Overdose and poisoning Flashcards
Why is it so important not to make a patient, who has ingested a corrosive substance, sick?
The liquid can be aspirated if the patient vomits, this can destroy the lungs
What should be referred to in the event of overdose or poisoning?
TOXBASE
and
UK National Poisons Information Servive
and
BNF
Important to know when a patient presents following overdose/ poisoning?
What did they take?
How much?
Time since ingestion
Clinical features and progress
Patient factors: weight, co-morbidities etc
What is given to treat organophosphate poisoning?
Atropine
Which medication, often used in overdose, causes arrhythmias classically?
TCAs
Ways to prevent poison absorption
- Charcoal given by mouth within 1hr: binds poisons in GI system and reduces absorption
- Gastric lavage: rarely used, suitable if within 1hr of ingestion, contraindicated if ingested substance is corrosive
Promoting vomiting is not recommended
Ways to promote active elimination of poison?
Repeated doses of charcoal
Haemodialysis
Alkalinisation of the urine e.g. for aspirin (salicylates)
Types of poisoning
- Unintentional: most common in small children e.g. tablets, house chemicals, plants
> Also occurs in drug packers who swallow drugs wrapped in packaging and the packagin leaks
- Self poisoning: most common form of poisoning in adults, drugs or poison often taken impulsively, suicidal intent is relatively uncommon but it is important to assess all patients for this
- Non-accidental poisoning of children: form of fabricated or induced illness in which a parent deliberately poisons a child, homicidal poisoning is rare
What is TOXBASE?
- Used for clinical guidance for a variety of sources of poisoning
- Useful to find the relevant information and print it off to put in the patients notes to guide future care
Psychiatric assessment following poisoning
Adults
- Admit patients who are seriously poisoned to a medical/ ICU ward
- Most patients who take overodses are not seriously ill and can be monitored in ED or clinical decisions unit
- Admitting a patient overnight may allow for a cooling off period even if there is no risk of toxicity
- Look for a cause of self harm and observe carefully due to risk of further self harm
Children
- Serious poisoning in children is uncommon butchildren can appear well even if not
- Admit to paeds ward for observation
- Healthy visitor may advise regarding poisoning prevention
- Children >6yrs: consider possibility of intentional self harm and assessment by CAMHS
Diagnosing poisoning
May not be possible to take a hx from the patient so collateral hx is often key
- Consult medical notes for any evidence or previous overdoses
- Examine for signs of poisoning e.g injection sites/ marks
- Exclude other diagnoses that may mimic overdose e.g. meningitis, head injury etc
- Chinese herbal medicines and herbal preparations can cause significant toxicity
What is a toxidrome?
Toxidrome describes a group of signs and symptoms and characteristic effects associated with exposure to a particular substance or class of substances
I.e. a syndrome associated with a particular toxin
e.g. coma, dilated pupils, divergent squint, tachycardia, increased tone and reflexes: TCA toxidrome
Supportive care in poisoning
- Protect airway: hypoxia and CO2 retention common, use ET tube if patient unconscious, nurse in recovery position to avoid aspiration in case of vomiting
- Hypotension: may result from hypovolaemia, arrhythmias, cardio-depressive drugs, treat according to the cause with fluids/ vasopressors as appropriate
- Arrhythmias: generally rare in poisoned patients, mainly associated with TCA overdose, b-blockers, digoxin, bronchodilators and amphetamines. Correct hypoxia , resp depression, metabolic acidosis and electrolyte abnormalities, anti-arrhythmic drugs are rarely needed
