Medical emergencies Flashcards
What is a HCIG test used for?
To see if someone is pregnant
What is an MSU test?
Mid stream urine sample
What are normal lactate levels?
0.5-1 mmol/L
During a paracetamol overdose, when should paracetamol and salicylate levels be taken?
How much paracetamol must the person have taken for these levels to be measured?
Take bloods within 4-8 hours of a single ACUTE (not staggered) paracetamol
Wait until 4 hours
They must have ingested >75mg/kg
What is the threshold for treatment for a paracetamol overdose?
100 mg/L at 4 hours
What are the two treatment options for a paracetamol overdose?
Activated charcoal
Acetylcysteine (Parvolex) injection 200 mg/mL
When would a paracetamol overdose be classed as staggered?
If it has been taken over the course of more than one hour
When would you give activated charcoal in paracetamol overdose?
Consider if the dose is more than 150mg/kg AND patient presents within 1 hour of ingestion.
What is the treatment regimen for acetylcytseine?
150mg/kg over 1-hour in 200mL dextrose 5% (or sodium chloride 0.9%)
then
50mg/kg over 4-hours in 500mL dextrose (or sodium chloride 0.9%)
then
100mg/kg over 16-hours in 1000mL dextrose (or sodium chloride 0.9%)
What is extremely common in acetylcysteine treatment (occurs in 20% of patients)?
Anaphylactoid reaction
NOT IgE mediated
What is extremely uncommon in acetylcysteine treatment and how do you treat it?
What do you do if the patient has previously had this?
- Anaphylactic reaction
- Chlorphenamine 10mg IV, once symptoms have settled then start with next infusion bag.
- If severe symptoms then consider Rantidine 50mg IV.
- For adults with previous anaphylactoid reactions or repeated anaphylactoid reactions these should be given before the acetylcysteine infusion.
How would you treat a Phenylephedrine overdose?
Activated charcoal if within 1 hour of ingestion
Diazepam - if agitated
How would you treat a guaifenesin overdose?
No specific treatment due to low toxicity
How would you treat amitriptyline overdose and what mg/kg would be considered to be a serious overdose?
What might the patient experience with this overdose?
Highly toxic by ingestion
15 mg/kg - serious
Treatment:
- Activated charcoal to eliminate
- Sodium bicarbonate and IV magnesium (to counteract cardiac arrythmias and metabolic acidosis)
Convulsions, hypotension, agitation, cardiac arrythmias
What would you need to test in an amitryptilline overdose?
Use a cardiac monitor and ECG due to QRS and QT prolongation risk
Describe the mechanism of action of acetylcysteine in paracetamol overdose
- Paracetamol has a toxic metabolite = NAPQI (n-acetyl-p-benzo-quinone imine)
- Usually conjugated with glutathione, which is synthesised from cysteine (rate limiting factor), glutamate and glycine (found in abundance in the liver)
- In overdose, hepatic glutathione stores are used up
- NAPQI builds up causing hepatotoxicity and cell death
- Cysteine is not well absorbed after oral administration. However, acetylcysteine is well absorbed and rapidly enters cells. It is a pro drug that converts to cysteine, providing the rate-limiting step for glutathione synthesis
What 3 amino acids are needed for glutathione production?
Which one is the rate limiting step?
Cysteine- rate limiting
Glutamate
Glycine
What is the max dose in IV paracetamol in mg/kg and what do you need to consider?
15 mg/kg (up to 1g QDS)
So max of 60 mg/kg in 24 hours
Important in lighter patients
<67 kg- dose is less than 4g a day
What is the ABCDE of assessing a patient in a medical emergency?
Airways and oxygenation
Breathing and ventilation
Circulation and shock management
Disability due to neurological deterioration
Exposure and examination
What are the signs and symptoms of anaphylaxis?
Depends on route of entry/contact
- Systemic allergens tend to cause cardiovascular problems
- Airway is first point of contact- bronchospasm may occur
- Reactions can be biphasic and develop again
- GI – abdominal pain, hyperperistalsis, faecal urgency/incontinence, nausea, vomiting, diarrhoea
- Oral – itching and swelling of the lips, tongue and palate
- Respiratory – short of breath, airway swelling, angioedema of tongue/throat, chest tightness, cough, wheeze, rhinitis, hoarse voice, stridor, cyanosis (late sign), respiratory arrest
- Cutaneous – rash, diffuse erythema, flushing, urticaria, pruritis, angioedema
- Cardiovascular, faintness, hypotension, arrhythmias, tachycardia, hypovolaemic shock, syncope, chest pain, cardiac arrest
- Ocular – peri-orbital oedema, erythema, conjunctival erythema, tearing
- Genito-urinary – uterine cramps, urinary urgency/incontinence
- CNS – confusion caused by hypoxia, decreased consciousness
What is the treatment for anaphylaxis?
• Remove the trigger:
- Food- stop eating it but no not induce vomiting
- Stings- remove it
- Drugs- stop infusion
• If removal of trigger not possible, do not delay treatment:
- IM adrenaline (IV is reserved for specialist environments)
• Stabilise airway
• High flow oxygen to ensure oxygenation and perfusion
• IV fluid to increase BP and increase perfusion and oxygen delivery
• Chlorphenamine IV – H1 antagonist to block histamine release from mast cells
• Hydrocortisone IV – can help prevent/shorten future reactions. Reduces vasodilation, decreases immune response (leukocytes and cytokines)
Why do you use adrenaline in anaphylaxis and how does it work?
