ACC Flashcards
what three main things present a risk to the patient undergoing surgery?
1) surgery itself - damage to structures, blood loss, complications
2) effects of anaesthesia
3) pre-existing disease
list some possible intra-operative problems that can happen
- fluid balance
- hypoxia
- pain
- PONV
- hypothermia
- anaphylaxis
- PE
- death
what “centre” controls PONV? how does it work?
the vomiting centre - linked to other parts of the brain responding to different stimuli, via different receptors.
- inner ear –> cerebellum (H1)
- emotion (fear) –> higher centres
- blood-borne emetic –> chemoreceptor trigger zone (5HT-3, D2, H1)
- pharynx/GI tract –> solitary tract nucelus (5HT-3, D2, H1)
blood borne emetics / GI tract interact between each other.
all these different pathways act on vomiting centre, mediated by 5HT-3, D2
I think?? maybe look this up to actually understand it
give an example of an antiemetic that works on serotonin pathways? indications?
ondansetron - useful for both PONV and for vomiting post acute opioid administration
give an example of an antiemetic that works on histamine (H1) pathways? indications?
cyclizine
commonly used for travel sickness
can cause tachycardia
give examples of antiemetics that work on dopamine (D2) pathways? indications?
domperidone = premedication if at risk of PONV metoclopramide = long term opioid use (counteracts gastric stasis procholperazine = vertigo
what 5 steps make up pre-op preparation?
1) optimise medical conditions
2) adjust medication
3) check Ix
4) check wt
5) EXPLAIN AND CONSENT
explain the ASA grading system
1) healthy individual
2) mild systemic disease not limiting activity
3) severe systemic disease limiting activity but not incapacitating
4) incapacitating systemic disease, life threatening
5) emergent case - expected survival <24hrs without surgery
(6 = brain stem dead, for organ retrieval)
how do the 5 ASA grades related to predicted mortality?
1 = 0.05% 2 = 0.5% 3 = 5% 4 = 25% 5 = 50%
what key conditions do you want to know about when asking the anaesthetic history in pre-op?
pts prev. experience and FHx relevant. * malignant hyperpyrexia * suxamethonium apnoea also: - previous airway problems - PONV (ask about travel sickness etc too)
what is malignant hyperpyrexia?
inherited skeletal muscle disorder that can be triggered by volatiles and suxamethonium.
causes hyperkalaemia, hypoxia, temperature, rhabdomyolysis.
can reverse with dantralene.
what is suxamethonium apnoea?
patient doesn’t have the enzyme to break down suxamethonium - use propofol instead.
inherited disorder of acetylcholinesterase.
what allergies is it important to ask about in pre-op assessment?
anaesthetic agents, analgesics, abx, latex, EGGS (propofol)
what is the protocol for peri-op adjustment if a patient is on: ACE inhibitors ?
stop as the anaesthetic will drop BP
what is the protocol for peri-op adjustment if a patient is on: angiotensin 2 receptor blockers ?
stop 24hrs before
what is the protocol for peri-op adjustment if a patient is on: ranitidine ?
increases pH so if aspiration occurs it’s less bad - continue
what is the protocol for peri-op adjustment if a patient is on: warfarin ?
stop.
if pt has AF use LMWH.
if thrombophilia/metallic heart valve (?) = stop 3-5 days before, use bridging protocol.
what is the protocol for peri-op adjustment if a patient is on: inhalers?
continue - should be brought with the patient into the anaesthetic room, and taken round to recovery.
what is the protocol for peri-op adjustment if a patient is on: clopidogrel?
stop 5 days before
what is the protocol for peri-op adjustment if a patient is on: beta blockers?
continue
what is the protocol for peri-op adjustment if a patient is on: PPIs?
continue
what is the protocol for peri-op adjustment if a patient is on: aspirin?
stop high does (200mg) - can continue 75mg only if spinal/epidural
what is the protocol for peri-op adjustment if a patient is on: steroids?
continue
what is the protocol for peri-op adjustment if a patient is on: insulin/oral hyperglycaemia?
insulin dependent people need a variable rate insulin infusion (sliding scale). avoid starving them - place first on the list!
what should you ask about at pre-op assessment for the CVS?
- HTN - well controlled? end organ damage?
- IHD - angina, MI
- pacemaker (causes problems for diathermy)
- PVD - exercise tolerance
- cerebrovascular disease - tight BP control needed to maintain perfusion
what should you ask about at pre-op assessment for resp system?
- COPD
- Asthma - inhalers, also can they take NSAIDs??
- OSA (STOP BANG)
- exercise tolerance - can they get up stairs without pause?
what other qus should you ask at pre-op assessment in terms of PMHx (apart from for CVS/resp)?
- GI - reflux (lying down?), liver disease
- DM
- thyroid
- DVT/PE
- rheumatoid
- social: smoking, alcohol, other drugs
what are the components of the STOP BANG score for obstructive sleep apnoea?
high risk if yes to 3+: Snoring Tiredness Observed apnoea Pressure (high BP)
BMI > 35
Age >50
Neck circumference >40cm
Gender - male
what medical conditions make airway assessment/management difficult?