- Convulsions: cause hypoxia > acidosis > cardiac arrest, caused by TCAs, mefenamic acid and theophylline (used to treat COPD), correct hypoxia and hypoglycaemia and consider giving IV lorazepam, buccal midazolam or rectal diazepam
- Hypothermia: check rectal temp, insulate and passively re-warm
- Hyperthermia: amphetamines, cocaine ecstasy, sympathomimetics, consider serotonin syndrome, convulsions and rhabdomyolysis common, actively cool and get expert help
Discuss use of activated charcoal in poisoning
If given within 1hr can reduce absorption of many drugs - actually little evidence to support use in overdose
- Decreases half life of some drugs
- Only used for substances that bind to it - e.g. iron, lithium, methanol, ethylene glycol and strong acids/ bases do not bind
- Messy and can cause vomiting and aspiration
Whole bowel irrigation following poisoning
Rarely performed and only done on expert advice
Aim is to empty bowel rapidly by giving fluid orally or via NG tube until rectal effluent is clear
- Has been used to remove packets from body packers and button batteries from children
- Saline is not used due to rsik of fluid overload and hypokalaemia
Polyethylene glycol electrolyte solution is used - this is the fluid used in bowel prep, it draws fluid out of the cells and thus acts as a laxative which speeds up gastric motility
Antidote for benzodiazepines
Flumazenil
Antidote for b-blockers
Glucagon
Atropine
Antidote for calcium channel blockers
Calcium, glucagon
Antidote for carbon monoxide poisoning
Oxygen
Digoxin antidote
Digoxin antibodies - digifab
Iron salt antidote
Desferrioxamine
Antidote for local anaesthetic toxicity
Intralipid
MDMA antidote
Dantrolene
Opioid antidote
Naloxone
Paracetamol antidote
Acetylcysteine
Serotonin syndrome antidote
Cyproheptadine
First-generation antihistamine with additional anticholinergic, antiserotonergic, and local anesthetic properties.
Tricyclic antidepressant antidote
Sodium bicarbonate
Intralipid
Warfarin antidote
Vitamine K
Prothrombin complex
Fresh frozen plasma
Substances used in opioid poisoning
- Includes morphine, diamorphine a.k.a. heroin, pethidine, codeine and methadone
- Acute opioid poisoning often occurs in recreational users, consider opioid poisoning in patients presenting with coma of unknown cause
Clinical features of opioid poisoning
Triad of (CPR)
- Coma
- Pinpoint pupils
- RR decreased
- Cyanosis, apnoea, convulsions and hypotension may also occur
- Resp depression can cause death within 1hr
- Delayed toxicity can occur with methadone which has a long duration of action
Management of opioid overdose
A-E
Naloxone is the antagnoist, it reverses respiratory depression and coma if given in sufficient dose
Naloxone has a much shorter 1/2 life than most opioids so it can wear off and resp. depression can return >> subsequent doses may be needed
Observe patient for a minimum of 6hrs following last dose of naloxine
Obsevre for up to 24hrs in methadone overdose
>>Try to persuade patient to stay in hospital, can be impossible <<
Salicylate (aspirin) poisoning features
<125mg/kg ingested + asymptomatic = harm unlikely
Features: tinnitus, vomiting, deafness, sweating, vasodilation, hyperventilation, dehydration, mixed metabolic acidosis and respiratory alkalosis
Management of salicylate (aspirin) poisoning
- If >125mg/kg ingested in past hr - consider activated charcoal
- >500mg/kg ingested in past hr - consider gastric lavage
- Measure plasma levels at least 2hrs after overdose and then every 2 hours until a peak has been reached
- Check U&E, clotting, ABG & VBG
Mild poisoning: asymptomatic patient with plasma level of <300mg/L + normal VBG - fit for discharge
Moderate poisoning 300-700mg/L: give sodium bicarbonate over 30mins to promote alkalinisation of urine and excretion of aspirin (increases excretion 18x)
Severe poisoning: CNS features, acidosis or plasma levels >700mg/L are associated with significant mortality, haemodialysis/ haemofiltration
How much paracetamol has to be ingested to cause severe toxicity?
Anything <75mg/kg is unlikely to cause severe toxicity
>150mg/kg ingested may cause severe liver damage
Calculating toxic dose of paracetamol in obese patient
Use an upper limit of 110kg if a patient weighs >110kg rather than their actual weight
Used to calculate both toxic dose and the dose af the antidote (acetylcysteine)
Pathophysiology of paracetamol poisoning
NAPQI is a metabolite of paracetamol, usually 5% of ingested paracetomal becomes NAPQI
NAPQI is conjugated by glutathione in the liver in normal circumstances
In overdose, glutathione is overwhelmed, NAPQI builds up and causes hepatotoxicity
Can also cause nephrotoxicity
Risk factors for paracetamol toxicity
It used to be the case that some patients e.g. those with existing liver damage were considered to be at high risk following paracetamol toxicity however this is no longer the case and all patients are treated as if high-risk
Clinical features of paracetamol toxicity
Hrs: N&V + abdo discomfort
24hrs: pain and tenderness over liver
2-4 days: jaundice > coma due to hypoglycaemia > bleeding
3-5 days: hepatic encephalopathy
50% have renal failure: haematuria, loin pain, proteinuria
Fatal cases: cerebral oedema, septicaemia, DIC
What is the most sensitive lab evidence of liver damage following paracetamol overdose?
INR
Discuss LFTs in paracetamol overdose
Normal until >18hrs then ALT and AST very high (>10,000U/L at 3-4 days)
Prolonged INR is most sensitive lab test
Paracetamol antidote
Acetylcysteine
Given IV in 5% glucose
Effective if given within 8hrs - if given later it is still worthwhile but less effective
Initial dose = 150mg/kg in 200mL glucose over 1hr, 50mg/kg in 500mL over 4hrs then 100mg/kg in 1L over 6hrs
Side effects of acetylcysteine
More likely if the plasma paracetamol levels are low
- Itching
- Rashes
- Nausea
- Bronchospasms
**If side effects occur, stop infusion and give antihistamine >> resume once reaction has settled
Staggered overdose of paracetamol
Do not use normogram
If in doubt, start treatment and get expert advice
When is liver transplant needed following paracetamol overdose?
Arterial pH < 7.3, 24h after ingestion
Or all of the following:
- prothrombin time > 100s
- creatine > 300umol/L
- grade III/IV encephalopathy
Management of paracetamol overdose
- Record time of ingestion (if unknown, commence treatment immediately)
- Record time bloods taken for plasma paracetamol levels
Within 4hrs ingestion: activated charcoal if <1hr, take blood at 4hrs and use normogram to decide whether to give acetylcysteine (give even if slightly below line)
Within 4-8hrs: use normogram to decide whether to give acetylcysteine, treatment mot effective when given <8hrs after ingestion
8-24hrs: start IV acetylcysteine if >150mg/kg taken, normogram less effective after 12-15hrs post ingestion… if in doubt treat
>24hrs: measure plasma levels, LFTs, U&E, creatinine, INR and ABG, if clinically jaundices/ hepatic tenderness - give acetylcysteine. If bloods normal and plasma levels low + asymptomatic >> no treatment needed
Staggered overdose: commence treatment and take bloods at least 4hrs after ingestion, if bloods normal and paracetamol level <10mg/L consider stopping treatment
Following paracetamol overdose, when should plasma levels be checked?
