Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

YEAR 5 ED > Poisoning > Flashcards

Poisoning Flashcards

1
Q

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)

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

In a patient presenting with poisoning, what are the most useful inv to do?

A
  • paracetamol and salicylate (aspirin) levels
  • blood glucose
  • ABG/VBG
  • U+Es
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are general features of carbon monoxide poisoning?

A
  • headache
  • malaise
  • N+V
  • vertigo
  • altered consciousness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Carbon monoxide poisoning can present with general features: headache, malaise, N+V, vertigo, altered consciousness. What additional features are present in severe poisoning?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What inv would you do in pt with suspected CO poisoning?

from RCEM

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

In CO poisoning, what are indicators of severity of the poisoning?

A
  • 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%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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?

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the 4 key questions you should ask a patient who has suspected CO poisoning?

A

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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How would you manage suspected CO poisoning?

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the theraputic dose of paracetamol for adults?

A

1g four times a day
Max 4g per day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What database can be used for posion information and management?

A

TOXBASE
(if really unsure can use NPIS - national poisons information service)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is paracetamol metabolised?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Using knowledge of paracetamol metabolism, explain why high levels of paracetamol become toxic and need therapeutic management

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are clinical features of paracetamol overdose?

A
  • 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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What inv would you do for paracetamol overdose?

A
  • 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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How is paracetamol overdose managed?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What does acetylcysteine do (in Mx of paracetamol overdose)?

A

Replenishes glutathione levels. This can then detoxify high levels of NAPQI by conjugating it.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are some ADRs of N-acetylcysteine?

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

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?

A
  1. Stop the infusion, give loratadine 10mg or promethazine 12.5mg IV, then restart at a slower rate
  2. Now N-acetylcysteine is given over 1 hour instead of 15 mins to reduce this ADR.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What investigations are needed 2 hours before completion of N-acetylcysteine for paracetamol overdose?

A

Repeat ALT LFTs and Paracetamol level.

21
Q

For paracetamol overdose, when should liver transplant be considered?

A
  • 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

22
Q

What are RF for paracetamol toxicity?

A
  • 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)
23
Q

In addition to pharmacological treatment, what is needed for pt who has intentional paracetamol overdose?

A
  • psychosocial assessment
  • specialist MH team need to review them
24
Q

What are RF for opiod overdose?

A
  • 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.
25
Q

What are clinical features of opiod overdose?

A

symptoms can range from mild to coma.
* decreased level of consciousness
* N+V
* constipation
* pruritis
* tiredness, increased drowsyness/somnolence
* confusion (esp in elderly)

note: overdose Sx can also just be side effects in a theraputic dose.

26
Q

A patient has a suspected opiod overdose. Apart from symptoms, what shoud you ask in the history?
(and why?)

A

Drug Hx
* review what opiods pt is taking and how it compares with prescription - GP and hospital doctor may prescribe opiates individually (without realising other doc has as well), and pt takes both = overdose.
* recreational drug use

PMHx
* assess RF for unintentional overdose
* e.g. chronic pain, palliative/bone mets, renal impairment, hepatic impairment

Psych Hx
* previous overdoses
* previous SH / suicide attempts

27
Q

What is the classical toxidrome of pt with an opiod overdose?

(you may see these on initial assessment and examination of pt)

A
  • reduced consciousness
  • respiratory depression
  • miosis
28
Q

What signs would you see in A-E assessment of pt with opiod overdose?

A

Airway
* may be speaking to you +/- slurred speech
* may be snoring / have noisy breathing if they have reduced consciousness.

Breathing
* low RR (bradypnoea) - due to resp depression. If < 12/minute = escalate.
* low oxygen sats

Circulation
* bradycardia - as opiods cause vasodilation and hypotension.

Disability
* miosis = pinpoint pupils
* reduced GCS - remember ‘if below 8, intubate’

Exposure
* look for track marks - in IVDU
* look for syringe driver and/or fentanyl patch - may be missed.

29
Q

A patient has presented with suspected opiod overdose. What differentials must you consider?

A
  • Hypoglycaemia
  • Post-itcal status
  • Overdose with other depressants e.g. alcohol, benzos?
  • Head injury or intracranial pathology
  • carbon dioxide narcosis - where too much CO2 is in the blood stream e.g. in COPD pts presenting with T2 resp failure
30
Q

What bedside investigations would you do for pt with suspected opiod overdose?

A
  • Obs - RR, O2 sats, HR, BP, temp
  • ABG - assess for evidence of T2 resp failure and acidosis
  • Cap blood glucose - rule out hypoglycaemia.
31
Q

What blood/lab inv would you do for pt with suspected opiod overdose?

A
  • FBC - obtain a baseline. Assess whether something else is going on
  • U+E - ?renal impairment causing opiod overdose?
  • LFTs - can pt metabolise opiod load. Have they got acute liver damage secondary to overdose?
  • Paracetamol levels - need to check for a mixed overdose. e.g. have they taken co-codamol and paracetamol.
32
Q

What is management of opiod overdose?

A
  • remove source if present e.g. patch or syringe driver
  • A-E approach of management - so ensure airway is supported.
  • Naloxone - initially 100-200 micrograms
  • Monitor closely - naloxone half life is short. It is shorter than half life of opiods so pt may initially improve then features of opiod overdose may recur if a further dose of naloxone is not given.
33
Q

A pt has a suspected opiod overdose. Naloxone is given but there is no improvement in features. What should next step be?