- Downs
- RA
- ankylosing spondylitis
- obesity
- dental abscess
what examination should be done as part of pre op assessment?
- listen to chest
- check teeth for loose/broken/crowns
- neck flexibility
- airway assessment
how do you assess the difficulty of a patient’s airway at pre-op assessment?
1) anatomy - small mouth/chin, large tongue, big neck, beard
2) mechanical limitation - limited mouth opening/neck movement
3) dentition - poor dentition, expensive dental work
what predictive tests can be used pre-op to assess the airway?
- Mallampati score assesses oropharynx
- extension of upper cervical spine <90 degrees = bad sign
- thyromental test - distance from tip of thyroid to tip of mandible at gull extension should be >6.5cm. <6cm means difficult laryngoscopy.
explain how the Mallampati score works
get patient to stick tongue out and open wide.
Class IV = soft palate not visible
Class III = soft palate only
Class II = uvula tip masked
Class I = pillars, soft palate and uvula all visualised.
Class III or IV will be difficult airway.
what are the three components of the anaesthetic triad?
- anaesthesia (unconsciousness)
- analgesia (local or systemic)
- muscle relaxation
define anaesthetisa
a pharmacologically induced, reversible state of sleep characterised by lack of pain, awareness of surroundings and memory of events
what are the 3 phases of general anaesthesia?
1) induction - usually IV, then secure/manage airway, then oxygenate (often pre-oxygenate as well)
2) maintenance
3) reversal
two routes - IV (propofol), inhaled (iso/sevo/desfluorane) - used for young kids, needle phobics
give some basic info on the different induction agents
- propofol - painful on injection
- sevofluorane - minimal vasodilation, almost no metabolism (taken up by and excreted via lungs), irritant, taken up in fat tissue (so get prolonged drowsiness)
- nitrous oxide - analgesic properties, low solubility means rapid onset and offset
Opioids - risk of respiratory depression
- remifentanil - tiny doses, breaks down spontaneously in 10-15s, used in TIVA
- alfentanyl - potent, rapid onset, duration 2-3 mins
- fentanyl - onset 1-2 mins, duration 10-15 mins
- morphine - causes more histamine release so not great for PONV, slow onset (10-15 mins) and causes constipation
what agents are used in maintaining anaesthesia?
gases - volatiles. nitric oxide/oxygen.
TIVA - propofol infusion + remifentanil infusion.
either method can involve paralysis + ventilation or spontaneous breathing.
give some basic info on the volatiles
- isofluorane = cheapest, maintains sedation, most irritant (coughing), not used for induction
- desfluorane = maintains sedation, wears off quickly
- sevofluorane = induces/maintains sedation
give some info on the use of muscle relaxants when under GA
will the patient breathe spontaneously?
if you do use muscle relaxants then you need to ventilate!
at what GCS level are you unable to maintain airway control?
8 or below
GCS 8 or lower ?? = AIRWAY MANAGEMENT NEEDED
what simple manoeuvres can be used in airway management?
- head tilt
- chin lift
- jaw thrust
list the different options for airway management
- simple manoeuvres
- oropharyngeal (guedel)
- nasopharyngeal (beware in base of skull #)
- supraglottic - LMA
- ET tube
also bag and mask ventilation
list three ways of determining correct placement of ET tube
1) chest movement
2) misting of mask
3) **trace on capnography
places tube shouldn’t be = oesophagus, endobronchial
briefly outline the mechanism of action of local anaesthetics
1) unionised LA enters the cell
2) LA becomes ionised
3) blocks Na channel so pain signals can’t be sent
what 4 different types of sites might be used for regional anaesthesia?
- peripheral nerve blocks
- plexus block
- epidural block
- spinal block
give some basic info on lidocaine
onset = immediate
duration = 15 minutes
used for = small procedure, lacerations, chest drains
give some basic info on bupivocaine
onset = 10 minutes
duration = 2hrs anaesthesia, 12hrs analgesia
used for = regional blocks
give some advantages for the use of regional anaesthesia
- avoids GA
- can be awake
- avoids airway problems
- less PONV
- better peri-operative pain control
what dermatome supplies the shoulder?
C5
what dermatome supplies the thumb?
C6
what dermatome supplies the middle finger?
C7
what dermatome supplies the little finger?
C8
what dermatome supplies the nipples?
T4
what dermatome supplies the umbilicus?
T10
what dermatome supplies the knee?
L4
what dermatome supplies the little toe?
S1
how do spinals work vs epidurals?
spinal goes through ligaments and dura into CSF. uses LA as a bolus, will last c.2 hrs.
epidural goes between the ligaments and dura (into the epidural space, obvs). LA give via a catheter as continuous infusion.
both allow operation below highest nerve root affected by block.
what are the 3 reasons you want muscle relaxation during surgery?
1) relaxes the opening to the trachea (glottis) for intubation
2) relax muscles for surgery
3) so patient doesn’t fight ventilation
what are the two main categories of muscle relaxants, and give examples of each?
Depolarising = suxamethonium. onset is within 30s so used only for EMERGENCIES.
