 3-5 g.
– Rarely causes respiratory depression but frequently results in tachycardia,
agitation and seizures (due to serotonin syndrome) .
What are the clinical presentations for benzodiazapines?
Drowsiness, confusion, dizziness
Slurred speech
Nystagmus, blurred vision
Hypotension
Ataxia, weakness, lack of coordination
Coma
Respiratory depression – even arrest
Cardiac arrest
Large doses – hypothermia, bradycardia, hypotension may occur
What is the clinical presentation of GHB?
Causes a rapid onset of CNS and respiratory depression
Other symptoms include myoclonic jerking, bradycardia, sweating,
agitation, vomiting, delirium, cheyne-stokes type breathing
Recreational doses 30-40 mg/kg
Can cause coma
Co-ingestion of other drugs, especially CNS depressants,
increased the risk of respiratory depression, apnoea and death
Recovery associated with brief period of agitation, delirium and
vomiting
what does Naloxone (Narcan ) do?
Opiate antagonist
Competes for the same receptors as opiates
Greater affinity
Shorter half life than opiates – this a problem
Administer after you have looked after the airway
Consider size of patient to determine initial dose
What are the types of opioid overdoses in the ‘Other opiod arm’ of the CPG
prescription
latrogenic
polypharmacy
unknown
what is the clinical presentation of alcohol intoxication/OD
CNS depression even coma
Loss of inhibition
Loss of judgement
Can add to the depressive effects of other CNS depressants
Vomiting, loss of airway protection
Increase in self-confidence
Agitation, aggression, disorientation
Slurred speech, Ataxia, nystagmus
Tachycardia, hypotension, hypothermia
Inhibition of Anti-diuretic Hormone (ADH) - Increase in urine production - Loss of fluid
volume – Possible hypotension – Dehydration - Loss of electrolytes etc.
What is the clinical presentation of alcohol poisoning?
– Confusion – Loss of coordination – Vomiting – Seizures – Irregular or slow breathing (less than eight breaths a minute) – Blue-tinged or pale skin – Low body temperature (hypothermia) – Stupor – when someone’s conscious but unresponsive – Unconsciousness – passing out – hypotension
Lose gag reflex
What are some cardiovascular complications of long-term alcohol abuse?
Cardiovascular – Afib, cardiomyopathy,
clotting problems
What are some GIT complications of long-term alcohol abuse?
Gastrointestinal – liver disease,
hepatitis, cirrhosis, oesophageal
varices, pancreatitis, chronic gastritis, GI
bleeds, enlarged liver
What are some additional complications of long-term alcohol abuse?
Malnutrition, Vitamin deficiency,
dehydration
Alcoholic ketoacidosis, electrolyte
imbalances
CNS - Memory problems (Wernicke’s
encephalopathy), subdural
haemorrhage
What are some of the management considerations of alcohol intoxicated patients?
- Hypoxia – breathing rate, depth, asphyxia,
- Hypovolemia / dehydration
- Analgesia
- Nausea and vomiting
- Aggression and compliance
- Competency to make own decisions
What are some of the pitfalls and dangers of alcohol intoxicated patients?
- Failure to regard ethanol intoxication as potentially life threatening
- Failure to detect and manage co-existing intoxications or other medical conditions in the intoxicated patient.
- Believing patient is competent to make own decisions re welfare
- Assault to the paramedics
- Crowds could also be a problem
- You may need to modify your behavior or language - You may elect to leave the scene
what are some of the physiological problems caused by alcohol withdrawl?
– Autonomic excitation – tremors, sweating, anxiety, agitation, tachycardia,
N&V, hyperthermia, hypertension
– Neuro-excitation – hyper-reflexia, hallucinations, seizures, nightmares
– Delirium tremens – severe form has 8% mortality
Present in 20% pts admitted to hospital
How do you manage alcohol withdrawal?
Resuscitation, supportive care and monitoring of all vitals
Get a good history
Exclude other non-toxicological causes e.g. hypoxia, metabolic
Establish an IV
Manage acute illness including dehydration and seizures
Is the withdrawal part of a medical plan?
Request MICA
What are some common sources of methanol?
– Antifreeze preparations – Automobile and furniture polish – Pesticides – Industrial products (oils, detergents) – Paint thinners – Methylated spirits (ethanol + methanol)
What are the clinical signs of methanol poisoning?
– Early symptoms are similar to ethanol intoxication CNS depression Loss of inhibition Ataxia Nausea
– Initial severe symptoms in 12-24 hours
(relates to amount ingested)
– Possibility of seizures
– Vision blurring or loss
– Metabolic acidosis
– Death
What is the management for methanol poisoning?
ABC’s are paramount
Pt is acidotic so will have respiratory compensation
– Hyperventilate to help blow off acid (remember respiratory unit)
MICA for intubation and possibly sodium bicarbonate
Treat seizures
Check BSL
Antidote = fomepizole – not available in Australasia
Quick transport – need dialysis
What are common stimulant & psychoactive drugs?
- MDMA / Ecstasy
- Methamphetamines
- Cocaine
what are the immediate S&S of MDMA/Ecstasy?
- Enlarged pupils
- Increased heart rate and blood pressure
- Increased energy
- Feeling of euphoria
- Teeth grinding and jaw clenching
- Anxiety and panic attacks
- Overheating and dehydration
- A ‘comedown’
- Nausea, vomiting and dizziness
- Visual distortions
- Paranoia
- Psychosis
- Serotonin syndrome
- Stroke.
what are the long-term S&S of MDMA/Ecstasy?