• Agonist of alpha and beta receptors • Increases BP, pulse and offsets the circulatory shock caused by the allergen • Causes fight or flight reaction: - Pupil dilation - Bronchodilation - HR and force increases so increases BP - Vasoconstriction in skin and viscera (may cause redness), vasodilation in skeletal muscles - Energy production
Adrenaline causes release of norepinephrine and activates:
- α1, stimulates phospholipase C increases inositol tri-phosphate which increases cytosolic Ca2+ leading to vasoconstriction or glandular secretion – vasoconstriction in skin and viscera
- β1 stimulates adenyl cyclase, converting ATP to cAMP, increasing intracellular Ca2+ leading to increased rate and force of contraction (heart) – increases blood pressure
- β2 stimulates adenyl cyclase, converting ATP to cAMP, leading to bronchodilation and vasodilation in skeletal muscle
- β receptor activation also suppresses histamine and leukotriene release from mast cells
What are the common substances that cause anaphylaxis?
- IgE mediated reactions- stings, food, ABX
- Complement mediated reaction – whole blood, immunoglobulins
- Mast cell activators- opioids via anaphylactoid reactions
- Non-immunological mast cell activators- radio contrast media, LMWH
- Modulators of arachidonic acid metabolism (aspirin, NSAIDs)
- Sulphiting agents
What kind of questions and counselling would you give someone with an Epipen?
a) Why/when did the GP initiated the Epipen?
b) Does she understand what it is for / reasons for use
c) What are her concerns? – active listening, explore using open questions – what triggered the last attack?
d) Was she shown how to use it?
e) Explain why it is used and how, can be given through clothing
f) Demonstrate to her how to use it – highlight PIL
g) Make sure you cover side effects and what to do, (don’t inject into fingers/hands)
h) Ensure she understands to keep it in the outer case and protect from light and to check it for discolouration/particulate matter
i) Advise to discuss with partner/family/friends so they are aware she carries an Epipen and would be confident to encourage her to use it
j) If used – call an ambulance / come to hospital to be reviewed
k) Check expiry – register epipen on manufacturing website and patient will get a text when it is due to expire
What is melaena?
Blood in faeces
Clopidrogel can increase risk of GI problems. True or false?
True
What is sigmoid adenocarcinoma?
Colon cancer
What is tricuspid regurgitation?
Disorder in which the valve does not close tight enough during systole
What is the PAR score ?
Patient at risk score
0-1- continue observations like normal
2- increased observations needed
3- urgent doctor review within 1 hour
4- immediate doctor review
What is the normal range for PAC02?
4.6-6
True or false. Fluoxetine increases risk of GI bleed?
True
If a patient has a GI bleed, it cannot be stopped straight away due to risk of discontinuation syndrome
What does AVPU stand for when assessing a patient’s neurological deterioration?
A- patient is awake
V - patient responds to verbal stimulation
P- patient respond to painful stimulation
U- patient is unresponsive
If a patient has a nose bleed, why might they need tachycardic?
Rebound tachycardia to maintain circulation
During a GI bleed, why do you get SOB?
Because of the blood loss
If a patient is on beta blockers, does this increase the severity of a GI bleed?
Yes- increases hypotensive risk
What age increases severity of GI bleed?
60
What are the symptoms of a GI bleed?
- bright red blood in vomit.
- cramps in the abdomen.
- dark or bright red blood mixed with stool.
- dizziness or faintness.
- feeling tired.
- paleness.
- shortness of breath.
- High HR
- Low BP
- Low haemaglobin
Do comorbidities increase severity of GI bleed?
Yes
What procedure would you go in a GI bleed patient once they are haemodynamically stable?
OGD- locates the bleed
What is the initial management of a GI bleed?
- Resuscitation (fluid) – if patient is not having active haematemesis or shock. 20-30 mL/kg Sodium chloride 0.9% to increase BP and circulating volume
- IV access
- Correct losses e.g. of blood and electrolytes
- Restore BP
- Routine bloods (INR, FBC, U&E, LFTs)
- OGD when patient is haemodynamically stable
What is the potential problem with sodium chloride as an IV fluid and what are the alternatives?
It can cause increased chloride levels and deranged electrolyte levels
Other fluid option- sodium lactate or colloids to expand plasma volume.
Hb could decrease even more if wrong fluid has been chosen/could get fluid overload if fluid goes to the wrong places
What is the difference between crystalloid and colloid fluids?
Crystalloids balance electrolyte composition, whereas colloids exert high oncotic pressure
List the 4 potential complications that can arise from incorrect fluid management?
- Overload – expanded circulatory volume causes increased strain on Left ventricle leading to heart failure and pulmonary oedema. Abdominal compartment syndrome and acute respiratory distress syndrome are also caused by excessive fluid resuscitation.
- Biochemical disturbances - use of sodium chloride 0.9% can lead to biochemical disturbances, hyperchloraemic acidosis and metabolic acidosis. This has been shown to increase morbidity and mortality.
- Haemodilution – decreased Hb concentration and reduced O2 carrying capacity will compromise tissue/organ perfusion. Dilutional coagulopathy.
- Infection – cannulae should be removed / not inserted if no IV fluids or drugs are required
What are the safest and riskiest of the following NSAIDs for GI bleed?
Ibuprofen – safest for GI bleed, would be NSAID of choice
Naproxen- worst for GI bleed
Diclofenac- cardiovascular risks
Ibuprofen
What could happen to absorption of drugs during a GI bleed?
Decreased absorption
If a patient is on diuretics during a GI bleed, would you continue them?
No - usually get low BP and volume
You cant to increase body volume at the start
If a patient has a GI bleed and is on iron tablets, would you continue them?
No as they cause black stools and constipation
It may obstruct bowels when using a camera to locate the bleed
Ibuprofen is not good for a patient with previous cardiac history. Why?
Causes sodium and water retention