A
  • Escalate to senior and discuss need for a CT head
  • This is needed to rule out intracranial pathology.
34
Q

What are long term management options for a patient who present with a:
1. intentional opiod overdose?
2. unintentional opiod overdose?

A
  1. need MH assessment and psych services if required. may need to involve Social services if children at home are involved.
  2. may need to go through STOPP/START criteria. Pt education. Referral to services for chronic pain or services for local drug cessation.
35
Q

What are complications of opiod overdose?

A

Resp depression –> death

Heroin OD = can lead to Acute lung injury.

36
Q

What are some salicylates people can overdose on?

A

Aspirin - main one.
Nsaids
Oil of wintergreen - in minty fragrances
Antacids
Anti-diarrhoeal meds

37
Q

How does mild and moderate salicylate poisoning affect the body?

A

Mild toxicity
* irritate gastric lining
* ototoxicity (causes reduced cochlear blood flow bc of vasoconstriction and changes to cochlear cells)

Moderate toxicity
* salicylates stimulate cerebal medulla - causes hyperventilation = leads to resp alkalosis
* salicylates are then metabolised = causes increased latic acid production = leads to metabolic acidosis = hyperventilation worsens as a response.

38
Q

What are clinical features of salicylate (aspirin) poisoning/overdose?

Split these into mild, moderate and severe if you can

A

Mild
* N+V
* epigastic pain
* tinnitus
* dizziness
* lethargy

Moderate
* sweating
* fever
* dyspnoea

Severe
* confusion
* convulsions
* coma

39
Q

What would be found on clinical examination in pt who has salicylate overdose?

A
  • warm peripheries
  • bounding pulse
  • cardiac arrythmia
  • acute pulmonary oedema

usually only present if toxicity is moderate or severe

40
Q

What inv would you do in a pt who has suspected salicylate overdose/poisoning?

A

Bedside
* pt general obs - RR, HR, temp, BP, GCS, O2 sats
* ECG - monitor for arrythmias
* Cap blood glucose - exclude hypoxia or ketoacidosis
* ABG - monitor acid-base balance

Lab inv
* plasma salicylate conc - 2 hours after ingestion and then every 2 hours until concentration peaks
* plasma paracetamol concentration - in case of a mixed overdose
* FBC - exclude infection
* U+Es - electrolyte disturbances
* LFTs - hepatic dysfunction
* Coagulation - INR and PT time (may increase if hepatic dysfunction)

Imaging
* CT head if pt has altered mental status and want to rule out intracranial pathology

40
Q

How does TOXBASE define mild, moderate and severe salicylate overdose?

i.e. what values?

A
  • Mild - less than 300 mg/L
  • Moderate - 300 - 700 mg/L
  • Severe - over 700 mg/L
41
Q

How is salicylate poisoning/overdose initially managed?

Note: there is no antidote for salicylate so need supportive care

A
  • A-E approach –> if severe toxicity - pt can lose control of airway so need to ensure it is patent and ventilation is maintained
  • Activated charcoal if present within 1 hour of ingestion of over 125mg/kg
  • IV fluid resus - use 0.9% sodium chloride
  • Potassium replacement –> as have hypokalaemia. This needs to be corrected before starting sodium bicarb.
  • Sodium bicarb - reduce transfer of salicylates to the CNS and enhances urinary excretion of salicylates = urine alkalinisation.
  • monitor urine pH.
42
Q

Once initial management of salicylate toxicity is completed, what are next steps for ongoing management?

A
  • cooling measures - some pts have hyperthermia
  • Haemodialysis - if pts have severe poioning with renal failure, severe metabolic acidosis or seizures
  • IV benzos - help with convulsions
  • CPAP - if they have acute pulm oedema or acute lung injury
  • Psych support - if OD was intentional
43
Q

What are complications of salicylate poisoning?

A

Complications are more likley with a higher ingested dose

  • ARDS - bilateral pulm odema with hypoxia.
  • Seizures - can use benzos to terminate them
  • Drug induced hepatitis
  • cardiac arrest - get prolonged QT –> leads to VT or VF –> cardiac arrest.
44
Q

A pt has OD of aspirin. A CXR is taken as he has SOB. What complication is shown?

A

Acute pulm odema
can see ‘bat wing shadowing in lung fields.

45
Q

What are clinical features of benzo overdose?

A
  • Reduced level of consciousness (including coma): if severe this can result in loss of airway tone and reflexes leading to hypoxia if left untreated.
  • Respiratory depression: decreased respiratory rate can result in hypoxia and inadequate tissue perfusion.
  • Hypotension
  • Bradycardia
  • Rhabdomyolysis
  • Hypothermia
  • blurred vision
  • slurred speech
  • ataxia
  • agitation
46
Q

What inv would you do in pt who has a suspected benzos overdose?

A

Vital obs
ABG/VBG
FBC
U+Es
LFTs
ECG
CK - rhabdomyolysis - when worried about a long lie or convulsions.
Plasma paracetamol conc
Toxicology screen
Cap blood glucose

47
Q

How is benzo toxicity managed?

A
  • A-E assessment and supportive care - maintain airway, oxyen, fluids etc.
  • Flumazenil is the antidote - only used for reversal of sedative effects. Used with caution (some websites say it’s not licesnced in UK) as it can cause convulsions and arryhthmias. Can cause withdrawal in pts who are dependent on benzos.
  • Activated charcoal can be used if present within an hour of ingestion
48
Q

ABG in salicylate poisoning?

A

initially a respiratory alkalosis followed by a raised/high anion gap metabolic acidosis

YEAR 5 ED (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions