Poisoning Flashcards by Tom Hosfield

Common poisoning methods

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

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History in poisoning

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

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Preventing absorption

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

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Activated charcoal

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

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Charcoal ineffective

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

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Complications of charcoal

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

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Gastric lavage

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

ie Iron

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SE of gastric lavage

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

Often very unpleasant and ineffective

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CI of lavage

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

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Increasing poison eliminaton

Multiple dose activated charcoal, urina alkanisation and haemodialysis

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Multiple dose activated charcoal

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

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MOA of multiple dose activated charcoal

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.

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Haemodialyisis

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

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Urine alkanisation

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

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Benzodiazepine antidote

Flumazenil

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Carbon monoxide antidote

High dose oxygen

Immediate management in OD

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

MDMA overdose

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

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

Paracetamol OD MOA

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

PC paracetamol OD

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

Poor prognosis in paracetamol OD

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

Invx paracetamol OD

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

Mx of paracetamol OD

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

N-acetyl cystine

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

Salicylate (Aspirin) PC

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

Invx salicylates

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

Mx of salicylate OD

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

Haemodialysis in salicylate OD

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

Opiate OD PC

Specific - bilateral pin point pupils, non-cariogenic pul oedema in heroin OD, rhabdomylosis PC = reduced respiratory rate, hypothermia, hypoglycaemia, hallucinations and covulsions

Mx opiate OD

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

Indications for Naloxone

GCS <10/15, RR <10 per minute Repeat when necessary or use continuous infusion

Naloxone Cautions

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

TCA OD PC

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

Mx TCA OD

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

Iron OD PC

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

Mx Iron OD

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

Prevention of self poisoning

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

Paracetamol OD >8hrs

Start NAC regardless

Severe iron poisoning

low GCS, convulsions, rectal bleeding or haematemasis | metabolic acidosis