Poisoning

Question 1

Common poisoning methods

Answer 1

Young person deliberate self harm or drug overdose
Chronic lead or iron poisoning
Accidental young children

OTC drugs which are easily available paracetamol, ibuprofen, prescription medications - SSRIs, TCA, opiates

Question 2

History in poisoning

Answer 2

At the time = when did it take place, what? - how much, symptoms, ever before?

Later = assess MH and suicide risk. Why? How are they feeling, PMHx. Psych referral

Question 3

Preventing absorption

Answer 3

Aims to reduced volume of poison entering the systemic circulation from the gut.

Methods = activated charcoal and gastric lavage

Cannot be used in patients who are unconscious of whose GCS is reduced due to risk of aspiration

Question 4

Activated charcoal

Answer 4

Evidence base only supports its use if within 1hr of ingestion of the poison.

Question 5

Charcoal ineffective

Answer 5

Alcohol, metal - iron, lithium, cyanides, hydrocarbons and insecticides

Question 6

Complications of charcoal

Answer 6

Tastes and looks awful. Aspiration pneumonitis due to vomiting can occur in 20%. Needs to be given with a laxative to prevent formation of briquettes. These are aggregates of charcoal and can precipitate a bowel obstruction

Question 7

Gastric lavage

Answer 7

Rarely used may be suitable for large/ life threatening poisoning which cannot be absorbed by charcoal

ie Iron

Question 8

SE of gastric lavage

Answer 8

Aspiration, gut perforation, water intoxication, pneumothorax, laryngospasm.

Often very unpleasant and ineffective

Question 9

CI of lavage

Answer 9

Hydrocarbon of a high aspiration potential or a caustic substance has been ingested (weakening of the oesophageal walls = perforation)

Question 10

Increasing poison eliminaton

Answer 10

Multiple dose activated charcoal, urina alkanisation and haemodialysis

Question 11

Multiple dose activated charcoal

Answer 11

50g of charcoal followed by further 25g 2hrly given with a laxative to prevent constipation

Shown no survival benefit only use patients with life threatening ingestion of theophylline, carbamazepine, quinine and phenobarbital

Question 12

MOA of multiple dose activated charcoal

Answer 12

Favour enterohepatic circulation, by using high levels of charcoal to bind all the drug in the gut, the drug will reenter the gut from the blood via passive diffusion down its concentration gradient.

Question 13

Haemodialyisis

Answer 13

Only useful if the drug has a small volume of distribution, present mainly in the blood. Useful for ethanol, lithium, salicylate and methanol

Question 14

Urine alkanisation

Answer 14

Can be used in phenobarbital and salicylate poisoning. Uses bicarbonate to ensure the pH of the urine is above 7.5

Question 15

Benzodiazepine antidote

Answer 15

Flumazenil

Question 16

Carbon monoxide antidote

Answer 16

High dose oxygen

Question 17

Immediate management in OD

Answer 17

Secure the airway is paramount. ECG, o2 sats, GCS, blood glucose, temperature and pupil size/reaction?

Question 18

MDMA overdose

Answer 18

PC = dilated pupils, hyponatremia, tachycardia, tremor, hypertension, hallucinations, trismus

Complications - seizures, rhabdomylosis, AKI, SIADH, cardiac arrythmias

Question 19

Paracetamol OD MOA

Answer 19

Paracetamol is broken down by the liver like so

• 30% sulphontransferase
• 55% paragluconide

The other 15% undergoes oxidation to NAPQI under normal conditions this is broken down by glutathione and excreted. In OD glutathione is depleted which leads to toxic NAPQI accumulating and causing cell damage and death

Question 20

PC paracetamol OD

Answer 20

Early (24hrs) - asymptomatic, N/V, non specific abdo pain

72 hrs post injection = peak may show jaundice, localised liver pain, raised PT, coagulopathy, encephalopathy and coma. This can lead to acute liver failure and death

Hypoglycaemia, metabolic acidosis

25% = ATN - oliguria and AKI

Question 21

Poor prognosis in paracetamol OD

Answer 21

PT/ INR rising after day 3
PT >180s at anytime
Bilirubin >70 
Metabolic acidosis
Encephalopathy grade III-IV
Creatinine >300, high lactate

Question 22

Invx paracetamol OD

Answer 22

Paracetamol levels - crucial for treatment
Clotting - INR and PT
LFTS - bill helps assess function, ALT >1000
U+E - renal function
ABG = metabolic acidosis?