Non-polarising = atracurium, rocuronium, vecuronium. onset 120-180s, duration 30mins. used routinely.
briefly explain the normal mechanism of muscle contraction (so you can understand how muscle relaxants work)
1) nerve impulse releases ACh to the neuromuscular junction (NMJ)
2) ACh binds to sites on muscles and open a pore for Ca2+ to cross membrane and cause contraction
how do non-depolarising muscle relaxants work (e.g . atracurium, rocuronium)
they competitively inhibit ACh by blocking binding site, preventing depolarisation.
- onset 1 minute.
how do depolarising muscle relaxants work?
- suxamethonisum is 2 ACh molecules bound together
- binds BOTH sites simultaneously
- causes contraction then keeps pore open preventing further contraction
- onset 30s, duration 3 mins - see muscle contractions then flaccid paralysis.
what drug can be used to reverse muscle relaxants? how does it work?
neostigmine
- ACh blockers
- causes build up of ACh at the receptor, and competition with the muscle relaxant for binding site
what drugs are used in theatre to speed up the HR? how do they work?
atropine, glycopyrrolate, hyoscine = anticholinergics, increase HR - these inhibit the vagus nerve as the parasymp. NS uses ACh as a neutrotransmitter.
dobutamine = beta-agonist (used in heart failure in ITU) - increases HR and contractility by stimulating beta adrenoreceptors in myocardial cells.
what drugs might you give to increase BP in theatre? (without raising heart rate)
- want to stimulate alpha adrenoreceptors
- causes vasoconstriction
- use alpha agonists to increase BP via increasing SVR (?)
- may cause decrease HR as body tries to correct
what drugs can you use in theatre to increase BP and HR?
e. g. ephedrine or adrenaline (very potent, therefore only @arrest/ITU).
- stimulate alpha and beta adrenoreceptors with combined alpha/beta agonist
briefly describe the WHO pain ladder
mild = paracetamol and NSAIDs mod = codeine and tramadol severe = morphine
who should you be careful about using paracetamol with?
liver failure low weight (elderly, children)
how do NSAIDs work?
inhibit cyclo-oxygenase (COX)
COX involved in release of prostaglandins, peripheral inflammation, rubor and dolor.
what are important side effects of NSAIDs?
peptic ulcers
AKI
blood thinning
list some different side effects for opioids, by systems
CNS - sedation, miosis CVS - bradycardia, hypotension resp - depression GI - N&V, constipation urinary - retention skin - itching
receptors for opioids found all over CNS, particularly descending pathways and brain
list the weak opioids
codeine = PO, *IM* - prodrug broken down to morphine tramadol = PO/IV - acts on NAd, opioid, serotonin
list the strong opioids
morphine (PO/IV)
oxycodone
methadone
buprenorphine
what modified release opioids options are there?
fentanyl patch
morphine sulphate tablet
oxycontin
explain the rule of thirds for fluid distribution
2/3rd is intracellular
1/3rd extracellular - which is 2/3 interstitial, 1/3 intravascular
what are the daily requirements per kg for an adult for: water, sodium, potassium, calories?
water = 30ml Na = 1-2mmol K = 1mmol kcal = 20kcal
explain the difference between crystalloids and colloids
crystalloids = ions or small molecules dissolved in water
colloids = larger insoluble molecules retained within plasma for longer e.g. blood, albumin (natural) or synthetic ones = starch, gelatin
what things do you need to know before prescribing fluids?
- haemodynamic status
- ongoing loss (bleeding, afebrile?) - sensible/insensible
- able to take orally
- weight
- renal function
- chemistry results
what are the steps on the respiratory support ladder?
1) O2 delivery
2) NIV
3) invasive ventilation
what are different oxygen delivery systems? give the O2 conc and flow for each
aim for 94-98% or 88-92% (if chronic T2 failure)
- nasal cannulae = 2-6l, 25-40%
- hudson mask = 4-15l, 35-70%
- Venturi = 4-15l, 24-60%
- NRBM = 15l, up to 80%
- closed/high flow = up to 100l, up to 100%
what’s the difference between T1 and T2 resp failure?
T1 resp failure = hypoxia w/o hypercapnia
T2 resp failure = hypoxia w/ hypercapnia
when do you use NIV?
used if supplemental oxygen is failing - resp failure!
delivered via mask, either tight fitting or hood.
what type of NIV is used for each of T1 vs T2 resp failure?
T1 - continuous CPAP
T2 = NPPV (noninvasive positive pressure ventilation - BiPAP biphasic)
pros and cons of CPAP?
Pros: - increase intrathoracic pressure - improves functional residual capacity (FRC) and oxygenation, reverses resp acid Cons: - discomfort might lead to non-compliance - gastric distension - aspiration - no impact on CO2
pros and cons of NPPV?
