Pt/w Deliberate Self Harm Flashcards
What are some early symptoms of paracetamol overdose?
FIRST 24 HOURS - NAUSEA AND VOMITING
- Symptoms of the actual overdose take quite a long time to occur (takes a while for NAPQ to build up)
- Usually when people are unwell when they come in is because they’ve ingested the pills with a lot of alcohol
What are some of the mid-symptoms of paracetamol OD and when do they occur?
24-72h
- MORE NAUSEA AND VOMITING
- RUQ pain (this occurs due to inflammation in the liver that stretched the liver capsule)
What are some of the LATE symptoms of paracetamol OD and when do they occur?
After 72h-SYMTOMS OF LIVER FAILURE
- Jaundice
- Encephalopathy (confusion/drowsines/irritability/seizures)
- Coagulopathy - bleeding, bruising
- Hypoglycaemia(glycogen not released from liver-another cause of seizures)
-AKI
If someone comes in with paracetamol OD what is important to find out in the history? (not including psych history)
How many tablets did they take?
Did they take anything else?
When did they take them?
Did they take them all at once or did they take breaks?
What makes treating paracetamol OD more difficult to treat?
What is deemed a large overdose?
If the person took a STAGGERED OVERDOSE
- this is if they took the tablets over a time period of 1 hour or longer (if you dont know-pressume it is staggered)
- Large overdose >10g
pathophysiology of paracetamol OD?
-Paracetamol is usually metabolised in the liver
-95% of paracetamol is metabolised to harmless metabolites (glucoronide and sulphate)
-5% of paracetamol is metabolised by the CYP450 system to NAPQ1 (harmful metabolite)
-NAPQ1 is then metabolised by GLUTATHIONE to harmless metabolites
-this pathway is saturated in OD
TOO MUCH PCM = NOT ENOUGH GLUTATHIONE.
-Build up of NAPQ1(toxic to hepatocytes> leading to hepatitis and liver failure)
What medications might decrease someones tolerance to paracetamol?
CP450 INDUCERS (crap GPs) because they encourage NAPQ to be produced
-Rifampicin (TB), some anti-convulstants and St Jonh’s Wort
What investigations are needed in someone who has taken a paracetamol OD
- PARACETAMOL LEVELS -take at 4 hours post dose
- THEN PLOT THIS on a graph of plasma paracetamol concentration vs time since ingestion (treat if ON or above line)
- LFTS usually normal until at least 18h post OD
- INR is often good to get - suggestive of liver damage if high
- ABG (lactic acidosis can occur)
When would you treat someone for paracetamol OD?
Paracetamol OD, treat if:
• Dose vs time line indicates you should (on or above line)
• If INR deranged
• If after 8 hours of ingestion (don’t bother with levels, just treat)
• Time of ingestion is UNKNOWN or STAGGERED (1+ hour)
• If symptoms of overdose start prior to 4 hours
What is the treatment for paracetamol OD and how do you decide how much to give an at what rate?
Side effects?
N-ACETYL CYSTEINE (NAC)
- The DOSE and infusion rate depends on the weight of the patient so refer to the table
- There is also different doses depending on whether it is the first, second or third infusion
- SE: can look like anaphylaxis: flushed (red hands and face), N+V, congested
IV infusion in 5% glucose (or 0.9% NaCl), 3 consecutive doses over 21 hours
- 150mg/kg in 200ml glucose over 1 hour
- 50mg/kg in 500ml over 4 hour
- 100mg/kg in 1L over 16 hours
(activated charcoal if less than 1hr)
Once the treatment is done what should we measure?
When can you stop treatment?
- After treatment measure Creatinine, ALT and INR (usually normal before 18 hours)
- Continue to treat with NAC until INR <1.3 and ALT less than 2 times the upper limit of normal
- If okay then stop treating and refer to PSYCH SERVICES
What are the complications of paracetamol OD?
COMPLICATIONS OF PARACETAMOL OD:
- Acute liver failure
- Cerebral oedema
- Renal failure
- Pancreatitis
How many paracetamol tables can be fatal?
- 150mg/kg is fatal equal to 24 tablets or about 12g
- If malnourished, 75mg/kg can be fatal
What groups of people have low levels of glutathione?
Alcoholics and malnourished (very low BMI)
What is the criteria for liver transplant after paracetamol OD:
KING COLLEGE Criteria for liver transplant: • pH <7.3 24 hours after overdose • PT > 100 secs(INR >6.5) • Creatinine > 300 •Grade 3 or 4 encephalopathy
What are common side effects of NAC?
