AC and trauma Flashcards
What is the antidote for the following overdoses:
- Paracetemol
- Opiate
- Aspirin
- Benzodiazepine
- Organophosphate
- Paracetemol: IV N-acetyl-cysteine
- Opiate: Naloxone
- Aspirin: Sodium bicarbonate
- Benzodiazepine: flumezanil
- Organophosphate: atropine
When should you measure paracetemol levels following ingestion
Paracetamol levels are measured 4 hours
post-ingestion, the result is then plotted on a graph and if the paracetamol level is
above a certain level, IV n-acetylcysteine is administered.
Which medications are the following side effects associated with:
- Constipation, respiratory depression, nausea, drowsiness
- Blurred vision
- Cough
- Tremor
- Rash
Morphine sulfate
Anti-muscarinic agents (atropine)
ACEi
b-adrenergic agonists (salbutamol)
Ampicillin and amoxicilin in glandular fever
What is your management of severe anaphylactic shock
Securing the airway and oxygen administration and IM or IV adrenaline with IV fluid resuscitation.
Call for help!
The dose of IM adrenaline is 500mcg or 0.5ml of 1 in 1000 adrenaline.
Give IV if patient circulation is very impaired
A nebulised bronchodilator with steroid and chlorpheniramne (antihistamine) given intravenously are also required
T/F non-ionic contrast agents can be safely used in the presence of renal impairment
F!
Non-ionic contrast agents are excreted by the kidneys and are nephrotoxic – the elderly, patients with myeloma and known renal impairment are all at risk.
When are non-ionic contrast agents contraindicated
They should be used with caution in patients with asthma
Iodine allergy is a contra-indication to their use
Contraindications to MRI?
Recent hip replacement (< 6 weeks), pacemaker, intracranial aneurysm clips and working with possible metal fragments are all contraindications to MR, as metal may move in the magnetic field.
T/F MRI is fine in pregnancy
F it’s a relative contraindiciation, especially in the 1st trimester
Alcohol withdrawal definition
Alcohol withdrawal occurs in patients who are alcohol dependent and who have stopped or reduced their alcohol intake within hours or days of presentation
Alcohol withdrawal risk factors and aetiology
Symptoms typically begin 6 to 12 hours after the patient’s last alcoholic drink, and may progress to life-threatening delirium tremens, with or without seizures
lcohol enhances inhibitory GABA activity and inhibits excitatory glutamate neurotransmission. Chronic alcohol exposure results in a compensatory reduction in GABA receptor function and upregulation of the glutamate NMDA receptors. Abrupt alcohol cessation leads to overactivation of the excitatory NMDA system relative to the GABA system.
Decrease in ethanol causes imbalance in these, resulting in excessive stimulation of SNS.
KINDLING: Multiple episodes of AWS increase the severity of subsequent AWS due to kindling phenomena.
Alcohol withdrawal epidemiology
.
Alcohol withdrawal history
When do the symptoms appear
What is delirium tremens and when does this commonly occur
Mild to moderate symptoms can start 6-12 hrs after their last drink, and peak at 24-36hrs.
Severe symptoms (seizures, psychiatric disturbance, deranged temp, BP or glucose) start 48-72hrs and peak at 5 days. -Hypertension is more commonly seen than hypotension
Delirium tremens is a life-threatening feature of severe alcohol withdrawal and generally occurs 48 to 72 hours after the last alcoholic drink: -Confusion -Hallucinations -Agitation -Disorientation (CHAD)
Alcohol withdrawal signs
Common symptoms are anxiety, nausea or vomiting, autonomic dysfunction, and insomnia
Can progress to seizures, psychiatric disturbances and delirium tremens
Alcohol withdrawal investigations
What are the 3 key electrolyte imbalances
What are indications for CT in a patient with alcohol withdrawal
VBG
- There may be a respiratory alkalosis due to hyperventilation which can reduce cerebral blood flow
- Metabolic acidosis is alcohol ketoacidosis is present
- Hypochloraemic metabolic acidosis with vomiting
Blood glucose
-Hypoglycaemia common due to poor nutrition of heavy alcohol use. Give with thiamine (but don’t delay whilst waiting for thiamine)
Raised MCV
Hypokalaemia in 50% from inadequate intake and GI losses due to dirrhoea
Hypomagnesia in 1/3 of people with chronic alcohol. HYPOCALCAEMIA AND HYPOKALAEMIA will not resolve until magnesium replacement is given
Hypophosphataemia (refeeding syndrome)
CT HEAD:
-If alcohol related seizure, or altered cognition
ECG, CXR
Amylase
Alcohol withdrawal management
Treatment plan individualised to patient’s symptom score (GMAWS), which determines whether patient commences oral benzodiazepine
1) Correct imbalances (remember hypoclacaemia and hypokalaemia won’t correct until you give magnesium)
2) Benzodiazepine (IV if in critical care environment) e.h chlordizepoxide
If alcohol withdrawal seizures occur, a fast-acting benzodiazepine (such as lorazepam [unlicensed indication]) should be prescribed to reduce the likelihood of further seizures.
