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Overdose and poisoning Flashcards

1
Q

Why is it so important not to make a patient, who has ingested a corrosive substance, sick?

A

The liquid can be aspirated if the patient vomits, this can destroy the lungs

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2
Q

What should be referred to in the event of overdose or poisoning?

A

TOXBASE

and

UK National Poisons Information Servive

and

BNF

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3
Q

Important to know when a patient presents following overdose/ poisoning?

A

What did they take?

How much?

Time since ingestion

Clinical features and progress

Patient factors: weight, co-morbidities etc

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4
Q

What is given to treat organophosphate poisoning?

A

Atropine

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5
Q

Which medication, often used in overdose, causes arrhythmias classically?

A

TCAs

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6
Q

Ways to prevent poison absorption

A
  • 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

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7
Q

Ways to promote active elimination of poison?

A

Repeated doses of charcoal

Haemodialysis

Alkalinisation of the urine e.g. for aspirin (salicylates)

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8
Q

Types of poisoning

A

- 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

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9
Q

What is TOXBASE?

A
  • 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
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10
Q

Psychiatric assessment following poisoning

A

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
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11
Q

Diagnosing poisoning

A

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
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12
Q

What is a toxidrome?

A

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

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13
Q

Supportive care in poisoning

A
  • 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
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14
Q

Discuss use of activated charcoal in poisoning

A

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
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15
Q

Whole bowel irrigation following poisoning

A

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

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16
Q

Antidote for benzodiazepines

A

Flumazenil

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17
Q

Antidote for b-blockers

A

Glucagon

Atropine

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18
Q

Antidote for calcium channel blockers

A

Calcium, glucagon

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19
Q

Antidote for carbon monoxide poisoning

A

Oxygen

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20
Q

Digoxin antidote

A

Digoxin antibodies - digifab

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21
Q

Iron salt antidote

A

Desferrioxamine

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22
Q

Antidote for local anaesthetic toxicity

A

Intralipid

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23
Q

MDMA antidote

A

Dantrolene

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24
Q

Opioid antidote

A

Naloxone

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25
Q

Paracetamol antidote

A

Acetylcysteine

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26
Q

Serotonin syndrome antidote

A

Cyproheptadine

First-generation antihistamine with additional anticholinergic, antiserotonergic, and local anesthetic properties.

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27
Q

Tricyclic antidepressant antidote

A

Sodium bicarbonate

Intralipid

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28
Q

Warfarin antidote

A

Vitamine K

Prothrombin complex

Fresh frozen plasma

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29
Q

Substances used in opioid poisoning

A
  • 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
30
Q

Clinical features of opioid poisoning

A

Triad of (CPR)

  1. Coma
  2. Pinpoint pupils
  3. 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
31
Q

Management of opioid overdose

A

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 <<

32
Q

Salicylate (aspirin) poisoning features

A

<125mg/kg ingested + asymptomatic = harm unlikely

Features: tinnitus, vomiting, deafness, sweating, vasodilation, hyperventilation, dehydration, mixed metabolic acidosis and respiratory alkalosis

33
Q

Management of salicylate (aspirin) poisoning

A
  • 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

34
Q

How much paracetamol has to be ingested to cause severe toxicity?

A

Anything <75mg/kg is unlikely to cause severe toxicity

>150mg/kg ingested may cause severe liver damage

35
Q

Calculating toxic dose of paracetamol in obese patient

A

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)

36
Q

Pathophysiology of paracetamol poisoning

A

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

37
Q

Risk factors for paracetamol toxicity

A

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

38
Q

Clinical features of paracetamol toxicity

A

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

39
Q

What is the most sensitive lab evidence of liver damage following paracetamol overdose?

A

INR

40
Q

Discuss LFTs in paracetamol overdose

A

Normal until >18hrs then ALT and AST very high (>10,000U/L at 3-4 days)

Prolonged INR is most sensitive lab test

41
Q

Paracetamol antidote

A

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

42
Q

Side effects of acetylcysteine

A

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

43
Q

Staggered overdose of paracetamol

A

Do not use normogram

If in doubt, start treatment and get expert advice

44
Q

When is liver transplant needed following paracetamol overdose?

A

Arterial pH < 7.3, 24h after ingestion

Or all of the following:

  • prothrombin time > 100s
  • creatine > 300umol/L
  • grade III/IV encephalopathy
45
Q

Management of paracetamol overdose

A
  1. Record time of ingestion (if unknown, commence treatment immediately)
  2. 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

46
Q

Following paracetamol overdose, when should plasma levels be checked?

A

4hrs after last ingestion

Immediately if patient presenting >4hrs after ingestion

47
Q

Paracetamol normogram

A

Important to use correct units - depends on the values used in lab

48
Q

TCA overdose

A

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

49
Q

ECG changes in TCA overdose

A

Sinus tachycardia initially

PR and QRS prolongationnas poisoning continues

Long PR and QRS helps to confirm TCA toxicity

Severe poisoning: ventricular arrhythmia and bradycardia

50
Q

Management of TCA overdose

A
  • 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
51
Q

Benzodiazepine poisoning

A

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

52
Q

Management of benzo overdose

A

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

53
Q

Lithium poisoning

A

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

54
Q

Investigations in lithium toxicity

A

>1.5mmol/L = toxic effects

Check for end organ damage (LFTs, U&E)

55
Q

Lithium toxicity management

A

**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
56
Q

Beta blocker poisoning

A

Causes bradycardia, hypotension, coma, convulsions and cardiac arrest

Can cause bronchospasm

ECG changes: prolonged QRS

Sotalol can cause torsades de pointes

57
Q

Management of beta blocker toxicity

A

Monitor obs

Venous acess

Atropine for bradycardia and hypotension

IV glucagon for cardiotoxicity

Consider intralipid in cardiac arrest

58
Q

Ethanol poisoning

A

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
59
Q

Management of ethanol poisoning

A
  • 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
60
Q

Ethylene glycol poisoning

A

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
61
Q

Management of ethylene glycol poisoning

A
  • 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
62
Q

Cyanide poisoning

A

Causes inhibition of cellular respiration, dizziness, confusion, arrhythmias and pulmonary oedema

Classical smell of bitter almonds on the breath

63
Q

Management of cyanide poisoning

A

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
64
Q

Carbon monoxide poisoning

A
  • 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
65
Q

Management of carbon monoxide poisoning

A
  • 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
66
Q

Button battery ingestion

A

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
67
Q

Cocaine toxicity

A

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
68
Q

Ecstasy toxicity

A

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
69
Q

Serotonin syndrome

A

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
70
Q

Body packers and stuffers

A

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

71
Q

Iron poisoning

A

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

72
Q

Management of iron poisoning

A

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

Acute (22 decks)

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