Common side effect of NAC:
-Rash (treat with anti-histamine chlorphenamine)
How would patients present with an amphetamine overdose?
Amphetamine overdose presents with sympathetic overdrive:
- euphoria
- agitated
- dilated pupils
- palpatations/arrhythmias and tachycardia, hypertension
- hyperpyrexia and sweating
- dehydration
- muscle rigidity
- rhabdomyalysis and AKI
- convulsions due to hyponatreamia from polydipsia (and increased ADH production)
- coma
- DIC
What would a blood gas show in amphetamine OD?
amphetamine OD-ABG would show metabolic acidosis
Acute management for amphetamine overdose?
Management for amphetamine overdose
- ABCDE assessment
- refer to TOXBASE (activated charcoal if within 1 hour)
SUPPORTIVE TREATMENT
• Cooling measures and consider dantrolene (muscle relaxant) if temp is over 39
• Correct electrolyte imbalance
• Sodium bicarbonate(metabolic acidosis)
• Diazepam for convulsions
• Metoprolol for narrow complex tachycardias
• Nifedipine (CCB) for hypertension
How does an opiate OD present?
Opiate OD presents with parasympathetic overdrive • Pinpoint pupils • Respiratory depression • Decreased GCS - potential coma • Hypotension
What would a blood gas show in opiate OD?
Opiate OD-ABG would show respiratory acidosis
Management for opiate OD?
Management for opiate OD
- ABCDE assessment (consider intubation)
- refer to TOXBASE
- IV 400microgram bolus of naloxone. Then infusion.
- Naloxone half life is shorter than morphine so may need to given more often
How does an tricyclic antidepressant OD present?
Tricyclic antidepressant OD CANNOT SEE, PEE, SPIT or SHIT (anticholinergic syndrome) • Dry skin and mouth • Dilated unreactive pupils • Urinary retention • Constipation
- Sedation and coma
- Seizures
- Hypertonia and hyperreflexia
- Severe hypotension/collapse
- Tachycardia
- Broad complex dysrhythmias (broad complex QRS seen on ECG)
What would an ABG show in tricyclic AD OD?
tricyclic AD OD-ABG would show metabolic acidosis
Acute management of tricyclic AD OD?
Management of tricyclic AD OD
- ABCDE assessment (intubation)
- Refer to TOXBASE
-IV sodium bicarbonate if QRS prolongation/dyssrhythmias/hypotension
(repeat every few minutes until BP improves and QRS complexes begin to narrow)
- Treat seizures with IV benzodiazepines (e.g. diazepam 5-10mg)
- Hyperventilate to maintain higher pH
What is important to include in a history for any overdose?
- What? When? Clinical features?
- Assess capacity
- Psychiatric history
How do you manage ANY OVERDOSE
- ABCDE assessment
- Vital signs including weight
- ECG and VBGs in everyone
REFER TO TOXBASE
Name the specific antidotes for the following overdoses
- Paracetamol OD
- TCADs OD
- benzodiazepine OD
- insulin OD
- local anaesthetic OD
- Carbon monoxide OD
- Iron
N- Acetyl-cysteine for Paracetamol
Sodium bicarbonate for TCADs arrhythmias
Flumazenil for benzodiazepines
Glucagon for hypoglycaemia
20% lipid emulsion for local anaesthetic toxicity
Oxygen for carbon monoxide
Desferrioxamine (chelation), consider whole bowel irrigation
How to do you treat bradycardia?
Give atropine for bradycardia
How do you treat beta blocker overdose?
Betablocker OD can be treated with glucagon
Whats the management for iron overdose?
1st line Whole-bowel irrigation
Chelation therapy with Deferoxamine (for severe cases)
***activated charcoal does not bind to iron-not indicated
What can you do to manage salicylate OD?
Activated charcoal if within 1 hour
- IV sodium bicarbonate in order to maintain blood pH at 7.5-8.0
- Dialysis if level >700 (or sizures/AKI/heart failure/cerebral odema/pulmonary odema)
How does a salicylate OD present?
- Hyperventilation
- Nausea
- Vomiting
- Tinnitus and headache.
If severe:
- Confusion
- Coma
- Seizures
- Hypoglycaemia
- Fever
What is the ABG in salicylate OD?
- Initially, hyperventilation>respiratory alkalosis
- Over 24 hours this progresses to a metabolic acidosis and hypokalaemia (SEVER OD)
- HIGH ANION GAP