Pros: - increase tidal volume - better CO2 clearance Cons: - discomfort might lead to non-compliance - gastric distension - failure
how does T1 resp failure work? how does CPAP help this?
inadequate oxygenation due to alveolar collapse (e.g. pneumonia), fluid in alveoli (L heart failure)
also V/Q mismatch
CPAP maintains minimum airway pressure. alveolus held open, fluid forced from lung.
how does T2 resp failure work? how does BiPAP help with this?
inadequate ventilation (effect of dead space) leads to limited alveolar expansion (e.g. COPD, muscular dystrophy)
BiPAP adds inspiratory pressure (IPAP) at inspiration and EPAP at expiration further expands the lung, holding any collapsing alveoli open so increasing the ventilation surface pressure
list some possible causes of respiratory failure
- infection = pneumonia
- collapse = atelactasis, pneumothorax
- fluid = pulmonary oedema
- not enough blood = thromboembolic disease
- not enough O2 = bronchospasm/obstruction, ARDS, increased metabolic demand
- loss of drive = central respiratory depression
how would you initially manage respiratory failure as an F1?
ABCDE !!!!!
assess oxygenation ± ventilation requirement
assess underlying problem
senior help early!!
what are some possible indications for invasive ventilation?
(either ET tube or tracheostomy)
1) airway protection
2) upper airway obstruction
3) neuromuscular paralysis
4) if it will improve SpO2, PaO2, FRC
list some possible complications /problems of invasive ventilation
- VAP = ventilator associated pneumonia
- VALI = VA lung injury
- need for sedation and muscle relaxation
- immobility - VTE risk
- O2 toxicity
what two things can you adjust when controlling invasive ventilation settings?
volume control = set a target volume, so pressure adjusts to meet this
pressure control = set a target pressure, therefore volume adjusts. used on ITU as protective of high pressure
list some possible indications for intubation
- emergency surgery (concerns re full stomach)
- history of severe reflux
- protect airway (blood, obstruction)
- poor facial access during surgery
- prone position
- planned ventilation due to e.g. need for paralysis, long operation, lung disease, if their obese, low GCS etc
list some things to check/do for each of ABCDE
A - secure airway (guedel, NP airway, ET/LMA)
B - resp. rates/sats - O2, salbutamol/ipatropium nebs
C - BP, HR, CRT, UO - fluid resus, vasopressors, catheterisation.
D - GCS, AVPU, BM - CT, IV dex
E - rash, burns, bleeding etc etc
what is the Canadian C Spine Score?
score used to determine need for CT scanning post neck injury.
use if patient is alert (GCS 15) and stable following trauma
outline the components of the canadian C spine score
if they have any ONE high risk factor = CT/imagine
if they have a LOW risk factor = assess ROM
if they can’t rotate neck actively (45 degrees L and R) = imaging.
if they can - no imaging.
(high/low risk factors on separate cards)
what are the high risk factors from the canadian C spine score?
- age 65 yrs +
- dangerous mechanism (see other card)
- paraesthesia in extremities
what are the low risk factors from the canadian C spine score?
- simple rear-end RTA
- sitting position in ED
- ambulatory at ANY TIME
- delayed (i.e. not immediate) presentation
- absence of midline C spine tenderness
what counts as a “dangerous mechanism” in the Canadian C spine rule?
- fall >2ft/5 stairs
- axial load to head (e.g. diving)
- high speed, rollover or ejection RTA
- bicycle collision with object (e.g. post, car)
- motorised recreational vehicles (e.g. quad bike)
what’s the difference between a burn and a scald? what age categories are high risk groups with burns?
burn = injury by thermal, chemical, electrical or radiation energy scald = contact with hot liquid or steam
kids <5 or adults >75 = high risk
what initial assessment should be done in a burns patient?
ABCDE, prevent hypothermia
assess need for fluid resus.
check nostrils for inhalational injury (smoke)
outline the rule of nines for burns
determines % body burnt (2nd/3rd degree only) arm = 9% head = 9% torso front = 18% torso back = 18% leg = 18% groin = 1%
what charts should you use for assess paediatric burns? how do they differ?
Lund and Browder - accounts for age and growth, head and leg are different.
for <1yr old head = 18%, leg = 14%.
for each extra year -1% for head, +0.5% for leg
what are the 5 different depths of burns? describe each one
NB - burns dynamic, should reassess in 24-72h
1) epidermal/superficial partial thickness = pain, red, glistening, NO blisters, brisk CRT.
2) superficial dermal = pale pink/mottled, swelling. SMALL blisters ± weeping, brisk CRT.
3) deep dermal = cherry red, blistering, dry, blotchy, no blanching, no cap refill, reduced senstion
4) full-thickness (3rd degree) = white/black, dry, no blisters, no cap refill, no sensation
5) fourth degree = incl. subcut fat, muscle + bone.
for each burn depth, how does it heal?
- epidermal/superficial partial thickness = heals in 1 wk, no scar
- superficial dermal = 3 wks, minimal scarring
- deep dermal = 3-8wks healing with scarring ± surgical Rx
- third degree = requires surgical repair/graft
- fourth degree = reconstruction/amputation
what Ix is needed for burns victims?
- bloods = FBC, crossmatch, carboxyhaemoglobin, serum glucose, U&E, ABG
- CXR
- cardiac monitoring (checking for dysrhythmias due to hypoxia/electrolyte disturbances)
- **circulation monitoring - BP can be difficult so unreliable. catheter for UO monitoring.
outline first aid for burns
stop burning and cool!