Delirium tremens is a medical emergency that requires specialist inpatient care. In patients with delirium tremens (characterised by agitation, confusion, paranoia, and visual and auditory hallucinations), oral lorazepam should be used as first-line treatment. If symptoms persist or oral medication is declined, parenteral lorazepam [unlicensed], or haloperidol [unlicensed] can be given as adjunctive therapy.
Thiamine supplementation is important to prevent Wernicke’s encephalopathy. Slow IV administration is best
Glucose should not be given before thiamine supplementation (unless critical hypoglycaemia) as this can precipitate Wernicke’s encephalopathy.
IV pabrinex for 5 days
Sort electrolyte imbalances and give benzo (chlordiazepoxide)
If mild to moderate, short electrolyte imbalances, they don’t need a benzo unless they get worse
Alcohol withdrawal complications and complications of management
Delirium tremens is a life-threatening medical emergency requiring urgent treatment
Chronic complications include cerebral atrophy and dementia, cerebellar degeneration, optic atrophy, peripheral neuropathy, myopathy. Indirect effects include hepatic encephalopathy, thiamine deficiency, causing Wernickes encephalopathy1 or Korsakoffs psychosis.2
Definition of burns
Skin cells exposed to too much energy in the form of heat, causing cellular necrosis
Aetiology and risk factor of burns
What factors determine burn severity
Degree of injury:
- Temp
- Duration
- Baseline structural integrity of the skin
Which is why children and elderly adults are at higher risk of injury as their skin is weaker
-------------------------- Cause: -Thermal: scalds, hot water, flames -Electrical: lightning strike, high voltage elecgtrical current -Chemical: acidic or alkaline substances ---------------
Burns increase capillary permeability, causing a tremendous amount of fluid to shift from the plasma to the interstitial space, which is called “third-spacing”.
Examination of burns
1st degree
2nd degree
3rd degree
4th degree
T/f 3rd and 4th degree burns are the most painful
1st degree=superficial burn. Only involves epidermis. E.g. simple sunburn. Red with no blisters.
2nd degree:
i. superficial partial thickness (epidermis and superficial demis)- red and blistered
ii. deep partial thickness (epidermis and deep dermis)- red or white, no blistered
3rd degree: full thickness burns: extending through and destroying entire dermis. Charred appearance and tense feel, usually surrounded by rim of 2nd degree burns
4th degree: extend beyond the dermis, destroying fascia, muscle or bone.
Because third and fourth degree burns destroy the entire skin, they destroy the skin nerve endings, and therefore can feel relatively painless.
What do electrical burns look like?
Should you still be alarmed even if the skin is quite normal? Why/not?
Due to their strength and velocity, electrical burns have an entrance and an exit wound, similar to a gunshot. But aside from that, the skin actually looks fine.
However internally, the muscles are injured and even heart can be severely damaged, so don’t let normal skin fool you.
Investigations of burns
Urine output should be monitored to make sure you’re not over-or-under-resuscitating the individual.
Carboxyhemoglobin levels are measured for carbon monoxide poisoning
If somebody has been exposed to CO during burn, how can you see that on a blood measurement
How would you manage
Also, If exposure to carbon monoxide is a concern, like in the setting of a closed house-fire, 100 percent oxygen is provided using a non-rebreather mask,
and carboxyhemoglobin levels are measured.
What is opioid overdose, what are the signs and symptoms
What investigation can you do
What must you bear in mind with administration of the antidote
Clinical features: Respiratory depression and lung oedema Bilateral miosis (pinpoint pupil) Altered mental status Seizures.
Altered mental status, respiratory depression, and miosis are the classic triad of opioid intoxication! However, the absence of miosis does not rule out opioid intoxication!
Look for needle marks, reduced GI motility
Can cause dysrhythmias ---------------------- Investigate: Trial naloxone ECG ------------------------------------- Naloxone has a dose-dependent duration of action (shorter than most opioids). Its quick metabolization can, therefore, lead to a renewed effect of opioids!
Which opioid receptor is responsible for causing analgesia, respiratory depressuin, GI dysmotility and miosis
Analgesia- mu and kappa
Mu: sedation, respiratory depression, euphoria, gastrointestinal dysmotility, and physical dependence.
Kappa: Kappa receptors mediate analgesia, miosis, diuresis, and dysphoria
How does respiratory depression result from mu receptors
u receptors cause a medullary decrease response to hypercarbia and a decrease in respiratory response to hypoxia, resulting in no stimulus to breathe and apnoea.
What is the maximum recommended dose of paracetemol
What is the consequence of taking a large dose
2X500mg tablets, 4 times in 24hr (4g)
Intake of >12g or >150mg/kg can cause hepatic necrosis.
