Poisoning Flashcards
(49 cards)
A patient with a potential poisoning has attended A+E.
What should be included in an inital assessment and monitoring?
(think about bedside tests/tests that get results quickly too)
- assess and record conscious level - use GCS
- check blood glucose (esp if they have confusion, coma or fits)
- RR and O2 sats
- ABG or VBG (esp if they are unconscious or breathing is abnormal)
- ECG
- BP
- Temp
In a patient presenting with poisoning, what are the most useful inv to do?
- paracetamol and salicylate (aspirin) levels
- blood glucose
- ABG/VBG
- U+Es
What are general features of carbon monoxide poisoning?
- headache
- malaise
- N+V
- vertigo
- altered consciousness
Carbon monoxide poisoning can present with general features: headache, malaise, N+V, vertigo, altered consciousness. What additional features are present in severe poisoning?
Coma with hyperventilation - pt has SOB and tachycardia.
Hypotension
Hypertonia
Hyperreflexia
Extensor plantars
Convulsions / seizures
Chest pain - due to angina or MI, arrythmias
hyperpyrexia
(v rare sign = cherry-red colouring of the skin)
What inv would you do in pt with suspected CO poisoning?
from RCEM
In addition to clinical assessment:
* Measure COHb - arterial or venous
* Blood glucose to rule out hypogylcaemia
* FBC, U+Es, CK, Trop, ABG
* Lactate
* 12 lead ECG
In CO poisoning, what are indicators of severity of the poisoning?
- new objective acute neurological signs - increased tone, upgoing plantars, coma
- needing ventilation
- ECG showing infarction or ischaemia
- clinically significant acidosis
- initial COHb greater than 30%
A patient has CO poisoning and has been given oxygen.They have a blood gas taken. Why might their ABG/VBG come back with COHb in normal levels?
- If they have been treated with high flow oxygen, COHb can come back normal.
- Giving oxygen speeds up the elimination of CO from the body - from a half life of 4-6 hours to a half life of aroiund 75 mins.
- So, if they have a mild CO poisoning, the results from the blood gas may come back normal.
What are the 4 key questions you should ask a patient who has suspected CO poisoning?
Use acronym COMA
C - co-habitees. Is anyone else in the house affected?
O - outdoors. Do symptoms improve outside the house?
M - maintenance. Are boilers and cooking appliances properly maintained?
A - alarm. Do you have a functioning CO alarm?
How would you manage suspected CO poisoning?
- A-E assessment
- 100% high flow oxygen via NRB mask. Should be given for at least 6 hours
- hyperbaric oxygen (HBOT) may be given if they have LOC, neurological signs, MI/arrhythmia, pregnant. HBOT is only given on a case-by-case basis.
What is the theraputic dose of paracetamol for adults?
1g four times a day
Max 4g per day
What database can be used for posion information and management?
TOXBASE
(if really unsure can use NPIS - national poisons information service)
How is paracetamol metabolised?
Paracetamol (95%) undergoes glucuronidation (where it conjugates with glucuronide) –> this makes it water soluble = is eliminated in the urine.
Remaining 5% = metabolised with cyp450 –> forms toxic metabolite NAPQI. NAPQI should bind to glutathione = makes it non-toxic = excreted in the urine.
Using knowledge of paracetamol metabolism, explain why high levels of paracetamol become toxic and need therapeutic management
- Paracetamol metabolises in the body via gluthathione dependent pathways
- Most conjugates with glucuronide (glucuronidation) and some will metabolise with cyp450 to form a toxic metabolite NAPQI.
- NAPQI normally binds to glutathione to become non toxic.
- With high leves of paracetamol, the production of NAPQI can exceed the detoxification capacity, as there is only a finite amount of glutathione available = NAPQI builds up
- excess NAPQI binds to hepatocytes = oxidative damage to hepatocytes, damage to proteins, DNA. Can lead to acute liver failure and death.
What are clinical features of paracetamol overdose?
- No symptoms - pt may come in/brought in straight after suicide attempt
- N+V
- Abdo pain
- RUQ tenderness
- can be asymptomatic until 24-72hrs.
Late features:
* moderate/severe abdo pain
* metabolic acidosis on ABG
* jaundice
* AKI, renal failure, oliguria
* hepatic encephalopathy
* coma
* bruising/ systemic haemorrhage (as clotting factors are deranged)
What inv would you do for paracetamol overdose?
- Paracetamol (and aspirin) level - after 4 hours ingesion
- LFTs - ALT is the most important. Take LFTs at presentation and repeat 2 hours before completion of acetylcysteine.
Other tests:
* glucose
* U+Es
* INR and prothrombin time
* phosphate
* ABG/VBG for met acidosis
How is paracetamol overdose managed?
If pt presents within an hour = activated charcoal
If plasma paracetamol concentration is above treatment line at 4 hours = give acetylcysteine
Other times acetylcysteine is given:
* there is a staggered overdose = not all tablets taken within an hour
* there is doubt over the time of paracetamol ingestion, regardless of the plasma paracetamol concentration;
* patients who present at 8+ hours and have ingested more than 12g, or more than 150 mg/kg of paracetamol.
* patients who present > 24 hours if they are clearly jaundiced or have hepatic tenderness, their ALT is above the upper limit of normal
What does acetylcysteine do (in Mx of paracetamol overdose)?
Replenishes glutathione levels. This can then detoxify high levels of NAPQI by conjugating it.
What are some ADRs of N-acetylcysteine?
- high risk of anaphylactoid reaction.
- can cause temporary rise in INR. Need to check it is stable to ensure changes to INR are not due to liver failure.
A patient has a anaphylactoid reaction to N-acetylcysteine whilst being treated for paracetamol overdose.
1. how do you manage this adverse effect?
2. how is this ADR managed now in NHS trusts?
- Stop the infusion, give loratadine 10mg or promethazine 12.5mg IV, then restart at a slower rate
- Now N-acetylcysteine is given over 1 hour instead of 15 mins to reduce this ADR.
What investigations are needed 2 hours before completion of N-acetylcysteine for paracetamol overdose?
Repeat ALT LFTs and Paracetamol level.
For paracetamol overdose, when should liver transplant be considered?
- INR > 3 at 48 hours post ingestion or 4.5 at any time
- Oliguira or creatinine > 200 umol/L
- Persistent acidosis (pH < 7.3), or lactate > 3
- Systolic BP < 80mmHg despite resuscitation
- Hypoglycaemia, severe thrombocytopenia or encephelopathy
- GCS < 15 not associated with sedative ingestion
See pic for shorter summary by King’s College on PM
What are RF for paracetamol toxicity?
- Hx of self harm - paracetamol is widely used and accessible
- Hx of frequent or repeated use of medication for pain relief - pt may not realise they are overdosing when taking different brands of medication
- Low body weight - if less than 50kg, pts can unintentionally overdose.
- CYP-p450 inducers - phenytoin, rifampicin etc can increase risk of liver injury following paracetamol overdose
- PMHx of glutathione deficiency - eating disorders, alcohol-use disorder, psych disorder, chronic illness (these can all lead to malnourishment which lead to higher risk of liver injury)
In addition to pharmacological treatment, what is needed for pt who has intentional paracetamol overdose?
- psychosocial assessment
- specialist MH team need to review them
What are RF for opiod overdose?
- IVDU and recreational drug use
- self harm and suicide attempt
- unintentional = chronic pain, palliative care pts, elderly (changing opiod or staring a new interacting medication), theraputic error, hepatic or renal impairment, CYP2D6 gene duplciation carrier.