- remove clothing, if stuck cool with water
- brush chemical powders way
- rinse in tap water (not ice as causes vasoconstriction) for 20 mins (beware hypothermia) - in medical setting, 10 mins irrigation w/cool sterile saline (longer for chemical burn)
- wrap with cling film (lengthways, not like around the whole arm - swelling)
how do you treat minor burns after first aid measures?
dressing + analgesia
- clean with soap and water
- leave blisters <1cm intact, aspirate large blisters
- non adhesive gauze dressing + re-examine at 48hrs
- if infection = daily wound inspection + dressing change + 7/7 fluclox
- give analgesia, check tetanus prophylaxis
what are you worried about in a major burns patient?
1) direct thermal injury - airway oedema/obstruction
2) CO poisoning
3) inhalation of smoke - pneumonia and oedema
what management would you do to cover A+B for a major burns patient?
Airway:
- check for indications of inhalational injury - hoarseness, singed nostril hairs, face/neck burns
- ET tube and ventilate if stridor, transfer to burns centre
Breathing:
- ABG (but don’t use PaO2 if CO poisoning)
- 100% O2 and COHb (carboxyhaemoglobin) levels - continue O2 until happy COHb levels normal (or at least <10% for >6h)
what causes fluid loss in burns?
heat increases capillary permeability leading to oedema + visible fluid loss exudates + blisters
what management would you do for C in a major burns patient?
- IV access and fluid replacement if >15% total surface area in adults, >10% in kids
Parkland formula = 4ml x kg x % total body area of Hartmanns
give half in first 8hrs, half in following 16hrs - don’t forget to calculate maintenance/other loss requirements
- give pain relief (strong opioids)
- warm all fluids to prevent hypothermia
at what % surface area burns would you want IV access and fluid replacement?
> 15% adults
10% kids
these are the people that warrant referral to burns unit as well.
when would you refer a patient to a specialised burns unit?
- age <5yrs or >60yrs
- site: face, hands, perineum, flexure (e.g. armpit)
- inhalational injury
- suspected NAI
- large area (>15% body surface area in adults, >10% BSA in kids)
what is flail chest?
life threatening injury where segment (3+) of rib cage breaks due to trauma - detaches from rest of chest wall so can’t contribute to rib expansion.
indicates pulmonary contusion, risk of PTX as well.
what would you see O/E in flail chest?
“paradoxical movement” - indrawing on inspiration
how do you manage flail chest?
ventilation with positive pressure - beware intubation + ventilation cos will exacerbate PTX/tension PTX
+ pain control (intercostal blocks)
+ pulmonary hygiene (clearing mucus/secretions)
what are the 5Hs and 4Ts (reversible causes of cardiac arrest?
Hypoxia Hypovolaemia Hypo/hyperkalaemia Hypothermia H+ ions - acidosis
Thrombosis (coronary/pulmonary)
Tamponade (cardiac)
Toxins
Tension PTX
(sometimes see 5Ts - separates coronary thrombosis from VTE)
what are the 5 sites of major haemorrhage? give brief Rx for each of the occult sites
“blood on the floor and four more”
- external (the floor)
- chest = chest drain for haemothorax
- pelvic # = if suspected, pelvic binder
- abdo/retroperitoneal = might need aparotomy
- thigh/long bones (femoral #) = splint!
what is the lethal triad of major trauma/haemorrhage?
hypothermia
acidosis (due to tissue hypoperfusion so lactic acid gets produced, worsened by hypoventilation in some cases)
coagulopathy
MUST DETECT THEM EARLY
any one of these = you’ve already f***ed it
management of major haemorrhage?
stop the bleeding! - splint, pressure, haemostatic agents (tranexamic avid IV), REBOA (rescusitative balloon occlusion of aorta - for chest/abdo/pelvis)
replace the fluid - fluids + blood + blood products (FFP, cryoprecipitate)
what blood products are given according to the major haemorrhage protocol (but see local guidelines)?
one unit RBCs
one unit FFP
one unit platelets
1:1:1 ratio in trauma
BUT - activate major haemorrhage protocol and just let the haematologist organise it all! first bag will contain the above in 1:1:1 then they’ll take it from there.
when fluid resus-ing, what’s a sensible target UO?
0.5 ml/kg/hr
so 70kg male = 35ml/hr
ideally want more like 1 ml/kg/hr but 0.5 is fine in trauma situ
what’s the overarching principle of wound management?
want to take a dirty, ragged wound and turn it into a nice clean wound that can be simply reconstructed
what are the key points/steps in wound/laceration management
- irrigation! w/0.9% saline or just tap water.