4hrs after last ingestion
Immediately if patient presenting >4hrs after ingestion
Paracetamol normogram
Important to use correct units - depends on the values used in lab
TCA overdose
TCAs are highly toxic
Anticholinergic effects: dry skin and mouth, dilated pupils, urinary retention, convulsions, drowsiness >> coma
Divergent squint (eye moves away)
Cardiotoxicity: prolonged PR and QRS >> ventricular arrhythmia
Pupils may be dilated and unreactive
10% have fits
ECG changes in TCA overdose
Sinus tachycardia initially
PR and QRS prolongationnas poisoning continues
Long PR and QRS helps to confirm TCA toxicity
Severe poisoning: ventricular arrhythmia and bradycardia
Management of TCA overdose
- A-E
- Observe continuously as rapid detrioration can occur
- Monitor ECG and check ABG
- Consider activated charcoal (<1hr)
- Lorazepam for seizures
- Correct hypoxia and acidosis to treat arrhythmias
- Sodium bicarbonate reduces free/ active TCA - may dramatically improve cardiac rhythm and output
- Cardiac arrest: consider intralipid
- In extreme cases cardiac bypass may be needed
Benzodiazepine poisoning
Rarely causes serious poisoning when taken in overdose but potentiate other CNS depressants e.g. elcohol, TCAs and barbiturates
Features: drowsiness, dizziness, ataxia, dysarthria (slurred speech)
Fatal poisoning is rare but can occur e.g. due to resp. depression in elderly with chronic COPD
Management of benzo overdose
Activated charcoal <1hr
Flumazenil - benzo antagonist, reverses effects of benzos within 1min
*Note flumazenil can cause convulsions and arrhythmias and may precipitate benzo withdrawal
**Not to be given to those who have take TCAs with benzos as can cause cardiac arrest 🫀❌**
Benzo metabolites can affect driving and congition for days so important to advise re this
Lithium poisoning
Often due to accumulation of therapeutic dose rather than self harm
N&V, coarse tremor, confusion, increased muscle tone, clonus
Can cause renal failure and coma in severe cases
Therapeutic index is 0.4-1
Toxicity if >1.5
Investigations in lithium toxicity
>1.5mmol/L = toxic effects
Check for end organ damage (LFTs, U&E)
Lithium toxicity management
**Activated charcoal does not bind lithium**
Whole bowel irrigation may be considered
Use standard supportive measure, treat seizures with lorazepam etc
- Haemodialysis for severe poisoning >> often has to be repeated due to rebound release of lithium from tissues
Beta blocker poisoning
Causes bradycardia, hypotension, coma, convulsions and cardiac arrest
Can cause bronchospasm
ECG changes: prolonged QRS
Sotalol can cause torsades de pointes
Management of beta blocker toxicity
Monitor obs
Venous acess
Atropine for bradycardia and hypotension
IV glucagon for cardiotoxicity
Consider intralipid in cardiac arrest
Ethanol poisoning
Disinhibition >> ataxia >> dizziness >> dysarthria >> drowsiness
Potentiates CNS depression of many drugs
Classical signs: odour, nystagmus, horizontal gaze
Severe poisoning:
- Patient may be comatose, have resp depression, hypotension, hypothermia, metabolic acidosis
- Death can occur due to reps failure or vomit aspiration
- Patients who have a blood alcohol level >350mg/dL are at a significant risk of death
Management of ethanol poisoning
- A-E
- Nurse in recovery position to protect airway
- Measure blood alcohol
- Check glucose every 1-2hrs in severe poisoning, correct hypoglycaemia with glucose
- Look for signs of injury e.g. head injury, low threshold for CT
- Long lie? Check CK for evidence of rhabdomyolysis
- Gastric lavage and charcoal are ineffective in ethanol intoxication
- Involve ICU and consider dialysis in extreme cases
Ethylene glycol poisoning
3 stages: alcohol like > high anion gap metabolic acidosis > AKI
- First 12hrs after ingestion the patient appears drunk but does not smell of alcohol
- Ataxia, nausea, vomiting, haematemesis followed by convulsions, coma and severe metabolic acidosis
- 12-24hrs after ingestion hyperventilation, pulmonary oedema, tachycardia, arrhythmias and cardiac failure may develop
- Acute tubular necrosis and renal failure
- Cranial nerve palsies
Management of ethylene glycol poisoning
- Do not give charcoal
- Consider gastric lavage if <1hr since ingestion
- ABGs, U&E, HCO3-, glucose, FBC, LFTs
- Read TOXBASE
- Observe for at least 6hrs after ingestion
- Monitor ECG, HR, BP, urine output
- Ethanol minimises toxicity
- Sodium bicarbonate reduces acidosis
- Correct hypocalcaemia
- Consider haemodialysis if severe
Cyanide poisoning