Question 23

Mx of paracetamol OD

Answer 23

NAC if dictated by paracetamol nomogram. Max efficacy @ 8hrs
Activated charcoal if within 1hr

Supportive - IV vit K/FFP if active bleeding?, ITU, liver transplant

Question 24

N-acetyl cystine

Answer 24

IV drip over 21hrs (Total dose 300mg/kg)

Anyone >100ml/L is treated

SE = anaphylactoid reaction involving urticaria, wheeze, hypotension. Not life threatening reduce infusion rate. If severe give antihistamines

Question 25

Salicylate (Aspirin) PC

Answer 25

Agitation, delirium, dizziness, sweating, vomiting, hyperventilation

Specific = tinnitus, mixed resp alkalosis and metabolic acidosis

Stimulate the respiratory centre increasing the depth and rate of breathing - resp alkalosis
Compensation leads to renal excretion of bicarb and K+ retention leading to metabolic acidosis. They also disrupt oxidative phosphorylation leading to lactic acid and ketone production

Question 26

Invx salicylates

Answer 26

Plasma salicylate level - dose dependent reaction
U+E - low K+, low bicarbo,
ABG = critical to manage acidosis and alkalosis

Question 27

Mx of salicylate OD

Answer 27

Activated charcoal within 1hr
Sodium bicarb to control acidosis and prevent salicylate crossing BBB and = seizures
Urinary alkinisation > 500mg/L

Question 28

Haemodialysis in salicylate OD

Answer 28

If pH <7.3, salicylate level >700mg/L or renal failure

Question 29

Opiate OD PC

Answer 29

Specific - bilateral pin point pupils, non-cariogenic pul oedema in heroin OD, rhabdomylosis

PC = reduced respiratory rate, hypothermia, hypoglycaemia, hallucinations and covulsions

Question 30

Mx opiate OD

Answer 30

Naloxone 1.2-2mg IV. Opiod receptor antagonist with higher affinity hence displaces the opioid and binds to the receptor.

Question 31

Indications for Naloxone

Answer 31

GCS <10/15, RR <10 per minute

Repeat when necessary or use continuous infusion

Question 32

Naloxone Cautions

Answer 32

Shorter t1/2 than most opioids pt may self discharge and hours later fall into a coma or collapse

In patients who are chronic opiates addicts or having long term opiates for palliative care naloxone will lead to rapid acute opiate withdrawal

• Muscle aches, diarrhoea, palpitations, fever, tremor, cramps. Even as severe as seizures and arrthymias

Question 33

TCA OD PC

Answer 33

Mild - tachycardia, sweating, dry mouth, dilated pupils, urinary retention all anticholinergic SE. Increased reflex and extensor plantar

Severe due to Na+ channel blockage. Wide QRS (>120ms) QTc prolongation, this can lead to life threatening arrythimas

Metabolic acidosis

Question 34

Mx TCA OD

Answer 34

Charcoal (multiple dose activated?)
If pH <7.4 or ECG signs of QRS widening give IV sodium bicarbonate

Prophylactic diazepam to prevent seizures as these may precipitate

Question 35

Iron OD PC

Answer 35

Unless >60mg of elemental iron has been consumed features are unlikely to present

PC 0-6hrs - N/V, abdo pain, bloody diarrhoea, GI fluid loss
2-72hrs - Black offensive stool, haematemsis, fits, low GCS, circulatory collapse
2-4days - Renal failure and acute liver necrosis

6 weeks post = intestinal strictures

Question 36

Mx Iron OD

Answer 36

Need to work out elemental iron dose consumed

If shock/coma or if iron >5mg/L give desferrioxime a chelation agent

SE - pul oedema, hypotension, ARDS, contraindicated in renal failure

Question 37

Prevention of self poisoning

Answer 37

Smaller quantities of drugs, safer alternatives, kept in a safe place away from children, weekly/daily prescriptions

Question 38

Paracetamol OD >8hrs

Answer 38

Start NAC regardless

Question 39

Severe iron poisoning

Answer 39

low GCS, convulsions, rectal bleeding or haematemasis

metabolic acidosis