- infiltrate with lidocaine
- remove debris, FBs, necrotic tissue - consider trimming ragged edges
- use absorbable sutures (Vicryl) to bring skin edges together (deep sutures), then interrupted nylon sutures for the superficial sutures (6’0 for face, 5’0 elsewhere)
- remove sutures after 5 days for face, upper limb/body 7-10 days, lower limb 14 days
list some alternatives to sutures in treating a wound/laceration
- steri-strips - good for non-hairy skin unlikely to get wet
- glue (e.g. Dermabond) - once bleeding stopped apply directly on top of apposed and dried skin edges, dry 30s, then apply another thin layer - don’t get glue IN the wound (cytotoxic) - “you can shower, but don’t soak/scrub”
briefly explain how you use lidocaine in treating a laceration (doses, ?adrenaline, max doses) etc
max dose of lidocaine = 3mg/kg
max dose of lidocaine w/adrenaline = 7mg/kg - used when vasoconstriction to stop bleeding is also helpful, or if you think you’ll exceed 3mg/kg
for suturing 1% lidocaine is good - strikes balance between toxicity vs waiting ages for it to work.
doses (plain lidocaine): 0.25% = 2.5mg/mL = allowed up to 1.12mL/kg 0.5% = 5mg/ml = allowed up to 0.56 ml/kg 1% = 10 mg/ml = allowed up to 0.28 ml/kg 2% = 20 mg/l = allowed up to 0.14 ml/kg
so 70kg pt can have up to 19.6ml of 1% lidocaine (plain)
outline motor scoring of GCS
6 = obeys commands 5 = localising response to pain 4 = withdraws to pain 3 = flexor response to pain 2 = extensor posturing to pain 1 = no response
outline verbal scoring of GCS
5 = oriented 4 = confused 3 = inappropriate speech/random words 2 = incomprehensible speech (just noises) 1 = none
outline eye opening scoring of GCS
4 = spont. 3 = in response to verbal command 2 = to pain 1 = nil
what are the components of the ATLS primary survey?
A = airway + give 100% O2 + immobilise C spine (jaw thrusts only - no head tilt/chin lift!!) B = breathing +/- ventilation C = circulation + haemorrhage control - apply direct pressure to visible haemorrhages (or indirect e.g. on femoral pulse if suspect bleeding from femoral #). 2x large boor cannula. ?pelvic binder. D = disability - check GCS/AVPU, pupils, gross neurology for spinal cord injury. BM. E = exposure - ensure body temp maintained, rewarm as needed. undress fully to check everywhere.
if there’s change to state of patient, or you treat a problem along the way, restart primary survey!
what are the 5 components of “damage control resuscitation” in trauma?
1) early haemostasis with surgery/splints/angiography
2) awareness and treatment of lethal triad
3) reduce excessive crystalloid/colloid use
4) early use of blood products in 1:1:1 ratio
5) hypotensive resus/”permissible hypotension”
what drug can be given in major haemorrhage to help limit bleeding? dose??
tranexamic acid IV - 1g over 10min, then 1g over 4hrs
ONLY if given within 3 hrs of initial injury.
antifibrinolytic properties.
what are the components of the secondary survey?
= a thorough head-to-toe exam once you’ve done your A-E and pt is responding to initial resus - esp. useful in an unconscious pt who can’t tell you that they’ve got v bad pain in their testicles…
mnemonic : survey Has = head/skull My = maxillofacial Critical = C spine Care = Chest Assessed = abdo Patient's = pelvis Priorities = perineum Or = orifices (PR/PV Next = neuro Management = MSK Decision? = diagnostic tests/definitive care
what is a tension pneumothorax? Rx?
- develops when penetrating injury creates one-way valve, forcing air from lung or through chest wall into thoracic cavity
- affected lung is collapsed + mediastinum displaced
needs immediate decompression of affected side = large bore cannula in 2nd intercostal space midclavicular line.
definitive treatment = chest drain.
what the difference between primary and secondary traumatic brain injury?
primary = occurs at time of impact secondary = occurs in mins-days later from neurophysiological consequences + anatomic damage e.g. raised ICP, cerebral oedema, expanding haematomas, seizures, infection
list the main cranial and intracranial injuries
cranial = skull #, C spine # intracranial = diffuse axonal injury, extradural bleed, subdural bleed, subarach bleed, intracerebral bleed, cerebral contusion
briefly how do you assess a head injury pt coming into A&E
A-E!!
special focus on GCS trends, pupil sizes and C spine protection.
unequal pupils less worrying if conscious but if in coma - not. good.
look for localising neurology
check for priapism and anal tone (spinal cord damage)
low BP + inappropriately low pulse rate = sympathetic disruption in C spine.
most importantly!! don’t make it worse - optimise ABC, don’t neglect other injuries and let BP, sats creep down etc
outline the NICE guidelines for imaging after a head injury
CT within 1 hr if any of:
- GCS less than 13 on initial assessment in the emergency department.
- GCS less than 15 at 2 hours after the injury on assessment in the emergency department.
- Suspected open or depressed skull fracture.
- Any sign of basal skull fracture (haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose, Battle’s sign).
- Post-traumatic seizure.
- Focal neurological deficit.
- More than 1 episode of vomiting.
CT within 8hr if:
- Age 65 years or older.
- Any history of bleeding or clotting disorders.
- Dangerous mechanism of injury (a pedestrian or cyclist struck by a motor vehicle, an occupant ejected from a motor vehicle or a fall from a height of greater than 1 metre or 5 stairs).