- Dependence / addiction
- Long-term problems with depression
- Impairments to memory and attention
- Liver problem
How does MDMA work?
MDMA/Ecstasy stimulates the body’s CNS. Onset of effects can take up to 60
minutes, people may therefore think the first pill isn’t working and take more.
How does Methamphetamine work?
• Methamphetamine increases the amount of the neurotransmitter dopamine, leading to high levels of that chemical in the brain.
What are the short-term effects of ICE?
- Feelings of pleasure and confidence
- Increased alertness and energy (often don’t sleep for days)
- Repeating simple things like itching and scratching
- Enlarged pupils and dry mouth
- Teeth grinding and excessive sweating
- Fast heart rate and breathing
- Reduced appetite
- Increased sex drive
- It takes several days to come down from ICE
What are long term effects of ICE?
Extreme weight loss due to reduced appetite Restless sleep Dry mouth and dental problems Regular colds or flu Trouble concentrating Breathlessness Muscle stiffness Anxiety, paranoia and violence Depression Heart and kidney problems Increased risk of stroke Needing to use more to get the same effect, Dependence on ice Financial, work or social problems Ice Psychosis
What are the short term effects of Cocaine
- Happiness and confidence
- Talking more
- Feeling energetic and alert
- Quiet contemplation and rapture
- Feeling physically strong, mentally sharp
- Reduced appetite
- Dry mouth
- Enlarged (dilated) pupils
- Higher blood pressure
- Faster heartbeat and breathing
- Higher body temperature
- Increased sex drive
- Unpredictable, violent behavior
- Indifference to pain
Whata re the long term effects of cocaine?
Regular use may eventually cause: • Insomnia and exhaustion • Depression • Anxiety, paranoia and psychosis • Sexual dysfunction • Hypertension and irregular heartbeat • Heart disease and death
What are the S&S of cocaine overdose?
- Nausea and vomiting
- Extreme anxiety
- Chest pain
- Panic
- Extreme agitation and paranoia
- Hallucinations
- Tremors
- Breathing irregularities
- Kidney failure
- Seizures
- Stroke
- Heart problems.
What are the common clinical symptoms of CNS stimulants?
Tachycardia and hypotension is common but hypertension and tachycardia also possible (adrenergic effect)
Dilated pupils (myadrisis) –adrenergic effect
Dysrhythmias
Diaphoresis – adrenergic effect
Agitation (adrenergic), hallucinations and paranoia
Dry mucous membranes – adrenergic effect
Fever, hyperthermia
Seizures, tremors, hyper-reflexia
Poly-pharmacy must always be considered with CNS stimulant use
Ingestion by children is potentially lethal
Known teratogenic effects, leading to miscarriage and fetal demise
What are some cardiovascular effects of CNS stimulants?
Toxicity results from sympathomimetic, vasospastic and sodium channel blocking
effects (cocaine).
Vasospasms also means poor myocardial perfusion as well as promotion of
platelet aggravation
Blocking of fast sodium channels results in dysrhythmias
Increased vascular dissection
Increased intracranial haemorrhage
Acute cardiomyopathy
Pulmonary oedema
What are some major complications of CNS stimulants?
Hyperthermia
– Can result from excited delirium (cocaine) or excessive exercise (MDMA)
– Further exacerbated by the environment they are in e.g. hot night club
– Can also be a sign of severe serotonin syndrome
What can hyperthermia lead to?
– Rhabdomyolysis
– Impaired consciousness,
– DIC (disseminated intravascular coagulation)
– and multi-organ failure
What are S&S of serotonin syndrome?
– Confusion, hallucinations
– Agitation or restlessness, anxiety, apprehension
– Dilated pupils
– Headache
– Changes in blood pressure and/or temperature
– Nausea and/or vomiting, diarrhoea
– Rapid heart rate, hypertension, increased RR
– Tremor, seizures
– Loss of muscle coordination or twitching muscles
– Shivering and goose bumps
– Heavy sweating, flushing
– Increased muscle tone, rigidity, hyper-reflexia
Life threatening if: • High fever • Seizures • Rigid muscles • Irregular heartbeat • Unconsciousness
what are some hallucingenic drugs?
- LSD - (Lysergic acid diethylamide)
- Magic mushrooms - psilocybin
- Mescaline - peyote cactus
what are S&S of psilocybin syndrome?
Onset usually within 1 hour lasting 4‐6 hours
– Nausea and vomiting (more rare, may happen before psychological effects)
– Heightened colour perception
– Emotional effects
– Changes in perception
– Anxiety
– Delusions
What are S&S of LSD?
Profound hallucinations – thoughts / perceptions dream like – sensory modalities confused – thoughts disconnected to reality – euphoria or dysphoria – anxiety / panic attacks – enhanced mood or depression – calmness or aggression – decreased libido?
What are the S&S of ketamine?
– Euphoria, relaxation, feeling detached from body – Hallucinations – Disorganised thoughts, confused – Anxiety, agitation, paranoia, panic – Nausea, vomiting – Slurred speech, get blurred vision, and lack of co-ordination – Sweating – more sensitive to touch
What are some S&S of high doeses of ketamine?
– be drowsy, have seizures or go into a coma
– have a near-death experience
– get amnesia, not be able to feel pain and have
stiff muscles
– become paranoid, experience panic, terror or
anxiety
– hallucinate and have bizarre or scary
experiences
– behave strangely.