Causes inhibition of cellular respiration, dizziness, confusion, arrhythmias and pulmonary oedema
Classical smell of bitter almonds on the breath
Management of cyanide poisoning
Supportive
- 100% oxygen
- Monitor ECG
- Charcoal/ gastric lavage if within 1hr
- Specific antidotes are dangerous in the absence of cyanide so only give if poisoning is moderate = severe
- Severe poisoning: give dicobalt edetate - in absence of cyanide this can cause facial, laryngeal and pulmonary oedema, vomiting, tachycardia and hypotension
- Mild poisoning: sodium thiosulfate or sodium nitrite
- High doses of hydroxocobalamin are useful and relatively safe in cyanide poisoning
Carbon monoxide poisoning
- Binds Hb and prevents O2 delivery from blood to the tissues
- Clinical features
- Early: headache, malaise, nausea, vomiting
- Severe: coma, hyperventilation, hypotension, increased muscle tone, convulsions
- Cherry red skin colouring may be seen in fatal CO poisoning but is rare in live patients
- Neurological and psychiatric problems may develop later
Management of carbon monoxide poisoning
- A-E
- Tight fitting mask with O2 reservoir for conscious patients - 100% oxygen
- IPPV for unconscious patients
- Record ECG, look for signs of MI
- Check COHb levels
- Correct metabolic acidosis by ventilation and O2
- Consider mannitol if cerebral oedema present
Button battery ingestion
Can get stuck and cause perforation
Management
See TOXBASE
- X-ray chest
- Remove any battery stuck in oesophagus
- Asymptomatic child with battery in stomach can be sent home
- If not passed in 2 days, review
- Batteries in ear: liaise with ENT
Cocaine toxicity
Chest pain due to MI, cerebral haemorrhage, pyrexia, rhabdomyolysis, renal failure, gut ischaemia and serotonin syndrome can occur
Manage:
- Same as for ecstasy - supportuve, manage fits, correct acidosis
- Treat chest pain with GTN and diazepam
- If ECG suggests MI consider angioplasty or thrombolysis
Ecstasy toxicity
Causes release of serotonin, catecholamines and other hormones Can cause serotonin syndrome
Manage:
- A-E
- Supportive, manage fits, correct acidosis, treat hyponatremia, cool patient down
- If temp >40 consider dantrolene
Serotonin syndrome
Increasingly recognised amongst those taking SSRIs
- Especially likely if they are recently started on medication or if it is taken with other drugs which increase release or availability of serotonin for example cocaine, ecstasy and amphetamines
- Serotonin syndrome can also occur after an acute overdose
Clinical features
- Altered mental status: confusion, hallucinations and agitation + drowsiness, reduced consciousness
- Neuromuscular features: rigidity, shivering, teeth grinding, hyper reflexia
- Autonomic: tachycardia, hypertension, flushing, diarrhoea, vomiting, hyperthermia
Treatment
- Supportive measures and seek advice from TOXBASE, diazepam may help with agitation, hypothermia, myoclonic jerking and fits
- Treat rhabdomyolysis with IV fluids
- Cyproheptadine is a serotonin receptors antagonist is limited evidence but a good theoretical basis for use in serotonin syndrome
Body packers and stuffers
Body packers: those who smuggle drugs wrapped in condoms foil latex. The packages can leak and whatever is inside the package can cause poisoning in the patient
- Features of toxicity depend on what has been packed in the body tried to establish the drug involved and the quantity packed inside the body check basic obs, abdominal x-ray can be used as a screening tool but is less sensitive than CT
- Isotonic laxatives and whole bowel irrigation made expulsion of packages
- Consider naloxone infusion if risk of opioid poisoning
Body stuffers are those who ingest drugs immediately prior to being apprehended by the police in order to avoid being caught with the drug in their possession – packaging is less likely to be robust and the risk of leakage is increased
Iron poisoning
Iron tablets may be ingested by children if confused for sweets
Serious poisoning is uncommon but fatalities can occur
Features: N, V, diarrhoea, abdo pain
Grey/ black stools ± blood
Hyperglycaemia and raised WCC may occur
Severe poisoning: haematemesis, drowsiness, convulsions, coma, metabolic acidosis, shock, hepatic encephalopathy, bowel infarction
Management of iron poisoning
Supportive measures
*Charcoal does not absorb iron*
Severe poisoning: desferrioxamine IVI - can cuase hypotension if given too quickly
Urine should turn orange/ red - confirms free iron has been bound and that desferrioxamine was required