- More than 30 minutes’ retrograde amnesia of events immediately before the head injury.
outline medical management of head injury
- avoid hypotension (no permissible hypotension here! = keep sys BP >90 - single ep low BP = worse outcomes for secondary brain injury
- avoid hypoxia/hypercapnia
- opiates - reduces stress of intubation, helps prevent surge in ICP
- mannitol - can reduce ICP in acute situ, but avoid if systemically hypotensive
- aggressively Rx any seizures (IV loraz/buccal midaz) - stress from seizure raises ICP
- raising head to 30 degrees helps jugular venous return
- avoid hyperglycaemia
refer to neurosurgery if needed
how do you quantify a patient’s aerobic fitness/functional capacity at pre-assessment?
METs = metabolic equivalents
1 MET = resting O2 consumption of a 40yo 70kg male.
walking indoors/100m level ground = 2-3 METs
2 flights stairs = 4 METs
strenuous sports = 10
briefly outline the steps involved in rapid sequence induction (RSI)
- NGT and IV access
- pre-oxygenate (for 3 mins)
- IV induction (Propofol)
- immediately give muscle relaxant (suxamethonium)
- cricoid pressure (attempts to prevent aspiration by occluding oesophagus)
- ET tube
list some absolute contraindications to “neuraxial anaesthesia” aka spinal/epidural
1) anticoagulant states - risk of pressure damage to cord from bleeding
2) local sepsis - might introduce it into CSF
3) shock/hypovolaemiac states
4) raised ICP (coning)
5) unwilling/uncooperative patient
6) fixed cardiac output states e.g. mitral/aortic stenosis
list some relative contraindications to neuraxial anaesthesia
- neuro disease (procedure might get blamed for change in functional state…)
- IHD
- spinal deformity/prev surgery
- bowel perforation (theoretical risk that increasing parasymp activity –> peristalsis and “peritoneal soiling”
list some oral analgesic options w/doses
- paracetamol 1g/6h
- NSAIDs - diclofenac 250mg/8h (risk of GI bleed so PPI cover, also caution in asthmatics)
- tramadol 50-100mg/4-6h PO/IV. less SEs than morphine but less potent.
- opioids e.g. codeine morphine
- neuropathic agents e.g. gabapentin
list some commonly used methods of analgesia, apart from tablets
IV - bolus or infusion. patient controlled analgesia (PCA) lets patient deliver boluses, reducing risks of cont infusion (don’t forget to programme in the max doses though!)
regional anaesthesia e.g. epidurals, LA or nerve blocks. boluses, continuous infusions. etc etc
transcutaneous fentanyl patches.
what are the different “levels of care”?
level 0 = normal ward care
level 1 = at risk ward patients, requiring additional staff time +/- support from critical care team
level 2 = HDU - high level of observation/intervention for a SINGLE failing organ system
level 3 = ITU/ICU - either advanced respiratory support alone, or support of any 2+ organs
step by step management of anaphylactic shock?
A-E !!
- secure airway, give 100% O2
- remove cause, consider raising feet
- IM adrenaline 0.5mg - repeated every 5 mins as needed until better (BP, pulse, resp function)
- secure IV access - chlorphenamine 10mg IV, hydrocortisone 200mg IV
- fluids if needed, treat wheeze as for acute asthma
- if still hypotensive admit to ICU, may need IVI adrenaline +/- aminophylline
if EpiPen administered at home can give 40mg prednisolone + dose of chlorphenamine (4mg/6h) orally.
if allergic reaction but not quite anaphylactic shock also try chlorphenamine +/- pred
flowchart for management acute STEMI?
- 12 lead ECG
- IV access, bloods for troponin, FBC, U&E, glucose, lipids
- aspirin 300mg unless GP/paramedics given
- morphine 5-10mg IV (+ metoclopramide 10mg IV - antiemetic)
- give primary onfirmed STEMI on ECG and available within 120mins
- if not fibrinolysis
flowchart for managing acute, severe pulmonary oedema
- sit them up
- give O2 100% (unless existing lung disease)
- IV access + monitor ECG (treat arrhythmias)
- start Ix whilst treating (CXR, ECG, U&E, ABG, trop etc)
- diamorphine IV
- furosemide 40-80mg IV slowly
- GTN 2 puffs (unless BP <90)
- do Ix, history, exam
- start nitrate infusion if BP >100 (isosorbidine dinitrate)
- if still getting worse - more furosemide, consider CPAP, increase nitrates
- if not working and/or BP <100 - ITU
arrhythmia and further ACS management should be in cardio cards
if not - need to add! back of OHCM
mnemonic for management of acute asthma attack?
OSHITME: Oxygen Salbutamol nebs (back to back, use oxygen driven nebs) Hydrocortisone IV Ipatropium nebs
(need senior help for the rest)
Theophylline
Magnesium sulphate
ESCALATE
pneumothorax, acute COPD, pneumonia, PE should all be covered in resp
add them if they’re not there!
meningitis, raised ICP and status epilepticus should be in neuro
add them if they’re not!
outline the flowchart for management of DKA
ABCDE, 2 large bore cannulae.
- if SBP <90 give 500ml saline bolus, no response give 2nd bolus + get ICU advice. if SBP >90 or response start fluids as below.
- tests: do VBG for pH, bicarb and lab glucose, ketones U&Es (for K and Na) as minimum
- insulin = add 50u actrapid to 50mL 0.9% saline, cont. infusion at 0.1u/kg/h – local protocols!
- check VBG for pH, bicarb, glucose and K+ at 1h, 2h and 2hrly after that
- assess need for K+ replacement
- consider need for catheter if no UO by 1h, consider NG tube if vomiting/drowsy, start all on LMWH
- when glucose <14 start 10% glucose at 125ml/hr alongside the saline - prevent hypoglycaemia
continue fixed rate insulin till ketones <0.3mmol/L, venous pH >7.3 and bicard >18
management for severe hypoglycaemia episode
IV = 200-300ml 10% dextrose
IM glucagon
PO glucagel
emergency management of diabetes insipidus?
- urgent plasma U&E and serum and urine osmolalities
- monitor UO carefully, check U&E twice/day
- IV fluids to keep up with UO++ - don’t lower Na too quickly if severely hyponatraemic (risk of cerebral oedema)
- if Na >/= 170 give 0.9% saline
- aim to reduce Na at rate of <12 mmol/L per day - any faster/use of 0.45% saline is dangerous!
- desmopressin IM can be given as a therapeutic trial
list some signs + symps of hypernatraemia
lethargy, thirst, weakness, irritability, confusion, coma and fits
+ signs of dehydration.
causes of hypernatraemia?
usually because water loss > sodium loss
- fluid loss without water replacement (e.g. D&V, burns)
- diabetes insipidus - suspect if urine+++++
- osmotic diuresis (can occur in DKA)
- iatrogenic (did your fluids wrong…)
- loads of niche stuff
management of hypernatraemia?
give water orally if you can.
IV glucose 5%, slowly, if not.
use UO and plasma Na as guide.
give 0.9% saline IV if hypovolaemic as causes less fluid shifting.
signs + symps of hyponatraemia
anorexia, nausea, malaise –> headache, irritability, confusion, weakness, reduced GCS and seizures
heart failure/oedema can indicate cause.
give some possible causes of hyponatraemia in a dehydrated patient, if urinary Na is >20mmol/L
sodium + water being lost via kidneys:
- addisons
- renal failure (diuretic phase)
- excess diuretics
- osmolar diuresis (hyperglycaemia, high urea)
give some possible causes of hyponatraemia in a dehydrated patient, if urinary Na is <20 mmol/L
sodium and water being lost somewhere apart from the kidneys…
- D&V
- burns
- small bowel obstruction
- trauma
- CF
- heat exposure
give some possible causes of hyponatraemia in a patient that isn’t dehydrated, but is oedematous
- nephrotic syndrome
- cardiac failure
- liver cirrhosis
- renal failure
give some possible causes of hyponatraemia in a patient that isn’t dehydrated, and isn’t oedematous
- SIADH (if urine osmolality >100mmol/kg)
- water overload (did your fluids wrong again… risk with giving 5% glucose without adding 0.9% saline)
- severe hypothyroidism
- glucocorticoid insufficiency (cortisol)
management of hyponatraemia
correct underlying cause - replace Na and water at same rate they were lost.
fluid restriction if asymptomatic chronic hypoatraemia e.g. in heart failure
acutely - cautiously give 0.9% saline but don’t correct Na too rapidly due to risk of central pontine myelinosis/cerebral oedema.
might use hypertonic saline in emergency but need senior help - risk of heart failure and central pontine myelinolysis/cerebral oedema
what would you see on ECG in hyperkalaemia?
- tall tented T waves
- small P waves
- wide QRS
- ventricular fibrillation
- fast and irregular!
at what level does hyperkalaemia become an emergency? what does emergency management involve?
> 6.5
use of insulin to drive K+ into cells - ALWAYS give with glucose.
use of calcium gluconate to stabilise cardiac membrane.
at what level does hypokalaemia become an emergency? how do you manage it?
<2.5
oral K+ supplement if mild.
switch thiazides to potassium sparing diuretics.
can give IV potassium if severe - careful! and NEVER as stat bolus.
signs/symps of hypokalaemia?
muscle weakness, hypotonia, hyporeflexia, cramps, tetany, palpitations, light-headedness (arrhythmias), constipation
what do you see on ECG in hypokalaemia?
small/inverted T waves, prominent U waves, long PR interval, depressed ST segments
list some possible causes of hypokalaemia
- diuretics
- D&V
- pyloric stenosis
- Cushing synd / steroids
- Conn’s synd
- alkalosis
etc
list some possible causes of hyperkalaemia
- oliguric renal failure
- potassium sparing diuretics
- rhambomyolysis
- metabolic acidosis (DM)
- excess K+ therapy
- Addison’s disease
- burns
- massive blood transfusion
- drugs - ACEi, seuxamethonium
- artefactual result!!
